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Hypercapnia During Oxygen Therapy in Airways Obstruction: a Reappraisal

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Hypercapnia During Oxygen Therapy in Airways Obstruction: a Reappraisal Thorax: first published as 10.1136/thx.41.12.897 on 1 December 1986. Downloaded from Thorax 1986;41:897-902 Editorial Hypercapnia during oxygen therapy in airways obstruction: a reappraisal Hypercapnia and acidosis after oxygen therapy in Table 1 Suggested causes of raised arterial carbon dioxide patients with acute exacerbations of chronic airways tension after oxygen therapy in patients with chronic obstruction is well recognised, and an understanding airways obstruction of its pathogenesis is essential if successful strategies Hypoventilation from reduced hypoxic ventilatory drive due to to limit the rise in arterial carbon dioxide tension the rise in arterial oxygen tension (Paco2) are to be designed. 2 Increased ventilation-perfusion mismatching: The acute rise in (a) loss of hypoxic vasoconstriction Paco2 during oxygen therapy was (b) development of collapsed alveoli first ascribed to reduced hypoxic drive (due to the rise 3 Haldane effect-displacement of carbon dioxide from in Pao2), an acquired insensitivity to carbon dioxide, oxygenated blood 4 Reduced slope of the carbon dioxide content curve for blood as and consequent hypoventilation.' This led to the carbon dioxide tension rises-reduction in effective partition introduction by Campbell of controlled oxygen ther- coefficient apy to give hypoxic patients a small increase in arterial oxygen tension (Pao2), sufficient to increase sig- copyright. nificantly the arterial oxygen saturation (Sao2), but not to depress seriously the ventilatory drive.2 Other Effect of oxygen during acute exacerbations of chronic mechanisms for this oxygen induced hypercapnia airways obstruction were considered (table 1) but were originally thought to be playing only a minor part. Recently new experi- Although clinically it was well recognised that high mental data3 in patients with acute respiratory failure inspired oxygen concentrations led to severe hyper- http://thorax.bmj.com/ have cast doubt on the classic explanation of hypo- capnia in acute exacerbations of chronic airways ventilation. Instead, it was suggested that the rise in obstruction, it was not until 1980 that Aubier et al alveolar oxygen tension reduces the adaptatory pul- made comprehensive measurements of gas exchange monary vasoconstriction that normally helps to main- in this condition.3 tain ventilation-perfusion (VA/() matching. Thus a deterioration in VA/( matching rather than hypo- METHODS ventilation became the favoured explanation for the Aubier et al looked at 22 patients with chronic airways hypercapnia. Interpretation of in data this field is obstruction during an episode of acute on chronic on September 30, 2021 by guest. Protected extremely difficult and there are inadequate experi- respiratory failure. All were severely hypoxic and mental data available to prove one or other of these hypercapnic (table 2). Ventilation was measured with hypotheses. a mouthpiece, one way valve, and pneumotachograph The purpose of this article is to discuss the possible (deadspace 75 ml). Ventilation, blood gases, mixed mechanisms of carbon dioxide retention after oxygen expired carbon dioxide, and cardiac output were mea- therapy and to re-examine the relevent data, particu- sured before and at the end of 15 minutes of breathing larly those of Aubier et al.3 The conclusions are at 100% oxygen. The physiological deadspace VDphys to variance with those of some other authors-namely: tidal volume (VT) ratio was calculated from the (a) release of hypoxic vasoconstriction has a minimal simplified equation: effect; (b) the major factor causing extra carbon diox- ide retention is decreased hypoxic drive due to the rise VDPhYS _ (PaCO2 -PECO2) in Pao2, as originally proposed; (c) the Haldane effect VT PaCO2 plays a smaller part in the steady state increase in where PECO2 = mixed expired CO2 tension. Paco2 than previously supposed. RESULTS They found3 that, initially, overall ventilation fell by 18% but then rose to 93% of the control level during Address for reprint requests: John R Stradling, Churchill Hospital, the 15th minute of oxygen administration. Although Oxford OX3 7LJ. the 7% fall in ventilation at the 15th minute was 897 Thorax: first published as 10.1136/thx.41.12.897 on 1 December 1986. Downloaded from 898 Table 2 Data on gas exchange in patients studied by VDphys falls more with a fall in VT than in normal Aubier et al3 with acute on chronic respiratory failure subjects, but this proportion is very variable.5 The before and after they had breathed 100% oxygen higher V/1 units contribute most to the change in VDphy. with VT.5 Thus in Aubier's experiment a small Air Oxygen % change fall in VDphys might have been expected with the fall in VT if VA/4 matching had remained unchanged. There Paco2 mm Hg (kPa) 65 (8 7) 88 (11 7) +35 V (1/min) 10.2 9.5 - 7 are, however, no relevant control data for estimating f (b/min) 32 31 - 3 this fall except from patients with stable chronic air- VT (ml) 341 323 - 6 ways obstruction, whose tidal volumes tend to be VDphy./VT (%) 77 82 + 6 higher. Read and Lee5 show that, on average, VDphys Paco2-arterial carbon dioxide tension; V-minute ventilation; falls 0-4 ml with each I ml fall in VT in patients with f-breathing frequency; VT-tidal volume; stable chronic airways obstruction. Presumably in the VDphy.