At least in healthy adult humans at rest, about 80% of ventricular filling is complete by the time atria contract. By definition, duration of diastole and consequently the time available for ventricular filling is reduced with a progressive elevation in HR, and the question in any situation therefore is how this might affect ventricular filling. During dynamic exercise in healthy adult humans, an increase in HR typically does not reduce ventricular filling as long as the rhythm is sinus and HR reaches about 180 bpm; rather, it is associated with an increase in ventricular filling (compared to baseline) providing that the rhythm is sinus and venous return is maintained or increased. An increase in SV is also made possible under these conditions by one or more of the following mechanisms acting in concert.
i) an increase in sympathetic outflow to the heart is normally associated with a positive lusitropic effect (i.e., acceleration of the rate of relaxation of ventricular myocardial cells) besides an increase in HR and an increase in the speed of conduction of cardiac impulse;
ii) an increase in HR in the 60-120 bpm range is typically associated with an increase in force of contraction secondary to an increase in intracellular calcium (frequency-force relationship or Treppe effect) providing that venous return is not affected;
iii) the sympathoexcitation that occurs during exercise also facilitates venous return by inducing constriction of the peripheral veins;
iv) contractions of skeletal muscles may contribute to maintaining venous return when valves in veins are competent.
How ventricular filling is affected by tachycardia in a given individual or experimental setting requires consideration of multiple factors including whether the rhythm is sinus or some other pathological rhythm, the extent of HR elevation, the presence or absence of an atrial kick effect contributing to ventricular filling, A-V valve function, ventricular diastolic function and pericardial pressure. Even in health, increases in ventricular rate beyond 180 bpm during intense exercise are not necessarily associated with a further increase in ventricular filling [Ganong]; further increases in cardiac output are achieved with a decrease in ventricular end-systolic volume, and an increase in HR. In individuals lacking the contribution of atrial contractions to ventricular filling such as in those with atrial fibrillation, ventricular filling has been observed to plateau at somewhat lower HRs (90-140 bpm) depending on the extent of the underlying disease, and the maximal cardiac output achievable is reduced compared to healthy age matched controls. If the atria are paced electrically to 180 bpm in healthy individuals at rest, little change occurs in cardiac output from baseline, because of a reduction in SV. This is because the rate of A-V nodal conduction (which is regulated by vagal and sympathetic influences) becomes limiting in the absence of an actual increase in cardiac sympathetic outflow and an actual decrease in cardiac vagal outflow; second, the positive lusitropic effects of sympathetic stimulation do not occur in this model.