Search

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.sub.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.sub.PT-AoT] of 6.5 [+ or -] 2.5 mmHg. The comparison of [IPD.sub.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 [+ or -] 2.3 mmHg (35%) of the maximal [IPD.sub.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 [+ or -] 1.5 mmHg (~60%) of the maximal [IPD.sub.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 fight ventricular pump function manifest in early and midsystole and a pressure-increasing energy wave arising from the fetal pulmonary vasculature in midsystole. fetal ventricular hydraulic power; fetal pulmonary trunk blood flow; fetal aortic trunk blood flow doi: 10.1152/ajpheart.00292.2010.

In midsystole, fetal pulmonary trunk (PT) and arterial (PA) blood flows characteristically fall, despite pulmonary blood pressure increasing, while ductus arteriosus (DA) flow continues to rise to a delayed peak. Wave intensity (WI) analysis indicates that midsystolic fetal PT and PA flow reductions are related to a very large midsystolic PA backward-running compression wave ([BCW.sub.ms]), which originates in the pulmonary microvasculature and is partially transmitted into the PT. This study tested the hypothesis that midsystolic augmentation of DA blood flow was related to transmission of the PA [BCW.sub.ms] into the DA. DA, PT, and PA WI analysis was performed in eight anesthetized late-gestation fetal sheep instrumented with DA, PT, and left PA micromanometer catheters to measure pressure (P) and transit-time flow probes to obtain blood velocity (U). In a subgroup (n = 5), the main PA was briefly occluded to abolish wave transmission from the lungs. WI was calculated as the product of P and U rates of change. PA and PT WI profiles both contained a prominent [BCW.sub.ms], ~5-fold larger in the PA (P < 0.005), which increased P but decreased U. By contrast, the DA WI profile demonstrated a large midsystolic forward-running compression wave ([FCW.sub.ms]), which increased DA P and U, and occurred 5 ms after PA [BCW.sub.ms]. Furthermore, both DA [FCW.sub.ms] and PT [BCW.sub.ms] were abolished by main PA occlusion. These results suggest that the fetal PA [BCW.sub.ms] undergoes retrograde transmission into the PT as a [BCW.sub.ms], but antegrade transmission into the DA as a [FCW.sub.ms] that augments midsystolic DA flow. ductus arteriosus blood flow; ductus arteriosus blood pressure; fetal central hemodynamics doi: 10.1152/ajpregu.00384.2009

Steady-state wave intensity (WI) analysis indicates that characteristic midsystolic falls in fetal pulmonary trunk (PT) and artery (PA) blood flow are due to an extremely large backward-running compression wave ([BCW.sub.ms]) that 1) originates from the pulmonary microvasculature by a combination of cyclical pulmonary vasoconstriction and vascular reflection of the forward-running compression wave ([FCW.sub.is]) associated with impulsive right ventricular ejection, and 2) is transmitted into the PT. However, no information is available about the dynamic properties of PA [BCW.sub.ms] and its contribution to beat-to-beat regulation of pulmonary hemodynamics. Accordingly, beat-by-beat WI analysis was performed during brief increases in ventricular contractility accompanying an extrasystole (ES) in nine anesthetized late-gestation fetal sheep instrumented with PT and left PA micromanometer catheters to measure pressure (P) and transit-time flow probes to obtain blood velocity (U). WI was calculated as the product of P and U rates of change. At steady state, the magnitude of PA [BCW.sub.ms], and its associated P and U changes ([DELTA]P and [DELTA]U, respectively), were similar to those of [FCW.sub.is]. The PA [FCW.sub.is] and [BCW.sub.ms], and their accompanying [DELTA]P and [DELTA]U, were all transiently potentiated after an ES. Beat-by-beat PA [FCW.sub.is]-[BCW.sub.ms] wave area, [DELTA]P and [DELTA]U relationships were highly linear ([R.sup.2] [greater than or equal to] 0.91) with slopes of 1.36-1.47 (P < 0.001), consistent with the presence of a vasoconstrictor component in PA [BCW.sub.ms]. PA-PT [BCW.sub.ms] area and [DELTA]P and [DELTA]U relationships were also linear ([R.sup.2] [greater than or equal to] 0.77) with slopes of 0.23-0.64 (P < 0.001). These results indicate that the fetal PA [BCW.sub.ms] contributes to beat-to-beat regulation of not only PA but also PT hemodynamics. fetal pulmonary blood flow; fetal pulmonary blood pressure; postextrasystolic potentiation

