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Neuromuscular Blocking Agents > The Basics > Flashcards

The Basics Flashcards

Info obtained from M&M Notecards

0
Q

Non depolarizing agents act as?

A

Competitive antagonists.

ACh receptors are bound but are incapable of inducing the conformational change necessary for ion channel opening.

Bc ACh is prevented from binding to it’s receptors, no end plate potential develops

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1
Q

Neuromuscular blocking agents are divided into two classes

A

De polarizing and blonde polarizing

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3
Q

De polarizing muscle relaxants act by?

A

Binding to ACh receptors, generating a muscle action potential.

These drugs are not metabolized by acetylcholinesterase, and their concentration in the synaptic cleft does not fall as rapidly, resulting in prolonged depolarization of muscle end plate

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4
Q

Phase I Block

A

the end plate cannot depolarize as long as the depolarizing muscle relaxant continues to bind to ACh receptors.

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5
Q

Phase II Block

A

after a period of time, prolonged end plate depolarization can cause ionic and conformational changes in the ACh receptor that clinically resembles that of non depolarizing muscle relaxants.

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6
Q

How does muscle denervation affect the NMJ?

A

it stimulates a compensatory increase in the number of ACh receptors and promotes expression of extra junctional ACh receptors:

leading to EXAGGERATED response to DEPOLARIZING muscle relaxants (w more receptors being depolarized)

but a RESISTANCE to NON depolarizing relaxants (more receptors that must be blocked)

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7
Q

How does Myasthenia Gravis affect the NMJ?

A

few ACh receptors lead to RESISTANCE to DEPOLARIZING relaxants and and INCREASED sensitivity to NON depolarizing relaxants

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8
Q

How does Eaton-Lambert Myasthenic Syndrome affect the NMJ?

A

decreased release of ACh

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9
Q

What is the definition of FADE with peripheral nerve stimulators?

A

Fade is a gradual diminution of evoked response during prolonged or repeated nerve stimulation, is indicative of a NONDEPOLARIZING blockade.

Adequate recovery correlates well with the absence of fade

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10
Q

What is Phase I Depolarization Block?

A

it does not exhibit fade during tetanus or TOF, and it does not demonstrate posttetanic potentiation.

If enough depolarizer is administered, the quality of the block changes to resemble a NONDEPOLARIZING block (Phase II block)

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11
Q

Succinylcholine: Mechanism of Action

A

DEPOLARIZING muscle relaxant (the only on in clinical use)

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12
Q

Succinylcholine: Dosage

A

1-1.5 mg/kg for intubation

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13
Q

Succinylcholine: Onset

A

30 - 60 seconds; typically lasts less than 10 minutes

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14
Q

Succinylcholine: Mechanism of Termination of Action

A

diffuses from NMJ, metabolized by psuedocholinesterases

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15
Q

Succinylcholine: Structure

A

two joined ACh molecules

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16
Q

Succinylcholine: two important drug interactions

A

CHOLINESTERASE INHIBITORS prolong the action of succinylcholine

NONDEPOLARIZING NMBA can antagonize a Phase I Block

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17
Q

Succinylcholine Contraindications

A

routine use of succinylcholine is relatively contraindicated in CHILDREN b/c of the risk of:

HYPERKALEMIA
Rhadbdomyolysis
Cardiac arrest from undiagnosed myopathies

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18
Q

Succinylcholine Side Effects:

A

CV: SCh stimulates ALL ACh receptors, which can lead to BRADY or TACHY. Brady occurs most frequently in children, but can occur in adults after second dose.

Fasciculations: denote the onset of paralysis

Hyperkalemia: normal m. releases K+ with SCh elevating the plasma K+ by 0.5 mEq/L. This can be life threatening with preexisting hyperkalemia or in pts who have suffered BURN injury or massive TRAUMA

M. Pains are sometimes noted post op

Elevation of ICP, Intragastic, and intraocular pressures

Masseter muscle rigidity occurs transiently

MH

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19
Q

NonDepolarizing NMBA are classified into which three categories?

