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Heart Failure - Pathophysiology (view source)

Revision as of 08:59, 30 June 2016

132 bytes added ,  08:59, 30 June 2016
→‎Compensatory Mechanisms
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==== Sympathetic Nervous System  ====
 
==== Sympathetic Nervous System  ====
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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)]].
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Decreased blood pressure stimulates release of noradrenaline. Increase heart rate and contractility by the effect on beta-receptors. Peripheral vasoconstriction is activated by its action on alpha-receptors. Sinus arrhythmias are abolished. Increased heart rate and rhythm imposed by the sympathetic nervous system increases the heart's oxygen consumption. As diastole is shortened the time available for blood to enter the coronary circulation is also shortened, decreasing blood flow to the myocardium. Resulting myocardial hypoxia may cause arrhythmias.
      
=== [[Cardiac Hypertrophy|Myocardial hypertrophy]]  ===
 
=== [[Cardiac Hypertrophy|Myocardial hypertrophy]]  ===
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