Apnea
Ann R. Stark
I. BACKGROUND
Definition. Apnea is defined as the cessation of airflow. Apnea is pathologic (an apneic spell) when absent airflow is prolonged (usually 20 seconds or more) or accompanied by bradycardia (heart rate <100 beats/minute) or hypoxemia that is detected clinically (cyanosis) or by oxygen saturation monitoring. Bradycardia and desaturation are usually present after 20 seconds of apnea, although they typically occur more rapidly in the small premature infant. As the spell continues, pallor and hypotonia are seen, and infants may be unresponsive to tactile stimulation. The level or duration of bradycardia or desaturation that may increase the risk of neurodevelopmental impairment is not known.
Classification of apnea is based on whether absent airflow is accompanied by continued inspiratory efforts and upper airway obstruction. Most spells are central or mixed apnea.
Central apnea occurs when inspiratory efforts are absent.
Obstructive apnea occurs when inspiratory efforts persist in the presence of airway obstruction.
Mixed apnea occurs when airway obstruction with inspiratory efforts precedes or follows central apnea.
Incidence. Apneic spells occur frequently in premature infants. The incidence of apnea increases with decreasing gestational age. Essentially, all infants <28 weeks’ gestational age have apnea. As many as 25% of all premature infants who weigh <1,800 g (˜34 weeks’ gestational age) have at least one apneic episode.
Onset. Apneic spells generally begin at 1 or 2 days after birth; if they do not occur during the first 7 days, they are unlikely to occur later.
Duration. Apneic spells persist for variable periods postnatally and usually cease by 37 weeks’ gestational age. In infants born before 28 weeks’ gestation, however, spells often persist beyond term postmenstrual age. In a study in which infants were monitored at home, significant apnea and/or bradycardia were recorded up to 43 weeks’ postmenstrual age in 20% of preterm infants who were free of spells for at least 5 days before discharge, and in 33% of those who had spells observed during that period. The clinical significance of these events is uncertain.
Term infants. Apneic spells occurring in infants at or near term are always abnormal and are nearly always associated with serious, identifiable causes, such as birth asphyxia, intracranial hemorrhage, seizures, or depression from medication. Failure to breathe at birth in the absence of drug depression or asphyxia is generally caused by irreversible structural abnormalities of the central nervous system (CNS).
II. PATHOGENESIS.
Several mechanisms have been proposed to explain apnea in premature infants, although those responsible for this disorder are unknown. Many clinical conditions have also been associated with apneic spells, and some may be causative.
Developmental immaturity of central respiratory drive is a likely contributing factor because apneic spells occur more frequently in immature infants.
The occurrence of apnea may correlate with brain stem neural function. The frequency of apnea decreases over a period in which brain stem conduction time of the auditory evoked response shortens as gestational age increases.
Breathing in infants is strongly influenced by sleep state. Active or rapid eye movement (REM) sleep is marked by irregularity of tidal volume and respiratory frequency. REM sleep predominates in preterm infants, and apneic spells occur more frequently in this state than in quiet sleep.
Chemoreceptor response
In preterm infants, hypoxia results in transient hyperventilation, followed by hypoventilation and sometimes apnea, in contrast to the response in adults. In addition, hypoxia makes the premature infant less responsive to increased levels of carbon dioxide. This suggests that immaturity of peripheral chemoreceptors may be involved in the pathogenesis of apnea. Although most infants do not appear to be hypoxemic before the onset of apnea, hypoxemia might play a role in prolonging the spell.
The ventilatory response to increased carbon dioxide is decreased in preterm infants with apnea compared with a matched group without apnea and is also decreased compared to term infants or adults. This suggests the possible contribution of immature central chemoreceptors to the pathogenesis of apnea.
Reflexes. Active reflexes invoked by stimulation of the posterior pharynx, lung inflation, fluid in the larynx, or chest wall distortion can precipitate apnea in infants. These reflexes may be involved in the apnea that is sometimes associated, for example, with vigorous use of suction catheters in the pharynx or with fluid in the upper airway during feeding.
Respiratory muscles. Ineffective ventilation may result from impaired coordination of the inspiratory muscles (diaphragm and intercostal muscles) and the muscles of the upper airway (larynx and pharynx).
Airway obstruction contributes to mixed and obstructive apneic spells. The site of this obstruction is usually the upper pharynx, which is vulnerable because of poor muscle tone, especially in REM sleep. Passive neck flexion, pressure on the lower rim of a face mask, and submental pressure (all encountered during nursery procedures) can obstruct the airway in infants and lead to apnea, especially in a small premature infant. Spontaneously occurring airway obstruction is seen more frequently when preterm infants assume a position of neck flexion.
Nasal obstruction can lead to apnea, especially in preterm infants who usually do not switch to oral breathing after nasal occlusion.
Gastroesophageal reflux is common in preterm infants. However, no association has been demonstrated between apnea of prematurity and gastroesophageal reflux.
Many inhibitory neurotransmitters are thought to play a role in the pathogenesis of apnea.
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