Lucan · Conditions

Hypertension

Australian guidance: Therapeutic Guidelines (eTG) Cardiovascular — Hypertension and blood pressure reduction; Atherosclerotic cardiovascular disease risk estimation

1. Definition and epidemiology

Hypertension is defined in Australia as sustained elevated blood pressure (BP) at or above 140/90 mmHg, with the decision to treat modulated by the patient's atherosclerotic cardiovascular disease (ASCVD) risk estimate. Epidemiological evidence establishes that the relationship between BP and cardiovascular risk is continuous from a systolic BP of 115 mmHg upward, such that there is no truly safe threshold. Approximately one in three Australian adults has elevated BP, and the condition accounts for a substantial proportion of the preventable burden of stroke, myocardial infarction, heart failure, and end-stage kidney disease.

2. Pathophysiology

The pathophysiology of primary (essential) hypertension involves a persistent imbalance between cardiac output and total peripheral vascular resistance, without a single identifiable cause. Robbins Ch 11 identifies several interacting mechanisms: increased sympathetic adrenergic tone, inappropriately activated renin-angiotensin-aldosterone system (RAAS), impaired pressure-natriuresis in the kidney, and structural vascular changes characterised by smooth muscle hypertrophy and endothelial dysfunction. Angiotensin II drives vasoconstriction via AT1 receptors, promotes sodium and water retention through aldosterone, and stimulates myocardial and vascular remodelling. Over time, sustained elevated intraluminal pressure accelerates endothelial injury, promotes lipid deposition, and amplifies atherosclerosis. In the kidney, hyaline arteriolosclerosis of afferent glomerular arterioles (nephrosclerosis) reduces the glomerular filtration rate and initiates a feedback loop that further sustains elevated BP. Cardiac adaptation produces concentric left ventricular hypertrophy, initially compensatory but ultimately a substrate for diastolic dysfunction and heart failure with preserved ejection fraction.

3. Clinical presentation and diagnostic criteria

Hypertension is largely asymptomatic until target-organ damage develops. Non-specific symptoms including headache and epistaxis are inconsistently associated. On examination, elevated BP readings must be confirmed on at least two separate occasions before a diagnosis is made. The preferred method of confirmation in Australia is 24-hour ambulatory BP monitoring (ABPM), which is reimbursed under the Medicare Benefits Schedule for the diagnosis of hypertension and is the most accurate method for identifying white-coat hypertension, masked hypertension, and nocturnal non-dipping patterns. Automated non-observed clinic BP measurement, where the patient rests alone for five minutes before an average of two to three readings is calculated, is the preferred clinic method. Fundoscopic examination may reveal hypertensive retinopathy. Secondary causes should be clinically screened via history and examination before investigation.

4. Investigations and AU-specific cutoffs

Initial investigations serve two purposes: confirming the diagnosis and screening for a secondary cause.

BP itself must be confirmed before treatment is considered. eTG's preferred clinic method is automated, non-observed measurement: the patient rests alone for at least 5 minutes, the first reading is disregarded, and the average of the second and third readings is taken. Twenty-four-hour ambulatory BP monitoring (ABPM) gives the most accurate picture of a patient's usual BP and is reimbursed by the Medicare Benefits Schedule for diagnosing hypertension; it is particularly useful when white-coat hypertension, masked hypertension, or nocturnal non-dipping is suspected. Home BP monitoring is a useful supplement to clinic readings.

Before investigating for a secondary cause, confirm the BP reading is accurate and exclude non-adherence with any existing BP-lowering drugs; if there is clinical suspicion of a secondary cause, investigate before starting drug therapy where possible, partly because some treatments (eg spironolactone) interfere with the aldosterone-renin ratio. Suspect secondary hypertension in apparent resistant hypertension, or with suggestive symptoms/signs (palpitations, haematuria, delayed femoral pulses, epigastric bruit), abnormal biochemistry (low potassium, elevated creatinine, proteinuria, haematuria), or abnormal imaging (renal artery stenosis on CT angiography, an adrenal mass). Primary aldosteronism, present even without hypokalaemia, is the most common curable secondary cause and accounts for around 10% of adults with hypertension; other causes include renal artery stenosis, renal parenchymal disease, thyroid dysfunction, Cushing syndrome, phaeochromocytoma, coarctation of the aorta, drug-induced hypertension, and obstructive sleep apnoea (a contributor to resistant hypertension specifically). Elevated BP in a child is likely to be secondary and needs specialist evaluation.

