A 21 year old female is brought to ICU extubated post Caesarian section for pre- eclampsia and foetal distress. The following are data from blood gas analysis.
Barometric pressure | 760 mm Hg | |
|
|
|
pH |
7.31 |
|
pO2 |
150 mm Hg |
20 kPa |
pCO2 |
42 mm Hg |
5.6 kPa |
HCO3- |
20.5 |
mmol/L |
Standard base excess |
-4.9 |
mmol/L |
a) Describe and explain the acid-base status.
b) If she had normal lung function, what should her PaO2 be?
c) Name three possible causes of her reduced oxygen transfer?
Q7.3a) Acute respiratory acidosis following previous compensated respiratory alkalosis of pregnancy. At 38 weeks pregnancy the normal PaCO2 is <30 mm Hg with compensatory HCO3- reduction. The blood gases therefore indicate acute CO2 retention, probably due to pain and narcotics.
Q7.3b) > 250 mm Hg.
Q7.3c) Potential explanations include loss of FRC post abdominal surgery, segmental collapse or consolidation, aspiration, pulmonary oedema.
Let us dissect these results systematically.
However, one should point out that the empirical rules for blood gas interpretation were developed from data collected in non-pregnant individuals, and do not account for the changes in homeostatic setpoints of pregnancy. Indeed, if we were to consider that the pregnant woman has well-compensated respiratory alkalosis at term (with a chronically decreased PaCO2, down to 30mmHg) we would expect the HCO3- to decrease by 5mmol/L, which would give us an expected HCO3- of 19mmol/L.
If this pregnant woman with a HCO3- of 19mmol/L were to suddenly develop a respiratory acidosis, the HCO3- would increase by 1mol/L for every 10mmHg of PaCO2 elevation. The expected HCO3- in this woman would therefore be slightly over 20mmol/L; ... which it is. Thus, there is probably no metabolic acid-base disturbance here.
The normal arterial oxygen for this woman should be well over 270, especilly if she had a normal PaCO2.
Why is the A-a gradient so great?
Apart from the guesses offered by the college ("loss of FRC post abdominal surgery, segmental collapse or consolidation, aspiration, pulmonary oedema") one can also suggest PE, amniotic fluid embolism and cardiomyopathy of pregnancy. In addition, merely being supine can cause modest hypoxia in pregnant women at term, though this is a pre-partum phenomenon.
AWE, ROBERT J., et al. "Arterial oxygenation and alveolar-arterial gradients in term pregnancy." Obstetrics & Gynecology 53.2 (1979): 182-186.
Milne, J. A. "The respiratory response to pregnancy." Postgraduate medical journal 55.643 (1979): 318-324.
Yeomans, Edward R., and Larry C. Gilstrap III. "Physiologic changes in pregnancy and their impact on critical care." Critical care medicine 33.10 (2005): S256-S258.
Fadel, Hossam E., et al. "Normal pregnancy: a model of sustained respiratory alkalosis." Journal of Perinatal Medicine-Official Journal of the WAPM 7.4 (1979): 195-201.