Succinylcholine Flashcards by Megan Manasco

Plasma cholinesterase abnormalities seen with

Profound liver disease (decreased production)

Drug induced

Genetically atypical

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Cardiac dysrhythmia with succ due to succ action at _____________________

Cardiac muscarinic cholinergic receptors where succ mimics Ach

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Succ and MH

First sign

Last sign

Increase in ETCO2

Hyperyrexia

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____________ gives succ small Vd

Poor lipid solubility

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NMJ has 3 types of _____________ receptors. Breakdown

Cholinergic nicotinic receptors

2 post synaptic on skeletal muscle
1 presynaptic on nerve endings

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Why fast twitch muscles equilibrate first

More Ach receptor sites

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Succ and cardiac rhythm- causes

Stimulates autonomic ganglia and muscarinic receptors causing change in cardiac rhythm (bradycardia) including cardiac arrest

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Obesity and succ

Have greater plasma cholinesterase activity so require larger dose

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______ of succ excreted unchanged in urine

10%

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Risk of hyperkalemia in 4 contraindicated pt peaks

7-10 days after injury

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How to somewhat prevent occurrence of cardiac dysrhythmia with succ

Pretreat with non depolarizer

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Single twitch response give what type of data

Post junctional

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4 factors influencing development of phase 2 block

Duration of drug exposure

Drug exposure

Muscle type (fast or slow)

Interaction with anesthetics

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NTS at NMJ for muscle contraction

Acetylcholine

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IV succ in children may result in deadly arrhythmias due to

Undiagnosed underlying myopathy

Rhabo and hyperkalemia

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Only with ___________ is plasma cholinesterase production too low to prolong succ

Severe liver disease

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Succinylmonocholine broken down into

Succinic acid and choline

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Succ pharmacokinetics (3)

Highly ionized

Water soluble at body pH

Poorly lipid soluble

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Dose required to block at diaphragm

2 times required to block adductor pollis and orbicularis oculi

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Succ pharmacological effect

Interrupt nerve impulse transmission at NMJ by mimicking Ach at NMJ

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Succ effect on IOP

Onset

Duration

Causes

Maximally increases 2-4 minutes

Lasts 5-10 minutes

Contraction of extraocular muscles and increased resistance to aqueous humor flow

INCREASES IOP

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Anticholinesterase typically used to reverse succ

Why

Endrophonium

Shortest duration of action

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Avoid succ in ESRD bc

Risk of hyperkalemia

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Basis of NM transmission

Flow of ions

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Succ MOA

Combines with cholinergic receptors of motor end plates causing depolarization then inhibits subsequent NM transmission

If pretreat with non depolarizer then give succ will get

More profound response to succ

Sites of action for succ

2 alpha subunits of nicotinic receptors

Muscle to monitor for diaphragm

Adductor pollicis

Fasiculations are caused by

Succ initially causes depolarization of skeletal muscle fibers

Due to hyperkalemia risk Succ is contraindicated in what 4 pt populations

Major burns Multiple traumas Extensive denervation of muscle Upper motor neuron injury

Dibucaine # 40-60

Prolonged succ block up to 30 minutes Heterozygous for atypical plasma cholinesterase

Depolarizing block is a ______ block

Phase 1

CV effects of succ enhanced by

Halogenated anesthetics

If give neostigmine to reverse pt with phase 1 block

It will worsen block to phase 2 bc less plasma cholinesterase

Initial sign of phase 2 block

Tachyphylaxix

Plasma cholinesterase low activity due to

``` Neostigmine Insecticides Glaucoma Myasthenia Gravis drugs Chemo ```

In these 2 circumstances succ can induce serious cardiac arrhythmias due to hyperkalemia

Electrolyte abnormalities Dig toxicity

Muscle damage with fasiculations causes

Hyperkalemia and muscle pains

Succ __________ cross lipid membranes like (4)

DOES NOT - BBB - renal tubulular epithelium - GI - placenta

TOF with succ

Each twitch decreased equally in size NO FADE

Succ short duration of action is due to __________ made in _______

Hydrolysis by plasma cholinesterases Liver

Changes in rhythm with succ result from

Vagal stimulation or hyperkalemia

Succ effect on myocardium

No direct effect

Myoglobinuria with succ seen with

MH Rhabdo Stains Muscle disease

Myasthenia gravis patients and succ

More resistant to succ to due lower number of fx Ach receptors Have to give more

Succ metabolism Compared to Ach

Hydrolysis by psudocholinesterases Slower than Ach

Succ and GI

Causes inconsistent increase in intragastric pressure r/t fasiculations Increases risk of aspiration of gastric contents

Cause of increased serum K+ levels with succ

Sustained receptor ion channel opening causes K+ leakage out of cell

TOF to check fast twitch

Orbicularis oculi Laryngeal

Adverse reactions of succ are due to

Ability to work on numerous sites of action bc similar to Ach which binds to several receptors

Plasma cholinesterase affects succ duration of action by

Controlling amounts hydrolysis before reaching NMJ

If use anticholinergic drug to reverse phase 2 block should be accompanied by

Anticholinergic drug

Treatment for hyperkalemia

IV Calcium Bicarbonate IV insulin Hyperventilation

Succ dose for laryngospasm

0.1 mg/kg

Pretreatment with non-depolarizer may prevent (4) But not

- dysrhythmia (bradycardia) - myalgia - increased intragastric pressure - increased IOP DOES NOT PREVENT HYPERKALEMIA

Huge plasma cholinesterase capacity causes

Most succ hydrolyzed before reaching NMJ

TOF check for slow twitch muscles

Adductor polices

Dibucaine # is indicator of

Quality of plasma cholinesterase not quantity

__________ muscles equilibrate more rapidly with plasma succ

Fast twitch muscles- laryngeal muscles Orbicularis oculi

Succ. IV Dose Onset Duration

1-1.5mg/kg 30-60 seconds 3-5 minutes

Diagnosis of phase 2 block

Peripheral nerve stimulator

Phase 2 block resembles Implication

Non-depolarizer block Why should ensure recovery from succ before giving non-depolarizer

Initial metabolite of succ

Succinylmonocholine Very weak NM activity

Ach binding with NMJ post junctional receptors causes

Opening of K+ receptors allowing ion flow

Succ causes increase of serum K+ by

0.5 mEq/L

When Ach released it binds to ____________ receptors on post synaptic membranes

Nicotinic cholinergic

Dibucaine # 20

20% inhibition of plasma cholinesterase activity Single dose of succ can last longer Homozygous for atypical plasma cholinesterase variant

Succ IM Dose Onset

3-4 mg/kg 1-2 minutes

Dibucaine # of 80 means

80% inhibition of plasma cholinesterase activity Normal

Tx for phase 2 block

Propofol gtt and leave on the vent until worn off

Plasma cholinesterase abnormalities cause

Slow to absent hydrolysis and prolongation of NMB

Pretreatment dose of non-depolarizer

1/10 intubating dose

Succ and open globe injuries

AVOID

Thought to be a cause of fasiculations with succ

Binding of succ to both alpha subunits on nicotinic cholinergic post synaptic receptors simultaneously

Cause of prolonged paralysis with succ

Plasma cholinesterase levels or atypical cholinesterases

Succ and preganancy

Plasma cholinesterase levels are decreased in pregnancy and several days postpartum More sensitive to succ

Last muscles paralyzed with succ First to recover

Intercostals and diaphragm last paralyzed and first to recover

Incidence of succ induced myalgia

About 50%

Ending of succ NMJ blockade due to

Diffusion away from NMJ bc low plasma cholinesterase level at NMJ

THE NM jx NTS

Acetylcholine