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Hypertension (High Blood Pressure) - Complete Overview

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1. Definition

• Correct classification requires averaging two or more readings obtained on two or more separate occasions.
• In children under 13, hypertension is defined relative to age-, sex-, and height-specific normative data (≥ 95th percentile).
• Two special patterns exist: white-coat hypertension (elevated in clinic, normal at home) and masked hypertension (normal in clinic, elevated at home) - each with ~15-25% prevalence.

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2. Causes

Primary (Essential) Hypertension - ~90-95% of cases

• Genetic factors: Polygenic inheritance; family history is a strong risk factor
• Dietary sodium excess and potassium insufficiency (nearly universal worldwide)
• Obesity and overweight (~75% of US adults)
• Physical inactivity
• Excess alcohol consumption
• Psychosocial stress
• Environmental exposures: Heavy metals (lead, mercury, cadmium, arsenic), air pollution (PM2.5 particulate matter raises SBP by ~3-5 mmHg)
• Age-related vascular stiffness
• Seasonal/geographic variation: Higher BP in cold seasons and at high altitudes

Secondary Hypertension - ~5-10% of cases

1. Hypertension is treatment-resistant
2. There is abrupt worsening of previously controlled BP
3. Disproportionate target organ damage exists
4. There are abnormal labs: unprovoked hypokalemia, proteinuria, left ventricular hypertrophy

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3. Pathophysiology

Key mechanisms:

• Reduced renal perfusion triggers renin release → Angiotensin I → Angiotensin II
• Angiotensin II causes vasoconstriction (raises TPR) and stimulates aldosterone
• Aldosterone promotes sodium and water retention → raised CO

• Increased catecholamines → tachycardia, increased cardiac contractility, vasoconstriction
• Triggers RAAS and promotes sodium retention

• Chronic high pressure causes vascular smooth muscle hypertrophy and remodeling
• Increased wall-to-lumen ratio → perpetuates elevated TPR
• Loss of arterial compliance/elasticity (especially in older patients)

• High sodium intake → volume expansion → increased CO
• Impaired pressure natriuresis (kidneys fail to excrete sodium despite high BP)

• Reduced nitric oxide (NO) production → impaired vasodilation
• Increased oxidative stress and inflammatory mediators

• Insulin resistance promotes sodium retention and SNS activity
• Leptin excess (in obesity) activates SNS

• Heart: Left ventricular hypertrophy (LVH), heart failure, coronary artery disease
• Brain: Stroke, hypertensive encephalopathy
• Kidneys: Nephrosclerosis, CKD
• Eyes: Hypertensive retinopathy
• Aorta: Dissection, aneurysm

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4. Symptoms

Most patients: No symptoms

When symptoms occur (usually from complications or severe elevation):

• Headache - typically occipital, worse in the morning (especially in severe hypertension)
• Dizziness and lightheadedness
• Visual disturbances (blurred vision, scotomas - from retinopathy)
• Palpitations
• Dyspnea (from left ventricular dysfunction)
• Chest pain (angina if coronary disease is present)
• Epistaxis (nosebleeds, though not specific)
• Tinnitus
• Fatigue

Hypertensive Urgency/Emergency Symptoms:

• Severe headache, nausea, vomiting
• Confusion, altered consciousness, seizures (hypertensive encephalopathy)
• Focal neurological deficits (stroke)
• Acute chest pain / back pain (aortic dissection)
• Pulmonary edema (acute heart failure)
• Acute kidney injury (oliguria, hematuria)
• Fundoscopic findings: papilledema, flame hemorrhages, cotton-wool spots

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5. Diagnosis (Di)

Blood Pressure Measurement

• Use a validated sphygmomanometer with appropriate cuff size
• Patient seated, arm at heart level, after 5 minutes rest
• Average of 2+ readings on 2+ occasions
• Home BP monitoring: Same threshold applies (SBP ≥130 / DBP ≥80)
• Ambulatory BP Monitoring (ABPM): Gold standard for confirming diagnosis

Workup for Newly Diagnosed Hypertension (Minimum Battery):

