Cardiac Rehabilitation in Decompensated Heart Failure

Heart failure is a progressive clinical syndrome in which the heart is unable to maintain adequate cardiac output to meet the body's metabolic demands. Decompensated heart failure represents an acute or subacute deterioration requiring hospitalization and is associated with significant morbidity, prolonged hospital stays, and high readmission rates. Beyond the primary cardiac impairment, patients with decompensated heart failure commonly develop secondary systemic consequences, including respiratory muscle dysfunction and peripheral skeletal muscle abnormalities, both of which contribute independently to exercise intolerance, symptom burden, and poor functional outcomes.

Inspiratory muscle weakness has been identified in approximately 30-50% of patients with heart failure and is believed to result from a combination of diaphragmatic underperfusion, chronic hyperventilation, and systemic inflammatory and catabolic processes. This weakness leads to increased work of breathing, ventilatory inefficiency, and heightened perception of dyspnea, creating a vicious cycle that further limits physical activity and accelerates functional decline. Inspiratory muscle training (IMT) targets this mechanism by applying progressive resistive loading to the inspiratory muscles, promoting improvements in diaphragmatic strength, ventilatory efficiency, and autonomic modulation. Several studies have demonstrated favorable effects of IMT on inspiratory muscle performance, exercise capacity, and quality of life in stable heart failure populations; however, evidence regarding its application during the acute decompensated phase remains limited.

Peripheral skeletal muscle dysfunction in heart failure is characterized by a shift from type I oxidative to type II glycolytic muscle fibers, reduced mitochondrial density, impaired oxygen utilization, and muscle atrophy driven by disuse, neurohormonal activation, and systemic inflammation. These changes are particularly pronounced during periods of decompensation and prolonged bed rest. Functional electrical stimulation (FES) offers a passive approach to muscle activation that bypasses the cardiovascular demand of voluntary exercise, making it a potentially suitable intervention for hemodynamically unstable or severely deconditioned patients. FES-induced muscle contractions have been shown to improve local blood flow, enhance oxidative enzyme activity, and promote favorable fiber-type remodeling in heart failure populations.

Despite the established individual benefits of IMT and FES, no study to date has investigated the combined application of these two modalities in patients hospitalized with decompensated heart failure. The physiological rationale for combining them is based on the concept of addressing both central (respiratory muscle) and peripheral (skeletal muscle) components of exercise intolerance simultaneously, which may produce additive or synergistic improvements in functional capacity and clinical outcomes compared to either intervention alone.

This study hypothesizes that the addition of combined IMT and FES to routine medical treatment will result in greater improvements in cardiac function, inspiratory muscle strength, and functional capacity compared to IMT alone or medical treatment alone in patients with decompensated heart failure. The findings may contribute to the development of early, comprehensive cardiac rehabilitation strategies for this high-risk population.

• Dyspnea Severity [Time frame: Baseline and 4 weeks]
• Quality of Life (Minnesota Living with Heart Failure Questionnaire Score) [Time frame: Baseline and 4 weeks]
• Functional capacity (6-minute walk test) [Time frame: Baseline and 4 weeks]
• Heart Rate [Time frame: Baseline and 4 weeks]
• Hand Grip Strength [Time frame: Baseline and 4 weeks]
• Maximum Expiratory Pressure [Time frame: Baseline and 4 weeks]
• Length of Hospital Stay [Time frame: During the hospitalization period (Up to 7 days)]
• Estimated peak oxygen uptake (VO₂max) [Time frame: Baseline and 4 weeks]
• Oxygen Saturation (SpO₂) [Time frame: Baseline and 4 weeks]