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CPAN Reviewer > Anesthesia Agents/ Adjuncts/ Reversal > Flashcards

Anesthesia Agents/ Adjuncts/ Reversal Flashcards

1
Q

What is ASA Score?

A

Rates physical status of patient assessed prior to receiving sedation/ anesthesia.

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2
Q

What are the different ASA Scores/ levels?

A

ASA 1 Healthy Pt
ASA 2 Healthy Pt with mild systemic disease (BMI>30)
ASA 3 Pt with severe systemic disease that limits activity
but not incapacitating (BMI>40)
ASA 4 Pt with severe systemic disease that is constant
threat to life

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3
Q

What are the different ASA Scores/ levels?

A

ASA 5 Pt not expected to survive without urgency
ASA 6 Pt brain dead to OR for organ harvest
ASA E Any emergency surgical procedure

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4
Q

What is general anesthesia?

A

State of reversible unconsciousness where protective reflexes are partially or completely lost.

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5
Q

What is monitored anesthesia care?

A

Relaxed, non-paralyzed state of analgesia and sedation
Pt maintains airway independently
Responds to verbal commands
!Administered by anesthesiologist/ CRNA

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6
Q

What is the 1st stage of anesthesia?

A

Begins with initiation and ends with loss of
consciousness
Protective reflexes maintained
!Patient feels conscious but drowsy
!Patient can follow simple commands
!Perception of pain is diminished

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7
Q

What is the 2nd stage of anesthesia?

A

!Delirium/ Excitation (highest risk stage)
!Begins with loss of consciousness and ends with loss of
protective reflex
!Breath holding
!Dilated pupils
!Irregular respirations
!Muscle tone intact

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8
Q

What is the 3rd stage of anesthesia?

A

Anesthetized - Surgical Anesthesia
Begins with regular breathing pattern to respiratory
cessation
Absent protective reflexes
No eyelash response, lid reflex
No spontaneous respiration
No response to surgical incision
Surgery occurs during this stage

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9
Q

What is the 4th stage of anesthesia?

A

Overdose (coding stage)
Depression of vital functions
Respiratory cessation
Cardiac / circulatory collapse

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10
Q

How does emergence from anesthesia occur?

A

!Reverse order of induction
Anesthesia agents titrated off
Influenced by
Duration of anesthesia
Use of other drugs
Physical status of patient

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11
Q

What is the patient at risk for during the anesthesia stage of delirium?

A

Vomiting
Laryngospasm
Cardiac arrest

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12
Q

Where is the HIGH blood flow area for volatile & gaseous inhalation agents?

A

Kidney
Liver
Brain
Heart
Endocrine glands

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13
Q

Where is the MODERATE blood flow area for volatile & gaseous inhalation agents?

A

Muscle
Skin

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14
Q

Where is the POOR blood flow area for volatile & gaseous inhalation agents?

A

Fat
Bone marrow
Avascular tissue

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15
Q

Part of body with slowest elimination of volatile & gaseous inhalation agents

A

!Fat group - serves as area for anesthesia to linger. Thus more fat takes longer to eliminate anesthesia.

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16
Q

Why is SEVOFLURANE ( volatile & gaseous inhalation agent) good for induction and pediatrics?

A

!Pleasant, non irritating odor

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17
Q

What are safety profiles of SEVOFLURANE ( volatile & gaseous inhalation agent)?

A

Does not sensitize myocardium
No effect on hepatic blood flow
Safe for pts with seizure disorder
(d/t minimal increase ICP)

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18
Q

What are precautions for SEVOFLURANE ( volatile & gaseous inhalation agent)?

A

!Potentiates neuromuscular blockade

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19
Q

How is SEVOFLURANE ( volatile & gaseous inhalation agent) degraded?

A

!Degraded through exposure with soda lime

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20
Q

What is HALOTHANE ( volatile & gaseous inhalation agent) good for induction and pediatrics?

A

!Pleasant non-irritating odor
Commonly used in pediatrics

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21
Q

What are precautions for HALOTHANE ( volatile & gaseous inhalation agent)?

A

Can cause:
!Increased ICP
Myocardial depression
Impaired AV node function
Halothane hepatitis

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22
Q

How is HALOTHANE ( volatile & gaseous inhalation agent) metabolized and excreted?

A

Metabolized in liver
Excreted 80% lungs, 20% kidneys

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23
Q

Why is ISOFLURANE ( volatile & gaseous inhalation agent) only used as maintenance anesthesia?

