Bedside monitoring of the QT interval

1998 ◽  
Vol 7 (3) ◽  
pp. 183-189 ◽  
Author(s):  
LK Rimmer

Cardiac repolarization, represented on the ECG by the QT interval, is of particular clinical interest in critical care. Once it is measured and corrected for changes in heart rate, the QT interval is known as the QTc. Measurement of the QT interval is important because a prolonged QT interval is associated with ventricular tachycardia and sudden cardiac death. Despite the serious complications associated with a prolonged QT interval, the interval is not routinely measured because a standardized method for measuring it has not been established and the length of QT interval critical to the development of ventricular tachycardia has not been determined. Much has been written about the conditions associated with prolonged QT intervals and specific actions to take when complications appear. Guidelines to be used for QT analysis in the clinical area, based on currently available information, include (1) procedures for measuring QT interval and calculating QTc, (2) procedures for QT analysis, (3) warning signs that indicate increased risk of ventricular tachycardia associated with a prolonged QT interval, and (4) actions to consider once increased risk is determined.

1996 ◽  
Vol 11 (S2) ◽  
pp. S40-S40
Author(s):  
William Brady ◽  
Daniel DeBehnke ◽  
Dennis Laundrie ◽  
Jeffrey A. Skiles

Objective: To determine the prevalence and outcome of out-of-hospital ventricular tachycardia (VT) cardiac arrest with a prolonged QT interval and to identify the subset with torsades de pointes (TdP).Methods: Design: Retrospective review. Setting: Fire department-based paramedic system. Participants: Non-traumatic VT cardiac arrest (1/91-12/94) with a supraventricular perfusing rhythm (SVPR) and a measurable QT interval. Interventions: QT interval was measured from a SVPR and corrected QT interval (QTc) was calculated (prolonged if ≥0.45 sec). VT was classified as polymorphic or monomorphic.Results: 190 patients met inclusion criteria. 51% of patients had a prolonged QTc (PQTc). The overall hospital discharge rate was 28.4%. No difference with respect to paramedic-witnessed arrests in each QTc group was found (25.8% normal QTc [NQTc] vs. 27.8% PQTc; p = 0.752). Patients with PQTc were less likely to be discharged from the hospital (19.6% vs. 37.6%; p = 0.01). Patients with PQTc were not more likely to have PVT (37% vs. 40%; p = 0.705). 16 (8.4%) patients had TdP. 27.8% of TdP and 26.8% of non-TdP patients were discharged (p = 0.912).


1998 ◽  
Vol 7 (5) ◽  
pp. 346-354 ◽  
Author(s):  
LK Rimmer ◽  
JD Rimmer

BACKGROUND: Prolonged cardiac repolarization is associated with ventricular tachycardia and sudden cardiac death. Repolarization, represented by the QT interval, is usually measured on a 12-lead ECG recording. Measurements of the interval on bedside monitor ECG recordings have not been compared quantitatively with measurements on 12-lead ECG recordings. OBJECTIVE: To determine if QT intervals and QTc values obtained by using monitor recordings are as accurate as those obtained by using 12-lead ECG recordings. METHODS: For each of 50 subjects, 2 ECG recordings were obtained, 1 with a 12-lead ECG and 1 with the bedside monitor, and QT intervals were measured manually. The QT intervals on each type of recording were compared on a lead-by-lead basis, the maximum QT interval and the QTc maximum determined with each method were compared, and the "best single leads" for determining the QTc were ascertained for each method. RESULTS: QT intervals, on a lead-by-lead basis; maximum QT intervals; and QTc maximum values measured on the monitor recordings were consistently longer than those measured on the 12-lead ECG recordings. When the monitor ECG leads I or II and the 12-lead ECG QTc maximum were examined for simple agreement by using 460 milliseconds as a cutoff, agreement was found in 82% to 84% of the sample, and false negatives were 12% and 8%, respectively. CONCLUSION: Recordings from leads I or II on the bedside ECG monitor should be used to measure the QT interval. Once prolonged QT values are detected, recordings obtained with a 12-lead ECG can be used to confirm the analysis.


