Cardiovascular Examination — Viva

Short Case Viva Defence

Candidate's opening statement (model answer)

"The cardiovascular system examination is the classic short case. My routine is a head-to-toe sequence that I perform in the same order every time: end of bed, hands, face, eyes, neck and JVP, praecordium (inspection, apex beat, thrills), the four-area auscultation, the dynamic manoeuvres, back, abdomen, and legs. I finish by stating the completion — blood pressure in both arms, temperature, oxygen saturation, fundoscopy, urinalysis, and the ECG, chest X-ray and echocardiogram. I then present a structured synthesis — a dominant finding, a diagnosis, and a confirmatory investigation. [1]

The three principles are: sequence before sophistication, characterise the murmur by timing first, and present with a hypothesis. The examiner forms a judgement before I pick up the stethoscope, so the hands, the face and the neck come first." [1]

Examiner probing questions and model answers

Q1: "Why do you start at the hands rather than the chest?" [1]

"Because the hands carry more cardiovascular information per square centimetre than any other region, and because the examination is head-to-toe — the stethoscope comes in the middle, not at the start. At the hands I assess clubbing and its cardiac causes (cyanotic congenital heart disease and infective endocarditis), the peripheral stigmata of endocarditis (splinter haemorrhages, Osler nodes, Janeway lesions), peripheral cyanosis, tendon xanthomata, and the radial pulse — rate, rhythm and character. The pulse character is the high-yield component: the bounding pulse of aortic regurgitation, the slow-rising pulse of aortic stenosis, the alternans of severe left ventricular failure, and the radiofemoral delay of coarctation. If I walk to the chest first I have missed all of these, and the examiner knows it." [1]

Q2: "How do you assess the JVP, and what does the waveform tell you?" [1]

"I position the patient at 45 degrees with the head turned slightly away and the neck muscles relaxed, and I use the right internal jugular vein as the reference — it is deep, medial to the sternocleidomastoid, and reliable. I measure the height as the vertical distance from the sternal angle to the top of the pulsation, in centimetres — the normal is less than 3, and a value above 4 is elevated. I then read the waveform: the a wave is atrial contraction, the v wave is venous filling against a closed tricuspid valve, the x descent is atrial relaxation, and the y descent is early ventricular filling. Cannon a waves — regular, large, intermittent waves — indicate complete heart block or atrioventricular dissociation (the atrium contracting against a closed tricuspid valve). Absent a waves occur in atrial fibrillation. A prominent systolic v wave indicates tricuspid regurgitation — the regurgitant jet fills the venous system in systole. I distinguish the JVP from the carotid pulse by four features: the JVP is non-palpable, varies with position, rises with abdominal pressure, and has a biphasic waveform; the carotid is palpable, fixed, and monophasic." [1]

Q3: "What does the apex beat character tell you?" [1]

"The apex beat is the bridge between the periphery and the auscultation. I localise the most lateral point of maximal cardiac impulse with the flat of the hand, and I assess two features: the position and the character. The normal position is the fifth intercostal space in the midclavicular line. Displacement laterally indicates ventricular dilatation — dilated cardiomyopathy, volume overload, severe mitral or aortic regurgitation, heart failure. The character has four patterns: a thrusting (heaving) apex indicates pressure overload — aortic stenosis, hypertension, hypertrophic cardiomyopathy; a tapping apex indicates mitral stenosis — the palpable loud first heart sound; a diffuse and hyperdynamic apex indicates left ventricular failure or a high-output state. The candidate who does not palpate the apex character has lost a pivotal discriminator — the thrusting non-displaced apex with a slow-rising pulse points to aortic stenosis; the tapping apex with a loud S1 points to mitral stenosis." [1]

Q4: "You hear a systolic murmur. How do you characterise it?" [1]

"I characterise it by timing first, then site, then radiation, then character, then grade, then the effect of the dynamic manoeuvres [5]. Timing is the single most reliable discriminator — I time the murmur against the carotid pulse. A systolic murmur at the upper right sternal edge radiating to the carotids, with a crescendo-decrescendo character, is aortic stenosis. A pansystolic murmur at the apex radiating to the axilla is mitral regurgitation. A pansystolic murmur at the lower left sternal edge, louder on inspiration, is tricuspid regurgitation. An ejection systolic murmur at the lower left sternal edge that gets louder on Valsalva is hypertrophic cardiomyopathy. I grade on the Levine scale — 1 is very faint, 4 is loud with a thrill, 6 is heard off the chest. A thrill always means grade 4 or above."

