Symptoms: The most common signs and symptoms of overdose with salbutamol are transient beta agonist pharmacologically mediated events, including skeletal muscle tremor, tachycardia, tenseness, headache, hyperactivity, peripheral vasodilatation and metabolic effects including hypokalaemia.
Hypokalaemia may occur following overdose with salbutamol. Serum potassium levels should be monitored.
Hyperglycaemia, agitation and hyperactivity have also been reported following overdose with salbutamol.
Lactic acidosis has been reported in association with high therapeutic doses as well as overdoses of short-acting beta-agonist therapy, therefore monitoring for elevated serum lactate and consequent metabolic acidosis (particularly if there is persistence or worsening of tachypnea despite resolution of other signs of bronchospasm such as wheezing) may be indicated in the setting of overdose.
Management: Asthmatic patients: Consideration should be given to discontinuation of treatment.
Monitor biochemical abnormalities, particularly hypokalaemia which should be treated with potassium replacement where necessary. β-adrenoceptor antagonists, even β1-selective antagonists, are potentially life-threatening and should be avoided.
Non-asthmatic patients: Monitor and correct biochemical abnormalities, particularly hypokalaemia.
The preferred antidote for overdosage with salbutamol is a cardioselective β-adrenoceptor blocking agent but due care and attention should be used in administering beta-blocking drugs in patients with a history of bronchospasm, as these drugs are potentially life-threatening. A non-selective β-adrenoceptor antagonist (e.g. nadolol, propranolol) will competitively reverse both hypokalaemia and tachycardia (β1-selective drugs will be largely ineffective).
The treatment of lactic acidosis in cases of salbutamol overdose should be undertaken in a specialist intensive care unit. Salbutamol therapy should be discontinued and appropriate supportive therapy should be commenced to treat the underlying condition. Lactic acidosis is treated indirectly by correcting the underlying causes and not by any treatment aimed directly at correction of lactic acidosis itself.