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Pathophysiologic Model

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Cardiovascular function results from the interplay of the heart, systemic vasculature, blood volume, and tissues in their functions as pump, transporting pathways, and oxygen carrying and consuming end-organs, and problems with structure or function of the filling and ejection mechanisms of the heart will lead to failing oxygen delivery and compensatory attempts, a complex disease condition known as heart failure (Porth, 2015). Dysfunction may involve initially primarily one ventricle only, though over time both sides may become affected. In left ventricular failure decreased cardiac output and outflow into the periphery leads to pulmonary congestion, evidenced by pulmonary edema and impaired gas exchange (Porth, 2015). As a result,…show more content…
Firstly, the hemodynamics model centers around the heart as a pumping organ, utilizing changes in heart rate and stroke volume or both, as explained by Frank and Starling, to respond and adapt to changes in pressure or volume exerted on it, with pathological ventricular remodeling as the compensatory outcome of long-term increases in preload and excessive pressure (Johnson, 2014). Heart rate is up- and down-regulated by the sympathetic, respectively parasympathetic nervous system, and stroke volume is controlled by preload, the blood volume in the ventricles right before systole, by afterload, the ejection force determined from systemic vascular resistance and ventricular wall tension, and by the contractile ability of the heart muscle (Porth, 2015). The contractility of the actin and myosin filaments is dependent on adenosine triphosphate (ATP) as energy source and on intracellular calcium release, and the diffusion of extracellular calcium ions across L-type calcium channels mediated through beta-adrenergic receptors to signal the chemical reaction leading to muscle shortening, as well as the removal of calcium through cell-membrane pumps to avoid signal overload (Porth, 2015). Pressure and volume overload will lead to ventricular hypertrophy, myocardial stiffness, restricted stroke volume, ventricular dilation and further…show more content…
Baroreceptors activate the sympathetic nervous system, with an increase in heart rate and blood pressure and vasoconstriction, causing beta receptor downregulation, and further increased adrenergic tone with pathological activation of the renin-angiotensin-aldosterone-system (Johnson, 2014). Angiotensin II releases catecholamine and stimulates renin release, which raises tone and pressure on the heart, and leads to aldosterone secretion, also increasing the pressure load on the heart; water and sodium retention through the presence of vasopressin and aldosterone add to preload (Johnson, 2014). This model is used to explain the compensatory mechanisms employed to maintain cardiac reserve, the ability of the heart to respond to increased needs; additional neurohormonal changes involve natriuretic peptides, atrial natriuretic peptide, brain natriuretic peptide and endothelin 1 (Johnson, 2014; Porth,
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