Left side heart failure
Increased MABP = increased aortic pressure, which means that the LVP must increase to overcome the increased aortic pressure so that valve will open
increased LVP caused by stronger force of contraction, will lead to LV hypertrophy and dilatation.
Eventually the hypertrophy becomes too severe that it distorts the normal myocyte, less beta-1 receptors = less sympathetic response
starling's law = length tension relationship, increased length too much, decreased ability to produce active tension
laplace's law: T=Pxr, increased R, has to increase T to get the same P, meaning need increased myocardial O2 demand
Heart starts pumping less effectively, starts to pool, will go into atria (increased LAP), and then into pulmonary circulation, causing pulmonary congestion and oedema.
increased pulmonary capillary hydrostatic pressure, shifts starling's equilibrium so that fluid shift into interstitum
decreased lung compliance, harder to expand => get dyspnoea
worse at night PND due to affect all parts of lung
crepitation at base of lung
frothy pink sputum