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(Chest. 2005;127:1867.)
© 2005 American College of Chest Physicians

CO2 Retention in Acute Severe Asthma

Vijo Poulose, MD, FCCP

Singapore

Correspondence to: Vijo Poulose, MD, FCCP, Department of Medicine, Changi General Hospital, 2, Simei St 3, Singapore 529889; e-mail: vijo_poulose{at}cgh.com.sg

To the Editor:

I applaud the authors for writing a comprehensive review on asthma (March 2004).1 However, I believe that further clarity needs to be given to their section on gas exchange (page 1083). The first paragraph states that the occurrence of hypercapnia is "a result of muscle fatigue and inability to maintain adequate alveolar ventilation." While muscle fatigue is undeniably a major cause of hypercapnia in acute severe asthma, it has to be pointed out that there are other factors that cause CO2 retention in these patients.2 I will limit this letter to the processes that create increase in dead space.

In addition to the low ventilation/perfusion (/) areas (which cause hypoxia), uneven distribution of ventilation gives rise to regions of alveolar hyperinflation and high / ratios, which cause increase in pulmonary dead space and CO2 retention. Alterations in regional perfusion from the increased intra-alveolar pressure and hypoxic pulmonary vasoconstriction are believed to contribute to this "dead space" effect. I had two patients with severe asthma in my ICU last year who had persistently high PaCO2 despite being intubated and receiving minute ventilation of > 10 L. In one of these patients, I even went to the extent of ordering a CT angiogram to eliminate the possibility of pulmonary embolism (which showed only hyperinflation). Needless to say, the PaCO2 came down to normal levels after the bronchospasm was corrected.

References

  1. Rodrigo, G, Rodrigo, C, Hall, JB (2004) Acute asthma in adults. Chest 125,1081-1102[Abstract/Free Full Text]
  2. McFadden, ER, Jr, Lyons, HA Arterial-blood gas tension in asthma. N Engl J Med 1968;278,1027-1032[ISI][Medline]




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