Figure 11-1: Tachycardia-dependent complete left bundle branch block. Negative, T waves become manifest (when the left bundle branch block disappears) in leads showing a predominant negative (S wave) deflection. The patient had "primary" conduction system disease with no other evidence of organic heart disease. These changes have been attributed to the type of long-term memory effects that become manifest after disappearance of an abnormal sequence of depolarization.

Figure 11-2: Vagal-induced AV nodal block in a young person without structural heart disease. All values are expressed in milliseconds. The uncorrected QT interval does not increase at the end of an 1860-ms (RR) pause. This can be due to the form of short-term cardiac memory whereby the QT interval "remembers" its prepause values because of the slow adjustment to abrupt changes in cycle length in otherwise normal subjects. Figure 11-3: Acute inferior (diaphragmatic) MI showing "indicative" ST-segment elevation in leads reflecting the inferior wall (II, III, and aVF). Reciprocal changes are seen in the diametrically opposed leads (I and aVL) located in the same (frontal) plane. V4R showed evidence of right ventricular MI. There was complete AV block with an AV junctional rhythm.

Figure 11-4: Early repolarization. This normal variant is characterized by narrow QRS complexes with J-point and ST-segment elevation in the chest leads. Left chest leads often show tall R waves with a distinct notch or slur in their downstroke (arrow in V5), while the right chest leads may display ST segments having a "saddleback" or "humpback" shape (arrow in V3).

Figure 11-5: A. Nonischemic ST-segment elevation in the right precordial leads in a young patient with the Brugrada syndrome. B. Epsilon wave of a patient with arrhythmogenic right ventricular dysplasia.

Figure 11-6: Nonspecific (nondiagnostic) ST-segment-T-wave changes, the most common abnormalities in ECG interpretation.

Figure 11-7: Acute extensive anterior wall MI showing abnormal ST-segment changes and hyperacute T waves.

Figure 11-8: Acute extensive Q-wave anterior MI. The top row shows abnormal ST-segment elevation at the moment of appearance of (small) q waves in V1, V2, and V3. Note that R waves are taller than q waves in leads (V2 and V3), where the reverse is expected. In the bottom row, Q waves are deeper, ST segments are less elevated, and ischemic T waves can be seen clearly.

Figure 11-9: Plots of ST-segment levels versus time from therapy in two selected patients with patency of the infarct-related vessel at 60 min. Note that a 50 percent decrease in ST-segment levels within 60 min occurred only when measurements were made from the peak ST-segment level (highest ST-segment level measurement within the first 60 min). Figure 11-10: Assessment of thrombolytic therapy in patients with acute MI by ST-segment monitoring. Plots of ST-segment levels versus time from initiation of therapy in two selected patients with angiographic reocclusion. Patient A showed wide ST-segment shifts in the first 40 min, angiographic and electrocardiographic reperfusion at 90 min, and reocclusion at 120 min that required coronary angioplasty (PTCA). Patient B had successful thrombolysis within 60 min of initiation of therapy. At 16 h, ST-segment elevation recurred, and PTCA was performed.

Figure 11-11: Acute nonspecific pericarditis showing ST-segment elevation in all leads except aVR and V1.

Figure 11-12: LAFB in a patient with primary conduction system disease. QRS duration: 0.10 s. At normal paper speeds (25 mm/s), the relationship between the peaks of the R waves (vertical lines) in simultaneously recorded leads II and III and aVL and aVR cannot be determined with the desired accuracy (see Fig. 11-13).

Figure 11-13: Derivation of electrocardiographic leads from a frontal plane QRS loop showing LAFB. Due to the counterclockwise rotation of the left superior loop, the peak of the R in aVL preceded the peak of this deflection in aVR (lower right). Furthermore, because the initial portion of the loop was inscribed on the positive half of the axis of lead III before it was inscribed on the positive half of the axis of lead II, the peak of the R in the former lead occurred before that in the latter lead. (From Castellanos A, Pina L, Zaman L, et al. Recent advances in the diagnosis of fascicular blocks. Cardiol Clin 1987; 5:469-488. Reproduced with permission from the publisher and authors.) Figure 11-14: LAFB with wide QRS complexes. Whereas panel A shows LAFB with RBBB, these conduction disturbances coexist with diffuse septal and inferoposterior fibrosis in panel B. Consequently, the expected small q wave and the wide S wave in lead I are not present. This pattern has been called "masquerading" bundle branch block because the standard leads suggest LBBB, while the chest leads are diagnostic of RBBB. Figure 11-15: Diagnosis of LAFB associated with MI. Diagnostic feature given in parentheses. A. LAFB and anteroseptal MI (QR or QS complex in right chest leads). B. LAFB and anterolateral MI (abnormal Q wave in leads I and V6). C. LAFB and anterolateral MI with electrical axis in the right superior quadrant (Q wave in leads I and V6). D. LAFB and inferior wall MI (QR or QS complexes and elevation of J point and ST segments in leads II and III).

