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... YLOR COLERIDGE. ('The Rime of the Ancient Mariner) ...... Experiment. 1 08. Table 8-1 : Rate of Penpheral Ruoff with FPHS Inflation at +4.0 Gz with the ...... have traditionally been reported in rnillirneters mercury (mmHg). As mercury is 13 - ...
FACTORS INFLUENCING THE CARDIOVASCULAR RESPONSE TO +Gz: IMPLICATIONS ON THE DESIGN OF LEE SZ~PPORT SYSTEMS FOR ACCELERATION PROTECTION

Martin R. Pecaric

A Thesis submitted in conformity with the requirements for the degree of Doctor of Philosophy Graduate Department of Exercise Sciences University of Toronto

O Copyright by Martin Pecaric 1999

1*1

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Für Elise

- L. VAN BEETHOVEN

Für Ann-Elise

- TC. MCGEE

Abstract Factors Influencing the Cardiovascular Response to +Gz: Implications on the Design of Life Support Systems for Acceleration Protection for the degree of Doctor of Philosophy, 1999

Martin R. Pecaric

Graduate Department of Exercise Sciences University of Toronto

Tactical aircrafl pilots can be exposed to high levels of headward acceleration. Resultant gravitoinertial forces (+Gz) impair vision and, if prolonged, may cause loss of consciousness (G-LOC). Current G-LOC countermeasures include a +Gz actuated regulator (G-valve) pressurizing a lower body garment (G-suit). Protection may also be augmented with positive pressure breathing during +Gz (PBG). Before an optimal strategy c m be proposed, a comprehensive investigation is required into how the various countermeasures and their timing affect the cardiovascular response and alter +Gz tolerance.

Six subjects were exposed to acceleration profiles ranging fiom +2.5 to +5.0 Gz in a human centrifuge. Subjects wore one of three lower body garments pressurized according to one of three different schedules. Pressurization was coincident with +Gz or

was delayed in 1.5 second intervals (maximum Iag of 4.5 seconds). When PBG was used,

pressure was applied according to one of two schedules. Tolerance to +Gz, based on changes in beat-by-beat heart level systolic blood pressure (SBP) indicated no significant improvernents from pressure schedules for the G-suits or PBG. Significant increases in

SBP occurred after a 3 to 4 second delay, and were delayed m e r with any lag in G-suit pressurization. The largest sustained improvements in SBP were recorded with the Gsuit providing the greatest coverage to the lower body.

A n uiferential analysis procedure estimated whole body blood flow (Qest) and resistive (Rest) changes. Flow dropped simuItaneously with G-suit inflation, but increased above baseline values after 2 to 3 seconds, primarily fiom an increased heart rate. Resistance rose rapidly with lower body pressurization, but immediatdy fell to values approaching pre-acceleratory levels. The data suggested that lower body pressurization resulted in an increased afterload concomitant with the forced emptying of

the underlying venous vasculature. Heterometnc autoregulation and a Bainbndge reflex

compensated for the increased aftedoad and augmented venous r e m , respectivefy. h s t decreased as blood settied into venous vessels not compressed by the lower body garment

and Qest remained elevated fiom a "rightward shifi" in vascular fünctioning. With the countermeasures G-LOC employed, the blood pressure control system seems to function more as a poor regulator than a servomechanistic system.

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.,. the machine does not isolate man _Fom the great problems of nature but plunges him more deeply inro them.

- ANTOINE DE SAINT-EXUPERY (Win4 Sand and Stars)

The self-same moment I could pray; AndfLom rny neck so j-ee The Albatross fil2 ofl and sank L ike lead into the sea.. ..

He went like one that hath been stunned, And is of sense forlorn: A sadder and a wiser man, He rose the rnorrow morn.

- SAMUELTAYLOR COLERIDGE ('The Rime of the Ancient Mariner)

Sometimes the greatest struggie resides in the acceptance that any written or spoken word f d s short of the mark when it cornes to expressing gratitude. Needless to Say, this is another of those moments. The completion of this work embodied the efforts of too many people for me to mention individually. For this I zm truly sorry. As any good story needs a beginning, every student requires a mentor. During

my thne at the Defence and Civil Institute of Environmental Medicine (DCIEM), Dr. Fred Buick provided more than just the necessities for graduate life. Thanks for your friendship, trust, and cornmitment. What good is science without data? Kudos to the subjects that devoted their tirne and bodies during the training and tedious data collection phases of this project

- your efforts and petechiae were beyond the cal1 of duty.

Special thanks to Mr. Mike

Jackson and the Iife support team at Carleton Technologies; Mr. Jim Maloan and Mr.

Tom Gee, the personnel in the Life Support Equipment Group, the aeromedical technicians, and the Medical Officers and support staff at DCIEM for their invaluable assistance. 1 am grateful to Drs. Uwe Ackerrnann, Robert Goode, Tom McLelIan, and Michael Plyley from the University of Toronto and to Dr. Duncan MacDougall from McMaster University for their constructive review of the manuscnpt. 1am very much indebted to my parents, farnily, and fitends who also have had to

endure the trials and tibulations of a graduate student. Without their love, support, and encouragement this never would have been possible. Finally, to Ann-Elise, my pillar of

strength, 1 couldn't have done it without you!

Table of Contents ..

Abstract ...................... . . .............................................................................................-13

Acknowledgements ......................................................... .....

........................*............. v

Table of Contents ................................. -. . . . . , List of Tables ..............

i

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List of Figures ...............................................................................................................

XII

List of Abbreviations ........ . .........................................................................................

xvi

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Chapter 1: Introduction 1 Physics of Flight ....................................................................................................... 1 Physiological Consequences......................................................................................3 1.2.1 Hydrostatic Effects of +Gz Exposure ....................................................... 3 1.2.2 Effects and Symptomology of +Gz Exposure ........................................... 6 ..................................... 7 1.2.3 Compensatory Mechanisms ............................. . . G-Tolerance............................................................................................................... 7 TraditionaI Methodologies Against +Gz Exposure .................................................. 8 1.4.1 The G-Suit.................................................................................................. 9 1.4.2 Aiiti-G Straining Maneuvers (AGSM) ..................................................... -9 Advanced +Gz Protection Systems ................... . . ................................................... 10 1.5.1 High Coverage Lower Body Garments ...................................................... 10 1.5.2 Positive Pressure Breathing During +Gz (PBG) ............................... .........10 G-valve Performance .......................... , . . ..... . . ...................................................... Il 1.6.1 Factors Infiuencing G-valve Responsiveness ............................................. I l 1.6.2 Demands from an Improved Flight Performance Envelope ....................... 12 1.6.3 Influences of Life Support System Design ................................................ 12 1.6.4 G-valve Responsiveness Studies............. ...... ...................................... 13 +Gz Tolerance Measurement: Vision and Blood Pressure ....................................... 14 1.7.1 Historical Bases for Modem Methodologies ......................................... 7 4 1.7.2 Detennining +Gz Tolerance Using Endpoints ........................... . . . ......15 Non-Invasive B lood Pressure Measurement: The Finapres ....................................17 1.8.1 Rationale ..................................................................................................... 17 1A.2 Clinical Validation ..................................................................................... 17 1.8.3 Implementation in Centrifuge Experirnents...................................... 1 9 Purpose of the Study ...................................... .......................................................... 19 1.10 Hypotheses .............................................................................................................. 20

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Chapter 2: Methodology 21 .......................................................... 21 Selection of Independent Treatment Variables Control of +Gz .......................................................................................................... 21 2.2.1 Selection of Acceleration Levels and the Hurnan Centrifiige......................21 2.2.2 The Acceleration Profile ............. . . . ......................................................23 ............................................................................................... Lower Body Coverage 24 Lower Body Pressurization ...................................................................................... 27 . . 2.4.1 G-suit Pressurization Schedules.................................................................27 2.4.2 G-valve Responsiveness .......................................................................... -28 Positive Pressure Breathing (PBG) ........................................................................... 30 Treaûnent Combinations Used in the Investigation................................................ 3 1 Experimental Design..................................................................................................33 2.7.1 Factors Influencing Experïmental Design ................................................. 33 2.7.2 Main Experimental Design ........................................................................ .JJ 2.7.3 Additional Conditions ............................................................................... -34 Subjects ..................................................................................................................... 35 2.8.1 Medical Screening...................................................................................... -35 2.8.2 Training ...................................................................................................... 36 Measurements ........................................................................................................... 37 2.9.1 Gravitoinertial Force, Mask Cavity, and G-suit Pressure .........................37 2.9.2 Blood Pressure ........................................................................................... 37 2.9.3 Heart Rate .................................................................................................. 37 2.9.4 Visual Light Loss Measurement................... . . . . .....................................-38 2.9.5 G-suit Pressure Cornfort, System Response, and Fatigue .........................39 2.9.6 Electromyographic and Ear Pulse Monitoring ...........................................40 2.10 Data Acquisition and Analyses ............................................................................... 41 2.10.1 Data Acquisition System ........................................................................ -41 2.10.2 Data Record Analysis Procedure ............................................................ -41 2.10.3 Parametric Statistics ................................................................................. 44 2.1 0.4 Nonparametric Statistics ................................... ... ................................. -46 -

CIL)

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47 Chapter 3: G-Tolerance Study 1 .Pressure Schedule Effects .............................................................................. 47 Selection of Profiles for Analysis Control of Treatment Variables ................................................................................. 47 Treatrnent EEects...................................................................................................... 48 .. 3.3.1 Subjective Measurement of +Gz Tolerance: Vision ..................................48 3 -3-2 Objective Measurement of +Gz Tolerance: Blood Pressure.....................48 G-suit Pressure Schedule and Acceleration Tolerance .............................................-53 Additional Factors and Issues ...................................................................................54 3 .5 .1 Fatigue Effects............................................................................................54 3.5.2 Cornfort During G-suit Pressurization.................................................... - 3 4 35 3 Variability of the Cardiovascular Response ............................................- 3 6 Treatment Levels in Relation to the Operational Environment ................................58 Findings Pertinent to Life Support Design ............................................................... 59

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60 Chapter 4: G-Tolerance Study II .G-valve Responsiveness 4.1 Selection of Profiles for Analysis..............................................................................60 4.2 Control of Treatment Variables...............................................................................1 4.2.1 Pressurization Delays and G-suit Pressures ..............................................61 4.3 Treatment Effects.....................................................................................................-62 4.3.1 Subjective Measurement of +Gz Tolerance: Vision..................................62 4.3 -2 Objective Measurement of +Gz Tolerance: Blood Pressure.....................65 4.3.3 Summary of Findings and The Effect of a Type I Error ............................67 4.4 G-valve Responsiveness and Acceleration Tolerance ...............................................69 ........-70 4.5 Quantification of the Delayed Blood Pressure Response ..................... . . . . 4.6 The Effect of Poor G-valve Response on Cardiac Emptying ...................................72 . . . ......74 4.7 Additional Factors and Issues ....................................................... 74 4.7.1 Ratings of System Responsiveness.......................................................... 75 4.8 Treatment Level in Relation to the Operational Environment.................................. 4.9 Findings Pertinent to Life Support Design ...............................................................79 3

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Chapter 5: G-Tolerance Study I11 .Lower Body Coverage 80 5.1 Selection of Profiles for Analysis..............................................................................80 5.2 Control of Treatment Variables................................................................................. 80 ...... 80 5.2.1 Coverage Condition and G-suit Pressures (P, ) ............................. ...................................................................................................... 5 -3 Treatment Effects 83 .. 83 5.3.1 Subjective Measurement of +Gz Tolerance: V ~ s ~.................................. on 5.3 -2 Objective Measurement of +Gz Tolerance: Blood Pressure..................... 86 89 5.3.3 Summary of Findings and The Effect of a Type I Error .......................... 5.4 Lower Body Coverage and Acceleration Tolerance .................................................. 90 5.5 Additional Factors and Issues ................................................................................... 94 5.5.1 Subjective Ratings of Comfoa .................................................................. -94 ....................................... 95 5.5.2 Cardiac Anomalies with FPHS ................ ...... 5.6 Treatment Level in Relation to the Operational Environment.................................. 96 5.7 Findings Pertinent to Life Support Design ............................................................... 99

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Chapter 6: G-Tolerance Study IV .Positive Pressure Breathing 100 6.1 Selection of Profiles for Analysis..............................................................................100 6.2 Control of Treatment Variables.............................................................................. 1 0 0 6.2.1 G-suit and Mask Cavity Pressure.............................................................. 100 6.3 Treatment Effects ...................................................................................................... 103 .. .................................. 103 6.3.1 Subjective Measurement of +Gz Tolerance: V~slon 6.3.2 Objective Measurement of +Gz Tolerance: Blood Pressure.....................107 6.4 PBG Schedules and Acceleration Tolerance.............................................................. 110 6.5 Treatment Level in Relation to the Operational Environment.................................. 113 6.6 Findings Pertinent to Life Support Design ...............................................................116

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Chapter 7: Implementation of a Simple Inferential Technique 117 7.1 Staternent of Requirement ......................................................................................... 117 7.2 Mathematical ModeIs of Cardiovascular Function: Roles in Research....................117 7.3 Models Used for Detemiining Flow and Peripheral Resistance ............................... 118 7.4 Assumptions of the Simple Mode1 Used .................................................................. 121 7.4.1 Assumption 1: The Pressure to VoIurne Relationship.............................. 121 7.4.2 Assumption 2: Capacitive Effects on the Rate of Blood Pressure Change...........................................-....................................................... 121 7.4.3 Asslunption 3 : Calculating Mean Pressure ...............................................122 7.5 Estimating Flow and Resistance................................................................................123 7.5.1 Estimating Systemic Arterial Blood Flow (Qest) ...................................... 123 7.5 -2 Estimating Resistance (Rest) ......................................................................125 7.6 Calculation of Flow and Resistance During +Gz........................ .... ....................1 2 5

......................................................

127 Chapter 8: Results of the Inferential Analyses 8.1 G-suit Schedules: Pressure. Flow. and Resistance Effects............................. .........127 8.1.1 Pressure ....................-. ............................................................................. 127 128 8.1.2 Flow ........................................................................................................ 8.1 -3 Resistance................................................................................................... 129 8.2 G-valve Responsiveness: Pressure, Flow. and Resistance Effects .......................... 132 8.2.1 Pressure .................................................................................................... 132 8.2.2 Flow ........................................................................................................... 132 8.2.3 Resistance................................................................................................... 134 8.3 Lower Body Coverage: Pressure, Flow, and Resistance Effects..............................135 8.3.1 Pressure .................................................................................................. 136 8.3.2 Flow ........................................................................................................... 137 8.3.3 Resistance................................................................................................... 137 8.4 PBG Schedules: Pressure, Flow. and Resistance Effects ......................................... 138 8.4.1 Pressure .................................................................................................... 138 8.4.2 Flow ........................................................................................................... 139 8.4.2 Resistance................................................................................................... 141 8.5 Support for the Inferential Analysis Methodology .................... .............................. 142 8.5.1 Cornparisons with Previous Findings ........................................................ 142 8.5.2 Cornparison with a Secondary Procedure ..................................................144 8.5 -3 Implications of the Cornparisons .........................................................,.....1 4 9 8.6 Summary of Findings ................................................................................................ 149

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Chapter 9: Homeostatic Blood Pressure Control and +Gz Protection 150 9.1 The Homeostatic Negative Feedback Control System.............................................. 150 9.1.3 Blood Pressure Control: A Negative Feedback System ............................ 150 9.1.2 Type of Controller Function......................................................................150 9.2 ZdentiQing the Primary Locus .................................................~...........................152 9.2.1 Support for A Venous Locus: Tissue Factors and Hydrostatics .............. 154 9.3 Hemodynamic Responses.........................................................................................159

9.4 9.5 9.6

9.7

61 9.3.1 The Bainbridge Mediated Response ...................................................1 Vascuiar and Cardiac Functioning ........................... . ............................................165 Temporal Effects On the Blood Pressure Response.................................................167 The Blood Pressure Control Process ........................................................................ 170 9.6.1 Factors AfTecting Blood Pressure Control ................................................. 170 9.6.2 Preferential Control During and Immediately Post Counterpressure Application .............................................................................................. 171 9.6-3 B lood Pressure Regulation ......................................................................1 71 9.6.4 Myogenic Factors ...................................................................................... 174 9.6.5 Integrated Neural Control: Possible Mechanism for Arrythmias .............174 Hypothetical Mode1 of the Cardiovascular Response .............................................. 176

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178 Chapter 10: Findings. Their Implications. and Future Research ................................................... 1 78 10.1 Current Issues in Life Support Systern Design 10.2 Findings In Relation to Experimental Hypotheses ................................................. 178 10.2.1 Effect of Lower Garment Pressurization ................................... 1 7 8 10.2.2 Effect of G-valve Responsiveness ......................................................... 1 79 10.2.3 Effect of Lower Body Coverage............................................................... 179 10.2.4 Effect of PBG Schedule........................................................................ 1 79 10.3 Tangible E1ements:Life Support System Design Factors........................................ 180 10.3.1 Vascular Effects........................................................................................ 180 10.3 -2 G-valve Responsiveness ..................................................................... 1 8 1 10.3.3 G-suit Design ....................................................................................... 1 82 10.4 Intangible Elements:Physiological Factors ........................................................... 1 82 10.4.1 Blood Pressure Control Mechanisms.................................................... 1 8 3 10.4.2 Variability in Subject Responses...............................................................183 10.5 Design Implications From Study Findings.......................................................... 1 84 10.6 Limitations of the Research................................................................................... 1 84 10.7 Future Research.................................................................................................. 1 85 10.7.1 Verification In A Wider Performance Envelope ....................................... 185 10.7.2 Additive Factors and +Gz Protection...................................................... 186 10.7.3 Development of the Full Pressure Half Suit ..................................... .......187

Annexes ....................................................................................................................

1 9 6

List of Tables Table 2- 1: Classification of the Extent of Visual Changes during the +Gz Plateau .......39 Table 2-2: Subjective Rating Scale used by Subjects to Evaluate G-suit Pressure Cornfort, System Response, and Fatigue..................................................................40 Table 2-3: Mirnimurn DZerences Required Between Means Before Being Considered for Post Hoc Analysis ..................... . . . ...............................................45 Table 3-1: Main Effect of G-suit Schedufe on nSBPELand nSBPHLat the +Gz Levels Used in the Experirnent ......................-..-...................................................... -5O Table 4-1: Delay x Time Interactions at the +Gz Levels Used in the Experirnent ......... 62 Table 4-2: Duration and Maximum DiEerence in G-suit Pressure Between Delay .. ................................................................................................................62 Cond~tions. Table 4-3: Delay x Time Interactions at the +Gz Levels Used in the Experiment ........66 Table 4-4: Delay x Tirne Interaction of G-suit Pressure Delay on nSBPHLat the +Gz Levels Used in the Experiment .........................................................................70 Table 4-5: Maximum Systolic Blood Pressure Change and Time to Maximum Systolic Blood Pressure fiom Onset of Profile for d l Delay Conditions ................. 72 Table 4-6: Calculation of the Delay in Cardiovascular Response Relative to Inflation of the G-suit ................... . . ...................................................................... 76 Table 5-1: Delay x Time Interactions with Different Levels of Lower Body Coverage at the +Gz Levels Used in the Experiment .......................................... 8 1 Table 5-2: Lower Body Counterpressure Coverage x Time Interactions on nSBPHl at the +Gz Levels Used in the Experiment ............................................................... 87 Table 5-3: Times to Intermediate Pressures in Subjects Exposed to + 5 0 Gz with Different Lower Body Gannents Pressurized by the Alar G-valve ......................... 98 Table 6-1 : PBG Schedule x Tirne Interactions on Mask Cavity Pressures (Pm)at 01 the +Gz Levels Used in the Experiment ............................................................ 1 Table 6-2: Target and Actual Pm Values Measured During the Last 5 Seconds of the Acceleration Profile for Al1 Conditions .............................................................. 103 Table 6-3: Main Effect of Time on nSBP, at the +Gz Levels Used in the Experiment .............................................................................................................. 1 08 Table 8-1 : Rate of Penpheral R u o f f with FPHS Inflation at +4.0 Gz with the Low and Nominal Pressurization Schedules ............................................................. 147 Table 9- 1: Intravascular and Extravascular (Bladder) Pressures at +.O, +4.5, and t5.0 Gz at the Level of the Abdomen, Mid-Thigh, and Mid-Calf with the Low, Nominal and High G-suit Pressurization Schedules.................................. 156 Table 9-2: CalcuIated Arterial and Vein Transmural Pressures at +4.0, t4.5, and +5.0 Gz at the Level of the Abdomen, Mid-Thigh, and Mid-Calf with the Low, Nominal and High G-suit Pressuization Schedules........................................ 157

List of Figures Figure 1.1: Alterations in the gravitational environment encountered during aerial ...............................................................................2 combat maneuvering........ ...... Figure 2-1 : Simulahg the high +Gz aircombat environment .......................................- 2 2 Figure 2-2: Graphical depiction of a rapid onset rate @OR) profile to +5 G z ..............2~ Figure 2-3 : The CSU 1 5/P and STMG G-suits .............................................................-25 Figure 2-4: The rnodified Full Pressure Half Suit (FPHS) .............................................. 26 Figure 2-5: The three G-suit pressure schedules used in the expenment........................28 Figure 2-6: Alterations in G-valve responsiveness via the introduction of delays into the pressurization schedule ........................... ...............................................3 0 31 Figure 2-7: PBG schedules used in this experiment........................................................ C)

Figure 2-8: Flow diagram outlining the independent variable combinations for each +Gz level................................................................................................................... 32 Figure 2-9: Lightbar and control column inside gondola of centrifuge.............................38 Figure 2-10: Schematic representation of the centrifuge gondola and Control Room configurations................................................................................................-42 Figure 2- 11: Software analysis procedure .......................................................................43 Figure 3-1: Mean ratings of worst and best peripheral and central light loss reported by subjects at +4.0. +4.5. and +5 .0 G z...................................................... 49 Figure 3-2: Changes in eye @anel A) and heart-level (panel B) systolic blood pressure fiom onset values collapsed across G-suit scheduie .................................. 51 Figure 3-3 : Mean subjective ratings of comfort with the three pressure schedules ........55 Figure 3-4: Experimental tracing from a subject exposed to a +4.5 Gz profile while wearing a STING G-suit inflated according to the high pressurization schedule..................................................................................................................... 57 Figure 3-5: G-suit pressure levels used in the experiment relative to requisite values (MIL-V-87255USAF) .................................................................................. 58 Figure 4-1 : Highest completed +Gz level by al1 subjects in each delay condition while wearing a STING G-suit pressurized according to the "Nominal" schedule or in the "Control" (nonpressurized) state.................................................61 Figure 4-2: Worst and best penpheral and central vision changes at +4.0 and +4.5 Gz with increasing delay in G-suit pressurization ...................................................64 Figure 4-3: Changes in heart-level systolic blood pressure f?om onset values with increasing delays in G-suit pressurization ................................................................66 Figure 4-4: Summary of the changes in with increasing deiays in G-suit 68 pressurization at +4.0. +4.5. and +5.0 Gz................................................................

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Figure 4-5: Tirne course of blood pressure changes with varying delays in G-suit . . pressunzation ........................................................................................................... 71 Figure 4-6: Hardcopy record i!lustrating the decrease in blood pressure for one cardiac cycle occurring irnmediately after G-suit inflation........................................73 Figure 4-7: Mean ratings of system responsiveness at +4.0. +4.5. and +5.0 Gz ...........75 Figure 4-8: Pressurehme profdes of d l deiay conditions used in the experiment .........-77 Figure 5-1: Differences in mean between G-suit pressures during accelerations to t4.0. t4.5. and +5.0 Gz .......................................................................................82 Figure 5-2: Mean subjective ratings of best and wose vision at +4.0 and +4.5 Gz .......84 Figure 5-3 : Normalized heart-level systolic blood pressure wiîh increasing Iower body coverage ...........................................................................................................86 Figure 5-4: in subjects wearing a CSU 15/P. STING. or FPHS G-suit pressurized according to the nominal schedule .........................................................88 Figure 5-5: Cardiovascular response to pressurization of the FPHS in two subjects exposed to +5.O Gz.....................................................................................92 Figure 5-6: Mean ratings of comfort with the three lower body garments at +4.0, +4SYand 3-50 Gz ..................................................................................................... 94 Figure 5-7: Cardiovascular response with a FPHS pressurized to 155 and 232 mmHg............................................................................................ .................... -96 Figure 5-8: Pressurehime profiles of Alar G-valve performance with subjects wearing the CSU 15P. STING. or FPHS ................................................................. 97 Figure 6-1 : Differences in mean mask cavity pressures (AI'. ) with no positive pressure breathing. Low. and High PBG schedules during accelerations to +4.0. +4.5. and +5.0 Gz............................................................................................ 102 Figure 6-2: Subject reports of best and worst vision at +4.0, +4.5 Gz and t5.0 Gz with three levels of PBG........................................................................................... 104 Figure 6-3: Norrnalized heart-level systolic blood pressure with no positive pressure breathing (No PBG). a Low PBG. and a High PBG schedule at +4.0, +4.5. and +5.0 Gz ..................................................................................................... 108 Figure 6-4: nSBP, and nSBPELresponses collapsed across G-suit and PBG schedules at +4.0. +4.5. and +5 .0 Gz ....................................................................... 109 Figure 6-5: Hardcopy records fiom one subject exposed to +5.0 Gz without and with PBG .................................................................................................................. 112 Figure 6-6: Regulator output pressures provided by the current United States Air Force (USAF) and proposed Canadian Air Force (High) PBG schedules................115 Figure 7- 1: Linear pressure:volume relationship ............................................................ -123 Figure 7-2: Inferring volume alterations fiom pressure changes.................................124 Figure 8-1 : Effect of G-suit pressurization schedule on mean merial pressure in subjects wearing a STMG lower body garment while exposed to +4.0 Gz .............127

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Figure 8-2: Effect of different lower body pressurization schedules on heart rate (HR) and pulse pressures (PP) during exposure to i4.0 Gz ....................................128 Figure 8-3: Alterations in estimated artenal blood flow at +4.0 Gz with the three P,, schedules used to pressurize the STING lower body garment ...........................129 Figure 8-4: Estimated resistance changes at +4.0 Gz with different presslinzation schedules.................-.-... ........-....... .. . . . . . .. . .. .. .. .............. . l 3 O Figure 8-5: Change in Rest values with different P, schedules at +4.0, +4.5, and +5.0 Gz ............................................ .........................................................................131 Figure 8-6: Effect of delayed G-suit pressuization of rnean arterial pressure in subjects wearing a STING lower body garment while exposed to +4.0 Gz ............. 132 Figure 8-7: Effect of lower body pressuization with and without delays at +4.0 Gz on heart rate (KR) and pulse pressures (PP) ..................................................... -133 blood flow at +4.0 Gz with various Figure 8-8: Alterations in estimated . artenal . delays in lower body pressunzation.. .............. ..-..... . - .............. ........................... 134 Figure 8-9: Estimated resistance changes at +4.0 Gz with increasing delay in . lower body pressunzation .......................................... ................................. 135 Figure 8- 10: Effect of lower body coverage on mean arterial pressure at +4.0 Gz. .......135 Figure 8-1 1: Effect of Lower body coverage on heart rate (HR) and pulse pressures (PP) during exposure to +4.0 Gz.............................-........ ..................... 136 Figure 8-12: Changes in estimated artenal blood flow at +4.0 Gz with the pressurization of different lower body ensembles................................................... 137 Figure 8-13: Estirnated resistance changes at +4.0 Gz with various levels of lower body coverage .......................................... .. .... ...... .. ... .... ... .. ...... .1 3 8 Figure 8-14: Effect of positive pressure breathing schedules on mean arterial pressure at +5.0 Gz ................................... . . . . . . . .. . ............................ .. 1 39 Figure 8- 15: Effect of lower body coverage on heart rate (HR) and pulse pressures (PP) during exposure to +4.O G z.............................................................. 140 Figure 8-16: Changes in estimated arterial blood flow at t5.O Gz with different PBG levels ................-................................................................................. . .. -.141 Figure 8-17: Effect of various PBG levels on estimated resistance changes at +5.0 L)L)

Figure 8-16: Mean cardiovascular response for the six subjects with exposure to +2.5, +3 .O, and +3.5 Gz in the unprotected (Control) state................................... 143 Figure 8-19: Calculation of peripheral runoff rate with inflation of the FPHS to 1O3 and 155 mmHg during a +4.0 Gz exposure................................. ....... ......... . - 146 Figure 8-20: Rate of vascular emptying with inflation of the FPHS according to the Low and Nominal schedi!les in one subject exposed to +4.0 Gz......................-- 148 Figure 9-1: Schema of a negative feedback system.........................................................150 Figure 9-2: Regulator and servomechanism systems ..................................................... 15 1

Figure 9-3: Effect of G-suit pressurization schedule on the cardiovascular response during a 10 second exposure to +4.0 Gz .......................-....-.-......... . .1 53 Figure 9-4: Vertical distances (h) fiom heart Ievel used to calculate internal vascular pressures ................................................................................................... 156 Figure 9-5: Cdculated pressure ciifferences across an artenal and vende wall with different pressurization schedules at t4.0, +4.5, and +5.0 Gz................................,158 Figure 9-6: Effect of extemal counterpressure on the underlying vascdature ................ 160 Figure 9-7: Changes in mean heart rate @IR)and mean pulse pressure (PP) at t5.0 Gz with varying schedules to the lower garment (panel A), delays in pressurization @anel B), and level of coverage (panel C) ........................................162 Figure 9-8: Rate of change in HR and SBP with three G-suit pressurization schedules ...................-.......-.........--... . .................... .. .. . .. ............... ...1 6 4 Figure 9-9: Effect of arteriolar vasoconstriction on the cardiac and vascular b c t i o n cuves. Note that flow wouid decrease with a rise in resistance ...............165 Figure 9-10: Increased flow and resistance necessitates a nghtward shift in the vascular function cuve ....................................................................................... ..166 Figure 9- 11: Schematical representation of the effect of counterpressure on the cardiovascular system ..................................... . ....... . ..... .. ...... ... . .. .1 69 Figure 9-12: Efferent inputs fiom pressure receptors to cardiac pacing control centers in the medulla oblongata .................................................. ........................ 172 Figure 9- 13: Ancillary reflexes during +Gz exposure to +4.0, +4.5, and +5.0 Gz.........-173 Figure 9- 14: Volume loading fkom lower body garment pressurization may transientfy impart additional signals tu the medulla .......................................... 175 Figure 9- 15: The time course of events that occur with the application of an extemal counterpressure ....................-......................................................................177

List of Abbreviations 1-B

power

A

area

a

nurnber of means to contrast

a,

centripetal acceleration (in dsec')

ag

rate of acceleration in fiee fa11 (9.8 1 m/sec2)

am

maneurvering acceleration

%V

family wise Type 1error rate

AGSM

anti-G straining maneuver

ANOVA

anaiysis of variance

PC

per cornparison Type 1error rate

B

Type II error rate

C

nurnber of pair-wise cornparisons

C a

arterial capacitance

Cao

aortic capacitance

CLL

central light loss

CLL Inter.

central light loss interrogation

CO

cardiac output

DBP

diastolic blood pressure

DCIEM

Defence and Civil Institute of Environmental Medicine

df

degrees of freedom

dfdenom

degrees of fieedom in denornhator

dfnu*

degrees of fieedom in numerator

dMAP1 dt

change in mean arterial pressure per given time interval

APgs

difference in G-suit pressure difference in mask cavity pressure

ASBPEL

change in eye-level systolic blood pressure from onset

ASBPHL

change in heart-level systolic blood pressure fiom onset

xvi

change in systolic blood pressure fiom G-suit pressure change in arterial volume per given time interval

ECG

electrocardiography

EMG

electromyography

F

F ratio

F,

force applied by an object at rest due to gravity (weight)

FI

gravitoinertial force

Fm

force due to maneuvering

FPHS

Full Pressure Half Suit

G

gravitoinertial force (direction unspecified)

+Gz

footward gravitoinertial force

G-LOC

G-induced loss of consciousness

h

hydrostatic distance

HR

heart rate

1

length of tube

LVEDV

left ventricular end-diastolic volume mass of an object

mean arterial pressure millirneters of mercwy

mean square n

sample size

n

viscosity

P

pressure

P

density

PBG

positive pressure breathing during +Gz p-value (Geisser-Greenhouse corrected) G-suit pressure input pressure

PLL

peripheral light loss

xvii

PLL Inter.

peripheral light loss interrogation end diastolic pressure

mask pressure maximum G-suit pressure mean circulatory pressure measured pressure output pressure systemic arterial pressure pulse pressure density ratio of blood to mercury (U13.6) reference pressure pressure at time (t) p v

venous pressure

Q

flow

Qest

estimated systemic arterial blood flow radius

RAP

rîght arterial pressure estimated resistance penpheral resistance

ROR

rapid onset rate

SBP

systolic blood pressure standard deviation standard error of the mean sum of squares stroke volume time of ejection United States Air Force angular velocity

arterial blood volume

xviii

ratio of treatment variance to enor variance mean constant pi (3.14 16)

chi square value aortic impedance

xix

INTRODUCTION 1.1 Physics of Ftight Due to earth's gravitational field, an object on the planet's surface is pulled toward its center. The rate of acceleration in free fa11 is constant (ad. If this motion is opposed (i.e., fiee fa11 is prevented), the inertial force exerted by the body at rest rnanifests itself as weight, usually expressed as:

F,=ms$ Fqn. 1-11 where F, is the force due to gravity in newtons, rn is the mass of the body in kilograrns, and a, the acceleration due to gravity (9.8 1 rn/secZ). As the mass of a body (m) remains constant, changes in weight (Le.. force) can ody be achieved by altering the magnitude of the acceleration vector (Smith, 1974).

Pilots of highly agile aircr& are exposed to a varying gravitational environment when perfomiing maneuvers requiring rapid alterations in direction and speed (Le., during aerial combat situations). Forces acting on the surfaces of the aircraft alter the direction of flight. According to Newtonian laws of motion, application of a force on a body results in an acceleration proportional to the applied force and inversely cornmensurate to the mass of the body:

where a,and Fm represent the acceleration and force due to maneuvering, respectively. If

a, is known (i.e., measured by an accelerometer), the applied maneuvering force may be calcdated:

A.

. .. -..--. - .

Fm= m a, Headward

hertid Force

Footward

Figure 1-1: AZterations in the gravitational environment encountered during aerial combat maneuvering. A. Directional change in flight path results in a headward acceleration and an equal, but opposite,footward inertial vector. B. The magnitude of the inertial force is the same as the accelerative force, and is referenced with respect to pilot orientation. Newton's third law States that for every action there is also an equal but opposite reaction (Figure 1- 1A). The inertial force (FI) encountered is usudly normalized with respect to that produced by gravity itself (Leverett Jr & Whinnery, 1985) and is expressed as G unis (Kaufinan et al., 1984):

F, =a,,, m /a, m Fqn. 1-41 As mass is a constant in both numerator and denominator, the formula then reduces to:

The magnitude of the gravitoinertial force vector is expressed as a dirnensionless multiple (Le., an accelerative force equivalent to hvice the earth's gravitational field would produce a 2 G gravitoinertial force). A system for referencing was introduced by Gel1 (1961). Acceleration in the

headward direction as shown in Figure 1-1B creates footward gravitoinertial forces (+Gz)

which, in tum, affect human physiology. In older generations of fighter aircraft, structural factors limited maneuvering performance. In today's era of science and technology, the physiological capacity of the pilot to endure the high gravitoinertial forces associated with irnproved aircraft agility is being shown to be the weak Link in aircombat situations (Burton et al., 1974). The aircraft have been designed to rapidly apply these forces and can sustain them for long durations (Gillingham & Knitz, 1974). Exposure to acceleration levels greater than +4 G z for prolonged periods will result in G-induced loss of consciousness (G-LOC) in unprotected individuals (Cochran et al., 1954). The incidence of G-LOC is high (Wood, 1988a) and is suspected as the cause of a number of mishaps involving the loss of both aircraft and pilot. Hence, it has become a prime concem to establish a means of increasing protection to the harsh +Gz environment (Wood et al., 1988).

1.2 Physiological Consequences

Factors influencing the physiological effects of accelerative force are: (i) intensity

of acceleration, (ii) duration of acceleration, (iii) rate of acceleration, (iv) area and site over which the force is applied, and (v) direction of acceleration with respect to the longitudinal axis of the human body (Leverett Jr, 1967). Physiological sequelae to an altered gravitational environment are dependent on the direction of the acceleration vector relative to the h m a n body.

1-2.1 Hvdrostatic Effects of +Gz Ex~osure

Pressure (P) is defined as the force per unit area (A):

P = FIA [Eqn. 1-61 Pressures measured at the bottom of a water column are the product of the fluid density (p) and the column height (h). Therefore, a 1 mm (0.001 meter) column of water

(p = 1000 N/m3) would produce 1 N/m2 or 1 pascal (Pa) of pressure. Blood pressures have traditionally been reported in rnillirneters mercury (mmHg). As mercury is 13-6 times denser than water, the reciprocal of this (U13.6) becomes the density ratio (pJ. Given that density is the weight per unit volume in a normal gravitational environment (i.e., a&, weight would change with any apparent alterations in the gravitational field, as seen with maneuvering acceleration (a&

To compensate for any variations in density, the

ratio of a,to a, is added to the equation. This ratio can be replaced by the magnitude of the resultmt gravitoinertial force (in G units), as seen in equation 1-4. Measurernents may not necessarily be made at the bottom of the fluid coluwi. Any measured pressure (Pm,) will be higher or lower than that recorded at a reference point (Pd), and is dependent on the distance (h, in mm) above or below P,,

. Pressures

above the reference point will be Iess, and those below will be greater than the reference pressure. Pm, (in mmHg) cari be esthated using the followuig equation: Pm,,= Pd + h G p, [Eqn. 1-71 Blood pressure determinations are not made at the bottom of the fluid filled vascular system, but at the level of the heart. For the average individual, mean artenal pressure (MAP) at the level of the heart is approximately 100 mmHg. In a nomal gravity environment (G equals 1), pressure will be 7.35 mmHg higher and 7.35 mmHg lower than the reference pressure at positions 100 mm below and above heart level, respectively. These hydrostatic gradients are produced in columns that lie in parallel with the gravitoinertial force.

If the distance (h) is increased to 300 mm (average heart-eye distance), M M measured at eye level would decrease by 22 mmHg to around 78 mmHg. Conversely, the

pressure measured at a point 300 mm below heart level would increase by this same amount (Le., to 122 rnmHg). Acceleration in the headward direction (as depicted in Figure

1B) widens these hydrostatic gradients. For every M e r 1 +Gz increment, mean arterid pressure would decrease or increase by an additional 22 mmHg (Stoll, 1956).

