What is the best definition of the term "hyperventilation"?

Abstract

Letter to the EditorWhat is the best definition of the term “hyperventilation”?Elapulli Sankaranarayanan PrakashElapulli Sankaranarayanan PrakashDivision of Basic Medical Sciences, Mercer University School of Medicine, Macon, GeorgiaPublished Online:01 Jun 2015https://doi.org/10.1152/advan.00078.2014MoreSectionsPDF (96 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat to the editor: In the context of a discussion about a patient with chronic obstructive pulmonary disease (COPD), a second-year medical student recently asked: What is the definition of hyperventilation? My initial response was that, when the CO2 production rate is constant, an individual who is hypocapnic (i.e., has a lower than normal CO2 tension in arterial blood) must have hyperventilated. This left me with the question as to whether hypocapnia is an essential feature of hyperventilation. In pulmonary physiology, the term “ventilation” is used to refer to the volume of gas flowing into the respiratory system per unit time. (5) Comroe et al. (1) defined ventilation as a cyclic process of inspiration and expiration in which fresh air enters the alveoli and an approximately equal volume of gas leaves the alveoli. Alveolar ventilation is defined as respiratory minute volume (or minute ventilation) minus ventilation of the anatomic dead space (5).However, historically, hypocapnia (a very likely consequence of an increase in alveolar ventilation) has been included as an essential feature of hyperventilation and alveolar hyperventilation (1, 3, 5). This is confusing because it does not logically follow the manner in which the term ventilation has been defined. Comroe et al. (1) defined hyperventilation as an increase in ventilation in excess of that required to maintain a normal Po2 and Pco2 in arterial blood (PaO2 and PaCO2, respectively). Plum (5) defined hyperventilation as a greater volume of ventilation than required by the metabolic demands of the body and suggested “one cannot call overbreathing hyperventilation so long as a patient breathing room air has either an arterial Pco2 above 40 mmHg or an arterial Po2 below 70 mmHg.” Whipp (5) defined hyperventilation as “an increase in ventilation out of proportion to any increase in metabolic V̇co2, therefore resulting in a low arterial Pco2. Hypocapnia is therefore a criterion by which to determine whether a subject is hyperventilating or not.” [Here, V̇co2 is expired CO2.] According to these definitions by Comroe et al. (1), Plum (3), and Whipp (5), a patient with COPD who has a PaO2 of 60 mmHg, PaCO2 of 46 mmHg, and whose respiratory minute volume is twice normal is not hyperventilating, and the increase in respiratory minute volume during exercise (hyperpnea) in a normal subject does not constitute hyperventilation if PaCO2 remains within the normal range. These definitions of hyperventilation are grounded in the notion that the functional significance of the process of ventilation is in part to maintain a Pco2 of 40 mmHg (in humans). In contrast, when hypocapnia is held as an essential feature of voluntary hyperventilation, it is grounded in a different teleological notion, which is that the functional significance of ventilation is to maintain CO2 elimination at the same rate as CO2 production without regard to PaCO2 and pH.Ingram et al. (2) studied the effect of voluntary “hyperventilation” (a term used by authors of this paper) on PaCO2 in patients with COPD and found that a small subset of patients had a PaCO2 > 40 mmHg despite a substantial increase in minute ventilation (see Table 2 in Ref. 2). The observed values of minute ventilation during voluntary hyperventilation were higher compared with baseline minute ventilation in eucapnic young adults. The high PaCO2 was associated with no change or a further increase in the ratio of Bohr's dead space and tidal volume. The observed PaCO2 values in hypercapnic patients after voluntary hyperventilation may or may not have been clinically significant; however, it is clear that when there is a significant mismatch between alveolar ventilation and pulmonary capillary perfusion, not only is O2 uptake by lungs impaired but CO2 elimination becomes less effective as well, despite a high respiratory minute volume and a presumed increase in alveolar ventilation.To summarize, my view is it is preferable that definitions for hyperventilation and hypoventilation follow the definition of ventilation in pulmonary physiology rather than be grounded in one of two implied teleological notions. Second, considering a broad range of physiological states and pathological states, including patients with COPD and substantial ventilation-perfusion mismatch, it is clear that an increase in respiratory minute volume does not necessarily result in a decrease in PaCO2. Third, as noted by West (4), defining hyperventilation as an increase in effective alveolar ventilation (i.e., alveolar ventilation that contributes to gas exchange) is not constructive since the latter is not measurable. Therefore, I suggest that the term hyperventilation be limited to refer to an increase in respiratory minute volume or total minute ventilation (i.e., the product of tidal volume and respiratory frequency) compared with baseline minute ventilation in age-matched healthy adults, regardless of PaCO2 or alveolar Pco2. Using hyperventilation as a synonym for hyperpnea is not a problem in and of itself. The more specific term alveolar hyperventilation is also best defined as an increase in alveolar ventilation in reference to resting alveolar ventilation in age-matched healthy adults, regardless of changes in PaCO2. Although measurements of pulmonary ventilation and anatomic dead space and therefore the calculation of alveolar ventilation are not feasible in routine clinical practice, practically, it is important to remember that when a patient with chronic bronchitis or emphysema whose breathing is labored and tachypneic also happens to be hypercapnic, it is suggestive of gross ventilation-perfusion mismatch. As previously suggested by West (4), in any given patient, determining whether hypercapnia is due to an absolute reduction in alveolar ventilation, absolute reduction in pulmonary blood flow, or gross ventilation-perfusion inequality is critical for appropriate management.DISCLOSURESNo conflicts of interest, financial or otherwise, are declared by the author(s).AUTHOR CONTRIBUTIONSAuthor contributions: E.S.P. drafted manuscript; E.S.P. edited and revised manuscript; E.S.P. approved final version of manuscript.REFERENCES1. Comroe JH, Forster RE, Dubois AB, Briscoe WA, Carlsen E. The Lung. Clinical Physiology and Pulmonary Function Tests. Chicago, IL: Year Book Medical, 1964, p. 28–51.Google Scholar2. Ingram RH, Miller RB, Tate LA. Arterial carbon dioxide changes during voluntary hyperventilation in chronic obstructive pulmonary disease. Chest 62: 14–18, 1972.Crossref | ISI | Google Scholar3. Plum F. Hyperpnea, hyperventilation, and brain dysfunction. Ann Intern Med 76: 328, 1972.Crossref | ISI | Google Scholar4. West JB. Causes of carbon dioxide retention in lung disease. N Engl J Med 284: 1232–1236, 1971.Crossref | ISI | Google Scholar5. Whipp BJ. Pulmonary ventilation. In: Comprehensive Human Physiology, edited by Greger R, Windhorst U. New York: Springer-Verlag, 1996, chapt. 100, p. 2036.Crossref | Google ScholarAUTHOR NOTESAddress for reprint requests and other correspondence: E. S. Prakash, Div. of Basic Medical Sciences, Mercer Univ. School of Medicine, 1550 College St., Macon, GA 31207 (e-mail: elapulli.[email protected]com). Download PDF Previous Back to Top FiguresReferencesRelatedInformation More from this issue > Volume 39Issue 2June 2015Pages 137-138 Copyright & PermissionsCopyright © 2015 The American Physiological Societyhttps://doi.org/10.1152/advan.00078.2014PubMed26031736History Published online 1 June 2015 Published in print 1 June 2015 Metrics