Neuro Flashcards
What is minimal level of cerebral metabolic rate of O2 consumption (CMRO2)?
3mL/100g/min (adults)
What is the average cerebral blood flow (CBF)?
What is the level for cerebral impairment?
50mL/100g/min
20-25mL/100g/min
How do you calculate cerebral perfusion pressure (CPP)?
What is normal values?
MAP - ICP or MAP - CVP
80-100 mmHg
Pressure auto regulation of cerebral vasculature keeps the CCP between what MAP values?
How does the vasculature respond to high or low MAP values?
What happens to these values during chronic HTN?
50-150 mmHg
High MAP = vasoconstriction (if too high, cerebral edema and hemorrhage can occur)
Low MAP = vasodilation (if too low, ischemia occurs)
They can reset
How is CBF affected by CO2?
How long does this effect last?
*lOw CO2 = vasOconstriction (decreases CBF/CPP)
Only CO2 (NOT HCO3) crosses the BBB
After 24-48 hours, CSF HCO3 compensates for PaCO2
How does CO2 affect the Hgb dissociation curve?
Low CO2 shifts curve to L –> decreased O2 unloading at the tissues
How does Hct effect CBF auto regulation?
Decreased Hct (hemorrhage) = decreased viscosity –> increased flow but decreased O2 carrying capacity
How do volatile anesthetics affect the CMR and CBF coupling?
Uncoupling –> decreased metabolic demand of brain with INCREASED CBF
- Decrease CMR
- Vasodilation of cerebral vasculature
Value for normal ICP?
Value for intracranial HTN?
10 mmHg
> 15 mmHg
Describe circulatory steal phenomenon?
Ischemic areas of the brain are already maximally dilated –> no increase in blood flow
There is increased blood flow to “NORMAL” perfused areas via vasodilation and this redistributes blood away from the ischemic areas
Effect of barbiturates on CNS?
Decreases CBF, ICP, CMRO2 INCREASES CPP (the decrease in ICP is greater than the decrease in MAP)
What is the Robin Hood Phenomenon?
“Normal” vessel vasoconstriction from decreased metabolic rate redistributes blood to ischemic areas which are maximally dilated already
Propofol effect on CNS?
Decreases CBF, ICP, CMRO2
What side effect must you monitor for with use of etomidate on CNS?
Myoclonic movements (NOT seizures)
*Also causes decrease of CBF, ICP (like propofol)
Ketamine effects on CNS?
When not to use ketamine?
INCREASES CBF, ICP, CMRO2
*Increased ICP (trauma, tumors)
Signs of increased ICP?
Headache Nausea/Vomiting Papilledema Focal neuro deficits Altered consciousness
What can occur if the ICP continues to rise (aside from herniation)?
Decreased CBF –> brain ischemia –> ischemia leads to cerebral edema/swelling –> further increases the ICP -> more ischemia and cycle repeats
What is Cushing triad of increased ICP?
1) HTN
2) Bradycardia
3) Irregular respirations
*Denotes extremely high ICP (last ditch effort of body to decrease ICP)
What are ways to decrease ICP?
1) Mannitol (osmotic diuretic –> hyperosmolar)
2) Hyperventilation (causes LOW CO2 = vasoconstriction of cerebral vasculature)
3) Corticosteroids (dexamethasone promotes repair of BBB and decreases inflammation and subsequent edema)
4) Loop diuretics
5) IV anesthetic agents (NOT inhaled gases)
Methods the brain uses to protect against ischemia?
1) Optimize CPP (increase MAP or decrease CVP)
2) Normoglycemia (less anaerobic metabolism and lactic acid production)
3) **Normocarbia
**Low PaCO2 = vasoconstriction = aggravates ischemia
**High PaCO2 = vasodilation = steal phenomena w/ focal ischemia
4) Hypothermia (32C) - decreases CMRO2 and CBF
5) **Magnesium (blocks excitatory neurotransmitters after traumatic injury)
also crosses BBB to prevent edema
6) Anesthetic agents (barbs, etomidate, propofol all lower CMR)
Why is TIVA a good choice for neuro cases?
Allows for intra-op NM monitoring if needed (can’t use long lasting paralytics)
During cranial cases, what 2 renal complications can occur and what area is usually involved in the brain?
Proximity to Pituitary gland
1) Cerebral salt wasting –> kidney looses ability to reabsorb Na and end up peeing out tons of Na and fluid
2) Central DI –> peeing out lots of water but holding onto Na
How do you differentiate b/w cerebral salt wasting syndrome and SIADH?
Urine studies
CSW: urine osmolarity is low + high flow rate
SIADH: very concentrated urine + low flow rate
With Conn syndrome, what 2 factors must be addressed intraoperatively?
1) Hemodynamic changes
Manipulation of adrenal gland can cause release of catecholamines
2) Hypokalemia
Avoid respiratory alkalosis (PaCO2 reflection of H+ levels)
Avoid sevoflurane use (induces polyuria)
Can prolong the action of NMB agents
