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.