Relevant bibliographies by topics / Bradycardia

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Academic literature on the topic 'Bradycardia'

Author: Grafiati
Published: 4 June 2021
Last updated: 31 January 2023

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Journal articles on the topic "Bradycardia"

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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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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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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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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 &lt; 0.001), glucocorticoid dose (estimate 4.820, 95% CI 2.048—7.592, p &lt; 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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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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Dissertations / Theses on the topic "Bradycardia"

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Smith-White, Margaret A. Medical Sciences Faculty of Medicine UNSW. "A functional study of neuropeptide Y mediated attenuation of vagal-evoked bradycardia." Awarded by:University of New South Wales. School of Medical Sciences, 2003. http://handle.unsw.edu.au/1959.4/19090.

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In the heart, neuropeptide Y (NPY) released during stimulation of the sympathetic nerve attenuates vagal-evoked bradycardia for a prolonged period. The inhibitory action of NPY is proposed as being Y2 receptor mediated. In rat and mouse, anaesthetised with sodium pentobarbitone, the selective Y2 receptor antagonist BIIE0246 reduced the inhibition of cardiac vagal activity evoked by a Y2 agonist, N-acetyl [Leu28, 31] NPY 24-36. BIIE0246 also reduced the inhibitory effect on vagal action evoked by stimulation of the sympathetic nerve. Deletion of the receptor in Y2 receptor-knockout mice abolished all NPY mediated inhibition of cardiac vagal-evoked bradycardia. These findings strongly support the proposal that NPY released during stimulation of the sympathetic nerve acts via Y2 receptors on the vagus nerve to decrease the slowing effect on the heart evoked by vagal stimulation. Examination of the structural components within NPY, using NPY, related PP peptides and structurally altered analogs, showed proline residues in the N-terminal polyproline region of NPY were found to influence the level of presynaptic activity while residues in the PP fold region further enhanced activity. NPY fragments, as long or longer than 3-36 NPY, possessed full inhibitory activity whereas short C-terminal analogs, such as 24-36 did not. The two leucine residues in agonist N-acetyl [Leu28, 31] NPY 24-36 was found to alter the structure and enhance the amphipathic nature of the a-helix in the shortened fragment. Arginine residues in the helix were also found to be important for activity. The leucine residues in N-acetyl [Leu28, 31] NPY 24-36 are proposed to stabilise the molecule producing an over all linear conformation. Although the conformation adopted by NPY at the receptor is unknown, it is plausible to suggest that the interaction between the proline residues and the a-helix stabilise the molecule in the same way that leucine substitution does in N-acetyl [Leu28, 31] NPY 24-36. Results obtained in Y2 receptor-knockout mice infer by their faster heart rates, an inhibitory role for the receptor in regions of the brain able to effect sympathetic outflow to the heart. Therefore knowledge of the structural requirements required of agonists and antagonists for Y2 receptor activation is likely to be of practical significance in drug design for the treatment of diseases affecting both parasympathetic and sympathetic innervation of the heart.
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Ruck, Sylvia A. "Induced Bradycardia Effects on Angiogenesis, Growth and Development in Early Development in Chicken Embryos, Gallus Domesticus." Thesis, University of North Texas, 2010. https://digital.library.unt.edu/ark:/67531/metadc33199/.

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Cardiac performance, angiogenesis and growth was investigated during early chicken development. Heart rate, and thus arterial pulse pressure and cardiac output, were altered with the bradycardic drug ZD7288. Heart rates at 72 h of development of control embryos and those dosed with chicken Ringer were not different at 171 bpm. Acute and chronic application of ZD7288 caused significant bradycardia. Chronic dosing of Ringer and ZD7288 changed neither eye diameter nor development rate. Chronic dosing of ZD7288 did not significantly alter CAM vessel density close to the embryo (2, 3 and 4 mm) but at farther distances (5 and 6 mm) chronic dosing with both Ringer and ZD7288 decreased vessel density by 13 - 16%. Chronic dosing with ZD7288 also reduced body mass by 20%. Thus, lowered heart rate and cardiac output had little effect on vessel density or developmental stage, but did reduce embryo growth.
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Manley, Elizabeth. "Apneic Bradycardia : terrestrial and aquatic responses in man under working conditions." Thesis, Rhodes University, 1989. http://hdl.handle.net/10962/d1001838.

