Sinoatrial Block Research Articles

Rarely seen cardiotoxicity of lithium overdose: Complete heart block

Introduction Serious cardiac toxicity due to lithium toxicity is uncommon and generally only occurs in individuals with underlying heart disease. Cardiac impairment may result in dysrhythmias, including sinus bradycardia, sinoatrial block, and first-degree atrioventricular block. This paper describes a patient with complete AV block in the course of chronic lithium treatment. Case report Fifty-seven year-old female was brought into the emergency department (ED) due to altered mental status and malaise by ambulance from hospice. She had hypertension, type-II diabetes mellitus, and depression. The caregivers told that she had been fine yesterday, had taken regular medications (lysinopril, furosemid, acetyl salicylic acid, oral antidiabetic tablets and lithium (300 mg tb/day)). Her vital signs were; blood pressure: 70/45 mmHg, pulse: 37 bpm, respiratory rate: 22 bpm, and oxygen saturation 86%. She was confused and unresponsive to verbal stimulation. Her EKG revealed total atrioventricular block. Initial biochemical results were unremarkable except for a lithium level of 2.2 mmol/l (therapeutic range 0.5–0.8 mmol/l) and an increased creatinine of 2.11 mg/dl. A transvenous pacing electrode was introduced into the right ventricle, which allowed rapid restoration of haemodynamic and neurological status. Her neurologic examination was completely normal in the follow-up period and she was discharged without sequelae. Conclusion In conclusion, emergency physicians should bear in mind that complete AV block can ensue in the course of lithium toxicity and it is an entity that should be included in the differential diagnosis.

Cardiac pacemaker function of HCN4 channels in mice is confined to embryonic development and requires cyclic AMP

Important targets for cAMP signalling in the heart are hyperpolarization-activated and cyclic nucleotide-gated (HCN) channels that underlie the depolarizing 'pacemaker' current, I(f). We studied the role of I(f) in mice, in which binding of cAMP to HCN4 channels was abolished by a single amino-acid exchange (R669Q). Homozygous HCN4(R669Q/R669Q) mice die during embryonic development. Prior to E12, homozygous and heterozygous embryos display reduced heart rates and show no or attenuated responses to catecholaminergic stimulation. Adult heterozygous mice display normal heart rates at rest and during exercise. However, following beta-adrenergic stimulation, hearts exhibit pauses and sino-atrial node block. Our results demonstrate that in the embryo, HCN4 is a true cardiac pacemaker and elevation of HCN4 channel activity by cAMP is essential for viability. In adult mice, an important function of HCN4 channels is to prevent sinus pauses during and after stress while their role as a pacemaker of the murine heart is put into question. Most importantly, our results indicate that HCN4 channels can fulfil their physiological function only when cAMP is bound.

Time Course of Effect of Piperazine Citrate on the Electrocardiogram of the Rat

The acute electrocardiographic (ECG) changes induced by 4 different doses of piperazine citrate (15, 30, 60, and 100 mg/kg) were determined in the anesthetized Wistar rat. A dose-dependent reduction in heart rate occurred, from 9.03%+/-2.97% at a dose of 15 mg/kg to 30.84%+/-3.4% at 100 mg/kg body weight. The P-R interval showed dose-dependent increases over values at equilibration, increasing from 10.69% +/-2.82% at 15 mg/kg to 24.79%+/-2.71% at 100 mg/kg. Similarly, the Q-T interval corrected for heart rate (Q-Tc) showed dose-dependent increases, from 4.7%+/-1.89% at 15 mg/kg to 29.40%+/-6.09% at 100 mg/kg. In comparison with values for controls, all these changes except those associated with 15 mg/kg were statistically significant (P<0.05). Piperazine did not have any effect on the duration of the QRS complex except at 100 mg/kg, the dose at which marked widening occurred in 3 of the 7 rats. Dysrhythmic phenomena, including various forms of atrioventricular (AV) block, sometimes with idioventricular rhythms, were also evident in the 3 rats. Severe bradycardia from sino-atrial depression and AV block was also observed. At this concentration (100 mg/kg), 3 of 7 rats died of complete heart block within 30 minutes of drug administration. It was concluded that piperazine citrate at the suggested antiarrhythmic dose (15 mg/kg intravenously) and even at four times that dose was associated with no ECG abnormality suggestive of cardiotoxicity. However, at 100 mg/kg very serious ECG aberrations can occur, with severe heart block and death.

