CBF & Its Regulation-1.2
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Transcript of CBF & Its Regulation-1.2
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Cerebral circulationerebral circulation
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Adult human brain weighs approx : 1350 gmabout 2% of body weight
Cranial vault rigid structure with a fixed total volumeBrain Tissue (80 %)Blood (12%)CSF (8%)
Recieves 12-15% of cardiac outputReflects brains high metabolic rate
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Normally brain consumes- 20% of total body O60% - to support neuronal activityto generate ATPS
Cerebral metabolic rate (CMR) measured interms of O consumption (CMR O )
Approx 3- 3.8mL/100g/min OR 50mL/min
Greatest in gray matter of cerebral cotrex
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CEREBRALCEREBRAL
METABOLISM:METABOLISM: 2% of body weight
17% of Cardiac output consumption at rest
20% of inspired oxygen
60% - for neuronal activity
40% - to maintain cellular integrity
CMR / CMRO 2 - 3-3.8ml/100g/min50ml/min
Cerebral glucose consumption - 5mg/100g/min
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cerebral blood flow
80% - Internal carotid arteries
20% - Vertebral arteries
Anterior n posterior communicatingarteries
Circle of Willis Communication between exl & int
carotids opthalmic arteries
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Circle of willis
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Physiology of CBF
Parallels with metabolic activity
Can vary from 10 300 ml/100g/min
Average 50ml/100g/min
Gray matter 80ml/100g/min
White matter- 20ml/100g/min
Total CBF- averages 750ml/min
< 20-25ml/100g/min- ischemia
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C BF
( m l / 1 0 0 g / m
i n )
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FACTORS CONTROLLING CBF
Intrinsic factors Myogenic Regulation
Metabolic Regulation
Neuronal Regulation
Hormonal Regulation
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FACTORS CONTROLLING CBF
Extrinsic factors Respiratory gas
Arterial BP Hematocrit Temperature
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SAFETY FACTOR
Normal brain receives
3x required oxygen
7x required glucose
Anoxia is the initial component of ischemia.
Hippocampus
cerebellem
Most sensitive to
hypoxic injury
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Cerebral perfusion pressure
CPP is the difference between Meanarterial pressure and intracranialpressure (or central venous pressure,which ever is greater)
CPP = MAP ICP
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CPP = MAP - ICP
Normal CPP 80 to 100mmHgMore dependent on MAP
ICP > 30mmHg compromise CPPCPP
< 50mmHg slowing of EEG25 40 mmHg flat EEG< 25 mmHg irreversible brain damage
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Cerebral auto regulation
Ability of the cerebral blood vessels to
alter their caliber in order to maintain aconstant flow in face of variations in
blood pressure
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Cerebral auto regulation
CBF is kept constant over a wide range of
MAP ( 50 160 mm Hg )
CPP = MAP CVP = MAP - ICP
MAP Cerebral vasoconstriction
MAP Cerebral vasodilatation
Constant CBF is maintained
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Cerebral auto regulation
graphPressures above160mmHg
Disrupts BBB
Cerebral edema
Haemorrhage
40 C B F
( m l / 1 0
0 g / m i n
)
60 120 180MAP (mmHg)
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Auto regulation
Autoregulatory changes take time
up to 60 sec
Large MAP changes may cause increasedCBF even in presence of intact autoregulation
In Hypertensive persons autoregulatory rangeshifts to higher pressure levels : 180 200mm Hg
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Dynamic v s Static
Dynamic auto regulation describes the
CBF response that takes place over
seconds in response to a sudden drop in
CPP.
Static / slower auto regulation is thesteady state achieved over 1 5 min
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Changes in autoregulation
Absent ( Vasomotor paralysis )brain traumasurgical retraction
high ICPbrain tumor seizures
Shift to rightSystemic hypertension
States of sympathetic activationShift to left
Volatile anesthetic agents
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FACTORS CONTROLLING CBF
Intrinsic factorsMyogenic Regulation
Metabolic Regulation
Neuronal Regulation
Hormonal Regulation
Extrinsic factorsRespiratory gas
Arterial BPHematocritTemperature
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Myogenic factors
Is the intrinsic response of smooth muscle cells in cerebralarterioles to changes in MAP
Protective mechanism againstexcessive pressure fluctuationat capillary level
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Metabolic regulation
NO
Hydrogen ions
potassium
adenosine
prostanoids
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Innervation
The sympathetic fibers arise mainly from thesuperior cervical ganglion
The parasympathetic from the sphenopalatineand otic ganglia
Sensory fibers from the trigeminal ganglion
The functional significance of neural innervationshas yet to be elucidated.
