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This is a clinician-written, evidence-based guide aligned to the MCC Examination Objectives. It is structured by clinical presentation — the way the MCCQE tests and the way patients actually present. Management reflects current Canadian guidelines (CMA, CFPC, CPS). Always cross-reference with institutional protocols and clinical judgment.
Key points
- Canadian threshold: HTN defined as >=140/90 in office (Hypertension Canada 2020) — different from ACC/AHA 2017 (>=130/80)
- Diagnosis requires: office BP >=140/90 on >=2 visits, OR ABPM daytime mean >=135/85, OR home BP mean >=135/85
- First-line agents: thiazide/thiazide-like (indapamide, chlorthalidone preferred over HCTZ), ACEi, ARB, long-acting DHP CCB (amlodipine)
- Hypertensive emergency = BP >=180/120 + acute target organ damage (encephalopathy, acute MI, aortic dissection, pulmonary oedema, AKI, eclampsia). IV treatment in ICU
- Always screen for secondary causes if: onset <30 or >55, resistant HTN, sudden worsening, hypokalaemia, or clinical features of a secondary cause
Approach to the Presentation
Blood pressure abnormalities encompass both hypertension and hypotension. Hypertension is the most common modifiable cardiovascular risk factor, affecting ~25% of Canadian adults. Canada uses Hypertension Canada guidelines (2020), which retain the office BP threshold of >=140/90 mmHg for diagnosis (unlike the ACC/AHA 2017 guideline that lowered the threshold to >=130/80). Out-of-office measurement (ABPM or home BP) is recommended to confirm the diagnosis and exclude white-coat hypertension. Hypotension as a primary presentation typically relates to shock (see Shock presentation), orthostatic hypotension, or medication effect.
Differential Diagnosis — Secondary Hypertension
| diagnosis | likelihood | key features | distinguishing test |
|---|---|---|---|
| Primary Hyperaldosteronism (Conn) | must-not-miss | HTN + hypokalaemia (may be normokalaemic). Resistant HTN, adrenal incidentaloma. Most common cause of secondary HTN | Plasma aldosterone:renin ratio (ARR). Confirm with salt loading or fludrocortisone suppression |
| Renal Artery Stenosis | must-not-miss | Resistant HTN, flash pulmonary oedema, worsening renal function on ACEi/ARB, abdominal bruit. Atherosclerotic (older, diffuse vascular disease) or fibromuscular dysplasia (young woman) | Renal artery duplex US, CTA, or MRA |
| Pheochromocytoma | must-not-miss | Paroxysmal HTN + classic triad: headache, palpitations, diaphoresis. May be episodic or sustained. Associated with MEN2, VHL, NF1 | Plasma free metanephrines (preferred) or 24h urine catecholamines/metanephrines |
| Pre-eclampsia | must-not-miss | New HTN (>=140/90) after 20 weeks gestation + proteinuria or end-organ dysfunction. Headache, visual changes, RUQ pain, oedema | BP + urine protein:creatinine ratio + CBC, LFTs, creatinine. Urgent obstetric assessment |
| Primary (Essential) Hypertension | common | ~90-95% of all HTN. Gradual onset, family history, associated with age, obesity, sedentary lifestyle, excess sodium/alcohol. No identifiable secondary cause | Diagnosis of exclusion after ruling out secondary causes where indicated |
| Chronic Kidney Disease | common | HTN with elevated creatinine, proteinuria, abnormal sediment. HTN may be both a cause and consequence of CKD | eGFR, urinalysis, urine ACR, renal ultrasound |
| Obstructive Sleep Apnoea | common | Resistant HTN, obesity, snoring, daytime somnolence, witnessed apnoeas. Most common cause of resistant HTN | STOP-BANG screening questionnaire, then polysomnography (sleep study) |
| Cushing Syndrome | less common | Central obesity, moon facies, buffalo hump, striae, proximal weakness, hyperglycaemia, easy bruising | Overnight dexamethasone suppression test or 24h urine cortisol or late-night salivary cortisol |
| Coarctation of the Aorta | less common | HTN in young patient, upper > lower extremity BP, radio-femoral delay, rib notching on CXR | Echocardiogram, CTA/MRA of thoracic aorta |
| Thyroid Disease | less common | Hyperthyroidism: systolic HTN with wide pulse pressure, tachycardia, tremor. Hypothyroidism: diastolic HTN, bradycardia, fatigue | TSH + free T4 |
Red Flags & Key History
Symptoms
Severe headache, visual changes, confusion (hypertensive encephalopathy)
Acute chest pain or dyspnoea (ACS, aortic dissection, acute pulmonary oedema)
New HTN in pregnancy >20 weeks (pre-eclampsia)
Episodic headache + palpitations + diaphoresis (phaeochromocytoma)
Resistant HTN (uncontrolled on >=3 drugs including diuretic) — consider secondary cause, especially primary hyperaldosteronism or OSA
Young patient (<30) with HTN — higher yield for secondary cause workup
Signs
BP >=180/120 + end-organ signs = hypertensive emergency
Abdominal bruit (renal artery stenosis)
Radio-femoral delay (coarctation)
Cushingoid features (Cushing)
Hypertensive retinopathy: AV nicking, flame haemorrhages, papilloedema (grade IV = malignant)
S4 gallop (LVH with diastolic dysfunction)
Approach to Investigation
First-line
