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Definition

Hypertensive emergenciesare severe elevations in BP, often higher than 220/140 mm Hg, complicated by clinical evidence of progressive target organ dysfunction. These patients require immediate admission and BP reduction (not necessarily to normal ranges) to prevent or limit further target organ damage. Examples include hypertensive encephalopathy, intracranial hemorrhage, acute myocardial infarction, acute left ventricular failure with pulmonary edema, dissecting aneurysm, acute renal failure, and eclampsia of pregnancy. Severe hypertension (urgencies)are marked elevations of BP, usually higher than 180/110mm Hg. Evidence of target organ damage is often present, but nonprogressive and manifesting symptoms may include head ache, shortness of breath, and pedal edema. Management in the emergency department (ED) with oral agents is suitable, depending on the individual's presentation, and follow-up within 24 to 72 hours is recommended.

Signs, symptoms, and diagnosis


Initial Assessment
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A brief but thorough history should address the duration as well as the severity of hypertension, all current medications, including prescription and nonprescription drugs and, of particular importance, the use of recreational drugs. A history of other comorbid conditions and prior cardiovascular or renal disease is essential to the initial evaluation. Direct questioning regarding the level of compliance with current antihypertensive medications may establish inadequacy of treatment or frank noncompliance. Historical information suggestive of neurologic, cardiovascular, and/or renal symptoms should be sought. Specific manifestations such as headache, seizures, chest pain, dyspnea, or edema should be assessed. The clinical characteristics of a hypertensive emergency are listed in Table 1

Table 1: Clinical Characteristics of the Hypertensive Emergency

Blood Funduscopic Pressure Findings (mm Hg) Usually >220/140 Hemorrhages, exudates, papilledema

Neurologic Status Headache, confusion, somnolence, stupor, visual loss, seizures, focal neurologic deficits, coma

Cardiac Findings Prominent apical pulsation, cardiac enlargement, congestive heart failure

Renal Symptoms Azotemia, proteinuria, oliguria

Gastrointestinal Symptoms

Nausea, vomiting

The level of BP alone does not determine a hypertensive emergency; rather, it is the degree of target organ involvement that will determine the rapidity with which BP should be reduced to a safer level to prevent or limit target organ damage. Initial therapy will be appropriate for a presumptive diagnosis based on the information available during the initial triage evaluation.

Table 2: Algorithm for Triage Evaluation

Severe Hypertension (Urgency) Parameter Asymptomatic Blood pressure >180/110 (mm Hg) Symptoms Headache, anxiety; often asymptomatic Symptomatic >180/110 Hypertensive Emergency Usually >220/140

Examination

Therapy

Plan

Shortness of breath, chest pain, Severe headache, shortness nocturia, dysarthria, weakness, of breath altered consciousness No target organ damage, no Target organ damage; Encephalopathy, pulmonary edema, clinical cardiovascular clinical cardiovascular renal insufficiency, cerebrovascular disease disease present, stable accident, cardiac ischemia Observe 3-6 hr; lower BP Baseline laboratory tests; Observe 1-3 hr; initiate, with short-acting oral intravenous line; monitor BP; may resume medication; increase agent; adjust current initiate parenteral therapy in dosage of inadequate agent therapy emergency room Arrange follow-up within 3Arrange follow-up Immediate admission to ICU; treat 7 days; if no prior evaluation in less than 72 to initial goal BP; additional evaluation, schedule hr diagnostic studies appointment

Physical Examination y y y y

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The physical examination should begin with an assessment of BP using an appropriately sized cuff in both upper extremities and in a lower extremity if peripheral pulses are markedly reduced. Brachial, femoral, and carotid pulses should be assessed. A careful cardiovascular examination, as well as a thorough neurologic examination, including mental status, should be conducted. This assessment will aid in establishing the degree of involvement of affected target organs and should provide clues to the possible existence of a secondary form of hypertension, such as renovascular hypertension. If a secondary cause of hypertension is suspected, appropriate blood and urine samples should be obtained before aggressive therapy is initiated. A careful funduscopic examination should be performed to detect the presence of hemorrhages, exudates, and/or papilledema.

