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Present your findings confidently and look the examiner in the eyes. Avoid using words "may be, I think, could be". §. Treat each case as new and do not let a ...

Global institute of medical sciences

CARDIOLOGY Dr.G.Bhanu Prakash

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CVD signs: Enlarged heart, swelling of the ankles or legs, unusual/ excess weight gain, wounds that do not heal well. CVD symptoms: Chest discomfort (pain, pressure, squeezing, heaviness, etc.) especially if brought on by exertion and relieved by rest, shortness of breath with minimal exertion or upon lying down, palpitation or irregular heart beats, severe dizziness or loss of consciousness, sudden weakness or paralysis of one part of the body, sudden slurring of speech or loss of vision, frequent nocturnal urination, unusual and progressive fatigue, leg pain/ discomfort with walking

Tips for clinical examination § § § § § § § §

§ §

Always introduce yourself and be courteous to the patients Ask for permission before examination Avoid hurting the patient Listen to the instruction carefully Do not forget to observe the patient first for examples hearing aid or dermatitis etc. Learn to describe the physical findings before giving the likely diagnosis Do not rush in the examination. Remember more than one signs may be present. (This may be associated or coincidental) Do not panic if you do not know the diagnosis. Give the physical findings and provide a list of differential diagnosis (you may want to classify the pathology as congenital or acquired; congenital may be inherited or non-inherited and acquired may be traumatic, nepotistic, inflammatory, iatrogenic etc.) Present your findings confidently and look the examiner in the eyes. Avoid using words "may be, I think, could be" Treat each case as new and do not let a bad case affect your subsequent examination

Dr.G.Bhanu Prakash

Global institute of medical sciences §


Avoid derogatory such as syphilis, cancer or multiple sclerosis. Use euphemism or medical jargons instead such as St.Louise's disease, neoplasm or demyelinating diseases Thank the patients and examiners at the end of the examination even if the whole thing go badly. Most cases have vascular diseases involving the eye or the visual pathway. Therefore, look for abnormal rhythm and left sided valvular disorders. The most likely cases are:         




atrial fibrillation mitral stenosis mitral incompetence aortic stenosis aortic incompetence a mixture of the above mechanical heart valve Marfan's syndrome with aortic incompetence carotid stenosis

Vascular Exam (Arterial Bruits or diminished pulses) 1. Abdominal aorta 2. Iliac artery 3. Femoral artery 4. Carotid artery 5. Subclavian artery Local Signs of Peripheral Vascular Disease 1. Decreased skin temperature 2. Shiny skin 3. Skin hairless over lower extremity (e.g. shin) 4. Dystrophic Toenails 5. Distal extremity color change with position a. Skin pallor when leg elevated b. Skin rubor when leg dependent

Dr.G.Bhanu Prakash

Global institute of medical sciences









1. 2. 3. 4. 5. 





Dr.G.Bhanu Prakash

Global institute of medical sciences


Areas of the heart Mitral  

apex should be 5th intercostal space and in mid-clavicular line

Tricuspid 

lower left sternal edge

Pulmonary 

upper left sternal edge ie left of manubrium

Aortic 

upper right sternal edge ie right of manubrium

Heart Sounds

1st Heart Sound, S1 This signals the onset of systole and is caused by the closure of the mitral and tricuspid valves with concomitant tensing of the left ventricular wall. The mitral valve closes slightly before the tricuspid valve but the two sounds are usually merged. Splitting is marked in tricuspid stenosis or right bundle branch block. NB The 1st sound can be identified by palpating the carotid pulse while auscultating - the upstroke of the carotid pulse closely follows the 1st heart beat.  

S1 is loud in mitral stenosis -> palpable tapping apex beat; also in tachycardia or hyperdynamic circulation S1 is soft in mitral regurgitation (and also when the PR interval is long); also in bradycardia and LVF

Dr.G.Bhanu Prakash

Global institute of medical sciences

2nd Heart Sound, S2 This separates systole and diastole. The sound is made by the closure of aortic and pulmonary valves. The aortic valve closes before the pulmonary valve and this splitting of the second sound is heard particularly during inspiration, as more blood is drawn into the right ventricle, a normal phenomenon. (This occurs because right heart venous return varies with respiration). During expiration the split sounds of S2 resynchronise. The sound of pulmonary valve closure (P2) is best heard over the pulmonary area as it is much quieter than that of aortic valve closure (A2). 

