Ahpra registration PHY0002298174
How these guides are written and reviewed →
Hypertension means blood pressure that stays higher than is healthy over time. It usually causes no symptoms, which is why it is often called a "silent" condition, but left unchecked it is the biggest modifiable cause of strokes, heart attacks and kidney disease. It is diagnosed with repeated readings and managed with lifestyle changes — less salt, more activity, a healthy weight and limiting alcohol — and medication when needed. Regular monitoring keeps it under control. This page explains high blood pressure and how it is managed.
Hypertension is the single largest modifiable contributor to global cardiovascular disease burden. Although managed predominantly in general practice, it sits at the foundation of every cardiac condition covered in this resource, and physiotherapy-led exercise prescription and lifestyle intervention have an established place in management.
Definition
Hypertension is defined by the National Heart Foundation of Australia (NHFA) as a clinic blood pressure of ≥ 140/90 mmHg, confirmed by ambulatory or home blood pressure monitoring. Australian guidelines retain the 140/90 threshold; this differs from the US ACC/AHA threshold of 130/80.
Severity is graded as grade 1 (140–159 / 90–99), grade 2 (160–179 / 100–109), and grade 3 (≥ 180/110). Isolated systolic hypertension (systolic ≥ 140, diastolic < 90) is common in older adults.
Pathophysiology
Hypertension reflects an imbalance between cardiac output and systemic vascular resistance, modulated by the renin-angiotensin-aldosterone system, the sympathetic nervous system, vascular endothelial function, sodium handling, and obesity-related neuro-humoral activation. Most cases are "primary" (essential) with multifactorial drivers; a minority have an identifiable secondary cause.
Co-morbidities
Obesity, type 2 diabetes, dyslipidaemia, chronic kidney disease, obstructive sleep apnoea, atrial fibrillation, heart failure (particularly HFpEF), and cognitive decline. The clustering of hypertension with these conditions defines cardiometabolic risk.
Prevalence
Approximately one in three Australian adults has hypertension; prevalence rises sharply with age, exceeding 60% in those over 65. A significant proportion of treated patients remain inadequately controlled, and a similar proportion of hypertensive Australians remain undiagnosed.
Causes and risk factors
Modifiable: excess sodium intake, low potassium intake, obesity, physical inactivity, excess alcohol, smoking, psychosocial stress, sleep disturbance, and obstructive sleep apnoea.
Non-modifiable: age, family history, male sex (until menopause), Aboriginal and Torres Strait Islander identity, and certain ancestral backgrounds (higher prevalence and earlier onset).
Secondary causes: renovascular disease, renal parenchymal disease, primary aldosteronism, phaeochromocytoma, Cushing’s syndrome, thyroid disease, obstructive sleep apnoea, coarctation of the aorta, and certain medications (NSAIDs, decongestants, oral contraceptives, corticosteroids, stimulants, liquorice).
Symptoms
Hypertension is overwhelmingly asymptomatic — it is often called a silent condition, because damage accumulates for years without warning. When symptoms occur they are usually a feature of severe or accelerated hypertension (headache, visual disturbance, chest pain, dyspnoea, neurological deficit) or of an underlying secondary cause.
Diagnosis
Why diagnosis matters
Blood pressure is the strongest modifiable risk factor for stroke and a major contributor to coronary disease, heart failure, kidney disease, atrial fibrillation, and vascular dementia. Each 10 mmHg reduction in systolic blood pressure produces approximately a 20% reduction in major cardiovascular events.
How the diagnosis is made
Diagnosis requires confirmation of elevated readings outside the clinic setting, using 24-hour ambulatory blood pressure monitoring (preferred) or structured home blood pressure monitoring. This identifies white-coat hypertension (in-clinic elevated, out-of-clinic normal) and masked hypertension (in-clinic normal, out-of-clinic elevated), each carrying different prognostic implications.1,2
Initial investigations
Targeted to assess cardiovascular risk, identify end-organ damage, and screen for secondary causes: urinalysis (proteinuria, haematuria), urine albumin-creatinine ratio, electrolytes and creatinine with eGFR, fasting lipids, fasting glucose or HbA1c, TSH, and ECG. Echocardiography for suspected left ventricular hypertrophy.
When to consider secondary hypertension
Young age at onset (< 30 years without family history), severe or resistant hypertension, sudden deterioration of previously controlled blood pressure, paroxysmal symptoms suggestive of phaeochromocytoma, hypokalaemia (primary aldosteronism), and clinical features of an endocrine cause warrant specialist referral and targeted investigation.
