To define heart failure in terms of systolic/diastolic function and severity.
To describe the pathological impact of heart failure on the systemic and pulmonary circulations.
To explain the issues with the compensatory mechanisms that are initiated to deal with low cardiac output and predict how these may worsen the underlying issue in heart failure.
the Raas system may be implemente dto increase BP to help increase venous return which can cause systemic hypertension, leading to more turbulence, a higher reynauld number causing increased risk of damage to vessel walls causing atherosclerosis or thrombosis to form potentially leading to myocardial infarcts due to vessel clogging or embolisms from distil areas to travel to the lung (PE) causing Death.
frank starlings mechanism is also used as a compensatory mechanism, it involves increasing venous return which causes an increase in preload which stretches myocin actin sarcomeres resulting in more recruitment and harder contraction allowing more blood to be expelled to systemic circulation per heart beat. however if this mechanism can be pathological if the myosin actin crossbridges are stretched too much causing them to uncouple from each other and rendering no contraction able to occur in that area of tissue, causing even greater heart failure.