Therole of increased afterload in the pathogenesis of the left heartfailure
Thisis usually necessary because with the reduced capability of the heartas a result of the heart failure the left ventricle needs to applymore pressure so as to be able to pump blood into the aorta(McMurray,Adamopoulos, Anker, Auricchio, Böhm, Dickstein, & Jaarsma,2012).This situation is usually so because the only time the aorta opens upto receive blood is when the pressure inside the left ventricle ismore compared to the one inside the blood vessel.Thevicious cycle of systolic heart failure
Systolicheart failure is caused by the disruption of the signals controllingthe contraction of the walls of the ventricles. This is usuallyreferred to as a decrease in the cardiac inotropy. The result of thiscondition is the shift of the Frank-Starling curve towards thedownside. It is then followed by the reduction in the stroke capacityas well as a considerable increase in the preload (Roger,Go, Lloyd-Jones, Adams, Berry, Brown, & Fox, 2011).This preload is normally measured in terms of the end-diastolicpressure of the ventricles. The preload increase is most often as aresult of the partial emptying of the ventricles. This mechanism isusually necessary because it helps to maintain the volume of theventricles, despite the fact that there has been a loss of inotropy.The sustained occurrence of this condition is what is known assystolic heart failure.Ifechocardiogram reveals an enlarged and dilated left ventricle, Whatis the cellular pathophysiology that led to this change?
Theincreased need of the left ventricle to use more pressure to pumpblood out of the heart could lead to a dilation of the leftventricle. This increased need could be as a result of high bloodpressure, leading to the constriction of the walls of blood vesselsor the failure of some cells of the heart (Tarone,Sbroggiò, & Brancaccio, 2013).
McMurray,J. J., Adamopoulos, S., Anker, S. D., Auricchio, A., Böhm, M.,Dickstein, K., … & Jaarsma, T. (2012). ESC Guidelines for thediagnosis and treatment of acute and chronic heart failure2012. Europeanjournal of heart failure, 14(8),803-869.
Roger,V. L., Go, A. S., Lloyd-Jones, D. M., Adams, R. J., Berry, J. D.,Brown, T. M., … & Fox, C. S. (2011). Heart disease and strokestatistics—2011 update a report from the American HeartAssociation. Circulation,123(4),e18-e209.
Tarone,G., Sbroggiò, M., & Brancaccio, M. (2013). Key role of ERK1/2molecular scaffolds in heart pathology. Cellularand molecular life sciences,70(21),4047-4054.