Pharmacology for Anaesthesia and Intensive Care

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9780521704632c11 CUFX213A/Peck 9780521618168 December 28, 2007 12:5

Section IICoredrugs in anaesthetic practice

Table 11.3.Pharmacological and physiological interactions of muscle relaxants.

Effect on blockade Mechanism

Pharmacological

Volatile anaesthetics prolonged depression of somatic reflexes in

CNS (reducing transmitter

release at the NMJ)

Aminoglycosides (large

intraperitoneal doses),

polymyxins and tetracycline

prolonged decreased ACh release possibly by

competition with Ca^2 +(which

unpredictably reverses the block)

Local anaesthetics variable low doses of local anaesthetic may

enhance blockade by causing a

degree of Na+channel blockade

Lithium prolonged Na+channel blockade

Diuretics variable variable effect on cAMP. May have

effects via serum K+

Ca^2 +channel antagonists prolonged reduced Ca^2 +influx leading to

reduced ACh release

Physiological

Hypothermia prolonged reduced metabolism of muscle

relaxant

Acidosis variable prolonged in most, but reduced for

gallamine. The tertiary amine

group of dTC becomes

protonated increasing its affinity

for the ACh receptor

Hypokalaemia variable acute hypokalaemia increases (i.e.

makes more negative) the resting

membrane potential. Non-

depolarizing relaxants are

potentiated while depolarizing

relaxants are antagonized. The

reverse is true in hyperkalaemia

Hypermagnesaemia prolonged decreased ACh release by

competition with Ca^2 +,and

stabilization of the post-

junctional membrane. When

used at supranormal levels (e.g.

pre-eclampsia) Mg^2 +can cause

apnoea via a similar mechanism

function. With only a single charged quaternary ammonium group, it is more lipid-

soluble than pancuronium and despite the metabolism of a similar proportion in

the liver, a far greater proportion is excreted in the bile. It may accumulate during

administration by infusion.