The Bezold-Jarisch reflex is a physiological response involving the heart and blood vessels that helps regulate the cardiovascular system and acts as a protective mechanism. It was initially described in 1867 by Albert von Bezold and Ludwig Hirt, and later confirmed and further explored by Adolf Jarisch in the late 1930s.
How the Reflex Works
The Bezold-Jarisch reflex begins with the activation of specialized sensory receptors located primarily in the inferoposterior wall of the left ventricle. These receptors include mechanoreceptors, which respond to mechanical changes like stretch and pressure, and chemoreceptors, sensitive to chemical substances such as serotonin and bradykinin. When stimulated, these receptors send signals along afferent nerve pathways, mainly unmyelinated C-fibers within the vagus nerves.
These signals travel to the brainstem, specifically to the nucleus tractus solitarii (NTS). The NTS processes this information and then sends efferent signals back to the heart and blood vessels. This efferent pathway involves an increase in parasympathetic activity and a decrease in sympathetic activity, leading to the reflex’s physiological effects.
Physiological Effects
Activation of the Bezold-Jarisch reflex leads to a triad of physiological outcomes. The first effect is bradycardia, a slowing of the heart rate. This occurs due to increased parasympathetic stimulation of the heart via the vagus nerve.
Systemic vasodilation follows, meaning blood vessels throughout the body widen. This widening reduces resistance to blood flow. The combined effect of a slower heart rate and widespread vasodilation results in hypotension, a decrease in overall blood pressure. This reduction in heart rate and blood pressure can help reduce the workload on the heart.
When the Reflex is Activated
The Bezold-Jarisch reflex can be triggered by various mechanical and chemical stimuli. One mechanical trigger is severe stretch of the ventricular walls, which can occur when the heart’s chambers are underfilled, as seen in severe hemorrhage or hypovolemia. In these situations, despite low blood volume, the ventricle may contract forcefully, activating the receptors.
Chemical triggers include substances like serotonin, bradykinin, and prostaglandins, which can be released during conditions such as myocardial ischemia (reduced blood flow to the heart muscle). The reflex is often observed in clinical scenarios such as inferior wall myocardial infarction, where the affected heart tissue stimulates the receptors. It also plays a role in vasovagal syncope, a common type of fainting, and can be activated during spinal anesthesia or coronary angiography.
Clinical Importance
The Bezold-Jarisch reflex is important in medical contexts due to its involvement in various conditions. In vasovagal syncope, the reflex can lead to a sudden and temporary loss of consciousness because of a rapid drop in heart rate and blood pressure. This response can be triggered by emotional stress or pain, causing a decrease in sympathetic outflow and an increase in parasympathetic activity.
In cardiology, the reflex is particularly relevant in cases of inferior wall myocardial infarction. It is thought to contribute to the bradycardia that can occur within the first hour of such an event, potentially explaining some instances of atrioventricular block. The reflex may also act as a protective mechanism by promoting vasodilation in the coronary arteries during ischemia, and its activation can be an indicator of successful reperfusion after a heart attack. Beyond these conditions, the reflex can influence responses to certain medical procedures, such as spinal anesthesia, where it might contribute to profound bradycardia and circulatory collapse.