THE FETAL AND NEONATAL CIRCULATION 



I&37 



Intra- uterine 



Uterus open 



22 



24 



26 



1 2 3 4 S 6 20 



Time (mln) 



fig. 16. In the guinea pig, of 54 days gestation, a) the fetal 

 heart slows when the uterus is opened; h) marked fetal brady- 

 cardia occurs following the maternal injection of noradrenaline 

 only after the uterine wall is opened. [From Martin & Young 

 (■33)-] 



blood supply to the fetus upon the susceptibility to 

 further asphyxia as shown in figure 16; after the 

 uterine wall was opened, to expose the fetus, the 

 uterine muscle contracted away from the incision 

 around the uterine blood vessels, and cardiac slowing 

 could be produced with a smaller dose of vasocon- 

 strictor substance in the maternal circulation than 

 when the fetus was in utero. 



Reduction in the uterine blood flow giving rise to 

 these various patterns of fetal heart rate changes may 

 be brought about in many ways. It follows the injec- 

 tion of either hypotensive (82, 194) or vasoconstrictor 

 (34) drugs into the maternal circulation; the effect 

 will be reversible or not according to the dose given 

 and the duration of action of the pharmacological 

 substance. Uterine blood flow may be markedly 

 reduced temporarily, by adrenaline or noradrenaline 

 in the maternal circulation, and this may be one 

 reason for the poor placental transfer of noradrenaline 

 which has been observed (168). In the guinea pig the 

 uterine blood vessels become sensitized to the action 

 of adrenaline as gestation proceeds and following the 

 administration of both estrogen and progesterone 

 (133). It is possible that there is a reduction in ma- 

 ternal placental blood flow before conversion of the 

 uterus from the spherical to oval shape (154, 157). 



The influence of uterine contraction on the fetal 

 heart rate has been most extensively studied and de- 

 pends upon the duration of the contraction, its fre- 

 quency and upon the intrauterine pressure developed 

 (7, 15, 109). It is probable that the first effect of any 



uterine contraction will be to upset the functional 

 countercurrent mechanism which enables the mater- 

 nal arterial blood in the intervillous space to reach 

 the base of the chorionic villi and enable final ar- 

 terialization of the umbilical venous blood. Hendricks 

 et at. (104) have made simultaneous recordings of the 

 intra-amniotic and intervillous pressures in the hu- 

 man and consider the sequence of events on the 

 maternal side of the placenta to be complicated be- 

 fore the oxygen supply to the fetus is impaired during 

 a contraction. They observed the pressures in the 

 intervillous pool and the amniotic cavity to be about 

 equal, both when the uterus was relaxed and during 

 systole; the increase in the intervillous pressure lagged 

 behind the intra-amniotic pressure rise during con- 

 traction. It is suggested that the intervillous volume is 

 slightly reduced during the early phase of contrac- 

 tion; but once the intra-amniotic pressure exceeds 

 that in the uterine vein, venous drainage will cease 

 and the intervillous volume become expanded as 

 the arterial inflow continues. The oxygen supply, 

 though slowed, may continue for a considerable time 

 during contraction, and the spongy structure of the 

 placenta and the large venous sinuses allows local 

 pressure differences to be distributed and prevent 

 retroplacental hemorrhage. The increased pressure 

 in the intervillous space will be transmitted to the 

 fetal vessels and, added to a reduced oxygen supply, 

 there will be a reduction in umbilical blood flow 

 as the resistance increases. Reynolds & Paul (159) 

 observed in the lamb, in utero, that rhythmic con- 

 tractions of low intensity which caused a rise of intra- 

 amniotic pressure of about 5 mm Hg caused an 

 equal rise in fetal blood pressure but no change in 

 heart rate: manual pressure on the uterus or the 

 application of weights, from 1 kg upward, caused 

 a rise of arterial pressure in the fetus which exceeded 

 the rise in amniotic pressure; this was asphyxial in 

 origin and accompanied by bradycardia. Strong 

 contractions induced by Pitocin, which raised the 

 intra-amniotic pressure more than 10 mm Hg, gave 

 similar vascular responses in the fetus (15, 159). 



The quantitative relationship between reduction 

 in maternal placental blood flow and the appearance 

 of fetal bradycardia has been supplied in the sheep 

 by Adams et al. (2); no change in fetal heart rate was 

 observed until the uterine blood flow, measured with 

 an electromagnetic flowmeter, was reduced to about 

 one-third of the control level following the injection 

 of adrenaline into the maternal circulation. This 

 relationship was readily predicted from the heart 

 rate changes occurring during the administration of 