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The focus of this research was the reappraisal in physiological and psychophysical terms of current equivocal theories regarding the onset, course and termination of apneic bradycardia. Sixteen healthy male subjects participated in four separate testing sessions . Maximal oxygen consumption (VO₂ max) was measured on land and underwater using an identical direct, continuous progressive cycle ergometer test. On each of two other occasions subjects exercised in either environment at 50, 70 and 90% of the appropriate VO₂ max, during which time heart rate was continuously recorded. An initial apneic bout at each exercise intensity was followed by performance of the same workload without apnea for an equivalent period of time. Ratings of perceived exertion (RPE) were also monitored. While apneic bradycardia occurred at each exercise intensity studied underwater, it was apparent only at 50% VO₂ max on land. With the exception of between 50 and 90% VO₂ max on land, the mean apneic heart rates did not differ with varying exercise intensity (p<0.05); nor did the lowest heart rate recorded, although this was lower underwater than on land. Apart from 70% VO₂ max on land, apneic heart rates were lower than the equivalent values measured during exercise without apnea. Land and underwater heart rates during apneic and non-apneic conditions did not differ until 90% VO₂ max. The effects of increasing exercise intensity upon the onset of bradycardia were evident in that it occurred earlier at 50% VO₂ max underwater than at the heavier workloads, and only at 50% VO₂ max on land. The mean breath-hold duration did not differ between the land and underwater environments, nor was it affected by increasing exercise intensity. The order in which breath-holds was performed did not alter the length of apnea. Land and underwater RPE did not differ and increased with increasing exercise intensity in both environments. During apneic exercise RPE was greater than the equivalent exercise without apnea. Twelve of the original 16 subjects were divided equally into two groups on the basis of vital capacity expressed relative to body surface area. Vital capacity was measured during the first laboratory session. Neither the mean heart rate response to apneic exercise at 50% V0₂ max in both environments, nor the lowest heart rates recorded differed between groups, prompting the conclusion that lung volume did not affect apneic bradycardia. Despite a longer breath-hold duration for Group A (large relative lung volume) than Group B (small relative lung volume), the onset point of bradycardia was the same for either group when expressed relative to total breath-hold duration
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Subramanian, Melanie. "Relative Bradycardia With Hypertension in Traumatic Brain Injury: A Marker for Mortality?" Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:17295909.

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Traumatic brain injury (TBI) is a leading cause of death in patients under 45 years of age. Hypertension has been shown to be associated with increased mortality in patients with moderate to severe traumatic brain injury (TBI). Furthermore, it is known that relative bradycardia is associated with increased mortality in hypotensive patients. We conducted a study to evaluate the relationship of initial heart rate (HR) with outcome in hypertensive TBI patients. This was a retrospective study of adult patients with moderate to severe blunt TBI (GCS <13) that presented to a Level I trauma center (2001-2011). Patients with hypertension, defined as an initial emergency department systolic blood pressure (SBP) ≥140 mmHg, were included in the analysis. The primary outcome was in-hospital mortality. Logistic regression analysis was used to control for age, injury severity, midline shift >5mm, pupil reflexes, hyperosmolar therapy, and blood transfusion. Secondary outcomes, including Glasgow Outcome Scale scores, were also analyzed. Of 490 patients with moderate to severe TBI, 53 patients were excluded. Of the remaining 437 patients, 223 (51%) presented with hypertension. Total in-hospital mortality was 31% in this group and the initial HR was significantly lower in the group that died (86±26 vs. 96±23; p=0.009). Bradycardia (HR≤60) upon presentation, which was identified in 21 (9%) patients, was associated with increased mortality (71% in HR≤60 vs. 27% in HR>60; p<0.001). Logistic regression identified bradycardia as an independent predictor of mortality (odds ratio 4.82; 95% confidence interval 1.36-17.10; p=0.015). Further subgroup analysis of relative bradycardia failed to identify HR between 60 and 90 as a predictor of mortality (p=0.113), although HR≤60 remained significant (p=0.006). The combination of initial hypertension and bradycardia in moderate to severe blunt TBI patients is associated with increased mortality.
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St-Hilaire, Marie. "Chémoréflexes laryngés induits par l'acide, l'eau vs le salin chez les agneaux nouveau-nés durant le sommeil calme." Mémoire, Université de Sherbrooke, 2004. http://savoirs.usherbrooke.ca/handle/11143/3789.

