Continued fetal oxygen deprivation produces a sequence from rapid breathing to primary apnea, gasping, and secondary apnea. Recognizing the limits of clinical distinction guides resuscitation at birth.
Primary apnea
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Insufficient fetal oxygen initially causes a brief period of rapid breathing. With continued asphyxia, respiratory movements cease and primary apnea begins.
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During primary apnea, heart rate falls and neuromuscular tone gradually diminishes, while blood pressure remains preserved.
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Tactile stimulation usually reinitiates respiration during this phase.
Progression to secondary apnea
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Continued asphyxia produces deep gasping respiration, a further fall in heart rate, falling blood pressure, and flaccidity.
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Breathing progressively weakens until the last gasp, followed by secondary apnea.
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During secondary apnea, the infant is unresponsive to stimulation and requires positive pressure ventilation to resume respiratory efforts.
Approach to apnea at birth
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Fetal hypoxia may cause primary and secondary apnea before delivery, so apnea at birth may represent either phase.
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The phases are clinically indistinguishable at birth: breathing is absent in both, and the heart rate may be below 100 beats per minute.
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Assume secondary apnea in an apneic infant at birth and institute full resuscitation without spending excessive time on tactile stimulation.