Hypertension

• Definition: sustained elevation of arterial pressure at or above 130/80 mmHg on repeated, properly measured readings (ACC/AHA 2017 Hypertension Guideline). Blood pressure is the product of cardiac output and systemic vascular resistance, so every cause of hypertension acts through one or both of these terms.
• Why it matters: pressure load is the dominant modifiable driver of atherosclerotic cardiovascular disease, and risk rises continuously and log-linearly with systolic pressure — there is no threshold below which risk abruptly disappears. Hypertension is the leading modifiable risk factor for stroke and a principal contributor to myocardial infarction, heart failure (both HFrEF and HFpEF), chronic kidney disease, atrial fibrillation, and aortic dissection.
• Silent disease: because the arterial tree tolerates high pressure without symptoms, damage accumulates in the heart, brain, kidney, and retina for years before presentation. This is the rationale for the USPSTF grade A recommendation to screen all adults 18 and older, with confirmation of elevated office readings outside the clinical setting before labeling and treating.

Epidemiology worth recalling

• Extremely common: prevalence rises steeply with age; under the 130/80 threshold roughly half of US adults qualify, and the majority of adults over 60 are affected.
• Isolated systolic hypertension predominates in older adults as large-artery stiffening widens pulse pressure; diastolic-predominant hypertension is more typical of younger patients with high sympathetic tone.
• Racial disparity: Black Americans develop hypertension earlier, reach higher pressures, and suffer disproportionate stroke, heart failure, and ESRD — a classic stem detail.
• Control rates are poor: a large fraction of hypertensive patients are undiagnosed, untreated, or treated but uncontrolled, which is why the exam repeatedly tests adherence, home monitoring, and combination therapy.

Secondary hypertension grouped by mechanism

• Renal parenchymal: chronic glomerulonephritis, diabetic nephropathy, polycystic kidney disease — sodium/volume retention plus inappropriate renin release. Most common secondary cause overall.
• Renovascular: atherosclerotic renal artery stenosis in older smokers; fibromuscular dysplasia ("string of beads") in young women. Reduced afferent perfusion → renin → angiotensin II.
• Mineralocorticoid excess: primary aldosteronism (adenoma or bilateral hyperplasia), congenital adrenal hyperplasia (11β- and 17α-hydroxylase), Liddle syndrome (constitutively active ENaC), licorice/glycyrrhetinic acid inhibiting 11β-HSD2.
• Catecholamine excess: pheochromocytoma/paraganglioma, cocaine or amphetamine use, MAO inhibitor plus tyramine.
• Other endocrine: Cushing syndrome, hyperthyroidism (high output), hyperparathyroidism, acromegaly.
• Mechanical: coarctation of the aorta.
• Sleep-disordered breathing: obstructive sleep apnea — intermittent hypoxia drives chemoreflex-mediated sympathetic surge; a leading cause of resistant hypertension.
• Drug-induced: NSAIDs (blunt prostaglandin-mediated natriuresis and vasodilation), combined oral contraceptives, glucocorticoids, calcineurin inhibitors, erythropoietin, decongestants, VEGF inhibitors, chronic alcohol, stimulants.

• Stem triggers for secondary workup: onset before age 30 or after 65, abrupt onset, resistant hypertension, spontaneous hypokalemia, abdominal bruit, or flash pulmonary edema.

• Core equation: MAP = cardiac output × systemic vascular resistance. Early essential hypertension is often a high-output, high-sympathetic state in young patients; over time output normalizes and resistance rises as arterioles remodel — the transition to a resistance-dominant phenotype.
• Renal pressure–natriuresis shift: the kidney normally excretes sodium until pressure normalizes. In hypertension the pressure–natriuresis curve is shifted rightward, so a higher pressure is required to excrete the same sodium load. This is why sodium restriction and diuretics work, and why every secondary cause that impairs sodium excretion (aldosteronism, renal disease, Liddle) produces hypertension.
• RAAS and sympathetic amplification: angiotensin II causes direct arteriolar vasoconstriction, aldosterone release, sympathetic facilitation, and — critically — growth-factor-like stimulation of vascular smooth muscle and cardiac myocyte hypertrophy and fibrosis. This trophic effect explains why RAAS blockade protects organs beyond its pressure effect.
• Endothelial dysfunction: reduced nitric oxide bioavailability with increased endothelin and reactive oxygen species shifts arterioles toward tonic constriction and promotes atherogenesis.

How chronic pressure becomes visible pathology

• Arterioles: chronic benign hypertension produces hyaline arteriolosclerosis — plasma protein insudation thickening the wall, narrowing the lumen, and causing downstream ischemia (nephrosclerosis, lacunar infarcts). Severe/malignant hypertension produces hyperplastic "onion-skin" arteriolosclerosis with fibrinoid necrosis, the lesion underlying malignant nephrosclerosis and hypertensive encephalopathy.
• Heart: pressure overload increases wall stress; sarcomeres add in parallel producing concentric LV hypertrophy. The stiff, hypertrophied ventricle relaxes poorly (diastolic dysfunction → HFpEF, S4 gallop) and outgrows its coronary supply, causing subendocardial ischemia and arrhythmia risk. Left atrial pressure rises → atrial fibrillation.
• Large arteries: repetitive stress degrades elastin, stiffening the aorta, raising systolic and pulse pressure, and predisposing to aneurysm and dissection.
• Autoregulation: cerebral vessels reset their autoregulatory range upward, which is why abrupt over-correction of chronic hypertension causes cerebral hypoperfusion.

