Bezold-Jarisch reflex

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Rim Halaby

Synonyms and keywords: Bezold's reflex, Bezold-Jarisch response, Jarisch-Bezold reflex, BJR.

Overview

The Bezold–Jarisch reflex involves a variety of cardiovascular and neurological processes which cause hypopnea (overly shallow breathing or an abnormally low respiratory rate) and bradycardia (abnormally low resting heart rate).[1]. A cardiovascular depressor 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 a slowing of the heart beat (bradycardia) and dilatation of the peripheral blood vessels with resulting lowering of the blood pressure. [2] [3] [4]

Historical Perspective

It is named for Albert von Bezold and Adolf Jarisch Junior.[5]. The concept was originated by Bezold in 1867, later revised by Jarisch in 1937.[6]

Physiology

Bezold-Jarisch reflex is the occurrence of bradycardia and hypotension through a pathway involving cardiac receptors, medullary centers and vagal afferent nerves.[7] Bezold-Jarisch reflex originates from inhibitory mechanoreceptors that are located in the left ventricle, particularly in the inferoposterior wall. The stimulation of these receptors occurs in the context of stretching and contraction of a poorly filled ventricle. Once stimulated, these mechanoreceptors stimulate parasympathetic pathways and inhibits the sympathetic pathways. The result of this reflex is a constellation of bradycardia, vasodilation and hypotension in addition to increase renin and vasopressin release.[6]

Below is a scheme that summarizes the physiology of Bezold-Jarisch reflex.

Clinical Implications

Bezold-Jarisch reflex plays a role in the following clinical conditions:

Acute Inferoposterior Myocardial Infarction

Bezold-Jarisch reflex is responsible for 61% of bradyarrhythmia that occur within the first 60 minutes of MI,[8] and it explains the occurrence of AV node block in the context of acute posterior or inferior myocardial infarction.[9] It is hypothesized that this reflex is a protective reflex that vasodilates the coronary arteries in the setting of posterior infarction associated with coronary vasospasm.[10]. Bradycardia in this setting may be treated with atropine.

Reperfusion Induced Bezold-Jarisch Reflex

Bezold-Jarisch reflex can occur in acute inferior MI after thrombolysis. In fact, it is a prognostic sign for early reperfusion as it occurs in 94% of cases of successful early thrmobolysis in inferior MI. In addition, it is a prognostic factor for coronary patency as it occurs in 89% of patent right coronary artery characterized by a TIMI flow grade of 3.[11]

Vasovagal Syncope

  • Prolonged upright posture results in some degree of pooling of blood in the lower extremities that can lead to diminished intracardiac volume. This phenomenon is exacerbated if the individual is dehydrated. The resultant arterial hypotension is sensed in the carotid sinus baroreceptors, and efferent fibers from these receptors trigger sympathetic autonomic signals that increase cardiac rate and contractility. However, pressure receptors in the wall and trabeculae of the underfilled left ventricle may then sense the stretching and contraction of the poorly filled ventricle, activating high-pressure C-fiber afferent nerves from these receptors. They may respond by activating the parasympathetic system that triggers paradoxical bradycardia and decreased contractility, resulting in additional and relatively sudden arterial hypotension. Hence, Bezold-Jarisch reflex results from the stimulation of vagal afferent pathways in response to sympathetic overactivity.
  • Inappropriate Bezold- Jarisch reflex must be suspected in the setting of unexplained syncope and should be investigated by tilt table test.


Medication Induced

It usually occurs in nitrate therapy and use of serotonin agonists.[12]

Anesthesia

  • The Bezold–Jarisch reflex has also been suggested as a possible cause of profound bradycardia and circulatory collapse after spinal anesthesia.[13]
  • Also, it is one of the complications of interscalene brachial plexus block.
Distribution of opioid OP4 receptors involved in the regulation of cardiovascular function. Various locations of OP4 receptors as suggested by functional studies are shown. Excitatory neurons are represented by solid lines, inhibitory neurons are represented by dotted lines. Abbreviations: CVLM - caudal ventrolateral medulla; NAmb - nucleus ambiguus; NTS - nucleus tractus solitarii; PVN - paraventricular nucleus; RVLM - rostral ventrolateral medulla.[14]
Distribution of opioid OP4 receptors involved in the regulation of cardiovascular function. Various locations of OP4 receptors as suggested by functional studies are shown. Excitatory neurons are represented by solid lines, inhibitory neurons are represented by dotted lines. Abbreviations: CVLM - caudal ventrolateral medulla; NAmb - nucleus ambiguus; NTS - nucleus tractus solitarii; PVN - paraventricular nucleus; RVLM - rostral ventrolateral medulla.[14]


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References

  1. Salo LM, Woods RL, Anderson CR, McAllen RM (2007). "Nonuniformity in the von Bezold-Jarisch reflex". Am. J. Physiol. Regul. Integr. Comp. Physiol. 293 (2): R714–20. doi:10.1152/ajpregu.00099.2007. PMID 17567718. Unknown parameter |month= ignored (help)
  2. A. von Bezold, Ludwig Hirt (1844-1907): Über die physiologischen Wirkungen des essigsauren Veratrine. Untersuchungen aus dem Physiologischen Laboratorium in Würzburg, 1867, 1: 73-122.
  3. A. Jarisch, C. Henze Über Blutdrucksenkung durch chemische Erregung depressorischer Nerven. Naunyn-Schmiedebergs Archiv für experimentelle Pathologie und Pharmakologie, 1937, 187: 706­-730.
  4. A. Jarisch Vom Herzen ausgehende Kreislaufreflexe. Archiv für Kreislaufforschung 1940, 7: 260-­274.
  5. Template:WhoNamedIt
  6. 6.0 6.1 6.2 Mark AL (1983). "The Bezold-Jarisch reflex revisited: clinical implications of inhibitory reflexes originating in the heart". J Am Coll Cardiol. 1 (1): 90–102. PMID 6826948.
  7. Aviado DM, Guevara Aviado D (2001). "The Bezold-Jarisch reflex. A historical perspective of cardiopulmonary reflexes". Ann N Y Acad Sci. 940: 48–58. PMID 11458703.
  8. Goldman, Lee; Anderson, Jeffrey L. "ST SEGMENT ELEVATION ACUTE MYOCARDIAL INFARCTION AND COMPLICATIONS OF MYOCARDIAL INFARCTION". Goldman: Goldman's Cecil Medicine (24th ed.). Saunders, an imprint of Elsevier Inc. p. 444. ISBN 978-1-4377-1604-7.
  9. Katz, Arnold M. (2001). Physiology of the heart (3. ed. ed.). Philadelphia [u.a.]: Lippincott Williams & Wilkins. p. 595. ISBN 0-7817-1548-2.
  10. Linden R.J. Function of Cardiac Receptors. Circulation. 1973; 48: 463-480
  11. Chiladakis JA, Patsouras N, Manolis AS (2003). "The Bezold-Jarisch reflex in acute inferior myocardial infarction: clinical and sympathovagal spectral correlates". Clin Cardiol. 26 (7): 323–8. PMID 12862298.
  12. eMedicine - Syncope : Article by M Silvana Horenstein, MD
  13. Tsai T. & Greengrass R. (2007). Textbook of Regional Anesthesia and Acute Pain Management: Spinal Anesthesia. (A. Hadzic, Ed.). New York: McGraw Hill Medical.
  14. Malinowska B. Godlewski G, Schlicker E. FUNCTION OF NOCICEPTIN AND OPIOID OP4 RECEPTORS IN THE REGULATION OF THE CARDIOVASCULAR SYSTEM, 2002, Bialystok, Poland

References


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