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Mise en contexte : Les chémoréflexes laryngés (CRI) sont déclenchés suite au contact entre un liquide et la muqueuse laryngée. Chez un organisme mature, ces CRL sont responsables de mécanismes de protection des voies aériennes inférieures (VAI) tels que déglutitions, toux et réaction d'éveil afin d'éviter l'aspiration. Par contre, chez un organisme immature comme c'est le cas chez les nouveau-nés, ces CRL associent apnée, bradycardie, laryngospasme, hypertension et redistribution du débit sanguin. En période néonatale, ces CRL, déclenchés en réponse à un reflux gastro-oesophagien acide, sont tenus responsables d'apnées du prématuré, de malaises graves du nourrisson (ALTE) et probablement de quelques cas de mort subite du nourrisson (MSN). Malgré leur pertinence clinique évidente, la revue de la littérature permet de constater que de nombreuses questions persistent concernant les CRL, principalement parce que les conditions expérimentales des études antérieures ne reflètent pas ce qui est vu en clinique. Ainsi, les CRL ont été étudiés le plus souvent en utilisant des modèles anesthésiés, en utilisant l'eau distillée, en se servant d'une trachéotomie pour l'injection des solutions et finalement en ne prenant pas en compte les stades de conscience. Une meilleure compréhension des CRL, en particulier déclenchés par des solutions acides, est donc nécessaire. But du projet : Le but de ce travail est d'étudier les CRL chez l'agneau nouveau-né sans sédation en réponse à l'acide, en comparaison à l'eau distillée et au salin durant le sommeil calme.
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Mateos, Juan Carlos Pachon. "Estudo comparativo dos parâmetros eletrofisiológicos da estimulação endocárdica septal com a estimulação cardíaca endocárdica convencional." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/98/98131/tde-12062012-074413/.

