Cardiovascular Examination — Clinical Case

DCE Short Case

Patient brief (provided to trainee)

Instruction: "Please examine this patient's cardiovascular system. Present your findings and offer a differential diagnosis." [1]

Patient: Mr James Whitfield, 72 years old, retired teacher, referred by his general practitioner for a murmur noted at a routine check and for exertional breathlessness over six months. [1]

Examination findings (trainee elicits):

• End of bed: comfortable at rest, no breathlessness, no cyanosis. Tall but not Marfanoid. No scars.
• Hands: no clubbing, no stigmata of endocarditis, no tendon xanthomata. Pulse 74, regular, slow-rising character. No radiofemoral delay.
• Face: arcus senilis. No malar flush. High normal dentition.
• Eyes: conjunctivae normal. Arcus senilis. No xanthelasma.
• Neck: JVP not elevated. Carotid pulse slow-rising and low-volume.
• Praecordium: apex beat in the fifth intercostal space at the midclavicular line, thrusting in character, not displaced. Systolic thrill at the upper right sternal edge.
• Auscultation: first heart sound normal. Second heart sound soft (A2 diminished). Ejection systolic murmur, grade 4 of 6, at the upper right sternal edge radiating to the carotids, crescendo-decrescendo, late-peaking. No diastolic murmur.
• Dynamic manoeuvres: murmur louder on squatting and passive leg raise; softer on Valsalva and hand grip.
• Back: lung bases clear. No sacral oedema.
• Abdomen: no hepatomegaly. No pulsatile liver.
• Legs: no peripheral oedema. All peripheral pulses present and symmetrical.
• Blood pressure 130/80 (narrow pulse pressure). [1]

Candidate's structured presentation (model)

Opening statement: [1]

"I have examined this patient's cardiovascular system. At the end of the bed he is comfortable at rest, with no breathlessness, no cyanosis and no distress. [1]

The hands show no clubbing and no stigmata of infective endocarditis. The pulse is regular at 74, of slow-rising character, with no radiofemoral delay. The face shows arcus senilis. The eyes show no xanthelasma. The JVP is not elevated. The carotid pulse is slow-rising and low-volume. [1]

The apex beat is in the fifth intercostal space at the midclavicular line and is thrusting in character, not displaced. 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, crescendo-decrescendo in character and late-peaking. There is no diastolic murmur. The murmur gets louder on squatting and passive leg raise, and softer on Valsalva and hand grip. [1]

The lung bases are clear. There is no hepatomegaly and no peripheral oedema. The peripheral pulses are all present and symmetrical. [1]

In summary, this 72-year-old man has a slow-rising pulse, a narrow pulse pressure, a thrusting non-displaced apex, a systolic thrill, and an ejection systolic murmur radiating to the carotids with a soft second heart sound and a late-peaking character. These findings are consistent with severe aortic stenosis. I would confirm this with an echocardiogram, and given the exertional breathlessness I would refer urgently to the heart team for the timing of aortic valve intervention." [1]

Completion: I would complete the examination by measuring the blood pressure in both arms, checking the temperature and oxygen saturation, performing fundoscopy and urinalysis, and requesting the 12-lead ECG (which may show left ventricular hypertrophy with strain), the chest X-ray (which may show aortic valve calcification), and the transthoracic echocardiogram (the definitive investigation). [1]

Examiner discussion questions

Q1: "What bedside features tell you the stenosis is severe?" [1]

"Five bedside features predict severe rather than moderate aortic stenosis. First, the slow-rising pulse (pulsus parvus et tardus) — the delayed and reduced systolic upstroke. Second, the soft or absent second heart sound — the calcified, immobile valve produces no audible A2. Third, the late-peaking murmur — as the stenosis worsens the murmur peaks progressively later in systole, closer to S2. Fourth, the thrill — grade 4 or above always has a thrill, and it indicates a significant gradient. Fifth, the narrow pulse pressure and the thrusting non-displaced apex (concentric hypertrophy rather than dilatation). I confirm the severity with the echocardiogram — the peak jet velocity at or above 4.0 metres per second, the mean gradient at or above 40 mmHg, and the aortic valve area at or below 1.0 cm squared — but the bedside signs predict it before the scan [3][4]."

Q2: "How did the dynamic manoeuvres help you?" [1]

"They confirmed that the murmur is aortic stenosis and not hypertrophic cardiomyopathy. The aortic stenosis murmur gets louder on squatting and passive leg raise (increased preload increases flow across the stenotic valve) and softer on Valsalva (reduced preload). Hypertrophic cardiomyopathy behaves oppositely — it gets louder on Valsalva and on standing, and softer on squatting and hand grip. Because this murmur got louder on squatting and softer on Valsalva, it is aortic stenosis. The manoeuvres are what distinguish the prepared candidate — the candidate who does not use them cannot make this distinction at the bedside [5]."

