Physiology of Cardiopulmonary Resuscitation

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Annu. Rev. Med. 1981.32:435-442. Downloaded from arjournals.annualreviews.org by PALCI on 10/25/08. For personal use only.

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PHYSIOLOGY OF CARDIOPULMONARY 1RESUSCITATION Myron L. Weisfeldt,

M. D. and Nisha Chandra,

.,7410

M. D.,

Peter Belfer Laboratoryfor MyocardialResearchand the CardiologyDivision, The Johns HopkinsMedicalInstitutions, Baltimore, Maryland21205 INTRODUCTION For 20 years external sternal compressionhas been used to create artificial circulation in patients following cardiac arrest (15), and the mechanism for the resulting movement of blood to the brain was thought to be understood. The arrested heart was viewedas a rubber ball filled with fluid with one-way valves at its entrance and exit. The heart is situated betweenthe sternum and the vertebral column, thus external chest compression movesthe sternum and was thought to compress the heart against the vertebral column. Such compression, like internal cardiac massage, movedblood from the left ventricle into the aorta as the aortic valve opened. Retrogradeflow was prevented by mitral valve closure. Followingthe period of compression the left ventricle filled with blood whenthe mitral valve opened. This widely held concept appeared inconsistent with a numberof observations in animal models (21) and man(17), but no alternative mechanisms for the movementof blood were suggested. In the dog arterial and venous pressures during chest compression were similar if not identical (21). fact, the high intrathoracic venouspressure was considered by some(17, 21 to point to an important injurious effect of "external massage." It was assumedthat the very high intrathoracic venous pressures were transmitted peripherally to the brain and caused brain injury. Only recently did it becomeclear that other mechanismsbeside cardiac compression operate during chest compression. These new suggestions (20) ~Supported by Grant No. P50-HL-17655-06 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland. 435

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are in part based on confirmation and extension of the earlier observations of the similarity of all intrathoraeic vascular pressures during sternal compression. Animportant stimulus to us in our studies was the workof Dr. J. Michael Criley and associates (8) dealing with "cough CPR." They demonstrated that by continuous coughing, an arrested patient could maintain himself in the conscious state as long as cough was continued. One ingredient in the coughis clearly a rise in intrathoraeie pressure. If this is the active factor in moving blood during cough, then it is a potent mechanism for the movementof blood to the brain.

ANIMAL STUDIES In extensive hemodynamicstudies (20) in large (20-40 kg) dogs we found that during chest compressionfollowing cardiac arrest there is essentially an equal rise in central venous, right atrial, pulmonaryartery, and aortic pressures. Diastolic pressures were also similar but slightly higher in the aorta than in the right atrium. These pressures in intrathoracic vascular structures were nearly equal to general intrathoraeie pressure as indexed by ¯ esophageal pressure. It was also clear that forward carotid flow occurred only during chest compression. Wewere seeking to identify the pumpwithin the chest responsible for movingblood through the circulatory system against the peripheral vascular resistance, but we could not find one. In any fluid-filled systemwith an appreciable resistance to flow (such as that present in the peripheral vascular bed), there must be a pressure gradient across the resistance to allow the fluid to flow through it. If there is a pumpresponsible for the generation of this pressure gradient across the resistance, there must be a pressure gradient across the pumpitself. Of course, normally whenthe heart is acting as a pumpthere is a substantial pressure gradient betweenthe aorta and the central veins. The lack of such a pressure gradient across the heart during chest compression eliminates the heart or compression of the heart as the sought-for pump. Hence we tried to identify the mechanismfor the generation of the peripheral arterial-venous pressure gradient that must be present across the resistance bed if there is to be forward flow of blood during cardiopulmonary resuscitation. By measuring peripheral pressures in the extrathoraeic carotid artery and the extrathoracic jugular vein, we confirmed that there was a pressure gradient across this resistance bed. As seen in Figure 1 intrathoracic arterial pressure in the aorta was transmitted relatively completely into the extrathoracic arterial bed; the intrathoracic venous pressure was not transmitted into the extrathoracic bed. This differential transmission of

