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Heart Failure - Pathophysiology (view source)
Revision as of 09:03, 30 June 2016
, 09:03, 30 June 2016→Sympathetic Nervous System
In heart disease, there is simultaneous activation of the sympathetic nervous system and withdrawal of parasympathetic influence. A decrease in systemic blood pressure is detected by baroreceptors (pressure receptors) and mechanoreceptors (stretch receptors) in the carotid sinus, aortic arch and atrial walls. Activation of these receptors causes an increase in sympathetic activity (and noradrenaline production) and a reduction in parasympathetic activity. Elevated sympathetic nervous system activity results in tachycardia, increased contractility, peripheral vasoconstriction and activation of the [[Renin Angiotensin Aldosterone System|renin-angiotensin-aldosterone system (RAAS)]].
In heart disease, there is simultaneous activation of the sympathetic nervous system and withdrawal of parasympathetic influence. A decrease in systemic blood pressure is detected by baroreceptors (pressure receptors) and mechanoreceptors (stretch receptors) in the carotid sinus, aortic arch and atrial walls. Activation of these receptors causes an increase in sympathetic activity (and noradrenaline production) and a reduction in parasympathetic activity. Elevated sympathetic nervous system activity results in tachycardia, increased contractility, peripheral vasoconstriction and activation of the [[Renin Angiotensin Aldosterone System|renin-angiotensin-aldosterone system (RAAS)]].
These effects are initially beneficial, as they act to increase cardiac output and systemic blood pressure. However, over time chronic activation of the sympathetic nervous system becomes detrimental. Noradrenaline stores become depleted, cardiac beta adrenergic receptors become downregulated and uncoupled and myocyte loss results from ischaemia and necrosis.
=== [[Cardiac Hypertrophy|Myocardial hypertrophy]] ===
=== [[Cardiac Hypertrophy|Myocardial hypertrophy]] ===