June 9, 2025 • 49 mins
Let’s Get Updated is an audio learning series that brings to life the key topics from Update in Anaesthesia—one topic at a time. Each episode guides you through a full reading of a selected topic, making it easy to listen and read along. Whether you’re preparing for exams or brushing up on essential concepts, this podcast is built for anaesthesia learners in all settings, especially low-resource environments. This is an independent educational project not affiliated with the World Federation of Societies of Anaesthesiologists (WFSA). Content is drawn from publicly available issues of Update in Anaesthesia.
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This episode features a full reading of “Cerebral Blood Flow and Intracranial Pressure” from Update in Anaesthesia, Volume 24, Number 2. Read along with the original article or simply listen in for a clear, guided walkthrough. Let’s get updated.
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(00:01):
Updating anaesthesia. Volume 24 #2 Cerebral blood flow
and intracranial pressure by Lisa Hill and Carl Ginwort.
(00:22):
Summary The normal adults call can be considered as a Bony box
of fixed volume containing brain, blood and cerebral spinal
fluid. An understanding of how these
components interact is essentialin managing normal patients
(00:46):
under anaesthesia and those withintracranial pathology.
These factors will be consideredin two sections, cerebral blood
flow and intracranial pressure. Cerebral blood flow.
(01:09):
The brain is unusual in that it is only able to withstand very
short periods of lack of blood supply, that is, ischemia.
This is because neurons produce energy that is ATP almost
entirely by oxidative metabolismof substrates including glucose
(01:34):
and ketone. Bodies with very limited
capacity for anaerobic metabolism.
Without oxygen, energy dependentprocesses cease, leading to
irreversible cellular injury if blood flow is not re established
(01:55):
rapidly, that is 3 to 8 minutes under most circumstances.
Therefore, adequate cerebral blood flow must be maintained to
ensure a constant delivery of oxygen and substrates and to
remove the waste products of metabolism.
(02:19):
Cerebral blood flow is dependenton a number of factors that can
be broadly divided into one, those affecting cerebral
perfusion pressure, and two, those affecting the radius of
(02:40):
cerebral blood vessels. This relationship can be
described by the Higgin poise well equation, which describes
the laminar flow of an incompressible uniformly viscous
fluid, so-called Newtonian fluid, through a cylindrical
(03:04):
tube with constant circular cross section.
Although blood does not fulfil all these criteria, it tends to
flow in a laminar manner at the level of capillaries.
The Hagen Poiseuille equation. Cerebral blood flow is equals to
(03:34):
delta P * π R to the 4th power divided by 8 ETA L, where delta
P is equals to cerebral perfusion pressure, R is equals
to radius of the blood vessels, ETA is equals to viscosity of
(03:59):
the fluid, that is, blood L is equals to the length of the tube
that is blood vessels and π is equals to a constant 3.14.
Let's take the equation again. Delta P times π R to the 4th
(04:21):
power divided by 8 ETA L. Some facts and figures.
Cerebral blood flow averages 50 meals per 100 grammes per
(04:42):
minute. That is ranging from 20 meals
per 100 grammes per minute in white matter to 70 meals per 100
grammes per minute in grey matter.
The adult brain weighs 1400 grammes or 2% of the total body
(05:07):
weight. Therefore, it can be seen that
cerebral blood flow is 700 mealsper minute or 15% of the resting
cardiac output. This reflects the high oxygen
(05:28):
consumption of the brain of 3.3 mils per 100 grammes per minute.
That is 50 mils per minute in total, which is 20% of the total
body consumption. This is often referred to as the
(05:48):
cerebral metabolic rate for oxygen or CMRO 2.
This is higher in the cortical grey matter and generally
parallels cortical electrical activity.
(06:08):
Cerebral perfusion Pressure Perfusion of the brain is
dependent on the pressure gradients between the arteries
and the veins and this is termedthe cerebral perfusion pressure.
This is the difference between the mean arterial blood pressure
(06:31):
MEP and the mean cerebral venouspressure.
The latter is difficult to measure and approximate to the
more easily measured intracranial pressure ICP.
So CPP is equals to MAP minus ICP.
(07:01):
MAP can be estimated as equal todiastolic blood pressure plus
1/3 pulse pressure, which is thedifference between systolic and
diastolic pressures and is usually around 900 millimetres
of mercury. Sorry and is usually around 90
(07:23):
millimetres of mercury. Intracranial pressure is much
lower and is normally less than 13 millimetres of mercury.
CPP is normally about 80 millimetres of mercury.
(07:45):
So to take it again, MEP is usually around 90 millimetres of
mercury, ICP is around 13 millimetres of mercury and CPP
is about 80 millimetres of mercury.
(08:05):
Clearly, cerebral perfusion pressure will be affected by
anything that changes the MEP orICP.
Blood loss causing hypertension will reduce MEP and CPP.
Hence the reduced level of consciousness seen in severely
(08:29):
shocked patients. While an intracerebral hematoma
will increase ICP with the same effect.
Clearly, if both coexist, the effect is a catastrophic fall in
CPP and the risk of brain ischemia.
(08:55):
An increase in cerebral perfusion pressure is usually
the result of an increase in theMAP.
The contribution made by reducing ICP is minimal except
in pathological states when ICP is very high.
(09:18):
In a normal brain, despite the potential for changes in MEP,
that is sleep, exercise, etcetera, cerebral blood flow
remains constant over a wide range of cerebral perfusion
pressures. This is achieved by a process
(09:38):
called auto regulation. Regulation of cerebral arterial
blood vessel calibre. This is regulated by 4 primary
factors 1. Cerebral metabolism 2.
(10:06):
Carbon dioxide and oxygen levels3 Auto regulation and four
neurohumeral factors. The radius of the arterial
vessels is particularly important because due to its
(10:28):
effect on the cerebral blood flow, an increased radius, that
is, vasodilatation, leads to an increase in cerebral blood
volume, which in turn increases intracranial pressure and
reduces cerebral perfusion pressure.
So a balance must be reached. Cerebral metabolism Changes in
(10:57):
cerebral blood flow and metabolism tend to follow each
other, local or global increasesin metabolic demand and met
rapidly by an increase in cerebral blood flow and
substrate delivery, and vice versa.
