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Journal articles on the topic 'Bradycardia'

Author: Grafiati

Published: 4 June 2021

Last updated: 31 January 2023

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1

Gautam, Binod, Ashmita Maharjan, and Suson Ghimire. "Bradycardia during laparoscopic surgeries: A cross-sectional study." Journal of Kathmandu Medical College 9, no. 1 (March 31, 2020): 5–12. http://dx.doi.org/10.3126/jkmc.v9i1.33515.

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Background: Bradycardia occurring during laparoscopic surgery potentially leads to cardiac arrest and adverse outcomes. Apart from the vagal reflex for its genesis, the knowledge on frequency and risk factors is limited. Objectives: To identify the bradycardia frequency and time points for its occurrence during laparoscopic surgeries. Methodology: In this hospital-based cross-sectional study, anaesthesia-related incident reports on bradycardia were collected from January to December 2019. Bradycardias (heart rate less than 60/minute) that occurred during laparoscopic surgeries were analyzed to characterize patient factors, the time point for occurrence, circumstantial events, management strategies, and outcomes. Results: Among 801 laparoscopic surgeries, 28 (3.4%) bradycardic incidents were identified, with one progressing to cardiac arrest. All bradycardias occurred in 26 patients undergoing laparoscopic cholecystectomy under general anaesthesia, with two patients each experiencing two bradycardic episodes. The mean patient age was 45 (±16.3) years and 17 (65.3%) were women. Fifteen (57.6%) patients had no co-morbidity. Controlled hypertension and hypothyroidism co-existed in seven (26.9%) and three (11.5%) cases respectively. Bradycardia occurred once each (3.5%) during laryngoscopy and endotracheal intubation. Six (21.4%) and twenty (71.4%) bradycardias respectively occurred before and during pneumoperitoneum. The mean of minimum heart rates was 43 (±8.8) per minute. Anticholinergics were administered in 25 (89.2%) incidents. Stopping surgery and pneumoperitoneum deflation included other major management strategies. The cardiac arrest case received chest compressions and adrenaline. Surgery resumed in all cases without adversity. Conclusion: Bradycardia occurs during laparoscopic surgery, more frequently during pneumoperitoneum and in healthy and younger females. Immediate cessation of surgical stimuli and atropine administration possibly prevent bradycardia from progressing to cardiac arrest.

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Rozloznik, Miroslav, Julian F. R. Paton, and Mathias Dutschmann. "Repetitive paired stimulation of nasotrigeminal and peripheral chemoreceptor afferents cause progressive potentiation of the diving bradycardia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 296, no. 1 (January 2009): R80—R87. http://dx.doi.org/10.1152/ajpregu.00806.2007.

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Hallmarks of the mammalian diving response are protective apnea and bradycardia. These cardiorespiratory adaptations can be mimicked by stimulation of the trigeminal ethmoidal nerve (EN5) and reflect oxygen-conserving mechanisms during breath-hold dives. Increasing drive from peripheral chemoreceptors during sustained dives was reported to enhance the diving bradycardia. The underlying neuronal mechanisms, however, are unknown. In the present study, expression and plasticity of EN5-bradycardias after paired stimulation of the EN5 and peripheral chemoreceptors was investigated in the in situ working heart-brain stem preparation. Paired stimulations enhanced significantly the bradycardic responses compared with EN5-evoked bradycardia using submaximal stimulation intensity. Alternating stimulations of the EN5 followed by paired stimulation of the EN5 and chemoreceptors (10 trials, 3-min interval) caused a progressive and significant potentiation of EN5-evoked diving bradycardia. In contrast, bradycardias during paired stimulation remained unchanged during repetitive stimulation. The progressive potentiation of EN5-bradycardias was significantly enhanced after microinjection of the 5-HT3 receptor agonist (CPBG hydrochloride) into the nucleus tractus solitarii (NTS), while the 5-HT3 receptor antagonist (zacopride hydrochloride) attenuated the progressive potentiation. These results suggest an integrative function of the NTS for the multimodal mediation of the diving response. The potentiation or training of a submaximal diving bradycardia requires peripheral chemoreceptor drive and involves neurotransmission via 5-HT3 receptor within the NTS.

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3

Cummings, Kevin J., Aihua Li, Evan S. Deneris, and Eugene E. Nattie. "Bradycardia in serotonin-deficient Pet-1−/− mice: influence of respiratory dysfunction and hyperthermia over the first 2 postnatal weeks." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 298, no. 5 (May 2010): R1333—R1342. http://dx.doi.org/10.1152/ajpregu.00110.2010.

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Neonatal rodents deficient in medullary serotonin neurons have respiratory instability and enhanced spontaneous bradycardias. This study asks if, in Pet-1−/− mice over development: 1) the respiratory instability leads to hypoxia; 2) greater bradycardia is related to the degree of hypoxia or concomitant hypopnea; and 3) hyperthermia exacerbates bradycardias. Pet-1+/+, Pet-1+/−, and Pet-1−/− mice [postnatal days (P) 4–5, P11–12, P14–15] were held at normal body temperature (Tb) and were then made 2°C hypo- and hyperthermic. Using a pneumotach-mask system with ECG, we measured heart rate, metabolic rate (V̇o2), and ventilation. We also calculated indexes for apnea-induced hypoxia (total hypoxia: apnea incidence × O2 consumed during apnea = μl·g−1·min−1) and bradycardia (total bradycardia: bradycardia incidence × magnitude = beats missed/min). Resting heart rate was significantly lower in all Pet-1−/− animals, irrespective of Tb. At P4–5, Pet-1−/− animals had approximately four- to eightfold greater total bradycardia ( P < 0.001), owing to an approximately two- to threefold increase in bradycardia magnitude and a near doubling in bradycardia incidence. Pet-1−/− animals had a significantly reduced V̇o2 at all Tb; thus there was no genotype effect on total hypoxia. At P11–12, total bradycardia was nearly threefold greater in hyperthermic Pet-1−/− animals compared with controls ( P < 0.01). In both genotypes, bradycardia magnitude was positively related to the degree of hypopnea ( P = 0.02), but there was no genotype effect on degree of hypopnea or total hypoxia. At P14–15, genotype had no effect on total bradycardia, but Pet-1−/− animals had up to seven times more total hypoxia ( P < 0.001), owing to longer and more frequent apneas and a normalized V̇o2. We infer from these data that 1) Pet-1−/− neonates are probably not hypoxic from respiratory dysfunction until P14–15; 2) neither apnea-related hypoxia nor greater hypopnea contribute to the enhanced bradycardias of Pet-1−/− neonates from approximately P4 to approximately P12; and 3) an enhancement of a temperature-sensitive reflex may contribute to the greater bradycardia in hyperthermic Pet-1−/− animals at approximately P12.

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4

García-Domingo, Mónica, José Ángel García-Pedraza, Juan Francisco Fernández-González, Cristina López, María Luisa Martín, and Asunción Morán. "Fluoxetine Treatment Decreases Cardiac Vagal Input and Alters the Serotonergic Modulation of the Parasympathetic Outflow in Diabetic Rats." International Journal of Molecular Sciences 23, no. 10 (May 20, 2022): 5736. http://dx.doi.org/10.3390/ijms23105736.

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Comorbid diabetes and depression constitutes a major health problem, worsening associated cardiovascular diseases. Fluoxetine’s (antidepressant) role on cardiac diabetic complications remains unknown. We determined whether fluoxetine modifies cardiac vagal input and its serotonergic modulation in male Wistar diabetic rats. Diabetes was induced by alloxan and maintained for 28 days. Fluoxetine was administered the last 14 days (10 mg/kg/day; p.o). Bradycardia was obtained by vagal stimulation (3, 6 and 9 Hz) or i.v. acetylcholine administrations (1, 5 and 10 μg/kg). Fluoxetine treatment diminished vagally-induced bradycardia. Administration of 5-HT originated a dual action on the bradycardia, augmenting it at low doses and diminishing it at high doses, reproduced by 5-CT (5-HT1/7 agonist). 5-CT did not alter the bradycardia induced by exogenous acetylcholine. Decrease of the vagally-induced bradycardia evoked by high doses of 5-HT and 5-CT was reproduced by L-694,247 (5-HT1D agonist) and blocked by prior administration of LY310762 (5-HT1D antagonist). Enhancement of the electrical-induced bradycardia by 5-CT (10 μg/kg) was abolished by pretreatment with SB269970 (5-HT7 receptor antagonist). Thus, oral fluoxetine treatment originates a decrease in cardiac cholinergic activity and changes 5-HT modulation of bradycardic responses in diabetes: prejunctional 5-HT7 receptors augment cholinergic-evoked bradycardic responses, whereas prejunctional 5-HT1D receptors inhibit vagally-induced bradycardia.

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5

Maltais-Bilodeau, Camille, Maryse Frenette, Geneviève Morissette, Dennis Bailey, Karine Cloutier, Camille Laberge, and David Simonyan. "2 Systemic glucocorticoids and bradycardia in critically ill children: a retrospective study." Paediatrics & Child Health 25, Supplement_2 (August 2020): e1-e1. http://dx.doi.org/10.1093/pch/pxaa068.001.

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Abstract Background Glucocorticoids are widely used in the pediatric population. They are associated with numerous side effects including repercussions on the cardiovascular system. The impact on heart rate is not well known, but bradycardia has been reported, mostly with high doses. Objectives We described the occurrence of bradycardias and the variation of heart rate in critically ill children receiving glucocorticoids. Design/Methods We conducted a retrospective study including 1 month old to 18 year old children admitted to the Pediatric Intensive Care Unit between 2014 and 2017, who received a glucocorticoid dose equivalent to 1 to 15 mg/kg/day of prednisone. We collected data on exposition to glucocorticoids, heart rate before, during and after the exposition, and interventions from the medical staff in response to bradycardia. The primary outcome was the occurrence of bradycardia and the secondary outcomes were the magnitude of heart rate variation and the clinical management of bradycardias. Results We included 92 admissions (85 patients). The median dose of glucocorticoid used was 2.80 mg/kg/day of prednisone (2.08—3.80). We found 70 cases (76%) with at least one bradycardia. Before treatment, all patients had a mean heart rate higher than the 5th percentile for age. During exposition to glucocorticoids, 8 patients (10%, n = 83) had a median heart rate ≤ 5th percentile. We noted 46 cases of bradycardia (50%) that led to an intervention from the medical staff, but no patient had a major event associated to bradycardia. We found a significant association between bradycardia and age (estimate -0.136, 95% CI -0.207—-0.065, p < 0.001), glucocorticoid dose (estimate 4.820, 95% CI 2.048—7.592, p < 0.001) and intravenous administration (estimate 8.709, 95% CI 1.893—15.524, p = 0.012). Conclusion In our study, most children hospitalized at the intensive care unit receiving standard doses of glucocorticoid experienced bradycardia. The majority of episodes led to an intervention from the medical staff. Presence of bradycardia was associated with younger age, higher dose and IV administration of glucocorticoids.

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Fortrat, Jacques-Olivier. "Zipf’s Law of Vasovagal Heart Rate Variability Sequences." Entropy 22, no. 4 (April 6, 2020): 413. http://dx.doi.org/10.3390/e22040413.

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Cardiovascular self-organized criticality (SOC) has recently been demonstrated by studying vasovagal sequences. These sequences combine bradycardia and a decrease in blood pressure. Observing enough of these sparse events is a barrier that prevents a better understanding of cardiovascular SOC. Our primary aim was to verify whether SOC could be studied by solely observing bradycardias and by showing their distribution according to Zipf’s law. We studied patients with vasovagal syncope. Twenty-four of them had a positive outcome to the head-up tilt table test, while matched patients had a negative outcome. Bradycardias were distributed according to Zipf’s law in all of the patients. The slope of the distribution of vasovagal sequences and bradycardia are slightly but significantly correlated, but only in cases of bradycardias shorter than five beats, highlighting the link between the two methods (r = 0.32; p < 0.05). These two slopes did not differ in patients with positive and negative outcomes, whereas the distribution slopes of bradycardias longer than five beats were different between these two groups (−0.187 ± 0.004 and −0.213 ± 0.006, respectively; p < 0.01). Bradycardias are distributed according to Zipf’s law, providing clear insight into cardiovascular SOC. Bradycardia distribution could provide an interesting diagnosis tool for some cardiovascular diseases.

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Ahmad, Munir, Muhammad Yasir, and Sehar Fatima. "DRUG INDUCED BRADYCARDIA." Professional Medical Journal 25, no. 06 (June 10, 2018): 908–13. http://dx.doi.org/10.29309/tpmj/2018.25.06.280.

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Background: Bradycardia in patients on rate slowing drugs i.e. beta blockers,digoxin and non dihydropyridine calcium channel blockers is common after discontinuation ofrate slowing drugs. Bradycardia persists in majority of patients, so bradycardia is not truly druginduced but due to underlying conduction system disease. Objectives: To determine the outcomein patients with bradycardia after discontinuation of rate slowing drugs in terms of frequencyof persistent bradycardia. Study Design: Descriptive cross-sectional. Place and Duration ofStudy: Cardiology Department, Faisalabad Institute of Cardiology, Faisalabad, from September2015 to March, 2016. Methodology: After written informed consent 95 patients who fulfilled theinclusion and exclusion criteria were selected for this study. Patients with bradycardia (heartrate less than 60 beats per minute) identified by pulse and electrocardiography (ECG) wereadmitted and culprit drug was discontinued. All admitted patients were followed everyday bydoing ECG and counting pulse twice. Patients, in whom bradycardia resolved, were discharged.Patients were monitored for persistent bradycardia after discontinuation of culprit drug for 5days. Results: Out of 95 patients 46 (48%) were male and 49 (52%) female, age range was25-85 years with mean age 61±11 years. Heart rate ranged 25-45 beats per minute with meanvalue of 31.28± 6.08, 72 (75.8%) patients were on beta blockers, 19 (20%) on calcium channelblockers and 4 (4.2%) patients were on digoxin. 73 (76.80%) patients had 30 AV block, 19(20%) 20 AV block while 3 (3.20%) had sinus bradycardia. Bradycardia persisted in 69 (72.60%)patients out of which 32 (69.6%) were male and 37(75.5%) female. Bradycardia resolved in 26(27.40%) patients in which 14 (30.4%) were male and 12(24.5%) were female. Conclusion:Persistent bradycardia is common in patients with drug induced bradycardia. Such bradycardiais not truly drug induced but is related to unmasking of subclinical conduction system diseaseby rate lowering drugs like beta blockers, calcium channel blockers and digoxin.

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8

Colombari, E., L. G. Bonagamba, and B. H. Machado. "Mechanisms of pressor and bradycardic responses to L-glutamate microinjected into the NTS of conscious rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 266, no. 3 (March 1, 1994): R730—R738. http://dx.doi.org/10.1152/ajpregu.1994.266.3.r730.

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Microinjection of increasing doses of L-glutamate (L-Glu, 0.03-5.0 nmol/100 nl) into the nucleus tractus solitarii (NTS) produced a dose-related pressor and bradycardic response. Prazosin virtually abolished the pressor response but produced no changes in the bradycardic response to L-Glu, indicating that bradycardia is not reflex in origin. The bradycardic response was blocked by atropine. In three different groups of rats, excitatory amino acid receptors in the NTS were blocked by increasing doses of kynurenic acid (0.5, 2.0, and 10.0 nmol/100 nl) and the pressor and bradycardic responses to L-Glu (1 nmol/100 nl) were reduced in a dose-related pattern. Reflex bradycardia induced by an increase in pressure caused by phenylephrine (iv) was also blocked by kynurenic acid. These data show that microinjection of L-Glu into the NTS of conscious rats produced pressor and bradycardic responses, which are due to the activation of two independent autonomic pathways. The data also indicate that the activation of both pathways is mediated by excitatory amino acid receptors. Considering that reflex bradycardia was also blocked by kynurenic acid, we suggest that L-Glu and excitatory amino acid receptors are part of the parasympathetic limb of the baroreceptor reflex. The pressor response to L-Glu is also mediated by excitatory amino acid receptors, but its physiological meaning is still unclear.

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Cardinal, René, Pierre Pagé, Michel Vermeulen, Caroline Bouchard, Jeffrey L. Ardell, Robert D. Foreman, and J. Andrew Armour. "Spinal cord stimulation suppresses bradycardias and atrial tachyarrhythmias induced by mediastinal nerve stimulation in dogs." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 291, no. 5 (November 2006): R1369—R1375. http://dx.doi.org/10.1152/ajpregu.00056.2006.

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Spinal cord stimulation (SCS) applied to the dorsal aspect of the cranial thoracic cord imparts cardioprotection under conditions of neuronally dependent cardiac stress. This study investigated whether neuronally induced atrial arrhythmias can be modulated by SCS. In 16 anesthetized dogs with intact stellate ganglia and in five with bilateral stellectomy, trains of five electrical stimuli were delivered during the atrial refractory period to right- or left-sided mediastinal nerves for up to 20 s before and after SCS (20 min). Recordings were obtained from 191 biatrial epicardial sites. Before SCS (11 animals), mediastinal nerve stimulation initiated bradycardia alone (12 nerve sites), bradycardia followed by tachyarrhythmia/fibrillation (50 sites), as well as tachyarrhythmia/fibrillation without a preceding bradycardia (21 sites). After SCS, the number of responsive sites inducing bradycardia was reduced by 25% (62 to 47 sites), and the cycle length prolongation in residual bradycardias was reduced. The number of responsive sites inducing tachyarrhythmia was reduced by 60% (71 to 29 sites). Once elicited, residual tachyarrhythmias arose from similar epicardial foci, displaying similar dynamics (cycle length) as in control states. In the absence of SCS, bradycardias and tachyarrhythmias induced by repeat nerve stimulation were reproducible (five additional animals). After bilateral stellectomy, SCS no longer influenced neuronal induction of bradycardia and atrial tachyarrhythmias. These data indicate that SCS obtunds the induction of atrial arrhythmias resulting from excessive activation of intrinsic cardiac neurons and that such protective effects depend on the integrity of nerves coursing via the subclavian ansae and stellate ganglia.

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Higuchi, S., A. Takeshita, H. Higashi, N. Ito, T. Imaizumi, H. Matsuguchi, and M. Nakamura. "Lowering calcium in the nucleus tractus solitarius causes hypotension and bradycardia." American Journal of Physiology-Heart and Circulatory Physiology 250, no. 2 (February 1, 1986): H226—H230. http://dx.doi.org/10.1152/ajpheart.1986.250.2.h226.

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It has been shown that saline microinjected into the region of the nucleus tractus solitarius (NTS) causes, but artificial cerebrospinal fluid (CSF) in the same volume does not cause, hypotension and bradycardia. This study was done to examine the possibility that the difference in effects between saline and artificial CSF may be due to the lack of calcium ions in saline. In anesthetized rats, saline or artificial CSF with or without calcium ions was microinjected into the region of the NTS. Saline microinjected in volumes of 0.2 and 0.5 microliter produced the volume-dependent decreases in arterial pressure and heart rate. Saline with added calcium ions and artificial CSF did not elicit the hypotensive and bradycardic response, but artificial CSF without calcium ions produced hypotension and bradycardia. These results suggest that the lack of calcium ions in the injected solutions is the factor that determines the hypotensive and bradycardic response. These results suggest that lowering the local availability of calcium to the NTS neurons results in hypotension and bradycardia.

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Chitravanshi, Vineet C., and Hreday N. Sapru. "Microinjections of urocortin1 into the nucleus ambiguus of the rat elicit bradycardia." American Journal of Physiology-Heart and Circulatory Physiology 300, no. 1 (January 2011): H223—H229. http://dx.doi.org/10.1152/ajpheart.00391.2010.

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Urocortins are members of the hypothalamic corticotropin-releasing factor (CRF) peptide family. Urocortin1 (UCN1) mRNA has been reported to be expressed in the brainstem neurons. The present investigation was carried out to test the hypothesis that microinjections of UCN1 into the nucleus ambiguus (nAmb) may elicit cardiac effects. Urethane-anesthetized, artificially ventilated, adult male Wistar rats, weighing between 300–350 g, were used. nAmb was identified by microinjections of l-glutamate (5 mM, 30 nl). Microinjections (30 nl) of different concentrations (0.062, 0.125, 0.25, and 0.5 mM) of UCN1 into the nAmb elicited bradycardic responses (26.5 ± 1, 30.1 ± 1.7, 46.9 ± 1.7, and 40.3 ± 2.6 beats/min, respectively). These heart rate responses were not accompanied by significant changes in mean arterial pressure. The bradycardic responses to maximally effective concentration of UCN1 (0.25 mM) were significantly ( P < 0.05) attenuated by prior microinjections of a selective antagonist (NBI 27914, 1.5 mM) for CRF type 1 receptor (CRF1R). Prior microinjections of ionotropic glutamate receptor (iGLUR) antagonists [d-(−)-2-amino-7-phosphono-heptanoic acid and 2,3-dioxo-6-nitro-1,2,3,4-tetrahydrobenzo-(f)quinoxaline-7-sulfonamide disodium] also attenuated the bradycardia elicited by UCN1 microinjections into the nAmb. Microinjections of NBI 27914 (1.5 mM) into the nAmb did not alter baroreflex responses. Bilateral vagotomy abolished the bradycardic responses to microinjections of UCN1 into the nAmb. These results indicated that 1) microinjections of UCN1 into the nAmb elicited bradycardia, 2) the bradycardia was vagally mediated, 3) activation of CRF1Rs in the nAmb was responsible for the actions of UCN1, and 4) activation of iGLURs in the nAmb also participated in the bradycardia elicited by UCN1.

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Pregerson, Brady. "BradyCardia." Emergency Medicine News 42, no. 10 (October 2020): 27. http://dx.doi.org/10.1097/01.eem.0000719132.08202.f7.

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Hayes, Denise D. "Bradycardia." Nursing 34 (May 2004): 4–12. http://dx.doi.org/10.1097/00152193-200405001-00002.

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MEE, CHERYL L. "Bradycardia." Nursing 26, no. 4 (April 1996): 25. http://dx.doi.org/10.1097/00152193-199604000-00009.

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MEE, CHERYL L. "Bradycardia." Nursing 26, no. 4 (April 1996): 25. http://dx.doi.org/10.1097/00152193-199626040-00009.

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Nandi, P. R., and B. Astley. "Bradycardia." Anaesthesia 40, no. 11 (November 1985): 1140. http://dx.doi.org/10.1111/j.1365-2044.1985.tb10635.x.

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BURKE, LAURA J. "BRADYCARDIA." Nursing 18, no. 9 (September 1988): 102–5. http://dx.doi.org/10.1097/00152193-198809000-00030.

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18

Kim, Albert M., and Nova Goldschlager. "Bradycardia." Journal of Electrocardiology 41, no. 3 (May 2008): 206. http://dx.doi.org/10.1016/j.jelectrocard.2008.02.021.

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Kemeç, Zeki, and Ali Gürel. "Acute kidney injury and sinus bradycardia associated with near-drowning." Ukrainian Journal of Nephrology and Dialysis, no. 4(68) (August 5, 2020): 18–22. http://dx.doi.org/10.31450/ukrjnd.4(68).2020.03.

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Acute kidney injury (AKI) occurs in different situations and may have a variable prognosis due to underlying cause, clinical setting and comorbidity. Near-drowning is known to lead to bradycardic rhythms which can lead to hypoxia because of hypoperfusion. AKI has a high risk of mortality and morbidity. However, sequelae of sinus bradycardia are related to its underlying etiology. Urinary, cardiovascular and respiratory disorders are more frequently seen after near-drowning. Near-drowning related AKI and sinus bradycardia are not reported together in the literature. We aimed to emphasize these complications in near-drowning patients.

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Deshmukh, Amrish, and Cevher Ozcan. "Symptomatic Long Pauses and Bradycardia due to Massive Multinodular Goiter." Case Reports in Cardiology 2017 (2017): 1–3. http://dx.doi.org/10.1155/2017/4201942.

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Sinus node dysfunction with symptomatic bradycardia or chronotropic incompetence is generally an indication for pacemaker implantation. However, in patients with symptomatic sinus bradycardia, the identification and treatment of underlying pathologies may avoid the need for permanent pacemaker implantation. We present a case of carotid sinus syndrome and severe obstructive sleep apnea due to a massive multinodular goiter in a patient who presented with recurrent sinus pauses and syncope. The patient was managed without pacemaker implantation but instead with thyroidectomy resulting in decompression of the carotid sinus and airway and resolution of bradycardic episodes.

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Kitchen, Amy M., Donal S. O'Leary, and Tadeusz J. Scislo. "Sympathetic and parasympathetic component of bradycardia triggered by stimulation of NTS P2X receptors." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 2 (February 2006): H807—H812. http://dx.doi.org/10.1152/ajpheart.00889.2005.

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We have previously shown that activation of P2X purinoceptors in the subpostremal nucleus tractus solitarius (NTS) produces a rapid bradycardia and hypotension. This bradycardia could occur via sympathetic withdrawal, parasympathetic activation, or a combination of both mechanisms. Thus we investigated the relative roles of parasympathetic activation and sympathetic withdrawal in mediating this bradycardia in chloralose-urethane anesthetized male Sprague-Dawley rats. Microinjections of the selective P2X purinoceptor agonist α,β-methylene ATP (25 pmol/50 nl and 100 pmol/50 nl) were made into the subpostremal NTS in control animals, after atenolol (2 mg/kg iv), a β1-selective antagonist, and after atropine methyl bromide (2 mg/kg iv), a muscarinic receptor antagonist. The bradycardia observed with activation of P2X receptors at the low dose of the agonist is mediated almost entirely by sympathetic withdrawal. After β1-adrenergic blockade, the bradycardia was reduced to just −5.1 ± 0.5 versus −28.8 ± 5.1 beats/min in intact animals. Muscarinic blockade did not produce any significant change in the bradycardic response at the low dose. At the high dose, both β1-adrenergic blockade and muscarinic blockade attenuated the bradycardia similarly, −37.4 ± 6.4 and −40.6 ± 3.7 beats/min, respectively, compared with −88.0 ± 11 beats/min in control animals. Double blockade of both β1-adrenergic and muscarinic receptors virtually abolished the response (−2.5 ± 0.8 beats/min). We conclude that the relative contributions of parasympathetic activation and sympathetic withdrawal are dependent on the extent of P2X receptor activation.

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Fashola, Yomi, Sanjeev Kaul, and Douglas Finefrock. "Bradycardia after Tube Thoracostomy for Spontaneous Pneumothorax." Case Reports in Emergency Medicine 2018 (2018): 1–3. http://dx.doi.org/10.1155/2018/6351521.

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We present the case of an elderly patient who became bradycardic after chest tube insertion for spontaneous pneumothorax. Arrhythmia is a rare complication of tube thoracostomy. Unlike other reported cases of chest tube induced arrhythmias, the bradycardia in our patient responded to resuscitative measures without removal or repositioning of the tube. Our patient, who had COPD, presented with shortness of breath due to spontaneous pneumothorax. Moments after tube insertion, patient developed severe bradycardia that responded to Atropine. In patients requiring chest tube insertion, it is important to be prepared to provide cardiopulmonary resuscitative therapy in case the patient develops a life-threatening arrhythmia.

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Cardoso, Leonardo Máximo, Débora Simões de Almeida Colombari, José V. Menani, Glenn M. Toney, Deoclécio Alves Chianca, and Eduardo Colombari. "Cardiovascular responses to hydrogen peroxide into the nucleus tractus solitarius." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 297, no. 2 (August 2009): R462—R469. http://dx.doi.org/10.1152/ajpregu.90796.2008.

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The nucleus tractus solitarius (NTS), a major hindbrain area involved in cardiovascular regulation, receives primary afferent fibers from peripheral baroreceptors and chemoreceptors. Hydrogen peroxide (H2O2) is a relatively stable and diffusible reactive oxygen species (ROS), which acting centrally, may affect neural mechanisms. In the present study, we investigated effects of H2O2 alone or combined with the glutamatergic antagonist kynurenate into the NTS on mean arterial pressure (MAP) and heart rate (HR). Conscious or anesthetized (urethane and α-chloralose) male Holtzman rats (280–320 g) were used. Injections of H2O2 (125 to 1500 pmol/40 nl) into the intermediate NTS of anesthetized rats evoked dose-dependent and transient hypotension (−18 ± 3 to −55 ± 11 mmHg) and bradycardia (−16 ± 5 to −116 ± 40 bpm). Injection of the catalase inhibitor 3-amino-1,2,4-triazole (100 nmol/40 nl) into the NTS also produced hypotension and bradycardia. Previous injection of the ionotropic l-glutamate receptor antagonist kynurenate (7 nmol/40 nl) attenuated by 48% the bradycardic response, without changing the hypotension evoked by H2O2 (500 pmol/40 nl) in anesthetized rats. The antioxidant l-ascorbate (600 pmol/80 nl) injected into the NTS attenuated the bradycardic (42%) and hypotensive (67%) responses to H2O2 (500 pmol/40 nl) into the NTS. In conscious rats, injection of H2O2 (50 nmol/100 nl) into the NTS also evoked intense bradycardia (−207 ± 8 bpm) and hypotension (−54 ± 6 mmHg) that were abolished by prior injection of kynurenate (7 nmol/100 nl). The results show that H2O2 into the NTS induces hypotension and bradycardia probably due to activation of glutamatergic mechanisms.

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Agrawal, Lakshminrusimha, and Chandrasekharan. "Chest Compressions for Bradycardia during Neonatal Resuscitation—Do We Have Evidence?" Children 6, no. 11 (October 29, 2019): 119. http://dx.doi.org/10.3390/children6110119.

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The International Liaison Committee on Resuscitation (ILCOR) recommends the initiation of chest compressions (CC) during neonatal resuscitation after 30 s of effective ventilation if the infant remains bradycardic (defined as a heart rate less than 60 bpm). The CC are performed during bradycardia to optimize organ perfusion, especially to the heart and brain. Among adults and children undergoing cardiopulmonary resuscitation (CPR), CC is indicated only for pulselessness or poor perfusion. Neonates have a healthy heart that attempts to preserve coronary and cerebral perfusion during bradycardia secondary to asphyxia. Ventilation of the lungs is the key step during neonatal resuscitation, improving gas exchange and enhancing cerebral and cardiac blood flow by changes in intrathoracic pressure. Compressing the chest 90 times per minute without synchrony with innate cardiac activity during neonatal bradycardia is not based on evidence and could potentially be harmful. Although there are no studies evaluating outcomes in neonates, a recent pediatric study in a hospital setting showed that when CC were initiated during pulseless bradycardia, a third of the patients went into complete arrest, with poor survival at discharge. Ventilation-only protocols such as helping babies breathe are effective in reducing mortality and stillbirths in low-resource settings. In a situation of complete cardiac arrest, CC reinitiates pulmonary flow and supports gas exchange. However, the benefit/harm of performing asynchronous CC during bradycardia as part of neonatal resuscitation remains unknown.

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25

Raman, Rajendra, Sarah Coppes, Tessa Hellingman, and Casper Laclé. "Junctional bradycardia caused by ciguatera intoxication." BMJ Case Reports 12, no. 5 (May 2019): e229354. http://dx.doi.org/10.1136/bcr-2019-229354.

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Ciguatera is a common but underreported tropical disease caused by the consumption of coral reef fish contaminated by ciguatoxins. Gastrointestinal and neurological symptoms predominate, but may be accompanied by cardiovascular features such as hypotension and sinus bradycardia. Here, we report an unusual case of junctional bradycardia caused by ciguatera in the Caribbean; to our knowledge, the first such report from the region. An increase in global sea temperatures is predicted to lead to the spread of ciguatera beyond traditional endemic areas, and the globalisation of trade in coral reef fish has resulted in sporadic cases occurring in developed countries far away from endemic areas. This case serves as a reminder to consider environmental intoxications such as ciguatera within the differential diagnosis of bradycardias.

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26

Edwards, G. L., A. K. Johnson, and J. D. Peuler. "Enhanced bradycardia but not renal sympathoinhibition during hemorrhage in rats with area postrema lesions." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 2 (August 1, 1994): H569—H573. http://dx.doi.org/10.1152/ajpheart.1994.267.2.h569.

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Hypotensive hemorrhage inhibits renal sympathetic nerve activity (SNA) and heart rate (HR) in rats. The area postrema (AP) is reported to modulate autonomic responses to arginine vasopressin (AVP) and may be a site where circulating AVP influences SNA and HR during hypotensive hemorrhage. We found a similar renal sympathoinhibition in AP-lesioned (APX) and sham-lesioned (Sham) rats during hypotensive hemorrhage and a greater bradycardia in APX compared with Sham rats. Further inhibition of renal SNA with AVP infusion was not observed in APX rats, although the bradycardic action of AVP infusion was comparable to that in Sham rats. Thus the AP attenuates bradycardia but not renal sympathoinhibition during hypotensive hemorrhage in normal rats. Nonetheless, an intact AP permits further reduction in renal SNA during infusion of AVP. If AVP contributes to hypotensive hemorrhage-induced renal sympathoinhibition, its action may occur at sites other than the AP or at the AP where such action is counterbalanced by sympathoexcitatory factor(s) also activated during hypotensive hemorrhage. Finally, enhanced bradycardia during hypotensive hemorrhage in APX rats suggests it may not be the site of action for AVP-induced bradycardia in intact rats.

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27

Roach, Daniel, Ela Thakore, and Robert S. Sheldon. "Large-magnitude, transient, bradycardic events in rabbits." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 277, no. 1 (July 1, 1999): R243—R249. http://dx.doi.org/10.1152/ajpregu.1999.277.1.r243.

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We propose that heart period sequences are organized similarly to sentences, with a lexicon of recurrent, similarly shaped words. These words should fulfill four criteria: universality, nonrandomness, central statistical tendencies, and specific associated physiology. Here we describe a large-magnitude, transient bradycardia (LMTB) and assess whether it constitutes a word. LMTBs were seen in 11 of 12 adult female rabbits. All shape parameters were different than those of the beat-randomized and phase-randomized surrogate sequences ( P < 0.05–0.001). LMTBs were 8.4 ± 2.9 beats and 2.64 ± 0.87 s long and were characterized by bradycardia of 77 ± 49 ms over 1.09 ± 0.49 s with a recovery to baseline over 1.56 ± 0.61 s. The LMTBs had a slower recovery than onset in 9 of 11 rabbits and were highly peaked in 10 of 11 rabbits ( P< 0.05). Scalar, magnitude, and shape parameters had values with central statistical tendencies. About 76% of LMTBs were accompanied by hypotension (mean −6.1 ± 3.9 mmHg) that lagged 2 beats behind the onset of the bradycardia and that correlated with the bradycardia (−10.5 ± 4.1 ms/mmHg). Thus transient bradycardic events are a distinct “word” in the lexicon of heart rate variability.

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28

Ahmad, Munir, Muhammad Yasir, and Sehar Fatima. "DRUG INDUCED BRADYCARDIA." Professional Medical Journal 25, no. 06 (June 9, 2018): 908–13. http://dx.doi.org/10.29309/tpmj/18.4793.

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29

Paula, Patrícia M. De, Jaci A. Castania, Leni G. H. Bonagamba, Hélio C. Salgado, and Benedito H. Machado. "Hemodynamic responses to electrical stimulation of the aortic depressor nerve in awake rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 277, no. 1 (July 1, 1999): R31—R38. http://dx.doi.org/10.1152/ajpregu.1999.277.1.r31.

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Changes in mean arterial pressure (MAP), heart rate (HR), and vascular resistance (hindquarter and mesenteric territories) in response to electrical stimulation (ES) of the aortic depressor nerve (ADN) were evaluated in conscious freely moving rats. Platinum electrodes were implanted into the ADN of all rats studied, and some of these animals were also implanted with miniaturized Doppler probes around the superior mesenteric artery and inferior abdominal aorta (hindquarter). In both groups, the femoral artery and vein were catheterized one day before the experiments. In the first group of rats ( n = 7), the control ES of the ADN in the range from 0.5 to 3.0 V (50 Hz, 10 ms) produced bradycardia and hypotension in an intensity-dependent manner, and treatment with methylatropine (intravenously) blocked the bradycardia but produced no significant changes in the hypotensive response. In a second group ( n = 6), ES of the ADN was performed with the intensity fixed at 3 V and the frequency of the stimuli varying from 10 to 50 Hz. In this group, the hypotensive response was frequency dependent, whereas the bradycardic response was not. In a third group of rats ( n = 6), ES of the ADN (2.5 V) produced hypotension (−35 ± 4 mmHg), minor changes in the mesenteric (+5 ± 14%), and vasodilation in hindquarter (−32 ± 6%) vascular beds. The data show that 1) ES of the ADN produces a fall in pressure, bradycardia, vasodilation in the hindquarter, and no changes in the mesenteric vascular resistance, 2) methylatropine blocked the bradycardia and produced no effect on the hypotensive response to ES of the ADN, and 3) the baroreceptor afferent fibers involved in the hypotensive response to ES of ADN are sensitive to the variation of the frequency of the stimuli, whereas the fibers involved in the bradycardic response are not.

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30

Abbas, Shahid, Sehar Fatima, Naeem Hameed, and Muhammad Qasim. "PERSISTENT BRADYCARDIA;." Professional Medical Journal 24, no. 11 (November 3, 2017): 1652–56. http://dx.doi.org/10.29309/tpmj/2017.24.11.666.

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Objectives: To determine the outcome in patients with bradycardia afterdiscontinuation of rate slowing drugs in terms of frequency of persistent bradycardia. StudyDesign: Descriptive study. Setting: Faisalabad Institute of Cardiology, Cardiology Department.Period: 2013-2014. Materials and Methods: Pulse and ECG were used to identify the patientsand after obtaining informed consent, total 95 patients of bradycardia were included fromemergency. Patients with persistent bradycardia were noted after 5 days of discontinuationof culprit drug. Results: Among total 95 patients, 46(48.4%) were male and 49(51.6%) werefemale. Patients with rate limiting drugs include β blockers 79(75.8%), CCBs 19(20%) anddigoxin 4(4.2%). Patients presented to hospital have sinus bradycardia 3(3.2%), 2nd degreeAV block 19(20%) and 3rd degree AV block 73(76.8%). After 5 days of discontinuation ofculprit drug, bradycardia persisted in 32(69.6%) male, 37(75.5%) female patients with sinusbradycardia persisted in 1(33.3%), 2nd degree AV block in 7(36.8%) and 3rd degree AV blockin 61(83.6%). Conclusion: In majority of patient on rate slowing drug, bradycardia persistedafter discontinuation of these drugs. Bradycardia was not truly drug induced, but it was due tounderlying conducting system disease which was unmasked by rate slowing drugs.

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31

Yamada, Atsushi. "Tachycardia/Bradycardia." Nihon Naika Gakkai Zasshi 100, no. 10 (2011): 3079–83. http://dx.doi.org/10.2169/naika.100.3079.

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32

Kim, Hyeon Ok, Chang Woo Chung, Hong Youl Kim, and Dong Ki Lee. "Severe Bradycardia." Korean Journal of Anesthesiology 24, no. 2 (1991): 446. http://dx.doi.org/10.4097/kjae.1991.24.2.446.

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33

Pelter, Michele M., and Mary G. Carey. "Symptomatic Bradycardia." American Journal of Critical Care 18, no. 2 (March 1, 2009): 173–74. http://dx.doi.org/10.4037/ajcc2009513.

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34

Altun, A., G. Aydyn, L. Bontempi, A. Curnis, M. Cerini, A. D'Aloia, A. Lipari, et al. "Bradycardia Pacing." Europace 13, Supplement 1 (January 31, 2011): i16—i17. http://dx.doi.org/10.1093/europace/euq475.

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35

Jacome, D. E. "Ictal bradycardia." Neurology 43, no. 9 (September 1, 1993): 1860. http://dx.doi.org/10.1212/wnl.43.9.1860.

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36

Fincham, R. W. "Ictal bradycardia." Neurology 43, no. 9 (September 1, 1993): 1860. http://dx.doi.org/10.1212/wnl.43.9.1860-a.

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37

Brown, Benjamin D., and David J. Fox. "Bradycardia pacing." Medicine 38, no. 9 (September 2010): 526–29. http://dx.doi.org/10.1016/j.mpmed.2010.06.013.

