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Volume Loop?
©@~~lill[f!]U©£IJU@[f!]® TO THe eDITOR
Communications for this section will be published as space and priorities permit. The comments should not exceed 350 words in length, with a maximum of five references; one figure 01' table can be printed. Exceptions may occur under particular circumstances. Contributions may include comments on articles published in this periodical, 01' they may be reports of unique educational character. Specific permission to publish should be cited in a covering letter or appended as a postscript.
Gastroesophageal Reflux Observed on Flow/Volume Loop? To the Editor: The Clinical Conference by Hughes and colleagues on "Aspiration and Occult Esophageal Disorders" (Chest 1981; 80:489-495) was very informative and interesting. Over the past few years, I have observed a flattening (blunting) of peak flow rates on both maximal inspiratory and maximal expiratory flow volume loops associated with a moderate decrease in the forced vital capacity. The utilization of PIF and PEF in the evaluation of intraand extrathoracic obstructive defects has been reported quite extensively; however, I have not read a report which eludes to gastroesophageal reflux or diaphragmatic hernia reflux being observed through pulmonary function testing. Is it possible that current roentgenographic techniques may be missing significant GE reflux by not having the patient perform a maximal inspiratory maneuver with precise timing of the exposure at peak inspiration? Is it also possible that the volume of GE reflux could be calculated from a forced inspiratory/expiratory flow volume loop? It seems feasible that, given a sufficient volume of GE reflux, as forced inspiratory and expiratory maneuvers are ~erformed, gastric contents (air or fluid) would be drawn mto and forced out of the esophagus in response to the negative and positive intrathoracic pressures being generated. It also seems feasible that the closing statement by Dr. Hughes that we should "add a careful GI history to the usual exposure history" be applicable to any patient undergoing a complete pulmonary evaluation.
David W. Robbins, RRT, Director, Respiratory Therapy and Cardiopulmonary Services, Coral Gables Hospital, Coral Gables, Florida
Running to Death To the Editor: In their article "Running to death" (Chest 1981; 79:34649) Waller and colleagues report the rhythm death of a 51-year-old jogger during diuretic therapy. Death followed his usual training run. He had previously sought medical advice when he developed "arm tiredness." While the authors describe coronary narrowing and healed myocardial infarction, they do not mention active lesions. We use the microlesions of Haerem! to link coronary narrowing to rhythm death. Haerem found ,that active piecemea:! necrosis of individual myocardial fibers was a useful
172 COMMUNICATIONS TO THE EDITOR
forensic tool that identified the myocardium which is vulnerable to sudden coronary death. In the absence of these microlesions, other causes of sudden death should be considered. An experienced marathon runner died suddenly at the finish of a 42 km race. He had been on diuretic therapy for years. Several weeks prior to death he sought medical advice for nonspecific weakness. He requested a serum potassium level which was reported as "normal." The coronary arteries were normal at autopsy. Myocardial contractionband necrosis was found, consistent with the known terminal episode of ventricular fibrillation. Lengthy attempts at cardiopulmonary resuscitation produced pulmonary hemorrhages with bone marrow embolization. Retrospective diet history disclosed that the runner had been avoiding beer and uncooked food during a six-week period of heavy training just prior to his last marathon. Both of these are good potassium sources. His motives were that alcohol was not consistent with serious training and raw fruits and vegetables contributed to the inconvenient bowel movement during long training runs, The similarities between these two, deaths is striking. Prodromal symptoms of "arm tiredness" or "nonspecific weakness" can be attributed to the body's inability to make glycogen during periods of potassium depletion, as described by KnocheJ.2 This should alert runners to increase their intake of potassium-rich foods and drinks. Potassium loss through sweat is one of the hazards of running; but when combined with a low-potassium diet and a potassium-losing diuretic it can be lethal! After a prodromal period of weakness, rhythm death usually strikes during the "cool down" period after a long run. In this light, I consider diuretic use and running to be incompatible. A more relevant title for the article by Waller and assodates wou1d he "Running to death during diuretic therapy."
Thomas J. Bassler, M.D., Department of Pathology, Centinela Hospital, Inglewood, California REFERENCES
1 Haerem JW. Myocardial lesions in sudden, unexpected coronary deaths. Am Heart J 1975; 90: 562-68 2 Knochel JP. Potassium depletion during training in the heat. Ann NY Acad Sci 1977; 301:175-82
Potential Diagnostic Value of Malondialdehyde (MDA) Levels in Pleural Effusions To the Editor: We read with special interest the report by Vladutiu and Brason describing the clinical usefulness of some tumor markers in pleural effusions (Chest 1981; 79:297301). We recently had the opportunity to measure the levels of malondlaldehyde (MDA) serially in pleural fluids. MDA is a stable metabolite of the prostaglandin synthesis, the levels of which are expected to reflect the inflammatory activity.1-3 The MDA levels in pleural fluid were measured according to Stuart et aI.2 The minimum amount of detectable MDA in this procedure was 4 !,-M/L. The reaction proved to be specific for MDA.4,5 Pleural effusion samples were obtained from eight patients with proven primary malignancy and from 23 patients with
CHEST, 81: 6, JUNE, 1982
Communications for this section will be published as space and priorities permit. The comments should not exceed 350 words in length, with a maximum of five references; one figure 01' table can be printed. Exceptions may occur under particular circumstances. Contributions may include comments on articles published in this periodical, 01' they may be reports of unique educational character. Specific permission to publish should be cited in a covering letter or appended as a postscript.
