Hypertensive emergency

A hypertensive emergency is severe hypertension (high blood pressure) with acute impairment of an organ system (especially the central nervous system, cardiovascular system and/or the renal system) and the possibility of irreversible organ-damage. In case of a hypertensive emergency, the blood pressure should be lowered aggressively over minutes to hours with an antihypertensive agent.

Several classes of antihypertensive agents are recommended and the choice for the antihypertensive agent depends on the cause for the hypertensive crisis, the severity of elevated blood pressure and the patient's usual blood pressure before the hypertensive crisis. In most cases, the administration of an intravenous sodium nitroprusside injection which has an almost immediate antihypertensive effect is suitable but in many cases not readily available. In less urgent cases, oral agents like captopril, clonidine, labetalol, prazosin, which all have a delayed onset of action by several minutes compared to sodium nitroprusside, can also be used.

It is also important that the blood pressure is lowered not too abruptly, but smoothly. The initial goal in hypertensive emergencies is to reduce the pressure by no more than 25% (within minutes to 1 or 2 hours) and then toward a level of 160/100 mm Hg within 2–6 hours. Excessive reductions in pressure may precipitate coronary, cerebral, or renal ischemia. The diagnosis of a hypertensive emergency is not only based on the absolute level of blood pressure, but also on the individual regular level of blood pressure before the hypertensive crisis. Individuals with a history of chronic hypertension may not tolerate a "normal" blood pressure.

Incidence

Hypertensive crisis affects upward of 500,000 Americans each year. Although the incidence of hypertensive crisis is low, affecting fewer than 1% of hypertensive adults, more than 50 million adult Americans suffer from hypertension.

According to a research published in 2006, hypertension prevalence is again on the rise with 28.6% of the U.S. population suffering it in 1999-2002. According to the study, incidence rates of hypertension range between 3% and 18%. These numbers depend on the age, gender, ethnicity, and body size.

According to Whelton, the incidence and prevalence of hypertension is about 50% higher in African-American adults than in white or Mexican-American populations. Also, Whelton adds that prevalence of hypertension has increased progressively in children and adolescents between 1988-2000. According to the study recent estimates indicate that approximately 1 billion adults have hypertension. The highest prevalence of hypertension is in Eastern Europe and the Latin American/Caribbean region.

As a result of the use of antihypertensives, the incidence of hypertensive emergencies has declined from 7% to 1% of patients with hypertension. The 1 – year survival rate has also increased. Before 1950, this survival rate was only 20%, and it is now more than 90% with the proper medical treatment. Hypertensive crises affect less than 1% of hypertensive adults in the United States.

Hypertensive crises more commonly occur among blacks and the elderly. Most patients who experience hypertensive crises have previously been diagnosed as hypertensive. Many of such patients have been prescribed antihypertensive therapy , but have inadequate blood pressure control.

Estimates indicate that approximately 1% to 2% of patients with hypertension develop hypertensive crisis at some point in their lifetime. Men are usually more affected by hypertensive crises than women.

The incidence of hypertensive crises has increased and hospital admissions tripled between 1983 and 1990, from 23,000 to 73,000 per year in the United States. The incidence of postoperative hypertensive crisis varies and such variation depends on the population examined. Most studies report and incidence of between 4% to 35%.

Terminology

Generally, the terminology describing hypertensive emergencies can be confusing. Terms such as hypertensive crisis, malignant hypertension, hypertensive urgency, accelerated hypertension and severe hypertension are all used in the literature and often overlap.

Hypertensive emergency as a specific term

The term hypertensive emergency is primarily used as a specific term for a hypertensive crisis with a diastolic blood pressure of 120 mm Hg and above plus end organ damage (brain, cardiovascular, renal) (as described above) in contrast to hypertensive urgency where as yet no end organ damage has developed. The former requires immediate lowering of blood pressure such as with sodium nitroprusside infusions (NOT injections) while urgencies (about 3/4 of cases with diastolic blood pressure of 120 mm Hg and above) can be treated with oral agents, with the goal of lowering the mean arterial pressure (MAP) by 20% in 1-2 days with further reduction to "normal" levels in weeks or months. The former use of oral nifedipine, a calcium channel blocker, has been strongly banned because it is not absorbed in a controlled and reproducible fashion and has led to serious and fatal hypotensive problems.

Hypertensive emergency as a generic term

Sometimes, although not very often, the term hypertensive emergency is also used as a generic term, comprising both hypertensive emergency as a specific term for a serious and urgent condition of elevated blood pressure and hypertensive urgency as a specific term of a less serious and less urgent condition (the terminology hypertensive crisis is usually used in this sense).

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.

Hypertensive emergency pathophysiology includes:

• Abrupt increases in systemic vascular resistance likely related to humoral. vasoconstrictors
• Endothelial injury
• Fibrinoid necrosis of the arterioles
• Deposition of platelets and fibrin
• Breakdown of the normal autoregulatory function.
• The resulting ischemia prompts further release of vasoactive substances completing a vicious cycle.

If the process is not stopped, a vicious of homeostatic failure begins, leading to loss of cerebral and local autoregulation, organ system ischemia and dysfunction and myocardial infarction.

