A hypertensive emergency, formerly known as malignant hypertension, is high blood pressure with potentially life-threatening symptoms and signs indicative of acute impairment of one or more organ systems (brain, eyes, heart, aorta, or kidneys). Hypertensive urgency is defined as having a systolic blood pressure over 180 mmHg or a diastolic blood pressure over 110 mmHg. Hypertensive emergency is defined as elevated blood pressure consistent with hypertensive urgency, plus evidence of impending irreversible organ damage. Signs of organ damage will be discussed below.
|Terminology||Systolic pressure||Diastolic pressure||End Organ Findings|
|Hypertensive Urgency||≥ 180 mm Hg||≥ 120 mm Hg||no|
|Hypertensive Emergency||≥ 180 mm Hg||≥ 120 mm Hg||yes|
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 or systolic blood pressure greater than or equal to 180 mmHg. Hypertensive emergency differs from hypertensive urgency in that, in the former, there is evidence of acute organ damage.
In 2000, it was estimated that approximately 1 billion people worldwide have hypertension, making it the most prevalent condition in the world. Approximately 60 million Americans suffer from chronic hypertension, with 1% of these individuals having an episode of hypertensive urgency. In emergency departments and clinics around the U.S., the prevalence of hypertensive urgency is suspected to be between 3-5%.
Risk factors for hypertensive emergency include age, obesity, noncompliance to anti hypertensive medications, female sex, Caucasian race, preexisting diabetes or coronary artery disease, mental illness, and sedentary lifestyle. 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, however hypertensive crises have a greater incidence in Caucasians.
With the usage of anti hypertensives, the rates of hypertensive emergencies has declined from 7% to 1% of patients with hypertensive urgency.
Many factors and causes are contributory in hypertensive crises. The most common cause in patients with diagnosed, chronic hypertension who have discontinued anti hypertensive medications.
Other common causes of hypertensive crises are autonomic hyperactivity such as pheochromocytoma, collagen-vascular diseases, drug use particularly stimulants, cocaine and amphetamines and their substituted analogues, monoamine oxidase inhibitors or food-drug interactions, glomerulonephritis, head trauma, neoplasias, preeclampsia and eclampsia, and renovascular hypertension. It is important to note that these conditions exist outside of hypertensive emergency, in that patients diagnosed with these conditions are at increased risk of hypertensive emergencies or end organ failure.
Signs and symptoms
The eyes may show bleeding in the retina, an exudate, cotton-wool spots, scattered splinter hemorrhages, or swelling of the optic disc called papilledema. The brain shows manifestations of increased pressure within the cranium, such as headache, nausea, vomiting, and/or subarachnoid or cerebral hemorrhage. Chest pain may occur due to increased workload on the heart resulting in a mismatch in the oxygen demand and supply to the heart muscle resulting in inadequate delivery of oxygen to meet the heart muscle's metabolic needs. People with hypertensive crises often have chest pain as a result of this mismatch and may suffer from left ventricular dysfunction. The kidneys will be affected, resulting in blood and/or protein in the urine, and acute kidney failure.
Other signs and symptoms can include:
- Chest pain
- Abnormal heart rhythms
- Nosebleeds that are difficult to stop
- Fainting or the sensation of the world spinning around them
- Severe anxiety
- Altered mental status
- Abnormal sensations
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 bleeding, aortic dissection, and pre-eclampsia or eclampsia.
|Kidney Biopsy showing thrombotic microangiopathy, a histomorphologic finding seen in malignant hypertension.|
The pathophysiology of hypertensive emergency is not well understood. 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
- Endothelial injury and dysfunction
- Fibrinoid necrosis of the arterioles
- Deposition of platelets and fibrin
- Breakdown of normal autoregulatory function
The resulting ischemia prompts further release of vasoactive substances including prostaglandins, free radicals, and thrombotic/mitotic growth factors, completing a vicious cycle of inflammatory changes. If the process is not stopped, homeostatic failure begins, leading to loss of cerebral and local autoregulation, organ system ischemia and dysfunction, and myocardial infarction. Single-organ involvement is found in approximately 83% of hypertensive emergency patients, two-organ involvement in about 14% of patients, and multi-organ failure (failure of at least 3 organ systems) in about 3% of patients.
In the brain, hypertensive encephalopathy - characterized by hypertension, altered mental status, and swelling of the optic disc - is a manifestation of the dysfunction of cerebral autoregulation. Cerebral autoregulation is the ability of the blood vessels in the brain to maintain a constant blood flow. 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. 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, with increased risk of intracranial bleeding.
In the heart, increased arterial stiffness, increased systolic blood pressure, and widened pulse pressures, all resulting from chronic hypertension, can cause significant damage. Coronary perfusion pressures are decreased by these factors, which also increase myocardial oxygen consumption, possibly leading to left ventricular hypertrophy. As the left ventricle becomes unable to compensate for an acute rise in systemic vascular resistance, left ventricular failure and pulmonary edema or myocardial ischemia may occur. 
In the kidneys, chronic hypertension has a great impact on the renal vasculature, leading to pathologic changes in the small arteries of the kidney. Affected arteries develop endothelial dysfunction and impairment of normal 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. The renin-aldosterone-angiotensin system can be activated, leading to further vasoconstriction and damage. During a hypertensive crisis, this can lead to acute renal ischemia, with hypoperfusion, involvement of other organs, and subsequent dysfunction. After an acute event, this endothelial dysfunction has persisted for years.
Several classes of antihypertensive agents are recommended, with the choice depending on the cause of the hypertensive crisis, the severity of the elevation in blood pressure, and the usual blood pressure of the person before the hypertensive crisis. In most cases, the administration of intravenous sodium nitroprusside injection which has an almost immediate antihypertensive effect, is suitable (but in many cases not readily available). Other intravenous agents like nitroglycerine, nicardipine, labetalol, fenoldopam or phentolamine can also be used, but all have a delayed onset of action (by several minutes) compared to sodium nitroprusside.
In addition, non-pharmacological treatment could be considered in cases of resistant malignant hypertension due to end stage kidney failure, such as surgical nephrectomy, laparoscopic nephrectomy, and renal artery embolization in cases of anesthesia risk.
It is also important that the blood pressure is lowered smoothly, not too abruptly. 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 a total of 2–6 hours. Excessive reduction in blood pressure can precipitate coronary, cerebral, or renal ischemia and, possibly, infarction.
The diagnosis of a hypertensive emergency 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. Individuals with a history of chronic hypertension may not tolerate a "normal" blood pressure.
Severe hypertension is a serious and potentially life-threatening medical condition. It is estimated that people who do not receive appropriate treatment only live an average of about three years after the event.
The morbidity and mortality of hypertensive emergencies depend on the extent of end-organ dysfunction at the time of presentation and the degree to which blood pressure is controlled afterward. With good 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 increases. 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.
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 crises than do men. The lifetime risk for developing hypertension is 86-90% in females and 81-83% in males.
Consequences of hypertensive emergency result after prolonged elevations in blood pressure and associated end-organ dysfunction. Acute end-organ damage may occur, affecting the neurological, cardiovascular, renal, or other organ systems. Some examples of neurological damage include hypertensive encephalopathy, cerebral vascular accident/cerebral infarction, subarachnoid hemorrhage, and intracranial bleeding. Cardiovascular system damage can include myocardial ischemia/infarction, acute left ventricular dysfunction, acute pulmonary edema, and aortic dissection. Other end-organ damage can include acute kidney failure or insufficiency, retinopathy, eclampsia, and microangiopathic hemolytic anemia.
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A summary of recommendations from the selected guidelines is presented in Table 2.
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