Gastroesophageal Reflux Observed on Flow/Volume Loop? To the Editor: The Clinical Conference by Hughes and colleagues on "Aspiration and Occult Esophageal Disorders" (Chest 1981; 80:489-495) was very informative and interesting. Over the past few years, I have observed a flattening (blunting) of peak flow rates on both maximal inspiratory and maximal expiratory flow volume loops associated with a moderate decrease in the forced vital capacity. The utilization of PIF and PEF in the evaluation of intraand extrathoracic obstructive defects has been reported quite extensively; however, I have not read a report which eludes to gastroesophageal reflux or diaphragmatic hernia reflux being observed through pulmonary function testing. Is it possible that current roentgenographic techniques may be missing significant GE reflux by not having the patient perform a maximal inspiratory maneuver with precise timing of the exposure at peak inspiration? Is it also possible that the volume of GE reflux could be calculated from a forced inspiratory/expiratory flow volume loop? It seems feasible that, given a sufficient volume of GE reflux, as forced inspiratory and expiratory maneuvers are ~erformed, gastric contents (air or fluid) would be drawn mto and forced out of the esophagus in response to the negative and positive intrathoracic pressures being generated. It also seems feasible that the closing statement by Dr. Hughes that we should "add a careful GI history to the usual exposure history" be applicable to any patient undergoing a complete pulmonary evaluation.
David W. Robbins, RRT, Director, Respiratory Therapy and Cardiopulmonary Services, Coral Gables Hospital, Coral Gables, Florida
Running to Death To the Editor: In their article "Running to death" (Chest 1981; 79:34649) Waller and colleagues report the rhythm death of a 51-year-old jogger during diuretic therapy. Death followed his usual training run. He had previously sought medical advice when he developed "arm tiredness." While the authors describe coronary narrowing and healed myocardial infarction, they do not mention active lesions. We use the microlesions of Haerem! to link coronary narrowing to rhythm death. Haerem found ,that active piecemea:! necrosis of individual myocardial fibers was a useful
172 COMMUNICATIONS TO THE EDITOR
forensic tool that identified the myocardium which is vulnerable to sudden coronary death. In the absence of these microlesions, other causes of sudden death should be considered. An experienced marathon runner died suddenly at the finish of a 42 km race. He had been on diuretic therapy for years. Several weeks prior to death he sought medical advice for nonspecific weakness. He requested a serum potassium level which was reported as "normal." The coronary arteries were normal at autopsy. Myocardial contractionband necrosis was found, consistent with the known terminal episode of ventricular fibrillation. Lengthy attempts at cardiopulmonary resuscitation produced pulmonary hemorrhages with bone marrow embolization. Retrospective diet history disclosed that the runner had been avoiding beer and uncooked food during a six-week period of heavy training just prior to his last marathon. Both of these are good potassium sources. His motives were that alcohol was not consistent with serious training and raw fruits and vegetables contributed to the inconvenient bowel movement during long training runs, The similarities between these two, deaths is striking. Prodromal symptoms of "arm tiredness" or "nonspecific weakness" can be attributed to the body's inability to make glycogen during periods of potassium depletion, as described by KnocheJ.2 This should alert runners to increase their intake of potassium-rich foods and drinks. Potassium loss through sweat is one of the hazards of running; but when combined with a low-potassium diet and a potassium-losing diuretic it can be lethal! After a prodromal period of weakness, rhythm death usually strikes during the "cool down" period after a long run. In this light, I consider diuretic use and running to be incompatible. A more relevant title for the article by Waller and assodates wou1d he "Running to death during diuretic therapy."
Thomas J. Bassler, M.D., Department of Pathology, Centinela Hospital, Inglewood, California REFERENCES
1 Haerem JW. Myocardial lesions in sudden, unexpected coronary deaths. Am Heart J 1975; 90: 562-68 2 Knochel JP. Potassium depletion during training in the heat. Ann NY Acad Sci 1977; 301:175-82
Potential Diagnostic Value of Malondialdehyde (MDA) Levels in Pleural Effusions To the Editor: We read with special interest the report by Vladutiu and Brason describing the clinical usefulness of some tumor markers in pleural effusions (Chest 1981; 79:297301). We recently had the opportunity to measure the levels of malondlaldehyde (MDA) serially in pleural fluids. MDA is a stable metabolite of the prostaglandin synthesis, the levels of which are expected to reflect the inflammatory activity.1-3 The MDA levels in pleural fluid were measured according to Stuart et aI.2 The minimum amount of detectable MDA in this procedure was 4 !,-M/L. The reaction proved to be specific for MDA.4,5 Pleural effusion samples were obtained from eight patients with proven primary malignancy and from 23 patients with
CHEST, 81: 6, JUNE, 1982