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Rishi Mugesh Kanna - One of the best experts on this subject based on the ideXlab platform.

  • Bezold–Jarisch Reflex causing bradycardia and hypotension in a case of severe dystrophic cervical kyphotic deformity: a case report and review of literature
    European Spine Journal, 2020
    Co-Authors: Soundararajan Dilip Chand Raja, Shanmuganathan Rajasekaran, K. S. Sri Vijayanand, Ajoy Prasad Shetty, Rishi Mugesh Kanna
    Abstract:

    Purpose A 17-year-old adolescent with neurofibromatosis and severe cervicothoracic deformity was identified to have thoracic inlet compression leading to bradycardia and hypotension, only during prone positioning, and we discuss its successful management. Methods Preoperative halo-gravity traction reduced the deformity from 126° to 91°. During prone positioning, sudden onset bradycardia was followed by asystole, which disappeared immediately on turning over to supine position. Surgery was called off after two additional failed attempts of prone positioning. Results A retrospective analysis of CT and MRI showed severe narrowing of the thoracic inlet. In this patient, the right thoracic inlet was severely narrow, and prone positioning caused a further dynamic compromise stimulating right vagal nerve. The right vagus supplies the sinoatrial node, which is the natural pacemaker of the heart, and its stimulation causes sympathetic inhibition. Bezold–Jarisch Reflex is a cardio-inhibitory Reflex occurring due to vagal stimulation resulting in sudden bradycardia, asystole, and hypotension. To facilitate prone positioning, the medial end of the clavicles, along with limited manubrium excision, was performed relieving the vagal compression. C2–T4 instrumented decompression followed by anterior reconstruction and cervical plating was performed. The postoperative period was uneventful, and the final deformity was 45°. Conclusion Bezold–Jarisch Reflex as a result of narrow thoracic inlet caused by cervical kyphosis and compensatory hyperlordosis of the upper thoracic spine has never been reported. This case highlights the need to introspect into thoracic inlet morphology in severe cervicothoracic deformities. Thoracic inlet decompression is an efficient way of addressing this unique complication.

  • bezold jarisch Reflex causing bradycardia and hypotension in a case of severe dystrophic cervical kyphotic deformity a case report and review of literature
    European Spine Journal, 2020
    Co-Authors: Soundararajan Dilip Chand Raja, Shanmuganathan Rajasekaran, Ajoy Prasad Shetty, K Sri S Vijayanand, Rishi Mugesh Kanna
    Abstract:

    A 17-year-old adolescent with neurofibromatosis and severe cervicothoracic deformity was identified to have thoracic inlet compression leading to bradycardia and hypotension, only during prone positioning, and we discuss its successful management. Preoperative halo-gravity traction reduced the deformity from 126° to 91°. During prone positioning, sudden onset bradycardia was followed by asystole, which disappeared immediately on turning over to supine position. Surgery was called off after two additional failed attempts of prone positioning. A retrospective analysis of CT and MRI showed severe narrowing of the thoracic inlet. In this patient, the right thoracic inlet was severely narrow, and prone positioning caused a further dynamic compromise stimulating right vagal nerve. The right vagus supplies the sinoatrial node, which is the natural pacemaker of the heart, and its stimulation causes sympathetic inhibition. Bezold–Jarisch Reflex is a cardio-inhibitory Reflex occurring due to vagal stimulation resulting in sudden bradycardia, asystole, and hypotension. To facilitate prone positioning, the medial end of the clavicles, along with limited manubrium excision, was performed relieving the vagal compression. C2–T4 instrumented decompression followed by anterior reconstruction and cervical plating was performed. The postoperative period was uneventful, and the final deformity was 45°. Bezold–Jarisch Reflex as a result of narrow thoracic inlet caused by cervical kyphosis and compensatory hyperlordosis of the upper thoracic spine has never been reported. This case highlights the need to introspect into thoracic inlet morphology in severe cervicothoracic deformities. Thoracic inlet decompression is an efficient way of addressing this unique complication.

