Cardiovascular · PANCE / PANRE

Hypertension

Persistently elevated BP ≥130/80 (ACC/AHA 2017); cornerstone modifiable cardiovascular risk factor.

Also known as: HTN, high blood pressure, essential hypertension, primary hypertension

Overview

Sustained elevation of arterial blood pressure ≥130/80 mmHg (ACC/AHA 2017 thresholds) based on average of ≥2 properly measured readings on ≥2 occasions. Stage 1: 130-139/80-89. Stage 2: ≥140/90. Hypertensive crisis: ≥180/120 (urgency if no end-organ damage; emergency if present).

Epidemiology

Affects nearly half of US adults under current guidelines. Leading modifiable risk factor for cardiovascular disease, stroke, CKD, and dementia worldwide.

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Risk factors

  • Non-modifiable: age, family history, Black race (earlier onset, more severe)
  • Modifiable: high sodium diet, low potassium intake, obesity, sedentary lifestyle, alcohol use, smoking, chronic stress, poor sleep / OSA
  • Secondary causes (~5-10% of cases) to consider especially in young, resistant, or rapidly accelerating HTN:
  • • Renal: renal artery stenosis (FMD in young women; atherosclerotic in older), CKD, glomerular disease
  • • Endocrine: primary hyperaldosteronism (Conn's — low K, metabolic alkalosis), pheochromocytoma (paroxysmal HTN, headache, sweating, palpitations), Cushing syndrome, hyperthyroidism
  • • Coarctation of aorta — upper-extremity HTN, lower-extremity hypotension, radio-femoral delay
  • • Obstructive sleep apnea (very common, under-recognized)
  • • Medications: NSAIDs, OCPs, decongestants, stimulants, SNRIs

Pathophysiology

Multifactorial: increased peripheral vascular resistance from inappropriate RAAS activation, sympathetic overactivity, endothelial dysfunction, vascular remodeling, and renal sodium handling abnormalities. Genetic predisposition interacts with dietary and lifestyle exposures.

Clinical presentation

Symptoms

  • Almost always asymptomatic — 'silent killer'
  • Severe HTN may produce: occipital headache, blurred vision, epistaxis, chest discomfort
  • Hypertensive emergency: neurologic deficits, chest pain (dissection, MI), dyspnea (flash pulmonary edema), oliguria

Signs / physical exam

  • Elevated office BP — confirm with ambulatory or home BP monitoring (rule out white-coat HTN)
  • Funduscopy: AV nicking, copper/silver wiring, hemorrhages, exudates, papilledema (hypertensive retinopathy stages I-IV)
  • Cardiac: S4 gallop from LVH; lateral PMI
  • Abdominal bruit (renovascular disease)
  • Asymmetric pulses or BP arm-to-arm differences (suggest dissection or coarctation)

Differential diagnosis

  • White-coat hypertension — Office BP elevated, ambulatory or home BP normal; ~20% of office HTN patients; no end-organ damage on workup
  • Masked hypertension — Office BP normal, out-of-office BP elevated; carries worse cardiovascular prognosis than white-coat; suspect with end-organ damage despite 'normal' office readings
  • Pseudohypertension (elderly) — Calcified non-compressible arteries cause falsely elevated cuff readings; persistent palpable radial pulse with cuff inflated above SBP (Osler maneuver)
  • Renal artery stenosis — Abdominal bruit, refractory HTN, ↑ creatinine after ACEi/ARB; FMD in young women, atherosclerotic in older men; renal artery Doppler or MRA
  • Primary hyperaldosteronism (Conn syndrome) — Hypokalemia, metabolic alkalosis, suppressed renin, elevated aldosterone-to-renin ratio; adrenal CT
  • Pheochromocytoma — Paroxysmal HTN with the '5 H's' — headache, hypertension, hyperhidrosis, heart palpitations, hyperglycemia; plasma or 24-h urine metanephrines
  • Cushing syndrome — Central obesity, moon facies, abdominal striae, easy bruising, proximal muscle weakness; 24-h urine free cortisol or dexamethasone suppression
  • Coarctation of the aorta — Upper-extremity HTN with weak/delayed femoral pulses; radio-femoral delay; rib notching on CXR (children/young adults)
  • Obstructive sleep apnea — Snoring, witnessed apneas, daytime somnolence, obesity; polysomnography; CPAP can lower BP
  • Drug or substance-induced — NSAIDs, OCPs, decongestants (pseudoephedrine), stimulants (cocaine, amphetamines), SNRIs, corticosteroids, licorice (mineralocorticoid effect)

Diagnostic workup

Labs

  • BMP (Cr, K, glucose), UA with albumin-to-creatinine ratio
  • Lipid panel, A1c, TSH
  • CBC
  • If secondary HTN suspected: aldosterone-to-renin ratio, 24-h urine metanephrines, renal artery Doppler/MRA, polysomnography

Imaging

  • 12-lead ECG — LVH (Cornell or Sokolow-Lyon criteria), prior MI
  • Echocardiogram if LVH on ECG, HF symptoms, or diagnostic uncertainty

