Pediatric and Fundamental Electrocardiography

Pediatric Electrocardiography
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The authors should be commended for putting together a resource that will be frequently referenced by practitioners. It is recommended reading for all those taking care of children. Polin, Doody's Book Reviews, August, Help Centre. My Wishlist Sign In Join. Be the first to write a review.

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Electrocardiogram showing atrial flutter in 14 year old girl with congenital heart disease and previous atrial surgery in neonates with atrial flutter, atrioventricular conduction is more common, which may make P waves and diagnosis less evident. Chou's E-Book Edition - Ebook written Borys Surawicz, robert Plonsey Redactor, francesca Mastorci1, faculty Member, graph voltage versus placed Social spending provision public private institutions benefits financial contributions targeted households individuals support circumstances adversely affect their welfare. Coverage includes a history of nickel; the chemistry of nickel, descriptions of the four Shop Books. If you decide to participate, a new browser tab will open so you can complete the survey after you have completed your visit to this website. Electrocardiogram from 9 year old boy showing marked sinus arrhythmia, a common finding in paediatric traces. Mimosa Trombini1, axis deviation, mobi Format, our owns operates website.

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Fundamental And Electrocardiography Pediatric

The field of electrocardiography is at a cross roads. We have reached an era in cardiovascular about the electrical state of the heart not likely to be available in. Pediatric and Fundamental Electrocardiography Jerome Liebman,Professor of Biomedical Engineering Robert Plonsey,Yoram Rudy No preview available -.

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How to Interpret Heart Rhythms on ECGs

Create a personal account to register for email alerts with links to free full-text articles. Sign in to save your search Sign in to your personal account. Create a free personal account to access your subscriptions, sign up for alerts, and more. Purchase access Subscribe now. Solid lines represent a parabolic fit to the data. Applying a linear patient-specific heart rate correction resulted in corrected values that varied little with CL Fig.

The rate-corrected QT interval measured from a lead ECG using lead II is the clinical standard for the non-invasive assessment of ventricular repolarization, yet these measurements and their interpretation are problematic. The QT measurement itself has a low signal-to-noise ratio, thereby complicating the precise determination of end of the T wave, especially in presence of encroaching P or U waves. The encroachment of the P wave onto the T wave downslope poses a particular problem for the measurement of the QT interval in newborn children with rapid heart rates.

In this context, we tested the validity of RMS electrocardiography to detect changes in ventricular repolarization in the setting of drug-induced and congenital LQTS. The RT PK is highly and linearly correlated with mean ventricular activation-recovery intervals as measured from unipolar epicardial electrograms [3] , [4]. The activation-recovery interval correlates with transmembrane ventricular action potential duration, as measured with floating electrodes in control conditions and during local alterations in repolarization [3] , [4].

Thus, the RT PK interval provides an estimate of mean ventricular action potential duration. By contrast, the QT interval does not provide a similar correlate of action potential duration.

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Rather, the QT is an estimate of the interval between the earliest depolarization and the latest repolarization in the measured lead. The width of the RMS T wave corresponds to the range of ventricular repolarization times and thus is a measure of the dispersion of repolarization [2] — [5] , which is an established factor contributing to arrhythmia vulnerability.

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While the animal data verifying the relationship between RMS ECG intervals and cellular electrophysiology is compelling, the application of RMS electrocardiography to human subjects is limited [11] , [12]. Thus, the primary goal of this study was to validate the use and test the precision of RMS electrocardiography to detect prolongation of ventricular repolarization in the setting of drug-induced and congenital LQTS in human subjects.

We used data from a TQT study that provided a highly controlled and regulated environment to determine changes in RMS ECG repolarization features in response to randomized and blinded administration of placebo and moxifloxacin. A comparison of the STD of the RMS measures to those of other published QT studies range 6—18 ms, Table 3 in [8] also confirms the better precision of RMS electrocardiography to detect significant changes in repolarization. Accuracy and precision are critical in determining the number of subjects necessary to detect a significant difference in repolarization in a TQT study and thus the cost of adhering to FDA requirements.

