Julius Jensen

Ventricular bigeminy (parasystole or reciprocal rhythm) in atrioventricular rhythm

Abstract In atrioventricular rhythm the normal auricular pacemaker is inhibited and there is uncovered a secondary center from which impulses activate the ventricle and, in uncompleted cases, the auricle as well. In certain cases, however, impulses from the secondary center are not conducted to the auricle. In such instances auricular escape occurs, the auricular center of highest automaticity becoming the pacemaker for the auricle. The rhythmicity of such a secondary auricular center is subject to the same influence that may affect other centers of impulse formation. In some cases the retrograde blocking of impulses from the ventricular center is incomplete, and the auricular pacemaker is discharged prematurely by those impulses which reach it just before the completion of its automatic period. Impulses from this pacemaker pass not only to the auricle but also toward the ventricle and produce premature ventricular contractions when not interfered with by refractory tissue. Beating of the ventricle in response to impulses both from the ventricular pacemaker and from the auricular center in such cases constitutes parasystole. Ten cases were studied, three of which are reported in detail. Reciprocal rhythm as an explanation of the records in these cases is considered but evidence against this interpretation is presented. It appears that cases of simple A-V rhythm, of so-called reciprocal rhythm, and of parasystole are fundamentally related; the precise mechanism in a given instance being determined by the state of retrograde conductivity from the ventricular pacemaker. These cases occur under circumstances associated with sinus depression and lowered conductivity. Digitalis in some instances appears to be a contributory factor.

The adrenalin test in hypertension

Abstract 1. 1. It appears from the literature that the response to adrenalin in the patient with hypertension differs from that of the normal person, but the evidence as to the variations in response is contradictory. 2. 2. Under approximately standard conditions series of subcutaneous injections of 1 c.c. of adrenalin were given to a number of normal persons, patients with hypertension, and others in whom the reaction was thought to throw light on the phenomena observed in hypertension. 3. 3. Persons with normal cardiovascular systems responded with a slow rise and a subsequent slower decrease of pressure. While the height of the excursion was but slightly accentuated after subsequent injections, the time consumed in reaching the maximum height of the pressure was markedly shortened. 4. 4. The cases of hypertension fell into two groups which were clinically 5. indistinguishable. In the first group no definite change could be ascribed to the first injection of adrenalin, while the other cases of marked hypertension responded with a brisk and intense increase of systolic blood pressure. When the test was repeated all the patients with hypertension responded with intense rises of pressure. In cases of early or intermittent hypertension the findings were like those of the former group of advanced hypertension, but less pronounced. 6. 5. Statistically it was found that the ratio of the difference and of the probable error of difference between the standard deviations from the average readings following the first and the repeated injections of adrenalin was significant in the first group, in those hypertensive patients in whom the response was absent on the first injection. 7. 6. The diastolic pressure decreased after all the injections but the time required to return to normal was longer in the patient with hypertension than in the normal person. It was not influenced by repetition of the test. The increase in heart rate and the occurrence of cardiac irregularities were not influenced by the state of hypertension or by repetition of the test. 8. 7. The blood pressure reaction of adrenalin in hypertension did not depend on the level of the blood pressure, the size of the heart, presence or absence of kidney disease, or the level of the blood calcium. No satisfactory explanation could be offered for the absence of response in some individuals with hypertension or for the change in response between first and subsequent tests. 9. 8. The clinical adrenalin reaction is not due to peripheral vasoconstriction. In fact a vasodilatation is present which indicates that the systolic rise is of cardiac origin. The intense increase in the patient with hypertension is thought to be related to the general instability of the hypertensive blood pressure. This instability is briefly discussed and considered mathematically.

The electrocardiogram in late middle life

Abstract Within the limits of our experience we may state: The following findings, some of which we have previously considered of doubtful significance, are not pathological. Diphasic or iso-electric P-waves in Lead I or inverted P-waves in Lead III, if they become upright on deep inspiration; slurring of QRS complexes, especially in Lead III and slight to moderate notching of R with the QRS interval below 0.10 seconds, “transverse heart,” isolated left axis deviation, moderate inversion of T-III (this last finding is very common). On the other hand, the following findings were not present in this series and must therefore be looked upon with suspicion. Indeterminate or inverted P-waves in Leads I or II, inverted P-waves in Lead III, if they do not become upright on deep inspiration. Inversion of T-waves in Leads I or I and II, or iso-electric T-waves in Leads I or II if they do not become upright on deep inspiration. A P-R interval exceeding 0.20 seconds, a QRS interval exceeding 0.10 seconds, or an S-T interval exceeding 0.34 or 0.36 seconds (the upper limit seems slightly uncertain). It is seen that for the proper evaluation of a doubtful finding deep inspiration and sometimes change in position may be necessary in any lead. Such thorough investigation should always be done when the electrocardiographic findings may be the determining factor in the diagnosis. This material does not indicate whether an isolated right axis deviation is definitely a pathological sign or whether the inverted wave in a transverse heart is always an S-wave. There do not seem to be any characteristic “age-changes” in the electrocardiogram.

The clinical value of theophylline in heart disease

Abstract 1. 1. In the heart-lung preparation, when the heart was made to fail with chloral hydrate, theophylline produced an increase in cardiac output, return of the dilated heart to its original size, and fall in venous pressure. 2. 2. In patients in congestive heart failure, theophylline in the usual dosage caused a significant fall of venous pressure and a shortening of the abnormally prolonged circulation time. 3. 3. The effect upon the coronary circulation is uncertain. The coronary vasodilation frequently observed may be secondary to myocardial stimulation. It has not been possible to demonstrate an effect upon the course of angina pectoris by giving theophylline by mouth. 4. 4. Theophylline has a dilator effect upon peripheral blood vessels. This may be a factor in the lowering of venous pressure. 5. 5. Theophylline increases the pulmonary circulation, especially when the lungs are congested from the left ventricular failure. 6. 6. It has not been demonstrated that theophylline changes vascular permeability. 7. 7. The therapeutic uses of the drug are discussed.