[Amitriptyline poisoning with severe cardiac arrhythmia. Cardiac arrhythmia treated with propranolol].
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Cardiac arrhythmias can present as benign ectopics or as life-threatening arrhythmias and sudden cardiac death. Clinical cardiac electrophysiology is the study of the electrophysiology of the heart and all aspects of management of cardiac arrhythmias. The invasive electrophysiological study was initially purely diagnostic, but recent advances in technology has allowed us to intervene and hence the term interventional electrophysiology. The interventional therapies include permanent pacing for bradyarrhythmias, arrhythmia surgery for arrhythmias, percutaneous catheter ablation and implantable devices for tachyarrhythmias. The treatment of bradyarrhythmias with permanent pacemaker implantation represents the first interventional therapy for patients with cardiac arrhythmias. From 1973 to June 1996, a total of 791 pacemakers have been implanted at the Singapore General Hospital. Previously, patients with tachyarrhythmias could only be cured by open heart surgery utilising intraoperative map guided surgery and ablation of the arrhythmia. Only 17 patients with supraventricular tachycardia (SVT) and 3 patients with VT have undergone this procedure. Catheter ablation has completely revolutionised the treatment of these patients. From October 1991 until December 1996, 860 patients have undergone radiofrequency (RF) catheter ablation for SVT and non-ischaemic VT. Ninety-eight per cent of the patients with SVT have been successfully ablated and 94% of the patients with VT were successfully ablated. RF ablation has become the technique of choice to cure patients with recurrent paroxysmal SVT due to AV re-entrant tachycardia using an accessory pathway, AV nodal re-entrant tachycardia, atrial tachycardia and atrial flutter. It is also used for AV nodal ablation followed by pacemaker insertion or AV nodal modification in patients with poorly controlled atrial fibrillation. Patients with idiopathic non-ischaemic VT arising from the left ventricle or right ventricular outflow tract can similarly be cured. For all these patients, RF ablation offers curative therapy, thus eliminating recurrent symptoms, life-threatening attacks, tachycardia cardiomyopathy and need for life-long drug therapy. For patients with resuscitated sudden cardiac death or at high risk for sudden death, the implantable cardioverter defibrillator (ICD) is the only technique that has significantly improved survival from sudden cardiac death. Since August 1992, 11 patients have had the ICD implanted, with 9 surviving. The 2 deaths were due to cardiac failure and not to sudden death. Thus the ICD can prevent sudden death, but the main limitation is the cost of the device and it is not suitable in patients who have severe heart failure. In conclusion, interventional electrophysiology represents a tremendous leap forward in the management of cardiac arrhythmias. With catheter ablation, it offers a safe curative therapy for patients with recurrent SVTs and VTs and with the ICD, prevents sudden cardiac death in patients who have been resuscitated from it or who are at risk for it. The future will see us improving our success in ablating patients with monomorphic ischaemic VT and even atrial fibrillation, and the role of prophylactic ICDs in high risk patients will be better defined.
Cardiac arrhythmia as an adverse effect of noncardiac drugs has been an issue of growing importance during the past few years. In this population-based study, we evaluated the risk for serious cardiac arrhythmias during the use of several noncardiac QTc-prolonging drugs in day-to-day practice, and subsequently focused on several specific groups of patients who could be extremely vulnerable for drug-induced arrhythmias. We performed a case-control study in which patients (cases), hospitalized for nonatrial cardiac arrhythmias from 1987 to 1998, were compared with their matched controls regarding current use of QTc-prolonging drugs. Odds ratios (OR) and 95% confidence intervals (CI) were calculated using multivariate conditional logistic regression, adjusting for potential confounding factors. Data were obtained from the PHARMO record linkage system. We identified 501 cases, 39 of whom used QTc-prolonging drugs. A statistically nonsignificant increased risk for arrhythmias (OR 1.2, 95% CI 0.8 to 1.9) was observed in patients who received QTc-prolonging drugs. A clearly increased risk of arrhythmias was, however, found in patients with a history of asthma (OR 9.9, 95% CI 1.0 to 100) and in patients using potassium-lowering drugs (OR 5.3, 95% CI 1.1 to. 25.9). Our data do not suggest that there is a strong overall association between the use of QTc-prolonging drugs and hospitalization for cardiac arrhythmias in the population at large. However, there appears to be clinically relevant associations of patients with a history of asthma and patients taking potassium-lowering drugs. The use of QTc-prolonging drugs should therefore be either avoided or monitored closely in these specific patients.
