Bezold–Jarisch reflex


Clinically, the Bezold-Jarisch reflex is an inhibitory reflex usually denoted as a cardioinhibitory reflex defined as bradycardia, vasodilation, and hypotension resulting from stimulation of cardiac receptors.

The Bezold-Jarisch reflex (BJR) was initially used an eponym for the triad of responses (apnea, bradycardia, and hypotension) following intravenous injection of veratrum alkaloids in experimental animals. The triad depends on intact vagi and is mediated through cranial nervous medullary centers controlling respiration, heart rate, and vasomotor tone.

The respiratory effects are mediated through pulmonary vagal afferents and the bradycardia and vasodepression through cardiac vagal afferents. The veratrum alkaloids activate all known receptors in the carotid–aortic and cardiopulmonary areas

The Bezold-Jarisch reflex originates from inhibitory mechanoreceptors in the left ventricle (particularly the inferoposterior wall). Stimulation of these inhibitory cardiac receptors by stretch (poorly filled ventricle), chemical substances or drugs increases renin and vasopressin release and parasympathetic activity and inhibits sympathetic activity. These effects promote reflex bradycardia, vasodilation and hypotension (Bezold-Jarisch reflex).

Clinical implications

Acute inferoposterior myocardial infarction

  • Cardioprotective effect: It is thought that the cardiodepressor Bezold-Jarisch reflex (BJR) acts as a protective reflex to vasodilate the coronary arteries in the setting of inferoposterior infarction associated with coronary vasospasm.
  • The BJR is thought to be responsible for up to 60% of bradyarrhythmia occurring within the first 60 minutes of infarction and for the occurrence of AV nodal block in the context of acute posterior or inferior myocardial infarction.
  • Reperfusion: The BJR in acute inferior myocardial infarction represents a reliable prognosticator of timely reperfusion and sustained coronary patency. It occurs in 94% of cases of successful early thrmobolysis in inferior MI; and 89% of patent right coronary artery.
  • Stimulation of vagal afferents in response to sympathetic overactivity may be the underlying pathogenetic mechanism promoting a BJR response. [Clin Cardiol. 2003]


  • The BJR has been implicated as a possible cause of profound bradycardia and circulatory collapse following spinal anesthesia and as a complication of interscalene brachial plexus block.

Vasovagal syncope

  • Prolonged upright posture results may result in lower extremity blood pooling; reduced venous return and diminished intracardiac volume. The resultant hypotension is sensed in the carotid sinus baroreceptors and triggers an increase in cardiac rate and contractility (sympathetic autonomic).
  • However, pressure receptors in the wall of the underfilled left ventricle 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 worsening of hypotension.

History of the Bezold–Jarisch reflex

1867Albert von Bezold (1836-1868) and Ludwig Hirt (1844-1907) showed that intravenous injection of a mixture of veratrum alkaloids, veratrine, causes a very large fall in blood pressure and heart rate, and arrest of breathing in animals. They attributed the depressor effect of veratrine in part to a reflex excited by stimulation of sensory nerve endings in the heart, the afferent pathways being in the vagus nerves. von Bezold and Hirt did not establish the reflex origin of the apnea.

1915William Cramer (1878-1945) described clearly the triad of apnea, bradycardia and hypotension which followed the intravenous injection of extracts of veratrum viride in cats. Cramer showed conclusively that the entire effect of small doses was reflex in nature, the afferent pathways being in the vagi, and that both reflex bradycardia and reflex peripheral systemic vasodilatation contributed to the hypotension. Cramer, influenced by Brodie and Russell’s demonstration in 1900 that electrical stimulation of the central ends of the pulmonary branches of the vagi caused apnea, bradycardia and hypotension, believed that the sensory receptors were in the lungs.

1937-1940 Adolf Jarisch, Jr (1891-1965) and colleagues investigated the effects of viscum album and of veratrine. They confirmed that the depressor effect was reflex in origin. Like von Bezold and Hirt, Jarisch believed that the sensory receptors were in the heart because the effect could be produced after removal of one lung and section of the vagus nerves to the other. They termed the response the Bezold effect

1947 – So, Cramer believed that the receptors for this effect were in the lung, but Jarisch argued that the receptors were located in the ventricle of the heart. In 1947 GS Dawes (1918-1996) using veratridine in cats, showed that the reflex apnea was caused by a mechanism separate from that mediating the hemodynamic changes. Dawes et al found that the reflex apnea produced by small doses of veratridine was due to an action upon sensory receptors in the lungs; and the reflex fall in blood pressure and heart rate was due to an effect upon receptors in the heart and, to a much smaller degree, the lungs.

1983Allyn L. Mark reviews the role of inhibitory cardiac sensory receptors in the clinical states of 1) bradycardia, hypotension and gastrointestinal disorders with inferoposterior myocardial ischemia and infarction, 2) bradycardia and hypotension during coronary arteriography, 3) exertional syncope in aortic stenosis, 4) vasovagal syncope, 5) neurohumoral excitation in chronic heart failure, and 6) the therapeutic effects of digitalis.

1997 – Somkiat Wattanasirichaigoon and Frank B. Pomposelli, Jr proposed that the Branham sign is an exaggerated Bezold-Jarisch reflex

Associated Persons
  • Albert von Bezold (1836-1868)
  • Ludwig Hirt (1844-1907)
  • William Cramer (1878-1945)
  • Adolf Jarisch, Jr (1891-1965)
  • Harris Miller Branham (1862-1936)
  • Geoffrey Sharman Dawes (1918-1996)

Alternative names
  • Bezold reflex, Bezold effect
  • Bezold-Jarisch effect, Bezold-Jarisch reflex, BJR
  • Bezold-Jarisch response, Jarisch-Bezold reflex


Historical references

Eponymous term review


the names behind the name

BA MA (Oxon) MBChB (Edin) FACEM FFSEM. Emergency physician, Sir Charles Gairdner Hospital.  Passion for rugby; medical history; medical education; and asynchronous learning #FOAMed evangelist. Co-founder and CTO of Life in the Fast lane | Eponyms | Books | Twitter |

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