Neurophysiology - CBF & Metabolism Flashcards
At rest, the brain consumes oxygen at an average rate of ______ ml oxygen per 100 g of brain tissue (…or ____ml/min)?
3.5 ; 50 ml/min
The brain weighs approx. _____ g?
1350
The brain utilizes _____% of total body glucose?
25%
What percentage of of the brain’s energy consumption is used to support electrophysiologic function (EEG)?
60%
What percentage of the brain’s energy consumption is used to maintain cellular homeostasis?
40%
The brain requires _____ and _____ for sustained function?
oxygen and glucose
In the complete absence of glucose, glycolysis could only be maintained for _____ min.?
5 min
How is the brain’s high demand for oxygen and glucose met?
By adequate blood flow
CBF is almost completely supplied by ______ and _________?
Internal carotid and vertebral arteries, which provide input to the circle of willis
What is the purpose of the circle of willis?
permits collateral blood flow in the event that a major vessel becomes occluded.
What contains most of the cerebral blood volume?
The veins and dural sinuses
What is the CMRO2 for the brain?
3.0-3.8 ml/100g/min
At normocarbia, global CBF is stable between _____?
45-65 ml/100g/min
Describe CBF-CMRO2 Coupling?
Cerebral blood flow is coupled to CMRO2 - meaning that the higher CMRO2, the higher the CBF
Identify 2 factors that decrease CMRO2 and 2 factors that increase CMRO2?
DECREASE (sleep, coma, general anesthesia)
INCREASE (sensory stimulation, mental tasks, epileptic activity)
Between ___ and ___ degrees C - CBF and CMRO2 increase.
37 and 42 degrees C
Above ____ degrees C, a dramatic reduction in CMRO2 occurs.
42 degrees C - hyperthermia beyond 42 denatures proteins and destroys neurons. At this point, CBF decreases
The brain receives what percentage of the cardiac output?
12-15%
CMRO2 decreases by ___ for each 1 degree C reduction in temperature.
6-7%
EEG suppression occurs at what temperature?
18-20 degrees C
In general anesthetics decrease CMRO2 except…?
Ketamine and N2O
Increasing plasma concentrations of anesthetics beyond the level of initial EEG suppression…?
Does not further decrease CMRO2; (The CMRO2 required to maintain cellular integrity i snot altered by anesthetics, only the electrophysiological aspects of CMRO2)
What is Cerebral Perfusion Pressure (CPP)?
CPP= MAP - ICP (or CVP, which ever is higher)
What are the primary factors that control CBF in the normal brain?
- Carbon dioxide
2. Oxygen
What law relates to CPP?
Ohm’s Law (Flow=P/R or P=FxR)
What is the most potent physiologic determinant of CBF?
Carbon dioxide-
- 1 mmHg increase in PaCO2 = CBF increases by 1-2 ml/100g brain tissue/min
- 1 mmHg decrease in PaCO2 = CBF decreases by 1-2 ml/100g brain tissue/min
Doubling the normal PaCO2 to 80 mmHg will….
Double the CBF, above 80 mmHg there is a plateau which reflects maximum vasodilation - also a reduction in CMRO2 occurs reflecting the anesthetic effect of extreme hypercarbia
Reducing normal PaCO2 to one-half (20mmHg) will…
Approx half the CBF - decreasing PaCO2 below 20 mmHg has no effect d/t maximal vasoconstriction
Evidence suggests that the normal brain will tolerate a ____% decrease in CBF without ischemic changes.
50%
What abolishes the normal effect of PaCO2 on the vasculature system?
Abnormal or pathologic states
The PaCO2 effects on CBF are not sustained. CBF will return to normal ….
Over a period of 6-8 hours (CSF pH gradually returns to normal d/t retention of bicarbonate - metabolic compensation)
What happens when PaO2 below 60 mmHg?
CBF increases rapidly (the vasodilation is mediated by acidic metabolic products like lactic acid)
What is cerebral autoregulation?
CBF is constant between a CPP of 50-150 mmHg
What are the 3 components of the cranium and their volumes?
- Brain - 80%
- Blood - 12%
- CSF - 8%
CPP above 150 results in?
Hypertensive encephalopathy d/t BBB disruption, edema, and ischemia
CPP below 50 mmHg results in?
maximal vasodilation and CBF becomes pressure dependent
Chronic HTN shifts curve to the _____?
Right, the brain becomes more tolerant of HTN, but it also becomes less tolerant of hypotension
What abolishes cerebral auto-regulation? Why is this significant?
CVAs, tumors, SAH, AVMs, trauma, volatile anesthetics
When autoregulation is impaired, CPP becomes dependent on blood pressure.
What is the effect of volatile anesthetics?
All cause a dose related increase in CBF and a decrease in CMRO2.
Beyond 1 MAC - direct cerebrovasodilation which increases CBF and cerebral blood volume.
Sevoflurane effects?
Like isoflurane, it causes little or no increase in ICP at concentrations up to 1.5 MAC
N2O effects?
When used alone with oxygen N2O is a potent vasodilator and may increase ICP
Clinically, it may be prudent to discontinue N2O in the case of a “tight brain”
Intravenous Anesthetics?
Most produce a reduction in both CMR and CBF, and autoregulation and CO2 responsiveness are preserved in during IV anesthetic drug use.
*Ketamine causes increased CBF and CMR
Barbiturates?
Decrease both CBF and CMRO2
Have a direct vasoconstrictive effect
Incremental doses of pentothal and may decrease CBF and CMRO2 by _____%?
55-60%
Propofol?
Reduces CMRO2 and secondarily decreases CBF, CBV, and ICP
Etomidate?
Reduces ICP without causing a decrease in CPP
Benzodiazepines?
Reduce CBF d/t a decrease in CVR and CMRO2
Flumazenil?
Flumazenil reverses the benzo effects and may increase CBF and CMRO2 above pre-midazolam levels. –> Should be used with caution in patients with impaired intracranial compliance.
Ketamine?
Increases CMR and CBF (increased CMR will lead to vasodilation)
Sub-anesthetic doses (0.2-0.3mg/kg) can increase CMR by 25%
Should be avoided as a single anesthetic agent in patients at risk of high ICP
Narcotics?
Minimal to modest depressive effects on CBF and CMRO2.
Local Anesthetics?
- Rapidly cross the BBB d/t lipid solubility
- In subtoxic doses, LAs cause a modest decrease in CMRO2 and CBF
- Toxic doses that induce seizure activity will increase CMRO2 and CBF
Muscle Relaxants?
Muscle relaxation in general can reduce ICP by preventing coughing and straining, which results in lowered CVP
*SUX may cause an increase in ICP d/t increased cerebral input d/t fasiculations - can give a defasiculating dose
Atracurium?
Causes histamine release
Metabolite laudanosine readily crosses the BBB (may cause seizures in large doses)
Pancuronium?
In pts with intracranial pathology and defective auto-regulation, can increase CBF and ICP d/t tachycardia and HTN
Vecuronium?
No cerebral effects - was the most common muscle relaxant used in neurosurgical patients.
Rocuronium?
Similar to Vecuronium