Initial Laboratory Studies y y

Initial laboratory studies should be limited and rapidly expedited. The urinalysis may reveal significant proteinuria, red blood cells, and/or cellular casts. Cellular casts are suggestive of renal parenchymal disease.

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Electrolyte abnormalities, particularly hypokalemia or hypomagnesemia, increase the risk of cardiac arrhythmias, and the chemistry panel will also provide evidence of renal or hepatic dysfunction, or both. The electrocardiogram should identify evidence of coronary ischemia, left ventricular hypertrophy, or both, and may reveal pulse deficits, raising the question of aortic dissection. When the clinical examination suggests cerebrovascular ischemia or hemorrhage, or if the patient is comatose, a computed tomography (CT) scan of the head should be immediately obtained.

Summary
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Most hypertensive crises are preventable. Hypertensive urgencies occur without evidence of progressive target organ damage. Hypertensive emergencies are complicated by evidence of progressive target organ damage. The levels of blood pressure readings alone do not determine action; this is determined by the degree of target organ damage.

Treatment
It is well recognized that patients presenting to emergency departments with hypertensive crises, BP higher than 180/110 mm Hg, these patients must not be allowed to wait their turn for initial evaluation those patients with a true hypertensive emergency.
This is best accomplished by using the initial triage evaluation to categorize patients into two groups: (1) those with severe hypertension (symptomatic or asymptomatic) and (2) those with an actual hypertensive emergency.

Emergency Department Treatment of Severe Hypertension Urgencies


Initial triage should quickly identify those patients who have an elevated BP without any evidence of significant target organ damage or any other impending cardiovascular events.8These patients clearly represent most of those seen in the ED. They are usually asymptomatic, although evidence of anxiety, headache, shortness of breath, or pedal edema may be observed. Physicians must also now be aware that aggressive dosing of oral agents may also necessitate a longer period of observation in the ED to minimize the risk of significant hypotension following discharge. Appropriate follow-up within 3 days should be scheduled and written instructions provided to the patient.
Table 3: Oral Agents for the Treatment of Hypertensive Agencies

Onset/Duration of Action (after discontinuation) 25 mg PO; repeat as needed; 15-30 min/6-8 hr SL 10-20 Captopril SL, 25 mg min/2-6 hr 0.1-0.2 mg PO, repeat hourly Clonidine as required to total dosage of 30-60 min/8-16 hr 0.6 mg Agent Dosage

Precautions Hypotension, renal failure, bilateral renal artery stenosis Hypotension, drowsiness, dry mouth

200-400 mg PO; repeat every 1-2 hr/2-12 hr 2-3 hr Amlodipine2.5-5 mg 1-2 hr/12-18 hr Labetalol SL, sublingual.

Bronchoconstriction, heart block, orthostatic hypotension Tachycardia, hypotension

Treatment for Hypertensive Emergencies


mean arterial pressure can be reduced within the first 30 to 60 minutes to 110 to 115 mm Hg. If this level is well tolerated and the patient is clinically stable, further gradual reductions toward a normal BP can be implemented over the next 24 hours. Excessively rapid reductions in BP have been associated with acute deterioration in renal function, ischemic cardiac or cerebral events, and occasional retinal artery occlusion and acute blindness. Therapy is often initiated before the results of laboratory studies are available. Although aggressive treatment is appropriate, initial therapy should be aimed at a partial reduction in BP in the first 30 to 60 minutes, rather than achievement of normotensive BP levels. Further progressive reduction in BP over the first 24 hours will depend on the clinical state of the patient and adequacy of target organ function.
Parenteral Agents