Often referred to as flow metabolism coupling, these
(11:23):
changes are thought to be controlled by several vasoactive
metabolism metabolic mediators including hydrogen ions,
potassium, carbon dioxide, adenosine, glycolytic
intermediates, phospholipid metabolites, and more recently,
(11:48):
nitric oxide. Next we get to Figure 1,
explaining the showing a graph illustrating coupling between
cerebral blood flow and CMRO 2. Kindly pause this recording and
(12:09):
go through Figure 1. Carbon dioxide and oxygen
levels. At normal tension, the
relationship between partial pressure of carbon dioxide in
arterial blood, that is PA CO2, and cerebral blood flow is
(12:32):
almost linear and at a PA CO2 of10.6 kilopascals, that is 80
millimetres of mercury, cerebralblood flow is approximately
doubled. No further increase in flow is
possible at this point as the arterioles are maximally
(12:52):
dilated. Conversely, at 2.7 kilopascals,
that is 20 millimetres of mercury, flow is almost halved
and again cannot fall further asthe arterioles are maximally
vaso constricted. These effects are regulated by a
(13:15):
complex and interrelated system of mediators.
The internal. The initial stimulus is a
decrease in brain extracellular pH brought about by an increase
in PA CO2 further mediated by nitric oxide.
(13:37):
Prostanoids. Cyclic nucleotides, potassium
channels, and a decrease in intracellular calcium
concentration as a final common mediator.
Arteriolar tone has an importantinfluence in how PA CO2 effects
(14:01):
cerebral blood flow. Moderate hypertension impairs
the response of the cerebral circulation to changes in PA
CO2, and severe hypertension abolishes it altogether in
response of the cerebral vesselsto carbon dioxide.
(14:26):
Let's take it again. The response of the cerebral
vessels to carbon dioxide can beutilised to help manage patients
with raised intracranial pressure, for example, after
traumatic brain injury. Hyperventilation reduces the PA
(14:48):
CO2 and causes vessel constriction of the cerebral
vessels, that is, reduces their radius and therefore reduces
cerebral blood volume and intracranial pressure.
However, if the partial pressureof carbon dioxide is reduced too
much, the resulting vaso constriction can reduce the
(15:12):
cerebral blood flow to the pointof causing or worsening cerebral
ischemia. Clearly, hypercapnia and the
resulting vasodilation, an increase in intracranial
pressure must be avoided. PA CO2 is therefore best
(15:34):
maintained at low normal levels to prevent raising intracranial
pressure, that is 35 to 40 millimetres of mercury 4.7 to 5
point 3K kilopascals. These carbon dioxide reactivity
(15:55):
may be lost in areas of the brain that are injured.
Furthermore, impaired cerebral carbon dioxide vaso reactivity
is associated with a poor outcome in patients with severe
head injury. Carbon dioxide reactivity is
(16:16):
generally preserved during inhalation anaesthesia that is
up to about 1 mark of volatile and can therefore be utilised to
help control intracranial pressure and brain swelling
during surgery. Next we get to Figure 2 talking
(16:41):
about the relationship between the cerebral blood flow and PA
CO2. Kindly go through it.
Oxygen has little effect on the radius of blood vessels at
partial pressures used clinically.
(17:05):
Next we get to Figure 3, explaining the relationship
between the cerebral blood flow and partial pressure of oxygen,
showing little effect on the cerebral blood flow in the
normal oximic range. Kindly pause this recording and
go through Figure 3. Cerebral blood flow increases
(17:31):
once the PACPA O2 drops below about 6.7 kilopascals so that
cerebral oxygen delivery remainsconstant.
Hypoxia acts directly on cerebral tissue to promote the
(17:52):
release of adenosine and in somecases prostanoids that
contribute significantly to cerebral vasodilatation.
Hypoxia also acts directly on cerebrovascular smooth muscle to
produce hyperpolarization and reduce calcium uptake, both
(18:18):
mechanisms enhancing vasodilatation.
Next, we get to Figure 4, explaining the relationship
between cerebral blood flow and cerebral perfusion pressure.
(18:38):
Kindly pause this recording to go through Figure 4.
The brain requires a constant flow of blood over a range of
pressures and this is achieved by the process of auto
regulation. Sorry, this we are under the
(19:00):
subsection titled Auto regulation, so let's take it
again. The brain requires a constant
flow of blood over a range of pressures and this is achieved
by the process of auto regulation.
(19:22):
The stimulus to autoregulation is cerebral perfusion pressure,
not MAP. In adults under normal
circumstances, that is ICP less than 10 millimetres of mercury,
(19:45):
CSPP and MAP are very similar, and CBF that cerebral blood flow
remains constant with a cerebralperfusion pressure of 60 to 160
millimetres of mercury. The higher the intracranial
(20:05):
pressure, the more cerebral perfusion pressure deviates from
the mean and arterial pressure and must be calculated.
The auto regulation curve is shifted to the right in chronic
hypertensive patients and to theleft in units and younger
(20:27):
children, gradually moving to adult values as they get older.
Auto regulation is thought to bea myogenic mechanism whereby
vascular smooth muscle constricts in response to an
increase in wall tension and to relax to a decrease in wall
(20:52):
tension. At the lower limit of auto
regulation, cerebral vasodilation is maximum and
below this level the vessels collapse and cerebral blood flow
falls passively with falls in mean arterial pressure.
(21:18):
At the upper limit, vessel constriction is maximum and
beyond this, the elevated intraluminal pressure may force
the vessels to dilate, leading to an increase in cerebral blood
flow and damage to the blood brain barrier.
(21:43):
Metabolic mediators such as adenosine may also be involved
in the low pressure range of autoregulation.
As with all the other mechanismsthat affect the radius of blood
vessels, autoregulation will also change the cerebral blood
(22:03):
volume and may affect intracranial pressure.
Pressure autoregulation can be impaired in many pathological
conditions, including patients with a brain tumour,
subarachnoid haemorrhage, strokeor head injury.
(22:29):
A loss of cerebral blood flow regulatory capacity can be
attributed either to damage of the control system, for example
cerebral vessels, or of the feedback mechanisms involved in
the brain's hemodynamic control.At this time, cerebral blood
(22:53):
flow becomes pressure dependent and thus small changes in MEP
can have profound changes in cerebral blood flow and cerebral
blood volume. Neurohumeral factors.
