LETTERS TO THE EDITOR

The assessment of radiation delivered to the target tissue (thyroid bed) was indirectly determined, but not in as great detail as another study [ 11. Of five patients in the other study [ 11, in only two was the thyroid or thyroid bed uptake mea- sured. The benefits of this method, although very interesting and theoretically promising, have not yet been established in the treatment of residual thyroid bed tissue in these pa- tients.

K. DAVID MCCOWEN, M.D. Major, Medical Corps Clinical Investigation Service Madigan Army Medical Center Tacoma, Washington 9843 1

References 1. Scott JS, Halnan KE, Shimmins J, et al.: Measurement of dose to thyroid carcinoma metastases from radioiodine therapy. Er J Radio1 43: 256, 1970.

ARTERIAL BLOOD OXYGEN TENSION IN PULMONARY EMBOLISM

To the Editor: In reviewing data from phase II of the Urokinase-Strep-

tokinase Pulmonary Embolism Trials, Bell et al. [l] reported that the average arterial oxygen tension (PaOp) was 60 mm Hg, and that 10 per cent of the patients had a PaO, greater than 80 mm Hg. This method of reporting PaOp values was also used in phase I of these trials [2]. In both reports, data are insufficient for evaluation and interpretation of the PaOp. In phase I, 11.5 per cent of the patients had a PaOa above 80 mm Hg. In both phase I and II, the concomitant arterial carbon dioxide tension (PaCO& fraction of inspired oxygen (FlOz), age of the patient and body temperature correction are omitted. For example, 44 per cent of the patients in phase II had a fever. If body temperature is not corrected for, a falsely low measurement of Pa02 may result [3]. An in- creased F102 may lead to an increased PaOp. I assume the values quoted are from samples taken while the patients were breathing room air, although this is not stated. By far, the most important omission is a specified carbon dioxide tension for each P02. The alveolar-air equation shows that an increased PC02 always leads to a decreased alveolar, and hence Pa02. The commonly used equation, slightly simplified and as- suming a normal respiratory quotient, is that alveolar oxygen tension (PA02) equals the partial pressure of inspired oxygen minus 1.25 times the PC02. For a given F102, the inspired PO2 is constant; on room air, at normal body temperature and at sea level, it is approximately 150 mm Hg. Thus the PA02 is 150 minus 1.25 (PC02). The normal PO2 difference between the alveoli and arterial blood is age-dependent. It ranges from 6 mm Hg in young adults to 18 mm Hg in elderly patients [4] when sampled with the subjects sitting; the values are higher with the subjects in the supine position. PA02 changes are reflected in the arterial blood in people with normal lungs; hence the individual alveolar-arterial gradient for oxygen, or P(A-a)O,, will remain essentially unchanged despite PC02 fluctuations. The P(A-a)02 will be increased when there is unequal ventilation-perfusion of the lung, such as in pulmo-

nary embolism and in most cases of acute and chronic lung disease. Both hyperventilation (low PC02) and ventilation- perfusion inequality with consequent hypoxemia are the rule in patients with pulmonary embolism. Thus, reporting the

Pa02 above 80 mm Hg, a value which may appear “normal,” is misleading without knowledge of the PC02 AND P(A-a)02. A patient with a PC02 of 20 and PO2 of 82 has the same el- evation of P(A-a)02 (43 mm Hg) as one with a PC02 of 40 and a PO2 of 57. Thus it may be incorrect to consider that 10 to 12 per cent of patients with angiographically-proved pul- monary embolism presented with a “normal” POP. It has been suggested in a review of phase I results that 90 mm Hg be considered the lower limit of normal [5], but this recom- mendation also omitted the factors just mentioned. A PO2 of 90 mm Hg on room air may be distinctly abnormal in a young patient with marked hyperventilation as may a PO2 above 100 mm Hg for any patient on supplemental oxygen. These comments about interpreting Pa02 values may well be ob- vious to many physicians. However, I have found that blood gas data, when presented in an isolated fashion, are all too often misapplied in diagnosing individual patients, particularly when the PaO2s are normal or near normal. This is apart from the common mistake of overinterpreting a low PO2 in patients with other parenchymal lung disease and suspected pulmo- nary embolism. A concomitant PaC02 with an age-corrected P(A-a)02, FlO2 and body temperature correction are neces- sary to evaluate accurately the Pa02 of any patient. I would be most interested if these investigators have this information about their 167 patients.

LAWRENCE MARTIN, M.D.

Assistant Professor of Medicine Case Western Reserve University School of Medicine Pulmonary Division Mt. Sinai Hospital of Cleveland Cleveland, Ohio 44 106 References

1. Bell WR, Simon TL. DeMets DL: The clinical features of submassive and massive pulmonary emboli. Am J Med 62: 355, 1977. 2. The Urokinase Pulmonary Embolism Trial: A National Cooperative Study. Circulation 47 (suppl II): 82, 1973. 3. Kelman GR, Nunn JF: Nomograms for correction of blood PO2. PC02 pH and base excess for time and temperature. J Appl Physiol 21: 1484, 1966. 4. Mellemgaard K: The alveolar-arterial oxygen difference: its size and components in normal man. Acta Physiol Stand 67: 10. 1966. 5. Sasahara AA: Current problems in pulmonary embolism. introduction. Prog Gardiov Dis 17: 162, 1974.

The Reply:

Martin’s comments about the arterial blood oxygen tension data are reasonable, straightforward and correct. We support his contention and agree with his remarks. The original typescript submitted to The American Journal of Medicine did not contain any information about arterial blood oxygen tension. These data were requested and inserted into the article by the late Editor. We agree that such data, presented in an isolated fashion, should not be overinterpreted in pa- tients suspected to have pulmonary emboli. However, we wish to emphasize that in our article about the clinical fea- tures of pulmonary emboli, we made no attempt to interpret or discuss the isolated data about arterial blood oxygen ten- sion.

WILLIAM R. BELL, M.D.

Hematology Division Department of Medicine The Johns Hopkins Medical Institutions Baltimore, Maryland 2 1205

166 July 1977 The American Journal of Medicine Volume 63