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Smoke inhalation injury and tissue dysoxia: what is the link?


Smoke inhalation injury is a frequent health threat contributing to significant pulmonary derangements. The objective of this study was to determine potential interdependencies between pulmonary shunt fraction (Qs/Qt), tissue oxygenation and cardiac performance in the acute phase of combined burn and smoke inhalation injury.


Following a 20%, third-degree burn, sheep (n = 10) were subjected to cotton smoke according to an established protocol (4 × 12 breaths, < 40°C). Before (BL) and after each set of cotton smoke inhalation, the Qs/Qt, mean pulmonary arterial pressure, cardiac index (CI), left ventricular stroke work index (LVSWI), O2 delivery index (DO2I), O2 consumption index (VO2I) and O2-extraction rate (O2-ER) were assessed. At the same time points, the arterio-venous SO2 difference and veno-arterial pCO2 gradient were determined.


One-way ANOVA with Student–Newman–Keuls post-hoc test, or linear regression when appropriate. Data are expressed as mean ± SEM, or Pearson correlation coefficient, respectively.


The burn injury led to an immediate and sustained decrease in CI (6.1 ± 0.2 vs 3.8 ± 0.6 l/min/m2), accompanied by a depression in LVSWI (75 ± 2 vs 28 ± 1 g/m/m2; P < 0.001 each). Smoke inhalation did not further impair these hemodynamic changes but led to a progressive increase in the Qs/Qt, up to a maximum of 85 ± 2% (P < 0.001 vs BL). Interestingly, the degree in Qs/Qt was inversely correlated with both the arterio-venous SO2 difference (r = -0.90) and the veno-arterial pCO2 gradient (r = -0.57). While the O2-ER remained unchanged, a more than 50% reduction in both DO2I (724 ± 41 vs 345 ± 43 ml/min2/m2) and VO2I (295 ± 16 vs 123 ± 9 ml/min2/m2) occurred (each P < 0.001 vs BL).


This study demonstrated that in the acute phase of combined burn and smoke inhalation injury (1) the deterioration in tissue oxygenation is linked with depressions in myocardial contractility and global oxygen transport as well as an increase in the Qs/Qt, and (2) the arterio-venous SO2 difference is more appropriate to mirror ventilation/perfusion mismatch compared with the veno-arterial pCO2 gradient.

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Westphal, M., Morita, N., Murakami, K. et al. Smoke inhalation injury and tissue dysoxia: what is the link?. Crit Care 8 (Suppl 1), P42 (2004).

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