Abstract
An elevated physiological dead space, calculated from measurements of arterial CO2 and mixed expired CO2, has proven to be a useful clinical marker of prognosis both for patients with acute respiratory distress syndrome and for patients with severe heart failure. Although a frequently cited explanation for an elevated dead space measurement has been the development of alveolar regions receiving no perfusion, evidence for this mechanism is lacking in both of these disease settings. For the range of physiological abnormalities associated with an increased physiological dead space measurement, increased alveolar ventilation/perfusion ratio (V′A/Q′) heterogeneity has been the most important pathophysiological mechanism. Depending on the disease condition, additional mechanisms that can contribute to an elevated physiological dead space measurement include shunt, a substantial increase in overall V′A/Q′ ratio, diffusion impairment, and ventilation delivered to unperfused alveolar spaces.
Abstract
A review of current understanding of factors accounting for abnormal physiological dead space measurements in disease http://ow.ly/Dnyw1
Footnotes
The online version of this article has been corrected. The correction is outlined in the erratum published in the October 2015 issue of the European Respiratory Journal [DOI: 10.1183/09031936.50137614].
Previous articles in this series: No. 1: Naeije R, Vachiery J-L, Yerly P, et al. The transpulmonary pressure gradient for the diagnosis of pulmonary vascular diseases. Eur Respir J 2013; 41: 217–223. No. 2: Hughes JMB, van der Lee I. The TL,NO/TL,CO ratio in pulmonary function test interpretation. Eur Respir J 2013; 41: 453–461. No. 3: Vonk-Noordegraaf A, Westerhof N. Describing right ventricular function. Eur Respir J 2013; 41: 1419–1423. No. 4: Hamzaoui O, Monnet X, Teboul J-L. Pulsus paradoxus. Eur Respir J 2013; 42: 1696–1705. No. 5: Prisk GK. Microgravity and the respiratory system. Eur Respir J 2014; 43: 1459–1471. No. 6: Dempsey JA, Smith CA. Pathophysiology of human ventilatory control. Eur Respir J 2014; 44: 495–512. No. 7: Petersson J, Glenny RW. Gas exchange and ventilation–perfusion relationships in the lung. Eur Respir J 2014; 44: 1023–1041. No. 8: Wagner PD. The physiological basis of pulmonary gas exchange: implications for clinical interpretation of arterial blood gases. Eur Respir J 2015; 45: 227–243.
Conflict of interest: None declared.
- Received July 27, 2014.
- Accepted September 29, 2014.
- Copyright ©ERS 2015
Jump To
- Article
- Abstract
- Abstract
- Introduction
- Bohr dead space
- Fowler dead space
- Physiological dead space
- Shunt contribution to physiological dead space
- V′A/Q′ heterogeneity contribution to physiological dead space
- Physiological dead space in an abnormal lung
- Physiological dead space during exercise
- Can “true” alveolar dead space also exchange CO2?
- Interaction between anatomical dead space and V′A/Q′ heterogeneity
- Diffusion impairment and physiological dead space
- Dead space measurements in ARDS
- Factors contributing to the elevated VD/VT in ARDS
- Abnormal exercise dead space measurements in heart failure
- Abnormal exercise dead space measurements in pulmonary hypertension
- Summary and conclusion
- Footnotes
- References
- Figures & Data
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