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NICU > Neuroanesthesia > Flashcards

Neuroanesthesia Flashcards

1
Q

ASA I (all surgery)

A

*Normal, healthy patient.
*0.08 % mortality within 48h
*0.06% mortality within 7 days

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2
Q

ASA II (all surgery)

A

II - mild systemic disease, no functional limitation
*0.27% mortality within 48h
*0.4% mortality within 7d

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3
Q

ASA III (all surgery)

A

III - severe systemic disease, definitive functional limitation
*1.8% mortality within 48h
*4.3% mortality within 7d

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4
Q

ASA IV (all surgery)

A

IV - severe systemic disease that is a constant threat to life
*7.8% mortality within 48h
*23.4% mortality within 7d

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5
Q

ASA V (all surgery)

A

V - moribund, expected to die within 24h with or without surgery.
*9.4% mortality within 48h
*50.7% mortality within 7d

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6
Q

ASA VI (all surgery)

A

VI- organ donor

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7
Q

WHat does the appendix “e” stand for in the ASA classification?

A

It means that emergency surgery is associated with 3x the risk compared to the given ASA % that are stated for elective surgey.

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8
Q

what factors determines CPP?

A

Cerebral perfusion pressure
- intact ?
- Blood pressure.
- ICP

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9
Q

Where should the srterial IV line be calibrated?

A

By meatus to etter reflect the intracranial BP.

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10
Q

How does the jugular venous pressure influence ICP?

A
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11
Q

What is the most potent cerebral vasodilator?

A

CO2.

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12
Q

What does hyperventilation create?

A

*Decreased CBV
*Decreased CBF

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13
Q

What is ETCO2?

A

End tidal Co2

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14
Q

How does ETCO2 correlate to arterial CO2?

A

Usually ETCO2 is approximately 5mmHg lower than in arterial blood.
The goal is PaCO2 30-35.

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15
Q

Why is the PaCO2 extra important in stereotactic surgery?

A

Due to the possible intracranial shifts when the bloodvolume changes.

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16
Q

WHy is hematocrit (Hct) important in neurosurgery?

A

Due to the O2 binding capacity in relation to the rheology.

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17
Q

What is the problem with hypOvolemia in neurosurgical cases?

A

It may impair blood flow.

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18
Q

What has to be thought of in prone position?

A

Excessive fluids can contribute to facial edema and PION in the worst case.

19
Q

Positioning changes!

A

During surgery, control of changes in position is necessary. It might be very dangerous to the patient.

20
Q

Postoperative nausea and vomiting must be avoided as much as possible.
Which anesthetic drugs should be avoided?

A
21
Q

What antiemetica might lower the seizure treshold?

A
22
Q

Why should inhalation anesthesia be avoided?

A

They REDUCE central metabolism by suppressing neuronal activity.
That might sound good BUT
They DISTURB CEREBRAL AUTOREGULATION and cause cerebral vasodilation.

23
Q

What is nitrous oxide doing in the brain?

A

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.

24
Q

What group of agents are primarily used today?

A

Halogenated agents like Isoflurane and Sevoflurane.
-all of which suppress EEG activity and provide cerebral protection.

25
Q

What drug is generally used for induction?

A

Propofol.
*unknown action. - but works as a sedative hypnotic.
*Short 1/2 life.
*no active metabolites.

26
Q

When Propofol is used as TIVA- total intravenous anethesia- What does it do to MAP and ICP?

A

It causes dose-dependent decrease in mean arterial blood pressure MAP and ICP.
* reduces CMRO2
* Reduces CBF and ICP
* Short 1/2 life.

27
Q

What barbiturate is usually used in induction?

A

Sodium thiopenthal.
* Rapid onset
* Short acting
* minimal effect on ICP, CBF and CMRO2

28
Q

What is the mechanism of Ketamine?

A
  • Its an NMDA receptor antagonist
  • It produces dissociative anesthesia.
  • Maintains cardiac output.
29
Q

Positives and NEGATIVES with nonsynthetic narcotics - morphine

A

+ : 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

30
Q

Why is histamine release not good in neuro-patients?

A
  • May cause hypotension
  • May cause cerebrovascular vasodilation
    ——CPP problems.—–
31
Q

What is good with synthetic narcotics?

A

They do not cause histamine release.

32
Q

Name two synthetic narcotics prominently used in neurosetting

A
  • Fentanyl
  • Remifentanil (ultiva)
33
Q

What is special with ultiva-remifentanyl?

A
  • Reduces CMRO2
  • Reduces CBV and ICP
  • Large doses might be toxic to the limbic system.
34
Q

What is special with Fentanyl?

A
  • Crosses BBB
  • Reduces CMRO2
  • Reduces CBV and ICP
  • May be given as bolus or infusion
35
Q

What is the action of Benzodiazepines and what are main (neuro) effects?

A
  • GABA agonists
  • Decrease CMRO2
  • Provide anticonvulsant action
  • Produce amnesia
36
Q

Name two commonly used paralytics

A
  • Succinylcholine
  • Rocuronium
37
Q

What is the only depolarizing agent used?

A

Succinylcholine.

38
Q

What side-effects make succinylcholin non-preferable in injuries or children/adolecsens?

A

Extra risk of Malignant hyperthermia.

39
Q

Which is the only non-depolarizing agent approved for rapid sequence intubation?

A

Rocuronium.

40
Q

What are anesthetic requirements for intraoperative evoked potential monitoring?

A

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.

41
Q

What is Malignant hyperthermia?

A

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!

42
Q

What is the incidence of Malignant hyperthermia?

A

Peds: 1:15000
Adults: 1:40000

43
Q

Treatment of Malignant hyperthermia?

A
  • 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.
44
Q
A

NICU (7 decks)

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