In a system comprïsed of rigid tubes, flow is unaffected by these hydrostatic gradients. However, the cardiovascular system contains elastic elements that collapse when extravascuiar pressure exceeds intemal blood vessel values, or expand with high transmural pressures. According to Poiseuille's Law, the flow of a Newtonian liquid through cylindrical tubes can be defmed using the equation:

Q= r(Pi - Po)r' / (8 n 1) Eqn. 1-81 Therefore, flow (Q) is affected by length of tube (l), radius of tube (r), pressure differential (input pressure minus output pressure, or Pi - Po)and liquid viscosity (n). Viscosity is the ratio of sheer stress to the rate of strain of the fluid, and x/8 is the constant of proportionality. The model does not perfectly predict flow through the vascular system as it assumes steady larninar flow. In addition, blood is a suspension and behaves similady, but not exactly like a Newtonian fluid such as water. However, the underlying principle can be used to examine the factors that govem flow through the vasculature @eme & Levy, 2983). Resistance to flow (R) is calculated as the pressure divided by flow. Removing the pressure and flow portions in equation 1-8, leaves:

R = 8 n l / ( n f l ) Fqn. 1-91 From the above equation, it is apparent that resistance is dependent only on the dimensions of the tube and charactenstics of the fluid. The length of the circulatory system is virtually constant, and the viscosity of blood does not Vary appreciably. The

main changes are produced from changes in the tube radius. Thus, the reduced vessel caliber in regions above the heart resuit in an increased resistance to flow. Flow dirninishes as intravascular pressures decline until pulsatile flow ensues. Further pressure

decreases completely collapse the blood vessels, and a cessation of blood flow occurs. Therefore, higher heart-level systemic arterial pressures are necessary to continue perfusing the vital cephalic regions (Le., the eyes and brain) as the +Gz level is increased.

In dependent regions, the apparent increase in the weight of the blood during sustained +Gz is evident in a downward (caudal) fluid translocation (Krutz et al., 1990).

Venous pooling in the lower extremities occurs after several minutes. The reduction in the effective blood volume is analogous to a hernorrhage condition, whereby the consequentid alterations in vascular function compromise both cardiac output (Lindberg & Wood, 1960) and venous return. Thus, for a given total penpheral resistance, changes in

systemic artend pressure would still result (Wood & Lambert, 1946). Additional blood

pressure declines can be attributed to the decreased resistance associated with the widening of the vessels in the lower regions (AGARD, 1990). Therefore, the associated footward fluid shift affects the total resistance of the system and alters the equilibrium point between venous return and cardiac output.

1.2.2 Effects and Sym~tomologvof +Gz Exposure

In order to perfùse the retina, blood pressure at eye-level must be in excess of 20 to 25 mmHg to overcome intra-ocdar pressures (Lambert, 1945). An unprotected pilot exposed to +3 to +4 Gz may encounter changes in the visual field. A gradud change in the gravitational environment initially affects peripheral vision, causing a narrowing of the vismi field. As the +Gz level is increased, eye-level blood flow is compromised. Perfiision to the retina is diminished or ceases, causing a situation in which the pilot can no longer see (i.e., blackout). At this +Gz level, an adequate blood supply to the brain is maintained. A relatively small increase in +Gz would M e r decrease blood flow to the brain to sub-critical levels. An interval exists between the acute cessation or near stoppage of brain blood flow and loss of cognitive brain function (Rossen et al., 1943).

After 5 to 7 seconds, the oxygen reserves in the blood and tissue are depieted and, ultimately, G-LOC results. A rapid onset of +Gz may cause G-LOC without the preceding visual changes if the acceleration is high enough and sustained for more than 5 to 7 seconds (Stoll, 1956).

1 -2.3 Cornpensatorv Mechanisms

With acceleration exposure, there is an immediate drop in head-level blood pressure. M e r 5 to 10 seconds, a rise in blood pressure occurs concurrent with an increase in heart rate. The response is mediated by the baroreceptor reflex. Baroreceptors are stretch receptors located in the carotid sinus and aortic arch (Bjurstedt et al., 1979; Kirchheim, 1976). Studies on anirnals have suggested that low pressure receptors may be located in the pulmonary vessels (Coleridge & Kidd, 1953), and right

and left atria (Paintal, 1953). Al1 are sensitive to changes in stretch. The decrease in blood pressure causes a lower firing fiequency propagated to the vasomotor center

(Komer, 1971). The vasomotor center and other reticular formation areas of the brain send impulses to the peripheral smooth musculature causing a higher tone (peripheral vasoconstriction). In addition, there is a concomitant increase in heart rate (Forster & Whhnery, 1988) and cardiac contractility (Sarnoff, 1960). However, the cardiovascular responses to high +Gz stress are of little help with onset rates greater than 1 +Gz/sec as

they are relatively slow responding (Dampney et al., 1971).

1.3 G-Tolerance Tolerance to headward acceleration can generally be defined as the ability to

maintain consciousness and at least a minimum field of vision compatible with useful psycliomotor performance (Buick, 1989). In research, three additional and more specific definitions are useful. G-intensity tolerance refers to the highest level of +Gz that an individual can withstand, usually for only a short period of time (e-g., the acceleration

level at which an endpoint is attained). G-duration tolerance emphasizes endurance capacity, measuring the length of time an individual can endure pre-determined +Gz levels (e-g., the duration fkom onset of acceleration until the thne an endpoint is reached). Gprotection refers to the extent of change fiom control (usually an unprotected state) in a measurable physiological metric in response to the application of a +Gz countermeasure.

The measure of G-protection need not be made at an individual's G-tolerance. This thesis is concemed with G-intensity tolerance.

Tolerance to +Gz requires adequate head-(evel blood pressure during +Gz exposure (Wood et al., 1988). Preserving head-level blood flow necessitates the reduction of the hydrostatic pressure gradient between the heart and head by: (i) decreasing the vertical distance between the h a r t and head; (ii) directly increasing blood pressure at the level of both head and heart; (iii) increasing blood pressure at heart-level brought on by venous pooling. Of these, only the latter two techniques are used in high performance aircraft. If a pilot is placed in a reclined position, the effect of the inertial vector is reduced and tolerance increased (Burton & Shaffstall, 1980; Cohen, 1983). However, the angle of the seat required to provide significant improvement would have to be at least 45 degrees fiom vertical, currently an irnpractical soIution to the problem. An alternative is to increase blood pressure at heart-level above normal values.

1.4 Traditional Methodologies Against +Gz Exposure

Systemic artenal pressures can be raised with the pressurization of a pneumatic counterpressure garment (anti-G-suit, or most cornmody referred to as G-suit) in combination with muscular straining. These traditional techniques have been successfully employed by aircrew for the past 40 years. Recent emphasis has been placed on finding improved methodologies due to the high, sustained +Gz capability of new generation tactical aircraft.

1-4.1 The G-Suit

The currently operational G-suit is comprised of five interco~ectingbladders enclosed in a fabric shell. The bladders are situated over the pilot's abdomen, thighs, and calves. A G-valve (a regulator sensitive to alterations in the +Gz level), pressurîzes the lower body pressure garment according to a preset schedule of 1.5 psi/+Gz (10.34

kPa/+Gz in S I units) beginning at +2 Gz.' Pressurization of the G-suit Limits venous congestion by controlling the blood vesse1 transmural pressure (Buick & Porlier, 1987) and assists venous return through an elevation of intra-abdominal pressure. A G-suit has also been shown to increase peripheral vascular resistance (Lindberg & Wood, 1960). AIthough G-intensity tolerance is improved by approximately 1 +Gz above a non-protected state (Burton et al., 1973; Wood, 1987), the cardiovascular mechanisms associated with these changes have yet to be fully elucidated.

1.4.2 Anti-G Straining Maneuvers (AGSM)

In addition to the protection provided by a lower body pressure garment, blood pressure can be M e r ïncreased if the pilot performs an anti-G straining maneuver

(AGSM). A straining maneuver involves the tensing of al1 the muscles of the body, particularly those of the legs, amis and abdomen, and the development of high intrapulmonary pressures by expiratory efforts against a closed/partially-closed glottis (Wood, 1947; Wood & Hallenbech, 1945; Wood et al., 1981). The respiratory component of the AGSM, coupled with isometric tensing of the musculature, requires proper execution and c m be very fatiguing to the pilot. A properly performed straining maneuver will, however, allow pilots to widistand gravitoinertial forces in the +9 G z range for short durations (Parkhurst et al., 1972). Pressure Ievels in Iife support system design have traditionally been expressed in empirical units. To convert units: 1 psi = 5 1.7 I5 mmHg = 6.985 kPa

1.5 Advanced +Gz Protection Systems

Current developments for improving +Gz tolerance include design of G-suits with greater surface coverage, and the implementation of positive pressure breathing during +Gz (PBG). 1S.1 H k h Coveraee Lower Bodv Garments

G-suits manufactured with larger bladders (greater surface coverage of the lower extremities) have demonstrated improved protection to +Gz (Green, 1993; Wood & Lambert, 1952). Increases in blood pressure were attributed to a higher peripheral vascular resistance and concomitant maintenance of thoracic blood volume (Sieker et al., 1953). Tolerance to +Gz was maximized using G-suits with the greatest surface area

coverage and pressurization to the highest tolerable pressures (Wood, 1988a).

1.5.2 Positive Pressure Breathinp Durinrr +Gz (PBG)

Positive pressure breathing requires a madified breathing regulator. The PBG regulator increases the gas pressure in the pilot's oronasd mask in proportion to the +Gz level. Mask pressures are determined by the pressure level inside the G-suit. A pressure sensor provides feedback to the breathing regulator and ensures that mask pressure is not raised in the absence of lower body counterpressure. Pressure breathing raises and maintains intrapulmonary pressure throughout the respiratory cycle (Buick et al., 1992). The imrnediate resultant increase in systernic artenal pressure approaches the applied innapleural pressure (Emsting, 1969). Aithough hi& intrathoracic pressures have been f o n d to reduce venous return, stroke volume, and

cardiac output (Ackles et al., 1978; Balldin & Wranne, 1980; Bjurstedt et al., 1979), the detrimental effects are partially countered with the pressurization of the G-suit (Bazett & Macdougall, 1942; Ernsting, 1969).

PBG Ievels less than 30 mmHg c m be used for 20 to 30 minute intervals at the cost of producing fatigue due to the added work during expiration (Ernsting, 1969). To recti@ this problem and allow exposure to higher levels of positive breathing pressures, a counterpressure jerkin or vest was developed. The jerkin provides force against the chest w&.

This limits lung expansion, aids expiration against an increased intra-pulmonary

pressure, and reduces the work of breathing (Ernsting, 1969). By Iimiting the expansion of the chest and providing a greater intrapleural pressure for a given airway pressure, the counterpressure jerkin increases pulse pressure and rehims arterial pressure to approximately 80% of the appiied intrapleural pressures (Emsting, 1969; Shaffistall& Burton, 1979). Full scale investigation of PBG was initiated in the early 1950s. PBG was found to improve both intensity (Clère et al., 1988; Pecaric & Buick, 1992) and duration (Burns & Balldin, 1988; ShafKstall & Burton, 1982) tolerance to +Gz. This would support PBG

as a viable alternative to the AGSM or possibly aid in augmenting acceleration protection through a combination of AGSM and assisted PBG. n i e curent PBG schedule used by the Unites States Air Force (USAF) has an application rate of 12 mm Hg/+Gz beginning at +4 Gz. A maximal pressure level of 60 mm Hg is provided by the regulator at +9 Gz (Bomar, 1985). Other studies (Pecaric & Buick 1992; Pecaric et al., 1995) have suggested that PBG commence earlier. Maximum pressures as high as 80 mmHg have been used in previous investigations (Pecaric & Buick, 1992).

1.6 G-valve Performance 1-6.1 Factors Influencing G-valve Res~onsiveness

Factors which influence the pressure output profile (pressure plotted as a function of time) from a G-valve c m be grouped into 2 categories: (i) extrinsic factors;

and (ii) intrinsic factors. Extrinsic factors alter pressure demands, while intrinsic factors

influence the G-valve's ability to meet these needs. Extrinsic factors include: (i) the rate of +Gz onset; (ii) the highest +Gz level attained (Le., plateau level) (iii) the pressure requirement for each +Gz increment (i.e., the G-suit schedule); and (iv) the design characteristics of the G-suit, specifically the volume of the G-suit and ifs resistance to

flow. Intrinsic factors are related to the actual design of the G-valve which control flow capacity, and include any electro/mechanical deiays in responsiveness.

1.6.2 Demands fiom an Imriroved Flight Performance Envelope

Early tactical aircraft were limited to short durations at high +Gz due to thrust limitations. Consequently, the performance of the G-valve was not a factor in +Gz protection. With technological advances in aircraft design, new generation aircraft are capable of maintaining high +Gz for extended durations. A critical repercussion of the improved aircraft performance envelope is the potential for an inadequate G-valve response. With rapid onset to +Gz, flow requirements rise in order to attain the requisite pressure level in a shorter time period. The "traditional" Alar anti-G valve has been s h o w to provide lower flow rates in cornparison to electronically controlled systems at

+Gz levels less than +6 Gz (i-e., within the normal +Gz envelope of the CF-18 aircraft). A "sluggish" response in a rapid +Gz onset environment wouid only M e r exacerbate

the flow inadequacies if design requirements of the life support system result in higher demands on the G-valve.

1.6.3 Influences of Life Sup~ortSvstern Desim

Life support systems are dependent on the G-valve's ability to pressurize a Gsuit as a fiuiction of the acceleration Ievel, and in a timely manner. When a "slow responding" G-valve is combined with an extended coverage G-suit (i-e., a G-suit with larger bladders), its apparent performance codd be M e r impaired. As a result, the time

necessary for the G-suit to attain its maximum pressure at a given +Gz ievel is delayed

(Lewis, 1955). Since the level of G-suit pressure provides the stimulus for the initiation of PBG, the pressure increase in the oronasal mask would also be af5ected. The potential to improve +Gz tolerance by increasing the pressure in the G-suit

has been reported in early investigations (Wood, 1988a; Wood & Lambert, 1952; Wood, 1987; Wood, 1990), leading to a greater flow requirement £kom the G-valve. Conversely, as lower body coverage increases, there is a higher risk of discornfort uskg traditional schedules, perhaps due to visceral displacement (lewis, 1955). Recent research using extended coverage G-suits (Ossard et al., 1994; Pnor, 1991) has proposed a decreased Gsuit pressure to minimize this problern. Both studies cited an improvement in comfort with a lower G-suit pressure, without compromised +Gz protection. Therefore, the

greater flow requirements imposed by larger bladder volumes may be negated by the decreased G-suit pressure schedule.

1-6.4 G-valve Responsiveness Studies

Several studies have exarnined the influence of G-valve responsiveness, but the fmdings fiom them are conflicting. A slow responding G-valve would logically be expected to decrease +Gz tolerance. The literature is varied dong this topic. Experiments using both mechanical (Burton et al., 1973;Burton et al., 1980) and electronic (Crosbie, 1983) G-valves have shown increases i n G-tolerance in the 0.4 to 1.3 +Gz range when using improved G-valves. Conversely, when Cammarota (1987) compared +Gz tolerance using the currently operational G-valve, a rapid response servo valve, and a servo valve programmed to anticipate the onset of +Gz by 0.5 seconds, no differences in either Gintensity or G-duration tolerance were found. Burton (1988) showed no difference in Gtolerance when G-valve output was delayed by as much as 3.3 seconds when subjects wore a traditional anti-G suit.

The lack of consistency may be due to the nature of the metrics used to assess changes in +Gz tolerance. Some investigations (Burton et al., 1973;Burton et al., 1980; Burton, 1988; Carnmarota, 1987; Crosbie, 1983) lacked objective physiological data to support their fmdings. The short acceleration profile durations, in combination with technological limitations, prevented detailed blood pressure r n o n i t o ~ g .Consequently, assessrnent of +Gz protection was usually based on subjective feedback regarding the amount of visual light loss o c c w g during the acceleration profile. To date, little ernpirical data provides insight as to how the various facets that comprise an acceleration protection system (Le., pressure schedule, surface coverage, and PBG level) affect the cardiovascular response to +Gz with and without alterations in G-valve responsiveness.

1.7 +Gz Tolerance Measurement: Vision and Blood Pressure 1.7.1 Historical Bases for Modern Methodologies The relationship between blood pressure and vision has been extensively studied in both laboratory and flight environments. Tolerance to +Gz was initially associated with the visual symptoms encountered by aircrew. An early report of a test pilot

experiencing a graying of the visual field and subsequent loss of consciousness occurred in

19 18 (Head, 1920). While flying in a +4.5 Gz turn, he "experienced the characteristic darkening of the sky". Through tnal and training, pilots became aware of these visual changes, and knew that increasing the +Gz level would lead to a M e r decrement in visual acuity and loss of consciousness. As the pilot c o d d not fly the aircraft without a visual reference, the symptomatic changes in vision became a pilot's primary indication of his ability to withstand the increased gravitational environment. Tt wasn't until the onset of the WW2 that these visual deficits were related to

systemic decreases in blood pressure. In 1946, Lambert and Wood (1 946) used puncture of the radial artery to correlate a drop in blood pressure with changes in vision. A strain

gauge manometer was used to activate a galvanometer. The subject was then placed inside the centrifuge with the wrist supported at the level of the heart or eye. The centrifuge was accelerated to various +Gz levels and Light signals were used to determine the extent

of visual light loss. Vision was found to be unimpaired if eye-level systolic blood pressure rernained above 50 mmHg. Systolic blood pressures less than 20 mmHg would result in complete loss of the visual field. Hence, blood pressure decreases were associated with the visual disturbances incurred during high +Gz exposure. Development of a near infia-red device for measuring pulsatile blood flow at the ear provided a secondary objective rneasure. Continuous recordings of intra-artenal blood

pressure and pulse amplitude during multiple +Gz exposures in various subjects have documented that loss of the ear pulse and zero arterial pressure at head level were aiways coincident events (Wood et al., 1988). In more than 50 incidents of loss of consciousness observed on the Mayo hurnan centrifuge and in-flight, a period of at least 4 seconds of zero or very near zero ear opacity pulse invariably preceded loss of consciousness (Wood et al., 1988). Direct intra-artenal pressure measurements (Lowry et al., 1953; Wood, 1988a; Wood & Lambert, 1946) recorded simultaneously with photoelectric plethysmographic tracings (Wood, 1987; Wood & Lambert, 1946) have confmed the physiological significance of these fmdings.

1.7.2 Determining +Gz Tolerance Usino End~oints

In evaluating the effect of a G-suit, Wood and Lambert (1946) used a hurnan centrifuge to increase the +Gz level while recording changes in reported visual syrnptoms; blood content of the ear, ear pulse amplitude, and blood pressure at the eye. Texmination of each exposure occurred when the subject had complete loss of the visual field. Predetermined changes in the magnitude of the physiological sipals were used to defhe

+Gz tolerance. The relative increase in G-intensity tolerance with a G-suit, as deterrnined

by the visual symptoms and the different techniques (blood content of the ear, ear pulse amplitude, and blood pressure) were 1.4, 1-5,1.7, and 1.7 G, respectively. The consistency of the four methods indicated the validity of using visual changes as a mesure of acceleration tolerance. The exposure of a subject to an increasing +Gz level until visual blackout was expenenced became a common technique of monitoring +Gz

tolerance in early centrifuge studies (Edelberg et al., 1956; Lund, 1947; Stoll, 1956; Zuidema et al., 1956). Lambert (1950) monitored the various stages of visual li&t loss in an aircraft and compared his results to those obtained fiom studies using a human centrifuge. A passenger in an aircraft was exposed to increasing acceleration levels in stages of 0.5 to 1.O

+Gz until they reported they had lost vision completely. Lights were mounted 23 degrees on either side of a fixation point. The visual field was reported as being clear, dirn, lost peripherally, or lost completely as detennined by the subject's response to light signals. Peripherd light loss was indicated by failure to respond to the peripheral lights. Complete loss of vision was recorded if the subject failed to respond to the peripheral lights and to another positioned at the fixation point of vision. Continuous recording of ear opacity and ear opacity pulse was performed using a photo-electric technique. Ear opacity was reduced to 50 percent or less of the control (measured pnor to acceleration)

in 75 percent of the exposures in which dimming of vision occurred, and in al1 conditions in which blackout was recorded. Visual syrnptoms, +Gz tolerance, and ear opacity

results were consistent with those reported during centrifiige investigations. The visual changes were found to occur in two stages. Peripheral light loss was expenenced early and at lower +Gz levels. A m e r increase in the gravitational force would cause visual blackout. The assessment of peripheral and central light loss is a proven technique and has been used in modem centrifuge studies (Balldin et al., 1989; Bums & Balldin, 1988;

Burton et al., 1980; Burton, 1988; Clère et al., 1988; Parkhurst et al.? 1972; Shaffçtall& Burton, 1979). Using a senes of lights strategically located in the visual field permits the subject to quanti@ the amount of light loss associated with +Gz levels lower than those producing complete visual blackout. It aiso provides a w h g of the irnpending +Gz limit that the subject can withstand. Hence, it is of vital importance that the subject identifies the varying degrees of light loss as he experiences +Gz levels approaching his tolerance lunit, and terminates the exposure before losing consciousness. The measurement of light loss provides valuable data in assessing the physiologicai state of

the subject and sirnulates the changes in visual acuity that effect pilot performance.

1.8 Non-Invasive BIood Pressure Measurement: The Finapres 1-8.1 Rationale

Difficulties and risks associated with catheterization procedures (sepsis, clotting, etc.) necessitated alternative methodologies for monitoring blood pressure. Although a standard method in clinical medicine, the Riva-Rocci/Korotkov method provided limited data in acceleration studies due to the relatively short duration of a +Gz exposure. It wasn't until the mid 1970's before a practical solution was achieved. A technique developed by Penaz (1 973) provided a beat-by-beat estirnate of systemic arterial pressure

using a finger cuff. The continuous analog output fiom the Finapres blood pressure monitoring system enabled simple, unobtrusive measurement of the various components of the pressure wavefom (Le., systolic and diastolic blood pressure, etc.).

1-8.2 Clinical Validation

Preferably, a non-invasive approach should provide robust and reproducible values comparable to its invasive counterpart. An investigatiori by Molhoek and colleagues (1984) on hypertensive patients using an early version of the Finapres unit indicated that both systolic and diastolic blood pressures were marginally underestimated

by the Penaz method when compared to values from an indwelling artenal catheter. The difference in blood pressure between the two techniques was thought to be caused by the

6 mmHg pressure gradient behveen the brachial artery and the arteries of the hand. Smith et al. (1985) found a strong correlation between ha-arterial blood pressure and the values measured using the Penaz technique. However, some offset in systolic values was noted which was amibuted to differences between arm and finger penpheral resistance. Shi et al. (1993) observed a very strong correlation between changes in intra-radial pressures and those deterrnined using an improved Finapres system. In subjects requested to perform a Valsalva maneuver, the Finapres underestimated both systolic and diastolic blood pressure components (Imholtz et al., 1988). Brachial artery to finger pressure differences showed lirnited deviation Erom those during the control period. With a straining maneuver, rnedian differences were at most 6 &g,

which were found to occur late d u ~ the g intrathoracic strain penod. A 7 mmHg

discrepancy was recorded during the post-release blood pressure overshoot. Most of the pressure drop was attributed to resistance differences between recording sites due to muscular tensing. Alterations in vascular resistance between the two recording sites during the maneuver was found to result in a spectral frequency shift, most of which could be removed with a simple filter (Wesseling et al., 1995). The rapid response of the Finapres system (a very short time constant of less than 10 rnilliseconds (Boehmer, 1987)) allowed accurate tracking of al1 components of the pulse contour. Thus, relative changes in blood pressures were only marginally affected. These large changes in vascular resistance dong the peripheral vascular tree would not be expected to occur in relaxed (i-e., nonstraining) individuals. Over 300 studies have used the Penaz technique for recording blood pressures at +1 Gz. The non-invasive methodology has been found to provide reliable and valid

measures of true changes in blood pressure. Data collected using this technique has been

used to track vasomotor responses (Shi et ai., L996), to calculate relative cardiac output changes fiom the pulse contour (Stok et al., 1993), in spectral anaiysis of baroreceptor function (Constant et al., 1995), and to record blood pressure variability during anesthesia and the proceeding recovery period (Omboni et al., 1993).

1-8.3 Irn~lementationin Centrifiige Ex~eriments

Evaluation of the Finapres system was first performed in the centnfbge by McKenzie and Glaister (1988). Finapres output during headward acceleration (+Gz) was measured with and without G-suit inflation. An onset rate of 1 +Gz/s was used. The values obtained fiom the Finapres unit were compared against values reported in the literature. The blood pressure monitoring system operated normaily up to the +9 Gz test limit. Improved tolerance was correlated with elevated systolic and diastolic blood pressures.

For the past decade, systems based on the Penaz technique have been successfully used in numerous acceleration investigations. Although slight offsets in values are evident, the general consensus remains that the non-invasive systems provide an accurate estimate of systemic blood pressure change.

1.9 Purpose of the Study A footward gravitoinertial force (+Gz) fiom headward acceleration produces

hydrostatic gradients in the fluid filled areas of the body. These, in tum, decrease

pemision pressures at head level and shift blood towards dependent regions. To compensate for the compromised blood pressures at head level, life support systems have been designed to counteract these adverse physiological sequelae. Individual facets of a life support system have been shown to influence tolerance to +Gz, including the level of pressure to the G-suit, the responsiveness of the G-valve, the arnount of lower body

surface coverage, and the level of applied PBG. A comprehensive investigation into how the various cornponents alter the cardiovascular response and, concornitantly, alter tolerance to +Gz is required before an optimal strategy can be suggested. The purposes of the smdy were to: 1. examine the changes in +Gz tolerance resulting fiom alterations in the various facets that comprise an acceleration protection system (G-suit pressure, G-valve responsiveness, lower body surface coverage, and PBG) using both objective and subjective measures; 2. atternpt to explain how these perturbations affect both cardiac and vascular functioning; and

3. suggest potential strategies for improving future protective systems.

1-10 Hypotheses

It was hypothesized that +Gz tolerance would: 1. increase with the increased level of pressure applied to the G-suit;

2. decrease with the increased delay in G-suit pressurization; 3. increase with increased lower body surface coverage; and

4. increase with the increased level of pressure applied by the PBG schedule.

METHODS 2.1 Selection of Independent Treatment Variables

The treatment variabIes used in the investigation included: (i) +Gz level; (ii) amount of lower body coverage; (iii) G-suit pressure schedule; (iv) G-valve responsiveness; and (v) PBG scheduie. 2.2 Controi of +Gz 2.2.1 Selection of Acceleration Levels and the Human Centrifuge

The +Gz leveis selected for the investigation ranged fiorn +2.5 Gz to - 6 0Gz, increasing in half +Gz incrernents. The lower limit (+2.5 Gz) was the minimum +Gz level at which the operational G-valve in the aircrafi provided pressure to the G-suit. The highest +Gz level at which al1 subjects could complete the majority of conditions (+5 Gz) established the upper +Gz limit of the study. Exposure to accelerative forces was performed with the passively girnbaled human centrifuge located at the Defence and Civil Institute of Environmental Medicine

(DCIEM), Toronto, Ontario. Subjects were seated in a gondola at the end of the 6.15 meter (20 foot) arm (Figure 2-1). The seatback angle of the chair was fmed at 22 degrees fiom vertical. A cornputer altered the radiai velocity of the gondola in order to produce the

requisite acceleration level. As the radius (r) of the inscribed circle was fixed (Le., the gondola position on the centrifuge ami never changed), the resultant radial acceleration and gravitoinertial force (G) were a function of the angular velocity (a)according to the equation 2- 1:

a, = G = n'r pqn. 3-11

As the gondola accelerated, the increase in c e n a g a i force rotated the gondola such that the subject was repositioned from the normal vertical orientation to a horizontal one. The head was then oriented towards the center of rotation. Consequently, the subject experienced headward acceleration and footward gravitoinertial forces (+Gz).

FRONTAL VlEW

tcninlugal Farce

Figure 2-1 :Simularing the high + Gz nircombat environment. A. Photograph of the human centrtfuge located at DUEM. B. Schematic representation of the gondola orientation. Gimbals allowed the gondola to rotate outwarh, such that the direction of the radial + Gz vector (i.e., centrifuga1force) was in-line with the Zongitudinal m i s of the 6.15 rneter centrifuge a m .

To ensure safety, the angular velocity of the arm was determined by a tachometer and compared with required values. An "enable switch" allowed the subject to begin and terminate an experimental condition. The gondola was equipped with a modified aircraft ejection seat and restraining hamesses, video and audio communications systems.

2.2.2 The Acceleration Profile

Rapid +Gz onset rate (ROR) profiles were used in the investigation (Figure 2-2). The gondola was k t accelerated gradually at 0.1 +Gzk to the standard baseline level of +1.4 Gz. Centrifuge arm revolutions increased such that the acceleration was altered fiom

The gondola was then immediately accelerated to peak baseline to +1.8 Gz at 0.2 +Gz/s.

+Gz at an effective acceleration rate of +2 Gz/s. The onset of +Gz resembled a haversine fimction, gently rounded at the Iow and peak +Gz levels, with the greatest rate of onset in-between these two points. This produced rapid, yet smooth changes in +Gz level. Provided the physiological end-point critena had not been reached (discussed later), the gondola was held at peak +Gz for 12 seconds. Following completion of the plateau or release of the enable switch, the gondola was decelerated at 1 +Gzkec to baseline +1.4

Gz, then eased to a fuIl stop. Profiles with varying +Gz plateau levels were repeated with alterations in the experimental treatment conditions.

+5 Gz plateau

-I

Baseline 3-1.4 Gz

Time (s) Figure 2-2: Graphieal depiction of a rapid onset rate (ROR) profle to +5 Gz. The omet rate was approximately 2 +W s e c and the plateau level was maintainedfor 12 secondrfor all treatment conditions. Note thatprofile onset was measured ut the time justprior to the gondola attaining + 1.8 Gz.

2.3 Lower Body Coverage Three G-suits (Figures 2-3 and 2-4) with increasing surface coverage were used in the protocol: 1. standard issue (CSU-1 S E , Irving Industries, Fort Erie, Ontario)

2. prototype extended coverage G-suit (STING, DCIEM, Toronto, Ontario)

3. experimentai full pressure half suit (FPHS, David Clark Company, Worcester PA) The STING G-suit (Figure 2-3) incorporated circumferentid bladders over the thighs and lower legs (Buick, 1993). Compared to the traditional CSU-1 5/P G-suit, abdominal coverage was similar. However, the extended coverage G-suit provided approximately 90% more surface coverage to the lower exwemities. The Full Pressure Half Suit (FPHS) maximized the amount of counterpressure applied to the lower body (Figure 2-4). It consisted of a nomex shell segmented into two compartments. Air was applied directly to each leg, and a larger bladder pressurized the entire abdominal area. Modification of the FPHS by the manufacturer was perfomed in order to improve subject cornfort and functionality. The original version of this garnient used in previous experiments (Beckrnan et al., 1955; Lewis, 1955) provided counterpressure posteriorly fiom the buttocks up to the level of the xiphesternal notch. Each garment was individually fitted to a subject. Tightening of G-suit laces was performed with the subject standing. A snug fit was ensured by hand tightening of the laces to remove excessive string length. A loop was tied at the end of the lacing. The hook on one end of a scaie (hst-t, Chatillon, NY) was then passed through the loop. Tension was produced by pulling on the fiee end of the scale until a reading of 4000 gm was registered. The lacing was then knotted at this kngth, and secured with an additional

piece of medical grade tape. Standardization in lacing tension ensured that there were no differences in the snugness of fit.

Figure 2-3: The CSU l5/P and S T ' . G G-suits. A. Frontal view of CSU-WP G-suit. B. Posterior view. C and D. S T N G G-suit. Note the increased bladder coveruge predominantly in the Zower extrernity regiom

Figure 2-1: The rnodzjîed Full Pressure HalfSuit (FPHS)). A. Frontal view. Note the extended bladder coverage encompassing thefeet. B. Posterior View C. Schematic representation. Air is supplied via the input hose at the level of the thigh. Pressure is W i e d directly to the lower extrernities below the reflected rubber seal. A large bladder provided pressure to the anterior abdominal region.

2.4 Lower Body Pressurization

Electronic (Le., cornputer) control of the G-valve output allowed manipulation of

the pressurization schedule. Changes in G-valve responsiveness were simulated with the addition of delays before pressurization of the lower body garment comrnenced. Fwther informatioli regarding the pressure regdators for G-suit pressurization and PBG, and their control, is located in Annex A.

2.4.1 G-suit Pressurization Schedules Pressure to the G-suit was provided as a fùnction of the acceleration Ievel. Three pressurization schedules prograrnrned into the G-valve control cornputer were:

1. Nominal Schedule: 2. Low Schedule: 3. High Schedule:

1.50 (Gz - 2) psi 1.00 (Gz - 2) psi 2.00 (Gz - 2) psi

The nominal schedule is currently employed in tactical aircraft. During an acceleration exposue, pressure to the G-suit comrnenced once the subject experienced more than +2 Gz and increased at a rate of 1.5 psi/+Gz. Selection of the Low schedule was based on the acceptable pressurization levels reported by Lewis and co-workers (1955) for subjects wearing the Full Pressure Half Suit. In their study, d l subjects reported severe epigastric pain when pressures ranged between 5 to 7 psi. Similar discomfort problems were reported in other investigations

(Becban et al., 1955; Cochran et al., 1954). Maximum pressures attained at +5 Gz using Low and Nominal schedule were less than or equal to 4.5 psi, thereby potentially reducing the likelihood of abdominal discomfort with the FPHS.

The High schedule provided an equally divergent change in pressure per +Gz when compared to the traditional G-suit schedule. In a prc-vicus PBG investigation, a similar G-suit pressurization schedule was used by Pecaric and Buick (1992). Subjects

easily tolerated the higher G-suit pressure while wearing CSU-15P G-suits. Although the modified G-suit pressure schedule did not improve +Gz tolerance, the effect of an increased pressure with an extended coverage G-suit required further study. Figure 2-5 provides a graphic depiction of the three G-suit schedules.

6.0

High

-

Nominal

4.5 -

Low

3.0 -

1.5 -

O

I

I

i

Figure 2 3 : The three G-suit pressure schedules used in the experiment. Pressure was applied to all G-suits beginning at +2 Gz. The rate ofpressurization dzffered, such that pressure was either O. 5 psi/G Zower (Loy) or higher (High) than the haditional schedule (nominal).

2.4.2 G-valve Res~onsiveness

In order to evaluate the effect of a delay in G-suit inflation, a "theoretically ideal" condition was established. In this experiment, a "No Delay" condition was simulated by tracking the signal fiom the centrifuge control cornputer to the centrifuge motor. Due to the mechanical delay between voltage input to the motor and the subsequently delayed

increase in centrifuge arm revolutions (+Gz), it was possible to apply pressure to the G-

suit slightIy ahead of the actual acceleration level (i.e., pressure to the G-suit preceded

+Gz). This type of rapid response simulated an advanced system in which pressure to the G-suit was govemed by the amount of deflection in the pilot's control stick (Preview Control concept). The mechanicd delay ( t h e from movement of the control stick until the aircraft's acceleration level was altered) would remove any pressurization delays encountered during inflation of the G-suit. This type of control system has been speculated to provide the best protection to +Gz (Goldenberg et al., 1987; Jacq & Damico, 2982). Discrete delay intervals were then introduced relative to the "No Delay" condition.

Burton (1 988) fomd that a 4.2 second delay was required before visual changes caused the subjects to teminate the +Gz profile. Visual endpoints, attained early into the acceleration profile, occurred very rapidly and to levels approaching blackout. Further delays would probably have increased the likelihood of G-LOC. As objective physiological measurements would most likely have been evident prior to these degradations in vision, a comparable delay of 4.5 seconds was set as the môllmum interval for this investigation. Inflation of G-suits using curent and future generation G-valves would have been completed in Iess than 4.5 seconds. Shorter delay intervals were required to simulate their performance. Burton, however, reported that visual changes were only evident with delays greater than 2 seconds. As a compromise, two intermediate delay intervais were selected between the "No Delay" and maximum delay conditions. Four responsiveness

conditions were, therefore, used in the study: 1. 2. 3. 4.

No Delay (G-suit pressure followed or slightly preceded +Gz) 1.5 second delay fiorn condition 1 3 .O second delay fiom condition 1 4.5 second delay from condition 1

The relationship between +Gz and pressure in the G-suit is shown in Figure 2-6.

In order to present both tracings using the sarne ordinate, units were normalized to percentages of maximum pressure and +Gz. Time zero (tO) denotes the interval in w-hich the centrifuge control input corresponded to the +2 G z equivdent, the t h e at which a preview control system wouid commence pressurization of the G-suit.

-+Gz

I

O

8

8

8

---

G-suit Pressure

8

Time (s) Figrre 2-6: A lterations in G-valve responsiveness via the introduction of delays into the presszrrization schedule. Note that in the No Delay condition G-suit infation precedes + Gz Al1 subsequent conditions were dehyed in 1.5 second incrernents.

2.5 Positive Pressure Breathing (PBG)

Pressure breathing was supplied by a cornputer controlled breathing regulator. Output fiom the regulator passed through a "Y" connector (Integrated Terminal Block, Gentex, Corp.) to a pressure sealing mask and helmet (TLSS, Gentex Corp.), and an upper body garment (Mustang Industries, Fort Erie, Ont.). This ensured that the pressure in the mask and jerkin were equal. The jerkin was fïtted such that the subject

could perform a vital capacity maneuver without the jerkin afEecting inspiration.

Positive pressure breathing, when applied, followed one of two schedules: 1. Low PBG Schedule: 12.5 (Gz - 3.5) rnrnHg 2. High PBG Schedule: 25.0 (Gz - 3.5) d g

The two schedules are shown in Figure 2-7. The High schedule has been proposed for irnplementation into CF-18 aircraft (Buick & Pecaric, 1993). The rate of pressurization was reduced by half in order to obtain the Low PBG schedule, one similar to that used by the United States Air Force (Bomar, 1985). Note that no pressure was provided to the oronasal mask for acceleration levels less than or equal to +3.5 Gz.

High

Low

USAF

Figure 2-7: PBG schedzrles used in rhis experimenr. The dope of the High schedzrle was twice that of the Low. The Low schedde was comparable to that used by USAF.

2.6 Treatment Combinations Used in the Investigation The resultant combinations used in the investigation are presented in Figure 2-8.

Al1 treatment combinations were not possible at each +Gz level. Only the "No PBG" condition was applicable for +Gz conditions at or below +3.5 Gz, as both pressure

breathing schedules commenced mask pressurization above this level. In addition, the

Kigh G-suit schedule was not used with the Full Pressure Half Suit, nor was a 4.5 second delay introduced when subjects wore this garment.

G-suit Coverage

G-suit Schedule

Pressure Delay

PBG Schedule

Pressure Delay

PBG Schedule

+(-)t

Pressure Schedule

G-suit Coverage

G-sui t Schedule

~(Lz-)

in Pressurîmtion

in Pressunzauon

Figure 2-8: Flow diag-am outlining the independent variable combinationsfor each + Gz level. Note that only the "No PBG" treatment was applicable at acceleration levels at or below +3.5 Gz. Only the Low and Nominal G-suitpressure schedules were used with the FPHS ensemble.