A

Pungent, irritating odor

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24
Q

What is the benefit of administering ISOFLURANE ( volatile & gaseous inhalation agent)?

A

Increases coronary blood flow

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25
Q

What are precautions for ISOFLURANE ( volatile & gaseous inhalation agent)?

A

Causes vasodilation - post operative shivering
Potentiates neuromuscular blockade

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26
Q

How is ISOFLURANE ( volatile & gaseous inhalation agent) metabolized and excreted?

A

Eliminated by exhalation
Excreted by kidneys

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27
Q

Why is DESFLURANE ( volatile & gaseous inhalation agent) used as maintenance anesthesia only?

A

Pungent, irritating odor

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28
Q

Why is the advantage of administering DESFLURANE (volatile & gaseous inhalation agent)?

A

!Rapid onset and offset due to extremely low solubility in blood

29
Q

What are precautions for DESFLURANE (volatile & gaseous inhalation agent)?

A

Causes vasodilation - post operative shivering
Potentiates neuromuscular blockade

30
Q

How is DESFLURANE (volatile & gaseous inhalation agent) metabolized and excreted?

A

Eliminated through exhalation

31
Q

What is an induction agent?

A

Administered to induce anesthesia so anesthesia is initiated easily without residual effects.

32
Q

What is etomidate (induction agent)?

A

Hypnotic only, no analgesic

33
Q

What is the side effect of Ketamine (induction agent)?

A

Hallucination

34
Q

What is important to know about propofol (induction agent)?

A

!Fat based
!Contraindicated with patients with sensitivity to soybean oil, egg, lecithin, glycerol

35
Q

What are anesthesia adjuncts?

A

Administered to enhance anesthesia but not considered anesthetics. May serve to reduce anxiety, sedate patient, reduce oral/ respiratory secretions.

36
Q

What is droperidol (anesthesia adjunct)?

A

Antiemetic

37
Q

What is dexmedetomidine (anesthesia adjunct)?

A

Non-opioid IV anesthetic
Controls stress, anxiety, and pain but no respiratory depression

38
Q

What is the important characteristic of muscle relaxants?

A

!Do not cross blood brain barrier

39
Q

Why are muscle relaxants needed?

A

To relax jaw and larynx during intubation
To relax skeletal muscle for surgery

40
Q

What prolongs the action of muscle relaxants?

A

Hypothermia

41
Q

What is the sequence of PARALYSIS for muscle relaxants?

A

Fine motor -> Gross motor
Eyes > Jaw > Hands > Limbs > Neck > Intercoastal Muscle > Diaphragm

42
Q

What is the sequence of RECOVERY for muscle relaxants?

A

Reverse of paralysis
Diaphragm > Intercoastal Muscle > Neck > Limbs > Hands > Jaw > Eyes

43
Q

What is succinylcholine (depolarizing muscle relaxant)?

A

!Causes muscle to contract by binding to muscle cell receptor sites, competes with acetylcholine
!Succinylcholine binds longer than acetylcholine
Ultra short acting (5-10 min)
Antinicotinic medication

44
Q

What are the effects of succinylcholine (depolarizing muscle relaxant)?

A

!Fasciculations
!Myalgia
Can stimulate vagal nerve - bradycardia
Mild histamine release - rashes on arms/ chest
Increase ICP
Increased release of k+ to extracellular fluid

45
Q

What is “defasciculation”?

A

Administration of non depolarizing muscle relaxant prior to succinylcholine to prevent muscle twitch/ fasciculation.

46
Q

29 y/o male admitted s/p fasciotomy for bilateral crush injuries of legs experiences partial laryngospasm when extubated. While preparing to intubate, anesthesia ask RN to administer succinylcholine 20mg IV. The RN shoud:

  1. refuse to administer medication
  2. request anesthesiologist to repeat dosage
  3. dilute drug with 10cc NS before administration
  4. titrate drug over 3 minutes
A

dilute drug with 10cc NS before administration

47
Q

How is succinylcholine (depolarizing muscle relaxant) eliminated in the body?

A

Broken down by plasma cholinesterase aka pseudocholinesterase

48
Q

Which part of the body produces pseudocholinesterase (depolarizing muscle relaxant)?

A

Produced by the liver
Pseudocholinesterase level directly related to albumin level

49
Q

Who can have pseudocholinesterase (depolarizing muscle relaxant) deficiency?

