Hypertension: Diagnosis & Management
A board-focused Step 2 CK lesson on hypertension covering 2017 ACC/AHA classification and diagnosis, when-to-treat thresholds driven by ASCVD risk, comorbidity-tailored drug selection, secondary-HTN pattern recognition, and hypertensive emergency vs urgency management. Built around classic vignette buzzwords and next-best-step decisions.
Overview & Pathophysiology
Hypertension (HTN) is the most prevalent modifiable cardiovascular risk factor and a leading driver of stroke, heart failure, CKD, and death. Blood pressure = cardiac output × systemic vascular resistance, so anything that raises volume, sympathetic tone, or vascular stiffness raises BP.
- Primary (essential) HTN — 90–95%: multifactorial (genetics, aging arterial stiffening, obesity, high sodium intake, RAAS and sympathetic overactivity). No single cause; typical onset ages 30–55.
- Secondary HTN — 5–10%: an identifiable cause. Suspect it with onset <30 or >55, resistant or malignant HTN, or specific lab/exam clues.
Sustained pressure produces target-organ damage: brain (stroke, encephalopathy), heart (LVH → HFpEF, CAD), kidney (nephrosclerosis, CKD), eyes (retinopathy), and large vessels (aneurysm, aortic dissection). Most patients are asymptomatic — HTN is caught on screening. That is why the boards emphasize accurate classification, evidence-based thresholds for starting drugs, tailoring agents to comorbidities, and recognizing hypertensive emergencies.
BP categories (adult, in-office, correct technique):
- Normal: <120 and <80 mmHg
- Elevated: 120–129 and <80
- Stage 1: 130–139 or 80–89
- Stage 2: ≥140 or ≥90
- Hypertensive crisis: >180 and/or >120
Making the diagnosis:
- Use the average of ≥2 readings on ≥2 separate visits (seated, rested, proper cuff).
- Confirm with out-of-office measurement — home BP monitoring or 24-h ambulatory BP monitoring (ABPM).
- White-coat HTN: high in office, normal out — confirm before treating.
- Masked HTN: normal in office, high out — do not miss.
Initial workup (risk + organ damage + secondary clues): BMP (Na, K, Cr, Ca), fasting glucose/HbA1c, lipid panel, TSH, urinalysis, and a 12-lead ECG (screen for LVH). Calculate the 10-year ASCVD risk — it decides therapy in Stage 1.
When to start medication (2017 ACC/AHA):
- Elevated / Stage 1, low risk (no clinical CVD and 10-yr ASCVD risk <10%): lifestyle alone, reassess in 3–6 months.
- Stage 1, high risk — established CVD, diabetes, CKD, or ASCVD risk ≥10%: lifestyle + one antihypertensive.
- Stage 2 (≥140/90): lifestyle + two first-line agents of different classes.
BP target: <130/80 mmHg for most adults, including diabetes, CKD, and known CVD.
Lifestyle (each lowers SBP a few mmHg):
- DASH diet (fruits, vegetables, low-fat dairy, low saturated fat)
- Sodium reduction (ideal <1500 mg/day; aim to cut ≥1000 mg/day)
- Weight loss (~1 mmHg per kg lost)
- Regular aerobic exercise, K⁺-rich diet, and limited alcohol (≤2 drinks/day men, ≤1 women)
Always confirm adherence and recheck before escalating therapy.
First-Line Drugs & Compelling Indications
| Class | Examples | Prefer in | Avoid / caution |
|---|---|---|---|
| Thiazide (chlorthalidone preferred) | chlorthalidone, HCTZ | osteoporosis, Black adults | gout, hypokalemia, hyponatremia |
| ACEi / ARB | lisinopril, losartan | DM + albuminuria, CKD, HFrEF, post-MI | pregnancy, bilateral RAS, hyperkalemia |
| Dihydropyridine CCB | amlodipine | Black adults, elderly systolic HTN | peripheral edema |
Vignette: A 54-year-old man presents for a routine visit. He is asymptomatic, does not smoke, and has no diabetes, CKD, or cardiovascular disease. Office BP is 136/86, confirmed on a repeat visit; home readings average 134/85. LDL and HbA1c are normal; 10-year ASCVD risk is 6%.
Diagnosis: Stage 1 hypertension, low cardiovascular risk.