2.7 Experirnental Design 2.7.1 Factors Influencing Emerimentai Design

Time constraints for the facility played a significant role on the number of experimentd sessions that could be completed. In order to meet these limitations, a design was developed that maxùnized the amount of information collected over the relatively short window available. The protocol was approved by the DCIEM Hurnan Subjects Ethics Committee. Due to time constraints upon the requisite facilities and from subject availability limitations, there was insufEcient time for a complete evaluation of the protocol by the University of Toronto 's Human Subjects Review Committee. This was brought to the attention of and discussed with the Office of Research Studies (meeting, University of Toronto, November 29, 1995).

2.7.2 Main Ex~erimentalDesim

Six subjects were exposed to al1 G-suit, G-suit pressure, time delay, and PBG combinations show in Figure 2-8 over 10 sessions (refer to Annex B for the experimental protocol assignment for one of the subjects). Each session was comprised of a "warmup" profile, 36 treatment conditions, and a "control series". Subjects "warmed-up" with a single exposure to G . 0 Gz prior to beginriing data collection in order to remove any first nin

effect (Denton, 1993). No pressure was supplied to the lower body garment during

this exposure and the data were not included in the subsequent analyses. Treatment conditions were grouped into three phases, each phase being comprised of 12 conditions. One minute separated each +Gz exposure, and a 5 minute rest interval followed the completion of a phase. The average subject received 45 +-Gzexposures/day, with the 10 sessions scattered over a two month period.

One control series was performed during each session, either before the start of a phase or at the end of the experiment (random assignment). This series of profiles consisted of centrifuge exposures beginniog at +2.5 Gz. No pressure was provided to the

Iower body garment. The acceleration plateau was increased in 0.5 +Gz increments until the subject reached hisher relaxed +Gz tolerance. This was defined as the +Gz plateau during which the subject experienced pre-syncopa1 symptoms and released the enable switch, or when early termination of the profile by the Run Director fiom a prolonged absence of an ear pulse (discussed later) resulted. Sessions were assigned using a semi-counterbalanced design to allow completion of al1 conditions with either the CSU-15/P or STING G-suits before beginning sessions with the alternate garment. This minimized the risk of inconsistent garment tightness associated with refitting of the G-suits. As the Full Pressure Half Suit was unavailable

until the later stages of the experiment, sessions using this garment were run as CSU-15/P

and STTNG conditions were nearing cornpletion.

2.7.3 Additional Conditions

The mechanical Alar valve provides a lower flow rate, which decreases as the pressure in the G-suit is increased. Therefore, the amount of "lag" increases as a fimction of time. As an electronic high-flow G-valve was used to pressurize the G-suits, time delays were simulated in relation to the centrifuge control input signal. This control strategy, in combination with an irnproved flow capability, resulted in difFerent pressure profiles (pressure plotted as a fùnction of t h e ) than found using the operational G-valve. DifEerences would have been expected to be M e r exacerbated with greater volume demands associated with increased lower body coverage and/or a higher pressurization schedule. As the performance characteristics of the mechanical G-valve used in the operational environment differed fiom it's electronic counterpart, a series of additional experimental conditions were necessary. A brief senes of acceleration exposures was conducted in order to: (i) quanti@ and compare the pressure profiles of the electronically and mechanically actuated G-valves; and (ii) to provide a basis for comparing the

cardiovascular response to +Gz in the two G-valve conditions shodd it have been necessary .

Three subjects were selected to undergo a single experimental session using one of the three G-suits. Subjects were exposed to three repetitions at each +Gz level, ranging fiom +2.5 to t5.O Gz with half +Gz uicrements. The currently operation G-vaive (Alar, Mode1 14050, high flow, Cleveland OH) pressurized the G-suit according to the Nominal G-suit pressure schedule. The computer controlled regulator provided PBG according to

the High schedule. A "warmup" exposure to +3.0 Gz preceded data collection. A series of controi nuis (no G-suit or PBG pressure) was randomly performed at either the start or the end of the experùnentd session.

2.8 Subjects

Al1 subjects were given a minimum of 24 hours separation between each day of data collection and were requested to: (i) refrain from consurning any aicoholic beverages

within 24 hours of a centrifuge run; (ii) have a restful evening the night before a test; (iii) perform no heavy exercise on the day of a test; and (iv) abstain fkom smoking, coffee and chocolate in the 3 hour penod before a test, and a meal in the hour preceding it. Subjects were selected fiom the DCIEM acceleration research panel. This team consisted of four male and two female personnel. The ages of the subjects used in the protocol ranged fiorn

24 to 45. Five of the subjects had prior experience in cenhifuge experiments. 2.8.1 Medical Screening Before beginning the study, all acceleration research subjects had: (i) received a preliminary +3 Gz exposure to determine their acceptability of +Gz and the centrifuge environment; (ii) received fidl medical screening; (iii) received a full briehg of the purpose

and methods of the study; (iv) read the protocol document; (v) provided informed consent in writing (&ex

C); and (vi) had received refiesher training in perfonning the

anti-G straining maneuver and in using positive pressure breathing. The centrifuge medical screening was comprised of a wide battery of tests in accordance with the standards set by the Medical Screening board of the institute (DCIEM/MAT, 1988) and

are detailed elsewhere (Whinnery & Gilhgham, 1983). 2.8.2 Traininq

Subjects received at least one session of familiarization training pnor to beginning the experiment. Al1 were fitted with a CSU- 15P or STING G-suit, upper pressure

garment, and pressure sealing rnask and helmet. They were exposed to the entire range of acceleration profiles with various combinations of G-suit pressurization, G-suit pressure delay, and PBG level. The conditions were comrnensurate with those used in the actual experiment. A bnef exposure to higher +Gz levels with the subject perfonning an anti-G straining maneuver was included for those requiring refamiliarization with this technique. A training session usually consisted of a minimum of 30 cennifbge profiles. Training was

repeated for subjects that had not recently participated in an experiment or had reported

any symptoms of motion sickness. Additional training was provided to the subject having lirnited centrifuge experience. The subject was given his initial pressure breathing indoctrination sessions at +1 Gz. These sessions were performed in the centrifuge gondola with increasing PBG

levels ranging from 10 to 30 mmHg. Once the subject felt comfortable with the procedure, pressure breathing was then introduced during acceleration exposures. Training was not considered complete until a subject was: (i) able to perform a proper anti-G straining maneuver; (ii) comfortable with the procedures and physiological measuring techniques used in the experiment; (iü) able to remain relaxed during the centrifuge profile despite experiencing varying levels of visual light loss; (iv) unperturbed by the response of the life support equipment, including long delays in G-suit

pressurization, increased G-suit pressures, and positive pressure breathing; and (v) able to complete a training session without signs or symptoms of motion sickness.

2.9 Measurements 2.9.1 Gravitoinertial Force. Mask Cavity. and G-suit Pressure

The +Gz level was measured using an acceierometer (Systron Donner, Model 43 10-20-AGIM, Concord CA) mounted at heart-level on the centrifuge gondola seat. Validyne (Model 1538N 1S4A, Northridge CA) pressure transducers were used to measure mask cavity and G-suit pressures. Mask (Pm)and G-suit (P,) pressures were monitored through p a s located in the oronasal mask and the abdominal bladder of the lower body garment, respectively. The transducers were oriented with the diaphragm fixed in a vertical plane to the gondola, preventing diaphragm displacement by +Gz. 2.9.2 Blood Pressure

Beat-by-beat blood pressure was measured during +Gz by the non-invasive Finapres (Ohmeda, Model 2300, Englewood CO) system (Kurki et al., 1987; Penaz, 1973; Wesseling et al, 1986). The fmger-cuff of the unit was placed around the middle phalynx of the second digit. The fmger was secured at heart level by vertical adjustment of an arm sluig positioned around the neck which supported the hand. Cuffpressure was controlled automatically to provide beat-by-beat recordings. 2.9.3 Heart Rate

Heart rate was continuously monitored using an ECG (Marquette Electronics Inc.,

Model Case 12, Milwaukee WI) output. The electrocardiogram was used to monitor the heart's elecû-ical activity, rhythm and rate. ECG electrodes were adhered to each shoulder, two on the lower abdomen below the costal margin, and one in the V5 position. A Medical Officer monitored the ECG waveform for abnormalities (premature

contraction, bigeminy, trigeminy, etc.) during +Gz exposure. If an ECG abnormality

occurred and introduced a risk to the subject, the experimental condition was terminated and the type of ECG abnormality recorded. Any significant ECG abnomality disqualified the subject from participating in m e r experirnentation until he/she was medically cleared to continue. 2.9.4 Visual Light Loss Measurement

A black lightbar was located 86.5 cm (34 inches) in fiont of the subject. Two

bilateral green lights were located 40.5 cm (16 inches) fiom the center. This inscribed a visual angle of 25 degrees fiom center and positioned the image near the optimal

sensitivity area of the retina (Coren et al., 1978). A red third LED was situated in the center of the visual field. This configuration is similar to that reported in the literature (Cohen, 1983; Lambert, 1950). Contrat was assisted by the du11 white colour of the interior of the gondola. An investigator in the centrifuge control room could selectively illuminate either series of LEDs or both. An illuminated light was extinguished via assigned buttons on the centrifbge control column (Figure 2-9).

Figure 2-9: Lightbar and control colurnn inside gondola of centrrfge. The "enable switch" was located on the fonvardpart of the control stick and two pushbutton switches on the top, aaft surface were used to extinguish the lightbar challenges.

While looking straight-ahead, the subject was required to respond to an illuminated light by selecting the appropriate bution on the control stick. The lights were randomly illuminzted Sy an investigator, with the peripheral lights comprishg the majority of challenges early into the profile. Once the subject could not see the peripheral Iipht (an extended period in which the subject did not respond to the challenge and indicating complete peripheral light loss), the investigator began prompting the subject with the centrally located red light. Absence of a response to both lights was deemed complete visual loss (Le., blackout). The lightbar system verified the extent of the symptoms encountered by the subject and provided a temporal synopsis of visual changes during the centrifuge profile. Upon completion of the profile, the subject provided M e r information using a pre-determined scale. Worst peripheral, worst central, best peripheral (if improved) and best central (if improved) were categorized according to the criteria in Table 2-1.

Table 2-1: Classzj?cationof the Extent of Visual Changes during the +Gr Plateau

-p.

Terminology

Extent o f Vision Lost

Clear Dirn Grey Cornpiete Loss

1% to 49% 50% to 99% 100%

0%

2.9.5 G-suit Pressure Cornfort. Svstem Res~onse.and Fatigue

In addition to reports of visuai changes, subjects were asked to rate the comfoa level of the pressurized G-suit, the speed of the life support system response, and their level of fatigue using the scales shown in Table 2-2. A numerical value was provided for each parameter, which was recorded by the Run Director (refer to Annex D).

Table 2-2: Subjective Rating Scale used by Subjects to Evaluate G-suit Pressure Cornfort, System Response, and Fatigue

2.9.6 Electromvoma~hicand Ear Pulse Monitoring

Subjects were insû-ucted and trairied to remain relaxed for al1 +Gz exposures. To ensure an individual did not employ the anti-G straining maneuver, EMG was monitored.

EMG electrodes were placed on the rectus abdominus and vastus lateralis muscles. The signal amplitude was increased using isolated pre-amplifiers (Gould, Model 11-5407-58, Cleveland OH) located inside the centrifuge gondola. The outputs were then fed to a universal amplifier (Gould, Model 13-4615-58, Cleveland OH) and displayed on a monitor. Visual inspection of the signal on a rnonitor ensured that the subject did not employ an anti-G straining maneuver during the +Gz profile. The acceleration profiles normally exposed hurnan subjects to +Gz levels below those potentially causing unconsciousness. However, there still existed the possibility of

a G-LOC occuning for subjects with low +Gz tolerance, inadequate protection and/or failure of the G-protection systern. In either case, loss of consciousness codd have occurred if the +Gz level was sustained for a long enough penod of time (Le., approximately 5-7 seconds). For this reason, monitoring of circulatory events at head level was necessary in order to terminate the run if a condition of possible unconsciousness was imminent. Ear opacity was measured fiom the upper pinna of one or both ears using an unobtnisive earpiece. The opacity units were powered by a medical-grade AC power supply. This technique has been previously described, and has been used extensively in previous DCIEM investigations (Buick et al., 1993; Wood & Buick, 1994). Therefore, although some exposures to +Gz were near levels which could

cause unconsciousness, the duration of the exposure was restricted for only long enough to d o w 3 seconds of obliterated ear pulse, thereby avoiding G-LOC. Neither the EMG nor the ear puise data were used in the subsequent analyses.

2.10 Data Acquisition and Analyses 2.10.1 Data Acauisition Svstem

The scientific instrumentation used for data collection was located in the centrifuge gondola. The analog outputs were fed through slip rings to a muiti-channel recorder (Gould, Mode1 ES 1000, Cleveland OH). Physical and physiologicai data were concurrently collected on two computers (Apple Cornputers, Macintosh IIci, Cupertino

CA) at either a high (1000 Hz) or low (100 Hz) sampling fiequency. Both computers were configured with 12-bit analog-to-digital boards (National hstruments, M I 0 16H, Austin TX) and LabVIEW software (National Instruments, Austin TX). The high sampling fiequency cornputer was configured with a 32-bit direct memory access controller board (National Instniments, NB-DMA2800, Austin TX) to increase data throughput. Two channels of data were continuously displayed to the investigator. Gain settings for each channel could be set independently using the gmphical user interface. The data, in voltage units, were stored as contiguous multiplexed files. Figure 2-10 is a schernatic representation of the integrated system.

2.10.2 Data Record Analvsis Procedure

The output voltages fiom the Finapres, accelerometer, and pressure transducers were converted to working units (rnmHg and G units). For each cardiac cycle, in-house

software packages determined systolic (SBP), diastolic (DBP), and pulse (PP) pressures, along with the respective time of occurrence for each parameter. The peak of the ECG R-wave was used to calculated heart rate (HR).

Control Room

Centrifuge Gondola

Centrlluge Controller

KM BR and G-vnlvc Control Valinges

I

I I I l

r-,,,-,,-, !

Event Mn rker

1 I I

J

I

f

70 Centrlfuge

-

1*

Lenen d

Wiring Pressue Transducer Direction of Flow

I

Data Acqulelllon Cornpulera

Figrrre 2- 10: Sclier~iaticrxpresentatioii oj'the ceri tr.(fugegorldola and Coritral Roor~iconfigurutioiis.

Cubic spline fit interpolation (Burden & Faires, 1985) was performed using the

values and times of occurrence for al1 of the physiological metrics (SBP, DBP, PP, and

ER) for each profile. Recalibration of the Finapres was required to obtain accurate tracking of biood pressures. This process was performed over several cardiac cycles

during which no measurements were made. Software control ensured that the recalibration only occuned after the +l Gz baseline measurements and before the start of the acceleration profile (tO). Consequently, data were not always available immediately pnor to profile onset (Figure 2-1 1 A).

Missing Data

SBP, DBP, PP, orHR

a

O @

O

0%

7.

0

a

EVENT MARKlER b

4

+1 Gz Baseline

tO

At +Gz

Cubic spiine fit

SBP, DBP, PP, or HR Mean Value (Baseline)

EVENT MAlXER

- -- -- - -I

I

I

I

l

f

I

l

I

l

t

,

I

I

I

(

I 1

l 1

i '

1 1 1

l

I

r

I

l

t

#

f i l

1

1

1

t-1

t-2 t-3

t-4

Figure 2-1 I : Sofrware anulysis procedure. A: Physiological parameter and the event marker status demarcuting + I Gz baseline and experimental regions. Due to Finapres recalibration, a region of missing data ocrurred between the end of the baseline period and thefirst value rneasuredfollowing the omet of the event marker ([O). B: The rnean baseline value was caZcuZated and added to the experimental data ar limes r-1, t-2, 1-3, and t-4. Thisprovided a cornplete data set, thereby allowing a cubic spline interpolationfor the entire + Gzprofle.

An additionai methodology was required in order to allow interpolation behueen

tO and the k t measured value. For each parameter, a mean d u e was calculated &orn a 10 second period immediately pnor to the start of the centrifuge profile (shown as "+1 Gz Baselineu). This value was then added to the data set at t-1, t-2, t-3, and t-4 seconds (Figure 2-1 1 B). Values codd then deteimined for the entire +Gz profile beginning at tO to t12 (twelve seconds afier event marker start) in O. 1 second increments. Changes in heart level blood pressures from onset of acceleration (tO) values were calculated (Le., normalized and designated as nSBPHL).To determine the corresponding eye Ievel equivalent (nSBPm), the nSBPHLand +Gz at each tirne interval was entered h t o equation 1-7. Measurements by Bums and Whinnery (1 984) indicated that the average distance between the aortic valve was 300 mm. This value was used to complete the calculations. 2.10.3 Parametric Statistics Parametric (+Gz, G-suit pressure, mask pressure, and blood pressure) data were analyzed using a 4 step procedure: 1) An omnibus (repeated measures analysis of variance, mi-ANOVA) test was performed on the data to determine if and where possible treatment effects occurred. To correct for violations in sphencity due to the repeated measures design, significant p values @S 0.05) were corrected using a Geisser-Greenhouse epsilon (E) correction factor. 2) Once main or interaction effects were determined, paired cornparisons were screened to ensure the differences between rneans was scientifically significant according to minimal delta values (refer toTab1e 2-3).

Table 2-3: MNiimum Dgerences Required Between Means Before Being Consideredfor Posr Hoc A n a b i s

I

Metric

,

Pm

-eGz

1

Minimum Delta 0.1 G 12.93 mmHg (0.25 psi)

I

3) Post hoc contrast analyses were used to test for statistical significance between conditions. Due to the low sample size, it was Unperative to balance the risk of

making Type 1errors against losses in sensitivity (Le., power). The per cornparison cntical value (c$,) was set at 0.01 in order to decrease the probability

of a family wise error (aFW). AS paired contrasts (a = 2) were being performed with 6 subjects, the corresponding cntical F value (with df = 1,s) equaled 16.3.

Using the critical F and the sample size, the relative ratio of treatrnent variance to error variance (o')was determined using the equation: &=(a-

1) (F - l ) / ( ( a - 1) (F - 1) +(a)(n)) p q n . 2-21

where a equals the number of conditions and n the sarnple size.

oz= 0.5604 This high w' value indicated that the treatment had to account for 56.04% of the total variance to be considered significant. This was well above the 15% level

Cohen (1977) uses to describe a "large effect". The sample size (n) and the calculated w'were then substituted into the next equation: @2 = n

0 '/

(1 - 02) pqn. 2-31 @-=

7.65

Taking the square root: @ = 2.77

U s h g 9= 2.76, a= 0.01 and a Pearson-Hartley chart, the correspondhg power (1-B) value (df,, = 1, df,,,,=

10) was 0.75. This is very close to the 0.80 level

that Keppel(1991) sees as being "a reasonable and realistic value". Due to the large nurnber of possible comparisons, this was considered an acceptable compromise between Type 1 and Type II error rates. The procedure was sensitive enough to detect differences in the Control data (Annex E) while maintaining control of the cumulative Type 1 error rate. 4) Family-wise Type 1error (aw)rate was then calculated for the number of comparisons (c) made: Eqn. 2-41 orRK = 1 - (1 - apC)C A farnily wise error rate (a,)

2 0.25 was considered an acceptable level of nsk, given the

low power from a small sample size and the number of possible païrwise comparisons. If the farnily wise error rate exceeded this value, the relative importance of a Type 1error on

the final conclusion fiom the analysis was considered, as suggested by Keppel(1991). 2.10.4 Nonriarametric Statistics Nonpararnetric data (subjective reports of visual light Ioss, G-suit pressure cornfort, system response, and fatigue) were analyzed using planned comparisons in the Friedman mode1 as descnbed elsewhere (Marascuilo & McSweeney, 1977; Siegel & Castellan Jr, 1987). A significant N2 ( p l 0.05) using the Friedman statistic was required before ali rankuigs were contrasted.

G-Tolerance Study 1- Pressure Schedule Effects 3.1 SeIection of Profiles for Analysis The simplest modification to an existing acceleration protection system is a change in the amount of pressure provided by the G-valve. To study the effect of varying the pressurization schedule, the influence of additional treatment effects (surface coverage, Gvalve responsiveness, and PBG schedule) must be controlled. Therefore, all conditions in which PBG was applied a d o r delays were introduced in lower body garment pressuization were eliminated. As the output fiom the G-valve is a function of the acceleration level and the rate of the pressurïzation (Le., slope), the greatest pressures and largest pressure differentials between schedules would occur at the highest +Gz levels used in the study (+4.0, +4.5, and +5.0 Gz). Al1 subjects had to complete exposures to these levels, in order to employ a statistical basis for assessing the changes in G-tolerance.

This was not possible in al1 coverage conditions. Subjects completed the requisite +Gz exposures with the STING and FPHS ensembles. To minimize the influence of coverage, the garment with the smallest surface area was selected (i-e., STING G-suit). Therefore,

profiles in which the treatment combinations matched these requirements were selected for the subsequent analyses.

3.2 Control of Treatment VariabIes At times t l to t10, differences in P, values were greater than 12.93 rnrnHg (0.25 psi) between each schedule (Annex F-1). 90 painvise comparisons (3 pairwise comparisons at each of 10 time intervals for the 3 +Gz levels) were subsequently performed. P, was found to be statistically different @ 1 0.01) at each time interval (tl to t10) between the three pressurization schedules at al1 +Gz levels. As al1 comparisons were significant, the am was calculated using the p-value corresponding to the lowest F ratio Uistead of the am Substituting this value into

equation 2-4, aw

=

1 - (1 - 0.00026)90 = 0.023 1. Consequently, even with a high

number of cornparisons, cumulative Type 1 errors needed no further consideration. Therefore, P, was signincantly diflerent (both statistically and scientificaily) between t 1 and t10 with each pressurization schedule and at the three +Gz levels.

3.3 Treatment Effects 3.3.1 Subjective Measurement of +Gz ToIerance: Vision Subjective responses indicated that vision was compromised as the +Gz level was increased (Figure 3-1). At +4.0 Gz, 4 out of the 18 profiles (3 schedules x 6 subjects) were completed with no observable effects on vision (i.e., the subject reported a clear central and clear penpheral field). This was decreased to only a single occurrence at +4.5 Gz. Al1 subjects reported visual decrements at +5.0 Gz. The number of visual blackout

occurrences (complete loss of central and peripheral vision) rose as the +Gz level increased. Out of the 18 profiles, there was 1 reported blackout at +4.0 Gz, 7 at +4.5 Gz, and 9 instances at +5.0 Gz. Vision Cid not irnprove for subjects experïencing visual blackout by the completion of the acceleration profile. Mean ratings of light loss seemed to suggest that the higher the G-suit pressure schedule, the better the associated visual field. Nonparametric analyses (Friedman Two-

Way Analysis of Variance By Rank), however, indicated that these were not statistically different at the three +Gz levels used in the experiment. 3 -3.2 Obiective Measurement of +Gz Tolerance: Blood Pressure

Omnibus evaluations of normalized heart level and eye level systolic blood pressure data (nSBP,

and nSBP,,

respectively) revealed that varying G-suit pressure

schedule only produced a significant main effect of Thne at al1 three +Gz levels (refer to Table 3-1). There were no main effects of Schedule, nor any Schedule x Tirne interactions.

BLACK

a

E

O

E

GREY

+4.0 Gz

1

Wont Ptriphenl

Woot Cenini

est ~criphcnl

Best Ccn[nl

h V)

CLMR L OW

NOMINAL

HIGH

I

I

I

LOW

NOMiNAL

HIGH

BL ACK

a

5

c . E .

GREY

5

CA

1 CLEAR

UB a i P m p i u n l

1 1

LOW

1

NOhlMAL

1

HIGH

LOW

~ c s tCenual

NOMINAL

UIGH

B LACK

=O

GREY

5.

V1

1 CL EAR

+ Bert Central

u scuPe"pl.ill 7- -

LOW

1

NOMWAL

Pressure Schedule

I

HIGH

LOW

Nohl l NAL

HIGH

Pressure Schedule

Figure 3-1: Mean ratings of worst and besî peripheral und cenhal light loss reported by subjects at +4.O, + 4 5, und +5.0 Gz.

Table 3-1: Main Effect of G-suit Schedule on nSB& and nSBP,, ar the +Gz Levels Used in the Ekperîment Change in Eye LeveI Systolic BIood Pressure Source

ss

df

MS

F

4.0

Time T h e x Subject Time Tirne x Subiect Time Time x Subject

13665.6 14 4772-720

10 50

1366.561 95.454

14.3 16

pg-;-e; 0.0046

28720.746 4718.842

2872.075 94.377

30.432

0.000 1

26252.844 (

10 50 10

( 2626.284 (

1

50

1

r

4.5 ¶

I

I

+GZ

5.0

1

I

1

5210.061

m

Change - in Heart Level Systolic BIood Pressure SS df +Gz Source 4.0 4.5 5.0

Time Time x Subject Time Time x Subject Time Time x Subject

I

I

25.194

104.201

1

1

0.0002

MS

F

Pg-g

26.758

0.0008

33 .254

0.0004

40.684

0.000 t

2554 1.579 4772.720

10 50

2 1945.994 4718.842

50

2554.158 95.454 2 194.599 94.377

42393.089 52 10.061

10 50

4239.309 104.20 1

1O

I

Transformations from heart to eye level (Table 3-1) only resulted in marginal differences in the sum of squares, without any changes in the error terms for al1 analyses. Consequently, the results were the same as the nSBP,, analyses, with only small alterations in the f d p, values. The data were collapsed across G-suit pressure schedule and are shown in Figure

3-2. The abscissa for both panels is the time fiom profile onset (i.e., the tirne at which the gondola attained H.75 Gz). n i e ordinates indicate changes in systolic blood pressure

in 11 mmHg increments, the approximate blood pressure required to produce a change of 0.5 +Gz in tolerance. The bottom panel (B) depicts changes in heart level systolic blood pressure (nSBPHL)fiom onset values. The top panel (A) is a mathematical adjustment of the heart level data to eye level values (nSBPa). Heart level pressures were compensated

for changes produced by hydrostatic infiuences and fiom a chznging +Gz level.

Normalized S ystolic Blood Pressure (mmHg)

Normalized S ystolic Blood Pressure (m mHg) I

O\ O\

k

W

W

I

h,

N

I

C

O

-

At al1 +Gz levels, pressurization of the G-suit was found to increase nSBP, over time. At approximately t6, blood pressure attained a plateau level and did not change for the remainder of the profile. Contrast analyses were used to compare nSBP,

at each

time interval against onset (tO) values. At +4.0 Gz, heart level pressure was unaffected by pressurization of the G-suit until t3 (nSBP,, 2 11 mmHg and p < 0.01). Significant

improvements were not found to occur until t5 and t2 at +4.5 and 5.0 Gz, respectively. Mean (+ SEM) nSBPHLduring the fkd 5 seconds of the profile were 3 1.3 (le 7.0), 25.9 (rt 6.4),and 41.8 (k 5.3) mmHg at each +Gz plateau. The absence of a signincant effect

at t9 during the +4.5 Gz profile was due to the variability of the blood pressure response in addition to a slight decrease at this interval. Given that nSBP, was higher before and

d e r t9 and that corresponding 02 was 0.5583, this finding could be amibuted to a loss of power with qcset at 0.01. Eye Ievel pressures (nSBPEL)were found to fall fiom baseline values with onset of acceleration exposure. Contrast analyses reveaied significant (nSBP, 2 11 mmHg and p l 0.0 1) decreases occurred within the first second of profile onset. The greatest decrements in eye level pressures were found 2 to 3 seconds into the acceleration profile, but a period

of rapid recovery followed before a steady state plateau was attained. However, nSBPEL never retumed to initial levels, remainhg significantly suppressed for the duration of the profile with exposures to +4.5 and +5.0 Gz. hcreasing +Gz plateaus resulted in mean nSBP,, decrements of 17.7,34.5, and 30.7 d

g fiom t6 to t 10. SEM values were the

same as those reported at heart level.

Calculated am for the 25 and 30 contrasts performed using the nSBP,

and

nSBPE, data was 0.222 and 0.260, respectively, suggesting that a slight risk of a Type 1 error was present. However, any false positive would likely have decreased the delay in the blood pressure response. Hence, the actual delay duration may have been greater than

that reported using this analysis procedure.

3.4 G-suit Pressure Schedule and Acceleration Tolerance

Tolerance to +Gz exposure, as defmed by vision or increases in systemic artenai pressures, was not affected by the pressurization schedule. With the omet of the acceleration, heart level blood pressure increased with G-suit pressurization, but did not attain maximum levels until approximately 5 to 6 seconds into the profile (i.e., several

seconds after complete inflation of the G-suit). This lag in blood pressure was evident with al1 three pressurization schedules (Figure 3-2). The mean nSBP, attained at the end

of the profile was not increased consistently with the greater suit pressures brought about fiom higlier +Gz exposure. The net increases in nSBP,, were not large enough to counter

the hydrostatically induced decreases in blood pressure to areas above the heart (i.e., eyelevel). This caused nSBPELto fall, even with no delay in G-suit pressurization, to nadir levels 2 to 3 seconds after G-onset. A rapid recovery over the next 2 to 3 seconds occurred, but systolic pressures never attained pre-acceleratory levels. Visual responses correlated well with these changes in nSBP,.

Subjective reports

also indicated no effect of G-suit pressurization schedule on vision. Given that exposure to increasing acceleration plateaus reduced estimated head level blood pressures, it was not surprising to fmd that vision progressively worsened as the +Gz plateau was raised. At +5 Gz, half of al1 experimental conditions resulted in blackout fiom which there were

no subsequent improvements in vision. Even with the highest head level pressures recorded at the end of the profile, retinal perfusion pressures rernained less than intraoccular pressure. Lightbar responses indicated that visual blackout occurred several seconds after nadir blood pressure levels were attained. The ability for subjects to respond to peripheral and central Iight challenges is thought to be due to the presence of oxygen reserves (Wood et al., 1987). The tirne course of events was consistent with that found after complete cervical artenal occlusion (Rossen et al., 1943). Not only was vision maintained for a brief period irnrnediately following +Gz exposure, but loss of

consciousness would aIso have been prevented had head level blood pressures temporarily fdlen below critical levels. Therefore, correlating alterations in a subject's visual field with blood pressure measurements must be made carefilly, taking into consideration the time delay in visio~?change due to the buf5ering effect of the reserves.

3.5 Additional Factors and Issues 3.5.1 Fatigue Effects

Ratings of fatigue were examined to ensure that the results were not affected by the large number of acceleration profiles subjects were exposed to during a single session. Fatigue ratings did not change in 5 of the 6 subjects. Al1 reported feeling "Not Tired" throughout each of their 3 sessions. The remaining individual indicated a change in status for only 1 of the 3 experimental periods. This occurred mid-way through the session, but

was only a single level increment. Given the lack of a change in their individuai reports, in combination with a counterbalanced design, the high number of profiles in an experimental session wodd not have innuenced the outcome of the investigation. Therefore, fatigue effects were not a factor in this experirnent and no M e r analysis was necessary on this measure. 3-5.2 Comfort During: - G-suit Pressurization

In the 1 8 profiles, the STING G-suit pressurized using the nominal schedule (1-5 psi/Gz) was found to cause discomfort for 1 subject at each +Gz level. Decreasing the pressure to the suit by 0.5 psi/Gz alleviated this discornfort. However, an increase in pressure by 0.5 psi/Gz above the nominal schedule produced discomfort in 3 to 5 of the subjects at each +Gz plateau. Subjects did not find the pressure intolerable with the highest presswization schedule. Mean subjective ratings are shown in Figure 3-3.

Intolerab ly

Un corn fortab 1 Low Schedule

a Nominal Schedule

t SignifÏcant Freidrnan resuIt (p ~ 0 . 0 5 )

m g ihSchedule

&

Tolerably

I

Uncom fortabl -CI

Cr

O C) *)'

a

3

C12

Cornfortable

Figrire 3-3: Mean subjective ratings of comfort with the three pressure schedules. AZthough Friedman analyses were signifcant at +1.O and +5.O Gz, dzrerences beîween ranks were not detected by the multiple contrasts. Nonparametric analyses indicated that G-suit pressure schedule did affect comfort ratings at +4.0 and t5.0 G z (N=6, di+ 2, LI'= 8.400, p= 0.0150), but the multiple cornparisons were not sensitive enough to detect these differences. The level of pressure to the G-suit should be a compromise between comfort and effectiveness, the latter defined by the increased blood pressures that are associated with improved tolerance to +Gz. In most cases, as long as the pressure to the G-suit is "tolerable", the effectiveness issue takes on the strongest weighting. Given there was M e difference in nSBP, with the pressurization schedules at the three +Gz levels tested, effectiveness becomes a less tangible component. Due to the relatively small sample size used in the experiment, the variability in the individual response to G-suit pressurization, and the interaction between G-suit pressure and a strainhg maneuver at high +Gz, a prudent level of pressurization should e n on the side of safety. The nominal pressurization schedule with the extended coverage G-suit posed minor discornfort problems (i.e., one subject did not rate it cornfortable at each +Gz level). Although a decrease in the G-valve pressure output of 0.5 psi/Gz albviated any cornplaint issues, a

low schedule may compromise flight safety if such a decision is based solely on subjective visual reports. The high pressurization schedule did produce more reports of discornfort. However, none of the subjects found the pressure to be intolerable and, thereby, increasing the pressure/+Gz may bear closer consideration. As the nominal pressurization schedule appears to produce eq~itablelevels of G-protection with extended coverage and requires no alterations to current specifications for Life support equipment, it may be the best compromise with the limited data available. Further experimentation will be required to address the unknown areas relating to this issue.

3.5.3 Variabilitv of the Cardiovascular Res~onse

The lack of a main effect fiom the various G-suit scheduies and the decreased blood pressure at +4.5 Gz rnay have resulted from the wide range of individual responses. Figure 3-4 exemplifies the amount of variability in nSBPHLwith G-suit pressurization. The bottom tracing shows the +Gz level, increasing at 2 Gz/s to a plateau level of +4.5

Gz. As the centrifuge passed through +1.75 Gz, the event marker was triggered to indicate "profile onset". The second panel depicts the rapid increase in G-suit pressure, achieving a maximum pressure of 258 mmHg as the gondola reached the plateau level. Systernic arterial blood pressure is shown on the upper panel. Note the long delay before peak systolic blood pressure was attained, almost 4 seconds after maximum G-suit pressurization occurred. The maximum blood pressure was not maintainedobut decayed to the pre-acceleratory value over several cycles. The blood pressure response was reflected in the amplitude changes measured by the ear pulses, thus validating the accuracy of the measure. Additionally, the lightbar responses during the profile confirmed that the subject's vision degraded towards the end of the profile. The point at which the subject stopped responding to central light loss interrogations (CLL Inter.) and peripherai light loss interrogations (PLL Inter.) is s h o w by the arrow. This was

consistent with the decreased blood pressure measured in the latter haif of the acceleration profrle.

CLL Inter. PLL Inter. Ear Pulse 1

Ear Pulse 2

Event Marker

Figure 3-41 Experimental tracingfiorn a subject exposed to a +4.5 Gz profie while wearing a STliVG G-suit inf ated according to the high pressur ization schedule. Note the lack of bloodpressure change with a high level of lower bod)pressurization and the resultant visual blackout during the latter stages of acceleration. CLL and PLL represent the central light and peripheral light interrogations, respectively.

3.6 Treatment Levels in Relation to the Operational Environment The requisite pressure output range specified for G-valves is showri in Figure 3-5.

The abscissa shows the +Gz level with G-valve outlet pressure plotted on the ordinate. The range of acceptance (maximum and minimum levels) is shown by the full lines. The mean pressures provided by each of the three schedules at +4.0, +4.5, and +5.0 G z are superimposed on the acceptance range. G-valve outlet pressures from the "nominal" schedule were at minimum range, while the Low and High schedules provided points on either side of the acceptable minimuai and maximum levels, respectively.

J Maximum Pressure

/ /

1

A Low Pgs Schedule

/ /

9 Nominal Pgs Schedule

7 /

,/, Nominal Pressu

Figure 3-5: G-suit pressure levels used in the experimenf relative to requisite values ( M L - V-87255 USAF). The nominal schedule follo wed the minimum pressure range, while the Low and High schedules providedpressures below and above minimum and maximum acceptances, respectively.

The +Gz levels used in the experiment comprised a small portion of the G-valve performance envelope. Differences in outlet pressures between the schedules increase with the acceleration input. The effects of different pressures at a given +Gz rnay not be evident until the subject is exposed to significady greater accelerations than those used in the expenment. However, these higher +Gz exposures rnay not be completable without the performance of a straining maneuver. C o d o n issues rnay also irnpede completion of higher +Gz exposures (Le., > +5 Gz), evident in the increasing reports of discomfort with the High schedule at accelerations Iess than or equal to +5 Gz. A schedule implementing a greater pressure slope may also produce discomfort at lower +Gz levels. 3.7 Findings Pertinent to Life Support Design

1. G-tolerance, as defined by alterations in nSBP,,

nSBPEL,or subjective reports of

Msual changes, was unaf5ected by alterations in G-valve outlet pressure at +4.0, +4.5, and +5 .O Gz.

2. Inflating the extended coverage G-suit with the Low, Nominal, or High pressure schedule resulted in a delayed and variable blood pressure response. 3. Visual deficits increased with +Gz regardless of the applied G-suit schedule, although

the buffering effect of the oxygen reserves rnay have transiently provided protection while blood pressure was at nadir levels. 4. Increasing G-suit pressure using a high schedule poses an increased risk of discomfort.

Although a lower G-suit pressure rnay alleviate discomfort issues in subjects wearing extended lower body garments, the current schedule rnay be the best compromise between comfort and flight safety.

CHAPTER 4

G-Tolerance Study 11 - G-valve Responsiveness 4.1 Selection of Profiles for Analysis When the inflation schedule to the G-suit was altered at +4.0,+4.5, and +5.0 Gz, there was a noticeable delay in the cardiovascular response even with rapid lower body pressurization. The lag in blood pressure rise was consistently present at al1 +Gz levels. A delayed increase in blood pressure may predispose a pilot to potential loss of

consciousness and, in combination with a slow responding G-valve, rnay pose a significant risk to flight safety. The rapid pressurization scheme used in the previous study may also have contributed to the resultant sluggish blood pressure response.

In order to assess the influences of G-valve responsiveness, conditions in which inflation of the G-suit was delayed2were exarnined. Acceleration exposures to +4.0, +4.5, and +5.0 Gz, in which the same lower body garment (STING) was pressurized

according to the intemediate (Le., Nominal) schedule, were selected. This combination of treatments ensured that one condition was the same as that used in the previous study and, thereby, senred as a reference for cornparison. The highest +Gz level completed by al1 subjects with varying delays is illustrated

in Figure 4- 1. Note that the highest +Gz plateau used in the expenment was +5 Gz. A subject was not necessarily at his/her G-intensity tolerance lirnit at this +Gz level. The control (no G-suit pressure, analogous to an infinite delay condition), is plotted furthest on the abscissa. As the delay increased, the highest +Gz level completed decreased. Subjects completed ail delay conditions at al1 +Gz levels with either no delay or a 1.5 second delay in suit pressurization. G-intensity tolerance fell to +4.5 Gz and +4.0 Gz

"ven though the No DeIay condition pressurized the G-suit just slightly ahead of the +Gz onset, for consistency and ease of reporting this configuration was deemed No Delay. Delays intervals were then referenced to this pressureltime profile.

