Neuro Physiology - Cerebral Blood Flow and ICP Flashcards
What is the Monroe-Kellie doctrine?
IMAGE
The skull is a fixed container with three types of content:
Brain 85%, Blood 5%, CSF 10%.
If one of these increases in volume, another must reduce otherwise ICP will rise.
Initially venous blood from the sinuses is pushed out of the skull.
Secondly, CSF via the foramen magnum
Thirdly, *arterial blood volume reduces *(but after a point this will not make much difference)
At this point, small increases in volume dramatically increase ICP, compressing brain parenchyma and causing ischaemia. Above 20mmHg there is focal ischaemia, and above 45-50mmHg there is global ischaemia.
Normal ICP is 8-12mmHg supine, directly related to ITP, with a respiratory swing. PEEP, coughing and straining all increase ICP.
What are the causes of increased ICP?
Increased CSF (Hydrocephalus)
Blockage, overproduction or
under-absorption
Mass effect of brain
Oedema, contusion, abscess, tumour
Increased intracranial blood volume
Venous obstruction (Venous sinus thrombosis)
Haemorrhage (IC/SA/SD/ED)
Benign intracranial HTN - unclear cause, associated with obesity
Draw and explain the intracranial pressure waveform
**Time (s) along X axis, mmHg along Y axis
Curve broadly similar to that of iABP, and is measured through an intracranial pressure transducer (Eg. Ventricular drain/SA bolt)
Three waves of gradually reducing amplitude
In normal physiology, the pulse wave has 3 components:
P1 - Percussive transmitted arterial pressure
P2 - Tidal Arterial wave reflecting off brain tissue, varying with compliance. Approx 80% amplitude of P1, and ends at point of dichrotic notch
P3 - Dicrotic wave Venous pressure wave, increases as CVP increases.
Respiration causes a variation in baseline pressure.
There are other slow (Lundberg) waves, usually pathological:
Type A - Plateau waves Rapid increase in baseline pressure to more than 50mmHg for 2-20 minutes, severely reduced compliance - always pathological
Type B 0.5-2 waves/minute, increases in pressure of around 20-30mmHg before returning to baseline, variable ICP usually present too. Can be due to vasospasm
Type C 4-8 waves/minute, up to 20mmHg, may be normal
How does CO2 affect intracranial pressure?
Hypercapnia causes vasodilation and increased cerebral blood flow.
Near-linear increase in blood flow until around 11kPa, with maximal vasodilation. At very low PaCO₂, the vasoconstriction is limited by the opposing vasodilation driven by the resultant ischaemia and hypoxia.
What is the effect of hyperventilation on patients with high ICP?
Hypocapnia causes vasoconstriction and reduces ICP.
However, the brain recalibrates its set point, with a return to previous pressure after about 4 hours.
When hyperventilation stops and CO₂ returns to baseline, the resulting vasodilation will be worse.
This should only be done in extremis as a temporising measure.
What is normal cerebral blood flow and what factors affect it?
IMAGE - Hagen-Poiseuille rearranged for flow
Volume of blood delivered to the brain per unit time, with normal flow of 0.5ml/g/minute, within the normal CPP range.
The factors affecting cerebral blood flow (Q) relate to the Hagen-Poiseuille equation.
Q = (π*Δ P*r⁴) / (8*n*L)
Δ P is the cerebral perfusion pressure (MAP - (ICP + CVP)), but can also be calculated via Ohm’s law (Cerebral blood flow x Cerebral vascular resistance)
r⁴ is blood vessel diameter, due vasoconstriction and dilation, with multiple factors including PaO₂ and PaCO₂
n is fluid viscosity
L is the blood vessel length, which is not easily changed
What are the effects of changing PaCO₂ on cerebral blood flow?
IMAGE - PaCO2 graph
Between 2kPa and 10kPa, blood flow increases linearly as a result of vasodilatation.
The graph plateaus at either end as a result of maximal vasodilation and constriction
Chronic hyperpanoea shifts the graph rightwards due to the compensatory buffering
Bicarbonate is actively pumped into the CSF to buffer the increased H+ ion concentration caused by chronic hypercapnoea.
What are the effects of changing PaO₂ on cerebral blood flow?
