Neuromuscular blocking agents Flashcards
When is neuromuscular blockade indicated?
- Endotracheal Intubation
- Surgery where muscle relaxation is essential
- Mechanical ventilation
What are the risks of incomplete reversal of neuromuscular blockade
- Very unpleasant for patient
- Hypoxia
- Aspiration
What can be used to reduced the risk of incomplete reversal of neuromuscular blockade?
Peripheral Nerve Stimulator
What is the premise of standard induction (versus RSI)
During standard induction the NDMR should only be administered once it has been confirmed that the airway can be maintained using simple mask ventilation
If the patient then proves impossible to intubate after being paralyzed, simple mask ventilation may be used to keep the patient oxygenated and anaesthetized.
What is the premise of RSI (versus standard induction)
Indicated in situations where the patient is at risk of aspiration of gastric contents.
Preoxygenation
Induction agent + depolarizing neuromuscular blocker
WITHOUT CHECKING FOR MASK VENTILATION
Sux wears off within a few minutes –>allowing spontaneous respiration to restart. The alveolar reservoir of oxygen should limit any hypoxia until spontaneous respiration restarts
When is maintenance of muscle paralysis indicated?
Surgery where muscle relaxation is essential
Mechanical ventilation in the ICU when lung compliance is low
Can repeated doses of non-depolarizing agent be administered during the surgery or in ICU to maintain paralysis?
If standard induction was used with a non-depolarizing muscle relaxant then repeated doses of the same agent can be used to maintain paralysis –> exact dose and frequency should be guided by the response to a nerve stimulator
Why should a peripheral nerve stimulator be used before administration of a non-depolarising muscle relaxant after SUX was used for RSI?
To ensure sux has worn off. If sux has not worn off, there is a possibility that succinylcholine apnoea is present.
If PNS is not used and paralysis is prolonged, it would be unclear which agent is responsible.
What is succinylcholine apnoea
Genetically abnormal plasma cholinesterase –> prolonged effects of this enzyme –>much slower metabolism of succinylcholine
What are the intubation and maintenance doses for vecuronium
Intubation dose: 0.1 mg/kg
Maintenance: 1 - 2 mg (Depends on PNS)
What is the intubating dose and maintenance dose of atracurium
Intubation: 0.5 mg/kg
Maintenance: 10 - 20 mg (Depends on PNS)
What is the intubating dose for succinylcholine
1 - 2 mg/kg
Can SUX be used to maintain neuromuscular blockade?
No
How does succinylcholine work?
Structurally related to acetylcholine –> produces muscle relaxation by first activating muscle fibres, then preventing a further response–> muscle fasciculation
What metabolizes succinylcholine?
Plasma pseudocholinesterase
What are the patient related and clinical contra-indications to the use of succinylcholine
Patient related contraindications: 1. Malignant hyperthermia 2. Anaphylaxis to succinylcholine 3. Succinylcholine apnoea (these conditions can still be triggered for the first time)
Clinical contraindications:
- Widespread denervation injury –> especially after burns/spinal cord injury
- Open, penetrating eye injury
Why is widespread denervation injury a clinical contra-indication?
During repolarization, K+ moves down its concentration gradient via nicotinic receptors into the extracellular environment. Normal rise in plasma potassium is about 0.5mmol rise which is clinically insignificant.
Burns/spinal cord injury –> disuse of muscle fibres with associated upregulation and proliferation of junctional and extrajunctional post-synaptic Ach nicotnic receptors. This leads to a more significant rise in plasma K+ –> VF –> asystole
Why is an open eye-injury a contra-indication to the use of succinylcholine
Contraction of the extra-ocular muscles following the use of succinylcholine result in a significant rise in intraocular pressureso that the contents of the eyeball may be compromised when there is an open eye injury
What are the adverse effects if SUX
- Bradycardia (especially after 2nd dose)
- ‘Sux’ pains
- Transient raised pressure in eye, stomach, cranium
What is the mechanism for bradycardia most common after a second dose of SUX and how is this prevented
The structural similarity of SUX to Ach –> cardiac muscarinic receptor stimulation –> bradycardia.
Prevention: pre-administration of an anti-cholinergic: atropine/glycopyrrolate
What are “sux pains”
Unco-ordinated muscle fasciculations –> pains in the jaw and neck most common
Persist for a day or two and are most likely in women
How do Non-depolarising neuromuscular blockers work?
These are all competitive antagonists of acetylcholine at the NMJ
What is the classification of non-depolarising muscle relaxants and what is this based on ?
Based on their structure:
Aminosteroids
- Vecuronium
- Rocuronium
- Pancuronium
Benzylisoquinoliniums
- Atracurium
- Cisatracurium
- Mivacurium