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At least 19 recordsLinked to original sources
PubMed1980

Hypertension secondary to bradycardia: blood pressure regulation under the effect of impaired cerebral blood flow and bradycardia.

Ninety-two patients of advanced age were studied in whom arterial hypertension was associated with chronic bradycardia, the cessation of bradycardia after pacemaker implantation was followed by a significant fall or permanent normalization of the high blood pressure. In three cases cerebral blood flow was found low, but it increased when the heart rate was normalized on pacing. In order to check the results obtained in humans, cerebral blood supply was restricted by carotids ligation, in some animals the vertebral artery of one side was also ligated. During obstruction of cerebral blood flow, bradycardia induced by av block or vagal stimulation was followed by an increase in arterial blood pressure. It is suggested that disturbances of cerebral blood flow associated with bradycardia have a decisive part in the pathogenesis of hypertension in old age.

Aged↗
PubMed1991

Bradycardia-dependent early afterdepolarizations in a patient with QTU prolongation and torsade de pointes in association with marked bradycardia and hypokalemia.

Endocardial monophasic action potentials (MAPs) were recorded at the right ventricular apex in a patient with QTU prolongation and torsade de pointes (TdP) in association with marked bradycardia and hypokalemia. There was a distinct hump on phase 3 repolarization of the MAPs characteristic of early afterdepolarizations (EADs), which was associated with marked prolongation of the QTU interval on the surface electrocardiogram. EAD amplitude was bradycardia dependent, and there was a strong correlation (r = 0.91) between the preceding RR interval and the amplitude of the EAD (percent of MAP amplitude). Intravenous administration of lidocaine or right ventricular pacing suppressed the ventricular premature complexes and TdP in association with the suppression of the EADs on the MAPs. Furthermore, these EADs were not recorded on the MAPs 1 month later when the QTU prolongation and TdP had disappeared. These findings suggest that the TU abnormality and QTU prolongation responsible for TdP were due to bradycardia-dependent EADs.

Action Potentials↗
PubMed1979

Atrial bigeminy with block associated with bradycardia and paroxysmal atrial fibrillation -- an important variant of the tachycardia-bradycardia syndrome.

Serial 2-channel 24 h dynamic ECGs in 7 patients who were referred with the "tachy-brady" syndrome for consideration for permanent cardiac pacing revealed: 1. atrial premature beats (APBs) which were conducted to the ventricles normally or aberrantly; 2. intermittent atrial bigeminy with block towards the ventricles (this rhythm mimicked sinus bradycardia with ventricular rates of 38-45 beats/min and the ectopic P waves were visible on only one of the ECG channels); 3. paroxysms of atrial fibrillation initiated by closely coupled APBs. These findings suggested that both the ventricular bradycardia and the atrial fibrillation were caused by frequent APBs and that pacing therapy was unnecessary. Disopyramide was given to 5 patients resulting in suppression of the arrhythmia and relief of symptoms. In one patient there was spontaneous resolution and one patient refused treatment. This variant of the "tachy-brady" syndrome can be successfully treated by suppression of abnormal atrial impulse formation without recourse to pacemaker implantation.

Adult↗
PubMed1993

Mechanism of the bradycardia produced in the cat by the anticholinesterase neostigmine.

Neostigmine evoked bradycardia in vagotomized, propranolol-treated cats. Heart rate decreased by 50% with 0.4 +/- 0.2 mg/kg (mean +/- S.D.) i.v. of neostigmine. The bradycardia was attenuated after acetylcholine (ACh) depletion in the cardiac parasympathetic pathway suggesting ACh release within this pathway was involved. The bradycardia was unchanged after preganglionic terminal degeneration suggesting ACh release was from cardiac ganglion cells. Edrophonium produced a much weaker bradycardia suggesting the anticholinesterase effect of neostigmine may not produce the bradycardia. The neostigmine-induced bradycardia was blocked by systemic atropine (ED50, 0.005 +/- 0.001 mg/kg), pancuronium bromide (ED50, 0.033 +/- 0.021 mg/kg), pirenzepine (ED50, 74.7 +/- 7.9 micrograms/kg), hexamethonium (ED50, 8.3 +/- 1.6 mg/kg) and d-tubocurarine (ED50, 8.6 +/- 3.0 micrograms/kg). The doses of hexamethonium and d-tubocurarine that blocked the neostigmine-induced bradycardia were significantly higher than required for blocking the bradycardia produced by vagus nerve stimulation. Hexamethonium (60 mg/kg i.v.) had no effect on the bradycardia produced by the muscarinic agonist methacholine (100-300 micrograms/kg/min i.v.). The dose of pirenzepine that blocked the neostigmine-induced bradycardia was lower than required for blocking the bradycardia produced by vagus nerve stimulation. McN-A-343 ([4-hydroxy-2-butynyl]-1-trimethyl ammonium m-chlorocarbanilate chloride) (1 mg/kg i.v.) did not produce bradycardia. These observations suggest neostigmine evokes bradycardia by activation of ACh receptors on cardiac ganglion cells producing ACh release and activation of cardiac M2 receptors. The low sensitivity of the neostigmine-induced bradycardia to pirenzepine, and the failure of McN-A-343 to evoke bradycardia, suggest the receptor on cardiac ganglion cells is not an M1-type.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1999

The efficacy of atropine in the treatment of hemodynamically unstable bradycardia and atrioventricular block: prehospital and emergency department considerations.

