Hypertension - systemic, primary and secondary
Description
- The largest single contributor to global cardiovascular death and the most treatable
- *A number, not a disease* - manage it as one component of absolute cardiovascular risk
Classification - the thresholds moved, and the documents disagree
| Source | Hypertension defined as | Treatment target |
|---|---|---|
| NHFA/CSANZ (Australia, 2016) | >=140/90 | <140/90; <120 systolic if high absolute risk and tolerated |
| ESC 2024 | >=140/90, plus a new category "elevated BP" 120-139/70-89 | Systolic 120-129 if tolerated |
| AHA/ACC 2025 | >=130/80 | <130/80 |
| *Australian 2026 guideline* | Heart Foundation/Stroke Foundation/Hypertension Australia; due 2026 - check before quoting a target | - |
- Know that the definitional threshold and the target are different questions, and that Australian practice has historically used 140/90 with risk-based intensification
Patterns
- Isolated systolic hypertension - elderly, arterial stiffening; the commonest pattern >60
- White coat hypertension - raised in clinic, normal out of clinic (~15-20%); not benign, but lower risk
- Masked hypertension - normal in clinic, raised out of clinic; higher risk than sustained hypertension because it goes untreated
- Resistant hypertension - BP above target on 3 drugs including a diuretic, at maximally tolerated doses
- Hypertensive urgency vs emergency - the discriminator is acute end-organ damage, not the number
Epidemiology
- ~1 in 3 Australian adults; only ~32% of those treated are controlled (the target of the National Hypertension Taskforce is 70% by 2030)
- Prevalence rises steeply with age; >60% over age 70
- 95% primary (essential); ~5-10% secondary - higher (up to 20-30%) in resistant, young-onset or abrupt-onset hypertension
- Aboriginal and Torres Strait Islander peoples: earlier onset, higher rates, greater renal and stroke burden
Aetiopathogenesis
Primary (essential)
- Polygenic + environmental: age, obesity, dietary sodium, alcohol, inactivity, low potassium intake, stress, low birth weight
- Mechanism: inc sympathetic tone + inc RAAS activity + renal sodium retention -> inc peripheral resistance
- -> arterial remodelling and stiffening -> self-reinforcing
Secondary causes - classify to remember
Renal
- Renal parenchymal disease - the commonest secondary cause overall (diabetic nephropathy, glomerulonephritis, PCKD, reflux nephropathy)
- Renovascular
- Atherosclerotic renal artery stenosis - older, smokers, vascular disease elsewhere; flash pulmonary oedema, AKI on ACEi/ARB
- Fibromuscular dysplasia - young women, "string of beads" on angiography
Endocrine
- Primary aldosteronism (Conn's) - *the commonest endocrine cause; 5-10% of all hypertension and up to 20% of resistant hypertension - and under-diagnosed*
- Hypertension + hypokalaemia (though most are normokalaemic), metabolic alkalosis
- Phaeochromocytoma/paraganglioma - episodic headache, palpitations, sweating, paroxysmal or labile BP
- Cushing's syndrome
- Congenital adrenal hyperplasia - 11-beta-hydroxylase and 17-alpha-hydroxylase deficiency (both cause hypertension with hypokalaemia; 21-hydroxylase deficiency does not)
- Acromegaly, thyrotoxicosis, hypothyroidism, hyperparathyroidism/hypercalcaemia
- Liddle syndrome, apparent mineralocorticoid excess (liquorice)
Vascular
- Coarctation of the aorta - radiofemoral delay, upper > lower limb BP, rib notching
Drugs and other
- Alcohol (a very common and reversible contributor), NSAIDs, corticosteroids, combined oral contraceptive, venlafaxine/SNRIs, ciclosporin/tacrolimus, VEGF inhibitors, decongestants, cocaine/amphetamines, liquorice, erythropoietin
- Obstructive sleep apnoea
- Polycythaemia vera, uraemia, pre-eclampsia, acute intermittent porphyria, hypercalcaemia, raised ICP
Diagnosis
Confirming the diagnosis
- *Never diagnose on a single clinic reading*
- Out-of-office measurement is required: ambulatory BP monitoring (preferred) or home BP monitoring
- ABPM thresholds: daytime average >=135/85, 24-hour >=130/80, night-time >=120/70
- Identifies white coat and masked hypertension; nocturnal non-dipping and reverse dipping are independently prognostic
- Correct technique: rested 5 min, seated, back supported, arm at heart level, correct cuff size (a small cuff on a large arm falsely elevates), average of 2-3 readings, both arms initially
