Pathophysiology of Congestive Heart Failure
The majority of patients with HF have symptoms resulting from an impairment of left ventricular myocardial function.12011, 6407 This pump dysfunction is associated with either myocardial injury (e.g., myocardial ischemia, cardiomyopathies, myocardial infarction) or hemodynamic overloading, (e.g., hypertension, valvular disorders), or both.
Heart failure may be associated with a wide spectrum of left ventricular functional abnormalities, which may range from normal left ventricular size and preserved ejection fraction, to severe dilatation and markedly reduced ejection fraction. In most patients, abnormalities of systolic and diastolic dysfunction coexist, regardless of ejection fraction. Patients with normal ejection fraction may have a different natural history and may require different treatment strategies than patients with reduced ejection fraction. Left ventricular dysfunction is generally a progressive process, beginning with stress on, or injury to the myocardium. The cardinal manifestation of this progression is cardiac remodeling, where mechanical, neurohormonal, and possibly genetic factors alter ventricular size, shape, and function.12011
Though the associated diseases are clear, the mechanisms responsible for decompensation have remained elusive. Several models have been generated to better understand the cascade of mechanisms involved in HF and the opportunities for intervention.12013 Initially, a cardiorenal model was proposed as the cause. In this model, abnormalities of renal blood flow resulted in excessive salt and water retention; this caused HF by fluid overload. This model held credence for many years, as the clinical signs of HF and peripheral and pulmonary edema were so closely associated with fluid overload. The advent of more accurate hemodynamic monitoring demonstrated to clinicians that HF was associated with both decreased cardiac output and increased peripheral vasoconstriction, findings that did not align with the more simplistic cardiorenal model. These findings led researchers to suggest that HF arose from an inability of the heart muscle to pump efficiently, termed the hemodynamic model for HF. While these 2 models explained some of the clinical symptoms of HF, they failed to explain why HF progressed.6407
Content on this page was last changed on December 16, 2009.
References:| 6407. | Francis GS. Pathophysiology of the heart failure syndrome. In: Topol EJ, ed. Textbook of Cardiovascular Medicine. Philadelphia, PA: Lippincott-Raven; 1998. |
| 12011. | Hunt SA, Abraham WT, Chin MH, et al. 2009 Focused update incorporated into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults. A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines Developed in Collaboration With the International Society for Heart and Lung Transplantation. J Am Coll Cardiol. 2009;53(15):e1-e90. |
| 12013. | Jessup M, Brozena S. Heart failure. N Engl J Med. 2003;348(20):2007-2018. |
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