Diagnostic algorithm

Compelling IndicationPreferred First-Line Class
Heart failure (HFrEF)ACEi/ARB + beta-blocker (evidence-based) + MRA + diuretic
Post-MI / CADBeta-blocker + ACEi/ARB
Diabetes mellitusACEi or ARB (renal protection)
CKD with proteinuriaACEi or ARB
Recurrent stroke preventionThiazide diuretic + ACEi
Black race (no compelling indication)Thiazide diuretic or CCB
PregnancyLabetalol, nifedipine, methyldopa (AVOID ACEi/ARB — teratogenic)
Resistant HTN (>3 drugs incl. diuretic)Add spironolactone; investigate secondary causes
Hypertension drug selection by compelling indication. When comorbidities are present, the choice of antihypertensive should target both BP and the comorbid condition.

Treatment

First-line

  • Lifestyle modifications (always foundational):
  • • DASH diet — fruits, vegetables, whole grains, low-fat dairy
  • • Sodium <1500-2000 mg/day
  • • Weight loss (each 1 kg ≈ 1 mmHg drop)
  • • Aerobic exercise 150 min/week moderate intensity
  • • Alcohol limit (≤2 drinks/day men, ≤1 women)
  • • Smoking cessation
  • Pharmacologic — initiate if stage 1 + ASCVD risk ≥10%, established CVD, DM, or CKD; or stage 2 regardless:
  • • First-line classes (any of, by representative agent):
  • • Thiazide diuretic — chlorthalidone (preferred over HCTZ for stronger CV outcome data), HCTZ, indapamide
  • • ACE inhibitor — lisinopril, enalapril, ramipril, benazepril
  • • ARB — losartan, valsartan, candesartan, telmisartan, irbesartan
  • • Dihydropyridine CCB — amlodipine, nifedipine ER, felodipine
  • • Black patients without HF/CKD: CCB or thiazide preferred first-line over ACEi/ARB monotherapy

Second-line / adjunct

  • Combination therapy if BP >20/10 mmHg above goal at diagnosis (start 2 drugs)
  • Add second drug from different class if monotherapy insufficient
  • Compelling indications (drug choice driven by comorbidity):
  • • HFrEF: ACEi or ARB + BB + MRA + diuretic
  • • Post-MI: BB + ACEi/ARB
  • • CKD with proteinuria: ACEi or ARB
  • • Diabetes: ACEi or ARB
  • • Recurrent stroke prevention: thiazide + ACEi
  • • BPH: alpha-blocker (doxazosin) — symptomatic relief but NOT first-line for HTN alone (ALLHAT)
  • Resistant HTN (BP uncontrolled on 3 drugs including a diuretic): add spironolactone (PATHWAY-2 trial); investigate secondary causes

Complications

  • Atherosclerotic cardiovascular disease: MI, stroke, peripheral arterial disease
  • Hypertensive heart disease: LVH → HFpEF → HFrEF, AFib
  • Chronic kidney disease — second leading cause of ESRD after diabetes
  • Hypertensive retinopathy
  • Aortic dissection
  • Hypertensive emergency with end-organ damage (encephalopathy, pulmonary edema, AKI)

PANCE pearls

  • Proper BP measurement: seated, back supported, feet flat, arm at heart level, no caffeine/exercise/smoking 30 min prior, appropriate cuff size. Average of ≥2 readings on ≥2 occasions.
  • ACEi cough (10-20% of patients, bradykinin-mediated) → switch to ARB. Angioedema → avoid both ACEi AND ARB (cross-reactivity ~10%).
  • Hypertensive urgency (≥180/120 no end-organ damage): oral therapy, gradual reduction over 24-48 h. Hypertensive emergency: IV therapy, reduce MAP 10-20% in first hour, then more gradually. Acute dissection: aggressive — SBP <120 in minutes.
  • Avoid sublingual nifedipine — unpredictable, can cause stroke or MI from rapid hypotension. Pulled from US market for this use decades ago.
  • Lower 'goal' to <130/80 in most patients per SPRINT (intensive control reduces CV events but increases AKI, syncope, electrolyte abnormalities).

Images

Left ventricular hypertrophy — chronic hypertension causes voltage criteria (Sokolow-Lyon, Cornell) and "strain" pattern
Left ventricular hypertrophy — chronic hypertension causes voltage criteria (Sokolow-Lyon, Cornell) and "strain" pattern

References

  • ACC/AHA 2017 — 2017 ACC/AHA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults (Whelton et al., Hypertension 2018)
  • SPRINT — A Randomized Trial of Intensive versus Standard Blood-Pressure Control (SPRINT Research Group, NEJM 2015)
  • ALLHAT — Major Outcomes in High-Risk Hypertensive Patients Randomized to ACEi, CCB, or Thiazide (ALLHAT Officers, JAMA 2002)
  • PATHWAY-2 — Spironolactone vs Placebo, Bisoprolol, Doxazosin for Resistant HTN (Williams et al., Lancet 2015)
  • JNC 8 — 2014 Evidence-Based Guideline for the Management of High Blood Pressure (James et al., JAMA 2014)

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