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Bradyarrhythmias and cardiac pacemakers in the elderly
Published in Wilbert S. Aronow, Jerome L. Fleg, Michael W. Rich, Tresch and Aronow’s Cardiovascular Disease in the Elderly, 2019
Naktal Hamoud, Fernando Tondato, Win-Kuang Shen
Although pacing is the mainstay of treatment for symptomatic SND, identifying and treating transient or reversible causes for SND comprise the first step in management. Vagally mediated SND may respond to atropine in the acute setting, but it needs to be treated only if the patient is symptomatic. Pharmacological therapy (atropine, isoproterenol) is effective only as a short-term emergency measure. Temporary percutaneous or transvenous pacing is necessary in patients with hemodynamically significant SND and bradycardia, to provide immediate stabilization prior to permanent pacemaker placement or to provide support when the bradycardia is precipitated by what is presumed to be a transient event, such as drug toxicity.
Electricity and Magnetism
Published in Sarah Armstrong, Barry Clifton, Lionel Davis, Primary FRCA in a Box, 2019
Sarah Armstrong, Barry Clifton, Lionel Davis
Transvenous pacing is achieved via a central vein under x-ray control and may be indicated after MI. The pulse duration is less than 1 ms, and the potential difference required is usually less than 4 V. There is a risk of microshock. Transvenous pacing should be considered preoperatively for bradyarrhythmiasthird-degree heart blocksecond-degree heart block if it is Mobitz II or if there are associated symptoms or extensive surgerybundle branch block if it is bifascicular or has a prolonged PR interval
Bradyarrhythmias
Published in Ian Mann, Christopher Critoph, Caroline Coats, Peter Collins, The Junior Doctor’s Guide to Cardiology, 2017
Ian Mann, Christopher Critoph, Caroline Coats, Peter Collins
Temporary pacing can be achieved either transcutaneously or by inserting a pacing wire through a transvenous sheath in a large vein (usually the femoral, jugular or subclavian vein). Transvenous pacing used to be carried out by general medical registrars, but current guidelines recommend insertion only by cardiologists or other appropriately trained specialists, due to the high rate of complications.
Loperamide toxicity: recommendations for patient monitoring and management
Published in Clinical Toxicology, 2020
William Eggleston, Robert Palmer, Pierre-André Dubé, Stephen Thornton, Andrew Stolbach, Diane P Calello, Jeanna M Marraffa
Loperamide is a nonprescription antidiarrheal that is safe when taken in therapeutic doses; but when taken in large quantities or combined with medications that alter its pharmacokinetics, it exerts opioid effects in the central nervous system. These include, euphoria, central nervous system depression, miosis, and respiratory depression. Patients with respiratory depression may be treated with naloxone. A continuous infusion of naloxone may be used for patients with recurrent respiratory depression. When taken in large doses, loperamide also causes cardiac toxicity, manifesting primarily as conduction disturbances and dysrhythmias. Conduction abnormalities include, but are not limited to, QT prolongation, QRS prolongation, polymorphic ventricular tachycardia, Torsades de Pointes (TdP), and Brugada pattern. Management includes close cardiac monitoring and standard Advanced Cardiac Life Support (ACLS) measures for life-threatening dysrhythmias. For patients with recurrent dysrhythmias, additional treatments such as transvenous pacing or amiodarone can be considered. Providers should include loperamide toxicity in their differential diagnosis for patients with a history of opioid use disorder with a new cardiac conduction disturbance. While individual practitioners may differ in their management of patients with loperamide toxicity, these are the positions and recommendations developed by the AACT and AAPCC, and endorsed by ACMT, after review of the issue and scientific literature, and are current at the time of this writing.
Cardiac arrhythmias, electrolyte abnormalities and serum cardiac glycoside concentrations in yellow oleander (Cascabela thevetia) poisoning – a prospective study
Published in Clinical Toxicology, 2019
Anandhi D., Vinay R. Pandit, Tamilarasu Kadhiravan, Soundaravally R., K. N. J. Prakash Raju
Our ED management included continuous hemodynamic assessment, cardiac monitoring, GI decontamination, correction of electrolyte abnormalities, administering atropine for severe bradycardia and temporary cardiac pacing for significant bradyarrhythmias. Hyperkalemia was treated with insulin-dextrose infusion. Digoxin specific Fab antibody fragments are not available in our hospital. The median duration of hospital stay was found to be 3 (IQR: 2–4) days. This was comparable to the study by Eddleston et al. in which he reported that each patient occupied a bed for 3–5 days [15]. Bose et al. observed a median hospital stay of five days [12]. In the present study, temporary transvenous pacing was done in 20% patients. Pirasath et al. reported that 3% required pacing and 3% expired [5]. Eddleston et al. reported that 40% of patients required specialized management [10]. Mortality rate was 5% in the present study. Bose et al. (1999) observed a case fatality rate of 4.6% among 300 patients in Eastern India [12]. A large Sri Lankan randomized controlled trial with 1647 oleander poisoning patients reported case fatality rate of 5% [13]. While other Sri Lankan studies reported mortality rate of 10% [15,19].
Takotsubo cardiomyopathy in the setting of complete heart block
Published in Baylor University Medical Center Proceedings, 2018
Aasim Afzal, John Watson, James W. Choi, Jeffrey M. Schussler, Manish D. Assar
A transvenous pacing wire was placed via the right femoral vein, and the patient returned to the intensive care unit. She remained 100% paced over the ensuing 48 hours and underwent placement of a biventricular permanent pacemaker via the left axillary vein on the third day of presentation (Figure 3). The patient was discharged the following day on angiotensin-converting enzyme inhibitor and beta-blocker therapy along with a LifeVest and instructions for a follow-up echocardiogram. During follow-up approximately 15 days after presentation, echocardiography showed an ejection fraction of 50%. Pacemaker interrogation revealed pacing >99%. Use of the wearable defibrillator was discontinued at this time. Subsequent 6-month follow-up showed 100% pacemaker dependence and an echocardiogram with an ejection fraction of 55%.