Left ventricular dysfunction after open repair of simple congenital heart defects in infants and children: Quantitation with the use of a conductance catheter immediately after bypass

Objective: Quantification of myocardial injury after the simplest pediatric operations by load-independent indices of left ventricular function, using conductance and Mikro-Tip pressure catheters (Millar Instruments, Inc., Houston, Tex.) inserted through the left ventricular apex. Methods: Sixteen infants and children with intact ventricular septum undergoing cardiac operations had left ventricular function measured, immediately before and after bypass. Real-time pressure-volume loops were generated by conductance and Mikro-Tip pressure catheters placed in the long-axis via the left ventricular apex, and preload was varied by transient snaring of the inferior vena cava. Results: Good quality pressure-volume loops were generated in 13 patients (atrial septal defects, n = 11; double-chambered right ventricle, n = 1; supravalvular aortic stenosis, n = 1; age 0.25 to 14.4 years, weight 3.1 to 46.4 kg). Their mean bypass time was 41 ± 14 minutes and mean aortic crossclamp time 27 ± 11 minutes. End-systolic elastance decreased by 40.7% from 0.34 ± 0.17 to 0.21 ± 0.15 mm Hg -1·ml -1·kg -1 ( p < 0.001). There were no significant changes in the slope of the stroke work–end-diastolic volume relationship, end-diastolic elastance, time constant of isovolumic relaxation, and normalized values of the maxima and minima of the first derivative of developed left ventricular pressure. Conclusion: Load-independent indices of left ventricular function can be derived from left ventricular pressure-volume loops generated by conductance and Mikro-Tip pressure catheters during the perioperative period in infants and children undergoing cardiac operations. Incomplete myocardial protection was demonstrated by a deterioration in systolic function after even short bypass and crossclamp times. Ignorance of the cause of postoperative myocardial dysfunction in the immature heart is compounded by the incomplete myocardial protection afforded by current cardioplegic strategies. 1,5 Investigations of the mechanisms and treatment of postoperative ventricular dysfunction are hampered by use of nonspecific clinical end points as indirect estimates of ventricular function, for example, requirement for inotropic agents, duration of ventilation, intensive care unit stay, and mortality. These clinical indices are relatively insensitive to changes in ventricular function and necessitate large cohorts of patients to detect even major differences in outcome from differing myocardial protective strat