Next best step: Lifestyle modification — DASH diet, sodium restriction, weight loss, aerobic exercise, limited alcohol — with reassessment in 3–6 months.
Why not start a drug? In Stage 1, pharmacotherapy is indicated only with clinical CVD, diabetes, CKD, or ASCVD risk ≥10%. With risk <10% and no comorbidity, starting medication now is premature. Had his risk been ≥10%, you would add a single first-line agent (thiazide, ACEi/ARB, or CCB).
Pheochromocytoma — the “5 P’s” (catecholamine-secreting tumor; a classic secondary-HTN vignette):
- Pressure — paroxysmal/episodic hypertension
- Pain — pounding headache
- Perspiration — drenching sweats
- Palpitations — tachycardia
- Pallor
Classic triad = episodic headache + sweating + palpitations. Screen with plasma free (or 24-h urine) metanephrines.
Manage in order: α-blockade first (e.g., phenoxybenzamine) to prevent hypertensive crisis, then β-blockade, then surgical resection. Never give a β-blocker first — unopposed α-stimulation triggers a hypertensive emergency. Recall the “rule of 10s”: ~10% bilateral, 10% extra-adrenal, 10% malignant, 10% familial (MEN 2A/2B, VHL, NF1).
Vignette: A 38-year-old woman has hypertension poorly controlled on three agents. She reports muscle cramps and fatigue and takes no diuretic. Labs: K⁺ 2.9 mEq/L, HCO₃⁻ 31 (metabolic alkalosis), Na⁺ 144.
Diagnosis: Primary hyperaldosteronism (Conn syndrome) — the most common endocrine / surgically correctable cause of secondary HTN and a leading cause of resistant hypertension. Classic triad = resistant HTN + hypokalemia + metabolic alkalosis (though many patients are normokalemic).
Next best step: Plasma aldosterone-to-renin ratio (ARR) — expect high aldosterone with suppressed renin. Confirm with a salt-loading/suppression test, then adrenal CT and often adrenal vein sampling to localize.
Treatment: unilateral adenoma → laparoscopic adrenalectomy; bilateral hyperplasia → mineralocorticoid receptor antagonist (spironolactone or eplerenone).
Secondary Hypertension at a Glance
| Cause | Vignette clues | Best test | Treatment |
|---|---|---|---|
| Primary aldosteronism | resistant HTN, hypokalemia, alkalosis | aldosterone:renin ratio | adrenalectomy or spironolactone |
| Renal artery stenosis | young ♀ (FMD) or older atherosclerotic; abdominal bruit; Cr rises after ACEi; flash pulmonary edema | duplex US, CTA/MRA | angioplasty (FMD); medical + statin (atherosclerotic) |
| Pheochromocytoma | episodic HTN, headache, sweating, palpitations | plasma/urine metanephrines | α- then β-block → resection |
| OSA | obese, snoring, daytime somnolence | polysomnography | CPAP, weight loss |
| Coarctation of aorta | young, ↑arm / ↓leg BP, radiofemoral delay, rib notching on CXR | echo, CT/MR angiography | surgical/catheter repair |
| Cushing syndrome | central obesity, striae, moon facies | dexamethasone suppression | treat underlying cause |
Hypertensive crisis = BP >180 and/or >120 mmHg. Split by acute target-organ damage:
- Emergency (WITH organ damage): encephalopathy, ischemic/hemorrhagic stroke, ACS, acute pulmonary edema, aortic dissection, AKI, retinopathy with papilledema, or eclampsia. → Admit; IV agents (labetalol, nicardipine, clevidipine, esmolol, nitroprusside).
- Urgency (NO organ damage): severe BP but asymptomatic. → Oral agents, gradual lowering over 24–48 h; avoid rapid drops.
How fast (emergency): reduce MAP by no more than ~25% in the first hour, then toward ~160/100 mmHg over the next 2–6 h, then to normal over 24–48 h — over-rapid correction causes cerebral/coronary/renal ischemia.
Key exceptions:
- Aortic dissection: lower fast — SBP 100–120, HR <60 within ~20 min; β-blocker (esmolol) first, then a vasodilator.
- Acute ischemic stroke: permissive HTN; treat only if >220/120 (or >185/110 if giving tPA).
- Eclampsia: magnesium + IV labetalol or hydralazine; deliver.
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