Tracing the "Disappearance" of Two Physical Signs

TRACING THE "DISAPPEARANCE" OF TWO PHYSICAL SIGNS JOSEPH HERMAN* We are prone to regard physical signs as the most enduring attributes of a disease because they are given to reproducibility and often to measurement . Taking a patient's pulse and determining that he or she has atrial fibrillation seems far more scientific than conducting a hermeneutic inquiry into what palpitations mean to him or her and the fears and expectations they engender [I]. Measurement enables specific action; one does not prescribe digitalis for a pounding in the chest, but if the pulse is totally irregular and there is a deficit over the radial artery one might be tempted to do so where an electrocardiograph is not available. The "disappearance' ' of two physical signs will be traced here in order to show the impermanency of even the "hardest" observations. Acute Emphysema In James B. Herrick's landmark paper of 1912, thought to give the first clear outline of myocardial infarction as a clinical event, a peculiar physical finding is mentioned: "The heart tones were very faint and there was a most startling and confusing hyperresonance over the chest, the area of heart dulness being entirely obscured" [2]. Herrick invokes the "acute emphysema—Lungenschwellung and Lungenstarrheit of von Basch—by which condition the heart sounds are obscured by overlapping air containing lungs." In the second edition ofDiseases ofthe Heart and Aorta by Arthur Douglass Hirschfelder, published in 1913, there is further reference to von Basch, who showed in animals that the dyspnea of heart failure is due to stasis in the pulmonary capillaries and veins: "Under these circumstances the elasticity of the lungs is probably diminished and the volume of the lung increases. The respiratory excursion decreases" [3]. Hirschfelder goes on Correspondence: 42 Harav Uzziel Street, Bayit V'gan 96424, Jerusalem, Israel. *Family Practice Unit, Department of Social Medicine, Hebrew University/Hadassah Medical School, Jerusalem, Israel.© 1996 by The University of Chicago. All rights reserved. 0031-5982/96/3903-0956$01.00 ectives in Biology and Medicine, 40, 1 ¦ Autumn 1996 55 to say that spirometrie investigations in cardiac dyspnea have demonstrated a tendency "for the lungs to assume the greatest possible volume (diaphragm descends lower and lower) just as is the case in emphysema" [3]. The third edition of Osier's Modern Medicine, edited by McCrae, appeared in 1927 and mentions Herrick's sign [4]. George Blumer's BedsideDiagnosis came out a year later and gives a slightly more detailed description of the finding: "In many cases an acute emphysematous distension of the thorax appears, producing a hyperresonant note with a prolonged wheezing respiratory murmur which maybe quite confusing" [5]. In 1932 McCrae edited and updated Osier's Principles and Practice ofMedicine, completely ignoring Herrick's sign [6] , as did White's Heart. Disease, published in 1935 [7] . Seven years later, however, there is a last echo of the hyperresonant note in The Principles and Practice of Cardiology by Bramwell and King: "Stagnation of blood in the lungs leads to an increase in the vascular bed. This gives rise to what has been termed 'secondary emphysema' with a reduction which may amount to 50 per cent in the vital capacity" [8]. In 1949, Tice laid the issue to rest, stating flatly that, in patients with myocardial infarction, "There is no change in percussion" [9]. Pulmonary physiologists have long been aware of certain reflexes arising in the vasculature of the lungs that can cause rapid, shallow breathing and bronchoconstriction [10]. Over 20 years ago, Interiano, et al., demonstrated that patients with myocardial infarction have a reduction in forced expiratory flow lasting up to four days. It correlated with chest X-ray signs of pulmonary congestion [H]. Both bronchoconstriction and vascular engorgement of the interstitium can narrow the airways and lead to airtrapping , wheezing and hyperresonance. In all, the half-life of Herrick's sign was about one generation. Its "disappearance " can be accounted for in a number of ways. First, it may have been observed in patients who would not have met today's criteria for myocardial infarction. Second, the disease itself may have changed over time, which is to say that it has a natural history independent of any particular sufferer...