Right Duct Lymph Flow in Experimental Heart Failure Following Acute Elevation of Left Atrial Pressure

Uhley, Herman N.; Leeds, Sanford E.; Sampson, John J.; Friedman, Meyer

doi:10.1161/01.res.20.3.306

Cited by 25 publications

(6 citation statements)

References 13 publications

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“…This has been demonstrated in an animal model. 31 Finally, chronic alterations in diastolic compliance of the left ventricle can limit increases in filling pressure during exercise. This would prevent pulmonary congestion and increase exercise capacity.…”

Section: Cardiac Medicationsmentioning

confidence: 99%

Exercise capacity in patients with severe left ventricular dysfunction.

Benge¹,

Litchfield²,

Marcus³

1980

Circulation

186

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SUMMARY Normal or near-normal exercise capacity has been thought to reflect normal left ventricular function. Many compensatory mechanisms could preserve exercise capacity in patients with severe left ventricular dysfunction. We evaluated exercise capacity using a treadmill exercise test in 26 patients with severe left ventricular dysfunction defined by a left ventricular ejection fraction of 30% or less by isotope ventriculography. One half of the patients had normal exercise capacity and a normal cardiothoracic ratio on chest x-ray. This study indicates that traditional predictors of left ventricular function that have been widely used in clinical evaluation of the patients with cardiac disease (cardiothoracic ratio and exercise capacity) can be normal in a significant number of patients with severe left ventricular dysfunction. Thus, left ventricular function cannot be accurately estimated using these traditional predictors and should be assessed quantitatively. The isotope ventriculogram appears to be ideal for this purpose.IN PATIENTS with suspected or established cardiac disease, normal or near-normal exercise capacity has generally been thought to reflect normal left ventricular function. The rationale for this assumption is based on studies that have shown a close linear correlation between maximal oxygen consumption and cardiac output. 1-4 Furthermore, the assumption that exercise capacity relates to the severity of heart disease has formed the basis of the most commonly used clinical classification of patients with heart disease (New York Heart Association).Although left ventricular dysfunction may alter exercise capacity, many compensatory mechanisms could preserve exercise tolerance despite severe left ventricular dysfunction, including preservation of absolute stroke volume, chronotropic competence, increased oxygen extraction, altered left ventricular compliance or augmented pulmonary lymphatic flow. Therefore, we reevaluated exercise capacity in patients with severe left ventricular dysfunction. If a substantial number of patients with severe left ventricular dysfunction and near-normal exercise tolerance could be identified, the concept that exercise capacity is a predictor of left ventricular performance would be challenged.

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Section: Cardiac Medicationsmentioning

confidence: 99%

Exercise capacity in patients with severe left ventricular dysfunction.

Benge¹,

Litchfield²,

Marcus³

1980

Circulation

186

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“…In the first set of studies of this report hydrostatic pressures were elevated by circulatory overload, while oncotic pressure remained essentially unchanged; in the second set, oncotic pressure was reduced under conditions of relatively stable hydrostatic pressure. Previous studies by others have been shown that the respective procedures produce marked elevation in pulmonary lymph flow rates from lungs, in vivo, in response to a presumed but not directly measured increase in rates of outward filtration (Uhley et al, 1967;Zarins et al, 1978).…”

mentioning

confidence: 88%

Morphometric studies of the alveolar epithelium in dog lungs in vivo after increased rates of outward filtration

DeFouw

Chinard

1983

Anat. Rec.

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Increased pulmonary artery pressures and decreased albumin concentrations were established in dogs, in vivo, by circulatory overload and by plasmapheresis. Each change, occurring singly, would be expected to produce an increase in outward filtration rate. The ultrastructure of the alveolar epithelium after the production of this presumed increase in filtration was evaluated by established morphometric techniques. The extent of extravascular fluid accumulation was assessed by multiple indicator-dilution studies and by light microscopic analysis. Previous studies from this laboratory (DeFouw and Berendsen, 1979;DeFouw, 1980) define increased alveolar surface densities, increased type I cell vesiculation, and depleted type I1 cell lamellar body contents after increased filtration had induced septal edema and alveolar flooding in isolated perfused dog lungs. In the present study septal edema and alveolar flooding were not detected. Nor were changes observed in either alveolar epithelial cells or in alveolar configurations. However, there was significant accumulation of extravascular fluid in cuffs around extraalveolar vessels. These results are consistent with the interpretation that the initial stage of cardiodynamic edema formation, namely, perivascular cuffing, is not associated with structural aberrations of the alveoli or their lining epithelial cells, in vivo. Since such changes were detected previously in isolated lungs after development of the final stages of edema, namely, septal fluid accumulation and alveolar flooding, additional studies of septal edema and alveolar flooding in intact animals are necessary to establish functional correlates to ultrastructural aberrations in severely edematous lungs.

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“…However, homeostasis of the extravascular fluid volume of the airways and lung also depends on effective lymph drainage from the lung. The pumping pressure in the lymphatic vessels close to the external jugular vein is approximately 17 cm H 2 O [56]. Thus, when this pressure is exceeded in the jugular veins, it is likely that pulmonary lymphatic drainage will be compromised, leading to an increase in the extravascular fluid volume and the appearance of respiratory symptoms.…”

Section: Exercise In Elderly People With Hfmentioning

confidence: 99%

Exercise and heart failure in the elderly

Kappagoda

Amsterdam

2012

Heart Fail Rev

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In this review, we will examine the physiological responses to exercise in elderly populations (age > 65 years) with and without evidence of heart failure. Aging per se in both men and women is associated with a ~40% lower maximum oxygen consumption in sedentary subjects. In trained individuals, this value is 25-32% lower. A smaller SV accounts for nearly 50% of these age-related differences, and the remainder is explained by a lower maximal HR and reduced oxygen extraction. Exercise training is also associated with an increase in the arteriovenous O(2) difference in previously sedentary elderly men and women, which probably contributes to the overall beneficial effect of training in the elderly. However, during vigorous exercise (125 W), the cardiac output in the elderly is dependent upon an age-related increase in end-diastolic volume and stroke volume, which "compensates" partially for the age-related decrease in heart rate. Hence, in elderly individuals, the stroke volume during exercise depends upon diastolic filling. The changes that occur in the heart are also associated with an overall reduction in efferent sympathetic nerve activity. Despite this decline, the metaboreflex initiated by receptors in exercising muscles remains the main determinant of sympathetic activation (to maintain blood pressure) during exercise in the elderly. It is recognized that aging is associated with the development of heart failure, particularly in women in whom its prevalence increases >twofold from age 65-69 (6.6%) to age 85 years (14%). Almost half the people presenting with heart failure appear to have normal left ventricular systolic function, a phenomenon that is more common in women. Exercise training in elderly people with and without heart failure appears to have a beneficial effect in terms of enhancing the quality of life and functional capacity. Mortality benefit in the latter has not been established with certainty.

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Right Duct Lymph Flow in Experimental Heart Failure Following Acute Elevation of Left Atrial Pressure

Cited by 25 publications

References 13 publications

Exercise capacity in patients with severe left ventricular dysfunction.

Exercise capacity in patients with severe left ventricular dysfunction.

Morphometric studies of the alveolar epithelium in dog lungs in vivo after increased rates of outward filtration

Exercise and heart failure in the elderly

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