Explain hypertension

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Hypertension

Hypertension (high blood pressure) is one of the most common and clinically significant chronic conditions worldwide. It is a sustained elevation of arterial blood pressure above normal thresholds that, over time, damages blood vessels and target organs.

1. Definition and Classification

The American College of Cardiology/American Heart Association (ACC/AHA) 2017 classification for adults is the current standard:

Category	Systolic (mmHg)		Diastolic (mmHg)
Normal BP	< 120	and	< 80
Elevated BP	120–129	and	< 80
Stage 1 Hypertension	130–139	or	80–89
Stage 2 Hypertension	≥ 140	or	≥ 90

When SBP and DBP fall in different categories, the higher classification applies. Diagnosis requires averaging two or more readings at two or more separate visits. In children under 13, hypertension is defined as BP at or above the 95th percentile for age, sex, and height. - Harrison's Principles of Internal Medicine 22E, p. 288

2. Epidemiology

By the criteria above, over 40% of adults in the United States are hypertensive. Prevalence rises with age and is highest in African Americans compared to European Americans, Asian Americans, and Latin Americans. Without treatment, approximately half of hypertensive patients die of ischemic heart disease or heart failure, and about one-third succumb to stroke. - Robbins & Kumar Basic Pathology, p. 311

3. Types of Hypertension

Primary (Essential) Hypertension

Accounts for 90–95% of all cases
No single identifiable cause; results from interplay of genetic and environmental factors
Compatible with long life unless a complication supervenes

Secondary Hypertension

Accounts for the remaining 5–10%. Known causes include:

Renal: Acute/chronic glomerulonephritis, polycystic kidney disease, renal artery stenosis, renin-producing tumors
Endocrine: Primary aldosteronism (Conn's syndrome), Cushing syndrome, pheochromocytoma, acromegaly, hypo/hyperthyroidism
Cardiovascular: Coarctation of the aorta, increased intravascular volume
Neurologic / Other: Obstructive sleep apnea, increased intracranial pressure, oral contraceptives/exogenous estrogen, sympathomimetics
Robbins & Kumar Basic Pathology, Table 8.1

4. Pathophysiology

Arterial blood pressure = Cardiac Output × Peripheral Vascular Resistance

Major factors influencing blood pressure

Lippincott Illustrated Reviews: Pharmacology - Figure 8.3

Two major regulatory systems keep BP in balance:

A. Autonomic Nervous System

Baroreceptors in the aortic arch and carotid sinuses detect pressure changes. A fall in BP triggers increased sympathetic and decreased parasympathetic output, causing vasoconstriction and raised cardiac output. Moment-to-moment regulation works through this reflex arc. - Lippincott Pharmacology, p. 292

B. Renin-Angiotensin-Aldosterone System (RAAS)

When renal baroreceptors detect reduced arterial pressure, the kidney releases renin, which converts angiotensinogen → Angiotensin I → Angiotensin II (via ACE). Angiotensin II:

Causes potent vasoconstriction (arterioles and veins)
Stimulates aldosterone secretion → increased renal Na⁺ reabsorption → increased blood volume
Preferentially constricts efferent renal arterioles, raising glomerular filtration pressure

C. Pathogenesis of Primary Hypertension

The exact trigger remains unknown, but the key mechanisms are:

Impaired renal sodium excretion - reduced Na⁺ excretion at normal pressure forces volume expansion and raises cardiac output; at the new elevated pressure, Na⁺ balance is restored but at the cost of chronically high BP
Increased vascular resistance - from vasoconstriction and structural thickening of vessel walls
Obesity and excess adiposity - may account for 65–75% of risk; mechanisms include increased sympathetic activity (partly via leptin signaling), elevated Angiotensin II and aldosterone, and physical renal compression
Genetic factors - familial clustering and twin studies confirm heritability; polymorphisms in the renin-angiotensin system, renal sodium transport genes, and endogenous pressor genes contribute
Environmental factors - high dietary sodium, stress, physical inactivity, smoking all amplify genetic predisposition

Guyton & Hall Textbook of Medical Physiology, p. 246–247; Robbins & Kumar Basic Pathology, p. 311

5. Vascular Pathology (Morphology)

Hypertension drives characteristic vascular injury:

Hyaline arteriolosclerosis - thickening of arteriolar walls with deposition of homogeneous pink hyaline material, luminal narrowing; caused by plasma protein leakage and increased ECM production in response to hemodynamic stress. In the kidney, this causes nephrosclerosis (glomerular scarring)
Hyperplastic arteriolosclerosis - seen in severe/malignant hypertension; "onion-skin" concentric laminated thickening of arteriolar walls with SMC layers and reduplicated basement membrane; may be accompanied by fibrinoid necrosis
Large vessel disease - accelerates atherogenesis; degenerative changes in large/medium arteries can cause aortic dissection and cerebrovascular hemorrhage
Robbins & Kumar Basic Pathology, p. 311

