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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↗
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↗
PubMed2001

Low-affinity M(2) receptor binding state mediates mouse atrial bradycardia: comparative effects of carbamylcholine and the M(1) receptor agonists sabcomeline and xanomeline.

Carbamylcholine, a nonselective muscarinic receptor agonist, and sabcomeline and xanomeline, functional M(1) receptor-selective agonists with high M(2) receptor affinities, were used to explore the relationship of the M(2) receptor affinity of these agonists to mouse atrial bradycardia and to understand the relationship of the high and low M(2) receptor affinity states to carbamylcholine-induced mouse atrial bradycardia. All three agonists produced bradycardia with sabcomeline (pEC(50) = 6.7) more potent than either carbamylcholine (pEC(50) = 5.9) or xanomeline (pEC(50) = 5.1). Sabcomeline and carbamylcholine produced a rapid, concentration-related bradycardia, which was antagonized by atropine with pK(B) values of 8.6 and 8.9, respectively. In addition, sabcomeline antagonized carbamylcholine-induced bradycardia (pK(B) = 7.48), indicating that sabcomeline was a partial agonist at M(2) receptors. In contrast, xanomeline (up to 10(-5) M), did not antagonize carbamylcholine-induced bradycardia, and atropine (3.0 x 10(-8) M) did not antagonize xanomeline-induced bradycardia, suggesting that xanomeline-induced bradycardia was not mediated by M(2) receptors. Analysis of receptor occupancy curves indicated that bradycardia resulted from the interaction of carbamylcholine with the low- rather than high-affinity state of the M(2) receptor and that sabcomeline was a partial agonist at M(2) receptors in mouse atria. In contrast, similar analysis for xanomeline using the receptor affinity of xanomeline at M(2) receptors (1.8 x 10(-8) M) was not consistent with classical receptor theory. These data document that 1) the low-affinity state of the M(2) receptor is responsible for muscarinic-induced atrial bradycardia, 2) sabcomeline was an M(2) receptor partial agonist, and 3) xanomeline-induced bradycardia was not mediated by activation of M(2) muscarinic receptors.

Animals↗
PubMedDate not supplied

Prolonged PR interval is a risk factor for bradycardia during spinal anesthesia.

BACKGROUND AND OBJECTIVES: Bradycardia occurs during 9%-13% of spinal anesthetics and may lead to cardiac arrest. Several risk factors for the development of bradycardia have been identified, but the risk conferred by presence of abnormalities detected on preoperative electrocardiogram (ECG) has not been examined. The authors undertook the study to correlate abnormal ECG findings with the incidence of bradycardia. METHODS: The data-base was previously collected from 952 patients undergoing spinal anesthesia. Patient records were reviewed and 537 had ECGs performed within 6 months of surgery. Intraoperative bradycardia was defined as a heart rate < 50 bpm (plus > 10% decrease from baseline). Abnormalities recorded from the ECG were prolonged PR interval (PR > 0.2 sec), atrial-ventricular conduction abnormalities, evidence of chamber hypertrophy, ischemia, and infarction. The findings were compared with incidence of bradycardia using contingency tables. Significant correlations were then evaluated with logistic regression. Significance was defined as P < .05. RESULTS: The incidence of bradycardia in this population was 12%. Patients with a prolonged PR interval had an increased incidence of bradycardia (25%, P = .01). Other ECG abnormalities did not correlate with increased incidence of bradycardia. Duration of PR interval did correlate significantly (P = .001) but poorly (r2 = 0.014) with baseline heart rate. However, logistic regression demonstrated that prolonged PR interval was a significant and independent predictor for bradycardia (odds ratio = 3.2, P = .01). CONCLUSIONS: Risk factors previously identified for the development of bradycardia during spinal anesthesia include: baseline heart rate < 60 bpm, ASA physical status 1 versus 3 or 4, use of beta-blocking drugs, sensory block height > or = T5, and age < 50. The results demonstrate that prolonged PR interval on the preoperative ECG is another significant and independent predictor for bradycardia.

Adult↗
PubMed1993

Cerebral hyperperfusion following episodes of bradycardia in the preterm infant.

The alterations in cerebral hemodynamics during and following 39 episodes with bradycardia of different severity have been studied by analysis of Doppler flow velocity waveforms amongst 16 stable preterm infants (range of conceptional age at the time of study 33-39 weeks; weight 1730-2820 g). Each episode with bradycardia has been classified as mild on seven occasions (heart rate between 100-120 beats/min), moderate on 15 occasions (80-100), or severe on 17 occasions (heart rate below 80) Depending on the severity of the bradycardia, the time-averaged mean flow velocity (V) could decrease by 80% below the preexistent baseline value and the end-diastolic velocity (D) dropped towards the zero line, whereas peak systolic velocities did not change The magnitude of the percentage decrease of V correlated positively with the severity of bradycardia, indicating a progressive decline of cerebral blood flow (CBF). Following bradycardia, V could increase up to 75% above the preexistent baseline value. Simultaneously, an increase of mean arterial blood pressure and D could be documented. Peak systolic velocities remained unaltered. The magnitude of the percentage increase of V following bradycardia depended both on the severity of bradycardia as well as on the drop in transcutaneous oxygen during the preceding bradycardia. Interpretation of these findings suggested that the transient cerebral hyperperfusion following bradycardia compensates for the hypoxic-ischemic episode, sustained during the preceding epoch of apnea and bradycardia.

Apnea↗
PubMed2003

Severe bradycardia during spinal and epidural anesthesia recorded by an anesthesia information management system.

BACKGROUND: Bradycardia and asystole can occur unexpectedly during neuraxial anesthesia. Risk factors may include low baseline heart rate, first-degree heart block, American Society of Anesthesiologists physical status 1, beta-blockers, male gender, and high sensory level. Anesthesia information management systems automatically record large numbers of physiologic variables that are combined with data input from the anesthesiologist to form the anesthesia record. Such large databases can be scanned for episodes of bradycardia. METHODS: To select spinal and epidural anesthetics that did not also involve general anesthesia, 57,240 automated anesthesia records were scanned. Obstetrical patients and patients younger than age 12 yr were excluded. The electronic records selected were then scanned for episodes of moderate (heart rate < 50 and >/= 40 beats/min) or severe (heart rate < 40 beats/min) bradycardia. RESULTS: A total of 6,663 cases (11.6%) met the inclusion criteria. Among the 677 cases of bradycardia (10.2%) were 46 cases of severe bradycardia (0.7%). In the final multivariate logistic regression analysis, baseline heart rate less than 60 beats/min (P </= 0.0001) and male gender (P </= 0.05) contributed significantly to risk for a severe bradycardia episode (odds ratio [OR]), 14.1 and 95% confidence interval [CI], 6.9-28.0, and OR, 2.1 and 95% CI, 1-4.3, respectively). For the 631 episodes of moderate bradycardia (9.5%), the final multivariate model included baseline heart rate less than 60 beats/min (OR, 16.2; 95% CI, 12.4-22.0), age younger than 37 yr (OR, 1.4; 95% CI, 1.1-1.7), male gender (OR, 1.4; 95% CI, 1.2-1.8), nonemergency status (OR, 1.7; 95% CI, 1.2-2.4), beta-blockers (OR, 1.6; 95% CI, 1.1-2.3), and case duration (OR, 2.0; 95% CI, 1.6-2.4) as significant risk factors. Time of occurrence of a bradycardia event was distributed widely across the entire duration of a case. CONCLUSIONS: Moderate or severe bradycardia may occur at any time during neuraxial anesthesia, regardless of the duration of anesthesia. Low baseline heart rate increases the risk for bradycardia.

Adult↗