Cerebral Perfusion and Intracranial Pressure Flashcards
What is the normal perfusion of cerebral blood flow?
55 to 60 mL/100g brain tissue per minute
What is the perfusion of cerebral blood flow in ischaemia?
20 mL/100 g/minute
At what perfusion does permanent damage occur?
When it drops below 10mL/100 g/minute
What is the cerebral perfusion pressure (CPP)?
It is the blood pressure gradient across the brain which determines cerebral blood flow
How do you work out the CPP?
CPP = MAP - ICP
This represents the pressure gradient driving cerebral blood flow (CBF) and hence oxygen and metabolite delivery.
How do you work out MAP?
MAP = DP + 1/3PP
MAP = 2/3DP + 1/3SP
DP - diastolic pressure
PP - pulse pressure
SP - systolic pressure
What is the effect of increased ICP on the CPP?
Increase ICP = decrease in CPP
Name three factors which regulate cerebral blood flow
- CPP
- Concentration of arterial CO2
- Arterial PO2
What is cerebral autoregulation?
The ability to maintain constant blood flow to the brain over a wide range of CPP (50-150 mm Hg)
What is the cerebral autoregulation when the CPP is low?
The cerebral arterioles dilate to allow adequate flow at the decreased pressure
What is the cerebral autoregulation when the CPP is high?
The cerebral arterioles constrict
In what pathological conditions can the cerebral blood flow not be autoregulated?
CPP exceeds 150 mm Hg, such as in hypertensive crisis, the autoregulatory system fails
- Exudation of fluid from the vascular system with resultant vasgoenic oedema
- Toxins like CO2 can cause diffuse cerebrovascular dilatation and inhibit proper autoregulation
- During the first 4-5 days of head trauma, many patients can experience disruption
What is cerebral oedema and what can it cause?
Increased brain volume as a result of an increase in water content
Prominent cause of subacute to chronic intracranial hypertension
What are the two different types of cerebral oedema?
Vasogenic oedema (extracellular) and cytotoxic oedema (intracellular)
Describe vasogenic oedema
- Increased capillary permeability
- Mainly white matter
- Extracellular fluid increased
- Plasma filtrate containing plasma protein
Describe cytotoxic oedema
- Cellular swelling (neuronal, glial and endothelial cells)
- Grey and white matter
- Increased intracellular after and sodium due to failure of membrane transport
- Extracellular fluid decreases
What is the blood brain barrier?
Endothelial tight junctions are the barrier to the passive movement of many substances in order to protect the sensitive neural tissue from toxic materials
It is composed of astrocytic foot processes wrapping around a capillary endothelium which contains tight junctions
How are materials transported across the endothelial cells?
- Lipid-soluble substances can penetrate all capillary endothelial cell membranes in a passive manner
- Amino acids and sugars are transported across the capillary endothelium by specific carrier-mediated mechanisms
What is the Monro-Kelly Doctrine?
It is the homeostatic intracerebral volume regulation, which stipulates that the total volume of the brain tissue, cerebrospinal fluid, and blood remains constant
When a new intracranial mass is introduced, a compensatory change in volume must occur through a reciprocal decrease in venous blood or CSF to keep the total intracranial volume constant
Describe the mechanisms for maintaining constant intracranial volume
Compliance vs elastance
Describe the elastance mechanism in maintaining constants intracranial volume
- Inverse of compliance
- Change in pressure for a given change in volume
- dP / dV
- Represents the accommodation to outward expansion of an intracranial mass
Describe compliance mechanism in maintaining constant intracranial volume
Change in volume observed for a given change in pressure
Describe how the venous system drains blood from the brain
It collapses easily and squeezes blood out through the jugular veins or through the emissary and scalp veins
Describe CSF exits the ventricles
Displaced from the ventricular system through the foramina of Luschka and Magendie into the spinal subarachnoid space
What happens when the compensatory venous and CSF pathways are exhausted?
Small changes in volume produce significant increase in pressure.
Homeostatic pressure-buffering mechanism offered by displacement of CSF and venous blood keeps compliance flat until ‘critical volume’ is reached
After this critical volume, small volumetric changes result in increases in pressure, and intracranial hypertension occurs.
Describe the relationship of change in volume and pressure with regards to compliance on the graph
During high compliance, an increase in volume causes a small increase in pressure.
With low compliance, there is a greater change in pressure for the same increase in volume.
After the critical volume, where there is no compliance, a small increase in volume will cause a massive increase in pressure
Name mechanism that decreases intracranial pressure
External ventricular drain (EVD) - drains CSF to reduce pressure
Describe the ICP waveforms from the pressure transducer of the EVD
P1 percussion wave - the arterial pulse transmitted through the choroid plexus into the CSF
P2 tidal wave - represents cerebral compliance, it can be thought of as a “reflection” of the arterial pulse wave bouncing off the springy brain parenchyma.
P3 dicrotic wave - closure of the aortic valve, which makes the trough prior to P3 the equivalent of the dicrotic notch
What are the different stages in lundberg waves?
- A waves
- B waves
- C waves
What are the A waves in the lundberg waves?
Abrupt elevation in ICP for 5 to 20 minutes followed by a rapid fall in the pressure to resting levels
The amplitude may reach as high as 50 to 100 mm Hg
What are the B waves in the lundberg waves?
Frequency of 0.5 to 2 waves per minute, are related to rhythmic variations in breathing
What are the C waves in the lundberg waves?
Rhythmic variations related to waves of systemic blood pressure and have smaller amplitude
What is Cushing’s reflex?
Physiological response to increased intracranial pressure (ICP) that results in Cushing’s triad:
- Hypertension
- Irregular breathing
- Bradycardia
How does the increased ICP cause the Cushing’s triad?
- Compression of cerebral arterioles
- Decreased CBF, activation of ANS
- Sympathetic response: A1 adrenergic receptors –> hypertension and tachycardia
- Aortic baroreceptors stimulate vagus nerve –> bradycardia
- Bradycardia also due to mechanical distortion of medulla
What are five ways to manage increased ICP
- Head end elevation: facilitate venous return
- Mannitol/ Hypertonic saline
- Hyperventilation: decrease CBF (temporary measure), reduce PCO2
- Barbiturate coma: decrease cerebral metabolism, CBF
- Surgical decompression
