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University Hospital of Wales Cardiff, Wales, UK
Correspondence to: Matt Wise, DPhil, University Hospital of Wales, Adult Critical Care, Heath Park, Cardiff, CF14 4XW, Wales, UK; e-mail: mattwise{at}doctors.org.uk
To the Editor:
Sinclair et al1 recently reported in CHEST (July 2006) the effects of acute hypercapnia on ventilation-perfusion matching in an animal model of acute lung injury. The authors cited two studies23 of ARDS patients in which the effects of acute hypercapnia, produced by low-tidal volume ventilation, on gas exchange were examined. While in experimental models hypercapnia improves gas exchange in normal lungs (where CO2 is usually added to inspired gases), hypercapnia as a consequence of protective lung ventilation led to impaired oxygenation as a result of increased shunting.23 In contrast, Mancini et al4 demonstrated improved oxygenation and reduced shunting in eight ARDS patients in whom hypercapnia had been induced by reducing tidal volumes from 10 to 12 mL/kg to 5 to 7 mL/kg. However, it would appear that improvement4 or deterioration23 in oxygenation and shunting correlated with changes in mean airway pressure rather than acute hypercapnia per se.
Sinclair et al1 hypothesized that the effects of hypercapnia on gas exchange in lung injury were largely unknown and may be beneficial, although they subsequently found no significant change. In their model, hypercapnia was induced by adding CO2 to inspired gases or adjusting minute ventilation through changes in rate rather than tidal volume (keeping the mean airway pressure constant). In our institution, we have used another method, the addition of dead space, to induce hypercapnia in ARDS patients.5 This approach also has the advantage that mean airway pressure is unaltered. No significant alteration was observed in PaO2, PaO2/fraction of inspired oxygen ratio, or shunting when acute hypercapnia was compared to normocapnia.5 Sinclair et al1 postulated that lung injury produced by the homogeneous depletion of a surfactant may abrogate the beneficial effects of CO2 on gas exchange that is observed in normal lungs; however, hypercapnia may be advantageous in patients with heterogeneous lung injury such as that caused by pneumonia. Although only two patients in our study had pneumonia as a cause of ARDS, neither showed improvement in gas exchange when they were acutely hypercapnic.
Footnotes
The authors have reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.
The author has reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.
References
University of Tennessee Health Sciences Center Memphis, TN
Correspondence to: Scott E. Sinclair, MD, FCCP, University of Tennessee, Department of Medicine, 956 Court Ave, H314, Memphis, TN 38163; e-mail: ssincla1{at}utmem.edu
To the Editor:
We appreciate the interest in our study on the effects of hypercapnic acidosis on gas exchange after saline solution lavage-induced lung injury. Findlay and Wise1 mention a study by Mancini and colleagues2 and correctly conclude that the changes in gas exchange in this study (ie, decreased shunt) are likely due to the differences in positive end-expiratory pressure (PEEP) [9 vs 16 cm H2O, respectively] and mean airway pressure (18 vs 21 cm H2O, respectively), and not due to modest differences in PaCO2 (39 vs 57 mm Hg, respectively) compared with other studies cited in their letter and in our article.3
In our study,3 although no significant differences in the clinical measurements of gas exchange were observed, low minute ventilation, which is produced by the reduction of respiratory rate, significantly reduced mean ventilation/perfusion distributions compared with inhaled carbon dioxide and eucapnia. Log SDs of ventilation and combined retention and excretion curves of the dispersion index were both increased during low minute ventilation, indicating the presence of unfavorable changes in ventilation distribution. Because tidal volumes and PEEP were kept constant between groups, there was no difference in shunt achieved by the technique of multiple inert gas elimination. Our protocol was designed to assess the effects of hypercapnic acidosis itself without the confounding effects of different tidal volumes, PEEP, or mean airway pressure.
In the study by Findlay and Smithies,4 hypercapnic acidosis was induced by adding dead space to the ventilatory circuit while keeping mean airway pressure constant. They reported no differences in PaO2, PaO2/fraction of inspired oxygen ratio, or shunt between the increased dead space group and control subjects. Rebreathing of dead space gas would dilute the fresh gas that reaches the alveolus, reducing the effective alveolar PO2. Therefore, the PaO2/fraction of inspired oxygen ratio would underestimate gas exchange in the increased dead space group. It would therefore be difficult to make meaningful comparisons between these groups without some independent method of assessing gas exchange efficiency.
References
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