Additional Tests When Secondary Cause Suspected:

• Plasma aldosterone/renin ratio (primary aldosteronism)
• Renal artery Doppler ultrasound / CT/MR angiography (renovascular disease)
• Polysomnography (OSA)
• 24-hour urine metanephrines (pheochromocytoma)
• Cortisol testing (Cushing's)
• Echocardiography (LVH, cardiac function)
• Fundoscopy (retinopathy grading)

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6. Treatment

A. Lifestyle / Non-Pharmacological Therapy (First-line for all patients)

B. Pharmacological Therapy

• Stage 1 hypertension (130-139/80-89) + high ASCVD risk (≥10% 10-year risk): Start drugs alongside lifestyle
• Stage 2 hypertension (≥140/90): Start drugs in ALL patients

• Hypertensive emergency: IV labetalol, nicardipine, or sodium nitroprusside; reduce MAP by no more than 25% in the first hour
• Pregnancy: Methyldopa, labetalol, nifedipine (ACEi/ARBs are contraindicated)
• CKD: ACEi or ARB preferred
• Heart failure with reduced EF: ACEi/ARB + beta-blocker + aldosterone antagonist

• General population: < 130/80 mmHg (2025 AHA/ACC Guideline, PMID 40811516)
• High-risk elderly: individualize (avoid excessive lowering)

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7. Forensic Importance

A. Sudden and Unexpected Death

• In individuals with a history of hypertension who die suddenly, autopsy may reveal only an enlarged heart (≥500 g) with marked left ventricular hypertrophy and minimal or absent coronary atherosclerosis.
• The mechanism of death in these cases is a cardiac arrhythmia, most likely ventricular fibrillation.
• Patients with LVH have significantly more ventricular premature contractions than normotensive individuals - this predisposes to lethal arrhythmias.
• Forensic pathologists recognize a significant subset of sudden deaths where hypertension-related LVH alone is the cause, without severe atherosclerosis.

B. Aortic Dissection

• Hypertension is the leading cause of aortic dissection - one of the most catastrophic sudden death causes in forensic practice.
• Dissection occurs when blood tracks between the middle and outer two-thirds of the aortic media, usually starting in the ascending aorta.
• At autopsy: intimal tear with sharp edges running transversely or longitudinally; dissection channel filled with blood.
• Also associated with cocaine and methamphetamine use (drug-induced hypertensive states), Marfan syndrome, and connective tissue disorders.

C. Hypertensive Retinopathy at Autopsy

• Retinal changes (silver-wiring, AV nicking, hemorrhages, papilledema) serve as evidence of chronic hypertension and can help establish pre-existing disease at autopsy.

D. Relevance in Manner of Death Determination

• Hypertension is commonly listed as a contributing cause of death on death certificates.
• In trauma deaths, pre-existing hypertension can complicate the picture - e.g., a minor head injury in a hypertensive person may trigger a hypertensive hemorrhagic stroke.
• Hypertension complicating natural disease deaths (cardiac deaths, stroke, renal failure) must be distinguished from trauma-related deaths.
• Drug-induced hypertensive crises (cocaine, amphetamines, certain medications) are of direct forensic relevance.

E. Estimation of Antemortem Hypertension

• Autopsy findings suggesting chronic hypertension:
  • LVH (heart weight > 400g in women, > 450g in men)
  • Hyaline arteriolosclerosis in kidneys (nephrosclerosis)
  • Hypertensive retinopathy changes
  • Aortic atherosclerosis (hypertension accelerates it)

F. Medico-Legal Aspects

• Inadequate management of hypertension leading to stroke or myocardial infarction can be grounds for medical negligence claims.
• Hypertension is relevant in fitness-for-duty assessments and insurance medicine.
• Identification of undiagnosed hypertension at autopsy (via organ changes) may clarify cause of death.

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Sources: Harrison's Principles of Internal Medicine 22E (2025); DiMaio's Forensic Pathology 3rd Edition; Brenner and Rector's The Kidney; 2025 AHA/ACC Hypertension Practice Guideline (PMID 40811516)