Circulatory responses to maternal hyperoxaemia and hypoxaemia assessed non-invasively in fetal sheep at 0.3–0.5 gestation in acute experiments

Fetal Ventricular Diastolic Filling Characteristics in a Primate Model: The Role of Fetal Heart Rate and Pulmonary Vascular Impedance

“…Unlike previous observational studies, we were able to demonstrate that the immediate increase in the TV V-max E/A ratio seen with hyperoxygenation was the result of a decrease in the Awave V-max, rather than the traditionally accepted increase in E-wave V-max. In line with a prior study of fetal sheep that demonstrated that hypoxia can augment atrial contractility, 10 our study suggests that an increase in fetal oxygenation can have an opposite effect on atrial contractility. Although some researchers indicate that the longitudinal increases in the E/A ratio during gestation are due to structural changes in the heart that lead to improved ventricular compliance and relaxation, 4,[11][12][13] we showed that the immediate changes in the E/A ratio seen with hyperoxygenation are independent of ventricular diastolic function.…”

Placental and fetal hemodynamics in prolonged pregnancies

“…high fetal cardiac output of 250–300 mL/kg/min), rapid heart rate, high fetal hemoglobin level and high oxygen affinity . Severe chronic fetal hypoxemia is characterized by hyperdynamic fetal circulation, redistribution of blood flow to vital organs, increased systemic venous pressure, a shift in cardiac output favoring the left ventricle and increased right ventricular afterload, whereas a reduced heart rate, increased peripheral resistance and reduced blood flow is typical for acute hypoxemia in animal and human fetuses . We hypothesized that subtle changes in Doppler measurements describing these parameters would identify fetuses unable to tolerate additional delivery‐related stress.…”

Fetal Venous Circulation

“…[6][7][8]99,100 The Pulsalility Index for Veins (PIV = (S − A)/V ta ) suggested by Hecher et al is probably the one most used and is a robust parameter for clinical work. 113,150,151 Although fetal reflexes and endocrine functions are not fully developed in the second trimester, the venous Doppler pattern induced by hypoxaemia is much the same as seen in older fetuses. In fetuses with congenital heart defects this is a common finding, especially if the defect involves valves or ventricular function.…”

“…A corresponding augmented nadir before the atrioventricular valves open to permit the second wave of diastolic filling 113 (Figure 19), is seen in terminally ill fetuses, particularly in the very premature and growth restricted fetuses. With increasing hypoxemia and acidosis, the myocardium becomes stiffer.…”

“…145 An increased pulsatility is usually due to an augmented a-wave 6 ( Figure 19). 113 A correlation between increased pulsatility in the ductus venosus and acidosis has been demonstrated in compromised pregnancies 145,152 and the sign of an augmented or negative a-wave has been suggested as part of a scoring system to assess congestive heart failure. 146 Similar changes are seen in the severely growth restricted fetus; 94,145,147−149 the systolic peak is maintained within normal ranges while the diastolic nadir is augmented, particularly in fetuses below 32 weeks of gestation.…”