The Bezold–Jarisch reflex (also called the Bezold reflex, the Jarisch-Bezold reflex or Von Bezold–Jarisch reflex[1]) involves a variety of cardiovascular and neurological processes which cause
hypopnea (excessively shallow breathing or an abnormally low
respiratory rate),
hypotension (abnormally low blood pressure) and
bradycardia (abnormally low resting
heart rate) in response to noxious stimuli detected in the cardiac ventricles.[2] The reflex is named after
Albert von Bezold and Adolf Jarisch Junior.[3] The significance of the discovery is that it was the first recognition of a chemical (non-mechanical) reflex.
History and physiology
von Bezold and Hirt described a reaction comprising a triad of bradycardia, hypotension, and apnea (hypopnea) resulting from an intravenous injection of an alkaloidal extract of
Veratrum viride or Viscum album in 1867.[4] This observation was comparatively neglected until Jarisch and Henze re-examined it in 1937; they identified the reaction as a chemoreflex acting via the
vagus nerve that was relayed in the
nucleus tractus solitarii (NTS), and termed it the Bezold reflex.[4] It is now usually called the Bezold–Jarisch reflex; however the bradycardia and hypopnea arise from anatomically distinct receptors in the heart and lung respectively[5] and whether hypopnea should be regarded as part of the reflex is disputed.[6][7] The afferent cardiac neurons relevant to the Bezold–Jarisch reflex have
cell bodies in the
nodose ganglion and the
dorsal root ganglion. They manifest two types of nerve endings in the heart: complex unencapsulated endings located in the
atrial and
ventricularendocardium and an endocardial nerve network throughout the surface of the endocardium. The axons include
myelinated fibers (A-fiber) and
unmyelinated fibers (C-fibers) which travel with the vagus and
sympathetic nerves. The myelinated afferents originating in the atria are attached to discrete receptor endings, whereas most of the unmyelinated fibers are located in the ventricles and the walls of the
coronary vessels.[8] Vagal afferent C fibers originating in the heart and lungs terminate in the NTS, while axons from the heart also inhibit sympathetic nervous activity via the
caudal ventrolateral medulla (CVLM) and possibly the
rostral ventrolateral medulla (RVLM).[8][7][9] The sites of the chemoreflex and
baroreflex input overlap and there is evidence that these reflexes modify each other, probably through the actions of excitatory and inhibitory neurotransmitters, such as
serotonin and
Gamma-Aminobutyric acid (GABA).[7][9]
Severe hemorrhage and hypovolemia: During severe
hemorrhage or profound
hypovolemia the ventricle can become relatively empty and trigger cardiac vagal afferent fibers to elicit the Bezold–Jarisch reflex resulting in paradoxical bradycardia, vasodilation, and hypotension.[6]
Myocardial ischemia: Chemoreceptors located in the ventricles respond to myocardial ischemia, resulting in an increase in blood flow to the myocardium and a decrease in the work of the heart. This appears to be a cardioprotective reflex, as coronary vasodilation occurs. The pathway for this cardioprotective reflex begins with receptors in the ventricles of the heart, which detect mechanical and chemical stimuli. Afferent unmyelinated C-fibers travel through the vagus to enhance the baroreceptor reflex mechanisms, inhibit sympathetic output, and inhibit vasomotor tone, leading to peripheral vasodilation. The Bezold–Jarisch reflex is thought to be responsible for the
sinus bradycardia that commonly occurs within the first hour following a
myocardial infarction,[13] and may explain the frequent occurrence of
atrio-ventricular (AV) node block in acute posterior or inferior myocardial infarction.[14] Bradycardia in this setting may be treated with
atropine.
Hypotension following injection of contrast media during coronary angiography[5]
Exertional syncope in aortic stenosis: in severe aortic stenosis exercise may cause a rise in left ventricular pressure which stimulates the Bezold–Jarisch reflex and results in reflex vasodilation and syncope.[15]
Spinal anesthesia: The Bezold–Jarisch reflex has been suggested as a possible cause of profound bradycardia and circulatory collapse after
spinal anesthesia[16] and interscalene
brachial plexus block.[17]
Vaso-vagal syncope: the role of the Bezold–Jarisch reflex in vaso-vagal
syncope is unclear. Upright posture results in pooling of blood in the
lower extremities that diminishes
venous return and results in a reduced
cardiac output. The resultant lowering of blood pressure is sensed by
carotid sinusbaroreceptors, and stimulates the
baroreflex to inhibit vagal activity and stimulate the sympathetic nervous system – this increases heart rate and
contractility, induces
vasoconstriction, and tends to restore blood pressure. However, if the Bezold–Jarisch reflex is activated due to the reduced ventricular volume this may trigger paradoxical
bradycardia and arterial
hypotension resulting in syncope. The importance of this mechanism is unclear since vaso-vagal syncope can be observed in
cardiac transplant patients who are presumed to lack cardiac
innervation.[6] If it operates this phenomenon would be expected to be exacerbated if the individual is
dehydrated. It has also been proposed that this mechanism accounts for the increased susceptibility to
orthostatic syncope of astronauts after space flights.[18]
^Goldman, Lee; Anderson, Jeffrey L. (2012-01-01). "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.
ISBN978-1-4377-1604-7.
^Katz, Arnold M. (2001). Physiology of the heart (3rd ed.). Philadelphia [u.a.]: Lippincott Williams & Wilkins. p. 595.
ISBN978-0-7817-1548-5.
^Tsai, Tony; Greengrass, Roy (2007). "Spinal Anesthesia". In Hadzic, Admir (ed.). Textbook of Regional Anesthesia and Acute Pain Management. New York: McGraw Hill Medical.
ISBN978-0-07-144906-9.
OCLC70051351.