Hypertension — Written Clinical Reasoning

SAQ 1 — Resistant Hypertension Workup and Management (20 marks, 30 minutes)

Prompt: Outline your assessment and integrated management plan for this patient, including how you would confirm the diagnosis, evaluate for secondary causes, and modify her pharmacotherapy. Justify each decision with reference to evidence. [1]

Model Answer

Problem list (4 marks):

1. Resistant hypertension — BP above target despite four agents (RAAS blocker + CCB + diuretic + beta-blocker) with confirmed adherence
2. Probable left ventricular hypertrophy (target organ damage on ECG) — indicates long-standing, inadequately controlled hypertension
3. Hypokalaemia (3.4 mmol/L) — on a thiazide, but also raises suspicion for primary aldosteronism
4. Obesity (BMI 31) — contributes to resistance
5. Stage 2 CKD (eGFR 62) with microalbuminuria — target organ damage [1]

Step 1 — Confirm true resistance and exclude pseudo-resistance (4 marks): [1]

• Confirm the BP reading is accurate. Arrange 24-hour ambulatory BP monitoring (ABPM) to exclude white-coat effect, which accounts for a substantial proportion of apparent resistance. Assess for a non-dipping pattern (which would suggest OSA).
• Confirm adherence. Although pharmacy refill data support adherence, I would have a non-judgemental conversation and consider urine antihypertensive drug screening if available — non-adherence is the single commonest cause of apparent resistance.
• Review lifestyle. Counsel on salt restriction (target under 5 g/day), weight loss (aim BMI under 25), and regular exercise. High salt intake alone can cause apparent resistance.
• Exclude drug and substance causes. Take a careful history for NSAIDs, sympathomimetics, decongestants, herbal supplements (especially liquorice), oral contraceptives, and recreational drugs. [1]

Step 2 — Evaluate for secondary causes (6 marks): [1]

Given the resistant hypertension, early age of onset (42), and hypokalaemia, secondary causes must be actively sought: [1]

• Primary aldosteronism is the priority. The hypokalaemia, although on a thiazide, combined with resistant hypertension, raises significant suspicion. I would measure an aldosterone-to-renin ratio (ARR). Importantly, the thiazide must be considered — it can cause hypokalaemia (falsely lowering the ratio) and the ACE inhibitor can suppress aldosterone. Correct hypokalaemia first. If the ARR is elevated, proceed to a confirmatory suppression test (oral sodium loading or saline infusion) per the Endocrine Society guideline (PMID 26934393). If confirmed, localise with adrenal CT and adrenal venous sampling before considering adrenalectomy.
• Obstructive sleep apnoea (OSA) is the commonest secondary cause in resistant hypertension. Although she reports no OSA symptoms, I would screen with the STOP-BANG questionnaire and consider a home sleep study given the resistant hypertension.
• Renal artery stenosis — less likely without abdominal bruit, abrupt creatinine rise, or flash pulmonary oedema, but I would consider renal artery Doppler if other workup is negative. Note the CORAL trial showed routine stenting does not benefit atherosclerotic stenosis.
• Phaeochromocytoma — unlikely without episodic symptoms (headache, sweating, palpitations), but plasma free metanephrines can be checked if there is any atypical feature. [1]

Step 3 — Pharmacological modification (6 marks): [1]

The immediate evidence-based change is to add spironolactone 25 mg daily: [1]

• The PATHWAY-2 trial (PMID 26414968) demonstrated that spironolactone is the most effective fourth-line agent in resistant hypertension, superior to placebo, bisoprolol, and doxazosin. She is already on four agents including bisoprolol, so adding spironolactone as a fifth agent is the evidence-based escalation.
• The hypokalaemia (3.4) further favours an MRA — it will correct the potassium and address the likely aldosterone excess.
• Monitor potassium and renal function at 1 week, 2 weeks, then monthly. The combination of ACE inhibitor + spironolactone raises hyperkalaemia risk; if K+ exceeds 5.5, reduce or hold.
• Titrate spironolactone to 50 mg if needed and tolerated. Watch for gynaecomastia (switch to eplerenone if symptomatic). [1]

I would also consider switching hydrochlorothiazide to chlorthalidone (a more potent, longer-acting thiazide-like diuretic) to improve volume control, and would reinforce dietary salt restriction. [1]

Her target BP should be under 130/80 mmHg given the target organ damage (LVH, CKD). The SPRINT trial (PMID 26551272) supports intensive control in high-risk patients, with attention to side effects. [1]

Communication and follow-up (no additional marks, but essential):

• Refer to a hypertension specialist / clinic for refractory management and to coordinate secondary workup.
• Reinforce adherence using a once-daily regimen where possible and a pill organiser.
• Arrange ABPM in 6–8 weeks to objectively assess response to spironolactone. [1]

SAQ 2 — Hypertensive Emergency (supplementary)

Prompt: A 64-year-old man known to have hypertension (non-adherent with medications) presents with BP 230/135 mmHg, confusion, papilloedema, and trace pulmonary oedema. Outline your immediate assessment and management. [1]

Model Answer

Diagnosis: Hypertensive emergency with encephalopathy and early pulmonary oedema — acute target organ damage. [1]

Immediate management:

1. Admit to HDU/ICU with continuous cardiac and BP monitoring, IV access, and hourly fluid balance.
2. Control BP gradually with IV antihypertensive: commence an IV labetalol infusion (or nicardipine infusion). Target a reduction in mean arterial pressure of no more than 25% in the first hour, then toward 160/100 mmHg over 2–6 hours. Do not normalise BP rapidly — chronic hypertension shifts the cerebral autoregulation curve rightward, and rapid reduction risks cerebral and myocardial hypoperfusion.
3. Investigations: FBE, U&E, troponin, ECG, urinalysis (malignant hypertension screen for microangiopathic haemolysis — blood film, LDH), CT brain (to exclude stroke/haemorrhage), chest X-ray.
4. Avoid: sublingual nifedipine (precipitous uncontrolled drop), rapid normalisation, and oral loading in the acute phase.
5. Transition to oral therapy once BP is stabilised and the patient is improving, and address non-adherence on discharge. [1]