Neonatal Apnea

Bodhankar Uday
Apnea Pathophysiology
There are currently thought to be three mechanisms of apnea of prematurity:

Central Apnea : A pause in alveolar ventilation due to a lack of diaphragmatic activity. In other words, there is no signal to breathe being transmitted from the central nervous system to the respiratory muscles. This is due to immaturity of brainstem control of central respiratory drive. The premature infant also manifests an immature response to peripheral vagal stimulation. For example, stimulation of laryngeal receptors in the adult results in coughing. However, stimulation of these same receptors in the premature infant results in apnea. Gavages feeds, aggressive pharyngeal suctioning and gastroesophageal reflux can induce this reflex apnea.
Obstructive Apnea : A pause in alveolar ventilation due to obstruction of airflow within the upper airway, particularly at the level of the pharynx. The pharynx collapses from negative pressure generated during inspiration, because the muscles responsible for keeping the airway open are too weak in the premature infant (ex. genioglossus and geniohyoid). Once collapsed, mucosal adhesive forces tend to prevent the reopening of the airway during expiration. Neck flexion will worsen this form of apnea.
Mixed Apnea : A combination of both types of apnea representing as much as 50% of all episodes. (5)

In brief following are the pathophysiologic mechanisms responsible for different types of apnea:
Central Apnea :
- Primary central respiratory center depression Decreased or inhibitory upper afferent input to the central respiratory center.Abnormal or hyperactive reflexes.Decreased or inhibitory lower afferent input to the central respiratory center.
- Hypoxemia

Obstructive Apnea:
Decreased or inhibitory upper afferent input to the central respiratory center.

Mixed Apnea:
- Decreased or inhibitory upper afferent input to the central respiratory center.
- Hypoxemia

- Decrease in arterial oxygen tension
- Decrease in heart rate
- Decrease in peripheral blood flow
- EEG changes suggesting CNS depression if apnea is severe
- Increase in venous pressure
- Decrease in muscle tone

Apnea has been classified into three types depending on whether inspiratory muscle activity is present. If inspiratory muscle activity fails following an exhalation, it is termed Central Apnea. If inspiratory muscle activity is present without airflow, this is termed Obstructive Apnea. If both central and obstructive apnea occurs during the same episode, this is termed Mixed Apnea. It is important to characterize a patient's apnea episodes into one or more types for treatment consideration.

The most common cause of apnea in the neonatal intensive care unit is apnea of prematurity, but it is necessary to initially investigate and rule out the following disorders:

- Infection: Sepsis especially in the first day of life and nosocomial infections and/or necrotizing enterocolitis in the first weeks of life.
- Temperature Regulation: Hypothermia or hyperthermia.
- Gastrointestinal: NEC or gastroesophageal reflux.
- Neurological: Intraventricular hemorrhage, intracranial hemorrhage, neonatal seizures, perinatal asphyxia or other pathology which could lead to increased intracranial pressure.
- Drugs: Prenatal exposure with transplacental transfer to the neonate of various drugs (narcotics, beta-blockers). Postnatal exposure to sedatives, hypnotics or narcotics.
- Metabolic: Hypercalcemia, hypoglycemia, hyponatremia or acidosis.
- Cardiovascular: Impairment of oxygenation from congestive heart failure and pulmonary edema (PDA, coarctation, etc.) or from shunting (cyanotic heart disease).
- Hematological: Anemia.
- Pulmonary: Impairment of oxygenation and ventilation from lung disease (surfactant deficiency, pneumonia, etc.).

Apnea is the most common problem of ventilatory control in the premature infant frequently prolonging hospitalization and needing cardiopulmonary monitoring. The standard definition of apnea is cessation of inspiratory gas flow for 20 seconds, or for a shorter period of time if accompanied by bradycardia (heart rate less than 100 beats per minute), cyanosis, or pallor.

This must be distinguished from periodic breathing which is three or more respiratory pauses of greater than 3 seconds duration with less than 20 seconds respiration between the pauses. Such a pattern generally unaccompanied by hypoxemia is thought to be benign.

Although there is considerable variation in incidence and severity of apnea in premature infants, both are inversely related to gestational age. Approximately 50% of infants less than 1500 grams birth weight require either pharmacologic intervention or ventilatory support for recurrent prolonged apneic episodes. The peak incidence occurs between 5 and 7 days postnatal age. Apnea of Prematurity is a specific diagnosis and usually resolves between 34 to 36 weeks postconceptual age.

The incidence of apnea and periodic breathing in the term infant has not been adequately determined. Approximately 50-60% of preterm infants have evidence of apnea: 35% present with central apnea, 5-10% with obstructive apnea, 15-20% with mixed apnea. Another 30% will have periodic breathing. (1)

Neonatal Apnea Neonatal Apnea 12/19/2001
Evaluation of the Apneic Infant (6) >>
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