Cardiac arrhythmias are probably more common in horses than in any other domestic animal species. The most frequent clinical complaint associated with cardiac arrhythmias is exercise intolerance. Physical examination is characterized by auscultation abnormalities such as fast or slow heart rate, irregular rhythm, extra sounds, long pauses, or abnormal heart sounds. The electrocardiogram is used to make a definitive diagnosis of the dysrhythmia. Other laboratory and cardiac function tests are employed to determine the etiology and to assess the significance of the arrhythmia. Antiarrhythmic therapy is given when clinical signs specifically related to the arrhythmia are present, when hemodynamic parameters are compromised by the arrhythmia, or when the ECG reveals abnormalities that put the patient at risk for development of more severe arrhythmias. The cardiovascular drugs most frequently used are digoxin and quinidine. Digoxin is most commonly used for supraventricular arrhythmias, especially arrhythmias characterized by fast heart rates. Quinidine is very effective for short-term treatment of ventricular and supraventricular arrhythmias but must be used with caution because of the potential for toxic side effects. The cardiac arrhythmias due to vagal tone (sinus arrhythmia, sinus block, sinus arrest, sinus bradycardia, wandering pacemaker, first-degree AV block, and second-degree AV block) that are found in resting horses are generally considered to be normal and generally do not require therapy.
Cardiac arrhythmias remain a major source of morbidity, mortality, and prolonged postoperative hospital stay in surgical patients. Recent studies in patients experiencing out-of-hospital cardiac arrest have expanded our knowledge in the management of cardiac arrhythmias. Future advances require additional studies focused on the unique proarrhythmic substrates in surgical patients, to provide a clear rationale for antiarrhythmic drug therapy in the perioperative period.
Cardiac arrhythmias, characterized by single or multiple reentrant circuits, represent a dynamic phenomenon in an excitable medium. In this review, we provide a brief overview of how cardiac action potential duration restitution, conduction velocity restitution, and intracellular calcium cycling regulate the dynamics of action potential excitation and wave propagation in relation to the genesis and maintenance of cardiac arrhythmias.
Cardiac arrhythmias may present in a variety of ways in the primary care setting. They may or may not be accompanied by related symptoms. Rhythm disturbances span the continuum of posing no risk to the patient to being life-threatening. The importance of a thorough history and physical examination to detect the presence of cardiovascular disease or related factors cannot be overemphasized. An ECG is essential for the accurate identification of cardiac arrhythmias. Evaluation and management of cardiac rhythm disturbances often requires collaboration with medical practitioners and possible specialist referral. The primary care nurse practitioner must be able to recognize the important red flags in clinical practice such as cardiac syncope, ischemia, or failure. Finally, an understanding of the diagnostic and therapeutic measures used for arrhythmia evaluation and management will facilitate appropriate patient education, counseling, and follow-up.
Cardiac arrhythmias are common in children, but most of them are benign and do not signify underlying heart disease. However, the main tachyarrhythmias (SVT and VT) can cause cardiovascular collapse, and should therefore be treated promptly. Drug treatment is generally effective and is appropriate in stable patients. DC shock is the treatment of choice in patients with compromised circulation. There is a wide array of antiarrhythmic drugs and though they are generally safe, most of them have the potential for serious adverse effects. Hence, there is a need to exercise caution and balanced judgement in prescribing them. It is perhaps best for the general duty paediatric staff to be familiar with a select few, and stick to them if possible. Management of most cases of cardiac arrhythmia in children is within the competence of non-cardiologist paediatric staff. But in some instances cardiology referral will be required, either for further investigations, for decision regarding longterm drug therapy, or for more technical management modalities.
