Abstract
Ventilatory depression and apnea are well-known early pulmonary responses to sepsis in infants, yet their underlying mechanisms are not understood. To further elucidate the pathophysiology, we induced Escherichia coli septicemia in young piglets and studied sequential changes in intrapulmonary shunt (QS/QT), physiological dead space (VD/VT), minute ventilation (VE), and blood gases for up to 6 h of lethal sepsis. Lung lymph was also collected by cannulating the right lymphatic duct and extravascular lung water (EVLW) was measured. Compared to the controls, QS/QT increased and PaO2 decreased significantly by 30 min after E. coli infusion, followed by a significant increase in PaCO2 by 45 min and a decrease in VE or apnea in 9 of the 13 septic piglets within 1 h. Lymph flow increased to 250% over baseline after 30 min of septicemia. EVLW and dry weight of the bloodless lung (EVLW/DWL) in the septic group also increased significantly within 1 h. Histology confirmed that interstitial edema developed by 1 h after E. coli infusion. These sequential data suggest that high-permeability pulmonary edema is a contributing factor in early ventilation-perfusion maldistribution in spontaneously breathing, young septic piglets. The latter in turn appears to be responsible for hypoxemia and subsequent ventilatory depression and apnea.
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Chuang, G.J.H., Gao, CX., Mulder, D.S. et al. The pathophysiology of septic ventilatory depression and apnea in infancy. Pediatr Surg Int 2, 271–277 (1987). https://doi.org/10.1007/BF00176197
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DOI: https://doi.org/10.1007/BF00176197