Though late decelerations share the same morphologic shape as early decelerations, they tend to appear late, after the onset and nadir of the contraction.

   Two varieties of late decelerations have been described, reflex and nonreflex. Reflex late decelerations are those which occur in the presence of normal FHR variability, whereas non-reflex late decelerations occur in association with diminished or absent FHR variability.
  
    The classically described cause of late decelerations is uteroplacental insufficiency (UPI). In UPI, there may be a problem with a uterine perfusion or uterine activity or there may be a problem with the placenta, or both.
  
    Uterine hyperactivity is associated with decreased time for intervillous space blood flow between uterine contractions. Similarly, maternal hypotension, even in the presence of normal uterine activity, will result in decreased volume of the intervillous space blood flow. Either of these factors may lead to a decrease in the maternal-fetal oxygen transfer.
  
    Placental dysfunction, too, may lead to a decreased maternal-fetal oxygen transfer, and/or a smaller volume of placental reserve in proportion to fetal need.
  
    Any of these causes may eventually lead to fetal hypoxemia and eventually myocardial depression. A vasovagal reflex leads to cardiodeceleration and continued hypoxemia may lead to lactic acidosis secondary to anaerobic metabolism.
  
   Reflex late decelerations are thought to be due to vagal stimulation by chemoreceptors in the head in response to low oxygen tension. This is accentuated by the decreased oxygen transfer during a uterine contraction. The hypoxemia results in increased sympathetic stimulation leading to increased systemic vascular resistance. The response to this increased pressure is a vagally mediated decrease in heart rate. This dual reflexive response may explain the delay in the heart rate following a contraction. Reflex late decelerations are associated with normal FHR variability because CNS system is intact.
  
   Nonreflex late decelerations, however, are associated with decreased or absent FHR variability. These decelerations are associated with a greater degree of relative hypoxemia and result in hypoxic depression of the myocardium coupled with the previously described vagal response. In reflex late decelerations, variability was maintained because the fetus was able to compensate, shifting oxygenated blood to vital organs (e.g., the heart), but in nonreflex late decelerations, the fetus is unable to compensate. It is these late decelerations which are more typically associated with fetal acidosis, and they are more commonly associated with placental dysfunction rather than uterine hypoperfusion or hyperactivity.
  
   The causes of UPI are varied, and many are reversible:

• Uterine hyperactivity
  
• Maternal hypotension
• Maternal hypertensive disorders
• Placental abruption
• Placenta previa
• IUGR
• Maternal DM
• Chorioamnionitis
• Postterm gestation
• Maternal anemia, SS anemia, etc.
• Rh isoimmunization
• Maternal cardiac disease
• Maternal smoking

See illustration below for an example of late deceleration. Please click to enlarge.