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A hypertensive emergency is severe hypertension with signs of damage to target organs (primarily the brain, cardiovascular system, and kidneys). Diagnosis is by BP measurement, ECG, urinalysis, and serum BUN and creatinine measurements. Treatment is immediate BP reduction with IV drugs (eg, clevidipine, fenoldopam, nitroglycerin, nitroprusside, nicardipine, labetalol, esmolol, hydralazine).
Target-organ damage includes hypertensive encephalopathy, preeclampsia and eclampsia, acute left ventricular failure with pulmonary edema, myocardial ischemia, acute aortic dissection, and renal failure. Damage is rapidly progressive and often fatal.
Hypertensive encephalopathy may involve a failure of cerebral autoregulation of blood flow. Normally, as BP increases, cerebral vessels constrict to maintain constant cerebral perfusion. Above a mean arterial pressure (MAP) of about 160 mm Hg (lower for normotensive people whose BP suddenly increases), the cerebral vessels begin to dilate rather than remain constricted. As a result, the very high BP is transmitted directly to the capillary bed with transudation and exudation of plasma into the brain, causing cerebral edema, including papilledema. Pathophysiology of other target-organ manifestations is discussed elsewhere in The Manual.
Although many patients with stroke and intracranial hemorrhage present with elevated BP, elevated BP is often a consequence rather than a cause of the condition. Whether rapidly lowering BP is beneficial in these conditions is unclear; it may even be harmful.
Very high blood pressure (eg, diastolic pressure > 120 to 130 mm Hg) without target-organ damage (except perhaps grades 1 to 3 retinopathy—see Overview of Hypertension : Diagnosis) may be considered a hypertensive urgency. BP at these levels often worries the physician; however, acute complications are unlikely, so immediate BP reduction is not required. However, patients should be started on a 2-drug oral combination (see Overview of Hypertension : Drugs), and close evaluation (with evaluation of treatment efficacy) should be continued on an outpatient basis.
BP is elevated, often markedly (diastolic pressure > 120 mm Hg). CNS symptoms include rapidly changing neurologic abnormalities (eg, confusion, transient cortical blindness, hemiparesis, hemisensory defects, seizures). Cardiovascular symptoms include chest pain and dyspnea. Renal involvement may be asymptomatic, although severe azotemia due to advanced renal failure may cause lethargy or nausea.
Physical examination focuses on target organs, with neurologic examination, funduscopy, and cardiovascular examination. Global cerebral deficits (eg, confusion, obtundation, coma), with or without focal deficits, suggest encephalopathy; normal mental status with focal deficits suggests stroke. Severe retinopathy (sclerosis, cotton-wool spots, arteriolar narrowing, hemorrhage, papilledema) is usually present with hypertensive encephalopathy, and some degree of retinopathy is present in many other hypertensive emergencies. Jugular venous distention, basilar lung crackles, and a 3rd heart sound suggest pulmonary edema. Asymmetry of pulses between arms suggests aortic dissection.
Testing typically includes ECG, urinalysis, and serum BUN and creatinine. Patients with neurologic findings require head CT to diagnose intracranial bleeding, edema, or infarction. Patients with chest pain or dyspnea require chest x-ray. ECG abnormalities suggesting target-organ damage include signs of left ventricular hypertrophy or acute ischemia. Urinalysis abnormalities typical of renal involvement include RBCs, RBC casts, and proteinuria.
Diagnosis is based on the presence of a very high BP and findings of target-organ involvement.
Hypertensive emergencies are treated in an ICU; BP is progressively (although not abruptly) reduced using a short-acting, titratable IV drug. Choice of drug and speed and degree of reduction vary somewhat with the target organ involved, but generally a 20 to 25% reduction in MAP over an hour or so is appropriate, with further titration based on symptoms. Achieving “normal” BP urgently is not necessary. Typical first-line drugs include nitroprusside, fenoldopam, nicardipine, and labetalol (see Table: Parenteral Drugs for Hypertensive Emergencies). Nitroglycerin alone is less potent.
Parenteral Drugs for Hypertensive Emergencies
Oral drugs are not indicated because onset is variable and the drugs are difficult to titrate. Although short-acting oral nifedipine reduces BP rapidly, it may lead to acute cardiovascular and cerebrovascular events (sometimes fatal) and is therefore not recommended.
Clevidipine is a new, ultra-short-acting (within 1 to 2 minutes), 3rd-generation Ca channel blocker that reduces peripheral resistance without affecting venous vascular tone and cardiac filling pressures. Clevidipine is rapidly hydrolyzed by blood esterases and, thus, its metabolism is not affected by renal or hepatic function. In recent trials, it has been shown to be effective and safe in the control of perioperative hypertension and hypertensive emergencies and was associated with lower mortality than nitroprusside. Starting dose is 1 to 2 mg/h, doubling the dose every 90 sec until approaching target BP, at which time dose is increased by less than double every 5 to 10 min. Clevidipine may thus be preferred over nitroprusside for most hypertensive emergencies, although it should be used with caution in acute heart failure with low ejection fraction as it may have negative inotropic effects. If clevidipine is not available, then fenoldopam, nitroglycerin, or nicardipine are reasonable alternatives.
