CBF
Regulation of Cerebral Blood Flow
cerebral perfusion pressure (CePP)
autoregulation
respiratory gas tensions
temperature
viscosity
autonomic influences
CePP = MAP - ICP
ex. 93 -10 = 83 mmHg
nl rangle: 80 - 100 mmHg
moderate to severe increase in ICP
may significantly compromise both CePP and CBF despite having a normal MAP
ex. ICP > 30 mmHg
CePP = MAP - ICP
93 - 33 = 60 mmHg
Since the normal range of CePP is 80 - 100 mmHg
Having a CePP of 60 mmHg may lead to cerebral impairment due to an moderaly to severe increase in ICP despite having a normal MAP.
constant cerebral blood flow despite changing cerebral perfusion pressures.
cerebral vasculature responds to changes to CePP usually within 10-60 seconds
abrupt changes in MAP may lead to changes to CBF
CBF is nearly constant when the MAP is between 60 - 160 mmHg
when the CBF is above or below the range of 60 -160 mmHg then the CBF is pressure dependant
Possible mechanisms involved
-myogenic: intrinsic response to smooth muscles in the cerebral aterioles with changes in MAP
-metabolic: metabolic demands dictate the arteriolar tone.
ex. when the demand (CMRO2) > supply (CBF)
metabolites help induce cerebral vasodilation in order to increase the CBF (supply)
possible mediators involved: nitric oxide, adenosine, prostaglandins, ionic gradients
RESPIRATORY GAS TENSIONS
-PaCO2
-PaO2
PaCO2
most important extrinsic influence on the CBF PaCO2 between 20-80 mmHg: the CBF is directly proportional to the PaCO2
changes in CBF +/- 1 to 2 ml/100gm/min: +/- 1mmHg PaCO2
effects are almost immediate due to the changes in pH of the CSF and cerebral tissue
the changes in pH are primarily from the CO2 concentration since it readily crosses the BBB
the effects of hypercarbia/hypocarbia diminish after 24-48 hrs due to the compensatory adjustments of HCO3- within the CSF
ex. hyperventilation: PaCO2 < 20 mmHg
(respiratory alkolosis: left shift on the O2 Dissociation Curve)
(left shift on the cerebral blood flow graph)
Therefore: decreased PaCO2 may suggest cerebral impairment even in normal individuals
PaO2
hyperoxia: has a minimal decrease (approximately 10%) in CBF
severe hypoxemia: has a profound increase in CBF
(PaO2< 50 mmHg)
CBF changes +/- 5-7% with every change +/- 1C in temperature
hyperthermia: increases CBF increases CMRO2 ex. @ 42C: oxygen demand and supply is increased with in CBF
hypothermia : decreases CBF decreases CMRO2 ex @ 20C: EEG is isoelectric
degree celcius CBF(ml/100gm/min) CMRO2
42 55
41 54
40 53
39 52
38 51
37 50 50ml 02/min
36 49
35 48
34 47
33 46
most important determining factor of blood viscosity is hematocrit levels
Increased hematocrit:
ex. polycythemia
increases blood viscosity and may reduce CBF
Decreased hematocrit
ex. anemia
decreases blood viscosity and may improve CBF
decreases oxygen carrying capacity
The combination of decreased oxygen carrying capacity and decreased CBF may lead to cerebral impairment due to decreased oxygen delivery (suppy) to meet the requirements of CMRO2 (demand)
optimal oxygen delivery
may occur at hematocrit of 30-34%
sympathetic tone : vasoconstricts intracranial vessels
parasympathetic tone: vasodilates intracranial vessels
noncholinergic/nonadrenergic tone: ex. seretonin, VIP
Cerebral physiology
-cerebral blood flow
regional cerebral blood flow (CBF) parallels cerebral metabolic activity (CMRO2)
CBF varies between 10ml blood/ 100 gm/min - 300 ml blood/ 100gm/min
average CBF: 50ml blood/ 100gm/min
grey matter: recieves 80 ml blood/min
white matter recieves 20 ml blood/min
Average brain 1500 gm
therefore: 1500gm x 50ml blood/100gm = 750 ml blood/ min
Decreased CBF may lead to cerebral impairment
CEREBRAL IMPAIRMENT: CBF: 20-25 ml blood/100 gm/min : slowing on EEG: CePP <50 mmHg
CBF: 15-20 ml blood/100 gm/min : isoelectric (flat)EEG CePP btn 25-40 mmHg
IRREVERSIBLE BRAIN DAMAGE: CBF: x< 10 ml blood/100 grm/min: CePP x< 25 mmHg
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