Abstract-The goals of electrocardiographic (ECG) monitoring in hospital settings have expanded from simple heart rate and basic rhythm determination to the diagnosis of complex arrhythmias, myocardial ischemia, and prolonged QT interval. Whereas computerized arrhythmia analysis is automatic in cardiac monitoring systems, computerized ST-segment ischemia analysis is available only in newer-generation monitors, and computerized QT-interval monitoring is currently unavailable. Even in hospitals with ST-monitoring capability, ischemia monitoring is vastly underutilized by healthcare professionals. Moreover, because no computerized analysis is available for QT monitoring, healthcare professionals must determine when it is appropriate to manually measure QT intervals (eg, when a patient is started on a potentially proarrhythmic drug). The purpose of the present review is to provide 'best practices' for hospital ECG monitoring. Randomized clinical trials in this area are almost nonexistent; therefore, expert opinions are based upon clinical experience and related research in the field of electrocardiography. This consensus document encompasses all areas of hospital cardiac monitoring in both children and adults. The emphasis is on information clinicians need to know to monitor patients safely and effectively. Recommendations are made with regard to indications, timeframes, and strategies to improve the diagnostic accuracy of cardiac arrhythmia, ischemia, and QT-interval monitoring. Currently available ECG lead systems are described, and recommendations related to staffing, training, and methods to improve quality are provided. Key Words: AHA Scientific Statements Ⅲ pediatrics Ⅲ electrocardiography Ⅲ torsade de pointes Ⅲ myocardial infarction Ⅲ tachyarrhythmias Ⅲ ischemia Ⅲ antiarrhythmic agents Ⅲ long-QT syndrome S ince the introduction of electrocardiographic (ECG) monitoring in hospital units Ͼ40 years ago, 1 the goals of monitoring have expanded from simple tracking of heart rate and basic rhythm to the diagnosis of complex arrhythmias, the detection of myocardial ischemia, and the identification of a prolonged QT interval. During the same 4 decades, major improvements have occurred in cardiac monitoring systems, including computerized arrhythmia detection algorithms, STsegment/ischemia monitoring software, improved noisereduction strategies, multilead monitoring, and reduced lead sets for monitoring-derived 12-lead ECGs with a minimal number of electrodes. 2,3 Despite these advances in technology, the need for human oversight in the interpretation of ECG monitoring data is as important today as it was 40 years ago for the following reasons. First, cardiac monitor algorithms are intentionally set for high sensitivity at the expense of specificity. As a result, numerous false alarms occur that must be evaluated by healthcare professionals so that overtreatment of patients will not occur. Examples of overtreatment are reported in the The American Heart Association makes every effort to avoid any actual or potential ...

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In 10 normal dogs, the right and left ventricular volumes and compliances were determined in the fresh post-mortem heart. With the use of a SigmaMotor pump, Ringer's solution at 23°C was simultaneously infused into both ventricles within an hour after death. When the ventricles were full but open to atmospheric pressure, the mean volumes were 35.8 ml/m 2 for the right and 23.1 ml/m 2 for the left ventricle; when the transmural pressure was increased by 10 mm Hg, the mean volumes were 56.9 ml/m-for the right and 41.9 ml/ m-for the left ventricle; at 20 mm Hg, the values were 60.8 and 48.5 ml/m-, respectively. The initial volumes and the increases in volume produced by increase in transmural pressure were affected by the position of the ventricular septum and by the presence of rigor mortis. With infusions into only one ventricle, right and left ventricular volumes were 20 to 74% greater at 10 mm Hg than the values when both ventricles were filled simultaneously. Compliance began to decrease 40 to 60 min after death; at 130 min after death (23°C), the change in volume when the transmural pressure was increased to 10 mm Hg was only about 1/5 of that immediately after death.ADDITIONAL KEY WORDS rigor mortis ventricular septum pressure-volume curves unilateral vs. bilateral filling• The purpose of these experiments was to study, in the fresh post-mortem heart, the volume-pressure relationships of the right and left ventricles of the dog. Such relationships previously reported are difficult to interpret, and are of uncertain relevance to conditions in vivo, because the effects of rigor mortis were not always considered and because in previous studies fluid was infused into only one ventricle at a time (1-3). In the present study we have found that volume-pressure relationships are highly dependent upon the state of filling of the contra-lateral chamber. Hence, the values of volume and compliance reported here, using the technique of simul- This study was supported by Public Health Service Research Crant HE 10382 from the National Heart Institute and the Ives Laboratories.Accepted for publication March 28, 1967. taneous biventricular filling, are probably physiologically more meaningful. MethodsTen mongrel dogs weighing between 12 and 23 kg were intravenously anesthetized with sodium pentobarbital, 27 mg/kg. A midstemal incision was rapidly made and the vessels, esophagus, and trachea were transected; the beating heart was then immersed in Ringer's solution at 23°C. The pericardium was incised and slipped to its insertion on the great vessels. The pericardium and other tissues were cut away leaving the atria and ventricles intact. With the use of Ringer's solution, blood was flushed from both ventricles. Polyethylene catheters, PE 240 (o.d. = 082 inches; i.d. = .062 inches), were inserted into the left and right ventricles via the atrioventricular valves. Heavy cotton suture, securely tied at the atrio-ventricular groove, closed off the ventricular inflow tracts. Two other polyethylene catheters, inserted in...

Left stellate or right stellate ganglion stimulation (LGSG or RSGS, respectively) is associated with ventricular tachyarrhythmias; however, the electrophysiological mechanisms remain unclear. We assessed 1) regional dispersion of myocardial repolarization during RSGS and LSGS and 2) regional electrophysiological mechanisms underlying T-wave changes, including T-peak to T-end (Tp-e) interval, which are associated with ventricular tachyarrhythmia/ventricular fibrillation. In 10 pigs, a 56-electrode sock was placed around the heart, and both stellate ganglia were exposed. Unipolar electrograms, to asses activation recovery interval (ARI) and repolarization time (RT), and 12-lead ECG were recorded before and during RSGS and LSGS. Both LSGS and RSGS increased dispersion of repolarization; with LSGS, the greatest regional dispersion occurred on the left ventricular (LV) anterior wall and LV apex, whereas with RSGS, the greatest regional dispersion occurred on the right ventricular posterior wall. Baseline, LSGS, and RSGS dispersion correlated with Tp-e. The increase in RT dispersion, which was due to an increase in ARI dispersion, correlated with the increase in Tp-e intervals (R(2) = 0.92 LSGS; and R(2) = 0.96 RSGS). During LSGS, the ARIs and RTs on the lateral and posterior walls were shorter than the anterior LV wall (P < 0.01) and on the apex versus base (P < 0.05), explaining the T-wave vector shift posteriorly/inferiorly. RSGS caused greater ARI and RT shortening on anterior versus lateral or posterior walls (P < 0.01) and on base versus apex (P < 0.05), explaining the T-wave vector shift anteriorly/superiorly. LSGS and RSGS cause differential effects on regional myocardial repolarization, explaining the ECG T-wave morphology. Sympathetic stimulation, in line with its proarrhythmic effects, increases Tp-e interval, which correlates with increases in myocardial dispersion of repolarization.

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This feasibility study of a novel myocardial activation-based ECGI using only the standard 12-lead ECG shows promise to localize the origin of PVC. This ECGI method yields activation estimates of isochrones on both ventricles from which the PVC origin location is derived. This method has the capability to localize the PVC from any part of the ventricular endocardium, intra-myocardium or epicardium.

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