Rory Childers

AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: part III: intraventricular conduction disturbances: a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society: endorsed by the International Society for Computerized Electrocardiology.

The present article introduces the second part of “Recommendations for Standardization and Interpretation of the Electrocardiogram.” The project was initiated by the Council on Clinical Cardiology of the American Heart Association and has been endorsed by the American College of Cardiology

AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the Electrocardiogram. Part III: Intraventricular Conduction Disturbances A Scientific Statement From the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society

The present article is the fourth in a series of 6 documents focused on providing current guidelines for the standardization and interpretation of the electrocardiogram (ECG). The project was initiated by the Council on Clinical Cardiology of the American Heart Association. The rationale for this project and the process for its implementation were described earlier.1 Abnormalities in the ST segment, T wave, and duration of the QT interval reflect abnormalities in ventricular repolarization. These abnormalities are common and often difficult to interpret. The U wave most likely represents an electricmechanical phenomenon that occurs after repolarization is completed. However, it is frequently included in discussions of repolarization and is discussed in this section. The ST segment corresponds to the plateau phase of the ventricular transmembrane action potential. Under normal conditions, the transmembrane voltage changes slowly during this phase and remains at approximately the same level in all ventricular myocardial cells. As a result, only small voltage gradients are present. This absence of pronounced voltage gradients is similar to that which occurs during electric diastole, ie, from the end of repolarization to the onset of the next depolarization, when ventricular myocardial cells are at their resting transmembrane potential of approximately 85 mV. This corresponds to the TP segment on the ECG. The absence of significant voltage gradients in ventricular myocardial cells during these 2 phases of the cardiac cycle explains why the ST and TP segments are normally nearly flat and at approximately the same level; that is, they are isoelectric. The T wave corresponds to the phase of rapid ventricular repolarization (phase 3) of the ventricular action potential.

Cellular telephone transmission of 12-lead electrocardiograms from ambulance to hospital

Currently, only single-lead, serial telemetry rhythm strips can be transmitted from ambulances. Triage of patients with chest pain and administration of thrombolytic therapy in ambulances is limited by the lack of specific electrocardiographic (ECG) diagnosis. A new technique is described using cellular telephone transmission of simultaneous 12-lead ECGs from ambulance to hospital to overcome this limitation. A portable 12-lead ECG installed in an ambulance was connected via modern link to a cellular telephone and digitized ECG information was transmitted to an ECG device in the hospital emergency room. Paramedics in the field placed adhesive patch electrodes and attached ECG wires. Field ECGs from 23 patients were compared with corresponding transmitted ECGs. There were no differences in heart rate, PR interval, QRS duration, QT interval or R- and T-wave axes. Baseline and transmitted ECGs had identical morphologic characteristics. Differences in R-wave amplitude in 5 transmitted tracings compared with hospital-recorded ECGs resulted in computer diagnosis of left ventricular hypertrophy by voltage, possibly due to differences in patient position. Twelve-lead ECGs can be easily transmitted from a moving ambulance using cellular telephones. This allows diagnosis before hospital arrival, improves prehospital triage of patients and may facilitate prehospital therapy with lidocaine or streptokinase. In addition, the cellular telephone link can convey both verbal and digitized information and thus improve on current telemetry systems.

Relation of electrocardiographic R-wave amplitude to changes in left ventricular chamber size and position in normal subjects