Nitroprusside is a venous and arterial dilator, reducing preload and afterload; thus, it is the most useful for hypertensive patients with heart failure. It is also used for hypertensive encephalopathy and, with β-blockers, for aortic dissection. Starting dose is 0.25 to 1.0 mcg/kg/min titrated in increments of 0.5 mcg/kg to a maximum of 8 to 10 mcg/kg/min; maximum dose is given for ≤ 10 min to minimize risk of cyanide toxicity. The drug is rapidly broken down into cyanide and nitric oxide (the active moiety). Cyanide is detoxified to thiocyanate. However, administration of > 2 mcg/kg/min can lead to cyanide accumulation with toxicity to the CNS and heart; manifestations include agitation, seizures, cardiac instability, and an anion gap metabolic acidosis. Prolonged administration (> 1 wk or, in patients with renal insufficiency, 3 to 6 days) leads to accumulation of thiocyanate, with lethargy, tremor, abdominal pain, and vomiting. Other adverse effects include transitory elevation of hair follicles (cutis anserina) if BP is reduced too rapidly. Thiocyanate levels should be monitored daily after 3 consecutive days of therapy, and the drug should be stopped if the serum thiocyanate level is > 12 mg/dL (> 2 mmol/L). Because the drug is broken down by ultraviolet light, the IV bag and tubing are wrapped in an opaque covering. Given some recent data showing increased mortality with nitroprusside compared to clevidipine, nitroglycerin, and nicardipine, nitroprusside should probably not be used when other alternatives are available.
Fenoldopam is a peripheral dopamine -1 agonist that causes systemic and renal vasodilation and natriuresis. Onset is rapid and half-life is brief, making it an effective alternative to nitroprusside, with the added benefit that it does not cross the blood-brain barrier. Initial dosage is 0.1 mcg/kg/min IV infusion, titrated upward by 0.1 mcg/kg q 15 min to a maximum of 1.6 mcg/kg/min.
Nitroglycerin is a vasodilator that affects veins more than arterioles. It can be used to manage hypertension during and after coronary artery bypass graft surgery, acute MI, unstable angina pectoris, and acute pulmonary edema. IV nitroglycerin is preferable to nitroprusside for patients with severe coronary artery disease because nitroglycerin increases coronary flow, whereas nitroprusside tends to decrease coronary flow to ischemic areas, possibly because of a “steal” mechanism. Starting dose is 10 to 20 mcg/min titrated upward by 10 mcg/min q 5 min to maximum antihypertensive effect. For long-term BP control, nitroglycerin must be used with other drugs. The most common adverse effect is headache (in about 2%); others include tachycardia, nausea, vomiting, apprehension, restlessness, muscular twitching, and palpitations.
Nicardipine, a dihydropyridine Ca channel blocker with less negative inotropic effects than nifedipine, acts primarily as a vasodilator. It is most often used for postoperative hypertension and during pregnancy. Dosage is 5 mg/h IV, increased q 15 min to a maximum of 15 mg/h. It may cause flushing, headache, and tachycardia; it can decrease GFR in patients with renal insufficiency.
Labetalol is a β -blocker with some α1-blocking effects, thus causing vasodilation without the typical accompanying reflex tachycardia. It can be given as a constant infusion or as frequent boluses; use of boluses has not been shown to cause significant hypotension. Labetalol is used during pregnancy, for intracranial disorders requiring BP control, and after MI. Infusion is 0.5 to 2 mg/min, titrated upward to a maximum of 4 to 5 mg/min. Boluses begin with 20 mg IV followed every 10 min by 40 mg, then 80 mg (up to 3 doses) to a maximum total of 300 mg. Adverse effects are minimal, but because of its β -blocking activity, labetalol should not be used for hypertensive emergencies in patients with asthma. Low doses may be used for left ventricular failure if nitroglycerin is given simultaneously.
A hypertensive emergency is hypertension that causes target-organ damage; it requires intravenous therapy and hospitalization.
Target-organ damage includes hypertensive encephalopathy, preeclampsia and eclampsia, acute left ventricular failure with pulmonary edema, myocardial ischemia, acute aortic dissection, and renal failure.
Do ECG, urinalysis, serum BUN and creatinine, and head CT for patients with neurologic symptoms or signs.
Reduce MAP by about 20 to 25% over the first hour using a short-acting, titratable IV drug such as clevidipine, nitroglycerin, fenoldopam, nicardipine, or labetalol.
It is not necessary to achieve “normal” BP urgently (especially true in acute stroke).
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