The Effects of Verapamil Hydrochloride on Electrocardiographic (ECG) Parameters of Domestic Donkey (Equus asinus)

Verapamil hydrochloride, a calcium channel blocker, has been used in domestic animals. Its effects on electrical activities of the heart of donkeys were studied in this preliminary research work. This experiment was carried out on 10 healthy donkeys ranging in age from 4 to 7 years and mean body weight of 155 ± 18.6 kg. The electrocardiogram (ECG) was recorded on a base apex lead before (for 3 days), during, and after verapamil injection (10, 20, 30, 40, 50, and 60 minutes). Verapamil hydrochloride (0.3 mg/kg body weight) was given via catheterizaion as an intravenous bolus over 2 minutes. Heart rate, rhythm, ECG morphology, amplitude, durations, and intervals were measured and taken into consideration and values were compared. Results showed that heart rate was significantly increased at the time of injection from 55 ± 10.7 before injection to 77.61 ± 12.6 beats per minute after injection (P < .05). Duration of P and T waves; P-R interval, and also P-R segment were increased (P < .05). However, duration of QRS complex, P-P and R-R intervals, and S-T segment were significantly decreased after verapamil injection (P < .05). Sinus arrest (2 cases), bradycardia (1 case), and wandering pacemaker (1 case) were recorded before treatment and verapamil injection did not affect these arrhythmias, except in one case in which sinus arrest disappeared. However, after injection of verapamil, four types of arrhythmias (wandering pacemaker [WPM], sinus tachycardia, 1st degree AVB, and 2nd degree AVB) were recognized. These arrhythmias (with the exception of tachycardia) can be related to the increase of vagal tone activity that might be attributed to the negative effect of verapamil on SA and atrioventricular block [AV] nodes.

Vomiting, fever, sinus bradycardia associated with sinoatrial block

第一次查房 心内科主治医师查房,入院半小时. 住院医师 汇报病史.患儿,男,6岁9个月.因呕吐、低热2 d入院.患儿于入院前2 d无明显诱因出现呕吐,时呈喷射性,为胃内容物,较频繁,每日十余次,与进食无关,伴发热,38℃左右.在当地医院考虑胃炎予抗感染、补液等对症治疗,症状无明显好转。

Die Erstbeschreibung des Sinusknotens vor 100 Jahren und die Rolle K. F. Wenckebachs

Hundred years ago, in 1907, A. Keith and M. Flack described histologically in the right atrium of different mammalian including human hearts a structure which they called sinu-auricular node and which they interpreted as the place where the heart beat originates. One year earlier K.F. Wenckebach had reported on an arrhythmia which he explained by polygraphic technique as "vein-atrial block" (today: sinoatrial block). To such an assumption he had to suppose that the heart action begins in the vena cava superior where he described a "small but interesting musculature" above the atrium as the morphological basis of the origin. Recently, with regard to the publication dates of these findings it was claimed (W. Ehrlich) that we should owe the honour of having discovered the sinus node morphologically to Wenckebach and not to Keith and Flack. Referring to the original publications it is shown that Wenckebach as well as Keith and Flack refered to different ideas. Wenckebach supposed the location of the origin of the heart beat in a macroscopically discernible muscle placed at the vena cava superior just above but separated from the right atrium. As the only connection capable of conduction between both he described a special bundle. On the contrary, Keith and Flack depicted as the place where the heart action begins a microscopically defined structur in the atrium at the junction of the vena cava superior with the sorrounding venous and atrial musculature being not separated from each other. Scientific progress corroborated the interpretation of Keith and Flack, while Wenckebach desisted only slowly from his position which, after all, proved incorrect.

Nonlinear oscillator model reproducing various phenomena in the dynamics of the conduction system of the heart

A dedicated nonlinear oscillator model able to reproduce the pulse shape, refractory time, and phase sensitivity of the action potential of a natural pacemaker of the heart is developed. The phase space of the oscillator contains a stable node, a hyperbolic saddle, and an unstable focus. The model reproduces several phenomena well known in cardiology, such as certain properties of the sinus rhythm and heart block. In particular, the model reproduces the decrease of heart rate variability with an increase in sympathetic activity. A sinus pause occurs in the model due to a single, well-timed, external pulse just as it occurs in the heart, for example due to a single supraventricular ectopy. Several ways by which the oscillations cease in the system are obtained (models of the asystole). The model simulates properly the way vagal activity modulates the heart rate and reproduces the vagal paradox. Two such oscillators, coupled unidirectionally and asymmetrically, allow us to reproduce the properties of heart rate variability obtained from patients with different kinds of heart block including sino-atrial blocks of different degree and a complete AV block (third degree). Finally, we demonstrate the possibility of introducing into the model a spatial dimension that creates exciting possibilities of simulating in the future the SA the AV nodes and the atrium including their true anatomical structure.