Cardiac arrhythmias were studied in twenty ASA class 1 patients under general anesthesia using halothane or isoflurane to supplement nitrous oxide in oxygen. The study began during the maintenance period, once the expiratory MAC value had reached a stable level of 1, and stopped one hour later. Both intubation and recovery periods were excluded. The end-tidal gas concentration was measured for carbon monoxide and vapours. The ECG was recorded on a magnetic tape. The incidence of arrhythmias was higher in the halothane group when compared to the isoflurane group (p less than 0.05). The main types of arrhythmias observed were supraventricular and ventricular ectopic beats. None of the arrhythmias observed were serious; in particular the ventricular beats were all unifocal and occasional. Heart rate measured at 10 min intervals tended to be more rapid in the isoflurane group.
Cardiac arrhythmias complicate many diseases affecting the heart and the circulation, and incorporate a multiplicity of underlying mechanisms. The evolution of scientific knowledge has made the complex changes produced by cardiovascular disease sufficiently understood at the organ, cellular, and molecular levels such that there is a diversity of therapeutic targets for pharmacological therapy and/or prevention. Moreover, the approach of rational drug design, in mechanism- and disease-specific fashion, facilitates targeting of therapy via molecular, structural and translational biology. Additional approaches, employing similar drug-design strategies but based on gene therapy and transcriptional and translational modification are on the horizon. Hence, there is reason to be optimistic regarding the design, testing and clinical availability of novel antiarrhythmic therapies.
Cardiac arrhythmias complicate many diseases affecting the heart and circulation, and they incorporate a multiplicity of underlying mechanisms. The evolution of scientific knowledge has made the complex changes produced by cardiovascular disease sufficiently understood at the organ, cellular, and molecular levels such that there is a diversity of therapeutic targets for pharmacological therapy and/or prevention. Moreover, the approach of rational drug design in mechanism-specific and disease-specific fashions facilitates the targeting of therapy using the methods of molecular, structural, and translational biology. Additional approaches, using similar drug design strategies but based on gene therapy and transcriptional and translational modification, are on the horizon. Hence, there is reason to be optimistic regarding the design, testing, and clinical availability of novel antiarrhythmic therapies.
Cardiac arrhythmias complicate many diseases affecting the heart and circulation, and they incorporate a multiplicity of underlying mechanisms. The evolution of scientific knowledge has made the complex changes produced by cardiovascular disease sufficiently understood at the organ, cellular, and molecular levels such that there is a diversity of therapeutic targets for pharmacological therapy and/or prevention. Moreover, the approach of rational drug design in mechanism-specific and disease-specific fashions facilitates the targeting of therapy using the methods of molecular, structural, and translational biology. Additional approaches, using similar drug design strategies but based on gene therapy and transcriptional and translational modification, are on the horizon. Hence, there is reason to be optimistic regarding the design, testing, and clinical availability of novel antiarrhythmic therapies.
Cardiac arrhythmias in the adolescent and young adult population are being seen with increasing frequency by cardiovascular nurses who predominantly care for adults. These patients include those with anatomically normal hearts and those with postoperative congenital heart disease. The treatment options available to these patients vary according to the rhythm abnormality being treated. In order to provide expert care to these patients and their families, the cardiovascular nurse must be aware of these specific rhythm abnormalities, their associated treatment options, and the nursing implications of caring for this often vulnerable patient population.
Cardiac arrhythmias are a cause of significant morbidity and mortality in patients with cardiac disease, and thus represent a major management problem. The recognition that antiarrhythmic drugs have the potential to aggravate as well as to attenuate arrhythmias has prompted clinicians to reconsider treatment strategies and weight the benefits of treatment against the risks. In this context, amiodarone has emerged as an effective antiarrhythmic agent and when used at the lowest effective dose has an acceptable side effect profile. This review focuses on the current clinical usage of amiodarone in a broad variety of cardiac arrhythmias, and addresses the risk-benefits arising from its use. It further discusses the current position of amiodarone in the management of sudden cardiac death.
