Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Anesthesia Pharm > Neuromuscular Blocking Drugs > Flashcards

Neuromuscular Blocking Drugs Flashcards

1
Q

Clinical uses of neuromuscular blockers

A

Facilitate tracheal intubation—2 x ED95
Improve surgical working conditions—90% suppression of single twitch response is usually sufficient
Mechanical ventilation of the lungs (ICU)
Laryngospasm—SCh 0.1 mg/kg IV (last resort→ first try PPV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Laryngospasm Treatment

A

SCh 0.1 mg/kg IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

NMBD Pharmacodynamics

A

The drug of choice is determined by the speed of onset and the duration of action needed. The drug is measured by the nerve stimulator
Muscle relaxants have equal potency (ED95) and the twitch response is decreased in the presence of volatile anesthetics (volatiles prolong the MR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Don’t redose a patient with NMBD until

A

you know how many twitches they have

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Giving NDNMBD after SCh

A

Don’t do it until twitches are back

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

NMBD effect on muscles

A

Small, rapidly moving muscles (ie vocal cords) are the first to relax. Diaphragm one of last to relax.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Onset of blockade

A

Depends on the fiber type and density of ACh receptors

Fast fibers that are dense in ACh receptors = blocked first

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Indicators of NMB effect

A

Orbicularis occuli = correlates most accurately with the vocal cords and diaphragm
Adductor pollicis = poor indicator of laryngeal relaxation The adductor pollicis can be blocked before the larynx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

NMBD Pharmacokinetics: limited volume of distribution

A

(quaternary ammonium groups- highly ionized water-soluble compounds, with limited lipid solubility), so Vd is similar to extracellular fluid volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

NMBD can’t cross lipid membranes

A

(such as BBB, placenta, GI epithelium, renal tubular epithelium)→ thus they don’t produce CNS effects, renal tubual reabsorption is minimal, oral absorption is ineffective, and maternal administration doesn’t harm baby

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

NMBD Plasma clearance and elimination

A

Are affected by age (decreased clearance), volatile agents (decrease clearance) and disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which NMBD is bad for renal patients?

A

pancuronium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Class: …curiums

A

Benzylisoquinolinium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Class: …roniums

A

Aminosteriods

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Mechanism of action of NMBD

A

Interrupt transmission of the nerve impulse at the NMJ (postsynaptic receptor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

NMBD Electrostatic attraction

A

+ nitrogen binds to – alpha subunit of receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

NMBD Lack of specificity

A

Skeletal muscle→ cardiac muscarinic receptors and autonomic ganglia nicotinic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

SCh Mechanism

A

Binds to and activates receptor (fasciculations). A depolarized postjunctional membrane cannot respond to subsequent release of ACh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Non-depolarizing NMBD

A

Bind to and block the receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Acetylcholine

A

Endogenous NT located in the central and peripheral nervous system. It is stored in synaptic vesicles and released into the synaptic cleft as packets (quanta). ACh binds to cholinergic receptors (nicotinic vs. muscarinic). ACh binds to receptor on the postsynaptic membrane and causes a change in membrane permeability to ions→ depolarization of skeletal muscle and contraction. ACh is rapidly hydrolyzed by acetylcholinesterase to acetic acid and choline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Succinylcholine dose, onset, and duration

A 
Dose = 1-2 mg/kg
Onset = 30-60 s (low lipid solubility)
Duration = 3-5 minutes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

SCh breakdown

A

SCh is not a substrate for acetylcholinesterase, it is instead broken down by plasma cholinesterases (not found at NMJ), so SCh has to diffuse away from NMJ to be hydrolyzed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Higher doses of SCh have what effect?