  • Bezold–Jarisch Reflex causing bradycardia and hypotension in a case of severe dystrophic cervical kyphotic deformity: a case report and review of literature
    European Spine Journal, 2020
    Co-Authors: Soundararajan Dilip Chand Raja, Shanmuganathan Rajasekaran, Ajoy Prasad Shetty, K Sri S Vijayanand, Rishi Mugesh Kanna
    Abstract:

    A 17-year-old adolescent with neurofibromatosis and severe cervicothoracic deformity was identified to have thoracic inlet compression leading to bradycardia and hypotension, only during prone positioning, and we discuss its successful management. Preoperative halo-gravity traction reduced the deformity from 126° to 91°. During prone positioning, sudden onset bradycardia was followed by asystole, which disappeared immediately on turning over to supine position. Surgery was called off after two additional failed attempts of prone positioning. A retrospective analysis of CT and MRI showed severe narrowing of the thoracic inlet. In this patient, the right thoracic inlet was severely narrow, and prone positioning caused a further dynamic compromise stimulating right vagal nerve. The right vagus supplies the sinoatrial node, which is the natural pacemaker of the heart, and its stimulation causes sympathetic inhibition. Bezold–Jarisch Reflex is a cardio-inhibitory Reflex occurring due to vagal stimulation resulting in sudden bradycardia, asystole, and hypotension. To facilitate prone positioning, the medial end of the clavicles, along with limited manubrium excision, was performed relieving the vagal compression. C2–T4 instrumented decompression followed by anterior reconstruction and cervical plating was performed. The postoperative period was uneventful, and the final deformity was 45°. Bezold–Jarisch Reflex as a result of narrow thoracic inlet caused by cervical kyphosis and compensatory hyperlordosis of the upper thoracic spine has never been reported. This case highlights the need to introspect into thoracic inlet morphology in severe cervicothoracic deformities. Thoracic inlet decompression is an efficient way of addressing this unique complication.

Robyn L. Woods - One of the best experts on this subject based on the ideXlab platform.

  • Do prostanoids or nitric oxide mediate sensitization of the von Bezold-Jarisch Reflex by B-type natriuretic peptide?
    Clinical and experimental pharmacology & physiology, 2011
    Co-Authors: Colleen J. Thomas, Atul D Sharma, Robyn L. Woods
    Abstract:

    Summary 1. Cardiac natriuretic peptides act on cardiopulmonary chemoreceptor afferents to enhance the von Bezold–Jarisch Reflex (BJR). Activity of the natriuretic peptide particulate guanylyl cyclase receptor is essential for full expression of the BJR. Whether natriuretic peptides act directly on cardiac afferents or they require another intermediate factor(s) for their effects on the BJR is unknown. Endogenous candidates tested as possible intermediates in the present study were prostanoids and nitric oxide (NO), plausible endogenous chemical mediators of cardiac chemoReflex activity. 2. Dose-dependent BJR bradycardia was evoked by the 5-HT3 receptor agonist, phenylbiguanide (range 5–89 μg/kg), in conscious instrumented adult sheep (n = 6). The influence of B-type natriuretic peptide (BNP; the most potent of the natriuretic peptides) on the BJR was assessed before and after blockade of prostanoids (using indomethacin, 1 mg/kg per h i.v.) or nitric oxide (using N-nitro-l-arginine (NOLA), 3 mg/kg bolus, then 3 mg/kg per h infusion i.v.). 3. On their own, indomethacin and NOLA did not significantly alter the BJR, showing that prostanoids and NO are not essential endogenous mediators of the BJR. As shown in previous studies, BNP (10 pmol/kg per min i.v.) infusion enhanced the BJR by 85 ± 36%, P 

  • Nonuniformity in the von Bezold-Jarisch Reflex
    American journal of physiology. Regulatory integrative and comparative physiology, 2007
    Co-Authors: Lauren M Salo, Robyn L. Woods, Colin R. Anderson, Robin M. Mcallen
    Abstract:

    The von Bezold-Jarisch Reflex (BJR) is a vagally mediated chemoReflex from the heart and lungs, causing hypopnea, bradycardia, and inhibition of sympathetic vasomotor tone. However, cardiac sympath...