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Fundamento: A estimulação endocárdica convencional do ventrículo direito em ápice ou na região subtricuspídea ocasiona grande alargamento do QRS e importante dessincronização do miocárdio comprometendo a função ventricular. Com o surgimento da estimulação bifocal do VD e com a necessidade de estimulação cardíaca menos deletéria, a estimulação septal do VD tem sido cada vez mais utilizada. Eventualmente têm sido relatados limiares de estimulação mais altos e ondas R menores na estimulação septal. Objetivo: Comparar os parâmetros eletrofisiológicos das estimulações apical e septal, no mesmo paciente, para verificar se existem diferenças que possam interferir na escolha do ponto de estimulação. Este não é um estudo de ressincronização, porém tem o objetivo de contribuir na busca de uma estimulação ventricular monofocal menos deletéria. Casuística e métodos: Estudo prospectivo controlado. Foram incluídos 25 pacientes, com 67,2 ± 9 anos, 10 (40%) mulheres, 15 (60%) homens, com indicações clássicas de marca-passo por bradiarritmias. As etiologias foram Degenerativa em 9 (36%), Insuficiência coronária em 8 (32%), Doença de Chagas em 7 (28%), e Valvopatia em 1 (4%) pacientes. Foram utilizados eletrodos de fixação ativa tanto no ápice e região subtricuspídea, como no septo IVD. Foram medidos e comparados os limiares de comando, impedância e onda R uni e bipolares no momento do implante (medida direta) e após seis meses de evolução (medida por telemetria). Resultados: No implante, as médias dos limiares de comando septais x apicais foram respectivamente 0,73 x 0,74V (unipolar) e 0,73 x 0,78V (bipolar). As médias das ondas R septais x apicais foram 10 x 9,9mV (unipolar) e 12,3 x 12,4mV (bipolar). As médias das impedâncias septais x apicais foram 579 x 621? (unipolar) e 611 x 629? (bipolar). Todas as diferenças entre parâmetros septais e apicais com teste t-pareado bicaudal foram não significativas (p > 0,1). Após seis meses do implante, as médias dos limiares de comando septais x apicais foram respectivamente 0,5 x 0,72V (unipolar) e 0,71 x 0,87V (bipolar). As médias das ondas R septais x apicais foram 11,4 x 9,5mV (unipolar) e 12 x 11,2mV (bipolar). As médias das impedâncias septais x apicais foram 423 x 426? (unipolar) e 578 x 550? (bipolar). As diferenças entre parâmetros septais e apicais após 6 meses com teste t-pareado bicaudal foram não significativas (p > 0,05), exceto quanto às médias dos limiares de estimulação unipolares septal x apical (p=0,02) com menores limiares septais. 27, Conclusão: Este estudo mostrou que não existem diferenças expressivas entre parâmetros eletrofisiológicos de estimulação septal e apical, quando comparadas no mesmo paciente. Estes dados sugerem que em relação aos parâmetros de estimulação não há restrições para a escolha da estimulação septal em ventrículo direito. Este estudo não tem o objetivo de testar a ressincronização ventricular, porém contribui na escolha de uma estimulação monofocal ventricular direita mais fisiológica e menos deletéria.
Background: The conventional endocardial pacing in right ventricular apex or subtricuspid area causes significant QRS enlargement and important left ventricular desynchronization with ventricular function damage. By the introduction of RV bifocal pacing and the need of a less deleterious ventricular stimulation right ventricular septal pacing has been increasingly used. However, despite rare, some authors have reported high pacing thresholds and low R wave in septal pacing. Objective: To compare the electrophysiological parameters of the apical and septal stimulation in the same patient, seeking for any difference that could affect the choice of the pacing point. This is not a resynchronization study however it has the aim to search for for a better monofocal ventricular pacing. Materials and methods: Prospective controlled study of 25 symptomatic patients (67.2 ± 9 years old, 10 [40%] female, 15 [60%] male) having permanent atrial fibrillation with high degree AV block and classical pacemaker indication. The etiologies were 9 (36%) aging, 8 (32%) coronary disease, 7 (28%) Chagas disease and 1 (4%) valvar cardiopathy. There were used active fixation leads both in septal and in apical locations. The generators were Biotronik Philos II DR and Entovis DR. There were measured and compared pacing thresholds, impedance and R wave uni and bipolar during implantation (direct measurement) and after six months of follow-up (telemetry measurement). Results: During implantation, the septal vs apical mean pacing threshold were respectively 0.73 vs 0.74V (unipolar) and 0.73 vs 0.78V (bipolar). Mean R wave septal vs apical were 10 vs 9.9 mV (unipolar) and 12.3 vs 12.4mV (bipolar). The mean impedance septal vs apical were 579 vs 621? (unipolar) and 611vs 629? (bipolar). All septal vs apical comparisons were non-significant (p > 0.1, two-tailed paired t-test). After six months the mean pacing threshold septal vs apical were respectively 0.5 vs 0.72V (unipolar) and 0.71 vs 0.87V (bipolar). The mean R wave septal vs apical were 11.4 vs 9.5mV (unipolar) and 11.2 vs 12mV (bipolar). The mean impedance septal vs apical were 423 vs 426? (unipolar) and 578 vs 550? (bipolar). Only the unipolar septal vs apical mean threshold had significant difference (p = 0.02) with lower septal value. Conclusion: This study showed no significant difference between electrophysiological septal and apical pacing parameters when the 29 comparison is done in the same patient. By this way there are no restrictions for the right ventricular septal pacing. Despite being a non-resynchronization study it may contribute for chosen a less deleterious right ventricular monofocal pacing.
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Lindholm, Peter. "Severe hypoxemia during apnea in humans : influence of cardiovascular responses /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-314-7/.

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Mosca, Nancy Walsh. "Holding premature infants during gavage feeding: Effect on apnea, bradycardia, oxygenation, gastric residual, gastrin, and behavioral state." Case Western Reserve University School of Graduate Studies / OhioLINK, 1995. http://rave.ohiolink.edu/etdc/view?acc_num=case1057766341.

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Montazeri, Ghahjaverestan Nasim. "Early detection of cardiac arrhythmia based on Bayesian methods from ECG data." Thesis, Rennes 1, 2015. http://www.theses.fr/2015REN1S061/document.

