Cardiovascular Examination — Written Clinical Reasoning

SAQ 1 — The Systematic Cardiovascular Examination and the Interpretation of an Aortic Stenosis Murmur (20 marks, 30 minutes)

Prompt: Outline your approach to the short-case instruction 'examine this patient's cardiovascular system', addressing: (a) the eleven-step routine and the key sign at each step; (b) the timing-based murmur framework and how you characterise an ejection systolic murmur at the upper right sternal edge radiating to the carotids; (c) the dynamic manoeuvres and how they confirm or refute aortic stenosis; (d) the findings that predict severe rather than moderate disease; and (e) the structured spoken presentation you deliver to the examiner. [1]

Model Answer

(a) The eleven-step routine and the key sign at each step (5 marks): [1]

The routine is head-to-toe and is performed in the same order every time so that no step is missed. The candidate who walks to the chest and listens has failed the question — the stethoscope comes in the middle of the examination, not at the start. [1]

Step 1, end of bed: I take five seconds to observe whether the patient is breathless, cyanosed, cachectic, Cushingoid or has a Marfanoid or Noonan body habitus, and I note any median sternotomy scar or device bump. [1]

Step 2, hands: I assess clubbing (cardiac causes are cyanotic congenital heart disease and infective endocarditis), the peripheral stigmata of endocarditis (splinter haemorrhages, Osler nodes, Janeway lesions), peripheral cyanosis, tendon xanthomata (familial hypercholesterolaemia), and the radial pulse for rate, rhythm and character. The four pulse characters I must recognise are the bounding (collapsing) pulse of aortic regurgitation, the slow-rising pulse of aortic stenosis, pulsus alternans of severe left ventricular failure, and radiofemoral delay of coarctation. I also check all the peripheral pulses. [1]

Step 3, face: I look for the malar flush of mitral stenosis and pulmonary hypertension, dysmorphic features (downslanting palpebral fissures and low-set ears in Noonan syndrome), poor dentition (endocarditis risk), and a high arched palate (Marfan syndrome). [1]

Step 4, eyes: I look for conjunctival pallor (anaemia), xanthelasma, corneal arcus (significant under 40), hypertelorism, blue sclerae (osteogenesis imperfecta with aortic root disease), and — from the history — ectopia lentis (Marfan syndrome). [1]

Step 5, neck: I assess the JVP for height (the vertical distance from the sternal angle, normal less than 3 cm) and waveform (cannon a waves in complete heart block, prominent v waves in tricuspid regurgitation, absent a waves in atrial fibrillation), and the carotid pulse for character and volume. [1]

Step 6, praecordium: I inspect for scars and visible impulses, I palpate the apex beat for position (normal is the fifth intercostal space in the midclavicular line; displacement indicates dilatation) and character (thrusting in pressure overload, tapping in mitral stenosis, diffuse and hyperdynamic in left ventricular failure), and I palpate for thrills and a right ventricular heave. [1]

Step 7, auscultation: I listen with the diaphragm and the bell at the four valve areas — the apex (mitral), the lower left sternal edge (tricuspid), the left upper sternal edge (pulmonary) and the right upper sternal edge (aortic) — identifying the first and second heart sounds, their splitting, any added sounds, and any murmurs. [1]

Step 8, dynamic manoeuvres: I use respiration, Valsalva, squat-to-stand and hand grip when I have identified a murmur, to distinguish the causes. [1]

Steps 9 to 11, back, abdomen, legs: I listen for basal crackles and pleural effusion, I palpate for hepatomegaly and a pulsatile liver (tricuspid regurgitation) and splenomegaly (endocarditis), and I check for peripheral oedema, the peripheral pulses and the deep vein thrombosis signs. I complete by stating that I would measure the blood pressure in both arms, the temperature and the oxygen saturation, perform fundoscopy and urinalysis, and request the ECG, the chest X-ray and the echocardiogram. [1]

(b) The timing-based murmur framework (4 marks): [1]

I classify every murmur by timing first, then site, then character [5]. Timing is the single most reliable bedside discriminator. I time the murmur against the carotid pulse — a murmur that coincides with the upstroke is systolic; one that follows it is diastolic.

