[Heart rate variability. Applications in psychiatry].

  • Servant D
  • Logier R
  • Mouster Y
 et al. 
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BACKGROUND: The autonomic nervous system sends messages through the sympathetic and parasympathetic nervous system. The sympathetic nervous system innervates the cardioaccelerating center of the heart, the lungs (increased ventilatory rhythm and dilatation of the bronchi) and the non-striated muscles (artery contraction). It releases adrenaline and noradrenaline. As opposed to the sympathetic nervous system, it innervates the cardiomoderator center of the heart, the lungs (slower ventilatory rhythm and contraction of the bronchi) and the non-striated muscles (artery dilatation). It uses acetylcholine (ACh) as its neurotransmitter. Sympathetic and parasympathetic divisions function antagonistically to preserve a dynamic modulation of vital functions. These systems act on the heart respectively through the stellar ganglion and the vagus nerve. The interaction of these messages towards the sinoauricular node is responsible for normal cardiac variability, which can be measured by monitoring heart rate variability (HRV). Heart rate is primarily controlled by vagal activity. Sensorial data coming from the heart are fed back to the central nervous system. HRV is an indicator of both how the central nervous system regulates the autonomic nervous system, and of how peripheral neurons feed information back to the central level. HRV measures are derived by estimating the variation among a set of temporally ordered interbeat intervals. The state of perfect symmetry, which, in medical parlance, is called respiratory sinus arrhythmia (RSA), can be described as a state of cardiac coherence. Obtaining a series of interbeat intervals requires a continuous measure of heart rate, typically electrocardiography (ECG). Commercially available software is then used to define the interbeat intervals within an ECG recording.

LITERATURE FINDINGS: The autonomic nervous system is highly adaptable and allows the organism to maintain its balance when experiencing strain or stress. Conversely, a lack of flexibility and a rigid system can lead to somatic and psychological pathologies. Several studies have shown a link between reduced HRV in postmyocardial infarction patients and increased risk for adverse cardiovascular events, including ventricular arrhythmias and sudden death. Recently, studies indicate that patients with depression and anxiety disorders exhibit abnormally low HRV compared with non-psychiatric controls. Reduced HRV seems indicate decreased cardiac vagal tone and elevated sympathetic activity in anxious and depressive patients and would reflect deficit in flexibility of emotional physiological mechanisms. A few studies have also revealed that biofeedback using respiratory control, relaxation and meditation techniques can increase HRV. For now, there is insufficient data to determine if paced respiration or subjective relaxation is necessary or sufficient for the efficacy of HRV biofeedback. Although the literature is modest, this review suggests that the use of biofeedback with relaxation and meditation approaches may result in increased HRV and parasympathetic activity. Limitations of the review literature have also been considered to identify areas for future research.

Author-supplied keywords

  • Anxiety Disorders
  • Anxiety Disorders: physiopathology
  • Arousal
  • Arousal: physiology
  • Autonomic Nervous System
  • Autonomic Nervous System: physiopathology
  • Biofeedback, Psychology
  • Biofeedback, Psychology: physiology
  • Death, Sudden, Cardiac
  • Depressive Disorder
  • Depressive Disorder: physiopathology
  • Heart
  • Heart Rate
  • Heart Rate: physiology
  • Heart: innervation
  • Homeostasis
  • Homeostasis: physiology
  • Humans
  • Meditation
  • Myocardial Infarction
  • Myocardial Infarction: physiopathology
  • Risk Factors
  • Stellate Ganglion
  • Stellate Ganglion: physiopathology
  • Vagus Nerve
  • Vagus Nerve: physiopathology

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  • D Servant

  • R Logier

  • Y Mouster

  • M Goudemand

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