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L'apnée est une complication fréquente chez les nouveaux-nés prématurés. L'un des problèmes les plus fréquents est l'épisode d'apnée bradycardie dont la répétition influence de manière négative le développement de l'enfant. C'est pourquoi les enfants prématurés sont surveillés en continu par un système de monitoring. Depuis la mise en place de ce système, l'espérance de vie et le pronostic de vie des prématurés ont été considérablement améliorés et ainsi la mortalité réduite. En effet, les avancées technologiques en électronique, informatique et télécommunications ont conduit à l'élaboration de systèmes multivoies de monitoring néonatal de plus en plus performants. L'un des principaux signaux exploités dans ces systèmes est l'électrocardiogramme (ECG). Toutefois, même si l'analyse de l'ECG a évolué au fil des années, l'ensemble des informations qu'il fournit n'est pas encore totalement exploité dans les processus de décision, notamment en monitoring en Unité de Soins Intensifs en Néonatalogie (USIN). L'objectif principal de cette thèse est d'améliorer la prise en compte des dynamiques multi-dimensionnelles en proposant de nouvelles approches basées sur un formalisme bayésien, pour la détection précoce des apnées bradycardies chez le nouveau-né prématuré. Aussi, dans cette thèse, nous proposons deux approches bayésiennes, basées sur les caractéristiques de signaux biologiques en vue de la détection précoce de l'apnée bradycardie des nouveaux-nés prématurés. Tout d'abord avec l'approche de Markov caché, nous proposons deux extensions du Modèle de Markov Caché (MMC) classique. La première, qui s'appelle Modèle de Markov Caché Couplé (MMCC), créé une chaîne de Markov à chaque dimension de l'observation et établit un couplage entre les chaînes. La seconde, qui s'appelle Modèle Semi-Markov Caché Couplé (MSMCC), combine les caractéristiques du modèle de MSMC avec le mécanisme de couplage entre canaux. Pour les deux nouveaux modèles (MMCC et MSMCC), les algorithmes récursifs basées sur la version classique de Forward-Backward sont introduits pour résoudre les problèmes d'apprentissage et d'inférence dans le cas couplé. En plus des modèles de Markov, nous proposons deux approches passées sur les filtres de Kalman pour la détection d'apnée. La première utilise les modifications de la morphologie du complexe QRS et est inspirée du modèle générateur de McSharry, déjà utilisé en couplant avec un filtre de Kalman étendu dans le but de détecter des changements subtils de l'ECG, échantillon par échantillon. La deuxième utilise deux modèles AR (l'un pour le processus normal et l'autre pour le processus de bradycardie). Les modèles AR sont appliqués sur la série RR, alors que le filtre de Kalman suit l'évolution des paramètres du modèle AR et fournit une mesure de probabilité des deux processus concurrents
Apnea-bradycardia episodes (breathing pauses associated with a significant fall in heart rate) are the most common disease in preterm infants. Consequences associated with apnea-bradycardia episodes involve a compromise in oxygenation and tissue perfusion, a poor neuromotor prognosis at childhood and a predisposing factor to sudden-death syndrome in preterm newborns. It is therefore important that these episodes are recognized (early detected or predicted if possible), to start an appropriate treatment and to prevent the associated risks. In this thesis, we propose two Bayesian Network (BN) approaches (Markovian and Switching Kalman Filter) for the early detection of apnea bradycardia events on preterm infants, using different features extracted from electrocardiographic (ECG) recordings. Concerning the Markovian approach, we propose new frameworks for two generalizations of the classical Hidden Markov Model (HMM). The first framework, Coupled Hidden Markov Model (CHMM), is accomplished by assigning a Markov chain (channel) to each dimension of observation and establishing a coupling among channels. The second framework, Coupled Hidden semi Markov Model (CHMM), combines the characteristics of Hidden semi Markov Model (HSMM) with the above-mentioned coupling concept. For each framework, we present appropriate recursions in order to use modified Forward-Backward (FB) algorithms to solve the learning and inference problems. The proposed learning algorithm is based on Maximum Likelihood (ML) criteria. Moreover, we propose two new switching Kalman Filter (SKF) based algorithms, called wave-based and R-based, to present an index for bradycardia detection from ECG. The wave-based algorithm is established based on McSarry's dynamical model for ECG beat generation which is used in an Extended Kalman filter algorithm in order to detect subtle changes in ECG sample by sample. We also propose a new SKF algorithm to model normal beats and those with bradycardia by two different AR processes
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Wung, Shu-Fen. "Bradyarrhythmias: Clinical Presentation, Diagnosis, and Management." W B SAUNDERS CO-ELSEVIER INC, 2016. http://hdl.handle.net/10150/621215.

