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Heart failure in dogs
By Mark D. Kittleson, DVM, PhD, DACVIM (Cardiology), Professor Emeritus, School of Veterinary Medicine, University of California, Davis

Heart failure is a clinical syndrome that occurs secondary to severe, overwhelming cardiac disease. It occurs because the heart is no longer able to maintain normal venous/capillary pressures, cardiac output, and/or systemic blood pressure. It is most commonly caused by a chronic disease that results in a severe decrease in myocardial contractility, severe regurgitation or shunting, or severe diastolic dysfunction. However, it is common to have all three abnormalities present simultaneously (but with one predominating). By far, the most common clinical manifestations seen with heart failure are directly due to edema and effusion (congestive or backward heart failure). Much less commonly, animals present because of signs referable to a decrease in cardiac output (forward heart failure). Very rarely, they present in cardiogenic shock (low blood pressure due to decreased cardiac output). This occurs because the cardiovascular system operates under a system of priorities. Its three primary functions are to maintain a normal blood pressure and normal cardiac output, both at a normal venous/capillary pressure. When the system is overwhelmed, it allows venous/capillary pressure to increase first (and so allows edema or effusion to form) and then allows cardiac output to fall. Only after cardiac output has fallen remarkably does cardiogenic shock occur. In acute heart failure, before any compensation has occurred, cardiogenic shock may predominate, but even in this situation, acute chordal rupture is the most common cause of acute heart failure in animals and results in an increased left atrial pressure and thus pulmonary edema.

Initial changes in cardiac chamber dimension (volume) or wall thickness that occur are best understood in relation to preload (the tension imposed by venous return on the ventricular walls at end-diastole) and afterload (the tension imposed on the ventricular walls at end-systole). Alterations in preload or afterload may be caused by structural cardiac abnormalities, systemic compensatory mechanisms, or both. Volume overload states, such as those that occur with chronic valvular disease/valvular insufficiencies, patent ductus arteriosus, atrial or ventricular septal defects, peripheral left-to-right shunts, anemia, or hyperthyroidism, cause an increase in preload that leads to ventricular growth and chamber enlargement (euphemistically called dilation) via eccentric myocyte hypertrophy. Pressure overload states, such as those that occur with pulmonary or systemic hypertension, and pulmonic or aortic stenosis, cause an increase in afterload (systolic intraventricular pressure) that leads to ventricular wall thickening via concentric hypertrophy. Neither volume nor pressure overload is synonymous with heart failure; either state may result in heart failure, depending on the severity of the overload and the degree of compensation.

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