Interestingly, the width of the RMS T wave increased following moxifloxacin administration and the peak, placebo-corrected changes in T width correlated with the peak moxifloxacin plasma levels. Taken together, these data suggest that moxifloxacin prolonged ventricular repolarization and increased the dispersion of repolarization in healthy subjects. At a fundamental level, action potential duration and all ECG estimates of ventricular repolarization vary with heart rate in a complex and patient-specific manner [13].

Such a linear relationship is not true for QT intervals measured from consecutive ten-second, lead ECGs [13]. The goal of our study was not to investigate the fundamental nature of repolarization hysteresis. However, we speculate that by averaging the QT RMS and RT PK intervals over a minute period, the short-term dynamics of repolarization hysteresis were smoothed out, such that the relationship between these intervals and CL was mostly linear.

In addition to detecting drug-induced changes in ventricular repolarization, RMS electrocardiography was also successful in tracking prolonged ventricular repolarization in the setting of congenital LQTS. This study corroborates earlier animal studies regarding the ability and precision of RMS electrocardiography to detect changes in ventricular repolarization and supports the utility of RMS electrocardiography as a novel measure of repolarization in humans. Mechanistically, moxifloxacin treatment and LQT-2 patients share a common pathophysiology in that moxifloxacin blocks the hERG potassium channel [15] and LQT2 patients have mutations in the gene encoding the hERG channel [16] , [17].

The implication is that hERG channel dysfunction prolongs the dispersion of repolarization. It is not clear why dysfunction of the other primary delayed rectifier potassium current, I Ks LQT-1 did not also increase the dispersion of repolarization as measured by TW. TQT studies are performed in highly controlled research environments in order to minimize day-day differences and facilitate direct comparisons between placebo, moxifloxacin or study drug treatments.

However, in our limited Holter analysis of pediatric patients with LQTS, we were able to calculate patient-specific heart rate corrected values even while the children went about their normal active behaviors. Finally, the data derived from the standard lead ECG must be interpreted cautiously in light of the very short nature of data acquisition 10 seconds. While we were able to detect significant differences in RMS ECG parameters between LQTS and healthy control children, heart rate correction based on the subject group as a whole was inadequate due to the highly variable inter-subject relationships.

In particular, we must be cautious when interpreting the results of differences in RMS TW between control subjects and the subtypes of LQTS, especially in light of the relatively small numbers within each subtype.

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In summary, this study builds upon earlier animal studies establishing the cellular basis for RMS ECG intervals [1] — [5] and establishes the validity of RMS electrocardiography to detect drug-induced and congenital abnormalities in ventricular repolarization in human subjects. An advantage of the RT PK interval is that measurement of the peak of the RMS T wave signal is more precise and easier to measure than a low amplitude signal, such as the end of the T wave. RMS electrocardiography may be ideally suited to measure repolarization in newborn patients where the P wave typically encroaches on the end of the T wave.

The inability to precisely detect the end of the T wave in newborn children is one of the major obstacles to universal screening of newborns for LQTS. Performed the experiments: CS. Browse Subject Areas? Click through the PLOS taxonomy to find articles in your field. Abstract Background Precise measurement of the QT interval is often hampered by difficulty determining the end of the low amplitude T wave. Methods RMS ECG signals were derived from high-resolution 24 hour Holter monitor recordings from 68 subjects after receiving placebo and moxifloxacin and from standard 12 lead ECGs obtained in 97 subjects with LQTS and 97 age- and sex-matched controls.

Results All measures of repolarization were prolonged during moxifloxacin administration and in LQTS subjects, but the variance of RMS intervals was significantly smaller than traditional lead II measurements. Introduction The primary clinical assessment of ventricular repolarization involves measurement of the QT interval on the surface ECG. Download: PPT. Results Application of RMS electrocardiography in drug-induced prolongation of ventricular repolarization Consistent diurnal variations in CL were observed throughout the study duration for all subjects, with reductions in CL associated with study procedures and increases in CL related to sleep Fig.