  • ANP, BNP, and CNP enhance bradycardic responses to cardiopulmonary chemoreceptor activation in conscious sheep
    American journal of physiology. Regulatory integrative and comparative physiology, 2001
    Co-Authors: Colleen J. Thomas, Clive N. May, Atul D Sharma, Robyn L. Woods
    Abstract:

    We demonstrated previously that atrial natriuretic peptide (ANP) enhances Reflex bradycardia to intravenous serotonin [5-hydroxytryptamine (5-HT)] (von Bezold-Jarisch Reflex) in rats. To determine ...

Deoclécio A. Chianca - One of the best experts on this subject based on the ideXlab platform.

  • Bezold–Jarisch Reflex in sino-aortic denervated malnourished rats
    Autonomic Neuroscience: Basic and Clinical, 2011
    Co-Authors: Vanessa Moraes Bezerra, Carlos Henrique Xavier, Luciano Gonçalves Fernandes, Leonardo Máximo Cardoso, Marco Antônio Peliky Fontes, Rodrigo Cunha Alvim De Menezes, Deoclécio A. Chianca
    Abstract:

    Abstract In this study we assessed the role of Bezold–Jarisch Reflex (BJR) in the regulation of blood pressure (BP) of malnourished (MN) and control rats (CN) with sino-aortic denervation (SAD). Fischer rats were fed diets containing either 6% (MN) or 15% (CN) protein for 35 days after weaning. These rats underwent sham or SAD and catheterization of femoral artery and vein for BP measurements and drug injection. Phenylbiguanide (PBG 5 μg/kg, i.v.) for activation BJR, produced bradycardia (− 317 ± 22 bpm for CN vs. −  372 ± 16 bpm for MN) and hypotension (− 57 ± 4 mm Hg for CN vs. − 54 ± 6 mm Hg for MN. After SAD, MN rats had reduced hypotensive (− 37 ± 7 mmHg for MN vs. − 82 ± 6 mm Hg for CN) and bradycardic (− 124 ± 17 for MN vs. −  414 ± 20 bpm CN) responses to BJR activation. To evaluate the contribution of the parasympathetic component due to BJR for the fall in BP, methyl atropine bromide, was given between two injections of PBG (5 μg/kg) separated by 10 min each other. Both bradycardic (− 216 ± 21 bpm before and − 4±3 bpm after for CN − 226±43 bpm before and − 9±20 bpm after for MN) and hypotensive (− 42±4 mm Hg before and − 6±1 mm Hg after for CN − 33±9 mm Hg before and − 5±2 mm Hg after for MN) responses were abolished in CN and MN groups. These data indicate that dietary protein malnutrition changes the relation between baroReflex and BJR required for maintenance of the BP during malnourishment.

  • Sympathoinhibition to Bezold-Jarisch Reflex is attenuated in protein malnourished rats.
    Neuroscience letters, 2010
    Co-Authors: Vanessa Moraes Bezerra, Carlos Henrique Xavier, Luciano Gonçalves Fernandes, Leonardo Máximo Cardoso, Marco Antônio Peliky Fontes, Deoclécio A. Chianca
    Abstract:

    Malnutrition affects cardiovascular Reflexes, including chemoReflex and baroReflex. In this study we assessed the hypothesis that malnourishment changes the responses in mean arterial pressure (MAP), heart rate (HR) and renal sympathetic nerve activity (RSNA) evoked from Bezold–Jarisch Reflex (BJR). Fischer rats were fed diets containing either (6% malnourished or 14% control) protein for 35 days after weaning. There were no differences in baseline MAP (102 ± 4 vs. 95 ± 3 mmHg) whereas higher baseline HR (478 ± 18 vs. 360 ± 11 bpm; P < 0.05,) and reduced sympathoinhibition (� RSNA = −54 ± 9 vs. −84 ± 7%; P= 0.0208) to BJR activation were found in malnourished rats. We conclude that malnutrition affects the sympathetic control of BJR. © 2010 Elsevier Ireland Ltd. All rights reserved.

