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Succinylcholine

The document discusses succinylcholine, a depolarizing neuromuscular blocker introduced in 1952, detailing its pharmacokinetics, mechanism of action, and clinical uses. It highlights the drug's rapid onset, duration of action, and potential side effects, including bradycardia and hyperkalemia. Additionally, it outlines contraindications and adverse effects associated with succinylcholine administration.

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Ankush Malhotra
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0% found this document useful (0 votes)
41 views1 page

Succinylcholine

The document discusses succinylcholine, a depolarizing neuromuscular blocker introduced in 1952, detailing its pharmacokinetics, mechanism of action, and clinical uses. It highlights the drug's rapid onset, duration of action, and potential side effects, including bradycardia and hyperkalemia. Additionally, it outlines contraindications and adverse effects associated with succinylcholine administration.

Uploaded by

Ankush Malhotra
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
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-There 02 types of neuromuscular

blockers.
Introduction
- This is depolarising neuromuscular
blocker.

Group Depolarising Muscle Relaxant

-Introduced by Thesleff and Foldes


History
in 1952.

➡ The ED95 of succinylcholine is


0.51 to 0.63 mg/kg
➡ Onset: 60 sec (1 mg/kg of
succinylcholine results in complete Chemical
suppression of response)
➡ Duration of action: 09 -13 mins
SCh is two molecules of
Acetylcholine
• Elimination: Elimination T1/2: 47 secs
➡ The drug is hydrolysed by plasma
cholinesterase into succinic acid and Pharmacokinetics ➡ Clear Aqueous solution
choline. ➡ 50 mg/ ml of drug
➡ Eighty percent of the administered dose ➡ Stored @ 4 degree centigrade
is hydrolysed before it reaches the NMJ.

Diluent ➡ Adult - No diluent


➡ Excretion: 2 – 10 % of the ➡ Paed - Use NS
administered dose is excreted Formulation and
unchanged in the urine. Administration
Preparation ➡ 2 ml vial
➡ 10 ml vial
➡ stimulates cholinergic autonomic Strength➡ 50 mg / ml
receptors on both sympathetic and
parasympathetic ganglia
Route➡ IV/ IM/ Sublingual

➡ muscarinic receptors in the sinus


node of the heart. Succinylcholine, a depolarizing
NMBD, produces prolonged
depolarization of the end plate
➡ Stimulation of cardiac Muscarinic region.
receptors in cardiac sinus ➡
Bradycardia.
➡ Common predominant vagal This mechanism results in
tone ( paediatric ) ➡ Desensitizationon the nAChR
➡ More incidence with second Sinus Bradycardia Succinylcholine ➡ Inactivationofvoltage-
gatedNa+channelsatthe
dose ➡ (hydrolysis products of
succinylcholine neuromuscular junction
(succinylmonocholine and ➡ Increases in K+permeability in the
CVS
Anaesthesia Blueprints
choline) may sensitize the heart to a surrounding membrane.
subsequent dose.

➡ The mechanism responsible for


Ref Millers Mechanism of Action ➡ Produces slightly prolonged
this likely involves relatively greater
stimulation of muscarinic receptors
Dr. Ankush Malhotra action as compared to acetylcholine
because its action is terminated
in the sinus node, thus suppressing only by diffusion out of the motor
Junctional Rythm end plate
the sinus mechanism and allowing
the emergence of the ➡ Subsequent metabolism by
atrioventricular node as the pseudocholinesterase in the plasma
pacemaker. (unlike Ach which is rapidly
degraded by acetylcholinesterase in
the NMJ).
➡ Decreases the threshold
of the ventricle to
VentricularDysrhythmias: • Sustained depolarization causes
catecholamine-induced
dysrhythmias all Ach receptors to be used up,
resulting in a failure of
depolarization and subsequent
➡ Increases the plasma K+ levels muscle relaxation.
by approximately 0.5 mEq/dL.
➡ This slight increase in K+ is well
tolerated by most individuals and • Used for endotracheal intubation:
generally does not cause Hyperkalemia 1 -1.5 mg / Kg at 60 sec
dysrhythmias.
➡ The increase in K+ results from • Drug of choice for Rapid sequence
the depolarizing action of intubation: 1- 1.5 mg/ Kg
succinylcholine
Uses and Dosage
• Used for end • Treatment of laryngospasm (0.1
Pharmacodynamics mg/Kg)
➡ It increases IOP.
➡ IOP inc within 01 mins ➡ Peak at Increased Intraocular Pressure • Use in ECT to minimize side effects
2-4 mind ➡ Subsides by 6 minutes. of violent muscle contractions (0.5
mg/Kg)

⬆ Increased Intragastric Pressure:


➡ Due Fasciculation of Abd • Arrhythmias-bradycardia after
Increased Intragastric Pressure
Muscles. second dose in children
• Increased ICP
• Increased IGP
• Increased IOP
Pre-treatment with nondepolarizing Increased Intracranial Adverse Effects
• Myalgia
NMBDs prevents ⬆ ICP Pressure: • Hyperkalaemia
• Myoglobinuria
• Masseter spasm
Myalgia
• Malignant Hyperthermia

➡ Increase in masseter muscle tone


• Open globe injury
of up to 500 g lasting 1 to 2 minutes Masseter Muscle Rigidity
• Burns patient after rst 24 hrs
is a normal nding in adults.
• Hyperkalaemia
Contraindication • Congenital Myopathies
Malignant Hyperthermia • Spinal cord injury
• Raised ICP/IOP
• Malignant Hyperthermia
➡ Incidence 0.06%
➡ Muscle relaxant cross-links with
IgE ➡ degranulation ➡ release of
histamine ➡ neutrophil
chemotactic factor ➡ platelet- Anaphylaxis
activating factor occur.
➡ Relase of mediators ➡ CVS
collapse ➡ Bronchospasm ➡ Skin
Reaction.
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