The short QT syndrome and sudden infant death syndrome

A three-week-old neonate with a shortened QT interval of 210 ms was admitted to the Southwest SIDS Research Institute (Texas, USA) for monitoring because of apnea. A wandering (shifting) pacemaker was present on admission (Figure 1), which was recognized as a frequent antecedent to symptomatic sinus node dysfunction (SND). There was also ST segment elevation and negative U waves (1). Finally, a 2:1 sinoatrial exit block was documented along with a junctional escape beat subsequent to vagotonic sinus arrest (2). With progressive default of the primary pacemaker the escape rhythm, atrioventricular dissociation developed (Figure 2). Asystole ensued following the development of critical SND: irregular sinus bradycardia consequent on episodic sinus inertia and/or third-degree sinoatrial exit block (Figure 3).

Sinoatrial block induced by timolol eyedrops

Sinoatrial block induced by timolol eyedrops

Sinoatrial block induced by timolol eyedrops

Sinoatrial block induced by timolol eyedrops

Intraoperative Transesophageal Ventricular Pacing in Pediatric Patients

Intraoperative Transesophageal Ventricular Pacing in Pediatric Patients

Digoxine-Josamycine : une interaction dangereuse chez l'enfant

Digitalis intoxication is usually accidental in children. We report the case of a young infant with congenital heart disease in whom the coadministration of digoxin and josamycin led to a 50% increase in the digoxin concentration, generating sinoatrial block and cardiac failure. Clinical and electrocardiographic symptoms very quickly resolved following immunotherapy with antidigitalis Fab fragments. Digoxin concentrations must be carefully monitored in patients concomitantly receiving macrolides to ensure that the digoxin dose can be readjusted if necessary.

The cardiovascular complications of intravenous regional anaesthesia.

Abstract In view of the uncertainty over the safety of intravenous regional anaesthesia the heart-rate, blood-pressure, and electrocardiogram were recorded seriany in 100 Bantu gold-miners in whom this form of anaesthesia was used for minor surgical procedures on the extremities. Changes in blood-pressure were infrequent and mild. In 31 patients the heart slowed by more than 10 beats per minute after release of the tourniquet, falling to less than 60 beats per minute in 27. One patient with sinus bradycardia developed sino-atrial block with cardiac standstill of short duration, a second developed an intermittent idioatrial tachycardia and premature atrial beats, and in 3 others sinus bradycardia was complicated by atrial escape beats, nodal rhythm, and premature ventricular beats respectively. These toxic effects were thought to be due either to direct myocardial depression or to increased vagal or decreased sympathetic tone, or to both of these mechanis. It is suggested that the cardiovascular depression caused by large doses of lignocaine may be aggravated by coexisting ischaemic heart disease. The importance of monitoring the patients carefully after release of the tourniquet and having facilities available for resuscitation is stressed.

Sinus arrest during adenosine stress testing in liver transplant recipients with graft failure: Three case reports and a review of the literature

Nuclear stress imaging is used frequently to evaluate patients with end-stage liver disease who are being considered for orthotopic liver transplantation. We present three patients who, following graft failure, developed sinus arrest during adenosine stress testing performed in anticipation of repeat liver transplantation. All had undergone uneventful adenosine stress imaging prior to initial transplantation. The mechanisms of action, pharmacokinetics, and pharmacodynamics of adenosine are reviewed, and possible reasons for this phenomenon are discussed. Finally, cautions regarding the use of adenosine and treatment of adenosine-induced sinoatrial and atrioventricular block are reviewed. Adenosine should be used with caution in patients following orthotopic liver transplantation due to an increased risk of sinus arrest. Should sinus arrest or atrioventricular block occur, it appears to respond readily to cessation of adenosine infusion and intravenous aminophylline with no significant sequelae.

