Schmidt H, Czerny H, Morgenstern J, Schulz J, Wernicke K
Z Geburtshilfe Perinatol. 1979 Apr;183(2):101-7.
Acute foetal hypoxia trials were conducted in 11 foetuses of sheep. The following parameters were determined continuously besides heart rate, art. pO2, arterial and venous blood pressure: cardiac output, stroke volume and system resistance. Acute foetal hypoxia was produced in two ways: 1) Compression of the maternal vena cava The arterial blood pressure in the foetus is increased. This is reflected mainly by the systolic blood pressure. This increase is provoked by the increase in stroke volume (up to 100%). This increase in stroke volume is so great that the cardiac output is increased despite the onset of deceleration. The system resistance remains unchanged. 2) Maternal hypoxia In contrast to foetal hypoxia as described above, the increase of stroke volume is not so pronounced at the onset of deceleration, and the system resistance is increased. After termination of maternal hypoxia there is an abrupt change of system resistance back to the original value. Both types of foetal hypoxia will subsequently not differ significantly from each other.