Parenteral therapy may be initiated in the ED if suitable supervision and monitoring of BP can be provided. More appropriately, the patient should be transferred to an intensive care unit (ICU) where continuous nursing supervision and monitoring of BP are available. A number of parenteral agents are effective in the immediate treatment of hypertensive emergencies ( Table 4 ).8,10,11
Table 4: Treatment of Hypertensive Emergencies

Agent

Dosage

Onset/Duration of Action (after discontinuation)

Precautions

Parenteral Vasodilators Nausea, vomiting; prolonged use may cause thiocyanate intoxication, Sodium 0.25-10 g/kg/min as IV Immediate/2-3 min methemoglobinemia, acidosis, cyanide nitroprusside infusion after infusion poisoning; bags, bottles, delivery sets must be light resistant Headache, tachycardia, vomiting, flushing, methemoglobinemia; requires Nitroglycerin 5-100 g as IV infusion * 2-5 min/5-10 min special delivery system because of drug binding to PVC tubing Tachycardia, nausea, vomiting, headache, 1-5 min/15-30 min, but increased intracranial pressure; Nicardipine 5-15 mg/hr as IV infusion may exceed 12 hr after hypotension may be protracted after prolonged infusion prolonged infusions Fenoldopam 0.1-0.3 g/kg/min as IV Headache, tachycardia, flushing, local <5 min/30 min mesylate infusion phlebitis, dizziness Tachycardia, headache, vomiting, 5-20 mg as IV bolus or 10- 10 min IV/>1 hr (IV); aggravation of angina pectoris, sodium 40 mg IM; repeat every 4-6 20-30 min IM/4-6 hr Hydralazine and water retention, increased intracranial hr (IM) pressure 0.625-1.25 mg every 6 hr Renal failure in patients with bilateral Enalaprilat Within 30 min/12-24 hr as IV injection renal artery stenosis, hypotension Parenteral Adrenergic Inhibitors

20-40 mg as IV bolus 5-10 min/2-6 hr every 10 min; up to 2 mg/min as IV infusion 500- g/kg bolus injection IV or 50-100 g/kg/min by infusion; may repeat bolus Esmolol 1-5 min/15-30 min after 5 min or increase infusion rate to 300 g/kg/min Phentolamine 5-10 mg as IV bolus 1-2 min/10-30 min Labetalol * Requires special delivery system. PVC, polyvinyl chloride.
Preferred Drugs

Bronchoconstriction, heart block, orthostatic hypotension, bradycardia

First-degree heart block, congestive heart failure, asthma

Tachycardia, orthostatic hypotension

The type of ongoing acute target organ damage will significantly affect the selection of parenteral agents for BP reduction. It is also important to keep in mind that it is not the absolute level of blood pressure, but rather the clinical status of the patient that determines the hypertensive emergency and influences the choice of antihypertensive agent ( Table 5 ).3,11
Table 5: Preferred Drugs for Select Hypertensive Emergencies

Emergency Aortic dissection AMI, ischemia Pulmonary edema Renal emergencies Catecholamine excess Hypertensive encephalopathy Subarachnoid hemorrhage Ischemic stroke

Drugs of Choice Target Blood Pressure Nitroprusside + Esmolol 110-120 SBP as soon as possible Nitroglycerin, nitroprusside, nicardipine Secondary to ischemia relief Improve symptoms 10%-15% in 1-2 Nitroprusside, nitroglycerin, labetalol hr Fenoldopam, nitroprusside, labetalol Target BP 20%-25% in 2-3 hr Control paroxysms 10%-15% in 1-2 Phentolamine, labetalol hr Nitroprusside 20%-25% in 2-3 hr

Nitroprusside, nimodipine, nicardipine 20%-25% in 2-3 hr Nitroprusside (controversial), 0%-20% in 6-12 hr nicardipine

AMI, acute myocardial infarction; SBP, systolic blood pressure.


There are significant exceptions to these initial recommendations; these are discussed in more detail later in the section on the treatment of select hypertensive emergencies.