(23:15):
A major difference between othersystemic circulations and the
cerebral circulation is the relative lack of humoral and
autonomic control on normal cerebral vascular tone.
The main action of the sympathetic nerves is
vasoconstriction that protects the brain by shifting the auto
(23:40):
auto regulation curve to the right.
In hypertension, the parasympathetic nerves
contribute to vasodilatation andmay play a part in hypertension
and reperfusion injury, for example after cardiac arrest.
(24:05):
Other factors. Blood viscosity.
This is directly related to hematocrit.
As viscosity falls, cerebral blood flow increases.
See the Hagen Pursuell equation.However, there will also be a
(24:29):
reduction in oxygen carrying capacity of the blood.
The optimal hematocrit is where there's a balance between flow
and capacity, usually about 30% temperature.
(24:53):
The cerebral metabolic rate of oxygen decreases by 7% for each
1% fall in body temperature and is paralleled by similar
reduction in cerebral blood flow.
At 27%, cerebral blood flow is approximately 50% of normal.
(25:19):
Sorry. At 27°C, cerebral blood flow is
approximately 50% of normal. By 20°C, cerebral blood flow is
about 10% of normal. The reduction in CMRO 2 is the
(25:43):
factor that allows cold patientsto withstand prolonged periods
of reduced cerebral blood flow without ischemic damage.
For example, during cardio pulmonary bypass, again because
of vasoconstriction, cerebral blood volume and ICP are
(26:07):
reduced. Although this has been tried to
help control high intracranial pressure, clinical trials have
been disappointingly ineffectivein showing an improved outcome.
Drugs cerebral metabolism can bemanipulated that is reduced and
(26:36):
consequently cerebral blood flow, cerebral blood volume and
intracranial pressure is reduced.
Infusions of the barbiturate thiopentone have been used to
help control high intracranial pressure after head injury.
(26:58):
However, there is little convincing evidence of benefit.
Anaesthetic drugs have a significant effect on cerebral
blood vessels. Volatile agents cause a
reduction in the tension of cerebral vascular smooth muscle
(27:18):
resulting in vasodilation and anincrease in cerebral blood flow.
Interestingly, many of the newerdrugs, that is isoflurane,
several fluorine also reduce neuronal function and metabolic
(27:39):
demands and as a result this canlead to uncoupling of flow
metabolism. This appears to be dependent on
the concentration of volatile and aesthetic given the
vasodilatation can be countered by mild hyperventilation to a
(28:03):
partial pressure of carbon dioxide at the low end of the
normal range, that is 4 to 4.5 kilopascals without serious risk
of cerebral ischemia. Intracranial pressure.
(28:23):
ICP intracranial pressure is important as it affects cerebral
perfusion pressure and cerebral blood flow.
Normal intracranial pressure is between 5 and 13 millimetres of
mercury. Because it is very dependent on
(28:46):
posture, the external auditory miathus is usually used as the
zero point. Some facts and figures
Constituents within the skull include the brain that is 80%
(29:07):
that under 1400 mils, blood 10 percent 150 mils, and cerebral
spinal fluid 10 percent 150 mils.
The score is a rigid box so if one of the three components
(29:32):
increases in volume then there must be compensation by decrease
in the volume of one or more of the remaining components.
Otherwise, the intracranial pressure will increase.
The term compliance is often used to describe this
(29:53):
relationship, but it is more accurately elastance, the
reciprocal of compliance, that is change in pressure for unit
change in volume. Compensatory mechanisms include
(30:15):
movement of cerebrospinal fluid into the spinal SAC, increase
reoptic of cerebrospinal fluid, and compression of venous
sinuses. OK increase reoptic of
cerebrospinal fluid and compression of venous sinuses.
(30:37):
These mechanisms reduce the liquid volume of the
intracranial contents. Next we get to Figure 5,
explaining the intracranial pressure elastance curve, that
is, the change in pressure by unit change in volume is in 4
(31:05):
stages, Stage 1 stroke 2 is the compensation phase and the stage
3 to 4 is the decompensated phase.
Stage 1 stroke 2 which is the compensation phase is explained.
(31:30):
Those as one of the intracranialconstituents increases in
volume, the other two constituents decrease in volume
in order to keep the intracranial pressure constant.
That is the phase of compression.
When we get to stage 3 to 4, that is the decompensated phase.
(31:54):
It says that when compensatory mechanisms are exhausted, small
increases in the volume of intracranial constituents cause
large increases in intracranial pressure.
The slope of the curve is dependent on which intracranial
constituent is increasing. If it is blurred or CSF, both of
(32:18):
which are poorly compressible, then the slope is steeper.
If it is brain tissue, such as atumour or edoema, the curve is
less steep as the tissue is compressible.
Cerebrospinal fluid. CSF cerebrospinal fluid is a
(32:46):
specialised extracellular fluid in the ventricles and
subarachnoid space which has a multitude of functions.
Functions of the CSF Mechanical protection of buoyancy.
(33:10):
The low specific gravity of CSF that is 1.007 reduces the
effective weights of the brain from 1.4 kilogrammes to 47
grammes, that is Archimedes principle.
This reduction in mass reduces brain inertia and thereby
(33:32):
protects it against deformation caused by acceleration or
deceleration forces. CSF provides a constant chemical
environment for neuronal activity.
(33:53):
CSF is important for acid base regulation for control of
respiration. CSF provides a medium for
nutrients after they are transported actively across the
blood brain barrier. CSF is produced as a rate at a
(34:19):
rate of 0.3 to 0.4 mills per minute, that is 500 mills per
day by the choroid plexus in thelateral 3rd and 4th ventricles.
CSF is produced by the filtration of plasma through
(34:44):
fenestrated capillaries, followed by active transport of
water and dissolved substances through the epithelial cells of
the blood CSF barrier. This is distinct from the blood
brain barrier, which consists ofendothelial cells linked by the
(35:09):
tight junctions, whose function is to protect the brain from
chemicals in the bloodstream. CSF formation is dependent on
the on the CPP and when this falls below 70 millimetres of
mercury, CSF production also falls because of the reduction
(35:34):
in cerebral and choroid plexus blood flow following production.
