Effect of Acute Mitral Insufficiency of Various Degrees on Mean Arterial Blood Pressure, Coronary Blood Flow Cardiac Output and Oxygen Consumption

Wégria, René; Muelheims, Gerhard H.; Jreissaty, Robert; Nakano, Jiro

doi:10.1161/01.res.6.3.301

Cited by 8 publications

(2 citation statements)

References 6 publications

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“…METHODS 17 dogs, ranging in weight from 15.5 to 25.6 kg (average, 20.4 kg) were anesthetized with i.v. sodium pentobarbital, [30][31][32][33][34][35][36][37][38][39][40] mg/kg, and a bilateral thoracotomy was performed under positive pressure respiration. The experimental preparation is illustrated in Fig.…”

Section: Introductionmentioning

confidence: 99%

Myocardial mechanics in aortic and mitral valvular regurgitation: the concept of instantaneous impedance as a determinant of the performance of the intact heart

Urschel¹,

Covell²,

Sonnenblick³

et al. 1968

J. Clin. Invest.

191

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A B STR A C T The effects on myocardial mechanics of acute, artificial aortic and mitral regurgitation were studied in the dog to determine the manner in which the changes in load induced by valvular regurgitation alter ventricular performance. With mitral and aortic regurgitant volumes of approximately the same magnitude as the forward stroke volume, immediate increases occurred in total stroke volume, left ventricular enddiastolic pressure, and peak ejection velocity, whereas contractility remained unchanged. Although calculated myocardial fiber tension rose, the rate of decline of tension during ejection was accelerated with regurgitation due to the more rapid decrease in ventricular size. Average tension therefore decreased relative to average pressure. As a consequence of the increased fiber length and this unloading, contractile element velocity, work, and power were increased. Despite unchanged contractility of the myocardium, the ejection fraction rose with both aortic and mitral regurgitation.When regurgitant beats were compared with control beats at a constant end-diastolic volume, ventricular stroke volume, work, power, and ejection fraction, as well as contractile element velocity, work, and power consistently increased. Thus, reduction of instantaneous impedance to ejection allowed the ventricle to empty further, reducing ventricular wall tension with a resultant Received for publication 5 June 1967 and in revised form 14 November 1967. increase in the velocity of shortening. External energy output was increased despite unchanged contractility and diastolic fiber length. It is concluded that the impedance to ejection and myocardial fiber tension during ejection govern the velocity and extent of contractile element shortening, and hence affect stroke volume, peak aortic flow rate, and ejection fraction. The alterations of ventricular function accompanying valvular regurgitation can be explained by an evaluation of the effects of these lesions on the instantaneous impedance to left ventricular ejection.

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Section: Introductionmentioning

confidence: 99%

Myocardial mechanics in aortic and mitral valvular regurgitation: the concept of instantaneous impedance as a determinant of the performance of the intact heart

Urschel¹,

Covell²,

Sonnenblick³

et al. 1968

J. Clin. Invest.

191

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show abstract

“…Although acutely induced aortic and mitral regurgitation have been shown to increase myocardial oxygen consumption (MVO 2 ) (3)(4)(5), the mechanism by which these increases are mediated has not been defined. It has recently become possible to define From the Cardiology Branch, National Heart Institute, Bethesda, Maryland 20014.…”

mentioning

confidence: 99%

Effects of Acute Valvular Regurgitation on the Oxygen Consumption of the Canine Heart

Urschel

Covell

Graham

et al. 1968

Circulation Research

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The effects on myocardial oxygen consumption and mechanics of acute, simulated aortic and mitral regurgitation were studied in open-chest, anesthetized dogs to determine how changes in the mechanical performance of the ventricle alter oxygen consumption. When regurgitation was induced acutely with effective stroke volume (total stroke volume less regurgitant volume) and heart rate held constant, left ventricular end-diastolic volume, total stroke volume, the ejection fraction, left ventricular wall tension, and the extent of shortening of the contractile element and the circumferential fibers all increased. With volumes of regurgitation approaching effective systemic blood flow, oxygen consumption increased only moderately, despite the increases in tension and shortening. When valvular regurgitation was induced while peak ventricular wall tension was held relatively constant, stroke volume doubled and the extent of both contractile element and circumferential fiber shortening increased. Confeactile element work in generating tension was unchanged; that which led to fiber shortening increased substantially. Myocardial oxygen consumption did not increase significantly. Thus, marked increases in the efficiency of the contractile elements and myocardial fibers occurred. The low energy cost per unit of work expended in shortening as opposed to that used for tension development therefore allows the excess stroke volume of valvular regurgitation to be maintained at only a small added oxygen cost to the ventricle.ADDITIONAL KEY WORDS aortic insufficiency mitral insufficiency cardiac energetics contractile element work myocardial tension• Although the effects of valvular regurgitation on cardiovascular dynamics have been studied intensively for many years (1, 2), relatively little information is available concerning the effects of these lesions on myocardial energy requirements. Although acutely induced aortic and mitral regurgitation have been shown to increase myocardial oxygen consumption (MVO 2 ) (3-5), the mechanism by which these increases are mediated has not been defined. It has recently become possible to define From the Cardiology Branch, with greater precision the relative importance of the various determinants of M\ 7 O2. These include the tension developed by the myocardium (6-9), the contractility of the myocardium as reflected in the velocity of shortening of the unloaded fibers (V maj ) (9-12) and myocardial shortening against a load (7, 13-15). Also the effects of acutely induced, simulated, aortic and mitral valvular regurgitation on myocardial mechanics have been examined (16) and such an approach now permits an analysis of the effects of these lesions on MV0 2 . MethodsA bilateral thoracotomy was performed in 11 dogs (avg wt, 20.7 kg) anesthetized with sodium

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Metabolism of the heart in cardiac failure

Scheuer

1970

Progress in Cardiovascular Diseases

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Effect of Acute Mitral Insufficiency of Various Degrees on Mean Arterial Blood Pressure, Coronary Blood Flow Cardiac Output and Oxygen Consumption

Cited by 8 publications

References 6 publications

Myocardial mechanics in aortic and mitral valvular regurgitation: the concept of instantaneous impedance as a determinant of the performance of the intact heart

Myocardial mechanics in aortic and mitral valvular regurgitation: the concept of instantaneous impedance as a determinant of the performance of the intact heart

Effects of Acute Valvular Regurgitation on the Oxygen Consumption of the Canine Heart

Metabolism of the heart in cardiac failure

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