Office BP (proper technique)Patient seated, rested 5 min, back supported, arm at heart level, correct cuff size. >=2 readings, >=2 visits. Use automated oscillometric device (BpTRU or similar preferred in Canada)
Out-of-office BP confirmationABPM (gold standard): daytime mean >=135/85 = HTN. Home BP monitoring: >=135/85 on average of duplicate readings morning and evening x 7 days. Essential to rule out white-coat HTN (~15-30% of apparent HTN)
Basic labsElectrolytes (K+ — low suggests hyperaldosteronism), creatinine/eGFR, urinalysis + urine ACR (proteinuria), fasting glucose/HbA1c, lipid panel
ECGLVH (Sokolow-Lyon, Cornell criteria), strain pattern, prior MI, arrhythmia
Second-line
EchocardiogramIf suspected LVH, HF, or valvular disease. More sensitive than ECG for LVH
Secondary HTN workup (when indicated)Plasma aldosterone:renin ratio (hyperaldosteronism), plasma free metanephrines (pheochromocytoma), renal artery imaging (RAS), TSH, overnight dexamethasone suppression (Cushing), polysomnography (OSA)
Specialist
Renal artery duplex US / CTA / MRAIf renal artery stenosis suspected (resistant HTN, abdominal bruit, Cr rise on ACEi/ARB)
Management Principles
Hypertension Canada 2020 Guidelines1
Lifestyle (all patients)
- DASH diet, sodium restriction <2000 mg/day
- Regular exercise: 30-60 min moderate intensity 4-7 days/week
- Weight loss if BMI >25, waist circumference targets
- Limit alcohol: <=2 standard drinks/day, <14/week (men), <9/week (women)
- Stress management
2
Pharmacotherapy — Canadian first-line agents
- Thiazide/thiazide-like: indapamide or chlorthalidone preferred over HCTZ (better outcome data)
- ACEi (ramipril, perindopril) or ARB (telmisartan, valsartan) — do NOT combine ACEi + ARB
- Long-acting DHP CCB: amlodipine
- Beta-blockers are NOT first-line for uncomplicated HTN in Canada (unlike some international guidelines) — reserved for specific indications (HF, post-MI, rate control for AF)
3
Compelling indications (Canadian-specific)
- Diabetes + HTN: ACEi or ARB first-line (renoprotective)
- CKD with proteinuria: ACEi or ARB
- Coronary artery disease: ACEi + beta-blocker
- Heart failure: ACEi/ARB/ARNi + BB + MRA + SGLT2i
- Black patients without compelling indication: thiazide or CCB first-line (Hypertension Canada recognizes differential drug response)
- Pregnancy: labetalol, nifedipine XL, or methyldopa. ACEi/ARBs are CONTRAINDICATED
4
Hypertensive emergency (>=180/120 + end-organ damage)
- Admit to ICU, arterial line for continuous BP monitoring
- IV agents: labetalol, nicardipine, nitroprusside, nitroglycerin, esmolol (choice depends on clinical scenario)
- Reduce MAP by no more than 25% in first hour, then toward 160/100 over next 2-6h, then normalise over 24-48h
- Aortic dissection exception: SBP <120 + HR <60 within 20 min (esmolol/labetalol FIRST)
- Stroke exception: only treat if >185/110 and thrombolysis planned, or >220/120 without thrombolysis
5
Hypertensive urgency (>=180/120 WITHOUT end-organ damage)
- Reinstate or uptitrate oral medications
- Do NOT rapidly reduce BP — risk of cerebral hypoperfusion
- Arrange close outpatient follow-up within 24-72h
Complications & Pitfalls
- Using ACC/AHA thresholds in a Canadian context: Canada defines HTN as >=140/90 (Hypertension Canada), not >=130/80 (ACC/AHA). Using the wrong threshold leads to overdiagnosis and unnecessary treatment
- Diagnosing HTN from a single office visit: Always confirm with a second visit or out-of-office measurements (ABPM or home BP). ~15-30% have white-coat HTN
- Failing to check K+ at baseline: Hypokalaemia suggests primary hyperaldosteronism — the most common cause of secondary HTN and frequently missed
- Beta-blocker as first-line for uncomplicated HTN: Not recommended in Canadian guidelines (unlike some international guidelines). This is a common exam distractor
- Rapidly lowering BP in hypertensive urgency: Risk of cerebral and coronary hypoperfusion — gradual reduction over days with oral agents is appropriate
MCCQE1 Exam Tips
- 1Canadian HTN threshold is >=140/90 (Hypertension Canada 2020), NOT >=130/80 (ACC/AHA). This is a critical distinction for the MCCQE1
- 2Confirm diagnosis with ABPM (>=135/85 daytime) or home BP (>=135/85 average). Do NOT diagnose from a single office visit
- 3Beta-blockers are NOT first-line for uncomplicated HTN in Canada — use thiazide, ACEi/ARB, or CCB. BB only for compelling indications (HF, post-MI, AF)
- 4Most common cause of secondary HTN: primary hyperaldosteronism. Screen with plasma aldosterone:renin ratio. Most common cause of resistant HTN: OSA
- 5Hypertensive emergency vs urgency: the distinction is END-ORGAN DAMAGE, not the BP number
- 6Pheochromocytoma: paroxysmal HTN + headache + palpitations + diaphoresis. Screen with plasma free metanephrines
- 7Pre-eclampsia: new HTN >20 weeks + proteinuria or end-organ dysfunction. Definitive treatment = delivery. Magnesium sulphate for seizure prophylaxis
- 8Aortic dissection BP management: beta-blocker FIRST (reduce shear), THEN vasodilator. Never vasodilator alone
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