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The relationship of fetal heart rate patterns to the fetal transcutaneous PO2
Continuous transcutaneous PO2 (tcPO2) monitoring of the human fetus was performed during 46 labors, 30 of which were complicated by abnormal fetal heart rate (FHR) patterns. FHR variability decreased with increases in the fetal tcPO2, and FHR variability increased with decreases in the fetal tcPO2. Analysis of the tcPO2 and FHR tracings provided an explanation for this apparent discrepancy. While rising fetal tcPO2 values were usually associated with decreased FHR variability, the pattern of late deceleration and decreased variability must still be considered an ominous pattern. The fetal tcPO2 declined during the deceleration and rose thereafter, with corresponding decreased FHR variability. Incomplete recovery of the fetal tcPO2 was associated with progressive acidosis. Repetitive and isolated late deceleration patterns showed markedly dissimilar fetal tcPO2 changes, suggesting different mechanisms may be involved in their production. Further studies are required before any definite conclusions can be drawn about the relationship of the FHR and the fetal tcPO2.
Continuous transcutaneous PO2 (tcPO2) monitoring of the human fetus was performed during 46 labors, 30 of which were complicated by abnormal fetal heart rate (FHR) patterns. FHR variability decreased with increases in the fetal tcPO2, and FHR variability increased with decreases in the fetal tcPO2. Analysis of the tcPO2 and FHR tracings provided an explanation for this apparent discrepancy. While rising fetal tcPO2 values were usually associated with decreased FHR variability, the pattern of late deceleration and decreased variability must still be considered an ominous pattern. The fetal tcPO2 declined during the deceleration and rose thereafter, with corresponding decreased FHR variability. Incomplete recovery of the fetal tcPO2 was associated with progressive acidosis. Repetitive and isolated late deceleration patterns showed markedly dissimilar fetal tcPO2 changes, suggesting different mechanisms may be involved in their production. Further studies are required before any definite conclusions can be drawn about the relationship of the FHR and the fetal tcPO2.