Following thrombolysis (or acute endovascular therapy), the blood pressure should be monitored closely (every 15 minutes for the first 2–3 hours, then every 30 minutes for 6 hours, and then hourly for the rest of the first day), and kept below 180/105 mmHg. Failure to control hypertension during this first day could result in a cerebral hematoma with rapid neurologic deterioration.

In our patient, we were able to reduce the blood pressure to an acceptable range after initiating an infusion of nicardipine, which was then continued for 24 hours in the NICU. The patient received intravenous rt-PA and improved substantially over the following day. On the second hospital day we restarted his ACE inhibitor and started a thiazide. Later the dose of the ACE inhibitor was progressively adjusted until blood pressure was normalized. His discharge NIH stroke scale was 3 and he only had minor symptoms and no disability 3 months later.

Ischemic Stroke—Not Candidate for Thrombolysis—First 24 Hours

Hypertension may be a physiological response in patients with acute brain ischemia (as indicated by the spontaneous resolution of hypertension typically seen after successful recanalization). Therefore, when the patient is not a candidate for acute recanalization therapy the prevailing thought is that it is better not to lower the blood pressure unless it is exceedingly high (above 220/120 mmHg). The concept of accepting high blood pressures (“permissive hypertension”) is based on the notion that lowering the blood pressure in these patients with persistent vessel occlusion could worsen the brain ischemia by reducing collateral flow. When allowing blood pressure to remain high, it is important to monitor patients for possible signs of congestive heart failure, acute kidney injury, and other complications of acute hypertension. That said, gradual and modest blood pressure reduction (by 10 or 15 mmHg) is probably safe, and studies are investigating whether this approach can be beneficial.

Ischemic Stroke—After the First 24 Hours

After the first day, we gradually start oral medications (beginning with any medications the patient was taking before admission if any had been prescribed) with the purpose of progressively achieving normotension while avoiding sudden drops in blood pressure. If the blood pressure control is not optimal upon discharge, we arrange for very close follow-up as outpatient until the goal of blood pressure normalization is reached.

Intracerebral Hemorrhage—First 24 Hours

Patients with intracerebral hemorrhage should be treated to achieve moderate blood pressure reduction (systolic blood pressure < 180–160 mmHg, mean arterial pressure < 130–110 mmHg). Although cerebral hematomas are surrounded by an area of hypoperfusion, these areas are not oxygen deprived as is typical of penumbral tissue, and there is no evidence that moderately reducing the blood pressure a few hours after hematoma onset can cause worsening ischemia. Moreover profound hypertension (especially when mean arterial pressure is over 140 mmHg) increases the risk of hematoma expansion. The possible value of more aggressive blood pressure reduction in these patients is currently being evaluated in prospective clinical trials.

We lower the blood pressure of patients with intracerebral hemorrhage starting as soon as the diagnosis is made, but try to do so gradually to avoid compromising cerebral perfusion. If intracranial pressure is monitored, rarely the case in clinical practice, the cerebral perfusion pressure should be maintained above 60 mmHg.

Intracerebral Hemorrhage—After the First 24 Hours

Similarly to ischemic stroke, after the first 24 hours we typically initiate oral antihypertensives, which are then titrated to achieve progressive normalization of the blood pressure before or shortly following discharge from the hospital.

Aneurysmal Subarachnoid Hemorrhage

Although there is no good evidence to guide the treatment of hypertension in acute aneurysmal subarachnoid hemorrhage, we prefer to treat hypertension with the goal of maintaining the systolic blood pressure below 160 mmHg before the aneurysm is secured, but we recognize that the evidence that blood pressure above those values is associated with higher risk of aneurysm rebleeding is not strong. Most patients with aneurysmal subarachnoid hemorrhage have elevated blood pressures due to the excessive sympathetic release that immediately follows the aneurysm rupture. Moreover, in these patients intracranial hypertension is common, and most patients with abnormal level of consciousness will need a ventriculostomy. Acutely lowering the blood pressure in patients with intracranial hypertension could compromise cerebral perfusion pressure. When intracranial pressure is known, the cerebral perfusion pressure should be kept above 60 mmHg.

Once the aneurysm is treated by means of clipping or endovascular coiling, we stop antihypertensives except for nimodipine (and low-dose beta-blocker in patients with history of heart disease previously on beta-blockers) anticipating the need to maintain adequate cerebral perfusion in a narrowed arterial bed from vasospasm.

What Drugs Should You Use?

We prefer labetalol or hydralazine in intermittent doses (both 10 mg IV) and we choose between them depending on the heart rate (if bradycardia, it is safer to use hydralazine). Enalaprilat is another reasonable option. If intermittent doses of these medications fail to control the hypertension, we place an arterial catheter and start an infusion of nicardipine (or sometimes labetalol). Clevidipine, a newer dihydropyridine calcium channel blocker, also appears to be a safe and effective agent for the acute control of severe hypertension. The most severe and refractory cases of acute hypertension may necessitate treatment with sodium nitroprusside. We prefer to avoid nitrates because their known venodilatory effect can increase intracranial pressure, although we are not so certain about the claimed deleterious effect on intracranial pressure with sodium nitroprusside. We also avoid very rapidly acting medications, such as sublingual nifedipine, because they can provoke excessive drops in blood pressure. Clonidine is not a safe option either in the hyperacute phase because the first dose can occasionally cause paradoxical hypertension. Table 21.1 lists the doses of the medications we use most often for the treatment of acute hypertension in ischemic and hemorrhagic stroke.

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