Extracorporeal Membrane Oxygenation Is Not First-Line Therapy for the Acute Respiratory Distress Syndrome

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Some patients with the acute respiratory distress syndrome (ARDS) experience severe impairments in gas exchange. We can use high fractions of inspired oxygen (FIO2) to counteract hypoxemia from ventilation-perfusion mismatch, but this may cause additional lung injury from oxygen toxicity. We can use positive end-expiratory pressure (PEEP) to counteract hypoxemia from elevated intra-pulmonary shunt, but this may cause circulatory depression and potentially damaging high airway pressures during inspiration. We can compensate for high dead space and CO2 retention by using larger tidal volumes and respiratory rates, but this may cause barotrauma and ventilator-induced lung injury from overdistention. How does the intensivist know when the benefit of an intervention outweighs potential harm?
What derangements in gas exchange represent credible threats to patients with ARDS? Most intensivists aim for normal arterial oxygenation but may tolerate PaO2s in the mid-50s or SpO2s in the high 80s. However, the limits of human tolerance of hypoxemia may far exceed these thresholds. When mountaineers without supplemental oxygen approach the summit of Mt. Everest, their PaO2s are in the low-mid 20s (1) (albeit with acclimation), and they survive this experience unless killed in a fall or an avalanche. A near-term fetus has a PaO2 in the mid-20s, and most thrive in this environment. ARDS patients are different from mountaineers and fetuses, but we really do not know how low is too low for PaO2 in patients with ARDS. It probably depends on several factors, such as age, comorbidities (e.g., atherosclerotic disease), hemoglobin concentration, and the altitude at which a patient is acclimated. Similarly, we do not know the acceptable limits of PaCO2. Most intensivists aim to maintain PaCO2s below 60 mm Hg and arterial pH > 7.30. However, in a striking report of their early experiences with mechanical ventilation with lower tidal volumes, New Zealand investigators reported five patients with PaCO2s greater than 80 mm Hg, three of whom survived (2). There are also animal data suggesting that acute hypercapnia with acidosis may mitigate acute lung injury (3).
Despite our lack of understanding of the safe limits of human tolerance in the ICU, intensivists often feel pressure to normalize (or decrease the abnormality) of blood gasses. Extra-corporeal membrane oxygenation (ECMO) (or extra-corporeal gas exchange, ECGE) offers an opportunity to maintain arterial oxygenation within normal limits without resorting to high FiO2s or PEEPs. Moreover, ECGE can maintain PaCO2 within normal limits without generous tidal volumes or rapid respiratory rates. With ECMO or ECGE, we can maintain acceptable gas exchange while resting the lung with small tidal volumes, low respiratory rates, and small-to-moderate PEEPs. This can “buy time” for other treatments such as antibiotics and for natural healing processes. Thus, there is a strong physiologic rationale for ECMO in ARDS.

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