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The de Winter electrocardiogram (ECG) pattern, marked by upsloping ST depression in leads V2-V6, ST elevation in lead aVR, and tall symmetric T waves, typically indicates left anterior descending artery (LAD) occlusion. Traditionally linked to LAD occlusion, it is rare in severe aortic stenosis and the Bezold-Jarisch reflex (BJR). We report an 83-year-old man with severe aortic stenosis who developed hypotension due to bleeding and exhibited the de Winter ECG pattern. This case highlights how severe aortic stenosis and BJR can lead to significant hemodynamic instability and ischemic ECG changes, resolving after hemodynamic stabilization.

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PURPOSE: The goal of this manuscript was to review the biological and clinical evidence that serotonin neurotransmission might play an important role in the  physiology and treatment of vasovagal syncope. METHODS: The authors reviewed PubMed and handsearches of secondary sources for papers related to the Bezold-Jarisch reflex and serotonin, the plausible involvement of the Bezold-Jarisch reflex in vasovagal syncope, and three lines of clinical evidence involving serotonin and the syncope. RESULTS: The Bezold-Jarisch reflex was first described following the infusion of veratrum alkaloids into animals in the 19th century. The reflex is triggered by serotonin stimulation chemoreceptors and mechanoreceptors in the the left ventricle. The afferent component of the reflex is carried by unmyelinated type C vagal nerve fibers, which results in parasympathetic efferent stimulation that causes bradycardia. The similarity of the combination of hypotension and bradycardia in the Bezold-Jarisch reflex and in vasovagal syncope led to the suggestion that the reflex was the cause of the syndrome.  Three lines of evidence implicate the serotonin 5HT3 receptors in the heart in the reflex. There is genetic and physiologic evidence for the serotonin 5HT1A and 5HT3 receptors and the serotonin reuptake transporter (SERT). Acute blockade of SERT induces vasovagal syncope in humans undergoing head-up tilt table testing, and SERT inhibition reduces hypotension and bradycardia during spinal anaesthesia. Finally, three randomized clinical trials of SERT inhibitors uniformly reported that they significantly reduce the likelihood of vasovagal syncope recurrences. CONCLUSION: Multiple lines of evidence implicate serotonin neurotransmission in the cause of vasovagal syncope.

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Acute coronary syndrome (ACS) presents significant diagnostic challenges, particularly in cases with atypical presentations and complex clinical scenarios. Here, we describe the case of a 59-year-old man who presented with presyncope, bradycardia, hypotension, and later syncope, attributed to the Bezold-Jarisch reflex. Electrocardiographic findings suggested both inferior and anterior wall infarction, with dynamic changes in T-wave morphology further complicating the diagnostic process. Despite a type A Wellens' pattern indicating critical stenosis in the proximal left anterior descending (LAD) artery, coronary angiography revealed a complete thrombotic lesion in the proximal right coronary artery (RCA), necessitating urgent intervention. Despite the Wellens pattern indicating LAD involvement, RCA revascularization took precedence due to immediate thrombotic risk. This case underscores the diagnostic challenges associated with conflicting clinical manifestations in ACS and highlights the importance of individualized management strategies integrating advanced diagnostic modalities to optimize outcomes. Understanding the interplay of complex clinical presentations and employing a nuanced approach to management are crucial in effectively navigating ACS scenarios.

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The Bezold-Jarisch reflex (BJR) is an inhibitory reflex characterized by bradycardia, hypotension, and apnea originating from ventricular mechanoreceptors. BJR is an uncommon but serious complication of neuraxial anesthesia. We present a case of a 33-year-old female undergoing combined spinal-epidural anesthesia prior to cesarean delivery who developed profound BJR, resulting in emergent actions. Within minutes of injection, she became severely bradycardic (HR: 17 bpm) and hypotensive (SBP: 30s mmHg) with bradypnea (RR: 6/min) and was treated with epinephrine. Fetal bradycardia prompted emergency cesarean section. Following delivery, the patient developed ventricular tachycardia, which was treated with intravenous fluids and cardiac monitoring. Both patient and neonate were discharged in stable condition on postoperative day four. This case illustrates the rapid maternal and fetal compromise associated with BJR during neuraxial anesthesia and the need for prompt recognition and treatment. Key steps include stopping anesthesia, intravenous fluid, left-lateral positioning, judicious vasopressors, fetal monitoring, and preparing for emergent delivery.

