Why is physiological dead space important

After all, physiological dead space is simply the difference between arterial and mixed expired pCO 2 divided by the arterial pCO 2. Thus, any gas exchange abnormality has the potential to increase dead space.

Some high-level perspective may be useful. First, it should be remembered that, since introduced by Riley and Cournand [ 4 ] more than 50 years ago, physiological dead space is a virtual concept wherein the lung is conceived as a two-compartment organ in which one compartment is normal and the other is completely unperfused. Physiological dead space, then, is the percentage of the tidal volume that must be distributed to the alveolus that is completely unperfused and which thus delivers no CO 2 to the expired gas to account for the difference between measured arterial and mixed expired pCO 2.

Physiological dead space in actual patients may be increased even when no alveoli are completely unperfused — as is the case here in the presence of a shunt. It is useful as a general parameter quantifying gas exchange disturbances but must not be overinterpreted as necessarily implying the existence of unperfused alveoli.

Second, as Niklason and colleagues show, the relationship between shunt and physiological dead space is nonlinear, especially when shunts are high. Normal log SDQ is less than 0. Fifth, Niklason and colleagues show that, for any given value of shunt, additional perturbations commonly seen in the intensive care unit influence arterial pCO 2 and therefore will increase calculated dead space.

These include a reduction in cardiac output and, separately, acidosis. This also means that a high cardiac output will reduce the dead space effect of shunt, as will alkalosis. In summary, the calculations of Niklason and colleagues serve to point out the complexity of gas exchange in critical illness and the challenges we face in trying to interpret apparently simple measurements as indicators of the lung's ability to carry out its primary responsibility — gas exchange.

Crit Care , R West JB: Ventilation-perfusion inequality and overall gas exchange in computer models of the lung.

Respir Physiol , 7: Bull Eur Physiopathol Respir , This chapter is most relevant to Section F6 v from the CICM Primary Syllabus , which expects the exam candidates to be able to "describe the physiological impact of increased dead space". This is a highly examinable topic which has come up twice in the past papers:.

The section from the 8th edition of Nunn's p. At a fundamental level, increasing the dead space functionally indistinguishable from hypoventilation:. Theoretically, it should not matter which dead space component has increased: this effect would be the same. However, functionally there may be some differences. Consider: let's say you have a patient who is breathing comfortably with tidal volumes of ml, of which there is ml of total dead space which is all anatomical.

Let's say you have now increased your dead space by introducing an extra ml of apparatus dead space into the respiratory circuit. Now, your alveolar ventilation remains the same, around ml, but now the tidal volume, moving ml of gas in and out of the respiratory circuit, is composed just of rebreathed gas.

No added oxygen is inhaled, unless it has mixed by diffusion with the contents of the apparatus. The evolution of bronchopulmonary dysplasia after 50 years. Care Med. Ochiai, M. A new scoring system for computed tomography of the chest for assessing the clinical status of bronchopulmonary dysplasia. Effective ventilation at conventional rates with tidal volume below instrumental dead space: a bench study. Wenzel, U. Comparison of different methods for dead space measurements in ventilated newborns using CO 2 -volume plot.

Intensive Care Med. Bourgoin, P. Assessment of Bohr and Enghoff dead space equations in mechanically ventilated children. Care 62 , — Frey, U. Specifications for equipment used for infant pulmonary function testing. Download references. You can also search for this author in PubMed Google Scholar. All authors were involved revising the manuscript and approved the final version.

Correspondence to Anne Greenough. The original online version of this article was revised due to a retrospective Open Access order. Reprints and Permissions. Williams, E. Physiological dead space and alveolar ventilation in ventilated infants. Pediatr Res Download citation.

Received : 17 November Accepted : 18 January Published : 18 February Anyone you share the following link with will be able to read this content:.

Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Advanced search. Skip to main content Thank you for visiting nature. Download PDF. This article has been updated. Abstract Background Dead space is the volume not taking part in gas exchange and, if increased, could affect alveolar ventilation if there is too low a delivered volume. Methods A prospective study of mechanically ventilated infants was undertaken.

Results Eighty-one infants with a median range gestational age of Conclusion Prematurely born infants with pulmonary disease have a higher dead space than term controls, which may influence the optimum level during volume-targeted ventilation.

Impact Measurement of the dead space was feasible in ventilated newborn infants. Introduction Newborn infants often require respiratory support with invasive mechanical ventilation, unfortunately such infants can develop chronic respiratory morbidity. Protocol Baseline demographic data were collected including gestational age, birth weight and sex.

Respiratory measurements An NM3 respiratory profile monitor Philips Respironics, CT , connected to a combined pressure and flow sensor with mainstream capnograph Capnostat-5 , was used [Fig. Full size image. Results Eighty-one infants were recruited into the study with a median range gestational age of Table 1 Baseline demographics of infants in each group. Full size table. Table 2 Dead space and alveolar ventilation parameter of infants in each group.

References 1. Article Google Scholar 2. Google Scholar 4. Article Google Scholar 5. Article Google Scholar 6. Article Google Scholar 7. Article Google Scholar 8.

Article Google Scholar 9. Article Google Scholar Google Scholar View author publications. Ethics declarations Competing interests The authors declare no competing interests. About this article. Cite this article Williams, E. Copy to clipboard.