Intracranial hypertension/hypotension question

Advanced Practice Columnist / Guide · Dec 19, 2014

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).

Advanced Practice Columnist / Guide · Dec 19, 2014

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.

Nurse_Bella · Dec 20, 2014

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.