It is estimated that in up to 83% of hypertensive emergency patients a single-organ involvement is found and two-organ involvement in nearly 14% of patients. Almost 3% of the patients are found with multi-organ failure which means failure of at least 3 organ systems.

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%). Less common presentations include. intracranial hemorrhage, aortic dissection, and eclampsia

Cerebral autoregulation is the ability of the blood vessels in the brain to maintain a constant blood flow. It has been shown that people who suffer from chronic hypertension can tolerate higher arterial pressure before their autoregulation system is disrupted and that they have an increased cerebrovascular resistance which makes them more at risk of developing cerebral ischemia if the blood flow decreases into normotensive ranges. On the other hand, sudden or rapid rises in blood pressure may cause hyperperfusion and increased cerebral blood flow, causing increased intracranial pressure and cerebral edema. Hypertensive encephalopathy is one of the clinical manifestations of cerebral edema and microhemorrhages seen with dysfunction of cerebral autoregulation and is characterized by hypertension, altered mentation, and papilledema.

In what concerns heart damage, this seems to be caused by an increased arterial stiffness, increased systolic blood pressure, and widened pulse pressures, all of these as results of chronic hypertension. The coronary perfusion pressures are decreased by these factors, which increase the myocardial oxygen consumption as well, leading to left ventricular hypertrophy. As the left ventricle is unable to compensate for an acute rise in systemic vascular resistance, left ventricular failure and pulmonary edema or myocardial ischemia may occur.

Chronic hypertension has a great impact on the renal vasculature as well as it may cause 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 blood pressure fluctuations. During a hypertensive crisis, this can lead to acute renal ischemia.

Endothelial injury occurs due to severe elevations of blood pressure and fibrinoid necrosis of the arterioles follow. The vascular injury leads to deposition of platelets and fibrin, and a breakdown of the normal autoregulatory function. Ischemia occurs as a result which prompts further release of vasoactive substances. This process completes the vicious cycle.

Many factors and causes contribute in hypertension crises. One main cause is the discontinuation of antihypertensive medications. Other common causes of hypertensive crises are autonomic hyperactivity, collagen-vascular diseases, drug use including cocaine and amphetamines, glomerulonephritis, head trauma, neoplasias, preeclampsia and eclampsia, renovascular hypertension.

During a hypertensive emergency uncontrolled BPs lead to progressive or impending end-organ dysfunction; therefore, it is important to lower the BP aggressively. Acute end-organ damage may occur including neurological, cardiovascular and other. Some examples of neurological damage include hypertensive encephalopathy, cerebral vascular accident/cerebral infarction, subarachnoid hemorrhage, and intracranial hemorrhage. Cardiovascular damages include myocardial ischemia/infarction, acute left ventricular dysfunction, acute pulmonary edema, and aortic dissection. Other end-organ damage include acute renal failure or insufficiency, retinopathy, eclampsia, and microangiopathic hemolytic anemia. Also, severe blood pressure leads to problems in the eye such as retinopathy or damage to the blood vessels in the eye.

Mortality

Severe hypertension is a serious medical condition with a general poor prognosis as it is estimated that people who do not receive appropriate treatment live up to three years after the diagnosis has been established.

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

The risks of developing a life-threatening disease affecting the heart or brain increase as the blood flow increase. Commonly, ischemic heart attack and stroke are the causes that lead to death in patients with severe hypertension. It is estimated that for every 20 mm Hg systolic or 10 mm Hg diastolic increase in blood pressures above 115/75 mm Hg, the mortality rate for both ischemic heart disease and stroke doubles.

Several studies have concluded that African Americans have a greater incidence of hypertension and a greater morbidity and mortality from hypertensive disease than non-Hispanic whites. It appears that hypertensive crisis is also more common in African Americans compared with other races.

Although severe hypertension is more common in the elderly, it may occur in children though very rarely. Also, women have slightly increased risks of developing hypertension crisis. The lifetime risk for hypertension is 86-90% in females and 81-83% in men.

Clinical history

The clinical history is focused on whether the end-organ dysfunction is present or not, the circumstances in which hypertension developed, and any other identifiable etiology. The clinical history is helpful in determining the type, severity, and treatment or management of the hypertensive event.

Both the history and physical examination determine the nature, severity, and management of the hypertensive event.

A complete clinical history should include detailed information on the type of medication that the patient takes. Commonly, details of antihypertensive drug therapy and compliance, intake of over-the-counter medication such as sympathomimetic agents and use of illicit drugs such as cocaine will be included in a complete clinical history.

The health care provider will need to know if the patient is taking any herbal or dietary supplements.

The duration and severity of preexisting hypertension, degree of blood pressure control, presence of previous end-organ dysfunction, particularly renal and cerebrovascular disease, and date of last menstrual period or other medical conditions such as prior hypertension, thyroid disease, Cushing disease or renal disease are other factors that are considered as part of a complete medical history in suspected of severe hypertension.

Another important part of the clinical history is to determine whether specific symptoms suggesting EOD are present such as chest pain, which indicates myocardial ischemia or infarction; back pain, which indicates aortic dissection; dyspnea, as indicator of pulmonary edema and congestive heart failure; and neurologic symptoms with indicators such as seizures, visual disturbances, altered level of consciousness.

See also

• Malignant hypertension
• Hypertension
• Hypertensive retinopathyde:Hypertensive Krise