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Neuronal regulation
-Adrenergic receptors in arterial smooth muscle
Postganglionic sympathetic fibers releasenoradrenaline
Causes smooth muscle contraction and
arterial constriction
Sympathetic innervation is responsible for vascular tone
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Sympathetic
Large & Medium sized arteries
normally overridden by autoregulation
Historically thought to have no role in cerebral circulation
Comes into play in states of excessive circulatoryactivity / pathologic states
Role in prevention of cerebral hge cerebral vasospasm
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Effect of CO 2 on CBF
CBF directly proportional to PaCO2 between tension 20 80 mmHg
1mmHg PaCO2- CBF by 1-2ml/100g/min
After 24 48 hrs CSF HCO 3 - compensation limits theeffects of hypocapnia/ hypercapnia
Persistent hyperventilation L/ODC cerebralimpairment
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Hypercarbia - CBF
The relationshipbetween PaCO2 andCBF is sigmoid
with plateaus below25 mmHg and above75 mmHg.
The slope isapproximately linear
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Mechanism of CO 2 on CBF
The mechanism of CO 2 induced changes in vessel caliber
An increase in perivascular H+ concentration
Associated NOS activation
An increase in intracellular cGMP
K+ efflux
A reduction in intracellular Ca + + resulting in dilation
NOS inhibition attenuates the
Cyclooxygenase inhibition CBF response to CO 2
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Effect of oxygen
Hyperoxia minimal decrease in CBF
10%
Severe hypoxia PaO 2 < 50mmHg
Increases CBF
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Haematocrit
in haematocrit
viscosity CBF
O 2 carrying capacity
haematocrit viscosity
CBF
Optimal haematocrit
30% to 34%
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Temperature
CBF changes 5- 7% per OC
Hypothermia CBF & CMR
Pyrexia has reverse effect
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Clinicalapplication
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Applied aspects
Effects of anesthetic drugs on CBFVolatile anesthetics
Induction agentsAnesthetic adjunctsVasopressorsVasodilatorsNeuromuscular blocking agents
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Volatile agents
Volatile agents dose dependent dilatation of
cerebral vessels
Impair auto regulation
Response to CO 2 retained
May increase cerebral blood volume
May result in elevated ICP
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HalothaneHas greatest effect onCBFCon.> 1% -abolishes auto
regulationGeneralized increasein CBFAt equivalent MACCBF up to 200%Prior hyperventilationto be initiated
IsofluraneCBFAuto regulation maintained upto 1 MAC
is > in sub cortical thanneocortical areas
At equivalent MACCBF up to 20%Simultaneous hyperventilationcan prevent in ICP
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Sevoflurane :CBF effects similar to isofluraneProduce slightly less vasodilationAuto regulation maintained up to 1.5 MAC
Desflurane:CBF similar to isofluranebut at >1 MAC > sevoflurane.Autoregulation progressively abolished as doseincreases
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Nitrous Oxide:When administered on its own- increasesboth CBF and metabolism.
when added to a background of another anesthetic, it increases CBF withoutchanging metabolism
It is a direct acting and potent cerebralvasodilator
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IV induction agents
Intravenous anesthetics reduce CBF ina dose dependent fashion
coupled to the reduction in metabolism
Once maximal suppression of
metabolism occurs, no further reductionin CBF occurs
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Barbiturates
Barbiturates maximal 50% reduction in CBFand metabolism
CO2 reactivity is maintained but is quantitativelyreduced compared to the awake response
Cerebral auto regulation maintained
intact
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Propofol
Propofol produces a coupled dose dependentreduction in CMRO 2 and CBF
High doses vasodilator effect overcomes thecoupling & CBF increases
Both CO2 responses and auto regulation are
maintained intact in the normal brainIn head injured patients static auto regulationmay be impaired by high propofol infusion rates
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Ketamine
Dilates the cerebral vasculature andincreases CBF ( 50 60%)
Increases in CBF, CBV, CSF volume canincrease ICP markedly in patients withdecreased IC compliance
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Opioids
Opioids at low doses produce very little effect onCBF (provided CO2 is not allowed to rise)
Auto regulation remains intactBP vasodilatation to maintain CBF
cerebral blood volume
increase intracranial pressure.
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Vasopressors
With intact auto regulation & BBB
in CBF occurs when
MAP150 160mmHg
In the absence of auto regulation,
vasopressors CBF
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Vasodilators
In the absence of hypotension
Cerebral vasodilatation
CBFWith Hypotension
CBF is maintained
CBV & ICP in patients with ICcompliance
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NMBD
No direct effect on CBF
Histamine releasing agents can causehypotension , CPP
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Thank you