Dynamic hyperinflation, intrinsic positive end-expiratory pressure, and respiratory rate.

In reviewing the article “Methemoglobinemia: Sudden Dyspnea and Oxygen Desaturation After Esophagoduodenoscopy,” in the August 2004 issue of RESPIRATORY CARE,1 I found the article suggested that, during the esophagoduodenoscopy procedure the patient’s blood oxygen saturation (measured via pulse oximetry) began to drop rapidly, and a saturation of 54% registered on the pulse oximeter while the patient was breathing 100% oxygen via non-rebreathing mask. The arterial blood gas analysis subsequently showed a PaO2 of 117 mm Hg. It is my understanding that a pulse oximeter is capable of reading only “functional” hemoglobin, that is, only the hemoglobin bound with or capable of binding with oxygen. If the PaO2 was 117 mm Hg, the oxyhemoglobin was 22.2%, and the methemoglobin was 77.4%, the oximeter should have been reading about 98%, since the maximum functional hemoglobin was 22.6% (100% –77.4% methemoglobin) and the actual oxyhemoglobin was 22.2%. The article gives the impression that a pulse oximeter can detect dysfunctional oxyhemoglobin states, when in fact the oximeter will often mislead practitioners about a patient’s true oxygen content when dysfunctional hemoglobin (ie, carboxyhemoglobin or methemoglobin) is present. Why was there a discrepancy with the pulse oximetry readings initially?