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Examination of circulatory dynamics and autonomic nerve activity in acute hemorrhage in diabetic (DM) rats revealed that despite decreased receptor sensitivity to arterial blood pressure, the DM rats experienced a decline in the heart rate and acceleration of the parasympathetic nerve activity at the sympathoinhibitory phase in response to bleeding (Bezold-Jarisch [B-J] reflex). To elucidate the involvement of the B-J reflex as a reaction to acute hemorrhage in DM rats by assessing c-Fos-positive cell (c-Fos) expression in the nucleus of the solitary tract (SolM), the primary relay nucleus of the baroreflex, Streptozotocin-induced DM and non-DM rats underwent controlled-graded bleeding or continuous phenylephrine infusion under conscious state. Changes in hemodynamics and autonomous nervous system caused by acute hemorrhage and continuous phenylephrine infusion were examined by analyzing blood pressure-heart rate variability. Furthermore, effects of hemorrhage and phenylephrine infusion on the expression of c-Fos in SolM were examined. DM rats showed increased c-Fos expression in response to acute blood loss in the SolM. Non-DM rats showed the same phenomenon in response to continuous phenylephrine infusion in the SolM. Significant interactions between DM and Non-DM rats were observed among hemodynamic and autonomic response to acute hemorrhage and continuous phenylephrine infusion. DM rats were sensitive to acute blood loss, and the circulatory system easily collapsed with accelerating parasympathetic activity in the form of the B-J reflex.

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Bioelectronic medicine is a novel field in modern medicine based on the specific neuronal stimulation to control organ function, cardiovascular, and immune homeostasis. However, most studies addressing neuromodulation of the immune system have been conducted on anesthetized animals, which can affect the nervous system and neuromodulation. Here, we review recent studies involving conscious experimental rodents (rats and mice) to better understand the functional organization of neural control of immune homeostasis. We highlight typical experimental models of cardiovascular regulation, such as electrical activation of the aortic depressor nerve or the carotid sinus nerve, bilateral carotid occlusion, the Bezold-Jarisch reflex, and intravenous administration of the bacterial endotoxin lipopolysaccharide. These models have been used to investigate the relationship between neuromodulation of the cardiovascular and immune systems in conscious rodents (rats and mice). These studies provide critical information about the neuromodulation of the immune system, particularly the role of the autonomic nervous system, i.e., the sympathetic and parasympathetic branches acting both centrally (hypothalamus, nucleus ambiguus, nucleus tractus solitarius, caudal ventrolateral medulla, and rostral ventrolateral medulla), and peripherally (particularly spleen and adrenal medulla). Overall, the studies in conscious experimental models have certainly highlighted to the reader how the methodological approaches used to investigate cardiovascular reflexes in conscious rodents (rats and mice) can also be valuable for investigating the neural mechanisms involved in inflammatory responses. The reviewed studies have clinical implications for future therapeutic approaches of bioelectronic modulation of the nervous system to control organ function and physiological homeostasis in conscious physiology.

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The Bezold-Jarisch reflex is a powerful inhibitory reflex initiated by activation of cardiopulmonary vagal nerves during myocardial ischemia, hemorrhage, and orthostatic stress leading to bradycardia, vasodilation, hypotension, and vasovagal syncope. This clinically relevant reflex has been studied by measuring heart rate (HR) and mean arterial pressure (MAP) responses to injections of a variety of chemical compounds. We hypothesized that reflex responses to different compounds vary due to differential activation of vagal afferent subtypes and/or variable coactivation of excitatory afferents. HR and MAP responses to intravenous injections of the transient receptor potential vanilloid-1 (TRPV1) agonist capsaicin and the serotonin 5-HT3 receptor agonist phenylbiguanide (PBG) were measured in anesthetized C57BL/6 mice before and after bilateral cervical vagotomy. Capsaicin and PBG evoked rapid dose-dependent decreases in HR and MAP followed by increases in HR and MAP above baseline. Bezold-Jarisch reflex responses were abolished after vagotomy, whereas the delayed tachycardic and pressor responses to capsaicin and PBG were differentially enhanced. The relative magnitude of bradycardic versus depressor responses (↓HR/↓MAP) in vagus-intact mice was greater with capsaicin. In contrast, after vagotomy, the magnitude of excitatory tachycardic versus pressor responses (↑HR/↑MAP) was greater with PBG. Although capsaicin-induced increases in MAP and HR postvagotomy were strongly attenuated or abolished after administration of the ganglionic blocker hexamethonium, PBG-induced increases in MAP and HR were mildly attenuated and unchanged, respectively. We conclude that responses to capsaicin and PBG differ in mice, with implications for delineating the role of endogenous agonists of TRPV1 and 5-HT3 receptors in evoking cardiopulmonary reflexes in pathophysiological states.