A

Increased duration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Decreased metabolism effect on SCh

A

Prolonged duration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Liver failure effect on SCh

A

Prolonged effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Phase I blockade with SCh

A

Prototypical effect. Decreased single twitch response, decreased amplitude during tetany (no fade between twitches), TOF ratio >0.7 (no fade), absence of posttetanic facilitation (can’t increase ACh with tetany to increase twitch response), enahanced block by anticholinesterase (neostigmine + no twitches = longer sux duration)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Phase II blockade with SCh

A

Nerve response resembles non-depolarizing block. There is fade (TOF and tetany) and there is posttetanic potentiation. Transition from phase I to phase II is abrupt (due to repeated doses/prolonged infusion and manifested as tachyphylaxis). Antagonized by anticholinesterases (now you can use neostigmine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Plasma cholinesterase

A

Degrades SCh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Effect of Anticholinesterases and Metoclopramide on SCh

A

Prolong Block

30
Q

Adverse side effects of SCh

A 
Bradycardia/Tachycardia
HYPERKALEMIA (SCh causes release of K+ from NMJ)
Myoglobinuria 
Increased IOP
Increased intragastric pressure
MH trigger
31
Q

Patients with already increased K+

A

3rd degree burns, muscular atrophy, MD, myalgia

Should avoid SCh

32
Q

Treatment of hyperkalemia

A

Insulin and glucose, calcium, bicarb and non-K sparring diuretics

33
Q

Non-depolarizing NMBD Mechanism of Action

A

Post-junctional nicotinic receptor (some action at the prejunctional receptor)
Compete with ACh at alpha subunits

34
Q

Characteristics of NDNMB

A

Decreased single twitch, fade with tetanus, TOF ratio <0.7, posttetanic potentiation, antagonized by anticholinesterases

35
Q

NDNMB Cardiovascular effects (rare)

A 
Histamine release (…curiums)→ decreases SVR, decreases BP, increases bronchoconstriction. 
Cardiac muscarinc receptors
36
Q

NDNMB Most likely to cause CV effects

A

Pancuronium

37
Q

Drugs that prolong NDNMB block

A

Volatile anesthetics, Aminoglycosides (antibiotics- mycins), Local anesthetics (high doses), Anti-dysrhythmics, Diuretics, and Ganglionic blockers (trimethaphan) (also delay onset)

38
Q

*Drugs that decrease NDNMB block duration

A

Phenytoin (and other seizure meds)

39
Q

NDNMBD Interactions: Hypothermia

A

Increase duration because slows hepatic enzymes

40
Q

NDNMBD Interactions: Hypokalemia

A

Hyperpolarizes cells causing resistance to SCh and sensitivity to NDNMBD

41
Q

NDNMBD Interactions: Hyperkalemia

A

Depolarizes cells so sensitize to SCh and resistant to NDNMBD

42
Q

NDNMBD Interactions: Magnesium

A

Decreases ACh release, enhancing the block

43
Q

NDNMBD Interactions: Combo with SCh

A

Defasiculating dose doesn’t effect block duration, but large dose SCh will prolong block

44
Q

NDNMBD Interactions: Steroid/isoquinolone

A

Synergy

45
Q

Pancuronium (about)

A

Very cheap, not good for intubating because long acting

CV effects at ED95

46
Q

Pancuronium (Dose, Onset, Duration, CV effects, Clearance)

A

Dose: 0.08-0.12 mg/kg intubation; 0.01 mg/kg maintenance
Onset: 3-5 minutes
Duration: 60-90 minutes
CV effects: increased HR, increased CO, increased MAP
Clearance: decreased up to 50% with renal failure

47
Q

Intermediate acting NDNMBDs (names)

A

Atracurium, Cisatracurium, Vecuronium, Rocuronium

CRAVe

48
Q

Intermediate acting NDNMBDs (about)

A

Intermediate acting NMBD have minimal cumulative effects because they are metabolized quickly. Minimal CV effects.

49
Q

Intermediate acting NDNMBDs (onset, duration, reversal)

A

Onset: 2-5 minutes
Duration: 20-45 minutes
Reversal: easily reversed with anticholinesterase. Spontaneous receovery sometimes without reversal.