Special Considerations in Select Hypertensive Emergencies


Aortic Dissection.

There is general agreement that at the time of diagnosis, and perhaps even when it is suspected, quickly controlling the systolic BP to lower than 120 mm Hg within 10 to 20 minutes supersedes the performance of any time-consuming techniques used to identify the dissection.

Acute Coronary Syndrome.

 

 

This situation includes patients presenting with unstable angina or myocardial infarction. Hypertension is often affected by acute adrenergic stimulation caused by ischemic chest pain or severe anxiety, but relief of chest pain is a priority, together with opening the coronary artery responsible in the case of a myocardial infarction for improved myocardial oxygen supply. The level of BP will determine the use of nitroglycerin or nitroprusside in this situation. Nicardipine can also be a useful alternative. A reduction of 10% to 20% over the first 1 to 3 hours will often be sufficient to alleviate chest pain. It is also an important step before consideration of thrombolytic therapy.

Congestive Heart Failure.

 

Congestive heart failure along with severe hypertension often results in pulmonary edema and a sharp reduction in effective circulating blood volume. In this setting, the agents of choice are those that reduce preload and afterload. The most effective is sodium nitroprusside or fenoldopam, although nitroglycerin can also be valuable, particularly if BP is not markedly elevated. Appropriate and timely use of a parenteral loop diuretic is also usually necessary.

Acute or Chronic Renal Failure.

  

A gradual reduction in BP of 20% to 25% during the first 1 to 3 hours is particularly helpful. Nitroprusside, labetalol, and nicardipine are all effective. Strong consideration should be given to fenoldopam as the agent of choice because of its favorable effects on renal function.12

Adrenergic Crises. 

   

Emergency caused by catecholamine excess includes the presence of a pheochromocytoma, cocaine or amphetamine intoxication, and dietary noncompliance in patients taking monoamine oxidase inhibitors. Care must be taken to select antihypertensive therapies that will not result in unopposed -adrenergic stimulation. Phentolamine may be useful as an initial agent to control paroxysms but is difficult to titrate for ongoing therapy. Beta blockers are generally avoided but labetalol has proved a useful agent with its alpha and beta blocking characteristics. When an occasional hypertensive crisis is observed secondary to clonidine withdrawal, immediate reinstitution of clonidine is appropriate. BP will often respond to one or two doses of clonidine, 0.1 to 0.2 mg.

Hypertensive Encephalopathy.

 

BP should be promptly lowered with nitroprusside or labetalol, with careful monitoring and frequent neurologic assessments. BP reduction can be associated with dramatic improvement in cerebral function. However, deterioration in neurologic function will require re-evaluation and consideration of other possible diagnoses.

Subarachnoid Hemorrhage.

 

Acute BP reduction is warranted in subarachnoid hemorrhage The agent of choice again would be sodium nitroprusside.

 

Nicardipine has also proved effective. Another dihydropyridine calcium antagonist, nimodipine, has demonstrated antihypertensive and anti-ischemic effects that may improve long-term outcomes of subarachnoid hemorrhage but not necessarily ischemic stroke.

Ischemic Stroke.  

First-line agents include nitroprusside, nicardipine, fenoldopam, and labetalol. Recommend avoiding reductions in mean arterial pressure higher than 10% in the first 1 to 3 hours or higher than 20% in the first 6 to 12 hours, with careful and frequent monitoring of neurologic status. The use of parenteral agents with short half-lives is most appropriate in this situation.

Summary
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Hypertensive emergencies warrant prompt ICU admission for rapid treatment and continuous blood pressure monitoring. Most hypertensive urgencies can be managed on an ambulatory basis. Excessive blood pressure reduction has been associated with acute deterioration of renal function, ischemic cardiac and cerebral events, and acute blindness. A decrease of 20% to 25% in mean arterial pressure from pretreatment blood pressure has been recommended.