In hypertensive emergencies, the BP should be lowered aggressively over minutes to hours. The pathophysiology of hypertensive emergencies is not well understood. However, an abrupt rise in vascular resistance seems to be a necessary initial step. The three major organ systems affected by high BP are the CNS, cardiovascular system, and renal system.

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.

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%. One-year mortality rate for an untreated hypertensive emergency is greater than 90%. Five-year survival rate among all patients presenting with a hypertensive crisis is 74%. Median survival is 144 months for all patients presenting to the ED with a hypertensive crisis.

Drug interactions - Monoamine oxidase inhibitors with tricyclic antidepressants, antihistamines, or tyramine- containing food; CNS - CNS trauma or spinal cord disorders, such as Guillain-Barré syndrome; Coarctation of the aorta; Preeclampsia/eclampsia; Postoperative hypertension.

Consider the context of the elevated BP (e.g.: severe pain often causes increase in BP). Screen for TOD: The patient's history, physical examination, laboratory studies, and diagnostic tests should be used to determine if TOD exists.

Patients without evidence of TOD may be discharged with follow-up.The misconception remains that a patient never should be discharged from the hospital with an elevated BP. As a result of this belief, patients are given oral medicines, such as nifedipine, in an effort to lower BP rapidly before discharge. This is not indicated and may be dangerous. Attempts to temporarily lower BP by using these medicines may result in a precipitous and difficult-to-correct drop in BP. Should this occur, target organ hypoperfusion may result. Furthermore, patients who present with high BP may have had this elevation for some time and may need chronic BP control but may not tolerate rapid return of BP to a "normal" level.

Patients with TOD usually require admission and rapid lowering of BP using intravenous (IV) medications. Suggested medication depends on the affected organ system. However, even in cases of hypertensive emergencies, the BP should not be lowered to normal levels. Rapid reduction in BP below the cerebral, renal, and/or coronary autoregulatory range will result in marked reduction in organ blood flow, possibly leading to ischemia and infarction. In general, the MAP should be lowered by no more than 20-25% in the first hour of treatment. If the patient remains stable, the BP should then be lowered to 160/100-110 in the next 2-6 hours. These BP goals are best achieved by a continuous infusion of a short-acting, titratable, parenteral antihypertensive agent along with constant, intensive patient monitoring.

Rapid BP reduction is indicated in the following circumstances: Acute myocardial ischemia (use Nitroglycerin and beta blockers IV); Congestive Heart Failure (CHF) with pulmonary edema (use Nitroglycerin, Laxix and Nitroprussive IV); Acute aortic dissection: In cases of acute aortic dissection, the SBP should be decreased as rapidly as possible to a goal of 100-110 mm Hg or lower using IV Labetolol or IV Nitroprusside with beta blockers like esmolol; Cerebral vascular accident: Evidence exists that patients who have acute strokes have better outcomes with higher BPs. Antihypertensive therapy is not routinely recommended for patients with acute stroke and HTN. The current recommendation by the American Stroke Association states that a patient with a recent ischemic stroke and a SBP >220 mm Hg or a DBP > 120-140 mm Hg can undergo cautious reduction of BP by about 10-15% (with IV nitroprusside or IV labetalol), if the patient is carefully monitored for neurologic deterioration related to the lower pressure; Intracranial hemorrhage (ICH): No evidence exists to suggest that HTN provokes further bleeding in patients with ICH.

Other causes and their treatments include: Monoamine oxidase (MAO)-tyramine interactions with acute hypertension - Phentolamine IV; Pheochromocytoma: use IV Phentolamine or IV Labetelol; Hypertensive encephalopathy: use Nitroprusside or Labetolol IV; Acute renal failure: use betablockers IV or Nicardipine or Beta-blockers IV; Eclampsia: IV Hydralazine, Labetalol, or IV Magnesium.