3. Cerebral Blood flow Flashcards
Composition
The brain weighs 2% of the human organism yet receives 15% of the cardiac output.
The intracranial contents consist of brain tissue (approximately 1,400–1,500 g),
blood (100–150 ml), CSF (110–120 ml) and extracellular fluid (<100 ml).
Normal cerebral blood flow (CBF)
Normal cerebral blood flow (CBF): normal CBF is 50 ml 100 g-1 of brain tissue per
minute, and is determined by the
Cerebral perfusion pressure (CPP).
The CPP = MAP – (CVP + ICP). The normal CPP is 70–80 mmHg.
Blood flow to grey matter is
more than twice that to white matter.
Autoregulation
Over a wide range of MAP,
typically between 50 and 150 mmHg,
autoregulation maintains normal flow.
The process is not instantaneous, and may take some seconds to complete.
The classic cerebral autoregulation curve is an oversimplification;
there is not a neat linear relationship between MAP and CBF at
each end of the curve, and changes in perfusion pressure may be regional.
Chronic hypertension shifts the autoregulatory curve to the right; drug-induced hypotension shifts it to the left (Figure 3.10).
The mechanisms which underlie autoregulation are
primarily myogenic, modulated by stretch receptors in vascular smooth muscle, and
metabolic, in which hydrogen ions and substances such as nitric oxide and adenosine
accumulate in the tissues at low flow and mediate vasodilatation.
PaCO2:
PaCO2: there is a linear relationship between PaCO2 and CBF in the range of partial
pressures from 3.5 to 10.0 kPa.
Below 3.5 kPa, cerebral vasoconstriction leads to tissue hypoxia (with subsequent reflex vasodilatation); at around 10.0–12.0 kPa there is a ceiling at which blood flow is maximal (at around 120 ml 100 g1 min1)
PaO2
: decreases in the partial pressure of oxygen below 8 kPa
are associated with sharp increases in CBF up to around 110 ml 10
0 g1 min1. At 4.0 kPa, CBF is
doubled. Hyperoxia is associated with decreases in CBF (Figure 3.12).
Temperature:
Changes in temperature are associated with altered requirements for
cerebral oxygen (the cerebral metabolic rate for oxygen, CMRO2),
Although the relationship is linear rather than exponential.
Thus, while at 37C, a 1 C drop in
temperature is accompanied by a fall in CMRO2 of 6–7%;
at a brain temperature of
15 C (during deep hypothermic circulatory arrest, for example), a further 1 C drop
results in a decrease in CMRO2 of only 1%.
CMRO2:
CBF is linked to CMRO2 by a mechanism that has not yet been fully
elucidated. There is a short lag time of 1–2 minutes.
Rheology
Rheology: lower plasma viscosity is associated with enhanced capillary flow,
although there is a balance between optimal rheology and oxygen delivery.
A haematocrit above 50% risks intravascular sludging and a reduction in CBF, and
a haematocrit below 30% is associated with decreased oxygen flux
Measurement of Cerebral Blood Flow
Kety–Schmidt method: this is an application of the Fick principle, which states that
flow is equal to the amount of a substance taken up or excreted by an organ, divided
by the arteriovenous (AV) concentration difference
itrous oxide is used as the
diffusible tracer. The subject breathes 10% N2O for 10 minutes, during which time
paired peripheral arterial and jugular venous bulb samples are taken
Transcranial Doppler ultrasonography
Transcranial Doppler ultrasonography: this gives a measure of the velocity of red
cells flowing through large cerebral arteries, most commonly the middle cerebral, and
can be used in clinical practice. The velocity can give an index of flow provided that
the diameter of the artery is determined independently, and provided that this
diameter changes little (as is the case with the major cerebral arteries).
Anaesthesia and Cerebral Blood Flow
IV agents
Intravenous induction agents: all except for ketamine reduce CMRO2, and as a
result CBF falls in tandem.
Autoregulation is not affected. Ketamine increases MAP,
which leads to a rise in blood flow
Anaesthesia and Cerebral Blood Flow
Volatile anaesthetic agent
Volatile anaesthetic agents: these uncouple CBF and CMRO2.
They reduce CMRO2 but are associated with a rise in CBF secondary to their capacity to
vasodilate the cerebral circulation and abolish autoregulation.
The response to changes in PaCO2 is unchanged.
This action is dose-dependent but can partly be
offset by the vasoconstrictor effect of hyperventilation. Autoregulation is abolished
by 1.5 MAC of all the agents bar sevoflurane. This has only 30% of the
vasodilatory potential of isoflurane and does not impair autoregulation. Nitrous
oxide increases CBF by increasing the CMRO2, while also affecting autoregulatory
mechanisms.
Opioid
Opioids: opioids have little direct effect,
but CBF will rise in response to CO2
retention should respiratory drive be depressed.
Arterial pressure:
chronic hypertension shifts the autoregulatory curve to the right,
while drug-induced hypotension shifts it to the left (Figure 3.10). If autoregulation is
attenuated by the use of volatile anaesthetics, then CBF and ICP will rise in parallel
with an increase in MAP.
Venous pressure
Venous pressure: Any of the many factors which increase venous pressure, such as
position, coughing, straining against a ventilator, impeded drainage from the head
and neck, volume overload or the use of IPPV and PEEP, will decrease CPP and
reduce CBF.