Cardiac arrhythmias are caused by alterations in the electrophysiologic properties of the cardiac cells, which affect the characteristics of the transmembrane potentials. The electrophysiologic properties that cause arrhythmias are automaticity, triggered activity, and reentrant excitation. Each of these mechanisms is described in terms of the characteristics of the transmembrane potentials and how these influence the appearance of the arrhythmia on the electrocardiogram.
Cardiac arrhythmias result from abnormalities in the initiation of impulses or in the conduction of these impulses through the heart. Arrhythmias caused by impulse initiation may be caused by either automaticity or triggered activity. Arrhythmias caused by abnormalities in conduction are often the result of reentrant excitation. These arrhythmogenic mechanism arise because of alterations in the transmembrane potentials of cardiac cells that are often caused by disease. These cellular mechanisms causing arrhythmias are the subject of this article.
Cardiac arrhythmias are ambiguous symptoms. Intracardiac as well as extracardiac alterations may be responsible. There is little direct information from the ECG concerning their pathophysiological mechanism. Bradycardic as well as tachycardic arrhythmias can be the result of two different fundamental disturbances: alterations of impulse formation (automaticity) or alterations of impulse conduction. Either one of these, or both of them acting together, may be responsible for the arrhythmia. Tachycardias due to disturbances of impulse formation may be brought about by enhanced firing of regular pacemakers (sino-atrial node, av-node, ventricular conduction system), by abnormal automaticity occurring in ordinary atrial or ventricular myocardium, or by triggered activity due to early or delayed afterdepolarizations. Bradycardic disturbances of impulse formation are primarily concerned with sino-atrial nodal function. Bradycardic conduction disturbances mainly impair sinoatrial or atrioventricular propagation causing partial or total conduction block. Tachyarrhythmias due to disturbances of conduction are generated by re-entry of excitatory waves either along anatomically preformed pathways or around functional obstacles (refractory zones) with excitable gaps being more or less pronounced. On the cellular level, altered activities of ionic channels or transport systems play a significant part. Such changes are caused by: alterations of electrolyte composition (potassium, sodium, calcium), acidosis or alkalosis, autonomic and hormonal influences, membrane active metabolites (long-chain acylcarnitine, lysophosphatidylcholine), drugs (class I and III antiarrhythmics, cardiac glycosides) and poisons. In disturbances of conduction other aspects like geometry of pathways or cable properties (anisotropic conduction, coupling resistances between cells) are of particular significance.(ABSTRACT TRUNCATED AT 250 WORDS)
A retrospective analysis was performed of 405 patients, over the age of 65 years, who had been admitted with proven myocardial infarction to a coronary care unit, to investigate the relationship between the serum potassium level on admission and the incidence of cardiac arrhythmias. On admission, 173 (42.7%) patients had a serum potassium of less than 4.0 mmol/l. During the first 24 hours in hospital, 57% of all patients exhibited a disturbance of cardiac rhythm. The incidence of total arrhythmias was independent of the initial serum potassium level, but the mortality rate was 46.2% in those patients with a serum potassium less than 4.0 mmol/l while it was 34.5% in those with a potassium of 4.0 mmol/l or greater. Twelve patients with a serum potassium less than 4.0 mmol/l experienced at least one episode of ventricular fibrillation (6.9%), but only 1 patient with a serum potassium of 4.0 mmol/l or greater had this arrhythmia. The difference in incidence of this arrhythmia was highly significant (p less than 0.001). No patient who experienced ventricular fibrillation was on existing cardiac medication with either a diuretic, beta-adrenoreceptor blocking drug or digoxin. There was no significant difference in the occurrence of other cardiac arrhythmias between low and normal serum potassium groups.