The dose is 5 - 10 mg IV as a bolus and then an infusion titrated against heart rate and blood pressure (starting at 5 - 10 mg/hour). The rationale for its use is that it increases cyclic AMP and activates myosin kinase independent of beta-receptors. Glucagon Glucagon had been used as antidote for beta-blocker poisoning in the past but its use has been largely superseded by insulin dextrose. It should be given prior to intubation, lavage, or any other procedure that might increase vagal tone and in patients who are nauseated or vomiting. This should be tried in all patients with bradycardia. Other effects In addition to their cardiac effects, beta blocking drugs may also cause hypoglycaemia (by inhibiting glycogenolysis) and /or bronchospasm (in susceptible individuals.) This leads to arrhythmias (ventricular tachycardia and heart block) and direct myocardial depression (see pharmacological properties). Some beta blocking drugs have significant effects on voltage gated ion channels (Na +, Ca 2+, K + ). This is occasionally important in therapeutics but is largely irrelevant to overdose. Lipid solubility alone will not lead to CNS effects and they may relate to Na+ channel blocking effects as they are particularly common with propranolol. (CNS effects) Only lipid soluble drugs will lead to direct CNS effects, though CNS symptoms may occur secondary to cardiac effects and decreased perfusion. This partial agonist effect rarely leads to significant problems and probably protects to some extent from the more serious class I and III antiarrhythmic effects. Intrinsic sympathomimetic activity (ISA) or partial agonist activityĭrugs with ISA may cause beta stimulation leading to tachycardia and hypertension. Though this may be important in determining adverse effects in therapeutic use, it does not have much influence in overdose, as selectivity is lost with high concentrations.
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