Assessment - three questions
A. Is it primary or secondary?
- Screen for secondary causes if:
- Onset <30 or >55 years, or abrupt onset
- Resistant hypertension
- Hypokalaemia (spontaneous or diuretic-provoked)
- Malignant/accelerated hypertension, end-organ damage out of proportion
- Symptoms or signs suggesting a specific cause
- Some now argue for screening ALL hypertensive patients for primary aldosteronism at least once
- Aldosterone:renin ratio (interpretation confounded by beta blockers, ACEi/ARB, MRA, diuretics - ideally washed out; verapamil SR, prazosin, hydralazine and moxonidine are BP-safe substitutes)
- Plasma or 24h urinary metanephrines; overnight dexamethasone suppression; renal artery imaging (CTA/MRA/duplex); polysomnography
B. Is there end-organ damage?
- Heart - ECG (LVH, strain), echo (LVH, diastolic dysfunction), NT-proBNP
- Kidney - eGFR, urine albumin:creatinine ratio (the earliest and cheapest marker)
- Eye - fundoscopy: AV nipping, silver wiring, haemorrhages/exudates (grade 3), papilloedema (grade 4 = emergency)
- Brain - stroke, TIA, cognitive impairment, white matter disease
- Vessels - peripheral pulses, bruits, ABI
C. What is the absolute cardiovascular risk?
- Australian CVD risk calculator (2023) - not BP alone
- Bloods: UEC, glucose/HbA1c, lipids, urate, TFT, FBE
Hypertensive emergency
- Severely raised BP with acute end-organ damage: encephalopathy, papilloedema, acute LV failure/pulmonary oedema, ACS, aortic dissection, AKI, microangiopathic haemolysis (malignant hypertension), eclampsia
- *Without end-organ damage it is "urgency" - the number alone does not warrant IV therapy*
Management
A. Lifestyle - in everyone
Ranked roughly by average BP reduction
| Intervention | Approximate systolic reduction |
|---|---|
| Dietary pattern change (DASH-type) | ~11 mmHg - the largest single measure |
| Weight loss | ~1 mmHg per kg lost, up to ~5-20 |
| Sodium restriction (<2 g/day sodium) | ~5-6 |
| Physical activity (150 min/week aerobic + resistance) | ~5-8 |
| Alcohol reduction | ~4 |
| Potassium-enriched salt substitute | ~4-5 (strong stroke-reduction evidence) |
- Smoking cessation - does not lower BP but is the largest cardiovascular gain
B. When to start drug therapy
- Immediately if BP >=160/100, or established cardiovascular disease, diabetes, CKD, or high absolute risk
- Otherwise trial lifestyle for 3-6 months first, then treat if still above target
- *Treat to a target, and start with two agents if BP is >20/10 above target*
C. Drug choice - Australian first-line options
ACEi or ARB, calcium channel blocker, or thiazide-like diuretic - all first line; beta blockers are NOT first line unless there is another indication
| Class | Prefer when | Avoid/caution |
|---|---|---|
| ACEi / ARB | Diabetes, CKD with albuminuria, HFrEF, post-MI, young | *Pregnancy (teratogenic), bilateral renal artery stenosis, hyperkalaemia. Never combine ACEi + ARB* |
| CCB (amlodipine) | Elderly, isolated systolic hypertension, African ancestry, pregnancy (nifedipine) | Ankle oedema, gum hypertrophy |
| Thiazide-like (indapamide, chlortalidone) | Elderly, isolated systolic, heart failure | Hyponatraemia, hypokalaemia, gout, glucose intolerance |
| Beta blocker | Angina, post-MI, HFrEF, AF rate control, aortopathy, pregnancy (labetalol) | Asthma, bradycardia, masks hypoglycaemia |
| Spironolactone | *4th-line agent of choice in resistant hypertension (PATHWAY-2)*; primary aldosteronism | Hyperkalaemia, gynaecomastia (eplerenone as alternative) |
- Single-pill combinations improve adherence and control - use them early
