Hypertension & Its Management

Hypertension is the single most important modifiable risk factor for cardiovascular and cerebrovascular mortality worldwide, and a perennial NEET PG favourite. This note covers definition and staging, white-coat and masked patterns, secondary causes, emergencies versus urgencies, and—most heavily tested—first-line drug selection with compelling indications in special populations.

Definition & classification

Hypertension is a sustained elevation of arterial blood pressure (BP) above a defined threshold, measured on at least two separate occasions in a properly seated patient after 5 minutes of rest. The threshold itself depends on the guideline used, and examiners exploit the difference between the older JNC framework and the 2017 ACC/AHA reclassification.

Category	ACC/AHA 2017 (mmHg)	JNC 7 (older, still examined)
Normal	<120 and <80	<120 and <80
Elevated	120–129 and <80	Prehypertension 120–139 or 80–89
Stage 1	130–139 or 80–89	Stage 1: 140–159 or 90–99
Stage 2	≥140 or ≥90	Stage 2: ≥160 or ≥100

High-yield: The ACC/AHA 2017 guideline lowered the diagnostic cut-off to 130/80, abolished "prehypertension," and is the most commonly tested modern threshold. JNC 8 (2014) focused on treatment goals and famously relaxed the target to <150/90 in adults ≥60 years without diabetes or CKD.

By aetiology hypertension is divided into:

• Primary (essential) hypertension — 90–95% of cases; no single identifiable cause; multifactorial (genetic predisposition, salt sensitivity, sympathetic overactivity, obesity).
• Secondary hypertension — 5–10%; an identifiable, often correctable cause. Suspect when onset is <30 or >55 years, hypertension is resistant/accelerated, or there are suggestive clues.

A few important clinical phenotypes:

• White-coat hypertension: elevated office BP (≥140/90) but normal out-of-office BP (home/ambulatory). Carries lower but not negligible risk.
• Masked hypertension: normal office BP but elevated out-of-office BP. Dangerous because it is missed; carries near-equivalent cardiovascular risk to sustained hypertension.
• Resistant hypertension: BP above goal despite three drugs (including a diuretic) at optimal doses, or controlled BP requiring four or more drugs.
• Isolated systolic hypertension (ISH): SBP ≥140 with DBP <90; typical of the elderly due to arterial stiffening.

High-yield: Ambulatory BP monitoring (ABPM) is the gold standard for diagnosing white-coat and masked hypertension and for detecting non-dipping. A normal night-time fall in BP is 10–20%; a non-dipper (<10% nocturnal fall) has higher cardiovascular risk and suggests secondary causes such as obstructive sleep apnoea or CKD.

Etiology & pathophysiology

BP is the product of cardiac output and systemic vascular resistance (BP = CO × SVR). Chronic elevation arises from a shift in the renal pressure-natriuresis relationship, sympathetic nervous system overactivity, and inappropriate activation of the renin-angiotensin-aldosterone system (RAAS).

• RAAS: Renin (from juxtaglomerular cells) converts angiotensinogen to angiotensin I; ACE (mainly pulmonary) converts it to angiotensin II—a potent vasoconstrictor that also stimulates aldosterone (sodium/water retention) and remodelling. This pathway is the target of ACE inhibitors and ARBs.
• Salt sensitivity: common in Indians, the elderly, obese, and CKD patients; explains efficacy of diuretics and salt restriction.
• Endothelial dysfunction: reduced nitric oxide bioavailability raises vascular tone.

End-organ damage (target-organ damage, TOD) results from sustained pressure load: left ventricular hypertrophy (concentric), accelerated atherosclerosis, nephrosclerosis, retinopathy, and small-vessel cerebral disease.

