Cardiomyopathy of Overload. Part 2
The systemic responses to impaired cardiac performance that generally predominate in this condition include salt and water retention, vasoconstriction, and sympathetic stimulation.
These responses probably represent the long-term effects of adaptive mechanisms, which by augmenting preload, maintaining blood pressure, and increasing the heart rate compensate for short-term reductions in cardiac output. When sustained in heart failure, however, these responses become deleterious.
Because these compensatory responses to low cardiac output lead to the most prominent symptoms of heart failure, until recently the major goal of therapy for this condition has been to rid the body of excess salt and water and to correct vasomotor abnormalities in the peripheral circulation. The use of diuretics to manage salt and water retention and vasodilators to overcome inappropriate vasoconstriction, however, fails to address directly the primary cardiac abnormalities in these patients. The cardiac glycosides have been the traditional agents used for inotropic therapy. Although Osler recognized almost a century ago that “degeneration and weakening” of the overloaded heart contribute to the clinical deterioration in congestive heart failure, only recently have clinical strategies for the care of these patients begun to address important and progressive abnormalities in the structure and function of the cells of the failing heart.
What Is Heart Failure?
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Since this article focuses on the state of the failing myocardium, rather than on alterations elsewhere in the body that result from impaired cardiac performance, heart failure is defined in terms of myocardial abnormalities. Thus, no effort is made to define this condition in terms of the clinical syndromes of heart failure, which — as already pointed out — are dominated by the circulatory consequences rather than the myocardial causes of the condition.
MacKenzie’s definition of heart failure as “exhaustion of the reserve force of the heart muscle” highlights the importance of myocardial abnormalities in patients with this condition. Of course, MacKenzie’s “reserve force” and the mechanism by which it might be “exhausted” in the failing heart could not be understood in terms of the knowledge of cardiac muscle that existed at the beginning of the century. It was not until the late 1960s, when myocardial contractility came to be appreciated as a manifestation of complex biochemical and biophysical processes in the myocardium, that our modern understanding of the pathophysiology of heart failure in terms of disordered myocardial-cell function became possible.