Many experimental studies have shown that
mechanical ventilation with high tidal volumes (Vt) or with a low end-expiratory volume allowing repeated end-expiratory collapse, can result in acute parenchymal
lung injury and probably an inflammatory response. Low volume ventilation with permissive
hypercapnia has been used in an attempt to avoid such injury in ARDS. Such management can affect oxygenation in many complex ways. The right-shift of the haemoglobin-
oxygen dissociation curve during acute
respiratory acidosis may increase venous
oxygen tension (PvO2) which could allow increased O2 uptake in ischaemic tissues.
Acidosis may reduce intrapulmonary shunt (Qs/Qt) by potentiating hypoxic pulmonary vasoconstriction, and there may also be direct and autonomically mediated effects of
hypercapnia both on the lung vasculature and on the airways. Cardiac output usually increases as a consequence of
hypercapnia and perhaps as a result of reduced intrathoracic pressure, further increasing PvO2 and CvO2, but the increase in cardiac output (CO) may tend to increase Qs/Qt as flow increases preferentially in unventilated lung. The reduction of mean airway pressure may directly increase Qs/Qt.
Hypercapnia may affect the distribution of systemic blood flow both within organs and between organs. Limited clinical studies suggest that tissue oxygenation is usually unchanged or improved during permissive
hypercapnia with increased CO, reduced arterio-venous O2 content difference and reduced blood
lactate concentration. However, acute
hypercapnia per se can reduce
lactate production. Further studies are required of this complex issue.