CNS - NMB - INTRO - Depolarizing NMB

23 important questions on CNS - NMB - INTRO - Depolarizing NMB

In which patients is succinylcholine contraindicated?

Succinylcholine is contraindicated in patients with excessively low levels of choline-esterase enzyme. It is also contraindicated in cases of bradycardia and malignant hyperthermia.

What is hyperkalemia associated with in the context of succinylcholine side effects?

Persistent depolarization of end-plates associated with efflux of intracellular K+. Hyperkalemia is a risk factor for cardiac dysarrhythmia and cardiac arrest.

What causes succinylcholine apnoea?

Succinylcholine apnoea is caused by:
  • Low levels of plasma cholinesterase enzyme (e.g., in liver disease or malnutrition).
  • Abnormal enzyme (e.g., genetic defect).
  • Failure of succinylcholine breakdown leads to apnoea.
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What can contracture and paralysis affect in relation to succinylcholine?

In muscle fibers supplied by multiple end-plates, e.g., extra-ocular muscle (six muscles that control movement of eyes).

What is the structural classification of Succinylcholine?

Succinylcholine is structurally a dicholine ester. It acts as an agonist at nicotinic receptors on NMJ, producing persistent depolarization resulting in muscle paralysis.

What is the treatment for succinylcholine apnoea?

Treatment includes:
  • Support respiration.
  • Phase I block: Blood transfusion to supply the enzyme (plasma ACHE).
  • Phase II block: Give Neostigmine + Atropine IV.

What are the effects of fasciculations due to succinylcholine?

  • Post-operative muscle pain and rhabdomyolysis due to unsynchronized muscle contractions.
  • Increased intra-ocular tension.
  • Increased intra-abdominal pressure and risk of gastric aspiration.

How is Succinylcholine hydrolyzed?

Succinylcholine is not hydrolyzed by AChE. It is hydrolyzed by non-specific plasma cholinesterase, i.e., Pseudocholinesterase.

What causes desensitization of nicotinic receptors to ACh in Phase II block?

Persistence of Succinylcholine at receptors causes desensitization of the nicotinic receptors to ACh. Although membrane potential eventually becomes repolarized, receptors fail to respond to normal physiological amounts of ACh followed by sustained muscle paralysis.

What causes succinylcholine to persist for a long period of time in Phase I block?

Succinylcholine persists for a long period due to the absence of plasma choline-esterase enzyme at the motor end-plate, leading to prolonged depolarization and failure of membrane potential to return to a repolarized state.

How do anticholinesterase agents affect Phase II block?

Anticholinesterase agents, e.g. Neostigmine, preserve ACh and eventually receptors will respond to ACh and the block is antagonized. Neostigmine potentiates Phase I block but antagonizes Phase II block.

What is the duration and onset of action for Succinylcholine?

Succinylcholine has an ultra-short duration of action of 5-10 minutes and a rapid onset of action within 1-2 minutes.

What is the onset and duration of action for suxamethonium?

Suxamethonium has the most rapid onset of action of any neuromuscular blocking drugs. It is ideal for fast onset and brief duration of action, about 2 to 6 mins following i.v doses of about 1mg/kg.

What is the result of the persistence of depolarization in Phase I block?

The persistence of depolarization leads to the failure of membrane potential to return to a repolarized state, resulting in no further impulse discharge or conduction, followed by flaccid skeletal muscle paralysis.

What is the action of Succinylcholine (Suxamethonium) chloride as a skeletal muscle relaxant?

Succinylcholine is a short-acting depolarizing skeletal muscle relaxant that acts by blocking transmission at the myoneural junction.

How does the hydrolysis of suxamethonium compare to ACH?

Hydrolysis of suxamethonium is much slower than for ACH, with prolonged depolarization.

How do anticholinesterase agents affect Phase I block?

Anticholinesterase agents, such as Neostigmine, preserve ACh by increasing depolarization, thereby potentiating the Phase I block.

How does Succinylcholine bind at the myoneural junction?

Succinylcholine binds to nicotinic receptors at the myoneural junctions resulting in depolarization of the skeletal muscles.

Can the action of suxamethonium be reversed?

Its action cannot be reversed. Recovery is spontaneous, and anticholinesterase such as neostigmine potentiate the neuromuscular block.

What role does Succinylcholine play as an acetylcholine agonist?

It acts as an acetylcholine agonist at nicotinic acetylcholine receptors at neuromuscular junctions, resulting in persistent depolarization of the motor end plate followed by muscle paralysis.

When should suxamethonium be given and what are its effects?

Suxamethonium should be given after anaesthetics induction because paralysis is usually preceded by painful muscle fasciculations. Tachycardia occurs with single dose and bradycardia occur with repeated doses.

What is the effect of Succinylcholine on muscle contractions?

It produces sustained muscle contractions lasting several minutes followed by skeletal muscle paralysis.

How does premedication with atropine affect suxamethonium use?

Premedication with atropine reduces bradycardia as well as the excessive salivation associated with suxamethonium use.

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