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Bradyarrhythmias are common clinical findings consisting of physiologic and pathologic conditions (sinus node dysfunction and atrioventricular [AV] conduction disturbances). Bradyarrhythmias can be benign, requiring no treatment; however, acute unstable bradycardia can lead to cardiac arrest. In patients with confirmed or suspected bradycardia, a thorough history and physical examination should include possible causes of sinoatrial node dysfunction or AV block. Management of bradycardia is based on the severity of symptoms, the underlying causes, presence of potentially reversible causes, presence of adverse signs, and risk of progression to asystole. Pharmacologic therapy and/or pacing are used to manage unstable or symptomatic bradyarrhythmias.
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Books on the topic "Bradycardia"

1

Lennon, Krystal. Euphoric Bradycardia. PublishAmerica, 2006.

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PILBERY. Standby Cpd: Symptomatic Bradycardia. Class Publishing, 2015.

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Jr, Joseph C. Kunz, and Michele G. Kunz. Zombie Notes Bradycardia/Heartblocks. Dickson Keanaghan, LLC, 2011.

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Swain, Una Gabriele. Heart rates and diving bradycardia in beaver. 1985.

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Burnett, Catherine. Effects of choline and exercise on resting bradycardia in rats. 1988.

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Burnett, Catherine. Effects of choline and exercise on resting bradycardia in rats. 1988.

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Publications, ICON Health. Bradycardia - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. ICON Health Publications, 2004.

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Katritsis, Demosthenes G., Bernard J. Gersh, and A. John Camm. Sinus nodal disease. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199685288.003.1459_update_003.

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Ramrakha, Punit, and Jonathan Hill, eds. Arrhythmias. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199643219.003.0010.

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The cardiac conduction system 478Bradycardia: general approach 480Sinus bradycardia 482Sinus pause 482Sick sinus syndrome 482Atrioventricular block 483Bundle branch block 484Tachycardia: general approach 486Tachycardia: emergency management 488Tachyarrhythmias: classification 490ECG diagnosis of tachyarrhythmias 492Supraventricular tachycardia 494...
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Gill, Harminder S., and Jaswinder S. Gill. Causes, diagnosis, and therapeutic strategy in bradyarrhythmias. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0157.

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Bradyarrhythmias (defined as a heart rate <60 beat/min) occur frequently in the critical care setting. Most are related to underlying disease processes and the multidrug therapies administered. Because of the intense monitoring of these patients, recognition is generally easy. Examination of the ECG will allow diagnosis of the type of bradycardia based on the sinus node, atrioventricular node and the infra-Hissian conducting system. The extent of conduction system disease can be estimated and this has an influence on the prognosis. Bradycardias causing haemodynamic collapse require treatment of underlying causes, resuscitation, and administration of atropine and epinephrine. If there is no response to these then either transcutaneous pacing, or temporary transvenous pacing is necessary. This can be followed by implantation of a permanent pacing system. The outcome of correctly diagnosing and treating a bradyarrhythmia is excellent as long as the causative pathology can be stabilized.
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Book chapters on the topic "Bradycardia"

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Hudson, Korin B., J. Aidan Boswick, and William J. Brady. "Bradycardia." In The ECG in Prehospital Emergency Care, 44–49. Oxford, UK: Blackwell Publishing Ltd., 2012. http://dx.doi.org/10.1002/9781118473740.ch8.

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Hsing, Jeffrey, and Paul Wang. "Bradycardia." In A Practical Approach to Cardiovascular Medicine, 204–11. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444393897.ch16.

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Good, Eric D., and Krit Jongnarangsin. "Bradycardia." In Practical Cardiology, 213–23. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-28328-5_17.