CSF then circulates through the ventricular system and the
subarachnoid species, aided by ciliary movements of the
appendimal cells. Resorption takes place mostly in
(35:59):
the arachnoid villi and granulations into the
circulation. The mechanism behind the
resorption is the difference between the CSF pressure and the
venous pressure. An obstruction in CSF
circulation, overproduction of CSF, or inadequate resorption
(36:23):
results in hydrocephalus pathological conditions, causing
a rise in volume of intracranialconstituents.
(36:43):
Any of the three intracranial constituents, that is, tissue,
blood, or CSF can increase in size and volume.
We get to Table one talking about the comparison of the
(37:04):
compositions of CSF and plasma. Kindly pause this recording to
go through Table 1. Effects of a raised intracranial
pressure. As intracranial pressure rises,
(37:28):
cerebral perfusion pressure falls, eventually to a point
when there is no cerebral blood flow.
No cerebral perfusion and brain death prior to this.
Brain structures begin to herniate, that is protrude
(37:51):
through an opening. Physiological compensatory
mechanisms occur to try and maintain cerebral blood flow.
Temporal lobe herniation beneaththe tentorium cerebelli that is
(38:13):
uncle herniation causes cradial nerve 3 palsy, that is
dilatation of pupil on the same side as lesion ipsilateral
followed by movement of the eye down and out.
(38:36):
Next we get to Figure 6, explaining the production,
circulation, and resorption of cerebrospinal fluid.
Kindly pause this recording to go through Figure 6.
(38:56):
Herniation of cerebellar peduncles through the foramen
magnum, that is, tonsillar herniation.
Pressure on the brain stem causes the caution reflex
hypertension bradycardia and chain strokes respiration that
(39:19):
is periodic breathing. Sub falsine herniation occurs
when the cingulate gyrus on the medial aspect of the frontal
lobe is displaced across across the midline under the free edge
(39:41):
of the false cerebrae and may compress the anterior cerebral
artery. Upward or cerebellar herniation
occurs with either a large mass or increased pressure in the
posterior fossa. The cerebellum is displaced in
(40:06):
an upward direction through the tentorial opening.
And causes significant upper brain stem compression.
Next we get to Table 2 explaining conditions causing
raised ICP. Kindly pause this recording to
(40:30):
go through Table 2. How can ICP be influenced?
Primary brain damage occurs at the time of a head injury and is
unavoidable except through preventable preventative
(40:53):
measures. The aim of management following
this is to reduce secondary brain damage which is caused by
reduction in oxygen delivery dueto hypoxemia that is low
arterial PAO 2 or anaemia, a reduction in cerebral blood flow
(41:18):
due to hypertension or reduced cardiac output and factors which
cause the raised ICP and reducedcerebral perfusion pressure.
The most important management strategy ensures A that is
(41:38):
airway and C spine protection intrauma, B that is breathing and
adequate oxygenation, and C thatis blood pressure and CPP.
Following this, further strategies to reduce
intracranial pressure and preserve cerebral perfusion are
(42:02):
required. Techniques that can be employed
to reduce intracranial pressure are aimed at reducing the volume
of one or more of the contents of the skull.
Often blood pressure needs to beaugmented with drugs that
(42:24):
produce arterial vessel constriction, such as
metaraminol or norepinephrine, which requires central venous
access following a head injury. When auto regulation is
impaired, if there is a drop in MAP from drugs or blood loss,
(42:48):
the resulting cerebral vasodilation increases cerebral
blood volume, which in turn raises intracranial pressure and
further drops the cerebral perfusion pressure.
This starts a vicious cycle, so by raising the MAPICP can often
(43:13):
be reduced. Measuring ICP Intracranial
pressure is traditionally measured by use of a ventricular
ostomy or external ventricular drain EVD, which involves A
(43:35):
catheter that is placed through a small hole in the skull, that
is burh hole into the lateral ventricle.
Intracranial pressure is then measured by transducing the
pressure in the fluid column. Ventriculostomies also allow
(43:55):
drainage of cerebral spinal fluid, which can be effective in
decreasing the intracranial pressure.
More commonly, intracranial pressure is now measured by
placing some form of measuring device, for example, a miniature
(44:16):
transducer within the brain tissue that is intraparenchymal
monitor. An epidural monitor can also be
used, but becomes increasingly unreliable at extremes of
pressure. The normal intracranial pressure
(44:39):
waveform is a triphysic wave in which the first peak is the
largest peak and the second and third peaks are progressively
smaller. When intracranial compliance is
abnormal, the second and third peaks are usually larger than
(45:02):
the first peak. In addition, when intracranial
compliance is abnormal and intracranial pressure is
elevated, pathological waves mayappear.
Lonberg described three types ofabnormal intracranial pressure
(45:23):
waves in 1960 that he named AB and C waves.
Although these can be identified, it is more common
nowadays to measure the mean intracranial pressure and use
this to calculate cerebral perfusion pressure.
(45:50):
Next, we get to Table 3 describing the strategies to
reduce intracranial pressure, talking about reducing brain
tissue volume, reducing blood volume, and reducing CSF value
volume. Kindly pause this recording to
(46:10):
go through Table 3. If intracranial pressure is not
measured directly, we can estimate it and therefore make
changes in the miniaturial pressure to maintain cerebral
perfusion pressure. Patient drowsy and confused.
(46:37):
That is GCS 9 to 13. ICP approximately 20 millimetres
of mercury. GCS less than or equal to 8 ICP,
approximately 30 millimetres of mercury.
(47:01):
Measuring the adequacy of cerebral perfusion.
This is difficult as ideally adequacy of cerebral perfusion
will be determined at a cellularlevel to determine whether
neurons are receiving adequate oxygen and nutrients.
(47:26):
Inferences about cerebral perfusion can be made by looking
at a variety of measured variables.
The first five techniques can beused at the bedside and are
often part of multimodal monitoring of head injured
patients. The latter techniques are more
(47:51):
invasive and generally restricted to research
programmes measuring ICP and calculating CPP, which is the
most common method. Jugular venous bulb oxygen
(48:12):
saturations, that is, SJ VO2 usually 65 to 75%, reflects the
balance between cerebral oxygen delivery and CMRO 2.
A low jugular venous bulb oxygensaturation reliably indicates
(48:36):
cerebral hyperfusion. Transcrania Doppler to measure
blood velocity and estimate cerebral blood flow.
Micro dialysis catheters to measure glucose, pyruvate,
(48:58):
lactate, glycerol, glutamate that is metabolic variables.
