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bacterial endocarditis and of arteriosclerotic aortic insufficiency are included here. Columns 6, 7 and 8

include cases of cardiac disease attributed to arteriosclerotic processes; in a few instances the Wassermann reaction was positive, and these patients, and possibly some others, may have been suffering from syphilitic myocarditis. This large group has been divided into three subdivisions, the first of which includes patients with a systolic blood-pressure less than 150 mm. Hg, the second patients with an unknown blood-pressure, and the third patients with a blood-pressure between 150 and 180 mm. Hg. Cases in which the systolic blood-pressure exceeded 180 mm. Hg are considered in the next two columns, the first of which includes cases without evidence of chronic nephritis and the second cases with nephritis. The headings of the remaining columns are self-explanatory.

The electrocardiographic abnormalities listed in table 1 have often been discussed as if they were in themselves significant. With the exception of auricular fibrillation, however, they have never been shown to increase the work of the heart, to interfere with its efficiency as a pump or to influence adversely its ability to maintain an adequate blood flow. In bundlebranch block one ventricle begins to contract some 0.03 second in advance of the other, but this slight asynchronism in the systole of its two chief chambers does not appear to diminish the mechanical efficiency of the heartbeat or to disturb it in other ways. The same may be said for the slight delay in the spread of the impulse over the ventricles which occurs in

other types of intraventricular block, and for the increase in the time which separates auricular and ventricular systole indicated by a lengthened P-R interval.2

Neither, so far as we know, do the changes in muscle activity which cause inversion of the T deflection, or the changes in muscle mass which apparently give rise to electrocardiographic preponderance seriously embarrass the heart.

The importance of the electrocardiographic abnormalities under discussion lies in their value as signs of myocardial change. They indicate that the disease has in some way attacked the heart muscle. One of the chief points that we wish to emphasize is that these electrocardiographic signs occur in a great variety of conditions (see table 1), and that their significance depends, therefore, upon the nature of the disease with which they are associated. The electrocardiogram should never be considered alone, but should always be interpreted in the light of all the other evidence that can be obtained. An inverted T deflection may be a sign of acute diphtheritic myocarditis, of acute rheumatic myocarditis, of myocardial changes due to toxic goiter, of syphilitic myocarditis, of coronary sclerosis or of digitalis intoxication according to the circumstances under which it occurs. Studies of the prog

2 When the P-R interval is greatly increased so that auricular systole coincides in time with the ventricular systole of the previous cardiac cycle, the auricles no longer contribute to ventricular filling by their contraction. Although a slight decrease in ventricular output occurs, this function of the auricles does not appear to be a very important one.

nostic value of inversion of the T deflection, or of any other electrocardiographic abnormality, apart from the nature of the disease which produced it, have, so it seems to us, comparatively little value. We may study with profit the prognostic value of such signs as albuminuric retinitis which occur in a single disease or in a small group of closely related diseases. But few would find value in the study of the prognostic value of such signs as fever or leucocytosis which have a great variety of causes. The electrocardiographic signs which we are discussing belong, in some measure, to the same class. They are not specific signs and their significance depends upon the circumstances under which they occur.

To discuss adequately the reliability, as signs of myocardial change, of the electrocardiographic abnormalities under discussion would require us to consider each one separately. Space for this discussion is not available.

Their value has often been questioned on the ground that they were dependent upon functional rather than upon structural changes, and because some of them may be produced by digitalis or through stimulation of the vagi. As an example of some of the opinions that have been expressed, we may quote Professor Wenckebach's remarks

at the last meeting of this Association. In discussing the significance of an increased P-R interval in influenza, he

said:

In such cases the diagnosis of myocarditis has not been made. Some of the influenzal cases are those of functional disorder of the heart, delayed conductivity or heart-block. This functional disorder may be set up by toxic agents or perhaps by fatigue. In influenza I have seen cases

of delayed conductivity. This was during convalescence, and the man was perfectly well afterward. Mackenzie has stated that there may be complete dissociation between auricles and ventricles, but not with complete recovery. Such cases may be myocarditis, but proof has to be given, and this cannot be given until the case is complete. We know that we can set up a heart-block with digitalis or a prolongation of the auriculoventricular interval, but none of us would admit that digitalis will set up myocarditis.

We have no desire to criticize these offhand remarks in the connection in which they were made; we give them as an example of the type of argument that is advanced against the general thesis that various electrocardiographic signs may give us reliable. evidence of myocardial disease. This kind of argument contains, so it seems to us, obvious fallacies. If myocarditis is defined as changes in the heart muscle which are visible to the naked eye, or which can be made visible by the aid of special stains and of the microscope, then the electrocardiographic signs in question are not direct evidence of myocarditis. But these signs indicate some sort of change in the myocardium. Are these changes less significant because they are made visible with a delicate galvanometer rather than with high-power lenses? They have the advantage, from the standpoint of the clinician, that they

can be made visible during life while microscopical changes can only be seen after death. The term "functional" is often used in the sense of "trivial," and disorders of function are considered less serious and less permanent than changes in structure. But many functional changes which are not accompanied by structural changes that can be made visible by

our present methods of histological examination are most serious and lasting (dementia præcox, for example). Structural changes, on the other hand, are not necessarily permanent and may be most fleeting; the solidified pneumonic lung recovers completely, and nearly all tissues have great powers of recovery and repair and of regeneration and compensatory growth. All acute lesions are accompanied by edema, infiltration with wandering cells, hemorrhage and other structural changes which may very quickly disappear. All functional disorders must be dependent upon underlying changes of one kind or another; whether these are visible or invisible, physicochemical or structural, does not in itself matter. In many diseases the postmortem examination is most illuminating, but in others it only serves to make death a greater mystery. The visibility of cellular damage is a question of the kind of injury, the grade of injury, and the adequacy of our methods of making the injury apparent to the eye, and is not a criterion of its seriousness. Nor does it seem to us that there is a fundamental difference between disorders of function and disorders of structure.

