Changes

== Compensatory Mechanisms  ==

== Compensatory Mechanisms  ==

==== Sympathetic Nervous System  ====

==== 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.

=== [[Cardiac Hypertrophy|Myocardial hypertrophy]]  ===

=== [[Cardiac Hypertrophy|Myocardial hypertrophy]]  ===

Although initially compensatory, increased myocardial mass associated with hypertrophy eventually leads to an increase in myocardial oxygen demand. The increase in oxygen demand outstrips the ability of the coronary circulation to provide sufficient oxygen, which results in myocardial ischaemia. This can result in damage to the myocardium (myocardial necrosis) with replacement by scar tissue (fibrosis), further compromising cardiac function.

Although initially compensatory, increased myocardial mass associated with hypertrophy eventually leads to an increase in myocardial oxygen demand. The increase in oxygen demand outstrips the ability of the coronary circulation to provide sufficient oxygen, which results in myocardial ischaemia. This can result in damage to the myocardium (myocardial necrosis) with replacement by scar tissue (fibrosis), further compromising cardiac function.

== Classification  ==

== Classification  ==