Hypertension

Meet the patient

A 52-year-old lorry driver turns up for an insurance medical feeling entirely well. He smokes fifteen a day, carries a BMI of 31, and his father died of a stroke at 58. The nurse records 168/96 mmHg; you repeat it after five minutes of seated rest and get 164/94, then 160/92 in the other arm.^[1]

He has never had his pressure checked. Fundoscopy is unremarkable and the heart sounds are normal, but the apex beat is thrusting and just displaced. The exam question is now live, and it is not "what is the number" — it is is this real, is there a cause worth finding, and has the pressure already done silent damage?^[5]

Everything below answers those three questions at consultant depth, ending in the one mantra you can repeat on any ward round: confirm before you treat, lower slowly, choose by comorbidity.^[1]

Two thresholds, one target — the guideline split

Both major guidelines land on the same treatment goal; they only disagree on the label. The 2018 ESC/ESH keeps the diagnosis at office BP at least 140/90 mmHg; the 2017 ACC/AHA dropped it to at least 130/80 mmHg.^[5][1]

The split is mostly semantic, but examiners test both columns, so learn both. The 2024 ESH update aligns the European systolic target to 130 to 139 mmHg when tolerated, narrowing the gap further.^[7]

^{[1] [5]}

Confirm before you treat — the white-coat and masked trap

Never start lifelong therapy on one clinic reading. Up to a third of clinic hypertension is white-coat (raised only with you in the room) and up to fifteen percent is masked (normal in clinic, high at home) — both are common and both mislead.^[5]

Confirm with ambulatory or home monitoring. The 2018 ESC/ESH out-of-office cut-offs to reproduce verbatim: 24-hour average under 130/80, daytime under 135/85, night-time under 120/70, home average under 135/85 mmHg.^[5]

^{[5] [1] [5]}

The 95/5 split — and when five becomes thirty

Ninety-five percent of hypertension is primary (essential) — no single cause, just the sum of genes, salt, weight, age and sympathetic tone. Five percent is secondary, but that five climbs to ten to thirty percent in anyone under 40 and in resistant hypertension, which is exactly where the hunt pays off.^[1]

Go looking when the patient is young, resistant to three drugs, hypokalaemic, carrying an abdominal bruit, describing paroxysms, or showing radio-femoral delay. A cause found is a cause fixed — sometimes surgically.^[5]

^[1]

Why the pressure rises — four mechanisms, four drug targets

Arterial pressure is cardiac output multiplied by systemic vascular resistance, and chronic hypertension locks one or both high. Four loops do the locking, and each one explains a drug class.^[1]

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• Renal pressure-natriuresis shifted right — the kidney now needs a higher pressure to excrete sodium; salt-sensitivity is why thiazides work in whoever is in front of you.
• RAAS overdrive — angiotensin II constricts and aldosterone retains sodium while wasting potassium; the target of ACE inhibitors, ARBs and spironolactone.
• Sympathetic overactivity — drives white-coat, sleep-apnoea and obesity hypertension, and is why beta-blockers and methyldopa still have jobs.
• Endothelial dysfunction and arterial stiffening — nitric oxide falls, endothelin rises, and a stiff aorta produces isolated systolic hypertension in the elderly.^[1]

A high resting heart rate rides on top of all of this as an independent prognostic signal — in high-risk cohorts it tracks cardiovascular harm beyond the pressure itself.^[14]

Untreated hypertension damages every vascular bed, slowly and silently. The heart hypertrophies, the brain strokes, the kidney scars, the retina burns, and the aorta tears.^[1]

Left ventricular pressure overload drives concentric LVH, then diastolic dysfunction and HFpEF, eventually HFrEF; the cerebral bed seeds lacunar infarcts and intracerebral bleeds; the renal bed develops arteriolar hyalinosis and CKD; the aorta dilates and dissects.^[1]

The retina is the one bed you can see, and its Keith-Wagener-Barker grades are pure exam marks.^[5]

^[5]

The silent killer speaks late — recognise the few who symptomise

Most hypertensives feel entirely well; symptoms mean the pressure is either very high or organ-damaging right now. Screen opportunistically from forty and at every pregnancy, pre-operative and diabetes visit.^[1]

• Early-morning occipital headache — rising intracranial pressure in encephalopathy.
• Visual blur or diplopia — grade 3 or 4 retinopathy on fundoscopy.
• Exertional dyspnoea, orthopnoea, ankle swelling — heart failure.
• Nocturia and frothy urine — nephropathy.
• Paroxysmal pressure with headache, sweat, palpitation and pallor — think phaeochromocytoma.^[1]

At the bedside — measure, then hunt for the cause

Examination rarely diagnoses hypertension; it stages it and leaks clues to a secondary cause. Spend two minutes doing it properly.^[1]

