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Permissive Hypoxemia : Is It Time To Change Our Approach? FREE TO VIEW

Mohamed Abdelsalam, MD
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Suez Chest HospitalSuez, Egypt

Correspondence to: Mohamed Abdelsalam, MD, ICU, Suez Chest Hospital, 137 Talhat Harb St, Suez, Egypt; e-mail: mohamedabdelsalam@hotmail.com



Chest. 2006;129(1):210-211. doi:10.1378/chest.129.1.210
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To the Editor:

Ahmed et al1 reported an interesting case of Wegener granulomatosis with diffuse alveolar hemorrhage in a 26-year-old woman. The patient was urgently intubated, sedated, paralyzed, and maintained on 100% oxygen and a positive end-expiratory pressure as high as 18 cm H2O. Despite the use of different modes of ventilation, including volume control, pressure control with inverse inspiratory/expiratory ratio, and high-frequency oscillatory ventilation, refractory hypoxemia persisted (arterial oxygen saturation [Sao2] < 80%), and the decision was made to start extracorporeal membrane oxygenation (ECMO). The patient seems to have fulfilled the blood gas criteria for ECMO. However, I am interested to know if there was any evidence of tissue hypoxia prior to the initiation of ECMO.

In general, criteria for ECMO are the existence of severe hypoxemia not responding to maximal conventional therapy. Most if not all ventilatory and nonventilatory strategies, including ECMO, focus primarily on the maintenance of satisfactory arterial oxygenation (often defined as an Sao2 > 90%), regardless of the adequacy of tissue oxygenation. It is often assumed that acute hypoxemia is poorly tolerated by critically ill patients because of increased risk of tissue hypoxia and death. It must be emphasized however, that tissue oxygenation is determined not only by Sao2 but also by hemoglobin concentration, cardiac output, oxygen affinity of hemoglobin, oxygen extraction, and metabolic demand of the body.23 Therefore, because of the presence of several factors that determine oxygen delivery and consumption, Sao2 alone cannot be expected to be a sensitive index of tissue oxygenation. To date, no large prospective randomized trial has been published to evaluate the relationship between acute hypoxemia, tissue oxygenation, and clinical outcome in critically ill patients and to demonstrate to what extent could such a relationship be modified by other parameters of oxygen delivery and consumption such as hemoglobin affinity and oxygen demand of the body.

As a result of the widely used lung protective ventilation, many patients with ARDS are now prone to hypercapnia and respiratory acidosis that can promote oxygen delivery and improve tissue oxygenation (due to right shift of oxyhemoglobin dissociation curve),4although the Sao2 may be relatively low. In addition, oxygen demand and consumption are often reduced in patients who receive mechanical ventilation because of sedation, muscle paralysis, and decreased oxygen cost of breathing.5 The beneficial effects of permissive hypercapnia, sedation, and muscle paralysis on oxygen delivery and consumption may partly explain why arterial hypoxemia is not necessarily associated with tissue hypoxia. In 1984, Lund et al6 reported a case of severe hypoxemia (Pao2 < 30 mm Hg) in a patient with ARDS who had no evidence of tissue hypoxia. Therefore, it may be difficult to determine a critical value of Sao2 that can define tissue hypoxia in all ICU patients, irrespective of the other parameters of tissue oxygenation. Instead, it may be more appropriate to assess tissue hypoxia in each individual patient (with blood lactate or mixed venous oxygen saturation) rather than using Sao2 as a surrogate marker of tissue oxygenation.

The concept that hypoxemia is probably well tolerated by ICU patients is further supported by the fact that multiorgan failure rather than tissue hypoxia is the leading cause of death in patients with ARDS. Interestingly, although refractory hypoxemia is the hallmark of ARDS, only a minority of patients who die do so because of respiratory failure.710 Ventilator-induced lung injury (including oxygen toxicity, volutrauma, and biotrauma) rather than hypoxemia may therefore explain the high incidence of multiorgan failure and death in patients with ARDS. The mortality rate from ARDS is approximately 40 to 50%.1113 However, in a recent study,14the mortality rate as low as 26% was reported. In the ARDS Network trial, lung-protective ventilation with low tidal volume has been shown to result in substantial reduction in mortality in patients with ARDS.15 It may be of interest to mention that improved outcome in the low tidal volume group was not due to improved arterial oxygenation. However, the higher mortality in patients who received large tidal volume ventilation did not result from hypoxemia and tissue hypoxia but probably from multiorgan failure induced by alveolar overdistension and biotrauma.

