Abstract
Background: End-tidal carbon dioxide pressure (PetCO2) is unreliable for monitoring PaCO2 in several conditions because of the unpredictable value of the PaCO2–PetCO2 gradient. We hypothesised that increasing both the end-inspiratory pause and the expiratory time would reduce this gradient in patients ventilated for COVID-19 with Acute Respiratory Distress Syndrome and in patients anaesthetised for surgery. Methods: On the occasion of an arterial blood gas sample, an extension in inspiratory pause was carried out either by recruitment manoeuvre or by extending the end-inspiratory pause to 10 s. The end-expired PCO2 was measured (expiratory time: 4 s) after this manoeuvre (PACO2) in comparison with the PetCO2 measured by the monitor. We analysed 67 Δ(a-et)CO2, Δ(a-A)CO2 pairs for 7 patients in the COVID group and for 27 patients in the anaesthesia group. Results are expressed as mean ± standard deviation. Results: Prolongation of the inspiratory pause significantly reduced PaCO2–PetCO2 gradients from 11 ± 5.7 and 5.7 ± 3.4 mm Hg (p < 0.001) to PaCO2–PACO2 gradients of −1.2 ± 3.3 (p = 0.043) and −1.9 ± 3.3 mm Hg (p < 0.003) in the COVID and anaesthesia groups, respectively. In the COVID group, PACO2 showed the lowest dispersion (−7 to +6 mm Hg) and better correlation with PaCO2 (R2 = 0.92). The PACO2 had a sensitivity of 0.81 and a specificity of 0.93 for identifying hypercapnic patients (PaCO2 > 50 mm Hg). Conclusions: Measuring end-tidal PCO2 after prolonged inspiratory time reduced the PaCO2–PetCO2 gradient to the point of obtaining values close to PaCO2. This measure identified hypercapnic patients in both intensive care and during anaesthesia.
Highlights
Lung involvement during SARS-CoV-2 infection frequently dominates the clinical picture of severe forms with both interstitial pneumonia related to the release of proinflammatory cytokines and vascular obstruction of thromboembolic origin [1]
Our hypotheses were that end-tidal PCO2 measured immediately after an inspiratory time (PACO2) prolonged by an inspiratory pause or recruitment manoeuvre could improve the estimation of PaCO2 and identify severe hypercapnia during mechanical ventilation in COVID Acute Respiratory Distress Syndrome (ARDS) patients or in patients anaesthetised for major surgery
From 8 April to 28 May 2020, 67 PACO2 were obtained for 34 patients (35 measures in 7 patients in the COVID group; 32 measures in 27 patients in the anaesthesia group)
Summary
Lung involvement during SARS-CoV-2 infection frequently dominates the clinical picture of severe forms with both interstitial pneumonia related to the release of proinflammatory cytokines and vascular obstruction of thromboembolic origin [1]. According to international recommendations for Acute Respiratory Distress Syndrome (ARDS) management, protective ventilation is the rule. This practice often induces hypercapnia and requires regular checks of arterial CO2 pressure (PaCO2) to adjust the level of ventilation. The monitoring of end-tidal CO2 pressure (PetCO2) is mandatory even if it underestimates the PaCO2, with a gradient around 4.5–13 mm Hg [2]. Our hypotheses were that end-tidal PCO2 measured immediately after an inspiratory time (PACO2) prolonged by an inspiratory pause or recruitment manoeuvre could improve the estimation of PaCO2 and identify severe hypercapnia during mechanical ventilation in COVID ARDS patients or in patients anaesthetised for major surgery
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