General Principles

Hypertension is defined as the presence of blood pressure (BP) elevation to a level that places patients at increased risk for target organ damage in several vascular beds including the retina, brain, heart, kidneys, and large conduit arteries (Table 3-1 and Table 3-2).

Table 3-1: Manifestations of Target Organ Disease
Organ SystemManifestation
Large vesselAneurysmal dilation
Accelerated atherosclerosis
Aortic dissection
CardiacAcute: Pulmonary edema, myocardial infarction
Chronic: Clinical or ECG evidence of CAD; LVH by ECG or echocardiogram
CerebrovascularAcute: Intracerebral bleeding, coma, seizures, mental status changes, TIA, stroke
Chronic: TIA, stroke
RenalAcute: Hematuria, azotemia
Chronic: Serum creatinine >1.5 mg/dL, proteinuria >1+ on dipstick
RetinopathyAcute: Papilledema, hemorrhages
Chronic: Hemorrhages, exudates, arterial nicking

CAD, coronary artery disease; LVH, left ventricular hypertrophy; TIA, transient ischemic attack.

Table 3-2: Classification of Blood Pressure for Adults Age 18 Years and Oldera
CategorySystolic Pressure (mm Hg)Diastolic Pressure (mm Hg)
Elevated blood pressure120–129<80
Hypertension, stage 1130–13980–89
Hypertension, stage 2≥140≥90

aNot taking antihypertensive drugs and not acutely ill. When systolic and diastolic pressures fall into different categories, the higher category should be selected to classify the individual’s blood pressure status.

Data from Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: a report of the American College of Cardiology/American Heart Association task force on clinical practice guidelines. J Am Coll Cardiol. 2018;71:e127-e248.  [PMID:29146535]


  • The following definitions and recommendations are based on the 2017 American College of Cardiology (ACC)/American Heart Association (AHA) guidelines. The 2018 European Society of Cardiology and European Society of Hypertension (ESC/ESH) guidelines and 2019 National Institute for Health and Care Excellence (NICE) guidelines do differ, particularly in terms of treatment thresholds.1,2
  • Normal BP is defined as systolic blood pressure (SBP) <120 mm Hg and diastolic blood pressure (DBP) <80 mm Hg; pharmacologic intervention is not indicated.
  • Elevated blood pressure is defined as SBP of 120–129 mm Hg and DBP of >80 mm Hg. These patients should engage in comprehensive lifestyle modifications to delay progression or prevent the development of hypertension. Blood pressure should be reassessed in 3–6 months.
  • In stage 1 hypertension (SBP 130–139 mm Hg or DBP 80–89 mm Hg), low-risk adults (no atherosclerotic cardiovascular disease [ASCVD] and 10-year cardiovascular disease [CVD] risk of <10%) should start with nonpharmacologic therapy and comprehensive lifestyle modifications. Blood pressure should be reassessed in 3–6 months. If not at goal, pharmacological therapy should be considered. In those with ASCVD or a 10-year CVD risk of ≥10%, pharmacologic therapy should be initiated in addition to lifestyle modification. Blood pressure should be reassessed in 1 month with a target of <130/80 mm Hg. If at goal, reassess every 3–6 months. If not at goal, assess for adherence and consider intensification of therapy.1,3
  • In stage 2 hypertension (SBP ≥140 mm Hg or DBP ≥90 mm Hg), pharmacologic therapy should be initiated in addition to lifestyle modification to lower BP to <130/80 mm Hg. Patients with BP levels >20/10 mm Hg above their treatment target will often require more than one medication to achieve adequate control, and a two-drug regimen may be initiated as initial therapy. Blood pressure should be reassessed in 1 month. If at goal, reassess every 3–6 months. If not at goal, assess for adherence and consider intensification of therapy.
  • If there is a disparity in category between systolic and diastolic blood pressures, individuals should be designated to the higher BP category.1,4
  • Hypertensive emergency is the association of substantially elevated blood pressure with evidence of acute end-organ damage (retina, brain, heart, large arteries, kidneys). It usually develops in patients with a previous history of elevated BP but may arise in those who were previously normotensive. Appropriate treatment of hypertensive emergency lowers blood pressure to prevent continued end-organ damage but does so slowly and gradually to prevent ischemic damage. Mean arterial pressure should be reduced by 10%–20% in the first hour and a further 5%–15% over the next 23 hours. Exceptions to gradual blood pressure lowering include acute ischemic stroke, acute aortic dissection, and intracerebral hemorrhage.5,6,7
    • Malignant hypertension is severe blood pressure elevation (largely BP >200/120) with associated advanced bilateral retinopathy.
    • Hypertensive encephalopathy is severe blood pressure elevation associated with lethargy, seizures, cortical blindness, and coma in the absence of other possible etiologies.
    • Other examples of clinical presentations of hypertensive emergencies include hypertensive thrombotic microangiopathy, acute coronary syndrome, acute stroke, cerebral hemorrhage, flash pulmonary edema, and aortic aneurysm/dissection.
  • Patients with severe asymptomatic hypertension who lack acute hypertension-mediated organ damage are not considered to have hypertensive emergency. Treatment with oral antihypertensive therapy in these patients is often appropriate as there is no proven benefit from rapid reduction of blood pressure in patients with severe asymptomatic hypertension.5,8,9
  • Isolated systolic hypertension, defined as an SBP ≥140 mm Hg and DBP <90, occurs frequently in the elderly (beginning after the fifth decade and increasing with age). Nonpharmacologic therapy should be initiated with medications added as needed and tolerated to lower SBP.
  • Resistant hypertension is defined as BP ≥130/80 in hypertensive patients on ≥3 antihypertensive agents, one of which is a diuretic, or controlled BP on ≥4 antihypertensive agents. All agents should be prescribed at maximally recommended (or maximally tolerated) doses. Causes of pseudoresistance should be ruled out prior to diagnosis with resistant hypertension (inaccuracy in BP measurement, white coat hypertension, poor adherence, or poor regimen).10,11 Potential causes of resistant hypertension include ingestion of exogenous substances (e.g., decongestants, oral contraceptives, appetite suppressants, sympathomimetics, venlafaxine, tricyclic antidepressants, monoamine oxidase inhibitors [MAOIs], chlorpromazine, some herbal supplements [e.g.: ma huang], steroids, NSAIDs, cyclosporine, caffeine, thyroid hormones, cocaine, alcohol use, erythropoietin) and secondary causes of hypertension.1
  • White coat hypertension is defined as blood pressure that is consistently elevated by office readings but does not meet diagnostic criteria for hypertension based on out-of-office readings.
  • Masked hypertension is defined as blood pressure that is consistently elevated by out-of-office measurements but does not meet the criteria for hypertension based on office readings.