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The concept of the Bezold-Jarisch reflex(BJR)has experienced more than 100 years,which is that the left ventricular unmyelinated vagus nerve input receptors are stimulated by drugs or me-chanical pull,the stimulation was then integrated by the vagus nerve afferent brain stem nucleus and trans-mitted to the vascular movement center to form vagal nerve output enhancement,leading to severe bradycar-dia,peripheral vasodatation,hypotension and even cardiac arrest,e.g,a cardiovascular inhibitory reaction.Although BJR is applied in clinical anesthesia,insufficient attention has been paid to it,resulting in absence of the mechanism analysis of related sudden severe bradycardia,hypotension,and even cardiac ar-rest in perioperative period.

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We present a novel description of Bezold-Jarisch Reflex (BJR) during cardiopulmonary exercise testing (CPET) in three young female patients with Group 1 pulmonary arterial hypertension (PAH). These three cases presented within 26 months, representing only 0.8% of 11,387 tests on patients with PAH undergoing CPET during this time frame.

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Objective: This study is aimed to analyze the characteristics of congenital anomalous origin of coronary artery in pediatric patients with syncope. Methods: A total of eight patients were retrospectively analyzed from August 2018 to August 2020 who were admitted to the Peking University First Hospital with the complaint of syncope and were diagnosed with congenital coronary artery disease. Results: In total, eight patients were included in the study with a median age of 12.5 ± 2.7 (8-16) years. In total, four of them were males, and four were females. Six of the eight patients were diagnosed with right anomalous coronary artery from the opposite sinus (R-ACAOS), while two patients were diagnosed with left anomalous coronary artery from the opposite sinus (L-ACAOS). The most frequent inducement was exercise, and the commonest prodromes were dizziness and blurred vision. Serum cardiac markers and exercise electrocardiography test (EET) were normal in seven of the patients. The majority of cases had abnormal electrocardiograms (ECGs), but only two of them manifested elevated/depressed ST-T segments. In total, seven patients had positive head-up tilt test (HUT). Echocardiography and coronary artery computed tomography angiography (CTA) were performed to aid the diagnosis. Coronary unroofing procedures were conducted in four patients, and none of them reported syncope after the surgery. The other four patients received routine medical treatment for vasovagal-like syncope. In total, two patients out of them became asymptomatic, and in the other two patients, episodes of syncope were reduced, but they still required medical treatment. Conclusion: Congenital coronary artery anomalies in children with syncope need prompt attention. Though ECG and echocardiography are the common methods for investigating cardiac syncope, they have limited ability to find coronary artery anomalies. When coronary artery anomalies are suspected, coronary CTA should be considered.

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This paper reviews the many functions of the vagus nerve, to understand how they interact in daily life and what might be accomplished by therapeutical electrical stimulation. A short historical introduction on the discovery and name-giving of the cranial nerves numbers 9-12 is followed by an overview of the functions that are under lower brain stem control: heart (rate, contractility), intestine (swallowing, peristalsis and glands secretions, feeling of satiety), lungs (bronchoconstriction, lung-irritant and stretch receptor signaling), blood pressure (by vascular wall stress sensing) and blood gases by specialized receptors. Key in the review is the physiology behind beat-by-beat heart rate variations, how everyday life is reflected in its variability, from exciting moments to quiet sleep, with the 'common faint' or vasovagal collapse as extreme example. Next, the recently proposed role of the vagus nerve in limiting inflammation is discussed. This has led to adoption of an earlier developed technique for epilepsy treatment, i.e., electrical stimulation of one vagus nerve bundle in the neck, but now for immune diseases like rheumatoid arthritis and the scope is even widening to depression and cluster headache. However, the problem in application of whole vagus nerve stimulation is the lack of specificity: there is no way to titrate the stimulation to an observable effect variable. All nerves in the bundle, incoming and outgoing, can be 'hit', leading to side-effects which limit the intended application.

