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Transseptal catheterization
Published in Debabrata Mukherjee, Eric R. Bates, Marco Roffi, Richard A. Lange, David J. Moliterno, Nadia M. Whitehead, Cardiovascular Catheterization and Intervention, 2017
ST segment elevation, accompanied by chest pain, hypotension, bradycardia, and diaphoresis, has been reported by a number of operators to occur during or immediately after transseptal access. While the phenomenon resembles a Bezold-Jarisch reflex, the mechanism is unclear. It occurs in slightly less than 1% of cases.[101] Although introduction of air with consequent right coronary embolization has been postulated,[117] coronary angiography during such episodes has failed to confirm this,[118] and a neurally mediated mechanism remains the likely etiology. The phenomenon is typically transient and may respond to atropine.
Orthotopic Cardiac Transplantation
Published in David Robertson, Italo Biaggioni, Disorders of the Autonomic Nervous System, 2019
The most widely recognized and clinically relevant consequence of cardiac denervation in human transplantation is the removal of afferent nociceptive fibres. The inability of patients to perceive myocardial ischemia (Gao et al., 1989; Schroeder and Hunt, 1992) necessitates frequent and costly coronary angiography to follow the course of graft coronary atherosclerosis. Because of C-fibre afferent pathway interruption, the Bezold- Jarisch cardiac inhibitory reflexes originating in cardiac sensory receptors (Mark, 1983) are absent in transplantation patients. Observations in transplant patients have confirmed a cardiac origin for various components of the Bezold-Jarisch reflex in man which were previously based mainly on animal model studies. Arrowood et al., (1989) showed that the afferent limb of the cardiac-depressor reflex could not be activated by intracoronary iodinated contrast in transplant patients, although this response is frequently seen in normally innervated subjects. Similarly, in autotransplanted dogs cryptenamine injection into the left ventricle does not activate the Bezold-Jarisch response (see Reinnervation-Animal Models, below). Scherrer et al., (1990a) surreptitiously but carefully recorded an episode of vasodilator-induced hypovolemic hypotension in an instrumented cardiac transplant patient. Depression of the patient’s muscle sympathetic nerve activity and of the remnant atrial heart rate (see Atrial Activity, below) occurred in the setting of profound hypotension, indicating strong vagal activation despite ventricular denervation. That afferent ventricular mechanoreceptor activation is not essential for this clinical example of the Bezold-Jarisch reflex was a new observation.
Cardiac Preload Control: An Important Function of Cardiac Chemical Receptors*
Published in Irving H. Zucker, Joseph P. Gilmore, Reflex Control of the Circulation, 2020
David M. Nganele, Thomas H. Hintze
In the face of a fall in blood pressure, the systemic arterial baroreflexes will attempt to increase pressure by increasing peripheral resistance and cardiac output and do the opposite when blood pressure is rising. The hypotension elicited by the Bezold-Jarisch reflex would be expected to unload the arterial baroreflexes. In one study, Chen (1979) varied the carotid sinus pressure after aortic nerve section and studied the extent of the hypotension and bradycardia to veratridine. He found that the effects of the Bezold-Jarisch reflex were influenced by the prevailing arterial baroreceptor input, varying inversely with the carotid sinus pressure. Other investigators have shown that the inhibition exerted by the cardiopulmonary receptors with vagal afferents is more pronounced after sinoaortic denervation. (Koike et al., 1975; Mancia et al., 1976). The early phases of myocardial infarction in humans may be accompanied by hypotension and bradycardia and this has been in part attributed to activation of the Bezold-Jarisch reflex (Webb et al., 1972; Esente et al., 1983). Thames et al. (1978) showed in the dog that brief occlusion of the left circumflex coronary artery caused a more profound depressor effect after sinoaortic denervation. Similar results have been reported by other investigators (Peterson and Bishop, 1974). In the cat, Hintze et al. (1984) showed that elimination of an arm of the baroreflex (ligation of the carotid arteries) potentiated the Bezold-Jarisch responses to PGI2 and AA. In dogs with total baroreflex denervation, stimulation of prostaglandin production by AA administration caused greater reductions in heart rate and blood pressures than before baroreflex denervation (Hintze and Kaley, 1984). These studies would indicate that there is an antagonism between the Bezold-Jarisch reflex and the systemic arterial baroreflexes. It would be expected therefore, that the arterial baroreflexes might modify the reflex control of preload by the Bezold-Jarisch reflex. This would be expected since the baroreflexes are thought to cause reflex venoconstriction, and to augment venous return and cardiac output in the face of reduced arterial pressure (Brunner et al., 1981; Rothe 1983).
