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Heart Failure - Pathophysiology (view source)
Revision as of 09:49, 30 June 2016
, 09:49, 30 June 2016→Compensatory Mechanisms
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.
===Natriuretic Peptides===
Natriuretic peptides include atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). The main site of manufacture, storage and release is the myocardium. Under normal circumstances, ANP and BNP are both manufactured by the atrial myocardium. In heart disease, BNP is manufactured predominantly in the ventricular myocardium. Both are released in response to increased chamber wall stress. These hormones counter regulate many of the above mechanisms, causing vasorelaxation and increased sodium loss. However, in congestive heart failure this counter regulatory system is overwhelmed by other vasoconstrictive and sodium retaining mechanisms.
Natriuretic peptides are useful biomarkers of cardiac disease, as levels are elevated in patients with clinically significant disease.
===Antidiuretic Hormone (ADH)===
===Antidiuretic Hormone (ADH)===