  • Effects of low-protein diet on the baroReflex and Bezold-Jarisch Reflex in conscious rats.
    Nutritional neuroscience, 2001
    Co-Authors: F.c. Tropia, Leonardo Máximo Cardoso, Maria Lúcia Pedrosa, Marcelo Estáquio Silva, Andrea Siqueira Haibara, Márcio Flávio Dutra Moraes, Deoclécio A. Chianca
    Abstract:

    The present study evaluated the effects of a low-protein diet (LP, 6% protein) on cardiovascular Reflexes of Male Fisher rats. Three experimental groups, and their respective controls (15% protein), were used. (1) Baroreceptor Reflex (BAR); (2) Bezold-Jarisch Reflex (BJR); and (3) Prazosin treated. Dietary restriction began after weaning (three weeks) and lasted for a period of five weeks, after which animals were subjected to the experimental protocols. The BAR group was evaluated through injections of phenylephrine (0.55.0 μg/Kg, i.v.) and sodium nitroprusside (0.77.0 μg/Kg, i.v.) while the BJR was evaluated through injections of serotonin (2.510μg/Kg, i.v.). Our results showed an increased baroReflex gain bradycardia for the LP group (-0.96 ± 0.34 vs. -2.12 ± 1.06 bpm/mmHg) and a larger bradycardia for the BJR the LP group (160 ± 18% greater than controls). Basal cardiovascular parameters were not different between LP and control rats, however LP animals treated with prazosin resulted in a larger fall ...

  • Microinjection of NMDA antagonist into the NTS of conscious rats blocks the Bezold-Jarisch Reflex.
    Brain Research, 1996
    Co-Authors: Deoclécio A. Chianca, Benedito H. Machado
    Abstract:

    The purpose of the present study was to evaluate whether or not cardiovagal excitatory and sympatho-inhibitory pathways of the Bezold-Jarisch Reflex at the NTS level were mediated by NMDA receptors. The Bezold-Jarisch Reflex was activated by intravenous (i.v.) injection of serotonin in conscious rats before and after microinjection of phosphonovaleric acid (AP-5), a selective NMDA antagonist, into the NTS. The Bezold-Jarisch Reflex was also activated before and after methyl-atropine (i.v.) in order to evaluate if the changes in mean arterial pressure were dependent on the bradycardic response. The data showed that AP-5 into the NTS produced a dose-dependent reduction in both bradycardic and hypotensive responses to activation of the Bezold-Jarisch Reflex. Methyl-atropine also blocked the bradycardic and hypotensive responses to Bezold-Jarisch Reflex activation. The data show that in conscious rats the cardiovagal component of the Bezold-Jarisch Reflex plays a major role in the cardiovascular changes produced by the activation of this Reflex and suggest that the neurotransmission of the cardiovagal component of the Bezold-Jarisch Reflex is mediated by NMDA receptors.

  • Short communication Microinjection of NMDA antagonist into the NTS of conscious rats blocks the Bezold-Jarisch Reflex
    1996
    Co-Authors: Deoclécio A. Chianca, Benedito H. Machado
    Abstract:

    The purpose of the present study was to evaluate whether or not cardiovagal excitatory and sympatho-inhibitory pathways of the Bezold-Jarisch Reflex at the Nq?S level were mediated by NMDA receptors. The Bezold-Jarisch Reflex was activated by intravenous (i.v.) injection of serotonin in consci~ous rats before and after microinjection of phosphonovaleric acid (AP-5), a selective NMDA antagonist, into the NTS. The Bezold-Jarisch Reflex was also activated before and after methyl-atropine (i.v.) in order to evaluate if the changes in mean arterial pressure were dependent on the bradycardic response. The data showed that AP-5 into the NTS produced a dose-dependent reduction in both bradycardic and hypotensive responses to activation of the Bezold-Jarisch Reflex. Methyl-atropine also blocked the bradycardic and hypotensive responses to Bezold-Jarisch Reflex activation. The data show that in conscious rats the cardiovagal component of the Bezold-Jarisch Reflex plays a major role in the cardiovascular changes produced by the activation of this Reflex and suggest that the neurotransmis,;ion of the cardiovagal component of the Bezold-Jarisch Reflex is mediated by NMDA receptors.

