THE GRAVITY OF BRONCHITIS IN ELDERLY MEN AND CUSPID INSUFFICIENCY, WITH REPORT BY ROBERT H. BABCOCK, M. D., CHICAGO. The advent of the season in which bronchitis begins to be more frequent makes the subject of this brief paper not unimportant. Not many weeks ago I was called by Dr. J. R. Hollowbush, of Rock Island, to see in consultation at WIll., Col. M., a portly vigorous man of sixty-two years, who had been a man of untiring strength and had prided himself upon his endurance, both mental and physical. He had smoked cigars to great excess and for twenty years had drunk three or four ounces of whisky every evening to promote sleep, since without it he was a victim of insomnia. He had been a good feeder, but not a gourmand and had taken a good deal of outdoor exercise. He had been wounded several times in the civil war, but had never been seriously ill and had not had syphilis. In March, 1902, he noticed for the first time that his breath was short in walking up hill and over uneven ground. Not long thereafter he developed a cough which had not left him up to the date of my visit in October. In August he had been in Rock Island and was so asthmatic that he consulted Dr. Hollowbush. The Doctor found the Colonel suffering from what appeared to be a widespread bronchitis of four months' standing. The chest was resonant, but full of both dry and most rales, cough being frequent and severe and the sputa copious and mucoid. The heart seemed healthy and body temperature was normal. Treatment gave some relief for a time, but in the fore part of October his patient's condition grew so alarming that the Doctor sought counsel. I found a tall, powerfully built man of indomitable will power who arose from his armchair to meet me although it was at once evident that he was very dyspneic. For five nights he had not slept without an opiate and for much of the time his restlessness, labored breathing, violent cough, occasionally bloody sputum and irregular, scarcely palpable pulse had presented a clinical picture of gravest import. The chest had been full of sonorous rales, but everywhere resonant and the thermometer had failed to show febrile temperature. Two nights before my arrival signs of tricuspid insufficiency had set in and the urine became scanty, but not albuminous. My examination revealed the following: Countenance suffused, labored respirations of thirty to the minute, a regular feeble pulse of 96 and mouth temperature of 101.9 F. Upon getting the patient undressed it was furthermore observed that the external jugulars were distended and showed a feeble systolic pulsation, while epi gastric pulsation could also be seen and felt. There was no other perceptible cardiac impulse. The radial arteries were stiff and the pulse was small and rapid. The liver was palpable about three fingers' breadth below the inferior costal margin, firm and rounded. There was no edema. Percussion elicited resonance of a rather tympanitic quality, over the left lung, excepting in the upper axillary and outer portion of the infraclavicular regions where the note was appreciably dull, and at the base behind, where there was a dull patch that cleared up after a few forcible inspirations. The right lung was resonant in front, but posteriorly there were indistinct areas of dullness and hyper-resonance that blended into each other in a way that gave the note a general wooden quality. Throughout both lungs, but chiefly in the right, were copious, sonorous and whistling rhonchi with here and there fine, crackling rales which in a few areas possessed a crepitant character. The abundance and intensity of the rales largely obscured the breath-sounds, but in some of the dull areas, particularly the left axillary region, the respiratory sound was distinctly bronchial. The heart could be outlined with difficulty, but was found considerably enlarged in all diameters. The first sound at the apex was accompanied by a distinct blowing murmur. This was found to have its maximum intensity in the tricuspid area and to be thence widely propagated. The aortic second tone was very loud and ringing, but seemed pure. The interpretation of these findings seemed to me as follows: There were a chronic arteriosclerosis and myocarditis which in March began to give premonitions of cardiac inadequacy under conditions of strain. Either secondarily or as a result of cold, a bronchitis declared itself soon thereafter which for want of proper treatment and care on the part of the patient went on until it became chronic, the condition discovered by Dr. Hollowbush in August. This predisposed to pneumonia which actually occurred and was present when I saw him, the pneumonia being in scattered areas and associated with areas of atelectasis and emphysema. The nature of the pneumonia was not altogether clear, but was believed to be a fibrinous one, which instead of being lobar as in young adults, had the lobular distribution not infrequently seen in the aged. It was, in a word, patchy. The infection was not probably a purely pneumococcus one, but was mixed, which might account for the clinical picture. Of course such a conclusion was conjectural, as the etiological factors concerned could only have been ascertained by an exploratory puncture of the lung with an aseptic needle and cultures made from the blood. and secretions thus obtained. At all events, the mildness of the infection was shown by the absence of cyanosis, the moderate degree of fever, 101.9°, which a few hours subsequently fell nearly 2°. As concerned the lungs, the real seriousness of the patient's condition appeared to lie, not in the pneumonia, which in its manifestations was mild, but in the extent of the bronchitis which involved the finer tubes and had led to areas of atelectasis. There was of course a possibility of an extension of the pneumonic process and of the development of a more intense infection. Consequently the outlook was uncertain and most grave. It was evident that aside from the state of the lungs very much depended upon the condition of the myocardium and its potential strength. Was the heart-muscle degenerated, and if so, how seriously? Leaving out of consideration the effect of the pneumonic toxins upon the heart, could it endure the mechanical strain to which it was subjected by the penumonia, bronchitis, atelectasis, and the severe fits of coughing? These were questions that had to be answered as far as possible. Judging from the stiffness of the vessels, the hypertrophy as well as the dilatation of the heart, and from the intensely ringing character