An important lesson to learn from the ARDS Network trial is that clinical outcome in ARDS is probably determined by the ability to avoid ventilator-induced complications rather than to improve arterial oxygenation. Over many years, maintenance of adequate arterial oxygen content (by improving oxygen saturation and optimizing hemoglobin concentration) has been a mainstay of supportive management of critically ill patients. In a large multicenter randomized controlled trial16 that compared restrictive transfusion strategy (hemoglobin, 7 to 9 g/dL) vs a liberal strategy (10 to 12 g/dL), it has been demonstrated that RBC transfusion used to augment oxygen delivery did not offer any survival benefit in critically ill patients with normovolemia when the hemoglobin concentration was > 7 g/dL. The Canadian trial has clearly shown that “permissive anemia” can be remarkably tolerated by critically ill patients. I think the most important lesson from the Canadian trial is the recognition that lowering of arterial oxygen content, as a result of anemia, is not necessarily associated with tissue hypoxia and death. However, it is not clear whether a reduction of oxygen content due to mild-to-moderate hypoxemia can also be well tolerated. Therefore, more studies are needed to compare a restrictive strategy of arterial oxygenation or permissive hypoxemia (Sao2 maintained between 82% and 86%) to a liberal oxygenation strategy (Sao2 maintained between 88% and 92%) in patients with ARDS and other diseases characterized by refractory hypoxemia.

Ahmed, SH, Aziz, T, Cochran, J, et al (2004) Use of extracorporeal membrane oxygenation in a patient with diffuse alveolar hemorrhage.Chest126,305-309. [CrossRef] [PubMed]
 
Guyton, AC, Hall, JE Transport of oxygen and carbon dioxide in the blood and body fluids.Textbook of medical physiology 10th ed.2000,463-473 W.B. Saunders. Philadelphia, PA:
 
Connie, CW, Hsia, MD Respiratory function of hemoglobin [abstract]. N Engl J Med. 1998;;338 ,.:239. [CrossRef] [PubMed]
 
Thorens, JB, Jolliet, P, Ritz, M, et al Effects of rapid permissive hypercapnia on hemodynamics, gas exchange and oxygen transport and consumption during mechanical ventilation for the acute respiratory distress syndrome.Intensive Care Med1996;22,179-181. [CrossRef] [PubMed]
 
Third European Consensus Conference in Intensive Care. Paris, France, December 7–8, 1995. Tissue hypoxia: how to detect, how to correct, how to prevent?Reanimation Urgencies,1996;5,161-320. [CrossRef]
 
Lund, T, Koller, ME, Kofstad, J Severe hypoxemia without evidence of tissue hypoxia in adult respiratory distress syndrome.Crit Care Med1984;12,75-76. [CrossRef] [PubMed]
 
Montgomery, AB, Stager, MA, Caricco, CJ, et al Causes of mortality in patients with the adult respiratory distress syndrome.Am Rev Respir Dis1985;132,485-489. [PubMed]
 
Steinberg, KP, McHugh, LG, Hudson, LD Causes of mortality in patients with the acute respiratory distress syndrome (ARDS): an update [abstract]. Am Rev Respir Dis. 1993;;147 ,.:A347
 
Wang, BM, Steinberg, KP, Hudson, LD Causes of mortality in patients with the acute respiratory distress syndrome (ARDS): 1981–1994 [abstract]. Am J Respir Crit Care Med. 1996;;153(suppl) ,.:A593
 
Stapleton, RD, Caldwell, ES, Hudson, LD, et al Causes and timing of mortality in patients with the acute respiratory distress syndrome (ARDS) [abstract]. Am J Respir Crit Care Med. 2001;;163 ,.:A449
 
Sloane, PJ, Gee, MH, Gottlieb, JE, et al A multicenter registry of patients with acute respiratory distress syndrome: physiology and outcome.Am Rev Respir Dis1992;146,419-426. [PubMed]
 
Doyle, RL, Szaflarski, N, Modin, GW, et al Identification of patients with acute lung injury: predictors of mortality.Am J Respir Crit Care Med1995;152,1818-1824. [PubMed]
 