The decision to start BP-lowering drug therapy weighs the confirmed BP against the patient's atherosclerotic cardiovascular disease (ASCVD) risk estimate: - Systolic BP 160 mmHg or more, or diastolic BP 100 mmHg or more: start drug therapy irrespective of ASCVD risk. - Established ASCVD: BP-lowering therapy, specifically with an ACEI or ARB, is recommended routinely. - High ASCVD risk (more than 10% risk of a cardiovascular event over 5 years on the Aus CVD risk calculator): treat with BP-lowering therapy alongside lifestyle change, unless contraindicated or clinically inappropriate (eg the patient is hypotensive). - Intermediate risk (5 to 10%): consider BP-lowering therapy alongside lifestyle change, in discussion with the patient about preferences. - Low risk (below 5%): BP-lowering drug therapy is not routinely required.

The Aus CVD risk calculator is the tool recommended by the Australian Chronic Disease Prevention Alliance (ACDPA); it is based on the PREDICT risk equation, derived from a large New Zealand cohort and adapted to the Australian context, and has replaced the older Framingham-based calculator. Its risk-category thresholds are 5% lower than the equivalent Framingham thresholds (eg PREDICT labels 10% risk as high, where Framingham labelled 15% as high), but the categories are considered clinically comparable because the Framingham equation likely overestimated risk. The calculator is validated for adults 45 to 79 years (35 to 79 years with diabetes; 30 to 79 years for First Nations people) without known ASCVD. People with moderate-to-severe chronic kidney disease (sustained eGFR below 45 mL/min/1.73m², or urine albumin-creatinine ratio above 25 mg/mmol in men or 35 mg/mmol in women) or familial hypercholesterolaemia are automatically considered high risk without formal calculation. Outside the validated age range, and in patients with established ASCVD (for whom risk estimation is not intended), use clinical judgement instead.

5. Management

All patients with elevated BP are advised to adopt lifestyle modification, which is complementary to drug therapy, not an alternative to it, and improves cardiovascular outcomes beyond its effect on BP alone. eTG-quantified measures include regular aerobic exercise (can reduce daytime BP by around 3.2/2.7 mmHg), reduced alcohol intake, moderate sodium restriction, a DASH-pattern diet, and weight loss in overweight patients (a 5 kg loss can reduce BP by around 7/3 mmHg). Treating obstructive sleep apnoea lowers BP but has not been shown to improve cardiovascular outcomes.

The general target for a treated patient is BP below 140/90 mmHg. In patients at high ASCVD risk, a target below 130/80 mmHg further reduces cardiovascular morbidity and may reduce mortality, though this extra benefit may not extend past age 80. Trial evidence supports an even lower target of 120/80 mmHg, but eTG cautions that the trial's method of BP measurement did not reflect real-world practice; aiming below 120 mmHg may be reasonable if the risk of adverse effects (eg falls) is low, with monitoring for hypotension, syncope, electrolyte abnormality, and worsening kidney function. Movement toward the target, even if it is not reached, still reduces ASCVD risk.

Drug therapy can start as a single drug at low-to-moderate dose, or two drugs at low dose; the two-drug approach is reasonable in any patient, and especially with high ASCVD risk or markedly elevated BP. Most patients need two or more drugs to reach target, and combination therapy is often more effective, and better tolerated, than high-dose monotherapy. At the time this guideline was last amended, fixed-dose combination products were not listed on the PBS for initiating treatment.

