a. Definition. Patients who consistently have systolic blood pressure >140 mm Hg or diastolic blood pressure >90 mm Hg are considered to be hypertensive.
b. Hypertension is an extremely common disorder in both outpatients and hospitalized patients. In general, hypertension in inpatients is a major concern when patients present with hypertensive urgency or emergency.
B. Essential Hypertension
a. Also called primary hypertension, essential hypertension is very common and increases in prevalence with age. One in three US adults, or 67 million adults (31%), have hypertension. Both genetic and environmental factors contribute to risk for developing hypertension.
b. Confirmation with out-of-office blood pressure monitoring (ambulatory or home monitoring) is helpful to rule out white-coat hypertension.
c. Evaluation of a patient with hypertension should include assessment of cardiovascular risk factors, signs or symptoms of secondary hypertension, and evidence of end-organ damage.
d. Treatment of essential hypertension should involve a combination of lifestyle modification and pharmacologic agents as outlined in the recent Eighth Joint National Committee (JNC 8) recommendations.
i. Lifestyle modification includes weight reduction, exercise, restriction of alcohol and sodium, and a DASH diet (high in fruits and vegetables, low in fat and dairy).
ii. Pharmacologic interventions
1. First-line agents include thiazide diuretics, calcium channel blockers (CCBs), angiotensin-converting enzyme (ACE) inhibitors, and angiotensin receptor blockers (ARBs).
2. Preferential agents when initiating therapy exist. For example, when starting treatment in patients of African descent without chronic kidney disease (CKD), CCBs and thiazides, instead of ACE inhibitors, are preferred.
3. Use of ACE inhibitors and ARBs is recommended in all patients with CKD regardless of ethnic background, either as first-line therapy or in addition to first-line therapy.
4. ACE inhibitors and ARBs should not be used in the same patient simultaneously.
5. CCBs and thiazide-type diuretics should be used instead of ACE inhibitors and ARBs in patients older than 75 years with impaired kidney function because of the risk for hyperkalemia, increased creatinine, and further renal impairment associated with these agents.
1. In patients 18 to 59 years of age without major comorbidities, and in patients 60 years or older who have diabetes, CKD, or both conditions, the goal blood pressure level is <140/90 mm Hg.
2. In patients 60 years or older who do not have diabetes or CKD, the goal blood pressure level is <150/90 mm Hg.
C. Causes of Secondary Hypertension. Although 95% of hypertensive patients have essential (primary) hypertension, causes of secondary hypertension must be considered in patients with characteristic signs or symptoms, with onset of hypertension at a very young or old age, or when the blood pressure is refractory to medical therapy. The causes of secondary hypertension can be remembered using the following memory aid:
One anatomic cause
Two renal causes
Three adrenal causes
Ethanol abuse or Estrogen use
a. One anatomic cause. Aortic coarctation, a congenital disorder characterized by aortic constriction at the origin of the left subclavian artery, usually presents in children or young adults and can lead to hypertension.
b. Two renal causes
i. Intrinsic renal disease. Almost any parenchymal kidney disorder can lead to hypertension, usually as a result of increased intravascular volume, increased endothelial reactivity, and/or increased activity of the renin-angiotensin-aldosterone system.
ii. Renal artery stenosis, a relatively common cause of secondary hypertension, is caused by atherosclerosis in older patients (most common) or fibromuscular dysplasia in young women (very infrequent). The stenosis leads to decreased renal blood flow, which stimulates renin release leading to systemic hypertension. This is a difficult diagnosis to make but should be suspected in patients with known atherosclerosis or risk factors for atherosclerosis (smokers), unexplained renal disease, history of flash pulmonary edema, and resistance of hypertension to medical therapy. Duplex Doppler ultrasonography is a reasonable initial imaging modality because it avoids iodinated contrast or gadolinium associated with computed tomographic angiography and magnetic resonance angiography. Conventional renal artery angiography remains the gold standard. Consider renal artery stenosis as the cause of hypertension if a patient shows a dramatic increase in serum creatinine (doubling or tripling) after starting ACE inhibitor therapy.
