assuming CO2 production remains constant. It is clear that is compromised either by decreasing the total (without changing the relative proportion of dead space and alveolar ventilation) or by keeping

the total constant and increasing the relative proportion of dead space to alveolar ventilation. A simple way to produce the latter circumstance is to change the pattern of breathing (i.e., decrease VT and increase frequency of breathing). With a lower VT, a larger proportion of each breath ventilates the fixed amount of anatomic dead space, and the proportion of alveolar ventilation to total ventilation must decrease.

In addition, if significant ventilation–perfusion mismatching is present, well-perfused areas may be underventilated, whereas underperfused areas receive a disproportionate amount of ventilation. The net effect of having a large proportion of ventilation go to poorly perfused areas is similar to that of increasing the dead space. By wasting this ventilation, the remainder of the lung with the large share of the perfusion is underventilated, and the net effect is to decrease the effective alveolar ventilation. However,

in many disease conditions, when such significant mismatch exists, any increase in PCO2 stimulates breathing, increases total minute ventilation, and can compensate for the effectively wasted ventilation.

Therefore, several causes of hypercapnia can be defined, all of which have in common a decrease in effective alveolar ventilation. Causes include a decrease in minute ventilation, an increase in the proportion of wasted ventilation, and significant ventilation–perfusion mismatch. However, by increasing the total minute ventilation, a patient often is capable of compensating for the latter two situations so CO2 retention does not result.

Decrease in alveolar ventilation is the primary mechanism that causes hypercapnia.

Increasing CO2 production necessitates an increase in alveolar ventilation to avoid CO2 retention. Thus, if alveolar ventilation does not rise to compensate for additional CO2 production, it will also result with hypercapnia.

As is the case with hypoxemia, pathophysiologic explanations for hypercapnia do not necessarily follow such simple rules so that each case can be fully explained by one mechanism. In reality, several of these mechanisms may be operative, even in a single patient.

Suggested readings

Cloutier M.M. Respiratory physiology 2nd ed. 2019; Elsevier Philadelphia.

Hsia C.C. Respiratory function of hemoglobin New England Journal of Medicine 1998;338: 239-247.

LoMauro A. & Aliverti A. Sex differences in respiratory function Breathe 2018;14: 131-140. Lumb A.B. Nunn’s applied respiratory physiology 8th ed. 2017; Elsevier Philadelphia. Petersson J. & Glenny R.W. Gas exchange and ventilation-perfusion relationships in the

lung European Respiratory Journal 2014;44: 1023-1041.

Mccormack M.C. & West J.B. Ventilation, blood flow, and gas exchange V.C. Broaddus, J.D. Ernst, T.E. King Jr., et al. Murray and Nadel’s textbook of respiratory medicine (7th ed.) 2021; Elsevier Philadelphia.

Robertson H.T. Dead space: the physiology of wasted ventilation European Respiratory Journal 2015;45: 1704-1716.

Schwartzstein R.M. & Parker M.J. Respiratory physiology: A clinical approach 2006;

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