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Bradycardia
Kinds of Bradycardia Selected AbstractsAdenosine A1 Antagonism Attenuates Atropine-resistant Hypoxic Bradycardia in RatsACADEMIC EMERGENCY MEDICINE, Issue 9 2003Justin L. Kaplan MD Abstract Objectives: To test the following hypotheses: Hypoxia induces bradycardia and hemodynamic compromise that are resistant to atropine but responsive to selective antagonism of the adenosine A1 receptor (A1AdoR). The mechanism for such attenuation is independent of the vagus nerve. Methods: Ten minutes after sham or actual bilateral cervical vagotomy, paralyzed ventilated rats were made hypoxic (5% fractional inspired oxygen, continued until death). Five minutes after beginning hypoxia, intravenous treatment with BG-9719, a selective A1AdoR antagonist (0.1 mg/kg); atropine (0.1 mg/kg); BG-9719 vehicle; or saline was initiated. These drug doses were based on pilot studies. Of the eight treatment groups (eight possible combinations of vagotomy status and drug/vehicle treatment), n= 8 in all except nonvagotomized, vehicle-treated rats (where n= 7). Results: Heart rate and left ventricular contractility decreased rapidly with hypoxia. Atropine had minimal effects in prolonging survival (from mean ± SEM of 15.5 ± 2.1 minutes to 20.2 ± 2.5 minutes, p = 0.94) and attenuating posthypoxic decreases in heart rate (p = 0.89) and contractility (p = 0.83) compared with saline. BG-9719 prolonged survival, however, from 14.4 ± 1.9 minutes (with vehicle treatment) to 37.2 ± 6.8 minutes (p < 0.001). Survival, heart rate, and contractility were preserved with BG-9719 compared with atropine and vehicle (p < 0.05, all comparisons). Vagotomy prevented the effects of BG-9719 on survival prolongation (p = 0.003), heart rate (p = 0.01), and contractility (p < 0.001) but did not affect those outcomes in saline-treated rats. Conclusions: Survival, heart rate, and contractility were better preserved with BG-9719 than atropine. A1AdoR selective antagonism, possibly because of its multiple mechanisms for attenuating hypoxic cardiac insufficiency, resulted in better hemodynamic and clinical outcomes. That attenuation seems to have a component of vagal mediation. [source] Bradycardia and sinus arrest during percutaneous ethanol injection therapy for hepatocellular carcinomaEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 3 2004A. Ferlitsch Abstract Background, Percutaneous ethanol injection (PEI) is an established method in the treatment of hepatocellular carcinoma (HCC) and considered a safe procedure, with severe complications occurring rarely. Cardiac arrhythmias have not been reported to date. Aim of the study was to investigate the occurrence of dysrhythmias during PEI. Patients and methods, Twenty-six consecutive patients with inoperable HCC were included. During ultrasound-guided PEI with 95% ethanol, electrocardiogram (ECG) monitoring was performed before starting and continuously during PEI. Results, During PEI a significant reduction in mean heart rate (> 20%) was seen in 15 of 26 (58%) patients. In 11 of 26 patients (42%) occurrence of sinuatrial block (SAB) or atrioventricular block (AVB) was observed after a median time of 9 s (range 4,50) from the start of PEI with a median length of 24 s (range 12,480). Clinical symptoms were seen in two patients, including episodes of unconsciousness, seizure-like symptoms in both and a respiratory arrest during PEI in one patient, requiring mechanical ventilation. In four of 12 patients with repeat interventions, dysrhythmias were reproducible during monthly performed procedures. There was a significant association between the occurrence of SAB or AVB and the amount of instilled alcohol (P = 0·03) and post-PEI serum ethanol levels (P = 0·03). Conclusions, Bradycardia and block formation occur frequently during PEI. These symptoms could be explained by a vasovagal reaction and/or the direct effect of ethanol on the sinus node or the right atrial conduction system. Ethanol dose is an important factor for the occurrence of SAB/AVB. ECG-monitoring seems mandatory during PEI. Prophylactic use of intravenously administered Atropine might be useful. [source] A novel approach to assessing percutaneous VX poisoning in the conscious guinea-pig,JOURNAL OF APPLIED TOXICOLOGY, Issue 5 2008Helen Mumford Abstract Nerve agents like VX (S-2-diisopropylaminoethyl-O-ethyl-methylphosphonothiolate) are potent irreversible acetylcholinesterase (AChE) inhibitors. Following percutaneous nerve agent exposure there is a slower rate of absorption, later onset and longer duration of signs of poisoning. Relatively little is known about the physiological effects of percutaneously applied nerve agent in unanaesthetised laboratory animals. Heart rate (ECG), brain electrical activity (EEG), body temperature, locomotor activity and clinical signs were monitored following percutaneous application of VX to conscious guinea-pigs. A fall in heart rate (bradycardia) preceded incapacitation following the highest VX dose, and occurred in the absence of incapacitation at the lower doses. Following the highest dose of VX (0.592 mg kg,1) three out of four animals died within 24 h. The lower two doses of VX (0.296 and 0.148 mg kg,1), produced extended periods of bradycardia in the absence of observable signs of poisoning. Bradycardia preceded, or occurred in the absence of, a temperature decrease; seizure-like EEG changes were not observed at any of the VX doses tested. Acetylcholinesterase activity was significantly inhibited in the blood and most brain areas at 48 h. There were significant dose-related decreases in body weight at 24 and 48 h following VX. This preliminary study suggests that decreased heart rate may be an early sign of the toxic effects of VX, whereas temperature and observable clinical signs are not good early indicators of percutaneous VX poisoning in this animal model. Future studies will use this model to assess the benefit of administering medical countermeasures in response to a defined decrease in heart rate. © Crown Copyright 2007. Reproduced with the permission of the Controller of HMSO. Published by John Wiley & Sons, Ltd. This article was published online on 5 December 2007. An error was subsequently identified. This notice is included in the online and print versions to indicate that both have been corrected [30 May 2008]. [source] Changes in Left Ventricular Repolarization and Ion Channel Currents Following a Transient Rate Increase Superimposed on Bradycardia in Anesthetized DogsJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 6 2000MICHAEL RUBART M.D. Electrical Remodeling of the Heart due to Rate. Introduction: We previously demonstrated in dogs that a transient rate increase superimposed on bradycardia causes prolongation of ventricular refractoriness