Hypertension Viva

Long Case Viva Defence

Candidate's opening statement (model answer)

"Mrs Chen is a 56-year-old office manager referred for uncontrolled hypertension. She was diagnosed at age 44 and despite treatment with four agents — perindopril 10 mg, amlodipine 10 mg, indapamide 1.5 mg, and bisoprolol 5 mg — her blood pressure today is 164/96. She is adherent (confirmed by pharmacy data). [1]

Her past history includes type 2 diabetes and stage 3a CKD (eGFR 55). She is a non-smoker with a BMI of 30. [1]

Her main problems are:

1. Resistant hypertension — BP above target despite four agents including a diuretic
2. Possible secondary cause — early age of onset (44), resistance, and a potassium of 3.3 on a thiazide raise suspicion for primary aldosteronism
3. Type 2 diabetes and CKD — target BP should be under 130/80
4. Likely target organ damage — I need to assess for left ventricular hypertrophy and retinopathy
5. Obesity contributing to resistance" [1]

Examiner probing questions and model answers

Q1: "What is your first priority?" [1]

"To confirm this is true resistant hypertension and not pseudo-resistance. I would arrange 24-hour ambulatory BP monitoring to exclude white-coat effect, which is the single commonest cause of apparent resistance. I would confirm adherence with a non-judgemental discussion and consider urine drug screening. I would also review for contributing factors — high dietary salt, NSAIDs, herbal supplements such as liquorice, and untreated OSA." [1]

Q2: "How would you screen for primary aldosteronism?" [1]

"Given the early age of onset, resistance, and hypokalaemia, primary aldosteronism is a real possibility — it is the commonest surgically curable cause of hypertension and is underdiagnosed. I would measure an aldosterone-to-renin ratio (ARR). I would correct the hypokalaemia first, as potassium deficiency suppresses aldosterone and can give a falsely low ratio. The ACE inhibitor she is taking can suppress aldosterone, so I would interpret the result in context — a clearly elevated ARR despite ACE inhibitor is highly suggestive, while a borderline result may require withdrawal of the ACE inhibitor and retesting. If the ARR is elevated, I would proceed to a confirmatory suppression test — oral sodium loading or saline infusion — per the Endocrine Society guideline. If confirmed, I would localise with adrenal CT, then adrenal venous sampling to distinguish unilateral adenoma from bilateral hyperplasia before considering adrenalectomy." [1]

Q3: "Her potassium is 3.3. What else could cause hypokalaemia in a hypertensive patient?" [1]

"The differential of hypokalaemia with hypertension includes: the thiazide diuretic she is taking (most common); primary aldosteronism (Conn syndrome — the key secondary cause to exclude); Cushing syndrome; renovascular hypertension with secondary hyperaldosteronism; and exogenous causes such as liquorice (inhibits 11-beta-hydroxysteroid dehydrogenase, causing apparent mineralocorticoid excess). I would distinguish these by the renin and aldosterone levels — primary aldosteronism shows low renin and high aldosterone; renovascular disease shows high renin and high aldosterone." [1]

Q4: "What is the evidence for adding spironolactone?" [1]

"The PATHWAY-2 trial, published in The Lancet in 2015, was a double-blind, placebo-controlled, crossover trial of 314 patients with resistant hypertension on three agents. It showed spironolactone was the most effective fourth-line agent — superior to placebo, bisoprolol, and doxazosin. The mechanism reflects the underlying pathophysiology: resistant hypertension is frequently driven by aldosterone-mediated sodium retention. I would start spironolactone 25 mg daily, titrating to 50 mg, and monitor potassium and renal function at one week, then monthly, because she is already on an ACE inhibitor and the combination raises hyperkalaemia risk." [1]

Q5: "What is her BP target and what evidence supports it?" [1]

