Neuromuscular Blocking Agents Flashcards by Shannon desmond

Structure of NMB

Quaternary Ammoniums
Structurally related to Ach
Synthetic Alkaloids
except Tubocuraine

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Structure of Succinylcholine

Two ACh molecules linked by acetate methyl groups

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Dose of Succinylcholine

1.0mg/kg

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How long does Succinylcholine take to work?

60 seconds

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How long does it take to recover 90% muscle strength?

9-13 minutes

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Metabolism of Succinylcholine

short action due to rapid hydrolysis

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Enzyme that breaks down Succinylcholine

butrylcholinesterase

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Metabolites of Succinylcholine

Succinylmonocholine and choline

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Succinylmonocholine is a

weak NMB; succinic acid and choline

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Where does recovery from succinylcholine motor blockade occur?

as it drifts away from NMJ down a concentration gradient

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Where is butyrylcholinesterase metabolized?

liver and found in plasma

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What is butyrylcholinesterase responsible for the metabolism of?

succinylcholine, mivacurium, procaine, chloroprocaine, tetracaine, cocaine and heroin

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Factors that decrease butyrylcholinesterase activity?

advance liver disease
age
malnutrition
pregnancy
burns
oral contraceptives
MAO inhibitors
echothiophate
cytotoxic drugs
neoplastic disease
anticholinersterase drugs

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Beta Blockers will

cause a mild prolongation of Succinylcholine

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Genetic variations with the administration of succinylcholine

will significantly prolongation

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Dibucaine

local anesthetic that inhibts typical PchE

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Reflects the typical PChE not quantity

dibucaine number

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Heterogenous for atypical gene

dibucaine number 40-60

Prolongs block 1.5-2times longer

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Homogenous for atypical gene

dibucaine number less then 30

prolonged for 4-8 hours

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Cardiac Side Effects of Succinylcholine

bradycardia,
tachycardia
junctional rhythm
sinus arrest
due to muscarinic receptors  on cardiac cells

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Cardiac effects due to succinylochine are more likely to occur

second dose within 5 minutes of first dose

pediatric patients

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Stimulation of autonomic ganglia may cause

ventricular dysrhythmias
tachycardia
increased BP

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Hyperkalemia

0.5-1mEq/L increase in plasma concentration
More severe in: burns, abdominal infectinos, metabolic acidosis, closed head injury and conditions with upregulation of nAChR (paraplegia, muscular dystrophy, Gullian-Barre)

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Myoglobinuria

damage to skeletal muscle especially pediatric patients

Most found to have muscular dystrophy or by malignant hyperthermia susceptible

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Increased intraocular pressure

peaks 2-4 minutes; pressure returns to normal by 6 minutes | not widely accepted in open eye injury

Increased intragastric and lower esophageal pressures

related to intensity of fasciculations of abdominal muscles Prevented by prior administration of ND-NMB does not increase risk of regulation

Increased intracranial pressure

can be attenuated with pre-treatment of ND-NMB

Masseter Spasm

trigger for MH

Myalgias

prominent in skeletal muscle of the neck, back and abdomen greater in young adults females and ambulatory surgery patients not well understood possible muscle injury to fasciculations pretreatment with ND-NMV lidocaine or NSAIDs myalgias occur even in absence of succinylcholine

Elderlys (sux)

onset slower due to decreased circulation reduced levels of PChE certain alzheimer medications may prolong actions

Pediatrics (suc)

avoided in pediatric patients (<5 yrs) Duchenne muscular dystrophy Cardiac arrest him from hyperkalemic rhabdomyolysis

Atricurium

Histamine Release

Structure of Cis

cis isomer of atracuurium

Onset of action of Cis

intermediate

Intubation Dose of Cis

0.1mg/kg

Cis is metabolized

by Hoffman elimination | No ester hydrolysis

Does cis cause histamine release?

DOA of Mivacurium

short acting non-deplorizing available

Intubating dose of mivacurium

0.15mg/kg

Mivacurium is metabolize by

butyrylcholinesterase 70-88% rate of succinylcholine monoester, dicarboxylic acid

Mivacurium produces

histamine release

Steriodal compounds include

pancuronium vecuronium rocuronium

Steriodal compounds structure

acetyl ester thought to facilitate interaction with NaChR | essential that one of two nitrogen atoms are quarternized

DOA of Pancuronium

Potent long acting neuromuscular blocking drug

Intubation dose of Pancuronium

0.08mg/kg

Onset time to max block of pancuronium

2.9 minutes

Majority of Pancuronium is cleared

by the kidney

Other small amount of Pan is

deacteylated by the liver

3-OH metabolite

Pancuronium | accumulation is responislbe for block prolongation

DOA of Vec

intermediate Acting

Intubating dose of VEc

0.1mg/kg

Onset time to max block of Vec

2.4 minutes

What drug is Vec similar

pancuronium without quaternized methyl group

What are the differences in properties between vec and pan?

slight decrease in potency loss of vagolytic properties Molecular instability (shorter DOA) increase lipid solubility

Where is Vec metabolized

principally by the liver | 3-OH metabolites has 80% of neuromuscular potency

DOA of Roc

Intermediate

Intubation dose of Roc

0.6mg/kg

Time to Max block in roc

1.7 minutes

Roc has a faster onset than

pan or vec

Roc potency is x times less potent then

pan or vec

Roc is primarily metabolized

in the liver | approximately 30% executed in the urine

NMB Potency increased

``` inhalational agents antibiotics hypothermia magnesium sulfate local anesthetic quinidine ```

Factors that decrease NMB potency

chronic anticonvulsant administration hyperparathyroidism and hypercalcemia (decreased atracurium sensitivity)

With NMB potency and onset

have an inverse relationship

Buffered Diffusion seen with

high density drugs | drug diffusion is impeded because it binds to high density receptors in a confined space

Autonomic Effects of NMB

block nicotinic receptors within sympathetic and parasympathetic nervous system bradycardia and hypotension histamine release (flushing, hypotension, reflex tachycardia and bronchospasm)

Vagolytic effects occur

pancurium block muscarinic receptors inhibition of negative feedback system where catecholamine release is modulated or prevented

Histamine Release

seen in benzylisoquinolinium (miv, atra, tubo) short duration slow administration or pretreatment with H1 and H2 blockers to reduce cardiovascular effects

Respiratory effects of NMB

related to histamine release in patients with reactive airways disease increasd airway resistance and bronchospasm

Allergic Reactions

cross reactivity =- food, cosmetics, disinfections, and industrial materials

treatment of allergic reaction

``` o2 IV epi intubation fluids sympathomimetic drug ```