Neuromuscular blocking agents
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List some reasons for using muscle relaxants
- To offset hypertonicity with ketamine
- To relieve muscle spasm
- To facilitate smooth muscle induction of anaesthesia in large animals
- To improve surgical conditions
What part of the neuromuscular junction do muscle relaxants block?
Describe the mechanism of action muscle relaxants
Muscle relaxants are competitive antagonists at the nicotinic acetylcholine. They need to block ~80% of the receptor sites as nicotinic receptors have a defensive mechanism by which only a few receptors need to be activated to cause muscle contraction.
Muscle relaxants cause rigid/flaccid muscle paralysis?
Flaccid muscle paralysis
Which muscles are the last to be affected and the first to recover from muscle relaxants?
The respiratory muscles
True or false: consciousness and perception of pain are normal when muscle relaxants are used?
What unwanted side effects can occur with muscle relaxants?
Fall in blood pressure and tachycardia
Describe the pharmacokinetics of muscle relaxants
- Mostly quaternary ammonium compounds
- Administered IV
- Rate of onset and duration vary
- Generally metabolised by the liver or excreted unchanged by the kidney
- Small volume of distribution (do not cross into protected organs e.g. CNS or placenta)
Why must a patient be mechanically ventilated when given muscle relaxants?
As they induce apnoea
What is the advantage of being able to 'top up' muscle relaxants or give an IV infusion for as long as needed?
It means they can maintain a long period of paralysis for surgery
Why should you be careful when removing the endotracheal tube from a patient that has been given muscle relaxants?
The lungs can start being expanded by the diaphragm and intercostal muscles before the airway is open (as these are highly sensitive and will be the last to recover). You should not take the endotracheal tube out before you are sure the patient can actually breathe on its own.
What are the different ways you can recover from a muscle relaxant?
- Spontaneously - as plasma concentration of relaxant declines the drug will move down its concentration gradient from the NMJ into the plasma
- Acetylcholinesterases - ACh is broken down by acetylcholinesterase so if this enzyme is inhibited ACh levels will increase, if ACh concentration increase to a sufficient level at the NMJ transmission will be restored
- Chemical antagonists - e.g. sugammadex
Why are anticholinesterases often given with antimuscarinic/anticholinergic drugs?
Increased acetylcholine concentrations in the body causes bradycardia, salivation, bronchoconstriction, urination and defecation. Anticholinergic drugs are given to try and reduce these side effects.
What factors can affect the NM blockade?
- Other drugs e.g. anaesthetics, antibiotics, anticholinesterases
- Hepatic/renal impairment
- Acid/base balance
- Electrolyte disturbances
- Myasthenia gravis
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