The history should focus on the presence of TOD, the circumstances surrounding the HTN, and any identifiable etiology. The history and physical examination determine the nature, severity, and management of the hypertensive event. Details of antihypertensive drug therapy and compliance
Assess whether specific symptoms suggesting TOD are present.
The physical examination should assess whether TOD is present.
Vitals
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BP should be measured in both the supine position and the standing position (assess volume depletion).
BP should also be measured in both arms (a significant difference suggests an aortic dissection).
ENT: The presence of new retinal hemorrhages, exudates, or papilledema suggests a hypertensive emergency.
Cardiovascular - Evaluate for the presence of heart failure.
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Jugular venous distension
Crackles
Peripheral edema
Abdomen - Abdominal masses or bruits
CNS
Level of consciousness
Visual fields
Focal neurologic signs
Causes
The most common hypertensive emergency is a rapid unexplained rise in BP in a patient with chronic essential HTN. Most patients who develop hypertensive emergencies have a history of inadequate hypertensive treatment or an abrupt discontinuation of their medications.
Lab Studies
Electrolytes, BUN, and creatinine levels to evaluate for renal impairment
CBC and smear to exclude microangiopathic anemia
Urinalysis
ECG
Imaging Studies
Chest radiography is indicated in patients with chest pain or shortness of breath.
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Cardiac enlargement
Pulmonary edema
Widened mediastinum
Head CT and/or brain MRI are indicated in patients with abnormal neurologic examinations or clinical concern for the following.
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Intracranial bleeding
Cerebral edema
Cerebral infarction
Chest CT scan, transesophageal echocardiography, or aortic angiography is indicated in cases where aortic dissection is suspected.
Prehospital Care
Address the manifestations of a hypertensive emergency, such as chest pain or heart failure. Reduction of BP may not be indicated in the prehospital setting.
Under most circumstances, attempting to treat HTN directly in the prehospital setting is unwise. In particular, rapid lowering of BP can critically decrease target organ perfusion.
Emergency Department Care
The fundamental principle in determining the necessary ED care of the hypertensive patient is the presence or absence of TOD.
Initial considerations (if the patient is not in distress)
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Place the patient who is not in distress in a quiet room and reevaluate after an initial interview. In one study, 27% of patients with an initial DBP higher than 130 mm Hg had their DBP fall below critical levels after relaxation without specific treatment.
Consider the context of the elevated BP (eg, severe pain often causes increase in BP).
Screen for TOD: The patient's history, physical examination, laboratory studies, and diagnostic tests, as outlined in Workup, 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 ED 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.
Acute lowering of BP in the narrow window of the ED visit does not improve long-term morbidity and mortality rates. The follow-up recommended for these situations by the Joint National Committee on High Blood Pressure is outlined in Follow-up.
Patients with TOD usually require admission and rapid lowering of BP using intravenous medications. Suggested medication depends on the affected organ system.
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 results 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% in the first hour of treatment. If the patient remains stable, the BP should then be lowered to 160/100-110 mm Hg in the next 2-6 hours. Please note the exceptions to this general rule listed below.
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 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.
Intravenous labetalol
Alternative – Intravenous nitroprusside with intravenous beta-blocker (eg, 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.
BP control affects the use of thrombolytic agents in ischemic stroke. SBP higher than 185 mm Hg or diastolic pressures higher than 110 mm Hg are contraindications to the use of tissue plasminogen activator (tPA) within the first 3 hours of an ischemic stroke.
The current recommendation by the American Stroke Association states that a patient with a recent ischemic stroke and a SBP higher than 220 mm Hg or a DBP higher than 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.
A precipitous fall in SBP may compromise cerebral perfusion and increase mortality. Do not exceed a 20% reduction in BP.
The controlled lowering of BP with intravenous nitroprusside or intravenous labetalol (in the absence of bradycardia) is currently recommended only when the SBP is higher than 200 mm Hg or the DBP is higher than 110.
Monoamine oxidase (MAO)-tyramine interactions with acute hypertension - Intravenous phentolamine
Pheochromocytoma
Intravenous phentolamine
Intravenous labetalol
Hypertensive encephalopathy: Do not exceed a 20% reduction in BP.