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Wide splitting occurs in o right bundle branch block o pulmonary stenosis Wide and fixed splitting (ie not varying with respiration) occurs when there is an atrial septal defect Reversed splitting (ie splitting increasing on expiration) occurs in o systemic hypertension o left bundle branch block o aortic stenosis  NB In aortic stenosis A2 is often soft or absent -> "single component 2nd sound" A2 is loud in systemic hypertension P2 is loud in pulmonary hypertension P2 is soft in pulmonary stenosis

3rd & 4th Heart Sounds These are low pitched (so heard best with the bell) and not usually heard. If either S3 or S4 is very loud a gallop/triple rhythm will result. Loud S3 rhythm = S1----S2--S3 ie crotchet-quaver-quaver Loud S4 rhythm = S4-S1-----S2 ie semiquaver-crotchet-crotchet

3rd Heart Sound, S3 This is produced by rapid ventricular filling and occurs in early-mid diastole ie soon after S2 Occurs normally in young fit adults with bradycardia eg athletes Occurs abnormally in 

 

patients with heart failure o left heart failure - S3 heard best in mitral area o right heart failure - S3 heard best in tricuspid area patients with high ventricular filling pressure mitral regurgitation

Dr.G.Bhanu Prakash

Global institute of medical sciences 

constrictive pericarditis o higher pitched and in early diastole => "pericardial knock" o occurs because ventricular filling is suddenly curtailed by constriction of pericardium

4th Heart Sound, S4 This is an atrial sound, occurring just before S1. It is always abnormal as it represents atrial contraction against a stiffened ventricle eg due to aortic stenosis or hypertensive heart disease. It may also occur in heart failure. Added Sounds

Ejection systolic clicks - usually due to aortic stenosis and systemic hypertension but can be to pulmonary stenosis or pulmonary hypertension. Mid-systolic clicks occur in mitral valve prolapse. Opening snap may occur in mitral or tricuspid stenosis. Prosthetic valves make noises on opening and closing. A pericardial friction rub is a creaking sound heard in systole or diastole which suggests pericarditis (could be viral, post MI, due to CTdisease, trauma or uraemia) so look for an associated pericardial effusion. Murmurs Murmurs are caused by turbulent blood flow; this may be due to a stenotic or regurgitant valve producing a high velocity jet; alternatively it may be due to increased flow velocity in a normal vessel or to normal velocity flow in a dilated or distorted vessel; non-pathological causes include the murmur of the hyperdynamic system in pregnancy or a minor anatomical distortion with no pathological consequences (innocent murmur). Bell is good when listening to low-pitched sounds eg mitral stenosis. Diaphragm is good when listening to high-pitched sounds eg aortic regurgitation.

Dr.G.Bhanu Prakash

Global institute of medical sciences

How to amplify murmurs Left heart murmurs are accentuated in expiration; right heart murmurs are accentuated in inspiration Performing the Valsalva manoeuvre (get patient to strain silently)  

amplifies the murmurs of mitral valve prolapse and hypertrophic obstructive cardiomyopathy softens the murmurs of mitral regurgitation and aortic stenosis

NB Sudden squatting has the opposite set of effects to performing the Valsalva manoeuvre. Mitral stenosis will be heard better if the patient rolls into the left lateral position. Aortic regurgitation will be heard better if the patient leans forward. Murmurs are also amplified by exercise due to increase in cardiac output.

Systolic murmurs 1) Ejection systolic murmur = crescendo-decrescendo murmur This originates from the outflow tract, waxing and waning with changing intra-ventricular pressure. It may be a flow murmur, common in childhood and pregnancy, or a pathological murmur as in     

aortic stenosis aortic sclerosis hypertrophic obstructive cardiomyopathy pulmonary stenosis atrial septal defect

2) Pansystolic murmur Of uniform intensity and merges with S2 although it may obscure both S1 and S2. It is usually caused by jets passing from a high pressure chamber to a low pressure chamber during systole ie mitral or tricuspid regurgitation. A pansystolic murmur also occurs when there is a ventricular septal defect. 3) Late systolic murmur This is caused by mitral valve prolapse or papillary muscle dysfunction. It is a high-pitched murmur of even intensity which starts halfway through systole with a mid-systolic click and terminates with A2. NB If the papillary muscle rupture has occurred posteriorly then this murmur will be loudest in the aortic area (instead of the mitral area where it is heard most of the time).

