Effects of venovenous extracorporeal membrane oxygenation on cardiac performance as determined by echocardiographic measurements.
We evaluated the effects of venovenous extracorporeal membrane oxygenation (ECMO) on cardiac performance by echocardiographic measurements in 15 infants. Heart rate and blood pressure were also recorded. Echocardiographic measurements included aortic and pulmonary peak blood flow velocities, pulmonary time to peak velocity, left ventricular shortening fraction, velocity of circumferential fiber shortening corrected for heart rate, and peak systolic wall stress before, during, and after venovenous ECMO. Pre-ECMO echocardiograms showed borderline or normal indexes of cardiac function. After initiation of venovenous ECMO, all infants had normalization and no infant had deterioration of cardiac performance. The inotropic agents dopamine and dobutamine were decreased from average doses of 12 and 3.6 micrograms/kg per minute, respectively, to 3.7 and 1.3 micrograms/kg per minute, respectively, within 8.8 hours of the institution of venovenous ECMO. During this time the mean arterial pressure remained stable, and the heart rate decreased (169 +/- 21 vs 136 +/- 15 beats/min; p < 0.001). During the course of ECMO there were no changes in left ventricular shortening fraction, velocity of circumferential fiber shortening corrected for heart rate, or aortic peak blood flow velocities. Pulmonary artery peak blood flow velocity (69 +/- 22 vs 92 +/- 28 cm/sec; p = 0.04) and pulmonary time to peak velocity improved (47 +/- 11 vs 65 +/- 16 msec; p = 0.026). We conclude that venovenous ECMO does not have deleterious effects on cardiac performance.
Strieper
M J
MJ
Children's Heart Center, Egleston Children's Hospital, Emory University, GA 30322.
Sharma
S
S
Dooley
K J
KJ
Cornish
J D
JD
Clark
R H
RH
D004452:Echocardiography; D015199:Extracorporeal Membrane Oxygenation / Q000379:methods; D005260:Female; D006439:Hemodynamics; D006801:Humans; D007231:Infant, Newborn; D008297:Male; D012131:Respiratory Insufficiency / Q000503:physiopathology / Q000628:therapy; D016277:Ventricular Function, Left