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Hypertension - Complete Detailed Information

1. Definition

Hypertension is defined as a sustained elevation of blood pressure (BP) above normal levels. The definition is, by necessity, arbitrary - Sir George Pickering first established that BP is distributed continuously in the population as a bell-shaped curve, with no true separation between normotension and hypertension. There is a direct, continuous relationship between cardiovascular risk and BP: the higher the BP, the higher the risk of stroke and coronary events.

Operational Definitions by Guideline:

Guideline	HTN Threshold
WHO/ESH (European)	≥ 140/90 mm Hg
ACC/AHA 2017 (US)	≥ 130/80 mm Hg
JNC 7 (older US guideline)	≥ 140/90 mm Hg

Diagnosis requires the average of two or more readings on two or more occasions, in adults not taking antihypertensive drugs and not acutely ill.

Park's Textbook of Preventive and Social Medicine, p. 424
Rosen's Emergency Medicine, p. 2306

2. Classification

WHO/ESH Classification (Adults)

Category	Systolic (mm Hg)		Diastolic (mm Hg)
Optimal	< 120	and	< 80
Normal	120-129	and/or	80-84
High Normal	130-139	and/or	85-89
Grade 1 Hypertension	140-159	and/or	90-99
Grade 2 Hypertension	160-179	and/or	100-109
Grade 3 Hypertension	≥ 180	and/or	> 110
Isolated Systolic HTN	≥ 140	and	< 90

Rule: When systolic and diastolic fall into different categories, assign the higher category.

ACC/AHA 2017 Classification

Category	Systolic (mm Hg)		Diastolic (mm Hg)
Normal	< 120	and	< 80
Elevated	120-129	and	< 80
Stage 1 HTN	130-139	or	80-89
Stage 2 HTN	≥ 140	or	≥ 90

This revision reflects increasing awareness of long-term cardiovascular risk even with modest BP elevations, supported by the landmark SPRINT trial.

Brenner and Rector's The Kidney, p. 2219
Rosen's Emergency Medicine, p. 2306

3. Etiology / Types

A. Primary (Essential) Hypertension (~90-95%)

No single identifiable cause. Multifactorial - genetic, environmental, and lifestyle factors interact.

B. Secondary Hypertension (~5-10%)

Identifiable underlying cause:

Renal: Chronic glomerulonephritis, chronic pyelonephritis, renovascular disease (renal artery stenosis), polycystic kidney disease (ADPKD)
Endocrine: Pheochromocytoma, primary aldosteronism (Conn's syndrome), Cushing's syndrome, hyperthyroidism, hyperparathyroidism
Vascular: Coarctation of the aorta
Pregnancy-related: Pre-eclampsia, eclampsia
Drug-induced: OCP, NSAIDs, corticosteroids, sympathomimetics, cocaine

In ADPKD specifically, hypertension is found in ~50% of 20-34-year-olds with normal renal function and nearly 100% with ESKD, driven by cyst expansion compressing the vascular tree and activating the RAAS.

Park's Textbook, p. 424
Brenner and Rector's The Kidney

4. Pathophysiology

BP = Cardiac Output (CO) × Total Peripheral Resistance (TPR)

Hypertension results from an increase in CO, TPR, or both.

Key Mechanisms:

A. Renin-Angiotensin-Aldosterone System (RAAS)

Renin (released by juxtaglomerular cells) cleaves angiotensinogen → Angiotensin I
ACE converts Ang I → Angiotensin II
Ang II: potent vasoconstrictor (raises TPR), stimulates aldosterone release (sodium/water retention, raises CO), promotes vascular remodeling
Ectopic renin synthesis and ACE-independent angiotensin II generation (via chymase) also contribute
Evidence of intrarenal RAAS activation is particularly strong in renovascular and ADPKD-related hypertension

B. Sympathetic Nervous System (SNS) Overactivity

Increases heart rate and CO
Causes arterial and venous vasoconstriction (raises TPR)
Stimulates renin release

C. Sodium Retention

Impaired renal sodium excretion raises plasma volume
"Pressure natriuresis" curve shifts rightward in hypertension

D. Endothelial Dysfunction

Impaired nitric oxide (NO)-mediated vasodilation
In ADPKD: impaired NO-associated endothelium-dependent vasorelaxation found in small resistance vessels before hypertension develops
Increased endothelin-1 (potent vasoconstrictor)

E. Vascular Remodeling

Chronic BP elevation leads to vascular smooth muscle hypertrophy, reduced lumen diameter
Further increases TPR creating a vicious cycle

F. Insulin Resistance / Hyperinsulinemia

Insulin promotes sodium retention, SNS activation, and smooth muscle proliferation
Brenner and Rector's The Kidney
Fischer's Mastery of Surgery

