How hypertension is tested on Step 1

Expect a young patient with severe or resistant hypertension and a clue to a secondary cause, a histology image of an arteriole, or a request for the best initial drug.

workspace_premium When to think secondary

Onset before 30 or after 55, resistant hypertension on three drugs, sudden worsening, low potassium, an abdominal bruit, or paroxysmal symptoms all suggest a secondary cause.

Stages and causes

Blood pressure is the product of cardiac output and systemic vascular resistance; most causes raise one or both.

Higher riskNormal< 120 and < 80 mm HgElevated120–129 and < 80Stage 1130–139 or 80–89Stage 2≥ 140 or ≥ 90Severe≥ 180 or ≥ 120 — emergency if end-organ damage
BP categories. Diagnosis requires repeated readings; home or ambulatory monitoring excludes white-coat hypertension.
Secondary causeClueTest
Primary aldosteronism (Conn)Hypokalemia, metabolic alkalosis, resistant HTNAldosterone-to-renin ratio (high aldosterone, low renin)
Renal artery stenosisAbdominal bruit; creatinine rise on ACE inhibitor; flash pulmonary edemaDuplex ultrasound, CT/MR angiography
Fibromuscular dysplasiaYoung woman; "string of beads"Angiography
PheochromocytomaEpisodic headache, sweating, palpitationsPlasma free metanephrines
Cushing syndromeCentral obesity, striae, hyperglycemiaDexamethasone suppression, 24-h urine cortisol
Coarctation of the aortaArm > leg pressure, rib notching; Turner syndromeEcho, CT/MR
Obstructive sleep apneaSnoring, daytime sleepiness, obesityPolysomnography
DrugsNSAIDs, decongestants, oral contraceptives, stimulants, cyclosporineHistory

Primary aldosteronism is the most common identifiable endocrine cause.

Pathology and end-organ damage

Chronic high pressure injures small arteries and drives remodeling of the heart and large vessels.

Hyaline arteriolosclerosisChronic benign hypertension, diabetes,agingPink, glassy thickened wallPlasma protein leakageNarrowed lumen → ischemiaBenign nephrosclerosis (granularkidneys)Hyperplastic arteriolosclerosisSevere (malignant) hypertensionConcentric "onion-skin" smooth musclelayersFibrinoid necrosis possibleAcute renal failureFlea-bitten kidneyvs
Arteriolosclerosis. Both are small-vessel diseases distinct from atherosclerosis of large arteries.
Hypertensive damageHeartConcentric LVH,HFpEF, CADBrainStroke; basalganglia bleedKidneyNephrosclerosis,CKDEyeAV nicking,papilledemaAortaDissection,aneurysm
End-organ damage. Charcot-Bouchard microaneurysms of lenticulostriate arteries cause hypertensive intracerebral hemorrhage.

Treatment

Lifestyle change (sodium restriction, weight loss, exercise, limiting alcohol, DASH diet) is the foundation. First-line drug classes are thiazides, ACE inhibitors or ARBs, and dihydropyridine calcium channel blockers.

Comorbidity or situationPreferred drug(s)Avoid
Diabetes with albuminuria, CKD with proteinuriaACE inhibitor or ARB—
HFrEFACE inhibitor/ARB/ARNI, β blocker, spironolactoneNon-DHP CCBs
After MI, anginaβ blocker, ACE inhibitor—
Black patients without CKD or HFThiazide or dihydropyridine CCB—
PregnancyLabetalol, nifedipine, methyldopaACE inhibitors, ARBs, aliskiren
Benign prostatic hyperplasiaα1 blocker (adjunct)—
OsteoporosisThiazide—
GoutLosartanThiazides, loop diuretics

Hypertensive emergency (severe BP with end-organ damage): lower mean arterial pressure by no more than about 25% in the first hour with IV labetalol, nicardipine, clevidipine, or esmolol.

Clinical application

Low potassium in a hypertensive patient points to excess mineralocorticoid.

functions Worked example — the low potassium

A 42-year-old has blood pressure 168/102 despite three drugs, serum K⁺ 3.0 mEq/L without diuretics, and bicarbonate 31 mEq/L. Plasma renin is suppressed. What is the most likely cause?

  1. Resistant hypertension plus hypokalemia and metabolic alkalosis suggests mineralocorticoid excess.
  2. Aldosterone increases ENaC activity in principal cells, retaining Na⁺ and wasting K⁺ and H⁺.
  3. Suppressed renin means the aldosterone is autonomous (not driven by RAAS).

Answer. Primary aldosteronism (adrenal adenoma or bilateral hyperplasia). Confirm with an elevated aldosterone-to-renin ratio; treat an adenoma surgically or bilateral disease with spironolactone or eplerenone.