"Given her diabetes and CKD, her target is under 130/80 mmHg. The SPRINT trial demonstrated that intensive BP control to a systolic under 120 mmHg, compared to under 140, reduced the composite of myocardial infarction, stroke, heart failure, and cardiovascular death by 25% and all-cause mortality by 27% in high-risk, non-diabetic patients. However, SPRINT excluded diabetics, and the ACCORD BP trial in diabetics did not show the same mortality benefit — so the target for diabetics is under 130/80 rather than under 120. I would titrate carefully, checking standing BP, because she is at risk of orthostatic hypotension on five agents." [1]

Q6: "How would you assess her target organ damage?" [1]

"I would perform a focused cardiovascular and systemic examination: fundoscopy for hypertensive retinopathy; cardiac auscultation for a fourth heart sound (indicating a stiff, non-compliant ventricle from diastolic dysfunction); assess for left ventricular heave (suggesting LVH); listen for renal and femoral bruits; check peripheral pulses including radio-femoral delay. I would order an ECG for voltage criteria of LVH (Sokolow-Lyon or Cornell), an echocardiogram to quantify left ventricular mass and diastolic function, urine albumin-to-creatinine ratio, and review her renal function. The presence and severity of target organ damage influences both her risk and the urgency of control." [1]

Short Case Discussion

Scenario: "Examine this patient's cardiovascular system"

Candidate presentation (model): [1]

"I examined Mr Thompson's cardiovascular system. He is comfortable at rest. There is no clubbing, pallor, or cyanosis. The radial pulse is regular at 76 beats per minute, normal volume and character. Blood pressure is 168/96 mmHg in the right arm, seated. The blood pressure in the left arm is 165/94 — no significant inter-arm difference. There is no radio-femoral delay. [1]

The JVP is not elevated. The apex beat is undisplaced in the 5th intercostal space, mid-clavicular line, and is thrusting in character, suggestive of left ventricular hypertrophy from pressure overload. There is no parasternal heave. On auscultation, the heart sounds are normal with a prominent fourth heart sound at the apex. There are no murmurs. The chest is clear. [1]

Examination of the abdomen reveals no renal or aortic bruits. Femoral and pedal pulses are present and symmetrical. Fundoscopy shows arteriolar narrowing and arteriovenous nipping, consistent with hypertensive retinopathy grade 2. [1]

In summary, these findings are consistent with long-standing hypertension with evidence of target organ damage — left ventricular hypertrophy indicated by the thrusting apex and fourth heart sound, and hypertensive retinopathy." [1]

Examiner: "What is the significance of the fourth heart sound?" [1]

"The S4 is a low-frequency sound produced in late diastole by atrial contraction ejecting blood into a stiff, non-compliant left ventricle. It indicates reduced ventricular compliance — in hypertension, this results from left ventricular hypertrophy and diastolic dysfunction. An S4 in a hypertensive patient is a marker of target organ damage and correlates with left ventricular hypertrophy on echocardiography." [1]

Examiner: "How do you measure blood pressure correctly?" [1]

"I use a validated, appropriately calibrated upper-arm cuff of the correct size — a cuff too small overestimates BP. The patient should be seated, relaxed, with the arm supported at heart level, feet flat on the floor, for at least five minutes before measurement. I avoid caffeine, exercise, and smoking for 30 minutes beforehand. I take at least two readings one to two minutes apart and record the average. I also check a standing BP after one to three minutes to detect orthostatic hypotension, especially in older or treated patients. To confirm a diagnosis, I arrange ambulatory or home BP monitoring, as single clinic readings are subject to white-coat effect." [1]

Examiner: "What is the grading of hypertensive retinopathy?" [1]

"The Keith-Wagener-Barker classification grades retinopathy into four levels. Grade 1: arteriolar narrowing. Grade 2: arteriovenous nipping (focal arteriolar constriction with vein compression at crossing points). Grade 3: flame-shaped haemorrhages, cotton-wool spots, and hard exudates. Grade 4: grade 3 changes plus papilloedema. Grades 1 and 2 are common in chronic hypertension; grades 3 and 4 indicate severe or malignant hypertension and are a hypertensive emergency." [1]