Neurocritical Care

21. Acute Hypertension After Stroke

A 56-year-old man with history of long-standing poorly controlled hypertension presents to the emergency department with sudden onset of a speech abnormality and right-sided weakness. Time from symptom onset is 70 minutes. First examination reveals a global aphasia, right heminopia, right hemiparesis (NIH stroke scale of 14).

Head CT scan shows a probable hyperdense dot sign in a Sylvian branch of the left middle cerebral artery with no evidence of acute infarction or hemorrhage. Blood pressure is initially 204/112 mmHg. He responds only briefly to two doses of 10 mg of intravenous labetalol each. The patient is potentially a candidate for intravenous thrombolysis, but after these two doses of labetalol, the blood pressure is back up to 194/106 mmHg. There are no other clinical or laboratory contraindications for intravenous thrombolysis.

What do you do now?

To know how—or even when—to treat hypertension in a patient with acute stroke, three pieces of information are needed. First, one needs to know the type of stroke, second, the time from the onset of symptoms and third, in acute ischemic stroke whether the patient is a candidate for thrombolysis (Figure 21.1). All recommendations mentioned here on blood pressure management are based on collective experience of experts in the field but, unfortunately, no clinical trials have evaluated this matter. Several clinical scenarios can be expected in the emergency department or neurosciences intensive care unit (NICU), and they are categorized as follows.

Ischemic Stroke–Candidate for Thrombolysis—First 24 Hours

Patients who are candidates for thrombolysis need to have their hypertension reliably controlled before they can be treated with rt-PA. Expert guidelines recommend reducing the systolic blood pressure below 185 mmHg and the diastolic blood pressure below 110 mmHg before infusing the thrombolytic. If these parameters cannot be reached and consistently maintained, intravenous rt-PA should not be administered. The same principle applies to endovascular recanalization therapies (mechanical clot retrieval or suctioning, intracranial stent placement). The rationale for deferring any type of acute recanalization therapies in patients with uncontrolled hypertension is that the risk of reperfusion hemorrhage is likely too high.

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FIGURE 21.1 Recommended algorithm for control of hypertension in patients with acute stroke. *Target should be 130/80 mmHg in patients with diabetes mellitus. Ideal blood pressure < 120/80 mm Hg. † If suspected increased intracranial pressure, then monitor intracranial pressure and maintain cerebral perfusion pressure > 60 mmHg. BP; blood pressure.

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.

TABLE 21.1 Options for the Treatment of Hypertension in Patients with Acute Stroke

Drug

Usual dose

Labetalol

10–20 mg IV over 1–2 minutes, may repeat after 10–15 minutes (maximum dose 300 mg over 24 hours)
Infusion: 2–8 mg/min

Hydralazine

10–20 mg IV over 1–2 minutes, may repeat after 10–15 minutes

Nicardipine

Infusion: 5 mg/hr, then can be titrated up to 15 mg/hr as needed

Sodium nitroprusside

Infusion: 0.3 mcg/kg/min, then can be titrated up to 10 mcg/kg/min as needed

KEY POINTS TO REMEMBER REGARDING ACUTE HYPERTENSION AFTER STROKE

· The goals of treatment of hypertension in acute stroke patients depends on the type of stroke and the time from symptom onset.

· Ischemic stroke patients receiving thrombolysis need strict and consistent control of hypertension to avoid hemorrhagic complications.

· Patients with ischemic stroke who are not candidates for recanalization therapies should have their hypertension managed more conservatively to avoid decrease in collateral cerebral blood flow.

· In patients with acute intracerebral hemorrhage moderate reductions of blood pressure are safe and may reduce the chances of hematoma expansion.

· In aneurysmal subarachnoid hemorrhage, we favor gradual blood pressure reduction during the first few hours which we maintain until the aneurysm is treated. Then blood pressure parameters should change upward to reduce the risk of ischemia if cerebral vasospasm develops.

Further Reading

Adams HP Jr, del Zoppo G, Alberts MJ, Bhatt DL, Brass L, Furlan A, Grubb RL, Higashida RT, Jauch EC, Kidwell C, Lyden PD, Morgenstern LB, Qureshi AI, Rosenwasser RH, Scott PA, Wijdicks EF; American Heart Association; American Stroke Association Stroke Council; Clinical Cardiology Council; Cardiovascular Radiology and Intervention Council; Atherosclerotic Peripheral Vascular Disease and Quality of Care Outcomes in Research Interdisciplinary Working Groups. Guidelines for the early management of adults with ischemic stroke: a guideline from the American Heart Association/American Stroke Association Stroke Council, Clinical Cardiology Council, Cardiovascular Radiology and Intervention Council, and the Atherosclerotic Peripheral Vascular Disease and Quality of Care Outcomes in Research Interdisciplinary Working Groups: the American Academy of Neurology affirms the value of this guideline as an educational tool for neurologists. Stroke 2007; 38:1655–1711.

Aiyagari V, Gorelick PB. Management of blood pressure for acute and recurrent stroke. Stroke 2009;40:2251–2256.

Anderson CS, Huang Y, Want JG, et al. Intensive blood pressure reduction in acute cerebral hemorrhage trial (INTERACT): a randomized pilot trial. Lancet Neurol 2008;7:391–399.

Geeganage C, Bath PM. Vasoactive drugs for acute stroke Cochrane Database Syst Rev. 2010; 7:CD002839.

Katzan IL, Furlan AJ, Lloyd LE, Frank JI, Harper DL, Hinchey JA, Hammel JP, Qu A, Sila CA. Use of tissue-type plasminogen activator for acute ischemic stroke: the Cleveland area experience. JAMA 2000; 283:1151–1158.

Marik PE, Varon J. Hypertensive crises, challenges and management. Chest 2007;131:1949–1962.

Morgenstern LB, Hemphill JC 3rd, Anderson C, Becker K, Broderick JP, Connolly ES Jr, Greenberg SM, Huang JN, MacDonald RL, Mess SR, Mitchell PH, Selim M, Tamargo RJ; American Heart Association Stroke Council and Council on Cardiovascular Nursing. Guidelines for the management of spontaneous intracerebral hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2010; 41:2108–2129.

Potter JF, Robinson TG, Ford GA, Mistri A, James M, Chernova J, Jagger C. Controlling hypertension and hypotension immediately post-stroke (CHHIPS): a randomized, placebo-controlled, double-blind pilot trial. Lancet Neurol. 2009; 8:48–56.

Rabinstein AA, Lanzino G, Wijdicks EFM. Multidisciplinary management and emerging therapeutic strategies in aneurysmal subarachnoid hemorrhage. Lancet Neurol 2010; 9:504–519.

Stead LG, Gilmore RM, Vedula KC, Weaver AL, Decker WW, Brown RD Jr. Impact of acute blood pressure variability on ischemic stroke outcome. Neurology 2006; 66:1878–1881.