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ESISTANCE


~ 0~85 I

I THORAX

ALL PRESSURES IN mmHg

Figure1 Representative pressuresrecordedduringconventional CPRwithforwardcarotid flow.Pressuresare thoserecordedduringcompression. Intrathoracicpressureswereindexed fromesophageal pressures.Thereis no significantpressuregradientacrossthe heart. The extrathoracic arterialpressureis similarto theintrathoracic aorticpressure.Theextrathoracic venous pressureis markedly lowerthanthe intrathoracicvenous (right atrial) pressure.There is an extrathoracic arterial-venous pressuregradientthat resultsin forwardflow.

the intrathoracic vascular pressure generated the extrathoracic arterialvenous pressure gradient required for forward flow.

Peripheral Arterial-VenousPressureGradient At least three general mechanismsare nowthought to contribute to the generation of the extrathoracic arterial-venous pressure gradient observed during conventional CPRin the dog. These factors are (a) various venous valving mechanismsare operating, (b) peripheral venous capacitance greater than arterial capacitance, and (c) arterial resistance to collapse greater than venous resistance. The most easily understood of these mechanisms is that of a valving mechanism.Veins at the thoracic inlet and other veins leading from the brain appear to have anatomic valves that prevent retrograde flow of blood during increases in intrathoracic pressures (9, 10, 16, 18). The valves along the extrathoracic veins, and the one at the thoracic inlet appear to be important. The secondfactor contributing to the generation of the peripheral arterial-venous pressure gradient is that venous capacitance is greater than arterial. Clearly, if the same amount of blood were to move from the intrathoracic arterial and from the intrathoracic venous systems into the extrathoracic arterial and venoussystems, arterial pressure wouldrise more



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than venous pressure because of the differences in extrathoracic arterial and venous capacitance. The third contributor to the peripheral arterial-venous pressure gradient is the difference in arterial and venousresistance to collapse. Venousstructures readily collapse wheninside pressures fall below surrounding pressures by even a small amount. Recently we showedthat the in vivo carotid artery at the thoracic inlet exhibits considerable intrinsic resistance to collapse. This resistance to collapse can be increased in the presence of vasoconstrictor agents (23). Resistance to collapse of the arterial vessels would allow blood flow to continue toward the brain despite surrounding intrathoracic pressures which exceed intravascular pressures. The veins would readily collapse at the exit to the high pressure region, i.e. at the thoracic inlet (1, 13). Blood returns from the periphery to the central circulation between compression cycles. Extrathoracic venous pressure rises (20) when blood flows from arteries to veins during compression. Between compressions intrathoracic pressure falls to near atmospheric, and an extrathoracic-tointrathoracic venous pressure gradient appears, which leads to flow into the chest. Right heart and pulmonaryblood flow is also diastolic, at least in part (7). With conventional CPR, fight heart compression maybe a component of the mechanism for pulmonary flow. Movement of Blood Through Direct Cardiac Compression As indicated previously, if direct compressionof the heart is the mechanism for forward movementof blood during chest compression, an arterialvenous pressure gradient across the heart must be produced during chest compression. The heart itself might serve as a pumpwithout an artefialvenous pressure gradient across the heart if there was a marked phase difference betweenhigh arterial and high venous pressures. But in our dog studies there was neither a systolic pressure gradient across the heart nor a markedphase difference in the rise and fall of arterial and right atrial pressures. In several of over 200 dogs we studied, a markedintrathoracic arterialvenous pressure gradient did exist in which aortic pressure was muchhigher than right atrial pressure with chest compression. The arterial pressure in these dogs exceeded 100 mmHg during chest compression,, which is far higher than usual for large dogs during conventional CPR.Thus, compression of the heart through sternal compressionof even animals with a chest structure such as the dog can result in direct cardiac compression. In the absence of an intrathoracic arterial-venous pressure gradient, even if the heart is physically compressed,cardiac compressionis not necessarily responsible for the peripheral or systemic blood flow (see Figure 1). The