Positron emission tomography, the distribution of radio
labelled water in the brain is monitored to indicate metabolic
activity. Functional Mr imaging
(49:24):
techniques. KT Smith's equation to determine
cerebral blood flow by using an innate carrier gas, that is
using xenon 133 and finally nearinfrared spectroscopy NIRS to
(49:46):
measure oxygenation in a localised cerebral field.
Updating anaesthesia. Volume 24 #2 Cerebral blood flow
and intracranial pressure by Lisa Hill and Carl Ginwort.
(00:22):
Summary The normal adults call can be considered as a Bony box
of fixed volume containing brain, blood and cerebral spinal
fluid. An understanding of how these
components interact is essentialin managing normal patients
(00:46):
under anaesthesia and those withintracranial pathology.
These factors will be consideredin two sections, cerebral blood
flow and intracranial pressure. Cerebral blood flow.
(01:09):
The brain is unusual in that it is only able to withstand very
short periods of lack of blood supply, that is, ischemia.
This is because neurons produce energy that is ATP almost
entirely by oxidative metabolismof substrates including glucose
(01:34):
and ketone. Bodies with very limited
capacity for anaerobic metabolism.
Without oxygen, energy dependentprocesses cease, leading to
irreversible cellular injury if blood flow is not re established
(01:55):
rapidly, that is 3 to 8 minutes under most circumstances.
Therefore, adequate cerebral blood flow must be maintained to
ensure a constant delivery of oxygen and substrates and to
remove the waste products of metabolism.
(02:19):
Cerebral blood flow is dependenton a number of factors that can
be broadly divided into one, those affecting cerebral
perfusion pressure, and two, those affecting the radius of
(02:40):
cerebral blood vessels. This relationship can be
described by the Higgin poise well equation, which describes
the laminar flow of an incompressible uniformly viscous
fluid, so-called Newtonian fluid, through a cylindrical
(03:04):
tube with constant circular cross section.
Although blood does not fulfil all these criteria, it tends to
flow in a laminar manner at the level of capillaries.
The Hagen Poiseuille equation. Cerebral blood flow is equals to
(03:34):
delta P * π R to the 4th power divided by 8 ETA L, where delta
P is equals to cerebral perfusion pressure, R is equals
to radius of the blood vessels, ETA is equals to viscosity of
(03:59):
the fluid, that is, blood L is equals to the length of the tube
that is blood vessels and π is equals to a constant 3.14.
Let's take the equation again. Delta P times π R to the 4th
(04:21):
power divided by 8 ETA L. Some facts and figures.
Cerebral blood flow averages 50 meals per 100 grammes per
(04:42):
minute. That is ranging from 20 meals
per 100 grammes per minute in white matter to 70 meals per 100
grammes per minute in grey matter.
The adult brain weighs 1400 grammes or 2% of the total body
(05:07):
weight. Therefore, it can be seen that
cerebral blood flow is 700 mealsper minute or 15% of the resting
cardiac output. This reflects the high oxygen
(05:28):
consumption of the brain of 3.3 mils per 100 grammes per minute.
That is 50 mils per minute in total, which is 20% of the total
body consumption. This is often referred to as the
(05:48):
cerebral metabolic rate for oxygen or CMRO 2.
This is higher in the cortical grey matter and generally
parallels cortical electrical activity.
(06:08):
Cerebral perfusion Pressure Perfusion of the brain is
dependent on the pressure gradients between the arteries
and the veins and this is termedthe cerebral perfusion pressure.
This is the difference between the mean arterial blood pressure
(06:31):
MEP and the mean cerebral venouspressure.
The latter is difficult to measure and approximate to the
more easily measured intracranial pressure ICP.
So CPP is equals to MAP minus ICP.
(07:01):
MAP can be estimated as equal todiastolic blood pressure plus
1/3 pulse pressure, which is thedifference between systolic and
diastolic pressures and is usually around 900 millimetres
of mercury. Sorry and is usually around 90
(07:23):
millimetres of mercury. Intracranial pressure is much
lower and is normally less than 13 millimetres of mercury.
CPP is normally about 80 millimetres of mercury.
(07:45):
So to take it again, MEP is usually around 90 millimetres of
mercury, ICP is around 13 millimetres of mercury and CPP
is about 80 millimetres of mercury.
(08:05):
Clearly, cerebral perfusion pressure will be affected by
anything that changes the MEP orICP.
Blood loss causing hypertension will reduce MEP and CPP.
Hence the reduced level of consciousness seen in severely
(08:29):
shocked patients. While an intracerebral hematoma
will increase ICP with the same effect.
Clearly, if both coexist, the effect is a catastrophic fall in
CPP and the risk of brain ischemia.
(08:55):
An increase in cerebral perfusion pressure is usually
the result of an increase in theMAP.
The contribution made by reducing ICP is minimal except
in pathological states when ICP is very high.
(09:18):
In a normal brain, despite the potential for changes in MEP,
that is sleep, exercise, etcetera, cerebral blood flow
remains constant over a wide range of cerebral perfusion
pressures. This is achieved by a process
(09:38):
called auto regulation. Regulation of cerebral arterial
blood vessel calibre. This is regulated by 4 primary
factors 1. Cerebral metabolism 2.
(10:06):
Carbon dioxide and oxygen levels3 Auto regulation and four
neurohumeral factors. The radius of the arterial
vessels is particularly important because due to its
(10:28):
effect on the cerebral blood flow, an increased radius, that
is, vasodilatation, leads to an increase in cerebral blood
volume, which in turn increases intracranial pressure and
reduces cerebral perfusion pressure.
So a balance must be reached. Cerebral metabolism Changes in
(10:57):
cerebral blood flow and metabolism tend to follow each
other, local or global increasesin metabolic demand and met
rapidly by an increase in cerebral blood flow and
substrate delivery, and vice versa.