that persists for hours after resumption of bradycardia. In this study, we examined changes in membrane currents that are associated with this phenomenon. Methods and Results: The whole cell, patch clamp technique was used to record transmembrane voltages and currents, respectively, in single mid-myocardial left ventricular myocytes from dogs with 1 week of complete AV block; dogs either underwent 1 hour of left ventricular pacing at 120 beats/min or did not undergo pacing. Pacing significantly heightened mean phase 1 and peak plateau amplitudes by ,6 and ,3 mV, respectively (P < 0.02). and prolonged action potential duration at 90% repolarization from 235 ± 8 msec to 278 ± 8 msec (1 Hz; P = 0.02). Rapid pacing-induced changes in transmembrane ionic currents included (1) a more pronounced cumulative inactivation of the 4-aminopyridine-sensitive transient outward K+ current, I to over the range of physiologic frequencies, resulting from a ,30% decrease in the population of quickly reactivating channels; (2) increases in peak density of L-type Ca2+ currents, Ica.I.' by 15% to 35% between +10 and +60 mV; and (3) increases in peak density of the Ca2+ -activated chloride current, ICl.Ca' by 30% to 120% between +30 and +50 mV. Conclusion: Frequency-dependent reduction in Ito combined with enhanced ICa.I. causes an increase in net inward current that may he responsible for the observed changes in ventricular repolarization. This augmentation of net cation influx is partially antagonized by an increase in outward ICa.Cl. [source] Bradycardia and asystolic cardiac arrest during spinal anaesthesia: A report of five casesACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 1 2000R. Z. Løvstad Sudden, severe bradycardia/asystolic cardiac arrest are considered infrequent, but are certainly the most serious complications of spinal anaesthesia. We report four cases of primary asystole and one of severe bradycardia in young to middle-aged, healthy patients scheduled for minor surgery at the day surgery unit. Bradycardia/asystole were not related to respiratory depression or hypoxaemia/hypercarbia; they occurred at different time intervals after the onset of spinal anaesthesia (10,70 min) and, apparently, were not dependent on the level of sensory block, which varied between T3 and T8. One patient was nauseated seconds before the asystole, otherwise there was no warning signs. All the patients were easily resuscitated with the prompt administration of atropine and ephedrine and, in the case of cardiac arrest, cardiac massage and ventilation with oxygen. One patient was treated with a small dose of adrenaline. Four patients had the surgery, as planned; one had the surgery postponed. All the patients were discharged from hospital in good health and did not suffer any sequelae. [source] Cooling Device for Bradycardia Based on Peltier Element for Accurate Anastomosis of Off-Pump Coronary Artery Bypass GraftingARTIFICIAL ORGANS, Issue 10 2002Yukio Kuniyoshi Abstract: Upon introducing off-pump coronary artery bypass grafting (CABG), the indications for CABG were expanded to include patients who previously had no operative indications. For accurate anastomosis, various devices and methods have been developed. Bradycardia is easily induced by drug administration. However, this method of achieving bradycardia also has adverse effects on cardiac function. We have developed a new device to decrease the heart rate by regional cooling of the sino-atrial node. The new device is incorporated with Peltier's element, which uses an electric charge to create a temperature gradient on both of its surfaces. In terms of the cooling ability of this device, its cooling surface is chilled from 25°C to 0°C within 30 s. During in vivo animal experiments, this device has been shown to decrease the myocardial temperature around the sino-atrial node to 15°C and suppress sino-atrial node activity, resulting in bradycardia to 60 beats/min level. In summary, the simple and easily applicable device for local cooling in combination with the application of diltiazem for effective heart rate reduction may be very helpful for the surgeon and may avoid disadvantages for critically ill patients. [source] Central Bromocriptine-Induced Tachycardia is Reversed to Bradycardia in Conscious, Deoxycorticosterone Acetate-Salt Hypertensive RatsBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 5 2001Saad Lahlou The present study investigated the effect of bromocriptine on heart rate and the principal site of action of this agonist in conscious, deoxycorticosterone acetate-salt hypertensive rats, in which altered central dopaminergic activity has been previously reported. Intravenous administration of bromocriptine (150 ,g/kg) increased heart rate (49±5 beats/min.) in uninephrectomized control rats, while it induced a significant bradycardia (50±6 beats/min.) in deoxycorticosterone acetate-salt hypertensive rats. In the latter animals, intravenous (500 ,g/kg) or intrathecal (40 ,g/rat at T9,T10) pretreatment with domperidone, a selective dopamine D2 receptor antagonist that does not cross the blood-brain barrier, reduced partially, but significantly, the bradycardiac responses to bromocriptine (reduction of about 44% and 48% of the maximal effect, respectively). In contrast, the bromocriptine-induced bradycardia was fully abolished by intravenous pretreatment with metoclopramide (300 ,g/kg), a dopamine D2 receptor antagonist that crosses the blood-brain barrier, or by combined pretreatment with intravenous and intrathecal domperidone. These results indicate that, in deoxycorticosterone acetate-salt hypertensive rats, bromocriptine decreases rather than increases heart rate, an effect that is mediated partly through a peripheral D2 dopaminergic mechanism and partly through stimulation of spinal dopamine D2 receptors. They further support the concept that, in normotensive, conscious rats, the central tachycardia of bromocriptine appears to predominate and to mask the bradycardia of this agonist at both peripheral and spinal dopamine D2 receptors. [source] Maternal methadone may cause arrhythmias in neonatesACTA PAEDIATRICA, Issue 5 2007Tarique Hussain Abstract Methadone treatment is a well recognised cause of QT interval lengthening in adults. In this case report, we present for the first time, clinically significant QT interval lengthening in a neonate secondary to maternal methadone treatment. Neonatal paediatricians should be aware of this important and potentially serious clinical phenomenon. Conclusion: Bradycardia, tachycardia or an irregular heart rate in an infant born to a mother on methadone treatment should not be ignored and a 12-lead electrocardiogram should be performed. Furthermore, there is also a need for a prospective study of QTc intervals in infants born