OBJECTIVE: To determine the efficacy of atropine therapy in patients with hemodynamically compromising bradycardia or atrioventricular block (AVB) in the prehospital and emergency department settings. METHODS DESIGN: Retrospective review of prehospital, emergency department, and hospital records. PARTICIPANTS: Prehospital patients with hemodynamically compromising bradycardia or AVB with evidence of spontaneous circulation who received atropine as delivered by emergency medical services personnel (advanced life support level). SETTING: Urban/suburban fire department-based emergency medical service system with on-line medical control serving a population of approximately 1.6 million persons. DEFINITIONS: Hemodynamic instability was defined as the presence of any of the following: ischemic chest pain, dyspnea, syncope, altered mental status, and systolic blood pressure less than 90 mmHg. Bradycardia was defined as sinus bradycardia, junctional bradycardia, or idioventricular bradycardia (grouped as bradycardia) while AVB included first-, second- (types I and II), or third-degree (grouped as AVB). The response that occurred within one minute following each dose of atropine was defined as none, partial, complete, or adverse. MAIN RESULTS: Of 172 patients meeting entry criterion complete data was available for 131 (76.1%) and constitutes the study population. The mean age was 71 years. Fifty-one percent were female. Forty-five patients had AVB and 86 bradycardia. Patients with AVB were more likely to have a presenting systolic blood pressure less than 90 mmHg than those with bradycardia. In the 131 patients, responses to atropine were as follows: 26 (19.8%) = partial, 36 (27.5%) = complete, 65 (49.6%) = none, and 4 (2.3%) = adverse. Patients presenting with bradycardia (compared to AVB) more commonly: (1) received a single dose of atropine; (2) a lower total dose of atropine in the prehospital interval; (3) were more likely to arrive in the ED with a normal sinus rhythm; and (4) were less likely to receive additional atropine or isoproterenol in the ED. Those patients who achieved normal sinus rhythm over the total course of care were likely to have achieved that rhythm during the prehospital interval. There was no difference between groups in the likelihood of leaving the ED with a normal sinus rhythm achieved during the ED interval. Acute myocardial infarction was more common in patients presenting with AVB (55.5%) than with bradycardia (23.2%, P = 0.001). CONCLUSIONS: Approximately one-half of patients who received atropine in the prehospital setting for compromising rhythms had either a partial or complete response to therapy. Adverse responses were uncommon. Those patients who presented with hemodynamically unstable bradycardia to EMS personnel responded more commonly to a single dose and a lower total dose of atropine compared to similar patients with AVB. Those patients who achieve normal sinus rhythm by ED discharge were likely to have achieved it during the prehospital interval.

Aged↗
PubMed2006

The ictal bradycardia syndrome: localization and lateralization.

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.

Adolescent↗
PubMed2006

Chronic myocardial infarction is a substrate for bradycardia-induced spontaneous tachyarrhythmias and sudden death in conscious animals.

INTRODUCTION: Patients with bradycardia can have severe tachyarrhythmias but it is unclear whether bradycardia alone can induce arrhythmias or whether an additional substrate is necessary. While several animal models of ventricular tachycardia (VT) exist, no model has been reported to mimic the clinical condition of spontaneous VT and sudden cardiac death (SCD) in the presence of bradycardia and chronic myocardial infarction (MI) in large animals without manipulation of the autonomic nervous system. We tested the hypothesis that MI and bradycardia cause more spontaneous sustained VT than does bradycardia alone. METHODS AND RESULTS: Sheep (42-56 kg) underwent atrioventricular (AV) node catheter ablation alone (n = 5) or AV node ablation and 150 minutes of angioplasty balloon occlusion of the left anterior descending coronary artery (n = 9). An implantable cardioverter defibrillator delivered rescue shocks and demand pacing at 90 beats per minute for the first week and at 40 beats per minute thereafter. Electrograms were continuously radiotelemetered and recorded for 6 weeks. Acute post-MI VT disappeared by day 4. The sudden bradycardia on day 8 triggered numerous premature ventricular contractions (PVCs) and episodes of sustained VT lasting >30 seconds during the next 5 weeks. There were 43 episodes of sustained VT and no spontaneous ventricular fibrillation (VF) with bradycardia alone. However, in the presence of both MI and bradycardia there were 970 episodes of VT/VF (P < 0.05) and three deaths at days 13, 15, and 34. The average 24-hour count of PVCs was similar at day 7 between the two groups but by days 11 and 40, the PVC counts were 35 times and 4 times greater, respectively, in the presence of bradycardia and chronic MI compared to bradycardia alone. No significant difference in the incidence of PVCs was detected because of large individual variation between the two groups (P = 0.21). A high PVC count did not appear to predict SCD. CONCLUSION: The combination of MI and bradycardia secondary to AV node ablation in sheep produces a higher incidence of VT than bradycardia alone, suggesting that this preparation can serve as a model for the study of VT and sudden cardiac death.