Often referred to as flow metabolism coupling, these
(11:23):
changes are thought to be controlled by several vasoactive
metabolism metabolic mediators including hydrogen ions,
potassium, carbon dioxide, adenosine, glycolytic
intermediates, phospholipid metabolites, and more recently,
(11:48):
nitric oxide. Next we get to Figure 1,
explaining the showing a graph illustrating coupling between
cerebral blood flow and CMRO 2. Kindly pause this recording and
(12:09):
go through Figure 1. Carbon dioxide and oxygen
levels. At normal tension, the
relationship between partial pressure of carbon dioxide in
arterial blood, that is PA CO2, and cerebral blood flow is
(12:32):
almost linear and at a PA CO2 of10.6 kilopascals, that is 80
millimetres of mercury, cerebralblood flow is approximately
doubled. No further increase in flow is
possible at this point as the arterioles are maximally
(12:52):
dilated. Conversely, at 2.7 kilopascals,
that is 20 millimetres of mercury, flow is almost halved
and again cannot fall further asthe arterioles are maximally
vaso constricted. These effects are regulated by a
(13:15):
complex and interrelated system of mediators.
The internal. The initial stimulus is a
decrease in brain extracellular pH brought about by an increase
in PA CO2 further mediated by nitric oxide.
(13:37):
Prostanoids. Cyclic nucleotides, potassium
channels, and a decrease in intracellular calcium
concentration as a final common mediator.
Arteriolar tone has an importantinfluence in how PA CO2 effects
(14:01):
cerebral blood flow. Moderate hypertension impairs
the response of the cerebral circulation to changes in PA
CO2, and severe hypertension abolishes it altogether in
response of the cerebral vesselsto carbon dioxide.
(14:26):
Let's take it again. The response of the cerebral
vessels to carbon dioxide can beutilised to help manage patients
with raised intracranial pressure, for example, after
traumatic brain injury. Hyperventilation reduces the PA
(14:48):
CO2 and causes vessel constriction of the cerebral
vessels, that is, reduces their radius and therefore reduces
cerebral blood volume and intracranial pressure.
However, if the partial pressureof carbon dioxide is reduced too
much, the resulting vaso constriction can reduce the
(15:12):
cerebral blood flow to the pointof causing or worsening cerebral
ischemia. Clearly, hypercapnia and the
resulting vasodilation, an increase in intracranial
pressure must be avoided. PA CO2 is therefore best
(15:34):
maintained at low normal levels to prevent raising intracranial
pressure, that is 35 to 40 millimetres of mercury 4.7 to 5
point 3K kilopascals. These carbon dioxide reactivity
(15:55):
may be lost in areas of the brain that are injured.
Furthermore, impaired cerebral carbon dioxide vaso reactivity
is associated with a poor outcome in patients with severe
head injury. Carbon dioxide reactivity is
(16:16):
generally preserved during inhalation anaesthesia that is
up to about 1 mark of volatile and can therefore be utilised to
help control intracranial pressure and brain swelling
during surgery. Next we get to Figure 2 talking
(16:41):
about the relationship between the cerebral blood flow and PA
CO2. Kindly go through it.
Oxygen has little effect on the radius of blood vessels at
partial pressures used clinically.
(17:05):
Next we get to Figure 3, explaining the relationship
between the cerebral blood flow and partial pressure of oxygen,
showing little effect on the cerebral blood flow in the
normal oximic range. Kindly pause this recording and
go through Figure 3. Cerebral blood flow increases
(17:31):
once the PACPA O2 drops below about 6.7 kilopascals so that
cerebral oxygen delivery remainsconstant.
Hypoxia acts directly on cerebral tissue to promote the
(17:52):
release of adenosine and in somecases prostanoids that
contribute significantly to cerebral vasodilatation.
Hypoxia also acts directly on cerebrovascular smooth muscle to
produce hyperpolarization and reduce calcium uptake, both
(18:18):
mechanisms enhancing vasodilatation.
Next, we get to Figure 4, explaining the relationship
between cerebral blood flow and cerebral perfusion pressure.
(18:38):
Kindly pause this recording to go through Figure 4.
The brain requires a constant flow of blood over a range of
pressures and this is achieved by the process of auto
regulation. Sorry, this we are under the
(19:00):
subsection titled Auto regulation, so let's take it
again. The brain requires a constant
flow of blood over a range of pressures and this is achieved
by the process of auto regulation.
(19:22):
The stimulus to autoregulation is cerebral perfusion pressure,
not MAP. In adults under normal
circumstances, that is ICP less than 10 millimetres of mercury,
(19:45):
CSPP and MAP are very similar, and CBF that cerebral blood flow
remains constant with a cerebralperfusion pressure of 60 to 160
millimetres of mercury. The higher the intracranial
(20:05):
pressure, the more cerebral perfusion pressure deviates from
the mean and arterial pressure and must be calculated.
The auto regulation curve is shifted to the right in chronic
hypertensive patients and to theleft in units and younger
(20:27):
children, gradually moving to adult values as they get older.
Auto regulation is thought to bea myogenic mechanism whereby
vascular smooth muscle constricts in response to an
increase in wall tension and to relax to a decrease in wall
(20:52):
tension. At the lower limit of auto
regulation, cerebral vasodilation is maximum and
below this level the vessels collapse and cerebral blood flow
falls passively with falls in mean arterial pressure.
(21:18):
At the upper limit, vessel constriction is maximum and
beyond this, the elevated intraluminal pressure may force
the vessels to dilate, leading to an increase in cerebral blood
flow and damage to the blood brain barrier.
(21:43):
Metabolic mediators such as adenosine may also be involved
in the low pressure range of autoregulation.
As with all the other mechanismsthat affect the radius of blood
vessels, autoregulation will also change the cerebral blood
(22:03):
volume and may affect intracranial pressure.
Pressure autoregulation can be impaired in many pathological
conditions, including patients with a brain tumour,
subarachnoid haemorrhage, strokeor head injury.
(22:29):
A loss of cerebral blood flow regulatory capacity can be
attributed either to damage of the control system, for example
cerebral vessels, or of the feedback mechanisms involved in
the brain's hemodynamic control.At this time, cerebral blood
(22:53):
flow becomes pressure dependent and thus small changes in MEP
can have profound changes in cerebral blood flow and cerebral
blood volume. Neurohumeral factors.
(23:15):
A major difference between othersystemic circulations and the
cerebral circulation is the relative lack of humoral and
autonomic control on normal cerebral vascular tone.
The main action of the sympathetic nerves is
vasoconstriction that protects the brain by shifting the auto
(23:40):
auto regulation curve to the right.
In hypertension, the parasympathetic nerves
contribute to vasodilatation andmay play a part in hypertension
and reperfusion injury, for example after cardiac arrest.