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factors responsible for forward flow are those factors generating the peripheral arterial-venous gradient. If cardiac compression and a rise in intrathoracic pressure both occur, the effects will likely be additive. Radionuclide angiographic studies charting the flow of blood through the chest (7) and angiograms performed during conventional CPR(18) support the early observations with regard to mechanism.The initial itow of blood followingthe rise in intrathoracic pressure is from the aorta, whichpartially collapses as blood is sucked toward the periphery from the aorta itself. Next, the valve structures of the heart open and blood movesfrom the lung and left atrium through the left ventricle into the aorta. There is little changein overall left ventricular size. This latter angiographic observation (18) strongly supports the notion that the heart is not compressedin the dog. Therefore, during CPRthe blood apparently circulates because the increased intrathoracic pressure is transmitted equally or nearly equally to all intrathoracic vascular structures. These intravascular pressures are unequally transmitted into the extrathoracic arterial and venous beds, which creates an extrathoracic arterial-venous pressure gradient and forward blood flow during the period of high thoracic pressure; During diastole (release of chest compression),blood flows into the lungs as a result of the extrathoracic venous-to-intrapulmonary pressure gradient. Compressionof the right ventricle during chest compression may aid in pulmonary flow. Overall then, the blood movesto and from the lungs by virtue of the changes in intrathoracic pressure. The heart serves only as a conduit for the passive movementand conduct of blood to and from the lungs. The valves of the heart are not of major significance with regard to extrathoracic blood flow. The mitral and the aortic valves must be open during systole, and the tricuspid and pulmonaryvalves must be open during diastole. During systole the tricuspid and pulmonaryvalves mayclose (although there are no data in this regard) and mayserve as ancillary valves in an additive fashion to the multiple venous valves in preventing retrograde flow. Our ownsuspicion is that the tricuspid valve, becauseof its large size and structure, is likely incompetent. Diastolic closure of the aortic valve maybe critically important in maintaining coronary blood flow.

STUDIES IN MAN Movement of Blood Wecannot yet draw any final conclusions as to the frequency or importance in manof the two mechanisms(chest compression or generalized increase in intrathoracic pressure) with conventional CPR.



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In a numberof patients we demonstrated (20) the presence of a pressure gradient at the thoracic inlet upon withdrawing intravascular catheters from the superior vena cava to the extrathoracic internal jugular vein. Since this pressure gradient does exist in manand since valves at this site can be demonstrated rather easily in manduring cough (9), this newly identified mechanismfor forward movementof blood is certainly operative. On the other hand some patients have readily measureable high arterial pressure with conventional CPR, pressures higher than those usually generated in man during conventional CPRand also higher than those in most dogs. It is our impression that most patients who have low radial artery pressure during CPRare probably able to moveblood through a mechanismrelated solely to the rise in intrathoracic pressure. It is not essential in the humanto think about these mechanismsin an exclusive fashion. Direct cardiac compressionis useful whenpossible; when it is not potent enough to maintain cerebral perfusion, manipulation of intrathoracic pressures would likely have a favorable additive effect on carotid blood flow (5). It must be emphasizedthat, where effective, direct cardiac compression has one particularly attractive feature. Withdirect cardiac compressionit is likely that the aortic diastolic pressure will be significantly higher than whenblood is movedsolely through manipulation ofintrathoracic pressure. In terms of coronary perfusion, this wouldclearly be a useful feature.

