Using Fetal Heart Rate Tracings to Assess Acidosis

During labor, lactic acid accumulation can lead to metabolic acidosis and a blunting of the vagal regulation of the fetal heart rate and consequent loss of accelerations, loss of variability between contractions, and other changes with possible long-term sequelae.

In monitoring labor, we want to know where we are on the spectrum of acidosis. Have we gone through the active phase, for example? Where are we in the second stage? Understanding where the fetus is on this spectrum prepares us to manage any changes—any additional acidosis related to fetal heart rate decelerations—that are superimposed on the background stress of the labor process.

Acidosis and Heart Rate Patterns

Research has confirmed not only degrees of hypoxemia and fetal base deficit values during the normal course of labor; it also has provided a window of knowledge into the changes in fetal acidosis in relation to particular fetal heart rate patterns.

Early decelerations are generally well tolerated by the fetus and probably do not result in any additional acidosis. These are believed to result from fetal head compression and a subsequent hormonal or vagal response.

Similarly, mild or moderate variable fetal heart rate decelerations, which are due to modest cord compression, are well tolerated if they occur at a reasonable frequency (such as every 3 minutes). The frequency of variable decelerations is critical as lactic acid generated during the variable deceleration may be cleared across the placenta during the periods between decelerations.

When variable heart rate decelerations are severe and of increasing frequency, however, the fetus can accumulate lactic acid—sometimes rapidly—depending on the frequency. A severe variable deceleration results from complete or near-complete umbilical cord occlusion and is typically defined as one that lasts for at least 60 seconds, during which the heart rate drops below 70 beats per minute

In a study we published this year with colleagues in Canada, we found that severe variable decelerations result in an increase in base deficit of 0.5 mmol/L per minute of cord occlusion. We also found, however, that metabolic acidosis is cleared at a rate of 0.1 mmol/L per minute of recovery, when fetal heart rate is normal and stress is reduced (Am. J. Obstet. Gynecol. 2009;200:200.e1-7).

Given these rates of acid accumulation and normalization, one can understand how acidosis may develop when repetitive, severe variable decelerations occur every 3 minutes, for instance. Past a certain frequency and severity, there simply isn't enough recovery time to allow the fetus to sufficiently correct the base deficit.

Although most of us will not actually be using these acid accumulation and recovery rates to calculate specific base deficits, an awareness of the principles can aid us in assessing fetal acidosis. The concept of recovery time is an important one. Again, knowing where your patient is on the spectrum of acidosis tells you how much “buffer time” you have if something goes wrong.

There is policy, sometimes attributed to midwives, that advocates letting the patient push only during every other contraction. Given what we've learned about the development of acidosis, when pushing is associated with severe variable decelerations, there may be an advantage to pushing every other contraction in order to permit sufficient recovery time and clearance of acid between the decelerations.

One of the signals that acidosis is progressing to a moderate level (approximately 8 mmol/L) is the change in severe variable decelerations from typical (having shoulders, a sharp drop, and a sharp rise) to atypical (a loss of shoulders, a U-shaped variable deceleration, or a slow return to baseline).

Another sign of moderate acidosis is a loss of variability between contractions. These heart rate patterns need more research, but in my experience a prolonged loss of variability between contractions (unrelated to the fetal sleep state) typically does not occur until the base deficit approaches 8 mmol/L or greater. Given that the risk of brain injury begins with a base deficit of 12 mmol/L, an observation of this change provides a buffer zone during which the patient can be even more closely monitored.

It used to be thought that late decelerations were extremely worrisome, but we have learned that these patterns are usually less threatening to the fetus's accumulation of metabolic acidosis than are severe variable decelerations.

When there is good baseline variability between the decelerations, the late deceleration often reflects a vagal-mediated response and probably involves no change in the level of acidosis. When there is a loss of variability between contractions, however, the late deceleration may reflect a hypoxia-induced response. Still, the rate of acidosis accumulation is typically less than it is with severe variable decelerations.