Bezold-Jarisch Reflex
What is the Bexold-Jarish Reflex? The Bezold-Jarisch Reflex (BJR) is a cardioinhibitory reflex involving a marked increase in vagal (parasympathetic) efferent discharge to the heart, elicited by stimulation of chemoreceptors, primarily in the left ventricle. This causes the heartbeat to slow (bradycardia) and the peripheral blood vessels to dilate, resulting in lower blood pressure.
The concept originated with German physiologist Albert von Bezold in 1867. In 1937, Austrian dermatologist Adolf Jarisch revised it.
Nagelhout – Nurse Anesthesia 7th ed.p.1037
The Bezold-Jarisch Reflex is a cardioinhibitory reflex mediated by intracardiac receptors responsive to volume, pressure, chemical stimuli, and the heart’s inotropic state. The afferent limb consists of unmyelinated vagal fibers, and the efferent limb augments vagal tone while simultaneously inhibiting sympathetic output. The net physiologic effect consists of vasodilation and bradycardia that, in some cases, may progress to asystole. In essence, activation of the BJR slows the heart down and allows adequate time to fill. Paradoxically, this occurs at the expense of cardiac output and systemic perfusion.
When the patient is surgically placed in the beach chair position, pooling blood in the lower extremities reduces venous return. Subsequent sympathetic activation, along with systemic absorption of epinephrine if included in a regional block, enhances the heart's inotropic state. An underloaded, hypercontractile ventricle may activate the BJR, leading to vagally mediated bradycardia and hypotension that may be difficult to remedy.
The first descriptions of hypotensive bradycardia episodes (HBEs) were historically in patients receiving spinal anesthesia for various surgeries. The mechanism involves sympathetic blockade; however, decreased sympathetic tone to the heart with decreased cardiac filling is a significant contributor. It has been proposed that epinephrine used with the local anesthetics for interscalene block may contribute to HBE by increasing cardiac hypercontractility and exacerbating the position-related hypovolemic state.
Prophylaxis to prevent HBE includes aggressive treatment of fluid deficits and blood loss. Minimize venous pooling in the upright position with support stockings. Avoid the use of local anesthetics containing epinephrine and consider the use of intraoperative beta-blockade in select patients.
Miller’s Anesthesia 9th ed.p.401
The Bezold-Jarisch Reflex responds to noxious ventricular stimuli sensed by chemoreceptors and mechanoreceptors within the LV wall by inducing the triad of hypotension, bradycardia, and coronary artery dilatation. The activated receptors communicate along unmyelinated vagal afferent type C fibers. These fibers reflexively increase parasympathetic tone. Because it invokes bradycardia, the Bezold-Jarisch reflex is considered a cardioprotective reflex. This reflex has been implicated in the physiologic response to cardiovascular conditions such as myocardial ischemia or infarction, thrombolysis, or revascularization and syncope. Natriuretic peptide receptors stimulated by endogenous ANP or BNP may modulate the Bezold-Jarisch reflex. Thus, the Bezold-Jarisch reflex may be less pronounced in patients with cardiac hypertrophy or atrial fibrillation.
Stoelting’s Anesthesia and Co-Existing Disease 7th ed.p.168
The exact mechanism responsible for bradycardia and asystole during spinal and epidural anesthesia is unknown. One proposed mechanism is the Bezold-Jarisch response, a paradoxical reflex-induced bradycardia resulting from decreased venous return and activation of vagal reflex arcs mediated by baroreceptors and stretch receptors. Another possible mechanism is the unopposed parasympathetic nervous system activity that results from the anesthetic-induced sympathectomy. Blockade of cardiac accelerator fibers originating from thoracic sympathetic ganglia (T1-4) may alter the balance of autonomic nervous system input to the heart and lead to relatively unopposed parasympathetic influences on the SA node and AV node. Secondary factors such as hypovolemia, opioid administration, sedation, hypercarbia, concurrent medical illnesses, and long-term use of medications that slow the heart rate could also contribute to the development of bradycardia.
Pharmacologic management should follow ACS protocols and include treatment with atropine, epinephrine, and/or dopamine as appropriate.
The following source should not be used for board references but is provided to further illustrate the concept of the Bezold-Jarisch reflex.
British Journal of Anaesthesia 2001; volume 86; p. 859–68
The following source should not be used for board references but is provided to further illustrate the concept of the Bezold-Jarisch reflex.
Reflex cardiovascular depression with vasodilation and bradycardia have been variously termed vasovagal syncope, the Bezold–Jarisch reflex, and neurocardiogenic syncope. The circulatory response changes from the routine maintenance of arterial pressure to parasympathetic activation and sympathetic inhibition, causing hypotension. This change is triggered by reduced cardiac venous return and through affective mechanisms such as pain or fear. It is probably mediated partly via afferent nerves from the heart but also by various non-cardiac baroreceptors, which may become paradoxically active. This response may occur during regional anesthesia, hemorrhage, or supine inferior vena cava compression in pregnancy; these factors are additive when combined. In these circumstances, hypotension may be more severe than that caused by bradycardia alone because of unappreciated vasodilation. Treatment includes restoring venous return and correcting absolute blood volume deficits. Ephedrine is the most logical choice of a single drug to fix the changes because of its combined action on the heart and peripheral blood vessels. Epinephrine must be used early in established cardiac arrest, especially after high regional anesthesia.