cesenahotel.info : Neurotrauma : Cerebral Perfusion Pressure
Cerebral Perfusion Pressure (CPP) is defined as the difference between the Mean Arterial Pressure (MAP) and the Intracranial Pressure (ICP). CPP = MAP - ICP. The cranium can absorb an additional cc fluid before ICP begins to rise whose perfusion pressure is dependent on the difference between MAP and CVP, the There is thus considerable debate as to whether ICP or CPP is a more. Use in patients with an intracranial pressure monitoring device. backing down on interventions raising the patient's MAP (e.g. pressors). ICP in one particular area of the brain), leading to gradients in CPP across different areas of the brain. the study investigators found that, among those TBI patients who survived
Because CBF is adjusted to meet the metabolic demand, oxygen by the grey matter is approximately five times more than by the white matter. Under aerobic conditions, oxidative phosphorylation produces 38 molecules of ATP for every molecule of glucose. Sixty per cent of the energy produced is utilized for the functioning of the neurons i. The lactate produced anaerobically is utilized to carry out the fundamental processes essential to maintain the cell structure.
Aerobic metabolism is restored if perfusion is re-established immediately, otherwise permanent cell death follows. The Monro—Kellie hypothesis states that the volume of the brain and its constituents inside the bony cranium is fixed and cannot be compressed.
To preserve a constant pressure in the box, the volume of the contents inside must be maintained. In adults, ICP is normally 5—15 mm Hg when supine and is posture-dependent, being lowest in the upright position. Increase in ICP above a critical level is not tolerated because it results in a decrease in the CPP of the brain and can also cause local compression of brain tissue against the tentorium, falx, and foramen magnum and ultimately herniation.Cerebral Perfusion
There are many ways that ICP is controlled. Volume buffering pressure—volume relationship Blood and CSF provide the main protection to the brain when the intracranial volume increases.
There is an initial compensation which prevents major changes in the intracranial compliance with minimal increases in ICP. In the presence of intracranial pathology, the volume of one component within the cranium increases e. C and D Decompensation phase—ICP increases rapidly with increasing intracranial volume as the buffers are exhausted.
Blood, despite being the smallest volume compartment within the cranium, has the most significant role in compensation for ICP changes as the cerebral venous volume can be changed very promptly and hence ICP can be modified almost immediately. Cerebral blood volume CBV can be increased by increasing the amount of blood flow that enters the cranium e. CSF is the fluid present extracellularly between the arachnoid and pia mater and in the ventricles, providing buoyancy to the brain.
It is produced mainly by the choroid plexus at a rate of 0. The production of CSF is constant, but if re-absorption is hampered or there is a mechanical obstruction to the CSF outflow, its volume increases causing an increase in ICP.
Spatial compensation occurs slowly and is significant in tumours which expand gradually but provides limited compensation for acute and sudden increase in ICP e. Reproduced with permission from Shardlow and Jackson. In the upright position in a normal brain, ICP and CVP at the level of the head are negative and therefore not accounted for. Autoregulation is believed to occur via a myogenic mechanism whereby an increase in MAP increases the transmural vessel tension causing depolarization of vascular smooth muscle and constriction of the precapillary resistance vessels.
The reverse happens when the MAP and transmural tension decreases. In chronic arterial hypertension, the upper and lower limits of autoregulation are both displaced to higher levels, shifting the curve to the right.
In hypertensive patients, cerebral hypoperfusion occurs at higher values of MAP compared with healthy individuals.
Cerebral perfusion pressure
Arterial carbon dioxide tension The relationship between and CBF is typically a sigmoid curve with lower and upper plateaus. It is fairly linear between 2. The upper plateau occurs at a of At this point, CBF is nearly doubled and cannot increase further. On the other hand, decreasing causes vasoconstriction with its maximum effect occurring at levels of 2.
Clinically, it is not recommended to decrease to such low levels and normocapnia should be maintained after brain injury. The blood—brain barrier BBB is permeable to carbon dioxide which readily diffuses across it and thereby decreases extracellular pH.
Cerebral perfusion pressure | BJA: British Journal of Anaesthesia | Oxford Academic
This affects the vascular smooth muscles directly causing dilatation. Decreasing the from 5. Prolonged hypocapnia has failed to show a beneficial role as CBF returns to the baseline after 6—8 h because of adaptation in the brain. The response of CBF to altering levels of is not very significant in clinical practise provided is maintained above 6.
Below this level, oxygen-sensitive ion channels in the vascular smooth muscles are activated and vasoactive substances, such as nitric oxide, adenosine, prostacyclin, angiotensin, vasopressin, and opioids, released. Imbalance in these mediators is responsible for the vasodilatation and increases in CBF during hypoxaemia.
Increasing oxygen will have the reverse effect and causes vasoconstriction which is not clinically significant. Flow-metabolic coupling CBF is very variable across the brain and largely dependent on neuronal activity. Increase in activity, either regional or general, causes an increase in the CMR which in turn results in proportional increases in blood flow.
The change occurs within seconds of increased functional cerebral activity. Those areas of the brain that are ischaemic, or at risk of ischaemia are critically dependent on and adequate cerebral blood flow, and therefore cerebral perfusion pressure. CPP should be maintained above mmHg Systemic hypotension is associated with poor prognosis Maintenance of an adequate Cerebral Perfusion Pressure is a cornerstone of modern brain injury therapy.
After brain injury, and especially in the multiply injured patient, cerebral blood flow may be lowered to the ischaemic threshold. To prevent further neuronal death the secondary brain injurythis flow of well oxygenated blood must be restored. There is no class I evidence for the optimum level of CPP, but mmHg is probably the critical threshold. Control of intracranial hypertension is discussed on the pages on intracranial pressure.
Even patients with one episode of hypotension during their ICU stay have a significantly reduced prognosis. Maintenance of an adequate MAP requires primarily a normovolaemic patient. Control of other sites of haemorrhage has the highest priority with oxygenation.
These patients should NOT be kept 'dry' with fluid restriction, but maintained in zero balance. Further elevation of MAP, once normovolaemia is achieved, is usually accomplished with norepinephrine, though dopamine may be used.