Dr.G.Bhanu Prakash

Global institute of medical sciences

Diastolic murmurs 1) Early diastolic murmur This is high-pitched and usually only heard as the "absence of silence" in early diastole. It occurs due to aortic or pulmonary regurgitation. The aortic regurgitation murmur is usually soft and is best heard with the patient leaning forward and in expiration. NB When pulmonary regurgitation is due to pulmonary hypertension caused by mitral stenosis then the early diastolic murmur is called a Graham-Steel murmur. 2) Mid-diastolic murmur This is low-pitched and rumbling; it starts after an opening snap. Caused by 

 

mitral stenosis (common) o exhibits pre-systolic accentuation in sinus rhythm o amplified by rolling the patient into the left lateral position rheumatic fever o thickens mitral valve leaflets o = Carey Coombs' murmur aortic regurgitation o regurgitant jet causes fluttering of anterior mitral valve cusp o = Austin Flint murmur tricuspid stenosis (rare) large atrioseptal defect

Other murmurs 1) Continuous, machinery murmur of patent ductus arteriosus. 2) Musical or "mewing" murmurs - characteristic of a hole in an aortic valve cusp due to endocarditis 3) Innocent murmur    

common in children or in pregnancy loudest in pulmonary area often low pitched and low intensity check them out with Echocardiograms and Doppler studies

    

? Marfan's -> aortic regurgitation ? Rheumatological disorders eg ank. spond -> aortic regurgitation ? Down's -> ASD or VSD ? Turner's -> coarctation of aorta ? Thyrotoxic -> predisposed to AF and high output heart failure

Dr.G.Bhanu Prakash

Global institute of medical sciences 

? Alcoholism -> dilated cardiomyopathy

Hands 

 

Clubbing o Cyanotic congential heart disease o Infective endocarditis Peripheral cyanosis and Perfusion Endocarditis is suggested by o Splinter haemorrhages o Osler's nodes = tender lumps in pulp of fingertips o Janeway lesions = red macules on wrist and hand Nicotine stains - peripheral vascular disease

Radial pulse - for rate and rhythm   

  

Irregularly irregular = atrial fibrillation (or multiple ectopics) Regularly irregular = 2nd degree heart block Water hammer pulse (= Collapsing) o strong radial pulse that taps hand on lifting of arm o indicates wide pulse pressure of aortic regurgitation Bounding pulse o CO2 retention o Liver failure o Sepsis Small volume thready pulse = shock Radio-radial delay - suggests coarctation or dissection Arterio-venous fistulae - buzzing - for dialysis

Carotid pulse - for character        

Normal Small volume - in low output states eg heart failure, shock, mitral stenosis Small Volume And Slow Rising pulse = aortic stenosis Collapsing (rapid up and rapid down) in aortic regurgitation (also AV fistula or hyperdynamic cicrulation) Bisferiens = collapsing and slow rising occurring in mixed aortic disease Pulsus alternans - LVF Jerky - hypertrophic cardiomyopathy Pulsus Paradoxus - pulse weakens in inspiration - indicates tamponade or constrictive pericarditis

Dr.G.Bhanu Prakash

Global institute of medical sciences Face  

Malar flush = mitral stenosis (also present in mixed mitral disease) ? Jaundice - poss. prosthetic valve causing mild haemolysis

Eyes 

Argyll-Robertson pupil o pupil constricted, does not react to light but does to accomodation o "the prostitute's pupil accomodates but does not react" o think of syphilitic aortic regurgitation & poss. aneurysm Xanthelasmata or corneal arcus = hyperlipidaemia

Mouth   

Cyanosis High arched palate of Marfan's -> aortic regurgitation Mucosal petechiae -> infective endocarditis

JVP Inspection of precordium    

Scars Deformity Pulsation Pacemaker boxes

Palpation  

Thrills Heaves o parasternal heave of RVH o apex beat may be  tapping (quick and light) - mitral stenosis  thrusting (diffuse and long) - mitral regurgitation  heaving (sharp and firm) - LVH & aortic stenosis Apex beat should be 5th intercostal space mid-clavicular line

Auscultation  

Remember to roll into left lateral position and to sit forwards Remember to listen on inspiration and on held expiration

Chest 

Listen at lung bases for fine inspiratory creps of pulmonary oedema (LVF)

Dr.G.Bhanu Prakash

Global institute of medical sciences Sacral oedema Abdomen      

Hepatomegaly - RVF Pulsatile hepatomegaly - tricuspid regurgitation Splenomegaly - endocarditis Pulsatile mass (not liver) - abdominal aneurysm Femoral arteries, radio-femoral delay (coarctation of aorta) and femoral bruits Also can listen for renal bruits

Peripherally    

Peripheral pulses Pitting oedema Peripheral vascular disease - cold feet, gangrene Varicose veins

Finally 

 

BLOOD PRESSURE o narrow pulse pressure indicates aortic stenosis o wide pulse pressure indicates aortic regurgitation o drop of > 10mm Hg in inspiration indicates pulsus paradoxus and either tamponade or constrictive pericarditis Fundi o hypertensive change  grade I copper wiring of arteries  grade II arteriovenous nipping  grade III flame or blot haemorrhages, cotton wool exudates  grade IV papilloedema o Roth' spots = retinal vasculitis indicative of endocarditis Urine - haematuria may indicate endocarditis Temperature chart - endocarditis

