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Treating Hypertension in Life-Threatening Conditions

Roberts, James R. MD

doi: 10.1097/01.EEM.0000669304.90657.87
    This patient presented to the ED with sudden onset of ripping chest pain, diaphoresis, and a blood pressure of 190/120 mm Hg. This chest x-ray demonstrated a widened mediastinum, a classic finding in aortic dissection. A beta blocker, such as IV esmolol, should be used first and immediately as anti-impulse therapy to decrease the blood pressure and cardiac output to lessen aortic shear forces and to decrease the pulse (60 bpm/min or less). After this is accomplished, an antihypertensive should be instituted to obtain a systolic blood pressure of 100-110 mm Hg or less. Nitroprusside or labetalol is most often used. The therapy should be instituted before the diagnosis is confirmed with a contrast CT scan or transesophageal ultrasound in addition to expedited consultation with a vascular surgeon.

    Most cases of severe hypertension—a blood pressure of 180/110 mm Hg or higher—are associated with stopping prescribed medications, usually in patients with essential hypertension. There is a general consensus that severe hypertension should be treated immediately in those with symptoms or evidence of end-organ damage or dysfunction. This is a hypertensive emergency, and immediate aggressive treatment may limit progression of organ damage. The symptoms prompting acute intervention for severe hypertension include headache, chest pain, nausea, dizziness, epistaxis, agitation, delirium, seizures, and focal neurological deficit.

    Hypertension without symptoms becomes less urgent, and acute intervention is not warranted immediately. The goal with both types of severe hypertension is to lower the blood pressure in a manner that does not produce severe hypotension.

    There are, however, specific etiologies that require more aggressive treatment of hypertension than for those with essential hypertension. These conditions include aortic dissection, toxemia in pregnancy, acute stroke, and myocardial infarction. These conditions are complicated and usually require admission, so early consultation with the appropriate specialty is imperative.

    Acute Aortic Dissection: Acute dissection of the aorta is frequently a fatal condition in which a longitudinal tear occurs in the media of the aorta. As blood enters the intramural space, there is further progression of the dissection. Aortic dissection can occur in the ascending aorta, termed a type A dissection by the Stanford classification, or distal to the subclavian artery, a type B dissection. The presence and type of aortic dissection can be confirmed with a contrast CT scan or transesophageal echocardiography. Treatment of hypertension and immediate consultation with a vascular surgeon are suggested, even before confirming the diagnosis.

    Early management of both types of acute aortic dissection involves controlling the pain and limiting the extension of the dissection using anti-impulse therapy, usually with beta blockers. Beta blockers can also lower the blood pressure. Type A dissections usually require surgery, while type B dissections generally do not and are usually managed medically or with endovascular treatment. Both types of aortic dissection require immediate control of hypertension.

    The treatment goal is obtaining a blood pressure of less than 120/80 mm Hg within 20 minutes. Often a combination of antihypertensive drugs is required. The best beta blocker is probably IV esmolol as the first intervention. This first-line anti-impulse therapy is given before blood pressure medications to reduce the velocity of the left ventricular contractions, decrease shearing stress, and minimize progression of the dissection. Importantly, the pulse rate should be lowered to 60 bpm. Labetalol can also be used for its beta and alpha blockade, but esmolol seems to be favored. If beta blockers do not quickly reduce the systolic blood pressure, another specific hypertension drug should be added, usually nitroprusside or nicardipine.

    Nicardipine has a number of advantages over nitroprusside, but neither should be used without first controlling the heart rate with beta blockade. Vasodilation can induce reflex activation of the sympathetic nervous system, leading to enhanced ventricular contraction and increased aortic stress. Direct vasodilators, such as hydralazine, should be avoided because they increase aortic wall stress. Pain is controlled with IV morphine.

    Acute Ischemic Stroke: Hypertension is common in acute ischemic stroke. Minimal data are available from randomized controlled trials specifically designed to guide blood pressure management in the acute phase of ischemic stroke. The perfusion pressure distal to the obstructed vessel is low in acute ischemic stroke, and the distal vessels are dilated. Because of impaired cerebral autoregulation, blood flow in these dilated vessels is thought to be dependent on the systemic blood pressure. Blood pressure is usually not lowered rapidly in the acute phase of ischemic stroke unless it is more than 185/110 mm Hg in patients who are candidates for reperfusion therapy.

    Acute treatment in patients who are not candidates for thrombolytic therapy is usually discouraged, but it has been suggested for blood pressure higher than 220/120 mm Hg. An emergency CT scan of the head is required to exclude CNS hemorrhage. The ischemic penumbra of an acute thrombotic stroke may be at risk if blood flow is reduced by lowering the blood pressure, causing irreversible damage.