Causes of secondary hypertension

Cause	Key clue / clinical pearl
Renal parenchymal disease	Most common secondary cause overall; raised creatinine, proteinuria
Renovascular (renal artery stenosis)	Young woman → fibromuscular dysplasia; older → atherosclerosis; abdominal bruit; rise in creatinine after ACEi
Primary hyperaldosteronism (Conn)	Hypertension + hypokalaemia + metabolic alkalosis; high aldosterone, low renin (↑ aldosterone:renin ratio)
Phaeochromocytoma	Episodic headache, palpitations, sweating; "rule of 10s"; raised plasma/urinary metanephrines
Cushing syndrome	Central obesity, striae, moon face; raised cortisol
Coarctation of aorta	Upper-limb hypertension, weak/delayed femoral pulses (radio-femoral delay); rib notching
Obstructive sleep apnoea	Obese, snoring, daytime somnolence; non-dipping
Drugs	OCPs, NSAIDs, steroids, decongestants, erythropoietin, cocaine

High-yield: The triad of hypertension + spontaneous hypokalaemia + metabolic alkalosis points to primary hyperaldosteronism (Conn syndrome). Screening test = plasma aldosterone-to-renin ratio (ARR); confirmation by saline suppression test; subtype localisation by adrenal venous sampling.

Clinical features

Most hypertension is asymptomatic—earning it the title "silent killer." When symptoms occur they reflect either very high pressure or established target-organ damage:

• Early-morning occipital headache, dizziness, epistaxis.
• Symptoms of complications: chest pain/dyspnoea (LVH, heart failure), visual disturbance (retinopathy), focal neurological deficit (stroke), claudication.
• Secondary-cause clues: episodic palpitations and sweating (phaeo), proximal weakness (Conn hypokalaemia), Cushingoid habitus.

Keith-Wagener-Barker classification of hypertensive retinopathy is a classic eponym:

1. Grade 1 — arteriolar narrowing (silver/copper wiring).
2. Grade 2 — AV nicking (Salus sign), focal spasm.
3. Grade 3 — flame haemorrhages, cotton-wool spots, hard exudates.
4. Grade 4 — Grade 3 + papilloedema (defines malignant/accelerated hypertension).

Diagnosis & investigation

Diagnostic flow: Accurate office measurement (correct cuff, seated, rested) → repeat on ≥2 visits → confirm with out-of-office measurement (ABPM or home BP) → assess target-organ damage and total cardiovascular risk → screen for secondary causes if clues present.

Baseline work-up for every newly diagnosed patient:

• Routine: fasting glucose/HbA1c, lipid profile, serum electrolytes (Na, K), urea, creatinine with eGFR, urinalysis (protein, blood), haemoglobin/haematocrit, serum uric acid.
• ECG — for LVH (Sokolow-Lyon: S in V1 + R in V5/V6 >35 mm) and ischaemia.
• Echocardiography — most sensitive for LVH; assesses diastolic dysfunction.
• Fundoscopy — retinopathy grading.
• Urine albumin:creatinine ratio — early renal damage.

Targeted secondary screening: ARR (Conn), plasma free metanephrines (phaeo), renal Doppler/CT or MR angiography (renal artery stenosis), overnight dexamethasone suppression (Cushing), polysomnography (OSA).

High-yield: A rise in serum creatinine >30% after starting an ACE inhibitor/ARB strongly suggests bilateral renal artery stenosis—these drugs are contraindicated there because efferent arteriolar dilatation drops glomerular filtration.

Management

Management combines lifestyle modification (for all) with pharmacotherapy guided by stage, total cardiovascular risk, and compelling indications.

Lifestyle modification (mnemonic: think DASH + WAVES)

• Diet — DASH diet (fruits, vegetables, low-fat dairy, low saturated fat).
• Alcohol reduction.
• Sodium restriction (<2 g sodium ≈ <5 g salt/day) — single most effective dietary measure.
• Weight reduction — ~1 mmHg fall per kg lost.
• Physical activity/aerobic Exercise (≥150 min/week).
• Smoking cessation (reduces overall CV risk).

High-yield: Approximate SBP reductions—weight loss ~5 mmHg, DASH diet ~11 mmHg, sodium restriction ~5–6 mmHg, exercise ~5–8 mmHg, alcohol moderation ~4 mmHg. DASH gives the greatest single dietary reduction.

First-line drug classes

The four first-line classes for uncomplicated hypertension are thiazide/thiazide-like diuretics, calcium-channel blockers (CCBs), ACE inhibitors, and ARBs. Beta-blockers are no longer first-line for uncomplicated hypertension (used when a compelling cardiac indication exists).

