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English Abstract
Journal Article
[Effects of permissive hypercapnia on cardiopulmonary function in acute lung injury model].
OBJECTIVE: To observe the effects of permissive hypercapnia on cardiopulmonary function in oleic acid induced acute lung injury (ALI) models.
METHOD: ALI models of pigs were induced successfully by infusing oleic acid, Swan-Ganz cathether was used for monitoring hemodynamics and different low tidal volumes were set for variable hypercapnia.
RESULTS: ALI was characterized by an increase in airway pressure and a decrease in static compliance (Cst), artery oxygen tension (PaO2), oxygenation index and cardiac output. There was also an increase in mean pulmonary artery pressure (mPAP), pulmonary vascular resistance (PVR), systemic vascular resistance (SVR) and shunt fraction. After using 0.98 kPa (1 kPa = 10.2 cmH2O) PEEP, some of cardiopulmonary functions were improved. While reduced tidal volume to 7.7 +/- 0.3 ml/kg and PaCO2 increased to 9.44 +/- 1.27 kPa (1 kPa = 7.5 mmHg), which caused neither a change in PaO2/FiO2, PaO2, Cst nor in SVR, PVR but an increase in cardiac output. Though ventilation setting did not change except for the reducing tidal volume to 6.1 +/- 0.6 ml/kg and PaCO2 reached 12.1 +/- 1.05 kPa, then various adverse effects on cardiopulmonary system were observed.
CONCLUSION: It seems that mechanical ventilation with permissive hypercapnia was safe at certain level.
METHOD: ALI models of pigs were induced successfully by infusing oleic acid, Swan-Ganz cathether was used for monitoring hemodynamics and different low tidal volumes were set for variable hypercapnia.
RESULTS: ALI was characterized by an increase in airway pressure and a decrease in static compliance (Cst), artery oxygen tension (PaO2), oxygenation index and cardiac output. There was also an increase in mean pulmonary artery pressure (mPAP), pulmonary vascular resistance (PVR), systemic vascular resistance (SVR) and shunt fraction. After using 0.98 kPa (1 kPa = 10.2 cmH2O) PEEP, some of cardiopulmonary functions were improved. While reduced tidal volume to 7.7 +/- 0.3 ml/kg and PaCO2 increased to 9.44 +/- 1.27 kPa (1 kPa = 7.5 mmHg), which caused neither a change in PaO2/FiO2, PaO2, Cst nor in SVR, PVR but an increase in cardiac output. Though ventilation setting did not change except for the reducing tidal volume to 6.1 +/- 0.6 ml/kg and PaCO2 reached 12.1 +/- 1.05 kPa, then various adverse effects on cardiopulmonary system were observed.
CONCLUSION: It seems that mechanical ventilation with permissive hypercapnia was safe at certain level.
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