Factors affecting use of the Doppler-determined time from flow onset to maximal pulmonary artery velocity for measurement of pulmonary artery pressure in children

Abstract

Measurement of the time from onset to maximal or peak velocity (TPV) of pulmonary artery (PA) flow has been proposed as a noninvasive means of determining PA pressure. The effects of age, heart rate, increased PA pressure and flow, pulmonary valve obstruction and altered PA vascular resistance on this measurement were evaluated. In 84 children, aged 1 day to 18 years, TPV was measured using continuous-wave Doppler echocardiography. The children were separated into 3 groups. Group I (n = 33) consisted of children with no cardiovascular abnormalities. Group II (n = 33) consisted of children with a variety of cardiovascular diseases producing varying PA pressures and flows. Group III (n = 18) consisted of children who had valvular pulmonic stenosis with PA to right ventricular gradients greater than 40 mm Hg. Doppler studies of group II and III patients were performed in conjunction with measurement of PA pressures and flows at the time of cardiac catheterization. In group I TPV showed a significant negative linear correlation with heart rate (r = −0.86, p < 0.001). The ratio of observed TPV to predicted TPV (TPVN) determined using the regression equation for TPV vs heart rate or TPV/TPVN was heart rate- and age-independent (p > 0.1) and ranged from 0.81 to 1.31 (mean 1.005). In group II TPV/TPVN was inversely related to the natural log of the PA pressures (systolic, r = −0.91; mean, r = −0.87; diastolic, r = −0.82; all p < 0.01), whether pressure elevation was due to increased flow, resistance or left atrial hypertension. It was not affected by increased flow in the absence of pressure elevation. In group III TPV/TPVN was prolonged beyond that expected for the PA pressures and beyond the group I range, but did not correlate with transvalvular pressure gradient. Changes in TPV/TPVN reflect changing PA input characteristics due to either decreasing vascular capacitance from pressure elevation or increased resistance from valvular obstruction.