  • The public health burden of hypertension is enormous. According to recent estimates from the National Health and Nutrition Examination Survey (NHANES) through the Centers for Disease Control and Prevention (CDC), hypertension affects an estimated 116 million American adults, up from 103 million per ACC/AHA guidelines in 2017.12,13 Of the population with hypertension, 73.9% of people with hypertension in the United States have uncontrolled hypertension. For nonhypertensive individuals aged 55–65 years, the lifetime risk of developing hypertension is 90%.14
  • Data derived from the Framingham Study have shown that hypertensive patients have a fourfold increase in cerebrovascular accidents and a sixfold increase in congestive heart failure (CHF) when compared with normotensive control subjects.14
  • Disease-associated morbidity and mortality, including ASCVD, stroke, heart failure (HF), and renal insufficiency, increase with higher levels of SBP and DBP. Elevated blood pressure is the strongest modifiable risk factor for CVD worldwide.15
  • Over the last 3 decades, aggressive treatment of hypertension has resulted in a substantial decrease in death rates from stroke and coronary heart disease (CHD). Although the incidence of end-stage renal disease (ESRD) has stabilized and hospitalizations for CHF have overall decreased,16 BP control rates remain poor, with 53% of treated hypertensive patients having BP above target goal.13


  • BP rises with age. Other contributing factors include obesity, decreased physical activity, increased dietary sodium intake, increased alcohol consumption, and lower dietary intake of fruits, vegetables, and potassium.
  • Of all hypertensive patients, more than 90% have primary or essential hypertension. The remainder have secondary hypertension due to renal parenchymal disease, renovascular disease, pheochromocytoma, Cushing syndrome, primary hyperaldosteronism, coarctation of the aorta, obstructive sleep apnea, and uncommon autosomal dominant or autosomal recessive diseases of the adrenal–renal axis, which result in salt retention.

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