-physiological deadspace. acutely ill patients studied by Aubier, whose tidal vol- significant, neither the frequency nor the VT changes umes were closer to their anatomical-plus-instrument responsible for this fall reached statistical significance. deadspaces, the physiological deadspaces could not Paco2 rose by 23 mm Hg (3-06 kPa) (35%), carbon have fallen much further. Nevertheless, from the data dioxide production remained unchanged (270 versus of Read and Lee, which probably overestimate, the 268 ml/min), and cardiac output rose slightly from 7 2 VDphys in Aubier's experiment might have been to 7 5 1/min. The calculated VDphys/VT ratio rose expected to fall to 256 ml (263-0 4 x (341-323)) had from 77% to 82% (p < 0-01). there been no change in VA/4 matching. So 60% of significantly the rise in PaCo2 after administration ofoxygen can be to a deterio- CONCLUSIONS ascribed to a fall in ventilation and 40% Aubier et al concluded that most of the rise in Paco2 ration in VA/0 matching because the actual VDphyscopyright. was due to a deterioration in VA/0 matching, on the was 265 ml, compared with a predicted value of basis of the following statements. (1) VE fell only 7% 256 ml. If the Haldane effect and slope change of the and thus could account for only 5 mm Hg (0-66 kPa) carbon dioxide content curve after oxygen therapy are of the rise in Paco2. (2) The Haldane effect calculated considered they would also be expected to raise the from Lenfant's nomogram4 accounted for 7 mm Hg VDphy. (by about 6 ml). This then virtually eliminates (093 kPa). (3) There was a significant rise in any need to invoke VA/0 changes to explain the http://thorax.bmj.com/ VDphy,/VT and, since VT did not change significantly, observed rise in PaCo2. VDphys must have changed. Thus VA/0 matching in Using the simpler approach favoured by West6 in the lungs must have worsened. analysing this sort of problem, we come to the same conclusions. If we assume that the anatomical dead- spaces in Aubier's patients were on average about CRITIQUE add the These statements are probably incorrect deductions 175 ml (mean age of patient 65 years) and from the data provided for the following reasons. instrument deadspace (75 ml) this leaves 91 ml (341-250) as the VT reaching th. alveoli. On the basis The conversion of changes in overall ventilation to on September 30, 2021 by guest. Protected expected changes in PaCo2 is extremely difficult and of the equation The classic way is via 'VA = f(VT-(VDanatomical and VDinstrumental)] depends on certain assumptions. the VA with air becomes 2-91 I/min and with oxygen the formula 2 26 1/min- ', a fall of 22%. This would be expected to kVC2 k.V0 2 PaCO2 = or. raise the Paco2 from 65 to 84 mm Hg (8-6 to li1 kPa), f X (VT - VDphys) VE X (I - VDphYS/VT) leaving only a further 4 mm Hg (0 53 kPa) to be expla- where k = a constant, VCO2 = carbon dioxide pro- ined by other mechanisms. The figure shows how as duction, f = frequency. With this approach, and the initial PaCo2 rises smaller and smaller falls in VA Aubier's data, the calculated VDphys is 263 ml (341 x are required to produce a given further rise in PaCo2. 0 77) for air and 265 ml (323 x 0.82) for oxygen. This is an obvious point but one often forgotten. In Hence VDph,5 did not change at all. The VDphys/VT addition, because the tidal volumes of the acutely ill ratio rose only because VT fell and the error made was patients in Aubier's study were so small and thus close to assume that a statistically insignificant change to the total deadspace, only very small falls in VT were could not be physiologically important. necessary to produce a physiologically significant fall The problem with this approach is in'trying to inter- in VA'. pret changes in VDphys/VT (or just VDphy5) to indicate The data of Aubier et al3 actually lend more changes in V/Q matching in the face of changing VT. support to the hypothesis that hypoventilation is the In normal subjects VDphys falls a little as VT falls. In cause of the hypercapnia than to the hypothesis patients with stable chronic airways obstruction that increasing VA/0 mismatch is responsible.
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