In our case report, we described the thoracoscopic repair of an iatrogenic lesion of the left main bronchus. This lesion was noticed by the surgeon because the inflated bronchial cuff of the left-sided double lumen tube was bulging through it. Repair was challenging because the right lung had to remain deflated to optimize visibility. But also the bulging bronchial cuff had to be deflated. Positive pressure ventilation through a double lumen tube with both cuffs deflated is inadequate. Therefore, to maintain oxygenation, we placed a 7F Arndt blocker behind the lesion and oxygenated the left lung with the Ventrain device. After the 20 minutes lasting closing procedure, the PaCO2 rose to 87 mm Hg while the PaO2 was 94 mm Hg.
In his letter, Professor Grocott stated that the maintained PaO2 indicated that the patient has been adequately oxygenated but that the significant hypercapnia suggested that the patient was grossly underventilated (and arguably might not have been ventilated at all). So although using the Ventrain through a 7F blocker (ID 1.12 mm) may have allowed the oxygenation needed to safely complete a 20-minute surgical procedure, this might similarly have been accomplished if free flow of oxygen had been provided to the bronchus without any ventilation at all.
We absolutely agree with Professor Grocott that during the repair of the left main stem bronchus ventilation was inadequate to clear all carbon dioxide produced but we disagree that ventilation was totally absent. Stock et al2 sampled the PaCO2 in anesthetized subjects and found that the PaCO2 increased 12 mm Hg in the first minute and then raised 3.4 mm Hg·minute−1 between minute 2 and 5. If we would extrapolate this linear increase in PaCO2 to 20 minutes apnea, the calculation shows that the PaCO2 would increase 76.6 mm Hg. A PaCO2 increase of 76.6 mm Hg after 20 minutes related to the measured PaCO2 of 87 mm Hg would implicate that the PaCO2 before repair would be ~10 mm Hg. We did not assess an arterial blood gas sample before we started the Ventrain use but we retrospectively determined the PETCO2 from the anesthetic report and found that it was 37 mm Hg.
Stock et al2 in the obstructed patient and Eger and Severinghaus3 in the unobstructed patients during apneic oxygenation determined that the rate of rise of PaCO2 averages 12–13.4 mL in the first minute (if the patient is not hyperventilated before apneic oxygenation) and 3–3.4 mL/min each minute thereafter.
As mentioned above there was subnormal removal of carbon dioxide in this case. A further contributory factor to this was the set phases of ventilation with intermittent equilibration as prescribed in the Ventrain User Manual, to prevent damage to the lung by hyperinflation.
When working with Ventrain, it is basically possible to estimate the volume of gas that has been insufflated each time by using intermittent capnometry.4 A sidestream capnographer can draw a sample from the breathing gas during equilibration and the value can be read off the display. That way one knows whether to use a higher or lower flow of the pressure-compensated oxygen source. However, the time required for the expiration depends on the resistance of the ventilation system, in particular on the ventilation catheter.
If the upper respiratory system is partially or completely obstructed, a very high intrapulmonary pressure could build up, eg, if the Ventrain was operated outside the limits specified in the manual.