Hypertensive Emergencies in Emergency Medicine Author: Christy Hopkins, MD, MPH; Chief Editor: David FM Brown, MD more...Updated: Mar 29, 2011Uncontrolled Blood PressureHypertensive emergencies encompass a spectrum of clinical presentations in which uncontrolled blood pressures(BPs) lead to progressive or impending end-organ dysfunction (EOD). In these conditions, the BP should belowered aggressively over minutes to hours.Neurologic end-organ damage due to uncontrolled BP may include hypertensive encephalopathy, cerebralvascular accident/cerebral infarction; subarachnoid hemorrhage, and/or intracranial hemorrhage. Cardiovascularend-organ damage may include myocardial ischemia/infarction, acute left ventricular dysfunction, acutepulmonary edema, and/or aortic dissection. Other organ systems may also be affected by uncontrolledhypertension, which may lead to acute renal failure/insufficiency, retinopathy, eclampsia, or microangiopathichemolytic anemia.With the advent of antihypertensives, the incidence of hypertensive emergencies has declined from 7% toapproximately 1% of patients with hypertension.  In addition, the 1-year survival rate associated with thiscondition has increased from only 20% (prior to 1950) to a survival rate of more than 90% with appropriatemedical treatment.History and physical examinationThe history and physical examination determine the nature, severity, and management of the hypertensive event.The history should focus on the presence of end-organ dysfunction, the circumstances surrounding thehypertension, and any identifiable etiology.The most common clinical presentations of hypertensive emergencies are cerebral infarction (24.5%), pulmonaryedema (22.5%), hypertensive encephalopathy (16.3%), and congestive heart failure (12%). Other clinicalpresentations associated with hypertensive emergencies include intracranial hemorrhage, aortic dissection, andeclampsia, as well as acute myocardial infarction.Not only should the patients duration and severity of preexisting hypertension -- including the degree of BPcontrol -- be evaluated, but the patients medication history should be assessed for details of antihypertensivedrug therapy and compliance, intake of over-the-counter (OTC) preparations such as sympathomimetic agents,and use of illicit drugs such as cocaine. In addition, it is important to elicit information about the presence ofprevious end-organ dysfunction, particularly renal and cerebrovascular disease, and any other medical problems(eg, thyroid disease, Cushing disease, systemic lupus). In female patients, determine the date of their lastmenstrual period.Patients may complain of specific symptoms that suggest end-organ dysfunction may be present. Chest painmay indicate myocardial ischemia or infarction, back pain may denote aortic dissection; and dyspnea maysuggest pulmonary edema or congestive heart failure. The presence of neurologic symptoms may includeseizures, visual disturbances, and altered level of consciousness (hypertensive encephalopathy)The physical examination should assess whether end-organ dysfunction is present. BP should not only bemeasured in both the supine position and the standing position (assess volume depletion), but it should also bemeasured in both arms (a significant difference may suggest aortic dissection).The presence of new retinal hemorrhages, exudates, or papilledema suggests a hypertensive emergency.Evaluate also for the presence of heart failure, which may be indicated jugular venous distention, crackles onauscultation, and peripheral edema. Central nervous system (CNS) findings may include changes in the patientslevel of consciousness and visual fields, and/or the presence of focal neurologic signs. Abdominal masses orbruits may be noted.
