Hemodynamic consequences of supraventricular tachycardias and their antiarrhythmic treatment

Complex adjustments in contractility, resistance, stroke volume and atrio-ventricular contraction relationships underlie the optimization of cardiac output during variations in sinus rate. In patients with intra AV nodal re-entry tachycardia and accessory pathway tachycardias, rate and loss of appropriately timed atrial transport reduce cardiac efficiency, but this is serious only when heart rates are very high. True atrial tachycardia, atrial fibrillation, and atrial flutter are often associated with cardiovascular disease. In atrial fibrillation and flutter, loss of atrial transport may be less important than the hemodynamic consequences of irregularity of ventricular systole. Antiarrhythmic management may ameliorate the consequences of the arrhythmia by reducing heart rate, restoring sinus rhythm or more controversially by regularizing ventricular contraction. Digoxin and antiarrhythmic surgery have little negative inotropic potential but most other antiarrhythmic drugs and ablation procedures depress myocardial function. Antitachycardia pacemakers may produce acute adverse hemodynamic effects depending upon the type of pulse trains delivered to terminate the tachycardia.