Ajoy Prasad Shetty - One of the best experts on this subject based on the ideXlab platform.

  • Bezold–Jarisch Reflex causing bradycardia and hypotension in a case of severe dystrophic cervical kyphotic deformity: a case report and review of literature
    European Spine Journal, 2020
    Co-Authors: Soundararajan Dilip Chand Raja, Shanmuganathan Rajasekaran, K. S. Sri Vijayanand, Ajoy Prasad Shetty, Rishi Mugesh Kanna
    Abstract:

    Purpose A 17-year-old adolescent with neurofibromatosis and severe cervicothoracic deformity was identified to have thoracic inlet compression leading to bradycardia and hypotension, only during prone positioning, and we discuss its successful management. Methods Preoperative halo-gravity traction reduced the deformity from 126° to 91°. During prone positioning, sudden onset bradycardia was followed by asystole, which disappeared immediately on turning over to supine position. Surgery was called off after two additional failed attempts of prone positioning. Results A retrospective analysis of CT and MRI showed severe narrowing of the thoracic inlet. In this patient, the right thoracic inlet was severely narrow, and prone positioning caused a further dynamic compromise stimulating right vagal nerve. The right vagus supplies the sinoatrial node, which is the natural pacemaker of the heart, and its stimulation causes sympathetic inhibition. Bezold–Jarisch Reflex is a cardio-inhibitory Reflex occurring due to vagal stimulation resulting in sudden bradycardia, asystole, and hypotension. To facilitate prone positioning, the medial end of the clavicles, along with limited manubrium excision, was performed relieving the vagal compression. C2–T4 instrumented decompression followed by anterior reconstruction and cervical plating was performed. The postoperative period was uneventful, and the final deformity was 45°. Conclusion Bezold–Jarisch Reflex as a result of narrow thoracic inlet caused by cervical kyphosis and compensatory hyperlordosis of the upper thoracic spine has never been reported. This case highlights the need to introspect into thoracic inlet morphology in severe cervicothoracic deformities. Thoracic inlet decompression is an efficient way of addressing this unique complication.

  • bezold jarisch Reflex causing bradycardia and hypotension in a case of severe dystrophic cervical kyphotic deformity a case report and review of literature
    European Spine Journal, 2020
    Co-Authors: Soundararajan Dilip Chand Raja, Shanmuganathan Rajasekaran, Ajoy Prasad Shetty, K Sri S Vijayanand, Rishi Mugesh Kanna
    Abstract:

    A 17-year-old adolescent with neurofibromatosis and severe cervicothoracic deformity was identified to have thoracic inlet compression leading to bradycardia and hypotension, only during prone positioning, and we discuss its successful management. Preoperative halo-gravity traction reduced the deformity from 126° to 91°. During prone positioning, sudden onset bradycardia was followed by asystole, which disappeared immediately on turning over to supine position. Surgery was called off after two additional failed attempts of prone positioning. A retrospective analysis of CT and MRI showed severe narrowing of the thoracic inlet. In this patient, the right thoracic inlet was severely narrow, and prone positioning caused a further dynamic compromise stimulating right vagal nerve. The right vagus supplies the sinoatrial node, which is the natural pacemaker of the heart, and its stimulation causes sympathetic inhibition. Bezold–Jarisch Reflex is a cardio-inhibitory Reflex occurring due to vagal stimulation resulting in sudden bradycardia, asystole, and hypotension. To facilitate prone positioning, the medial end of the clavicles, along with limited manubrium excision, was performed relieving the vagal compression. C2–T4 instrumented decompression followed by anterior reconstruction and cervical plating was performed. The postoperative period was uneventful, and the final deformity was 45°. Bezold–Jarisch Reflex as a result of narrow thoracic inlet caused by cervical kyphosis and compensatory hyperlordosis of the upper thoracic spine has never been reported. This case highlights the need to introspect into thoracic inlet morphology in severe cervicothoracic deformities. Thoracic inlet decompression is an efficient way of addressing this unique complication.