61

with delays of 3.0 and 4.5 seconds, respectively. Without suit pressurization (Control), al1 subjects completed the +3.5 Gz condition.

0.0 s

1.5 s

3.0 s

4.5 s

Control

Condition Figure 4-1: Highest completed +Gz level by al1 subjects in each d e l q condition while wearing a STING G-suit pressurized according to the "Nominal"schedule or in the "Control"(nonpressurized) state. In order to statistically evaluate the changes that occurred with increasing delay in G-suit pressurization, only conditions completed by al1 subjects could be used. Hence, al1 delay conditions were used in the subsequent analyses at +4.0 Gz, the longest delay condition (4.5 seconds) could not be used at +4.5 Gz, and only the No DeIay and 1.5 second delay conditions were evaluated at +5.0 Gz.

4.2 Control of Treatment Variables 4.2.1 Pressurization D e l a ~ and s G-suit Pressures

Graphical representation of the P, conditions may be found as Amex F-2. Omnibus analyses (rm-ANOVAs) of the G-suit pressures measured at each tirne interval revealed strong Delay x Time interactions (Table 4-1).

Table Cl: Delay x Time Interactiom at the +Gz Levels Used in the Experiment Source

4.5

1

5-0

1

Delay x Time DeIay x Time x Subject Delay x T h e DeIay x Time x Subject Delay x Time Dclav x Thne x Subiect

1067.579 194320.687

578.966

Evaluation of the P , values for each time interval identified 37 paired comparisons in which the difference in mean pressure (APd was greater than 12.93 mmHg (0.25 psi). Ali paired comparisons were found significantly different (AP, 2 12.93 mmHg and p I 0.01). Using the smallest p-valve, a ,

=

1 - (1 - 0.00472)37= 0.1606, resulted in a low

risk for making a cumulative Type I error. The duration of any signif~cantdserence between delay conditions and maximum pressure difference (Pm=) are shown in Table 4-2 for each +Gz level. In al1 comparisons, pressures were always greater for the condition

with the shortest delay. Comparative differentials in pressure may be found in Annex G. Table 4-2: Dzrration and Maximum Drfference in G-suit Pressure Between Delay Conditions r

+Gz

DeltaPressure

4

Duration (s) Pm, (mmHg) Duration (s) Pm, (mmHg)) Duration (s) Pm, (mmIfg)

4.5

5

Conditions Compared (Delay in seconds) 0 . 0 v s 1 . 5 ~ 0 . 0 v s 3 . 0 0.0vs4.5 1.5vs3.0 1.5vs4.5 3 113 3 113 3

4 149

3

6

111

154

4 149

4 111

5 153

3.0vs4.5

3 83

168

4.3 Treatment Effects

4.3.1 Subjective Measurement of +Gz Tolerance: Vision There was a statistically significant effect of delay on worst penpheral light loss during the +4.0 Gz profile (N=6, df= 3, x2= 9.293, p= 0.0256). One of the six subjects experienced complete loss of peripheral vision with No Delay or a 1.5 second delay in G-

suit pressurization. In cornparison with the longer delay conditions (i-e., 3.0 and 4.5 seconds), three and four subjects experienced this level of visual degradation, respectively. Subjects reported having experienced greater peripheral vision impairment with the No Delay condition when compared to a 1.5 second delay in G-suit pressurization (Figure 4-

2). Three subjects experienced peripheral greying in the No Delay condition, while only one subject indicated similar changes in this parameter with a slight (1 -5 second) delay. Conkast analyses only detected a significant difference in worst peripheral light loss between the 1.5 second and 4.5 second delay conditions. Peripheral vision irnproved by the end of the profde such that four, two, and three of the six subjects reported a clear field with a 1.5,3.0, and 4.5 second delay in pressurization. However, no subject experienced an improvement in penpheral vision with the No Delay condition. Subsequently, mean ratings of light loss were highest in

this condition. A Friedman analysis indicated that there was an effect of delay on best peripheral vision (N=6: df= 3, K

'= 11.364, p= 0.0099), but post hoc contrasts failed to

confïrm that any differences existed.

Central vision was similarly affected by delays in suit pressurization. ??ie worst degradation of central vision occurred with the longest delay, with one subject reporting visual blackout. Vision was least a e c t e d by a 1.5 second delay in pressurization, resulting in only dimrning of the central field in three subjects. In al1 conditions other than

the 1.5 second delay, at least one subject experienced central greying during the acceleration profile. These changes were nof however, statistically different.

BLACK

CLEAR

BLACK

V1

E

= O

GREY

E

2 œ

.-4 >

DIM

CLEAR

I

0.0 s

1.5 s

3.0 s

0.0 s

4.5 s

Signifiant Freidman d

1

3.0 s

1

4.5 s

Delay

Delay

t

I

1.5 s

t

@s

O

os)

* Signiticandy different from 1.5 s dday (p c O 0s) Figure 4-2: Worst and best peripheral and central vision changes at +1.0 and +4.5 Gz with increasi~gdelay in G-suitpressurization.

There was no improvement in central vision with the No Delay condition, with one subject reporting central greying. In al1 other delay conditions, the profile was completed with al1 subjects experiencing an irnprovement in central vision. Mean ratings were again highest in the No Delay configuration; Although the Friedman analysis was significant for best central light loss @=6, df= 3, kt2= 11.000, p= 0.0017) between the four delay conditions, limited contrast sensitivity failed to detect differences between the

Vision degraded as the acceleration level was increased. At +4.5 Gz, 3 subjects experienced blackout with No Delay in pressurization while only 1 subject reported the same extent of visual deficit with either a 1.5 or 3.0 second delay. Vision did not improve for al1 subjects experiencing blackout. There was a significant improvement in central vision m=6,di+ 2, K 2= 8.588, p= 0.01 36). Light loss was rated greatest in the No Delay condition. Contrasts using mean ranks were insensitive to dserences between delay conditions. By +5.0 Gz, 4 and 3 subjects reported experiencing visual blackout with the No Delay and 1.5 second delay conditions, respectively. With both delay configurations, al1 subjects experienced no improvement in vision by the time the acceleration profile was completed. Parametric analyses could not be performed on these data due to the insensitivity of the Sign Test with such a small sample size.

4.3 -2 Obiective Measurement of +Gz Tolerance: Blood Pressure The average nSBP,, response at the three +Gz levels used in the experiment are

shown in Figure 4-3. With the onset of acceleration, nSBPHLonly increased once G-suit pressurization commenced, and rose until it was approximately 30 to 40 mmHg greater than at the start. The greatest differences in heart-level systolic pressure between delay conditions occurred between t4 and t6. Midway through the acceleration exposure (i-e., t5), the longer delay conditions produced the greatest differences in nSBP,.

However, within

two to four time intervals systolic blood pressure increased to No Delay values. This finding was consistent with al1 delays and at all +Gz levels. Analysis of variance on nSBPHLdata revealed that varying the delay in G-suit pressure produced a Delay x Time interaction at al1 three +Gz levels (refer to Table 4-3).

r0.0 s DELAY & 1.5 s DELAY

Time Since Profile Onset (s)

Figure 4-3: Changes in heart-level systolic blood pressure Porn onset values with increusing delays in G-suit pressuriration. Pnor to performing contrast analyses, differences in nSBP,

between delay conditions of

11 mmHg or greater were evident in o d y 36 of the possible 100 comparisons. The cumulative family-wise error rate (aw)with an cxPc of 0.0 1 was 0.3036, indicating that the presence of a Type 1error in the data set was likely to have occurred. Table 1-3: Delay x Time Interaction of G-suit Pressure Delay on nSBP,, at the + Gz Levels Used in the Experiment +Gz

4.0 4.5 5.0

Source

SS

7997.787 Delay x T h e Delay x Tirne x Subject 7241.621 7161.388 Delay x Time 4740.158 Delay x T h e x Subject 2564.855 Delay x T h e Delay x Time x Subject 2613.068

df

MS

30 150

266.593

20 100 10 50

1

F 5.522

Pg-g 0.0084

358.069 47.402

7.554

0.0026

256.486 52-26 1

4.908

0.0205

1

48.277

Figure 4 4 illustrates the time intervals at which significant differences in blood pressure were found between delay conditions at al1 +Gz levels (refer to Annex G for a description of the plotting methodology). Examination of the paired contrasts indicated that at +4.0 and +4.5 Gz nSBPHLwas elevated for a single time interval if pressure to the G-suit was delayed by 1.5 seconds fiom the No Delay condition. The duration was lengthened to 2 seconds with exposure to the +5.0 Gz profile. Differences in nSBP,, either occurred 4 or 5 seconds after profile onset (i-e., afier complete pressurization of the G-suit) . With longer delays, the magnitude and duration of the difference in the normalized systolic blood pressure was increased from the No Delay values. There were, however, no significant changes in nSBPm between the 1.5 second and 3.0 second delay conditions at either +4.0 or t4.5 Gz conditions. Nor was nSBPmaf3ected when the delay was increased from 3.0 to 4.5 seconds at +4.0 Gz. During the latter portion of the acceleration profile (t8 to t IO), there were no differences in heart level systolic blood pressures between conditions at al1 +Gz levels-

4.3 -3 S u m m q of Findings and The Effect of a Tvoe 1 Error

The G-suit pressure profile was reflected in the blood pressure response. The longer the delay condition, the geater the t h e required before a significant difference in blood pressure occurred. However, differences in blood pressure lagged those found in the measured P, values and were briefer in duration (Le., 1 to 4 s vs 3 to 6 s, respectively). Blood pressure was the same during the final few seconds of acceleration exposure in all delay conditions at al1 +Gz levels. Therefore, delays in Iower body pressurization did not cause prolonged differences in systemic blood pressure. Given that oxygen reserves (Wood et al., 1987) would compensate for any insufficiencies in

perfusion pressure (Rossen et al., 1943), the presence of a possible Type 1error would not affect the outcome of the analysis.

Figure 4-4: Summary of the changes in nSBPHLwith increashg delays in G-suit pressurization at +4.0, -+4.5, and +5.O Gz.

4.4 G-valve Responsiveness and Acceleration Tolerance

Tolerance to +Gz was significantly afFected with increasing delays in G-suit pressiilization. If tolerance to +Gz was based on visual symptoms alone, the No Delay condition would appear to be sub-optimal. With no delay in G-suit pressurization, central and peripheral vision were least improved by the end of the profile (Figure 4-2). However, it was cornmon for subjects to report that vision became progressively worse during the acceleration profile. Based on best vision, optimal protection was afforded by

a system that delayed pressure to the G-suit by 1.5 seconds. This, however, was not supported by the blood pressure data (Figure 4-4). Heart level values were either the same or temporarily higher in the No Delay condition when compared to the 1.5 second delay response. With either a 3.0 or 4.5 second delay, vision was either the sarne or slightly worse than conditions with a 1.5 second delay. There were, however, no differences in final heart level blood pressures with any of the treatrnent levels (Figure 44) Therefore, the correlation between G-tolerance measurement techniques was very poor. As found in the previous analysis, the effect of temporary differences in head level blood pressures may be negated by the oxygen reserves. Visual syrnptoms would not only be caused by alterations in local perfusion pressures, but also by the duration of the changes and the t i m e at which they occurred. As there were no means to ascertain the time interval at which vision was altered during the acceleration profile (except for instances where blackout could be determined), decisions regarding optimal inflation scheduling should not be made soleiy on light loss values. Closer examination of Figure 4-3 revealed blood pressure did not reach maximum levels until well after complete pressukation of the lower body garment. A quiescent period in the nSBP, response occurred during or immediately &er G-suit presswization.

This effect was exacerbated by long delays, and blood pressures during this penod may

even have dropped below pre-acceleratory levels. A rapid increase in heart level systolic blood pressure followed, during which the greatest changes in nSBP, were found. The slope of this phase was usually greatest with the longest delays. Consequently, the diminished systolic blood pressure resulting from a long delay was quickly rectified by

the end of the profile (Figure 4-4). However, as the +Gz level increased, this delay in blood pressure response reduced acceleration tolerance (Figure 4-1). The duration of this signifcant lag in blood pressure response mented M e r study.

4.5 Quantification of the Delayed Blood Pressure Response As al1 significant increases in nSBP,

were delayed relative to the time at which G-

suit pressurization commenced, it was imperative to quanti@ this lag in the cardiovascdar response and to confirm that the delay was consistent across dl conditions. As al1 subjects completed +4.0 G z with al1 delay conditions, this profile was selected for this purpose.

Table 4-4: Maximum Systolic Blood Pressure Change and Time fo Maximum Systolic BZood Pressure j-om Orner of Profle for all Delay Conditions

For each subject, the maximum systolic blood pressure change and the tune of maximum pressure from profile start was recorded with each delay condition. The average maximum change in nSBP, was 36.3 (k2-61rnmHg. As seen in Table 4-4, there was little difference in maximum pressure increase for the four delay conditions.

However, the t h e course for blood pressure change rose as the duration of the delay increased. With a 4.5 second delay, maximum pressure change occurred near or at the end of the acceleration profile (Le., 10 seconds Çorn profile onset).

Time From Profile Onset (seconds) Figure 4-51 Time course of blood pressure changes with varying delays in G-suit pressurization. The thin lines represent G-suifpressurization and the bold line the change in nSBP,, . Using tirne fo 90% maximum G-suit and nSBPHL(dashed Zine), the lime hg was rhen calnrlated. The arrow denotes a 3.1 second deZuy in the No Delay condition. The delay in blood pressure response was quantified by calculating the time difference between G-suit inflation and t h e to maximum systolic blood pressure for each subject for dl delay conditions. Due to the haversine nature of the G-suit pressure profile, it was difficult to determine when the G-suit was completely infIated. Therefore,

the time to 90% maximum was used. Figure 4-5 depicts the average response for each delay condition. The mean change in systolic blood pressure is plotted as a percentage of

the maximum value. The same was done for G-suit pressure. The 90% reference point is indicated by the dashed line. The delay in blood pressure response is the difference between G-suit press~zationand the increase in systolic blood pressure to 90% of its

maximum value ( s h o w by the arrow). In the No Delay condition, blood pressure was found to lag G-suit pressurization by 3.1 seconds. The lag in nSBP,

ranged fkom 3.1

seconds to 3.9 seconds in al1 delay conditions (Table 4-5). The average delay for all conditions was 3.4 t 0.3 seconds.

Table 4-51 Calcularion of the Delay in Cardiovascular Response Relative to Inflation of the G-suif A. Time 90% Pressure

(Seconds from Onset)

1

Delay

1 No Delay

X 1.9 3.3 4.7 6.1

IB.

Time 90% SBP Max 1 (Seconds f7om Onset)

SEM 0.O

X

SEM

5.0

0 .O 0.1

7-2 8 -4

0 -9 0.6

O .O

9.2

0.5 0.2

Lag Pet-iod (E3 - A) (Seconds)

X

SEM

3.1

O -9 O -6 0.5 O -2

3 -9 3 -7 3.1

4.6 The Effect of Poor G-valve Response o n Cardiac Emptying

Figure 4-6 demonstrates the deleterious effect of a delay in G-suit pressure on the cardiovascular response in a subject exposed to +4.5 Gz. G-suit was pressurized according to the nominal schedule, but onset of inflation was delayed by 3.0 seconds.

The delay before P, is applied is depicted by the arrow between the bottom and middle panel. G-suit pressure rapidly attained the target pressure of 193 mmHg. The corresponding rise in blood pressure, however, was delayed due to what appeared to be a missed or "dropped" cardiac cycle. Evaluation of the ECG (top panel) showed normal sinus rhythm throughout the profile. Significant decreases in pulse amplitude of both earpieces (EP 1 and EP2) during the same period confirmed that the blood pressure monitoring system was functioning properly. Hence, the "dropped" wavefom was not

an abenation, but was a result of the delayed increase in lower body presswïzation. Of the three "dropped" waveforms from the 54 +Gz exposures, al1 occurred in exposures with delays.

-- _--_ I .

,*.

-

k-1

c

-

i

Figure 4-6: Hardcopy record i l l ~ a t i n the g decrease in bloodpressure for one cardiac cycle occurring immediately ufter G-suit inflation. Subject wore extended coverage (STING) G-suit w ith a 3.0 second delay in pressurization. Note what appears to be a "dropped beat': but the ECG indicates normal sinus rhythm. The decreased in heart level SBP was also reflected in both ear pulse amplitude changes. Total time between maximum G-suit pressure to steady state bloodpressure (BP la& was almost 4 seconds. Blood pressure then rose over the following four cardiac cycles, reached a steady state, then oscillated for the remainder of the profile. The time between complete

pressurization of the G-suit and attainment of a steady state blood pressure (BP lag) was almost 4 seconds. The subject was able to complete the entire profile, but expenenced visuai blackout (as reflected by the state of the interrogation lights) for the latter half of the acceleration plateau. Therefore, a delay in G-suit inflation may exacerbate the decline

in cardiac emptying that occurs with iower body pressurization. However, the time for blood pressure to attain maximum levels was not altered. The effect of this transient sequela on tolerance to +Gz has yet to be determined.

4.7 Additional Factors and Issues

4.7.1 Ratings of Svstern Responsiveness Subjective ratings of system responsiveness at +4.0 Gz indicated a difference between conditions (N=6, df= 3 N 2= 14.118, p= 0.0027). Post hoc analyses detected difXerences in subjective ratings between the No Delay condition and the 3.0 and 4.5 second delay conditions (Figure 4-7). All subjects reported that the No Delay condition responded adequately or slightly faster than expected, while only one subject felt the system's response was adequate with a delay in pressurization of 3.0 seconds. Two subjects felt that a 4.5 second delay was slightly slower than expected, and the remainder found it to respond unacceptably slow. Ratings of system responsiveness was significantly different at +4.5 Gz (N=6, df= 2 H ~ 8.400, = p= 0.0150), but post hoc analyses were unable to detect differences

between rankings. However, 5 of 6 subjects found the No Delay condition to respond adequately or slightly faster than expected, while one subject found this condition to be unacceptably slow. With a 1.5 second delay, system responsiveness was rated either faster than expected or slightly slower than anticipated. The longest delay condition (3.0 seconds) was found to be either slower than expected or unacceptably slow.

o +4.5 Gz a +$.O Gz

rDifferent ftom No Delay Condition

As Expected

SIower Than Expected

Unacceptablq Slow

3.0 s

1.5 s

4.5 s

Delay Interval Figure 4- 7: Mean ratings of system responsiveness ut +4.0,

+4.5, und t 5.0 Gz.

No statistical difference was f o n d in the rating of the systemrsperfom~ance between the two conditions at +5.0 Gz. Four of six subjects found that the system responded at the correct speed in the No Delay condition, with one reporting a slightly faster and one subject a slightly slower responsiveness than expected. Three of six subjects felt the system responded adequately with a 1.5 second delay in G-suit pressurization, while the remainder found the systern to respond slightly slower than expected.

4.8 Treatment Level in Relation to the Operational Environment The demand for the G-valve to provide the requisite pressure faster rose with the IeveI of acceleration exposure. This fmding contrasted with those of the previous study, in which al1 subjects were able to complete the +5.0 Gz profile regardless of G-valve performance (i.e., final outlet pressure). Delays in G-suit pressurization resulted in

~ i ~ c a n tdifferent ly levels of lower body pressure ( P d for bnef periods (Annex G). These varied f?om approximately 80 to 170 mmHg and occurred early into the acceleration profile. The Iargest differentials were present at the highest +Gz Ievel a n d o r

with the longest delay period. In order to gain insight as to how the delays used in the experiment compare with those present in the operational environment, the pressure time profile was detemiined for each condition. Mean G-suit pressures at each +Gz plateau were plotted as a function of time for all delay conditions in which aLl subjects completed the profite. In addition, the average G-suit pressures measured us ing the conventional Alar G-valve for one subject wearing the STMG G-suit were also included. As the output pressures fkom the curre~tlyoperational G-valve were approximately 13 mmHg above expected values at

al1 +Gz levels, this made it dificult to determine which delay best depicted its output response. In addition, the rate of onset to each +Gz plateau was not constant during the initial onset phase of the profile. The "rounding off' of the +Gz level as the gondola approached the plateau portion of the profile made it impossible to determine when

maximum pressure was attained. Thus, the G-suit pressures (successive dashed lines) and +Gz (fine solid line) were plotted as percentages of their final values (refer to Figure 4-8). The pressure/time profile for the Alar G-valve is shown by the bold solid line. Time to 90% of maximum pressure was used as the cnterion for attaining the target Gsuit pressure. Delay times, measured with 0.1 second resolution (Table 4-6), were determined as time to 90% pressure minus time to 90% of maximum +Gz.

Table 4-6: Time to 90% offinal G-valve output pressure relative tu the acceleration level (in seconds) for each dehy condition andfor the operational G-valve (Alar) *

C;z 4.0

No Delay

4.5 5 .O

-0.5 -0.5

-0.6

1.5 s 0.8 1.O 1.O

3.0 s 2.2

4.5 s 3.6

2.4

-

-

-

Alar 1.7 1.4 1.3

O

2

4

6

8

10

Tirne From Proflle Onset (s) Figure 4-8: Pressure/time profiles of all delay conditions used in the experiment. The +Gz level @ne solid line) and G-suit pressures (dashedfor the cornputer controlled G-valve and bold solid line for the Alar) are plotted as percentof maximum levels. m e operational G-valve was found to lag the acceleration input by approximately 1.5 seconds at al2 + Gz levels.

Figure 4-8 and Table 4-6 show that the computer controlled G-valve inflated the G-suit ahead of the acceieration in the "No Delay" cmdition. "Pre-inflation" of the Gsuit was approximately 500-600 rnilliseconds ahead of the +Gz input. For the remaining configurations, the computer provided a consistently increasing delay in G-suit pressurization. In contrast, the response of the Aiar G-valve pressurized the G-suit slightly faster than the 1.5 second delay configuration during initial +Gz onset. However, as the gondola neared the plateau level, the operational G-valve was unable to keep up with the pressure demands. Therefore, using 90Y0maximum pressure as a standard, the mechanical valve reached this level approxhately 1.5 seconds after peak

+Gz was attained. This delay in responsiveness was comparable to an intermediate state, between the 1.S and 3.0 second conditions tested in the expenment. As the extnnsic factors that altered the pressure demands (rate of acceleration onset, +Gz plateau, pressure schedule, and G-suit volume and resistance) were kept constant, the intrinsic factors were responsible for the delays found with the operational (Alar) G-valve. The mechanical principles that actuate the Alar G-valve, in addition to a lower flow capability, were responsible for the different pressure/time profiles between the G-valves used in this study. Given the cumulative effect of delay with the time

required for the cardiovascular response to occur, the operational G-valve could predispose the pilot to a decreased tolerance to +Gz. An irnproved flow capability, whereby the delay in G-suit pressurization lags the +Gz level by less than 1.O second would greatly reduce this risk. Reducing the delay to less than 1.O second (via high flow G-valves or "preview" control systems) only marginally improves the initial rise in blood pressure and could possibly have a detrimental effect on +Gz tolerance towards the end of the acceleration profile.

79 4.9 Findings Pertinent to Life Support Design Delays in presswization of the extended coverage G-suit significantly affected the ability of subjects to cornplete the acceleration profiles. With increasing acceleration plateaus, pressure/time profiles that lagged +Gz by more than 1 second (i.e., the 3.0 and 4.5 second delay conditions) could decrease tolerance.

Increases in nSBP, only occurred 3 to 4 seconds d e r complete pressurization of the G-suit. This delay was additive with lags introduced by the G-valve. Differences in h e m level systolic blood pressures were shorter in duration than those for P ,.

There were no changes in maximum systolic blood pressures between delay

conditions at al1 +Gz levels tested. Pre-pressurization of the G-suit did not significantly improve tolerance to +Gz in cornparison to a slight lag in inflation (Le., 1.5 second condition). Vision was reported to have been worse in the No Delay condition by the end of the acceleration profile, perhaps indicating a deleterious effect when combined with extended Lower body coverage. No irnprovements in visual field were found to occur for al1 subjects experiencing blackout, irrespective of the length of pressurization delay. Subjects perceived differences in systern responsiveness once pressurization was delayed by more than 2 seconds from +Gz (3.0 and 4.5 second delay conditions). Best ratings were consistent with a system that responds as quickly as possible. The response charactenstics of the current anti-G valve, in combination with an extended coveraee lower bodv ~arment.mav influence tolerance to +Gz.

CHAPTER 5

G-Tolerance Study III - Lower Body Coverage 5.1 Selection of Profiles for Analysis Delays in the presstukation of the G-suit caused additive lags in the cardiovascular response to +Gz. Tolerance to +Gz diminished when pressure to the Gsuit lagged by more than 2 seconds. There was, however, no irnprovement with pre-

inflation (No Delay condition) of the G-suit when compared with a slight (1.5 second) lag in pressurization in subjects wearing an extended coverage G-suit. The time necessary to

pressurize a larger lower body garnient would be expected to M e r delay the cardiovascular response. Possible flow restriction resulting fiom differences in lower garment construction may also influence tolerance to +Gz. However, a larger area of lower body counterpressure rnay also improve tolerance via a greater increase in blood pressure. Acceleration exposures to +4.0, +4.5, and t5.0Gz in which the lower body garment was altered were subsequently exarnined. Profiles in which the G-suit was i d a t e d according to the intermediate (Le., Nominal) schedule without a delay in pressurization were selected. This combination of treatments again ensured that one condition was the same as that used in the previous studies. The three G-suit conditions were cornpared at +4.0 and +4.5 Gz. The traditional G-suit was excluded fiom the +5 Gz analyses, as the data set was not complete at this acceleration level.

5.2 Control of Treatment Variables 5.2.1 Coveraee Condition and G-suit Pressures P,,$

The results of the omnibus testing (rm-ANOVAs) performed on the G-suit pressures measured at each time interval revealed strong Coverage x Time interactions

(Table 5-1). Graphical representation of the pressure/time profiles with the different Gsuits may be found in Amex F-3.

Table 5-1: DeZq x Time I&eractions with D%ferent Leveis of Lower Body Coverage al the +Gz Levels Used in the Expriment 1 +CZ / Source I ss 1 d f 1 MS 1 F 1 PP-P I I

4.0

-

4.5 r

I

1

I

Cover x Time Cover x Time x Subiect Cover x Tirne Cover x Time x Subiect Cover x Time Cover x Time x Subject

I

1

1704.525 420.265 1990.798 703.534 1543.617 397.969

I

1

1

20 100 20 IO0 IC

50

1

1

I

1

--

I

85.226 4.203 99.540 7.035 154362 7.959

20.279

0.0001

14.149

0.0001 m

I

1

19.394

1

1

0.0006

I

Out of 70 possible paired comparisons (30 at +4.0, 30 at +4.5, and 10 at +5.0 Gz), only 10 P, values differed by more than 12.93 rnmHg (0.25 psi) at any time

interval. Contrast analyses found al1 paired comparisons to be significant (AP, 2 12.93

mmHg and p I 0.01). Using the lowest p-value, aw = 1 - (1 - O.O0407)1O = 0.0400, the probability of a false positive fmding was very remote. Figure 5-1 indicates where mean differences in G-suit pressure between coverage conditions at each tirne interval during the three +Gz profiles occurred. Each G-suit was compared against the others, with the amplitude of the pressure difference again represented on the Y axis. hP, was only calculated if the contrast was statistically significant and the difference in G-suit pressures was larger than 12.95 rnmHg. At +4.0 Gz, significant differences in G-suit pressures were found between the lower body ensembles. However, these were only evident during profile onset and lasted for 1 to 2 seconds. The greatest dwerentiais were found with the FPHS, the mean pressure to this ensemble behg 25.3 and 21 -5 rnrnHg less than that recorded in the CSU 15/P and STNG garments, respectively. Pressurization of the STmG G-suit was

FPHS

Figure 5-1: Dz$2erencesin mean P, between G-suit pressures during accelerations to t4.0,+4.5,and + J O Gz.

slightly slower in cornparison to the operational CSU 15/P, resulting in a 13 mmHg pressure difference one second after profile omet. There were no signifïcant differences in pressure between coverage conditions d e r t3. Slow filling of the FPHS resulted in the same trend across d l +Gz levels. At +4.5 Gz, pressure was again lower in this suit (maximum AP, 25.7 mmHg in cornparison to

the STING and CSU 15/P garments). However, the difference in pressure was only present for 2 seconds during profile onset. G-suit pressurization was not significantly different between G-suit conditions after t4 (i.e., 4 seconds after profile onset). The small AP,, found at +4.0 Gz between the CSU 15P and the STING G-suit was not present at +4.5 Gz. With exposure to +5.0 Gz, AP, was less pronounced. Pressure to the FPHS was on average 28.1 mmHg less than that in the STING garment, but only at t2. At al1 other time intervals, there was no difference in the pressurization level between

gamients.

5.3 Treatment Effects 5 -3.1 Subiective Measurement of +Gz Tolerance: Vision During the +4.0 Gz profile, subjects experienced significant changes in vision. Friedman analyses revealed that the different levels of lower body coverage affected both worst peripheral (N=6, df= 2, N'= 8.588, p= 0.0136) and best peripheral (N=6, df= 2,

EI'=10.2 11, p= 0.006 1) vision reported at the end of the profile. Three of the six subjects expenenced complete loss of peripheral vision while wearing the CSU 1 5 P Gsuit, while only one subject had the same level of decrement with the SïTNG garment. Peripheral dimming was the worst peripheral change to have occurred with the FPHS in four of the six subjects, while the rernaining two subjects did not experience any degradation in thek visual field. However, contrast analyses were unable to confimi differences existed in worst peripherd light loss between G-suit conditions. Only one subject wearing either the CSU-lS/P or FPHS reported irnprovements in peripheral vision

by the end of the profüe. Post hoc contrasts did indicate a significant difference in best peripheral light loss between the CSU 15/P and FPHS conditions. Mean ratings of visual change are shown in Figure 5-2.

+4.0 Gz

BLACK

*

E

= O

Worst Periphedt

+ ~ o scentni t t

Berr~eri~heml~

--O- Best centnlt

GREY

E

z L

a

z

>

r

d

DIM

CLEAR

I

I

L

CSU 15/P

ST [NG

I

FPHS

L

I

CSU1S/P

STING

1

FPHS

Coverage

Coverage

BLACK

E

O

Ea m

GREY

ëi

2

5

DIM

*

C L EAR

Worst ~ e r i p h e n l t Besr ~cripheraf

c I

CSU 15/P

ST ING

fPHS

I

CSU LSIP

I

FPHS

Coverage

Coverage

t S ignificant Freidman result (p

ST ING

0.05)

* SignificantIy dierent from CSU 151P (p 10.05) Figure 5-2: Mean subjective ratings of best and worse vision at + 4 O and +4.5 Gr.

Central vision was also found to be significantly af3ected by the arnount of lower body coverage (worst reported central vision (N=6, df= 2,

x2= 9.579, p= 0.0083), best

central vision (N=6, dl+ 2, H'= 7.538, p= 0.023 1)). Two of six subjects wearing the

CSU 15/P experienced either greying or visual blackout, while the remaining four only reported dimming of the central field. With the STING garment, the worst level of central vision compromise was greying in two subjects. Two subjects indicated dirnming of the central field and two had no visuai symptorns. O d y one subject reported dirnming while wearing the FPHS, the rest experienchg no degradation in their vision. Central light loss was found to only irnprove with the CSU-15/P G-suit for two individuals. The subject

that reported visual blackout reported no improvement by the conclusion of the profile. Contrast analyses indicated that worst central vision was statistically different between the FPHS and the CSU 15/P coverage conditions.

Reported visual changes were more pronounced at +4.5 Gz. Worst and best peripheral vision was significantly altrred by lower body coverage (N=6, df= 2, K 2 = 10.000, p= 0.0067; Y *= 9.500, p= 0.0087, respectively). Five of six subjects

experienced complete loss of penpheral vision while wearing either the CSU 1 5 P or STING ensembles. Vision did not improve during the remainder of the profile. The

remaining subject reported greying to have occurred, which irnproved to a dim visual field when the individuai wore the CSU 1 5 P G-suit. The same pattern occwred in central vision. Both worst and best central vision were affected by G-suit condition (N=6, d e 2, ~1'= 19.500, p= 0.0087; t12= 9.294, p= 0.0096, respectively). There were little

differences in mean values (Figure 5-2) between subjects fitted with the STING or CSU 1 5 R . Four of 6 and 3 of 6 subjects indicated having lost complete central vision

(blackout) with the STING and CSU 15/Pgamients, respectively. Vision did not irnprove by the end of the profile. Only one individual reported experiencing blackout with the FPHS. Vision d s o did not irnprove during the +Gz exposure. For the remaining

5 subjects, al1 reported a clear central field by the end of the profile. Limited contrast sensitivity failed to detect differences between the mean ranks for any of the light loss measures at +4.5 Gz. Visual data was not statistically analyzed at +5.0 G z due to the inability to fmd differences between the FPHS and STING conditions with a low sample size. However,

the same trends were noted in light loss. With the STMG G-suit, 4 subjects reported experiencing visual blackout, while 2 subjects experienced the same symptcms with the

FPHS. In al1 cases, vision was not improved by the end of the profile. 5.3 -2 Objective Measurement of +Gz Tolerance: Blood Pressure

The average nSBPHLresponse to hcreasing lower body coverage at the three +Gz

levels used in the experiment are shown in Figure 5-3.

Low Covenge -O- Nominai Coversge High Coverage

[email protected]

x+SEM

Tirne Since Profile Onset (s)

Figure 5-3: Norrnalized heart-level systolic bloodpressure with increasing Zower body coverage.

The three lower body coverage conditions produced varying changes in nSBP,. Pressurization of the standard CSU 15/P G-suit (low coverage) produced the smallest change in hem level systolic blood pressures fkom onset values. The extended coverage STING G-suit (nominal coverage) irnproved the nSBP,

response by approximately 10

mmHg above those measured with the CSU 15P. The largest improvements were produced using the Full Pressure Half Suit (hi& coverage). Results of the omnibus testing (rm-ANOVAs) o n these data indicated weak Coverage x T h e interactions (Table 5-2) at al1 three +Gz levels.

Table 5-2: Lower Body Cornterpressure Coverage x Time Interactions on nSBP, af the + Gs Levels Used in the Experiment +Gz

4.0 4.5 5.O

Sou rce Coverage x Time Coverage x Time x Subject Coverage x T h e Coverage x Tirne x Subject Coverage x Time Coverage x Time x Subject

SS

df

MS

F

3414.519 4369.864 6564.677 8255.043 3984.495 3686.562

20 100

170.739 43.699 328.234 82.550 398.450 53.731

3.907

Pg-g 0.0401

3.976

0.04 18

7.416

0.0135

20 100 10 50

The 49 out of the possible 70 comparisons, in which AnSBP,

differed by 1 1

mmHg or more, were selected for post hoc contrast. aF, calcuiated for d l possible paired cornparisons was 0.3888. indicating a nsk of Type 1error. Figure 5-4 inclicates the t h e intervals at which AnSBP,

between the coverage conditions were significantly different.

As blood pressures were always higher with greater lower body coverage, AnSBP, values were deterrnined relative to the garment producing the largest effect (Le., STING values were always subtracted from FPHS data, etc.). With exposure to +4.0 Gz, nSBP, was significantly higher (AnSBP,

2 11 mmHg

and p l 0.01) with the STNG G-suit in cornparison to the CSU 15/P at only one tirne

period 05). On average, systolic blood pressures were increased by 18.5 mmHg with the

10

Figure 5-4: dnSBPHLin subjects wearing a CSU 15/RSTING, or FPHS G-suit pressurized according to the nominal schedule.

extended coverage suit. Although the FPHS did produce M e r increases in nSBPHL fkom the STNG G-suit, these were not statistically significant. At t7 where a AnSBPH, of 15.7 mmHg occurred between the FPHS and STMG garments (Figure 5-3), the size of the coverage effect was small (o'= 0.2 16). Comparatively, w2 equaled 0.6728 at t5

(STING vs CSU 1YP). In contrast with the CSU 15P, the FPHS did significantly improve nSBPm by 29.1 rnmHg at t6. By the end of the profile (t9 and t10) nSBP,, was not different between coverage conditions. When the profile plateau was raised to +4.5 Gz, the initial hcreases in nSBP, with the STING G-suit above those measured with the CSU 15/P were no longer evident.

Variability in bIood pressure was greater with little improvement above levels found at +4.0 Gz. The FPHS bnefly produced significant increases in nSBPm (AnSBPm 2 11 mmHg and p l 0.01) at tg. In cornparison against the CSU 1 5 P ensemble, the amplitude

of the change in blood pressure was higher and the duration longer with FPHS. The mean increase in nSBP,, was 30.1 mmHg fiom t8 to t10. Pressurization of the FPHS did produce a significantly higher AnSBPm at +5.0 Gz than that found with the STMG G-suit. Improvement occurred early in the profile (t4) and was maintained for the duration of the exposure. The magnitude of the effect was a mean increase of 25.6 d

g between t4 and t10.

5.3.3 Summarv of Findings and The Effect of a Twe I Error With exposure to +4.0 and +4.5 Gz, any differences in nSBPHLbetween the three coverage conditions were very bnef in duration, potentially even shorter taking into consideration the possibility of a false positive event. Added to this is the buffering capacity of the oxygen reserves. Therefore, blood pressure should not be considered

different between coverage conditions at these two acceleration levels.

Blood pressure was, however, higher when subjects wore the FPHS compared to that measured with a SïTNG garment with exposure to +5.0 Gz. This difference in

nSBP, was present for most of the acceleration profile, and would be little af6ected by the presence of a Type 1error in any of the significant comparisons.

5.4 Lower Body Coverage and Acceleration Tolerance G-suit pressures with the various lower body garments were found to differ during the initial onset of +Gz, but mean values differed by less than 0.25 psi (12.93 &g)

at the end of the accelera5on profile. This would indicate that resistive and/or

volume dserences between the G-suits affected G-valve performance. The FPHS was

always slowest to idlate, resulting in the 0.5 psi (25.5 mmHg) underpressurization found imrnediately &ter profile onset when compared to the other two G-suits. Pressure/time profiles did not differ between STING and CSU-1 5/P ensembles. Tolerance to +Gz was affected by the amount of lower body coverage. As the

+Gz Ievel was increased, the standard CSU 15/P was found to produce only marginal improvernents in nSBP,, (Figure 5-3). Consequently, it was not surprishg that one subject terminated the +5.0 Gz exposure while wearing this garment. Even though it provided a greater arnount of lower body counterpressure, the STMG G-suit was ineffective at improving tolerance to +Gz beyond that provided by the standard (CSU 15B) garment at both +4.0 and +4.5 Gz. There were little differences in either the

AnSBP, or reported light loss values. The only interval during which the STMG G-suit increased systolic blood pressure enough to potentially improve tolerance by 0.5 Gz (Le.,

AnSBP,

> 11 mmHg) occurred five seconds following profile onset at +4.0 Gz.

