How can tachycardia lead to fetal compromise?

Tachycardia in the fetus refers to an abnormally high heart rate, which can significantly impact fetal health. One of the primary concerns with fetal tachycardia is its effect on ventricular filling. When the heart beats too rapidly, there is insufficient time between beats for the ventricles to fill adequately with blood. This leads to decreased stroke volume and, consequently, a reduction in cardiac output.

Decreased cardiac output can result in diminished perfusion and oxygen delivery to the fetal tissues, which is particularly critical given that the fetus is reliant on the placental circulation for oxygen. As tissue oxygenation decreases, the fetus may experience hypoxia, which can lead to further complications such as fetal distress, impaired growth, or neurological issues. This is why decreased tissue oxygenation due to ventricular filling issues is directly linked to potential fetal compromise in cases of tachycardia.

Other options do not accurately reflect the physiological consequences of fetal tachycardia. Increased fetal movement, improved circulation, and supported fetal development do not align with the pathological effects of a rapid heart rate, which primarily results in compromised oxygenation and nutrient delivery to the fetus.