Cerebral Blood Flow and Intracranial Pressure

Last updated on May 5, 2023

Take home messages

Intracranial pressure is often examined, and an easy place to collect lots of extra marks
Understanding the factors that influence intracranial pressure is crucial to managing patients with head trauma effectively
In district general hospitals where intracranial pressure monitoring isn't available, you may have to 'assume' a raised pressure to be on the safe side

A spot of history

A long long time ago, before anaesthesia and CT scans - or medicine really - if you behaved strangely it was 100% because there was a demon in your head and the best way to release it was with a drill to the skull.

Preferably while wearing an upside down funnel, and with your ODP balancing the controlled drugs book on their head.

*The Extraction of the Stone of Madness*, a painting by Hieronymus Bosch depicting trepanation (c. 1488–1516) Image credit

This procedure dates back as far as 10,000 years ago, and amazingly, the mortality rate (for an unsterile, unguided drill to the skull in a field) is believed to only have been around 60%.

While the techniques and indications have evolved and improved somewhat, the underlying principle for a lot of intracranial pathology is the same:

The skull is a closed box

Enter the Monroe-Kellie doctrine

The skull is a fixed container with a lot of little holes, and one big one at the bottom. Inside said fixed box of bone there exist three types of content:

Brain 85%
Blood 5%
CSF 10%

They live in a constant harmonious balance wherein if any one of them increases in volume, to avoid a harmful rise in intracranial pressure, one or both of the others must decrease in volume to compensate.

Otherwise you get this graph:

Note that normal pressure, when lying supine, is approximately 8-12mmHg
Above 20mmHg there starts to be focal ischaemia, and above 45-50mmHg there is global ischaemia

What are the causes of raised intracranial pressure?

This is a very common exam question, either in the SOE or the OSCE. The key to a strong answer is, as always, to categorise.

Increased CSF in the brain:

Overproduction
Underabsorption
Blockage of drainage
All three of these can lead to Hydrocephalus

Mass effect of the brain itself:

Oedema
Contusion
Abscess
Tumour

Increased intracranial blood volume:

Venous obstruction
Venous Sinus Thrombosis
Haemorrhage

Benign intracranial hypertension:

Unclear cause
Associated with obesity

What happens when intracranial pressure starts to increase?

There are three main compensatory mechanisms in place to deal with increasing intracranial pressure.

Initially venous blood is pushed out of the skull, reducing the volume of venous blood in the great veins and sinuses

This is why it's a good idea to avoid jugular central lines, and anything else that might obstruct venous drainage such as tube ties (use tape instead).

Secondly, cerebrospinal fluid is extruded via the foramen magnum

There's a total volume of approximately 150ml of csf, with around 125ml of this in the subarachnoid space (both brain and spinal cord), and only about 25ml in the ventricles.

Thirdly the volume of arterial blood starts to reduce

This is where it becomes seriously bad news, because the blood supply to an already stressed brain decreases.

After a certain point, there won't be anything else that can be removed to accomodate the expanding volume, and only very small increases in volume will dramatically increase intracranial pressure, causing compression of the brain parenchyma and ischaemia.

What are the clinical features of raised intracranial pressure?

Headache, worse on straining or bending over
Nausea and vomiting
Papilloedema
Reduced GCS or irritability
Bulging fontanelle in infants

The Cushing Reflex is a preterminal sign

Raised intracranial pressure leads to hypoperfusion
The brain releases vasoactive mediators to increase blood pressure
This increased blood pressure causes a reflex bradycardia, and further increases intracranial pressure
The increasing pressure leads to herniation of brainstem through foramen magnum, stretching the cranial nerves
This is known as coning
Hypotension, apnoea and fixed dilated pupils follow once cushing’s reflex fails

Talk to me about cerebral blood flow

As one might expect, the brain receives rather a lot of blood in order to sustain all of those thoughts and decisions, and ends up receiving around 25% of the cardiac output.

The golden number to remember is 50 ml of oxygen per 100g of brain tissue per minute.

Factors influencing cerebral blood flow relate to the Hagen Poiseuille equation:

Pressure gradient

Cerebral Perfusion Pressure = Mean Arterial Pressure – (ICP + CVP)

Where ICP = intracranial pressure and CVP = central venous pressure
Also CPP = Cerebral blood flow x Cerebral vascular resistance
This is essentially Ohm’s law (V=IR)

Blood vessel diameter

Again similar to Ohm's law, the blood vessel diameter dramatically affects the resistance to blood flow

The main factors that induce vasoconstriction and dilation are PaCO2 and PaO2

PaCO2

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.

PaO2

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.

What is flow-metabolism coupling?

The rate at which the brain consumes oxygen for metabolism is the cerebral metabolic rate or oxygen utilisation or CMRO2

Usually around 3ml/100g/minute
5ml/100g/minute in young children

Flow-metabolism coupling is where perfusion is adjusted to match the metabolic demand of a given region of the brain, or the brain as a whole

There is a linear relationship between CBF and CMRO2
Ischaemia occurs below 20ml/100g/minute

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 pulse waves, each with gradually reducing amplitude.

