What is the Monroe-Kellie doctrine?
The skull is a fixed container with three types of content
- Brain 85%
- Blood 5%
- CSF 10%
If any one of these increases in volume, to avoid a rise in intracranial pressure, one or both of the others must decrease in volume to compensate. In the case of bleeding, initially venous blood is pushed out of the skull, reducing the volume of venous blood in the sinuses. Secondly, CSF is extruded via the foramen magnum. Thirdly the volume of arterial blood starts to reduce.
However after a certain point this will no longer suffice and only small increases in volume will dramatically increase intracranial pressure, causing compression of the brain parenchyma and ischaemia.
Normal ICP is 8 – 12 mmHg supine, and it is directly related to intrathoracic pressure, meaning it has a respiratory swing. PEEP, coughing and straining all cause intracranial pressure to increase.
Above 20mmHg there starts to be focal ischaemia, and above 45-50mmHg there is global ischaemia.
What are the causes of raised intracranial pressure?
Increased CSF in the brain:
- Blockage or over production or under absorption
Mass effect of brain itself:
Increased intracranial blood volume:
- Venous obstruction
- Venous Sinus Thrombosis
Benign intracranial hypertension:
- Unclear cause
- Associated with obesity
Can you draw and explain the intracranial pressure waveform?
This essentially looks a lot like the invasive arterial pressure waveform, measured through an intracranial pressure transducer such as a ventricular drain or subarachnoid bolt.
It has three waves, with gradually reducing amplitude.
- Transmitted arterial pressure
- Due to arterial wave reflecting off brain tissue, so varies with brain compliance
- Approximately 80% amplitude of P1
- Ends at point of dicrotic notch
- Dicrotic wave
- Venous pressure wave, increases as CVP increases
This is a larger variation in baseline pressure with the respiratory cycle.
Also known as Lundberg waves, these are usually pathological.
Type A – Plateau waves
- Rapid increase of baseline pressure to more than 50mmHg for between 2 and 20 minutes
- Demonstrate severely reduce compliance
- Always pathological
- 0.5 to 2 waves per minute
- Increases in pressure of around 20-30mmHg before returning to baseline
- Variable ICP usually present as well
- Sometimes due to vasospasm
- 4 to 8 waves per minute
- Up to 20mmHg
- May be normal
How does carbon dioxide affect intracranial pressure?
Hypercapnia causes vasodilatation and therefore increased cerebral blood flow. Across the normal range of PaCO2, this results in a near-linear increase in cerebral blood flow.
However above 11kPa, maximal vasodilatation is reached, and so there is minimal further increase in cerebral blood flow, and the graph levels out. At low PaCO2 this also occurs, as the vasoconstriction caused by hypocapnia is opposed by vasodilation induced by the resulting ischaemia and hypoxia.
Low CO2 tries to vasoconstrict, causing hypoxia which tries to vasodilate
Should we hyperventilate patients with high intracranial pressure?
Hypocapnia causes vasoconstriction and reduces ICP but only temporarily. If this process is prolonged the brain will recalibrate its set point and the pressure will return to its previous level within about four hours.
Then when the hyperventilation stops, and the CO2 rises, the resulting vasodilatation would be even worse than before. Therefore this should only be done in extremis as a temporising measure.
What is normal cerebral blood flow, and what factors affect it?
This is the volume of blood delivered to the brain per unit time, and normal flow is 50ml/100g/minute.
Factors influencing cerebral blood flow relate to the Hagen Poiseuille equation:
- Cerebral Perfusion Pressure = MAP – (ICP + CVP)
- Also CPP = Cerebral blood flow x Cerebral vascular resistance
- This is essentially Ohm’s law
Blood vessel diameter
- This is due to vasoconstriction and dilation, with multiple influencing factors:
Cerebral blood flow increases linearly with PaCO2 as a result of vasodilatation, between 2kPa and 10kPa. The graph plateaus at either end as a result of maximal vasodilatation and vasoconstriction.
In chronic hypercapnoea the graph is shifted to the right as a result of compensatory buffering. Bicarbonate is actively pumped into the CSF to buffer the increased hydrogen ion concentration caused by chronic hypercapnoea.
Cerebral blood flow is stable above a PaO2 of 8kPa. Below this, vasodilatation causes a rapid increase in cerebral blood flow. This response is very strong and will overpower any vasoconstriction caused by other mechanisms.
Autoregulation is the process by which an organ regulates its own blood flow, independent of perfusion pressure (within limits). Both the brain and kidney demonstrate autoregulation.
Between 50 and 150mmHg of mean arterial pressure, the cerebral blood flow remains at 50ml/100g/min.
This graph shifts to the right in chronic hypertension, emphasising the importance of maintaining sufficient MAP in known hypertensive patients.
What effect does temperature have on CMRO2?
As temperature decreases CMRO2 decreases, which is part of the rationale behind targeted temperature management in out of hospital arrest patients. The graph has two linear segments, changing gradient at 27°C.
- 7% reduction for every 1°C temperature drop
- At 27°C it will be 30% of baseline metabolic rate
- At 17°C it will be 10% of baseline
What effect do anaesthetic agents have on CMRO2?
The dashed line is the graph depicting flow-metabolism coupling.
Inhalational agents induce a dose-dependent vasodilatation apart from sevoflurane. At 1.5 MAC cerebral autoregulation is disrupted. Nitrous causes vasodilatation and also increases CMRO2.
Propofol and Thiopentone reduce CMRO2 and cerebral blood flow. Ketamine increases CMRO2 and cerebral blood flow, but flow to a greater extent. It is generally avoided in patients with raised intracranial pressure however it is often used for head trauma patients where cardiovascular stability is the priority.
What are the management options for raised intracranial pressure?
- Noradrenaline to maintain perfusing pressure
- IV induction agents (propofol, thiopentone, etomidate)
- dose dependent decrease in cerebral blood flow, pressure and metabolic rate
- Reduce blood flow and metabolic rate but not pressure
- Opiates can decrease CMRO2 in large doses
- NMBA are useful to prevent coughing and straining
- Suxamethonium causes a transient increase in ICP, attenuated by induction agents
- Volatile agents
- Increase ICP due to cerebral vasodilatation, but also reduce CMRO2
- Can be used at MAC <1
- N2O and Ketamine
- Vasodilates and increases CMRO2, increasing ICP
- Osmotic diuretic, filtered and not reabsorbed
- Withdraws water from brain across BBB
- Free radical scavenger and reduces CSF production
- 0.5 – 1ml/kg of 20% solusion
- Phenytoin used to prevent convulsions, it is a membrane stabiliser that prevents sodium and calcium influx during depolarisation
- Maintain oxygenation
- Prevent secondary brain injury
- Decrease ICP
- Optimise CPP
- PaCO2 4.0-4.5
- Hypocapnoea should be avoided to prevent vasoconstriction
- Aid venous drainage
- 30 degrees head up
- Head in midline
- No collars or tube ties
- PEEP minimal
- Not shown to improve mortality however avoiding pyrexia does improve outcome
Immediate neurosurgery is the only definitive treatment
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