Review therapy at 4 to 6 weeks (sooner for high ASCVD risk or very elevated BP), checking adverse effects, adherence, and whether the BP target has been reached. If a patient on monotherapy has not reached target, add a low dose of a second, different-class drug rather than increasing the first drug's dose — this is usually more effective. If a patient on two drugs has not reached target and both are tolerated, uptitrate one drug to its maximum dose, then the second, before adding a third; if BP is still above target 4 to 6 weeks after that, look for non-adherence or a secondary cause (eg a BP-raising drug) before adding a third agent. Pharmacologically complementary combinations: an ACEI or ARB with a thiazide or thiazide-like diuretic, an ACEI or ARB with a calcium channel blocker, or an ACEI/ARB plus a dihydropyridine calcium channel blocker plus a thiazide/thiazide-like diuretic as a triple combination. Do not combine an ACEI with an ARB except on specialist advice, and avoid a beta-blocker with verapamil or diltiazem because of the risk of heart block.

If a combination of tolerated first-line drugs does not adequately control BP, add a second-line drug and consider screening for secondary hypertension if this has not already been done. Spironolactone has the best evidence as add-on therapy for resistant hypertension; the PATHWAY-2 trial found it more effective than a beta-blocker or an alpha-blocker when added to three BP-lowering drugs at maximum dose. A rapid or marked BP response to spironolactone can itself point to underlying primary aldosteronism.

For patients with established ASCVD, BP-lowering therapy with an ACEI or ARB is recommended routinely as part of the overall secondary-prevention approach, alongside the other elements of cardiovascular risk management (eg lipid-modifying therapy, addressed in a separate eTG topic not reviewed here).

6. Pharmacology and AU PBS notes

Dose ranges below are eTG's suitable ranges for uncomplicated elevated BP in non-pregnant adults: start low-to-moderate and increase slowly, with a lower starting dose in older patients or those with reduced kidney or liver function.

First-line classes, of broadly similar efficacy, chosen according to comorbidity and tolerability: - ACE inhibitors (ACEIs): captopril 12.5 to 50 mg twice daily, enalapril 5 to 40 mg daily, fosinopril 10 to 40 mg daily, lisinopril 5 to 40 mg daily, perindopril arginine 5 to 10 mg daily (or perindopril erbumine 4 to 8 mg daily), quinapril 5 to 40 mg daily, ramipril 2.5 to 10 mg daily, trandolapril 1 to 4 mg daily. Preferred with heart failure with reduced ejection fraction (HFrEF), chronic kidney disease (especially diabetic nephropathy), or after myocardial infarction. Avoid in bilateral renal artery stenosis and in a history of angioedema. Monitor for hypotension, kidney impairment, and hyperkalaemia; a rise in creatinine of up to 25%, or a within-range rise in potassium, can be transient and does not automatically require stopping the drug. Avoid the "triple whammy" of an ACEI/ARB plus a diuretic plus an NSAID (including COX-2 inhibitors), which risks acute kidney injury, especially with pre-existing kidney disease, dehydration, or older age. - Angiotensin II receptor blockers (ARBs): candesartan 8 to 32 mg daily, eprosartan 600 mg daily, irbesartan 150 to 300 mg daily, losartan 50 to 100 mg daily, olmesartan 20 to 40 mg daily, telmisartan 40 to 80 mg daily, valsartan 80 to 320 mg daily. Similar cardio- and renoprotective profile to ACEIs, without the cough; weigh the risk carefully before prescribing after an ACEI-related angioedema, since the reaction can recur. Same monitoring and triple-whammy caution as ACEIs. - Dihydropyridine calcium channel blockers: amlodipine 5 to 10 mg daily, felodipine modified-release 5 to 20 mg daily, lercanidipine 10 to 20 mg daily, nifedipine modified-release 30 to 120 mg daily. Useful with stable angina. Peripheral oedema (from fluid redistribution, not retention) should not be treated with a diuretic; reduce the dose or stop if it persists. - Thiazide and thiazide-like diuretics: chlortalidone 12.5 to 25 mg daily, hydrochlorothiazide 12.5 to 50 mg daily, indapamide 1.25 to 2.5 mg daily (or modified-release 1.5 mg daily). At antihypertensive doses these act mainly as vasodilators rather than diuretics. Not recommended first-line under 65 years because of new-onset diabetes risk; avoid in gout. Check plasma sodium and potassium 3 to 6 weeks after starting; hypokalaemia and hyponatraemia are uncommon at these doses.

