Defined as systolic BP ≥ 140 mm Hg and/or diastolic BP ≥ 90 mm Hg based on three measurements separated in time in adults (see Table 1). Classified as 1° or 2°. A major risk factor for stroke and MI.
1° (ESSENTIAL) HYPERTENSION
Hypertension with no identifiable cause. Represents 95% of cases of HTN. Risk factors include a family history of HTN or heart disease, a high sodium diet, smoking, obesity, ethnicity (African-Americans > whites), and advanced age.
- HTN is usually asymptomatic until complications develop.
- Patients should be evaluated for end-organ damage to the brain (stroke, dementia), eye (cotton-wool exudates, hemorrhage, retinopathy), heart (LVH), and kidney (proteinuria, CKD). Renal bruits may signify renal artery stenosis as the cause of HTN.
- Quantify overall risk: Fasting glucose, HBA1c, lipid profile.
- Assess end-organ damage: ECG to check for LVH or past MI, urinalysis for proteinuria or hematuria; BUN/creatinine.
- Exclude secondary causes (as required): U&Es, Ca2+, renal ultrasound, 24-hour urine metanephrine, renin, aldosterone, urinary cortisol.
- 24-hour ambulatory BP monitoring (ABPM) may be useful sometimes (ie, “white coat” or borderline hypertension).
Treatment of HTN— ABCDMnemonic
Diuretics (typically thiazide diuretics)
- Begin with lifestyle modifications (weight loss, exercise, smoking cessation, diet improvement, limit alcohol and salt intake).
- BP goals vary by category and ASCVD (see Table 1).
- Diuretics, CCBs, ACEIs, and β-blockers have been shown to ↓ mortality in uncomplicated HTN. They are first-line agents unless a comorbid condition requires another medication (see Table 2).
- For patients who are not African-American, including those with diabetes, → ACEI/ARB (nephroprotective), thiazide, CCB.
- For African American patients, including those with diabetes, → thiazide, CCB.
- For patients ≥ 18 years of age with CKD → ACEI/ARB (nephroprotective).
- If BP goal is not reached within 1 month of commencing treatment, ↑ dose of initial drug or add a second drug, and if goal BP cannot be reached with two drugs, add and titrate a third drug. Poorer outcomes are seen if ACEIs and ARBs are used together.
- Periodically test for end-organ complications, including renal complications (BUN, creatinine, urine protein-to-creatinine ratio), hypertensive retinopathy (eye exam), and cardiac complications (ECG evidence of LVH).
Hypertension 2° to an identifiable organic cause (∼5% of cases). See Table 3 for the diagnosis and treatment of common causes.
Causes of 2° hypertension—Mnemonic
Hyperaldosteronism (Conn syndrome)
Stenosis of renal arteries
Renal causes (renal artery stenosis, PKD)
Endocrine (Conn syndrome, Cushing syndrome, hyperparathyroidism, pheochromocytoma)
Coarctation of the aorta
A spectrum of clinical presentations in which there is a severe increase in BP (usually > 180/120 mm Hg) that can lead to end-organ damage.
Present with end-organ damage revealed by acute kidney injury, severe chest pain (ischemia, MI), back pain (aortic dissection), stroke, severe headache with changes in mental status (hypertensive encephalopathy), and blurred vision. Other symptoms include nausea and vomiting, seizures, shortness of breath, and severe anxiety.
- Hypertensive urgency: ↑ BP with mild to moderate symptoms (headache, chest pain, nausea and vomiting) without end-organ damage.
- Hypertensive emergency: ↑ BP with signs or symptoms of impending end-organ damage such as acute kidney injury, intracranial or retinal hemorrhage, papilledema, stroke, or ECG changes suggestive of ischemia, MI, or pulmonary edema.
Hypertensive emergencies are diagnosed on the basis of the extent of end-organ damage, not BP measurement.
- Hypertensive urgency: BP can be reduced gradually over 24–48 hours with oral antihypertensives (eg, β-blockers, clonidine, ACEIs) (see Table 4).
- Hypertensive emergency: BP must be reduced immediately to prevent imminent organ damage. Treat with IV medications (labetalol, nitroprusside, nicardipine) with the goal of lowering mean arterial pressure by no more than 25% over the first 2 hours to prevent cerebral hypoperfusion or coronary insufficiency.