Arterial oxygen saturation in relation to metabolic acidosis in fetal lambs.
OBJECTIVE
We studied the relationship between preductal arterial oxygen saturation and metabolic acidosis in 18 chronically instrumented fetal lambs (gestational age 119 to 133 days) in two experimental designs. In the first group the onset of metabolic acidosis was determined. In the second group the progression of metabolic acidosis was studied as was the cardiovascular and hormonal changes resulting from hypoxemia.


METHODS
In nine fetal lambs maternal fraction of inspired oxygen was lowered stepwise by increasing flows of nitrogen delivered into the trachea through a small indwelling catheter (group 1), and in nine fetal lambs maternal blood flow was reduced stepwise by means of a vascular occluder (group 2).


RESULTS
Baseline arterial oxygen saturation values ranged from 26% to 67% with normal pH and extracellular fluid base excess values in both groups 1 and 2. In both groups pH and extracellular fluid base excess started to decrease below 30% arterial oxygen saturation, with a progressive decrease below 20% arterial oxygen saturation to an end value for pH of 7.14. In some fetal lambs pH and extracellular fluid base excess decreased initially at 20% to 30% arterial oxygen saturation and then stabilized at the lower level. Fetal heart rate in group 1 increased during hypoxemia from 155 to 179 beats/min. In group 2 baseline fetal heart rate was 153 beats/min and fell with every step change in arterial oxygen saturation but subsequently increased to 172 beats/min by the end of the period of hypoxemia. Baseline values for epinephrine, norepinephrine, dopamine, cortisol, and mean arterial pressure were not related to baseline arterial oxygen saturation levels, and each of these variables was increased at the end of hypoxemia in group 2.


CONCLUSIONS
Preductal arterial oxygen saturation can reach values between 20% and 30% before anaerobic metabolism starts. During the progressive acidosis blood pressure was increased, which can be attributed to a strong rise in catecholamines.
Nijland
R
R
Department of Obstetrics and Gynaecology, University of Nijmegen.
Jongsma
H W
HW
Nijhuis
J G
JG
van den Berg
P P
PP
Oeseburg
B
B
D000138:Acidosis / Q000097:blood* / Q000209:etiology; D000818:Animals; D002245:Carbon Dioxide / Q000097:blood; D002395:Catecholamines / Q000097:blood; D005110:Extracellular Space / Q000502:physiology; D005260:Female; D005315:Fetal Diseases / Q000097:blood* / Q000209:etiology; D006863:Hydrogen-Ion Concentration; D000860:Hypoxia / Q000150:complications; D010100:Oxygen / Q000097:blood*; D012756:Sheep; D014599:Uterus / Q000098:blood supply
D002395:Catecholamines; D002245:Carbon Dioxide; D010100:Oxygen