Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3014238 | Revista Española de Cardiología | 2010 | 15 Pages |
Abstract
The optimizations needed to meet these conflicting demands result in reduced capacity to compensate for increased afterload or pressure. Unfortunately, a large number of pathologic processes can result in acute and or chronic increases in afterload stress. As afterload stress rises, right heart failure may develop, and hemodynamic instability and death can occur abruptly. Several biochemical pathways have been identified that may participate in adaptation or maladaptation to excessive pressure loads.
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Authors
Clifford R. Greyson,