Laboratory evaluationObtain electrolyte levels, as well as measurements of blood urea nitrogen (BUN) and creatinine levels to evaluatefor renal impairment. A dipstick urinalysis to detect hematuria or proteinuria and microscopic urinalysis to detectred blood cells (RBCs) or RBC casts should also be performedA complete blood cell (CBC) and peripheral blood smear should be obtained to exclude microangiopathic anemia,and a toxicology screen, pregnancy test, and endocrine testing may be obtained, as needed.Malignant hypertensionMalignant hypertension and accelerated hypertension are both hypertensive emergencies, with similar outcomesand therapies. Malignant hypertension may or may not be associated with clinical conditions present inhypertensive urgency. A patient with malignant hypertension always has retinal papilledema (as seen in the imagebelow), as well as flame-shaped hemorrhages and exudates. Other clinical features of malignant hypertensionmay include encephalopathy, confusion, left ventricular failure, intravascular coagulation, and impaired renalfunction, with hematuria and weight loss.The pathologic hallmark of malignant hypertension is fibrinoid necrosis of the arterioles, which occurssystemically, but specifically in the kidneys. These patients develop fatal complications if untreated, and morethan 90% will not survive beyond 1-2 years. See Malignant Hypertension.Papilledema. Note the swelling of the optic disc, with blurred marginsTo see complete information on Hypertension, please go to the main article by clicking here.Management of Hypertensive EmergenciesApproximately 3-45% of adult patients have at least one incident of increased BP during their stay in theemergency department (ED). The fundamental principle in determining the necessary ED care of the hypertensivepatient is the presence or absence of end-organ dysfunction. Many patients present to the ED with elevated BPs;however, only a small proportion of patients will require emergency treatment. An important point to remember inthe management of the patient with any degree of BP elevation is to "treat the patient and not the number."The primary goal of the emergency physician is to determine which patients with acute hypertension are exhibitingsymptoms of end-organ damage and require immediate intravenous (IV) parenteral therapy. In contrast, patientspresenting with acutely elevated BP (systolic BP [SBP] >200 mm Hg or diastolic BP [DBP] >120 mm Hg) withoutsymptoms that are sustained throughout the ED stay and whose BP stays significantly elevated to this level ondischarge should have initiation of medical therapy and close follow-up in the outpatient setting. Thus, optimal control of hypertensive situations balances the benefits of immediate decreases in BP against therisk of a significant decrease in target organ perfusion. The emergency physician must be capable ofappropriately evaluating patients with an elevated BP, correctly classifying the hypertension, determining theaggressiveness and timing of therapeutic interventions, and making disposition decisions.Acutely lowering BP in the ED for clinical situations other than those listed below is controversial and generallyshould be avoided.PharmacotherapyAn important point to remember in the management of the patient with any degree of BP elevation is to "treat thepatient and not the number." In patients presenting with hypertensive emergencies, antihypertensive drug therapyhas been shown to be effective in acutely decreasing blood pressure. 
Sodium nitroprusside is a commonly used medication. It is a short-acting agent, and the BP response can betitrated from minute to minute. However, patients must have constant monitoring in an intensive care unit. Thepotential exists for thiocyanate and cyanide toxicity with prolonged use or if the patient has renal or hepaticfailure.Diazoxide may also be used in hypertensive crisis. Small boluses of 100 mg are administered every 5 minutes,as indicated. Diazoxide is not preferred with concomitant congestive heart failure or low cardiac output.Labetalol, an alpha- and beta-blocking agent, has proven to be quite beneficial in the treatment of patients withhypertensive emergencies. Labetalol is particularly preferred in patients with acute dissection. Boluses of 10-20mg may be administered, or the drug may be infused at 1 mg/min until the desired BP is obtained. Once anadequate BP level is obtained, oral hypertensive therapy should be initiated, and patients are gradually weanedfrom parenteral agents.Fenoldopam, a peripheral dopamine-1-receptor agonist is given as initial IV dose of 0.1 µg/kg/min titrated every 15minutes.Clevidipine, a dihydropyridine calcium channel blocker, is administered intravenously for rapid and precise BPreduction. It is rapidly metabolized in the blood and tissues and does not accumulate in the body. Initiate IVinfusion of clevidipine at 1-2 mg/h; titrate the dose at short intervals (ie, 90 s) initially by doubling the dose.As the BP approaches its goal, increase the clevidipine dose by less than double, and lengthen the time betweendose adjustments to every 5-10 minutes. An approximately 1-2 mg/h increase produces an additional 2-4 mm Hgdecrease in SBP. Typically, the