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Synopsis: Low-tidal-volume ventilation, as part of a lung-protective strategy for managing patients with ARDS, has recently been shown to decrease mortality. However, using lower tidal volumes may increase the risk of lung collapse, particularly when applied in other clinical settings.
Source: Kallet RH, et al. Respir Care. 2001;46(1):49-52.
Kallet and associates report the case of a 35-year-old man with the acute respiratory distress syndrome (ARDS) complicating hemorrhagic pancreatitis and abdominal compartment syndrome. This patient was managed with the currently recommended lung-protective mechanical ventilation strategy that incorporates the use of small tidal volumes and attempts to keep end-inspiratory plateau pressure below 35 cm H2O in order to prevent ventilator-induced lung injury. While receiving tidal volumes of 4.5 mL/kg and 20 cm H2O of positive end-expiratory pressure (PEEP), the patient abruptly desaturated while being turned, and a chest radiograph revealed total right lung collapse. Large amounts of tenacious secretions were removed by fiberoptic bronchoscopy, but hypoxemia recurred and repeat chest x-ray showed partial reinflation of the right lower lobe but new left upper lobe collapse. The tidal volume was increased to 7 mL/kg, and PEEP was increased to 30 cm H2O for 2 breaths every 3 minutes. Although these intermittent PEEP breaths increased end-inspiratory plateau pressure from 38 to 50 cm H2O, oxygenation improved and the lung remained fully inflated for the next 10 days. The patient eventually succumbed to multiple organ failure, but lung collapse did not recur.
Comment by David J. Pierson, MD, FACP, FCCP
Within the last several months, a large randomized controlled trial of lung-protective, low-tidal-volume ventilation vs. traditional management in ARDS was published showing convincingly that using the new strategy reduced mortality.1 This landmark paper confirmed the results of several case series and smaller randomized trials over the previous decade, and marked the first time that any specific approach to mechanical ventilation made a real difference in ultimate patient outcomes in ARDS. Appropriately, ICU clinicians everywhere are adopting the lung-protective ventilatory approach, or at least moving in that direction. However, as we use tidal volumes only about half as large as those we have used for more than 20 years, several related phenomena are becoming apparent.
First, because patients with ARDS have respiratory distress, and because low tidal volumes fall even shorter than larger ones in satisfying the air hunger of such patients, more sedation is often required, along with greater temptation to use muscle relaxants to achieve patient-ventilator synchrony. Patient distress and the need for more sedation are further augmented by the hypercapnia that often develops during lung-protective ventilation. It remains to be seen whether using higher doses of opioids, benzodiazepines, and other agents (including paralytic agents) to make patients appear more confortable also prolongs weaning and delays extubation once their ARDS has improved. In my experience, however, we are spending a lot more time and energy at the bedside dealing with sedation and patient-ventilator synchrony than we did before adoption of the new strategy.
Another downside of low-tidal-volume ventilation is the potential for lung collapse. Our traditional use of 10-12 mL/kg tidal volumes evolved from the demonstration nearly 40 years ago that anesthetized persons with normal lungs developed widespread atelectasis and impaired arterial oxygenation when ventilated with small tidal volumes and without intermittent sigh breaths.2 Now that low-tidal-volume ventilation is in vogue for patients with ARDS, there seems to be a tendency for clinicians to use smaller tidal volumes in other patients as well—which is a definite mistake. Using tidal volumes of 7 or 8 mL/kg in someone without intrinsic lung disease, who is ventilated after cardiac surgery or a drug overdose and does not have diffuse acute lung injury, amounts to an invitation for the development of lobar collapse—or at least to greater impairment of oxygenation—which may delay weaning and invite other complications.
Patients with ARDS need small tidal volumes to avoid ventilator-induced parenchymal lung damage. Individuals with obstructive lung disease such as advanced chronic obstructive pulmonary disease or acute asthma should also receive small tidal volumes, in order to prevent further hyperinflation, hemodynamic compromise, and barotrauma. However, all other patients should still be ventilated with tidal volumes of 10-12 mL/kg.
In the report summarized above, Kallet et al fall somewhat short of demonstrating that the patient’s lung collapse was due solely to low-tidal-volume ventilation. Atelectasis did not develop until more than a week into the patient’s course, despite the use of low tidal volumes for several days before the event. Although usual clinical criteria for ventilator-associated pneumonia were absent at the time of the event, lung collapse was associated with an increase in secretions, suggesting the possibility of lower respiratory infection. The atelectasis went away when several things were done, including institution of ventilation with larger tidal volumes, and did not recur.
Whatever the mechanisms for atelectasis and its correction in this specific case, I think the point is well taken that current ventilator management for patients with ARDS probably increases the likelihood of lung collapse, particularly in the presence of copious or especially viscous airway secretions. This is not a reason to go back to larger tidal volumes in managing ARDS, but should increase our awareness of the potential complication of lung-protective ventilation addressed by Kallet et al in this report.
1. ARDS Network. N Engl J Med. 2000;342(18):1301-1308. Critical Care Alert 2000;4:63-65.
2. Bendixen HH, et al. Anesthesiology. 1964;25:297-301.