Effects of pulmonary vascular obstruction on right ventricular afterload

We compared the effects of three forms of vascular obstruction: positive end-expiratory pressure (PEEP), ensnarement of the left main pulmonary artery (SN), and pulmonary thromboembolism (EMB) on right ventricular afterload. We measured right ventricular and pulmonary arterial pressures and flow in open-chested dogs under anesthesia (n = 8). Pulmonary artery input impedance (Z(in)) was calculated by Fourier analysis of the pressure and flow waves. Characteristic impedance (Z(c)) and pulmonary arterial compliance (C(a)) were estimated from Z(in) with a lumped parameter model. Although PEEP, SN, and EMB all increased mean pulmonary arterial pressure, PEEP had negligible effect on Z(c) and C(a), whereas SN increased Z(c) but decreased C(a) (+24% and -49%, respectively), and EMB decreased both Z(c) and C(a) (-33% and -39%, respectively). These changes of Z(c) affect wave reflection and alter the energy transmission ratio, which is the ratio of hydraulic power output in the measured and forward waves (Ẇ(m)/Ẇ(f)). Under control conditions, Ẇ(m)/Ẇ(f) was 62% and was not affected significantly by SN (59%) or by PEEP (46%), but it fell significantly to 30% after EMB. Stimulation of these experiments in a mathematical model suggested that the increase of Z(c) with SN was due to an active neurohumoral effect; all other responses were consistent with passive mechanical effects. In additional experiments, we tested the effects of meclofenamate (n = 6) and ketanserin (n = 6) and of atropine and vagotomy (n = 5) on the response to SN and EMB. The serotonin antagonist, ketanserin, blunted the increase of Z(c) to SN, but none of the interventions significantly affected the response of Z(c) or C(a) to EMB. We conclude that SN had different effects on right ventricular afterload than does EMB. SN appears to involve an active neurohumoral mechanism that is attenuated by ketanserin and acts to reduce the adverse effects of wave reflection.