Neuromuscular blocking drugs Flashcards

1
Q

Neuromuscular blocking drugs

What do they do?

What does they result in?

Potentially what issue?

A
  • NMBDs interrupt transmission of nerve impulses at the neuromuscular junction
  • Results in complete paralysis of striated muscles while consciousness is retained, there is no analgesia, and spontaneous respiration ceases
  • Potentially an animal welfare issue
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2
Q

4 indications for NMBDs?

A
  • Position the eyeball centrally without traction
    • Aids for intraocular or corneal surgeries
    • Most common indication in vet med
  • Relax resp. muscles to allow mechanical ventilation (rare indication)
    • Sometimes in small animal ICU
  • Relax the muscles for neurological or orthopedic surgeries (rare indication)
  • Aid intubation (humans)
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3
Q

What are the 3 minimum requirements for NMBD’s regarding ventilation and monitoring?

A
  • Use mechanical ventilation (cuffed tube, etc.)
  • Monitor cardiovascular, resiratory systems, and oxygenation
    • Eye position, pupillary reflex, etc. will not be available
    • Tachycardia and high blood pressure is the only sign they can show in response to noxious stimuli
  • Monitoring end tidal agent (e.g. ISO) is useful but not mandatory
    • If not available, use high fresh gas flow and keep ISO vaporizer around 1%
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4
Q

Contraindications for NMBDs?

A
  • If there is no possibility to ventilate and monitor the patient
  • If animal remains conscious
    • Conscious experience of complete muscle paralysis is EXTREMELY DISTRESSING even without pain
  • If there is insufficient analgesia during surgery
    • NMBDs should not be used to “cover” the lack of analgesia
  • If the personnel in charge does not have a complete understanding of the use of NMBDs
  • It cannot be overemphasized that NMBDs MUST NOT be used as a sole agent for any kind of procedure (painful or nonpainful)
  • Nevertheless, they MUST NOT be used as a sole agent for euthanasia
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5
Q

Neuromuscular junction

Consists of?

Function (5 steps)?

A
  • NMJ consists of a prejunctional motor nerve ending a highly folded postjunctional membrane of the skeletal muscle and a synaptic cleft between them
  • Function
    • An impulse arrives at the motor terminal (Ca2+ influx)
    • Release of acetylcholine neurotransmitter
    • ACh binds to nicotinic cholinergic receptors on the postjunctional membranes (opening K+ and Na+ channels)
    • The resulting ion influx triggers an action potential that leads to muscle contraction
    • ACh is rapidly metabolized by the enzyme acetylcholinesterase in the synaptic cleft
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6
Q

Mechanism of action: depolarizing and non-depolarizing NMBDs

A
  • Depolarizing NMBDs act as an agonist on the nicotinic ACh receptors, thus causing muscle membrane depolarization
  • Non-depolarizing NMBDs act as a competitive antagonist on the nicotinic ACh receptors, thus stabilizing muscle membranes
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7
Q

Order of muscle relaxation

A
  • Ocular muscles are the most sensitive and will be paralyzed first even at low doses
  • Diaphragm is the most resistant–last to complete blockade and first to recover
  • All other muscles are between
  • Typical order of onset:
    • Eyes > larynx > diaphragm
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8
Q

Drugs that potentiate NMBD effect?

A
  • Inhalational anesthetics
  • Aminoglycoside antibiotics
  • Local anesthetics
  • Cardiac antiarrhythmic drugs
  • Diuretics
  • Magnesium
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9
Q

What are some other factors that influence the depth of NMBD effect?

A
  • Hypothermia
  • Electrolyte abnormalities
  • Acid-base disorders
  • Age
  • Thermal burn
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10
Q

NMBD chemical properties

A
  • Water-soluble drugs
  • Do not cross lipid barriers easily
  • Therefore less likely to:
    • Cross BBB or placental barrier
    • Adsorb from GI tract
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11
Q

Histamine release:

Occurs when?

Which NMBDs are more likely to cause it?

May cause what?

Treatment?

A
  • Rare complication; mostly at high doses
  • More likely to cause it:
    • Atracurium
    • Succinylcholine
  • Histamine may cause
    • Bronchoconstriction
    • CV: vasodilation, (-) inotropy, tachycardia
  • Treatment: e.g. low dose epinephrine
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12
Q

What are the side effects of NMBDs at the ANS?

A
  • Nicotinic ACh receptors are also found in the ANS
  • Interactions with older NMBDs (e.b. pancuronium) are possible; those may have side effects related to ANS function
  • Unlikely with modern NMBDs
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13
Q

Classification/examples of NMBDs

A
  • Depolarizing
    • Succinylcholine
  • Non-depolarizing
    • Long-acting (>30 min): pancuronium
    • Imtermediate acting (10-30 min): atracurium, cisatracurium, rocuronium, vecuronium
    • Short-acting: rapacuronium
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14
Q

Succinylcholine (SCh): general

A
  • Cause sustained membrane depolarization on the end plate
  • This will initially lead to muscle fasciculation, then the postjunctional Na channels close and remain closed until SCh is present
  • This mechanism prevents neuromuscular transmission
    • Called the phase-1 block
  • After prolonged or high dose SCh administration another type of block (phase-2) may develop which is similar to the non-depolarizing blockade
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15
Q

Adverse effects of Succinylcholase?

A
  • Cardiac arrhythmias (bradycardia, sinus arrest)
  • Hyperkalemia
  • Fasciculation, myalgia, myoglobinuria
  • Elevated intra-ocular and intra-gastric pressures
  • May trigger malignant hyperthermia
  • Not a preferred NMBD in vet med
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16
Q

Intermediate-acting non-depolarizing NMBDs: general

A
  • Non-depolarizing NMBDs have less adverse effects than SCh
  • Preferred for vet med: atracurium, cisatracurium, rocuronium, vecuronium
  • Cumulative effects are less likely and recovery is rapid
  • Little or no cardiovascular effects
17
Q

Atracurium

A
  • Mixture of 10 stereoisomers
  • Eliminated via
    • Plasma esterase enzyme
    • Spontaneous degradation (Hofmann elimination)–this depends on plasma pH and temperature
  • Laudanosine is the major metabolite and it decreases the seizure threshold
  • May cause histamine release at high doses
18
Q

Cisatracurium

A
  • 1 of the 10 isomers of atracurium (represents ~15%)
  • Elimination is mostly organ dependent (80% by Hofmann elimination)
  • Laudanosine production is less
  • Kind of a better but more expensive version of atracurium
19
Q

Rocuronium

A
  • Excellent NMBD
  • No. 1 choice in the vet med Uni. Vienna
  • Can be antagonized with Sugammadex
  • Mostly eliminated by the liver, partially by the kidneys
  • Recovery is fast
  • Antagonist is normally not needed
20
Q

Monitoring the effects of NMBDs

A
  • Residual postoperative neuromuscular blockage may be assoc. with significant impairment of respiratory and pharyngeal muscle fx and increased risk for postoperative pulmonary complications
  • It is impossible to be sure that residual blocking effects are not present only by examining the clinical signs
  • Sustained ability to hold the head or stand may indicate that the patient recovered enough to protect the airway
  • Monitoring the neuromuscular function with peripheral nerve stimulators is necessary
  • Acceptable neuromuscular recovery is a TOF ratio >/= 0.9
21
Q
A