2020 ◽  
Vol 8 ◽  
pp. 232470962094840
Author(s):  
B K Anupama ◽  
Soumya Adhikari ◽  
Debanik Chaudhuri

Recent reports have suggested an increased risk of QT prolongation and subsequent life-threatening ventricular arrhythmias, particularly torsade de pointes, in patients with coronavirus disease-2019 (COVID-19) treated with hydroxychloroquine and azithromycin. In this article, we report the case of a 75-year-old female with a baseline prolonged QT interval in whom the COVID-19 illness resulted in further remarkable QT prolongation (>700 ms), precipitating recurrent self-terminating episodes of torsade de pointes that necessitated temporary cardiac pacing. Despite the correction of hypoxemia and the absence of reversible factors, such as adverse medication effects, electrolyte derangements, and usage of hydroxychloroquine/azithromycin, the QT interval remained persistently prolonged compared with the baseline with subsequent degeneration into ventricular tachycardia and death. Thus, we highlight that COVID-19 illness itself can potentially lead to further prolongation of QT interval and unmask fatal ventricular arrhythmias in patients who have a prolonged QT and low repolarization reserve at baseline.


Blood ◽  
2002 ◽  
Vol 100 (6) ◽  
pp. 2249-2252 ◽  
Author(s):  
Chern-En Chiang ◽  
Hsiang-Ning Luk ◽  
Tsui-Ming Wang ◽  
Philip Yu-An Ding

Abstract Arsenic trioxide (As2O3; ATO) has recently been found to be very effective for relapsed acute promyelocytic leukemia. Several articles reported prolongation of QT interval or ventricular arrhythmias in patients receiving ATO. However, the QT-prolonging effect has not been confirmed and the direct membrane effect of ATO has never been studied. In the present investigation, using conventional action potential recording technique, we found that ATO dose dependently prolonged action potential duration (APD) in guinea pig papillary muscle with a slow pacing frequency. Parenteral administration of ATO prolonged QT interval and APD in guinea pig hearts. Intravenous infusion of clinically relevant doses of ATO prolonged QT interval and APD dose dependently. These studies suggest that ATO has a direct effect on cardiac repolarization. Patients who are receiving ATO should avoid concomitant administration of other QT-prolonging agents or conditions in favor of delaying cardiac repolarization.


2017 ◽  
Vol 35 (5) ◽  
pp. 804.e5-804.e6 ◽  
Author(s):  
Max Wentlandt ◽  
Stephen C. Morris ◽  
Steven H. Mitchell

2021 ◽  
Author(s):  
Tibor Hornyik

Proarrhythmia - the triggering of arrhythmias following drug therapy - is a rare, but potentially lethal side-effect of various drugs, and therefore, a major safety concern during drug development. Most often proarrhythmia is caused by the drugs’ potential to interact with various K+-channels in the heart, leading to a prolongation of cardiac repolarization that is usually observed on the ECG as prolonged QT interval (drug-induced acquired long QT syndrome; aLQTS). Although drug-induced long-QT-related proarrhythmia is most frequently found in patients with impaired cardiac repolarization due to disease-induced structural and/or electrophysiological remodelling of the heart; most cellular, tissue and whole animal model systems used for drug safety screening are based on normal, healthy models. This approach has serious limitations; therefore, novel animal models that mimic the pathophysiological conditions under which drugs display the highest proarrhythmic risk - such as models with impaired cardiac repolarization - would be desirable for proarrhythmia safety testing. The aims of the present study: Drug-induced (HMR-1556 to block IKs) acquired LQTS, and various transgenic (congenital) LQTS rabbit models with impaired cardiac repolarization due to cardio-selective overexpression of loss-of-function mutations of human KCNH2 (HERG-G628S, α-subunit of IKr, loss of IKr, LQT2), KCNE1 (KCNE1-G52R, β-subunit of IKs, decreased IKs, LQT5)[1] or both KCNQ1 and KCNE1 transgenes (LQT2-5) were used to investigate: - the proarrhythmic potential of SZV-270, a novel antiarrhythmic drug candidate with combined Class I/B and Class III effects (acquired LQTS model). - the electrophysiological characteristics of a newly generated, double-transgenic LQT2-5 rabbit model - the utility of transgenic LQT2, LQT5 and LQT2-5 rabbit models for more reliable prediction of drug-induced ventricular arrhythmias Main findings: The acquired LQTS rabbit proarrhythmia model with pharmacologically reduced repolarization reserve (by the IKs inhibitor HMR-1556) was able to predict the known torsadogenic potential of the IKr blocker dofetilide, while indicated no SZV-270-induced proarrhythmia risk. This advantageous electrophysiological effect of the SZV-270 - prolongation of ventricular repolarization without increased arrhythmia risk - is assumed to be attributed to its combined IKr (Class III) and INa (Class I/B) blocking characteristics. Transgenic LQTS rabbit models reflected patients with clinically ‘silent’ - normal QT interval (LQT5) - or 'manifest' - prolonged QT interval (LQT2 and LQT2-5) - impairment in cardiac repolarization reserve capacity due to different pathomechanisms. The LQTS animals were more sensitive in detecting IKr - (LQT5) or IK1/IKs - (LQT2 and LQT2-5) blocking properties of drugs compared to healthy wild type (WT) animals. Impaired QT-shortening capacity at fast heart rates was observed due to disturbed IKs function in LQT5 and LQT2-5. Importantly, the transgenic LQTS models did not only show more pronounced changes in different proarrhythmia markers in response to potassium channel blockers but also exhibited higher incidence, longer duration and more malignant type of ex vivo arrhythmias than WT. Conclusions: Drug-induced and transgenic LQTS rabbit models reflect human pathophysiological settings - patients with reduced repolarization reserve - that favour drug-induced arrhythmia formation. As they demonstrate increased sensitivity to different specific ion-channel blockers (IKr-blockade in LQT5 or in HMR-1556 induced acquired LQTS model, IK1 - and IKs - blockade in LQT2 and LQT2-5), their combined use could provide more reliable, and more thorough prediction of (multi-channel-based) pro-arrhythmic potential of novel drug candidates especially in the setting of impaired cardiac repolarization reserve.