The electrocardiographic abnormalities under discussion are often transient when they occur in acute diseases; the structural changes which occur in acute disease are likewise often temporary. Whether the electrocardiographic changes are directly dependent upon the structural changes is difficult to determine and not profitable to discuss. In chronic diseases the electrocardiographic changes and also the structural changes are, for the most part, permanent, and it is

probable that in a great many instances, though not in all, the former are directly dependent upon the latter.

The argument that digitalis may produce heart-block, and that, therefore, heart-block is not necessarily due to myocardial injury, is a valid one only because digitalis block is chiefly vagal. A similar argument might be advanced to prove that inversion of the T deflection does not indicate myocardial changes. It is true that digitalis does not produce myocarditis; the changes to which it gives rise are not visible with the microscope. But they are, nevertheless, real; we see them with the string galvanometer. Digitalis is a powerful poison and can kill by its action on the heart. If it were produced, not by a large plant like the foxglove but by a bacterium that could grow in the body, it might produce a disease as fatal as diphtheria. If this were the case, what name should we give to the type of heart disease that it produced? The lack of seriousness of the myocardial changes produced by digitalis lies in our ability to remove them by stopping the drug. They are not permanent, but their lack of permanency does not depend upon their invisibility or upon the fact that they are "toxic." Each individual poison has its own peculiarities, the cause of which is not always understood.

Whether the electrocardiographic abnormalities mentioned are or are not evidence of structural heart disease, it would seem wise to treat the patient who displays them as if his myocardium were attacked by the disease from which he is suffering. If this is an acute infectious disease and

the electrocardiographic abnormality is transient, a slow and guarded convalescence and frequent subsequent examinations would seem to be indicated. If the disease is chronic and the electrocardiographic abnormality is permanent the same principles should apply as when the patient has a real valve lesion, cardiac enlargement or some other structural cardiac abnormality.

TREATMENT

In the treatment of patients with heart disease electrocardiographic observations are often of great value. The changes in the P-R interval and in the form of the T deflection, which digitalis produces, enable us to control the administration of this drug in a way which is not possible without the aid of the string galvanometer. It is insufficiently realized that digitalis may produce serious cardiac poisoning without giving rise to nausea or vomiting or other of the common symptoms of digitalis intoxication. The occurrence of complete dissociation with a high ventricular rate is a common event; it is difficult or impossible to recognize this dis

turbance without graphic methods, and its recognition is of great importance. The continuance of digitalis after complete dissociation has developed was followed in one of our recent cases, and in other cases that we know of by sudden death, possibly due to ventricular fibrillation.

A similar type of complete dissociation is produced by adrenalin when this drug is injected directly into the heart or intravenously.

The treatment of patients with syphilitic heart disease with arsphenamine is frequently followed by striking changes in the form of the ventricular complex. The exact nature of these changes is uncertain, but it is probable that they indicate cardiac damage of some sort.

In the treatment of auricular fibril

lation with quinidin, electrocardiographic observations are essential. This drug gives rise to the most complicated disturbances of the heart's rhythm and to high-grade disturbances of intraventricular conduction. These disturbances disturbances

cannot be recognized without electrocardiographic records, and it is impossible to give this drug intelligently without electrocardiographic control.

Effort Syndrome, Its Clinical Course

O

BY WILLIAM B. PORTER, Roanoke, Virginia

NE is impressed by conditions

which occur in large numbers during a pandemic upheaval such as the late war, but interest tends to lag when the daily routine of civil life is resumed. DaCosta (1) described in 1867 a condition observed in soldiers which he termed "soldier's heart." A similar condition was described by McLean (2) in 1867, by Myers (3) in 1870, by McCarty (4) in 1898 and by Tyson (5) in 1906. Since Tyson's contribution no specific mention of the syndrome has been made in medical literature until the beginning of the late war.

Prior to 1914 there was a group of young men and women who were found principally in the hands of the neurologist, relegated to that motley throng composing neurasthenia. Soon there developed a general feeling that "neurasthenia" was an unsatisfactory diagnosis. In fact such a diagnosis was looked upon as an expression of ignorance. In an effort to more satisfactorily catalog these individuals the tuberculosis sanatoria began to harbor many of them as cases of incipient tuberculosis. As a result of an innocent cardiac murmur heard by an enthusiastic listener, a prolonged rest treatment for heart disease was not infrequently instituted, this treatment usually resulting in no happy termination.

Soon after the beginning of the late war there was discovered a class of

patients suffering from precordial pain, shortness of breath, fatigue, palpitation, giddiness and fainting attacks. On examination the extremities were found to be cold and clammy with a dappled, cyanotic discoloration of the hands. There was a coarse tremor of the hands, and free sweating in the axilla. Examination of the cardiovascular apparatus revealed a rapid pulse which was easily accentuated by exertion. The apex beat was diffuse and forcible, giving a confusing impression of cardiac hypertrophy. Systolic murmurs and thrills were often present. The systolic blood pressure in the majority was elevated, especially after induced tachycardia. In the more severe cases, precordial hyperesthesia was marked and its distribution was in many instances characteristic of that observed in true angina pectoris.

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There was no disease encountered during the late war which attracted such a host of brilliant investigators as did the condition variously styled "effort syndrome," "irritable heart, "soldier's heart," "D. A. H.," and "neuro-circulatory asthenia." Cohn in an article published in 1919 on the "Cardiac Phases of the War Neurosis," stated that more than 250 contributions had appeared on this one phase of war medicine.

The intense interest manifested was due not only to the determined effort to do justice to the invalided soldier,

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