Class	Prototype	Mechanism	Notable adverse effect
Thiazide diuretic	Hydrochlorothiazide, chlorthalidone	↓ Na reabsorption at distal tubule	Hypokalaemia, hyperuricaemia/gout, hyperglycaemia, hypercalcaemia, hyponatraemia
Dihydropyridine CCB	Amlodipine, nifedipine	Vascular smooth-muscle relaxation	Ankle/pedal oedema, flushing, headache
Non-DHP CCB	Verapamil, diltiazem	Cardiac rate/contractility ↓	Bradycardia, constipation (verapamil); avoid with beta-blocker
ACE inhibitor	Enalapril, ramipril	Blocks ACE → ↓ angiotensin II	Dry cough (bradykinin), hyperkalaemia, angioedema; teratogenic
ARB	Losartan, telmisartan	Blocks AT1 receptor	Hyperkalaemia; teratogenic; no cough
Beta-blocker	Metoprolol, bisoprolol	↓ Cardiac output, ↓ renin	Bradycardia, fatigue, bronchospasm, mask hypoglycaemia

High-yield: ACE-inhibitor cough is due to bradykinin/substance P accumulation and is the classic reason to switch to an ARB (which does not cause cough). Angioedema is a more serious, life-threatening ACEi effect; ARBs carry a small cross-reactive risk.

Compelling indications (very high-yield)

Condition	Preferred drug(s)	Reason
Diabetes with albuminuria / CKD	ACE inhibitor or ARB	Renoprotective; reduce intraglomerular pressure & proteinuria
Heart failure (HFrEF)	ACEi/ARB (or ARNI) + beta-blocker + MRA (spironolactone)	Mortality benefit
Post-myocardial infarction	Beta-blocker + ACE inhibitor	Mortality benefit
Stable angina	Beta-blocker or CCB	Anti-anginal
Atrial fibrillation (rate control)	Beta-blocker or non-DHP CCB	Rate control
Isolated systolic HTN (elderly)	Thiazide or DHP CCB	Best evidence in elderly
Pregnancy	Labetalol, methyldopa, nifedipine	Fetal safety
Benign prostatic hyperplasia	Alpha-blocker (add-on)	Dual benefit

High-yield: In a diabetic with proteinuria/CKD, the drug of choice is an ACE inhibitor or ARB—do not combine the two (ONTARGET trial showed increased renal harm). In pregnancy, ACEi/ARBs are absolutely contraindicated (fetal renal dysgenesis, oligohydramnios); use labetalol, methyldopa, or nifedipine.

Choosing initial therapy & escalation

Stepwise approach:

1. Initiate lifestyle changes for all; start drug therapy at Stage 2 (or Stage 1 with high CV risk/established disease).
2. First drug by patient profile: ACEi/ARB in younger (<55 yr) non-Black patients and in diabetics/CKD; CCB or thiazide in older or Black patients.
3. Step up to two drugs (e.g., ACEi + CCB, or ACEi + thiazide) if not at goal—single-pill combinations improve adherence.
4. Three drugs: ACEi/ARB + CCB + thiazide.
5. Resistant HTN: add spironolactone (mineralocorticoid receptor antagonist)—the evidence-based fourth drug (PATHWAY-2 trial).

High-yield: For resistant hypertension on three drugs including a diuretic, the fourth agent of choice is spironolactone. Always first exclude pseudo-resistance (poor adherence, white-coat effect, improper measurement) and secondary causes.

Hypertensive emergency versus urgency

This distinction is a classic single-best-answer question.

Feature	Hypertensive emergency	Hypertensive urgency
BP	Usually >180/120	>180/120
Target-organ damage	Present (encephalopathy, MI, ACS, pulmonary oedema, aortic dissection, AKI, eclampsia, papilloedema)	Absent
Treatment route	IV, in ICU	Oral, outpatient
Goal	Reduce MAP by ~10–20% in 1st hour, then ~25% over 24 h	Gradual reduction over 24–48 h

High-yield: The cardinal rule—do NOT lower BP too fast. In hypertensive emergency, dropping MAP by more than ~25% in the first hour risks watershed cerebral, coronary, and renal ischaemia because autoregulation is shifted rightward.

Drug choices in emergencies:

• Hypertensive encephalopathy / general: IV labetalol, nicardipine, or sodium nitroprusside.
• Aortic dissection: IV beta-blocker (esmolol/labetalol) first to reduce shear stress (dP/dt), then add nitroprusside. Beta-blockade before vasodilator is essential.
• Acute pulmonary oedema: IV nitroglycerin + loop diuretic; avoid beta-blockers.
• Phaeochromocytoma crisis: Phenoxybenzamine (alpha-blockade) FIRST, then beta-blocker—never beta-block first (unopposed alpha causes a hypertensive crisis).
• Eclampsia: IV labetalol or hydralazine + magnesium sulphate for seizure prophylaxis.