(24:05):
Other factors. Blood viscosity.
This is directly related to hematocrit.
As viscosity falls, cerebral blood flow increases.
See the Hagen Pursuell equation.However, there will also be a
(24:29):
reduction in oxygen carrying capacity of the blood.
The optimal hematocrit is where there's a balance between flow
and capacity, usually about 30% temperature.
(24:53):
The cerebral metabolic rate of oxygen decreases by 7% for each
1% fall in body temperature and is paralleled by similar
reduction in cerebral blood flow.
At 27%, cerebral blood flow is approximately 50% of normal.
(25:19):
Sorry. At 27°C, cerebral blood flow is
approximately 50% of normal. By 20°C, cerebral blood flow is
about 10% of normal. The reduction in CMRO 2 is the
(25:43):
factor that allows cold patientsto withstand prolonged periods
of reduced cerebral blood flow without ischemic damage.
For example, during cardio pulmonary bypass, again because
of vasoconstriction, cerebral blood volume and ICP are
(26:07):
reduced. Although this has been tried to
help control high intracranial pressure, clinical trials have
been disappointingly ineffectivein showing an improved outcome.
Drugs cerebral metabolism can bemanipulated that is reduced and
(26:36):
consequently cerebral blood flow, cerebral blood volume and
intracranial pressure is reduced.
Infusions of the barbiturate thiopentone have been used to
help control high intracranial pressure after head injury.
(26:58):
However, there is little convincing evidence of benefit.
Anaesthetic drugs have a significant effect on cerebral
blood vessels. Volatile agents cause a
reduction in the tension of cerebral vascular smooth muscle
(27:18):
resulting in vasodilation and anincrease in cerebral blood flow.
Interestingly, many of the newerdrugs, that is isoflurane,
several fluorine also reduce neuronal function and metabolic
(27:39):
demands and as a result this canlead to uncoupling of flow
metabolism. This appears to be dependent on
the concentration of volatile and aesthetic given the
vasodilatation can be countered by mild hyperventilation to a
(28:03):
partial pressure of carbon dioxide at the low end of the
normal range, that is 4 to 4.5 kilopascals without serious risk
of cerebral ischemia. Intracranial pressure.
(28:23):
ICP intracranial pressure is important as it affects cerebral
perfusion pressure and cerebral blood flow.
Normal intracranial pressure is between 5 and 13 millimetres of
mercury. Because it is very dependent on
(28:46):
posture, the external auditory miathus is usually used as the
zero point. Some facts and figures
Constituents within the skull include the brain that is 80%
(29:07):
that under 1400 mils, blood 10 percent 150 mils, and cerebral
spinal fluid 10 percent 150 mils.
The score is a rigid box so if one of the three components
(29:32):
increases in volume then there must be compensation by decrease
in the volume of one or more of the remaining components.
Otherwise, the intracranial pressure will increase.
The term compliance is often used to describe this
(29:53):
relationship, but it is more accurately elastance, the
reciprocal of compliance, that is change in pressure for unit
change in volume. Compensatory mechanisms include
(30:15):
movement of cerebrospinal fluid into the spinal SAC, increase
reoptic of cerebrospinal fluid, and compression of venous
sinuses. OK increase reoptic of
cerebrospinal fluid and compression of venous sinuses.
(30:37):
These mechanisms reduce the liquid volume of the
intracranial contents. Next we get to Figure 5,
explaining the intracranial pressure elastance curve, that
is, the change in pressure by unit change in volume is in 4
(31:05):
stages, Stage 1 stroke 2 is the compensation phase and the stage
3 to 4 is the decompensated phase.
Stage 1 stroke 2 which is the compensation phase is explained.
(31:30):
Those as one of the intracranialconstituents increases in
volume, the other two constituents decrease in volume
in order to keep the intracranial pressure constant.
That is the phase of compression.
When we get to stage 3 to 4, that is the decompensated phase.
(31:54):
It says that when compensatory mechanisms are exhausted, small
increases in the volume of intracranial constituents cause
large increases in intracranial pressure.
The slope of the curve is dependent on which intracranial
constituent is increasing. If it is blurred or CSF, both of
(32:18):
which are poorly compressible, then the slope is steeper.
If it is brain tissue, such as atumour or edoema, the curve is
less steep as the tissue is compressible.
Cerebrospinal fluid. CSF cerebrospinal fluid is a
(32:46):
specialised extracellular fluid in the ventricles and
subarachnoid space which has a multitude of functions.
Functions of the CSF Mechanical protection of buoyancy.
(33:10):
The low specific gravity of CSF that is 1.007 reduces the
effective weights of the brain from 1.4 kilogrammes to 47
grammes, that is Archimedes principle.
This reduction in mass reduces brain inertia and thereby
(33:32):
protects it against deformation caused by acceleration or
deceleration forces. CSF provides a constant chemical
environment for neuronal activity.
(33:53):
CSF is important for acid base regulation for control of
respiration. CSF provides a medium for
nutrients after they are transported actively across the
blood brain barrier. CSF is produced as a rate at a
(34:19):
rate of 0.3 to 0.4 mills per minute, that is 500 mills per
day by the choroid plexus in thelateral 3rd and 4th ventricles.
CSF is produced by the filtration of plasma through
(34:44):
fenestrated capillaries, followed by active transport of
water and dissolved substances through the epithelial cells of
the blood CSF barrier. This is distinct from the blood
brain barrier, which consists ofendothelial cells linked by the
(35:09):
tight junctions, whose function is to protect the brain from
chemicals in the bloodstream. CSF formation is dependent on
the on the CPP and when this falls below 70 millimetres of
mercury, CSF production also falls because of the reduction
(35:34):
in cerebral and choroid plexus blood flow following production.
CSF then circulates through the ventricular system and the
subarachnoid species, aided by ciliary movements of the
appendimal cells. Resorption takes place mostly in
(35:59):
the arachnoid villi and granulations into the
circulation. The mechanism behind the
resorption is the difference between the CSF pressure and the
venous pressure. An obstruction in CSF
circulation, overproduction of CSF, or inadequate resorption
(36:23):
results in hydrocephalus pathological conditions, causing
a rise in volume of intracranialconstituents.
(36:43):
Any of the three intracranial constituents, that is, tissue,
blood, or CSF can increase in size and volume.
