Mechanism of Acute Experimental Heart Failure

Harrison, Tinsley R.; Friedman, Ben; Resnik, Harry

doi:10.1001/archinte.1936.00170090092007

Cited by 36 publications

(2 citation statements)

References 18 publications

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“…per gram per hour. Comparable values were obtained by Harrison, Friedman and Resnik (13), in dogs with the chest and pericardium open. The procedure they employed causes considerable surgical shock.…”

Section: Oxygen Consumption Of the Heartsupporting

confidence: 60%

Studies on the Mechanism of the Increased Oxygen Consumption in Patients With Cardiac Disease

Resnik

Friedman²

1935

J. Clin. Invest.

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Since the introduction of accurate methods for measuring oxygen consumption, that function has been repeatedly observed to be increased in persons with congestive heart failure (1, 2, 3, 4) and to decline as improvement occurs (4). The mechanisms underlying these changes have not been clearly defined. In studying a group of patients with heart failure we were impressed with the constancy and magnitude of the alterations in metabolic rate and attempted to identify some of the factors responsible for them.This group of patients consisted of individuals with heart disease due to hypertension, syphilis or rheumatic infection. Most of the patients were moderately decompensated, a few had severe failure and a smaller number were without congestive phenomena or had symptoms due to neuroses. The usual measures used in treating heart failure were employed, i.e., rest, sedation, digitalis, diuretics and limitation of fluids. Venesection, thoracentesis and abdominal tapping were resorted to as occasion demanded. Observations were made at frequent intervals under, the usual "basal " conditions with the patient sitting in a wheel chair. The oxygen consumption was measured by gas analysis of the expired air, duplicate determinations being made as a rule. The metabolic rates were calculated on the basis of the edema-free weight, using the Boothby and Sandiford modification of DuBois' standard tables (16). In order to minimize the factor of nervousness and apprehension the subjects were trained for one or. two days prior to the beginning of the observations. Twenty-five patients were studied. They have been classified in three groups, depending on the response to treatment. Group I consists of 13 individuals who showed marked improvement as evidenced by three criteria, i.e., a loss of weight of at least 5 pounds, an increase in vital capacity of 10 per cent or more and the disappearance of paroxysmal dyspnea. Most of the subjects in this group had moderate or advanced congestive failure at the beginning of the observations. In Group II are six persons who claimed subjective relief but in whom the objective evidences of improvement, although demonstrable, were not sufficient to meet the standards for Group I. In general, the patients in this group were not as severely decompensated as those in Group I. Those in Group III showed either doubtful or no improvement and include the patients with well compensated heart disease or with symptoms due to neuroses.The results are shown in Table I. The data recorded are the initial level of the metabolic rate and the change in the rate as improvement occurred. In all but two patients the metabolic rate was 10 per cent or more above the calculated normal, when congestive failure was present, and tended to decline with improvement. The highest metabolic rates were found in Group I, where they ranged between 15 and 60 per cent above normal, with an average of 32 per cent above normal. The greatest change in rate with improvement in the clinical state was noted in this group, the average decrea...

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Section: Oxygen Consumption Of the Heartsupporting

confidence: 60%

Studies on the Mechanism of the Increased Oxygen Consumption in Patients With Cardiac Disease

Resnik

Friedman²

1935

J. Clin. Invest.

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“…It is suggested that the only hemodynamic disturbance constant to all types of heart failure is that the cardiac output is reduced relative to the inflow load. 6. It is pointed out that hypervolemia may be either primary and a cause of cardiac failure or, much more commonly, secondary and a result of heart failure.…”

Section: The Classi/ication Of Heart Failurementioning

confidence: 99%

Experimental Hypervolemic Heart Failure: Its Bearing on Certain General Principles of Heart Failure

1950

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Infusion of large volumes of fluid into normal dogs produces a progressive rise in venous pressure with an initial parallel rise in cardiac output succeeded by a fall. On the basis of these experiments and other considerations which are discussed, it is concluded that the cardinal hemodynamic defect common to all types of heart failure is a disproportion between inflow load and cardiac output. The various general circulatory disorders are classified as primary disorders of filling and primary disorders of emptying with various subgroups.

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Survey of Techniques for Measuring Myocardial Microperfusion

Eichstädt

Félix

1983

Radiological Functional Analysis of the Vascular System

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Mechanism of Acute Experimental Heart Failure

Cited by 36 publications

References 18 publications

Studies on the Mechanism of the Increased Oxygen Consumption in Patients With Cardiac Disease

Studies on the Mechanism of the Increased Oxygen Consumption in Patients With Cardiac Disease

Experimental Hypervolemic Heart Failure: Its Bearing on Certain General Principles of Heart Failure

Survey of Techniques for Measuring Myocardial Microperfusion

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