• Cardiac — a thrusting, displaced apex and a fourth heart sound mean LVH; an aortic diastolic murmur means root dilatation.
• Fundoscopy — the Keith-Wagener-Barker grades, live and visible.
• Abdomen — an epigastric bruit (renal artery stenosis, present in about half), palpable kidneys (polycystic), an expansile aorta.
• Peripheral — radio-femoral delay or an arm-to-leg BP gap (coarctation), absent foot pulses.
• Neuro — residual focal deficit, cognitive screening.^[1]

Investigations — confirm, stage, chase the clue

Three jobs: confirm severity, stage the end-organ damage, and chase a secondary cause only when a clue points to one. Blind panels are not the answer.^[1]

First-line for every new hypertensive: a 12-lead ECG (LVH by Sokolow-Lyon — S in V1 plus R in V5 or V6 at least 35 mm), echocardiogram, urea, creatinine, eGFR, electrolytes, fasting glucose, HbA1c, lipids, TSH, urinalysis with albumin-to-creatinine ratio, and renal ultrasound.^[5]

Then chase the clue: renin and aldosterone for Conn; 24-hour metanephrines for phaeo; overnight dexamethasone suppression for Cushing; CT or MR angiography for renal artery stenosis and fibromuscular dysplasia; polysomnography for sleep apnoea.^[1]

Quantify the ten-year risk with a validated equation — the AHA PREVENT tool extends risk prediction across diverse populations and is the modern adjunct to SCORE2 and ASCVD when you are deciding whom to treat.^[15]

Lifestyle first — the cheapest millimetres of mercury

Every patient gets lifestyle advice at every visit; it is the foundation, not the preamble. The gains are real and they are measurable.^[1]

• Sodium under 2 g per day — roughly 3 to 4 mmHg systolic.^[16]
• DASH diet — fruit, vegetables, low-fat dairy and wholegrain over a control diet; about 3 mmHg systolic and 3 diastolic across 30 trials.^[17]
• Weight loss — about 1 mmHg systolic per kilogram lost.^[18]
• Aerobic exercise — about 8 mmHg systolic in established hypertension and less at normal pressures; 150 minutes a week is the usual prescription.^[19]
• Alcohol cut by half in heavier drinkers — about 5 mmHg systolic when intake falls from six or more drinks a day; stop tobacco.^[20]

Drug by comorbidity — the table that earns its marks

Four classes share first line — ACE inhibitor, ARB, calcium-channel blocker, thiazide-like diuretic — and the class is chosen by the patient in front of you, not by habit.^[5]

Across 147 trials the benefit tracks the fall in pressure, not the class: any of the four prevents events per millimetre of mercury lowered, which is why combination beats escalation.^[8]

^[5]

Combine early — the ACCELERATE and ASCOT evidence

Most patients need two drugs, so start combined and titrate rather than crawl up one agent. ACCELERATE proved initial benazepril plus amlodipine controlled pressure earlier than monotherapy escalation, and ASCOT-BPLA showed an amlodipine-based regimen outperformed an atenolol-based one across both older and younger patients.^[12][13]

This is exactly why beta-blockers are no longer first line for uncomplicated hypertension — reserve them for a separate indication such as post-MI, HFrEF or atrial fibrillation rate control.^[5]

The step ladder — monotherapy to spironolactone

Step up every four weeks until target, combining before you max any single drug. A single-pill combination beats a handful of tablets for adherence.^[5]

^[5]

Resistant hypertension — spironolactone is the fourth drug

Resistant hypertension is pressure above target on three or more drugs at optimal dose including a diuretic. Before reaching for a fourth agent, exclude non-adherence, the white-coat effect, over-the-counter NSAIDs, and an undiagnosed secondary cause.^[10]

PATHWAY-2 settled the choice: spironolactone 25 to 50 mg daily beat bisoprolol, doxazosin and placebo as the fourth-line agent. Serum potassium exceeded 6 mmol per litre in 6 of 285 patients on spironolactone, so recheck it after starting.^[10]

Targets — how low, for whom

Lower is better, but only as far as the patient tolerates. The target moves with the phenotype.^[5]

• Most adults — under 140/90 mmHg; 130 to 139 systolic if tolerated.
• Diabetes, CKD or high cardiovascular risk — under 130/80 mmHg.
• Fit, younger, high-risk — intensive to systolic 120 to 129 mmHg when tolerated, on the SPRINT evidence.
• Over-eighties — 130 to 149 systolic, guided by standing BP and falls.^[5]

SPRINT drove the intensive case: a systolic target under 120 mmHg cut cardiovascular events by about a quarter and all-cause mortality by just over a quarter in high-risk, non-diabetic adults.^[9]

HOPE-3 makes the prevention point from the other end — lowering pressure in intermediate-risk people without established disease reduced events, and the benefit was driven entirely by those starting above 143 mmHg systolic.^[11]

Emergency vs urgency — the discriminator is the organ, not the number

A hypertensive emergency is severe BP plus acute target-organ damage; everything else is urgency. The number does not decide this — the brain, heart, kidney, eye or aorta does.^[1]

