In chronic heart failure, shortness of breath is driven by respiratory and metabolic factors in skeletal muscle rather than central hemodynamics alone, suggesting therapies must target these peripheral factors to improve symptoms.
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Peripheral factors merit targeted symptom trials in chronic HF; hypothesis-generating and requires prospective validation before practice change.
Severe shortness of breath is a prominent symptom in acute heart failure (pulmonary oedema) and is related to left atrial pressure. A reduction of this pressure almost always leads to an improvement in symptoms. Patients with chronic heart failure complain of both shortness of breath and tiredness even when fluid overload has been corrected by the appropriate use of diuretics. Shortness of breath under these circumstances is not related simply to central haemodynamics but is determined more by the interaction of changes in respiratory pattern and the metabolic consequences of reduced perfusion of exercising skeletal muscle. An important clinical consequence is that when such patients are optimally treated with diuretics, further improvement of symptoms would not be expected from drugs which merely alter central haemodynamics without influencing other factors such as skeletal muscle blood flow on exercise, or lung perfusion.
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P. A. Poole‐Wilson (1988) studied this question.
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