Neuromuscular blocking agents

• To offset hypertonicity with ketamine
• To relieve muscle spasm
• To facilitate smooth muscle induction of anaesthesia in large animals
• To improve surgical conditions

Acetylcholine receptors

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.

Flaccid muscle paralysis

The respiratory muscles

True

Fall in blood pressure and tachycardia

• 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)

As they induce apnoea

It means they can maintain a long period of paralysis for surgery

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.

• 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

Increased acetylcholine concentrations in the body causes bradycardia, salivation, bronchoconstriction, urination and defecation.  Anticholinergic drugs are given to try and reduce these side effects.

• Other drugs e.g. anaesthetics, antibiotics, anticholinesterases
• Hepatic/renal impairment
• Age
• Temperature
• Acid/base balance
• Electrolyte disturbances
• Myasthenia gravis