[An experimental study on the pathophysiology of septic ventilatory depression].
Ventilatory depression and apnea are well-known early pulmonary responses of sepsis in infants, yet their underlying mechanisms are not understood. To further elucidate the pathophysiology, we induced Escherichia coli septicemia in piglets and studied the sequential changes in intrapulmonary shunt (QS/QT), physiological dead space (VD/VT), minute ventilation (VE), and blood gases for up to 6 hours of lethal sepsis. Lung lymph was also collected and extravascular lung water (EVLW) was measured. Histology confirmed that interstitial edema developed 1 hour after E. coli infusion. These data suggest that high permeability pulmonary edema and hypoxemia following early intrapulmonary shunt increase may be the causes of septic ventilatory depression.
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D000818:Animals; D001784:Blood Gas Analysis; D004195:Disease Models, Animal; D004927:Escherichia coli Infections; D005260:Female; D000860:Hypoxia / Q000209:etiology; D008297:Male; D011654:Pulmonary Edema / Q000209:etiology; D012126:Respiratory Dead Space; D012127:Respiratory Distress Syndrome, Newborn / Q000209:etiology*; D018805:Sepsis / Q000150:complications* / Q000503:physiopathology; D013552:Swine