5. Risk Factors

Non-modifiable:

Age: Prevalence rises markedly with age (isolated systolic HTN predominates in elderly)
Genetics/Family history: 30-60% heritability
Race: Higher prevalence and severity in Black populations
Sex: Men more affected before age 55; women more affected after menopause

Modifiable:

Obesity: BMI > 30 strongly associated; visceral fat promotes inflammation and SNS activation
High sodium intake: Directly raises plasma volume
Physical inactivity
Alcohol excess: > 2 drinks/day raises BP
Smoking: Raises BP acutely; major CV risk multiplier
Stress/psychological factors
Dyslipidaemia, diabetes: Co-morbid risk amplifiers

Epidemiology:

Global prevalence: ~1.13 billion (2015); ~26-31% of adults worldwide
"Rule of halves" (Hypertension iceberg): Only ~half of hypertensives are aware; only half of those are on treatment; only half of treated patients are adequately controlled - a major public health gap
Park's Textbook of Preventive and Social Medicine, p. 423-425

6. Clinical Features

Symptoms

Hypertension is largely asymptomatic ("the silent killer") - symptoms arise only from target organ damage (TOD).

Possible non-specific complaints:

Headache (classically occipital, morning) - though evidence for causal link is weak
Dizziness, fatigue
Epistaxis (no proven causal link with BP level)
Blurred vision (hypertensive retinopathy)
Chest pain, dyspnea (cardiac involvement)

Signs

Elevated BP on repeated measurement
Fundoscopy - Keith-Wagener-Barker (KWB) grading of retinopathy:
- Grade I: Arterial narrowing, increased light reflex
- Grade II: AV nipping (nicking)
- Grade III: Flame hemorrhages, cotton wool spots
- Grade IV: Papilledema (hypertensive emergency)
Cardiomegaly, left ventricular heave
Fourth heart sound (S4) - due to LVH
Renal bruits (renovascular HTN)
Radio-femoral delay (coarctation)

7. Target Organ Damage (TOD)

Chronic hypertension damages multiple organs. Organ damage should be evaluated separately from BP level, as markedly high pressures may exist without damage, and damage may occur with only moderate elevation.

Organ	Damage
Heart	Left ventricular hypertrophy (LVH), diastolic dysfunction, heart failure (HFpEF), coronary artery disease, MI, atrial fibrillation
Brain	Ischemic stroke, hemorrhagic stroke, lacunar infarcts, hypertensive encephalopathy, vascular dementia
Kidneys	Hypertensive nephrosclerosis, proteinuria, CKD, ESKD
Eyes	Hypertensive retinopathy (grades I-IV), retinal artery occlusion, CRAO
Aorta/Vessels	Aortic dissection, aortic aneurysm, peripheral arterial disease (PAD)
Placenta	Pre-eclampsia, IUGR, premature birth

Hypertension carries a 2.5-fold age-adjusted risk of PAD in men and 3.9-fold in women.

Textbook of Family Medicine 9e
Rosen's Emergency Medicine

8. Investigations / Workup

Baseline (Initial Evaluation)

To assess TOD and cardiovascular risk:

Urinalysis: Proteinuria, hematuria, casts
Serum creatinine/eGFR: CKD
Electrolytes: Hypokalemia (hyperaldosteronism)
Fasting glucose: Diabetes
Lipid profile: Dyslipidemia
ECG: LVH (Sokolow-Lyon criteria), ischemia, arrhythmia
Echocardiography (if clinically indicated): LVH, diastolic dysfunction

Blood Pressure Measurement:

Office-based (at least 2 readings, 2 occasions)
24-hour Ambulatory BP Monitoring (ABPM): Class I recommendation (ACC/AHA) - superior to office measurement; detects white-coat hypertension and masked hypertension
- Correction factors: Office 130/80 ≈ ABPM 125/75; Office 140/90 ≈ ABPM 130/80
Home BP monitoring: Useful adjunct

Secondary HTN Workup (if suspected):

Plasma aldosterone:renin ratio (Conn's)
24-hour urine catecholamines/metanephrines (pheo)
Renal doppler/MRA (renovascular)
Overnight dexamethasone suppression test (Cushing's)
Renal ultrasound (PKD)

9. Management

Step 1: Lifestyle Modifications (Non-pharmacological)

For all patients (and alone for Stage 1 without high CV risk):

