Heart failure (HF) is a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood. The cardinal manifestations are dyspnea, fatigue and fluid retention.
The clinical syndrome of HF may result from disorders of the pericardium, myocardium, endocardium, or great vessels, but coronary artery disease, hypertension, and dilated cardiomyopathy are the main causes of HF in the Western world.
The majority of patients with HF have symptoms due to an impairment of LV myocardial function. Heart failure may be associated with a wide spectrum of LV functional abnormalities, which may range from patients with normal LV size and preserved EF (diastolic dysfunction) to those with severe dilatation and/or markedly reduced EF (systolic dysfunction).
There is no single diagnostic test for HF because it is largely a clinical diagnosis based on a careful history and physical examination. The most useful elements from the history and physical examination are a past history of heart failure (LR + 5.8), paroxysmal nocturnal dyspnea (LR + 2.6), presence of a third heart sound (LR + 11), presence of abdominojugular reflux (LR + 6.4) and presence of jugular venous distention (LR + 5.1).[1]
This update will not focus on standard HF therapies like ACE inhibitors, ARBs, diuretics and beta-blockers but instead will focus on newer agents and the role of brain natriuretic peptide (BNP) measurement in the diagnosis and management of HF. For more detailed information readers are referred to the ACC/AHA 2005 updated HF guidelines.[2]
|