We get to Table one talking about the comparison of the
(37:04):
compositions of CSF and plasma. Kindly pause this recording to
go through Table 1. Effects of a raised intracranial
pressure. As intracranial pressure rises,
(37:28):
cerebral perfusion pressure falls, eventually to a point
when there is no cerebral blood flow.
No cerebral perfusion and brain death prior to this.
Brain structures begin to herniate, that is protrude
(37:51):
through an opening. Physiological compensatory
mechanisms occur to try and maintain cerebral blood flow.
Temporal lobe herniation beneaththe tentorium cerebelli that is
(38:13):
uncle herniation causes cradial nerve 3 palsy, that is
dilatation of pupil on the same side as lesion ipsilateral
followed by movement of the eye down and out.
(38:36):
Next we get to Figure 6, explaining the production,
circulation, and resorption of cerebrospinal fluid.
Kindly pause this recording to go through Figure 6.
(38:56):
Herniation of cerebellar peduncles through the foramen
magnum, that is, tonsillar herniation.
Pressure on the brain stem causes the caution reflex
hypertension bradycardia and chain strokes respiration that
(39:19):
is periodic breathing. Sub falsine herniation occurs
when the cingulate gyrus on the medial aspect of the frontal
lobe is displaced across across the midline under the free edge
(39:41):
of the false cerebrae and may compress the anterior cerebral
artery. Upward or cerebellar herniation
occurs with either a large mass or increased pressure in the
posterior fossa. The cerebellum is displaced in
(40:06):
an upward direction through the tentorial opening.
And causes significant upper brain stem compression.
Next we get to Table 2 explaining conditions causing
raised ICP. Kindly pause this recording to
(40:30):
go through Table 2. How can ICP be influenced?
Primary brain damage occurs at the time of a head injury and is
unavoidable except through preventable preventative
(40:53):
measures. The aim of management following
this is to reduce secondary brain damage which is caused by
reduction in oxygen delivery dueto hypoxemia that is low
arterial PAO 2 or anaemia, a reduction in cerebral blood flow
(41:18):
due to hypertension or reduced cardiac output and factors which
cause the raised ICP and reducedcerebral perfusion pressure.
The most important management strategy ensures A that is
(41:38):
airway and C spine protection intrauma, B that is breathing and
adequate oxygenation, and C thatis blood pressure and CPP.
Following this, further strategies to reduce
intracranial pressure and preserve cerebral perfusion are
(42:02):
required. Techniques that can be employed
to reduce intracranial pressure are aimed at reducing the volume
of one or more of the contents of the skull.
Often blood pressure needs to beaugmented with drugs that
(42:24):
produce arterial vessel constriction, such as
metaraminol or norepinephrine, which requires central venous
access following a head injury. When auto regulation is
impaired, if there is a drop in MAP from drugs or blood loss,
(42:48):
the resulting cerebral vasodilation increases cerebral
blood volume, which in turn raises intracranial pressure and
further drops the cerebral perfusion pressure.
This starts a vicious cycle, so by raising the MAPICP can often
(43:13):
be reduced. Measuring ICP Intracranial
pressure is traditionally measured by use of a ventricular
ostomy or external ventricular drain EVD, which involves A
(43:35):
catheter that is placed through a small hole in the skull, that
is burh hole into the lateral ventricle.
Intracranial pressure is then measured by transducing the
pressure in the fluid column. Ventriculostomies also allow
(43:55):
drainage of cerebral spinal fluid, which can be effective in
decreasing the intracranial pressure.
More commonly, intracranial pressure is now measured by
placing some form of measuring device, for example, a miniature
(44:16):
transducer within the brain tissue that is intraparenchymal
monitor. An epidural monitor can also be
used, but becomes increasingly unreliable at extremes of
pressure. The normal intracranial pressure
(44:39):
waveform is a triphysic wave in which the first peak is the
largest peak and the second and third peaks are progressively
smaller. When intracranial compliance is
abnormal, the second and third peaks are usually larger than
(45:02):
the first peak. In addition, when intracranial
compliance is abnormal and intracranial pressure is
elevated, pathological waves mayappear.
Lonberg described three types ofabnormal intracranial pressure
(45:23):
waves in 1960 that he named AB and C waves.
Although these can be identified, it is more common
nowadays to measure the mean intracranial pressure and use
this to calculate cerebral perfusion pressure.
(45:50):
Next, we get to Table 3 describing the strategies to
reduce intracranial pressure, talking about reducing brain
tissue volume, reducing blood volume, and reducing CSF value
volume. Kindly pause this recording to
(46:10):
go through Table 3. If intracranial pressure is not
measured directly, we can estimate it and therefore make
changes in the miniaturial pressure to maintain cerebral
perfusion pressure. Patient drowsy and confused.
(46:37):
That is GCS 9 to 13. ICP approximately 20 millimetres
of mercury. GCS less than or equal to 8 ICP,
approximately 30 millimetres of mercury.
(47:01):
Measuring the adequacy of cerebral perfusion.
This is difficult as ideally adequacy of cerebral perfusion
will be determined at a cellularlevel to determine whether
neurons are receiving adequate oxygen and nutrients.
(47:26):
Inferences about cerebral perfusion can be made by looking
at a variety of measured variables.
The first five techniques can beused at the bedside and are
often part of multimodal monitoring of head injured
patients. The latter techniques are more
(47:51):
invasive and generally restricted to research
programmes measuring ICP and calculating CPP, which is the
most common method. Jugular venous bulb oxygen
(48:12):
saturations, that is, SJ VO2 usually 65 to 75%, reflects the
balance between cerebral oxygen delivery and CMRO 2.
A low jugular venous bulb oxygensaturation reliably indicates
(48:36):
cerebral hyperfusion. Transcrania Doppler to measure
blood velocity and estimate cerebral blood flow.
Micro dialysis catheters to measure glucose, pyruvate,
(48:58):
lactate, glycerol, glutamate that is metabolic variables.
Positron emission tomography, the distribution of radio
labelled water in the brain is monitored to indicate metabolic
activity. Functional Mr imaging
(49:24):
techniques. KT Smith's equation to determine
cerebral blood flow by using an innate carrier gas, that is
using xenon 133 and finally nearinfrared spectroscopy NIRS to
(49:46):
measure oxygenation in a localised cerebral field.
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