DASH diet (Dietary Approaches to Stop Hypertension): Rich in fruits, vegetables, low-fat dairy; low sodium
Sodium restriction: < 2.3 g/day (ideally < 1.5 g/day) - reduces SBP by 2-8 mm Hg
Weight loss: 1 mm Hg SBP per kg lost
Regular aerobic exercise: 30 min/day, 5 days/week - reduces SBP by 4-9 mm Hg
Alcohol moderation: ≤ 2 drinks/day (men), ≤ 1 (women)
Smoking cessation: Not directly lowers BP but eliminates multiplicative CV risk
Stress management

Step 2: Pharmacotherapy

BP Target Goals (ACC/AHA 2017):

General: < 130/80 mm Hg
High-risk patients (CVD, CKD, diabetes): < 130/80 mm Hg
SPRINT trial demonstrated that an intensive SBP target of < 120 mm Hg (vs. < 140 mm Hg) significantly reduced cardiovascular events and mortality

First-Line Drug Classes:

Drug Class	Examples	Key Indications	Key Side Effects
Thiazide/Thiazide-like diuretics	Hydrochlorothiazide (HCTZ), Chlorthalidone, Indapamide	First choice in uncomplicated HTN; HF, edema	Hypokalemia, hyperuricemia, hyperglycemia, hyponatremia
ACE Inhibitors (ACEi)	Enalapril, Lisinopril, Ramipril	HTN + DM + CKD (renoprotection), HTN + HFrEF, post-MI	Dry cough (10-15%), angioedema, hyperkalemia, teratogenic
Angiotensin Receptor Blockers (ARBs)	Losartan, Valsartan, Olmesartan	Same as ACEi (use when ACEi cough); CKD proteinuria	Hyperkalemia, angioedema (rare), teratogenic
Calcium Channel Blockers (CCBs)	Amlodipine (DHP), Verapamil/Diltiazem (non-DHP)	HTN + angina, elderly, isolated systolic HTN, Black patients	Pedal edema, flushing (DHP); bradycardia, AV block (non-DHP)
Beta-blockers	Metoprolol, Bisoprolol, Atenolol, Nebivolol	HTN + angina, HFrEF, post-MI, AF, migraine	Bradycardia, bronchospasm, fatigue, cold extremities, depression

Notes:

Chlorthalidone is superior to HCTZ in reducing BP and cardiovascular events
Thiazides lose efficacy when eGFR < 30 mL/min (use loop diuretics instead, except indapamide and metolazone)
ACEi/ARB + CCB combination abrogates CCB-induced pedal edema
Each antihypertensive drug reduces SBP by approximately 8-10 mm Hg on average

Compelling Indications for Specific Drugs:

Condition	Preferred Drug
DM + Proteinuria/CKD	ACEi or ARB
HFrEF	ACEi/ARB + BB + diuretic + MRA
Post-MI	ACEi + BB
Stable Angina	BB or CCB
Atrial Fibrillation	BB or non-DHP CCB (rate control)
Pregnancy	Methyldopa, Labetalol, Nifedipine (avoid ACEi/ARB)
Black patients	Thiazides + CCB preferred; ACEi/ARB less effective as monotherapy
Pheochromocytoma	Alpha-blocker first, then BB
Primary Aldosteronism	Mineralocorticoid receptor antagonist (spironolactone)

Combination Therapy:

Most patients require 2-3 drugs
Preferred combinations: Thiazide + ACEi/ARB; CCB + ACEi/ARB; CCB + Thiazide
Single-pill fixed-dose combinations (SPC) improve adherence
Triple combination SPCs (ARB + CCB + HCTZ) are FDA-approved for initial treatment in moderate-to-severe HTN
Goodman & Gilman's The Pharmacological Basis of Therapeutics
Brenner and Rector's The Kidney

10. Hypertensive Crisis

A. Hypertensive Emergency

BP typically ≥ 180/120 mm Hg with acute target organ damage (TOD)
Requires immediate IV treatment in ICU/critical care
TOD manifestations:
- Hypertensive encephalopathy: Confusion, seizures, papilledema
- Hemorrhagic or ischemic stroke
- Aortic dissection: Immediate BP reduction mandatory (target SBP < 120 mm Hg within minutes)
- Acute pulmonary edema / Hypertensive HF: IV nitroglycerin + diuretics
- Acute MI / ACS
- Acute kidney injury
- Eclampsia / Pre-eclampsia

IV Drugs Used in Hypertensive Emergency:

Drug	Use Case
Labetalol IV	Most emergencies, aortic dissection, pregnancy
Nicardipine IV	Stroke, post-op HTN
Nitroprusside IV	Aortic dissection, severe HTN (caution: cyanide toxicity)
Nitroglycerin IV	ACS, acute pulmonary edema
Esmolol IV	Aortic dissection, perioperative
Hydralazine IV	Pre-eclampsia/eclampsia
Clevidipine IV	Perioperative