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Kusumoto, Fred M. "Bradycardia." In ECG Interpretation: From Pathophysiology to Clinical Application, 139–54. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-88880-4_10.

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Kusumoto, Fred. "Bradycardia." In ECG Interpretation, 139–57. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-40341-6_10.

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Fok, Henry, Kerry Layne, and Adam Nabeebaccus. "Bradycardia and Malaise." In 100 Cases in Acute Medicine, 164–67. 2nd ed. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003241171-57.

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Aktas, Mehmet K., and Ryan Mandell. "Cardiac Conduction and Bradycardia." In Clinical Cardiac Electrophysiology in Clinical Practice, 1–15. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-5433-4_1.

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Upadhyay, Gaurav A., and Jagmeet P. Singh. "Bradycardia and Pacemakers/CRT." In MGH Cardiology Board Review, 423–38. London: Springer London, 2013. http://dx.doi.org/10.1007/978-1-4471-4483-0_25.

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Patrinos, Mary Elaine, and Richard J. Martin. "Apnea, Bradycardia, and Desaturation." In Manual of Neonatal Respiratory Care, 619–25. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-39839-6_76.

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Chatterjee, Neal A., Gaurav A. Upadhyay, and Jagmeet P. Singh. "Bradycardia and Pacemakers/CRT." In MGH Cardiology Board Review, 323–38. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-45792-1_16.

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Conference papers on the topic "Bradycardia"

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Sahoo, Nibedita, P. Unnikrishnan, Smita Vimala, and Ajay P. Hrishi. "Ictal Bradycardia: A Missed Etiology for Intraoperative Bradycardia." In 19th Annual Conference of the Indian Society of Neuroanaesthesiology and Critical Care (ISNACC). Thieme Medical and Scientific Publishers Private Limited, 2018. http://dx.doi.org/10.1055/s-0038-1636386.

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Wang, Qingjie, Sanjay Kharche, Gareth Jones, Cunjin Luo, Chengchun Tang, and Henggui Zhang. "Calcium leak induced sinus bradycardia." In 2015 Computing in Cardiology Conference (CinC). IEEE, 2015. http://dx.doi.org/10.1109/cic.2015.7411109.

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Patil, Kaustubh, and Rajesh Radhakrishnan. "Leadless pacing: Addressing barriers for bradycardia therapy in India." In 2013 IEEE Point-of-Care Healthcare Technologies (PHT). IEEE, 2013. http://dx.doi.org/10.1109/pht.2013.6461343.

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Yutsis, P. I., and M. J. Bucksbaum. "Computerized polygraphic audiovisual monitoring in infants with apnea-bradycardia." In Proceedings of the Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1988. http://dx.doi.org/10.1109/iembs.1988.95041.

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Loganathan, Prakash Kannan, Prashant Mallya, and Vrinda Nair. "682 Hypoxia and Bradycardia episodes in neonatal elective intubations." In Royal College of Paediatrics and Child Health, Abstracts of the RCPCH Conference–Online, 15 June 2021–17 June 2021. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2021. http://dx.doi.org/10.1136/archdischild-2021-rcpch.141.

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Pravisani, G., A. Beuchee, L. Mainardi, and G. Carrault. "Short term prediction of severe bradycardia in premature newborns." In Computers in Cardiology, 2003. IEEE, 2003. http://dx.doi.org/10.1109/cic.2003.1291258.

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Archer, D., J. Ferdous, and Y. Alderazi. "E-017 Prolonged bradycardia after carotid angioplasty and stenting." In SNIS 14TH, Annual Meeting, July 24–27, 2017, The Broadmoor, Colorado Springs, CO. BMA House, Tavistock Square, London, WC1H 9JR: BMJ Publishing Group Ltd., 2017. http://dx.doi.org/10.1136/neurintsurg-2017-snis.89.

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Ge, D., G. Carrault, and A. I. Hernandez. "Online Bayesian apnea-bradycardia detection using auto-regressive models." In ICASSP 2014 - 2014 IEEE International Conference on Acoustics, Speech and Signal Processing (ICASSP). IEEE, 2014. http://dx.doi.org/10.1109/icassp.2014.6854439.

