MH During Anaesthesia
What happens when MH occurs during surgery?
The cardinal features of malignant hyperthermia result from an uncontrollable increase in intracellular calcium ions within the skeletal muscles. This initially leads to an increase in metabolic rate as compensatory mechanisms kick in.
The clinical signs are attributed directly to an increase in CO2 production, increased oxygen utilisation and the sympathetic response to increased metabolic activity.
The commonest features are therefore signs of increased CO2 production, which manifest differently according to whether the patient is breathing spontaneously or whether there is controlled ventilation, along with an increase in heart rate.
The increase in metabolic activity will increase heat production but this really takes off when the compensatory mechanisms are overcome. Here, intracellular calcium concentration increases sufficiently to cause interaction between the myofilaments. Contractile activity is energetically inefficient with 40% of the energy only going towards contractile activity with the rest liberated as heat. The minor perturbations of membrane integrity that accompany contractile activity are exaggerated with sustained intracellular calcium increase and will lead to clinically significant leak of intracellular contents including potassium irons, myoglobin and creatine kinase.
The body temperature during a fulminant MH crisis can increase by 0.5° C every 10 minutes. When the body temperature exceeds 39.5°C protein function can be affected and this becomes increasingly significant with further increases in body temperature. Proteins affected include those of the coagulation pathway and their dysfunction can lead to disseminated intravascular coagulation
If an MH reaction is allowed to develop this far it may not be possible to save the patient because the increase in intracellular calcium can lead to mitochondrial failure, with a vicious cycle of continuing calcium release. The muscle damage also leads to muscle swelling, compartment syndrome and ischaemia of the muscles which further compounds the muscle injury. When the blood supply to the muscle is compromised the therapeutic agent dantrolene will not reach it’s site of action within skeletal muscle cells.