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Tyberg JV, Smith ER. Ventricular diastole and the role of the pericardium. Herz. 1990;15(6):354-61
Tyberg, J. V., & Smith, E. R. (1990). Ventricular diastole and the role of the pericardium. Herz, 15(6), 354-61.
Tyberg, J V, and Smith, E R. "Ventricular diastole and the role of the pericardium." Herz vol. 15,6 (1990): 354-61.
Tyberg JV, Smith ER. Ventricular diastole and the role of the pericardium. Herz. 1990 Dec;15(6):354-61. PMID: 2279730.
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Herz. 1990 Dec;15(6):354-61.

Ventricular diastole and the role of the pericardium.

Herz

J V Tyberg, E R Smith

Affiliations

  1. Department of Medicine, University of Calgary, Alberta, Canada.

PMID: 2279730

Abstract

In order to understand the mechanics of left ventricular (LV) diastolic filling it has become important to understand the role of the pericardium. This is because it has been demonstrated that the LV pressure-volume relationship can be shifted by previously unrecognized changes in pericardial "pressure" and, therefore, LV end-diastolic pressure (LVEDP) may be ambiguous as a measure of preload. The key to this understanding is to appreciate that (except in the case of pericardial effusion or tamponade) the pericardium impedes cardiac filling by exerting a stress, not by raising the pressure in the pericardial fluid, and that the magnitude of this stress is variable and relatively great. When animals or humans are volume loaded acutely, this stress is approximately equal to right ventricular (RV) filling pressure. Thus, while it may not be possible to estimate true preload from simple measurements of LVEDP, subtracting RV filling pressure from LVEDP may provide a useful estimate of transmural LVEDP. As an example of the effect of the pericardium, recent laboratory results indicated that the decrease in stroke volume which resulted from acute pulmonary embolization could be explained by reductions in LV preload. Transmural LVEDP and end-diastolic volume decreased in spite of the fact that LVEDP rose markedly. Since LVEDP increased while stroke volume decreased, it might have been concluded that contractility had decreased. However, this was shown not to be the case, since the reduction in stroke volume only corresponded to the reductions in transmural LVEDP and end-diastolic volume. Thus, appropriately accounting for pericardial constraint may allow many changes in LV systolic performance, hitherto thought to represent changes in contractility, to be explained on the basis of preload changes and the Frank-Starling mechanism.

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