Although exercise-induced changes in electrocardiographic R-wave amplitude have been ascribed to changes in left ventricular (LV) size, QRS axis, heart rate and ischemia, the physiologic mechanism remains unclear. To clarify the relation between R-wave amplitude and changes in LV size and position, simultaneous 9-lead electrocardiograms and targeted M-mode echocardiograms were recorded from 15 normal subjects. Recordings were made at rest, during Valsalva maneuver and during methoxamine infusion. LV diastolic dimension increased with methoxamine and decreased with Valsalva maneuver (p less than 0.001). R-wave amplitude in leads V5 and V6 varied directly with LV dimensions (p less than 0.001). The correlation coefficient between the change in R-wave amplitude in V5 or V6 and the change in LV dimension was 0.81 (p less than 0.01). No significant changes in R-wave amplitude were seen in electrocardiographic leads I, II, III, aVR, aVL, aVF or V1. Distance from the chest wall to the LV posterior wall correlated with change in R-wave amplitude (r = 0.79, p less than 0.001). Change from supine to left lateral position moved the left ventricle closer to the lateral chest wall in association with a 41 +/- 8% increase in R-wave amplitude in V5 and V6 (p less than 0.001). In conclusion, there is a direct and a dynamic relation between R-wave amplitude and LV chamber size. Chamber size and distance from the left ventricle to leads V5 or V6 interact as major determinants of R-wave amplitude.

Time-related changes in the Q-T interval in acute myocardial infarction: Possible relation to local hypocalcemia

In 63 patients with either acute transmural or nontransmural myocardial infarction, the Q-T interval was prolonged beyond normal limits on at least 1 of the 5 days after infarction in 27 patients (8 with transmural and 19 with nontransmural infarction). The time-related changes in the corrected Q-T (Q-Tc) interval were defined for the entire sample and showed significant expansion, maximal on day 2, from a preinfarction control value. By day 5, the Q-Tc interval was no longer significantly prolonged and was not expanded beyond normal limits in any patient. Various possible causes of Q-T prolongation in myocardial infarction are local hypothermia, local conduction delay, neurogenic effect and local hypocalcemia. Collateral evidence suggests that the letter may contribute significantly to prolongation.

Sinus nodal echoes: Clinical case report and canine studies

Abstract Sinus nodal echoes are illustrated in (1) a case report, and (2) a study of the effects of atrial premature beats after atrial drive in dogs. When atrial premature beats confront the sinus node while it is still refractory, 3 types of response may be seen: (1) Complete interpolation—the subsequent sinus beat (or escape) comes precisely at the expected time; (2) incomplete interpolation—the subsequent sinus beat is delayed; and (3) sinus echoes—the sinus beat appears earlier than expected. In all 3 instances the node is entered, but the pacemaker fails to be reset. Although the echo has the form of a sinus beat, it is followed by a pause, presumably as a result of repenetration of the sinus node through pathways unused during exit. The curves characterizing the expansion by vagal stimulation of the nodal refractory period and total echo circuit time are defined, together with the latency of cholinergic effect on nodal refractoriness, sinus automaticity and exit conduction of the echo. The secondary concealment zone of a completely interpolated atrial premature beat is established. Atrial preexcitation (before the echo) sometimes evokes a second echo. The limiting factor on sustained sinoatrial reciprocation thus appears to be total echo circuit time rather than refractoriness of atrium or echo entrance pathways. The repetitive echoes seen in this study may be the basis for some clinical cases of sinus or atrial tachycardia.

R Wave of the Surface and Intracoronary Electrogram During Acute Coronary Artery Occlusion

Increases in electrocardiographic R-wave amplitude in humans have been described with positive and negative dynamic exercise test findings, episodes of variant angina and myocardial ischemia and infarction. The role of factors other than acute reversible ischemia in the genesis of these R-wave size alterations is unclear. To evaluate the contribution of acute ischemia to changes in R-wave size in the absence of other confounding variables, electrocardiograms were recorded before and during coronary angioplasty balloon inflation. The frontal leads and V1, V2, V5 and V6 were recorded during the last 10 seconds of coronary occlusion in 20 patients and intracoronary epicardial electrograms were recorded continuously during balloon inflation in 10 patients. Inflations were 8 +/- 2 atm for 52 +/- 36 seconds. Chest pain occurred in 26 of 30 patients with balloon inflation and ST elevation occurred in 22. No significant increases in R amplitude were noted in any lead or in the sum of the R waves in all leads, including intracoronary electrograms. In contrast, R amplitude tended to decrease. The initial decrease in both surface and epicardial R amplitude was similar to the first of the biphasic changes observed in animal models. An increase in R-wave amplitude is not by itself always a marker for myocardial ischemia, but depends on severity and duration of the process.

