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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)

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2
Q

Laryngospasm Treatment

A

SCh 0.1 mg/kg IV

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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)

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4
Q

Don’t redose a patient with NMBD until

A

you know how many twitches they have

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5
Q

Giving NDNMBD after SCh

A

Don’t do it until twitches are back

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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.

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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

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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

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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

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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

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11
Q

NMBD Plasma clearance and elimination

A

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

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12
Q

Which NMBD is bad for renal patients?

A

pancuronium

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13
Q

Class: …curiums

A

Benzylisoquinolinium

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14
Q

Class: …roniums

A

Aminosteriods

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15
Q

Mechanism of action of NMBD

A

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

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16
Q

NMBD Electrostatic attraction

A

+ nitrogen binds to – alpha subunit of receptor

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17
Q

NMBD Lack of specificity

A

Skeletal muscle→ cardiac muscarinic receptors and autonomic ganglia nicotinic receptors

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18
Q

SCh Mechanism

A

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

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19
Q

Non-depolarizing NMBD

A

Bind to and block the receptor

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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

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21
Q

Succinylcholine dose, onset, and duration

A 
Dose = 1-2 mg/kg
Onset = 30-60 s (low lipid solubility)
Duration = 3-5 minutes
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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

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23
Q

Higher doses of SCh have what effect?

A

Increased duration

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24
Q

Decreased metabolism effect on SCh

A

Prolonged duration

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25
Liver failure effect on SCh
Prolonged effect
26
Phase I blockade with SCh
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)
27
Phase II blockade with SCh
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)
28
Plasma cholinesterase
Degrades SCh
29
Effect of Anticholinesterases and Metoclopramide on SCh
Prolong Block
30
Adverse side effects of SCh
``` Bradycardia/Tachycardia HYPERKALEMIA (SCh causes release of K+ from NMJ) Myoglobinuria Increased IOP Increased intragastric pressure MH trigger ```
31
Patients with already increased K+
3rd degree burns, muscular atrophy, MD, myalgia | Should avoid SCh
32
Treatment of hyperkalemia
Insulin and glucose, calcium, bicarb and non-K sparring diuretics
33
Non-depolarizing NMBD Mechanism of Action
Post-junctional nicotinic receptor (some action at the prejunctional receptor) Compete with ACh at alpha subunits
34
Characteristics of NDNMB
Decreased single twitch, fade with tetanus, TOF ratio <0.7, posttetanic potentiation, antagonized by anticholinesterases
35
NDNMB Cardiovascular effects (rare)
``` Histamine release (…curiums)→ decreases SVR, decreases BP, increases bronchoconstriction. Cardiac muscarinc receptors ```
36
NDNMB Most likely to cause CV effects
Pancuronium
37
Drugs that prolong NDNMB block
Volatile anesthetics, Aminoglycosides (antibiotics- mycins), Local anesthetics (high doses), Anti-dysrhythmics, Diuretics, and Ganglionic blockers (trimethaphan) (also delay onset)
38
*Drugs that decrease NDNMB block duration
Phenytoin (and other seizure meds)
39
NDNMBD Interactions: Hypothermia
Increase duration because slows hepatic enzymes
40
NDNMBD Interactions: Hypokalemia
Hyperpolarizes cells causing resistance to SCh and sensitivity to NDNMBD
41
NDNMBD Interactions: Hyperkalemia
Depolarizes cells so sensitize to SCh and resistant to NDNMBD
42
NDNMBD Interactions: Magnesium
Decreases ACh release, enhancing the block
43
NDNMBD Interactions: Combo with SCh
Defasiculating dose doesn’t effect block duration, but large dose SCh will prolong block
44
NDNMBD Interactions: Steroid/isoquinolone
Synergy
45
Pancuronium (about)
Very cheap, not good for intubating because long acting | CV effects at ED95
46
Pancuronium (Dose, Onset, Duration, CV effects, Clearance)
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
Intermediate acting NDNMBDs (names)
Atracurium, Cisatracurium, Vecuronium, Rocuronium | CRAVe
48
Intermediate acting NDNMBDs (about)
Intermediate acting NMBD have minimal cumulative effects because they are metabolized quickly. Minimal CV effects.
49
Intermediate acting NDNMBDs (onset, duration, reversal)
Onset: 2-5 minutes Duration: 20-45 minutes Reversal: easily reversed with anticholinesterase. Spontaneous receovery sometimes without reversal.
50
Atracurium (about)
Good for renal failure patients | pH = 3.2, so don’t mix it with thiopental or it will form crystals
51
Atracurium (dose, onset, duration)
Dose: 0.5 mg/kg (over 30-60 seconds) to decrease histamine Onset: 3-5 minutes Duration: 20-35 minutes
52
Atracurium (clearance)
Clearance: hoffamann elimination (spontaneous metabolism), ester hydolysis, pH dependent. Hypothermia increases duration bc it decreases Hoffmann elimination. Alkalosis = increased degradation Acidosis = decreased degradation
53
Atracurium (side effects)
Histamine release and CV effects from histamine
54
Atracurium (clinical considerations)
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
Cisatracurium
Isoform of atracurium (no histamine release and no laudanosine) Great for kidney and renal failure patients
56
Cisatracurium (Dose, onset, duration)
``` Dose = 0.1-0.15 mg/kg; infusion 1-2 mcg/kg/min Onset = 2-3 minutes Duration = 20-45 minutes ```
57
Cisatracurium (clearance)
Hoffmann elimination (no laudanosine)
58
Vecuronium (about)
10 mg powder- reconstitute to 1 mg/ml
59
Vecuronium (dose, onset, duration)
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
Vecuronium (clearance)
Metabolized by liver and kidney, so lasts longer in patients with renal and hepatic dysfunction.
61
Vecuronium (Peds vs. elderly)
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
Rocuronium (about)
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
Rocuronium (dose, onset, duration)
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
Rocuronium (clearance)
No metabolites because cleared unchanged by the liver and kidneys
65
Mivacurium (about)
Only short acting non-depolarizing MR Used to be used for peds intubations Not made anymore!
66
Mivacurium (dose, onset, duration)
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
Mivacurium (clearance)
Plasma cholinesterase | Hepatic/renal dysfunction doesn’t affect clearance
68
Choose the NMBD: Renal failure and severe hepatic failure
Mivacurium, Cisatracurium, Atracurium
69
Choose the NMBD: Long Cases
Pancuronium
70
Choose the NMBD: Pseudocholinesterase deficient
Rocuronium
71
Choose the NMBD: Most cases
Rocuronium and Vecuronium
72
Choose the NMBD: RSI
Rocuronium

Anesthesia Pharm (11 decks)

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