Figure 11-16: Type of nonspecific intraventricular conduction delay known as peri-infarction block. The patient had an evolving inferior wall MI. The wide (0.14-s) ventricular complexes show a predominantly terminal delay (arrows) and notching (more evident in the inferior leads) without a typical LBBB or RBBB morphology. Figure 11-17: Nonspecific intraventricular conduction delay characterized by very wide (0.17-s) QRS complexes not showing a typical RBBB or LBBB pattern. Figure 11-18: Premature atrial beats showing increasing degrees of (incomplete and complete) LPFB aberration. The first beats in all panels are escape beats with the same morphology as that of sinus beats. The second, aberrantly induced ventricular complexes show different degrees of right-axis shift with an increase in size of the R waves in leads II and III. Note that the fundamental characteristic of LPFB was not right-axis deviation (beyond +90°) but an inferior-axis shift. (From Castellanos A, Myerburg RJ. The Hemiblocks in Myocardial Infarction. New York: Appleton-Century-Crofts; 1976. Reproduced with permission from the publisher and authors.)

Figure 11-19: LPFB with RBBB. A. No MI. B. Anteroseptal MI (note q wave in V2). C. Inferior MI (note ST-segment elevation and T-wave inversion in leads II and aVF with slight ST-segment depression in lead I). The differences in QRS complexes between A and C are not very marked because pure LPFB may produce an almost abnormal Q wave in the inferior leads.

Figure 11-20: Pure (without RBBB) LPFB (third row) and LAFB (second row) occurring during acute anterior wall MI. Pre- and postfascicular block QRS morphologies are shown in the top and bottom rows, respectively.

Figure 11-21: Morphologic characteristics of complete LBBB complicated by acute anterior MI. A. Abnormal ST-segment elevation without q waves (QRS duration: 0.14 s). B. Abnormal ST-segment elevation, obtained from another patient, persisted after the appearance of abnormal Q waves (QRS duration: 0.13 s).

Figure 11-22: Morphologic features of complete LBBB complicated by acute inferior MI. There is abnormal ST-segment elevation in leads II, III, and aVF (QRS duration: 0.14 s). AV block is also present.

Figure 11-23: A. Complete LBBB with old anterior MI. Abnormal Q waves are present in lead I (QRS duration: 0.18 s). B. Pacing-induced complete LBBB pattern in a patient with old anterior MI. There are abnormal Q waves in lead I after spikes (QRS duration: 0.20 s). Note resemblance between natural and artificial (electrically induced) QRS patterns. Figure 11-24: Wolff-Parkinson-White syndrome in a patient with a left free-wall accessory pathway. A. Sinus rhythm with fusion beats showing different degrees of preexcitation. B. Maximal preexcitation during atrial fibrillation. Note marked change in QRS duration and electrical axis.

Figure 11-25: Wolff-Parkinson-White syndrome in a patient having a posteroseptal accessory pathway. Note short PR intervals with negative delta waves in leads III and aVF (false pattern of inferior MI). Lead V2 shows all-positive QRS complexes. Figure 11-26: Wolff-Parkinson-White syndrome in a patient with a right free-wall accessory pathway. Note LBBB "pattern" characterized for diagnostic (of accessory pathway location) purposes by a QRS duration greater than 0.09 s in lead I with rS complexes in leads V^ and V2. The electrical axis is approximately +15°. Figure 11-27: Wolff-Parkinson-White syndrome in a patient with a right anteroseptal accessory pathway. Note LBBB pattern (as defined in Fig. 11-26). The most important difference with the latter is that the electrical axis points more vertically, toward +60°, thereby being located within the range of the axis (+30 to +120°) reported for right anteroseptal accessory pathways.

Figure 11-28: Useful algorithm to predict accessory pathway location from the 12-lead ECG. Step 1: Analysis of R/S ratio in V2. Step 2: Existence of positive (+) delta wave in lead III (initial 40 ms). Step 3: Existence of positive or negative (-) delta wave in V1 (initial 60 ms). Step 4: Delta-wave polarity in aVF (initial 40 ms) or analysis of R/S ratio in V1 (± = biphasic or isoelectric). The accuracy of the algorithm for each location in 187 prospective patients is also shown at the bottom. LAL, left anterolateral; LL, left lateral; LP, left posterior; LPL, left posterolateral; LPS, left posteroseptal; MS, midseptal; RA, right anterior; RAL, right anterolateral; RAS, right anteroseptal; RL, right lateral; RP, right posterior; RPL, right posterolateral; RPS, right posteroseptal. (From Chiang et al.105 Reproduced with permission from the publisher and authors.) Figure 11-29: QRS changes (location of the electrical axis and polarity of lead V1) produced by pacing from right ventricular apex (RVA), right ventricular outflow tract (RVOT), great cardiac vein (GCV), and middle cardiac vein (MCV). Figure 11-30: ECG taken on a patient with pulmonary emphysema showing slight right-axis deviation with small rS complexes in lead I, an electrically vertical heart position, overall tendency to low voltage, and rS complexes in all chest leads. (From Lemberg and Castellanos.151 Reproduced with permission from the publisher and authors.) Figure 11-31: ECG from a patient with RV enlargement (volume overload in type) due to a small atrial septal defect (ostium secundum). Right-axis deviation was associated with an incomplete RBBB pattern (rsR' complexes in lead V1). (From Lemberg and

Castellanos.151 Reproduced with permission from the publisher and authors.) Figure 11-32: ECG from a patient with RV hypertrophy due to pure mitral stenosis showing P "mitrale," right-axis deviation, an all-positive deflection (R wave of only approximately 5 mm) in V1, and rS complexes from V2 to V6. (From Lemberg and

Castellanos.151 Reproduced with permission from the publisher and authors.)