Sinus node dysfunction following targeted disruption of the murine cardiac sodium channel gene Scn5a

We have examined sino-atrial node (SAN) function in hearts from adult mice with heterozygous targeted disruption of the Scn5a gene to clarify the role of Scn5a-encoded cardiac Na+ channels in normal SAN function and the mechanism(s) by which reduced Na+ channel function might cause sinus node dysfunction. Scn5a+/- mice showed depressed heart rates and occasional sino-atrial (SA) block. Their isolated peripheral SAN pacemaker cells showed a reduced Na+ channel expression and slowed intrinsic pacemaker rates. Wild-type (WT) and Scn5a+/- SAN preparations exhibited similar activation patterns but with significantly slower SA conduction and frequent sino-atrial conduction block in Scn5a+/- SAN preparations. Furthermore, isolated WT and Scn5a+/- SAN cells demonstrated differing correlations between cycle length, maximum upstroke velocity and action potential amplitude, and cell size. Small myocytes showed similar, but large myocytes reduced pacemaker rates, implicating the larger peripheral SAN cells in the reduced pacemaker rate that was observed in Scn5a+/- myocytes. These findings were successfully reproduced in a model that implicated i(Na) directly in action potential propagation through the SAN and from SAN to atria, and in modifying heart rate through a coupling of SAN and atrial cells. Functional alterations in the SAN following heterozygous-targeted disruption of Scn5a thus closely resemble those observed in clinical sinus node dysfunction. The findings accordingly provide a basis for understanding of the role of cardiac-type Na+ channels in normal SAN function and the pathophysiology of sinus node dysfunction and suggest new potential targets for its clinical management.

Mental retardation, keratoconus, febrile seizures and sinoatrial block: a previously undescribed autosomal recessive disorder

Clinical GeneticsVolume 67, Issue 5 p. 448-449 Mental retardation, keratoconus, febrile seizures and sinoatrial block: a previously undescribed autosomal recessive disorder D Kirby, D KirbySearch for more papers by this authorAP Jackson, AP JacksonSearch for more papers by this authorG Karbani, G KarbaniSearch for more papers by this authorYJ Crow, Corresponding Author YJ Crow Dr Y.J. Crow Department of Clinical Genetics St James's University Hospital Leeds LS9 7TF UK Tel.: +44 113 2066658 Fax: +44 113 2467090 e-mail: yanick.crow@leedsth.nhs.ukSearch for more papers by this author D Kirby, D KirbySearch for more papers by this authorAP Jackson, AP JacksonSearch for more papers by this authorG Karbani, G KarbaniSearch for more papers by this authorYJ Crow, Corresponding Author YJ Crow Dr Y.J. Crow Department of Clinical Genetics St James's University Hospital Leeds LS9 7TF UK Tel.: +44 113 2066658 Fax: +44 113 2467090 e-mail: yanick.crow@leedsth.nhs.ukSearch for more papers by this author First published: 22 February 2005 https://doi.org/10.1111/j.1399-0004.2005.00429.xCitations: 5Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume67, Issue5May 2005Pages 448-449 RelatedInformation

An analysis of abnormal distribution and trend of ECG derived from medical examination

目的 分析比较我市行政事业单位人员体格检查中异常心电图的分布与变化趋势,为心血管病流行病学的研究提供依据.方法回顾近年3次体检共11714例次心电图资料,从异常心电图的分布情况,年龄、性别及3次结果分类统计,予以横向及纵向的比较.结果(1)各项指标在异常心电图中所占比例依次为窦性心律失常41%,ST-T异常24%、其他心律失常13%、室内阻滞10%、R波高电压7%、房室或窦房阻滞等.(2)各项指标除窦性心律失常外,均随年龄增加而递长.(3)各项指标异常率除ST-T异常外,男女比较均为男性＞女性.(4)各项指标在3次体检对比中无变化.结论心血管病的患病率随年龄的增加而增高,同时男性患病的危险性高于女性。

Prevention of primary ventricular fibrillation in acute myocardial infarction with prophylactic lidocaine

