[Hemodynamics in ventricular arrhythmias and in their treatment]

The hemodynamic consequences of ventricular tachyarrhythmias are influenced by age, underlying cardiac disease, left ventricular ejection fraction, and possibly by atrial natriuretic peptide. Severity and frequency of the rhythm disorder play, of course, a major role, e.g., monomorphic or polymorphic ventricular premature complexes (VPC), rare or frequent VPC, ventricular tachycardia, ventricular flutter or fibrillation, torsade de pointes, and tachycardia, etc. The therapeutic approach with antiarrhythmic drugs or cardiac pacemakers in cases of conduction disturbances have an additional impact on cardiac performance. Compared to ventricular pacing, a significant higher cardiac output was observed during AV sequential (so called "physiological") pacing evaluated by radionuclide ventriculography. Especially in patients with a reduced left ventricular ejection fraction, the negative inotropic effects of antiarrhythmic drugs are of major importance. A decrease of cardiac output may occur under beta-blocking agents, propafenone, flecainide and particularly disopyramide. On the other hand, amiodarone does not impair cardiac output significantly during acute high dose loading and longterm therapy. In general, negative inotropic effects of antiarrhythmic substances are overestimated; they may even be neglected as long as the antiarrhythmic agent leads to effective suppression of the symptomatic ventricular tachyarrhythmia.