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Case 31-2004: A Four-Year-Old Boy with Hypoxemia
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     To the Editor: In Case 31-2004 (Oct. 14 issue),1 which involves a four-year-old boy with the hepatopulmonary syndrome, the minimal increase in the partial pressure of arterial oxygen (from 52 mm Hg while the boy was breathing room air to 69 mm Hg while he was breathing 100 percent oxygen), after nearly a quintupling of the fraction of inspired oxygen (from 0.21 to 1.0), uncovers a fascinating aspect of this patient's physiology that is not touched on in the discussion: the shunt is dynamic and worsens with oxygen supplementation. The ratio of the partial pressure of arterial oxygen to the fraction of inspired oxygen, an excellent correlate of the shunt fraction, deteriorated from 248 while the boy was breathing room air to 69 while he was breathing 100 percent oxygen.2 This is consistent with the pathogenesis of hypoxemia in the hepatopulmonary syndrome, since as a potent pulmonary vasodilator, oxygen can further dilate capillaries and hinder diffusion to the center of the vessel.

    According to Table 4 of the article, with a true shunt there is no response to 100 percent oxygen supplementation, but the patient did have a "minimal response." Although supplementation with 100 percent oxygen will not correct a true shunt, it certainly can correct the hypoxemia caused by a true shunt, provided that the shunt does not exceed a certain fraction of total cardiac output. Anesthesiologists who initiate one-lung ventilation during surgery can often completely reverse or prevent shunt-induced hypoxemia with oxygen supplementation.

    Nir Hoftman, M.D.

    University of California at Los Angeles

    Los Angeles, CA 90095-1722

    nhoftman@mednet.ucla.edu

    References

    Case Records of the Massachusetts General Hospital (Case 31-2004). N Engl J Med 2004;351:1667-1675.

    Covelli HD, Nessan VJ, Tuttle WK III. Oxygen derived variables in acute respiratory failure. Crit Care Med 1983;11:646-649.

    Dr. Kinane and a colleague reply: Dr. Hoftman suggests a potential alternative mechanism: the shunt fraction is increased by the inhalation of 100 percent oxygen in the hepatopulmonary syndrome, but this increase is masked by other mechanisms. If we use oxygen as a test gas to estimate the right-to-left shunt, we find that the percentage of hemoglobin saturation associated with a 50 percent shunt is 87.5; this would correspond to a partial pressure of arterial oxygen of 53 torr while the subject breathed ambient air. During breathing of 100 percent oxygen, the well-ventilated 50 percent of the lung would add an additional 1.7 ml of oxygen per 100 ml of blood. This would raise the arterial oxygen saturation to 92 percent, corresponding to a partial pressure of arterial oxygen of 65 torr. These values are similar to the values in our patient, with no need to invoke an alternative mechanism.

    T. Bernard Kinane, M.D.

    Daniel C. Shannon, M.D.

    Massachusetts General Hospital

    Boston, MA 02114