Pulse wave

Pulse waves

Percussive
Transmitted arterial pressure

Tidal
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

As well as the three pulse waves in each beat, there are two other patterns in the pressure waveform:

Respiratory wave

This is a larger variation in baseline pressure with the respiratory cycle and is totally normal.

Slow waves

Also known as Lundberg waves, these are usually pathological, but not always.

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

Type B

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

Type C

4 to 8 waves per minute
Up to 20mmHg
May be normal

These images are beautifully represented in Dr Nick Mark's fabulous ICU one pager infographic, which you can find here, or in the resources section below.

How does carbon dioxide affect intracranial pressure?

Hypercapnia causes vasodilatation and therefore increased cerebral blood flow as detailed above.

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 hypocapnoea is opposed by vasodilation induced by the resulting ischaemia and hypoxia.

Low CO2 tries to vasoconstrict, causing hypoxia which overrides it and forces the vessels to vasodilate

Should we hyperventilate patients with high intracranial pressure?

This seems like a logical plan on the face of it - by hyperventilating our patient we could theoretically induce a degree of vasoconstriction that would reduce intracranial blood volume and therefore intracranial pressure.

However there is a problem with this:

It's a very temporary effect, and the brain rapidly recalibrates its set point for PaCO2 and will vasodilate again within a matter of a few hours
Then when the hyperventilation stops, and the CO2 rises, the resulting vasodilatation would be even worse than before

Therefore hyperventilation should only be done in extremis as a temporising measure, for example in the ambulance when you're fifteen minutes away from definitive surgery.

For all other scenarios, the focus should be on maintaining a low-normal PaCO2, and preventing avoidable vasodilatation.

Aim for PaCO2 of 4-4.5kPa

Autoregulation

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

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.

Intravenous agents

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?

This is a common question at a variety of points during the FRCA exam journey, so it's worth investing some time to build a slick answer.

The categories we would suggest are pharmacological, non-pharmacological and surgical.

Pharmacological

Noradrenaline - to maintain perfusing pressure
IV induction agents (propofol, thiopentone, etomidate) - cause a dose dependent decrease in cerebral blood flow, pressure and metabolic rate
Benzodiazepines - reduce blood flow and metabolic rate but not pressure
Opiates - can decrease CMRO2 in large doses
Muscle relaxants - useful to prevent coughing and straining

Just note that suxamethonium causes a transient increase in ICP, attenuated by induction agents such as thiopentone.

Volatile agents - slight theoretical increase in ICP due to cerebral vasodilatation, but also reduce CMRO2 - Can be used at MAC <1
N2O and Ketamine - Vasodilates and increases CMRO2, increasing ICP
Barbiturates - deep thiopentone coma used in refractory seizures
Phenytoin - used to prevent convulsions, it is a membrane stabiliser that prevents sodium and calcium influx during depolarisation
IV fluids:

Mannitol

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% solution

Hypertonic saline

2-3ml/kg of 5% NaCl
Hypertonicity draws fluid out of the interstitium into the blood to be drained away

Non-pharmacological

Main priorities

Maintain oxygenation
Prevent secondary brain injury
Decrease ICP
Optimise CPP

Ventilation

PaCO2 4.0-4.5
Hypocapnoea should be avoided to prevent vasoconstriction

Aid venous drainage

Posture
30 degrees head up
Head in midline
No collars or tube ties
PEEP minimal

Cooling is controversial

Not shown to improve mortality however avoiding pyrexia does improve outcome

Surgical

Immediate neurosurgery is the only definitive treatment for raised intracranial pressure

Debulking
Drainage - via external ventricular drain
Craniectomy

Apparently

You can put a needle through the orbit into the lateral ventricle and drain CSF that way...

Syllabus

PB_BK_69 Intracranial pressure: cerebrospinal fluid, blood flow

A Free Final CRQ

Our wonderful colleagues over at FRCA-revision have put together a whole series of high yield CRQ questions for the Final FRCA, and they also have a fantastic SBA and MCQ bank for the Primary. Tap the image below to go straight to the CRQ on intracranial pressure.

Useful Tweets and Resources

If you haven't already discovered Dr Nick Mark's amazing infographics over at ICU one pager - you simply must check them out

Cerebrospinal fluid shooting out in acute hydrocephalus with elevated intracranial pressure pic.twitter.com/hzqCbRmgQk
— Oren Gottfried, MD (@OGdukeneurosurg) April 19, 2023

From our #neuroanaesthesia series, our #cognitiveaid on effectively managing elevated intracranial pressure. #cognitiveaids #ascar #anaesthesia #anesthesia #icu #anesthesiology #icu #icunurse #ernurse #erdoc #icudoctor #foamed #medicalstudent #medicalschool pic.twitter.com/13JVuPPGwz
— ascargroup (@ascargroup) January 11, 2023

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References and Further Reading

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