Cardiac & Resuscitation, Patient Care

Blood Pressure Management Goals in Stroke Care

Issue 5 and Volume 43.

Blood pressure management goals in stroke care

You arrive at a small rural emergency healthcare facility to transport a 72-year-old female who presents to the ED with the worst headache of her life. She’s to be transported to a tertiary center with neurosurgical services.

Upon further questioning you determine her headache was sudden onset with maximum intensity.

When reviewing her history and medications, you note that she’s currently on Coumadin (warfarin) with an international normalized ratio (INR) of 3.5, with the following vital signs noted on the monitor upon entering the room: blood pressure of 209/75 mmHg; heart rate of 66; respiratory rate of 16; SpO2 of 98% on a nasal cannula at 2 Lpm.

The facility’s staff report a substantial decline in the patient’s level of consciousness since her arrival with a current Glasgow coma scale of 11.

You review the CT of her head and note blood in the sulci, confirming the diagnosis of subarachnoid hemorrhage.

You and your partner discuss management strategies to maximize the patient’s outcome during the hour-long transport.

During interfacility transports where the type of stroke is known, you’ll often have very different blood pressure goals depending on if the stroke was identified as ischemic or hemorrhagic.

Blood Pressure Goals: Clot Vs. Bleed

Hypertension is a common problem afflicting all races and genders worldwide.1

In many circumstances, hypertension is often over-treated, in both the hospital and prehospital setting. Many clinicians feel the need to intervene with an elevated blood pressure despite the patient not displaying any indication of end-organ damage.

In cases where hypertension is stumbled upon with other medical issues, no emergent treatment is indicated. These types of patients can follow up with their primary care provider for evaluation and management on a long-term basis with oral antihypertensive medications.2

In the setting of a patient with stroke symptoms, there are some major differences in the patient’s blood pressure management.

During interfacility transports where the type of stroke is known, you’ll often have very different blood pressure goals depending on if the stroke was identified as ischemic or hemorrhagic.

The problem with ischemic strokes is they will generally have an ischemic penumbra surrounding the core of the stroke. This is an area that’s at risk for death; thus, having an elevated blood pressure is beneficial at minimizing the stroke size through collateral circulation. (See Figure 1.)

When antihypertensive medications are administered that rapidly lower this type of patients’ blood pressure too far, the patient will often take a turn for the worse and have a worse neurological outcome.3

The use of tissue plasminogen activator (tPA) in acute stroke remains controversial, but almost all would agree that if tPA is administered, managing blood pressure is a crucial component if the patient is extremely hypertensive. For the patient who won’t be receiving tPA, there doesn’t appear to be any benefit in reducing the systolic blood pressure < 220 mmHg.4,5

Patients who will be receiving tPA require a more aggressive strategy to reduce the risk of post-reperfusion bleeding that can be caused by the tPA.

If the patient has a systolic blood pressure > 185 mmHg or a diastolic blood pressure that’s > 110 mmHg, IV antihypertensive medications are indicated. With reperfusion therapy being time-sensitive, the clinician should aggressively work to reduce the blood pressure to a safe level to start the administration of tPA.2

There’s a very distinct difference between an ischemic stroke and a hemorrhagic stroke in the way blood pressure is managed.

The first major difference is that a hemorrhagic stroke doesn’t have an ischemic penumbra, so they’re not as sensitive to blood pressure changes as the ischemic stroke is. There’s still a need to have adequate perfusion to overcome a potential increase in intracranial pressure, so dropping the patient’s blood pressure too far would be harmful as well.

The interesting thing about hemorrhagic strokes is that even though patients are more likely to die in the acute event; if the patient does survive and receive a high level of neurocritical care, they’re more likely to have a favorable neurological outcome.

Some key components of having a favorable neurological outcome are a high-quality neuroprotective intubation (if performed), good post-intubation management maintaining euoxemia, eucapnia, good sedation and analgesia, and positioning with the patient’s head elevated.

Importantly, if there’s any coagulopathy, especially those caused by medications such as Coumadin (warfarin), then this needs to be aggressively addressed.

Another extremely important goal to achieve during the management of this patient is to correct their INR. A patient with an INR of 3.5 (such as the patient described in this case) will experience a worsening of the bleed. In this case we would want to institute a two-pronged approach for managing the coagulopathy.

Since Coumadin (warfarin) is a vitamin K antagonist, it’s reasonable to administer vitamin K to this patient. The route recommended in a position paper by the American College of Emergency Physicians is to give this medication by slow IV infusion. Since it takes 24 hours to see an increase in factor II, the reversal with vitamin K alone will take too long to provide much benefit.

The co-administration of plasma, which contains all of the vitamin K-dependent clotting factors, will allow for immediate reversal and should be administered as soon as possible.

The other option is to administer prothrombin complex concentrates (PCCs), but PCCs aren’t likely to be available from the sending facility and they’re prohibitively expense to stock for most transport agencies, unlike blood and plasma.

Since these patients don’t have an ischemic penumbra and we’re worried about rebleeding caused by hypertension, then a fairly rapid reduction in blood pressure is indicated. This is in stark contrast to the ischemic stroke, where mild and slow blood pressure reduction is the strategy of choice.

There’s some debate in the literature, but a safe range seems to be a reduction to a systolic blood pressure that measures between 140–160 mmHg. Both the Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial (INTERACT) and Antihypertensive Treatment of Acute Cerebral Hemorrhage (ATACH) trials both demonstrated that the rapid reduction to this range is safe.6

There are several choices of antihypertensive medications in these situations, although most would shy away from using medications like nitroglycerine or hydralizine. Some clinicians use an IV angiotensin-converting enzyme (ACE) inhibitors, such as enalaprilat, but by far the favored medications are either IV labetalol or the IV calcium channel blocker nicardipine. The later drug is often being preferred for its ease in titration.

Remember to first manage the patient’s pain with analgesics before starting antihypertensives, as there’s often a component to hypertension caused by the pain associated with a stroke. Once pain management is accomplished, the patient’s blood pressure can be better managed.

Summary

With early, aggressive management, stroke patients can have a better outcome than we’ve ever seen in the past.

Proper initial management of stroke includes selecting the correct stroke facility and optimizing all aspects of the patient’s care, including blood pressure goals.

References

1. Chobanian AV, Bakris GL, Black HR, et al. The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: The JNC 7 report. JAMA. 2003;289(19):2560–2572.

2. Wolf SJ, Lo B, Shih RD, et al. Clinical policy: Critical issues in the evaluation and management of adult patients in the emergency department with asymptomatic elevated blood pressure. Ann Emerg Med. 2013;62(1):59–68.

3. Fischer U, Cooney MT, Bull LM, et al. Acute post-stroke blood pressure relative to premorbid levels in intracerebral haemorrhage versus major ischaemic stroke: A population-based study. Lancet Neurol. 2014;13(4):374–384.

4. He J, Zhang Y, Xu T, et al. Effects of immediate blood pressure reduction on death and major disability in patients with acute ischemic stroke: The CATIS randomized clinical trial. JAMA. 2014;311(5):479–489.

5. Sandset EC, Bath PM, Boysen G, et al. The angiotensin-receptor blocker candesartan for treatment of acute stroke (SCAST): A randomised, placebo-controlled, double-blind trial. Lancet. 2011;377(9767):741–750.

6. Owens WB. Blood pressure control in acute cerebrovascular disease. J Clin Hypertens (Greenwich). 2011;13(3):205–211.