Therefore, implementation of an extended G-suit pressurized according to the nominal (1.5 psi/G) schedule may not substantially improve relaxed +Gz tolerance in aircrew exposed to low accelerative forces.

In order to induce the largest increases in G tolermce, a full pressure G-suit must be worn. This lower body garment both improved nSBPHLand minimized the extent of visual light loss, the effects being most noticeable at the highest +Gz level. Dserences in heart level blood pressures increased in duration and magnitude with +Gz. At t5.0 Gz, blood pressure was significantly higher than that found with the STING G-suit, and this difference existed fiom just after attainrnent of the +Gz plateau (t4) and was rnaintained for the duration of the profile. This would indicate that the effectiveness of this gannent may be influenced by the pressure/time profile and fmal pressure provided by the Gvalve (i.e., the pressurization schedule). Given that all subjects reported the FPHS to be either "slightly uncornfortable" or "ùitolerable" with the nominal pressurization schedule, it may be inadvisable to M e r increase the final pressure above these levels. In addition to raising the mean blood pressure during the +Gz profile, the FPHS eEect was less variable across the acceleration levels (refer to SEM values in Figure 5-3). Even though differences between mean nSBPHLmay have been large (i.e., 38 d

g between FPHS and

CSU 15/P at t4 during the t4.5 Gz exposure), the increased variability with the latter garment, coupled with a small sample size, made it very diEcult to detect the coverage effect. Consequently, the FPHS may have been more effective at lower +Gz levels, and provided an improved blood pressure response for longer durations.

The cardiovasculv response witl a full pressure half suit can be seen in Figure 5-5. Tracings for two subjects exposed to t5.0 Gz are shown. The G-suit was pressurized according to the nominal schedule. Note that the increase in blood pressure fiom profile onset was approximately the same for both subjects (80 d g ) . Systolic blood pressure increased rapidly in Subject A with inflation of the G-suit to 232 m d g ,

and kept rising for 3 cardiac cycles after complete pressurization of the lower garment. This lag in response corresponded to a delay of approximately 2.5 seconds. A steady state followed, with systolic blood pressures of 200 m g . Blood pressure was then rnaintained at this level for the duration of the profile. The subject reported expenencing

peripheral greying and centrai dimmuig, wîthout any improvements in vision during the

+Gz exposure. The response for Subject B differed substantially. Initial systolic blood pressure values were approximately 40 mmHg higher at profile onset. Pressurization of the FPHS caused SBP to increase to 240 mmHg, but the rise was much slower for this subject and took place over 6 cardiac cycles. Increases in blood pressure were delayed by 4.5 seconds fkom the time of complete lower body pressurization to the time at which maximum values were reached, alrnost twice as long as that noted for Subject A. Blood pressure did not achieve steady state, as a secondary decline followed. The rate of the decrease was similar to the rate of blood pressure nse following complete pressuization of the G-suit.

During the latter stages of the acceleration exposure, the intersystolic interval was lengthened and cardiac arrhythmia was evident. Large decreases in blood pressure resulting fkom the rhythnl anomalies were reflected in the amplitude of the ear pulse. The subject reported only dirnrning of the peripheral visual field, which cleared by the end of the profile. In al1 conditions, pressure to the three lower body garments was the same at the +Gz plateau. Therefore, differences in the cardiovascular response were due to the effect

of coverage. Figure 5-3 indicated that the magnitude of the blood pressure changes was greater with a higher level of lower body counterpressure. The increases in blood pressure took place over several cardiac cycles, with the greatest improvements occurring only after complete pressurization of the garment (Figure 5-5). The slow cardiovascular

response with varying levels of coverage was consistent with that found using different pressure levels, and with delays introduced in the pressure/time profile. This would irnpiy that the underlying mechanism(s) responsible for the increases in blood pressure

may be the same for d l factors pertaining to lower body pressurization (pressure, delay, and coverage). However, the cardiovascular response also demonstrated a secondary

decrease in blood pressure in subjects wearing the FPHS. Effective use of counterpressure may prove to be advantageous during the short term, but could aiso lead to a declining level of protection if the duration of the acceleration profile is extended. Further evaluation of the data is required before this hypothesis can be confkmed.

5.5 Additional Factors and Issues 5.5.1 Subiective Ratings of Comfort

Mean subjective ratings of comfort with the three G-suits at +4.0, +4.5, and +5.0

Gz are shown in Figure 5-6. The data for the CSU 15P garment was included in the +5.0

Gz analysis as the one subject that terminated the profile early experienced complete pressurization of the suit, and was dius capable of providing an accurate response.

C S U ISlP

5S n N G FPHS

t

Significant Freidrnan result (p 5 0.05)

Slightly Uncornfortable

Cornfortabte -

Figure 5-6: Mean ratings of comfort with the three lower body garments at +1.0, + 4.5, and +5.O Gz.

Cornfort was not appreciably different with the three lower body garments at +4.0 Gz. There was a difference in reported comfort levels at +4.5 Gz (N=6,df= 3 H'=

7.000, p= 0.0302). Surprisingly, the STING G-suit was ranked the most comfortable, while al1 individuals found the FPHS either "uncomfortabIe" or "intolerable" with its

pressurization. Post hoc analyses did not fmd ciifferences in these rankings. Subjects rated al1 G-suits less intrusive at +5.0 Gz. There was no effect of lower body garnient on their ratings.

5.5.2 Cardiac Anomalies with FPHS

Pressurization of the FPHS caused significant cardiac rhythm anomalies in 2 of the

6 subjects. The arrhythmias were usually incurred at the highest acceleration level(+5 Gz) and with the highest level of pressure applied to the garment (Le., nominal schedule). After a period of prolonged post-nin bradycardia in one of these individuals, it was decided that al1 conditions were not to be completed. The other subject fuiished al1 treatrnent combinations with this garment. Figure 5-7 demonstrates the cardiovascular response of the latter to a +5 Gz profile with the FPHS pressurized according to the Low (tracing A) and Nominal (tracing

B) schedules. Both exposures were completed 10 minutes apart, with 3 profiles interspersed between them. Inflation of the FPHS with the Low schedule resulted in a delayed blood pressure rise (tracing A). The subject reported experiencing visual blackout, which can be verified by the lightbar responses.

Maximum systolic pressures were higher with the Nominal pressurization schedule (tracing B), but sinus bradycardia occurred during the plateau portion of the

g extended asystolic intervals were lower than those exposure. Blood pressures d u ~ the recorded with the Low schedule. Note that vision was compromised to the same degree (i.e., blackout) and that the subject failed to respond to the lightbar challenges approximately 2 seconds earlier into the acceleration profile. Use of the FPHS garment has been shown to have caused simcant

rhythm

disturbances in past studies (Cochran, 1954). Wood (1 990) postulated that depressor

reflexes fkom the aortic arch may have mediated this response. He concluded that very effective garments may provoke Iife threatening arrhythmogenic mechanisms, which should not be disregarded in the development of life support systems for high +Gz protection. Consequently, the use of the FPHS with al1 aircrew should be implemented with extrerne caution. Sinus Btadycardia

Figure 5-7: Cardiovascular revonse with a FPHS pressurized to 155 and 232 mmHg. Same subject at +S. O Gz. Note the sinus bradycardia with the higher schedule and that visual blackout occurred earlier into the profile.

5.6 Treatment Level in Relation to the Operational Environment Given that the amount of lower body coverage does improve tolerance to +Gz, irnplementation of a G-suit such as the FPHS may benefit pilots in the operational

environment. As the design of this lower body garment differs significantly fiom that currently used with the aircraft, the ability of the standard Alar G-valve to adequately pressurize a large volume garment has yet to be determined. A low flow fiom the Gvalve, coupled with higher resistance, could produce significant delays and pressure drops that may negate the positive improvements fiom greater counterpressure. To determine the pressure time profile for the respective garments, three subjects were exposed to +5.0 Gz while wearing one of the three G-suits pressurized with the

Alar G-valve. Mean pressures measured over three consecutive profiles were then plotted against time and are shown in Figure 5-8.

-----CSU 15P

- STiNG

O

1

2

3

4

5

6

7

8

FPHS

9

1

0

Time Since Profile Onset (s) Figure j-8:Pressure/time profiles of Alar G-valve performance with subjects wearing the CSU IS/P, STING, or FPHS. As thefinal pressures (P,J differed at the end of the profile, time to intermediate pressure levels were used to assess coverage effects. Time to a G-suit pressure of 200 mmHg (tJOdis represented by the dashed line, indicating that it took almost 5 seconds afler profile onset before pressure in the FPHS attained this levez.

The mean pressure over the fmal second (tg to t10) was taken as the maximum

(Pmaavalue. This was found to differ between coverage conditions, with Pm, falling as the level of counterpressure increased. Time to intermediate pressure of 50, LOO, 150, and 200 mmHg (t,,, t,,, t,,,, and tZo0) were subsequently selected. The time to 90% of

maximum pressure (bw.)was also detemiioed. The results are shown in Table 5-3. Table 5-3: Times to Intermediate Pressures in Subjects Eqosed to +5.O Gz with Dzfferent Lower Body Guments Pressurized by the AZar G-valve

Pm, values indicated that the performance of the Alar G-valve was affected by the design of the G-suits. The lower pressures found with the STING and FPHS were most likely due to increased resistance to flow. By the end of the profile, the FPHS had not achieved a steady state pressure (Figure 5-8). Times to the various pressure levels did not differ much between the STTNG and CSU 15/P, but the FPHS took significantly longer to attain the same G-suit pressures. Time to 90% (ho./.)provided a very conservative indication as to how long it took to pressurize the garment to 90% of its final value. Subtracting the time required for the acceleration profile to attain 90% of its target value (i.e., 2.5 s), the delay in G-suit pressurization fiom the +Gz input c m then be deterrnined and evaluated against previous conditions. In the preceding study, subjects expenenced a decrease in tolerance once the delay in pressurization was longer than 2.5 s (analogous to the 3 second delay condition) while wearing the STING lower garment. Given the 3 second delay in the G-suit pressurehime profile found with the AlarEPHS, any gains in tolerance provided by the additional lower body coverage could be negated by delays in garment pressurization.

Therefore, augmentation of the flow capabilities of the current operational G-valve andlor an improved design of the FPHS to decrease flow restrictions may be required. 5.7 Findings Pertinent to Life Support Design

1. Tolerance to +Gz was aBected by the amount of lower body coverage. 2. Increases in nSBP,, were delayed with respect to pressurization of the G-suit, but

attained higher levels in proportion to the counterpressure surface area. 3. The blood pressure response in subjects wearing a FPHS was much more variable in

cornparison to exposures with the STMG and CSU 154' ensembles. Some of the varïability could be due to a secondary decrease in blood pressure found to occur in some individuals. 4. Pressurization of the FPHS could provoke arrhythmogenic mechanisms in some

aircrew. 5. Inflation of the FPHS with a nominal pressure schedule produced higher levels of

discornfort than with the STING and CSU 25/PG-suits. A more aggressive schedule would likely be intolerable and unacceptable to aircrew. 6 . Use of the current operational G-valve with larger volume lower body g m e n t s

produces hcreasing delays in pressurization that rnay negate any potential improvements in +Gz tolerance.

CHAPTER 6

G-Tolerance Study IV - Positive Pressure Breathing 6.1 Selection of Profiles for Analysis The cardiovascular response to +Gz was found to be similar with different G-suit pressure schedules if delays were introduced before inflation of the garment was commenced, or if the arnount of coverage provided by the G-suit was altered. These factors involved the lower body, with no perturbations imposed on regions above the abdomen. As positive pressure breathing during +Gz (PBG) is being introduced as a means of improving tolerance to +Gz, it is unknown as to whether the cardiovascular response is af5ected by the associated increased intrathoracic pressures. As PBG only began at +Gz levels greater than +3.5 Gz, exposures to +4.0, +4.5, and +5.0 G z could o d y be used. Treatment conditions were selected for statistical and comparative purposes. Of the three possible G-suits used in the expenmental matrix, conditions in which subjects wore the STTNG garrnent were analyzed. Selection of runs with the Nominal pressurization schedule was consistent with treatments examined in

previous studies. As dl subjects had to have completed al1 runs with this garment and to avoid introducing G-valve responsiveness effects, the No Delay situation was chosen.

6.2 Control of Treatment Variables

6.2.1 G-suit and Mask Cavitv Pressure

G-suit time/pressure profiles (Pd may be found in Annex F-4. The increase in variance in the High PBG condition was due to a 48 mmHg overpressurization in one of the six subjects. This did not significantly alter mean measured P, from target levels. Changes in the averaged blood pressure response in this condition should only be marginally affected by the difference in lower body garment pressure. Furthemore, larger

differentials produced by changes in P, schedule were ineffective in raising systemic blood pressures (Snidy 1). Omnibus testing (rm-ANOVAs) performed on the mask cavity pressures measured at each time interval revealed strong PBG x T h e interactions (Table 6-1).

Table 6-1: PBG Schedule x Time Interactions on Mask C m i Pressures ~ (Pd at the +Gz LeveZs Used in the fiperiment +cz

4.0 L

4.5 5 .O

1

Source PBG x Tinte PBG x T h e x Subject PBG x Time PBG x Time x Subject PBG x Time PBG x Time x Subject

SS 839.016 174.460

3271.650 208.276 7254.7 10 297.329

1 1 1

df 20 100 20 100 20 100

MS

F

Pg-g;

41.95 1

24.046

0.000 1

78.541

0.0001

121.998

0.0001

1.745 I

163.583 2.083 362.736 2.973

I

Differences in mean mask pressures (AP,) were calculated between PBG conditions at each tirne interval. 72 out of a possible 99 paired comparisons (33 at each +Gz level) differed by more than 5 mmHg at any time interval. Contrast analyses found

al1 paired comparisons to be significant (AP, 2 5 mmHg and p 5 0.01). The probability o f family wise Type 1error (aFw) was 1 - (1 - 0.0 1)"

= 0.5 150, hdicating

the need for

cautious interpretation of the post hoc analyses. Figure 6-1 shows the mean differences at each t h e interval for the three PBG schedules. A€', in mask cavity pressure (Mm)

was only calculated if the contrast was statistically significant and the difference mask pressures was larger than 5 mmHg. At +4.0 Gz, significant differences were found between pressure breathing schedules. The low PBG schedule produced significantly higher (AP, t 5 mmHg and p l

0.01) mask cavity pressures above the No PBG condition for transient periods. Significance did not occur until5 seconds after profile onset fkom baseline +Gz, was not evident at t8 and tg, and was higher by the end of the profile. The High PBG schedule provided raised mask cavity pressures above those measured with either the No PBG and

Figrrre 6-1: Dzzerences in mean mark cmity pressures (Md with no positive pressure breathing, Lo W. and High PBG schedules during exposures to + 4.0, +4.5, and +5.0 Gz.

Low PBG conditions. Significantly higher pressures (AP, > 5 mmHg and p S 0.0 1) occurred at t3 and were rnaintained for the duration of the profile. At 4-4.5 and +5.0 Gz, the PBG scheddes differed (AP, 2 5 mmHg and pS 0.01) just after profile onset (t2 or t3). Significantiy higher pressures were produced by the Low and High PBG scheddes in

cornparison to the No PBG condition. The High PBG mask pressures were also raised above Low PBG schedule values. Accuracy of the final pressures provided by the PBG regulator was assessed by cornparing the cdculated target values against the mean Pmvalues measured during the last

5 seconds (t6 to t10) of the profile. This data can be found in Table 6-2. Table 6-2: Target and Actual Pm Values Measured During the Las&5 Seconds of the Accelemtion Profile for AZZ Conditions +Cz

PBG Schedule None LOW H igh None Low High None

4 .O

4.5

5.0

Low

High

1 Target (mmHg) 0.00 6.25 12.50

1

Actual (mmHg) SEM (mmHg) Error (mmHg) O. 17 - i -20 - 1.20 4.03 10.3 1

0.20 0.28

-2.22 -2.19

0.00 12.50 25.00

-1 .O6 1 1.O4 22-92

O. 16 O -24 0.42

- 1.O6 - 1.46 -2.08

0.00 18.75 37.50

-1.12 17.25 3 5 -46

0.20 0.30 0.5 1

-1.12 - 1.50 -2.04

At the end of the profile, mask cavity pressures were found to be very reproducible (Iow SEM) with the three PBG schedule at al1 +Gz levels. The error (Actual - Target) was found to be very small. Pm,on average, was no more than 2.2 d

g below target levels. These findings indicated that the regulator provided

appropriate, reproducible mask pressures during ali conditions and at al1 +Gz levels. 6.3 Treatment Effects

6.3.1 Subjective Measurement of +Gz Tolerance: Vision

Mean subjective ratings of visual light loss during exposure to +4.0, +4.5, and +5.0 Gz are shown in Figure 6-2.

BLACK

z

+4.0 Gz

11

+

Wont P c r i p h 4

Worst C e d

Best C e n d

Bat R r i p h e d

GREY

NONE

HIGH

LOW

NONE

LOW

HIGH

BLACK

VJ

= C

GREY

C

h

V1 d

Q

3 VJ

>

a-

DIM --)- Worst Peripheral B a t Rriphenl CLEAR

'

I

NONE

I

I

LOW

I

HIGH

NONE

I

r

1

I

LOW

H IGH

BLACK

rn Y

GREY

C

* CLEAR

Wost Peripheral

t Besr C e n a l

BestEkriphenl

I

1

NONE

L

LOW

PBG Schedule

H IGH

NONE

1

LOW

H IGH

PBG Schedule

Figure 6-2: Subject reports of best and worst vision at + 1.0,+ 1.5 Gz and +5.0Gz with three levels of PBG.

During the +4.0 Gz profile, peripherai vision was compromised most without

PBG and with the low PBG schedule. Without PBG, two subjects reported their worst syrnptoms as either clear or dimmed. Three individuals experienced greying, while one reported complete loss of the penpheral visual field. With the low PBG schedule, 4 subjects reported little change in vision (Le., clear or dim peripheral fields), with the remahhg two subjects experiencing peripheral black out. Al1 subjects reported their worst level of peripherai light loss as clear o r dirn with the high PBG schedule. These ratings were not found to be statistically different. Peripheral vision did not improve in the No PBG condition for any of the subjects. With the low PBG schedule, one subject reported a change from dim to clear in their visual state. The two individuals that had lost complete peripheral vision indicated no improvement by the end of the acceleration profile. A high PBG schedule cleared a dimmed visual field for three of the four subjects with compromised peripheral vision. nie effect of PBG schedule on best reported

peripheral light loss was significant (N=6, df= 2, K'= 6.706, p= 0.0350), but contrast cornparisons of the mean ranking were not sensitive enough to c o n f m where these changes occurred.

The extent of central vision degradation was less than that found for the peripheral field. Two subjects reported greying as their worst symptoms without PBG, while only one individual had central vision compromised to diis level. No subjects experienced central greying with the high PBG schedule. Vision did not improve for any of the 4 subjects that reported central changes in the No PBG condition, while 2 of 3 individuals stated the central vision did irnprove by the end of the acceleration profile with the Low PBG schedule. The lone subject that reported central dirnming indicated no improvement with the Hiph PBG schedule. Mean ratings were not found to be statistically significant

for both worst and best central light loss.

The same pattern of light Ioss was evident at +4.5 Gz, but the extent of visual degradation was greater. Five of the six subjects expenenced cornplete loss of peripheral vision with No PBG, while 4 and 3 of the six individuals had the sarne symptornology with the Low and High PBG schedules, respectively. Only one subject cornpleted the

profde with no alterations in central vision, and that occurred with the High PBG schedule. Vision did not improve for any of the subjects that reported complete loss of the penpheral visual field in either the No PBG or Low PBG conditions. With the High PBG scheduie, one individual did indicate that they did regain peripheral vision, but that it was grey at the end of the acceleration profile. Results of the Friedman analyses suggested that worst and best peripheral light loss reports were not af5ected by the PBG schedule. Friedman analyses indicated significant effects of PBG on central vision changes

(worst reported central vision ( W 6 , df= 2,

x:'=9.500, p= 0.0087), best central vision

(N-6, df= 2, EI 2= 8.400, p= 0.01 50)). 4 out of the 6 subjects had expenenced complete loss of their central visual field in the No PBG condition. This level of visud degradation was not found in any individuals with either the Low or High PBG schedules, as 3 of the 6 subjects reported only greying. Central vision was not improved without PBG by the

end of the acceleration profile. Contrast analyses were unable to detennine which conditions differed for both measures. Vision was M e r degraded with exposure to +5.0 Gz. In al1 subjects, peripheral vision was completely lost with no PBG or the Low PBG schedule. Peripheral vision did not improve by the end of the profile. With a High PBG schedule, only 3 of the 6 subjects experienced the same extend of visual change. Two individuals reported their worst peripheral vision as grey, while one only encountered dunming. Peripheral vision was not regained by the 3 subjects expenencing penpheral blackout, and only one of six

had any improvernent by the end of the profile. Worst and best reported peripheral

changes were signif~cant(N=6, df= 2, ~ ~ 6 . 0 0p= 0 ,0.0498 for both measures), but the mean rankings were not found to be different by the post hoc contrasts. Central vision was completely lost (i-e., blackout) in 4 and 3 of the six subject with either No PBG or the Low PBG schedule, respectively. Vision was never regained by the end of the profile. With either condition, worst central vision was reported to be grey in the remaining individuals. A High PBG schedule resulted in greying of the central field for two of the six subjects, with the rest experiencing only dùnming. Vision was only improved for one subject initially reporting central dimming, which improved to

clear by the end of the profile. Similar to the peripherd changes, central vision was found to be different by the Friedman analyses (worst reported cenbal vision (N=6, df= 2, Hz= 9.500, p= 0.0087), best central vision (N=6, df= 2, N

'= 8.400, p= 0.0150)),

but no

differences were identified between mean ranks by the post hoc comparisons.

6.3 -2 Obiective Measurement of +Gz Tolerance: Blood Pressure The average nSBP,

response to positive pressure breathing at the three highest

+Gz levels used in the experiment are shown in Figure 6-3.

The normalized heart level systolic blood pressure (nSBP,)

response to PBG did

not differ much at al1 +Gz ievels. At +4.0 Gz, mean nSBPHLincreased at the same rate

with al1 PBG schedules, attained a maximum level at t5 or t6, and either remained at this level or fell slightly during the rernainder of the profile. The same pattern was found at +4.5 Gz. nSBPHLwas not increased fiom +4.0 Gz levels and a greater drop in blood

pressure occurred during the fmal few seconds of +Gz exposure. Srnall irnprovernents in

nSBPHLwere evident at +5.0 G z during the middle of the profile. These differences were not rnaintained and blood pressures were the same by t10.

+4.0 Gz No PBG

+Low PBG Schedule

---*---

High PBG Schedule

Z

SEM

Time Since Profile Onset (s)

Figure 6-3: Normalized heari-leve l systoIic blood pressure w ith no positive pressure breathing (Nc PBG), a Low PBG, and a High PBG schedule ai +4.0, + 4.5,and + 5.0 Gz. Results of the omnibus testing (rm-ANOVAs) on these data confirmed that there was little effect of PBG schedule on the blood pressure response. Only a main effect of Time was significant at each +Gz level (no main effect of PBG or a PBG x Time

interaction). Table 6-3 is a sumrnary of the main Thne effects at al1 three +Gz levels. Table 6-3: Main Effeci of Time on n S f i ut the + Gz Levels Used in the Ekperiment

1

4.0

1

1

l

4.5

I

SS

Source

+Gz

I

Time Tirne x Subieet Tirne Time x Subiect

-

Time x Subject

1

981.166 43.812

I

1

48 11.432 175.624 109.101

df

MS

F

Pz-g

10 50

98.1 17 0.876

1 1 1.975

0.0001

I

1

48 1.143 3.512

10 50

1

50

1

2.182

1

1

1

I

0.000 1

136.981

1

1

PBG Effect (Hearr Level) 4 P g Effect ( H e m Level)

I....~..~Ys I

~

.

.

~

~

.

PBG E f f a (Eye Level) Pgs Effcct (Eyc Levei) ~

D

~

~

~

Time Since Profile Onset (s)

Figure 6-4: nSBPHLand nSBP,, responses collapsed across G-suitand PBG schedules at + 4 0 , -1-4.5,and t5.O Gz.

Data were collapsed across PBG schedule at each +Gz level. Mean heart level systolic blood pressures (nSBPHL) were used to calculate eye level equivalents (nSBPEL) by compensahg for hydrostatically induced changes. Both data sets are shown in Figure 6-4. In addition, the cardiovascular response fiom the initial investigation (effect of dBerent levels of lower garment pressurization, collapsed across P, schedule) were added to the graph. At each time interval, the mean blood pressures were plotted and the standard error of the mean is shown with the heart level values. Eye level variance was the same as that measured at heart level. From the figure, it is apparent that the cardiovascular response was similar between the two treamients (P,, and PBG schedule). The length of the delay in blood pressure increase was the sarne in both instances. Heart level values were raised over time and attained a steady state level at al1 +Gz levels after approximately 5 to 6 seconds after profile onset. Eye level equivalents were found to decrease sharply durhg the first few seconds of +Gz exposure, rose quickly over the next 2 seconds yet never retumed to baseline values. As the +Gz level increased, eye level pressures were progressively diminished. Variability (SEM) in systolic blood pressures was less with the three PBG schedules compared to that produced by the G-suit pressurization schedules. 6.4 PBG Schedules and Acceleration Toierance

When PBG was used at each +Gz level, the mask cavity pressures (Pm)provided

by the regulator differed by at least 5 mmHg a few seconds after profüe onset. At the +Gz plateau, target values were reproducibly attained. Thus, any changes in the cardiovascular response fiom that measured in the No PBG condition would have been attributable to the added positive pressures fiom the two PBG schedules. As seen fiom Figure 6-3, there were no significant improvements in blood

pressures produced with PBG. The lack of a large improvement in nSBPHLmay have

been due to the relatively low mask pressures attained at +4.0 G z (Le., 6.25 and 12.5 mmHg with the Low and High PBG schedules, respectively). However,

Pm was raised to

25 mmHg at +4.5 Gz with the High schedule, but nSBPHLwas the same for ail conditions. Only ai +5.0 Gz were any increases in nSBPHLevident. At t3 and t4, mean nSBP, was temporarily raised above levels measured with no pressure breathing or a Low PBG schedule. This difference was quickly reduced over the succeeding tirne intervals and mean systolic blood pressures were the same by the end of the acceleration profile. The transitory nature of the blood pressure response was not found to be statistically significant, perhaps due to the large variability associated with the effect. When the blood pressure data were collapsed across PBG schedule, the cardiovascular response was very similar to that found with the G-suit schedule data. Heart level pressures were always slow to increase, while eye-level equivalents dropped dramatically during profile onset. The net effect was a temporary decrease in head level pressures during the initial few seconds of +Gz exposure, then nSBP,

recovered over the

next few seconds before a steady state level was attained. As heart level values never increased enough to counter the added hydrostatic falls at head level with increasing +Gz, perfusion pressures and, consequently tolerance to +Gz, was reduced. Analyses of the visual reports of light loss seemed to indicate that PBG did improve vision with the High PBG schedule. At al1 +Gz levels, perïpheral and central light loss ratings were best with the highest mask pressures. Consequently, the small transitory increase in systolic blood pressure found with the High PBG schedule would have occurred at the moment eye level pressures were most susceptible to the largest decreases (tl to t4). This rnay explain the improved visual field without a large change in systolic blood pressure across the entire acceleration profile. Figure 6-5 depicts how this may have occwed for one subject. Two tracings

fÎom the same individual exposed to +5.0 Gz are shown. The G-sL& was pressurized

according to the nominal schedule and attained 232 mmHg during the plateau stage of the acceleration exposure. During the first profile, no mask pressure was provided by the

PBG regulator. Systolic blood pressure (SBP) rose with G-suit pressurization and continued to increase for 3 to 4 cardiac cycles d e r complete pressurization of the lower body garment. After attaining a peak SBP, blood pressures decreased slightly over tirne. Note that the subject expenenced blackout at the end of the profile, at the time indicated by the arrow. The change in SBP attributed to the inflation of the G-suit (ASBPpF)was calculated as the merence from the onset blood pressure and a mean approximated from the steady state level. Consequently, with pressurization of the G-suit, systolic blood pressure was found to increase by approximately 44 mmHg from the onset value. With the high PBG schedule, the lag in the blood pressure response was of the sarne duration (4 seconds in both occasions). However, the increase in SBP at the peak of the response was greater by 22 mmHg over that found in the no PBG condition. This improved cardiovascular response would indicate that almost 60% of the rnask cavity pressure was translated into an increase in blood pressure. This value is very sirnilar with that found in the literature (Ernsting, 1969; Prior, 1989). This rise in blood pressure was not maintained, as a greater rate of decrease followed in cornparison to the No PBG state. By the end of the profile, there was no difference in normalized blood pressure between conditions. The improved visual field may have been due to either the transitional increase in blood pressure or, perhaps, due to the slightly higher baseline value. Ln either case, a marginal and temporary improvement in +Gz tolerance could be due to the introduction of PBG.

6.5 Treatment Level in Relation to the Operational Environment

PBG did not substantially improve relaxed +Gz tolerance at or below +5.0 Gz if systolic blood pressure was used as a comparative measure. However, subjects did

report decreased visual impairment with the High positive pressure breathing schedule. Given that a pilot relies on vision to perform flight duties, any improvement in vision would enhance safety and operationai effectiveness. With an extended coverage (STING) G-suit inflated accordhg to the nominal presswization schedule, the greatest visual deficits occurred in the No PBG condition at

al1 +Gz levels (Figure 6-2). In order to benefit from the implementation of positive pressure breathing, the PBG schedule must produce at least a change in the visual field at a +Gz Ievel at which vision is degraded enough to a u e n c e flight operations. The reported visual disturbances at +4.0 G z without PBG met this criterion. At this +Gz plateau, the High PBG condition provided a mask cavity pressure of only 12.5 m d g . However, peripherd vision was greatly improved with this schedule, in contrast to changes that occurred with either no pressure breathing or the Low PBG condition. Thus, a PBG schedule should be aggressive enough to provide this level of mask cavity pressure in order to improve vision and, ultimateiy, flight operations.

Potential loss of effectiveness can be seen in Figure 6-6. Two bold lines are used to represent the curent United States Air Force (USAF) schedule and one proposed for the Canadian Air Force (Wigh). For reference, the Low PBG (fine line) condition was added. The pressure output from a PBG regulator is s h o w on the ordinate as a function of +Gz. Pressure to the oronasal mask is detennined by the cut-in (Le., starting +Gz) and rate of pressure increase (slope). A change in cut-in and/or dope c m be used to alter the final output pressure. The Iate cut-in and shallow slope of the USAF schedule resulted in

no pressure output at +4.0 Gz. Consequently, any benefit of PBG at the low +Gz levels was lost completely. If the intent of implementing PBG is to improve +Gz intensity tolerance, an aggressive (early cut-in with high slope) would prove most effective.

High

Low

USAF

Figure 6-6: Regulaor outpur pressures provided by the m r e n r United States Air Force (USAF) andproposed Canadian Air Force (High)PBG schedules. The Low condition used in the experiment was uddedfor rejerence. Note that any benefls of PBG are lost at + 4 O Gz due to the laie start and shallow dope of the USAF schedule. Using mean ratings, penpheral light loss at +5.0Gz with the High PBG schedule was only slightly worse than the visual symptoms reported at +4.0 Gz without pressure breathing (Figure 6-2). This wodd indicate that PBG couid improve tolerance by slightly less than 1 +Gz in the relaxed state.

Even wiîh an aggressive PBG schedule, vision degraded with increasing +Gz plateaus. Based on subjective data, better vision correlated with higher output pressures fkom the PBG regulator. By +5.0 Gz, subjects began reporting visual blackout in the High PBG condition. The rate of pressure increase with the High schedule may not compensate for hydrostatically induced head level pressure decreases. As to whether or not higher mask pressures would alleviate these symptoms at and above +5.0 Gz remains

6.6 Findings Pertinent to Life Support Design 1. Subjective reports of worst and best vision did indicate that positive pressure breathing did improve tolerance to +Gz. Higher mask cavity pressures correlated

with a decrease in visual symptoms. 2. PBG did not significantly alter the cardiovascular response to +Gz. Both heart and eye level blood pressures were delayed with respect to pressurization of the G-suit, but attained similar leveIs with the three PBG conditions used. 3. In order to derive an improvement in +Gz tolerance, a PBG schedule should require

early pressure supply to the mask cavity and increase at a high rate. Schedules that have a late cut-in andlor shallow dope may provide little benefit to aircrew at low acceleration levels (St5.0 Gz).

CHAPTER 7

Implementation of a Simple Inferential Mode1 7.1 Statement of Requirement Improved +Gz tolerance, as defmed by alterations in systotic blood pressure a d o r reported visual statu, indicates the potential operational benefits attributable to changes in the dtfferent aspects of a life support system (pressure, coverage, G-valve responsiveness, and PBG). What remains unknown are how these variations in the life support system parameters affect the determinants and components of the blood pressure response. What are the time courses for their respective changes, and to what extent are underlying mechanisms involved? As invasive techniques could not be used, measurements of flow and resistance could not be performed. Therefore, a methodology was required that was based on the interdependent nature of pressure, flow, and resistance (Le., blood pressure, cardiac output, and total penpheral resistance in the cardiovascular system). If an estirnate of flow (Le., a change in volume over a known tirne interval) could be determined fiom components of the blood pressure waveform, alterations in resistance could then be calcufated. Thus, die respective changes in these two variables (flow and resistance) are not measured, but inferred.

7.2 Mathematical Models of Cardiovascular Function: RoIes in Research Developing models of responses to perturbations of the cardiovascular system has taken place for most of this century. Techniques have included the generation of electrical andogs that range in complexity fi-om a single element b a i s to multi-element structures incorporating Navier-Stokes equations for predictive purposes in which measurements were difficult or impossible to perform (Jaron et al., 1984). Others (Wamer et al., 1953; Wesseling et al., 1993; Self et al., 1994) have attempted to extract additional information nom blood fiow and/or pressure signds already recorded.

The degree of predictive accuracy required of a model is dependent on its objective. As the final output of the model is a mathematical estimation, the precision with which the final prediction matches the actual value is detennined by the degree of

detail andor the validity of the model. Consequently, a simple rnodel may provide as accurate an estimate as that fiom a cornplex variant whose underlying assumptions are not met.

7.3 Modeis Used for Determining Flow and Peripheral Resistance For the purpose of estirnating cardiac output fiom the systemic artenal pressure waveform, various models have been developed around the principal factors affecting lefi ventricular outflow (Le., the stroke volume), primarily the aortic impedance (Zo), aortic capacitance (C,), and peripheral resistance (R,).Two such models (Kouchoukos et al., 1970; Wesseling et al., 1993) are briefly described below. A third methodology (Self et al., 1994) involved the actual rneasurement of both systernic flow and pressure in order to predict changes in total peripheral resistance. Kouchoukos et al. (1970) employed an unconected pulse contour method in which the area under the systolic portion of the wavefonn was used. The calculation required subtracting end diastolic pressure (Pa from each pressure point during systole

(Pt). Beat-by-beat stroke volume (SV) was determined by dividing the integrated pressure value by aortic irnpedance (Zo): SV= 1/Z,

It .

eject

(Pt - Pd) dt [Eqn. 7-11

where &,=, is the time of ejection This simple model provided very reasonable approximations of cardiac output, and was based on the assumption that a linear relationship existed between systolic area and stroke volume. A variation of this model was subsequently used in humans by Jansen and CO-workers(1990). Accuracy was improved with the addition of an equation that

compensated for changes in mean pressure and heart rate, and when corrections for nonlinearity in the systolic area-stroke volume relationship were applied. No corrections were made for changes in peripheral resistance. Outputs from the two methodologies were uncalibrated. The addition of an absolute cardiac output measuring technique (Fick,

dye-, or thennodilution) was necessary in order to convert the pulse contour calculations to physiologicaily relevant equivalents (van Goudoever et al., 1995). Spranger et al. (199 1) and Stok et al. (1 993) used portions of the systemic arterial pressure pulse to provide estimations of venû-icular outflow and total peripheral resistance. Wesseling et al. (1993) used a three element model to calculate flow (Q) fiom the arterial pressure waveform. The mode1 contained the three major properties of the aorta

and artenal systern (Zo, Ca,, and R,). Two of the rnodel parameters (Z, and Cao)were derived fiom pressure-area relationships. Rp was assumed to have a negligible effect on systolic uiflow into the rnodel, and was defmed as the ratio of average pressure to average flow. Cornputations using a series of equations provided a simulated aortic flow output fiom the artenal pressure profile, referred to as "Modelflow". The area under the flow curve during systole provided an estimate of stroke volume. Cardiac output was computed as SV multiplied by instantaneous heart rate. Once calibrated with a thennodilution technique, the methodology was found to accurately track changes in patient state with or without vasoactive drug applications. Self et al. (1994) attempted to quanti@ the changes in total peripheral resistance (R,)

and arterial cornpliance (Cm) during non steady state +Gz stress. They modelled

cardiovascular function as a two element windkesseI system. Clinically instnunented, sedated baboons were exposed to difEerent levels of gravitational stress ranging fkom +2 to +9 Gz. The area under the output curve of a flowrneter, irnplanted at the aortic root,

provided beat-by-beat estimates of stroke volume. It was assumed that total flow had a capacitive and resistive cornponent, and that both & and C, were constant throughout a

cardiac cycle. This allowed the formation of two matrices which, when solved simultaneously, provided estirnates of & and C , changes. The data indicated a decrease

in aortic blood pressures concomitant with a drop in &. During the compensatory stages of the acceleration exposure, aortic blood pressure and total peripheral resistance rose in parallel. With low to moderate gravitational stress (Le., c +6 Gz), capacitance was found to marginally increase (< 5% change fÏom baseline levels). Although a useful methodology with primate models, the requirement for a concise measurement of aortic blood flow limits its application in human subjects.

During this experiment, the average rate of pressure increase to the lower body garment was greater than 150 mmHg/s during a +5 Gz exposure. Total penpheral resistance would not be expected to remain constant with high levels of counterpressure (Sieker et al., 1953). During inflation of the G-suit, the rate of peripheral runoff (outflow fiom the d e s through the capillaries) decreased and end diastolic pressures rose dramatically during a cardiac cycle (refer to panel A of Figure 5-5). This violates the basic assurnption of little or no change in %, and introduces an unknown error into the Wesseling et al. (1993) and Self et al. (1994) models. One solution to this problem would be to employ a methodology less influenced by changes in &. Pulse contour techniques have been shown to be unaEected by resistance changes (van Goudoever et al., 1995). Alterations in end diastolic pressure (PeJare incorporated into the SV calculations for each cardiac cycle (see equation 7-1). A

simple model could then be used that assumes a linear pressure-volume relationship, then calculates the % pararneter based on the average pressure to average fiow ratio (Modelflow technique). If this combined model provides a sirnilar pattern of estimated flow and resistance response as found in other studies, they could then become the basis for identifying the underlying events that comprise the cardiovascular response to a perturbation.