Primary ventricular fibrillation (VF) during an acute myocardial infarction (AMI) occurs with a high incidence and mortality rate with or without thrombolysis. The incidence varies from 2% to 19% depending on the definition of "primary." Primary VF in this study refers to fibrillation occurring in the absence of shock or pulmonary edema. Mortality rate, when primary VF occurs, is 2 to 4 times greater than when it does not. Prevention of VF has been impeded by the publication of the 1996 recommendations of the American Heart Association and American College of Cardiology against the use of prophylactic lidocaine based on meta-analysis studies implying toxicity. This observational study of 4,254 patients with AMI reports the incidence and mortality rates of primary VF over 32 years. Of the 4,254 patients, 4,150 received prophylactic lidocaine, and 104 patients did not receive prophylactic lidocaine due to the 1996 guidelines, after which administration of prophylactic lidocaine was governed by physician choice. The incidence of primary VF was 0.5% among the 4,150 who received prophylactic lidocaine and 10% among the 104 who did not (p <0.0001). Among the 4,150 receiving prophylactic lidocaine, sinoatrial block occurred in 0.5% and complete infranodal atrial ventricular block occurred in 0.2%, all secondary to the site of infarction (concurrent serum lidocaine levels were < 4 microg/ml). Asystole was an agonal rhythm in 4%; these patients had been off lidocaine for 48 hours. Mortality rates were 10.5% in patients without primary VF and 25% in patients with VF (p <0.001). Thus, prophylactic lidocaine markedly decreased the incidence of VF in 4,150 patients with AMI to 0.5% compared with trials before and after thrombolysis (2% to 19%) and with the 104 patients in this study who did not receive prophylactic lidocaine (10%). No lidocaine-induced sinoatrial or atrial ventricular block or asystole occurred.

Clinical characteristics of hypervagotonic sinus node dysfunction.

BackgroundSinus node dysfunction (SND) is caused not only by intrinsic sinus node disease, but also by the extrinsic factors. Among the extrinsic factors, autonomic imbalance is most common. Symptomatic SND usually requires permanent pacemaker therapy. However, the clinical characteristics and patient response to medical therapy for hypervagotonic SND have not been properly clarified.Materials and MethodsThirty two patients (14 men, 18 women, 51 ± 14 years) with hypervagotonic SND were included in this study, but those patients who had taken calcium antagonists, beta-blockers or other antiarrhythmic drugs were excluded. Hypervagotonic SND was diagnosed if the abnormal electrophysiologic properties of the sinus node were normalized after the administration of atropine (0.04 mg/kg).ResultsThe presenting arrhythmias were 16 cases of sinus bradycardia (50.0%), 12 of sinus pause (37.5%), 3 of sinoatrial block (9.4%) and 1 of tachy-bradycardia (3.1%). Nine (28.1%) patients had hypertension, 7 (21.9%) smoked, 2 (6.3%) had diabetes mellitus, and 1 (3.1%) had hypercholesterolemia. Among the patients, 3 had no remarkable symptoms, 13 had dizziness, 7 had syncope, 3 had weakness and 6 had shortness of breath. Twenty five (78.1%) patients were treated with theophylline, 1 patient with tachy-bradycardia syndrome was treated with digoxin and propafenone, and 6 (18.8%) were treated with no medication. During the 43±28 month follow-up, 25 patients remained asymptomatic, but 6 who took no medication developed mild dizziness. One patient needed permanent pacemaker implantation owing to recurrent syncope despite of theophylline treatment.ConclusionThese results show that hypervagotonic SND has a benign course and most of the patients can be managed safely without implanting a pacemaker. (Ed note: I like the abstract. It is short and direct, as it should be.)

Electrocardiographic changes and cardiac pathology in canine babesiosis

The main purpose of this study was to describe electrocardiographic (ECG) changes in canine babesiosis, and to relate these to clinical severity, outcome and cardiac pathology. Four groups of dogs with babesiosis were studied: mild to moderate anemia, severe anemia, concurrent autoagglutination and concurrent complications. Lead II ECG was recorded at admission for 1 minute in all dogs (121). A six lead ECG was recorded in 88 dogs. Full necropsy was performed on 16 dogs (5 died on arrival, 11 had ECG recording). The following ECG changes were recorded in relatively high prevalence: sinoatrial blocks or sinus arrest (7%), ventricular premature complexes (7%), low R-amplitude (23%), prominent Q (13%), axis deviations (40%), prolonged QRS (32%), ST depression and coving (28%), large T (42%), and notched R (28%). Differences between groups were minor. There was a significantly higher prevalence of sinus bradycardia and irregular rhythm in the non-survivors. Gross pathological changes were pericardial effusion and hemorrhages. Histological changes were hemorrhages, necrosis, inflammation and fibrin microthrombi. The only correlation between pathology and ECG was low R-amplitude and pericardial effusion. The ECG changes were similar to the pattern described for myocarditis and myocardial ischemia, and together with the histopathological findings indicated that the heart suffers from the same pathological processes described in other organs in canine babesiosis, namely inflammation and hypoxia. As the clinical application of the ECG changes found in this study was limited, cardiovascular assessment should be based on functional monitoring rather than ECG.