Cahill et al deserve congratulations for a rare well-designed study that contained a large cohort.
This letter could be all praise, but critical analysis is also important. The article robustly shows fetal heart rate decelerations remain “center stage” with deceleration area that best correlates to fetal acidemia rather than deceleration categories. This is not surprising, given the muddled categorization of decelerations, which is not criticism of this article.
Given negative predictive value of 99.2% for acidemia (<7.10) and 95% for composite neonatal morbidity, “normal deceleration area” means a 0.8% (of 1.8% acidemic in this study) chance of the fetus being acidemic (ie, 45% of acidemic babies undetected) and worse for morbidity (57% undetected of 8.8% with composite morbidity). Improvement, but not a silver bullet on its own! Reasons could be that the decelerations are much deeper and wider during pushing in second stage for which a mental adjustment occurs during visual cardiotocography interpretation. Thus, the same deceleration area cut-off seems inappropriate for both first and second stage. Importantly, in the presence of fetal compromise (eg, growth retardation, preeclampsia, diabetes mellitus) smaller deceleration areas would be abnormal.
Cahill et al imply continuance of visual interpretation of cardiotocography; therefore, categorization of decelerations is not just an academic/semantic issue but forms the crucial pattern-recognition framework/edifice. Their article mentions the pathophysiology of decelerations as “well-described”; instead, it is seriously befuddled. The experimental biophysiologists who asserted for a few decades that all rapid decelerations are due to cord compression (hence variable) have now performed a U-turn. Benign mechanisms that include head compressions also cause rapid decelerations; so why are “early decelerations” misconceived to be gradual? This amounts to changing the reality to suit definitions/convictions. Disproven theories must be relinquished (Sir Karl Popper). The British categorization before 2007 was different (Figure 1), which made early decelerations majority. This primarily “timing-based” categorization of decelerations has robust pathophysiologic basis that distinguishes between hypoxic and nonhypoxic decelerations (Figures 1 and 2) and was the low-lying fruit (highly significant) immediately picked by Hon and Caldeyro-Barcia. This distinction is lacking in the current (primarily rapid vs gradual) categorization, with many detrimental consequences. It imposes a flawed framework that is incompatible with science. It makes a 3-tier system dysfunctional. Substitutions like deceleration area or width/depth do not compensate for loss of meaning from the nondistinction of hypoxic vs nonhypoxic decelerations. It also leads to a questionable “meme” that it is the recurrent decelerations that (commonly) cause/worsen fetal hypoxemia/acidemia from reduced fetal cardiac output. But we know that the etiology of fetal hypoxemia predominantly is a contraction-induced drop in uteroplacental perfusion (not cord compression or decelerations) because of preexisting compromise or excessive uterine action. Decelerations that primarily cause/worsen acidemia is unproved and unlikely. Decelerations mostly are a reflection, rather than a cause, of fetal hypoxemia.