to mothers receiving methadone. [source] Cardio-respiratory reflexes evoked by phenylbiguanide in rats involve vagal afferents which are not sensitive to capsaicinACTA PHYSIOLOGICA, Issue 1 2010A. Dutta Abstract Aim:, Stimulation of pulmonary C fibre receptors by phenylbiguanide (PBG, 5-HT3 agonist) produces hypotension, bradycardia and tachypnoea or apnoea. However, tachypnoeic or apnoeic responses are not consistent. Therefore, this study was undertaken to delineate the actions of PBG on respiration and compared with those evoked by capsaicin (TRPV1 agonist). Methods:, Blood pressure, respiratory excursions and ECG were recorded in urethane anaesthetized adult rats. The effect of PBG or capsaicin was evaluated before and after ondansetron (5-HT3 antagonist), capsazepine (TRPV1 antagonist) or bilateral vagotomy. In addition, their effect on vagal afferent activity was also evaluated. Results:, Bolus injection of PBG produced concentration-dependent (0.1,100 ,g kg,1) hypotensive and bradycardiac responses, while there was tachypnoea at lower concentrations (0.1,3 ,g kg,1) and apnoea at higher concentrations (10,100 ,g kg,1). After vagotomy or after exposure to ondansetron both tachypnoeic and apnoeic responses were abolished along with cardiovascular responses. However, capsazepine (3 mg kg,1) did not block the PBG-induced reflex responses. Capsaicin (0.1,10 ,g kg,1), on the other hand, produced a concentration-dependent apnoea, hypotension and bradycardia but tachypnoea was not observed. Ondansetron failed to block the capsaicin-induced reflex response while bilateral vagotomy abolished bradycardiac and hypotensive responses and attenuated the apnoeic response. In another series, vagal afferent activity and cardio-respiratory changes evoked by PBG were blocked by ondansetron. However, capsaicin failed to activate the PBG-sensitive vagal afferents even though cardio-respiratory alterations were observed. Conclusions:, The present observations indicate that PBG produced tachypnoea at a lower concentration and apnoea at a higher concentration involving vagal afferents which are different from those excited by capsaicin. [source] Experience With Implantable Loop Recorders for Recurrent Unexplained SyncopeCONGESTIVE HEART FAILURE, Issue 2008Michele Brignole MD Knowledge of what occurs during spontaneous syncope is the gold standard for evaluation. Initially, implantable loop recorders (ILRs) were used in patients with unexplained syncope at the end of unsuccessful full, conventional work-up. In pooled data regarding 247 patients, a correlation between syncope and electrocardiographic findings was found in 84 patients (34%); of these, 52% had a bradycardia or asystole at the time of the recorded event, 11% had tachycardia, and 37% had no arrhythmia. Presyncope-electrocardiography correlation was observed in another third of the patients; presyncope was much less likely to be associated with an arrhythmia than was syncope. The diagnostic yield was similar in patients with and without structural heart diseases and was higher in older than in younger patients. Recent studies showed that ILR implantation can be safely performed in an early phase of the diagnostic evaluation,provided that patients at risk for life-threatening events are carefully excluded,in the patients who have a severe presentation of syncope (because of high risk of trauma or high frequency of episodes) which can be a benefit of a mechanism-specific therapy. Congest Heart Fail. 2008;14:7,12. ©2008 Le Jacq [source] Circulatory effects of apnoea in elite breath-hold diversACTA PHYSIOLOGICA, Issue 1 2009F. Joulia Abstract Aim:, Voluntary apnoea induces several physiological adaptations, including bradycardia, arterial hypertension and redistribution of regional blood flows. Elite breath-hold divers (BHDs) are able to maintain very long apnoea, inducing severe hypoxaemia without brain injury or black-out. It has thus been hypothesized that they develop protection mechanisms against hypoxia, as well as a decrease in overall oxygen uptake. Methods:, To test this hypothesis, the apnoea response was studied in BHDs and non-divers (NDs) during static and dynamic apnoeas (SA, DA). Heart rate, arterial oxygen saturation (SaO2), and popliteal artery blood flow were recorded to investigate the oxygen-conserving effect of apnoea response, and the internal carotid artery blood flow was used to examine the mechanisms of cerebral protection. Results:, The bradycardia and peripheral vasoconstriction were accentuated in BHDs compared with NDs (P < 0.01), in association with a smaller SaO2 decrease (,2.7% vs. ,4.9% during SA, P < 0.01 and ,6% vs. ,11.3% during DA, P < 0.01). Greater increase in carotid artery blood flow was also measured during apnoea in BHDs than in controls. Conclusion:, These results confirm that elite divers present a potentiation of the well-known apnoea response in both SA and DA conditions. This response is associated with higher brain perfusion which may partly explain the high levels of world apnoea records. [source] B2 kinin receptors mediate the Indian red scorpion venom-induced augmentation of visceral reflexes via the nitric oxide cyclic guanosine monophosphate pathwayACTA PHYSIOLOGICA, Issue 4 2009S. Kanoo Abstract Aim:, This study was performed to delineate the kinin (receptor)-dependent pathways in the Indian red scorpion (Mesobuthus tamulus; MBT) venom-induced pulmonary oedema as well as the augmentation of cardio-pulmonary reflexes evoked by phenyldiguanide (PDG). Methods:, In urethane-anaesthetized adult rats, the effect of venom on the PDG reflex responses (blood pressure, heart rate and respiration rate) and the pulmonary water content was ascertained using various antagonists(des- Arg, B1 receptor antagonist; Hoe 140, B2 receptor antagonist; N, -nitro- l -arginine methyl ester (l -NAME), nitric oxide (NO) synthase inhibitor; methylene blue, soluble guanylate cyclase inhibitor; and glibenclamide, K+ATP channel blocker). The effect of phosphodiesterase V inhibitor (sildenafil citrate) on the reflex response and the pulmonary water content was also examined and compared with venom-induced responses. Results:, Intravenous injection of PDG (10 ,g kg,1) evoked apnoea, bradycardia and hypotension lasting >60 s. Exposure to MBT venom (100 ,g kg,1) for 30 min augmented the PDG reflex responses by two times and increased the pulmonary water content, significantly. Hoe 140 blocked the venom-induced responses (augmentation of PDG reflex and increased pulmonary water content) whereas des-Arg did not. l -NAME, methylene blue or glibenclamide also blocked the venom-induced responses. Furthermore, sildenafil citrate (that increases cGMP levels) produced augmentation of PDG reflex response and increased the pulmonary water content as seen with venom. Conclusion:, The