Relationships between left ventricular volume, ejected fraction, and wall stress

Rr, Taylor; He, Chao; Rh, McDonald

doi:10.1152/ajplegacy.1966.211.3.674

Cited by 36 publications

(7 citation statements)

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“…The high pressure and tension development by isovolumic contractions originating from the high LVEDP in the dogs with an aorto-caval fistula tFig. 1) and the higher ejected fraction, SV/EDV, in ejecting beats, also are not unexpected since both isovolumic pressure development (11) and muscle fiber shortening, and hence SV/ EDV (16), are influenced by ventricular filling. The most striking of the present results, however, is that in only one of the seven animals with an aorto-caval fistula, circulatory congestion, and marked fluid retention, was left ventricular contractility depressed below the normal range, as judged by tension-velocity relations, Vmax, and isovolumic tension development.…”

Section: Discussionmentioning

confidence: 91%

“…Received for publication 16 November 1967 and in revised form 12 January 1968. g/kg of initial body weight (normal 5.25 + 0.56 g/kg) (P < 0.001), which reflected moderate ventricular hypertrophy, and ventricular internal volume at a given filling pressure was increased proportionally. Therefore, the ventricular contractile state usually was normal in the dog with a large aorto-caval fistula, and it is proposed that mechanisms for fluid retention that results in circulatory congestion were activated because of the large hemodynamic burden despite normal myocardial contractile properties.…”

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confidence: 99%

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Left ventricular function in experimental aorto-caval fistula with circulatory congestion and fluid retention

Taylor¹,

Covell²,

Ross³

1968

J. Clin. Invest.

108

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A B S T R A C T The mechanical properties of left ventricular contraction were described in terms of tension, velocity, length, and time in closed-chest, sedated dogs in which a large aorto-caval fistula had resulted in circulatory congestion, and the results were compared with those in normal dogs. Instantaneous contractile element velocity was calculated from left ventricular pressure and its first derivative during isovolumic left ventricular contractions produced by sudden balloon occlusion of the ascending aorta during diastole. A range of ventricular end-diastolic volumes was induced and heart rate was controlled at 150 beats/min. Wall tension (stress) was derived from ventricular pressure and volume, the latter being obtained from the pressure-volume relation of the passive ventricle. Extrapolated velocity at zero tension, Vmax, averaged 3.0 circ/sec in the normal dogs and 2.9 circ/sec in the seven dogs with an aortocaval fistula and fluid retention; in only one of these seven animals was Vmax below the lower limit of normal of 2.7 circ/sec. Isovolumic tension (PO) in dogs with aorto-caval fistulas tended to be slightly greater than normal at low ventricular filling pressures, and there was no difference in P. between the two groups of animals at high ventricular filling pressures. Time to peak pressure averaged 151 ± 6 (SE) msec (normal 139 ± 3). Left ventricular weight averaged 6.32 ±0.23 Dr. Taylor is a

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Section: Discussionmentioning

confidence: 91%

mentioning

confidence: 99%

Left ventricular function in experimental aorto-caval fistula with circulatory congestion and fluid retention

Taylor¹,

Covell²,

Ross³

1968

J. Clin. Invest.

108

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“…For example, isovolumic contractions of the hyperthyroid left ventricle at spontaneous heart rate and filling pressure developed less tension than did contractions of the normal ventricle (Table I). This can be accounted for by the lower left ventricular end-diastolic pressure, end-diastolic volume and muscle fiber length (23,36,37) TENSION g /cm2 FIGURE 3 Contractile element velocity (VcE) plotted against tension at 10 msec intervals throughout isovolumic left ventricular contractions in representative normal, hypothyroid, and hyperthyroid dogs. The time from the first appearance of mechanical activity is indicated once on each curve.…”

Section: Discussionmentioning

confidence: 99%

Influence of the thyroid state on left ventricular tension-velocity relations in the intact, sedated dog

Taylor¹,

Covell²,

Ross³

1969

J. Clin. Invest.

108

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The mechanical properties of left ventricular contraction were described in terms of tension, velocity, length, and time in closed-chest, sedated normal, hypothyroid, and hyperthyroid dogs. Heart rate was controlled at 150 beats/min, and instantaneous contractile element velocity was calculated from left ventricular pressure and its first derivative during isovolumic left ventricular contractions, produced by sudden balloon occlusion of the ascending aorta during diastole. Wall tension was derived from ventricular pressure and volume, the latter being obtained from the pressure-volume relation of the arrested ventricle, and tension-velocity relations were analyzed over a range of ventricular enddiastolic volumes. At any level of ventricular volume, the hypothyroid state was associated with a displacement of the tension-velocity relation of the left ventricle downwards and to the left, and the time to peak tension was prolonged (154 msec, normal 139 msec). In the hyperthyroid state, the tension-velocity relation of the left ventricle was displaced upwards and to the right, and the time to peak tension was reduced (80 msec). The changes in the tension-velocity relations indicate that the inotropic state of the left ventricle in the intact dog varies directly with the animal's thyroid state. This influence on myocardial contractility necessarily constitutes an important and integral part of the response of the intact circulation to altered thyroid state.

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“…1b, Fig. 2b,2g) [10-13]. Although these parameters cannot differentiate between increased contractility and decreased afterload because of their load dependence, the relatively load-independent peak systolic pressures/ESV (for both the right and left ventricles) appear to support the former (Fig.…”

Section: Discussionmentioning

confidence: 99%

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et al. 2004

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R128 CI = cardiac index; CO = cardiac output; CVP = central venous pressure; EDV = end-diastolic volume; EF = ejection fraction; ESV = end-systolic volume; HR = heart rate; LVEDVI = left ventricular end-diastolic volume index; LVEF = left ventricular ejection fraction; LVESVI = left ventricular endsystolic volume index; MAP = mean arterial pressure; PAC = pulmonary artery catheter; PWP = pulmonary artery wedge pressure; RVESVI = right ventricular end-systolic volume index; SBP = systolic blood pressure; SV = stroke volume; TPR = total peripheral resistance; SVI = stroke volume index. AbstractIntroduction Resuscitation with saline is a standard initial response to hypotension or shock of almost any cause. Saline resuscitation is thought to generate an increase in cardiac output through a preloaddependent (increased end-diastolic volume) augmentation of stroke volume. We sought to confirm this to be the mechanism by which high-volume saline administration (comparable to that used in resuscitation of shock) results in improved cardiac output in normal healthy volunteers. Methods Using a standardized protocol, 24 healthy male (group 1) and 12 healthy mixed sex (group 2) volunteers were infused with 3 l normal (0.9%) saline over 3 hours in a prospective interventional study. Individuals were studied at baseline and following volume infusion using volumetric echocardiography (group 1) or a combination of pulmonary artery catheterization and radionuclide cineangiography (group 2). Results Saline infusion resulted in minor effects on heart rate and arterial pressures. Stroke volume index increased significantly (by approximately 15-25%; P < 0.0001). Biventricular end-diastolic volumes were only inconsistently increased, whereas end-systolic volumes decreased almost uniformly. Decreased end-systolic volume contributed as much as 40-90% to the stroke volume index response.

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Relationships between left ventricular volume, ejected fraction, and wall stress

Cited by 36 publications

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Left ventricular function in experimental aorto-caval fistula with circulatory congestion and fluid retention

Left ventricular function in experimental aorto-caval fistula with circulatory congestion and fluid retention

Influence of the thyroid state on left ventricular tension-velocity relations in the intact, sedated dog

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