Always consider renal artery stenosis as the cause of hypertension when a patient shows a dramatic increase in serum creatinine after starting ACE inhibitor therapy for hypertension.
c. Three adrenal causes
i. Primary hyperaldosteronism, a relatively common cause of secondary hypertension, is caused by an aldosterone-secreting adenoma or bilateral adrenal hyperplasia. Primary hyperaldosteronism should be suspected in a hypertensive patient with hypokalemia without diuretic therapy.
Primary hyperaldosteronism should be suspected if a hypertensive patient is hypokalemic and not taking diuretics.
ii. Cushing’s syndrome. Excess glucocorticoids (from any cause) will often cause the patient to be hypertensive. Usually, other clinical manifestations of glucocorticoid excess (e.g., round facies, buffalo hump) are present to aid in making the diagnosis.
iii. Pheochromocytoma is a rare norepinephrine- and epinephrine-secreting tumor that may be malignant and can also lead to headaches and glucose intolerance. It is most commonly—but not always—located near the adrenals.
d. “Five CENTS”
i. Calcium. Hypercalcemia is an uncommon cause of hypertension but should be considered in those who have underlying diseases apt to lead to hypercalcemia (see Chapter 76).
ii. Ethanol abuse, estrogen use, or use of other drugs and toxins. The most common causes of secondary hypertension are the use of alcohol and oral contraceptives. Pregnancy can also lead to hypertension. Over-the-counter preparations, such as ephedrine-containing medications and other cold remedies, commonly raise blood pressure. Certain illicit drugs, such as cocaine and methamphetamines, are also common culprits.
iii. Neurologic disease. Any process that leads to increased intracranial pressure can lead to the triad of hypertension, bradycardia, and irregular respiration (known as Cushing’s triad).
iv. Thyrotoxicosis. Patients with hyperthyroidism can also be hypertensive.
v. Sleep apnea (obstructive) is strongly associated with hypertension, possibly by upregulation of the sympathetic nervous system.
D. Hypertensive Crises: Urgencies and Emergencies
a. Hypertensive urgencies are situations in which the patient has systolic blood pressure >220 mm Hg or diastolic blood pressure >120 mm Hg but without evidence of end-organ damage. Urgencies are usually treated with oral antihypertensive agents (e.g., labetalol, clonidine, or captopril) in the emergency department. After their blood pressure is lowered to an acceptable level, these patients may be discharged but warrant very close follow-up.
Sublingual or short-acting nifedipine should be avoided in almost all patients because it often causes rebound hypertension.
i. Examples. The following situations qualify as hypertensive emergencies:
1. Hypertensive encephalopathy (altered mental status)1
2. Intracranial hemorrhage
3. Aortic dissection
4. Myocardial infarction
5. Unstable angina
6. Hypertensive nephropathy (progressive acute kidney injury with proteinuria and hematuria)
ii. Treatment of hypertensive emergencies usually requires admission to the intensive care unit (ICU) and the administration of parenteral antihypertensives (e.g., nitroglycerin, nitroprusside, labetalol). To minimize organ hypoperfusion, blood pressures should not be lowered by more than 25% over the first 1–2 days (i.e., not lower than 170/110 mm Hg). Treatment of target organ damage should occur in conjunction with blood pressure control.
Suggested Further Readings
Berlowitz DR, Foy CG, Kazis LE, et al. Effect of intensive blood-pressure treatment on patient-reported outcomes. N Engl J Med 2017;377:733–44.Find this resource:
Calhoun DA, Jones D, Textor S, et al. Resistant hypertension: diagnosis, evaluation, and treatment. Circulation 2008;117:e510.Find this resource:
James PA, Oparil S, Carter BL, et al. 2014 Evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8). JAMA 2014;311:507–20.Find this resource:
Johnson W, Nguyen M-L, Patel R. Hypertension crisis in the emergency department. Cardiol Clin 2012;30:533–43.Find this resource:
SPRINT Research Group. A randomized trial of intensive versus standard blood-pressure control. N Engl J Med 2015;373:2103–16.Find this resource:
1 Malignant hypertension is an outdated term that implies hypertension associated with encephalopathy and accompanied by papilledema. It is a form of hypertensive emergency.