Hypertension

Written 24th February 2020 - Last Update 28th September 2026

Hypertension

See Secondary Hypertension for the fuller secondary-cause work-up.

The most common condition requiring long-term drug therapy in Australia. Hypertension is associated with stroke, coronary heart disease, kidney disease, heart failure, and atrial fibrillation. Target organs that can be damaged: heart (failure, LVH, ischaemic disease), kidney (insufficiency), retina (retinopathy), blood vessels (peripheral vascular disease, aortic dissection), brain (cerebrovascular disease).

Diagnosis (adults ≥18): repeated measurements of diastolic > 90mmHg and/or systolic > 140mmHg.

Classification (clinic BP)

CategorySystolic (mmHg)Diastolic (mmHg)
Optimal<120and80–84
Normal120–129and/or85–89
High-normal130–139and/or90–99
Grade 1 (mild)140–159and/or100–109
Grade 2 (moderate)160–179and/or≥110
Grade 3 (severe)≥180and/or—
Isolated systolic≥140and<90

Malignant hypertension: diastolic > 120mmHg with exudative vasculopathy in the retinal and kidney circulations. Refractory hypertension: BP > 140/90mmHg despite maximal dosage of two drugs for 3–4 months.

Criteria for diagnosis by measurement method

MethodSystolic (mmHg)Diastolic (mmHg)
Clinic≥140and/or≥90
ABPM daytime (awake)≥135and/or≥85
ABPM night-time (asleep)≥120and/or≥70
ABPM over 24 hours≥130and/or≥80
HBPM≥135and/or≥85

Consider out-of-clinic measurement (ABPM/HBPM) for: suspected white-coat or masked hypertension; marked variability in clinic readings; autonomic/postural/post-prandial/ drug-induced hypotension; confirming true resistant hypertension; suspected nocturnal hypertension or absent nocturnal dipping (e.g. sleep apnoea, CKD, diabetes).

A diagnosis of hypertension should be based on BP measured on at least 2 occasions, one or more weeks apart (sooner if severe).

Causes

  • Essential (90–95%).
  • Secondary (~5–10%) — see Secondary Hypertension:
    • Renal (<3%) — glomerulonephritis, reflux nephropathy, renal artery stenosis.
    • Endocrine (0.3–1%) — primary aldosteronism (Conn syndrome), Cushing syndrome, phaeochromocytoma, oral contraceptives.
    • Coarctation of the aorta.
    • Immune disorders (e.g. polyarteritis nodosa).
    • Drugs (e.g. NSAIDs, corticosteroids).
    • Pregnancy.

History

Usually asymptomatic. Recognise the two acute presentations:

  • Hypertensive emergency: BP > 220/140mmHg with acute target organ damage — heart failure, acute pulmonary oedema, acute MI, acute renal failure, major neurological change, hypertensive encephalopathy, papilloedema, stroke.
  • Hypertensive urgency: BP > 180/110mmHg with headache/visual disturbance, or moderate target organ damage.

Symptoms suggesting a secondary cause: phaeochromocytoma (frequent headaches, sweating, palpitations); sleep apnoea (obesity, snoring, daytime somnolence); hypokalaemia (muscle weakness, cramps, hypotonia); hypothyroidism (tiredness, weight gain, bradycardia); hyperthyroidism (heat sensitivity, weight loss, tachycardia); Cushing syndrome (central obesity, skin pigmentation, round flushed face).

Medications/substances associated with hypertension: NSAIDs, stimulants, COCP, HRT, corticosteroids, SNRIs, MAOIs, clozapine, bupropion, decongestants, diet pills; excessive alcohol, liquorice, caffeine, cocaine, amphetamines.

Also take a full personal/family/lifestyle history: duration of raised BP and previous levels; current/previous antihypertensive therapy and tolerability; family/personal history of CKD, diabetes, dyslipidaemia, stroke, early-onset coronary heart disease (<55 in men, <65 in women), low birth weight; modifiable lifestyle factors (smoking, diet, weight, exercise, recreational drugs, alcohol); psychosocial factors that could affect care effectiveness; symptoms of end-organ damage/CVD (IHD, heart failure, cerebrovascular or peripheral arterial disease, nocturia, haematuria).

Examination

Two or more readings sitting, in both arms. Standing BP. Carotid/renal artery bruits; palpate for enlarged kidneys. Waist circumference, height, weight. Pulse rate/rhythm, apex, S3/S4, signs of LVF. To assess for coarctation of the aorta: compare the volume/timing of radial and femoral pulses, compare BP in the arm and leg, and compare BP between the two arms (radio-femoral delay is the key sign).

Investigations

All patients: urine dipstick for blood (send for microscopy if positive); urinary albumin/creatinine ratio (ACR — highly recommended for all, mandatory in diabetes); fasting lipids (total, LDL, HDL, triglycerides); UEC with eGFR; Hb/haematocrit; 12-lead ECG (AF, LVH, evidence of prior ischaemia).

ACR reference ranges (first-void spot urine, mg/mmol): microalbuminuria 2.5–25 (male) / 3.5–35 (female); macroalbuminuria above these. Proteinuria is defined as >500mg/ day protein excretion — use a 24-hour collection if spot urine falls in the macroalbuminuria range.

