Effects of Slow-paced Breathing on Heart Rate Variability in Patients With Heart Failure

Physiological Link Between Slow-Paced Breathing and Autonomic Nervous System Regulation

Although conventional breathing exercises (e.g., diaphragmatic breathing and deep breathing) facilitate lung expansion, prevent premature alveolar and airway collapse, and maintain normal respiratory function and adequate gas exchange, these techniques primarily focus on the quantity of breathing and respiratory muscle activity. In contrast, slow-paced breathing (SPB) is a controlled breathing technique that primarily regulates the breathing frequency and maintains a fixed inspiratory-to-expiratory ratio, allowing synchronization with intrinsic cardiovascular oscillations to enhance cardiopulmonary function and autonomic regulation. Slow-paced breathing, also referred to as slow breathing, resonance frequency breathing, or paced breathing, is considered a method that influences autonomic nervous system (ANS) function through modulation of respiratory frequency.

The interaction between respiration and cardiovascular regulation is mediated through the autonomic nervous system, which regulates heart rate, blood pressure, and respiratory patterns. This physiological coupling is known as respiratory sinus arrhythmia (RSA), which is considered one of the primary contributors to HRV. Under normal RSA conditions, heart rate slightly increases during inspiration and decreases during expiration. This phenomenon reflects parasympathetic modulation of cardiac activity and serves as an important physiological indicator of vagal function.

The interaction between respiratory and cardiovascular systems involves three major components: the respiratory network, the cardiovascular network, and their central synaptic interactions. The respiratory network within the central nervous system generates respiratory commands that activate respiratory motor neurons, leading to respiratory muscle activity. During this process, two major types of afferent feedback signals are generated from the lungs: chemical feedback and mechanical feedback. Chemical feedback is mediated through the aortic arch and carotid bodies, which detect changes in oxygen, carbon dioxide, and hydrogen ion concentrations and transmit these signals back to the brain. Mechanical feedback occurs through lung expansion during inspiration, which activates lung stretch receptors; meanwhile, respiratory-induced changes in intrathoracic pressure also generate afferent signals transmitted to the central nervous system.

Meanwhile, the cardiovascular network regulates cardiac activity and vascular smooth muscle function through the autonomic nervous system, resulting in changes in heart rate and vascular resistance. The vascular system determines systolic arterial pressure (SAP) and diastolic arterial pressure (DAP), leading to alterations in blood pressure and arterial blood conditions. Changes in blood pressure stimulate baroreceptors located in the aortic arch and carotid sinus, which subsequently transmit sensory information back to the brain. Ultimately, these signals are integrated within the nucleus tractus solitarius (NTS) in the brainstem, resulting in respiratory-mediated modulation of cardiovascular autonomic control

Inclusion criteria

• Patients diagnosed with heart failure during hospitalization and who are clinically stable.

Exclusion criteria

Respiratory distress at rest with the utilization of accessory neck muscles (neck breathing pattern).

Presence of an implanted cardiac pacemaker. Chronic pulmonary diseases, such as chronic obstructive pulmonary disease (COPD), pulmonary hypertension, pulmonary fibrosis, or exercise-induced asthma.

Current use of mechanical ventilation. Severe aortic stenosis. Aortic dissection. Acute myocarditis, pericarditis, or infective endocarditis. Inability to walk independently due to orthopedic, neurological, or other medical conditions.

Inability to understand the study protocols or cooperate, such as individuals with psychiatric disorders, dementia, or a history of stroke.