• Typical stem: an overweight middle-aged or older adult — often Black, often with snoring/daytime somnolence, high-sodium diet, or NSAID use — found to have elevated readings at a routine or unrelated visit. Symptoms are absent; the diagnosis is made by measurement, not by complaint.
• Nonspecific symptoms occasionally reported: occipital headache on waking, dizziness, epistaxis. These correlate poorly with pressure and should not be used to titrate therapy.

Findings of end-organ damage, each with its mechanism

• S4 gallop and sustained, laterally non-displaced apical impulse: atrial contraction into a stiff, concentrically hypertrophied LV. Displacement and an S3 suggest progression to dilated, failing ventricle.
• Loud A2: high aortic closing pressure.
• Retinal changes (Keith–Wagener–Barker grading): arteriolar narrowing and copper/silver wiring from arteriolosclerosis, AV nicking where the thickened arteriole compresses the shared-adventitia venule, then flame hemorrhages, cotton-wool spots (nerve-fiber-layer infarcts), and hard exudates; papilledema defines the malignant phase.
• Renal: usually silent; microalbuminuria is the earliest marker, later a rising creatinine with bland urine sediment.
• Abdominal or flank bruit: renovascular disease.
• Radio-femoral delay with weak lower-extremity pulses and upper-extremity hypertension: coarctation.
• Episodic pallor, palpitations, headache, diaphoresis: pheochromocytoma.
• Muscle weakness, cramps, polyuria: hypokalemia of primary aldosteronism.

Emergency presentations (end-organ damage in evolution)

• Hypertensive encephalopathy: headache, vomiting, confusion, seizure, papilledema — breakthrough of cerebral autoregulation with vasogenic edema (posterior-predominant on MRI, PRES).
• Tearing chest/back pain with pulse or BP differential: aortic dissection.
• Acute dyspnea with pulmonary edema, chest pain with ischemic ECG changes, oliguria with hematuria and schistocytes, or acute neurologic deficit.

Step 2 — stage it (ACC/AHA 2017).

• Normal: <120 and <80. Elevated: 120–129 and <80.
• Stage 1: 130–139 or 80–89. Stage 2: ≥140 or ≥90. Classify by the higher of the two numbers.
• Hypertensive crisis: ≥180 and/or ≥120 — urgency without acute target-organ injury, emergency with it.

• Exceptions requiring rapid, aggressive lowering: aortic dissection — beta blockade (esmolol/labetalol) first to blunt dP/dt, then a vasodilator, targeting systolic pressure near 120 within about 20 minutes; never vasodilate before rate control (reflex tachycardia worsens shear).
• Pheochromocytoma crisis: phentolamine or nicardipine; alpha blockade must precede beta blockade to avoid unopposed alpha vasoconstriction.
• Hypertensive urgency without organ damage: oral agents and close outpatient follow-up, not IV therapy.

Chronic management (ACC/AHA 2017)

• All patients: lifestyle therapy as already outlined in this article.
• Drug initiation: stage 1 with clinical ASCVD, diabetes, CKD, or 10-year ASCVD risk ≥10%; all stage 2. Stage 2 with pressure far above goal warrants starting two agents from different classes, preferably as a single-pill combination, since monotherapy rarely achieves goal.
• Compelling indications: ACE inhibitor or ARB (lisinopril, losartan) for CKD with albuminuria (KDIGO) and for diabetes with albuminuria (ADA Standards of Care); beta blocker plus RAAS blocker post-MI; guideline-directed HFrEF therapy takes precedence.
• In Black adults without CKD or heart failure, ACC/AHA favors a thiazide-type diuretic (chlorthalidone) or dihydropyridine CCB (amlodipine) as initial therapy.
• Resistant hypertension (uncontrolled on three agents including a diuretic at maximal tolerated doses): confirm adherence and correct technique, stop interfering drugs, then add spironolactone, the best-supported fourth agent (PATHWAY-2).

Cardiac

• LV hypertrophy → HFpEF: pressure overload, concentric hypertrophy, impaired relaxation. Signal: S4, ECG voltage criteria, exertional dyspnea with preserved EF. LVH is independently arrhythmogenic and a strong predictor of sudden death.
• Coronary disease and MI: accelerated atherosclerosis plus increased myocardial oxygen demand and reduced subendocardial perfusion.
• Atrial fibrillation: left atrial pressure/volume overload and fibrosis.

