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About Search. Enable Autosuggest. Patients were maintained in a 30 degrees head-up position. Maintenance of PEEP to levels of 40 cm H2O pressure for as long as 18 hours did not increase ICP in patients with either normal or low intracranial compliance, and did not increase ICP in the absence of pulmonary disease.
However, it would be a stretch to describe this as a consequence of positive pressure ventilation per se. In fact, well managed positive pressure ventilation actually prevents these sorts of outcomes. In any case, the discussion of these matters lends itself more properly to a whole chapter dedicated to open-lung and lung-protective ventilation. Lung lymphatics are thin single cell interstitial conduits which rely on the negative pressure of spontaneous breathing.
It would, therefore, make sense that positive pressure ventilation should impede or reverse this process, and therefore inhibit the clearance of foreign materials and toxins from the lung. The pressure in lymphatic vessels, in general, appears to be around 4mmHg, which ends up being higher than the intrathoracic central venous pressure on spontaneous ventilation which therefore favours the emptying of these sewer-like vessels into the central circulation.
Obviously, such a low pressure system will be highly susceptible to even small changes in intrathoracic pressure. For various reasons anaesthetised animals appear to have borne the brunt of medical violence in research on lymphatic drainage during mechanical ventilation. This is probably because the favoured method of determining lymphatic flow from the lungs is to remove and weigh them.
Unfortunately, many of the researchers ended up with wildly different results. In contrast, Mondejar et al found that lymphatic drainage of extravascular lung water and thoracic duct flow increased with increasing PEEP when the dogs had pulmonary oedema.
Where humans are concerned, what should we believe, and which opinion should the CICM exam candidate regurgitate?
In summary, the authors hold that the pulmonary lymphatics are one one hand filled by positive pressure pushing fluid out of the alveoli and into the interstitium, and on the other hand have their drainage impaired by the increased pressure in the central venous circulation.
The net effect is increased lymph production but decreased lymph flow. This is demonstrated by more cruel animal experiments. Soni and Williams quote a couple of excellent studies which illustrate the point nicely. Haider et al induced lung injury in mechanically ventilated dogs. The volume of lymph produced by the lung increased, but the flow in the thoracic duct decreased, resulting in some degree of oedema. With the thoracic duct open as a fistula i. Remarkably, Dugernier et al were able to demonstrate the same phenomenon in humans.
Patients with pancreatitis were selected to undergo thoracic duct drainage. In this manner, lymph was drained from these patients, in a volume ranging from ml to 15,ml over 10 days. Lung function and chest X-ray appearance improved, which was interpreted as the consequence of improved pulmonary lymphatic drainage. The cynic might point out that a man armed with enough frusemide to produce a negative balance of 15 litres might also have cleared the lungs up nicely, but this would only serve to muddle the discussion.
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