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Low-tidal-volume ventilation reduces mortality in patients with ARDS, but there are often challenges in implementing lung-protective ventilation, such as acidosis from hypercapnia. In a patient with severe ARDS we achieved adequate ventilation with a very low tidal volume (4 mL/kg ideal body weight) by inducing mild hypothermia (body temperature 35–36°C).
- acute respiratory distress syndrome
- mechanical ventilation
- lung-protective ventilation
- tidal volume
- permissive hypercapnia
ARDS is defined as an acute onset of severe respiratory distress with bilateral infiltrates on chest radiograph, an absence of left-atrial hypertension, a pulmonary capillary wedge pressure of ≤ 18 mm Hg, no clinical signs of left-heart failure, and severe hypoxemia (PaO2/FIO2 ≤ 200 mm Hg).1 The current standard practice for the management of ARDS includes lung-protective ventilation, which entails low tidal volume (VT) (6 mL/kg ideal body weight), plateau pressure ≤ 30 cm H2O, and modest PEEP.
Low-VT ventilation is the only ventilation strategy that has been shown to reduce mortality in patients with ARDS.2 In the ARDS Network trial,2 patients were randomized to either low VT (≤ 6 mL/kg predicted body weight) and plateau pressure ≤ 30 cm H2O or conventional ventilation with higher VT. Low VT had a 9% absolute reduction in mortality risk, more ventilator-free hospital days, and more days free from nonpulmonary-organ failure. However, we do not know if further lowering VT or airway pressure would further improve survival.
In addition to lung-protective ventilation, many unproven strategies have been attempted to improve oxygenation in patients with severe ARDS, including alveolar recruitment, airway pressure-release ventilation, high-frequency oscillatory ventilation, and high-frequency percussive ventilation. Other strategies include paralysis (which recently was found to improve survival in early stages of ARDS, possibly by improving patient-ventilator synchrony and decreasing barotrauma and biotrauma),3 inhaled nitric oxide, inhaled prostacyclin (which improves ventilation-perfusion matching), extracorporeal membrane oxygenation, and positioning maneuvers such as prone position.
Barriers to the use of low-VT ventilation in patients with ARDS include hypercapnia and acidosis. We hypothesized that inducing hypothermia might allow very-low-VT ventilation by decreasing carbon dioxide production and thus decreasing respiratory acidosis. There have been case reports on hypothermia as an adjunct in treating patients with ARDS. One patient with ARDS and sepsis had improved oxygenation with hypothermia.4 Wetterberg and Steen reported the successful use of hypothermia and a buffer infusion in a patient with ARDS.5 However, neither of those patients underwent hypothermia in order to allow low-VT ventilation.
A 29-year-old man was admitted to the intensive care unit after an aspiration event. He was intubated on arrival to the hospital. His arterial blood gases (pH 7.33, PaCO2 44 mm Hg, and PaO2 109 mm Hg on 100% oxygen) and chest radiograph (Fig. 1) were consistent with ARDS. His oxygenation continued to worsen, and he was paralyzed to improve patient-ventilator synchrony and to achieve lung-protective ventilation. His temperature rose to 38.4°C after he was admitted to the intensive care unit. He was actively cooled to 35–36°C in an effort to decrease carbon dioxide production. By achieving a temperature of 35–36°C we were able to decrease VT to 4 mL/kg ideal body weight (Table 1). The other ventilator settings were held constant (PEEP 12 cm H2O, FIO2 0.60, respiratory rate 28 breaths/min). His hemodynamic variables were: blood pressure range 117–147/68–76 mm Hg, central venous pressure range 8–10 mm Hg, heart rate range 98–108 beats/min. His plateau pressure dropped from 23 cm H2O to 18 cm H2O with low-VT ventilation. While there was an increase in his PaCO2, his pH remained stable despite the low VT (see Table 1). His pH and PaCO2 tolerated the 4 mL/kg VT, and ventilator settings were maintained.
After 6 days of hypothermia we rewarmed the patient to evaluate for clinical improvement. Over the course of 8 hours his temperature increased from 35.9°C to 37.9°C, pH decreased from 7.41 to 7.24, and PaCO2 increased from 48 mm Hg to 71 mm Hg. Over the next 24 hours we again cooled him to 35.7°C, and his pH increased to 7.43 and PaCO2 decreased to 40 mm Hg. We made no ventilation changes during this period.
Because of worsening hypoxemia, despite paralysis and lung-protective ventilation, we initiated inhaled nitric oxide therapy and his oxygenation dramatically improved. We transitioned to inhaled prostaglandin, and then to an oral phosphodiesterase inhibitor. He was eventually extubated and discharged from the hospital.
We hypothesize that hypothermia and paralysis allowed us to use a very low VT and a low plateau pressure by decreasing the metabolic rate and carbon dioxide production and thus preventing a substantial PaCO2 increase and acidosis. While it is likely that an even lower VT could be achieved with a greater degree of hypothermia, our target was very mild hypothermia of 35–36°C, in order to avoid the complications of hypothermia, which include higher infection rate and coagulopathy. We believe that even very mild hypothermia reduces the metabolic rate enough to achieve low-VT ventilation. Our patient's acidosis was relatively mild (pH 7.31) and was well tolerated on a VT of 4 mL/kg ideal body weight. It would be interesting to further investigate mild hypothermia as a means of achieving low-VT ventilation and lower plateau pressure in patients with severe ARDS.
While our approach in this patient was to minimize CO2 production, other authors have proposed unconventional methods to improve CO2 removal, such as decreasing airways dead space. In a laboratory study in sheep, Rossi et al developed a modified method of transtracheal gas insufflation that they called intratracheal pulmonary ventilation.6 A continuous flow of fresh gas is delivered at the carina, so the upper-airways dead space is bypassed. In healthy sheep, intratracheal pulmonary ventilation allowed lowering VT to as low as 1 mL/kg while maintaining normocapnia. Similarly, during continuous apneic ventilation, oxygen is usually delivered at the carina while maintaining a stable level of hypercapnia.7
A different and fascinating method of removing CO2 is artificial blood filtration. Gattinoni et al used venovenous extracorporeal membrane oxygenation to remove most of the metabolic carbon dioxide in ARDS patients.8 More recently, Cressoni et al, in a sheep model, found that half of metabolic CO2 production could be removed with a commercial hemofilter and a replacement solution containing sodium hydroxide.9
Both approaches (lowering CO2 production and increasing CO2 removal) may permit low-VT ventilation and thus decrease the risk of lung injury. In a paralyzed patient, inducing hypothermia to 35–36°C is a safe and low-risk strategy that can be a useful adjunct to other strategies for managing ARDS.
- Correspondence: Ulrich Schmidt MD PhD, Surgical Intensive Care Unit, Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, 55 Fruit Street, Gray 4, Boston MA 02114. E-mail: .
To avoid potential conflict of interest, Editor in Chief Dean Hess was blinded to the peer review process, deferring to Associate Editor Richard Branson.
The authors have disclosed no conflicts of interest.
- Copyright © 2011 by Daedalus Enterprises Inc.