IMED3001 Study Guide - Final Guide: Hemodynamics, Heart Failure, Nuclear Dna
15 Dec 2020
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Atherosclerotic plaques, valvular stenosis, systemic hypertension, or aortic coarctation. Addition of volume workload to chambers, eg: lv in ar; la and lv in. Diversion of blood from one part of the heart to the other through congenital or acquired defects. Conduction defects or arrhythmias eg: af or vf. Rupture of the heart or a major vessel. Aetiology: pressure or volume overload or trophic signals. Nuclear enlargement (squared off appearance) and increased mitochondria. Synthesis of abnormal protein and additional nuclear dna. Molecular changes: expression of immediate early genes, shift to a gene expression pattern resembling that in foetal cardiac development. Failure of pump, end stage of chronic heart disease, acute haemodynamic stresses etc. Frank starling mechanism, myocardial adaptations, activation of neurohumoral systems. Ischaemic heart disease (ihd), hypertensive heart disease (hhd), Congestion of pulmonary circulation, stasis of blood in left sided chambers and hypoperfusion .
