Vagal tone

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Vagal tone refers to activity of the vagus nerve, an important component of the parasympathetic branch of the autonomic nervous system. This division of the nervous system is not under conscious control and is largely responsible for regulation of the body at rest. Vagal activity results in diverse pleiotropic effects, including: lowered heart rate, changes in vasodilation/constriction, and glandular activity in the heart, lungs, and digestive tract. Because the vagus nerve is importantly involved in heart rate regulation though its action on pacemakers in the heart, vagal tone is easily assessed by heart rate.

In this context, tone specifically refers to the continual nature of baseline parasympathetic action that the vagus nerve exerts. While vagal input is continual, the degree of stimulation it exerts is regulated by a balance of inputs from both divisions of the autonomic nervous system and reflects the general level of parasympathetic activity. Vagal tone is typically considered in the context of heart function, but also has utility in assessing emotional regulation and other processes that alter, or are altered by parasympathetic activity.[1][2]

Vagal innervation of the heart[edit]

Heart rate is controlled largely by the heart's internal pacemaker activity. In normal hearts the main pacemaker is a collection of cells on the border of the atria and vena cava called the sinoatrial node. Heart cells exhibit automaticity, or the ability to generate electrical activity independent of external stimulation. As a result, these cells spontaneously generate electrical activity that is subsequently conducted throughout the heart, resulting in a regular heart rate. This is termed sinoatrial pacemaking.

Without external stimulation sinoartial pacing results in a heart rate of approximately 100 beats per minute. However, branches of the vagus nerve acts on this node and slow its conduction. This is mediated by the neurotransmitter norepinephrine and downstream changes to calcium handling by heart cells.

Respiratory sinus arrhythmia[edit]

Vagal tone is not directly measured, instead it is inferred by measuring processes that the vagus nerve alters - specifically heart rate and heart rate variability. Increased vagal tone (and thus vagal action) is associated with a diminished and more variable heart rate. Vagal tone generally serves as a measure of parasympathetic nervous system activity that promotes "rest and digest".

An ECG showing respiratory sinus arrhythmia

Respiratory sinus arrhythmia (RSA) is typically a benign, naturally occurring variation in heart rate that occurs during the breathing cycle. It is characterized by an increased heart rate during inhalation and a diminished heart rate during exhalation.

During inhalation intra-thoracic pressure lowers due to the downward movement of the diaphragm and the expansion of the chest cavity. Atrial pressure is also lowered as a result of this, enabling more blood to return to the heart. As more blood enters the heart, the vasculature and atria expand, triggering baroreceptors (pressure) which act to suppress vagal tone. Subsequently, heart rate increases.

During exhalation, the diaphragm contracts and decreases the size of the chest cavity, causing a subsequent increase in intra-thoracic pressure. This increased pressure inhibits venous return to the heart and thus less atrial expansion and activation of baroreceptors occurs. As these baroreceptors are no longer acting to suppress vagal tone, heart rate decreases.

These changes in thoracic pressure and subsequent venous return are collectively termed the thoracic pump.

Accompanying changes in the vasculature (pressure, and blood oxygenation) around the heart, including the carotid and pulmonary artery, also exert effects on vagal tone.

Heart rate (HR) (top trace) and tidal volume (Vt) (lung volume, second trace) plotted on the same chart, showing how heart rate increases with inspiration and decreases with expiration.

On an electrocardiogram, RSA is detectable as changes in the P-P interval, or the distance between P waves. This corresponds to the initiation of depolarization of the atria and indicates the beginning of a new electrical cycle in the heart.

Because RSA is the result of breathing, this arrhythmia is not present when breath is held.

Age related changes in RSA[edit]

RSA is pronounced in children, but without sufficient cardiovascular exercise it gradually disappears as a person approaches his/her teenage years. Typically, expression of RSA decreases with age; however, adults in excellent cardiovascular health, such as endurance runners, swimmers, and cyclists, are likely to have a more pronounced RSA. Professional athletes typically maintain very high vagal tone and RSA levels. RSA also becomes less prominent in individuals with diabetes and cardiovascular disease.[3]

Biological findings[edit]

Studies have shown that the efficiency of pulmonary gas exchange is improved by RSA, suggesting that RSA may play an active physiological role. The matched timing of alveolar ventilation and its perfusion with RSA within each respiratory cycle could save energy expenditure by suppressing unnecessary heartbeats during expiration and ineffective ventilation during the ebb of perfusion (delivery of blood from arteries to capillaries for oxygenation and nutrition).[4][5]

RSA or heart rate variability in synchrony with respiration is a biological phenomenon, which may have a positive influence on gas exchange at the level of the lung via efficient ventilation/perfusion matching.[6]

Historically, respiratory sinus arrhythmia was believed to be pathological, and extended bed rest was traditionally prescribed until work by Sir James Mackenzie disproved this idea.[7]

Psychological findings[edit]

Due to age differences in expression of RSA, the majority of vagal tone research as it relates to social behavior and human psychology has focused on children. Typically, researchers are concerned with baseline vagal tone, treating it either as a potential predictor of behavior or examining its relationship with mental health (particularly emotion regulation, MDD, anxiety, and internalizing and externalizing disorders).[8][9]

Research indicates that children with more secure attachments with their mothers exhibited greater empathetic responsiveness, less social inhibition, and higher vagal tone, again highlighting the vagus nerve's regulatory effect on emotional and social function.[2]

References[edit]

  1. ^ Heathers, J. (2006). "Introduction to vagal tone". 
  2. ^ a b Diamond LM, Fagundes CP, Butterworth MR (2012). "Attachment style, vagal tone, and empathy during mother–adolescent interactions". Journal of Research on Adolescence. 22 (1): 165–184. doi:10.1111/j.1532-7795.2011.00762.x. 
  3. ^ "Respiratory sinus arrhythmia and diseases of aging: Obesity, diabetes mellitus, and hypertension". Biological Psychology. 74: 212–223. doi:10.1016/j.biopsycho.2006.07.006. Retrieved 2014-11-06. 
  4. ^ Ben-Tal, A; Shamailov, SS; Paton, JFR (2012). "Evaluating the physiological significance of respiratory sinus arrhythmia: looking beyond ventilation-perfusion efficiency". J Physiol. 590 (8): 1989–2008. doi:10.1113/jphysiol.2011.222422. 
  5. ^ Hayano, J (1996). "Respiratory sinus arrhythmia. A phenomenon improving pulmonary gas exchange and circulatory efficiency". Circulation. 94 (4): 842–7. doi:10.1161/01.cir.94.4.842. 
  6. ^ Yasuma F, et al. (Feb 2004). "Respiratory sinus arrhythmia: why does the heartbeat synchronize with respiratory rhythm?". Chest. 125 (2): 683–90. PMID 14769752. doi:10.1378/chest.125.2.683. 
  7. ^ Moorhead R. (Jan 1999). "Sir James Mackenzie (1853-1925): views on general practice education and research". Journal of the Royal Society of Medicine. 92 (1): 38–43. PMC 1297041Freely accessible. PMID 10319040. 
  8. ^ Connell, A.M.; Hughes-Scalise, A.; Klostermann, S.; Azem, T. (2011). "Maternal depression and the heart of parenting: Respiratory sinus arrhythmia and affective dynamics during parent–adolescent interactions". Journal of Family Psychology. 25 (5): 653–662. doi:10.1037/a0025225. 
  9. ^ Rottenberg, Jonathan; Clift, April; Bolden, Sarah; Saloman, Kristen (2007). "RSA fluctuation in major depressive disorder". Psychophysiology. 44: 450–458. doi:10.1111/j.1469-8986.2007.00509.x.