results indicate that venom-induced responses involve B2 kinin receptors via the NO-dependent guanylate cyclase-cGMP pathway involving K+ATP channels. [source] Electrosurgery, Pacemakers and ICDs: A Survey of Precautions and Complications Experienced by Cutaneous SurgeonsDERMATOLOGIC SURGERY, Issue 4 2001Hazem M. El-Gamal MD Background. Minimal information is available in the literature regarding the precautions implemented or complications experienced by cutaneous surgeons when electrosurgery is used in patients with pacemakers or implantable cardioverter-defibrillators (ICDs). The literature pertinent to dermatologists is primarily based on experiences of other surgical specialties and a generally recommended thorough perioperative evaluation. Objective. To determine what precautions are currently taken by cutaneous surgeons in patients with pacemakers or ICDs, and what types of complications have occurred due to electrosurgery in a dermatologic setting. Methods. In the winter of 2000, a survey was mailed to 419 U.S.-based members of the American College of Mohs Micrographic Surgery and Cutaneous Oncology (ACMMSCO). Results. A total of 166 (40%) surveys were returned. Routine precautions included utilizing short bursts of less than 5 seconds (71%), use of minimal power (61%), and avoiding use around the pacemaker or ICD (57%). The types of interference reported were skipped beats (eight patients), reprogramming of a pacemaker (six patients), firing of an ICD (four patients), asystole (three patients), bradycardia (two patients), depleted battery life of a pacemaker (one patient), and an unspecified tachyarrhythmia (one patient). Overall there was a low rate of complications (0.8 cases/100 years of surgical practice), with no reported significant morbidity or mortality. Bipolar forceps were utilized by 19% of respondents and were not associated with any incidences of interference. Conclusions. Significant interference to pacemakers or ICDs rarely results from office-based electrosurgery. No clear community practice standards regarding precautions was evident from this survey. The use of bipolar forceps or true electrocautery are the better options when electrosurgey is required. These two modalities may necessitate fewer perioperative precautions than generally recommended, without compromising patient safety. [source] Anaphylaxis: Clinical concepts and research prioritiesEMERGENCY MEDICINE AUSTRALASIA, Issue 2 2006Simon GA Brown Abstract Anaphylaxis is a severe immediate-type hypersensitivity reaction characterized by life-threatening upper airway obstruction bronchospasm and hypotension. Although many episodes are easy to diagnose by the combination of characteristic skin features with other organ effects, this is not always the case and a workable clinical definition of anaphylaxis and useful biomarkers of the condition have been elusive. A recently proposed consensus definition is ready for prospective validation. The cornerstones of management are the supine position, adrenaline and volume resuscitation. An intramuscular dose of adrenaline is generally recommended to initiate treatment. If additional adrenaline is required, then a controlled intravenous infusion might be more efficacious and safer than intravenous bolus administration. Additional bronchodilator treatment with continuous salbutamol and corticosteroids are used for severe and/or refractory bronchospasm. Aggressive volume resuscitation, selective vasopressors, atropine (for bradycardia), inotropes that bypass the ,-adrenoreceptor and bedside echocardiographic assessment should be considered for hypotension that is refractory to treatment. Management guidelines continue to be opinion- and consensus-based, with retrospective studies accounting for the vast majority of clinical research papers on the topic. The clinical spectrum of anaphylaxis including major disease subgroups requires clarification, and validated scoring systems and outcome measures are needed to enable good-quality prospective observational studies and randomized controlled trials. A systematic approach with multicentre collaboration is required to improve our understanding and management of this disease. [source] Adenosine A1 Antagonism Attenuates Atropine-resistant Hypoxic Bradycardia in RatsACADEMIC EMERGENCY MEDICINE, Issue 9 2003Justin L. Kaplan MD Abstract Objectives: To test the following hypotheses: Hypoxia induces bradycardia and hemodynamic compromise that are resistant to atropine but responsive to selective antagonism of the adenosine A1 receptor (A1AdoR). The mechanism for such attenuation is independent of the vagus nerve. Methods: Ten minutes after sham or actual bilateral cervical vagotomy, paralyzed ventilated rats were made hypoxic (5% fractional inspired oxygen, continued until death). Five minutes after beginning hypoxia, intravenous treatment with BG-9719, a selective A1AdoR antagonist (0.1 mg/kg); atropine (0.1 mg/kg); BG-9719 vehicle; or saline was initiated. These drug doses were based on pilot studies. Of the eight treatment groups (eight possible combinations of vagotomy status and drug/vehicle treatment), n= 8 in all except nonvagotomized, vehicle-treated rats (where n= 7). Results: Heart rate and left ventricular contractility decreased rapidly with hypoxia. Atropine had minimal effects in prolonging survival (from mean ± SEM of 15.5 ± 2.1 minutes to 20.2 ± 2.5 minutes, p = 0.94) and attenuating posthypoxic decreases in heart rate (p = 0.89) and contractility (p = 0.83) compared with saline. BG-9719 prolonged survival, however, from 14.4 ± 1.9 minutes (with vehicle treatment) to 37.2 ± 6.8 minutes (p < 0.001). Survival, heart rate, and contractility were preserved with BG-9719 compared with atropine and vehicle (p < 0.05, all comparisons). Vagotomy prevented the effects of BG-9719 on survival prolongation (p = 0.003), heart rate (p = 0.01), and contractility (p < 0.001) but did not affect those outcomes in saline-treated rats. Conclusions: Survival, heart rate, and contractility were better preserved with BG-9719 than atropine. A1AdoR selective antagonism, possibly because of its multiple mechanisms for attenuating hypoxic cardiac insufficiency, resulted in better hemodynamic and clinical outcomes. That attenuation seems to have a component of vagal mediation. [source] The Ictal Bradycardia Syndrome: Localization and LateralizationEPILEPSIA, Issue 4 2006Jeffrey W. Britton Summary:,Purpose: Previous studies have established the importance of the insular cortex and temporal lobe in cardiovascular autonomic modulation. Some investigators, based on the results of cortical stimulation response, functional imaging, EEG recordings of seizures, and lesional studies, have suggested that cardiac sympathetic and parasympathetic function may be lateralized, with