Hypertension

Why hypertension prevalence increases with age

Arterial stiffness increases with age → systolic BP rises → widened pulse pressure → higher HTN prevalence.

Learning objective: pathophysiology of hypertension

Hypertension results from increased cardiac output, increased systemic vascular resistance, or both—driven by genetics, sympathetic activation, RAAS, sodium retention, endothelial dysfunction, and vascular remodeling.

Primary vs secondary hypertension

Primary HTN = 90% of cases, multifactorial

How chronic hypertension damages organs

Chronic HTN causes LV hypertrophy, CKD, retinopathy, stroke, PAD, and aortic aneurysm/dissection due to increased wall stress and vascular remodeling.

Law of Laplace in hypertensive heart disease

Wall stress = (Pressure × Radius) / (Wall thickness). Chronic pressure overload → LV hypertrophy → reduced wall stress per sarcomere.

Arteriolar changes in chronic hypertension

Hyaline arteriolosclerosis (long‑standing HTN), hyperplastic arteriolosclerosis (severe HTN), necrotizing arteriolitis (malignant HTN).

Retinopathy findings in hypertension

AV nicking, cotton‑wool spots, flame hemorrhages, papilledema (in malignant HTN).

BP Classifications

Normal: <120/<80

Elevated: 120-129/<80

Stage 1 HTN: 130-139/80-89

Stage 2 HTN: >140/>90

When to start medications for HTN

Stage 1 HTN: start 1 drug, Stage 2: start two drugs

First‑line agents: thiazides, ACE inhibitors, ARBs, calcium channel blockers.

Compelling indications: heart failure what drugs?

Use BB, ACEI/ARB, aldosterone antagonist

Compelling indications: post‑MI what drugs

Use BB, ACEI/ARB, aldosterone antagonist

Compelling indications: diabetes

ACEI/ARB preferred to reduce nephropathy progression

Compelling indications: chronic kidney disease

ACEI/ARB reduce proteinuria and slow CKD progression

Hypertensive emergency vs urgency

Emergency = BP >180/110 with organ damage. Urgency has no organ damage

Phechromocytoma Tx

Surgical removal of tumor. Start with irreversible Alpha blocker (phenoxybenzamine), then give beta blocker

Obstructive sleep apnea and HTN

Repeated hypoxia → sympathetic surges → persistent hypertension.

Pheochromocytoma physiology

Catecholamine‑secreting tumor → episodic HTN, palpitations, sweating, anxiety

Coarctation of the aorta clues

Arm BP >20 mmHg higher than legs, rib notching, delayed femoral pulses.

Why ACE inhibitors lower BP

Block Ang II → vasodilation + reduced aldosterone → lower SVR and preload.

Why ARBs lower BP

Block AT1 receptor → prevent vasoconstriction and aldosterone release.

Why calcium channel blockers lower BP

Block L‑type Ca channels → arteriolar vasodilation → decreased SVR.

Why beta‑blockers lower BP

Reduce HR and contractility → lower CO

Alcohol and hypertension

Excess alcohol increases sympathetic tone and raises BP.

Consequence of too low BP

Shock(organs not perfused), Kidney failure, Anoxic encephalopathy, lactic acidosis

Consequences of too high BP

Intracranial hemorrhage, stroke, vascular disease, kidney damage, heart disease, retinopathy

Secondary HTN causes

Sleep apnea, drugs, CKD, primary aldosteronism, Renovascular disease, chronic steroids/cushings syndrome, phenochromocytoma, coarctation of aorta, thryid disease