Management
Treatment goals
NHFA targets are < 140/90 mmHg for most adults, with < 130/80 mmHg considered for higher-risk patients (established CVD, diabetes, CKD with proteinuria) where tolerated. Office targets should be interpreted alongside out-of-clinic readings.3,4
Lifestyle and exercise
Lifestyle measures reduce blood pressure independently and amplify pharmacological effects. These include weight loss (a 1 mmHg fall per kg lost in overweight adults), DASH-style or Mediterranean dietary pattern, sodium restriction to < 2 g/day, increased potassium-rich foods (unless contraindicated), regular aerobic exercise (150 minutes per week of moderate intensity), reduced alcohol intake (≤ 10 standard drinks per week and ≤ 4 per occasion under current Australian guidelines), and smoking cessation.5,6,7,8,9
Exercise prescription should combine moderate-intensity aerobic activity, dynamic resistance training, and (with emerging evidence) isometric exercise such as wall-sit or handgrip protocols, which have particularly large blood-pressure-lowering effects in recent meta-analyses.
Pharmacological therapy
Initiated when blood pressure remains elevated despite lifestyle measures, or earlier in patients with established cardiovascular disease, target-organ damage, or high absolute CVD risk. Initial therapy is typically a single agent from one of four classes (ACE inhibitor, ARB, calcium channel blocker, thiazide diuretic), with low-dose combination therapy increasingly favoured as first-line in moderate-to-severe hypertension.
Resistant hypertension
Resistant hypertension (uncontrolled despite three drugs at optimal doses including a diuretic) warrants reassessment for adherence, secondary causes (particularly OSA, primary aldosteronism, renovascular disease), and consideration of mineralocorticoid receptor antagonist as fourth-line therapy. Renal denervation has re-entered guidelines as an option in selected centres.
Identifying hypertensive emergency
Severely elevated blood pressure (typically ≥ 180/120 mmHg) with acute target-organ damage — encephalopathy, acute coronary syndrome, acute heart failure, aortic dissection, stroke, acute kidney injury — is a medical emergency requiring controlled in-hospital reduction. Asymptomatic severe hypertension is managed urgently but does not require IV therapy.
Medications
ACE inhibitors and angiotensin receptor blockers
Perindopril, ramipril, enalapril (ACEi); irbesartan, candesartan, telmisartan (ARB). First-line in younger patients, those with diabetes, CKD with proteinuria, and heart failure. Side effects: cough (ACEi only), hyperkalaemia, rise in creatinine, angioedema (rare), contraindicated in pregnancy.
Calcium channel blockers
Amlodipine, felodipine, lercanidipine (dihydropyridines) are first-line in older patients and effective in combination with ACEi/ARB. Side effects: peripheral oedema, headache, flushing.
Thiazide and thiazide-like diuretics
Indapamide (preferred in current guidelines), chlorthalidone, hydrochlorothiazide. Effective particularly in older and salt-sensitive patients. Side effects: hyponatraemia, hypokalaemia, hyperuricaemia, glucose intolerance.
Other agents
Mineralocorticoid receptor antagonists (spironolactone, eplerenone) for resistant hypertension. Beta-blockers no longer first-line for uncomplicated hypertension but indicated in patients with concurrent coronary disease, heart failure, or atrial fibrillation. Centrally-acting agents (moxonidine, clonidine) and alpha-blockers (prazosin) are reserved for refractory cases.
Multi-system manifestations
Target-organ damage
Chronic untreated or under-treated hypertension produces left ventricular hypertrophy and diastolic dysfunction, accelerated atherosclerosis, chronic kidney disease, retinopathy, and cognitive impairment. Reversal or stabilisation of these is a key goal of treatment.
Concurrent conditions to address
OSA, type 2 diabetes, dyslipidaemia, and obesity should be screened for and managed in parallel. Aspirin is no longer routinely recommended for primary prevention but is core to secondary prevention in established CVD.10
Living with hypertension
Home blood pressure monitoring
Patients should be taught structured home blood pressure monitoring using a validated upper-arm device, with seven days of twice-daily readings (morning and evening, after five minutes seated) and an average calculated excluding day one. This supports diagnosis, adherence, and titration.
Adherence and inertia
Non-adherence and clinical inertia (failure to up-titrate when targets are not met) are the principal reasons for under-treatment in Australia. Single-pill combination therapy improves adherence and is increasingly first-line.
Nutrition
DASH-style or Mediterranean dietary pattern, sodium ≤ 2 g/day (≤ 5 g salt), increased potassium from fruit, vegetables, legumes, and dairy (unless contraindicated by CKD), and moderation of alcohol.
Sleep and stress
Address sleep duration (< 7 hours associated with higher BP), screen for and treat OSA, and incorporate stress-reduction strategies (mindfulness-based interventions, structured exercise) which have modest but measurable effects.
