Cardiology > Essential Hypertension   

Background

Essential hypertension—also known as primary hypertension—is a chronic elevation of systemic arterial blood pressure without a clearly identifiable secondary cause. It is defined as a systolic BP ≥130 mm Hg or a diastolic BP ≥80 mm Hg, measured on at least two different occasions. Essential hypertension accounts for the vast majority of hypertension cases and is a major modifiable risk factor for cardiovascular and renal morbidity and mortality.

II) Classification/Types

Based on AHA/ACC Guidelines: 

• • • Normal BP: <120/80 mm Hg 

• • • Elevated BP: 120–129/<80 mm Hg 

• • • Stage 1 Hypertension: 130–139/80–89 mm Hg 

• • • Stage 2 Hypertension: ≥140/90 mm Hg 

• • • Hypertensive Crisis: ≥180/120 mm Hg (urgency vs emergency based on organ damage) 

By Etiology: 

• • Essential (primary) hypertension: ~90–95% of all cases; idiopathic 

• • Secondary hypertension: ~5–10%; caused by an underlying condition or drug 

III) Pathophysiology 
Essential hypertension is a multifactorial disorder driven by genetic and environmental factors. It involves: 

• • Increased systemic vascular resistance 

• • Overactivation of the sympathetic nervous system 

• • Enhanced RAAS activity 

• • Endothelial dysfunction 

• • Sodium retention and volume expansion 

• • Vascular remodeling and arterial stiffness 
    Chronic exposure to elevated BP damages target organs including the heart, brain, kidneys, and vasculature. 

IV) Epidemiology

• • Affects ~45% of U.S. adults 

• • Prevalence increases with age 

• • More common in African American populations 

• • Strong correlation with obesity and sedentary lifestyle 

• • Major contributor to cardiovascular morbidity, CKD, stroke, and premature death 

Etiology

I) Causes

• • No specific cause identifiable in essential hypertension 

• • Result of cumulative genetic susceptibility and lifestyle/environmental factors 

II) Risk Factors

• • Age >55 

• • Family history of hypertension 

• • High sodium intake 

• • Low physical activity 

• • Obesity or central adiposity 

• • Excess alcohol use 

• • Tobacco use 

• • Low potassium diet 

• • Chronic psychological stress 

• • Insulin resistance/metabolic syndrome 

 Clinical Presentation

I) History (Symptoms)
Most patients are asymptomatic for years
When symptoms occur, they may include: 

• • Occipital headaches (especially in the morning) 

• • Dizziness or lightheadedness 

• • Palpitations 

• • Fatigue 

• • Blurred vision 

• • Epistaxis (rare) 

• • Symptoms of complications: chest pain, dyspnea, confusion (suggest target organ damage) 

II) Physical Exam (Signs)

• • Elevated BP measured accurately on ≥2 visits 

• • Retinal changes: AV nicking, hemorrhages, papilledema (in severe HTN) 

• • Displaced apical impulse (suggests LVH) 

• • S4 gallop 

• • Bruits (suggestive of vascular disease) 

• • Peripheral edema (if heart failure or nephropathy present)

     

 
Differential Diagnosis (DDx)

• • Secondary hypertension 

• • White coat hypertension 

• • Pseudohypertension (elderly with calcified arteries) 

• • Drug-induced hypertension 

• • Anxiety-related or stress-induced BP elevation 

• • Hypertensive urgency/emergency 

• • Pain-related transient BP elevation 

 Diagnostic Tests

Initial Evaluation: 

• • Accurate BP measurements using validated equipment 

• • Confirm diagnosis with HBPM or ABPM 

• • Assess for cardiovascular risk and end-organ damage 

Baseline Investigations: 

• • Basic metabolic panel (BMP): electrolytes, renal function 

• • Fasting glucose or HbA1c 

• • Lipid profile 

• • Urinalysis: proteinuria, hematuria 

• • TSH: screen for thyroid dysfunction 

• • ECG: LVH, arrhythmias, ischemia 

If secondary cause suspected (less likely in essential HTN): 

• • Plasma aldosterone/renin ratio 

• • Renal ultrasound or Doppler 

• • 24-hour urinary catecholamines/metanephrines 

• • Sleep study (if OSA suspected) 

Treatment

I) Initial Approach

• • Confirm BP diagnosis 

• • Estimate ASCVD risk 

• • Educate patient on disease, risk, and monitoring 

• • Decide on pharmacologic vs non-pharmacologic strategy based on stage and comorbidities 

II) Non-Pharmacologic Management
Lifestyle modification is cornerstone therapy:

• • DASH diet 

• • Sodium restriction: <2.3 g/day (ideal <1.5 g/day) 

• • Weight loss: ~1 mm Hg BP reduction per 1 kg lost 

• • Aerobic physical activity: 150 minutes/week 

• • Limit alcohol intake: ≤2 drinks/day (men), ≤1 (women) 

• • Smoking cessation 

• • Stress reduction 

• • Limit caffeine 

III) Pharmacologic Therapy 

First-line agents: 

• • Thiazide-type diuretics: Chlorthalidone preferred 

• • ACE inhibitors or ARBs 

• • Calcium channel blockers: Dihydropyridines like amlodipine 

Agent choice depends on comorbidities and patient profile: 

• • CKD or diabetes: ACEi or ARB 

• • Black adults: Thiazide or CCB preferred 

• • Post-MI or heart failure: Beta-blockers + ACEi/ARB 

• • Elderly patients: Start low dose and titrate slowly 

Combination therapy: 
Often required for stage 2 hypertension or inadequate control with monotherapy 

• • Fixed-dose combinations improve adherence 

• • Monitor BP every 2–4 weeks during titration 

 Patient Education, Screening, Vaccines

Education: 

• • Hypertension is a lifelong condition 

• • Importance of lifestyle modification and medication adherence 

• • Home BP monitoring for trend assessment 

• • Warning signs of hypertensive crisis 

Screening: 

• • Begin screening at age 18 

• • Recheck every 2 years if BP <120/80 

• • Annually if BP ≥120/80 or if at risk 

Vaccinations: 

• • Follow adult immunization schedule 

• • Emphasize influenza, pneumococcal, and COVID-19 vaccines 

• • Encourage preventive care and health maintenance 

Consults/Referrals

• • Primary care: Ongoing management and risk modification 

• • Cardiology: Resistant hypertension or cardiac complications 

• • Nephrology: Advanced CKD or suspected renovascular hypertension 

• • Endocrinology: Suspected adrenal causes 

• • Sleep medicine: If obstructive sleep apnea suspected 

• • Hypertension specialist: If BP remains uncontrolled on ≥3 medications 

Follow-Up

• • Short-term: Reassess BP every 1–4 weeks until goal achieved 

• • Long-term: Every 3–6 months once stable 

• • Labs: Monitor renal function and electrolytes, especially with ACEi/ARB or diuretics 

• • Prognosis: 

• • • Excellent with early detection and treatment 

• • • Poor outcomes with uncontrolled BP: increased risk for stroke, MI, heart failure, CKD, and premature death