Zilberberg, MD, Epstein, SK Acute lung injury in the medical ICU: co-morbid conditions, age, etiology and hospital outcome.Am J Respir Crit Care Med1998;157,1159-1164. [PubMed]
 
The National Heart, Lung, and Blood Institute ARDS Clinical Trials Network.. Higher versus lower positive end-expiratory pressures in patients with the acute respiratory distress syndrome.N Engl J Med2004;351,327-336. [CrossRef] [PubMed]
 
The ARDS Network.. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome.N Engl J Med2000;342,1301-1308. [CrossRef] [PubMed]
 
He’bert, PC, Wells, G, Blajchman, MA, et al A multicenter, randomized, controlled clinical trial of transfusion requirements in critical care.N Engl J Med1999;340,409-417. [CrossRef] [PubMed]
 

Figures

Tables

References

Ahmed, SH, Aziz, T, Cochran, J, et al (2004) Use of extracorporeal membrane oxygenation in a patient with diffuse alveolar hemorrhage.Chest126,305-309. [CrossRef] [PubMed]
 
Guyton, AC, Hall, JE Transport of oxygen and carbon dioxide in the blood and body fluids.Textbook of medical physiology 10th ed.2000,463-473 W.B. Saunders. Philadelphia, PA:
 
Connie, CW, Hsia, MD Respiratory function of hemoglobin [abstract]. N Engl J Med. 1998;;338 ,.:239. [CrossRef] [PubMed]
 
Thorens, JB, Jolliet, P, Ritz, M, et al Effects of rapid permissive hypercapnia on hemodynamics, gas exchange and oxygen transport and consumption during mechanical ventilation for the acute respiratory distress syndrome.Intensive Care Med1996;22,179-181. [CrossRef] [PubMed]
 
Third European Consensus Conference in Intensive Care. Paris, France, December 7–8, 1995. Tissue hypoxia: how to detect, how to correct, how to prevent?Reanimation Urgencies,1996;5,161-320. [CrossRef]
 
Lund, T, Koller, ME, Kofstad, J Severe hypoxemia without evidence of tissue hypoxia in adult respiratory distress syndrome.Crit Care Med1984;12,75-76. [CrossRef] [PubMed]
 
Montgomery, AB, Stager, MA, Caricco, CJ, et al Causes of mortality in patients with the adult respiratory distress syndrome.Am Rev Respir Dis1985;132,485-489. [PubMed]
 
Steinberg, KP, McHugh, LG, Hudson, LD Causes of mortality in patients with the acute respiratory distress syndrome (ARDS): an update [abstract]. Am Rev Respir Dis. 1993;;147 ,.:A347
 
Wang, BM, Steinberg, KP, Hudson, LD Causes of mortality in patients with the acute respiratory distress syndrome (ARDS): 1981–1994 [abstract]. Am J Respir Crit Care Med. 1996;;153(suppl) ,.:A593
 
Stapleton, RD, Caldwell, ES, Hudson, LD, et al Causes and timing of mortality in patients with the acute respiratory distress syndrome (ARDS) [abstract]. Am J Respir Crit Care Med. 2001;;163 ,.:A449
 
Sloane, PJ, Gee, MH, Gottlieb, JE, et al A multicenter registry of patients with acute respiratory distress syndrome: physiology and outcome.Am Rev Respir Dis1992;146,419-426. [PubMed]
 
Doyle, RL, Szaflarski, N, Modin, GW, et al Identification of patients with acute lung injury: predictors of mortality.Am J Respir Crit Care Med1995;152,1818-1824. [PubMed]
 
Zilberberg, MD, Epstein, SK Acute lung injury in the medical ICU: co-morbid conditions, age, etiology and hospital outcome.Am J Respir Crit Care Med1998;157,1159-1164. [PubMed]
 
The National Heart, Lung, and Blood Institute ARDS Clinical Trials Network.. Higher versus lower positive end-expiratory pressures in patients with the acute respiratory distress syndrome.N Engl J Med2004;351,327-336. [CrossRef] [PubMed]
 
The ARDS Network.. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome.N Engl J Med2000;342,1301-1308. [CrossRef] [PubMed]
 
He’bert, PC, Wells, G, Blajchman, MA, et al A multicenter, randomized, controlled clinical trial of transfusion requirements in critical care.N Engl J Med1999;340,409-417. [CrossRef] [PubMed]
 
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