Eponym for a triad of responses (apnea, bradycardia, and hypotension)
A cardiovascular decompressor reflex involving a marked increase in vagal (parasympathetic) efferent discharge to the heart, elicited by stimulation of chemoreceptors, primarily in the left ventricle & hypopnea. This causes a slowing of the heart beat (bradycardia) and dilatation of the peripheral blood vessels with resulting lowering of the blood pressure.
Reflex cardiovascular depression with vasodilation and bradycardia has been variously termed vasovagal syncope, the Bezold–Jarisch reflex and neurocardiogenic syncope
The concept was originated by a German physiologist Albert von Bezold in 1867, later revised by an Austrian dermatologist Adolf Jarisch in 1937.
Miller’s Anesthesia 7 th Ed.p. 409
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 thought of as a cardioprotective reflex. This reflex has been implicated in the physiologic response to a range of 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 5 th Ed.p.74-5
The underlying mechanism responsible for bradycardia and asystole during spinal and epidural anesthesia is not known. Proposed theories include reflex-induced bradycardia resulting from decreased venous return and activation of vagal reflex arcs mediated by baroreceptors and stretch receptors in the sinus node resulting in a paradoxical Bezold-Jarisch response. 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 resulting in the emergence of 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 development of bradycardia.The following source would not be used for board references, but is here to further illustrate the concept of the Bezold-Jarisch reflex.
British Journal of Anaesthesia 2001; volume 86; p. 859–68
Reflex cardiovascular depression with vasodilation and bradycardia has been variously termed vasovagal syncope, the Bezold–Jarisch reflex and neurocardiogenic syncope. The circulatory response changes from the normal maintenance of arterial pressure, to parasympathetic activation and sympathetic inhibition, causing hypotension. This change is triggered by reduced cardiac venous return as well as through affective mechanisms such as pain or fear. It is probably mediated in part 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 the restoration of venous return and correction of absolute Blood volume deficits. Ephedrine is the most logical choice of single drug to correct 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.
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