[Physiology and pathophysiology of postnatal pulmonary adaptation. 2: Pathophysiology]

Subject of this review is the pathophysiology of the respiratory distress syndrome (RDS), the apnea, and the sudden-death infant syndrome (SIDS). The fatality rate of the RDS yet amounts to 24%. Preterm infants are preferably involved because of their deficient surfactant synthesis. The lack of surfactant causes atelectases, hyaline membranes, lung oedema, and augmentation of respiration work. Only towards the very end of gestation the amount of surfactant of the fetal lung increases rapidly so that the normal postnatal respiration is guaranteed. RDS produces a pathological circulatory situation with insufficiency of the right heart and congestion. The atrial natriuretic hormone is increased about tenfold in the serum of RDS-infants. Modern treatment of the RDS uses instillations of exogenous surfactants before the first breath. Apneic attacks are observed predominantly during REM-sleep. They seem to have pathological value only if they exceed 15 seconds. Infants with recurrent apnoea breathe periodically, they were mostly preterm newborns. Probably, the cause of recurrent apneic attacks are central regulatory deficits and adenosine may play an important pathological role as neurotransmitter. Arrhythmias of the heart including the QT-syndrome observed in SIDS-infants at risk may have the same central pathophysiological source.