Multiple classes of xenobiotics have the potential to influence the function of the cardiovascular system. When evaluating the hemodynamic consequences of any toxic exposure and initiating treatment of such abnormalities, the clinician must consider the mechanism by which the toxin exerts its effect. This review focuses on diagnosis and management of toxicity related to common classes of antiarrhythmic drugs and the centrally acting hypertensives. Beta blockers, calcium channel blockers, cardiac glycosides, sodium channel and potassium channel blockers, and clonidine and centrally acting alpha2 agonists are described in relation to principles of toxicity, immediate stabilization, diagnosis and definitive therapy, and disposition and outcome. Tables include classes of antiarrhythmics, various beta-blocker properties, standard dosing regimen for hyperinsulinemia/euglycemia, calcium channel blockers, botanical and animal sources of cardiac glycosides, P-glycoprotein inhibitors, and various alpha agonists. Figures show the mechanisms for beta-receptor activation, hyperinsulinemia/euglycemia, and cardiac glycosides. An electrocardiogram demonstrating digitalis effect is also provided. T
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