7.4 Assumptions of the Simple Mode1 Used The assumptions address: -the relationship behveen pressure and volume with heart level measurements -the capacitive effect on the rate of blood pressure change ~calculationof the mean arterial pressure during a cardiac cycle

7.4.1 Assurn~tion1:The Pressure to Volume Relationshi~

Using the Penaz technique, memurement of the continuous blood pressure waveform was made at the finger by the Finapres system. Any change in pressure must be attributed to an alteration in artenal blood volume. The elastic properties of the arterïal wall govem the relationship between volume and pressure. This relationship has

been shown to be rnostly linear during static infusions of blood into the aorta (Hdock & Benson, 1937). Regions of nonlinearity were found only at very low and high infusion volumes, either below 60 mrnHg or above 225 rnmHg, respectively. This is consistent with a more recent study of the aortic pressure-area relationship (Langewouters et al.,

1984). Given the range of blood pressure values measured at the level of the heart during the investigations:

The relatiomhip beîween bloodpressure and vesse1 volume can be assumed to be linear when measzrrements are made at the level of the heart.

7.4.2 Assurn~tion2: Ca~acitiveEffects on the Rate of Blood Pressure Change As the measurements were perforrned in a dynamic environment (i.e., blood pressure was changing continuously), capacitive effects may have prevented pressures fiom attaining their steady state levels. The capacitance of the system will only affect the

rate at which MAP will change, and its influence decreases in srnail vessels (Berne &

Levy, 1983). Vessels with small capacitance (rigid vasculature) will have a faster rate of

pressure increase for the same volume input. Capacitance also falls with distance fiom the hem. Therefore, equilibriurn will be attained much faster in the digital artery than in a larger, more elastic vessel such as the aorfa. This is confumed by the nature of the pressure waveform measured by the Finapres, in which there is little delay in pressure nse during the rapid ejection phase of the cardiac cycle (Figures 3-4,4-6, and 5-5). Systole is significantly delayed when pressures are recorded in more proximal regions such as the aortic arch (Remington & O'Brien, 1970). Calculations of relative cardiac outptït changes have been successfidly accomplished (Stok et al., 1993) using a pulse contour methodology with peripheral (i.e., fmger) blood pressure measurements. Thus:

Capacitive effects can be comidered negligible when rneasurements are performed using the digital artery. Therefore, for a given volume input into the digital artery, any dynamically measured pressure (SBP, DBP, or MAP) should be very similar to steady state final pressures.

7.4.3 Assumption 3: Calculating Mean Pressure

Based on the previous discussion, mean artenal pressure (MAP) is dependent only on the mean volume of blood in the vessel. Detemination of this value can be made by calculating the area under the blood pressure/time curve and dividing by the time interval involved. This process is very complicated, but can be adequately approximated using the systolic and diastolic components recorded during a cardiac cycle using the following formula:

MAP= 1/3 (SBP-DBP) + DBP [Eqn. 7-21 This leads to the next assumption:

U 4 P can be adequately approximated using equation 7-2.

Calculations based on the substitution of blood pressure components into equation 7-2 have been shown to be a good representatïon of mean arterid pressure (Berne and Levy,

1983). This method has been applied in numerous studies to facilitate calculation of flow or resistance parameters (Ackles et al., 1978; Goodman et al., 1992; Fraser et al., 1994).

7.5 EstMating Flow and Resistance 7.5.1 Estimatine Svstemic Artenal Blood Flow (O&

If assumptions 1 and 2 hold, this would then allow the application of ratios to ider aiterations in one variable to the relative change in thc other. This is shown in Figure 7-1. A pressure (P 1) is measured with a volume (VI) in the vessel (point A). If the pressure is found to ïncrease (P2), it can be inferred that the volume in the vessel rose to V2. In other words, if blood pressure is found to have doubled, a proportional rise would be expected to have occurred in the vessel volume.

Pl

-

P2

Pressure

Figure 7-1: Linear pressureivolume relationship. Ifassumptions I and 2 hoZd, a change in rneasuredpressure fiom PI fo PZ would resulîfiom a volume change Rom VI to v2. Point A can be replaced by the minimum pressure immediately pnor to the start of ventncular outflow (diastolic blood pressure). At this t h e , the blood volume in the vessel is lowest. During the rapid ejection phase of the cardiac cycle, volume into the

systemic arteriai system exceeds the volume that leaves the arterioles. Arterial volume (synonymous to pressure) increases and attains a maximal value (systolic blood pressure or Point B in this event). Figure 7-2 depicts the volume change associated with these two components of the blood pressure waveform. The rise in pressure from Pl (DBP) to P2 (SBP) is brought about by an increase in volume fiom V I to V2. Pulse pressure (the difference between SBP and DBP) corresponds to a net volume increment. Under normal cardiac pacing conditions, approximately 80% of the stroke volume is represented in the volume ulcrement (Berne & Levy, 1983).

Pressure Figure 7-2: Inferring volume alterationsfrom pressure changes. Points A and B can be replaced by the diûstolic (DBP) and systolic (SBP)components of the bZoodpressure waveform, respectively. The increase inpressure_fi.ornPI (DBP) to P2 (SBP) is brought about by a rise in vohme from VI to V2.

Flow is defmed as the change in volume over t h e , and can be calculated as the product of SV and instantaneous heart rate (as per the Modelflow practice). The latter is easily determined using the R-R interval fkom the ECG. Thus flow can now be approximated using the following equation: Q, = SBP-DBP / R-R Interval pqn. 7-31

which reduces to:

7.5.2 Estimatine Resistance

Resistance can be caiculated fiom the systemic arterial blood flow (Q,,) and the pressure difference between the arterial vascular bed and that at the heart. The vascular bed pressure can be representzd by subtracting right atrial pressure (RAP) from mean arterial pressure (MAP). Thus resistance c m be determined using the equation:

L, = (MAP - RAP) / Q,,,[Eqn. 7-51 If RAP is considered to remain constant at approximately O rnmHg, the equation can be sirnplified to:

it,=

Qat

CEqn- 7-61

7.6 Calculation of Flow and Resistance During +Gz As previously described, data were grouped by +Gz plateau and by treatrnent (i.e.

P,, Delay, Coverage, and PBG). The following procedure was applied to each data set to allow estimation of flow and resistance: Step 1. Systolic (SBP) and diastolic (DBP) blood pressure components were selected fiom each cardiac cycle during a +Gz profile for each subject. Step 2. The R-R interval between successive cardiac cycles was used to detemiine heart rate (HR). HR was calculated using the equation:

HR (bpm) = 60 / R-R interval (in seconds) [Eqn. 7-71 Step 3. Spline fit interpolations were perfomed on the SBP, DBP, and HR data for each subject during each +Gz profiIe. The resultant curve was decimated to provide a sample every Il1O of a second. Thus, values were obtained fi-om tO to t 10 in 0.1 second increments.

Step 4: Data at each tirne interval (tO to t10) was then used to calculate the respective

mean SBP, DBP, and HR for the subject pool.3 Step 5. At each time interval ,xSBP and xDBP was used to estimate the average mean arterial pressure (xMAP) using equation 7-2. Step 6. The average pulse pressure (xPP) was calcdated as the difference between

xSBP and xDBP (fkorn Step 4). Step 7. xQ, was calcdated by substituting xHR and xPP values into equation 7-4. Step 8- xR,was the found by substituting xMAP and xQ, into equation 7-6. Step 9. xMAP, xQ,

%,,

xHR, and xPP were then normalized with respect to tO

(Le. expressed as percentages of profile onset values). Step 10. Data for the variables listed in Step 9 were then plotted as a function of time. This produced a series of graphs for each treatment at each +Gz 1evel.j

Note that a mean value is signified with an "x" infront of the variable. Mean systolic pressure would be written as xSBP. "ornparison of the changes in the respective measures were then performed based on visual inspection.

CHAPTER 8

Results of the Inferential Analyses 8.1 G-suit Schedules: Pressure, Flow, and Resistance Effects 8.1.1 Pressure

In Figure 8- 1, the three curves depict the average change in mean arterial pressure with the Low, Nominal, and High G-suit pressure schedules at +4.0 Gz. Time is plotted on the abscissa, and the percentage uicrease or decrease on the ordinate a i s . The black

bar above the x -axis indicates the time at which inflation to the STING G-suit began and attained 90% of maximum pressure. Note that no delays in pressurization were introduced. (An index of variability in MAP and its components is provided in Annex H.

Note that the data were plotted in discrete 1 second intervals, and the resultant loss of resolution with respect to the shape of the response curve).'

0

1

2

3

4

5

6

7

8

9

1

0

Tirne Slnce P r d i h Onset (s)

Figure 8-1: Effect of G-suitpressurization schedule on mean arferialpressure in subjects wearing a STING lower body garment while exposed to +4.0 Gz. With G-suit pressurization, there was a rapid increase in MAP. Upon complete inflation of the lower body garment (end of black bar), a transient period of little

improvement followed. Artenal pressure then rose to a steady state level. There was little dzerence in MAP produced by the different pressurization schedules at any time

* Given that the spline fit approximation provided a clear and concise representation of the response curve, the addition of any measure of variability proved to be very difficult and provided minimal assistance in the interpretation of the results. Consequently, the latter was not incorporated into the figures.

during the +Gz profile. By the end of the acceleration profile, lower body p r e s s ~ z a t i o n

ïncreased MAP by 34% to 38% fiom pre-acceleratory levels. 8.2.2 Flow

Changes in the two metrics used to calculate the resultant flow (heart rate and pulse pressure) are shown in Figure 8-2. Visuai inspection of the response curves indicates that heart rate rose for several seconds &er complete pressurization of the lower body garment. Peak heart rate was highest with the High G-suit schedule. There was little ciifference in the maximum heart rate between the Nominal and Low conditions.

However, peak heart rate occurred later during the acceieration profile with the Low schedule. By the end of the profile, there was little difference in HR between schedules. Pulse pressure fell during G-suit pressurization, due to DBP rising faster than the SBP component of the blood pressure waveform (figure in Annex H). Progressively g larger decreases in pulse pressure resulted, with the greatest rate of decline o c c ~ with

the highest pressurization Ievel applied to the lower body garment. Minimum pulse pressure was concomitant with complete inflation of the G-suit. Pulse pressures then rapidly returned to baseline values within 2 seconds. By the end of the profile, there was o d y a slight change in PP fkom onset levels with any of the inflation schedules. bu Pgs

-- ----

-

Nom Pgs

pp

HtPgs

--•

-

Lou Pgs

-

------.Nom Pgs

Hi Pgs

-10%

0

1

2

3

4

5

6

?

8

Tlme Since Profile Onset @)

9

1

0

0

1

2

3

4

5

6

7

8

9

1

0

Tirne Since Profite Onset ( 8 )

Figure 8-2: Effect of dzfferentlower body pressurization schedules on hearr rate (HR) and pulse pressures 0during exposure to + 4.O Gz.

The resultant product of heart rate and pulse pressure was used to estimate systemic arterial 80w (43. In Figure 8-3, flow was found to be significantly affected by lower body pressurization. Minimum flow levels were found to occur with complete pressurization of the G-suit. Q, was reduced by 8%, 14% and 24% with the Low, Nominal, and High schedules, respectively. Flow then rose rapidly over the next 2 seconds anci surpassed baseline values by approximately 20% for al1 conditions. There

was little difference in flow between conditions after t3. A slow decline in Q, ensued for the duration of the acceleration profile. At t10, flow was augmented fiom preacceleratory values by approximately 12%. Qeçf

----Lw

Pgs

-----

Nam Pxs

-

Hi Pgs

1

Figure 8-3: Alterotions in estimated arterial bloodflow at + 4 O Gz with the three P, scheddes used to pressurize the S T ' G lower body garmenl. 8.1-3 Resistance

Having calculated pressure (MAP) fkom components of the blood pressure waveform and estimated flow (Q,), resistance was caiculated as the quotient of these MO variables. The estirnated resistance (R,) change over tirne is s h o w in Figure 8-4. PressuTization of the G-suit caused a rapid initial rapid nse in resistance. R, peaked within one cardiac cycle fkom the time at which lower body pressure was maximized for al1 conditions and al1 +Gz levels. There was a proportional increase with the level of pressure applied. Estirnated resistance rose by 3 1%, 47%, and 68% with the

Low, Nominal, and High schedules, respectively. The large increase in resistance was not, however, rnauitained. A rapid decline followed and a nadir was found to occur between t5 and t6. Nadir values were approximately 10% higher than those calculated at profde omet. Subsequently, resistance began a slow, oscillating increase for the remainder of the acceleration profile. The net change was only a 20% increase by the end of the profile for

al1 conditions.

Figure 8-4: Estimated resistance changes at +4.0 Gr with different pressurization schedules.

In order to test for consistency in the calculated change in resistance, &,values were calculated for the three pressurization schedules at dl +Gz levels. Figure 8-5 reveals that the pattern of response was very similar at al1 +Gz levels. Pressurization of the Gsuit resulted in an initiai rapid increase in resistance, coïncident with the application of lower body counterpressure. R, peaked within one cardiac cycle fkom the time at which G-suit pressure was maximized for all conditions and dl +Gz levels. Resistance was not, however, maintained. A rapid decline followed and a nadir was found to occur between t5 and t6. Subsequently, resistance began a slow, oscillating increase for the remainder of the acceleration profile. At +4.5 Gz, the net improvement in resistance was increased by an additional 5% above that found at +4.0 Gz. By +5.0 Gz, there was little difference in resistance with any of the pressurization schedules. R, did not increase appreciably between schedule conditions, nor was the maximum resistance different fiom values

---A

..... Nom P g

Low Pgs

~70%

-Hi Pgs

+4,0 Gz

-80% al

+70%

>

+60%

3 a L.

5

al

al

-

+50°h +40%

L

a +30% O

Q)

g

+IO%

C

C

3

+IO%

a

h

100% O

1

2

3

4

5

6

7

8

9

1

0

fime Since Profile Onset (s)

Figure 8-5: Change in L t values with different Pgs schedules at + 4 0, + 4 5, and +5.O Gz. Note that resistance is only temporarly increased wirh G-suit pressurization (black bar) and that there is little dzfference in values by the endfo the accelerution profile.

cdculated at +4.5 Gz. The oniy gain was a marginal improvement by the end of the profile. Temporal changes in resistance were found to produce a consistent pattern that was maffected by the Ievel of acceleration stress.

8.2 G-valve Responsiveness: Pressure, Flow, and Resistance Effects 8.2.1 Pressure Changes in mean artenai pressure at +4.0 Gz with delayed pressurization of the

STING lower body garnient are shown in Figure 8-6. The arrows denote the t h e at which G-suit pressure attained 90% of the maximum level. The highest rate of blood pressure rise occurred with G-suit pressurization, which was then followed by a transient period of Little improvernent. A secondary rise in artend pressures followed. By the end

of the acceleration profile, mean arterial pressure approached steady state in al1 but the 4.5 second delay condition. Lower body pressurization increased MAP by 35% to 45% from pre-acceleratory levels.

0

1

2

3

4

5

6

7

8

9

1

0

Tlme Since Profile ûiset (8)

Figure 8-6: Effect of delayed G-suitpressurization of mean arterial pressure in subjects wearing a STBVG Zower body garment while exposed to + 1.O Gz. 8.2.2 FIow

Measured heart rate and pulse pressure responses are illustrated in Figure 8-7. Heart rate rose for several seconds after complete pressurization of the lower body

gamient, artained a maximum level shortly afler, and decreased for the remainder of the profile. Peak and final heart rates were progressively higher with longer delays. Pulse pressure decreased with delay in G-suit pressure. Progressively larger decreases in PP occurred, with the greatest rate o f decline resulting with pressurization of the lower body garment. Minimum pulse pressure was synchronous with complete inflation of the Gsuit. This effect was exacerbated with a delay ui G-suit inflation. Pulse pressures then rapidly returned to baseline values within a couple seconds. By the end of the profile, there was only a slight change in PP from onset levels for any of the delay conditions.

O

I

Z

l

J

5

6

7

8

9

Tirne Since Profile Onset 6 )

1

0

0

1

2

3

4

5

6

7

8

9

1

0

Tirne Since Profile Onset (s)

Figure 8- 7: Eflecf of lower bod) pressurization with and without delays al + 1.O Gz on heart rate (HR) and pzdse pressures (PP). The arrows denote the tinte at which the Gsuit was iniated to 90% of rnuximum pressure. From Figure 8-8, flow ( 4 3 was found to be marginally affected by a delay in lower body pressurization. However, once the G-suit was inflated, flow fell dramatically for the duration equivalent to that of one cardiac cycle. Q, subsequently rose above baseiine levels, then declined towards a steady state for al1 but the 4.5 second delay

condition. Higher flow was produced at the end of the profile in conditions with longer delays in lower body pressurization.

0

1

;

3

4

;

6

7

8

9

1

0

Time Slnce Profile Onset @)

Figwe 8-8: Aiterations in estimared arterial bloodflow ut + 4 O Gz with various delays in Io wer body pressurization.

8.2.3 Resistance The effect of a delay in G-suit pressurization on the caiculated resistance estimate is shown in Figure 8-9. The peak R, value in each condition was always consistent with

the attainment of maximum G-suit pressure. As f o n d previously, the rapid increase in estimated resistance was followed by a syrnmetrical decline. Afier a nadir, a secondary slow rise occurred. A delay was found to shifi the peak resistance by the length of the lag in G-suit pressurization. The maximum & values appeared to be increased with long delays as ktrose by 83% with a 4.5 second delay in G-suit pressurization. The highest estimated resistance was 47%, 40% and 55% above starting values with the No Delay, 1.5 second, and 3.0 second delay conditions, respectively. There was, however, little diffèrence between conditions by the end of the acceleration profile. The Iongest delay in G-suit pressurization (4.5 seconds) did not attain the final resistance values found with the No Delay and 1.5 second conditions. The net improvements in the estimated

resistance by the end of the profile were low, as the final increases were only 20% to 30% above pre-acceleratoq- levels.

Figure 8-9: Estirnated resistance changes ut + 1.0 Gz with increusing delay in Zower body pressurization.

8.3 Lower Body Coverage: Pressure, Flow, and Resistance Effects 8.3.1 Pressure

The average change in mean arterial pressure at +4.0 Gz with different lower

gannent ensembles is displayed in Figure 8-10. The lower body garments were al1 pressurized according to the nominal schedule and no delays were introduced. The larger volume of the FPHS resulted in the G-suit pressure attaining 90% of maximum pressure slightly Iater (0.4 s) into the profile than with the STNG and CSU 15P. The black bar indicates the tirne at which this g m e n t attained the requisite 90% level.

I

-10%

0

1

2

3

4

5

6

7

8

9

1

0

Time SInce Proflie Onset (s)

Figure 8-10: Eflect of lower body coverage on mean arterial pressure ut + 1.0Gz. Gsuits were pressurized with the nominal schedule and no deZuys were introduced

With G-suit pressurization, there was a rapid increase in MAP in subjects wearing the STING and FPHS. However, the CSU 1 5 P caused a slower rate of change in blood pressure. Coverage had a significant effect on mean artenai pressure imrnediately after complete application of counterpressure. MAP was always highest in subjects wearing the FPHS and lowest with the CSU 15P ensemble. By the end of the acceleration profile, lower body pressurization increased MAP by 26%, 34%, and 49% £kom preacceleratory levels with the CSU 15P, STING, and FPHS, respectively.

8.3.2 FIow

Measured heart rate and pulse pressure responses are indicated in Figure 8-1 1.

The pattern of heart rate changes was similar between the STMG and FPHS. Comparatively, peak heart rate was higher and extended in subjects wearing the CSU 15P. HR by the end of the profile rose by 16% above pre-acceleratory values. A slight increase was found with the STRuG garment, while heart rate feil below baseline values in subjects wearing the FPHS.

-10% 0

1

2

3

4

5

6

7

8

Tlrne Since Profile Onset 6 )

9

I

I

O

0

1

2

3

4

5

6

7

E

9

1

0

lime Sinca Profile Omet (s)

Figure 8-11: Effeci of lower body coverage on heart raie (HR) and pulse pressures (PP) during exposure tu +B. O Gr. As found in previous analyses, pulse pressure fell during G-suit pressurization. The declines in PP were progressively larger with the greatest rate of decrease occurring

with the greatest level of surface coverage (Le., FPHS). Minimum pulse pressure was concomitant with complete inflation of the G-suit. Pressurization of the CSU 15P,

STING, and FPHS ensembles suppressed PP by 18%, 23%, and 32%, respectively. Pulse pressures then rapidly returned to baseline values within 2 to 3 seconds. By the end of the profile, there was only a slight change (< 10%) in PP from onset levels. Alterations in systemic artenal flow (Q,,) are shown in Figure 8- 12. Flow was found to be significady affected by lower body coverage only during the initial stages of the acceleration profile. Minimum flow levels were again found to occur with complete pressurization of the G-suits. Q, was reduced by 6%, 15% and 23% with the CSU 1SR,

STING, and FPHS, respectively. Flow then rose rapidly over the next 2 seconds and surpassed baseline values. By the end of the profile, flow appraached steady state. The greatest increases in Q, (+15%) was found with the CSU 1 W. Flow rose by 10% with the STING garment, and by only 5% with the Full Pressure Half Suit.

Figure 8-12; Changes in estimated arterial bloodflow at + 4.0 Gr with the pressurimîion of dzyerent lower body ensembles. 8.3 -3 Resistance

With a change in the ai1~un-i of lower body coverage, the shape of the R, curve

(Figure 8-13) was the same as found previously. There was a rapid initial rise, coincident with the G-suit attaining rnaxirnum pressure. Estimated resistance peaked within one

cardiac cycle. With greater surface area coverage, the peak &,values rose by 18%, 47%, and 74% for the CSU 15P, S m G , and FPHS g m e n t s , respecûvely. Resistance then

fell in al1 conditions in proportion to the peak values until a nadir was reached. The resistive improvements that occurred early with the CSU 15/Pand S m G garments were almost cornpletely abolished. Contrary to that found with changes in G-suit pressure schedule, the recovery during the last 4 seconds of the profile was affected by lower body coverage. By the end of the acceleration plateau, esthated resistance was always highest with the FPHS . Ln general, the final resistance increase was aimost twice than found with

the STING G-suit. The STING garrnent, in tuni, provided a 10% improvernent in resistance above that found with the CSU 15/P.

0

1

2

3

4

5

6

7

8

9

1

0

Time Since Profile Onset (s)

Figure 8-13; Estimated resistance changes at +4.0 Or with various Zevels of lower body coverage. 8.4 PBG Schedules: Pressure, Flow, and Resistance Effects

As there was no significant changes in nSBP with PBG at al1 +Gz levels, inferential analyses were performed on the +5.0 Gz data, the acceleration level at which the regulator provided the highest mask cavity pressures.

8.4.1 Pressure

Mean arterial pressure responses are shown in Figure 8-14. With G-suit pressurization, there was a rapid increase in M M in the two pressure breathing

conditions. A temporary significant effect of PBG on mean arterial pressure was evident b e d i a t e i y after complete application of counterpressure. The greatest increase in

MAP was produced with the High PBG schedule, while a small improvement occurred with the Low PBG condition. By mid-profile, these differences in MAP were no longer present. There was a 50% increase in MAP by the end of the acceleration profile in al1

three conditions.

0

1

2

3

4

5

6

7

8

9

1

0

Time Slnœ Profile Onset (s)

Figure 8-14: Effect of positive pressure breathing schedules on mean arterial pressure at +5.0 Gz. Subjects wore the STNG G-suit inflated according tu the nominal G-suif pressur ization schedule. No deZays in lower body garment pressurizat ion were introduced. 8.4.2 Flow

Measured heart rate and pulse pressure responses are indicated in Figure 8-15. The pattern of heart rate changes was sirnilar for al1 conditions. Peak heart rate was higher with the Low PBG and No PBG conditions. HR decreased in al1 conditions for several seconds after attaining maximal levels, then increased over the final 3 seconds of

+Gz exposure. By the end of the profile rose HR by 15%, 18%, and 13% with No PBG, the Low PBG schedule, and Hi& PBG schedule, respectively.

Pulse pressure again fell rapidly during G-suit pressurization. With the addition of PBG, the extent of the decrease was Iessened. Without PBG, pulse pressure at the

nadir was 37% less than starting values. A Low and High PBG schedule caused decreases of 33% and 30% respectively. During the recovery period from t2 until t5, PP was always greater with the High PBG condition. The Low PBG schedule provided some improvement above the No PBG condition. At t6, pulse pressures had returned to b a s e h e values. Large fluctuations were present for the remainder of the profile in al1 conditions, with PP falling below starting levels over the fuial few seconds. HR

.......

No PBC

-Lou

PBC

""

pp

HI& PBG -20%

-

1

o

T h e Since Prof lia Onçet (s)

.......No PBG

-LowPBG

" "

1

L

,

I

~

3

n

4

I

I

5

6

I

7

i

H 1% PBC

.

I

l

9

1

. 1

Tirne Slnce Prof ik, Onset (s)

Figure 8-15: Effect of lower body coverage on heart rate (HR) and pulse pressures (PP) during exposure to +4.0 Gz. The pattern of flow changes during the acceleration profile was sirnilar across al1 conditions (Figure 8-1 6). Minimum flow levels were again found to occur wiîh complete pressurization of the G-suit. Q, fell by 26%, 21% and 20% in the No PBG, Low PBG,

and High PBG conditions, respectively. From t2 to t5, flow was consistently higher with the High PBG schedule. The Low PBG schedule improved Q,,, fiom the No PBG schedule during this penod. Peak flow was increased by 25% to 3 1% above starting levels in the three conditions. After t5, a downward trend in estimated flow was found to occur. By the end of the acceleration profile, Q, was highest in the No PBG condition. Flow was lightly less with a Low PBG schedule and below baseline with the High condition.

0

Time SInœ Profile Onset (s)

Figure 8-16: Changes in estimated arterial bloodfIow at +5.O Gr with dzflerent PBG leve ls.

8.4.3 Resistance

Calculated resistance estimates were plotted in Figure 8- 17. The pattern of resistive changes was consistent with that produced with different pressure schedule, delays, and coverage. The shape of the response c u v e was unaffected by the addition of intrathoracic pressure. The rate of resistance increase was the same for al1 conditions, with a slight difference in peak R, values. Resistance was again maxunized just after

complete inflation of the Lower body garment. This was also the time at which mask cavity pressure reached its greatest level. Even though mask and G-suit pressures remained constant, there was a subsequent decrease in resistance. A secondary increase in

ktfollowed during the Latter stages of the acceIeration profile.

Final estimated resistance

values appeared to be af5ected by the PBG schedule. Compared to the values at the start of the profile, & levels by the end of the profile were 22%, 32%, and 50 % greater in the No PBG, Low PBG, and High PBG conditions, respectively.

NoPBG

PBC

-Lam

""' Hi@ PBC

i

-

t 0

o

S 1

s 2

l 3

l 4

i 5

i

l 6

i 7

i

l

1

l 9

l 1

I 0

l i m e S i n a i Profile Onset (s)

Figure 8-17: Effect of various PBG Zevels on estintated resistance changes at +5.O Gs.

8.5 Support for the Inferential Analysis Methodology Implementation of a spline fitting procedure provided a means to transform nondiscrete data to a continuous format, thereby improving the ability to examine responses that occur over a very short duration. This was M e r irnproved with the addition of an inferential methodology, which provided a basis for evaluating changes in critical cardiovascular components that could not be measured directly. However, it would be ill-advised to draw conclusions f?om the data without first validating the outcome of this procedure against previous findings. 8S.1 Com~arisonsWith Previous Findings

Figure 8-1 8 s ~ ~ l l ~ a r ithe z e saverage cardiovascular response of the six subjects with exposure to t2.5,t3.0,and +3.5 Gz in the unprotected (Control) state. Cornparison of the resistance changes with the Self et al. (1994) data indicated that the sequence of events was identical over the course of the comrnon +3.0 Gz profile. In both studies, resistance in the unprotected state was found to decrease during profile onset, attained nadir levels fiom which a slow recovery followed. The amplitude of the resistive changes using the simple contour mode1 were, however, darnpened in cornparison to those reported by Self and CO-workers. This may have four possible explanations: (i) the lower

-10%

1

0

1

2

1

1

b

5

6

1

1

7

1

1

1

4

9

1

0

Time Sinc8 Profile Onset (s)

-10% 0

I 1

I

I

2

I

j

J

I 6

5

~ 7

I 8

1 1

9

I 0

0

2

1

4

m >

-g 6

5

6

7

8

9

1

0

fime Since Profile ûiset (s)

Tlme Since Protlb Onset (s)

-..-

--

+Ll

cZ

...-. 3.0 Cr +

+ LW.

-

* 3.5 G r

'30%

8

=9 0

*20%

LL O

m +IO% d

a C

5

100%

e -10% O

I

Z

3

4

5

6

7

1

1

Tlme Since Profila Onset (s)

9

1

0

Time Sinco Proflie aiset

(s)

Figure 8-18: Mean cardiovascular response for the sk subjects with expusure to +2.5, t3.0,and +3.5 Gz in the unprotected (Control) state.

baseiïne (reference +Gz Level) used in the Self investigation to calculate percentage changes in resistance; (ii) the potential for general anesthesia to producing marked alterations in peripheral vascular tone, thereby confounding the effects of +Gz stress;

(iii) inaccuracies in the simplified model that result in an overestimation of the flow (Qa component fiom a decreased arterial cornpliance with higher blood pressures; andlor (iv) the tendency for lower resistance values when mean data are used in the cornputations (see Amex E). Using a thoracic irnpedance plethysrnography method, Welch (1994) assessed beat-by-beat cardiac function during +Gz exposure with and without pressurization of a G-suit. Calcdated resistance values were found to fa11 for several seconds folIowing complete pressurization of the lower body garment. The increases in artenal systolic blood pressures during the early portion of the +Gz plateau were attributed to an improved flow (Q) component. During the later stages of the gravitational stress, resistance values climbed while flow values dropped. Heart rate rose during the early stages of acceleration exposure, but later declined while systolic blood pressures increased. Concomitantly,stroke volume index remained very constant throughout the profile. These responses are identical to those computed with the simplified pulse contour model.

8.5.2 Com~arisonwith a Secondary Procedure

There is admittedly a potential for error with the simplified pulse contour methodology. Cardiac pacing is never synchronous to the onset of the profile, and the response to any treatment will Vary between individuais. Consequently, al1 responses are marginally affected by heart rate and the lag interval between profile start and the event of the frst cardiac cycle. Use of a mean response would filter out individual differences and

may be influenced by large deviations fiom a "central tendency". This is especidy tnie

with the small sample size ( ~ 6used ) in this investigation. Small errors may also have

been introduced due to changes unaccounted for by the basic assumptions (i.e., increases

in R U ,alterations in pre-ejection penod, etc.). A significant argument in support of the applied analyses resides in the

consistency of response found at al1 +Gz levels. This can be seen in the changes in estimated resistance values. Note that with al1 treatrnents (G-suit pressure schedule, Gvalve responsiveness, G-suit coverage, and PBG), maximum Ievels were consistent with the G-suit attaining maximum pressure. nie shape of the response c u v e was also found to be very similar across al1 treatments. The reproducibility was especially evident in Figure 8- 17, in which the lower body garment was pressurized to the same level on three separate occasions. The temporal pattern of resistance changes was the sarne in al1 conditions. The discovery of a rapid rise and fa11 in resistance with pressurization of the lower body g m e n t remains a critical fmding fiom the analysis procedure. To substantiate this result, a second technique was used to ascertain these changes in resistance. The blood pressure response was re-exarnined for one subject wearing the FPHS during a t4.0 Gz exposure. The garment was inflated according to the Low or Nominal schedule, without

any delays in pressurization. The resultant effect on the blood pressure response c m be seen in Fi-we 8- 19. A stmight line was drawn f?om the dicrotic notch (close of aortic valve) to the succeeding diastoiic point for each cardiac cycle. The slope of the line (decrease in BP/unit time) estimated the average rate of peripheral nuioff, a metric found to be predorninantly af5ected by resistance (Berne & Levy, 1983). This methodology removed any errors associated with estimates of stroke volume, and did not require accurate tirne stamping of the systolic and diastolic pressure points.

FPHS Pressurized to 155 mmHg

Profüe Onset Max Pg,

Figure 8-19: Calculation of peripheral runoffrate with N?fation of the FPHS to 1O3 and 15.5 mmHg during a + 4 0 Gz exposure. Note the lower dope (i.e. less runoff/sec afrer complete presurization of the garment (Mmc l&). Rare of runoff then increased over the next 2 to 3 cardiac cycles.

Hardcopy information was enlarged, then scanned into a graphics package (MacDraw Pro, Clark, Santa Clara, CA) for the two profdes. The software calculated the angle (9)fiom horizontal. The tangent of the Înscribed angle provided the slope of the line. Note that a vertical line would represent a "no resistance" condition, while an infinite resistance value would exist if the line was horizontal. The dope was then converted to working units (rnmHg/sec). The rate of runoff was caiculated for the fust 10 cardiac cycles of each +Gz exposure (Table 8-1).

Table 8-1:Raie of Peripheral Runofwith FPHS Inflation ut +4.0 Gz with ihe Lo w and Nominal Pressurimiion Schedules. Schedule

Low 103 mmHg

Cardiac Cycle 1 2 3 4 5 6 7

8 9 1O 1

3

Nom inal 155 mmHg

3 4 5 6

1 --

1

0

Tan $

57.0 58.6 55.1 62.6 65.8 72.9 66.8

1.540 1.638 1.433 1.929 2.225

Runoff (mmHdsec)

66.7 66.9 70.7

2.333 2.323 2.344 2.856

30.80 32.76 28.66 3 8.58 44.50 65.00 46.66 46.46 46.88 57.12

47.7 4 1.8 49.1 50.1 62.7 71.0

1.O99 0.894 1.154 1.196 1.937 2.904

2 1.98 17.88 23 .O8 23 -92 38.74 58.08

3.250

Figure 8-20 shows the rate of vascular emptying (Le., peripheral runoff) plotted as a function of cardiac cycle. The units of the ordinate have been inverted in order to transform alterations in peripheral run off into resistance changes. Note that the abscissa is independent of tirne, as cardiac pacing was not identical in both conditions. Thus,

maximum G-suit pressures (Max P,) occurred prior to cycles #3 and #2 for the Low and

Nominal SChedules, respectively. Resistance was highest at the interval irnrnediately afker complete inflation of the

FPHS. Over the next 3 to 4 cardiac cycles, resistance fell to nadir values. A secondary Licrease in resistance then followed. These fmdings are consistent with those determùied

using the inferentiai methodology (Figure 8-4). As would have been expected, the

maximum resistance was higher with the Nominal pressurization schedule. The parallel nature of the response indicates a very similar course of resistive change incurred with the

two treatrnent conditions.

Card iac Cycle

Figure 8-20: Rate of vascular emptying with infation of the FPHS according to the Low and Nominal schedules in one subject exposed to +4.O Gz

8.5.3 Implications of the Comuarisons Although the methodology used in the inferential analysis may be prone to some errors, there can be little argument agauist the type of information that can be gleaned

fiom the anaiysis. Thus, the ability to examine the course of change in critical elements of the cardiovascular response in a continuous manner far outweighs the limitations associated with this approach.

8.6 Summary of Findings 1. Different G-suit pressure scheduies had Iittle effect on blood pressure, sysremic flow, and vascular resistance.

2. The pattern of temporal changes in pressure, flow, and resistance were similar when

deIays in G-suit pressurization were introduced. However, the respective meîrics lagged No Delay values by the length of the imposed delay.

3. The largest changes in the cardiovascular response were found to occur with the FPHS. Estimated resistance was higher throughout the acceleration exposure with this garment. There was little difference found between the STING and CSU 15/P ensembles. 4. PBG had little influence on the cardiovascular response.

5. With ail treatments, resistance rapidly increased with pressurization of the lower body garment. This was consistent with a large drop in pulse pressure. M e r attaining a

maximum level, resistance dropped immediately to near pre-acceleratory values. By the end of the profile, al1 treatment conditions resulted in a minor increase in both resistance and flow.

CEFAPTER 9

Homeostatic Blood Pressure Control and +Gz Protection 9.1 The Homeostatic Negative Feedback Control System 9.1.1 Blood Pressure Control: A Negative Feedback Systern

Inputs for a large number of cardiorespiratory receptors are integrated by the blood pressure control system into autonomie responses. The closed-loop behavior of any biological homeostatic system is dependent on its individual components. Typically, a negative feedback control requires the continuous monitoring of an output variable by some feedback transducer, which provides afferent information to the controllhg system. The iatter establishes a setpoint and calculates the error between desired and measured values. The error information is used to alter the state of an effector, which then

influences the controlled process again. A simplified schema of a negative feedback control system is illustrated in Figure 9-1. Note that the setpoint (reference) can be rnodified through independent extemal comrnands.

Command

-

Controlling Sy stem Disxwbance

Reference

f Controller

Eficror

L

M

Conrrolled Process

Figure 9-1: Schema of a negative feedbuck systern. A disturbance changes the conirol process. The resulrant effect on the output variable (C) is sensed by a transducer and isfed back to the control system. î l e dzfference between reference (R) and outpur (C) is the error (e), which determines the magnitude of the effector output (W. (Frorn Korner, 1971) 9.1.2 T-me of Controller Function

The controller can firnction as a regulator or as a servomechanism. The distinction between the two are shown in Figure 9-2. A regulating system attempts to return the output towards the original state while a servomechanism attempts to modio the output

in order to track the disturbance. The diffèrence between output and the desired steady state is reflected in the error (e). The blood pressure regulating system has been shown to have both regulator and servomechanism tendencies (Korner, 1971).

SERVOMECRANLSM Figure 9-2: Regulator and servornechunisrn systems. The dflerence beiween the desired REGULATO R

steady state value and current stare determines the ewor term (e).

Input fiom the baroreceptors is central to the control of the blood pressure regulating system. Aortic and carotid sinus signals are used to provide information about pressure changes in the systernic circulation during every cardiac cycle. However, peripherai inputs fiom arterial chemoreceptors, pulm~naryarterial baroreceptors, cardiac and pulmonary mechanoreceptors, in addition to somatic and visceral sensory inputs, are

al1 sampled and integrated by the controlling system (Komer, 1971). Thus, the net changes in heart rate and vascular tone fiom an extemal perturbation will be dependent on the location and magnitudes of the various afferent inputs. Additionally, the peripheral signals may affect autonomic function through changes in setpoint and/or gain of the artenal baroreceptor reflex. Therefore, critical to the design and evaluation of +Gz protective equipment is: (i) the identification of the pnmary locus of the disturbances induced by both accelerative forces and the applied countermeasure(s); (ii) the determination of the underlying hemodynarnics induced by the perturbations; (iii) the examination of the associated changes in both cardiac and vascular functioning; (iv) the evaiuation of the temporal responses to the perturbation; and (v) the identification of possible alterations in the blood pressure control process (i.e., baroreceptor setpoint and

the type (regulator vs servomechanism) of system response) by ancillary reflexes.

