Myocardial contractility of the canine left ventricle during unsynchronized dual chamber pacing.

The influence of changes of left ventricular (LV) myocardial contractility on the decrease of cardiac output during atrial fibrillation was investigated in dogs using the slope (Ec) and the length intercept (Lo) of the LV end-systolic force-length relationship. The hearts of nine healthy adult mongrel dogs were instrumented with ultrasonic crystals and a micromanometer, after which pharmacologic autonomic blockade was instituted. The LV diameter and pressure data were recorded during inferior vena caval occlusion. Hemodynamic parameters were measured during pacing from the right atrial appendage at a pacing rate 30 beat/min greater than the natural heart rate using a cardiac stimulator (atrial pacing), and during simultaneous pacing from the right atrial appendage and right ventricular apex at the same rate (unsynchronized dual chamber pacing). Cardiac hemodynamics in the absence of synchronized left atrial contraction were simulated by unsynchronized pacing. During atrial pacing, the cardiac output (1.68 +/- 0.25 vs 1.57 +/- 0.21 l/min, p < 0.005) and Ec (110.1 +/- 58.5 vs 81.8 +/- 30.8 g/cm, p < 0.05) were significantly greater than during normal sinus rhythm, whereas the stroke volume (12.4 +/- 2.4 vs 15.1 +/- 3.1 ml, p < 0.005) and LV end-diastolic volume (16.6 +/- 2.7 vs 19.5 +/- 3.4 ml, p < 0.005) were significantly smaller. Lo did not change during pacing. During unsynchronized dual chamber pacing, cardiac output (1.46 +/- 0.17 vs 1.68 +/- 0.25 l/min, p < 0.005), stroke volume (10.8 +/- 1.7 vs 12.4 +/- 2.4 ml, p < 0.005), and LV end-diastolic volume (15.0 +/- 2.0 vs 16.6 +/- 2.7 ml, p < 0.05) were significantly smaller than during atrial pacing. However, Ec and Lo were similar during both types of pacing. These findings suggest that the decrease of cardiac output and stroke volume during atrial fibrillation is chiefly due to the decrease of LV end-diastolic volume through loss of left atrial contraction, and is not due to a change of LV myocardial contractility.