QTc prolongation is associated with impaired right ventricular function and predicts mortality in pulmonary hypertension

BACKGROUND In rodent models of pulmonary hypertension (PH) and right ventricular hypertrophy (RVH), the QTc interval is prolonged, reflecting downregulation of repolarizing Kv channels in RV myocytes. The significance of QTc prolongation in human PH is unknown. We hypothesized that QTc prolongation occurs in human PH, is associated with RVH and decreased RV function, and predicts adverse prognosis. METHODS Patients receiving a PAH-specific therapy (a prostanoid, endothelin-receptor antagonist and/or a phosphodiesterase-5 inhibitor), who had a 12-lead electrocardiogram (ECG) (n=202) were compared to age- and sex-matched controls (n=100). The duration of QTc on ECG was correlated with invasive hemodynamics (n=156) and with the status of the RV, as measured by Brain Natriuretic Peptide (NT-proBNP, n=145) and magnetic resonance imaging (n=24). Survival of the entire PH cohort and a subgroup with WHO Groups 1 and 4 PAH was prospectively determined from the Social Security Death Index. RESULTS QTc intervals were longer in PH vs. controls (454.8 ± 29 ms vs. 429.8 ± 18 ms, p<0.001) and did not differ based on PAH-specific therapy. NT-proBNP increased proportionately with QTc and was higher for those in the upper quintile (QTc ≥ 480 ms) vs. those with QTc<480 ms (4004 ± 6682 pg/mL vs. 1501 ± 1822 pg/mL, p<0.001). The QTc interval also correlated directly with increasing RV end-diastolic volume (r=.67, p<0.001) and mass (r=.0.51, p<0.05), and inversely with RV ejection fraction (r=-.49, p<0.05). In the entire PH cohort and WHO Groups 1 and 4 subgroup, QTc ≥ 480 ms and cardiac index were independent predictors of mortality. CONCLUSIONS QTc prolongation in PH patients reflects the status of the RV and is an independent predictor of mortality.

Change in ventricular cavity size: differential effects on QRS and T wave amplitude.

Although many factors have been reported to change the R wave amplitude of the electrocardiogram (ECG), few observations have been made of the associated changes in T wave amplitude. We hypothesized that changes in R and T wave amplitude should parallel each other. To test this hypothesis, R and T wave amplitudes were measured in 15 normal subjects during increased and decreased left ventricular dimensions induced by infusion of methoxamine and by Valsalva maneuver, respectively, as well as during changes in the proximity of the left ventricle to the chest wall (i.e., shift in patient position from supine to left lateral position). Simultaneous nine-lead ECGs and two-dimensional-guided M mode echocardiograms of the left ventricle were recorded at rest and under each experimental condition. R wave amplitude increased as the left ventricular lateral wall moved closer to the V5 and V6 electrodes. Alterations in R wave amplitude seen with changes in left ventricular chamber size were primarily caused by radial movement of the left ventricle in relation to the chest wall. Proximity of the left ventricle to the chest wall was therefore a major determinant of R wave amplitude. In contrast, T wave amplitude varied directly with alterations in left ventricular chamber size but was unaffected by changes in proximity to the recording electrode on the chest wall. Left ventricular chamber size, and possibly the associated alteration in endocardial-to-epicardial surface area ratio, appeared to be the major determinants of T wave amplitude.

Rate-dependent right precordial Q waves: “Septal focal block”

Rate-dependent pathologic Q waves in leads V 1 to V 3 were seen in two patients with myocardial infarction. Months later this conduction defect could be recalled with atrial premature beats, or as a continuing rate-dependent phenomenon. It is suggested that these cases represent a focal block in the septal fibers of the left bundle branch system and that this defect could underlie the transient right precordial Q waves seen in myocardial infarction or ischemia, as well as the fixed Q waves of many patients without septal infarction at autopsy.