IMPROVEMENT OF CPR Wehave explored two basic strategies for improving peripheral perfusion during CPR. Both depend on the general principle of moving blood by raising intrathoracic pressure. Thefirst strategy is to increase intrathoracic pressure per se. Increasing intrathoracic pressure through clamping of the endotracheal tube, while continuing chest compression augmentedcarotid blood flow in a mannerparalleling the increase in intrathoracic vascular pressures (20). During these experiments in the dog it soon becameapparent that one of the limitations of such manipulation of intrathoracic pressure was the occurrenceof carotid arterial collapse. Carotid arterial collapse will occur whenthe intraarterial pressure falls belowthe sumof the extraarterial pressure (intrathoracic pressure) and the resistance of the artery to collapse. Whencarotid collapse occurs there can, in fact, be a reduction in flow through the increase in intrathoracic pressure. With merely clamping the airway, there is a markedinitial increase in extrathoracic carotid pressure and flow with the first chest compression. These benefits dissipate rapidly with subsequent compression cycles, undoubtedly because venous return is inhibited by the continuously high intrathoracic pressure following clamping of the airway. To take advantage



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of this mechanismfor increase in blood flow without inhibiting venous return, the technique of high airway pressure ventilation synchronouswith chest compression was developed. Such techniques were shownpreviously to improve hemodynamicsand animal survival (22), but the mechanismwas unclear and the results doubted (12, 14). The second approach to augmenting blood flow during cardiopulmonary resuscitation is related to abdominal binding. Someyears ago abdominal binding was proven useful in improving the hemodynamicsof cardiopulmonary resuscitation (19). Onelarge study in dogsreported significant benefits in survival and hemodynamicswithout any significant untoward complications. In contrast, another study seemedto showa higher incidence of liver rupture resulting from abdominal binding (11). In the dog we were able to showsignificant augmentationof carotid blood flow through abdominal binding. Abdominalbinding likely improves carotid blood flow for a number of reasons. First, with conventional CPR abdominal binding alone increases esophageal pressure and vascular pressures during chest compression, which mayreflect a greater rise in intrathoracic pressure. Secondly, abdominalbinding maydirect blood flow away from organs below the diaphragm. Thirdly, abdominal binding increases the circulating blood volume(20).

SYNCHRONOUS VENTILATION COMPRESSION

AND CHEST

Using carotid blood flow measuredwith a cannulating flow probe as the sole end-point for assessing efficacy, we compared conventional CPR(chest compression alone at a rate of 60/min with ventilation interposed after every fifth compression) with a new approach. This new approach includes high airway pressure ventilation synchronous with chest compression at variable rates. Venous return is allowed to occur by interrupting both ventilation and compression between each ventilation-compression cycle (diastole). Synchronousventilation and chest compression alone approximately doubles carotid flow (3). There is an additive beneficial effect from abdominal binding and also from volume loading. It should be noted that in some dogs synchronous ventilation and compression provides a lower carotid blood flow than conventional CPR. In these animals the carotid artery collapses. Carotid collapse can be prevented or reversed in most dogs by abdominalbinding, which likely increases the circulating blood volume. In addition, we have most recently found that negative diastolic airway pressure will reverse carotid collapse in somedogs (2), probably because pulmonaryblood flow increases whenthe negative diastolic airway pressure supplies more blood for subsequent circulation.

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Wehaveappliedabdominal binding(6) andventilation at high airway pressuressynchronous with chest compression (4) for brief periodsto smallnumber of patients. Although the results of these studies are encouraging, suchfactors as adequacy of ventilationandthe benefits or complications of these procedures remainto be explored.