of the aortic second tone, it was inferred that the aorta was sclerotic and the heart-muscle in a state of chronic myocarditis. Furthermore, the history of beginning dyspnea, of effort in the previous spring seemed to indicate that the potential energy of the myocardium was on the wane, even before the advent of the bronchitis. These considerations made me very apprehensive regarding the heart's ability to much longer endure the strain of mechanical interference with pulmonary circulation incident to the state of the lungs and cough, even if it did not succumb to the pneumonic complication. My apprehension was increased by the discovery of the relative tricuspid insufficiency which showed that the right ventricle had already begun to yield to the strain and the regurgitation was thought to indicate a serious degree of cardiac weakness. Further reflection in the light of the subsequent history of this case has led me to change the view then held concerning this relative incompetence of the tricuspid valve under conditions prevailing in this instance. It was shown by Wilkinson King many years ago that when the right ventricle is overburdened as during prolonged, severe physical exertion, the thinness of its wall permits such a degree of dilatation that the tricuspid valve is no longer able to shut off the auriculoventricular orifice. This has been termed "the safety-valve action" of the tricuspid, for the reason that the resulting reflux into the auricle relieves the overtaxed ventricular wall and prevents its diastolic arrest. In the case under discussion the myocardium was presumably diseased and this degeneration involved the right as well. as the left ventricle rendering it abnormally liable to disastrous overstrain. The establishment of tricuspid regurgitation acted therefore as a safety-valve and shifted the burden on to the right auricle and great venous system and prevented paralysis of the weakened ventricle. This safety-valve action of relative tricuspid incompetence is frequently seen in patients with chronic bronchitis and emphysema. and serves, I believe, to prolong life. It is a measure of the strain to which the ventricle is subjected and hence of the degree of pulmonary congestion, but is not in itself a sign of bad omen. It is said to occur far more often than is generally believed and serves to tide many a patient over a period of storm and stress that otherwise would wreck his frail craft. If in the present case the pneumonic infection had been intense and expended on the nerve centers and myocardium, nothing could have prevented the heart, whether healthy or degenerated, from yielding, but as it was it appeared to be the mechanical strain rather than the toxemia that was dangerous. During the day of my visit the patient's condition showed signs of beginning improvement; temperature and pulse fell somewhat and his distress grew perceptibly less. The treatment instituted included the administration of digitalis, appropriate expectorants and as complete physical rest as the active nervous man could be induced to maintain. The expectorants were prescribed not with a view to the pneumonic element, but for the long-standing bronchitis. Physical rest was regarded as a sine qua non of recovery since it was believed that the heart could not long tolerate the strain of his frequently getting up to wait on himself and walk about. The subsequent history of the case is not known to me in detail, but convalescence proceeded slowly and two weeks after I saw him his condition was reported by the nurse as satisfactory, pulse being 66 and his temperature normal. It is presumable, therefore, that the pneumonia had cleared up, but whether or not some of his previous bronchitis remained I am unable to state. One thing is tolerably certain I think; namely, that in spite of this man's naturally robust physique he will not again be as vigorous as before in consequence of the strain which his degenerated heart underwent through the long continuance of his bronchitis and the subsequent pneumonia. The foregoing case illustrates the gravity of bronchitis in elderly men and teaches some instructive lessons from which I think several conclusions may be drawn. (1) Bronchitis in elderly although robust men may readily become chronic. Presuming on their previously good health and vigor, they think they can easily throw off their cold and hence are apt to ignore medical aid until after the bronchitis has become settled and obstinate. (2) The cardiovascular degenerations so often present and unrecognized in elderly men increase the tendency of bronchitis to become chronic. This is because the stiffened arteries and chronic myocarditis, even though the heart remains potentially equal to the demands of everyday life, tends to the production of pulmonary and bronchial congestion which, when bronchitis once sets in, renders it less amenable to ordinary treatment. Moreover, the physician who may perchance be consulted is apt to overlook the influence of cardio-vascular changes and contents himself with prescribing expectorants, whereas he should at the same time lessen the congestion by a brisk calomel cathartic. He should also in many cases inhibit exercise and attention to business that the heart may be relieved of unnecessary strain. (3) Another element of danger in the bronchitis of elderly men is pneumonia. In most cases the bronchitis predisposes to a pneumonia which may develop after the lapse of weeks or months, as in the case narrated. There is, however, the possibility that the bronchitis, which sets in abruptly and severely, may be but an attendant or manifestation of pneumococcus infection and may obscure the signs of pneumonia when this is lobular. (4) A fourth danger lies in the effect of the bronchitis upon the heart. Chronic myocarditis develops so insidiously that one may not always be able to detect it and can not foresee how little extra strain may be required to seriously impair its potential strength. Even should pneumonia not ensue, the mechanical strain of the bronchitis, especially if it leads to atelectasis and emphysema, and of repeated violent attacks of coughing is capable of seriously damaging the degenerated right ventricle, the dilatation of which aggravates the already existing congestion. (5) Should such dilatation lead to relative tricuspid insufficiency, this is not to be regarded as a sign of danger per se, since it is in reality a safety-valve which for a time protects the ventricle from disastrous overdistention. The tricuspid regurgitation is a |