Cerebrovascular — hypertension is the top risk factor

• Lacunar infarcts: lipohyalinosis of penetrating arterioles supplying basal ganglia, internal capsule, thalamus, pons — pure motor or pure sensory syndromes.
• Intracerebral hemorrhage: rupture of Charcot–Bouchard microaneurysms, classically in the putamen. Emergency.
• Hypertensive encephalopathy/PRES: autoregulatory breakthrough with vasogenic edema. Emergency.
• Vascular cognitive impairment from chronic small-vessel ischemia.

Treatment-related

• ACE inhibitors: dry cough (bradykinin), angioedema (emergency if airway involved), hyperkalemia, AKI when efferent tone is removed in bilateral renal artery stenosis, fetal toxicity.
• Thiazides: hyponatremia, hypokalemia, hypomagnesemia, hyperuricemia/gout, hyperglycemia, hypercalcemia, sulfa cross-reaction.
• Dihydropyridine CCBs: dose-dependent ankle edema (precapillary dilation), flushing, reflex tachycardia; non-dihydropyridines: bradycardia, AV block, constipation.
• Beta blockers: bradycardia, fatigue, bronchospasm, masked hypoglycemia; abrupt withdrawal causes rebound tachycardia/ischemia.
• Spironolactone: hyperkalemia, gynecomastia. Hydralazine: reflex tachycardia and drug-induced lupus. Clonidine: rebound hypertension on withdrawal. Nitroprusside: cyanide/thiocyanate toxicity with prolonged high-dose infusion or renal failure.
• Over-rapid BP lowering: watershed cerebral, retinal, or renal ischemia.

• Elevated office reading is not a diagnosis. The single best next step in an asymptomatic patient with one high reading is repeat measurement plus out-of-office confirmation (ABPM or home monitoring) — the USPSTF grade A pathway. This is how white-coat hypertension is excluded; conversely, masked hypertension (normal office, high home readings) carries real risk and does require treatment.
• Hypokalemia with metabolic alkalosis and hypertension in a patient not on a diuretic = primary aldosteronism until proven otherwise. Best next step: plasma aldosterone-to-renin ratio. High aldosterone with low renin; contrast with renovascular disease where both are high, and Liddle syndrome where both are low.
• Rise in creatinine after starting an ACE inhibitor points to bilateral renal artery stenosis — angiotensin II was maintaining efferent arteriolar tone and thus GFR. A small, stable creatinine bump (under roughly 30%) is expected and acceptable, not a reason to stop.
• Never give a beta blocker first in suspected pheochromocytoma or cocaine-associated hypertension — unopposed alpha stimulation worsens vasoconstriction. Phenoxybenzamine/phentolamine (or a benzodiazepine plus CCB for cocaine) comes first.
• In aortic dissection, rate control precedes vasodilation. Esmolol or labetalol first to reduce dP/dt; a vasodilator alone provokes reflex tachycardia and higher aortic shear.
• Lower pressure gradually in chronic hypertensive emergency (about 25% MAP reduction in the first hour, per ACC/AHA) because cerebral autoregulation has reset upward — except in dissection, where rapid control is the goal.
• Pregnancy: labetalol, nifedipine, or methyldopa (ACOG). ACE inhibitors and ARBs are absolutely contraindicated; captopril's short half-life makes it handy for rapid titration in non-pregnant patients only.
• Classic distractor: treating "hypertensive urgency" (≥180/120, asymptomatic) with IV drugs or rapid oral loading. Oral therapy and close follow-up are correct; end-organ damage, not the number, defines an emergency.

• Definition: BP ≥130/80 mmHg (Stage 1: 130-139/80-89; Stage 2: ≥140/90)
• Prevalence: Most common cardiovascular disease; affects ~1 billion people worldwide
• 90-95% is essential HTN (no identifiable secondary cause); 5-10% is secondary
• Major CVRF for MI, stroke, HF, CKD, and aortic dissection
• JNC 8 guidelines recommend individualizing therapy by age, comorbidities, and CV risk

• Asymptomatic in majority of cases; often discovered incidentally
• HTN crisis: severe headache, blurred vision, chest/back pain, altered mental status, dyspnea (malignant HTN with end-organ damage)
• Buzzwords: "Hypertensive urgency" (≥180/120, no symptoms) vs. "hypertensive emergency" (end-organ damage present)

1. 1.Confusing white-coat HTN with true HTN: White-coat HTN (elevated office, normal home BP) does NOT require pharmacotherapy; home/ambulatory monitoring essential for diagnosis
2. 2.Over-treating young patients: Overly aggressive BP control in young/middle-aged patients may increase CV risk (J-curve effect); target SBP typically 130-140 mmHg depending on age/tolerance
3. 3.Missing secondary causes: Always screen for secondary HTN in sudden-onset HTN, young age (<30), resistant HTN, or abnormal labs (↓K+, ↓renin)

• ACE inhibitors or ARBs (especially with DM, CKD, post-MI)
• Thiazide diuretics (HCTZ) or chlorthalidone
• Calcium channel blockers (CCBs; amlodipine, diltiazem)
• Beta-blockers (reserve for specific indications: CAD, post-MI, HF, arrhythmia)