1990 ◽  
Vol 10 (1) ◽  
pp. 66-72
Author(s):  
Makoto TOHYAMA ◽  
Hideyoshi FUJIHARA ◽  
Ryo KIMURA ◽  
Kazunori SATO

2016 ◽  
Author(s):  
Gary Green ◽  
Sally Graglia

Wide-complex tachycardias (WCTs) should always alert the emergency physician to a potentially immediate or rapidly developing, life-threatening scenario. The approach to these patients should follow general emergency medicine principles. The review covers the pathophysiology, stabilization and assessment, diagnosis and treatment, and disposition and outcomes of WCT. Figures show a basic electrocardiogram (ECG) tracing, an ambulatory monitoring strip of a patient with recurrent presyncope showing repetitive monomorphic ventricular tachycardia, a 12-lead ECG of a rapid wide QRS tachycardia due to an antidromic atrioventricular reciprocating tachycardia in a patient with Wolff-Parkinson-White (WPW) syndrome, an example of pacemaker-mediated tachycardia, ventricular tachycardia occurring in the context of QT prolongation consistent with torsades de pointes, a 12-lead ECG in a patient with WPW syndrome showing a rapid, irregular ventricular rate and wide QRS complexes of atrial fibrillation with a short refractory period, an ECG representative of tricyclic antidepressant overdose, and an algorithm for identifying patients with systolic heart failure and left ventricular ejection fraction less than or equal to 35% who are candidates for an implantable cardioverter-defibrillator. Tables list causes of regular WCT, causes of prolonged QT interval, common medications with potential QT prolongation activity, pharmacologic treatment options for stable patients with WCT, Kindwall and colleagues’ criteria for ventricular tachycardia, Brugada and colleagues’ criteria for ventricular tachycardia, Vereckei and colleagues’ aVr algorithm for the diagnosis of ventricular tachycardia, and a comparison of self-reported sensitivities, specificities, and test accuracies of the algorithms presented by Kindwall, Brugada, and Vereckei and their colleagues.   Key words: prolonged QT interval, supraventricular tachycardia, ventricular tachycardia, wide-complex tachycardias   This review contains 8 highly rendered figures, 8 tables, and 59 references.


2021 ◽  
pp. 126-130
Author(s):  
N. A. Skuratova ◽  
A. I. Zaryankina ◽  
A. A. Kozlovsky ◽  
S. S. Ivkina

The article presents a clinical case of a 16-year-old girl with clinical manifestations of congenital long QT interval syndrome in the form of syncope which were primarily diagnosed as epileptic syndrome for which the patient was taking anticonvulsant drugs having qualities of secondary prolongation of QT interval. At the same time, the data of family anamnesis (sudden death of the mother at a young age) in combination with typical manifestations of disease and electrocardiographic signs (prolonged QT interval measured from the standard electrocardiogram, paroxysms of spindle-shaped ventricular tachycardia accompanied with syncope conditions) made it possible to diagnose congenital long QT interval syndrome and implant an electric cardiac pacemaker.


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