clinical aspects of cerebral perfusion and ICP Flashcards
what % of cardiac output is cerebral outflow
15%
what is the normal cerebral blood flow average
55-60mL/100brain tissue per minute
when does ischaemia occur
when cerebral blood flow at 20ml/100g/minute
when does permanent damage occur
when cerebral blood flow drops below 10ml/100g/minute
what is the most important factor that determines cerebral blood flow at any given time
cerebral perfusion pressure (CPP)
= the effective blood pressure gradient across the brain
what does an increased ICP do to the CPP
causes it to decrease
what are the three factors that regulate cerebral blood flow under physiological conditions
CPP
concentration of arterial CO2
arterial PO2
what is cerebral auto regulation
the ability to maintain constant blood flow to the brain over a wide range of CPP
how does cerebral auto regulation occur
CPP low - cerebral arterioles dilate to allow flow at decreased pressure
CPP high - cerebral arterioles constrict to allow flow at increased pressure
when can the autoregulatory system fail
if CPP exceeds 150mm/Hg
- eg hypertensive crisis
vasogenic oedema from exudation fluid from the vascular system
toxins (eg CO2) diffuse cerebrovascular dilation and inhibits autoregualtion
during first 4-5 days of head trauma
what is cerebral oedema
state of increased brain volume as a result of an increase in water content
what can cerebral oedema cause
subacute to chronic intracranial hypertension
what is the blood brain barrier
barrier composed of astrocytic foot processes wrapping around a capillary endothelium composed of tight junctions
what is the specific role of the endothelial tight junctions in the brain
stop passive movement of substances to the neural tissues to protect i from toxic materials
what materials can be naturally transported across the BBB and how
lipid-soluble substances
- penetrate all capillary endothelial cell membranes in a passive manner
amino acids and sugars
- transported across the capillary endothelium by specific carrier-mediated mechanisms
what is the total volume of the brain/blood/CSF and what re their respective volumes
total = 1700mL
brain - 1400mL
blood - 150mL
CSF - 150mL
what is the moro-kelly doctrine
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
ie 100ml mass - 100ml decrease in blood/CSF in skull
what is compliance
change in volume observed for a given change in pressure
dV/dP = change in volume/change in pressure
what is elastance
inverse of compliance
change in pressure observed fro a given change in volume
dP/dV
= change in pressure/change in volume
**represents the accommodation to outward expansion of an intracranial mass
how can blood be displaced from the brain
venous system collapses easily and squeezes venous blood out through the jugular veins or through the emissary and scalp veins
how can CSF be displaced from the brain
displaced from the ventricular system through the foramina of Luschka and Magendie into the spinal subarachnoid space
when can small changes in volume produce significant changes in pressure
when a critical volume is reached - any small increase in volume over this level will cause drastic increases in pressure
how can ICP be measured
manometry
connected to electric monitor to see ICP waveforms
what are the waves seen ICP manometry
Lundberg waves:
A waves
B waves
C waves
when are A waves seen
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
when are B waves seen
related to rhythmic variations in breathing
Frequency of 0.5 to 2 waves per minute
what are C waves
Rhythmic variations related to waves of systemic blood pressure and have smaller amplitude
what is Cushing’s reflex and what does it involve
a vasopressor response
triad:
hypertension
irregular breathing
bradycardia
what is the physiology that causes the triad in Cushing’s response
Increased ICP more than MAP causes compression of cerebral arterioles
Decreased CBF activates autonomic nervous system
Sympathetic response:
alpha-1 adrenergic receptors -> Hypertension and tachycardia
Aortic baro-receptors stimulate vagus nerve -> Bradycardia
Bradycardia also due to mechanical distortion of medulla
how is raised ICP managed
Head end elevation: facilitate venous return
Mannitol/ Hypertonic saline
Hyperventilation: decrease CBF (temporary measure)
Barbiturate coma: decrease cerebral metabolism, CBF
Surgical decompression
