Pulmonary blood velocity patterns in lamb models of pulmonary vascular impairment

Summary To provide a comprehensive picture of the interaction between abnormal pulmonary hemodynamics and pulmonary blood velocity patterns in the young, we have developed infant animal models of pulmonary hypertension and/or elevated pulmonary blood flow. This report focuses on relationships between selected velocity waveform shape-dependent variables — i.e., the time between the onset of systole and peak velocity (rise time), the time during which velocity remains at >90% of that peak (90% time), and flow reversal patterns — and traditional hemodynamic indications of pulmonary vascular impairment, i.e., elevated pulmonary artery pressure and pulmonary vascular resistance. Studies were performed on 36 anesthetized, open-chest, one-month-old lambs with normal pulmonary circulations or with abnormal conditions that had been initiated during the first few days of life via (1) a central venous injection of monocrotaline pyrrole (hypertension) or (2) a side-to-side anastomosis between the common carotid artery and jugular vein (elevated flow). Animals with large shunts (shunt open cardiac output/shunt closed cardiac output >2.1) had both elevated pressures and flows. The tightest correlations (linear and log-linear) were found between unindexed pulmonary vascular resistance and waveform variables, the most reliable being 90% time (r = -0.838), 90% time + rise time (r = -0.838), and 90% time × rise time (r = -0.824). The best correlate to mean pulmonary artery pressure was 90% time + rise time (r = -0.713). Combined rise time and 90% time variables yielded results that exceeded 90% sensitivity and specificity levels in diagnosing elevated pulmonary vascular resistance (>700 dyne-sec/cm5). Absence of flow reversal in central and anterior regions was an indicator of markedly elevated pulmonary artery pressures (mean >28mmHg). The findings of this report (1) demonstrate the successful development of animal models that mimic a broad spectrum of relevant pulmonary hemodynamics in infants and children with compromised pulmonary circulations and (2) point to shape variables that should improve noninvasive assessment of elevated pulmonary vascular resistance.