Prognosis
With sustained treatment and target achievement, cardiovascular event risk approaches that of normotensive peers. Outcomes are strongly determined by long-term adherence and concurrent risk factor management.
Role of the physiotherapist
The physiotherapist supports blood-pressure control through structured aerobic and resistance exercise — a first-line lifestyle intervention — alongside weight management and activity coaching, and integrates cardiovascular risk-factor education into every programme.
Warning signs
Part 1 · References
- Stergiou GS, Palatini P, Parati G, et al. 2021 European Society of Hypertension practice guidelines for office and out-of-office blood pressure measurement. J Hypertens 2021;39(7):1293–1302.
- National Heart Foundation of Australia. Guideline for the diagnosis and management of hypertension in adults 2016. Melbourne: NHFA; 2016.
- McEvoy JW, McCarthy CP, Bruno RM, et al. 2024 ESC guidelines for the management of elevated blood pressure and hypertension. Eur Heart J 2024;45(38):3912–4018.
- SPRINT Research Group. A randomized trial of intensive versus standard blood-pressure control. N Engl J Med 2015;373(22):2103–2116.
- Cornelissen VA, Smart NA. Exercise training for blood pressure: a systematic review and meta-analysis. J Am Heart Assoc 2013;2(1):e004473.
- Edwards JJ, Deenmamode AHP, Griffiths M, et al. Exercise training and resting blood pressure: a large-scale pairwise and network meta-analysis of randomised controlled trials. Br J Sports Med 2023;57(20):1317–1326.
- Sacks FM, Svetkey LP, Vollmer WM, et al. Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. N Engl J Med 2001;344(1):3–10.
- He FJ, Li J, MacGregor GA. Effect of longer term modest salt reduction on blood pressure: Cochrane systematic review and meta-analysis of randomised trials. BMJ 2013;346:f1325.
- Roerecke M, Kaczorowski J, Tobe SW, Gmel G, Hasan OSM, Rehm J. The effect of a reduction in alcohol consumption on blood pressure: a systematic review and meta-analysis. Lancet Public Health 2017;2(2):e108–e120.
- Pengo MF, Soranna D, Giontella A, et al. Obstructive sleep apnoea treatment and blood pressure: which phenotypes predict a response? A systematic review and meta-analysis. Eur Respir J 2020;55(5):1901945.
References are numbered in citation order (Vancouver/BMJ style) and were current at the time of writing. Guidelines are living documents — verify against the latest version before clinical use.
Supervised exercise, breathing technique and self-management education are the mainstay of cardiorespiratory physiotherapy for this condition.
Clinical evidence
Part 1 covers the same condition without the technical detail. What follows is the evidence base behind it, written for clinicians — the literature, the reasoning and the gaps.
For clinicians: this summary supports clinical reasoning and is not a protocol. Check current guidelines and local policy before applying it, and read it alongside the key references and guidelines directory.
Framing. The 2024 ESC guideline reframed blood pressure as a continuous risk factor with an "elevated" category below the hypertensive threshold, and lowered the systolic target for most treated adults toward 120–129 mmHg where tolerated — a direction set by SPRINT, in which intensive control reduced cardiovascular events and mortality at the cost of more adverse events.1,2,3 Exercise is not adjunctive advice in this setting: it is an antihypertensive intervention with a measurable dose–response.
Exercise as antihypertensive therapy
- Aerobic training lowers resting blood pressure by roughly 3–5 mmHg systolic on average, with substantially larger reductions (around 8/6 mmHg) in people who are hypertensive at baseline.4
- Isometric resistance training produced the largest reductions in a network meta-analysis of exercise modalities — around 8/4 mmHg — ahead of aerobic, dynamic resistance and combined training, using simple protocols such as wall squats or handgrip holds.5
- Dynamic resistance and combined training also lower blood pressure and should not be withheld; the older advice to avoid strength work in hypertension is not supported for controlled patients.5
- Post-exercise hypotension — a fall of up to 10 mmHg persisting for hours after a single session — contributes to the chronic effect and explains why session frequency matters more than session length.4
Non-exercise lifestyle evidence
- The DASH dietary pattern with sodium reduction produced blood-pressure falls comparable to single-drug therapy, with the largest effect at the lowest sodium intake.6
- Sodium reduction alone lowers blood pressure in a dose-dependent manner in both hypertensive and normotensive people.7
- Reducing alcohol intake lowers blood pressure in heavier drinkers, with benefit proportional to the reduction achieved.8
- Out-of-office measurement is essential: home and ambulatory monitoring identify white-coat and masked hypertension, which change management in a substantial minority.1,9
- Obstructive sleep apnoea is a leading contributor to resistant hypertension and to non-dipping nocturnal patterns; treating it produces modest but real blood-pressure reduction.10
Physiotherapy implications
- Measure properly and act on it: correct cuff size, seated and rested, arm supported at heart level, repeat readings, and check both arms at first assessment. A single high reading is not a diagnosis.1
- Prescribe the modality that suits the patient — isometric protocols are attractive because they are brief, equipment-light and home-deliverable, and can be combined with aerobic work rather than replacing it.5
- Avoid maximal isometric effort and Valsalva in uncontrolled hypertension, aortopathy or proliferative retinopathy; teach continuous exhalation through effort and progress load gradually.