9.2 Identifling the frimary Locus Elevating systemic artenal pressure (Pa fiom the mean circulatory pressure (P.,) level c m only be achieved fiom a translocation of blood fiom the venous to the artenal side of the circulatory system (Guyton et al., 1973). P, will rise with an increase in resistance andor flow. P, would continue to climb untif a new steady state level is attained, thereby increasing bIood volume in the arterial tree and reducing venous values

(Levy, 1979). Pressurization of a G-suit at +4.0 Gz (Figure 9-3A) caused systernic blood pressure to increase above starting levels. During this period, the flow deched (Figure 9-3D) and the increased arterial pressure could be attributed to a rise in total peripheral

resistance (Figure 9-3E). The drop in pulse pressure (Figure 9-3C) resulted fiom the inability of the left ventricle to pump a normal stroke volume against the increased aflerload. However, heterometric autoregdation (Samoff, 1960) returned stroke vo lurne (Le., pulse pressure) rapidly to normal. This was due to the attended rise in ventricular

diastolic volume and, therefore, a more optimized myocardial fiber length (Frank-Starling mechanism). Panels A through E in Figure 9-3 revealed that the magnitude and time course of the associated cardiovascular response was dependent on the extent of the applied counterpressure and its resultant effect on the underlying vasculature. If mechanicd compression of the tissue was equivalent to vasoconstriction of the peripheral arteriolar vessels, a new steady state blood pressure should have been attained, assuming the perturbation did not trigger a compensatory reflex response. However, resistance fell quickly following complete inflation of the lower body garment (Panel E), flow increased (Panel D) and systemic arterial pressures continued to rise (Panel A). From t3 onwards, flow was elevated above startkg values (Panel D). Therefore, the locus of the applied counterpressure was not prharily the traditional site for controlling systernic resistance

MAP

w -

5 Q

Figure 9-3: Effect of G-suit pressurization schedule on the cardiovascular response during a 10 second exposure to + 4.0 OThe STlhrG garment was infirated by either the Low (----), Nominai (=4 or High ( ) schedules, and no delays were introduced. Note that al[ tracings are locked at t 0 .

Tlme Since Profile Onset (s)

(i-e.,the arterioles). The rise in flow following complete pressurization of the lower body garment suggests that a significant portion of blood located in underlying venous vasculature was rnobilized. 9.2.1 S u ~ p o rfor t A Venous Locus: Tissue Factors and Hvdrostatics

Factors that influence the efficacy of an external counterpressure include the amount of pressure lost through tissue and the intemal vessel pressures. The former is afTected by the distance of the underlying vasculature fiom the point of counterpressure application, vessel composition, and wall thickness. The efficiency of the counterpressure then resides in the difference between interna1 and extemal vascular pressures. Intravascular pressures fa11 from the high pressure systemic tree to the low pressure venous side, creating differentials throughout the circulatory system. Additional changes are introduced by hydrostatic effects resultant from acceleration exposure. Al1 factors sigrilficantly alter the ability of an extemal pressure to deform the underlying vasculature. As counterpressure is applied by a circumferential bladder, pressure m u t be transferred through tissue before it reaches the walls of the vasculature. Inevitably, pressure losses result. These will increase with distance fkom the point of application. Therefore, counterpressure would be greatest in vessels that lie very superficial to the point of application. The effectiveness of external counterpressure would not only rely on the daerence between intemal and external (Le., transmural) pressure, but dso on the characteristics of the vessel wall. The amount of vascular deformation would depend on composite structure and wall thickness. Principal components (smooth muscle, elastic tissue, and fibrous tissue) and wall thicknesses differ throughout the vasculature. Pressures are very high in the aorta and the arteries. They are primaily comprised of an elastic structure and wall thicknesses are

increased to reduce the associated tensile stresses. Further down the arterial tree, penpheral arteries become muscular in character. At the arterioles, the muscular layer predominates and wall thickness dramatically nses. nius, the systemic arterial vasculature is very ngid and there is little change in volume with an increase in intemal pressures. Venous vessels are significantly thinner than their merial counterpart and are approximately 20 times more capacitant. Thus, for a given intemal pressure (Pi), a significantly higher transmural pressure would be required to alter the caliber of a vesse1 in the systemic artenal tree. Hydrostatic calculations (Eqn. 1-7) may be used to determine intemal pressures in the underlying vasculature distal to the point of measurement (i.e., heart level). Intemal pressures throughout the circulatory system are influenced by the gravitoinertial force (G) and hydrostatic distance (h). Counterpressure garments, however, are inflated according to a schedule solely based on the level of applied acceleration. Therefore, the extemal compressive force will differ as a function of +Gz and, therefore, will determine the vasculature most affected by the applied pressure. A sirnplified cardiovascular mode1 can be used to evaluate the possible action of a

mechanical pressure on the underlying vasculature. Assumuig intemal pressures of 100 mmHg and 5 rnmHg in a heart-level artery and vein respectively ,hydrostatic effects can

be predicted at the abdomen, thigh, and calf Approximate distances (from the aortic valve to the umbilicus, rnid-thigh, and mid-calf) of 30 cm, 50 cm and 65 cm were used in the calculations (Figure 9-4). These values corresponded to points rnidway through the

respective bladders of a traditional lower body garment design. Calculated intravascular pressures and extravascular pressures with the three pressurization schedules are shown in Table 9- 1.

art Level

Bladde

, ' ->!

I

,/-

Figure 9-4: Vertical distances @) fiom heurt level used to calculute infernal vasailar pressures. Note that artenal pressures are approxirnately 100 mmHg higher than venous values. Intravascular pressures rise with the acceleration (+Gz)level and vertical distance

Table 9-1: Intravascular and Extravasczrlar (Bladder) Pressures at +4.0, +- 4.5, and + 5. O Gz at the Level of the Abdomen, Mid-Thigh, and Mid-Calfwith the Low,Nominal and High G-suit Pressurization Schedules

1I

htravascuiar Press. (rnrnHg

1 1

Artery

1 Heart Level 1

100.00

Abdomen

188.24

I G z I I

1

Site

t

Abdomen Mid-Calf Abdomen

Mid-Thigh Mid-Caif

1 I

1 1 1

Bladder Pressure ( r n m ~ ~ )

I

Vein

291.18 199.26 3 15.07

2 10.29 283.82 338.97

fiom the hem. However, the extemal counterpressure is constant at each site, varying in accordance with the inflation schedule. The difference between bladder and intravascular pressures was used to estimate the transmural pressures, assurning complete transmission

of counterpressure (Table 9-2 and Figure 9-5). Negative values indicate that G-suit

pressure would not collapse the underlying vasculature. Positive values only suggest a potential for the applied extemal pressure to reach and deform the affected vessel.

Table 9-2: Calculated Arterial and Vein Transrnural Pressures at +3.0, +4.5, and +5.O Gz at the Level of the Abdomen, Mid-Thigh, and Mid-Calfwith the Low, Nominal and High G-suit Presstirkation Schedules Site

C;z

4 4 4 4.5 4.5 4.5 5 5 5

1

I

1

Abdomen Mid-Thigh Mid-Calf Abdomen Mid-Thigh Mid-Calf Abdomen Mid-Thigh Mid-Cali

l~rtet-y Transmural Press. ( m m ~--g ) lVein Transmural Press. (mmHg) -High Nominal Low Nominal High Low 1

]

I

1

I

-84.84 -143.66 -187.78 -70.01 -136.19 -185.82 -55.19 -128.72 -183.87

1

1

-33.14 -91.96 -136.08 -5.39 -71.57 - 121-20 22-36 -51.17 -106.32

I

1

18.56 -40.26 -84.38 59.24 -6.94 -56.57 99.91 26.38 -28.77

1

1

10.16 48.66 -92.78 24.99 -41.19 -90.82 39.81 -33.72 -88.87

I

1

6 1.86 3 .O4 -4 f .O8 89.6 1 23-43 -26.20 117.36 43 -83 - 1 1.32

1

1

1

1

1

113.56 54.74 10.62 154.24 88.06 38.43 194.91 121.38 66.23

With a low pressurization schedule, bladder pressures never exceeded estimated intravascular artery pressures at al1 sites, irrespective of the acceleration level. The same was true with a nominal schedule, with the exception of the abdominal site at +5.0 Gz.

The level of pressure inside the abdominal bladder exceeded that inside the underlying vasculature by approximately 22 mmHg. However, this pressure differential may not be enough to counter the pressure losses through the deep ninning, elasticized tissue. Consequently, a higher pressure level is required before changes in vascular diameters are imposed on an artery. Bladder pressures d i d however, exceed intravascular pressures at +4.5 and +5 .O Gz with the High inflation schedule. This was only true for the abdominal

bladder, as negative values were calculated at both mid-thigh and rnid-calf levels. Consequently, inflation of the lower body garment with any of the pressurization schedules would marginally influence the caliber of the hi& pressure arterial bed. Any

Arîery

Vein

I

Artery

Vein

@ I

Anery I 8t

Abdomen

+5.0 Gz

t

I

1

1 I

I l I

I

-

Low Pgs

1

n I-

NomPgs

HighPgs

Law Pgs

iVo m Pgs

High Pgs

Figure 9-5: Calculuted pressure dzrerence across an arterial and venule wall with the dzfferentpressurisation schedules at +1.0, + 4.5, and + 5.O Gz. Note that a negative value indicates that G-suit pressure was l e s than intvavasulur pressure.

changes would, therefore, reside on the lower pressure side of the circulation (Le., downstream fiom the arterioles). The effects of extemai counterpressure are much more pronounced on the venous side. Even with a Low inflation schedule, bladder pressures begin to exceed intravascdar pressures calculated in the vein. During an exposure to +5 Gz, extravascular pressures with a Mgh inflation schedule exceed calcuiated intemal pressures by 195, 121, and 66 mmHg at the abdomen, mid-th@, and nid-calf, respectively. As the pressure inside the

bladders increased, extravascular pressures in distal sites would be expected to defom the low pressure vessels. The greater the pressure provided by the schedule, the larger the

area of influence. Due to the cornpliant nature and close proximity of the underlying venous vasculature to the point of counterpressure application, tissue losses would be significantly less than that on the artenai side. Such high transrnural pressures would

most likely collapse the vesse1 walls.

These fmdings are consistent with those reported by Wood and associates (1944). They concluded that the most important factor determinhg the amount of acceleration

protection afforded by a G-suit was the amount of pressure applied to the abdomen and trunk. Inflation of bladders located in this region accounted for the greatest proportion of the acceleration tolerance improvement. Pressurization of the legs alone did little to protect the subject, on average increasing tolerance by only 0.2 +Gz.

9.3 Hemodynamic Responses Although a lower body garment may begin to exert some influence on the merial

side with an aggressive (Le., high rate of pressure increase) inflation schedule, the focus of the vascular response originates on the venous side of the circulatory system. As the greatest proportion of the circulating blood volume is contained in the high capacitance venous vasculature, a significant volume shift would be expected to occur during the initial

Pressure Garment 232 mmHg

Cutaneous Tissue

Cutaneous Tissue

Pressure Garment 232 mmHg

Pressure Garmen 232 mmHg

Vein

Artery

Figure 9-6: Effect of external courtterpressure on the underlying vasculature. Top panel indicutes the mid-thigh level pressure distributions within a deep artery and a superficial vein during exposure to +5 Gz. Counterpressure was applied by a circumferential G-suit bladder inflated to 232 mmHg. Note that even without tissue losses, extrmiascular pressure does not exceed intravascular values for the artery. The net effect is shown in the bottom panel. ExtravascuIar pressures collapse only the vein. Valves ensure unidirectionalflow of blood towards the right atrium.

pressurization of the lower body garrnent. This contrasts sharply with the negligible fluid translocation that occurs with alterations in arteriole caliber (Guyton et al., 1973). Before any alterations in caliber (Le., resistance) can take place, the fluid inside the vessel must either be compressed or redistributed. Although blood is not a true Newtonian fluid, it's primary component is water. As water is not compressible, the radius of the underlying vessel can not be altered without a concomitant blood volume redistribution. Figure 9-6 demonstrates the primary action of the counterpressure. The unidirectional valves found in the venous system ensure blood moves centrally, towards the right atrium.

9.3.1 The Bainbridge Mediated Remonse

Figure 9-7 surnmarizes the changes in mean heart rate (HR) and pulse pressure

(PP)with varying pressure to the lower garment, different delays in pressurization, and altered amounts of coverage. The data were measured at +5.0 Gz., the acceleration level that would have produced the greatest perturbations on the cardiovascular system.

In al1 instances, HR rose during the early portions of the profile, attained a peak

value, and declined. Pulse pressure decreased bnefly with pressurization of the lower body, then rapidly increased back to pre-acceleratory values. If PP is assumed to be an accurate representation of the stroke volume (Berne & Levy, 1983), the only effect of the treatments was to transitionally impede stroke volume during pressurization of the lower body garment (i-e., increase afterload). Stroke volume retumed to pre-acceleratory levels over one to two cardiac cycles (heterometric autoregulation) and remained fixed at this value for the remainder of the profile. Changes in cardiac output (SV x ER), outside of the time interval during which SV was depressed fiom pre-acceleratory levels, would be totally attributed to alterations in heart rate.

A. Pressure Effect at +5.0 Gz

-

HR

B. Delay Effect a t t5.0 Cz --

oovconds

IJswal&

-10%

I

,

PP

0

1

-

00~0~rd.s

f

m 41

m

U)

0'2 -20%

2

-a -c

0 -3-

Q m

$

. . y .

a Q -50% 0

1

2

3

i

5

6

7

9

1

0

lïme SInce Profile Onset (s)

2

3

1

5

6

1

1

9

1

0

Tlme SInce Profile Onset (s)

C. Coverage Effect at +5.0 Gz

Figure 9-7: Changes in mean heart rate (XR) and mean pulse pressure (PP) at + 5.O Gz with varying schedzdes to the lower garment @anel A), deluys in pressurirarion @anel B), and level of coverage @anel C). Note that HR increases during the early stages of the profie, whereas PP exhibits an initial decrease before returning to preacceleratory levels.

The data are consistent with fluid loading experiments performed on conscious dogs (Vatner & Boettcher, 1978). Translocation of blood from the peripheral venous vascuiature due to extravascular compression would have been expected to increase blood flow to the right atrium, thereby producing an abrupt nse in right atrial filling pressure

and eliciting the Bainbridge response (distention of B stretch receptors in either the left or right atrium resulting in cardiac acceleration). As cardiac contractility (inotropic effect) is not altered by the Bainbridge reflex, changes in cardiac output (Le., flow) were proportional to alterations in heart rate while stroke volume remained the same. This was found to occur in al1 treatment conditions (Figure 9-7). Further support of the invoked Bainbridge response is reflected in the sequence of cardiac pacing changes in relation to the systolic blood pressures alterations. The rates of change in cardiac pacing (dHR/dt) and systolic blood pressure (ÇISBP) were calculated for the three G-suit schedule conditions at +4.0 Gz and plotted over time (Figure 9-8). Note

that peak W d t was consistent with pressurization of the lower body garment (end of black bar on abscissa) and was greatest with the High schedule. Peak dSBPldt occurred much later into the profile than peak dHR/dt, and maximum values rose with the level of pressure applied to the lower body garment. Closer examination suggests that the changes seen in the blood pressure response

are very simila. to that occurring in heart rate, but with a delay introduced. A lag in blood pressure rise would have been expected during the translocation of blood fiom the venous circulation (right ventride) to the systernic arterial side (left ventricle). A minimal delay of I cardiac cycle would constitute a one second fag if heart rate was 60 bpm. Patterson

and CO-workers(19 14) demonstrated the sequence of events following a sudder, augmentation of nght atrial filling pressure (RAP) in an isolated heart preparation. A rapid increase in RAP resuited in a delayed rise in left ventncular end diastolic volume

(LVEDV). Aortic pressures did not change appreciably, falling transiently during the

Low Pgs Scheclule 15-

-SBP --IiR

-

:Il ,

lligh Pgs Schedulc

Nominal Pgs Srhedule 251

xn.

20.

i

0 1 2 3 4 5 6 7 8 9 1 0 Timc Since I'rofiIc Onset (s)

Tinic Sincc Profile Onsct (s)

Tinic Sincc Profile Onwt (s)

Figure 9-8: Rate of change in HR and SBP with three G-suit puessurizaiion schedules. Noie that peak dHWd is consistent with the tirne the lower body garment attains 90% mawirnui~rpressure (end of black bar) and nraxinzum dNR/dt incieases with Pgs schedule. Concommitantly, the rate of SBP raiseis decreased and bloodpressure falls transiently with the High schedule. With a greater pressure io the lowera body gument, cardiac deceleration occurs for longer. durations.

initial cardiac cycles following volume loading. This short lag in the artenal pressure response may have been due to the shortened lefi ventricular filling time associated with the increased heart rate. Therefore, the delay in the systemic blood pressure response can be attributed to two factors: (i) the time required for heterometric autoregdatory compensation fiom an increased afterload; and (ii) the time required to translocate blood

fiom the affected site of counterpressure (Le., venous side) to the systernic vascular tree. With the Nominal and High schedules, blood pressure rose fiom t4 to t6 wfiile

heart rate was decreasing. This suggests that a carotid sinus baroreceptor reflex was not a factor in the blood pressure response. Eye level systolic pressures (Figure 6-4) never exceeded pre-acceleratory levels. Additionally, the Bainbndge reflex has been shown to be prepotent over the baroreceptor reflex when blood volume is raised (Berne & Levy, 1983). 9.4 Vascular and Cardiac Functioning

Assuming no ancillary factors are involved in the cardiovascular response, a rise in

peripheral resistance mediated by a change in arteriolar caliber would be expected to shifi 8

- Control Venus Renirn (VR)

Control Cardiac Output (CO) c - -

-

-

L

O

I

2

3

4

5

6

7

8

9

Venous Pressure (mmHg)

Figure 9-9: Effect of arteriolar vasoconshiction on the cardiac and varcularfunction curves. Note that flaw wodd decrease with a rise in resistance.

the cardiac output curve downward due to the increased afterload (Figure 9-9) in steady state conditions (Guyton, 1973).

A change in resistance (R) wodd also influence the vascular f i c t i o n curve as seen

in equation 9- 1:

The fluid translocated due to a srnaller arteriolar vesse1 diameter would not alter mean circulatory pressure (P,,), flow (Q), or the arferial to venous capacitance C, / (C, +

C,) relationship. Therefore, the new response converges on the same X-intercept, but resistance alters the slope of the linear portion of the response. A new equilibnum wodd be reached (Le., a shift f?om point A to point B in Figure 9-9) in which the increased peripheral resistance would invoke a decrease in flow (cardiac output).

9 8

-

FLuid-Loding \

Control CO

\ -,

--Res istance 5 4

-

2

-

1

0

1

2

3

.

1

5

6

7

8

9

1 0 1 1

Venous Pressure (mmHg)

Figure 9-10: fncreased JIow and resistance necessitates a rightward shzfi in the vascular fùnction ctlrve. Thus, counterpressure would sim ulute af i i d Zoadirzg condition.

Inferential analyses, however, indicated that both flow and resistance were higher

than baseIine values throughout the latter portions of the acceleration profile. Resistance would again decrease the slope component of the vascular function curve, thereby reducing the flow for a given P,. If pressurization of the G-suit reduced the arterial: venous capacitance ratio, a flatter slope would occur concomitant with a decreased flow. Consequently, the o d y rernaining variable is Pm,. For both flow and resistance to nse, a signîficant rightward shift in the vascular fùnction c u v e would be required (Figure 9-1 O). Counterpressure must, therefore, increase Pm.while havùig a minimal influence on the Ca to C , ratio. Cardiac and vascular function curves indicate that a large increase in mean circulatory pressure (P,,) would be required in order to invoke a rise in both resistance and flow. Hydrostatic calculations revealed that the low pressure venous structures would be most influenced by an external mechanical counterpressure. As the greatest proportion of the blood volume (approximately 85%) is located in the systemic veins (Guyton, 198l), an attendant result of such a perturbation would be a large increase in

Pm,. Alterations in blood volume have been known to increase Pm,to levels as hi& as 40 to 50 rnmHg (Guyton et al., 1973). This would be analogous to a volume loading condition, and is consistent with the cardiac pacing changes found to have resulted during the acceleration profile (discussed previously).

9.5 Temporal Effects On the Blood Pressure Response Application of counterpressure uiduced changes in resistance primarily due to compression of the underlying venous vessels. However, resistance was found to rise quickly, but Sien fall to values approaching pre-acceleratory levels. In order to have increased resistance, blood must have been shified fiom the vessels underlying the lower body gannent. Some of the translocated fluid wodd have resided in the systemic arterial bed, thus causing the rise in Pa. However, the artenal:venous capacitance ratio is

approximately 1:19 (Berne & Levy, 1983) and the greatest proportion of the translocated blood would have returned to the venous vasculature not collapsed by the G-suit (i.e., to areas superior to the site of application). The diarneter of these vessels would as a result have increased, thereby significantly decreasing total peripheral resistance (Eqn. 1-9). Additionally, a rise in puhonary pressures would also have resdted in a higher RAP. Recruitment and distention of the capillary bed would subsequently have decreased the pulmonary component of the total penpheral resistance (West, 1985). Pulmonary resistance has been found to drop by as much as 75% in certain physiological states such

as exercise (Guyton, 198 1). A schematic representation of the circulatory system is shown in Figure 9-1 1.

Without counterpressure inflation (top panel), systemic blood pressure is controlled by the variable artenal resistors R,,&,and b).Extemal compression (lower panel)

discharges the underlying venous capacitor (C,,), indicated by the decreased distance between plates (horizontal lines). The translocated blood pools in the unaffected venous regions (C,, and Cv2)and the pulmonary circulation (C,). Thus, the temporal effect of the blood redistribution was a reduction in TPR fiom maximum levels due to the coincident rise in venous vesse1 caliber. This would explain the rapid, symrnetrical decrease in resistance that ensued immediately upon complete inflation of a lower body garment (Figures 8-4,8-5, 8-9, 8-13, 8-17). Further evidence of this temporal influence is found with the introduction of PBG. Positive pressure breathing has been s h o w to increase systemic arterial pressures similarly to that measured with a straining maneuver. The change in blood pressure was mainly atûibuted to the transmission of the applied pressure to the left ventricle, thereby improving cardiac eEciency. The raised intrathoracic pressure is also believed to constrict the greater vesseis located in the thoracic cavity. This was confirmed using section radiography by Kiiburn and Sieker (1960). They found positive pressures of

Arteriat System

$

Pre-Gsuit Inflation

2:

G-suit Inflation

Venou a S ystem Arterial System

51 Auium

Venou s System

Figure 9-11: Schernatical representation of the efect of counterpressure on the cardiovascular systern. Without counterpressure inflation (top panel), bZood pressure is controlled by the variable arterial resistors (Rai, Raz, and Ra3). External compression (bottom panel) discharges the underlying venous capacitor (CvZ), indicated by the decrease disrance beiweenplates @orizontullines) The translocated bloodpools in the unaffected systernic venous (CvIand C,d andptilmonq (Cp) circulations.

24 to 28 c&,O

(17.6 - 20.6 mmHg) decreased cardiac diameter and caused a "striking

degree of narrowing of the pulmonary veins in the right hemithorax" . In this study, PBG with lower body counterpressure was found to transiently alter pressure, flow, and resistance (Figures 8-14,8-16, and 8-17, respectively). At the highest acceleration level

(+5 Gz), the PBG regulator provided 32 mmHg of pressure to the oronasal mask. Assuming no pressure tosses, the consequent intrathoracic pressure Ievels would still be insuficient to dter the resistance in the systemic arterial bed. Therefore, any resistive increases would only occur as a result of changes in the low pressure vasculature. Additional blood translocated from the associated pulrnonary vessels (Le., discharging capacitor C, in Figure 9-1 1) would be stored in the remaining capacitive sites, primarily in

the high capacitive venous side (C,, and C,J.

Therefore, the translocation of blood fiorn

areas affected by the perturbation(s) will transiently impart an influence in the blood pressure response. However, the highly capacitive venous vasculature will negate most of the resistive increase produced by the application of a counterpressure andor a positive ainvay pressure.

9.6 The Blood Pressure Control Process 9.6.1 Factors Affecting Blood Pressure Control

Every cardiorespiratory input converges on the motoneuron pool of the bulbar area. The rise in blood pressure following the introduction of a disturbance (+Gz, G-suit pressurization, and PBG) requires the controller to integrate the information from these afferent inputs and determine a new setpoint. The resultant autonomic reflex then &ers

the activity of every circulatory autonomic effector. The response fkom changes in one or more inputs will either be greater, the same, or less than normally produced h o u & the arterial baroreceptor inputs alone, the principal feedback signals to the system. However, preferential engagement of particular inputs may occur and the blood pressure control

systern response c o d d differ during the various stages of the response to acceleration exposure.

9.6.2 Preferential ControI During and Immediatelv Post Counterpressure An~lication

Initial blood pressure increases with lower body counterpressure were consistent with a rise in heart rate. However, blood pressure continued to increase while heart rate

fell (Figures 8-1 and 8-2, respectively) even though head level pressures were below preacceleratory values (Figure 3-2A). The lack of correlation between the two responses indicated that preferential engagement of different blood pressure control inputs occurred. Monnation from the left and right atria wouid have provided rate-sensitive information at

the time of the a-wave, and the degree of pulrnonary and systernic venous filling during the v-wave (Gauer & Henry, 1963). As the volume loading reflex would ovemde the inotropic afTierent input associated with the pressor reflex during fluid infusion (or with lower body pressurization during +Gz), changes in contractility would also have been repressed (Berne & Levy, 1983). The Bainbridge reflex was prepotent over the pressor reflex during and irnmediately after G-suit inflation. Therefore, the change in blood pressure and concomitant fluid redistribution was not a direct result of efferent changes produced by the blood pressure control system. This would indicate that the controller h c t i o n e d as a servomechanical system (Figure 9-2) during this stage of the acceleration exposure.

9.6.3 Blood Pressure Replation Blood pressure rose for several seconds after cornplete presswization of the lower body garment. During this period, resistance decreased in a symmeûical manner and attained nadir levels. Assurning al1 afferent inputs responsible for the resultant Bainbridge response retumed to pre-inflation Ievels at this tirne, the principal afferents become those

from the baroreceptors. For the remainder of the acceleration profile, systemic pressures either slightly decreased or remained at the new steady state level. Low fiequency oscillations were evident for the remainder of the acceleration pronle. The cycling may be due to the conflict of efferent signals to the ponto-medullary cardiac pacing control area fiom the aortic arch and carotid sinus baroreceptors. Wood (1990) postulated that the baroreceptors would be in direct cornpetition when a G-suit providing high acceleration protection is employed. The pressor response fiom a decrease in head level pressure would be opposed by an uihibitory signal fiom the aortic arch receptor as a consequence of a very high drîving pressure (Figure 9-12). This is believed to be at least one of the causes of the low fiequency oscillation in systernic pressures that begin several seconds after +Gz exposure found in other investigations (Buick et al., 1993). Low Head Loref Ressure Carotid Sinus €3aroreceptor

J+ L

1

I

Aortic Aich Baroreceptor

High Driving Pressure

Figure 9-12: Efferent inputsfiom pressure receptors to cardiac pacing c o n ~ ocenters l in the rnedulla oblongata. Cornpetition between baroreceptors receptors rnay be present when carotid sinus pressures do not increase while central (aortic arch) values rise above setpoint levels The conflict between baroreceptor inputs would also have affected the setpoint of the regulatory systern. If the aortic arch receptor is prepotent, blood pressure would fa11 during the latter stages of the acceleration profile (Figure 4-8,6-5),resulting in a "regulator" type action. If the carotid receptor input supersedes aortic arch signals, there would be little change fiom the new equilibrium value (Figure 5-7) and the bbod pressure response would be servomechanistic in nature.

Secondary

Secondary

Secondary

o

.'

.

l

.

i

B

9

,

a

Time Shce Profile Onset (s)

Figure 9-13: Effects of ancillary reflexes on resistance during +Gz exposure fo +4.0, +4.5, and +5.0 Gz. Note that peak resistance was always higher with lengthier deluys, even though the pressure in the lower body garment was the same. A slow secondary rise in resistance followed cornpzete pressurization of the G-suit.

9.6.4 Mvogenic Factors

A second type of integrdon occurs peripherally during a general disturbance.

This is performed by the vascular smooth muscle and includes both autonornic and local effects (Korner et al., 1967). This is evident in the resistance changes following al1 delay conditions at the highest +Gz level, shown in Figure 9- 13. After nadir resistance levels were attained, a slow secondary resistance increase always followed. Initially, it would appear that the secondary rise was due to a continued pressor response. Given that the volume loading effect would have been absent d u ~ the g latter half of the acceieration profile, a pressor response should also have been present and a blood pressure rise should have resulted. However, systemic arterial pressures remained the sarne (Figures 8- 1,8-10, and 8-14), flow decreased (Figures 8-3,812, 8-16) and heart rate either fell or remained constant (Figures 8-2, 8-1 1, and 8- 15) d u ~ this g penod. Thus, local myogenic factors rnay have been predorninant in the peripheral vasculature in response to the sudden rise in perfusion pressures associated

with the increased acceleration environment (Jones & Berne, 1965).

9.6.5 Intemated Neural Control: Possible Mechanism for Arrythrnias

In order to provide high acceleration tolerance, a very effective lower body garment must elevate arterial pressures. As a direct result, the high driving pressure would be expected to trigger a reflex response mediated by the aortic arch baroreceptor. Pressurization of the FPHS in previous studies (Cochran, 1954) was believed to elicit a strong vagal response, resulting in the significant rhythm disturbances recorded during acceleration exposure. Pressurization of the FPHS garment induced similar arrhythmias in this study (Figure 5-7). However, large changes in heart level pressures were not required to permit subjects to complete the highest acceleration levels (+5 Gz),nor were excessively high

levels of pressure introduced into the garment. Greater increases in systemic pressures were produced with very effective arterial occlusion gaments without invoking the same pacing disturbances found with the FPHS. Therefore, the potential exists that other factors may also have influenced sinus pacing of the heart. Inferential analysis indicated that the greatest blood pressure, flow and resistance changes were produced using this ensemble (Figures 8- 10,8-12,843).

Therefore, a

significantly larger volume of blood would have been mobilized and have entered the atria, inducing a saonger Bainbridge response f?om the higher atrial pressures. The vagal response associated with the pacing disturbances immediately post loading may be due to the summed inputs fiom the atrial and aortic arch receptors (Figure 9-14). This is

consistent with the onset of the asystolic event shown in Figure 5-7. Thus, a rapid change in atrial fdling pressures may play a contributing role in the associated arrhythmias. _VolumeLoading In creased Swerch

Carotid Sinus Batoreceptor

-

High Driving Pressure

Pest Loading Low Head Level Pressure caratid Sinus Baroreceptor

High Driving Pressure

Atrial Receptors

Decreared Srretch (Posr Loading)

Figure 9-14: Volume Zoadingfrorn Zower body garment pressurization may transiently impart additional signuls &O the m e d h Note the potential for a spong vagal responsefiom additive afferenf inputsfrom the atrial and aortic arch receptors immediately post Zoading.

9.7 Hypothetical Mode1 of the Cardiovascular Response

Autonomie control of the cardiovascular system includes numerous integrative receptor inputs, bulbar and suprabulbar mechanisms, in addition to local factors. The components al1 form part of the closed-loop response to a disturbance, and rnay or may not be involved during the time dependent changes that result during +Gz exposure.

Thus, it is impossible to attribute the blood pressure response at any given interval to

any one individual mechanism. However, a general mode1 can by hypothesized from the data collected during the study. Hydrostatic calculations indicated that the pressures in the lower body garment may have been high enough to cause some arterial compression at the level of the abdominal bladder. However, G-suit bladder pressures fell below arterial intravascular pressures in caudal regions, whereby the extemal counterpressure would only have collapsed the underlying venous structures. Emptying of the capacitive side of the vasculature required the mobilization of blood from the venous vessels, and effectively increased blood volume. The influx of a large bolus of blood into the heart invoked a Bainbridge response (Le., heart rate rose while stroke volume remained the same). Resistance fell as the transposed blood resettled into the highly cornpliant venous vascuIahue not directly affected by the applied counterpressure. The diarneter of these venous vessels increased, thereby negating most of the resistance changes occurring in the lower extremities and splanchnic bed. A new equilibrium point was reached on the vascular and cardiac function curves, and the control setpoint (Le., reference value) was altered. Blood pressure either remained elevated (servornechanism response) or decreased towards, but ncver attaining, pre-acceleratory levels (regulator action) via ancillary reflexes that changed flow and resistive components of the cardiovascular system. These events are sumrnarized in Figure 9- 15.

7

/f Perip heral Vasculatur e

(

Extravascu lar Pressure Venous Compression Fluld Translocation f Effective Blood Volume f Reslstance

Volume Shlft t o Un affected Veno us Vessels

C

?Atrlal Stretch

1

f Vessel Caliber

Limited Arterial Compression

Atrial Receptors

f

+ Fiesistanc e

(

1

1

Syrnpethetle Actlvlty ( Arteriolar Caliber f Reslstance

y

Some Arlerlal Compression

c

+Atrlal Stretch

L ocal Vascula r Reflex

b Heart Rate

f Heart Rate B a h bridge Re flex

( /

Myocardial Tissue

1

[

Afterload

bStmkeVolume t Cardiac Output

II

1

'a

Normallred SV

f ~ a r d l a cOutput

1

1

Heferometric Autoregulation Ar terial Blood Pressure Total Resistance

Increaslng

I

lncreasing

I

D ecreaslng

Flow

Stari External Counterpressure

Decreaslng lncreaslng

I ncreaslng

0 ecreaslng

Counterpressure

Figure 9-15: The tinie course of everlts that occitr with the application ormi exte~mlcouiileipressu~r The pattern of cliange iil pressure, Jlow and resistarice r~esults,fivi~~ a co~?iplex iiilteractiori betivee~ivasculai aiid reflex rdespoiises.

CHAPTER 10

Findings, Their Implications, and Future Research 10.1 Current Issues in Life Support System Design Exposure to +Gz continues to be a problem in modem tactical aircraft.

Maxirnizing the ability of a life support system to protect against acceleration-induced sequelae is pivotal to irnproving both flight effectiveness and safety. Some researchers

have suggested orientation of the pilot into a prone position as the ultimate protection strategy for reducbg the deleterious hydrostatic effects of +Gz on the cardiovascular system (Wood 1986, Wood, 1987; Wood, 1988a; Wood, 1988b). However, current airhrnes have and may continue to incorporate an upright seat configuration, due primarily to the extensive cockpit re-engineering required to convert to this type of crewstation. As a result, life support systems should address both current and future requirements, the former being the purpose of this investigation.

10.2 Findings In Relation to Experimental Hypotheses 10.2.1 Effect of Lower Garment Pressurization

It was hypothesized that +Gz protection would increase with the level of pressure applied to the G-suit. The study found that G-tolerance, as defined by aiterations in nSBPm, nSBP,, ,or subjective reports of visual changes, was unaf5ected by aiterations in G-valve outlet pressure in subjects wearing an extended coverage (STNG) G-suit. Although resistive changes were induced, these were transient in nature. Application of a higher pressure level to the lower body garment o d y managed to increase subject discornfort, and was ineffective in producing a long term alteration in resistance.

10.2.2 Effect of G-valve Resuonsiveness With an increased delay in G-suit pressurization, it was hypothesized that tolerance to +Gz would decrease. Delays in presswization of the extended coverage Gsuit did significantly a e c t the ability of subjects to complete the acceleration profiles. There were no changes in maximum systolic blood pressures, however, between delay conditions cornpleted by al1 subjects. With increasing acceleration plateaus, pressure/Gme profiles that lagged +Gz by more than 1 second were found to decrease tolerance. Prepressurization of the G-suit did not significantly improve tolerance to +Gz Ui cornparison with a slight lag in inflation (Le., 1-5 second condition).

10.2.3 Effect of Lower Body Coverage It was also hypothesized that protection to +Gz would increase with the level of lower body coverage. Tolerance to +Gz was found to be affected by the arnount of lower body coverage. Increases in nSBP,

and resistance were in proportion to the

counterpressure surface area. However, pressurization of the FPHS provoked arrhythrnogenic mechanisms in some subjects.

10.2.4 Effect of PBG Schedule With increasing levels of PBG, it was hypothesized that tolerance to +Gz would increase. Based on subjective reports of visual changes, positive pressure breathing did improve protection. However, PBG did not significantly alter heart and eye level blood pressures by the end of the acceleration exposure. Both metrics attained similar values

with the three conditions used, possibly due to the relatively low positive pressures generated by the schedules. Resistance response curves were also unaected by the introduction of different Ievels of intrathoracic pressure.

10.3 Tangible Elements: Life Support System Design Factors

Many factors govern the cardiovascular response to +Gz. Some c m be altered

and, in tum, will influence the degree of protection provided (Le., tangible variables)These include the effect of external counterpressure on the underlying vasculature, the responsiveness of the G-valve, and the design of the lower body garment. Al1 of these elements must be considered during the early stages of development of an acceleration protection system.

10.3.1 Vascular Effects

Hydrostatic calculations and the t h e dependent physiological changes indicated that the prirnary locus of counterpressure was the venous vasculature, with a minimum influence imposed on the systemic resistance vessels. Specific targeting of the latter, with significant increases in systemic pressures, has been accomplished with progressive occlusion type garments during WWII (Wood et al., 1945; Wood & Lambert, 1952). Although an effective countermeasure, these G-suits were also found to cause significant discomfort and were not accepted by the pilot community. The extent of lower body coverage was subsequently decreased and the p r e s s k t i o n levels reduced (Wood, 1987). Arterial occlusion suits would today face the same acceptability issues that presided 50 years ago. Even though acceleration tolerance could be improved with such a garment, the losses in operational effectiveness from the added discomfort could negate any possible benefit. Better protection can be af3orded by the life support system %y

simply replacing the traditional CSU 1 5 P suit with an extended or full coverage suit. However, the appropnate level of coverage and pressure could, in itself, be limited by the dynamics of the cardiovascular response. The FPHS has been s h o m to induce rhythm disturbances during acceleration exposure. However, lower pressure levels may reduce the risk of arrhythmias while still increasing tolerance above levels found with other

garments. Therefore, the best possible compromise is a lower body ensemble that provides the greatest surface coverage, while still being an acceptably cornfortable and

safe alternative to aircrew.

