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Heart Failure - Pathophysiology (view source)
Revision as of 09:39, 30 June 2016
, 09:39, 30 June 2016→Compensatory Mechanisms
== Compensatory Mechanisms ==
== Compensatory Mechanisms ==
=== Sympathetic Nervous System ===
In heart disease, there is simultaneous a shift of autonomic balance from one of parasympathetic dominance to one of sympathetic dominance. 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. A drop in signals from these receptors in response to perceived hypoperfusion leads to an increase in sympathetic activity (and noradrenaline production) and a reduction in parasympathetic activity. Increased adrenergic activity is mediated via cardiac beta and vascular alpha effects. 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 a shift of autonomic balance from one of parasympathetic dominance to one of sympathetic dominance. 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. A drop in signals from these receptors in response to perceived hypoperfusion leads to an increase in sympathetic activity (and noradrenaline production) and a reduction in parasympathetic activity. Increased adrenergic activity is mediated via cardiac beta and vascular alpha effects. 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.
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.
=== [[Renin Angiotensin Aldosterone System|Renin-angiotensin-aldosterone system]] ===
Causes sodium and water retention by the kidney as well as vasoconstriction. Angiotensin is also recognised as a substance that causes modification and growth in cardiac myocytes and fibroblasts, influencing myocardial remodelling and hypertrophy.
Causes sodium and water retention by the kidney as well as vasoconstriction. Angiotensin is also recognised as a substance that causes modification and growth in cardiac myocytes and fibroblasts, influencing myocardial remodelling and hypertrophy.