  • Bezold–Jarisch Reflex causing bradycardia and hypotension in a case of severe dystrophic cervical kyphotic deformity: a case report and review of literature
    European Spine Journal, 2020
    Co-Authors: Soundararajan Dilip Chand Raja, Shanmuganathan Rajasekaran, Ajoy Prasad Shetty, K Sri S Vijayanand, Rishi Mugesh Kanna
    Abstract:

    A 17-year-old adolescent with neurofibromatosis and severe cervicothoracic deformity was identified to have thoracic inlet compression leading to bradycardia and hypotension, only during prone positioning, and we discuss its successful management. Preoperative halo-gravity traction reduced the deformity from 126° to 91°. During prone positioning, sudden onset bradycardia was followed by asystole, which disappeared immediately on turning over to supine position. Surgery was called off after two additional failed attempts of prone positioning. A retrospective analysis of CT and MRI showed severe narrowing of the thoracic inlet. In this patient, the right thoracic inlet was severely narrow, and prone positioning caused a further dynamic compromise stimulating right vagal nerve. The right vagus supplies the sinoatrial node, which is the natural pacemaker of the heart, and its stimulation causes sympathetic inhibition. Bezold–Jarisch Reflex is a cardio-inhibitory Reflex occurring due to vagal stimulation resulting in sudden bradycardia, asystole, and hypotension. To facilitate prone positioning, the medial end of the clavicles, along with limited manubrium excision, was performed relieving the vagal compression. C2–T4 instrumented decompression followed by anterior reconstruction and cervical plating was performed. The postoperative period was uneventful, and the final deformity was 45°. Bezold–Jarisch Reflex as a result of narrow thoracic inlet caused by cervical kyphosis and compensatory hyperlordosis of the upper thoracic spine has never been reported. This case highlights the need to introspect into thoracic inlet morphology in severe cervicothoracic deformities. Thoracic inlet decompression is an efficient way of addressing this unique complication.

Shanmuganathan Rajasekaran - One of the best experts on this subject based on the ideXlab platform.

  • Bezold–Jarisch Reflex causing bradycardia and hypotension in a case of severe dystrophic cervical kyphotic deformity: a case report and review of literature
    European Spine Journal, 2020
    Co-Authors: Soundararajan Dilip Chand Raja, Shanmuganathan Rajasekaran, K. S. Sri Vijayanand, Ajoy Prasad Shetty, Rishi Mugesh Kanna
    Abstract:

    Purpose A 17-year-old adolescent with neurofibromatosis and severe cervicothoracic deformity was identified to have thoracic inlet compression leading to bradycardia and hypotension, only during prone positioning, and we discuss its successful management. Methods Preoperative halo-gravity traction reduced the deformity from 126° to 91°. During prone positioning, sudden onset bradycardia was followed by asystole, which disappeared immediately on turning over to supine position. Surgery was called off after two additional failed attempts of prone positioning. Results A retrospective analysis of CT and MRI showed severe narrowing of the thoracic inlet. In this patient, the right thoracic inlet was severely narrow, and prone positioning caused a further dynamic compromise stimulating right vagal nerve. The right vagus supplies the sinoatrial node, which is the natural pacemaker of the heart, and its stimulation causes sympathetic inhibition. Bezold–Jarisch Reflex is a cardio-inhibitory Reflex occurring due to vagal stimulation resulting in sudden bradycardia, asystole, and hypotension. To facilitate prone positioning, the medial end of the clavicles, along with limited manubrium excision, was performed relieving the vagal compression. C2–T4 instrumented decompression followed by anterior reconstruction and cervical plating was performed. The postoperative period was uneventful, and the final deformity was 45°. Conclusion Bezold–Jarisch Reflex as a result of narrow thoracic inlet caused by cervical kyphosis and compensatory hyperlordosis of the upper thoracic spine has never been reported. This case highlights the need to introspect into thoracic inlet morphology in severe cervicothoracic deformities. Thoracic inlet decompression is an efficient way of addressing this unique complication.

