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Regulation of Cerebral Blood Flow Listen to Audio brain1_0.jpg cerebral perfusion pressure (CePP) autoregulation respiratory gas tensions temperature viscosity autonomic influences Cerebral Perfusion Pressure 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. Autoregulation 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) TEMPERATURE 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 VISCOSITY 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% AUTONOMIC INFLUENCES 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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