Correspondence  |   August 2011
“Life-threatening” Hypoxemia in One-lung Ventilation
Author Affiliations & Notes
  • Ravi S. Tripathi, M.D.
  • †Ohio State University Medical Center, Columbus, Ohio.
Article Information
Correspondence   |   August 2011
“Life-threatening” Hypoxemia in One-lung Ventilation
Anesthesiology 8 2011, Vol.115, 438. doi:10.1097/ALN.0b013e318223bbad
Anesthesiology 8 2011, Vol.115, 438. doi:10.1097/ALN.0b013e318223bbad
To the Editor:
In January's Anesthesiology, Rozéet al.  1 describe a thorough and step-wise approach to the management of hypoxemia in one-lung ventilation. Although we agree that “life-threatening” hypoxemia should be treated with resumption of bipulmonary ventilation, we question the definition of life-threatening hypoxemia based only on an arterial oxygen saturation (Spo2) less than 90%.
Physiologically, end-organ injury caused by inadequate oxygen delivery (DO2) is dependent on the product of arterial oxygen content (Cao2) and cardiac output. Spo2is only a single component of Cao2,along with hemoglobin concentration. Thus, in addition to Spo2, we would like to illustrate the importance of considering hemoglobin concentration and cardiac output before aborting one-lung ventilation.
We agree that an Spo2less than 90% may be tolerated poorly in an anemic patient; however, for patients with a normal or high hemoglobin concentration, oxygen content can be maintained at much lower oxygen saturations. It is well known that polycythemia is a compensatory mechanism for hypoxia in people native to high altitudes, with their hemoglobin concentrations being on average 5 g/dl higher than that of their counterparts residing at sea level.2 Transfusion of erythrocytes is associated with known complications, but increasing hemoglobin concentration via  transfusion is associated with decreased work of breathing and minute ventilation in ventilated patients with chronic obstructive pulmonary disease3 and increased successful weaning from mechanical ventilation in anemic patients with chronic obstructive lung disease.4 
With regard to overall oxygen delivery, cardiac output is another key factor. Although Rozéet al.  comment briefly on the development of right ventricular dysfunction with hypoxic pulmonary vasoconstriction, vigilance should be kept to maintaining a normal cardiac output in the face of decreased oxygen saturation. Increased cardiac output is a known compensatory mechanism to hypoxia5 with additional beneficial effects separate from increased oxygen delivery, such as decreased dead-space ventilation. In addition, although Rozéet al.  discuss the use of vasodilators to treat hypoxic pulmonary vasoconstriction, dobutamine has been shown to increase oxygen delivery significantly more than does prostacyclin.6 Pharmacologic assistance may be needed to maintain a sufficient cardiac output, and patients with low cardiac output states may indeed require oxygen saturations much greater than 90%.
Although in a different population than those with one-lung ventilation but having similar physiologic principles, recommendations for management of patients with acute respiratory distress syndrome requiring extracorporeal life support include maintenance of an Spo2greater than 80% and a arterial oxygen concentration of 40 mmHg, provided oxygen content is adequate (hematocrit more than 40%) and cardiac function is not threatened.1We have applied similar principles to patients with acute respiratory distress syndrome without extracorporeal life support. In the event of satisfactory hemoglobin concentrations and cardiac function, we have accepted an Spo2between 85% and 90% in patients with severe acute respiratory distress syndrome without finding evidence of end-organ malperfusion. In an extreme case, we cared for an 42-yr-old, previously healthy woman with H1N1 infection with superimposed Pseudomonas pneumonia. This patient did not achieve an Spo2greater than 90% for more than 10 days despite advanced ventilation maneuvers and pharmacologic therapies (including inhaled nitric oxide); however, oxygen delivery was maintained through cardiac output and oxygen content (hemoglobin goal, more than 12 g/dl). The patient recovered from the acute pathophysiology with no long-term end-organ damage or signs of neurologic impairment.
A complete discussion of mechanisms to increase organ oxygenation is beyond the scope of this letter. Essentially, vigilant consideration must be given to a myriad of parameters, including peak and plateau airway pressures, tidal volumes, rate of cycle delivery or flow, inspired oxygen concentrations, acid-base, markers of end-organ perfusion, cardiac output or ventricular function, and hemoglobin concentration, rather than choosing an Spo2of 90% as an arbitrary point of discontinuation of a surgical procedure, sometimes treating “life-threatening” disease.
†Ohio State University Medical Center, Columbus, Ohio.
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