Goal in most emergencies: Reduce MAP by no more than 20-25% in the first hour; further gradual reduction over 24-48 hours (to avoid ischemia from rapid hypoperfusion)

Exception - Aortic dissection: Rapid reduction to SBP < 120 mm Hg within minutes

B. Hypertensive Urgency

BP ≥ 180/120 mm Hg without acute TOD
No evidence supports acute BP reduction in the ED
Risk: Rapid BP lowering (e.g., sublingual nifedipine, IV clonidine) causes relative hypoperfusion - particularly dangerous in cerebrovascular circulation
Management: Resume/restart oral medications; arrange prompt outpatient follow-up
The most important step is ensuring ongoing care and medication adherence

⚠ Important clinical point: "Asymptomatic hypertension" often has vague symptoms (headache, dizziness). These are unrelated to the BP level. Acute BP reduction in the absence of TOD lacks rationale, offers no outcome benefit, and may cause harm.

Rosen's Emergency Medicine
Brenner and Rector's The Kidney
Comprehensive Clinical Nephrology, 7th Edition

11. Special Populations

Population	Considerations
Elderly	Isolated systolic HTN common; start low, go slow; avoid orthostatic hypotension; CCBs and thiazides preferred
Pregnancy	Target < 140/90; safe drugs: methyldopa, labetalol, nifedipine; never ACEi/ARB (teratogenic)
CKD	ACEi/ARB for proteinuria; loop diuretics when eGFR < 30; tight BP control slows progression
Diabetes	Target < 130/80; ACEi or ARB preferred for renoprotection
Black patients	Thiazides + CCBs more effective; ACEi/ARBs less effective as monotherapy
Ischemic heart disease	BB + CCB (amlodipine); ACEi for LV dysfunction
Heart failure	ACEi/ARB + BB + diuretic + MRA (ARNI if HFrEF)

12. Hypertension in Specific Diseases

Renovascular Hypertension

Due to renal artery stenosis (atherosclerotic or fibromuscular dysplasia)
Mechanism: Reduced renal perfusion → renin release → Ang II → systemic vasoconstriction and aldosterone release
Treatment: ACEi/ARB (caution in bilateral stenosis), revascularization (angioplasty ± stent)

ADPKD-related Hypertension

Present in ~50% of 20-34 year olds with normal renal function
Mechanism: Cyst expansion compresses renal vasculature → RAAS activation; polycystin dysfunction impairs vascular smooth muscle and endothelial function
Early detection with ABPM critical; target < 110/75 (HALT-PKD trial)

Pulmonary Hypertension (different entity)

Defined as mean pulmonary arterial pressure (mPAP) > 20 mm Hg
5 WHO groups (arterial, venous, hypoxia, CTEPH, multifactorial)
Managed separately from systemic hypertension

13. Prevention

Primary Prevention (Population Strategy):

Reduce dietary sodium at population level
Promote physical activity, weight control, healthy diet
Address alcohol and tobacco use
Regular BP screening starting at age 18

Secondary Prevention (High-Risk Individuals):

Rigorous antihypertensive treatment reduces:
- Stroke by ~35-40%
- MI by ~20-25%
- Heart failure by ~50%
- Renal failure progression

The "Rule of Halves" Challenge:

The major public health challenge remains closing the detection-treatment-control gap. In most developed countries: ~50% aware → ~50% of those treated → ~50% of those adequately controlled. In developing countries, the gap is far wider.

Park's Textbook of Preventive and Social Medicine

Summary Table: Key Numbers

Parameter	Value
Normal BP	< 120/80 mm Hg
HTN threshold (WHO)	≥ 140/90 mm Hg
HTN threshold (ACC/AHA)	≥ 130/80 mm Hg
Global prevalence	~1.13 billion
Essential HTN proportion	~90-95%
Secondary HTN proportion	~5-10%
SBP reduction per kg weight loss	~1 mm Hg
SBP reduction from DASH diet	~8-14 mm Hg
SBP reduction per antihypertensive drug	~8-10 mm Hg
Safe MAP reduction in emergency (1 hr)	No more than 20-25%

Sources:

Park's Textbook of Preventive and Social Medicine, 26e (Epidemiology, Classification, Risk Factors)
Goodman & Gilman's The Pharmacological Basis of Therapeutics (Drug classes, mechanisms)
Brenner and Rector's The Kidney (Pathophysiology, RAAS, Drug selection)
Rosen's Emergency Medicine (Hypertensive emergency/urgency, BP measurement)
Comprehensive Clinical Nephrology, 7th Edition (Classification, malignant HTN)
Textbook of Family Medicine 9e (HTN and PAD, risk factors)
Fischer's Mastery of Surgery (Renovascular hypertension)

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