    Overall, however, acute blood pressure reduction does not have an identifiable or proven beneficial effect on functional outcome. But treatment is recommended to lower the systolic pressure prior to lytic intervention. The reduction of blood pressure in both cases should be done cautiously, aiming for a 15 percent reduction over the first 24 hours or more quickly if lytics are used. No good evidence supports using any specific antihypertensive agent to achieve recommended blood pressure goals. Medications suggested for treating hypertension in acute ischemic stroke are labetalol, nicardipine, or clevidipine, all given intravenously.

    Hemorrhagic Stroke: Managing blood pressure in patients with spontaneous cerebral hemorrhage or subarachnoid hemorrhage is complicated by the risks of reducing cerebral perfusion v. the benefit of possibly reducing further bleeding. For patients with acute intracranial hemorrhage, it is usually suggested to slowly lower hypertension to a systolic blood pressure of 140 mm Hg. This degree of blood pressure reduction appears to be safe and may improve functional outcome. For those with hemorrhagic stroke who have a systolic blood pressure above 220 mm Hg, aggressive reduction with IV drugs is suggested.

    The goal is a systolic blood pressure of 140-160 mm Hg. IV agents for controlling blood pressure include nicardipine, clevidipine, labetalol, esmolol, or enalaprilat. Studies have suggested that aggressively lowering the blood pressure for acute hemorrhagic stroke is associated with reduced hematoma size, but a long-term benefit for most clinical outcomes is unproven. For patients with cerebellar hemorrhage, surgical removal of the clot with cerebellar decompression is advised for patients with hemorrhage greater than 3 cm in diameter.

    Acute Coronary Syndrome: Severe hypertension associated with acute coronary syndrome, including acute MI, is treated with intravenous nitroglycerine, clevidipine, nicardipine, or IV metoprolol or esmolol. There are no specific guidelines on when to treat hypertension in such patients. It seems reasonable to lower severe hypertension in patients with acute coronary syndrome with the medications listed, but further specifics are lacking in the medical literature.

    Withdrawal of Short-Acting Antihypertensive Agents, Clonidine, or Propranolol: The sudden withdrawal of these medications can be associated with severe hypertension. Generally, the reinstitution of recently discontinued drugs lowers the blood pressure adequately.

    Severe Hypertension in Pregnancy: The rapid treatment of severe hypertension in pregnancy is suggested, and often requires preantral therapy. Severe hypertension should be treated to prevent maternal vascular complications, such as stroke and heart failure, but there is no consensus about the optimal blood pressure threshold for initiating therapy. It is generally suggested that antihypertensive therapy should be initiated for a systolic pressure greater than 150-160 mm Hg or a diastolic pressure greater than 100-120 mm Hg.

    One can initiate treatment at lower levels for women who have a headache, chest discomfort, shortness of breath, or confusion. Severe hypertension, with a systolic blood pressure greater than 160 mm Hg, seems to predict adverse cerebral events. There is no high-quality evidence supporting physician recommendations for the treatment of hypertension in pregnancy. Intravenous labetalol and hydralazine are most often recommended. Nifedipine (not immediate release) or methyldopa is also appropriate.

    Thoracic aortic aneurysm. A: PA chest radiograph of a 77-year-old woman shows a left mediastinal mass contiguous with the contour of the aorta (arrow). B: CT shows an aneurysm of the proximal descending aorta with extensive mural thrombus (T). Adjacent rim of high attenuation represents an atelectatic lung (arrow). C: Coronal CT shows a fusiform aneurysm involving the junction of the aortic arch and descending aorta; this is the most common location of atherosclerotic thoracic aortic aneurysms. D: CT after placement of endovascular stent graft shows the metallic stent, enhancing aortic lumen, and surrounding low-attenuation thrombus. There is no evidence of leak. E: Coronal CT shows overlapping stents. Note persistent thrombus (T). F: Sagittal CT shows normal appearance of overlapping stents.

    It is usually recommended to avoid using angiotensin II receptor blockers, ACE inhibitors, and nitroprusside. The optimal targeted blood pressure following treatment in pregnancy is 130-150/80-100 mm Hg. It is generally suggested that reducing the mean arterial pressure of no more than 25 percent over two hours is reasonable. Options for the treatment are best initiated with consultation with an OB/GYN.

    ED Use of Esmolol for Acute Aortic Dissection

    Esmolol Premixed Injection: Supplied as single-use bags of 2,500 mg/250 mL (10 mg/mL).

    Esmolol Double-Strength Premixed Injection: Supplied as single-use bags of 2,000 mg/100 mL (20 mg/mL).

    Dosing for Acute Aortic Dissection: Esmolol is the preferred agent. The dose is 250-500 mcg/kg IV loading dose, then infuse at 25 to 50 mcg/kg/minute; titrate to maximum dose of 300 mcg/kg/minute).

    Onset of action is one to two minutes. Duration of action is 10-20 minutes. A re-bolus should be given before each upward dose titration.

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    Dr. Robertsis a professor of emergency medicine and toxicology at the Drexel University College of Medicine in Philadelphia. Read the Procedural Pause, a blog by Dr. Roberts and his daughter, Martha Roberts, ACNP, PNP, at, and read his past columns at

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