Arthur J. Merrill

THE CARDIAC OUTPUT IN PATIENTS WITH CHRONIC ANEMIA AS MEASURED BY THE TECHNIQUE OF RIGHT ATRIAL CATHETERIZATION

Many patients with circulatory failure either from hemorrhage or heart failure have anemia. In these patients, the cardiac output may be within normal limits and yet the circulation may be inadequate. The question immediately arises as to what is the effect of anemia on the requirements of the tissues of the body for blood. Before it can be determined whether a given patient with anemia has an adequate circulation, it is necessary to know how anemia per se affects the cardiovascular system and what level of cardiac output should be expected for a given hemoglobin concentration. Studies on the circulation were, therefore, carried out on patients with chronic anemia in whom the picture was not complicated by shock and by the marked decrease in total blood volume which are so often present in the acute anemia produced by hemorrhage.

Concentration of renin in renal venous blood in patients with chronic heart failure

Abstract 1.1. Renal venous blood was obtained from five normal subjects and eleven patients with fixed chronic congestive failure. A catheter introduced into the antecubital vein was threaded through the venous system into the renal vein. Dogs were used for the assay of renin. 2.2. No renin was detected in the renal venous blood or arterial blood of the normal subjects. It is to be noted that the dog is only about one-fourth as sensitive to renin as the cat. 3.3. Significant amounts of renin were found in the renal venous blood of eight of the eleven patients with chronic heart failure. No renin was detected in the arterial blood. 4.4. The finding of increased concentration of renin in the renal venous blood of patients with chronic congestive failure is additional evidence in support of the finding that the renal blood flow is greatly reduced in chronic heart failure. 5.5. The well maintained blood pressure in the presence of a low cardiac output, the sudden changes in venous pressure produced by relieving pericardial tamponade and by improvement of the circulation by digitalis, and the marked fall in renal blood flow out of proportion to the fall in cardiac output all suggest that active vasoconstriction is present in patients with heart failure. No final conclusion can be reached at this time as to whether renin is responsible for some of the observed vasoconstriction. ∗ ∗The hypertensin used for renin standardization was furnished through the courtesy of Dr. K. G. Kohlstaedt, of the Lilly Research Laboratory.

THE EFFECT OF VENESECTION AND THE POOLING OF BLOOD IN THE EXTREMITIES ON THE ATRIAL PRESSURE AND CARDIAC OUTPUT IN NORMAL SUBJECTS WITH OBSERVATIONS ON ACUTE CIRCULATORY COLLAPSE IN THREE INSTANCES

The mechanisms by which the body compensates for a decrease in blood volume have not been thoroughly studied in man. All physicians are aware that from 500 to 1000 ml. of blood can be removed from a person of average size without producing any symptoms, if the body is horizontal. If the blood is removed rapidly, hemodilution plays little part in the immediate adjustment. Do the arterioles constrict, maintaining the arterial pressure at a normal level at the expense of blood flow to the tissues? Is the atrial pressure maintained at the normal level by venous constriction? Or is it possible that up to a certain point, the heart can function effectively with a falling atrial pressure so that the circulation can be maintained without either arteriolar or venous constriction in spite of a moderate decrease in blood volume? The purpose of this paper is to describe the changes in the circulation in normal subjects caused by moderate loss of blood from the body, either as the result of venesection or by pooling blood in the extremities through the application of venous tourniquets. During the experiments, acute circulatory collapse (primary shock) occurred in three instances and quantitative observations were made on the changes occurring in the circulation.

Mechanisms of salt and water retention in heart failure

Abstract The concept is proposed that edema in heart failure is caused by retention of salt and water produced by a diminished ability of the kidney to excrete salt and water. This disturbance in the kidney is the result of an inadequate cardiac output which is both relatively and absolutely reduced in patients who have chronic cardiac edema at rest, and is relatively reduced as compared with general or specialized tissue demands in other cardiac subjects with edema, i.e., those who fail with exertion, hyperthyroidism, anemia or beri-beri, and who may have a normal or elevated resting cardiac output. The inadequate cardiac output, through one or more mechanisms, causes the kidney to excrete less salt and water. It also produces a reduction in renal plasma flow and filtration rate by a contraction of the efferent arterioles of the kidney effected by some humoral substance. The reduced filtration rate corresponds closely to the reduction in sodium excretion and evidence is presented which indicates that the lowered filtration rate may be one of the causes of the reduction in sodium excretion. In advanced stages of heart failure the reduction in salt and water excretion is probably produced by at least two other means—the adrenal cortex is definitely stimulated and the pars intermedia of the pituitary probably also plays a part. Much work needs to be done to evaluate the role of these various factors both in renal hemodynamics and sodium excretion. Too little is known of the effect of changes in the intracellular electrolytes on edema formation and cardiac physiology to warrant any speculation as to the part taken by them.

Renal hemodynamics, sodium and water excretion in supine exercising normal and cardiac patients.

Diminished sodium excretion is one of the factors underlying edema formation in congestive heart failure. The clinical improvement and disappearance of the edema in some cardiac patients treated with bed rest alone suggests the importance of exercise as a potentiating factor in the sodium retention. Exercise studies carried out in normal and cardiac patients in the upright position by other investigators are open to question since the upright position itself is a factor in diminished sodium excretion. In order to exclude postural effects completely, it became necessary to study renal hemodynamics and electrolyte and water excretion in supine exercising subjects.