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Open Access

Vd/Vt test in the detection of pulmonary dysfunction in sepsis

  • K Cala1,
  • V Pilas1 and
  • N Vucic1
Critical Care20048(Suppl 1):P20

https://doi.org/10.1186/cc2487

Published: 15 March 2004

Keywords

Oxygen Partial PressurePulmonary Vascular ResistanceDead SpaceArterial OxygenMinute Ventilation

Dyspnea and tachypnea are the leading signs of pulmonary dysfunction in sepsis. With regards to present knowledge of pathophysiology and pathogenesis of the pulmonary dysfunction, the real reasons for this phenomena are still not researched enough. It is our assumption that one of the underlying causes is in the increased ventilation of the physiological dead space due to the mismatch of the pulmonary ventilation and perfusion. In sepsis, equal to change in systemic, there are changes in pulmonary circulation, often with pulmonary hypotension and decreased pulmonary vascular resistance. To investigate this we used a simple test to measure the ventilation of the dead space using the Vd/Vt test.

Patients and methods

In 20 patients having conventional criteria for sepsis and tachypnea > 20/min we measured dead space ventilation using Bohr's Principle. The patients with chronic pulmonary disease (asthma, COPD) were not eligible for the study. According to Bohr the ratio of the dead space (Vd) ventilation to tidal volume (Vt) is a measurable variable denoted as Vd/Vt = (PaCO2 - PECO2)/PaCO2. Normal values are 0.20–0.40. To measure it we used a direct method with certain technical innovations. The subjects breathed through an oronasal mask and one-way valve. Expired air was collected in a 5-l balloon in order to provide adequate mixture of dead space and alveolar air. The concentration of CO2 on the end of the balloon (PECO2) was measured with an RGM 'Ohmeda' capnograph (infrared technique) together with minute ventilation. Arterial oxygen partial pressure (PaO2) was measured simultaneously from arterial blood using a conventional method.

Results

In all subjects an increased (> 0.40) Vd/Vt index was found (0.50 ± 0.05). Minute ventilation was also increased (13 ± 1.4 l). We compared these results with arterial oxygen (PaO2) partial pressure and found a high degree of negative linear correlation for the Vd/Vt index and PaO2 (r = -0.7512, P < 0.01). A positive linear correlation for the Vd/Vt index and MV (r = 0.5862, P < 0.01) was also found.

Discussion and conclusion

We believe that our results indicate that dyspnea and tachypnea in sepsis are mostly a result of the increased physiological dead space ventilation and that this test is useful for early detection and objectification of the pulmonary dysfunction in sepsis. The simplicity of this method makes it suitable for large-scale clinical use.

Authors’ Affiliations

(1)
CH Sveti Duh, Zagreb, Croatia

Copyright

© BioMed Central Ltd. 2004

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