The ejection systolic murmur at the upper right sternal edge radiating to the carotids is the murmur of aortic stenosis. I confirm the character — crescendo-decrescendo — and grade it on the Levine scale (1 is very faint, 4 is loud with a thrill, 6 is heard with the stethoscope off the chest). I then look for the associated signs: the slow-rising pulse (pulsus parvus et tardus), the thrusting non-displaced apex (concentric left ventricular hypertrophy from the pressure overload), the soft or absent aortic component of the second heart sound (the calcified, immobile valve), and the ejection click (present only if the valve is still mobile, typically in a bicuspid valve). I distinguish it from the other ejection systolic murmurs: pulmonary stenosis is at the upper left sternal edge with radiation to the left lung field; hypertrophic cardiomyopathy is at the lower left sternal edge and responds characteristically to the dynamic manoeuvres [3].

(c) The dynamic manoeuvres (4 marks): [1]

The dynamic manoeuvres change the preload, the afterload or the heart rate and shift the murmur in a diagnosis-specific way. For the aortic stenosis murmur I perform: [1]

• Squatting and passive leg raise (increased preload and afterload) — the aortic stenosis murmur gets louder (increased flow across the stenotic valve).
• Valsalva strain phase (reduced preload) — the aortic stenosis murmur gets softer.
• Hand grip (increased afterload) — the aortic stenosis murmur gets softer. [1]

The critical distinction is from hypertrophic cardiomyopathy, which behaves oppositely: it gets louder on Valsalva and on standing (reduced ventricular filling brings the septum and the mitral leaflet closer, increasing the dynamic outflow tract obstruction) and softer on squatting and hand grip. The aortic stenosis murmur that gets louder on Valsalva does not exist — if a left-sided systolic murmur gets louder on Valsalva, it is hypertrophic cardiomyopathy or mitral valve prolapse, not aortic stenosis [5]. The mitral regurgitation and VSD murmurs get louder on hand grip (increased afterload increases the regurgitation), which also distinguishes them from aortic stenosis.

(d) The findings that predict severe rather than moderate disease (4 marks): [1]

The bedside markers of severe aortic stenosis are [3][4]:

1. The slow-rising pulse (pulsus parvus et tardus) — the delayed and reduced systolic upstroke.
2. The soft or absent second heart sound (the calcified, immobile valve produces no audible A2).
3. The late-peaking murmur — as the stenosis worsens, the murmur peaks progressively later in systole, closer to S2. This is a high-yield bedside sign of severity.
4. The thrill (grade 4 or above) and the sustained, thrusting, non-displaced apex (concentric hypertrophy rather than dilatation).
5. Paradoxical splitting of S2 in very severe disease. [1]

The severity is confirmed by the echocardiogram — the peak jet velocity (severe at or above 4.0 m/s), the mean gradient (severe at or above 40 mmHg) and the aortic valve area (severe at or below 1.0 cm squared) — but the bedside signs predict the severity before the scan. The teaching point is that the candidate who presents the slow-rising pulse, the soft S2 and the late-peaking murmur is presenting severe aortic stenosis, not just aortic stenosis. [1]

(e) The structured spoken presentation (3 marks): [1]

I present in the structured template. "I have examined this patient's cardiovascular system. At the end of the bed the patient is comfortable at rest. The hands show no clubbing and no stigmata of endocarditis; the pulse is regular at 72, of slow-rising character, with no radiofemoral delay. The face and eyes show arcus senilis. The JVP is not elevated. The carotid pulse is slow-rising and low-volume. The apex beat is in the fifth intercostal space in the midclavicular line and is thrusting in character; there is a systolic thrill at the upper right sternal edge. On auscultation the first heart sound is normal and the second heart sound is soft; there is an ejection systolic murmur, grade 4 of 6, at the upper right sternal edge radiating to the carotids. The lung bases are clear; there is no hepatomegaly and no peripheral oedema. In summary, this patient has the slow-rising pulse, the thrusting non-displaced apex, the systolic thrill and the ejection systolic murmur radiating to the carotids with a soft second heart sound — these findings are consistent with severe aortic stenosis. I would confirm this with an echocardiogram, assess for symptoms (angina, syncope, exertional dyspnoea) with a careful history and an exercise test if asymptomatic, and refer to the heart team for the timing of intervention." [1]

