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You are in Home >> Resources >> Clinical anaesthesia >> Malignant Hyperthermia

Pathophysiology of malignant hyperthermia

Created: 23/6/2004

Trigger agent administered to patient

[i] All potent inhalational agents
[ii] Succinylcholine

Leads to increased cytoplasmic free calcium

Rigidity - may or may not be present
Masseter spasm
Total body rigidity

Resulting in increased oxygen consumption/increased carbon dioxide production/increased heat production.


Cell damage

Resulting in leakage of cell contents (potassium, myoglobin, creatine kinase [creatine phosphokinase])

Compensatory mechanisms

Heat loss (sweating, cutaneous vasodilatation)
Increased circulating catecholamines (increased heart rate, cutaneous vasoconstriction, increased systemic vascular resistance)
Increased cardiac output - may not meet with O2 demands (decreased mixed venous oxygen content, decreased arterial oxygen content depends on shunt, lactic acidosis)
Increased ventilation - may not be sufficient compensation (increased respiratory drive, increased end tidal carbon dioxide.

Temperature rise- related to:

 Severity of stimulus
 Environmental temperature
 Starting temperature
 Amount of vasoconstriction vs. vasodilatation

Secondary systemic manifestations

Cardiac arrhythmias
Disseminated intravascular coagulation
Renal failure


Related examination questions

1.The following features are essential to diagnose malignant hyperthermia:

a) muscle rigidity
b) hypercapnia
c) renal failure
d) body temperature greater than 38 degrees C
e) family history


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