Malignant hypertension

Hypertensive emergency formerly ref2242ed to as malignant hypertension.

Acute severe hypertension with blood pressure elevations above 180/110-120 mmHg can result in acute injury to the heart, brain, and microvasculature.

Acute severe hypertension accounts for an estimated 4% of all ED visits, and as a frequent reason for hospitalizations.

A cute severe hypertension emergencies have steadily increased during the past 20 years, but in-hospital mortality has improved ranging between 0.2 and 11%.

Acute severe hypertension is more common in persons older than 60 years of age, black, uninsured or underinsured who live in low income areas.

Refers to hypertension with acute impairment of one or more organ systems, especially the central nervous system, cardiovascular system and/or the renal system.

Both absolute blood pressure level and the pace of the rise of blood pressure determines the risk of acute hypertension mediated target organ damage.

Hypertensive urgency refers to the absence of acute organ damage, but is a condition that is 2 to 3 times were common than hypertensive emergency.

The relative incidence of hypertensive crisis is less than 1% annually, and affects upward of 500,000 Americans each year.

A significant cause of serious morbidity in the US.

The incidence of postoperative hypertensive crisis varies and is between 4% to 35%.

The diagnosis is not based solely on an absolute level of blood pressure, but also on the typical blood pressure level of the patient before the hypertensive crisis occurs.

Episodes of severe acute hypertension associated with increased risk of stroke and fatal or non-fatal cardiovascular events.

In contrast to acute hypertensive changes do not appear to be associated with adverse short term outcomes.

Can result in irreversible organ damage.

The blood pressure should be slowly lowered over a period of minutes to hours with an antihypertensive agent.

Papilledema must be present before a diagnosis of malignant hypertension can be made.

The retina may demonstrate retinal hemorrhage or exudates.

The brain may manifest with increased intracranial pressure, headache, vomiting, and/or subarachnoid or cerebral hemorrhage.

Patients will usually suffer from left ventricular dysfunction.

Patients may have hematuria, proteinuria, and acute renal failure.

Other signs and symptoms that patients may experience include: Chest pain, arrhythmias, epistaxis, dyspnea, headache, vertigo, anxiety, altered mental status, paresthesias, nausea, and vomiting.

Chest pain requires immediate lowering of blood pressure.

Less urgent side effects can be treated with oral agents.

Initial goal is to lower the mean arterial pressure (MAP) by 20% in 1–2 days with further reduction to normalized levels in weeks or months.

The pace and intensity of blood pressure reduction depends on the presence of aortic dissection, eclampsia, pheochromocytoma crisis, and intracerebral hemorrhage, all of which require more aggressive approach approaches.

In patients with ischemic stroke more conservative management to involve avoid infarction hypo perfusion is required.

The use of oral nifedipine, a calcium channel blocker, is strongly discouraged because it is not absorbed in a controlled and reproducible fashion and can lead to serious hypotensive problems.

Hypertension staging: Systolic Pressure (mm Hg) Diastolic Pressure (mm Hg) Normal < 120 < 80 Pre-hypertension 120-139 80-89 Hypertension stage 1 140-159 90-99 Hypertension stage 2 ≥ 160 ≥ 100 Hypertensive crisis – emergency ≥ 180 ≥ 120

The term hypertensive emergency is primarily used as a specific term for a hypertensive crisis with a diastolic blood pressure greater than or equal to 120 mmHg and/or systolic blood pressure greater than or equal to 180mmHg.

Hypertensive emergency differs from hypertensive crisis in that, in the former, there is evidence of acute organ damage.

Pathophysiology of hypertensive emergency is not well understood.

Associated with failure of normal autoregulation and an abrupt rise in systemic vascular resistance are typical initial components of the disease process.

Hypertensive emergency pathophysiology includes:

Abrupt increase in systemic vascular resistance, likely related to humoral vasoconstrictors.

Presence of endothelial injury.

Fibrinoid necrosis of the arterioles with platelet and fibrin deposition.

Breakdown of normal autoregulatory function

Ischemia prompts further release of vasoactive substances and homeostatic failure begins, with loss of cerebral and local autoregulation, organ system ischemia and dysfunction, and myocardial infarction.

