Artificial respiration and kidney function disorder--a vicious circle?

Acute lung disease is commonly associated with interstitial pulmonary edema and a tendency towards partial or total alveolar collapse. To counteract this tendency mechanical ventilation is successfully used in most cases. Mechanical ventilation, however, leads to a harmful retention of water and salt, which may worsen interstitial pulmonary edema and further impair gas exchange. This problem seems to be less known. A survey of the effects of currently used modes of mechanical ventilation on excretory function and hemodynamics of the kidneys is given together with a short review of the possible afferent and efferent mechanisms which mediate the renal response to mechanical ventilation. Some clinical suggestions are made to break through the vicious cycle between mechanical ventilation and kidney function.     

Effect of nalbuphine on respiration

The respiratory depressant effects of 0.25 mg/kg nalbuphine were analyzed in detail in seven healthy volunteers by determining the CO2 response (Read's method) and the mouth occlusion pressure (Whitelaw's method) before and 10, 30 and 60 min after administration of the drug. Minute ventilation VE (PACO2 = 55 mm Hg) decreased after nalbuphine by a maximum of 36.4% (P less than 0.05). Simultaneously, the slope of the right-shifted CO2 response curve was diminished by 21.1% (NS) while the mouth occlusion pressure decreased by 36.3% (P less than 0.05), respectively. There were only slight changes in mean inspiratory flow rate. These findings demonstrate that nalbuphine does not lead to relevant impairment of central respiratory regulation or respiratory mechanics.