Neuroanesthesia Flashcards
ASA I (all surgery)
*Normal, healthy patient.
*0.08 % mortality within 48h
*0.06% mortality within 7 days
ASA II (all surgery)
II - mild systemic disease, no functional limitation
*0.27% mortality within 48h
*0.4% mortality within 7d
ASA III (all surgery)
III - severe systemic disease, definitive functional limitation
*1.8% mortality within 48h
*4.3% mortality within 7d
ASA IV (all surgery)
IV - severe systemic disease that is a constant threat to life
*7.8% mortality within 48h
*23.4% mortality within 7d
ASA V (all surgery)
V - moribund, expected to die within 24h with or without surgery.
*9.4% mortality within 48h
*50.7% mortality within 7d
ASA VI (all surgery)
VI- organ donor
WHat does the appendix “e” stand for in the ASA classification?
It means that emergency surgery is associated with 3x the risk compared to the given ASA % that are stated for elective surgey.
what factors determines CPP?
Cerebral perfusion pressure
- intact ?
- Blood pressure.
- ICP
Where should the srterial IV line be calibrated?
By meatus to etter reflect the intracranial BP.
How does the jugular venous pressure influence ICP?
What is the most potent cerebral vasodilator?
CO2.
What does hyperventilation create?
*Decreased CBV
*Decreased CBF
What is ETCO2?
End tidal Co2
How does ETCO2 correlate to arterial CO2?
Usually ETCO2 is approximately 5mmHg lower than in arterial blood.
The goal is PaCO2 30-35.
Why is the PaCO2 extra important in stereotactic surgery?
Due to the possible intracranial shifts when the bloodvolume changes.
WHy is hematocrit (Hct) important in neurosurgery?
Due to the O2 binding capacity in relation to the rheology.
What is the problem with hypOvolemia in neurosurgical cases?
It may impair blood flow.
What has to be thought of in prone position?
Excessive fluids can contribute to facial edema and PION in the worst case.
Positioning changes!
During surgery, control of changes in position is necessary. It might be very dangerous to the patient.
Postoperative nausea and vomiting must be avoided as much as possible.
Which anesthetic drugs should be avoided?
What antiemetica might lower the seizure treshold?
Why should inhalation anesthesia be avoided?
They REDUCE central metabolism by suppressing neuronal activity.
That might sound good BUT
They DISTURB CEREBRAL AUTOREGULATION and cause cerebral vasodilation.
What is nitrous oxide doing in the brain?
It potently vasodilate. Increase CBF and also a little the cerebral metabolism.
Contributes to postoperative nausea and vomiting N/V.
EXCEPT FOR THAT! It is uterly dangerous in the setting of air embolus or pneumocephalus, where it fills the air space and increase the pressure A LOT.
What group of agents are primarily used today?
Halogenated agents like Isoflurane and Sevoflurane.
-all of which suppress EEG activity and provide cerebral protection.
What drug is generally used for induction?
Propofol.
*unknown action. - but works as a sedative hypnotic.
*Short 1/2 life.
*no active metabolites.
When Propofol is used as TIVA- total intravenous anethesia- What does it do to MAP and ICP?
It causes dose-dependent decrease in mean arterial blood pressure MAP and ICP.
* reduces CMRO2
* Reduces CBF and ICP
* Short 1/2 life.
What barbiturate is usually used in induction?
Sodium thiopenthal.
* Rapid onset
* Short acting
* minimal effect on ICP, CBF and CMRO2
What is the mechanism of Ketamine?
- Its an NMDA receptor antagonist
- It produces dissociative anesthesia.
- Maintains cardiac output.
Positives and NEGATIVES with nonsynthetic narcotics - morphine
+ : Increase CSF absorption and minimally reduce cerebral metabolism.
- :
* Cause dose-dependent respiratory depression —hypercarbia in the non-ventilated patient.
*N/V postop.
* Cause histamine release
* Can accumulate in renal or hepatic insufficient patient and cause confusion
Why is histamine release not good in neuro-patients?
- May cause hypotension
- May cause cerebrovascular vasodilation
——CPP problems.—–
What is good with synthetic narcotics?
They do not cause histamine release.
Name two synthetic narcotics prominently used in neurosetting
- Fentanyl
- Remifentanil (ultiva)
What is special with ultiva-remifentanyl?
- Reduces CMRO2
- Reduces CBV and ICP
- Large doses might be toxic to the limbic system.
What is special with Fentanyl?
- Crosses BBB
- Reduces CMRO2
- Reduces CBV and ICP
- May be given as bolus or infusion
What is the action of Benzodiazepines and what are main (neuro) effects?
- GABA agonists
- Decrease CMRO2
- Provide anticonvulsant action
- Produce amnesia
Name two commonly used paralytics
- Succinylcholine
- Rocuronium
What is the only depolarizing agent used?
Succinylcholine.
What side-effects make succinylcholin non-preferable in injuries or children/adolecsens?
Extra risk of Malignant hyperthermia.
Which is the only non-depolarizing agent approved for rapid sequence intubation?
Rocuronium.
What are anesthetic requirements for intraoperative evoked potential monitoring?
INDUCTION:
* Minimize pentothal or use etomidate
*! Use TIVA NOT inhalation.
+ Obs nondepolarizing muscle relaxants have little effect on evoked potentials!
+ Propofol has mild effect on evoked potentials,
*continous infusion should be used, not boluses.
* Obs! SSEPs can be affected by hyper or hypothermia and by changes in BP.
+ Hypocapnia, down to end tidal CO2 21 has no effect on peak latencies
+ Antiepileptic drugs have NO effect on SSEPs.
What is Malignant hyperthermia?
Idiopathic block of Ca 2+ re-entry into SR.
Genetic predisposal
Body O2 consumption raise by 2-3 times.
Fulminant form -muscle ridgidity so intubation is impossible.
+ if progressing; DIC, pulomnary edema, Rhabdomyolysis, cardiac arrest and death
!!!! Frequently associated by use of Succinylcholine!
What is the incidence of Malignant hyperthermia?
Peds: 1:15000
Adults: 1:40000
Treatment of Malignant hyperthermia?
- Eliminate offending agent
- DANTROLENE SODIUM - 2.5mg/kg iv up to 10mg/kg until symtoms subside.
- Hyperventialtion w 100% oxygen.
- Cooling
- Bicarbonate for acidosis
Procainamide for arrythmias - Diuresis - volume loadinga nd osmotic diuresis.