Veratrum parviflorum poisoning: identification of steroidal alkaloids in patient blood and breast milk
Published in Clinical Toxicology, 2022
Jared T. Seale, Joseph E. Carpenter, Matthew D. Eisenstat, Emily A. Kiernan, Brent W. Morgan, Daniel P. Nogee, Xinzhu Pu, Colin A. Therriault, Michael Yeh, Owen M. McDougal
In April 2015, two patients presented to a Georgia hospital with Veratrum poisoning resulting from erroneous identification of V. parviflorum as Allium tricoccum [11]. In addition to a Bezold-Jarisch reflex, neurological symptoms including taste disturbance, vertigo, dysarthria, and vision changes were observed. These neurological symptoms have not been reported for previous cases of toxicity with V. viride or V. album [12–16,18,19]. Analysis of V. parviflorum plant biomass identified verazine, veratramine, veratridine, and cyclopamine, all of which have been previously observed in Veratrum species [11]. Due to the appearance of atypical neurological symptoms and a lack of information regarding the phytochemical profile of V. parviflorum, it was hypothesized that additional steroidal alkaloids, beyond those previously detected from patients, may be observed. The present study investigated eight cases of V. parviflorum poisoning resulting from the misidentification of plant material. Patient serum and breast milk was collected over the course of inpatient treatment and analyzed using high performance liquid chromatography-quadrupole time of flight mass spectrometry (HPLC-QTOF).
Short-term transcutaneous non-invasive vagus nerve stimulation may reduce disease activity and pro-inflammatory cytokines in rheumatoid arthritis: results of a pilot study
Published in Scandinavian Journal of Rheumatology, 2021
AM Drewes, C Brock, SE Rasmussen, HJ Møller, B Brock, BW Deleuran, AD Farmer, M Pfeiffer-Jensen
To the best of our knowledge, this is the first exploratory report examining the short-term effect of n-VNS directed at therapeutically manipulating the cholinergic anti-inflammatory pathway in RA. We demonstrated a small but significant reduction in disease activity in participants with active disease, which was associated with a reduction in IFN-γ. The reduction in disease activity was mediated by a decrease in the number of swollen and tender joints, as well as in CRP. Such effects were not seen in those participants with low disease activity, suggesting that this effect was specific to those RA patients with marked inflammation. This may be due to the fact that they already had a very low inflammation level and therefore a decrease in disease severity was more difficult to obtain. In addition, disease activity was negatively associated with baseline CVT. The observed decrease in systolic BP is a physiological response to increased parasympathetic tone. Given the lack of standardized VNS paradigms (long term vs short term and invasive, aural vagal stimulation and n-VNS), an obvious limitation exists since there is no consensus on the best cardiovascular outcome parameter. It has been shown that n-VNS has limited effects on C-fibres. Consequently, there is expectedly constrained stimulation of the Bezold–Jarisch reflex following n-VNS, which would have inhibited sympathetic activity, leading to bradycardia, vasodilatation, and hypotension (25). In contrast to previous studies where no effect on HR and BP is reported, we saw a reduction in systolic BP following n-VNS.
Special maternal care bundle to attenuate post-spinal hypotension in cesarean section: A randomized controlled clinical trial
Published in Egyptian Journal of Anaesthesia, 2023
Abdelrhman Alshawadfy, Shaimaa A. Dahshan, Ahmed A. Ellilly, Ahmed M. Elewa
Spinal anesthesia-induced hypotension is the pathophysiological response to sympathectomy caused by the neuro-axial blockade. Peripheral vasodilatation and parasympathetic activation predominate. A pregnant uterus compresses the vena cava, and lower leg venous blood accumulation reduces cardiac output and venous return [2]. Furthermore, higher sympathetic block inversely decreases the compensatory mechanisms via baroreceptors resulting in cardioinhibitory reflexes, such as the Bezold-Jarisch reflex. Chemoreceptors located on cardiac vagal afferents are the site of this reflex, which is mediated by 5-HT or 5-HT3 agonists. As a result, hypotension, dizziness, vomiting, nausea, and bradycardia commonly occur with spinal anesthesia [4].