Additional tests for selected patients (assessing asymptomatic organ damage, CVD, or CKD): echocardiography (LVH, left atrial dilatation, suspected concomitant heart disease); carotid ultrasound (asymptomatic atherosclerosis, especially in older adults); renal artery duplex/CT angiography (suspected renovascular hypertension — fibromuscular dysplasia in young women, atherosclerotic renal artery disease in older patients, or a renal/femoral bruit); ankle-brachial index (PAD risk factors — an index <0.9 is diagnostic); plasma aldosterone/renin ratio (primary aldosteronism occurs in 5–10% of hypertensive patients and isn’t excluded by normal potassium — consider especially in moderate-severe or treatment-resistant hypertension, or hypokalaemia; refer to a specialist if suspected); plasma/urinary metanephrines or catecholamines (episodic catecholamine excess/hypertension suggestive of phaeochromocytoma). A 2022 prospective Melbourne general-practice study found primary aldosteronism in 14% of newly diagnosed, treatment-naive hypertensive patients, with hypokalaemia present in only 30% of cases — a reminder that relying on hypokalaemia alone as a trigger for screening will miss most cases.

Lifestyle risk factor management

Assess and manage in all patients; assess the patient’s readiness to change first.

FactorTarget
Physical activity150–300 min/week moderate intensity (or 75–150 min vigorous), plus muscle-strengthening ≥2 days/week
Weight controlWaist circumference <94cm (men), <90cm (Asian men), <80cm (women); BMI <25kg/m²
DietTotal fat 20–35% of energy intake; salt ≤6g/day (primary prevention) or ≤4g/day (secondary prevention); 5 serves vegetables + 2 serves fruit daily
SmokingCessation
Alcohol≤2 standard drinks/day, ≤4 on any one occasion

A 5kg weight reduction (if overweight) yields roughly a 7/3mmHg BP drop.

Cardiovascular risk and treatment threshold

The 2023 Australian CVD risk guideline governs when to start therapy. Assess ages 45–79 (35–79 with diabetes; First Nations 30–79) with the Aus CVD Risk Calculator — categories low <5%, intermediate 5–<10%, high ≥10%. Established CVD, moderate-to- severe CKD, and familial hypercholesterolaemia bypass the calculator as automatic high risk; diabetes no longer does (it’s now a calculator input).

  • At high calculated risk: start BP-lowering and lipid-modifying therapy regardless of individual BP grade.
  • Regardless of calculated risk: start drug treatment for persistent BP ≥160/100.

See Cardiovascular Risk Assessment for the full calculator.

Medication management

First-line drug classes: ACE inhibitors, ARBs, dihydropyridine calcium channel blockers, thiazide diuretics — similar efficacy as monotherapy despite different mechanisms. When combination therapy is needed, ACE inhibitor/ARB + calcium channel blocker is the superior combination.

Stepped approach:

  1. Start a first-line drug at a low-moderate dose. If not tolerated, switch class, again starting low-moderate.
  2. If target not reached after 3 months: add a second drug from a different class at a low-moderate dose (rather than up-titrating the first) — maximises efficacy while minimising adverse effects.
  3. If still not at target after 3 months, and both drugs are well tolerated: increase the dose of one (excluding thiazides) to the maximal recommended dose before increasing the other.
  4. If still not at target after 3 months: consider a third drug class at low-moderate dose. Reassess for non-adherence, secondary hypertension, treatment-resistance from sleep apnoea, undisclosed alcohol/recreational drug use, or high salt intake.
  5. If BP remains elevated despite this, seek specialist advice.

ACE inhibitors and ARBs: similar efficacy. ACEi clearly prevent nephropathy onset and reduce mortality in early diabetes, and prevent coronary heart disease in hypertension. ARBs better prevent kidney failure in advanced diabetic nephropathy but are inferior for coronary heart disease prevention. Monitor renal function after starting — a creatinine rise up to 25% is acceptable; more warrants dose reduction. Monitor potassium (rises).

Dihydropyridine CCBs (amlodipine, felodipine, lercanidipine): vasodilators, useful for stable angina + hypertension together; can cause peripheral oedema that may not respond to diuresis.

Thiazides: monitor sodium/potassium after 3–6 weeks; associated with new-onset diabetes; may exacerbate gout.

Treatment-resistant hypertension: uncontrolled (>140/90) despite 3 drugs, one of which is a diuretic.

Drug class contraindications

Drug classCompelling contraindicationsPossible contraindications
ACE inhibitors / ARBsPregnancy, angioedema, hyperkalaemia, bilateral renal artery stenosisWomen of childbearing potential
Dihydropyridine CCBs—Heart failure
Thiazide diuretics (low-dose, first-line)GoutGlucose intolerance, metabolic syndrome, hypercalcaemia, hypokalaemia
Beta-blockers (not first-line therapy)Asthma, bradycardia, grade 2–3 AV block, uncontrolled heart failureType 1/2 diabetes, metabolic syndrome, glucose intolerance, athletes/active patients, COPD (except vasodilator beta-blockers), depression