Physiologic Basis of Fetal Heart Monitoring

Neural Control of Fetal Cardiac Activity

     Fetal oxygenation affects the functionof the fetal brain which in turn affects the function of the cardiovascular system.  The fetal heart has intrinsic activity based on inherent tissue automaticity.  Cardiac contractions are mediated by signals arising at the sinoatrial node, passing to the atrioventricular node, and continuing throughout the ventricles.  As the autonomic nervous system fully develops by 24 to 28 weeks, several extrinsic parameters begin to influence cardiac rate.  The effects seen are a result of changes mediated by chemoreceptors, baroreceptors, circulatory catecholamines, central nervous system influences, and hormones.  The sympathetic and parasympathetic nervous systems exert their complex yin-yang effects on a second-by-second basis. 

Sympathetic simulation results in norepinephrine release contributing to increases in both chronotropy, inotropy, and systemic vascular resistance.  Parasympathetic stimulation influences fetal heart rate (FHR) by decreasing rate and by providing an oscillating effect that contributes to variability.  The components of this cardiac regulatory system make up a pathway from the fetal cerebral cortex through the cardiac integratory center in the medulla oblongata, the vagus nerve, and the cardiac conduction system.  The complex interaction between the factors above result in the variation of the fetal rate.  This pathway is dependent upon the physiologic status of the fetal brain.  Any factor that affects the fetal brain, such as oxygenation,  will alter this pathway.  Therefore, changes in fetal oxygenation will correspondingly be reflected in a variation of cardiac activity.  It is this concept that is the basis for fetal heart monitoring.  By evaluating the patterns of cardiac activity, fetal oxygenation status and physiologic integrity may be inferred. 

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