Apnea in preterm newborns: determinants, pathophysiology, effects on cardiovascular parameters and treatment

Apnea, especially in preterm newborns (AoP) is one of the common problems encountered at neonatal units. Numerous factors are likely to play a role in the etiology of apnea. Recent data sugest a role for genetic predisposition of AoP. It seems, that physiological rather than pathological immaturity of the respiratory, or cardiorespiratory control, play a major part in the pathophysiology of AoP. Immaturity of the brainstem, cerebral cortex, receptors of the lungs and the airways as well as of the chemoreceptors contribute to the development of apnea in preterm newborns. Several neurotransmitters (GABA, adenosin, endorphins) and their maturational changes are including in pathogenesis of apnea, too. The instability of the upper airway in preterm infants, asynchrony of musculature of the upper airway and diaphragm, pathological changes in the upper airway and malformations of the central nervous system might also contribute to the occurrence and severity of AoP. In newborns, apnea occurs more frequently in active sleep than in quiet sleep and the frequency of apnea in active sleep is higher in the warm conditions. Durations of apnea correlate with the body heat loss. Cardiovascular changes during apnea - bradycardia, peripheral vasoconstriction and various changes in peripheral blood flow and pressure occur together with changes in ECG. The standard clinical management of apnea includes non-pharmacological treatment (eliciting arousal reactions and reflex breathing by mechanical skin, or mucosa stimulations), pharmacological treatment (methylxanthines are preferred) and application of continuous positive airway pressure (CPAP) or in severe apnea - mechanical ventilation