Q5: "What are the dynamic manoeuvres, and which murmur is the manoeuvre-dependent one?" [1]

"The dynamic manoeuvres change the preload, the afterload or the heart rate, and the murmur shifts in a diagnosis-specific way. Inspiration increases right-sided venous return — right-sided murmurs get louder. Expiration increases left-sided return — left-sided murmurs get louder. Valsalva strain reduces preload and afterload. Squatting increases preload and afterload. Standing reduces preload and afterload. Hand grip increases afterload. Passive leg raise increases preload. The critical manoeuvre-dependent murmur is hypertrophic cardiomyopathy — it is the only left-sided systolic murmur that gets louder on Valsalva and on standing, when every other left-sided murmur gets softer. The physiology is that reduced ventricular filling brings the hypertrophied basal septum and the anterior mitral leaflet closer, increasing the dynamic outflow tract obstruction. Squatting and hand grip make it softer. The single sentence: the murmur that gets louder on Valsalva and on standing is hypertrophic cardiomyopathy." [1]

Q6: "What is the Austin Flint murmur, and how do you distinguish it from mitral stenosis?" [1]

"The Austin Flint murmur is a low-pitched mid-diastolic rumble at the apex that occurs in severe aortic regurgitation when the regurgitant jet impinges on the anterior mitral leaflet, vibrating it and partially obstructing the mitral inflow. It mimics mitral stenosis, but I distinguish it by three features: there is no opening snap, the first heart sound is soft rather than loud (in mitral stenosis the taut stenotic valve snaps shut, producing a loud S1), and the obvious early diastolic murmur and the wide pulse pressure of aortic regurgitation are present. The candidate who hears a mid-diastolic rumble in a patient with a collapsing pulse and an early diastolic murmur should recognise the Austin Flint mechanism, not call it mitral stenosis." [1]

Q7: "What are the common examination traps?" [1]

"There are several. First, walking to the chest and listening before examining the hands, face and neck — the examination is head-to-toe and the stethoscope comes in the middle. Second, not timing the murmur — a murmur described without saying systolic or diastolic gives no useful information. Third, not using the dynamic manoeuvres — the candidate who hears a systolic murmur and does not perform Valsalva or squat-to-stand cannot distinguish aortic stenosis from hypertrophic cardiomyopathy. Fourth, calling an innocent flow murmur pathological — a soft, short, vibratory murmur at the left sternal edge in a young well patient with no radiation and no thrill is innocent. Fifth, not palpating the apex character — the apex is the bridge between the periphery and the auscultation. Sixth, presenting findings without a synthesis — a list of observations fails; a synthesis with a dominant finding, a diagnosis and a confirmatory investigation passes. Seventh, stopping at the chest and not completing the examination. Eighth, forgetting the body habitus — the tall thin patient with a high arched palate and an aortic regurgitation murmur has Marfan syndrome, and the diagnosis changes the management [6]."

Q8: "How do you present the findings?" [1]

"I present in the structured template — opening sentence, end of bed, hands and pulse, face and eyes, neck and JVP, praecordium and apex, auscultation summary, the rest of the examination, and the synthesis. The synthesis names the dominant finding, offers the diagnosis, and states the confirmatory investigation. The candidate who lists findings without synthesising them has performed the examination but not passed the case." [1]

Short Case Discussion — The Marfan Syndrome Patient

Examiner instruction: "This 24-year-old tall man has been referred with a murmur. Examine his cardiovascular system." [1]

Candidate's model answer: [1]

"At the end of the bed this patient is tall and thin, with an arm span that appears to exceed his height and long, slender fingers — a Marfanoid habitus. There is no median sternotomy scar. The hands show no clubbing and no stigmata of endocarditis; the pulse is regular, of large volume and collapsing in character — consistent with aortic regurgitation. The face shows a high arched palate. The eyes show no xanthelasma. The JVP is not elevated. The carotid pulse is bounding. The apex beat is thrusting and displaced to the sixth intercostal space in the anterior axillary line. On auscultation there is a high-pitched early diastolic murmur at the left sternal edge, best heard with the patient sitting forward, breath held in expiration. There is also an ejection systolic flow murmur. The lung bases are clear. There is no hepatomegaly and no peripheral oedema. In summary, this tall, thin man with the Marfanoid habitus has a collapsing pulse, a thrusting displaced apex and an early diastolic murmur at the left sternal edge — consistent with aortic regurgitation from aortic root dilatation in Marfan syndrome. I would confirm the diagnosis with an echocardiogram to assess the aortic root and the valve, and I would arrange genetic testing for the FBN1 mutation and family screening [6]."

Examiner: "What else would you look for?" [1]

"I would assess for the other features of Marfan syndrome — the skeletal features (pectus excavatum or carinatum, scoliosis, the wrist and thumb sign), the ocular features (ectopia lentis — upward lens dislocation, on fundoscopy or slit-lamp), and the cardiovascular features (aortic root aneurysm, mitral valve prolapse). I would measure the aortic root diameter on the echocardiogram and arrange serial imaging — the threshold for prophylactic aortic root repair in Marfan syndrome is 5.0 cm, lower than in the non-syndromic patient, because of the intrinsic wall weakness. I would screen the first-degree relatives with echocardiography. The teaching point is that the cardiovascular examination is never just about the heart — the body habitus changes the diagnosis and the management." [1]