50
Q

Atracurium (about)

A

Good for renal failure patients

pH = 3.2, so don’t mix it with thiopental or it will form crystals

51
Q

Atracurium (dose, onset, duration)

A

Dose: 0.5 mg/kg (over 30-60 seconds) to decrease histamine
Onset: 3-5 minutes
Duration: 20-35 minutes

52
Q

Atracurium (clearance)

A

Clearance: hoffamann elimination (spontaneous metabolism), ester hydolysis, pH dependent. Hypothermia increases duration bc it decreases Hoffmann elimination.
Alkalosis = increased degradation
Acidosis = decreased degradation

53
Q

Atracurium (side effects)

A

Histamine release and CV effects from histamine

54
Q

Atracurium (clinical considerations)

A

pH: pH = 3.2, so don’t mix it with thiopental or it will form crystals.
Temperature: hypothermia increases duration bc it decreases Hoffmann elimination.
Peds vs. elderly: peds dose decrease by 50%, elderly can get same dose because Hoffmann elimination
Laudanosine: metabolites due to Hoffmann elimination. Can evoke seizures from continuous atracurium

55
Q

Cisatracurium

A

Isoform of atracurium (no histamine release and no laudanosine)
Great for kidney and renal failure patients

56
Q

Cisatracurium (Dose, onset, duration)

A 
Dose = 0.1-0.15 mg/kg; infusion 1-2 mcg/kg/min 
Onset = 2-3 minutes 
Duration = 20-45 minutes
57
Q

Cisatracurium (clearance)

A

Hoffmann elimination (no laudanosine)

58
Q

Vecuronium (about)

A

10 mg powder- reconstitute to 1 mg/ml

59
Q

Vecuronium (dose, onset, duration)

A

Dose: 0.08-0.12 mg/kg; 0.01 mg/kg q 15-20 min maintenace: 1-2 mcg/kg/min (pt on seizure meds)
Onset: 2-3 minutes
Duration: 20-45 minutes

60
Q

Vecuronium (clearance)

A

Metabolized by liver and kidney, so lasts longer in patients with renal and hepatic dysfunction.

61
Q

Vecuronium (Peds vs. elderly)

A

Peds onset of vec is quicker and duration is longer; elderly- duration is longer because decreased liver/kidney blood flow and onset is the same.

62
Q

Rocuronium (about)

A

Only non-depolarizing MR that can mimic the onset of SCh, but you must use max dose (1.2 mg/kg)
No histamine release

63
Q

Rocuronium (dose, onset, duration)

A

Dose: 0.6-1.2 mg/kg; 5-12 mcg/kg/min
Onset: similar to SCh with high dose (onset with low dose ~ 2m)
Duration: 20-45 minutes

64
Q

Rocuronium (clearance)

A

No metabolites because cleared unchanged by the liver and kidneys

65
Q

Mivacurium (about)

A

Only short acting non-depolarizing MR
Used to be used for peds intubations
Not made anymore!

66
Q

Mivacurium (dose, onset, duration)

A

Dose: 0.15-0.2 mg/kg; 4-10 mcg/kg/min
Onset: 2-3 minutes
Duration: 10 minutes
(Duration increased with atypical cholinesterase)

67
Q

Mivacurium (clearance)

A

Plasma cholinesterase

Hepatic/renal dysfunction doesn’t affect clearance

68
Q

Choose the NMBD: Renal failure and severe hepatic failure

A

Mivacurium, Cisatracurium, Atracurium

69
Q

Choose the NMBD: Long Cases

A

Pancuronium

70
Q

Choose the NMBD: Pseudocholinesterase deficient

A

Rocuronium

71
Q

Choose the NMBD: Most cases

A

Rocuronium and Vecuronium

72
Q

Choose the NMBD: RSI

A

Rocuronium

Anesthesia Pharm (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions