Anesth Analg 2004;99:955
© 2004 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000131700.62287.0D
LETTERS TO THE EDITOR
Interpretation of PO2 via FIO2
Leo Stemp, MD
East Granby, CT
To the Editor:
I would like to comment on a minor oversight by the editorial board that was germane to an article and a letter in the February 2004 issue of Anesthesia & Analgesia. That is, in both the article and the letter, a PO2 is noted without concomitant mention of the FIO2.
In Papadimos et al.’s report (1) on a suspected case of malignant hyperthermia, they stated: "The arterial blood gas before one-lung ventilation was pH 7.36, PaCO2 43 mm Hg, PaO2 475 mm Hg..." There is no notation of the FIO2.
In the letter by Sen et al. (2) regarding a case of oculocutaneous albinism, they stated: "Clinically, the patient appeared well oxygenated. Arterial blood gas analysis showed PaO2—104 mm Hg..." Again there was no note of the FIO2.
As a critical care physician, lung function is of paramount importance to me, and any PaO2 is considered in that light. In fact, I consider the SpO2 to be the real fifth vital sign, and I record it as such in my daily notes and presentations. However, the PaO2 (or SpO2) only tells half the story, and the unimportant half at that. It is actually the A-a gradient where the money is. The A-a gradient is a standard qualitative and quantitative marker of the severity of lung disease (or lack thereof). The PaO2 or SpO2, as measures of a patient’s "health," are uninterpretable in isolation, i.e., without some feel for the A-a gradient, which is garnered from stating the associated FIO2.
Thus, in the report by Papadimos et al. (1), the very high PaO2 noted suggests that the patient was likely being ventilated with 100% oxygen. But in the case reported in the letter by Sen et al. (2), given the apparent oxygenation problems, the reader might well assume that the patient may have been ventilated with a high FIO2. In that case, the patient’s PaO2 of only 104 would signify a major problem, in contrast to the authors’ assertion.
My point is that the PO2 or SpO2 mean nothing without notation of the associated FIO2. The fact that both authors made no mention of the FIO2 attests to lack of understanding of this point on the part of many physicians, including anesthesiologists. And even if the significance of the A-a gradient is understood intuitively by physicians, the authors’ lack of purposeful notation of the FIO2 attests to their lack of understanding of the importance of communicating a feel for the A-a gradient. To put it in perspective, in a case presentation I would no sooner mention a PaO2 without an FIO2 than I would fail to note a patient’s age or gender.
References
- Papadimos TJ, Almasri M, Padgett JC, Rush JE. A suspected case of delayed onset malignant hyperthermia with desflurane anesthesia. Anesth Analg 2004; 98: 548–9.[Abstract/Free Full Text]
- Sen I, Thapa D, Gombar KK. Oculocutaneous albinism and spurious pulse oximetry [letter]. Anesth Analg 2004; 98: 553.[Free Full Text]
Response
Thomas J. Papadimos, MD
Medical College of Ohio, Toledo, Ohio
In Response:
I would like to thank Dr. Stemp for his comments. The patient in our case report (1), as he surmised, was on an FIO2 of 1.0, and I regret the oversight of such documentation on our part. I would like to reassure Dr. Stemp that in my practice as a critical care physician I also record the FIO2 and SpO2 in my daily notes, and I agree with him as to the importance of the alveolar to arterial oxygen tension gradient (A-a gradient). To have knowledge of the PaO2 is indeed without meaning if one does not know the alveolar O2 [PAO2 = (PB – PH2O) x FIO2 – PaCO2/0.8]. The A-a gradient, along with shunt fraction, can help one with delineation of major physiologic causes of hypoxemia (hypoventilation, V/Q mismatch, low FIO2, diffusion impairment, and right to left intracardiac shunt). The A-a gradient has been of assistance in critical care medicine since the first suggestion in 1946 that it be used for quantifying pulmonary O2 transfer disruption without the requirement of mixed venous blood sampling (2). However, we must keep in mind that in the context of the acutely ill patient or patient under anesthesia, the A-a gradient varies independently with changes in FIO2, SaO2, and SvO2 (3–6). Again, I would like to thank Dr. Stemp for a point well taken.
References
- Papadimos TJ, Almasri M, Padgett JC, Rush JE. A suspected case of delayed onset malignant hyperthermia with desflurane anesthesia. Anesth Analg 2004; 98: 548–9.
- Lilienthal JL, Riley RL, Proemmel DD, et al. An experimental analysis in man of oxygen pressure gradient from alveolar to arterial blood during rest and exercise at sea level and at altitude. Am J Physiol 1946; 147: 199–216.[Free Full Text]
- Peris LV, Boix JH, Salom JV, et al. Clinical use of the arterial/alveolar oxygen tension ratio. Crit Care Med 1983; 11: 888–91.[Medline]
- Lecky JH, Ominsky AJ. Postoperative respiratory management. Chest 1972; 62 (Suppl): 50S–57S.
- Seigel JH, Farrell EJ, Miller M, et al. Cardiorespiratory interactions as determinants of survival and the need for respiratory support in human shock states. J Trauma 1973; 13: 602–19.[Medline]
- Kanber GJ, King FW, Eschar YR, et al. The alveolar-arterial oxygen gradient in young and elderly men during air and oxygen breathing. Am Rev Respir Dis 1968; 97: 376–81.[Medline]
Response
Indu Sen, MD,
Deepak Thapa, MD, and
Kanti K. Gombar, MD
Department of Anaesthesia and Critical Care, Government Medical College and Hospital, Chandigarh, India
In Response:
We thank Dr. Leo Stemp for his comments. I fully agree with him that FIO2 should always be mentioned along with PaO2 in arterial blood gas analysis. The detailed ABG report was pH 7.4, PaO2 104 mm Hg, PaCO2 37 mm Hg, SaO2 99% at FIO2 0.34. In this patient, we increased the concentration of delivered oxygen at first instance of low SpO2 only and FIO2 was lowered back to 0.34, as arterial oxygen saturation immediately picked up on changing the probe site. This continued, though there were no clinical indications of poor ventilation/perfusion of tissues and this female had normal preoperative pulmonary reserves. ABG analysis was done to eliminate any undetected abnormality and also for academic interest. However, this is one case report in which we could not find any pathological reason for intraoperative variations in SpO2. Future detailed workup of patients with oculocutaneous albinism on herbal remedies may give us more information.
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