Hypertension (HTN)

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Hypertension (HTN)

Definitions

  • 2017 ACC/AHA: ≥ 130/80 mmHg

  • JNC 8 & ISH: ≥ 140/90 mmHg

  • Children:

    • <13 y: ≥ 95th percentile or ≥130/80 (whichever lower)

    • ≥13 y: ≥130/80

Classification (2017 ACC/AHA)

  • Normal: <120/<80

  • Elevated: 120–129/<80

  • Stage 1: 130–139 or 80–89

  • Stage 2: ≥140 or ≥90

Epidemiology

  • Affects 1/3–1/2 adults in US

  • Primary HTN: 90% (multifactorial)

  • Secondary HTN: 10% (renal, endocrine, vascular, drugs, OSA)

  • ↑ prevalence with age, obesity, African American race, and family history

Risk Factors

  • Nonmodifiable: age, family history, race/ethnicity

  • Modifiable: obesity (most important), high salt intake, low K⁺ intake, alcohol, smoking, inactivity, stress, uncontrolled DM

Clinical Features

  • Usually asymptomatic until complications

  • Possible early nonspecific symptoms: headache (morning), dizziness, tinnitus, chest discomfort, epistaxis

  • Target organ damage:

    • Brain → stroke, TIA, cognitive decline

    • Heart → LVH, CAD, HF, MI

    • Kidneys → CKD, proteinuria

    • Eyes → retinopathy

Subtypes

  • White coat HTN: high in clinic, normal outside

  • Masked HTN: normal in clinic, high outside

  • Isolated systolic HTN: SBP ≥140, DBP ≤90 (common in elderly)

  • Resistant HTN: uncontrolled ≥130/80 on ≥3 drugs or requires ≥4

Secondary Hypertension Causes

  • Renal: renal artery stenosis, CKD, glomerulonephritis, polycystic kidney


  • Endocrine: Conn (hyperaldosteronism), Cushing, pheochromocytoma, hyperthyroidism, hyperparathyroidism, acromegaly

  • Vascular: coarctation of aorta

  • Others: OSA, drugs (NSAIDs, OCPs, steroids, cocaine, sympathomimetics)


Diagnosis

  1. Office BP ≥130/80 on ≥2 visits

  2. Confirm with ABPM or HBPM

  3. Evaluate risk + organ damage

    • Labs: CBC, electrolytes, Cr/eGFR, glucose, lipids, TSH, urinalysis, UACR

    • ECG (± echo, fundoscopy)


  4. Consider secondary workup if: young age, abrupt onset, resistant HTN, severe HTN, abnormal labs

    ADPCKD CAUSE 2ry HTN

Management

Lifestyle (for all patients)

  • Weight loss (1 mmHg ↓ per kg lost)

  • DASH diet (fruits, vegetables, whole grains, low sat fat)

  • ↓ Na⁺ (<1.5 g/day), ↑ K⁺ intake (unless CKD)

  • Exercise (aerobic 150 min/week)

  • Limit alcohol (♂ ≤2 drinks, ♀ ≤1/day)

  • Stop smoking


Pharmacological

  • First line: ACEIs, ARBs, thiazides, CCBs

  • Add based on comorbidities:

    • CHF/MI: ACEI/ARB + β-blocker + diuretic + aldosterone antagonist

    • CKD/DM with albuminuria: ACEI/ARB

    • Stroke: thiazide + ACEI/ARB

    • Black patients (no CKD/CHF): thiazide or CCB

  • Avoid: ACEI + ARB combo

  • Resistant HTN: add spironolactone, evaluate secondary causes

    HTN+COMORBIDITY

Target BP

  • Most adults: <130/80

  • CKD (if tolerated): SBP <120

  • Elderly (>65 y): individualized, often <130 systolic

STEP2 NOTE:

  • Patients with severe hypertension or evidence of end-organ damage should be prescribed antihypertensive therapy immediately.  For those with only mild blood pressure elevations, the diagnosis should first be confirmed outside of a health care setting with ambulatory blood pressure monitoring or home measurement.

  • For hypertensive patients with systolic blood pressure (BP) <20 mm Hg and/or diastolic BP <10 mm Hg above target, 1-drug antihypertensive therapy is often adequate.  However, a single agent is unlikely to be adequate for those with baseline BP ≥20/10 mm Hg above target, and 2-drug therapy is likely to be required.

  • Fibromuscular dysplasia is a noninflammatory and nonatherosclerotic condition that presents most commonly in women age 15-50.  The condition affects primarily the renal arteries and causes hypertension.  Involvement of the cerebrovascular arteries (eg, carotid, vertebral) can cause symptoms of brain ischemia (eg, transient ischemic attack, amaurosis fugax, stroke) or nonspecific symptoms (eg, headache, pulsatile tinnitus, dizziness).

  • Excessive alcohol intake (ie, >2 drinks/day) and binge drinking (ie, ≥5 drinks in a single sitting) are associated with increased incidence of hypertension, higher blood pressure, and failure to respond to appropriate antihypertensive therapy.  In contrast, moderate alcohol intake is associated with lower blood pressure.

  • Onset of hypertension at a young age (ie, age <30) should raise suspicion for a secondary cause.  In addition to hypertension, features suggesting intranasal cocaine use include epistaxis and tremor.  A urine drug screen should be considered in a young patient with unexplained hypertension.

  • Obstructive sleep apnea (OSA) is a common cause of secondary hypertension due to the production of catecholamines during apneic episodes.  The hypertension is often resistant to medications, but treatment of the underlying OSA (eg, nocturnal continuous positive airway pressure) often leads to resolution.  Other cardiovascular complications of OSA include pulmonary hypertension, right-sided heart failure, coronary heart disease, and arrhythmias.

  • Hyperparathyroidism is a cause of secondary hypertension and should be suspected in patients who have hypertension associated with hypercalcemia, renal stones, abdominal pain, or neuropsychiatric symptoms.  Other cardiovascular manifestations of hyperparathyroidism include left ventricular hypertrophy, arrhythmias, and vascular and valvular calcification.

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