Cardiovascular · PANCE / PANRE

Hypertension

Written & clinically reviewed by Ryan Busch, PA-C · Updated August 2026 · Report an error

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.

Try two board-style Hypertension questions

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Question 1CardiovascularMedium
A 62-year-old man presents with acute confusion and headache. His blood pressure is 218/128 mm Hg, fundoscopy shows papilledema, and his serum creatinine has risen acutely from 0.9 to 2.4 mg/dL. He is alert but disoriented to time and place. Which of the following is the most appropriate initial antihypertensive agent?
  • AOral nifedipine
  • BIntravenous nicardipine
  • CIntravenous furosemide
  • DOral captopril
Reveal answer & full explanation
Correct answer: B — Intravenous nicardipine
  • AOral nifedipine
  • BIntravenous nicardipine✓
  • CIntravenous furosemide
  • DOral captopril

Why Intravenous nicardipine is correct

  • This patient has a hypertensive emergency: severely elevated blood pressure with acute end-organ damage (encephalopathy with confusion, papilledema, and acute kidney injury).
  • The goal is a controlled, titratable reduction of mean arterial pressure by no more than about 25% in the first hour, then gradual normalization over 24-48 hours, because abrupt drops can cause cerebral, renal, or coronary hypoperfusion and ischemic stroke.
  • Intravenous nicardipine is a titratable dihydropyridine calcium channel blocker that allows this smooth, controlled reduction and is a guideline-preferred agent (labetalol is the other first-line choice).

Why the others are wrong

  • Oral nifedipine — oral immediate-release nifedipine causes a rapid, unpredictable, and uncontrolled blood pressure drop that has precipitated strokes and myocardial infarction; it is contraindicated in hypertensive emergencies.
  • Intravenous furosemide — treats volume overload and may be adjunctive in pulmonary edema, but this patient has no signs of fluid overload, and aggressive diuresis can worsen the hypoperfusion driving his acute kidney injury.
  • Oral captopril — has too slow and unpredictable an onset for an emergency requiring minute-to-minute titration, and an ACE inhibitor is risky in the setting of acute kidney injury.
Question 2CardiovascularMedium
A 48-year-old woman is evaluated for hypertension that has remained difficult to control on two agents. She takes no diuretics. Blood pressure is 168/104 mm Hg and serum potassium is 3.1 mEq/L with high-normal serum sodium. The plasma aldosterone-to-renin ratio is markedly elevated at 40. Renal function is normal and there are no cushingoid features. Which of the following is the most likely diagnosis?
  • AEssential hypertension
  • BPheochromocytoma
  • CRenovascular hypertension
  • DPrimary hyperaldosteronism
Reveal answer & full explanation
Correct answer: D — Primary hyperaldosteronism
  • AEssential hypertension
  • BPheochromocytoma
  • CRenovascular hypertension
  • DPrimary hyperaldosteronism✓

Why Primary hyperaldosteronism is correct

  • Resistant hypertension with spontaneous (non-diuretic) hypokalemia and a markedly elevated aldosterone-to-renin ratio is the classic screen-positive picture for primary hyperaldosteronism (Conn syndrome).
  • Autonomous aldosterone secretion drives sodium retention (hypertension, high-normal serum sodium) and renal potassium wasting (hypokalemia) while suppressing renin, producing the high ratio.
  • A positive screen is confirmed with an aldosterone-suppression test (saline infusion or fludrocortisone), then adrenal CT and adrenal venous sampling to localize (per Endocrine Society guidance).

Why the others are wrong

  • Essential hypertension — does not cause spontaneous hypokalemia or an elevated aldosterone-to-renin ratio. Trap: premature closure on the most common cause of hypertension while ignoring the potassium and the ratio.
  • Pheochromocytoma — catecholamine excess produces episodic hypertension with headache, palpitations, and diaphoresis; it does not suppress renin or raise the aldosterone-to-renin ratio, and spontaneous hypokalemia is not part of the syndrome. Trap: reaching for any secondary cause of resistant hypertension without matching the specific electrolyte and hormone pattern.
  • Renovascular hypertension — causes secondary hyperaldosteronism with HIGH renin, so the aldosterone-to-renin ratio is low or normal, not 40. Trap: confusing primary (low-renin) with secondary (high-renin) aldosteronism.
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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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Related Cardiovascular diagnoses

Acute Coronary Syndrome (ACS)Stable AnginaHeart Failure with Reduced Ejection Fraction (HFrEF)Heart Failure with Preserved Ejection Fraction (HFpEF)Atrial FibrillationAtrial FlutterHyperlipidemiaAortic StenosisMitral RegurgitationAortic Regurgitation (AR)Mitral Stenosis (MS)Mitral Valve Prolapse (MVP)Infective Endocarditis (IE)Acute Pericarditis

Differentials & related conditions

Primary Hyperaldosteronism (Conn Syndrome)PheochromocytomaCushing SyndromeCoarctation of the AortaObstructive Sleep Apnea (OSA)

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