sympathetic representation lateralized to the right insula, and parasympathetic, to the left. These studies have suggested that ictal bradycardia is most commonly a manifestation of activation of the left temporal and insular cortex. However, the evidence for this is inconsistent. We sought to assess critically the predictable value of ictal bradycardia for seizure localization and lateralization. Methods: In this study, we reviewed the localization of seizure activity in 13 consecutive patients with ictal bradycardia diagnosed during prolonged video-EEG monitoring at Mayo Clinic Rochester. The localization of electrographic seizure activity at seizure onset and bradycardia onset was identified in all patients. In addition, we performed a comprehensive review of the ictal bradycardia literature focusing on localization of seizure activity in ictal bradycardia cases. Results: All occurrences of ictal bradycardia in the 13 identified patients were associated with temporal lobe,onset seizures. However, no consistent lateralization of seizure activity was found at onset of seizure activity or at onset of bradycardia in this population. Seizure activity was bilateral at bradycardia onset in nine of 13 patients. The results from the literature review also showed that a predominance of patients had bilateral activity at bradycardia onset; however, more of the ictal bradycardia cases from the literature had left hemispheric localization of seizure onset. Conclusions: Ictal bradycardia most often occurs in association with bilateral hemispheric seizure activity and is not a consistent lateralizing sign in localizing seizure onset. Our data do not support the existence of a strictly unilateral parasympathetic cardiomotor representation in the left hemisphere, as has been suggested. [source] Embryonic Arrhythmia by Inhibition of HERG Channels: A Common Hypoxia-related Teratogenic Mechanism for Antiepileptic Drugs?EPILEPSIA, Issue 5 2002Faranak Azarbayjani Summary: ,Purpose: There is evidence that drug-induced embryonic arrhythmia initiates phenytoin (PHT) teratogenicity. The arrhythmia, which links to the potential of PHT to inhibit a specific potassium channel (Ikr), may result in episodes of embryonic ischemia and generation of reactive oxygen species (ROS) at reperfusion. This study sought to determine whether the proposed mechanism might be relevant for the teratogenic antiepileptic drug trimethadione (TMO). Methods: Effects on embryonic heart rhythm during various stages of organogenesis were examined in CD-1 mice after maternal administration (125,1,000 mg/kg) of dimethadione (DMO), the pharmacologically active metabolite of TMO. Palatal development was examined after administration of a teratogenic dose of DMO and after simultaneous treatment with DMO and a ROS-capturing agent (,-phenyl- N -tert-butyl-nitrone; PBN). The Ikr blocking potentials of TMO and DMO were investigated in HERG-transfected cells by using voltage patch-clamping tests. Results: DMO caused stage-specific (gestation days 9,13 only) and dose-dependent embryonic bradycardia and arrhythmia at clinically relevant maternal plasma concentrations (3,11 mM). Hemorrhage in the nasopharyngeal part of the embryonic palate (within 24 h) preceded cleft palate in fetuses at term. Simultaneous treatment with PBN significantly reduced the incidence of DMO-induced cleft palate, from 40 to 13%. Voltage patch-clamping studies showed that particularly DMO (70% inhibition), but also TMO, had Ikr blocking potential at clinically relevant concentrations. Conclusions: TMO teratogenicity, in the same way as previously shown for PHT, was associated with Ikr -mediated episodes of embryonic cardiac arrhythmia and hypoxia/reoxygenation damage. [source] Cardiovascular effects of noradrenaline microinjected into the dorsal periaqueductal gray area of unanaesthetized ratsEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2005Gislaine Garcia Pelosi Abstract The periaqueductal grey area (PAG) is a mesencephalic region that is involved in the modulation of cardiovascular changes associated with behavioural responses. Among the neurotransmitters present in the PAG, noradrenaline (NA) is also known to be involved in central nervous system cardiovascular regulation. In the present study we report the cardiovascular effects of the microinjection of NA into the dorsal portion of the PAG (dPAG) of unanaesthetized rats and the peripheral mechanism involved in their mediation. Injection of NA in the dPAG of unanaesthetized rats evoked a dose-dependent pressor response accompanied by bradycardia. The magnitude of the pressor responses was higher at more rostral sites in the dPAG and decreased when NA was injected into the caudal portion of the dPAG. The responses to NA were markedly reduced in urethane-anaesthetized rats. The pressor response was potentiated by i.v. pretreatment with the ganglion blocker pentolinium and blocked by i.v. pretreatment with the vasopressin antagonist dTyr(CH2)5(Me)AVP. The results suggest that activation of noradrenergic receptors within the dPAG can evoke pressor responses, which are mediated by acute vasopressin release. [source] Somatic and visceral afferents to the ,vasodepressor region' of the caudal midline medulla in the ratEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 6 2003Jason R. Potas Abstract Previous research has found that the integrity of a restricted region of the caudal midline medulla (including caudal portions of nucleus raphé obscurus and nucleus raphé pallidus) was critical for vasodepression (hypotension, bradycardia, decreased cardiac contractility) evoked either by haemorrhage or deep pain. In this anatomical tracing study we found that the vasodepressor part of the caudal midline medulla (CMM) receives inputs arising from spinal cord, spinal trigeminal nucleus (SpV) and nucleus of the solitary tract (NTS). Specifically: (i) a spinal,CMM projection arises from neurons of the deep dorsal horn, medial ventral horn and lamina X at all spinal segmental levels, with approximately 60% of the projection originating from the upper cervical spinal cord (C1,C4); (ii) a SpV,CMM projection arises primarily from neurons at the transition between subnucleus caudalis and subnucleus interpolaris; (iii) a NTS,CMM projection arises primarily from neurons in ventrolateral and medial subnuclei. In combination, the specific spinal, SpV and NTS regions which project to the CMM receive the complete range of somatic and visceral afferents known to trigger vasodepression. The role(s) of each specific projection is discussed. [source] Role of GABAergic neurones in the nucleus tractus solitarii in modulation of cardiovascular activityEXPERIMENTAL PHYSIOLOGY, Issue 9 2010Jasenka Zubcevic GABAergic neurones are interspersed throughout the nucleus tractus