500
THE:
AMERICAN
XEART
JOURNAL
The arterial and venous pressures of clinical congestive failure cannot be reproduced in this schema by weakening the heart alone. Mechanisms which cause an increase of Btatie blood pressure, such as general vasoconstriction, pressure on vessels from without, or the insertion of additional fluid within the vessels, must be introduced before the pressure relations of clinical congestive heart failure can be produced. The behavior of the schema has suggested clinical considerations which raised doubt whether the venous congestion of “congestive heart failure” was brought about in the manner commonly believed. This prompted the clinical investigations reported in the following paper. AUTHORS. Starr, Isaac: Role of the “Static Blood Pressure” Venous Pressure, Especially in Heart Failure. Studies. Am. J. M. SC. 199: 40, 1940.
II.
in Abnormal Increments Clinical and Experimental
of
The pressure remaining throughout the circulation after the cessation of cardiac action, the “static blood pressure, ” has been measured promptly after death in sixty-four patients. Necropsies were performed in forty-four of these cases. In persons dying of prolonged congestive heart failure the static blood pressure averaged 20.3 cm. H,O. In persons dying without heart disea’se it averaged 7.6 cm. This difference is large enough to account for the major part, in some instances for all, of the high venous pressure found in cases of congestive failure during life. Obviously, therefore,, the larger part of the increase of venous pressure found in cases of congestive failure should not be attributed directly to any difference of cardiac function, for the abnormality persists when the heart is no longer functioning. Well-known theoretical conceptions in congestive failure have been restudied and reassessed in the light of this new information. AUTHOR. Freundlich, Right
J., and Lepeschkin, Axis Deviation Types
Systemic Studies E.: of Electrocardiograms.
of Chest Leads in Left and Cardiologia 3: 331, 1939.
Eighty cases with left and twenty-seven with right axis deviation were studied; none had myocardial infarction or prolonged QRS. Sixteen chest points were used, and the “indifferent” electrode was on the left leg. In the left axis deviation with upright T,, the chest leads resembled the normal. However, when T, was inverted, the QRS was upright and the T wave was inverted in the right anterior chest surface, and QRS was inverted and T was upright on the left side; the transition between these two areas was abrupt. This configuration occurred with enlarged left ventricle and old or recent heart failure. When T, is isoelectric the chest leads of left axis deviation were intermediate. Right axis deviation also showed two types of chest leads. In one type QRS was inverted over the entire anterior che’st, with T inverted or isoelectric except In the second type, QRS on the right side of in the left anterior axillary line. the chest was mainly up with T inverted, and on the left side it was mainly down with the T wave up. KATZ. Liideritz, in the was
Between B. : The Relation Human Electrocardiogram.
QRS Duration and the Form of S-T Segment Arch. f. Kreislaufforsch. 5: 223, 1939.
Five hundred normal electrocardiograms found to vary between 0.06 to 0.12
were second
analyzed. The duration with a typical distribution
of QRS curve