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Das, Subhasish, Bahman Moraffah, Ayan Banerjee, Sandeep K. S. Gupta, and Antonia Papandreou-Suppappola. "Bradycardia Prediction in Preterm Infants Using Nonparametric Kernel Density Estimation." In 2019 53rd Asilomar Conference on Signals, Systems, and Computers. IEEE, 2019. http://dx.doi.org/10.1109/ieeeconf44664.2019.9049007.

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Altuve, M., G. Carrault, A. Beuchee, P. Pladys, and A. I. Hernandez. "On-line apnea-bradycardia detection using hidden semi-Markov models." In 2011 33rd Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2011. http://dx.doi.org/10.1109/iembs.2011.6091085.

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Reports on the topic "Bradycardia"

1

Claus, Ana, Borzooye Jafarizadeh, Azmal Huda Chowdhury, Neziah Pala, and Chunlei Wang. Testbed for Pressure Sensors. Florida International University, October 2021. http://dx.doi.org/10.25148/mmeurs.009771.

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Currently, several studies and experiments are being done to create a new generation of ultra-low-power wearable sensors. For instance, our group is currently working towards the development of a high-performance flexible pressure sensor. However, with the creation of new sensors, a need for a standard test method is necessary. Therefore, we opted to create a standardized testbed to evaluate the pressure applied to sensors. A pulse wave is generated when the heart pumps blood causing a change in the volume of the blood vessel. In order to eliminate the need of human subjects when testing pressure sensors, we utilized polymeric material, which mimics human flesh. The goal is to simulate human pulse by pumping air into a polymeric pocket which s deformed. The project is realized by stepper motor and controlled with an Arduino board. Furthermore, this device has the ability to simulate pulse wave form with different frequencies. This in turn allows us to simulate conditions such as bradycardia, tachycardia, systolic pressure, and diastolic pressure.
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Harris, Gregory, Brooke Hatchell, Davelin Woodard, and Dwayne Accardo. Intraoperative Dexmedetomidine for Reduction of Postoperative Delirium in the Elderly: A Scoping Review. University of Tennessee Health Science Center, July 2021. http://dx.doi.org/10.21007/con.dnp.2021.0010.

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Background/Purpose: Post-operative delirium leads to significant morbidity in elderly patients, yet there is no regimen to prevent POD. Opioid use in the elderly surgical population is of the most significant risk factors for developing POD. The purpose of this scoping review is to recognize that Dexmedetomidine mitigates cognitive dysfunction secondary to acute pain and the use of narcotic analgesia by decreasing the amount of norepinephrine (an excitatory neurotransmitter) released during times of stress. This mechanism of action also provides analgesia through decreased perception and modulation of pain. Methods: The authors developed eligibility criteria for inclusion of articles and performed a systematic search of several databases. Each of the authors initially selected five articles for inclusion in the scoping review. We created annotated literature tables for easy screening by co-authors. After reviewing the annotated literature table four articles were excluded, leaving 11 articles for inclusion in the scoping review. There were six level I meta-analysis/systematic reviews, four level II randomized clinical trials, and one level IV qualitative research article. Next, we created a data-charting form on Microsoft Word for extraction of data items and synthesis of results. Results: Two of the studies found no significant difference in POD between dexmedetomidine groups and control groups. The nine remaining studies noted decreases in the rate, duration, and risk of POD in the groups receiving dexmedetomidine either intraoperatively or postoperatively. Multiple studies found secondary benefits in addition to decreased POD, such as a reduction of tachycardia, hypertension, stroke, hypoxemia, and narcotic use. One study, however, found that the incidence of hypotension and bradycardia were increased among the elderly population. Implications for Nursing Practice: Surgery is a tremendous stressor in any age group, but especially the elderly population. It has been shown postoperative delirium occurs in 17-61% of major surgery procedures with 30-40% of the cases assumed to be preventable. Opioid administration in the elderly surgical population is one of the most significant risk factors for developing POD. With anesthesia practice already leaning towards opioid-free and opioid-limited anesthetic, the incorporation of dexmedetomidine could prove to be a valuable resource in both reducing opioid use and POD in the elderly surgical population. Although more research is needed, the current evidence is promising.
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