Clinical meaning
Hypertension is defined by the 2017 ACC/AHA guidelines as BP ≥130/80 mmHg (replacing the previous JNC8 threshold of 140/90). Sustained elevated pressure causes endothelial dysfunction, reduces nitric oxide bioavailability, promotes vascular smooth muscle hypertrophy and arterial stiffening. The left ventricle undergoes concentric hypertrophy to overcome increased afterload, eventually progressing to diastolic then systolic dysfunction. Target organ damage affects the brain (lacunar infarcts, hemorrhagic stroke), heart (LVH, coronary artery disease, heart failure), kidneys (nephrosclerosis, proteinuria), eyes (hypertensive retinopathy), and peripheral vasculature (atherosclerosis, aortic dissection). Diagnosis requires confirmation with out-of-office measurements to exclude white-coat hypertension, which affects 15-30% of patients with elevated office readings.
Diagnosis & workup
Diagnostics & workup: - Office BP measurement: proper technique (rest 5 min, feet flat, arm at heart level, appropriate cuff size); average of ≥2 readings on ≥2 occasions - Ambulatory blood pressure monitoring (ABPM): gold standard for confirming HTN diagnosis; 24-hour average ≥125/75 confirms HTN; identifies white-coat HTN and masked HTN - Home blood pressure monitoring (HBPM): average ≥130/80 confirms HTN; instruct morning/evening readings for 7 days - BMP with creatinine and eGFR (renal function), fasting lipid panel, fasting glucose or HbA1c, urinalysis with spot urine albumin-to-creatinine ratio - TSH, serum calcium (screening for secondary causes) - 12-lead ECG for LVH (Sokolow-Lyon criteria: S in V1 + R in V5/V6 ≥35mm) - Screen for secondary HTN if onset <30 years, resistant HTN (uncontrolled on 3+ drugs), sudden worsening, or clinical clues (hypokalemia → aldosteronism; paroxysmal HTN with triad → pheochromocytoma)