- Anticipate medication effects in session: beta blockade blunts heart-rate response (prescribe by RPE), diuretics and alpha blockers cause postural hypotension, and ACE inhibitors and ARBs contribute to dizziness with dehydration and heat.
- Defer exercise and refer when resting blood pressure is around 180/110 mmHg or higher, and stop the session for exertional hypotension, headache with visual change, chest pain or new neurological symptoms. Note that sources differ: this 180/110 mmHg figure comes from exercise-in-hypertension guidance and applies to deferring training; the ATS six-minute-walk statement sets a relative caution at 180/100 mmHg for testing, as stated on the six-minute walk test page. Both are guidance rather than a threshold that decides for you.
- Screen for secondary and contributing causes to route back to the GP: snoring and witnessed apnoeas, high alcohol intake, NSAID and decongestant use, and very young onset or abrupt loss of control.1,10
Clinical reasoning
- Blood pressure is a treatment target rather than a symptom — most patients feel nothing, so adherence rests on explanation rather than experience.
- An isolated in-clinic elevation warrants out-of-office confirmation, not immediate escalation.9
- Established target-organ damage — left ventricular hypertrophy, albuminuria, retinopathy, prior stroke — changes the intensity of the whole programme and the appetite for high-load work.
- Frame exercise dose in the same language as pharmacotherapy: frequency, intensity, duration and expected millimetres of mercury.4,5
Evidence gaps
- Isometric training trials are numerous but small and short, with little long-term or hard-outcome data.5
- Optimal exercise dose for blood pressure in older, frail and multimorbid populations is undefined.
- Durability of exercise-induced reduction after supervision ends is poorly characterised.
- Whether exercise-attributable blood-pressure reduction translates into the same event reduction as drug-attributable reduction has never been tested directly.
References for the clinical evidence summary
- McEvoy JW, McCarthy CP, Bruno RM, et al. 2024 ESC guidelines for the management of elevated blood pressure and hypertension. Eur Heart J 2024;45(38):3912–4018.
- National Heart Foundation of Australia. Guideline for the diagnosis and management of hypertension in adults 2016. Melbourne: NHFA; 2016.
- SPRINT Research Group. A randomized trial of intensive versus standard blood-pressure control. N Engl J Med 2015;373(22):2103–2116.
- Cornelissen VA, Smart NA. Exercise training for blood pressure: a systematic review and meta-analysis. J Am Heart Assoc 2013;2(1):e004473.
- Edwards JJ, Deenmamode AHP, Griffiths M, et al. Exercise training and resting blood pressure: a large-scale pairwise and network meta-analysis of randomised controlled trials. Br J Sports Med 2023;57(20):1317–1326.
- Sacks FM, Svetkey LP, Vollmer WM, et al. Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. N Engl J Med 2001;344(1):3–10.
- He FJ, Li J, MacGregor GA. Effect of longer term modest salt reduction on blood pressure: Cochrane systematic review and meta-analysis of randomised trials. BMJ 2013;346:f1325.
- Roerecke M, Kaczorowski J, Tobe SW, Gmel G, Hasan OSM, Rehm J. The effect of a reduction in alcohol consumption on blood pressure: a systematic review and meta-analysis. Lancet Public Health 2017;2(2):e108–e120.
- Stergiou GS, Palatini P, Parati G, et al. 2021 European Society of Hypertension practice guidelines for office and out-of-office blood pressure measurement. J Hypertens 2021;39(7):1293–1302.
- Pengo MF, Soranna D, Giontella A, et al. Obstructive sleep apnoea treatment and blood pressure: which phenotypes predict a response? A systematic review and meta-analysis. Eur Respir J 2020;55(5):1901945.
Corrections: If something on this page is wrong, out of date or unclear, we want to know. Email reception@inspireclinic.au with the page name and what you believe is incorrect. Substantive corrections are made promptly, and the guide’s version and last-updated date are changed to reflect it.