  • bezold jarisch Reflex causing bradycardia and hypotension in a case of severe dystrophic cervical kyphotic deformity a case report and review of literature
    European Spine Journal, 2020
    Co-Authors: Soundararajan Dilip Chand Raja, Shanmuganathan Rajasekaran, Ajoy Prasad Shetty, K Sri S Vijayanand, Rishi Mugesh Kanna
    Abstract:

    A 17-year-old adolescent with neurofibromatosis and severe cervicothoracic deformity was identified to have thoracic inlet compression leading to bradycardia and hypotension, only during prone positioning, and we discuss its successful management. Preoperative halo-gravity traction reduced the deformity from 126° to 91°. During prone positioning, sudden onset bradycardia was followed by asystole, which disappeared immediately on turning over to supine position. Surgery was called off after two additional failed attempts of prone positioning. A retrospective analysis of CT and MRI showed severe narrowing of the thoracic inlet. In this patient, the right thoracic inlet was severely narrow, and prone positioning caused a further dynamic compromise stimulating right vagal nerve. The right vagus supplies the sinoatrial node, which is the natural pacemaker of the heart, and its stimulation causes sympathetic inhibition. Bezold–Jarisch Reflex is a cardio-inhibitory Reflex occurring due to vagal stimulation resulting in sudden bradycardia, asystole, and hypotension. To facilitate prone positioning, the medial end of the clavicles, along with limited manubrium excision, was performed relieving the vagal compression. C2–T4 instrumented decompression followed by anterior reconstruction and cervical plating was performed. The postoperative period was uneventful, and the final deformity was 45°. Bezold–Jarisch Reflex as a result of narrow thoracic inlet caused by cervical kyphosis and compensatory hyperlordosis of the upper thoracic spine has never been reported. This case highlights the need to introspect into thoracic inlet morphology in severe cervicothoracic deformities. Thoracic inlet decompression is an efficient way of addressing this unique complication.

  • Bezold–Jarisch Reflex causing bradycardia and hypotension in a case of severe dystrophic cervical kyphotic deformity: a case report and review of literature
    European Spine Journal, 2020
    Co-Authors: Soundararajan Dilip Chand Raja, Shanmuganathan Rajasekaran, Ajoy Prasad Shetty, K Sri S Vijayanand, Rishi Mugesh Kanna
    Abstract:

    A 17-year-old adolescent with neurofibromatosis and severe cervicothoracic deformity was identified to have thoracic inlet compression leading to bradycardia and hypotension, only during prone positioning, and we discuss its successful management. Preoperative halo-gravity traction reduced the deformity from 126° to 91°. During prone positioning, sudden onset bradycardia was followed by asystole, which disappeared immediately on turning over to supine position. Surgery was called off after two additional failed attempts of prone positioning. A retrospective analysis of CT and MRI showed severe narrowing of the thoracic inlet. In this patient, the right thoracic inlet was severely narrow, and prone positioning caused a further dynamic compromise stimulating right vagal nerve. The right vagus supplies the sinoatrial node, which is the natural pacemaker of the heart, and its stimulation causes sympathetic inhibition. Bezold–Jarisch Reflex is a cardio-inhibitory Reflex occurring due to vagal stimulation resulting in sudden bradycardia, asystole, and hypotension. To facilitate prone positioning, the medial end of the clavicles, along with limited manubrium excision, was performed relieving the vagal compression. C2–T4 instrumented decompression followed by anterior reconstruction and cervical plating was performed. The postoperative period was uneventful, and the final deformity was 45°. Bezold–Jarisch Reflex as a result of narrow thoracic inlet caused by cervical kyphosis and compensatory hyperlordosis of the upper thoracic spine has never been reported. This case highlights the need to introspect into thoracic inlet morphology in severe cervicothoracic deformities. Thoracic inlet decompression is an efficient way of addressing this unique complication.