Intracranial hypertension/hypotension question


Hi fellow nurses!

I am a new grad one month into my first job at the neuro ICU. I am still finding myself confused about blood pressure as it relates to neuro compared to the rest of the body. In conditions such as subarachnoid hemorrhage, I've noticed that it's important to keep their blood pressures high, but at the same time they are given nimodipine to prevent vasospasms. Doesn't nimodipine also lower/control blood pressure and if so, why are we vasodilating them while at the same time wanting to keep them hypertensive? I guess I'm thinking of it in terms of someone having hypertension as a condition by itself without neuro involvement, so that's skewing my reasoning on this concept. My preceptor wasn't sure of the answer, along with the charge nurse, and when I asked one of the doctors, he just confused me more. Can anyone explain it better? What is the role of blood pressure in the brain for someone with a neuro condition? Do they have to be hypertensive or hypotensive and how does that relate to the cerebral prefusion?

If anyone can help me grasp this concept, I'd really appreciate it :)

Thanks a bunch!!!

juan de la cruz, MSN, RN, NP

9 Articles; 4,338 Posts

Specializes in APRN, Adult Critical Care, General Cardiology. Has 31 years experience.

Since you mentioned SAH, I think you should focus your thought on that condition and why blood pressure is important for patients in this particular condition. Be aware that institutional practice may vary depending on provider preference and not everyone will follow the literature to the book.

Majority of SAH's are aneurysmal in origin. The bleed is typically caused by rupture of an aneurysm in the cerebral arterial circulation. In the acute presentation, the goal is to keep BP under control (under 140 systolic at our institution) to prevent further bleeding. In cases where there is intra-ventricular extension causing hydrocephalus, an external ventricular drain is placed to relive this pressure.

There are two accepted modalities to treat cerberal aneurysms: coiling and clipping. Coiling is a Neuro IR procedure that involves embolization of the aneurysm via coil. Clipping involves a craniotomy and is performed by a Neurosurgeon. Once an intervention is done, the aneurysm is called "secured" and no longer at risk for rupture that could lead to further SAH.

Unfortunately, that's not where the problems for these patients end. Cerebral vasospasm is a serious consequence of SAH's after an aneurysmal rupture. It typically occurs on day 3-4 and peaks at day 10 following the bleed. Vasospasm causes the arterial lumen to narrow and compromise arterial blood flow to the brain. Neurosurgeons have used the Triple H therapy (hypervolemia, HTN, hemodilution) as a way to counteract the effect of cerebral vasospasm.

Another mainstay of therapy is cerebroselective Calcium Channel Blockers (Nimodipine) which ironically can lower the BP. In some institutions (such as ours), another Calcium Channel Blocker called Verapamil is injected directly into the artery that is having spasms by a Neuroradiology Interventioanalist. Calcium Channel Blockers relax smooth muscle and that's how they lower BP and prevent spasm.

In our institution, we "vasopress" patients to a set SBP goal during the vasospasm risk phase. The thought behind this is that if you increase blood pressure, you get better blood flow through the cerebral arteries that are spasm-ing. The goal SBP tends to be arbitrary. There is no single answer to how high BP should be because we really don't see that an SBP of 160 is better than 170 since we're not monitoring actual flow in the artery as BP changes. However, in some patients, you could clearly see neurologic deficits when BP is allowed to drift to a low level (i.e., less than 140).

juan de la cruz, MSN, RN, NP

9 Articles; 4,338 Posts

Specializes in APRN, Adult Critical Care, General Cardiology. Has 31 years experience.

Alternatively, you could also use Cerebral Perfusion Pressure (CPP) as target number in determining BP goals in patients where there is a concern for compromise in brain perfusion. We know that CPP = MAP - ICP. However, we don't always know what the patient's ICP is unless there is an EVD or similar ICP monitor.


23 Posts

Thanks so much Juan de la Cruz!! You explained it very well :) It's an interesting concept and one that I see quite frequently on the floor, so I was really wondering about the patho behind the disease and what exactly the role of BP is in this condition.