To determine hemodynamic effects of crying, 12 newborn infants recovering from the respiratory distress syndrome (RDS) were studied.
When crying, the range of inspiratory esophageal pressure was - 18.8 to −32.5 cm H2O and the range of expiratory pressure was +6.2 to +34.4 cm H2O. The esophageal pressure remained positive for a mean value of 66% of the respiratory cycle. There was a mean significant increase in heart rate of 19 beats/min. The systolic and diastolic blood pressures increased significantly at the beginning of strain to 115 and 135% of the respective control values. There was a progressive decrease in systolic and diastolic pressures during the period of strain and the systolic pressures reached values significantly less than control. With the decrease in systolic and diastolic pressures, there were pronounced reductions in pulse pressures. Three infants reached pulse pressure values less than 1% of control when cries were sustained for nine cardiac cycles.
There was a significant mean decrease in arterial oxygen tension (PaO2) of 16.8 mm Hg. There were no changes in arterial carbon dioxide tension (PaCO2), pH, or base excess.
Speculation Asphyxiated nconates and infants with RDS often have a compromised circulation with hypoxemia and hypotension. This study suggests that the circulatory status in such infants may be further compromised by extended periods of crying. In three patients who were relatively stable and normovolemic, a profound decrease in pulse pressure was observed when the cry included seven or more cardiac cycles. These transient periods of no aortic flow might be of clinical significance in critically ill infants. The decreased frequency of crying observed in critically ill neonates may be beneficial to both oxygenation and hemodynamic stability.