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- Essential hypertension (HTN) is HTN without an identifiable cause; it is also known as primary HTN and benign HTN. Although its importance as a risk factor for cardiovascular and other morbidity and mortality is well-established, there is significant and increasing controversy regarding recommended thresholds for diagnosis and treatment.
- HTN is defined (Joint National Committee [JNC] 8) as ≥2 elevated BPs (1).
- Age <60 years: systolic BP (SBP) ≥140 mm Hg and/or diastolic BP (DBP) ≥90 mm Hg at ≥2 visits
- Age ≥60 years: SBP ≥150 mm Hg and/or DBP ≥90 mm Hg at ≥2 visits
- With diabetes or chronic kidney disease (CKD): SBP ≥140 and/or DBP ≥90 mm Hg
- Synonym(s): benign, chronic, idiopathic, familial, or genetic HTN; high BP
- Isolated systolic HTN is common.
- Therapy has been shown to be effective and beneficial at preventing stroke, although target SBP is higher than in younger patients (~150 mm Hg systolic), and adverse reactions to medications are more frequent (2)[A]. The benefit of therapy has been conclusively demonstrated in older patients for SBP ≥160 mm Hg. More aggressive targets may be appropriate for higher risk individuals (2)[A].
- Measure BP during routine exams for >3 years of age.
- Defined as SBP or DBP ≥95th percentile on repeated measurements
- Pre-HTN: SBP or DBP between 90th and 95th percentile
- Elevated BP during pregnancy may represent chronic HTN, pregnancy-induced HTN, or preeclampsia. ACE inhibitors and angiotensin II receptor blockers (ARBs) are contraindicated.
- Maternal and fetal mortality are reduced with treatment of severe HTN. Evidence is not clear for treatment of mild HTN (see topic “Preeclampsia and Eclampsia (Toxemia of Pregnancy)”).
- Preferred agents: methyldopa, labetalol, hydralazine, or nifedipine
Incidence and prevalence is higher among men. Depending on the definition used, 32–46% of adults in the United States have HTN.
Etiology and Pathophysiology
- >90% of cases of HTN have no identified cause.
- For differential diagnosis and causes of secondary HTN, see “Hypertension, Secondary and Resistant.”
BP levels are strongly familial, but no clear genetic pattern exists. Familial risk for cardiovascular diseases (CVDs) should be considered.
Family history, obesity, alcohol use, excess dietary sodium, stress, physical inactivity, tobacco use, insulin resistance