6. Clinical Presentation and Complications

Hypertension is called the "silent killer" because it is usually asymptomatic until target-organ damage occurs. End-organ damage affects:

Organ	Complication
Heart	Left ventricular hypertrophy, heart failure, coronary artery disease, MI
Brain	Stroke (hemorrhagic and ischemic), hypertensive encephalopathy
Kidneys	Nephrosclerosis, chronic kidney disease
Eyes	Hypertensive retinopathy
Peripheral vasculature	Peripheral artery disease (2.5× risk in men, 3.9× in women)

A small subset (~5%) present with hypertensive crisis (BP > 180/120 mmHg), which may be:

Urgency: Severely elevated BP without acute target-organ damage
Emergency: Severely elevated BP with acute damage (aortic dissection, hypertensive encephalopathy, acute pulmonary edema, MI)

7. Diagnosis

Confirm with average of ≥2 readings at ≥2 separate visits
White coat hypertension (elevated only in office) can be identified with ambulatory blood pressure monitoring (ABPM) or home monitoring
Assess for secondary causes: renal function, urinalysis, electrolytes, lipid panel, thyroid function, aldosterone-to-renin ratio if primary aldosteronism suspected
Screen for end-organ damage: ECG/echo for LVH, fundoscopy, urinary albumin

8. Treatment

Lifestyle Modifications (First-line for all stages)

Weight loss (obesity accounts for a large portion of risk)
Regular aerobic exercise
DASH diet (high in fruits, vegetables, low-fat dairy; low in sodium)
Sodium restriction (< 2.3 g/day)
Alcohol moderation
Smoking cessation

Pharmacologic Treatment

First-line drug classes (per ACC/AHA and Brenner & Rector's The Kidney):

Drug Class	Examples	Key Use
Thiazide/thiazide-like diuretics	Chlorthalidone (preferred), HCTZ	First-line monotherapy; chlorthalidone is more potent than HCTZ
ACE inhibitors	Lisinopril, enalapril	First-line; preferred in CKD, diabetes, heart failure
Angiotensin Receptor Blockers (ARBs)	Losartan, valsartan	Alternative to ACE inhibitors (avoid ACE inhibitor cough)
Calcium channel blockers (CCBs)	Amlodipine, diltiazem	First-line; useful in elderly, isolated systolic hypertension

Combination strategies:

ACE inhibitor/ARB + CCB or thiazide are highly effective combinations
ACE inhibitor/ARB + CCB reduces pedal edema (a common CCB side effect)
Triple-pill combinations (ARB + CCB + HCTZ) are FDA-approved for moderate-to-severe hypertension
Do NOT combine ACE inhibitor + ARB (dual RAAS blockade increases adverse effects)

Special populations:

CKD or proteinuria: ACE inhibitor or ARB preferred (renoprotective)
Diabetes: ACE inhibitor or ARB; BP target generally < 130/80 mmHg
Heart failure with reduced EF: ACE inhibitor/ARB, beta-blocker, aldosterone antagonist
Pregnancy: Labetalol, nifedipine, methyldopa are safe; ACE inhibitors and ARBs are contraindicated

BP targets:

General: < 130/80 mmHg (ACC/AHA 2017)
If existing CV disease or 10-year CVD risk > 10%: < 130/80 mmHg
Elderly (cautious approach): may target < 150/90 mmHg depending on frailty
Brenner and Rector's The Kidney; Lippincott Illustrated Reviews Pharmacology; Comprehensive Clinical Nephrology 7e

9. Hypertension in Special Contexts

Hypertension in Pregnancy

Preeclampsia is defined as BP ≥ 140/90 mmHg after 20 weeks' gestation (confirmed on two readings ≥ 4 hours apart) plus proteinuria ≥ 300 mg/24h, or, in the absence of proteinuria, thrombocytopenia, renal insufficiency, impaired liver function, pulmonary edema, or cerebral/visual symptoms. Severe hypertension (≥ 160/105) can herald eclampsia (seizures) and must be treated urgently. - Brenner and Rector's The Kidney, Table 48.3

Resistant Hypertension

BP that remains above goal despite three optimally dosed drugs from different classes (including a diuretic). Obstructive sleep apnea is a common reversible cause; CPAP has been shown to reduce BP in resistant hypertension. - Textbook of Family Medicine 9e

Summary

Hypertension is a sustained elevation in blood pressure (≥ 130/80 mmHg by ACC/AHA criteria) affecting >40% of U.S. adults. The vast majority (~90–95%) is primary/essential, with no single cause but driven by RAAS activation, sympathetic overactivity, impaired renal sodium handling, obesity, and genetic factors. It silently damages the heart, brain, kidneys, and blood vessels. Treatment begins with lifestyle modification and, when indicated, pharmacotherapy with thiazide diuretics, ACE inhibitors/ARBs, or CCBs - chosen based on comorbidities and patient profile. With proper management, hypertension-related morbidity and mortality are substantially reduced.

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