10.3.2 G-valve Res~onsiveness

The responsiveness of the G-valve may be instrumental in detemiinhg the extent of protection af5orded by the life support system due to the added 3 to 4 second delay required for blood pressure to attain maximum levels. The extended delay in the systemic blood pressure response with lower body counterpress~zationcan be attributed to two factors: (i) the time required for heterometnc autoregdation to compensate fiom an increased afterload; and (ii) the time taken to translocate blood fiom the af5ected underlying venous vessels to the systemic side of the vascular tree. This leaves little additional thne before oxygen reserves are depleted. Given the ability of combat aircrafl to attain high +Gz levels rapidly, the flow capability of the G-valve should be sufficient to allow pressurization of the lower body garment to 90% of maximum pressure within a few seconds of attaining the peak +Gz level. The data indicated that the traditional Alar valve was unable to meet this requirement at the acceleration levels tested. Electronic systems have demonstrated better responsiveness (Crosbie, 1983; Meeker et al., 1985; Meeker et al., 1987), in addition to providing flexibility in output scheduling (Frazier et

al., 1988). The time course of the blood pressure increase firom pre-acceleratory values was consistent with and without the introduction of delays in lower body pressurization. Thus, the tirne differential between systemic pressures attaining identical maximum values between conditions was a iinear function of the length of delay. Oxygen reserves acted as

a protective buffer during the initial exposure to +Gz, compensating for rninor shortcomings in G-valve responsiveness. Thus, there was no improvement in acceleration

tolerance gained by providing pressure to the G-suit ahead of the +Gz level (i.e., "preview control" concept). Implementation of preview control requires sarnpling of the pilot's input to the control stick in addition to several aircraft parameters. The data is then introduced into a computer and comparator. Following a complex senes of calcuiations, the computer provides a predicted +Gz level, and inputs this information into an electronic G-valve. This allows the G-valve to provide pressure to the G-suit slightly ahead of the anticipated acceleration profile (Farrell et al., 1996). The fmdings of this study suggest that there would be litde benefit in introducing this concept as part of a Me support system, only adding unnecessary costs and complexity.

10.3.3 G-suit Desim

Although G-valve performance is predominantly responsible for any delays in pressurization, the design of the lower body garment bears some scrutiny. This was evident by the delayed pressurization associated with the FPHS g m e n t , even though a high flow elecbonic G-valve was used. Restrictions to flow, ballooning bladders, and

poor garment fitting produce extra demands of the G-valve, leading to longer delays and reduced final pressure levels. These factors ment dmost as much attention as the surface coverage, given that poor garment design can significantly reduce the overall protection afforded by a life support system (Lambert et al., 1944).

10.4 Intangible Elements: PhysiologicaI Factors

A successfid +Gz protection system increases systemic pressures at head level.

Although components of the life support system play a significant role, physiological factors ultimately determine the time course of the blood pressure response. The elements include the blood pressure control mechanisms and the varïability associated with individual responses, both of which greatly influence the speed and magnitude of the

cardiovascular response. These are out of the reach of the currently employed strategies

and, thus, can be considered intangible issues. However, their importance on future life support system design must not be overlooked.

10.4.2 Blood Pressure Controi Mechanisms

Two main controlluig mechanisms were critical in detennining the blood pressure response to acceleration exposure with G-suit pressurization. The early response to +Gz was governed by the Bainbridge reflex. This reflex was prepotent over the baroreceptor

inputs and took several cardiac cycles to complete. Blood pressure was elevated above pre-acceleratory values, and conthued tg rise while heart rate declined. During the latter stages of the acceleration exposure, blood pressure usually decreased. Hence, a new setpoint in the control system was established at a level less than the maximum systernic arterial pressure recorded imrnediately following pressurization of the lower body garment. Therefore, the controller rnay act as a poor regdator rather than a servomechanism, the ideal response required to maximize the protection afforded by a protection system.

10.4.2 Variability in Subiect Res~onses

A wide range of responses was measured within the subject pool. Some

individuals -ernonstrated little change in systemic blood pressures from pre-acceleratory levels with pressurization of a G-suit, while others indicated a significant improvement. Thus, the level of protection afTorded by any life support equipment may predominantly be influenced by an individual's response to both the stress (+Gz) and the applied countermeasure (Le., level of coverage, pressure, and PBG). This would suggest that the life support system should be designed based on the needs of the individual aircrew member or, altematively, requires some closed-loop capability. A "personal" life support system can be introduced into the aircraft using programmable, electronically controlled

hardware, although the additional costs and Ume required to "tailor" the system may not be practical. A closed-loop life support system, which compensates for individual

differences could, potentially, alleviate this necessity. For such a system to be implemented successfully, a real-time feedback signal must be present that provides the controller instantaneous status idormation. However, as seen by the long delay in the blood pressure response, no obvious cardiovascular metrics c m be used for this purpose. Alternative measurements rnust be substituted for the closed-loop control signal and, as such, may not be applicable replacements andor be dificult to implement.

10.5 Design Implications From Study Findings From the findings of the investigation, the optimal acceleration protection system for an upright crewmember should include a d o r rneet the following criteria:

is based on a G-suit that provides the greatest Iower body surface coverage possible; incorporates a G-valve that can pressurize the above garment to 90% of the

maximum required or tolerable pressure within 1.5 seconds of attaining

-

the peak +Gz level; and implements a PBG schedule that begins at +3.5 Gz and increases pressure to the oronasal mask by at least 25 mmHg/+Gz.

10.6 Limitations of the Research The analysis procedure used in this investigation detected small differences in the

independent variables (Le., G-suit and rnask pressures) with time and treatment condition (Coverage, Delay, G-suit and PBG schedule). Statisticaliy significant changes in the cardiovascular response (i.e., blood pressure) during +Gz stress were more difficuit to

identifjr. This was primarily due to between-subject variability, as most of the withinsubject variance (fatigue, c a r y -over and anticipatory effects, etc.) were removed by normalizing the blood pressures with respect to profile onset values. Despite large differences befween means (i-e., ASBP > 1 1 mmHg) produced by the various treatment conditions, contrasts were unable to detect these changes. This was most likely due to the low sample size (n=6) and tight control over Type 1error rate (ap,=0.01).

10.7 Future Research

This study addressed some of the key issues pertinent to life support design at moderate acceleration levels. However, these fmdings require verification in areas of the operational environment that could not be simulated due to limitations of the centrifuge, experimental design, and tirne constraints. As each of the factors that influence acceleration protection was studied independently, the potential for an additive effects necessitates M e r study. Additionaily, the results of this body of work indicate areas of potential development that may prove beneficial in the design of new protective garmentry.

10.7.1 Verification In A Wider Performance Envelope

Given that tactical aircraft can expose aircrew to as much as +9 Gz with onset rates as high as +15 Gdsec, only part of the aircraft performance envelope was assessed.

In order to elirninate the variance created by having subjects employ an anti-G straining maneuver and to identie the effect of al1 possible treatment variables, data were collected in relaxed subjects exposed to a maximum of +5 Gz. With the best combination of

treatment variables, subjects rnay have been able to complete slightly higher accelerations levels in the relaxed state. Greater G-suit pressures would be introduced with increased +Gz plateaus and, potentially, affect the relative contribution of the arterial and venous

vascular beds. Therefore, a follow-up investigation codd be used to confimi the consistency of the blood pressure response with exposures above those used in the present study. It is strongly suggested that additional instrumentation be used to confirm the cardiovascular changes associated with lower garment pressurization. Flow and volume detemination techniques such as Doppler (Rushmer et al., 1966; Kmtz et al.,

1973) and tetrapolar impedance plethysmography (Montgomery et al., 1988; Montgomery et al., 1989; Krutz et ai., 1990) could be used to ven@ the time dependent fluid shifis S e r r e d fiom the data. The rate of acceleration onset for al1 acceleration profiles was +2 Gdsec, the highest possible with the passively girnbaled centrifuge at DCIEM. Suffice to Say, the examination of higher onset rates codd not be examined in the present facility. High onset +Gz potentially increases caudal pooling, which codd be exacerbated by a delay in G-suit pressurization. A greater blood volurne in the lower body compartments may influence the resultant cardiovascular response following innation of the lower body garment. Altematively, such an investigation may be used to confîtm the fmdings of this study in an environment that closely sirnulates the performance capabilities of the modem tactical aircrafi.

10.7.2 Additive Factors and +Gz Protection

Investigation of the various parameters that comprise an acceleration protection system indicates that each facet c m influence tolerance to +Gz. Collectively, these factors may be additive, meriting M e r study of their cornbined influence on the cardiovascular response. An "ultimate" condition for assessment against the currently operational configuration is strongly recommended. The former would provide greatest lower body coverage (i.e., FPHS) idiated to the highest acceptable pressure with minimal lag in the pressurehime profile, and introduce an aggressive PBG schedule. The latter

condition would require subjects to Wear the traditional CSU- 1S R garment, pressurized

by the Alar G-valve according to the nominal schedule, and would exclude PBG. Cornparison of the cardiovascular response between these two conditions, in combination with the results of this study, would provide an empincal basis for defining the potential

interactions between life support systern parameters.

10.7.3 Development of the Full Pressure Half Suit The Full Pressure Half Suit provided the best potential gains in acceleration tolerance. Design of the garment ensured the sarne kvel of pressure was introduced to the abdominal area as that applied to the lower extremities. However, this may have accounted for the discornfort reported by al1 the subjects. Compartmentalization of this

gannent, with lower pressures applied to the abdominal bladder, may irnprove acceptability. Electrocardiographic (Chimoskey, 1970; Whinnery, 1982) and echocardiographic (Jennings et al., 1985; Mitaka et al., 1989) study of cardiac f i c t i o n should also be conducted in order to examine the pathophysiologic episodes frequently associated with the use of this garment (Cochran, 1954; Wood, 1990). This would ensure safe implementation of this lower body garment into the operational environment should it prove to be a viable alternative.

References Ackles KN Porlier JAG, Holness DE, Wright GR, Lambert JM,McArthur WJ (1978). Protection against the physiological effects of positive pressure breathing. Aviat. Space Environ. Med. 49:753-758. AGARD (1990). High G Physiological Protection Training. North Atlantic Treaty Organization, Advisory Group for Aerospace Research and Development, AMP Working Group No. 14, AGARDograph No. 322, December. Balldin UI, Wranne B (1980). Hemodynamic effects of extreme positive pressure breathing using a two-pressure flying suit. Aviat. Space Environ. Med. 5 1:85 1-855. Balldin UI, Dahlback, GO, Lasson, LE (1989). Full coverage anti-g suit and balanced pressure breathing. Forsvarets Forskningsanstalt, FOA Report No. C50065-5 A, Febmary. Bazett HC, Macdougall GR (1942). Pressure breathing at altitude: practical methods for its use. Report to the Associate Committee of Aviation Medicine Research, National Research Council, Canada. Boehmer RD (1987). FINAPRES. Ohmeda Monitoring Systems, Englewood, CO. Beckman EC, Slaughter CK, Wood EH (1955). Measurements to evaluate the effectiveness of the full pressure half suit in applying external pressure to the body. US. Naval Air DeveIopment Center, Report No. NADC-MA-5502, March. Berne RM, Levy MN (1983). Phvsiologz (2nd ed.). St. Louis: C.V. Mosby. Bjurstedt H, Rosenharner G, Lindborg B, Hesser CM (1979). Respiratory and circulatory responses to sustained positive-pressure breathing and exercise in man. Acta Physiol. Scand. 105:204-2 14. Bomar J (1985). Breathing systerns integration in the USAF Advanced Life Support System (ALSS). In: Symposium on Integration of the Aircrewman: His Equipment and the Crewstation. Air Standards Coordinating Committee, 26th Meeting of ASCC Working Party 61, Aerospace Medical and Life Support Systems, Farnborough U.K. Air Standards Coordinating Cornmittee 98- 108. Buick F, Porlier JAG (1987). Tactical life support system: design considerations for protection against high +Gz. Defence and Civil Institute of Environmental Medicine, Technical Report No. 87-Tech. Report-2 1, June. Buick F (1989). +Gz protection in the future - a review of scientific Iiterature. Defence and Civil Institute of Environmental Medicine, Technical Report No. 89-TR-47, November. Buick F, Hartley J, Pecaric M (1992). Maximum intra-thoracic pressure with anti-G straining rnanoeuvers and positive pressure breathing during +Gz. Aviat. Space Environ. Med. 63 ~670-677. Buick, F (1993). "STING" Programme - prefiminary andysis of G-suit study. Defence and Civil Institute of Environmental Medicine, Technical Memorandum HPDS 93/12, September. Buick F, Pecaric M (1993). "STING" Program - preliminq analysis of PBG schedule study. Defence and Civil Institute of Environmental Medicine, Technical Mernorandum KPDS 93/ 18, Novem ber. Buick F, Maloan J, Welch V, Pecaric M, Wood EH (1993). Ear opacity: indicator of circulatory changes at head Ievcl for objective measurements of unprotected and protected human +Gz tolerance. Aviat. Space Environ. Med. 64:46 1.

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Annexes

The Computer Controlled Life Support System A.l The Pressure-Regulating System

PBG and G-suit pressures were controlled using a modified life-support system (Altitude and Acceleration Protection System (AAPS), Carleton Technologies, Orchard

Park, NY). The AAPS system (Figure A-1) was composed of an electro-mechanical breathing re,gdator (EMBR), a .electronically controlled G-valve, and an electronic control unit (ECU). Carleton AAPS S ystem

-+

,"

Figure A-1: Schematic of the AAPS life-support system. The system was composed of an electro-mechanical breathing regulator (EMBR), an electronic G-valve, and an electronic control unit (ECU).Tramducers sensing cabin pressure (Pcab), output pressure (Peut), supplypressure (Psup), andflow (FI) were located inside the EMBR. A pressure ~ansducerand accelerometer in the G-valve provided + Gr and G-suit pressure information to the ECU. A discrete input to the ECU via a toggle switch prevented the processor in the ECUfiom cornputing internal command schedules. The Iife-support system was configured in such a way that an externd discrete input to the system's ECU could be applied via a toggle switch. When a discrete signal

was received, the ECU ignored the intemal transducer signals and used two externally supplied cornmand voltages (pressure breathing and G-suit pressure) to compute the appropriate rnicroprocessor output signals to the drive amplifiers. The externally supplied command signals were limited so that the respective maximum output pressures

fiom the PBG regulator and G-valve were 90 mmHg (48.18" H20 ) and 12 psi (620

mmHg), regardless of the actual command value. The pressure regulating system was then calibrated. A variable DC power supply was used to determine the pressure delivered by the EMBR and G-valve at dBerent input voltages. Regression analyses were used to formulate equations that were then incorporated into the software control algorithm.

A.2 Controi Inputs and Safety Instrumentation

EMBR and G-valve output were measured as pressures in the oronasal rnask cavity (Pmask) and in the G-suit input hose (Pgsuit), respectively, using calibrated

variable reluctance pressure transducers (DP- L 5, Validyne, Northridge, CA). Output from the EMBR also supplied pressure to a counterpressure upper garment wom by the subjects. Due to an improved signal-to-noise ratio fiorn the Pgsuit transducer, the output from the variable reluctance transducer was used as the control input to the computer instead of the AAPS intemal pressure transducer signal. The AAPS accelerometer analog output was not used as the +Gz control input. Installation of the system in the centrifuge required attaching the pressure regulators (G-valve and EMBR) to the side of

the gondola seat, which left them lower than heart-level. Correspondingly, the +Gz levels at the G-valve were slightly higher than nominal heart-level values. The +Gz level was

subsequently measured via an external accelerometer (43 10-20-AGIM, Systron Donner, Concord, CA) already mounted at the appropriate position on the centrifuge gondola seat (Figure A-2).

!

Mask

Accelerorneter

Figure A-2: Conho/ instrumentation and subject sufity switches. The centrifuge + Gz Ievel was measured using an external accelerorneter. Oronasal mask (Pmask) and Gsuit (Pgsuit) pressures were monitored using variable reluetance pressure rrnnsducers. Two switches, a subject "enable"and a s o f i a r e "override" button, were used to terminate mask andor G-suit pressurization. The centrifuge operations computer could not initiate the acceleration profile until the subject engaged an "enable" switch. Engagment of the switch indicated that the subject was prepared to begin a +Gz exposure and he/she was required to keep the switch in the depressed position until the centrifuge profile was completed. The subject could teminate the profile at any t h e by releasing the "enable switch", at which time the centrifuge was decelerated to H . 4 Gz at a rapid rate. This procedure was used to

minimize the liklihood of encountering a loss of consciousness episode. A software "override" switch was also available to the system operator. The

"enable" and "ovemde" switches provided +5 VDC signals to the control computer. If

either switch was disengaged, the output pressures fkom the life-support equipment were reduced according to criteria designed to provide the greatest protection and cornfort to the subject.

A.3 The Controller Computers

Two cornputers were used to control the blood pressure monitoring and life support systems, provide event marker status to the data acquistion software, and monitor the system safety parameters. In order to improve systern speed, the tasks were divided such that o p b a l control of the life-support system was ensured. Correspondingly, a high level controller was used to gather necessary information £tom the system operator and then commanded the iow level computer to provide the necessary pressures to the subject. A short description of the hardware and software comprising each controuer is given below.

A.3.1 High Level Controller

The analog voltages fiom the "enable" and "override" switches, accelerometer, and centrifuge control computer (Vrpm) were fed to a multifunction board (MI016H, National Instruments, Austin, TX) of a computer (Macintosh IIX, Apple Computers, Cupertino, CA). A 32-bit direct memory access controller board (NB-DMA2800, National Instruments, Austin, TX) sped up data transfer. Graphical software (LabVTEW, v2.2, National Instruments, Austin, TX) was used to develop a real-time instrument control program. Part of the front panel display is shown in Figure A-3. The computer operator could change any of the fiont panel controls with a mouse. This allowed rapid alteration of the experimental pararneters between successive acceleration profiles.

The hardware/software received the multiple control input signals and converted the analog data to working units (+Gz units). The software continuously rnonitored the status of the software "ovemde" switch. The system operator could terminate the software routine by engaging the "ovemde" switch. The pressure schedule pararneters for both the G-suit and PBG pressures, including any necessary timed delays in pressurization, were entered by the system operator using the graphical user intefiace.

Ring indicators dlow opcrator full flcxibiliiy in sclccling options

\ G-s&t

c 'Tcxi inforniotion provides

G-suit Delay

G-suit Schedule

'PI A: CSU 15P B: STING C: FPHS

1: NONE 2: 0.50psi BELOW Noininal 3: Nominal 4: 0.50 psi ABOVE Nominal

1

A: 0,00 s Dclay : 1.50 s Delay C: 3.00 s Dclay D: 4.50 s Dclay

PBG Schedrile ---

---

dI

1: No PBG 2: STING / 2 3: STlNG

t

GO

Protocol Enable

Main S t d S t o p Switcli:

(i) 1:inaprcs cantrol routines (ii) Eveiit Marker rouiincs (iii) Signnl Acquisition rouiincs

Figure A-3: Front panel of high level contialler with re@iunce information. In this example, the subject worc the CSU-I j / P G-suit, no pivssure was applicd, no dclay in piesslrrizaiioiz or PBG was r*equired. This designutcd a contiol condition.

These parameters were converted into an 8-bit code and sent via a digital input/output port to the low level control computer. Once the program was initiated ("Go" button), the software automatically initiated start-up on the Finapres blood presssure monitoring unit. Once the blood pressure signal was satisfactory, the operator began the event marker cycle by selecting the "Protocol" button. Each experimental series aiways began with a 10 second control. The subject had been instructed to rernain as relaxed as possible during the control period, and was specifically told to refrain from moving or contracthg any muscle groups. Three seconds prior to onset of the control period, the software provided an auditory waming tone. A series of commands were sent to the blood pressure monitoring system to ensure that no calibrations occurred during this interval. During the control penod, a +5 volts signal was provided to the data acquisition systems fiom the high level controller to assist in data analysis procedures. The intemal clock/timer on the multifunction board accurately ensured a 10 second interval, afier which the event marker voltage returned to zero. Once the control period was completed, the software waited until the +Gz level, determined by the centrifuge accelerometer increased above +1.25 Gz. From that thne onward, until the +Gz level fell below this value, the operator entered experimental parameters could not be changed. A second event marker cycle was triggered by the Vrpm signai. Once the

centrifuge computer provided a voltage equivalent to 2.0 +Gz, the high level controller provided a second +5 VDC output to the data acquisition systems. The event marker remained at this level until the +Gz level fell below +2.0 Gz, at which tirne it retunied to

the O volt level The high level controller also provided cornmands to the blood pressure monitoring system, attempting to keep it fiom recalibrating during the acceleration profile. Once the centrifuge profile was completed (event marker retum to O volts), the software

started a second tirner which kept track of elapsed time. A 45 second interval (rest) was encoded into the software before the next control penod was initiated. A temporal representation of the event marker and timer cycles is shown in Figure A-4.

EVENT MARKER

0

G, End of Profile

+1 Gz Control

€? Vrpm= t3.0 Cz

G, Accelerometer- +UO Cz

Start Rest Interval

Figure A-4: Event maker time cycle. The tirne cycle is intiated with return of event marker to O volts. Rest cycle duration is set to 45 seconds and is preceeded with an auditory warning. Onset of controlperiod is represented with event marker voltage increase. During the + 1 Gz control, voltage remains at 5 voltsfor 10 seconds before returning to base voltage. SofhYare then monitors statzrs of Vrpm signal and initiates second voltage rise at +2 Or equivalent. Event marker status remains high until accelerometer voltagefalk below +2 Gz.

A.3.2 Low Level Controller The andog voltages fiom the so&are "ovemde" switck accelerometer, centrifuge control cornputer (Vrpm), and G-suit pressure transducer were fed to a multifunction board (MI0 16H, National Instruments, Austin, TX) of a second cornputer (Macintosh IIci, Apple Cornputers, Cupertino, CA). Labview software (v2.2, National Instnunents,

Austin, TX) was again used to develop an instrument control program. A simple front panel design (Figure A-5) required the system operator to simply start the program at the beginning of an experimental session and then terminate the program using a mouse entered input.

Select GO and Start with ARROW

Reselect GO to Stop Program

Figure A-5: Thefiont panel of the low Zevel conh-oller. The systern operator initiated and terminated the sofhare algorithm with a mouse input.

The software decoded the parameter information provided by the high level controller. The PBG and G-suit pressure schedules, along with delay information were integrated into the software algorithms. A ring buffer was used to control the time delay

in G-suit pressure. Control input signals were converted to working units. Based on information provided by the control inputs, the required mask and G-suit pressures were then calculated. The pressures (Preq) were then converted to the necessary control voltage inputs to the ECU (Figure A-6). The control voltages were supplied by the mdtifunction board to the AAPS system. The software loop could be interrupted using the ovemde feature. If the switch was engaged, the output pressures fkorn the Life-

support equipment were reduced according to critena designed to provide the greatest protection and cornfort to the subject.

Low Level Controller LabVIEW Sofware

High Levef Controller

Mdti function Board A/D

Conversion ---

-

-

Digital

m Port

Multifmiction Board

LabVBW Sofware

AJD Conversion

Digital I I 0 Pm

Figure A-6: The rnziltzficnction board and Lab VIEW s o f i a r e environment of the conirol cornputer. Analog voltages were acquired by the multzjÙnction board, converted to working units, and used tu calculote the required mask and G-suil pressures. The resultant control voltage was then supplied to the ECU

Sample Exposure Schedule

Volunteer Consent Form 4 July 95

VOLUNTEER CONSENT - PROTOCOL #L- 1 18 - Amendment #I The Effect of Changes in Timing of G-suit Pressurization on the Cardiovascular Response to +Gz: Rate of G-suit Pressurization and the Human Cardiovascuhr Response to +Gz Principal Lnvestigator: M. Pecaric MSc, Co-investigators: F. Buick PhD, I Maloan BSc Aerospace Life Support TechnoIogy Section

1.

of (name) (addtess) hereby volunteer to participate as a test subject in a DCIEM experiment designed to examine the effects of changes in timing of G-suit pressurization on the cardiovascular response to +Gz. I have read experimencd protocol #L118, this arnendment, and the description of the associated risks, and have had the opportunity to ask questions of the Investigator(s) and DCIEM physician. 1 have been informed to my satisfaction of ail details of the procedures by one of the Investigators. 1 have been told that the risks of +Gz exposure inciude: temporary neurological and visual effects including G-

induced loss of consciousness (G-LOC). tissue trauma, cardiovascular stress, respiratory changes, and other associated possible risks. 1 have been given examples of potential mirior and remote risks associated with the experiment and consider these risks acceptable. In addition, 1 undersund chat this smdy. or any research. may involve risks that are currently unforeseen. 1 understand and accept these risks. For CF mernbers onlv: 1 understand that 1 am considered to be on duty for disciplinary. administrative and Pension Act purposes dunng my participation in this experiment. 1 understand that a medical interview, examination. and rests will be required before any participation begins. 1 agree to provide responses to questions that are to the best of my knowledge, truthful and complete. Furthermore, 1 agree to advise the Investigator(s) of any heaith status changes since my initial assessment (including, but not Iimited to, virai illnesses, new prescription or 'over-the-counter' medications, and new risk of pregnancy). 1 have been advised that the medical information I reveal and the experîmental data conceniing me will be treated as confidential ('Protected B' IAW CF Security Requirements). and it wilI not be reveaied to anyone other than the Investigators without my consent except as data unidentified as to source. 1 am aware of the requirement ro sign a separate consent fonn for invasive medical procedures.

For female sub-iects: 1 have been inforrned chat tiis experiment could be potentially h m f u l to a fetus. Therefore. 1 consent to the administration of a pregnancy test as part of the medical procedure prior to commencement of this experiment. 1 understand that this result and al1 discussion pertaining to this matter wilt be treated as confidentid between physician and subject. If 1 have any concern regarding a possible pregnancy, I will consult a DCIEM physician before undenaking or resurning any phase of the experiment. Furthermore, 1 will take appropriate precautions to prevent pregnancy for the duration of the entire experiment. 1 am aware that 1 will remain relaxed and be protected by an anti-G suit and, during some conditions, positive pressure breathing. 1 understand that the typical experiment will require 3 to 6 sessions of approxirnately 2 hrs each. In addition, several preIiminary training sessions may be required until 1 am able to perform al1 the techniques properly. 1 accept compensation as outlined in the subject information package.

1 agree to: (i) not consume any alcoholic beverages within 24 hrs of a centrifuge run; (ii) have a restful evening the ~ g h before t a test; (iii) perform no heavy exercise on the day of a test; and (iv) abstain from smoking, coffee and chocolate in the 3 hr period before a test, and a med in the hour preccding it.

1 understand that a blood donation less than 30 days in advance of commencement is a contraindication to my participation in the study. In the event of a loss of consciousness episode as a result of +Gz exposure, 1 shail refrain frorn driving or operating heavy machinery for a penod of 4 hrs following the experimental session. If tmsponation is required because of this recommendation, the Investigators shall make such arrangements, the cost of which, where necessary, will be borne by DCIEM. Should G-induced loss of consciousness occur when a physician is not in attendance, then the physician will be notified. 1 understand that 1 am free to refuse to participate and may withdraw my consent without prejudice or hard feelings at any time. Should 1 withdraw my consent, my participation as a subject will cease immediately - unless the Investigator(s) determine that such action would be dangerous or impossible (in which case my participation will cease as soon as it is safe to do so). 1 also understand that the Investigator(s), their designate, or the physician(s) responsible for the experiment rnay terminate my participation at any time, regardless of my wishes. 1 understand and agree that if I should require medicai treatment as a resuit of rhis scudy, this will be provided or coordinated by the physician assigned to this study. 1 understand that a Flight Surgeon shalI be present during al1 exposures involving the use of the experimental hiil pressure hdf suit and, hereby. consent to whatever emergency medical intervention deemed necessary by the attending medical personnel or their consultants. 1 will go with the lnvestigator to seek immediate medical attention if either I or the Investigacor considers that it is requi red-

NOTES: For Militarv oersonnel on Dermanent strength of CFEME: Approval in principle by Cornmanding Officer is given in Memorandum 3700-[(CO CFEME), 18 Aug 94; however. members must still obtain their Section Head's signature designating approval to participate in this particular experiment. For other militarv wersonnel: Al1 other military personnel m u t obtain their Cornmanding Officer's signature designating approval to participate in this experiment. For civilian oersonneI at DCIEM: Signature of Section Head is required designating approval to participate in this experiment.

Volunteer

Witness

Name: Signature: Date:

This subject is fit to participate in this experiment as outlined in the protocol 1 with the limitations appended beIow: PhysiciadMed Officer Name: Signature: Date: Limitations:

Section Head 1 Commanding Officer's Signature: Date:

Investigator

%irin R u p o ~ r 1. Unrcagiibly Slow 2 Sli rly Slo*rcr lbm Eipcctoû

4. Sliwy Puia Thin hpsctd 5. U n ~ a c p r b l yFa

Annex E

A n a b i s Sensitivity and Control Data A series of control (Le., no pressurization of the G-suit) runs to +2.5, M.0, and

t3.5 G z were randornly selected for each subject fiom the 4 experimental sessions in wliich the STTNG garment was wom. The spline fit interpolation of the heart level systolic blood pressure (SBP,)

data at the highest acceleration level completed by al1

subjects (+3.5 Gz) is shown in panel A of Figure E-1 . Individual differences were evident at the onset of the acceleration profile (t0). Systolic blood pressures were found to oscillate during the +Gz exposure, yet there was little difference between starting and ending levels. The data were then normalized (nSBP,)

with respect to profile omet (tO) values

(Panel B), thereby negating any differences between subjects prior to profile onset (i.e., carry over effects, fatigue and anticipatory effects, and any individual differences). The

mean response for the +Gz exposure was then determined dong with an index of variability (SEM) as shown in panel C. Note that the oscillation in blood pressure response was darnpened, but it was still present during +Gz. By the end of the acceleration profile, mean systolic pressures did not change fiom onset values. The mean nSBP,

responses for the three +Gz levels are shown in Figure E-2.

The magnitude and fiequency of oscillation were consistent across the acceleration levels selected. There were srna11 differences between conditions at each time interval (Le., below scientifically relevant differentials of 11 r n d g ) for most of the +Gz exposure. However, at t9 the mean SBP, was much lower at +2.5 Gz than that recorded at +3.0 and +3.5 Gz. According to the analysis protocol, omnibus testing was then performed using a 2 way (three +Gz x 11 time interval) repeated measures analysis

Time Since Profile Onset (s)

Figure E- 1: SpZine fit interpolation of the sysiolic blood pressure response wiih exposure to +3.5 Gz in subjects wearing an unpressurized G-suit. A. Individual subject data. B. Data normalized wiih respect to profie onset values. C. Average response and variability (SEW.

Time Since Profile Onset (s)

Figure E-2: Mean nS& response wifh expusure fo +2.5, +3. O, and + 3.5 Gz in the control (no G-suitpressurizarion)esszrization condition. of variance (rm-ANOVA). There were no main effects of +Gz level or Tirne, nor was an interaction present (see Table E-1).

Table E-1: Effect of + Gz and Time un nSBPxLin the Conirol Data Type III Sums of Squares Source Subject +Gz Level +GzLevel ' Subiect ---

-

Tirne Tirne ' Subject

+GzLevel 'Tirne +Gz Level ' Tirne ' Subiect

df

Sum of Squares

Mean Square

5

1 718.360

2 10 10 50 20 100

382.254 4632.907 678.393 2528.1 92 979.404 7876.653

343.672 191.127 463.291 67.839 50.564 48.970 78.767

-

-

GG

F-Value

P-Value

.413

.6727

5538

1.342

.2351

.3000

A22

.8880

S592

Although the rneans differed by over 11 m d g at tg, a closer examination of the individual responses was required. Figure E-3 shows the nSBP, for each of the six subjects ( i) at each +Gz level. To the right of the distribution is the group mean ( O ) , with the bars indicating the SEM. The difference between mean values could rnostly be

atûibuted to subject variability rather than to the effect of +Gz. The variability was the same as that found at other time intervals (refer to panel C in Figure E-1). No M e r analysis was, therefore, required for these data.

Figure E-3: nSBPHL(W )for each of the six subjects (SI ta S6) at each control + Gz level afier 9 S. To the righr of the disiribution is the group mean (O), with the bars indicating the SEM. Systolic blood pressures may not have changed during +Gz exposure between control conditions at the level of the heart, but pressures would be expected to f d l in cephalad regions due to hydrostatic influences. The same data set was subsequently converted to eye level equivalents using equation 1-7. Normalized eye level systolic blood pressure (nSBPEL)responses are depicted in Figure E-4. Note that nSBPELvalues

Time Since Profile Onset (s)

Figure E-4: Norrnalized eye level systolic blood pressure (nSBP,J response with control exposures tu t2.5,+3.0, and +3.5 Gz.

were aiready less at tO than heart level equivalents by approximately 39 mmHg due to the effect of a t1.75 Gz inertial force. During the +Gz profile, nSBP, values decreased in proportion to the applied acceleration stress. The relative position of the lines remained steady throughout the course of the exposure. Omnibus testing indicated a main effect of +Gz level and Time (see Table E-2). Consistent with the mean response seen in Figure E-4, there was no interaction present.

Table E-2: Effect of +Gz and T h e on n W E ,in the Control Daia Type III Sums of Squares

Source

df

Subjecî

5

+GzLevel +GzLevel ' Subject

Sum of Squares

Mean Sauare

1718.360

343.672

2

7024.31 2

3512156

1O

4632.907

463,291

Time

1O

13809.485

1380.949

Time ' Subject

50

2528.1 92

50.564

20

2303.585

115.179

100

7876.653

78.767

+GzLevel 'Tirne +Gr Level * Tirne 'Subject

F-Value

P-Value

ffi

1 7.581 27.311

1 1

(

-0099

-0130

.O001

.O001

-1124

.2768

1 1,462

Dependent: nSBP at Eye Level

Data were then collapsed across Tirne. Mean nSBP, (kSEM) at +2.5, i3.0, and +3.5 Gz were 54.66 (k 1.44), 62.03 (+ 1-46},and 69.25 (k I .86) rnmHg lower than heart

level values at profile onset, respectively. A minimum differential was only present between the t2.5 Gz and +3.5 Gz conditions. Contrast analyses tested for differences between +Gz levels. As two means were compared (i.e., a = 2), the df.,

was fixed at 1.

To maxknize the sensitivity of the paired analyses, a non-pooled error term was selected

as described by Keppel(1991). A non-pooled term uses only the variance associated with the paired cornparison, such that the df,.,.

equals n-1 . This fixed the cntical F value

at 16.3 for dl cornparisons, main and interaction alike. Contrast analyses found the hnSBPELof 14.6 mmHg to be significant (F(1,5)= 18.3 1, p < 0.0 1). To examine the effect of Tirne, the data were collapsed across +Gz. Contrasts were used to compare blood pressures each tirne interval (tl to t10) against values

measured at profile onset (tO). Calculated nSBPa values at all time intervals were different (F(1,5) 2 57.3, p S 0.01) from those measured at profile onset (see Figure E-5). The smallest differential (AnSBPR of 13.5 rnmHg) occurred between tO and t 1.

* Significant at p 5 0.01

Figure E-5: Surnrnary of contrast analyses comparing nSB& onset values (tO).

af tl to t10 against profle

The control data indicated that there was little effect of +Gz on systolic blood pressure values measured at the level of the heart. However, the hydrostatic influences of acceleration exposure produced a significant decrease in cephalad regions. Perfuçion pressures at head level were found to decrease immediately after profile onset, and these changes were afEected by the magnitude of the +Gz level. Contrast analyses were able to detect main effect dBerences with a, set at 0.0 1. Tt was also necessary to test the sensitivity of the analysis when an interaction occurred. To change blood pressures above control (Le., an unprotected state) levels, the G-suit is innated accordhg to a preset pressurization schedule. As the pressure to the Gsuit is a fünction of both the schedule and +Gz level, the potential for the largest effect

would occur at the highest acceleration level(+3.5 Gz). Subsequently, the control condition at +3.5 Gz was compared against the blood pressure response with the G-suit pressurized according to one of the three inflation schedules (Low, Nominal, or High). Note that no delay was introduced in lower garment pressurization. The resultant changes in nSBP, are shown in Figure E-6.

Time Since Profile Onset (s)

Figure E-6: Change in n W H Lin either the conhol condition or with the STNG G-suit pressurized by one of the three P, schedules in subjects exposed [O c 3 . j Gz. The omnibus output is shown in Table E-3. There were main effects of Condition and Tirne. In addition, a Condition x Time interaction was also significant.

Table E-3: Summary of Omnibus Test on nSBP,, in Conîrol and G-suit Pressurization Conditions at +3.5 Gz Type III Sums of Squares df

Subject

5

6691.351

3

8429.T74

15

5119.207

Condition Condition ' Subiect Time -

Time 'Subject Condition ' Time Condition 'Time ' Subject Dependent: nSBPhl

1

10

1 1

50 30 f 150

Mean Square

Sum of Squares

Source

1

7556.405

2809.925

1

1

341.280 755.641

3184.094

63.682

431 9.090

143.970

6004.820

F-Value

P-Value

GG

8.233

.O018

.O036

.O001

1 .O009

.O001

-0387

1338.270

40.032

1

11.866 3.596

1

The difference between condition means was caiculated at each tirne interval. Of

the 66 possible comparisons (6 at each time interval x 11 intervals), 20 pairs of means were at least 11 mmHg apart (i.e., ASBP,

2 11 mmHg). Contrast analysis detected 6

significantly diflerent occurrences (F(1,S) 2 16.3, p 5 0.0 1) between Control and one of the presswized G-suit conditions at t7, t8, or t 10 (see Figure E-7). Lowering the crpc to 0.05 would have reduced the cntical F to 6.6 1, thereby increasing the number of significant differences to 16. However, calculation of the a , indicates the great nsk associated with the higher apcvalue. Due to the high number of paired comparisons

(c = 20), or,

increased fkom 0.182 to 0.642. Such a strong possibility of at least one

Type 1error using a,

makes it ciifficult to interpret the treatment effect, knowing

= 0.05

that some of the si@icant

findings may have resulted by chance alone. Consequently,

selection of the lower ccpCvalue reduces thk risks at the cost of Iosing statistical power. Given that differences in blood pressure were still detected with ccpc= 0.00 1, this was considered an acceptable compromise.

O

+

-10

,

tO

l

tl

l

I

t2

t3

A

* significant fkom ControI ( p c 0.01)

y

1

I

t4

t5

I

I

t6 t7 Time Interval

1

1

t8

t9

Control LowPgs

Nom Pgs

High Pgs

1

t10

Figure E-7: Significant mean nSBPHLincreuses ivith lower body garment pressurization fiom control vahes. Bars indicate SEMfor the highest and lowest means ut each time interval.

AMYEX F-1

Study 1: G-suit Pressuref'ïime Profiles

AMYEX F-2

Study II: G-suit Pressure/Time Profiles

ANN'EX F-3

Study III: G-suit Pressure/Time Profiles

ANNEX F-4

Study IV: G-suit Pressurernime Profiles

Comparative Pressure Differences Between Delay Conditions Figures G-1 and G-2 illustrate the significant mean differences in G-suit pressure between the delay conditions at each time interval during the +4.0, +4.5, and +5.0 Gz exposures. Time fiom profile onset is represented on the X axis, the magnitude of the AP, on the Y, and the conditions of cornparison on the 2. The Y value is the algebraic subtraction of the second condition from the fxst. In the initial series, P,, with the 1.5 second delay was subtracted fiom the No Delay values. The resdtant values were then plotted at each time interval. Conditions were classsed according to the differences in

delay duration: (A) 1.5 seconds; (B) 3.0 seconds; or (C) 4.5 seconds.

Figure G-l : Dzxerences in G-suit pressure between delqv conditions at +4 O Gz.

Figure G-2: Dzrerences in mean P, between delay conditions at + 4 5 and +5. O G.

Blood Pressures with the Low, Nominal, and High Pgs Schedules

175

1

175

1

Nomiral Pgs Schedule

High Pqs ScheduIe

'Iime (s)