Approximately 83% of patients with malignant hypertension have single organ involvement, two-organ involvement in about 14% of patients, and multi-organ failure in about 3% of patients.

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.

People who suffer from chronic hypertension can tolerate higher arterial pressure before their autoregulation system is disrupted.

Hypertensives also have an increased cerebrovascular resistance which puts them at greater risk of developing cerebral ischemia if the blood flow decreases into a normotensive range.

Sudden rises in blood pressure may cause hyperperfusion and increased cerebral blood flow, causing increased intracranial pressure and cerebral edema.

Hypertensive encephalopathy is characterized by hypertension, altered mentation, and papilledema.

Factors and causes contributory in hypertensive crises: discontinuation of antihypertensive medications, autonomic hyperactivity, collagen-vascular diseases, drug use, glomerulonephritis, head trauma, neoplasias, preeclampsia and eclampsia, and renovascular hypertension.

Uncontrolled blood pressure leads to progressive or impending end-organ dysfunction.

Uncontrolled blood pressure may cause acute end-organ damage affecting the neurological, cardiovascular, renal, or other organ systems.

May precipitate neurological damage include hypertensive encephalopathy, cerebral vascular accident/cerebral infarction, subarachnoid hemorrhage, and intracranial hemorrhage, cardiovascular system damage including myocardial ischemia/infarction, acute left ventricular dysfunction, acute pulmonary edema, and aortic dissection, acute renal failure or insufficiency, retinopathy, eclampsia, and microangiopathic hemolytic anemia. He

Treatment in most extreme cases is with intravenous sodium nitroprusside.

In less urgent cases, oral agents like captopril, clonidine, labetalol, or prazosin can be used, but all have a delayed onset of action compared to sodium nitroprusside.

Non-pharmacological treatment is considered in resistant malignant hypertension due to end stage renal failure, such as: nephrectomy, and renal artery embolization in cases of anesthesia risk.

Blood pressure is lowered smoothly, not too abruptly.

In hypertensive emergencies reduction of 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 a total of 2–6 hours.

Aggressive reduction in blood pressure can precipitate coronary, cerebral, or renal ischemia and, possibly, infarction.

Relative incidence rates of hypertension range between 3% and 18% of the population, depending on the age, gender, ethnicity, and body size.

The incidence of hypertensive emergencies has declined from 7% to 1% of patients with hypertension due to the use of antihypertensive medications.

The 1–year survival rate for malignant hypertension has also increased to more than 90% with proper medical treatment.

Approximately 1% to 2% of patients with hypertension develop hypertensive crisis at some point in their lifetime.

Men are more commonly affected by hypertensive crises than women.

Estimated that people who do not receive appropriate treatment only live an average of about three years after the event, but with good blood pressure control and medication compliance, the 10-year survival rate of patients with hypertensive crises approaches 70%.

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.

Hypertensive crisis is also more common in African Americans compared with other races.

Severe hypertension is more common in the elderly.

It may rarely occur in children.

Women have slightly increased risks of developing hypertension crises than do men.

The lifetime risk for hypertension is 86-90% in females and 81-83% in males.

Patient with acute severe hypertension should be admitted to intensive care unit and treated with IV anti-hypertensive agents.

The most commonly used intravenous antihypertensive agents or labetalol, nitroglycerin, nicardipine, hydralazine, and nitroprusside.

Hydralazine among the above medications has the most unpredictable effects and it is not the first option.

Guidelines for treatment suggest that blood pressure be decreased by no more than 20-25% during the first hour and then to 160/100 to 110 mmHg during the ensuing 2-6 hours.

Rapid reduction in blood pressure is associated with an increased risk of death.

Most patients can tolerate normalization of blood pressure within 48-72 hours.

In patients with symptoms that are presumed to be related to hypertension but do not reflect target organ damage such as headache, atypical chest pain, or epistaxis, choosing an oral agent with faster onset of action such as clonidine, labetalol, captopril, prazosin, or nitroglycerin are acceptable.

Nifedipine is avoided owing to unpredictable blood pressure reduction.

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