- Typical escalation: ACEi/ARB + CCB -> add thiazide-like diuretic -> add spironolactone
- Then: beta blocker, alpha blocker, centrally acting agent (moxonidine, methyldopa), hydralazine, minoxidil
- Renal denervation - an option in genuinely resistant hypertension in selected centres
D. Special situations
- Pregnancy - labetalol, methyldopa, nifedipine; *ACEi, ARB and MRA are contraindicated*; treat >=140/90; aspirin from 12 weeks if pre-eclampsia risk
- CKD - ACEi/ARB with albuminuria; add SGLT2i; finerenone in diabetic kidney disease
- Diabetes - ACEi/ARB first; target <130/80
- Elderly/frail - individualise; treat (HYVET, SPRINT show benefit even in the old) but watch postural hypotension and falls
- Primary aldosteronism - adrenalectomy for a unilateral adenoma (after adrenal vein sampling), MRA for bilateral hyperplasia
- Phaeochromocytoma - *alpha blockade (phenoxybenzamine/prazosin) BEFORE beta blockade* - unopposed alpha stimulation precipitates hypertensive crisis
E. Hypertensive emergency
- IV therapy in a monitored setting: GTN (pulmonary oedema), esmolol/labetalol (dissection, with a vasodilator), hydralazine or labetalol (eclampsia), sodium nitroprusside, clevidipine
- *Reduce MAP by no more than 20-25% in the first hour*, then to ~160/100 over 2-6 h
- Faster correction -> cerebral, coronary and renal hypoperfusion (autoregulation is shifted rightward)
- Exceptions requiring rapid control: aortic dissection (target SBP <120 and HR <60 within minutes), eclampsia, and acute pulmonary oedema
- *In acute ischaemic stroke do NOT lower BP* unless >220/120, or thrombolysis/thrombectomy planned (then <185/110)
F. Adherence - the commonest cause of "resistant" hypertension
- Simplify to once-daily single-pill combinations
- Ask directly and non-judgementally; consider urine or serum drug-level screening in true resistance
- Home BP monitoring improves control
Associations
- Stroke - the strongest association of all (both ischaemic and haemorrhagic)
- Ischaemic heart disease, heart failure (both HFrEF and HFpEF), LVH, atrial fibrillation
- Aortic dissection and aneurysm
- CKD and ESKD; hypertensive nephrosclerosis
- Hypertensive retinopathy, retinal vein/artery occlusion
- Vascular dementia and cognitive decline - mid-life hypertension is a leading modifiable dementia risk factor
- Obstructive sleep apnoea, obesity, metabolic syndrome, T2DM
- Pre-eclampsia - and a doubled lifetime cardiovascular risk afterwards
- Erectile dysfunction, peripheral arterial disease
Natural history & complications
- Continuous log-linear relationship with cardiovascular risk from 115/75 upward - no threshold below which risk stops falling
- Every 20/10 mmHg increase roughly doubles cardiovascular mortality
- A 10 mmHg systolic reduction gives approximately: dec stroke ~27%, dec coronary events ~17%, dec heart failure ~28%, dec all-cause mortality ~13%
- Untreated: progressive LVH -> diastolic dysfunction -> HFpEF; nephrosclerosis -> CKD -> ESKD
- Malignant/accelerated hypertension untreated: ~1-year mortality historically >80%; near-normal with treatment
- Blood pressure control rates remain poor worldwide - the gap is detection, adherence and therapeutic inertia, not the availability of effective drugs
- Primary aldosteronism carries excess cardiovascular and renal risk beyond that explained by the BP, and it is reversible - which is why finding it matters
🔒
6 more sections, plus exam facts
Premium unlocks every note across every specialty, and the full exam fact library behind it.
Get premium access