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 accounts for a substantial proportion of apparent resistance — alongside non-adherence, the single commonest cause overall. 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 335 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]