Definition/Introduction
Cerebral perfusion pressure (CPP) is the net pressure gradient that drives oxygen delivery to cerebral tissue. It is the difference between the mean arterial pressure (MAP) and the intracranial pressure (ICP), measured in millimeters of mercury (mm Hg). Maintaining appropriate CPP is critical in managing patients with intracranial pathology, including traumatic brain injury, and with hemodynamic distress, such as shock. Normal CPP lies between 60 and 80 mm Hg, but these values can shift to the left or right depending on individual patient physiology. Because CPP is a calculated measure, MAP and ICP must be measured simultaneously, most commonly invasively. Maintaining adequate CPP in clinical situations of intracranial pathology with deranged ICP or hemodynamically unstable conditions decreases the risk of ischemic brain injury.
- CPP = MAP - ICP
Physiology
CPP and ICP: The CPP, at its most basic, is dependent on the ICP and mean arterial pressure, and its normal range is 60 to 80 mm Hg. Under normal conditions, the ICP is between 5 and 10 mm Hg and thus has less impact on CPP than on MAP in clinical situations not involving intracranial pathology. ICP is usually directly measured via intracranial pressure transduction. Physiologically, ICP is a function of intracranial compliance. Intracranial compliance is the relationship between ICP and the volume of the intracranial cavity, including cerebrospinal fluid (CSF), brain tissue, and arterial and venous blood. Because the skull is a fixed, rigid anatomic space, ICP increases as intracranial volume increases and intracranial compliance decreases. As the ICP increases (or intracranial compliance decreases), the CPP decreases.
Several mechanisms help keep ICP within the normal range for as long as possible during periods of changing intracranial volume and compliance. As volume adds to the intracranial space, CSF can move into the spinal subarachnoid space, leaving the ICP relatively unchanged. As volume increases (a growing space-occupying lesion, brain tissue edema, or blood), this mechanism becomes overwhelmed, and ICP increases sharply.
Cerebral blood flow (CBF) is also a critical factor in ICP homeostasis. Cerebral autoregulation ensures a steady blood flow to the brain across a wide range of physiologic changes and disturbances. When blood pressure decreases, autoregulation causes cerebral vasodilation, increasing CBF and cerebral blood volume, thereby maintaining ICP and CPP. When blood pressure increases, autoregulation causes cerebral vasoconstriction and a decrease in CBF, thereby reducing cerebral blood volume and maintaining ICP and CPP. Too much alteration outside of normal CBF ranges can lead to brain ischemia and injury.[1]
CPP and MAP: Because ICP within normal ranges is relatively small, the CPP is much more dependent on mean arterial pressure. MAP is the average blood pressure over 1 cardiac cycle and can be measured directly via invasive hemodynamic monitoring or calculated as the systolic blood pressure plus 2 times the diastolic blood pressure divided by 3. The normal MAP range is 70 to 100 mm Hg.
The mean arterial pressure is much more likely to change during day-to-day activities such as exercise, rest, and stress. However, if ICP remains constant, the mean arterial pressure can vary across its relatively wide normal range without dramatically increasing or decreasing CPP. CPP and CBF remain relatively unchanged across a wider range of MAP (50 to 150 mm Hg) than normal due to cerebral auto-regulation and vasoconstriction or vasodilation of cerebral vasculature.
For patients with hypertension, the autoregulatory setpoint shifts; therefore, a lower mean arterial pressure relative to the patient’s normal mean arterial pressure causes vasodilation, increasing CBF. Patients with mean arterial pressure above normal at baseline have autoregulatory vasoconstriction in response to an increase in their relative normal MAP, returning CBF to baseline. Thinking about CBF and CPP in the context of the patient’s normal MAP is clinically relevant regarding the management of intracranial pathology and hemodynamic derangements.
Issues of Concern
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Issues of Concern
Monitoring cerebral perfusion pressure requires measuring both the MAP and the ICP. The MAP can be measured directly using invasive hemodynamic techniques, most often by cannulating a peripheral artery, such as the radial or femoral artery. The MAP can also be measured indirectly using a noninvasive blood pressure cuff and the previously mentioned formula, based on the systolic and diastolic blood pressures.
Intracranial pressure is usually measured invasively using an intracranial pressure transducer. The most common and most accurate method is with an intraventricular monitor. As such, intraventricular ICP measurement is the current gold standard.[2] An intraventricular catheter is inserted through a hole drilled in the skull and into the lateral ventricle to measure CSF pressure 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 subdural monitors.
ICP can be measured noninvasively by several methods, most commonly transcranial Doppler ultrasonography (TCD). TCD uses a temporal window to measure blood flow velocity in 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 of the ICP through an intraventricular catheter provides continuous, accurate CPP measurements.
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 is within the normal range, it is important to remember that each patient’s brain tissue has a CPP that is “normal” in the context of that individual’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 widely available.
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 decreases, causing further injury via ischemic mechanisms. 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 of at least 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 with ICP and cerebral autoregulation, MAP goals should be set 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 care for patients with conditions in which CPP is an important vital sign bear responsibility to understand the implications of this value and to articulate these issues to members of the interprofessional healthcare team. This encourages accurate diagnosis, prompt intervention, and improved patient monitoring, resulting in the best possible outcomes.
References
Armstead WM. Cerebral Blood Flow Autoregulation and Dysautoregulation. Anesthesiology clinics. 2016 Sep:34(3):465-77. doi: 10.1016/j.anclin.2016.04.002. Epub [PubMed PMID: 27521192]
Zhang X, Medow JE, Iskandar BJ, Wang F, Shokoueinejad M, Koueik J, Webster JG. Invasive and noninvasive means of measuring intracranial pressure: a review. Physiological measurement. 2017 Jul 24:38(8):R143-R182. doi: 10.1088/1361-6579/aa7256. Epub 2017 Jul 24 [PubMed PMID: 28489610]
Needham E, McFadyen C, Newcombe V, Synnot AJ, Czosnyka M, Menon D. Cerebral Perfusion Pressure Targets Individualized to Pressure-Reactivity Index in Moderate to Severe Traumatic Brain Injury: A Systematic Review. Journal of neurotrauma. 2017 Mar 1:34(5):963-970. doi: 10.1089/neu.2016.4450. Epub 2016 Jun 27 [PubMed PMID: 27246184]
Level 1 (high-level) evidenceKawoos U, McCarron RM, Auker CR, Chavko M. Advances in Intracranial Pressure Monitoring and Its Significance in Managing Traumatic Brain Injury. International journal of molecular sciences. 2015 Dec 4:16(12):28979-97. doi: 10.3390/ijms161226146. Epub 2015 Dec 4 [PubMed PMID: 26690122]
Level 3 (low-level) evidenceDepreitere B, Güiza F, Van den Berghe G, Schuhmann MU, Maier G, Piper I, Meyfroidt G. Pressure autoregulation monitoring and cerebral perfusion pressure target recommendation in patients with severe traumatic brain injury based on minute-by-minute monitoring data. Journal of neurosurgery. 2014 Jun:120(6):1451-7. doi: 10.3171/2014.3.JNS131500. Epub 2014 Apr 18 [PubMed PMID: 24745709]
Level 2 (mid-level) evidence