therapeutic response is achieved with 4-6 mg/h, although severe hypertensionmay require higher doses. Most patients have received maximum doses of 16 mg/h or less; experience is limitedwith short-term dosing as high as 32 mg/h. Because of lipid load restrictions, do not exceed 1000 mL or anaverage of 21 mg/h within a 24-hour period; experience is limited with use beyond 72 hours.Neurologic emergenciesRapid BP reduction is indicated in neurologic emergencies, such as hypertensive encephalopathy, acute ischemicstroke, acute intracerebral hemorrhage, and subarachnoid hemorrhage.In hypertensive encephalopathy, the treatment guidelines are to reduce the MAP 25% over 8 hours. Labetalol,nicardipine, esmolol are the preferred medications; however, nitroprusside and hydralazine should be avoided.For acute ischemic stroke, the preferred medications are labetalol and nicardipine. Withhold antihypertensivemedications unless the SBP is >220 mm Hg or the DBP is >120 mm Hg, UNLESS the patient is receiving IV orintra-arterial (IA) fibrinolysis; then, the goal BP is an SBP of < 185 mm Hg and DBP < 110 mm Hg. Aftertreatment with fibrinolysis, the SBP should be maintained < 180 mm Hg and the DBP at < 105 mm Hg for 24hours.For acute intracerebral hemorrhage, the preferred medications are labetalol, nicardipine, and esmolol; avoidnitroprusside and hydralazine. The treatment is based on clinical/radiographic evidence of increased intracranialpressure (ICP). If there are signs of increased ICP, maintain the MAP just below 130 mm Hg (or SBP < 180 mmHg) for the first 24 hours after onset. In patients without increased ICP, maintain the MAP < 110 mm Hg (or SBP< 160 mm Hg) for the first 24 hours after symptom onset. Recent evidence shows that in cases of acute intracerebral hemorrhage, early intensive BP control is welltolerated and can reduce hematoma growth in patients treated within 6 hours after the onset of intracerebralhemorrhage.[10, 11] The target systolic pressure for these studies was 140 mm Hg and routine IV medicationswere used. The target SBP was maintained over 7 days. [10, 11]In subarachnoid hemorrhage, nicardipine, labetalol, and esmolol are also the preferred agents; again, nitroprussideand hydralazine should be avoided. Maintain the SBP < 160 mm Hg until the aneurysm is treated or cerebralvasospasm occurs. Although oral nimodipine is used to prevent delayed ischemic neurologic deficits, it is NOTindicated for treating acute hypertension.Cardiovascular emergenciesRapid BP reduction is also indicated in cardiovascular emergencies, such as aortic dissection, acute coronarysyndrome, and acute heart failure.In aortic dissection, the preferred medications are labetalol, nicardipine, nitroprusside (with beta-blocker), esmolol,
In aortic dissection, the preferred medications are labetalol, nicardipine, nitroprusside (with beta-blocker), esmolol,and morphine sulfate. However, avoid beta-blockers if there is aortic valvular regurgitation or suspected cardiactamponade. Maintain the SBP at < 110 mm Hg, unless signs of end-organ hypoperfusion are present. Thepreferred treatment includes a combination of narcotic analgesics (morphine sulfate), beta blockers (labetalol,esmolol), and vasodilators (nicardipine, nitroprusside). Calcium channel blockers (verapamil, diltiazem) are analternative to beta blockers. For acute coronary syndrome, beta blockers and nitroglycerin are the preferred drugs. Treatment is indicated if theSBP is >160 mm Hg and/or the DBP is >100 mm Hg. Reduce the BP by 20-30% of baseline. Note thatthrombolytics are contraindicated if the BP is >185/100 mm Hg.In acute heart failure, the preferred medications are IV or sublingual nitroglycerin and IV enalaprilat. Treat withvasodilators (in addition to diuretics) for a SBP !140 mm Hg. Cocaine toxicity/pheochromocytomaDiazepam, phentolamine, and nitroglycerin/nitroprusside are the preferred drugs. However, avoid beta-adrenergicantagonists before administering phentolamine.Hypertension and tachycardia from cocaine toxicity rarely require specific treatment. Alpha-adrenergic antagonists(phentolamine) are the preferred agents for cocaine-associated acute coronary syndromes.Pheochromocytoma treatment guidelines are similar to that of cocaine toxicity. Only after alpha blockade canbeta blockers be added for BP control.Preeclampsia/eclampsiaThe preferred medications are hydralazine, labetalol, and nifedipine. Avoid - Nitroprusside, angiotensin-convertingenzyme inhibitors, esmolol. In women with eclampsia or preeclampsia, the SBP should be < 160 mm Hg and theDBP should be < 110 mm Hg in the antepartum and intrapartum periods. If the platelet count is less than 100,000cells mm3 , the BP should be maintained below 150/100 mm Hg. Patients with eclampsia or preeclampsia shouldalso be treated with IV magnesium sulfate to avoid seizures. Perioperative hypertensionNitroprusside, nitroglycerin, and esmolol are preferred. Target the perioperative BP to within 20% of the patientsbaseline pressure, except if there is the potential for life-threatening arterial bleeding. Perioperative beta blockersare the first choice in patients undergoing vascular procedures or in patients with an intermediate or high risk ofcardiac complications.