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Evidence indicates that the activation of the parasympathetic branch of the autonomic nervous system may be effective in treating inflammatory diseases. Previously, we have described that baroreflex activation displays anti-inflammatory properties. Analogous to the baroreflex, the Bezold-Jarisch reflex also promotes parasympathetic activation with simultaneous inhibition of the sympathetic system. Thus, the present study aimed to evaluate whether the activation of the Bezold-Jarisch reflex would also have the ability to reduce inflammation in unanesthetized rats. We used lipopolysaccharide (LPS) injection (5mg/kg, i.p.) to induce systemic inflammation in male Wistar Hannover rats and phenylbiguanide (PBG) administration (5µg/kg, i.v.) to activate the Bezold-Jarisch reflex. Spleen, heart, hypothalamus, and blood samples were collected to determine the levels of cytokines. Compared to baseline, PBG reduced the arterial pressure (115±2 vs. 88±5mmHg) and heart rate (380±7 vs. 114±26bpm), immediately after its administration, confirming the activation of the parasympathetic system and inhibition of the sympathetic system. From the immunological point of view, the activation of the Bezold-Jarisch reflex decreased the plasma levels of TNF (LPS: 775±209 vs. PBG + LPS: 248±30pg/ml) and IL-6 levels in the spleen (LPS: 39±6 vs. PBG + LPS: 24±4pg/mg of tissue). However, it did not change the other cytokines in the plasma or the other tissues evaluated. These findings confirm that the activation of the Bezold-Jarisch reflex can modulate inflammation and support the understanding that the cardiovascular reflexes regulate the immune system.

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Background: When exposed to repetitive umbilical cord occlusions (UCO) with worsening acidemia, fetuses eventually develop cardiovascular decompensation manifesting as pathological hypotensive arterial blood pressure (ABP) responses to fetal heart rate (FHR) decelerations. Failure to maintain cardiac output during labor is a key event leading up to brain injury. We reported that the timing of the event when a fetus begins to exhibit this cardiovascular phenotype is highly individual and was impossible to predict. Objective: We hypothesized that this phenotype would be reflected in the individual behavior of heart rate variability (HRV) as measured by root mean square of successive differences of R-R intervals (RMSSD), a measure of vagal modulation of HRV, which is known to increase with worsening acidemia. This is clinically relevant because HRV can be computed in real-time intrapartum. Consequently, we aimed to predict the individual timing of the event when a hypotensive ABP pattern would emerge in a fetus from a series of continuous RMSSD data. Study Design: Fourteen near-term fetal sheep were chronically instrumented with vascular catheters to record fetal arterial blood pressure, umbilical cord occluder to mimic uterine contractions occurring during human labor and ECG electrodes to compute the ECG-derived HRV measure RMSSD. All animals were studied over a ~6 h period. After a 1-2 h baseline control period, the animals underwent mild, moderate, and severe series of repetitive UCO. We applied the recently developed machine learning algorithm to detect physiologically meaningful changes in RMSSD dynamics with worsening acidemia and hypotensive responses to FHR decelerations. To mimic clinical scenarios using an ultrasound-based 4 Hz FHR sampling rate, we recomputed RMSSD from FHR sampled at 4 Hz and compared the performance of our algorithm under both conditions (1,000 Hz vs. 4 Hz). Results: The RMSSD values were highly non-stationary, with four different regimes and three regime changes, corresponding to a baseline period followed by mild, moderate, and severe UCO series. Each time series was characterized by seemingly randomly occurring (in terms of timing of the individual onset) increase in RMSSD values at different time points during the moderate UCO series and at the start of the severe UCO series. This event manifested as an increasing trend in RMSSD values, which counter-intuitively emerged as a period of relative stationarity for the time series. Our algorithm identified these change points as the individual time points of cardiovascular decompensation with 92% sensitivity, 86% accuracy and 92% precision which corresponded to 14 ± 21 min before the visual identification. In the 4 Hz RMSSD time series, the algorithm detected the event with 3 times earlier detection times than at 1,000 Hz, i.e., producing false positive alarms with 50% sensitivity, 21% accuracy, and 27% precision. We identified the overestimation of baseline FHR variability by RMSSD at a 4 Hz sampling rate to be the cause of this phenomenon. Conclusions: The key finding is demonstration of FHR monitoring to detect fetal cardiovascular decompensation during labor. This validates the hypothesis that our HRV-based algorithm identifies individual time points of ABP responses to UCO with worsening acidemia by extracting change point information from the physiologically related fluctuations in the RMSSD signal. This performance depends on the acquisition accuracy of beat to beat fluctuations achieved in trans-abdominal ECG devices and fails at the sampling rate used clinically in ultrasound-based systems. This has implications for implementing such an approach in clinical practice.