solitarii (NTS), and their tonic activity is crucial to the maintenance of cardiorespiratory homeostasis. However, the mechanisms that regulate the magnitiude of GABAergic inhibition in the NTS remain unknown. We hypothesized that the level of GABAergic inhibition is proportionally regulated by the level of excitatory synaptic input to the NTS from baroreceptors. Using the in situ working heart,brainstem preparation in normotensive and spontaneously hypertensive rats, we blocked GABAA receptor-mediated neurotransmission in the NTS with gabazine (a specific GABAA receptor antagonist) at two levels of perfusion pressure (low PP, 60,70 mmHg; and high PP, 105,125 mmHg) while monitoring the immediate changes in cardiorespiratory variables. In normotensive rats, gabazine produced an immediate bradycardia consistent with disinhibition of NTS circuit neurones that regulate heart rate (HR) which was proportional to the level of arterial pressure (,HR at low PP, ,57 ± 9 beats min,1; at high PP, ,177 ± 9 beats min,1; P < 0.001), suggesting that GABAergic circuitry in the NTS modulating heart rate was arterial pressure dependent. In contrast, there was no significant difference in the magnitude of gabazine-induced bradycardia in spontaneously hypertensive rats at low or high PP (,HR at low PP, ,45 ± 10 beats min,1; at high PP, ,58 ± 7 beats min,1). With regard to thoracic sympathetic nerve activity (tSNA), at high PP there was a significant reduction in tSNA during the inspiratory (I) phase of the respiratory cycle, but only in the normotensive rat (,,tSNA =,18.7 ± 10%). At low PP, gabazine caused an elevation of the postinspiration phase of tSNA in both normotensive (,,tSNA = 23.7 ± 2.9%) and hypertensive rats (,,tSNA = 44.2 ± 14%). At low PP, gabazine produced no change in tSNA during the mid-expiration phase in either rat strain, but at high PP we observed a significant reduction in the mid-expiration phase tSNA, but only in the spontaneously hypertensive rat (,,tSNA =,25.2 ± 8%). Gabazine at both low and high PP produced a reduction in the late expiration phase of tSNA in the hypertensive rat (low PP, ,,tSNA =,29.4 ± 4.4%; high PP, ,tSNA =,22.8 ± 3%), whereas in the normotensive rat this was only significant at high PP (,,tSNA =,42.5 ± 6.1%). Therefore, in the spontaneously hypertensive rat, contrary to the GABAA receptor-mediated control of HR, it appears that GABAA receptor-mediated control of tSNA in the NTS is arterial pressure dependent. This study provides new insight into the origin of GABAergic inhibition in NTS circuitry affecting heart rate and sympathetic activity. [source] ,And the beat goes on' The cardiac conduction system: the wiring system of the heartEXPERIMENTAL PHYSIOLOGY, Issue 10 2009Mark R. Boyett The cardiac conduction system (CCS), consisting of the sino-atrial node, atrioventricular node and His,Purkinje system, is responsible for the initiation and co-ordination of the heart beat. In the last decade, our understanding of the CCS has been transformed. Immunohistochemistry, used in conjunction with anatomical techniques, has transformed our understanding of its anatomy; arguably, we now understand the position of the sino-atrial node (not the same as in medical textbooks), and our new understanding of the atrioventricular node anatomy means that we can compute its physiological and pathophysiological behaviour. Ion channel expression in the CCS has been shown to be fundamentally different from that in the working myocardium. Dysfunction of the CCS has previously been attributed to fibrosis, but it is now clear that remodelling of ion channels plays an important role in dysfunction during ageing, heart failure and atrial fibrillation. Differences in ion channel expression may even be responsible for the bradycardia in the athlete and differences in heart rate among different species (such as humans and mice). Recent work has highlighted less well-known components of the CCS, including tricuspid, mitral and aortic rings and even a third (retro-aortic) node. These additional tissues do not participate in the initiation and co-ordination of the heart beat and instead they are likely to be the source of various life-threatening arrhythmias. During embryological development, all parts of the CCS have been shown to develop from the primary myocardium of the linear heart tube, partly under the influence of the transcription factor, Tbx3. [source] A clinical prospective comparison of anesthetics sensitivity and hemodynamic effect among patients with or without obstructive jaundiceACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 7 2010L.-Q. YANG Background: To compare isoflurane anesthesia in patients with or without hyperbilirubinemia undergoing hepatobiliary surgery. Methods: Forty-two patients with obstructive jaundice and 40 control patients with normal liver function scheduled for hepatobiliary surgery under isoflurane anesthesia were studied. Anesthesia was induced with propofol (1.5,2 mg/kg) and remifentanil (2 ,g/kg). After tracheal intubation, anesthesia was titrated using isoflurane in oxygen-enriched air, adjusted to maintain a bispectral index (BIS) value of 46,54. Ephedrine, atropine and remifentanil were used to maintain hemodynamic parameters within 30% of the baseline. The mean arterial blood pressure (MAP), heart rate (HR), drug doses and the time taken to recover from anesthesia were recorded. Results: Demographic data, duration and BIS values were similar in both groups. Anesthesia induction and maintenance were associated with more hemodynamic instability in the patients with jaundice and they received more ephedrine and atropine and less remifentanil and isoflurane (51.1±24.2 vs. 84.6±20.3 mg/min; P for all <0.05) than control patients. Despite less anesthetic use, the time to recovery and extubation was significantly longer than that in control. Conclusion: Patients with obstructive jaundice have an increased sensitivity to isoflurane, more hypotension and bradycardia during anesthesia induction and maintenance and a prolonged recovery time compared with controls. [source] New Glaucoma Medications in the Geriatric Population: Efficacy and SafetyJOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 5 2002Gary D. Novack PhD Glaucoma can be considered a disease of the aging eye. Most medications used to treat glaucoma are in topical eyedrop form and may cause numerous untoward systemic effects in older persons. In recent years, several new ocular hypotensive medications have become available. These medications are being used more commonly because there is a growing trend by ophthalmologists to aggressively lower intraocular pressure. Therefore, geriatricians require a comprehensive knowledge of medications used to treat glaucoma, in addition to an understanding of their mechanism of