Experimentally, a typical ∼2-min cord clamp-to-ventilation interval in preterm lambs is accompanied by increased hemodynamic lability of the birth transition. However, whether this lability is related to development of asphyxia after cord clamping, or can be avoided with a shorter clamp-to-ventilation interval, is unknown. To address these questions, anesthetized preterm fetal lambs (gestation 127 ± 2 days) were instrumented with ductus arteriosus and left pulmonary artery flow probes to obtain right ventricular (RV) output, brachiocephalic trunk and aortic isthmus flow probes to measure left ventricular (LV) output, and aortic trunk catheters for pressure measurement and blood gas analysis. With hemodynamics recorded continuously, fetuses were delivered onto the ewe's abdomen and the cord clamped for 1.5 min before ventilation (n = 8), with aortic sampling at 15, 30, 45, and 60 s, or for 0.5 min, with sampling at 15 s (n = 4). With 1.5-min cord clamping, an asphyxial state (Po2 < 10 mmHg) was evident at ≥45 s, with bradycardia and marked falls in LV and RV outputs (by 60% and 50%, P < 0.001), followed after ventilation onset by tachycardia and LV and RV output surges (4- and 3-fold, P < 0.001). By contrast, heart rate and outputs remained stable after 0.5-min cord clamping, with no postventilation change in heart rate or RV output, and a lesser rise in LV output (22%, P < 0.005). In preterm lambs, rapid development of an asphyxial state within 45 s in the cord clamp-to-ventilation interval increased hemodynamic lability of the birth transition, which was reduced with a shorter (∼0.5 min) cord clamp-to-ventilation interval.

support-information-section). Key pointsr Controversy exists about the physiological mechanism(s) underlying decreases in cardiac output after immediate clamping of the umbilical cord at birth. r To define these mechanisms, the four major determinants of ventricular output (afterload, preload, heart rate and contractility) were measured concurrently in fetal lambs at 15 s intervals over a 2 min period after cord clamping and before ventilation following delivery.r After cord clamping, right (but not left) ventricular output fell by 20% in the initial 30 s, due to increased afterload associated with higher arterial blood pressures, but both outputs then halved over 45 s, due to a falling heart rate and deteriorating ventricular contractility accompanying rapid declines in arterial oxygenation to asphyxial levels.r Ventricular outputs subsequently plateaued from 75 to 120 s, associated with rebound rises in ventricular contractility accompanying asphyxia-induced surges in circulating catecholamines.r These findings provide a physiological basis for the clinical recommendation that effective ventilation should occur within 60 s after immediate cord clamping.