scholarly journals Torsades de pointes in the PACU after outpatient endoscopy: a case report

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Andrew Schaar ◽  
Mark Liu ◽  
Michael Patzkowski
Keyword(s):  
Ventricular Fibrillation ◽  
Long Qt Syndrome ◽  
Torsades De Pointes ◽  
Long Qt ◽  
Rare Presentation ◽  
Case Presentation ◽  
Outpatient Procedure ◽  
Qt Syndrome ◽  
Lower Endoscopy ◽  
Insight Into

Abstract Background This case demonstrates the severe electrolyte derangements that may present after a common therapy such as a bowel preparation for an outpatient procedure and the rare yet potential detrimental outcomes of those abnormalities. It also highlights the implications of long QT syndrome regarding pharmacology and treatment. Case presentation We present a case of 48 year-old female with severe electrolyte derangements and long QT syndrome (LQTS) leading to Torsades de Pointes (TdP), pulseless ventricular fibrillation, and unsynchronized defibrillation in the post anesthesia care unit (PACU) after uneventful upper and lower endoscopy. This led to an unanticipated intensive care unit admission for aggressive electrolyte repletion, cardiology consultation, and implantable cardioverter defibrillator (ICD) placement. Conclusions This is a rare presentation after an outpatient procedure that would have had a detrimental outcome if not promptly diagnosed and treated appropriately. Therefore, we aim to provide further insight into the diagnosis and treatment of severe hypokalemia and long QT syndrome resulting in Torsades de Pointes and ventricular fibrillation.

scholarly journals Vomiting, electrolyte disturbance, and medications; the perfect storm for acquired long QT syndrome and cardiac arrest: a case report

2022 ◽  
Vol 16 (1) ◽  
Author(s):  
K. D. Tiver ◽  
D. Dharmaprani ◽  
J. X. Quah ◽  
A. Lahiri ◽  
K. E. Waddell-Smith ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Long Qt Syndrome ◽  
Torsades De Pointes ◽  
Long Qt ◽  
Case Presentation ◽  
Electrolyte Disturbance ◽  
Electrolyte Disturbances ◽  
Acquired Long Qt Syndrome ◽  
Qt Syndrome ◽  
Proper Consideration

Abstract Background Acquired long QT syndrome is an important and preventable cause of cardiac arrest. Certain medications and electrolyte disturbance are common contributors, and often coexist. In this case, we report five contributors to cardiac arrest. Case presentation This case is of a 51-year-old Caucasian female patient who presented with vomiting associated with hypokalemia and hypomagnesemia. She subsequently received ondansetron and metoclopramide, on the background of chronic treatment with fluoxetine. She then suffered an in-hospital monitored cardiac arrest, with features of long QT and torsades de pointes retrospectively noted on her prearrest electrocardiogram. She was diagnosed with acquired long QT syndrome, and her QT interval later normalized after removal of offending causes. Conclusions This case highlights the importance of proper consideration prior to prescribing QT prolonging medications, especially in patients who have other risk factors for prolonged QT, such as electrolyte disturbances and pretreatment with QT prolonging medications.

A rare indication of permanent pacemaker implantation in children: congenital long QT syndrome

2020 ◽  
Vol 30 (12) ◽  
pp. 1880-1881
Author(s):  
Mehmet Taşar ◽  
Nur Dikmen Yaman ◽  
Huseyin Dursin ◽  
Murat Şimşek ◽  
Senem Özgür
Keyword(s):  
Sudden Death ◽  
Long Qt Syndrome ◽  
Pacemaker Implantation ◽  
Torsades De Pointes ◽  
Permanent Pacemaker ◽  
Long Qt ◽  
Permanent Pacemaker Implantation ◽  
Qt Syndrome ◽  
Congenital Lqts ◽  
Congenital Long Qt Syndrome

AbstractCongenital Long QT Syndrome (LQTS) is a dangerous arrhythmic disorder that can be diagnosed in children with bradycardia. It is characterised by a prolonged QT interval and torsades de pointes that may cause sudden death. Long QT syndrome is an ion channelopathy with complex molecular and physiological infrastructure. Unlike the acquired type, congenital LQTS has a genetic inheritance and it may be diagnosed by syncope, stress in activity, cardiac dysfunction, sudden death or sometimes incidentally. Permanent pacemaker implantation is required for LQTS with resistant bradycardia even in children to resolve symptoms and avoid sudden death.

scholarly journals Peripartum Cardiomyopathy Presenting with Syncope due to Torsades de Pointes: a Case of Long QT Syndrome with a Novel KCNH2 Mutation

