Annotations
Of cardiac output and congestive heart failure
It is generally accepted and taught that the clinical and pathophysiologic manifestations of congestive heart failure (CHF) are due to low cardiac output (C.O.) and that these manifestations disappear when cardiac output is increased. This may be so, but a reduction in C.O. cannot be the sole factor. To rationalize the concept t h a t low cardiac output is responsible for the clinical manifestations of CHF in instances when the cardiac output actually is high, the terms "high" and "low" cardiac output types of CHF were introduced. Yet, it is well known that the C.O. of normal man can be either extremely high or low, but CHF is absent. Compare the C.O. of normal man running 100 meters with that at 3:00 A.M. when he is in a deep sleep. Furthermore, when the manifestations of CHF are present, these manifestations are similar regardless of the magnitude of C.O. at rest. Exercise in a patient with CHF may increase cardiac output, but the CHF worsens; it does not improve. This situation is again rationalized by stating that, even though the C.O. increased, the increased needs for blood produced by the exercise exceeded the C.O. so that the state of CHF worsened. Again, this may be so, but is it? Furthermore, a patient with CHF placed in a hot and humid environment has an increase in C.O. even at rest, yet his state of CHF worsens.1 2 The metabolic needs for blood are not increased to the degree of the increase in circulatory
American Heart Journal
dynamics. In spite of the increase in C.O. produced by the hot and humid environment, the pathophysiologic state of CHF is extremely worsened. It does not improve. There is no doubt that the clinical state of chronic CHF originates in the heart, but the mechanisms of the pathophysiology remain to be explained, and the role of cardiac output itself, alone, needs careful consideration and analysis. The role of the central and autonomic nervous systems in CHF needs investigation. Finally, even though the mechanism of the pathophysiology of the clinical state of CHF is not well understood, when therapy is properly and elegantly instituted and compliance is religiously obtained, the therapeutic response is astonishingly favorable.
G. E. Burch, M.D. Tulane University School of Medicine and Charity Hospital New Orleans, La. REFERENCES
1. Burch, G. E.: Influence of a hot and humid environment on the patient with coronary heart disease, J. Chronic Dis. 4:350, 1956. 2. Burch, G. E., and Miller, G. C.: The effects of warm, humid environment on patients with congestive heart failure, South. Med. J. 62:816, 1969.
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Of cardiac output and congestive heart failure
It is generally accepted and taught that the clinical and pathophysiologic manifestations of congestive heart failure (CHF) are due to low cardiac output (C.O.) and that these manifestations disappear when cardiac output is increased. This may be so, but a reduction in C.O. cannot be the sole factor. To rationalize the concept t h a t low cardiac output is responsible for the clinical manifestations of CHF in instances when the cardiac output actually is high, the terms "high" and "low" cardiac output types of CHF were introduced. Yet, it is well known that the C.O. of normal man can be either extremely high or low, but CHF is absent. Compare the C.O. of normal man running 100 meters with that at 3:00 A.M. when he is in a deep sleep. Furthermore, when the manifestations of CHF are present, these manifestations are similar regardless of the magnitude of C.O. at rest. Exercise in a patient with CHF may increase cardiac output, but the CHF worsens; it does not improve. This situation is again rationalized by stating that, even though the C.O. increased, the increased needs for blood produced by the exercise exceeded the C.O. so that the state of CHF worsened. Again, this may be so, but is it? Furthermore, a patient with CHF placed in a hot and humid environment has an increase in C.O. even at rest, yet his state of CHF worsens.1 2 The metabolic needs for blood are not increased to the degree of the increase in circulatory
American Heart Journal
dynamics. In spite of the increase in C.O. produced by the hot and humid environment, the pathophysiologic state of CHF is extremely worsened. It does not improve. There is no doubt that the clinical state of chronic CHF originates in the heart, but the mechanisms of the pathophysiology remain to be explained, and the role of cardiac output itself, alone, needs careful consideration and analysis. The role of the central and autonomic nervous systems in CHF needs investigation. Finally, even though the mechanism of the pathophysiology of the clinical state of CHF is not well understood, when therapy is properly and elegantly instituted and compliance is religiously obtained, the therapeutic response is astonishingly favorable.
G. E. Burch, M.D. Tulane University School of Medicine and Charity Hospital New Orleans, La. REFERENCES
1. Burch, G. E.: Influence of a hot and humid environment on the patient with coronary heart disease, J. Chronic Dis. 4:350, 1956. 2. Burch, G. E., and Miller, G. C.: The effects of warm, humid environment on patients with congestive heart failure, South. Med. J. 62:816, 1969.
673
