Cerebral Perfusion Pressure

Issues of Concern

Monitoring cerebral perfusion pressure requires measuring both the MAP and the ICP. The MAP can be measured directly through invasive hemodynamic means, most often cannulation of a peripheral artery such as the radial or femoral artery. The MAP can also be measured indirectly with a noninvasive blood pressure cuff and by applying the previously mentioned formula using the systolic and diastolic blood pressures.

Intracranial pressure is usually measured invasively through an intracranial pressure transduction device. The most common and most accurate method is with an intraventricular monitor. As such, intraventricular measurement of ICP is the current gold standard.[2] An intraventricular catheter is inserted into a hole drilled into the skull and then into the lateral ventricle to measure the pressure of the CSF directly. The advantage of an intraventricular catheter is that CSF can be removed, if needed, to decrease ICP in the acute setting. Disadvantages include the risk of bleeding, infection, and difficulty with proper placement if the ICP is very high. Other options include intra-parenchymal and sub-dural monitors.

ICP can be measured non-invasively by several methods, including, most commonly, transcranial Doppler ultrasonography (TCD). TCD utilizes a temporal window to measure the velocity of blood flow through the middle cerebral artery. Systolic and diastolic flow velocity and mean flow velocity are used to calculate a pulsatility index. The pulsatility index has been reported to correlate strongly with ICP in some studies and poorly correlate with ICP in others. Therefore, using TCD alone as a substitute for direct ICP measurement is not recommended.[3][4]

Ideally, invasive monitoring of the MAP through an arterial cannula and invasive monitoring of the ICP through an intraventricular catheter will give a continuous and accurate calculation of CPP.

Clinical Significance

Two general categories of pathologic derangement exist wherein management of CPP is vital: intracranial pathology, where ICP management is most important, and hemodynamic instability/shock, where MAP management is most important.

Intracranial pathology includes space-occupying lesions such as tumors, epidural and subdural hematoma or acute intraparenchymal hemorrhage, and cerebral edema as seen after ischemic injury, traumatic brain injury, or severe hepatic encephalopathy. In these cases, adequate CPP is dependent on lowering the ICP back to a reasonably normal range as quickly as possible while maintaining an adequate MAP. While CPP has a range of normal, it is important to remember that each patient’s brain tissue has a CPP that is “normal” in the context of that individual patient’s physiology, which may be influenced by other medical problems such as hypertension or vascular disease. There is a push towards more dynamic management of CPP using the patient’s auto-regulatory capacity.[5]  These methods involve more frequent and sophisticated monitoring and may not be available for widespread use.

For example, in the setting of substantial traumatic brain injury, significant cerebral edema can decrease intracranial compliance and overcome initial CSF shunting measures, producing an elevated ICP (intracranial hypertension). Auto-regulatory mechanisms may or may not function normally, and if ICP remains elevated, CPP will decrease, causing further injury through an ischemic mechanism. In this case, in addition to initiating ICP lowering measures, it is important to avoid hypotension (MAP – ICP = CPP), and in some cases, allowing hypertension is reasonable.

In cases of hemodynamic instability, the ICP is relatively stable as cerebral autoregulation is intact. In the setting of hypotension, the MAP decreases due to blood loss (hemorrhagic shock), intravascular leak (distributive shock), or decreased cardiac output (cardiogenic shock), and the CPP decreases as well. The relationship between MAP and CPP drives resuscitation guidelines to recommend maintaining a MAP greater than or equal to 65 mm Hg. Assuming a normal ICP, this threshold should guarantee a CPP of 55 to 60, the minimum needed to prevent cerebral ischemic injury. As in the case of ICP and cerebral auto-regulation, MAP goals should be within the context of an individual patient’s baseline hemodynamic function. Patients with untreated hypertension should have higher MAP goals to maintain appropriate CBF and CPP.

Nursing, Allied Health, and Interprofessional Team Interventions

Clinicians and other medical/ancillary staff who deal with patients suffering from conditions where CPP is an important vital sign bear a responsibility to understand the ramifications of this value and be able to articulate issues to the members of the interprofessional healthcare team. This will encourage accurate diagnosis, prompt intervention, and improved monitoring of patients, resulting in the best possible outcomes. [Level 5]