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El reflejo de Bezold Jarisch es un reflejo cardioinhibitorio que juega un papel en la homeostasis cardiovascular. Consiste en la triada dada por hipotensión, bradicardia y vasodilatación periférica que puede ser desencadenada tanto por estímulos mecánicos, como químicos. Se considera que el mecanismo eferente contrarresta e inhibe los efectos del influjo simpático y, por el contrario, activa los efectos producidos por el sistema parasimpático. Durante la cirugía neurológica, la disminución de la presión intracraneal posterior a la extracción de colgajo óseo en la craneotomía, el uso de medicamentos osmóticos para disminuir el edema cerebral e incluso la posición del paciente durante el procedimiento suponen situaciones más propensas a la aparición del reflejo.

The Bezold Jarisch reflex is a cardioinhibitory reflex that plays a role in cardiovascular homeostasis. It consists of a triad given by hypotension, bradycardia, and peripheral vasodilation that can be triggered by both mechanical and chemical stimuli. The efferent counteracting mechanism is considered to inhibit the effects of sympathetic influx and, conversely, activates the effects produced by the parasympathetic system. During neurological surgery, the decrease in intracranial pressure after bone flap extraction in the craniotomy, the use of osmotic medications to decrease cerebral edema and even the position of the patient during the procedure supposes situations more prone to reflex appearance

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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.

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BACKGROUND: The Bezold-Jarisch reflex is a depressor reflex of the heart due to the preferential distribution of vagal nerves in the inferior wall of the left ventricle. We report a case of Stanford type A acute aortic dissection, in which coronary spastic angina caused the Bezold-Jarisch reflex in the acute phase. CASE REPORT: A 53-year-old man presented with left chest pain and cold sweating. An electrocardiogram was normal and the high-sensitivity cardiac troponin T level was negative. A diagnosis of Stanford type A acute aortic dissection was made based on computed tomography (CT); there was no evidence of ischemic heart disease on coronary CT angiogram obtained simultaneously. While waiting for emergency surgical repair, chest pain worsened, followed by bradycardia and hypotension, along with ST-segment elevations in the inferior leads, all of which were resolved by conservative treatment. During surgery, no evidence to suggest an extension of the dissection to the ostium of the right coronary artery was observed. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: The present case highlights the importance of recognizing the Bezold-Jarisch reflex because this depressor reflex may require different management than other conditions.

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Acute inferior myocardial damage can induce transient bradycardia and hypotension-the Bezold-Jarisch reflex, which is explained by the preferential distribution of vagal nerves in the inferior wall of the left ventricle. We report a 76-year-old man who showed a perfusion defect in the inferior wall with redistribution on exercise scintigraphy with thallium-201. Of note, during exercise at an intensity of 100 watts, the patient's heart rate transiently decreased from 122 to 95 bpm in sinus rhythm, accompanied by ST-segment depression. A diagnosis of coronary spastic angina was made since no stenotic lesions were observed on conventional coronary angiography.

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