Second-line classes: - Spironolactone 12.5 to 50 mg daily (or amiloride 2.5 to 5 mg daily if not tolerated — not registered in Australia as a single-drug product, available via the Special Access Scheme) for resistant hypertension. Check kidney function and potassium before starting; do not use if potassium is 5 mmol/L or more. Recheck kidney function and potassium 1 to 2 weeks after starting, given hyperkalaemia risk, which is higher still with an ACEI/ARB or kidney disease. - Beta-blockers: atenolol 25 to 100 mg daily, metoprolol tartrate 25 to 100 mg twice daily. Not first-line for uncomplicated hypertension, being less effective than the first-line classes at reducing stroke risk, but useful with stable angina, after myocardial infarction, or with HFrEF. Taper rather than stop abruptly (halve the dose every 2 to 3 days) to avoid rebound hypertension or tachyarrhythmia. - Alpha-blockers: prazosin 0.5 mg twice daily, increasing to a maintenance dose of 1 to 10 mg twice daily. Not first-line, being associated with more cardiovascular events (especially heart failure) than other classes; can improve urinary flow in men with coexisting benign prostatic hypertrophy. Risk of postural hypotension, particularly after the first dose. - Non-dihydropyridine calcium channel blockers: diltiazem modified-release 180 to 360 mg daily, verapamil modified-release 120 to 480 mg daily. Useful with stable angina; contraindicated with left ventricular failure or an ejection fraction of 40% or less. - Centrally acting alpha-2 agonists: methyldopa 125 mg twice daily increasing to up to 500 mg three times daily, or clonidine 50 micrograms twice daily increasing to up to 300 micrograms twice daily — now used mainly for pregnancy-associated hypertension; taper clonidine (halve every 2 to 3 days) to avoid severe rebound hypertension 12 to 36 hours after abrupt cessation. Moxonidine 200 micrograms daily increasing to up to 300 micrograms twice daily is avoided in heart failure, given an association with increased mortality in the MOXCON trial. - Direct-acting vasodilators (minoxidil, then hydralazine if minoxidil is not tolerated): reserved for BP that is uncontrolled, or drugs that are not tolerated, on other classes. Minoxidil is always co-prescribed with a loop diuretic (to prevent fluid retention) and usually a beta-blocker (to prevent reflex tachycardia).

PBS: at the time this eTG topic was last amended (February 2025), fixed-dose antihypertensive combination products were not listed on the PBS for initiating treatment, although they may reduce pill burden and improve adherence once therapy is established; check the current PBS schedule for listing and any authority requirements before prescribing.

7. Complications and monitoring

Target-organ damage from sustained hypertension spans multiple systems: cardiovascular (left ventricular hypertrophy, heart failure, coronary artery disease, aortic dissection), cerebrovascular (ischaemic and haemorrhagic stroke, hypertensive encephalopathy), renal (nephrosclerosis progressing to chronic kidney disease), and ocular (hypertensive retinopathy). Hypertensive urgency (severe elevation without end-organ damage) and hypertensive emergency (with acute organ damage including aortic dissection, myocardial ischaemia, or stroke) require different approaches; emergencies require urgent parenteral therapy.

Monitoring schedule: - Confirm target BP is reached four to six weeks after initiating or adjusting therapy. - Renal function and electrolytes at baseline and one to two weeks after starting an ACEI, ARB, or potassium-sparing diuretic, and after each dose escalation. - Annual review of BP control, electrolytes, renal function, uACR, and lipid profile in stable patients. - Screen for target-organ damage with ECG and fundoscopy at baseline and when clinically indicated. - Reassess ASCVD risk every two years in intermediate-risk patients; formal recalculation not required once drug therapy is established. - First Nations patients: reassess ASCVD risk annually given higher baseline risk and earlier onset.

Written for Australian practice and grounded in the guidance named above. Study material only — not medical advice. Always check against current guidelines.