The Bezold-Jarisch reflex is a cardiovascular control mechanism originating in the heart that results in a rapid change in circulatory state. This reflex triggers a sudden, coordinated drop in both the heart rate and the systemic blood pressure. The concept was introduced by Albert von Bezold and Ludwig Hirt in 1867, and later confirmed by Adolf Jarisch Jr. in the late 1930s, leading to the current eponym.
The Physiological Pathway
The reflex arc begins with sensory receptors, primarily mechanoreceptors and chemoreceptors, located within the heart. These receptors are concentrated in the inferoposterior wall of the left ventricle. They are especially sensitive to intense mechanical stimulation, such as a vigorous contraction of a poorly filled or volume-depleted ventricle.
The afferent (incoming) arm of this reflex is composed largely of unmyelinated vagal C-fibers. When stimulated, these fibers transmit sensory signals via the vagus nerve (Cranial Nerve X) up to the brainstem. Specifically, the signals travel to the nucleus tractus solitarii (NTS) in the medulla, which acts as the central processing center for the reflex.
The efferent (outgoing) arm of the reflex dictates the physiological response. Central processing results in increased parasympathetic activity to the heart, while simultaneously inhibiting sympathetic nervous system outflow. This dual action creates the characteristic triad of the reflex: a decrease in heart rate (bradycardia), a reduction in the heart’s contractile force, and widespread peripheral vasodilation. The collective effect of these changes is a rapid and often profound drop in systemic blood pressure.
Situations That Activate the Reflex
The Bezold-Jarisch reflex can be triggered by scenarios that disrupt the mechanical or chemical environment of the left ventricle. One recognized trigger is acute, severe hemorrhage, particularly in its early stages. During significant blood loss, the ventricle becomes underfilled, and the vigorous contraction of the small remaining volume activates the mechanoreceptors, leading to a paradoxical decrease in heart rate and blood pressure.
Myocardial ischemia, such as a heart attack, is another potent trigger. Chemoreceptors in the ventricular wall respond to the chemical changes associated with a lack of oxygen, especially in the inferoposterior region of the heart. Activation of the reflex in this context is thought to be cardioprotective, resulting in coronary vasodilation to increase blood flow and decrease the heart’s workload.
The reflex may also be activated by pharmacological agents and clinical procedures. For example, the intravenous injection of contrast media during cardiac angiography can stimulate the receptors. Certain anesthetic agents or drugs that affect the serotonin (5-HT3) receptors on the vagal nerve endings can also trigger the reflex.
Spinal and epidural anesthesia can also initiate the Bezold-Jarisch reflex. These regional anesthesia techniques can cause a blockade of the sympathetic nervous system, resulting in the pooling of blood in the lower body. This reduces the amount of blood returning to the heart, leading to a poorly filled, hypercontractile ventricle which then activates the reflex.
Clinical Importance and Treatment
The Bezold-Jarisch reflex is clinically significant because it can lead to acute circulatory collapse and serves as a diagnostic clue in several conditions. It contributes to the symptoms seen in vasovagal syncope (common fainting). In this scenario, a sudden pooling of blood or a strong emotional stimulus leads to ventricular underfilling and vigorous contraction, triggering the reflex and causing the patient to lose consciousness due to the rapid drop in blood pressure.
The reflex is also implicated in shock, especially those involving severe volume depletion. The paradoxical bradycardia and hypotension seen in profound hypovolemia can worsen the patient’s condition by further reducing cardiac output. In acute inferior wall myocardial infarction, the reflex is a frequent complication and a reliable indicator of the specific location of the heart damage.
When the reflex results in symptomatic bradycardia and hypotension, immediate medical management is necessary to restore adequate circulation. The primary treatment involves restoring the volume in the heart with fluid administration. In cases of severe bradycardia, an anticholinergic drug, such as atropine, is administered to block the excessive parasympathetic activity and increase the heart rate. Treating the underlying cause—blood loss, ischemia, or an anesthetic effect—is also a necessary part of the overall strategy.