Animals↗
PubMed2005

Carotid angioplasty and stent-induced bradycardia and hypotension: Impact of prophylactic atropine administration and prior carotid endarterectomy.

OBJECTIVE: We compared the physiologic effect of selective atropine administration for bradycardia with routine prophylactic administration, before balloon inflation, during carotid angioplasty and stenting (CAS). We also compared the incidence of procedural bradycardia and hypotension for CAS in patients with primary stenosis vs those with prior ipsilateral carotid endarterectomy (CEA). METHODS: A total of 86 patients were treated with CAS at 3 institutions. Complete periprocedural information was available for 75 of these patients. The median degree of stenosis was 90% (range, 60%-99%). Indications for CAS were severe comorbidities (n = 49), prior CEA (n = 21), and prior neck radiation (n = 5). Twenty patients with primary lesions were treated selectively with atropine only if symptomatic bradycardia occurred (nonprophylactic group). Thirty-four patients with primary lesions received routine prophylactic atropine administration before balloon inflation or stent deployment (prophylactic group). The 21 patients with prior CEA received selective atropine treatment only if symptomatic bradycardia occurred (prior CEA group) and were analyzed separately. Mean age and cardiac comorbidities did not vary significantly either between the prophylactic and nonprophylactic atropine groups or between the primary and prior CEA patient groups. Outcome measures included bradycardia (decrease in heart rate >50% or absolute heart rate <40 bpm), hypotension (systolic blood pressure <90 mm Hg or mean blood pressure <50 mm Hg), requirement for vasopressors, and cardiac morbidity (myocardial infarction or congestive heart failure). RESULTS: The overall incidence of hypotension and bradycardia in patients treated with CAS was 25 (33%) of 75. A decreased incidence of intraoperative bradycardia (9% vs 50%; P < .001) and perioperative cardiac morbidity (0% vs 15%; P < .05) was observed in patients with primary stenosis who received prophylactic atropine as compared with patients who did not receive prophylactic atropine. CAS after prior CEA was associated with a significantly lower incidence of perioperative bradycardia (10% vs 33%; P < .05), hypotension (5% vs 32%; P < .05), and vasopressor requirement (5% vs 30%; P < .05), with a trend toward a lower incidence of cardiac morbidity (0% vs 6%; not significant) as compared with patients treated with CAS for primary carotid lesions. There were no significant predictive demographic factors for bradycardia and hypotension after CAS. CONCLUSIONS: The administration of prophylactic atropine before balloon inflation during CAS decreases the incidence of intraoperative bradycardia and cardiac morbidity in primary CAS patients. Periprocedural bradycardia, hypotension, and the need for vasopressors occur more frequently with primary CAS than with redo CAS procedures. On the basis of our data, we recommend that prophylactic atropine administration be considered in patients with primary carotid lesions undergoing CAS.

Aged↗
PubMed2003

Impact of bradycardia on cerebral oxygenation and cerebral blood volume during apnoea in preterm infants.

Apnoea in prematurity is a common problem in neonatology; and it is the impaired oxygen delivery during apnoea, which can harm the brain. The aim of this study was to evaluate the effect of bradycardia (below 80 beats min(-1)) on 'cerebral haemoglobin oxygenation index' (cHbD) and cerebral blood volume (CBV) during apnoea in stable preterm infants measured by means of near infrared spectroscopy. Twenty-six episodes of mixed and central apnoea with bradycardia (bradycardia group) in 20 preterm infants were compared to 26 episodes of mixed and central apnoea without bradycardia (non-bradycardia group) in 19 preterm infants. cHbD decreased significantly more in the bradycardia group (-11.33 micromol 1(-1) after 30 s) than in the non-bradycardia group (-6.36 micromol 1(-1) after 30 s) (p < 0.05). CBV decreased significantly in the bradycardia group (p < 0.05), whereas CBV did not change significantly in the non-bradycardia group. Peripheral oxygen saturation (SaO2) decreased similarly in both groups. The aggravation of decrease of cHbD and the decrease of CBV during bradycardia in association with apnoea could be explained by decrease in cerebral blood flow, which caused decrease in cerebral oxygen delivery. This decrease of oxygen delivery during bradycardia might worsen long-term neurodevelopmental outcome in preterm infants with apnoea.

