Neonatal Apnea



  • Apnea of infancy
    • An unexplained episode of cessation of breathing for 20 seconds or longer or a shorter respiratory pause associated with bradycardia, cyanosis, pallor, and/or marked hypotonia in infants with gestational age (GA) of 37 weeks or more at the onset of apnea
  • Apnea of prematurity (AOP)
    • The cessation of breathing for >20 seconds or if <20 seconds is accompanied by oxygen desaturation or bradycardia in infants born <37 weeks GA.
  • Periodic breathing
    • A normal neonatal breathing pattern, defined by ≥3 pauses, each ≥3 seconds, with <20 seconds of regular respiration between pauses
  • Classification of apnea based on respiratory effort and airflow
    • Central apnea
      • No evidence of obstruction to airflow but absent chest wall motion
      • Caused by decreased central nervous system (CNS) stimuli to respiratory muscles
    • Obstructive apnea
      • Characterized by absent airflow but persistent chest wall motion
      • Often caused by pharyngeal instability, neck flexion, or nasopharyngeal occlusion
    • Mixed apnea (most frequent in preterm infants)
      • Obstructive apnea preceding (usually) or following central apnea


  • Apnea and bradycardia occur in ~2% of all healthy term infants.
  • AOP is inversely correlated to GA. It occurs in <10% of neonates 34 to 35 weeks GA and in almost all neonates <28 weeks GA at birth.

Risk Factors

  • Prematurity is the most common cause of apnea.
  • Risk factors common to both AOP and apnea of infancy are as follows:
    • Maternal medications, such as magnesium sulfate, prostaglandins, or narcotics
    • Age (first 30 days of life)
    • Infections: upper respiratory tract infections
    • Gastroesophageal reflux disease (GERD)
    • Anemia
    • Cardiac arrhythmias
    • CNS insult (hemorrhage, seizure, tumors)
    • Immunizations (after DTaP injection)


  • Immature respiratory control in neonates
    • Immature structural development of central respiratory network in the brainstem
    • Enhanced sensitivity to inhibitory neurotransmitters (such as γ-aminobutyric acid [GABA]) and neuromodulators (such as adenosine, serotonin, and prostaglandin) that can lead to apnea
    • Low functional residual capacity predisposing to hypoxia when short apneas occur
  • Hypoxic ventilatory depression
    • Increased peripheral chemoreceptor sensitivity, leading to more unstable breathing (such as periodic breathing) or decreased sensitivity, which prolongs apnea when it does occur
  • Impaired hypercapnic ventilatory response
    • Prolonging expiratory time (but not increasing frequency or overall tidal volume) may lead to less minute volume as well as uncoordinated movements of respiratory muscles in response to hypercapnia, resulting in apnea.
  • Laryngeal chemoreflex
    • Activation of laryngeal chemoreceptors (via superior laryngeal nerve afferents) as seen in GERD can result in apnea, bradycardia, and hypotension.
  • Sleep state
    • Neonates spend majority of their time in active sleep. Apneas are more common during active sleep when breathing is irregular and chest wall and upper airway muscles are inactivated.
  • Upper airway obstruction
    • Hypotonic pharynx in preterm infants with additional loss of upper airway tone during active sleep

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