An important point to remember in the management of the patient with any degree of BP elevation is to 'treat the patient and not the number'.
In patients presenting with hypertensive emergencies, antihypertensives have 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 be titrated from minute to minute (in countries where appropriate facilities exist, of course). However, patients must have constant monitoring in an intensive care unit. The potential exists for thiocyanate toxicity and cyanide toxicity with prolonged use, or if the patient has renal or hepatic failure.
Diazoxide may also be used in hypertensive crisis. Small boluses of 100mg are administered every 5 minutes, as indicated. Diazoxide is not preferred with concomittant 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 with hypertensive emergencies. Labetalol is particularly preferred in patients with acute dissection. Boluses of 10-20mg may be administered, or the drug may be infused at 1mg/min until the desired BP is obtained. Once an adequate BP level is obtained, oral antihypertensive therapy should be initiated, and patients are gradually weaned off parenteral agents.
Fenoldopam, a peripheral dopamine-1-receptor agonist, is given as an initial IV dose of 0.1 μg/kg/min, titrated every 15 minutes.
Clevidipine, a dihydropyridine calcium channel blocker, is administered intravenously for rapid and precise BP reduction. It is rapidly metabolized in the blood and tissues and does not accumulate in the body. Initiate IV infusion of clevidipine at 1-2mg/h; titrate the dose at short intervals (ie 90s) initially by doubling the dose. As the BP approaches its goal, increase the clevidipine dose by less than double, and lengthen the time between dose adjustments to every 5-10 minutes. An approximately 1-2mg/h increase produces an additional 2-4mmHg decrease in SBP. Typically, the therapeutic response is achieved with 4-6mg/h, although severe hypertension may require higher doses. Most patients have received maximum doses of 16mg/h or less; experience is limited with short-term dosing as high as 32mg/h. Because of lipid load restrictions, do not exceed 1000mL or an average of 21mg/h within a 24-hour period; experience is limited with use beyond 72 hours.
Rapid BP reduction is indicated in neurologic emergencies, such as hypertensive encephalopathy, acute ischemic stroke, acute intracerebral hemorrhage, and subarachnoid hemorrhage.
In hypertensive encephalopathy, the treatment guidelines are to reduce the MAP 25% over 8 hours. Labetalol, nicardipine, and esmolol are the preferred medications; however nitroprusside and hydralazine should be avoided.
For acute ischemic stroke, the preferred medications are labetalol and nicardipine. Withhold antihypertensive medications unless the SBP is >220mmHg or the DBP is >120mmHg unless the patient is receiving IV or intra-arterial fibrinolysis; then, the goal BP is an SBP of <185mmHg and DBP <110mmHg. After treatment with fibrinolysis, the SBP should be maintained <180mmHg and the DBP at <105mmHg for 24 hours.
For acute intracerebral hemorrhage, the preferred medications are labetalol, nicardipine, and esmolol; avoid nitroprusside and hydralazine. The treatment is based on clinical/radiographic evidence of increased intracranial pressure (ICP). If there are signs of increased ICP, the MAP is to be maintained just below 130mmHg (or SBP <180mmHg) for the first 24 hours after onset. In patients without increased ICP, maintain the MAP <110mmHg (or SBP <160mmHg) for the first 24 hours after symptom onset. Recent evidence shows that in cases of acute intracerebral hemorrhage, early intensive BP control is well tolerated and can reduce hematoma growth in patients treated within 6 hours after the onset of intracerebral hemorrhage. The target systolic pressure for these studies was 140mmHg and routine IV medications were used. The target SBP was maintained over 7 days.
In subarachnoid hemorrhage, nicardipine, labetalol, and esmolol are also the preferred agents; again, nitroprusside and hydralazine should be avoided. Maintain the SBP <160mmHg until the aneurysm is treated or cerebral vasospasm occurs. Although oral nimodipine is used to prevent delayed ischemic neurologic deficits, it is not indicated for treating acute hypertension.
Rapid BP reduction is also indicated in cardiovascular emergencies, such as aortic dissection, acute coronary syndrome, and acute heart failure.
In aortic dissection, the preferred medications are labetalol, nicardipine, nitroprusside (along with a beta-blocker), esmolol, and morphine sulfate. However avoid beta-blockers if there is aortic valvular regurgitation or suspected cardiac tamponade. Maintain the SBP at <110mmHg, unless signs of end-organ hypoperfusion are present. The preferred treatment includes a combination of narcotic analgesics (morphine sulfate), beta-blockers (labetalol, esmolol), and vasodilators (nicardipine, nitroprusside). Calcium channel blockers (verapamil, diltiazem) are an alternative to beta-blockers.
For acute coronary syndrome, beta-blockers and nitroglycerin are the preferred drugs. Treatment is indicated if the SBP is >160mmHg and/or the DBP is >100mmHg. Reduce the BP by 20-30% of baseline. Note that thrombolytics are contraindicated if the BP is >185/100mmHg.
In acute heart failure, the preferred medications are IV or sublingual nitroglycerin and IV enalaprilat. Treat with vasodilators (in addition to diuretics) for a SBP > or = 140mmHg.