High-yield: Sodium nitroprusside can cause cyanide/thiocyanate toxicity, especially in renal/hepatic impairment or prolonged infusion—watch for metabolic acidosis and altered mentation.

Complications

• Cardiac: LVH → diastolic and later systolic heart failure; accelerated coronary disease/MI; atrial fibrillation.
• Cerebrovascular: ischaemic and haemorrhagic stroke (hypertension is the strongest risk factor for intracerebral haemorrhage), hypertensive encephalopathy, vascular dementia. Charcot-Bouchard microaneurysms in lenticulostriate vessels rupture to cause basal ganglia bleeds.
• Renal: hypertensive nephrosclerosis, chronic kidney disease, malignant nephrosclerosis.
• Vascular: aortic aneurysm and aortic dissection, peripheral arterial disease.
• Ocular: hypertensive retinopathy, choroidopathy.

Key differentials

When a young patient or a resistant case presents, distinguish secondary causes:

• Phaeochromocytoma vs panic/thyrotoxicosis — episodic catecholamine surge with raised metanephrines distinguishes phaeo.
• Conn syndrome vs secondary hyperaldosteronism (renal artery stenosis, diuretic use) — renin is low in Conn, high in secondary forms.
• Coarctation vs essential hypertension — radio-femoral delay and arm–leg BP gradient.
• White-coat vs sustained hypertension — ABPM is decisive.
• Cushing vs metabolic syndrome — cortisol excess testing.

Recently asked / exam angle

• ACC/AHA 2017 cut-off of 130/80 and JNC 8 relaxed target <150/90 for ≥60 years are repeatedly asked—know which guideline gives which number.
• Mechanism-based MCQs: ACEi cough = bradykinin; DHP CCB = ankle oedema; verapamil = constipation; thiazide = hyperuricaemia/hypercalcaemia/hyperglycaemia (the "hyper" cluster) with hyponatraemia/hypokalaemia.
• Drug of choice scenarios: diabetic nephropathy → ACEi/ARB; pregnancy → labetalol/methyldopa/nifedipine; resistant HTN 4th drug → spironolactone; aortic dissection → beta-blocker first; phaeo → alpha-blocker first.
• Conn syndrome biochemistry (hypokalaemia + alkalosis, high aldosterone:renin ratio) and the confirmatory/localisation tests.
• Emergency vs urgency: presence of target-organ damage and the rule of not dropping MAP >25% in the first hour.
• Eponyms: Keith-Wagener-Barker retinopathy grades and Charcot-Bouchard microaneurysms.

Rapid revision

1. ACC/AHA 2017 diagnoses hypertension at ≥130/80; JNC 8 target is <150/90 in adults ≥60 years (else <140/90).
2. ABPM is the gold standard; it diagnoses white-coat and masked hypertension and detects non-dippers.
3. Masked hypertension (normal office, high out-of-office) carries risk similar to sustained hypertension.
4. Four first-line classes: thiazide, CCB, ACEi, ARB—beta-blockers are NOT first-line for uncomplicated HTN.
5. ACEi/ARB are renoprotective and the drug of choice in diabetes with proteinuria/CKD; never combine the two.
6. ACEi cough = bradykinin; switch to ARB. Angioedema is the dangerous ACEi effect.
7. Thiazides cause hypokalaemia, hyperuricaemia, hyperglycaemia, hypercalcaemia, hyponatraemia.
8. Conn syndrome: hypertension + hypokalaemia + alkalosis, high aldosterone:renin ratio; screen with ARR.
9. Resistant HTN 4th drug = spironolactone (PATHWAY-2).
10. Pregnancy: use labetalol, methyldopa, nifedipine; ACEi/ARB are teratogenic and contraindicated.
11. Hypertensive emergency = TOD present → IV drugs; lower MAP by only ~10–25% in the first hour.
12. Aortic dissection → beta-blocker before vasodilator; phaeochromocytoma → alpha-blocker before beta-blocker.