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J Thorac Cardiovasc Surg 2008;135:1371
© 2008 The American Association for Thoracic Surgery
Invited Commentary |
[Slides] Some time ago I was interested in the laboratory with pursuing arteriovenous extracorporeal membrane oxygenation as an artificial placenta to mature newborn lamb lungs. We did not recognize then the importance of barotrauma, and we evaluated the shunt required to normalize PO 2. We early learned that by increasing the shunt, we could change PO 2, but the numbers required to do that required a great strain on the heart.
The importance of this paper has been to confirm the concept that Gattinoni brought to us of the "baby lung." We must remember the ARDS patient shown on this computed tomographic scan, the importance of the defunctionalized lung that does not ventilate as opposed to the ventilated lung, which may be as little as a third of each lung. Sixty-six percent of this patient's lung would not be ventilated and 33% would be ventilated, so even at a reserved low-volume ventilation, that translates into about 18 mL/kg or high ventilation volume to the normally ventilated lung, which we know from ARDSNet to be counterproductive.
You have appropriately dissociated oxygenation and MV. Extrapulmonary gas exchange replaces MV, which enables a therapeutic window to protect the ventilation. The key to your study, of course, is the low-resistance oxygenator that is now commercially available in Europe and the fact that less than 20% of the CO needs to be diverted into this oxygenator to achieve almost 300 mL of carbon dioxide removal. While you ventilated with a PEEP of 19, your end-inspiratory pressure was only 21. Your tidal volume was a third of the "optimized" ventilated group and a fifth of the conventionally ventilated group. Your minute volume was only 1 L, at a rate of 6. Your model probably is not the same that we see clinically with ppARDS, but that is okay. I think what you have demonstrated is lung protection, which is the hallmark of treating this terrible problem.
I have two questions for you. Have you looked at various forms of ventilation of your animals that might in fact even improve on the outcomes that you had with the current experimental group? In other words, have you tried continuous positive airway pressure as a ventilatory method for these animals, extubating them very early?
Finally, have you measured cytokines in animals that did not have anything other than the iLA associated with it? Early on in my career, there was a lot of criticism about using artificial lung membranes in patients with injured lungs for fear that cytokines would in fact be elaborated.
Dr Iglesias. Thank you for your questions. To address the second question, I performed a study accepted in the Journal of Thoracic and Cardiovascular Surgery where we placed the iLA in axillary vascular access and then we measured the cytokine response and did not find a systemic inflammatory response in this type of pigs. It was done undergoing nothing for us. It practically inhaled the pigs.
I did not understand your first question.
Dr Griffith. Could you forecast perhaps an even better form of assisted ventilation to work in concert with the iLA, such as spontaneous continuous positive airway pressure?
Dr Iglesias. I refer this question to Dr Macchiarini.
Dr Macchiarini. Thank you for the question. Yes, we did, in the sense that as soon as you get on the iLA, you need to adapt the ventilation and try the best setting in the sense that some respond very well to pressure control and some to volume control. We found that for the type of pneumonectomy that we did, a very simple pneumonectomy, the pressure control ventilation was the simplest to manage. Whether or not this was because we had such a high level of PEEP, I cannot tell you that, but it is a little bit parallel to what we saw in the clinical experience on severe ppARDS. I would suggest that from the experimental and clinical experience, so long as you reach the target to reduce the tidal volumes as low as you can, you might use either of the ventilation modes. We can go even further. We tried to not ventilate the patients at all in the clinical setting but simply keeping in place the tracheostomy tube or the tracheal tube and putting a very low flow of oxygen, doing a sort of apneic oxygenation. It did work as well. So there is a very large variability among patients. You might try to use the best one adapted to the patient, as long as you reach very low tidal volumes.
Dr Nasser K. Altorki (New York, NY). How long were the pigs generally treated on the extracorporeal membrane oxygenator? Were they also on some ancillary measures, such as steroids, or were they just treated simply by the oxygenator?
Dr Iglesias. We treated with iLA in a total of 5 pigs among the 15 pigs in which we induced ARDS by surfactant depletion.
Dr Altorki. How many days were they on it after the ARDS induction?
Dr Iglesias. Ninety minutes, more or less.
Related Article
J. Thorac. Cardiovasc. Surg. 2008 135: 1362-1371.
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