Q3: "He has exertional breathlessness. What is the significance?" [1]

"The symptom triad of severe aortic stenosis is angina, syncope and exertional breathlessness (heart failure). Once symptoms develop, the natural history turns a corner — the mortality climbs steeply, and intervention is indicated. The exertional breathlessness means he is a symptomatic patient with severe aortic stenosis — Stage D in the ACC/AHA classification — which is a class I indication for aortic valve replacement. I would not delay for medical optimisation, because no drug slows the progression of calcific aortic stenosis [3]."

Q4: "What is your management plan?" [1]

"First, the transthoracic echocardiogram to confirm the severity, the valve morphology (tricuspid calcific versus bicuspid), the left ventricular function, and the pulmonary artery pressure. Second, given the symptomatic severe aortic stenosis, urgent referral to the multidisciplinary heart team for the decision between surgical aortic valve replacement (SAVR) and transcatheter aortic valve implantation (TAVI), integrating the surgical risk, the age, the life expectancy, the anatomical suitability and the comorbidities. Third, I would assess the coronary arteries (a CT coronary angiogram or an invasive angiogram if intervention is planned). Fourth, I would optimise the medical therapy — statin for the concomitant coronary disease risk, blood pressure control, and avoidance of vasodilators that may precipitate collapse in the fixed-output state. The teaching point is that the symptomatic patient with severe aortic stenosis needs valve intervention, not medical therapy." [1]

Q5: "How do you distinguish aortic stenosis from an innocent flow murmur?" [1]

"The innocent flow murmur is soft (grade 1 or 2), short, vibratory, at the left sternal edge (not the upper right), with no radiation, no thrill, normal heart sounds (a normal A2), no pulse-character abnormality (a normal-volume, normal-rising pulse), and it occurs in a young, well patient with no symptoms. This patient has the opposite — a loud (grade 4), long, late-peaking murmur at the upper right sternal edge radiating to the carotids, with a thrill, a soft A2, and a slow-rising pulse. The candidate who calls the innocent murmur pathological, or the pathological murmur innocent, has made a serious error." [1]

Q6: "What is the single most important lesson from this case?" [1]

"The single most important lesson is that the bedside examination predicts the severity before the echocardiogram. The slow-rising pulse, the soft second heart sound, the late-peaking murmur and the thrill are the markers of severe aortic stenosis, and the candidate who presents them — and synthesises them into a diagnosis of severe aortic stenosis confirmed by echocardiogram — has demonstrated the integrated clinical reasoning that the examination is testing. The corollary is the dynamic manoeuvres: the candidate who uses them fluently distinguishes aortic stenosis from hypertrophic cardiomyopathy at the bedside, and that is what the examiner is looking for." [1]

DCE Short Case 2 — The Mitral Stenosis Patient

Instruction

"Please examine this 40-year-old woman's cardiovascular system. She has migrated from South Asia and presents with progressive exertional breathlessness." [1]

Examination findings: Malar flush. No clubbing. Pulse irregularly irregular (atrial fibrillation at 90). JVP not elevated. Apex beat tapping, non-displaced. Loud first heart sound. Opening snap. Low-pitched mid-diastolic rumble at the apex, best heard with the bell in the left lateral position. No thrill. Lung bases clear. [1]

Presentation template

"I have examined this woman's cardiovascular system. At the end of the bed she has a malar flush and is comfortable at rest. The hands show no clubbing. The pulse is irregularly irregular at 90 — atrial fibrillation. The face shows a malar flush. The JVP is not elevated. The apex beat is tapping and non-displaced. On auscultation the first heart sound is loud, there is an opening snap, and there is a low-pitched mid-diastolic rumble at the apex, best heard with the bell in the left lateral position. The lung bases are clear. In summary, this woman with the malar flush, the atrial fibrillation, the tapping apex, the loud first heart sound, the opening snap and the mid-diastolic rumble has mitral stenosis — almost certainly rheumatic in origin given her South Asian background. I would confirm this with an echocardiogram to assess the valve area and the mean gradient, and I would assess for pulmonary hypertension." [1]

Discussion

Examiner: "What is the cause of her mitral stenosis?" [1]

"Mitral stenosis is almost always rheumatic. The rheumatic mitral valve has the characteristic echo appearance — the hockey-stick deformity of the anterior leaflet, the commissural fusion, and the fish-mouth orifice. The atrial fibrillation is a common complication — the dilated, stressed left atrium is arrhythmogenic, and the new atrial fibrillation with rapid ventricular response can precipitate acute pulmonary oedema by shortening the diastole (mitral stenosis is a diastolic disease, and less filling time means a higher left atrial pressure). I would confirm the diagnosis and the severity with the echocardiogram and arrange the anticoagulation given the high embolic risk [4]."