action profiles of untoward effects and possible interactions with other diseases or medications. Therefore, we performed a review of the medications recently introduced into clinical practice. We selected drugs approved by the U.S. Food and Drug Administration between 1996 and September 2001. The safety profiles of these agents and their untoward side effects were reviewed by class: topical carbonic anhydrase inhibitors (brinzolamide: ocular tolerance, taste perversion), ,-adrenoceptor antagonists (timolol: bradycardia and bronchospasm), ,-adrenergic agonists (brimonidine: oral dryness, headache, and fatigue), and prostaglandin analogs (latanoprost, bimatoprost, travoprost, and unoprostone isopropyl: ocular hyperemia, iris color changes). The function of this review is to make geriatricians more aware of the efficacy and untoward effects of medications recently introduced into clinical practice. We recommend that geriatricians perform a medication review on all medications their patients use, including eye drops. [source] Fetal and offspring arrhythmia following exposure to nicotine during pregnancyJOURNAL OF APPLIED TOXICOLOGY, Issue 1 2010Yu Feng Abstract Although recent studies have demonstrated prenatal nicotine can increase cardiovascular risk in the offspring, it is unknown whether exposure to nicotine during pregnancy also may be a risk for development of arrhythmia in the offspring. In addition, in previous studies of fetal arrhythmia affected by smoking, only two patterns, bradycardia and tachycardia, were observed. The present study examined acute effects of maternal nicotine on the fetal arrhythmia in utero, and chronic influence on offspring arrhythmia at adult stage following prenatal exposure to nicotine. Nicotine was administered to pregnant ewes and rats. In the fetal sheep, intravenous nicotine not only induced changes of fetal heart rate, but also caused cardiac cycle irregularity, single and multiple dropped cardiac cycles. Although maternal nicotine had no influence on fetal blood pH, lactic acid, hemocrit, Na+, K+ levels and plasma osmolality, fetal blood PO2 levels were significantly decreased following maternal nicotine in ewes. In offspring rats at 4,5 months after birth, prenatal exposure to nicotine significantly increased heart rate and premature ventricular contraction in restraint stress. In addition, arrhythmias induced by injection of nicotine were higher in the offspring prenatal exposure to nicotine in utero. The results provide new evidence that exposure to nicotine in pregnancy can cause fetal arrhythmia in various patterns besides tachycardia and bradycardia, the possible mechanisms for nicotine-induced fetal arrhythmia included in utero hypoxia. Importantly, following exposure to nicotine significantly increased risk of arrhythmia in the adult offspring. The finding offers new insight for development of cardiac rhythm problems in fetal origins. Copyright © 2009 John Wiley & Sons, Ltd. [source] A novel approach to assessing percutaneous VX poisoning in the conscious guinea-pig,JOURNAL OF APPLIED TOXICOLOGY, Issue 5 2008Helen Mumford Abstract Nerve agents like VX (S-2-diisopropylaminoethyl-O-ethyl-methylphosphonothiolate) are potent irreversible acetylcholinesterase (AChE) inhibitors. Following percutaneous nerve agent exposure there is a slower rate of absorption, later onset and longer duration of signs of poisoning. Relatively little is known about the physiological effects of percutaneously applied nerve agent in unanaesthetised laboratory animals. Heart rate (ECG), brain electrical activity (EEG), body temperature, locomotor activity and clinical signs were monitored following percutaneous application of VX to conscious guinea-pigs. A fall in heart rate (bradycardia) preceded incapacitation following the highest VX dose, and occurred in the absence of incapacitation at the lower doses. Following the highest dose of VX (0.592 mg kg,1) three out of four animals died within 24 h. The lower two doses of VX (0.296 and 0.148 mg kg,1), produced extended periods of bradycardia in the absence of observable signs of poisoning. Bradycardia preceded, or occurred in the absence of, a temperature decrease; seizure-like EEG changes were not observed at any of the VX doses tested. Acetylcholinesterase activity was significantly inhibited in the blood and most brain areas at 48 h. There were significant dose-related decreases in body weight at 24 and 48 h following VX. This preliminary study suggests that decreased heart rate may be an early sign of the toxic effects of VX, whereas temperature and observable clinical signs are not good early indicators of percutaneous VX poisoning in this animal model. Future studies will use this model to assess the benefit of administering medical countermeasures in response to a defined decrease in heart rate. © Crown Copyright 2007. Reproduced with the permission of the Controller of HMSO. Published by John Wiley & Sons, Ltd. This article was published online on 5 December 2007. An error was subsequently identified. This notice is included in the online and print versions to indicate that both have been corrected [30 May 2008]. [source] Electrocardiographic Findings, Device Therapies, and Comorbidities in Octogenarian Implantable Defibrillator RecipientsJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 3 2010JAMES D. DANIELS M.D. Implantable Defibrillators in Octogenarians.,Background: The use of implantable cardioverter-defibrillators (ICDs) in octogenarians is poorly defined. Objective: To assess baseline electrocardiographic (ECG) findings, arrhythmia episodes, and development of severe nonarrhythmic illness or death in patients aged ,80 years at ICD implantation, and to compare them with younger patients. Methods: Medical records and device interrogations for 199 patients ,70 years old who underwent ICD implantation were reviewed. Patients were divided into 3 groups based on age at the time of implant: age 70,74 (group 1; 88 patients), age 75,79 (group 2; 67 patients), and age ,80 (group 3; 44 patients). Results: ECGs: Octogenarians were more likely to have sinus bradycardia (SB) (P = 0.047) and left bundle branch block (LBBB) (P = 0.043) compared to younger patients. There was no difference among groups in the proportion of patients with atrial fibrillation or any degree of AV block. Therapies: There was no difference between age groups in any therapy (P = 0.78), appropriate therapy (P = 0.54), or inappropriate therapy (P = 0.21) per patient-year. There was no difference between groups in time-to-first therapy of any type (P = 0.71). Nonarrhythmic death/morbidity: There was no difference between groups in time to death or serious illness. Conclusion: Our study is the first to evaluate in detail the therapies received by octogenarians after ICD