Comprehensive and Detailed Explanation From Exact Extract NCC-Recommended Sources
NCC-recommended physiology references (AWHONN, Simpson & Creehan, Menihan, Creasy & Resnik) consistently state that the primary mechanism by which tachysystole affects fetal oxygenation is reduced uteroplacental perfusion, specifically through impaired intervillous space reperfusion.
During a normal contraction cycle, the fetus receives oxygen between contractions, when the uterus relaxes and maternal blood re-enters the intervillous space. AWHONN’s Fetal Heart Monitoring Principles & Practices explains that tachysystole—defined as more than five contractions in 10 minutes averaged over 30 minutes—shortens or eliminates the relaxation phase, preventing adequate placental reoxygenation.
Simpson & Creehan highlight that “tachysystole decreases uteroplacental blood flow and interferes with replenishment of oxygenated maternal blood in the intervillous space.” Menihan emphasizes that fetal hypoxemia in tachysystole results from interrupted perfusion, not from altered oxygen transport or maternal hemodynamic changes. Creasy & Resnik confirm that uterine overactivity reduces intervillous perfusion during contractions and impairs fetal oxygen exchange.
Thus, the physiologic problem is failure of the intervillous space to reperfuse, which compromises fetal oxygenation.
[References:, AWHONN – Fetal Heart Monitoring Principles & PracticesSimpson & Creehan – Perinatal NursingMenihan – Electronic Fetal MonitoringCreasy & Resnik – Maternal-Fetal MedicineMiller’s Pocket Guide, ====================================================]
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