Coupling between the heart and arterial system in heart failure

Article Abstract:

Unlike a heart attack, which typically occurs as an acute crisis when an important coronary artery becomes blocked, heart failure is a chronic condition in which the heart muscle is simply unable to perform the workload imposed upon it. While the events leading to a heart attack itself may be complex, the actual attack results in the deprivation in part of the heart muscle of proper blood flow. The understanding of heart failure is more difficult, and involves complex interactions of the entire circulatory system, including the heart muscle, the blood vessels, and the kidneys. In a detailed article, the authors discuss the relationship between the workload of the heart and the function of the arterial system. In a properly functioning system, the arteries and the heart interact to produce optimal performance. To define a properly functioning system in mathematical terms, equations were constructed using many physiological parameters such as elastance, the change in pressure in some elastic container for some unit change in volume. Both the system of arteries and the heart itself may be considered elastic containers. It has been found that in healthy individuals the elastance of the heart is twice as large as the elastance of the arterial system. This permits the heart to pump blood with a volume per individual stroke that is best for maximum efficiency. Normal individuals have a ventricular ejection fraction of more than 60 percent, meaning that with each stroke more than 60 percent of the blood is pumped out of the heart's ventricles. Patients with an ejection fraction of 40 to 59 percent are impaired, but do not have heart failure; these individuals have an elastance of the heart that is about the same as the elastance of the arterial system. This means that the heart muscle can still maximize the work done pumping the blood on each stroke, but at the cost of greater inefficiency of the muscle. Patients with an ejection fraction of less than 40 percent have heart failure. In these patients, the elastance of the heart is less than half the elastance of the arteries. In such a case, not only is the heart working inefficiently, it is also no longer possible for the heart to develop maximum potential in the pump stroke. (Consumer Summary produced by Reliance Medical Information, Inc.)

Heart muscle, Myocardium

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Peripheral adaptations in congestive heart failure: a review

Article Abstract:

The basic physiological principles of heart failure are straightforward. The heart cannot pump enough blood to supply the organs of the body with oxygen, and the vessels of the lungs are congested with blood limiting flow through the lungs. The physiological details of heart failure are significantly more complex, however. Patients with congestive heart failure have low tolerance for exercise, but experiments have shown that it is not possible to correlate the exercise tolerance of any individual patient with various indicators of heart performance. In cases where the patient has received a heart transplant, the presence of a healthy new heart does not immediately improve exercise tolerance. Heart transplant patients improve their tolerance for exercise only slowly over time. These observations suggest that heart failure actually involves more than just the heart. Heart failure develops slowly, and physiological changes also involve the peripheral blood vessels and the skeletal muscle. Peripheral blood vessels lose their ability to dilate as blood flow increases. Patients with heart failure have increased amounts of noradrenaline in their blood, but drugs that inhibit the synthesis of noradrenaline do nothing to relax the abnormal constriction of arteries. It seems that an important regulator of blood vessel constriction in healthy individuals is less significant for heart failure patients. The muscle itself seems to be changed in heart failure, and much of this change may result from chronic inactivity. Even when drugs can strengthen the heart and improve blood flow, the performance of the muscles does not immediately improve. Experiments have suggested that the flow of blood within the muscle itself is altered, which does not permit adequate oxygen supply to the muscle fibers that need it most. The circulatory system involves a great many different factors that must respond to changing conditions. In cases of heart failure, even when the heart is aided by drugs or a heart transplant is performed, the rest of the circulatory system may take weeks or months to readapt and to provide healthy responses to the demands of exercise. (Consumer Summary produced by Reliance Medical Information, Inc.)

Peripheral circulation

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Circulatory abnormalities and compensatory mechanisms in heart failure

Article Abstract:

The heart and the circulatory system are more than merely a pump and a system of tubes to carry blood. Both the heart and the blood vessels adapt to the changing needs of the body. For example, when a person exercises, the majority of the blood flow is directed to the muscles, and the blood flow to the kidney is reduced. The constriction of the kidney blood vessels, however, keeps the blood pressure in the kidney constant, despite decreased flow. The complexities of compensation of blood flow contribute to the difficulties in understanding the physiological details of heart failure. In heart failure, the heart can no longer keep up with the workload imposed on it, but it is not a failure of the heart alone. Heart failure is the failure of the entire system of circulation to compensate for changing demands of the body. In a person with moderate heart failure, the heart may be able to keep up with demands while at rest, but the cardiovascular system may fail to adequately compensate for the changes required by exercise. As a result, the patient becomes breathless and tired very quickly. Much research on patients with moderate heart failure have focused on the heart itself. The constant increased stress on the heart produces many effects; one of the most readily noticeable is the increase in size of the muscular ventricles of the heart. The heart muscle loses some of its ability to contract, but new research has indicated that this is not a direct consequence of the enlargement, but is related to biochemical changes that occur in the heart muscle cells themselves. Less is known about how the circulatory system changes in heart failure. The ability to respond to changes in the demands made on the muscles may result from an increase of stiffness in the blood vessels of the muscle, but the precise cause remains uncertain. The net result is that when a patient with heart failure exercises, the blood vessels of the muscles do not dilate, while the blood vessels of many internal organs do constrict. The total output of the heart does not rise normally, and the proportional increase of blood flow to the muscles fails to occur. (Consumer Summary produced by Reliance Medical Information, Inc.)

Causes of

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