Adolph R. Berger

Comparison of intracardiac and intravascular temperatures with rectal temperatures in man.

A study of intracardiac and intravascular temperatures was undertaken with the thought that such measurements might provide further information concerning the mechanisms which normally maintain body temperature within its narrow limits and also that they might help to explain the deviations from normal temperature in certain disease states. Whereas the temperature of the peripheral tissues may vary widely, homeothermic man maintains the temperature of the deep tissues, or of a critical deep tissue, fairly constant under widely varying conditions of heat loss and heat gain (2). The identity of the critical deep tissue is not completely understood but a considerable body of evidence places it in the diencephalon and in normal man small variations in its temperature are thought to initiate compensating mechanisms which return the temperature of the body to the homeothermic norm. Generally, rectal temperature has been considered to indicate deep tissue, and critical tissue, temperatures but often rectal temperature appears to be a lagging and unsatisfactory index; witness the onset, when the body is heated, of such compensating mechanisms as peripheral vasodilatation and sweating before a rise in rectal temperature has occurred; and conversely, in subjects who are cooled, the presence of vasoconstriction and pilomotor activity before a fall in rectal temperature has taken place. It seemed desirable, therefore, to look for some other index of critical deep tissue temperature. Considerations of the mixing of blood in the left ventricle, probably in proportion to the volume flow and temperature of the blood from all organs,

Intracardiac and Intravascular Potentials Resulting from Electrical Activity of the Normal Human Heart

Electrical records were made from the interior of the right heart and attached vessels in 14 normal subjects. Technics differed somewhat from those previously reported in that simultaneously recording string galvanometers were used exclusively, and tracings were made whenever the catheter-electrode was moved within the heart. Previously unreported large positive QRS deflections were found in records from the lower part of the right atrium, from the pulmonary artery, and in two instances from within the right ventricle itself close to the base. The possible anatomical origin of these is discussed.

Comparison of the Hemodynamic Effects of Mercurial Diuretics and Digitalis in Congestive Heart Failure

The non-xanthine-containing mercurial diuretic mercaptomerin (Thiomerin), a noncardiotonic agent, was given repeatedly to 14 patients with congestive heart failure until all edema fluid had been eliminated. There resulted relief of subjective symptoms and removal of the characteristic physical signs of circulatory congestion to the point where subjects were considered in “cardiac compensation”; reduction of the elevated intracardiac pressures, in the right atrium, right ventricle, and pulmonary artery; variable changes in cardiac function (cardiac output) and cardiocirculatory (arterial-mixed venous oxygen difference) function, with improvement toward normal in half of the patients and no change in the other half.In subjects in whom full mercurial diuresis alone improved the cardiac and cardiocirculatory functions, subsequent digitalization produced no further improvement in these functions. These patients were in a first or second episode of cardiac decompensation.In subjects in whom full diuresis alone did not alter the cardiac and cardiocirculatory dynamics, subsequent digitalization produced an increase in cardiac output and a decrease in A-V oxygen difference toward normal values. These subjects usually had had one or several previous episodes of congestive failure.When there was persistent chronic congestive heart failure, neither mercurial diuretic nor digitalis therapy altered the low cardiacoutput or the high A-V oxygen difference. Removal of the edema and vascular congestion by diuresis alone nevertheless produced subjective improvement.In those patients in whom an increase in cardiac output occurred as the mercurial diuretic eliminated edema and lowered the elevated intracardiac pressures, the response may be considered consistent with Starlings law of the heart in man in congestive heart failure.The data clearly make the point that it is the circulatory congestion that produces the symptoms and the physical signs traditionally considered characteristic of congestive heart failure. Removal of the circulatory congestion, however accomplished, relieves the symptoms and physical signs of congestive heart failure, regardless of whether or not cardiac function is improved toward the normal.Circulatory congestion does not necessarily indicate, nor correlate with, the status of cardiac function.

Cardiovascular Dynamics, Blood Volumes, Renal Functions and Electrolyte Excretions in the Same Patients during Congestive Heart Failure and after Recovery of Cardiac Compensation

Largely on the basis of acute observations in cardiac patients during congestive heart failure and in noncardiac control subjects, two assumptions have been made: (a) that congestive heart failure develops as cardiovascular and renal functions change from the type found in the control subjects to the type found in decompensated cardiac patients, and (b) that a return to, or toward, the normal occurs in these functions as cardiac compensation is regained. That these assumptions are not necessarily valid is indicated by the herein reported simultaneous measurements of cardiovascular dynamics, renal functions, blood volumes and electrolyte excretions in eight patients during cardiac decompensation and after recovery of compensation.