A

Inherited
Advanced age, renal failure, malnutrition, hepatic disease

50
Q

What is the effect of pseudocholinesterase deficiency (depolarizing muscle relaxant)?

A

!Prolonged paralysis that can lead to ventilation in PACU
!Tincture of time

51
Q

Patient had recent (past 2-4 days) neuromuscular injury. Why can’t patient receive succinylcholine (depolarizing muscle relaxant)?

A

Can cause life threatening levels of K+ release
(e.eg. major burns, multiple trauma, CVA, denervation of muscles, recent spinal cord injury - within 6 months)

52
Q

Patient has chronic illness. Why can’t patient receive succinylcholine (depolarizing muscle relaxant)?

A

Risk for hyperkalemia
(e.g. prolonged immobilization, atrophy, critically ill)

53
Q

Other medical conditions when patient can not be administered with succinylcholine (depolarizing muscle relaxant)?

A

Children with muscular dystrophies
!History or family history of malignant hypothermia because succinylcholine can trigger MH

54
Q

Patient developed respiratory failure and required intubation. Succinylcholine IV to be administered as part of rapid sequence intubation. Perianesthesia RN knows to have which drug ready to counteract fasciculations?

  1. benzodiazaphines
  2. non-depolarizing muscle relaxants
  3. antihistamines
  4. sustained released anticonvulsants
A

non-depolarizing muscle relaxants

55
Q

What are non-depolarizing muscle relaxants?

A

Blocks acetylcholine from binding to muscle receptor sites. Thus muscle is unable to contract.

56
Q

What medications enhance NDMR paralysis?

A

Aminoglycosides
! Calcium Channel Blockers
Clindamycin
Lithium
Magnesium
Tetracycline
Volatile anesthetics

57
Q

What physiological factors enhance NDMR paralysis?

A

Respiratory Acidosis
!Hypothermia
Dehydration
HYPERcapnia
Hypokalemia
Hyponatremia
HYPERmagnesemia

58
Q

What are considered NDMR antagonists?

A

!Caffeine Hypocapnia
Reversal agents HYPERkalemia
Epinephrine HYPERnatremia
Norepinephrine Respiratory Akalosis
Theophylline

59
Q

Name the long acting NDMRs?

A

!Tubocurarine
!Doxacurium
!Pancuronium
!Pipecuronium

60
Q

What are NDMR reversal agents?

A

!Anticholinesterase agents - inhibit breakdown of acetylcholine

61
Q

What are common NDMR reversal agents?

A

!Sugammadex - reverses rocuronium and vecuronium
Neostigmine - must be given with glycopyrrolate
Edrophonium - must be given with atropine
Pyridostigmine - given with glycopyrrolate

62
Q

What to watch out for in administering Sugammadex (NDMR reversal agent)?

A

!Decreases serum concentration of estrogen and progestin derivatives

63
Q

What is the mechanism of action for neostigmine (NDMR reversal agent)?

A

Neostigmine binds to acetylcholinesterase, thus increases the number of acetylcholine

64
Q

What is the mechanism of action for Sugammadex (NDMR reversal agent)?

A

Sugammadex binds to NDMR, thus acetylcholine can occupy receptor sites

65
Q

Why atropine or glycopyrrolate is administered with the NDMR reversal agent?

A

Significant increase in vagal tone can lead to profound bradycardia/ asystole.
Atropine and glycopyrrolate are anticholinergics.

66
Q

Patient reversed with endrophonium and atropine. The reason for atropine administration is:

  1. decrease likelihood of vomiting
  2. promote acetylcholine release
  3. enhance onset of nueromuscular reversal
  4. minimize muscarinic stimulation
A

minimize muscarinic stimulation

67
Q

What is residual paralysis (in NDMR)?

A

Reversal agent wears off before the breakdown of NDMR
!common sign fish mouth breathing

68
Q

What type of medication is glycopyrrolate?

A

Anticholinergic
A quaternary amine used in anesthesia to decrease salivary and tracheal secretions, per National Library of Medicine

69
Q

Why is glycopyrrolate given with neostigmine?

A

Neostigmine binds to acetylcholinesterase, thus increases the number of acetylcholine and reverses NDMR agent. Neostigmine is cholinergic with s/e bradycardia and bronchospasm. Glycopyrrolate is anticholinergic.

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