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Cardiac rehabilitation in patients with heart failure

Author
Ileana L Piña, MD, MPH
Section Editor
Stephen S Gottlieb, MD
Deputy Editor
Susan B Yeon, MD, JD, FACC

INTRODUCTION

Patients with heart failure (HF) often have limited exercise capacity because of dyspnea and fatigue [1]. Symptoms of exercise-induced dyspnea resemble those of deconditioning-related dyspnea and these symptoms make patients fearful of being active and may interpret deconditioning as worsening of their disease. (See "Skeletal muscle dysfunction and exercise intolerance in heart failure".) Exercise training improves functional capacity and quality of life in patients with HF.

This topic will discuss cardiac rehabilitation, including exercise training in patients with HF. Measurement of peak oxygen uptake to assess exercise capacity and prognosis in HF and cardiac rehabilitation programs are discussed separately. (See "Exercise capacity and VO2 in heart failure" and "Cardiac rehabilitation programs".)

RATIONALE

Although exercise training of heart failure (HF) patients was previously discouraged due to concerns of worsening symptoms and detriment to the disease process itself, evidence supports a role for exercise training in this population as a means of reversing cardiac and skeletal muscle abnormalities, and improving functional status, quality of life, and clinical outcomes [2].

It was previously thought that exercise limitation in patient with HF was due entirely to cardiac dysfunction. However, drugs that improve cardiac output may not acutely improve exercise tolerance [3-6]. Thus, factors in addition to the low cardiac output and reduced skeletal muscle blood flow contribute to poor exercise tolerance and fatigue. (See "Inotropic agents in heart failure with reduced ejection fraction" and "ACE inhibitors in heart failure with reduced ejection fraction: Therapeutic use".)

Observations since the 1980s have documented improvements in exercise function for patients with HF with a low rate of complications. These observations were followed by a series of studies that demonstrated that significant biochemical and functional abnormalities in skeletal muscle are present in patients with HF and play a large role in the exercise intolerance [1]. Inactivity is in part responsible, leading to muscle atrophy. In addition, skeletal muscle utilizes high-energy phosphates in an inefficient manner; as a result, lactic acid accumulates at a more rapid rate than in normal controls, contributing to muscle fatigue and limited exercise capacity. Skeletal muscle dysfunction can also involve the respiratory muscles, which may contribute to fatigue and dyspnea on exertion [7]. These biochemical and functional abnormalities, when added to deconditioning, can result in even greater impact on physical function. The importance of skeletal muscle dysfunction provides part of the rationale for the use of cardiac rehabilitation in patients with HF.

                          

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Literature review current through: Nov 2016. | This topic last updated: Mon Feb 08 00:00:00 GMT+00:00 2016.
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