A patient at 220/120 who is chronic and asymptomatic is urgency; a patient at 180/120 with tearing chest pain or a new hemiparesis is an emergency. The two are managed completely differently.^[5]

^{[1] [5]}

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^[1]

Do not crash the BP — the shifted autoregulation rule

Emergency drugs — pick by the organ in trouble

No single drug fits every emergency; match the agent to the target-organ syndrome. All are titrated, in HDU or ICU, with intra-arterial monitoring.^[1]

^[1]

Scenario-specific targets — the exam favourites

Each emergency carries its own number and its own order of operations. Memorise the target, not the general rule.^[1]

• Intracerebral haemorrhage — intensive lowering to systolic under 140 mmHg within 1 hour improved functional outcome over the old under-180 target.^[21]
• Ischaemic stroke with thrombolysis — systolic above 185 or diastolic above 110 mmHg before treatment is a contraindication to lysis.^[22]
• Phaeochromocytoma — alpha-blockade with volume expansion first, beta-blocker second.^[23]
• Eclampsia — magnesium sulphate, about 4 g IV loading then 1 g per hour; delivery follows once the mother is stable.^[24][25]

Pregnancy — the teratogenic trap

ACE inhibitors and ARBs are absolutely contraindicated in pregnancy. The safe antihypertensives are labetalol, nifedipine and methyldopa.^[1]

Seizures in pre-eclampsia mean eclampsia. Magnesium sulphate halves the risk of eclampsia compared with placebo; give about 4 g IV loading then 1 g per hour, and deliver once the mother is stable.^[24][25] In women at high risk, aspirin 81 mg daily from 12 weeks of gestation reduces pre-eclampsia.^[26]

Preventable harm — what good treatment actually stops

The evidence ledger — trials that changed practice

^{[9] [10] [6] [8]}

Regional practice — same evidence, local flavour

Exam pearls — the high-yield one-liners

• Confirm before you treat — clinic systolic at least 140 mmHg plus out-of-office readings before you commit anyone to more tablets.^[10]
• First line is ACE inhibitor, ARB, CCB or thiazide-like — every class lowers pressure by about the same per millimetre, so choose by comorbidity.^[8] Never combine an ACE inhibitor with an ARB — ONTARGET showed more renal harm and hypotension with no cardiovascular gain.^[6]
• Targets — under 140/90 for most; intensive to systolic 120 to 129 when tolerated in high-risk, non-diabetic adults (SPRINT: about a quarter fewer cardiovascular events and deaths).^[9]
• Resistant hypertension — add spironolactone 25 to 50 mg daily; it beat bisoprolol, doxazosin and placebo as the fourth drug (PATHWAY-2).^[10]
• Phaeochromocytoma — alpha-blockade with volume expansion first, then beta-block.^[23]
• Pregnancy — no ACE inhibitor or ARB; eclampsia is magnesium sulphate, about 4 g IV loading then 1 g per hour, plus delivery; aspirin 81 mg daily from 12 weeks in high-risk women.^[24][26]

Ward-round test

A 30-year-old with BP 170/110, spontaneous hypokalaemia and an abdominal bruit — what is the single most likely diagnosis, and which drug must you avoid jumping to?ShowHide

Think primary aldosteronism (Conn) — hypertension with spontaneous or diuretic-induced hypokalaemia, suppressed renin and raised aldosterone. Screen with a plasma aldosterone-to-renin ratio before starting any ACE inhibitor, ARB or diuretic, all of which distort the result.^[1]

BP 200/120 with tearing back pain and unequal arm pressures — what is your first drug, and what is the target?ShowHide

This is acute aortic dissection until proven otherwise — urgent CT aortogram, and beta-block first (IV labetalol or esmolol) to drop dP/dt, targeting systolic under 120 mmHg within 20 minutes and heart rate under 60, before adding a vasodilator. Vasodilating first reflexively tachycardics the patient and worsens the dissection.^[1]

Above target on an ACE inhibitor, amlodipine and a full-dose thiazide — what is the next move, and which trial backs it?ShowHide

This is resistant hypertension — pressure above target on three drugs including a diuretic. Add spironolactone 25 to 50 mg daily on top of the maximally tolerated three; it beat bisoprolol, doxazosin and placebo as the fourth agent in PATHWAY-2. Serum potassium exceeded 6 mmol per litre in 6 of 285 patients on spironolactone, so recheck it after starting.^[10]

A paroxysm of severe BP with headache, sweating and pallor — name the syndrome, the screening test, and the blockade order.ShowHide

This is phaeochromocytoma (the 5 Ps — Pressure, Pain, Perspiration, Palpitation, Pallor). Screen with 24-hour urinary fractionated metanephrines, and when you treat, alpha-block first (phenoxybenzamine or phentolamine), then beta-block — reversing the order provokes hypertensive crisis from unopposed alpha stimulation.^[1]

References26ShowHide

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