An analysis of causes of right axis deviation based partly on endocardial potentials of the hypertrophied right ventricle

Abstract 1. 1. The physiologic and anatomic reasons for deviation of the electrical axis to the right are reviewed. 2. 2. In certain patients with myocardial infarction, right axis deviation results when the infarct is so oriented that the left arm is in effect a semidirect lead from the cavity of the left ventricle, and is more negative during ventricular excitation than the right arm. 3. 3. Considerations and data are presented which make it doubtful that the hypertrophied right ventricle, except in rare instances, can cause right axis deviation by itself. Rather, it appears to have its dominant effect on the electrocardiogram by changing the position of the heart in the thorax. 4. 4. In certain diseases characterized by a large right ventricle and conditions in the thorax which favor rotation of the heart about its long axis, it is believed that extreme rotation of this organ with almost complete reversal of the electrical fields of the two ventricles in the thorax may occur. 5. 5. When excitation of all the ventricular muscle requires less than 0.1 second, and right axis deviation is accompanied by a late R′ in leads from the right side of the precordium, the deviation and the deflection are probably caused by a delay in propagation of excitation across the free wall of the right ventricle, this delay being distal to the bundle branch. Under such circumstances the R′ may be somewhat exaggerated in size and duration by late components contributed by the base of the right ventricle, particularly if it is hypertrophied.

Anomalous Atrioventricular Excitation Produced by Catheterization of the Normal Human Heart

During the withdrawal of a catheter-electrode through the right ventricle of 2 normal subjects the electrogram displayed briefly a short P-R interval and an aberrant QRS. In the simultaneously recorded standard lead, the phenomenon simulated what is seen in the Wolff-Parkinson-White syndrome. The findings are presented in support of the physiologic, rather than anatomic, explanation for anomalous atrioventricular excitation.

Rapidly progressive glomerulonephritis in a patient with rheumatoid arthritis during treatment with high-dosage D-penicillamine.

A patient with advanced rheumatoid arthritis and severe clinical manifestations of rheumatoid vasculitis died of acute renal failure after 30 months of treatment with high-dosage D-penicillamine. She had had no signs of adverse drug reactions until the terminal illness. Although streptococcal pharyngitis was diagnosed late in her disease, penicillamine-induced immune complex glomerular damage is considered more likely than poststreptococcal glomerulonephritis, because her microscopic hematuria preceded diagnosis of pharyngitis. Postmortem examination disclosed findings suggestive of rapidly progressive glomerulonephritis of immune complex pathogenesis. The short period of microscopic hematuria and the rapidity of development of renal failure before death emphasize the need for frequent monitoring of renal function and prompt discontinuation of D-penicillamine treatment upon detection of otherwise unexplained hematuria. There is urgent need for early immunological evaluation, renal biopsy, and vigorous therapeutic measures.

AURICULAR FLUTTER OF ELEVEN YEARS' DURATION WITH OBSERVATIONS ON ESOPHAGEAL ELECTROCARDIOGRAMS

Excerpt Auricular flutter in subjects without other evidence of cardiac disease is usually paroxysmal in type. Parkinson and Bedford1had five cases of this nature, and Friedlander and Levine had th...

SOLITARY MYOCARDIAL ABSCESS IN SUBACUTE BACTERIAL ENDOCARDITIS

Excerpt On occasion a case of subacute bacterial endocarditis is encountered which presents an unusual feature or combination of features. It is the purpose of this communication to record an insta...

Case Report Echocardiographic Observations in Patients with Friedreich’s Ataxia

Echocardiography was performed on 11 patients with Friedreichs Ataxia. Eight of 11 had asymmetric septal hypertrophy and systolic anterior motion of the anterior leaflet of the mitral valve at rest or after inhalation of amyl nitrite. Two patients had concentric left ventricular hypertrophy. In view of this high incidence of hypertrophic cardiomyopathy, echocardiography is suggested as part of the routine evaluation of the patient with Friedreichs Ataxia.