A

Benzylisoquinilinium (tend to release histamine)
Steroidal (tend to be VAGOlytic)
Chlorofumarates

20
Q

Nondepolarizers: what can prolong the block?

A

hypothermia, respiratory acidosis, hyokalemia, hypocalcemia, hypermagnesemia

21
Q

Nondepolarizers: Hepatic Clearance

A

can impact PANCURONIUM and VECURONIUM

22
Q

Nondepolarizers: Renal Excretion

A

significant in clearing DOXACURIUM, PANCURONIUM, VECURONIUM, and PIPECURONIUM

23
Q

Atracurium is what type of nondepolarizer?

A

benzylisoquinoline

24
Q

Atracurium: Metabolism and Excretion

A

undergoes ester hydrolysis from nonspecific esterase’s and HOFMANN ELIMINATION

(spontaneous b/d dependent on physiologic pH and temperature)

25
Q

Atracurium: Dosage

A

0.5 mg/kg for intubation; intermediate duration

26
Q

Atracurium: Side Effects

A

HISTAMINE release - hypotension, tacky, bronchospasm

LAUDANOSINE Toxicity - b/d of Hofmann elimination that can cause CNS excitation and is metabolized by liver

Prolonged action - at abnormal pH and temperature

27
Q

Cisatracurium is what type of nondepolarizer?

A

Benzylisoquinoline

a stereoisomer of atracurium

28
Q

Cisatracurium: metabolism and excretion

A

same as atracurium

undergoes ester hydrolysis from nonspecific esterase’s and HOFMANN Elimination

29
Q

Cisatracurium: dosage

A

0.1 - 0.15 mg/kg for intubation; intermediate duration

30
Q

Cisatracurium: Side Effects

A

Laudanosine Toxicity - significantly lower levels than with atracurium

Prolonged action - at abnormal pH and temp

31
Q

Pancuronium is what type of nondepolarizer?

A

Steroidal

32
Q

Pancuronium: Metabolism and Excretion

A

excretion is primarily renal (40%); limited liver metabolism and bile clearance

33
Q

Pancuronium: Dosage

A

0.08 - 0.12 mg/kg for intubation; LONG duration

34
Q

Pancuronium: Side Effects

A

HTN and TACHYcardia - caused by VAGAL blockade and SYMPATHETIC stimulation

Arrhythmias

35
Q

Vecuronium is what type of nondepolarizer?

A

steroidal

36
Q

Vecuronium: Metabolism and Excretion

A

excretion is primarily biliary and secondarily renal (25%)

limited liver metabolism

37
Q

Vecuronium: Dosage

A

0.08 - 0.12 mg/kg for intubation; Intermediate duration

38
Q

Vecuronium: Side Effects

A

can precipitate if administered with THIOPENTAL

possible prolonged duration in LIVER FAILURE

Active metabolites can lead to prolonged duration after long infusion

39
Q

Rocuronium is what type of nondepolarizer?

A

steroidal

40
Q

Rocuronium: Metabolism and Excretion

A

no metabolism;

excreted primarily by the liver and slightly by the kidneys

41
Q

Rocuronium: Dosage

A
  1. 45 - 0.9 mg/kg IV for routine intubation
  2. 9 - 1.2 mg/kg IV for rapid intubation

1-2 mg/kg IM (onset, 3-6 min)

Intermediate duration at lower dose range

42
Q

Rocuronium: Side Effects

A

prolonged action at higher dosage range

43
Q

Gantacurium is what type of nondepolarizer?

A

Chlorofumarate

44
Q

Gantacurium: Metabolism and Excretion

A

Cysteine adduction and ester hydrolysis

45
Q

Gantacurium: Dosage

A

0..2 mg/kg for intubation with onset in 1-2 mins

Duration of action is 5-10 mins (can be accelerated by edorphonium or exogenous cysteine)

46
Q

Gantacurium: Side Effects

A

Histamine release at higher dosages

47
Q

Gancurium is available in the US? True or False

A

False

Neuromuscular Blocking Agents (1 decks)

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