The Signs of Different Conditions Aortic Stenosis (Uncomplicated)   

  

Observation - more likely to be male Hands - nil Radial pulse o normal o AF (irregularly irregular) Carotid pulse - slow rising pulse Face - nil JVP - normal

Dr.G.Bhanu Prakash

Global institute of medical sciences 

Thrills o

aortic areas  2nd R intercostal space (classical aortic area)  4th L intercostal space/sternal edge whch is along the line of LV ejection  over apex (along line of LV ejection)


normal position 5th intercostal space in mid-clavicular line heaving character due to LVH Auscultation o 1st HS normal o Ejection systolic click may precede murmur o Ejection systolic murmur  loudest sitting forward  loudest in expiration  radiates to carotids and apex o 2nd HS  may be soft or absent  paradoxical splitting may occur during expiration such that P2 occurs before A2 but A2 may not be audible anyway o No diastolic murmurs o 4th HS may be present just before 1st HS Peripherally nil of note Blood pressure o narrow pulse pressure eg 120/80 or 110/80 o o

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Mitral Regurgitation (Uncomplicated)  

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Observation - nil Hands o look for signs of endocarditis ie splinter haemorrhages (transilluminate them), Osler's nodes, Janeway lesions Radial pulse - may find AF Face - normal in uncomplicated mitral regurgitation (but malar flush of mitral stenosis if mixed mitral disease) Carotid o usually normal character o in severe disease may get a small volume jerky pulse due to shortened ejection volume and time JVP o usually normal o raised if subsequent pulmonary hypertension Thrill possible in mitral area Heaves o in severe regurgitation may develop a parasternal heave due to left atrium enlargement o may also have RV Heave if pulmonary hypertension has developed

Dr.G.Bhanu Prakash

Global institute of medical sciences 

Apex displaced laterally and down thrusting Auscultation o 1st HS - soft or normal o Pan-systolic murmur  loudest at apex in left lateral position  radiates to the axilla  may obscure aortic component of 2nd HS o 2nd HS may be obscured (but if there is pulmonary hypertension it could be loud and late) o 3rd HS often present o o

Abnormalities of the JVP 1) Raised JVP with normal waveform   

right heart failure fluid overload bradycardia

2) Raised JVP with absent pulsation 

SVC obstruction - full dilated jugular veins, no pulsation, oedematous face and neck

3) Large a wave   

tricuspid stenosis - atria contracts against stiff tricuspid and so pressure in atria rises higher than normal pulmonary hypertension - there are generally higher pressures on the right side of the heart pulmonary stenosis

4) Extra-large a wave = Cannon wave Occurs when atrium contracts against closed tricuspid eg      

complete heart block atrial flutter single chamber pacing nodal rhythm (AV node is in charge) ventricular extra-systole ventricular tachycardia

ie any condition in which the atria and the ventricles are not conducting in appropriate rhythm 5) Absent a wave 

atrial fibrillation

6) Systolic waves = combined c-v waves = big v waves 

tricuspid regurgitation (c-v wave because the pressure in the right atrium is raised throughout ventricular systole - tip is to watch for earlobe movement!)

Dr.G.Bhanu Prakash

Global institute of medical sciences

7) The slow y descent occurs in tricuspid stenosis (if the HR is so low as to allow the length of descent to be appreciated!) 8) Paradoxical JVP = Kussmaul's sign Normally the JVP should rise on expiration and fall on inspiration. When the JVP rises on inspiration it indicates   

pericardial effusion constrictive pericarditis pericardial tamponade

Right Ventricular Failure ·

R side heart failing


Pooling blood IVC< V


Raised JVP




Ankle oedema




Signs of what caused it

Pericardial Disease ·

Pericarditis o


friction rub

Tamponade o

JVP raised


very reduced heart sounds §


apex beat impalpable


Dr.G.Bhanu Prakash

Global institute of medical sciences

Aortic Stenosis ·

Narrowing imposes a pressure load on LV


Restricts LV outflow


Midsystolic harsh ejection murmur


Max at aortic area


Loudest sitting and expiration Blood Pressure Classification in Adults Category





What does a blood pressure of 170/80 indicate?