IMAGE - PaO2 graph
Above a PaO₂ of 8kPa, cerebral blood flow is unchanged.
Below this, vasodilation causes a rapid increase in cerebral blood flow.
This reponse overpowers any vasoconstriciton caused by other mechanisms.
Describe cerebral autoregulation
IMAGE (Graph)
The process by which an organ regulates its own blood flow, independent of perfusion pressure (within limits)
Between 50-150mmHg MAP, cerebral blood flow remains at 50ml/100g/min
Graph shifts to the right in chronic hypertension, hence why chronic hypertensives benefit from a higher target MAP
What is flow-metabolism coupling?
GRAPH
CMRO₂ = Cerebral metabolic rate of oxygen utilisation (Usually 3ml/100g/minute)
Perfusion is matched to the CMRO₂ of a given region of the brain, or the brain as a whole
There is a linear relationship between CBF (Cerebral blood flow) and CMRO₂
Ischaemia occurs below a CBF of 20ml/100g/minute.
What effect does temperature have on CMRO₂?
GRAPH
CMRO₂ decreases with decreasing temperatures, and is the rationale behind targeted temperature management post OOHCA.
The graph has two linear segments, changing gradient at 27°C.
If 100% CMRO₂ is at 37°C
7% reduction per 1°C
At 27°C it is 30% of baseline
At 17°C it will be 10% of baseline
What effect do anaesthetic agents have on CMRO₂?
GRAPH
Inhalational agents:
Dose-dependent vasodilation (other than sevoflurane)
At 1.5 MAC cerebral autoregulation is disrupted
Nitrous causes vasodilation, but also increases CMRO₂.
Intravenous agents:
Propofol/Thio reduce CMRO₂ and CBF
Ketamine increases CMRO₂ and CBF, but flow to a greater extent.
Textbooks often advise avoiding ketamine in raised ICP, but its cardiovascular stability offsets this effect.
What are the clinical features of raised ICP?
Headache (worse in the morning, and on straining/bending over), nausea, vomiting, papilloedema, reduced GCS
Bulging fontanelle in infants
Coning Cerebral herniation of brainstem through foramen magnum, stretching the cranial nerves
Preterminal sign of cushing reflex (hypertension/bradycardia), followed by hypotension, apnoea and fixed dilated pupils.
How can ICP be monitored?
Continuous measurement, in conjunction with MAP allows calculation of CPP
Extradural fibreoptic probe (Via burr hole)
Easy to position, low infection rate
CSF cannot be drained, liable to drift
Subarachnoid bolt via burr hole
More accurate
High infection rate, easy to position
**External ventricular drain
**Allows transduction of pressure & release of fluid
Infection rate 3-5%, much higher than other methods
How can raised ICP be managed pharmacologically?
Noradrenaline to maintain CPP
IV induction agents (propofol, thiopentone, etomidate) - dose dependent decrease in CBF, ICP, and CMRO₂.
Benzodiazepines/Barbiturates Reduce CBF and CMRO₂, but not ICP (Eg. Thiopentone coma in seizures)
Opiates decrease CMRO₂ in large doses
NMBA to prevent coughing and straining
Suxamethonium - transient rise in ICP (attenuated by induction agents)
Volatiles increase ICP due to cerebral vasodilatation, but reduce CMRO₂. Can be used at MAC < 1
N₂O and Ketamine vasodilate and increase CMRO₂, increasing ICP
Mannitol osmotic diuretic, filtered and not reabsorbed, draws water from brain across BBB. Free radical scavenger and reduces CSF production.
0.5-1ml/kg of 20% solution
Hypertonic Saline draws fluid from the interstitium into the blood to be drained away
2-3ml/kg of 5% NaCl
Phenytoin membrane stabiliser that prevents Na and Ca influx during depolarisation, narrow therapeutic window requiring monitoring of levels, and an enzyme inducer.
Side effects:
Idiosyncratic - Gum hyperplasia, hirsutisim, acne, blood dyscrasias
Dose dependent - Hypotension, N&V, confusion, headache, drowsiness
CPP - Cerebral perfusion pressure
CBF - Cerebral blood flow
ICP - Intracranial pressure
CMRO₂ - Cerebral metabolic rate of Oxygen utilisation
NMBA - Neuromuscular blocking agents