Apnea↗
PubMed1994

Bradycardia during anesthesia in infants. An epidemiologic study.

BACKGROUND: The frequency and morbidity of bradycardia during anesthesia in infants are not well documented. This study sought to determine the frequency of bradycardia during anesthesia in infants (0 to 1 yr) compared to that in older children, describe causes and morbidity, and identify factors that influence its frequency. METHODS: Computerized information abstracted from 7,979 anesthetic records of patients ages 0-4 yr undergoing noncardiac surgery were examined for the presence or absence of intraoperative bradycardia. To study bradycardia in infants, 4,645 anesthetics in patients aged 0-1 yr were considered. Those with bradycardia to heart rates less than 100 beats/min were examined for causes, morbidity, and treatment of the bradycardia. For analysis of influencing factors, the frequency of bradycardia in infants was related to age, sex, race, ASA physical status, surgical site (body cavity), complexity (major or minor) and duration, type of primary anesthetist, type of supervising anesthesiologist, and anesthetic agents. Logistic regression was used to estimate the significance (P < 0.05) and odds ratios for each. RESULTS: The frequency of bradycardia was 1.27% in the 1st yr of life, but only 0.65% in the third and 0.16% in the 4th yr, a significant difference. Causes of bradycardia in infants included disease or surgery in 35%, the dose of inhalation agent in 35%, and hypoxemia in 22%. Morbidity included hypotension in 30%, asystole or ventricular fibrillation in 10%, and death in 8%. Treatment involved epinephrine in 30% and chest compression in 25%. Associated factors included an ASA physical status of 3-5 (vs. 1 or 2) and longer (vs. shorter) surgery. Bradycardia was less than half as likely when the supervising anesthesiologist was a member of the Pediatric Anesthesia Service as with other anesthesiologists (P < 0.001). CONCLUSIONS: Bradycardia is more frequent in infants undergoing anesthesia compared to older children and is associated with substantial morbidity. It is more likely in sicker infants undergoing prolonged surgery and less likely when a pediatric anesthesiologist is present.

Age Factors↗
PubMed1998

Role of adenosine receptors in the paradoxic bradycardia response of rats to inferior vena cava occlusion during an infusion of isoproterenol.

BACKGROUND: In susceptible humans, vasodepressor reactions are induced by restriction of venous return (upright tilting) and administration of isoproterenol. Because paradoxic bradycardia is a major manifestation of vasodepressor reactions, and allowing for extrapolation between paradoxic bradycardia in rats and vasodepressor reactions, we examined whether adenosine receptors mediate the paradoxic bradycardia reaction. METHODS AND RESULTS: Paradoxic bradycardia was induced in rats by inferior vena cava occlusion during an isoproterenol infusion. We studied whether dipyridamole, an adenosine transport inhibitor, and aminophylline (nonselective) or DPCPX (selective) A1 antagonists augmented or inhibited paradoxic bradycardia, respectively, during inferior vena cava occlusion. The maximum changes in R-R during 60 seconds of inferior vena cava occlusion were that (1) in control, the rate accelerated (DeltaR-R, -9.7+/-0.8 ms, P<0.001); (2) during isoproterenol (0.8 microg . min-1), paradoxic bradycardia occurred (DeltaR-R, +92.0+/-32.0 ms, P<0.001); (3) during isoproterenol but after dipyridamole, paradoxic bradycardia occurred at a much lower dose of isoproterenol (0.2 microg . min-1), and the magnitude was increased at all doses (at 0.8 microg . min-1 isoproterenol, DeltaR-R, +195.6+/-27.6 ms, P<0.001 versus isoproterenol alone, DeltaR-R, +92.0+/-32 ms); (4) during isoproterenol and dipyridamole, atropine did not block paradoxic bradycardia, but cervical vagotomy inhibited paradoxic bradycardia (DeltaR-R, +5.6+/-1.8 ms, P<0.001 compared with isoproterenol and dipyridamole alone); and (5) during isoproterenol alone, aminophylline or DPCPX blocked paradoxic bradycardia (DeltaR-R, -5.4+/-1.0 ms, and DeltaR-R, -2.6+/-0.5 ms, respectively, each P<0.001 compared with isoproterenol alone). CONCLUSIONS: The adenosine A1 receptor mediates the paradoxic bradycardia reflex during inferior vena cava occlusion in the face of isoproterenol via vagal afferents.

Adenosine↗