Dr.G.Bhanu Prakash

Global institute of medical sciences

Pure Systolic Hypertension 

Have the patient roll on their left side. o Listen with the bell at the apex. o This position brings out S3 and mitral murmurs. Have the patient sit up, lean forward, and hold their breath in exhalation. o Listen with the diaphragm at the left 3rd and 4th interspace near the sternum. o This position brings out aortic murmurs Murmurs and Extra Sounds

Systolic Ejection


Systolic Click Late Systolic

Innocent/Physiologic Aortic/Pulmonic Stenosis

Mitral/Tricusp Regurgitation

Mitral Valve Prolapse

Early Diastolic

Mid Diastolic

Opening Snap Diastolic Rumble

Aortic Regurgitation

Mitral/Tricusp Stenosis

Mitral Stenosis

Dr.G.Bhanu Prakash

Global institute of medical sciences

Ejection Sound



Aortic Valve Disease

Normal in Children Heart Failure

Physiologic Various Diseases

Murmur Grades Grade





very faint, only heard with optimal conditions



loud enough to be obvious



louder than grade 2



louder than grade 3



heard with the stethoscope partially off the chest



heard with the stethoscope completely off the chest yes

Occlusion Location A. Aortoilliac Occlusive Disease (Leriche's Syndrome) 1. Bilateral leg diminished pulses throughout 2. Slow wound healing legs 3. Impotence B. Iliofemoral Occlusive Disease 1. Unilateral leg diminished pulses throughout 2. Buttock claudication may be present C. Femoropopliteal Occlusive Disease 1. Thigh and calf claudication 2. Normal femoral pulses in groin A. Ankle-Brachial ratio > 0.9: Normal B. Ankle-Brachial ratio 0.5 to 0.9: Claudication C. Ankle-Brachial ratio < 0.5: Resting ischemic pain

Chronic Venous Insufficiency

Venous Insufficiency Venous Stasis

Risk Factors


A. Obesity B. Congestive Heart Failure C. Diabetes Mellitus Symptoms and Signs A. Initial Changes

Dr.G.Bhanu Prakash

Global institute of medical sciences



1. Varicose veins 2. Tan or reddish brown skin color changes 3. Weeping and excoriated skin 4. Pedal edema B. Later Changes 1. Lipodermatosclerosis a. Induration at medial ankle to mid-leg C. Advanced Changes 1. Brawny edema above and below fibrotic area 2. Ulcerations Complications A. Venous Stasis Ulcers 1. More common in older women 2. Chronic and often recurrent B. Postphlebitic Syndrome 1. Chronic leg edema 2. Deep Venous Thrombosis 3. Pigmentation 4. Ulceration Diagnosis

Abdominal Aortic Aneurysm Causes A. B. C. D. E.

Associated with Atherosclerosis in only 25% of patients Aortic Dissection Mycotic Infection Cystic Medial Necrosis Ehlers-Danlos Syndrome

A. B.

Asymptomatic in 75% of AAA Abrupt onset severe pain unrelieved by position change 1. Suggestive of aneurysm enlargement or rupture Aortic Rupture (20% present ruptured) 1. Free Intraperitoneal Rupture (Catastrophic) a. Acute pain b. Cardiovascular Collapse c. Sudden Death 2. Sentinal Bleed (small posterolateral wall tear) a. Acute pain (constant) b. Syncope


c. d. e.

Pulsatile abdominal mass Hemodynamically stable with tachycardia Needs Emergent Intervention before full rupture

Dr.G.Bhanu Prakash

Global institute of medical sciences

Findings suggestive of occlusion A. B. C.

Proximal lower extremity pressures less than arms Proximal femoral pressure 20-30 mmHg

Edema evaluation

Pitting edema Brawny edema Dependent edema Non-Pitting edema I.


Examiner impresses thumb into skin over bony surface 1. Tibia 2. Fibula 3. Sacrum B. Withdraw thumb C. Measure depth of pit and record in millimeters II. Interpretation A. Pitting Edema B. Non-Pitting edema (Brawny edema) 1. Myxedema 2. Chronic inflammation 3. Chronic Venous Stasis III. Edema Distribution A. Dependent Edema (fluid shift in response to gravity) 1. Standing patient accumulates fluid in feet and ankles 2. Bed-bound patient collects fluid posteriorly (sacrum) B. Chronic Leg edema (Brawny edema) 1. Tissue becomes fibrotic and fails to pit Chest Pain  A heart attack.  Lung problems like pneumonia, bronchitis, or an injury.  A hiatal hernia - known in medical terms as gastroesophageal reflux disease (GERD).  Heartburn.  Shingles.  A pulled muscle.  Mitral valve prolapse. A common disorder, especially in women, in which the mitral valve of the heart fails to close properly. In most people, this is not a serious problem.  Anxiety.  Swallowing too much air.

Dr.G.Bhanu Prakash