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The underlying mechanism involves the nervous system slowing the heart rate and dilating blood vessels, resulting in low blood pressure and thus not enough blood flow to the brain. [2] Diagnosis is based on the symptoms after ruling out other possible causes. [3] Recovery from a reflex syncope episode happens without specific treatment. [2]
Gastric nerve connections to the spinal cord and brain medulla oblongata, which regulate the movements of the stomach. The cranium dysfunction mechanical changes in the gut can compress the vagus nerve at any number of locations along the vagus, slowing the heart. As the heart slows, autonomic reflexes are triggered to increase blood pressure ...
In most cases, vagal tone is not measured directly. Instead the processes affected by the vagus nerve – specifically heart rate and heart rate variability – are measured and used as a surrogate for vagal tone. Increased vagal tone (and thus vagal action) is generally associated with a lower heart rate and increased heart rate variability.
The cervical cardiac branches (sometimes ambiguously called superior cardiac branches) of vagus nerve, two or three in number, arise from the vagus, at the upper and lower parts of the neck. The upper branches are small, and communicate with the cardiac branches of the sympathetic. They can be traced to the deep part of the cardiac plexus.
Norepinephrine (Levophed) is the most common first-line vasopressor for people who don't respond well to other hypotension treatments such as fluid resuscitation. Atropine is administered for bradycardia. It acts on the vagus nerve so it's not effective in heart transplant patients as the vagus nerve is severed during the transplant. [11]
The CVMs, which send motor fibers to the heart via the vagus nerve, are responsible for tonic inhibitory control of heart rate. Thus, an increase in pulmonary stretch receptor activity leads to inhibition of the CVMs and an elevation of heart rate (tachycardia). This is a normal occurrence in healthy individuals and is known as sinus arrhythmia.
The reflex was originally demonstrated by Bainbridge in 1915 who observed an increase in heart rate following infusion of blood or saline into the jugular vein of anaesthetized dogs. [6] The response was reduced by cutting the cardiac sympathetic nerves and abolished by cutting the vagus nerve and he therefore concluded that it was a neural reflex.
The vagus nerve is also responsible for regulating inflammation in the body, via the inflammatory reflex. [7] Efferent vagus nerve fibers innervating the pharynx and back of the throat are responsible for the gag reflex. In addition, 5-HT 3 receptor-mediated afferent vagus stimulation in the gut due to gastroenteritis is a cause of vomiting. [8]
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