Why does a fetus' heart rate exhibit bradycardia (abnormally slow heart rate) in response to hypoxia (low oxygen levels), whereas a normal person's heart rate typically increases, exhibiting tachycardia (abnormally fast heart rate)?

From the Guidelines

A fetus's heart rate decreases in hypoxia due to a protective "diving reflex" mechanism that conserves oxygen during stress, which is distinct from the adult physiological response of increased heart rate in hypoxia. This difference in response is crucial for understanding fetal monitoring during labor. In adults, hypoxia triggers the sympathetic nervous system to increase heart rate, enhancing cardiac output to deliver more oxygen to tissues 1.

Fetal Physiological Response to Hypoxia

In contrast, fetuses have evolved a different physiological adaptation to cope with hypoxia. When a fetus experiences hypoxia, the "diving reflex" causes peripheral vasoconstriction, redirecting blood flow to vital organs (brain, heart, adrenal glands), while simultaneously slowing the heart rate to reduce oxygen consumption. This bradycardia is mediated by increased vagal (parasympathetic) tone and is a critical survival mechanism. The fetal myocardium is also more sensitive to hypoxia than adult heart tissue, and slowing the heart rate helps prevent cardiac damage.

Clinical Implications

The use of oxygen during pregnancy should follow the same general principles as the use of oxygen for other patients, aiming to achieve normoxaemia (saturation 94–98%) 1. However, there is no evidence to suggest that maternal 'hyperoxaemia' is beneficial to the mother or fetus, and caution should be exercised when considering maternal oxygen administration as a first-line intrauterine resuscitation measure 1.

Key Points

• The fetal heart rate response to hypoxia is a decrease in heart rate, not an increase like in adults.
• This response is due to a protective "diving reflex" that conserves oxygen during stress.
• The use of oxygen during pregnancy should aim to achieve normoxaemia (saturation 94–98%).
• There is no evidence to support the use of maternal oxygen administration as a first-line intrauterine resuscitation measure.

From the Research

Fetal Heart Rate Response to Hypoxia

• In contrast to adults, where heart rate increases in response to hypoxia, a fetus's heart rate may decrease in response to hypoxia due to the activation of a chemoreflex response via the vagus nerve, which helps reduce fetal myocardial workload 2.
• This decrease in heart rate is a compensatory mechanism to reduce oxygen demand and prevent anaerobic metabolism in the fetal myocardium 2.
• The fetus has a unique physiology that allows it to adapt to hypoxic conditions, including the presence of fetal hemoglobin, which has a higher affinity for oxygen than adult hemoglobin 3.

Mechanisms of Fetal Heart Rate Changes

• The principal mechanisms underlying fetal heart rate changes in response to hypoxemia include alterations in the distribution of blood flow, which permit the fetus to deal with reduced oxygen levels 4.
• The fetus may also exhibit changes in motility and behavior in response to hypoxemia, including suppressed movements during acute hypoxemia 4.
• The pathophysiological interpretation of fetal heart rate tracings is based on the application of knowledge of fetal responses to intrapartum mechanical and/or hypoxic stress in clinical practice 3.

Clinical Implications

• The timely recognition of the speed of onset of intrapartum hypoxia and preexisting uteroplacental insufficiency on fetal heart rate tracing is crucial to improve perinatal outcomes 3.
• In cases of acute fetal hypoxia, which manifests as a prolonged deceleration on the fetal heart rate tracing, immediate intervention is required to optimize perinatal outcome 2.
• Interventions for intrapartum fetal heart rate abnormalities may include corrective measures to optimize oxygenation, such as addressing reversible causes of reduced fetal oxygen delivery 5.