The synthesis is what earns the pass — a dominant finding (the ejection systolic murmur radiating to the carotids), a diagnosis (severe aortic stenosis), and a confirmatory investigation (the echocardiogram). A list of unconnected observations fails the case; a synthesis passes it. [1]

SAQ 2 — The Dynamic Manoeuvres and the Manoeuvre-Dependent Murmur (10 marks)

Prompt: A junior colleague asks you to explain: (a) the physiological basis of each dynamic manoeuvre used in cardiac auscultation; (b) how each manoeuvre shifts the common murmurs and the single manoeuvre-dependent murmur that it is critical not to miss; and (c) how you would use the manoeuvres at the bedside to distinguish aortic stenosis from hypertrophic cardiomyopathy in a young patient with a systolic murmur. [1]

Model Answer

(a) The physiological basis of each manoeuvre (4 marks): [1]

Each dynamic manoeuvre changes the preload (venous return), the afterload (systemic vascular resistance), or the heart rate, and the murmur shifts in a predictable way [5]:

• Inspiration increases the venous return to the right heart (the negative intrathoracic pressure), making right-sided murmurs (tricuspid and pulmonary) louder.
• Expiration increases the venous return to the left heart, making left-sided murmurs (mitral and aortic) louder.
• Valsalva strain phase (forced expiration against a closed glottis) raises the intrathoracic pressure, reducing the venous return (preload) and the afterload; murmurs dependent on preload and flow (aortic stenosis, mitral regurgitation) get softer.
• Standing up from squatting reduces the preload and the afterload.
• Squatting down from standing increases the preload (venous return from the legs) and the afterload (compression of the leg vessels).
• Isometric hand grip increases the afterload (systemic vascular resistance) without changing the preload.
• Passive leg raise increases the preload (venous return from the legs) and is the manoeuvre of choice in the patient who cannot squat. [1]

(b) How each manoeuvre shifts the common murmurs (4 marks): [1]

The critical manoeuvre-dependent murmur is hypertrophic cardiomyopathy — it is the only left-sided systolic murmur that gets louder on Valsalva and on standing (reduced ventricular filling brings the hypertrophied basal septum and the anterior mitral leaflet closer, increasing the dynamic outflow tract obstruction) and softer on squatting and hand grip (increased filling and afterload reduce the obstruction). Every other left-sided systolic murmur gets softer on Valsalva and on standing. [1]

Mitral valve prolapse is the classic that moves: the click and the late systolic murmur move earlier and longer on standing (less preload brings the prolapse earlier in systole) and later and shorter on squatting. [1]

Aortic stenosis gets louder on squatting and passive leg raise (increased preload increases flow across the stenotic valve) and softer on Valsalva. [1]

Mitral regurgitation, aortic regurgitation and VSD get louder on hand grip (increased afterload increases the regurgitant volume) and softer on amyl nitrate (reduced afterload). [1]

Right-sided murmurs (tricuspid and pulmonary regurgitation or stenosis) get louder on inspiration (Carvallo sign). [1]

(c) Distinguishing aortic stenosis from hypertrophic cardiomyopathy (2 marks): [1]

At the bedside, I first assess the pulse and the apex: aortic stenosis gives a slow-rising pulse and a thrusting non-displaced apex; hypertrophic cardiomyopathy may give a jerky or bisferiens pulse and a double or triple apex impulse. I then perform the dynamic manoeuvres. I ask the patient to strain (Valsalva) and to stand from squatting: if the murmur gets louder, it is hypertrophic cardiomyopathy; if it gets softer, it is aortic stenosis. I then ask the patient to squat and to perform hand grip: if the murmur gets softer, it is hypertrophic cardiomyopathy; if it gets louder, it is aortic stenosis. The disciplined use of the four manoeuvres — Valsalva, squat, stand, hand grip — distinguishes the two at the bedside, and I confirm with the echocardiogram. The teaching point is the single sentence: the murmur that gets louder on Valsalva and on standing, when every other left-sided murmur gets softer, is hypertrophic cardiomyopathy. [1]