Excerpt from Hypertensive Emergencies

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Background

Approximately 50 million people in the United States are affected by hypertension (HTN).¹ New data show an increased lifetime risk of developing HTN and an increased risk of cardiovascular complications associated with blood pressures (BPs) previously considered to be normal. Given this information, the Joint National Committee (JNC-7) has introduced a new classification system for HTN.²

• Prehypertension - Systolic blood pressure (SBP) 120-139 mm Hg or diastolic blood pressure (DBP) 80-89 mm Hg
• Stage I HTN - SBP 140-159 mm Hg or DBP 90-99 mm Hg
• Stage II HTN - SBP >160 mm Hg or DBP >100 mm Hg

Hypertensive crises encompass a spectrum of clinical presentations where uncontrolled BPs lead to progressive or impending target organ dysfunction (TOD). The clinical distinction between hypertensive emergencies and hypertensive urgencies depends on the presence of acute TOD and not on the absolute level of the BP.

Hypertensive emergency

Hypertensive emergencies represent severe HTN with acute impairment of an organ system (eg, central nervous system [CNS], cardiovascular, renal). In these conditions, the BP should be lowered aggressively over minutes to hours.

Hypertensive urgency

Hypertensive urgency is defined as a severe elevation of BP, without evidence of progressive TOD. These patients require BP control over several days to weeks.

Emergency department considerations

Optimal control of hypertensive situations balances the benefits of immediate decreases in BP against the risk of a significant decrease in target organ perfusion. The ED must be capable of the following:

• Appropriately evaluating patients with an elevated BP
• Correctly classifying the HTN
• Determining the aggressiveness and timing of therapeutic interventions
• Making disposition decisions

An important point to remember in the management of the patient with any degree of BP elevation is to "treat the patient and not the number."

Pathophysiology

The pathophysiology of hypertensive emergencies is not well understood. Failure of normal autoregulation and an abrupt rise in systemic vascular resistance are typically initial steps in the disease process. This is followed by endovascular injury, with fibrinoid necrosis within the arterioles. If the process is not stopped, a cycle of ischemia, platelet deposition, and further autoregulatory dysfunction ensues. The 4 major organ systems affected by high BP are the CNS, cardiovascular system, renal system, and gravid uterus.

Single-organ involvement is found in approximately 83% of patients presenting with hypertensive emergencies. Two-organ involvement is found in 14% of cases, and multiorgan involvement (>3 organ systems) is found in approximately 3% of patients presenting with a hypertensive emergency.³

The most common clinical presentations of hypertensive emergencies are cerebral infarction (24.5%), pulmonary edema (22.5%), hypertensive encephalopathy (16.3%), and congestive heart failure (12.0%). Less common presentations include intracranial hemorrhage, aortic dissection, and eclampsia.³

Central nervous system

Cerebral autoregulation is the inherent ability of the cerebral vasculature to maintain a constant cerebral blood flow (CBF) despite changes in blood pressure. As mean arterial pressure (MAP) increases, the cerebral endothelium is disrupted and the blood-brain barrier can become interrupted. Fibrinoid material deposits in the cerebral vasculature and causes narrowing of the vascular lumen. The cerebral vasculature then attempts to vasodilate around the narrowed lumen. This leads to cerebral edema and microhemorrhages. Patients with chronic HTN can tolerate higher MAPs before they have disruption of their autoregulation system. However, such patients also have increased cerebrovascular resistance and are more prone to cerebral ischemia when flow decreases.

Hypertensive encephalopathy is one of the clinical manifestations of cerebral edema and microhemorrhages seen with dysfunction of cerebral autoregulation. Without treatment, hypertensive encephalopathy can lead to cerebral hemorrhage, coma, and death.

Cardiovascular system

HTN affects the structure and function of the coronary vasculature and left ventricle. HTN also activates the renin-angiotensin-aldosterone system, causing systemic vasculature constriction. This results in increasing myocardial oxygen demand by increasing the left ventricular wall tension and leads to left ventricular hypertrophy and coronary compression. During hypertensive emergencies, the left ventricle cannot overcome systemic vascular resistance. This leads to left ventricular failure and pulmonary edema or myocardial ischemia.

Renal system

Chronic HTN causes pathologic changes to the small arteries of the kidney. The arteries develop endothelial dysfunction and impaired vasodilation, which alter renal autoregulation. When the renal autoregulatory system is disrupted, the intraglomerular pressure starts to vary directly with the systemic arterial pressure, thus offering no protection to the kidney during BP fluctuations. During a hypertensive crisis, this can lead to acute renal ischemia.

Frequency

United States

Hypertension affects approximately 25% of the population in the United States.⁴ The prevalence of HTN increases with advancing age. More than half of people aged 60-69 years and approximately three quarters of people aged 70 years or older are affected by this disease.² Hypertensive crises affect about 500,000 Americans or approximately 1% of hypertensive adults.¹

International

Worldwide, approximately 1 billion people have HTN.²

Mortality/Morbidity

Death from both ischemic heart disease and stroke increase progressively as the BP increases. For every 20 mm Hg systolic or 10 mm Hg diastolic increase in blood pressures above 115/75 mm Hg, the mortality rate from both ischemic heart disease and stroke doubles.²

The morbidity and mortality of hypertensive emergencies depend on the extent of TOD on presentation and the degree to which BP is controlled subsequently. With BP control and medication compliance, the 10-year survival rate of patients with hypertensive crises approaches 70%.¹

• The 1-year mortality rate for an untreated hypertensive emergency is 79%.⁵
• The 5-year survival rate among all patients presenting with a hypertensive crisis is 74%.⁶ 

Race

Hypertension develops at an earlier age, leads to more clinical sequelae, and is more common and severe in African Americans compared with age-matched non-Hispanic whites. Hypertensive crises are also more common in African Americans when compared with other races.

The prevalence and incidence of HTN in Mexican Americans are similar to or lower than those in non-Hispanic whites. In general, Mexican Americans and Native Americans have lower BP control rates than non-Hispanic whites and African Americans.

Sex

Overall, the prevalence and incidence of HTN is slightly higher in men than in women. Hypertensive crises are 2 times more frequent in males than in females.

Age

Hypertensive crises are more common among elderly persons.

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