Precise identification of end-diastole (ED), corresponding to the end of diastole and start of systole, is crucial for accurate assessment of cardiac function. The aims of this study were to develop a new algorithm based on peak curvature ([K.sub.p]) for detecting ED as a 'corner' in left ventricular pressure (LVP) signals, and to compare this approach with 'gold-standard' ED obtained by manual annotation ([ED.sub.man]) and ED calculated with previously described algorithms that use an LVP first-derivative threshold (dP/[dt.sub.0] or dP/[dt.sub.100]), the peak LVP second-derivative ([d.sup.2] P/[dt.sup.2.sub.p]) or ECG R-wave peak ([ECG.sub.R]). Using customized software, all algorithms were applied to data derived from 213 large animal studies spanning a wide range of animal ages (fetus to adult), heart rates, inotropic states, and loading conditions. Differences between [ED.sub.man] and each algorithm were then compared after defining an acceptance region for the ED detection based on [ED.sub.man] interobserver variability. ED detected with [K.sub.p] was the most accurate (p < 0.001) and least variable (p < 0.001), with 97% of measurements within the acceptance region and difference from [ED.sub.man] of (1.5 [+ or -] 4.2) ms. By contrast, ED was often detected early with dP/[dt.sub.0] and dP/[dt.sub.100], and late with [d.sup.2] P/[dt.sup.2.sub.p] and [ECG.sub.R]. These results indicate that the peak curvature algorithm using LVP provides accurate and reliable detection of ED. Index Terms--Curvature, end-diastole (ED), feature detection.

The physiological basis of a characteristically low blood flow to the fetal lungs is incompletely understood. To determine the potential role of pulmonary vascular interaction in this phenomenon, simultaneous wave intensity analysis (WIA) was performed in the pulmonary trunk (PT) and left pulmonary artery (LPA) of 10 anesthetized late-gestation fetal sheep instrumented with PT and LPA micromanometer catheters to measure pressure (P) and transit-time flow probes to obtain blood velocity (U). Studies were performed at rest and during brief complete occlusion of the ductus arteriosus to augment pulmonary vasoconstriction (n = 4) or main pulmonary artery to abolish wave transmission from the lungs (n = 3). Wave intensity (d/w) was calculated as the product of the P and U rates of change. Forward and backward components of d/w were determined after calculation of wave speed. PT and LPA WIA displayed an early systolic forward compression wave ([FCW.sub.is]) increasing P and U, and a late systolic forward expansion wave decreasing P and U. However, a marked midsystolic fall in LPA U to near-zero was related to an extremely prominent midsystolic backward compression wave ([BCW.sub.ms]) that arose ~5 cm distal to the LPA, was threefold larger than the PT [BCW.sub.ms] (P < 0.001), of similar size to [FCW.sub.is] at rest (P > 0.6), larger than [FCW.sub.is] following ductal occlusion (P < 0.05) and abolished after main pulmonary artery occlusion. These findings suggest that the absence of pulmonary arterial midsystolic forward flow which accompanies a low fetal lung blood flow is due to a [BCW.sub.ms] generated in part by cyclical vasoconstriction within the pulmonary microcirculation. fetal pulmonary vascular interaction; fetal pulmonary blood flow; fetal pulmonary blood pressure

This study undertook a detailed examination of the ventricular-vascular interaction of the predominant [beta]-adrenergic agonist dobutamine using wave intensity analysis. Eight anesthetized open-chest ewes were instrumented with an aortic micromanometer to measure central aortic blood pressure (P) and an ultrasonic flow probe to obtain ascending aortic blood velocity (U). Hemodynamics were recorded during incremental dobutamine infusion (0.5, 1, 2.5, 5, 7.5, and 10 [micro]g x [kg.sup.-1] x [min.sup.-1]). Wave intensity (d[I.sub.w]) was calculated as the product of the rates of change of P and U with customized software using ensemble-averaged signals. Forward and backward components of d[I.sub.w], P, and U were determined after calculation of wave speed. As well as the typical initial forward compression wave (FCW), midsystolic backward compression wave (BCW), and late-systolic forward expansion wave ([FEW.sub.es]), two minor and previously unheralded waves were also detectable in the wave intensity profile at baseline. The first was an early systolic backward expansion wave (BEW), which reduced P but increased peak U. The second was a mid-systolic forward expansion wave ([FEW.sub.ms]), which reduced P and U. During dobutamine infusion FCW d[I.sub.w] increased 18-fold (P < 0.001), but BCW d[I.sub.w] rose 12-fold (P < 0.001) while [FEW.sub.es] d[I.sub.w] fell by 70% (P < 0.001). However, the latter changes were accompanied by a 44-fold increase in BEW d[I.sub.w] (P = 0.005) that augmented the initial aortic forward flow and a >100-fold rise in [FEW.sub.ms] d[I.sub.w] (P < 0.001) that produced earlier and enhanced aortic blood deceleration. These findings provide new insights into the ventricular-vascular interaction of dobutamine. hemodynamics; wave propagation; arterial circulation; blood velocity