PULMONARY BLOOD VELOCITY PATTERNS IN LAMB MODELS OF PULMONARY VASCULAR IMPAIRMENT

To provide a comprehensive picture of the interaction between abnormal pulmonary hemodynamics and pulmonary blood velocity patterns in the y oung, we have developed infant animal models of pulmonary hypertension and/or elevated pulmonary blood flow. This report focuses on relation ships between selected velocity waveform shape-dependent variables - i .e., the time between the onset of systole and peak velocity (rise tim e), the time during which velocity remains at >90% of that peak (90% t ime), and flow reversal patterns - and traditional hemodynamic indicat ions 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 pulmonar y circulations or with abnormal conditions that had been initiated dur ing the first few days of life via (1) a central venous injection of m onocrotaline pyrrole (hypertension) or (2) a side-to-side anastomosis between the common carotid artery and jugular vein (elevated flow). An imals with large shunts (shunt open cardiac output/shunt closed cardia c output >2.1) had both elevated pressures and flows. The tightest cor relations (linear and log-linear) were found between unindexed pulmona ry vascular resistance and waveform variables, the most reliable being 90% time (r = -0.838), 90% time + rise time (r = -0.838), and 90% tim e x rise time (r = -0.824). The best correlate to mean pulmonary arter y pressure was 90% time + rise time (r = -0.713). Combined rise time a nd 90% time variables yielded results that exceeded 90% sensitivity an d specificity levels in diagnosing elevated pulmonary vascular resista nce (>700 dyne-sec/cm(5)). Absence of flow reversal in central and ant erior regions was an indicator of markedly elevated pulmonary artery p ressures (mean >28 mmHg). The findings of this report (1) demonstrate the successful development of animal models that mimic a broad spectru m of relevant pulmonary hemodynamics in infants and children with comp romised pulmonary circulations and (2) point to shape variables that s hould improve noninvasive assessment of elevated pulmonary Vascular re sistance.