Literature Cited 1. Brecher, G. A. 1952. Mechanism of ve12. Harris, L. C., Kirimli, B., Safar, P. nousflowunderdifferent degreesof as1967. Ventilation-cardiac compression piration. Am.J. Physiol. 169-423 rates and ratios in cardiopulmonary 2. Chandra,N., Cohen,J. M., Tsitlik, J., resuscitation. Anesthesiology28:806-12 Weisfeldt,M. L. 1979. Negativeairway 13. Holt, J. P. 1941.Thecollapse factor in pressure between compressions augthe measurementof venous pressure. mentscarotid flow during CPR.CircuAm.J. Physiol. 134:292 lation 59 &60:II-46 14. Jude, J. R. 1963. Discussion.Surgery 3. Chandra,N., Rudikoff,M., Tsitlik, J., 53:193-94 Weisfeldt, M.L. 1979. Augmentation of 15. Kouwenhoven,W. B., Jude, J. R., earotid flow during eardiopulmonary Knickerbocker, G. C. 1980. Closed resuscitation (CPR)in the dog by siheart cardiac massage.J. Am.Med.Asmultaneouscompressionand ventilasoc. 173:1064--67 tion with43:422 high airwaypressure. Am.J.. 16. MacKenzie,J. 1894. The venous and Cardiol. liver pulses, and the arhythmie(sic) 4. Chandra,N., Rudikoff, M., Weisfeldt, contractionof the cardiac cavities, d. M. L. 1980. Simultaneouschest comPathol.Bacteriol. 2:113 pression andventilation at high airway 17. MacKenzie,G. J., Taylor, S. H., Mcpressure during cardiopulmonary resusDonald, A. H., Donald, K. W. 1964. citation. Lancet1:175-78 Hemodynamic effects of external car5. Chandra,N., Snyder, L., Tsitlik, J., diac compression.Lancet 1:1342-45 Weisfeldt,M.L. 1980. Non-invasive as18. Niemann, J. T., Garner, D., Rossisted circulation bysynchronized cycliborough, J., Criley, J. M. 1979. The cal highintrathoracic pressuresupport. mechanism of bloodflow in closed chest Circ. Res. 28:161A cardiopulmonaryresuscitation. Circu6. Chandra,N., Snyder,L., W¢isfeldt,M. lation 59 &60:I1-74 L. 1979. Abdominalbinding during 19. Redding, J. S. 1971. AbdominalcomCPRin man.Circulation 59 &60:II-45 pression in cardiopulmonary resuscitation. AnesthesiaAnalgesia50:668-75 7. Cohen, J. M., Alderson, P. O., Van Aswegen, A., Chandra,N., Tsitlik, J., 20. Rudikotf, M. T., Manghan,W.L., EtfWeisfeldt,M.L. 1979.Timingof intraron, M., Freund,P., Weisfeldt, M. L. thoracic bloodflow duringresuscitation 1980. Mechanisms of blood flow durng with highintrathoracic pressure. Circucardiopulmonary resuscitation. Cir ,~lation 61:345-52 lation 59 &60:II-196 8. Criley,J. M., Blaufuss,A.N., Kissel,G. 21. Weale,F. E., Rothwell-Jackson,R. L. L. 1976. Cough-inducedcardiac com1962.Theet~eieneyof cardiac massage. pression. J. Ar~ Med. Assoc. Lancet 1:990-92 236:1246-50 22. Wilder, R. J., Weir, D., Rush,B. F., 9. Fisher, J., Chandra, N., Eaton, L., Ravitch, M. M. 1963. Methodof coorWeisfeldt, M. L. 1980. Venoushemodydinating ventilation and dosed chest cardiac massage in the dog. Surgery namicsduring coughin man.Circ. Rex 28:168A 53:186-94 10. Franklin,K. J. 1927.Valvesin veins: an 23. Yin,F. C. P., Cohen,J. M., Tsitlik, J., historical survey.In Proc.R. Soc. Med., Weisfeldt, M.L. 1979.Arterial resisSect. History Med.,pp. 4-6 tance to collapse: A determinantof pe11. Harris, L. C., Kirimli, B., Safar, P. ripheral flow resulting fromhigh intra1967.Augmentation of artificial circuthoracic pressure. Circulation 59 & lation during cardiopulmonary resusci60:I1-196 tation. Anesthesiology28:730-34


