Distensibility of the dog left ventricle

Hefner, Lloyd L.; Coghlan, H. Cecil; Jones, William B.; Reeves, Tim

doi:10.1152/ajplegacy.1961.201.1.97

Cited by 69 publications

(23 citation statements)

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“…Variations in heart rate have been demonstrated to alter ventricular end-diastolic compliance (Braunwald et al, 1960), but in our study, heart rate did not change during CPPV. CPPV may alter neurohumoral stimuli, but evidence indicates that changes in circulating catecholamines and autonomic discharge to the heart do not decrease ventricular end-diastolic compliance (Wiggers, 1927;Mitchell et al, 1960;Hefner et al, 1961;Wildenthal et al, 1969a;Wildenthal et al, 1969b). Changes in coronary perfusion pressure or coronary blood flow can alter ventricular end-diastolic compliance (Cross et al, 1961), but these variables did not change during CPPV in our study.…”

Section: Discussioncontrasting

confidence: 60%

Continuous positive-pressure ventilation decreases right and left ventricular end-diastolic volumes in the dog.

Fewell¹,

Abendschein²,

Carlson³

et al. 1980

Circulation Research

178

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SUMMARY We investigated the mechanism(s) responsible for the decreased cardiac output during continuous positive-pressure ventilation (CPPV). Seven dogs were anesthetized with chloralose-urethane, intubated, and ventilated using a volume ventilator. We measured heart rate, stroke volume, and the determinants of stroke volume: left and right ventricular end-diastolic volumes, isovolumic and ejection phase indices of myocardial contractility, and pulmonary and systemic arterial pressures. Myocardial blood flow was estimated using radioactive microspheres. Variables were measured during a control period of intermittent positive-pressure ventilation (IPPV), 8-20 minutes after the initiation of CPPV using 12 cm H 2 O positive end-expiratory pressure (PEEP), and 8-20 minutes after the removal of PEEP. CPPV decreased cardiac output but did not affect total or regional myocardial blood flow or the ratio of subendocardial to subepicardial blood flow. Isovolumic and ejection phase indices of myocardial contractility, heart rate, and systemic arterial pressure did not change during CPPV. Right and left ventricular end-diastolic and end-systolic volumes decreased markedly during CPPV. We conclude that CPPV decreases cardiac output in accordance with Starling's law by decreasing preload. Circ Res 46: 125-132, 1980CONTINUOUS positive-pressure ventilation (CPPV) is used to increase the arterial Po 2 in patients with acute respiratory failure and hypoxemia refractory to usual oxygen therapy (Ashbaugh et al., 1969;Mclntyre et al., 1969;Kumar et al., 1972;Falke et al., 1972). Although CPPV usually improves the arterial Po-2, it also decreases cardiac output and may actually decrease the amount of oxygen transported to the tissues (Lutch and Murray, 1972).Studies on animals (Tucker and Murray, 1972;Jones and King, 1973) and humans (Cournand et al., 1948;Powers et al., 1973) have demonstrated that CPPV decreases the cardiac output, but the mechanism is unclear. It generally was believed that cardiac output falls due to decreased venous return (Cournand et al., 1948;Ashbaugh and Petty, 1973;Qvist et al., 1975). If this were true, the effective or transmural filling pressure of the right atrium (right atrial pressure minus pleural pressure) would be expected to decrease during CPPV. However, several investigators have reported that transmural right and left atrial pressures, measured rel- ative to lateral pleural or esophageal pressure, do not decrease, but stay the same or actually increase during CPPV (Scharf et al., 1977;Zarins et al., 1977;Cassidy et al., 1978). This suggests that decreased venous return is not the primary factor producing the decrease in cardiac output. A decrease in cardiac output in the presence of constant or increasing transmural atrial pressures may indicate a decrease in myocardial contractility. Lozman et al. (1974) and Powers and Dutton (1975) have suggested that ventricular dysfunction occurs during CPPV and may be related to decreased subendocardial blood flow.The purpose of the present study was to c...

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Section: Discussioncontrasting

confidence: 60%

Continuous positive-pressure ventilation decreases right and left ventricular end-diastolic volumes in the dog.

Fewell¹,

Abendschein²,

Carlson³

et al. 1980

Circulation Research

178

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“…Such an element might be "passive" or might represent the degree of Circulation Research, Vol. XXIII, August 1968 persistent interaction in the contractile element. Other types of studies have suggested that the contractile element has viscous properties (8).…”

Section: Discussionmentioning

confidence: 99%

“…• During the past forty years a variety of considerations have suggested that the diastolic pressure-volume relationship for the mammalian ventricle might vary as a result of some change in the characteristics of the myocardium (1)(2)(3)(4)(5)(6)(7)(8). Moreover, it was recognized early that under appropriate conditions variability in the pressure-volume relationship would influence both the performance of the heart as well as any evaluation of performance which employed measurement of enddiastolic pressure as an index of fiber length.…”

mentioning

confidence: 99%

Some Mechanical Properties of Isolated Mammalian Cardiac Muscle

Hoffman

Bassett

Bartelstone

1968

Circulation Research

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Isolated preparations of mammalian cardiac muscle have been employed to study possible mechanisms responsible for changes in diastolic compliance. Muscles have been studied at rest and during isometric and afterloaded contractions, at fixed initial length and during programmed, cyclic changes in length, and under the influence of paired stimulation, catecholamines, and elevated extracellular calcium concentrations. The results obtained indicate that, although there is a series viscous element in cardiac muscle, which accounts for stress-relaxation, some changes in compliance apparently result from alterations in the extensibility of the contractile element. This conclusion is based primarily on experiments showing shifts in the apex of the length-tension curve produced by action of inotropic agents which alter diastolic compliance and on experiments showing that the rate and extent of relaxation of afterloaded contractions depend on the extent of shortening during contraction. • During the past forty years a variety of considerations have suggested that the diastolic pressure-volume relationship for the mammalian ventricle might vary as a result of some change in the characteristics of the myocardium (1-8). Moreover, it was recognized early that under appropriate conditions variability in the pressure-volume relationship would influence both the performance of the heart as well as any evaluation of performance which employed measurement of enddiastolic pressure as an index of fiber length. A change in the pressure-volume or lengthtension relationship might result either from an alteration in the contractile elements or

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“…However, all of the studies have been performed in the condition with the pericardium removed. On the other hand, in acute volume overload, the pericardium protects the heart from overdistension and contributes to elevation of left ventricular diastolic pressure at any given volume through pericardial restraint (Hefner et al 1961; Spotnitz and Kaiser 1971;Glantz et al 1978 ; Shirato et al 1978Shirato et al , 1982Janicky and Weber 1980). Furthermore, previous study in our laboratory has shown that the pericardium modifies the end-systolic pressure-segment length relationship of canine left ventricle in acute volume overload (Kanazawa et al 1983).…”

mentioning

confidence: 83%