Wave intensity analysis of right ventricular and pulmonary vascular contributions to higher pulmonary than aortic blood pressure in fetal lambs

Abstract

Although fetal pulmonary trunk (PT) blood pressure may exceed aortic trunk (AoT) pressure, the specific mechanism(s) underlying this pressure difference remain undefined. To evaluate the potential role of ventricular and vascular factors in the generation of a fetal PT-AoT pressure difference, nine anesthetized late-gestation fetal sheep were instrumented with PT and AoT micromanometer catheters to measure high-fidelity pressure and transit-time flow probes to obtain blood velocity. The PT-AoT instantaneous pressure difference (IPD(PT-AoT)) was calculated from PT and AoT pressure profiles. PT and AoT wave intensity (WI) was derived from the product of the appropriate pressure and velocity rates of change. While diastolic pressures were near identical, systolic PT pressure exceeded AoT pressure (P < 0.001), with a maximal IPD(PT-AoT) of 6.5 +/- 2.5 mmHg. The comparison of IPD(PT-AoT) with wave-related PT and AoT pressure changes indicated that 1) a greater pressure-generating effect of the PT forward-running compression wave arising from impulsive right ventricular contraction in early and midsystole accounted for 2.3 +/- 2.3 mmHg (35%) of the maximal IPD(PT-AoT) and 2) a larger pressure-generating effect of a large midsystolic backward-running compression wave transmitted into the PT from the pulmonary vasculature contributed 4.0 +/- 1.5 mmHg ( approximately 60%) of the maximal IPD(PT-AoT). These results indicate that the higher PT than AoT blood pressure observed in fetal lambs is a systolic phenomenon principally related to the combination of a relatively higher level of right ventricular pump function manifest in early and midsystole and a pressure-increasing energy wave arising from the fetal pulmonary vasculature in midsystole.

Wave intensity analysis in the great arteries – What has been learnt during the last 25 years? Part 1

“…This wave is also transmitted into the Da as a FCW (FCWpulm_foet_Da) and is responsible for augmentation in Da mid-systolic blood flow, a mechanism that supports foetal right-to-left flow at a period in the cardiac cycle where pT and pa flows are decreasing 67 . The comparative assessment of foetal pT and ascending aortic pressure and flow velocity profiles indicated that the higher mean pressure routinely observed in the pT is entirely due to systolic differences 65 . WIa investigation revealed that these differences were because of a larger FCWpulm than FCWao and a larger BCWpulm_foet_pT than BCWao, signifying that both ventricular and vascular components are responsible for the augmentation of foetal systolic pT pressure 65 .…”

“…The comparative assessment of foetal pT and ascending aortic pressure and flow velocity profiles indicated that the higher mean pressure routinely observed in the pT is entirely due to systolic differences 65 . WIa investigation revealed that these differences were because of a larger FCWpulm than FCWao and a larger BCWpulm_foet_pT than BCWao, signifying that both ventricular and vascular components are responsible for the augmentation of foetal systolic pT pressure 65 .…”

“…Notwithstanding, often the FCWpulm presents a second, mid-systolic peak that might be related to the structural immaturity of the foetal myocardium and the resulting poor coordination between lV and RV systolic function 65 . In addition, the presence of a prominent mid-systolic BCW (BCWpulm_foet_pT) has been observed in the foetal pT and temporally associated with the onset of the characteristic mid-systolic plateau in pT blood flow 63 .…”

A step toward clinically applicable noninvasive coronary wave intensity analysis

“…Four possible wave types exist: 1) forward-running compression waves that increase pressure and velocity, 2) forward-running decompression waves that decrease pressure and velocity, 3) backwardrunning compression waves that increase pressure but decrease velocity, and 4) backward-running decompression waves that decrease pressure but increase velocity. Identifying such waves and studying their sequence and magnitude throughout the cardiac cycle can provide a wealth of information regarding physiological mechanisms underlying measured pressure and flow/velocity signals (1,17,21,22).Characterization of coronary arterial flow patterns using wave intensity analysis was first performed in anesthetized dogs by Sun et al (27), via passage into the circumflex artery of a thin micromanometer-tipped catheter to measure highfidelity pressure and a guidewire with a Doppler sensor mounted on its tip to obtain velocity. An important finding arising from initial studies was that backward-running compression waves, generated within the myocardium during the isovolumic contraction and early ejection periods, were key actuators of systolic flow impediment, as they countered the forward flow-promoting effects of an aortic forward-running compression wave generated in the early phase of ventricular ejection (26,27).…”

“…Four possible wave types exist: 1) forward-running compression waves that increase pressure and velocity, 2) forward-running decompression waves that decrease pressure and velocity, 3) backwardrunning compression waves that increase pressure but decrease velocity, and 4) backward-running decompression waves that decrease pressure but increase velocity. Identifying such waves and studying their sequence and magnitude throughout the cardiac cycle can provide a wealth of information regarding physiological mechanisms underlying measured pressure and flow/velocity signals (1,17,21,22).…”