2012 ◽  
Vol 51 (5) ◽  
pp. 461-464 ◽  
Author(s):  
Orie Nishimoto ◽  
Morihiro Matsuda ◽  
Kei Nakamoto ◽  
Hirohiko Nishiyama ◽  
Kazuya Kuraoka ◽  
...  
Keyword(s):  
Long Qt Syndrome ◽  
Torsades De Pointes ◽  
Peripartum Cardiomyopathy ◽  
Long Qt ◽  
Qt Syndrome

scholarly journals Dobutamine Infusion for Unmasking Long QT Syndrome and Torsades de Pointes

2009 ◽  
Vol 32 (6) ◽  
pp. E78-E81 ◽  
Author(s):  
Fang Quan ◽  
Gao Peng ◽  
Cheng Kangan ◽  
Hu Dayi ◽  
Li Cuilan ◽  
...  
Keyword(s):  
Long Qt Syndrome ◽  
Torsades De Pointes ◽  
Dobutamine Infusion ◽  
Long Qt ◽  
Qt Syndrome

scholarly journals Prolonged QTc: "Mind the Gap"

2014 ◽  
Vol 2 (1) ◽  
pp. 44-45
Author(s):  
Ahmad Mursel Anam ◽  
Raihan Rabbani ◽  
Farzana Shumy ◽  
M Mufizul Islam Polash ◽  
M Motiul Islam ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Long Qt Syndrome ◽  
Qt Interval ◽  
Torsades De Pointes ◽  
Junior Doctors ◽  
Long Qt ◽  
Acquired Long Qt Syndrome ◽  
Prolonged Qt Interval ◽  
Prolonged Qt ◽  
Qt Syndrome

We report a case of drug induced torsades de pointes, following acquired long QT syndrome. The patient got admitted for shock with acute abdomen. The initial prolonged QT-interval was missed, and a torsadogenic drug was introduced post-operatively. Patient developed torsades de pointes followed by cardiac arrest. She was managed well and discharged without complications. The clinical manifestations of long QT syndromes, syncope or cardiac arrest, result from torsades de pointes. As syncope or cardiac arrest have more common differential diagnoses, even the symptomatic long QT syndrome are commonly missed or misdiagnosed. In acquired long QT syndrome with no prior suggestive feature, it is not impossible to miss the prolonged QT-interval on the ECG tracing. We share our experience so that the clinicians, especially the junior doctors, will be more alert on checking the QT-interval even in asymptomatic patients. DOI: http://dx.doi.org/10.3329/bccj.v2i1.19970 Bangladesh Crit Care J March 2014; 2 (1): 44-45

Pauses after burst pacing provoke afterdepolarizations and torsades de pointes in a patient with long QT syndrome

Heart Rhythm ◽  
2004 ◽  
Vol 1 (6) ◽  
pp. 720-723 ◽  
Author(s):  
Paulus Kirchhof ◽  
Stephan Zellerhoff ◽  
Gerold Mönnig ◽  
Eric Schulze-Bahr
Keyword(s):  
Long Qt Syndrome ◽  
Torsades De Pointes ◽  
Long Qt ◽  
Qt Syndrome

A Candidate Locus Approach Identifies a Long QT Syndrome Gene Mutation

2003 ◽  
Vol 5 (2) ◽  
pp. 97-104 ◽  
Author(s):  
Theresa A. Beery ◽  
Macaira Dyment ◽  
Kerry Shooner ◽  
Timothy K. Knilans ◽  
D. Woodrow Benson
Keyword(s):  
Potassium Channel ◽  
Long Qt Syndrome ◽  
Family Members ◽  
Torsades De Pointes ◽  
Sudden Onset ◽  
Coding Region ◽  
Long Qt ◽  
Candidate Locus ◽  
Qt Intervals ◽  
Qt Syndrome

Long QT syndrome is an inherited disorder that results in lengthened cardiac repolarization. It can lead to sudden onset of torsades de pointes, ventricular fibrillation, and death. The authors obtained a family history, performed electrocardiograms, and drew blood for DNA extraction and genotyping from 15 family members representing 4 generations of an affected family. Seven individuals demonstrated prolonged QT intervals. The authors used polymorphic short tandem repeat markers at known LQTS loci, which indicated linkage to chromosome 11p15.5 where the potassium channel, KCNQ1, is encoded. Polymerase chain reaction was used to amplify the coding region of KCNQ1. During survey of the KCNQ1 coding region, a G-to-A transition (G502A) was identified. DNA from all clinically affected but from none of the clinically unaffected family members carried the G-to-A transition. The candidate locus approach allowed an efficient mechanism to uncover the potassium channel mutation causing LQTS in this family.

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