Sensitivity and afterload independence of zero-load aortic flow

The computed zero-load flow is the expected aortic flow when the aortic pressure is zero, thus eliminating the effect of afterload on ventricular ejection. Zero-load flow was computed in 15 anesthetized dogs (sodium pentobarbital 25 mg/kg, iv) by studying the response of left-ventricular pressure or aortic pressure, and aortic flow to the change in aortic input impedance induced by partial snare occlusion of the aorta. The waveform and peak value of zero-load flow were computed from a theoretical model of the left ventricle and verified by measurements of aortic flow in the first beat after transection of the aorta. To study the sensitivity, changes of zero-load flow were computed under the enhanced inotropic state produced by isoproterenol (0.1 μg/kg/min), and under the depressed contractile state induced by propranolol (0.15 mg/kg). Administration of isoproterenol resulted in an increase in the peak zero-load flow by 143.9% (p<0.001), compared with a 50.6% increase (p<0.05) in peak dp/dt. The difference of the variations was statistically significant in a paired t test. After injection of propranolol, peak zero-load flow decreased by 32.0% (p<0.005). Afterload independence of zero-load flow was studied by computing zero-load flow before and after increasing arterial pressure by partial aortic occlusion or injection of 5 mg methoxamine. After injection of methoxamine in denervated dogs, the peak zero-load flow increased by 11.2% (N.S.), while input resistance increased by 153% (p<0.025). The peak zero-load flow decreased by 8% (N.S.) after partial aortic occlusion, while cardiac output decreased by 26.7% (p<0.001). These results may suggest that the computed peak zero-load flow is an afterload independent index of the pumping capability of the left ventricle in the intact heart.