placement. The higher incidence of SB and LBBB might influence the number of pacing sites in octogenarian patients. Very elderly patients have similar rates of arrhythmic episodes and development of severe comorbidities as septuagenarians, and they should not be denied ICD implantation based solely on age. (J Cardiovasc Electrophysiol, Vol. 21, pp. 236,241, March 2010) [source] SCN5A Mutation Associated with Cardiac Conduction Defect and Atrial ArrhythmiasJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 5 2006PÄIVI J. LAITINEN-FORSBLOM Ph.D. Introduction: We aimed at identifying the molecular defect underlying the clinical phenotype of a Finnish family with a cardiac conduction defect and atrial arrhythmias. Methods and Results: A large Finnish family was clinically evaluated (ECG, 24-hour ambulatory ECG, echocardiography). We performed linkage analysis with markers flanking the SCN5A gene and subsequently sequenced the SCN5A gene. Five family members had atrial arrhythmias and intracardiac conduction defects, and due to bradycardia needed a pacemaker when adolescents. No heart failure or sudden cardiac death was observed. Left ventricle dilatation was seen in one individual and three individuals had a slightly enlarged right ventricle. Premature death due to stroke occurred in one subject during the study, and two other members had suffered from stroke at young age. Linkage analysis favored the role of the SCN5A gene in disease pathogenesis, and direct sequencing disclosed D1275N mutation. This alteration was present not only in all six affected individuals, but also in two young individuals lacking clinical symptoms. Conclusions: Cardiac conduction defect and atrial arrhythmias in a large Finnish family appear to result from the SCN5A D1275N mutation. Although no sudden cardiac death was recorded in the family, at least three affected members had encountered brain infarction at the age of 30 or younger. [source] Phytanic Acid Accumulation Is Associated with Conduction Delay and Sudden Cardiac Death in Sterol Carrier Protein-2/Sterol Carrier Protein-x Deficient MiceJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 11 2004GEROLD MÖNNIG M.D. Introduction: The sterol carrier protein-2 gene encodes two functionally distinct proteins: sterol carrier protein-2 (SCP2, a peroxisomal lipid carrier) and sterol carrier protein-x (SCPx, a peroxisomal thiolase known as peroxisomal thiolase-2), which is involved in peroxisomal metabolism of bile acids and branched-chain fatty acids. We show in this study that mice deficient in SCP2 and SCPx (SCP2null) develop a cardiac phenotype leading to a high sudden cardiac death rate if mice are maintained on diets enriched for phytol (a metabolic precursor of branched-chain fatty acids). Methods and Results: In 210 surface and 305 telemetric ECGs recorded in wild-type (C57BL/6; wt; n = 40) and SCP2 null mice (n = 40), no difference was observed at baseline. However, on diet, cycle lengths were prolonged in SCP2 null mice (262.9 ± 190 vs 146.3 ± 43 msec), AV conduction was prolonged (58.3 ± 17 vs 42.6 ± 4 ms), and QRS complexes were wider (19.1 ± 5 vs 14.0 ± 4 ms). In 11 gene-targeted Langendorff-perfused hearts isolated from SCP2 null mice after dietary challenge, complete AV blocks (n = 5/11) or impaired AV conduction (Wenckebach point 132 ± 27 vs 92 ± 10 msec; P < 0.05) could be confirmed. Monophasic action potentials were not different between the two genotypes. Left ventricular function studied by echocardiography was similar in both strains. Phytanic acid but not pristanic acid accumulated in the phospholipid fraction of myocardial membranes isolated from SCP2 null mice. Conclusion: Accumulation of phytanic acid in myocardial phospholipid membranes is associated with bradycardia and impaired AV nodal and intraventricular impulse conduction, which could provide an explanation for sudden cardiac death in this model. [source] Changes in Left Ventricular Repolarization and Ion Channel Currents Following a Transient Rate Increase Superimposed on Bradycardia in Anesthetized DogsJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 6 2000MICHAEL RUBART M.D. Electrical Remodeling of the Heart due to Rate. Introduction: We previously demonstrated in dogs that a transient rate increase superimposed on bradycardia causes prolongation of ventricular refractoriness that persists for hours after resumption of bradycardia. In this study, we examined changes in membrane currents that are associated with this phenomenon. Methods and Results: The whole cell, patch clamp technique was used to record transmembrane voltages and currents, respectively, in single mid-myocardial left ventricular myocytes from dogs with 1 week of complete AV block; dogs either underwent 1 hour of left ventricular pacing at 120 beats/min or did not undergo pacing. Pacing significantly heightened mean phase 1 and peak plateau amplitudes by ,6 and ,3 mV, respectively (P < 0.02). and prolonged action potential duration at 90% repolarization from 235 ± 8 msec to 278 ± 8 msec (1 Hz; P = 0.02). Rapid pacing-induced changes in transmembrane ionic currents included (1) a more pronounced cumulative inactivation of the 4-aminopyridine-sensitive transient outward K+ current, I to over the range of physiologic frequencies, resulting from a ,30% decrease in the population of quickly reactivating channels; (2) increases in peak density of L-type Ca2+ currents, Ica.I.' by 15% to 35% between +10 and +60 mV; and (3) increases in peak density of the Ca2+ -activated chloride current, ICl.Ca' by 30% to 120% between +30 and +50 mV. Conclusion: Frequency-dependent reduction in Ito combined with enhanced ICa.I. causes an increase in net inward current that may he responsible for the observed changes in ventricular repolarization. This augmentation of net cation influx is partially antagonized by an increase in outward ICa.Cl. [source] Pacing in Right Ventricular Dysplasia after Disconnection SurgeryJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2 2000CHUEN TANG M.B.B.S. Pacing in Right Ventricular Dysplasia. This report describes a 33-year-old patient with arrhythmogenic right ventricular (RV) dysplasia who had a dual chamber pacemaker implanted at age 23 years for drug-induced bradycardia. Pacing was continued after right ventricular free-wall disconnection (RVFVVD) at age 24 years. Her pacemaker was not replaced after battery depletion 7 years later. She presented the following year in severe right-sided heart failure. Her old pacemaker generator was replaced. This was followed by rapid resolution of her clinical failure and return to a full, active, physical lifestyle. This observation suggests the potential benefit of dual chamber pacing in patients with RV dysplasia after RVFWD. [source] | |||||||||||||||||||||||||||||||||||||||||||