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38

Kirkwood, Graeme, David J. Fox, and Benjamin D. Brown. "Bradycardia pacing." Medicine 42, no. 10 (October 2014): 615–19. http://dx.doi.org/10.1016/j.mpmed.2014.07.005.

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39

Nikolaidou, Theodora, David J. Fox, and Benjamin D. Brown. "Bradycardia pacing." Medicine 46, no. 10 (October 2018): 646–51. http://dx.doi.org/10.1016/j.mpmed.2018.07.002.

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40

ELDER, ANNEMARIE N. "SINUS BRADYCARDIA." Nursing 24, no. 11 (November 1994): 48–50. http://dx.doi.org/10.1097/00152193-199411000-00018.

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MIRACLE, VICKIE, and JENNIFER M. SIMS. "SINUS BRADYCARDIA." Nursing 26, no. 7 (July 1996): 43. http://dx.doi.org/10.1097/00152193-199607000-00013.

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42

MIRACLE, VICKIE, and JENNIFER M. SIMS. "SINUS BRADYCARDIA." Nursing 26, no. 7 (July 1996): 43. http://dx.doi.org/10.1097/00152193-199626070-00013.

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43

Craig, Karen Jean. "Symptomatic bradycardia." Nursing 40, no. 12 (December 2010): 72. http://dx.doi.org/10.1097/01.nurse.0000390688.56631.47.

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44

Miller, Michelle S., Kevin M. Shannon, and Glenn T. Wetzel. "Neonatal bradycardia." Progress in Pediatric Cardiology 11, no. 1 (May 2000): 19–24. http://dx.doi.org/10.1016/s1058-9813(00)00032-1.

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45

Nikolić, George. "Sudden bradycardia." Heart & Lung 40, no. 2 (March 2011): 177–79. http://dx.doi.org/10.1016/j.hrtlng.2010.07.002.

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46

Eckert, S., H. M. Mertens, H. Mannebach, and U. Gleichmann. "Bradycardia factitia." DMW - Deutsche Medizinische Wochenschrift 113, no. 12 (March 25, 2008): 469–71. http://dx.doi.org/10.1055/s-2008-1067665.

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47

Freysz, Marc, Quadiri Timour, Lucien Bertrix, and Georges Faucon. "Propofol bradycardia." Canadian Journal of Anaesthesia 38, no. 1 (January 1991): 137–38. http://dx.doi.org/10.1007/bf03009178.

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48

Hrishi, AjayPrasad, Unnikrishnan Prathapadas, Smita Vimala, and KarenRuby Lionel. "Ictal bradycardia: A missed etiology for intraoperative bradycardia." Neurology India 66, no. 1 (2018): 237. http://dx.doi.org/10.4103/0028-3886.222862.

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49

Machado, B. H., and M. J. Brody. "Mechanisms of pressor response produced by stimulation of nucleus ambiguus." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 259, no. 5 (November 1, 1990): R955—R962. http://dx.doi.org/10.1152/ajpregu.1990.259.5.r955.

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We showed previously that activation of nucleus ambiguus (NA) induced bradycardia and increased arterial pressure. In this study, we compared responses produced by electrical and chemical (glutamate) stimulation of NA and adjacent rostral ventrolateral medulla (RVLM). Equivalent pressor responses were elicited from both areas. However: 1) The response from RVLM was elicited at a lower frequency. 2) Regional vascular resistance changes were different, i.e., electrical stimulation of NA increased vascular resistance in hindquarters much more than the renal and mesenteric beds. In contrast, electrical and chemical stimulation of RVLM produced a more prominent effect on the renal vascular bed. 3) Bradycardia was elicited from NA at lower current intensity. 4) Glutamate produced bradycardia only when injected into NA. Studies in rats with sinoaortic deafferentation showed that bradycardic response to activation of NA was only partly reflex in origin. We conclude that 1) NA and RVLM control sympathetic outflow to regional vascular beds differentially and 2) the NA region involves parasympathetic control of heart rate and sympathetic control of arterial pressure.

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50

López, Cristina, Miriam Gómez-Roso, José Ángel García-Pedraza, María Luisa Martín, Asunción Morán, and Mónica García-Domingo. "Fluoxetine oral treatment discloses 5-HT1D receptor as vagoinhibitor of the cardiac cholinergic neurotransmission in rat." Canadian Journal of Physiology and Pharmacology 97, no. 2 (February 2019): 90–98. http://dx.doi.org/10.1139/cjpp-2018-0390.

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Although depression and cardiovascular diseases are related, the role of antidepressants such as fluoxetine (increasing serotonin levels) within cardiac regulation remains unclear. We aimed to determine whether fluoxetine modifies the pharmacological profile of serotonergic influence on vagal cardiac outflow. Rats were treated with fluoxetine (10 mg/kg per day; p.o.) for 14 days or equivalent volumes of drinking water (control group); then, they were pithed and prepared for vagal stimulation. Bradycardic responses were obtained by electrical stimulation of the vagal fibers (3, 6, and 9 Hz) or i.v. acetylcholine (ACh; 1, 5, and 10 μg/kg). The i.v. administration of 5-hydroxytryptamine (5-HT; 10 and 50 μg/kg) inhibited the vagally induced bradycardia. 5-CT (5-HT1/7 agonist) and L-694,247 (5-HT1D agonist) mimicked the serotonin inhibitory effect while α-methyl-5-HT (5-HT2 agonist) was devoid of any action. SB269970 (5-HT7 antagonist) did not abolish 5-CT inhibitory action on the electrically induced bradycardia. Pretreatment with LY310762 (5-HT1D antagonist) blocked the effects induced by L-694,247 and 5-CT. 5-HT and 5-CT failed to modify the bradycardia induced by exogenous ACh. Our outcomes suggest that fluoxetine treatment modifies 5-HT modulation on heart parasympathetic neurotransmission in rats, evoking inhibition of the bradycardia via prejunctional 5-HT1D in pithed rats.

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