Figure 11-33: ECG from a 17-year-old patient who had RV enlargement (pressure overloading in type) due to severe pulmonic stenosis. Note extreme right-axis deviation, overall high voltage, and qR complexes in lead Vj without an incomplete RBBB pattern.

(From Lemberg and Castellanos.151 Reproduced with permission from the publisher and authors.)

Figure 11-34: Electrocardiographic manifestations of early hyperkalemia. The nonprolonged QRS complex is followed by a peaked T wave having a very narrow base. Uncorrected and corrected QT intervals of 0.32 and 0.44 s, respectively (^). Hyperkalemia with hypocalcemia characterized by prolongation of the QT interval at the expense of the ST segment preceding the narrow-based T wave. Uncorrected and corrected QT intervals of 0.52 and 0.53 s, respectively (B).

Figure 11-35: Advanced hyperkalemia. The wide (0.14-s) QRS complexes are followed by peaked T waves (best seen in lead V3). The hyperkalemia-induced ST-segment elevation in lead V^ (arrows), known as the dialyzable currents of injury, disappeared after appropriate treatment.

Figure 11-36: Electrocardiographic manifestations of hypokalemia (upper strip) and hypercalcemia (lower strip).

Figure 11-37: ECG obtained from a patient with hypothermia. The characteristic Osborn wave (arrows) is the terminal deflection inscribed between the slender part of the QRS complexes and the beginning of the ST segment. Note that it is not easy to determine where the ST segment starts. In addition, there is marked prolongation of the QT interval. Figure 11-38: Identification of improper connections of a single cable from the electrocardiographic machine to the corresponding electrodes placed on the patient's limbs. Note that aVR, aVL, and aVF invariably refer to whatever morphology is recorded when, while the ECG is being obtained, the corresponding knobs are turned in this order (regardless of whether the cables were attached properly or improperly). On the other hand, RA (right arm), LA (left arm), and LL (left leg) or LF (left foot) correspond to the normal morphology recorded by the cables so labeled. This method, based solely on the analysis of the unipolar extremity leads, is simpler than the method based on the study of the bipolar standard leads but is useful only when a single cable is misconnected. A. Normal. B. Since LA appears in aVR and RA appears in aVR (with LF being in its normal position), the right arm and left arm cables must have been switched. C. Since LF appears in aVR and RA appears in aVF (with LA in its normal position), the right arm and left leg cables must have been switched. D. Since LA appears in aVF and LF appears in aVL (with RA in its normal position), the left arm and left leg cables must have been switched. Figure 11-39: Identification of improper connections of the right leg (RL) (ground) cable. C can be regarded as almost equal to the control tracing because the RL (ground) and left leg (LL) cables were switched. The corresponding morphologies are not identical to the control morphologies because a very small difference in potential between both legs does exist. The latter is seen in A. Because the RL and RA cables were switched, lead II (RA-LL) records the difference in potential between both legs, which seems to be approximately 0.15 mV. The latter results in an almost straight line interrupted by a small blip. In addition, lead I represents the mirror image of normal lead III, and lead III is the normal lead III. In B, where the LA and RL cables have been switched, lead III (LA-LL) records almost a straight line. In addition, lead I is the normal lead II, and lead II is the normal lead II. [From Castellanos A, Saoudi NC, Schwartz A, et al. Electrocardiographic patterns resulting from improper connection of the right leg (ground) cable. PACE 1985; 8:364-368. Reproduced with permission from the publisher and authors.]

' Figure 11-40: The spatial vectorcardiographic loops cannot be analyzed routinely in space with presently available techniques. Therefore, it is customary to study their projections in three planes seen as depicted in this figure. Note that (1) the frontal plane conforms to Einthoven's view of his equilateral triangle, (2) the horizontal plane is seen in such a way that the anterior surfaces of the heart and sternum are displayed in the inferior portions of the paper (in contrast to other noninvasive, nonelectrical methods), and (3) the sagittal plane is viewed from the right side of the patient. (From Lemberg and Castellanos.151 Reproduced with permission from the publisher and authors.)

' Figure 11-41: Method used to derive the morphology of a unipolar precordial lead (in this example lead Vg) from the planar projection of the spatial QRS and ST-T loops on the horizontal plane. First (leftpanel), a line is drawn from the estimated location of the corresponding electrode to the point of origin of the loops. Thereafter, a perpendicular to this line passing from the point of origin is drawn. This divides the thorax into a negative area (for V6) that is located beyond the perpendicular line and a positive area that is located between the perpendicular line and the electrode. Thus, in the top right schematic, the small part of the loop located beyond the perpendicular line produces the small q wave in V6. The other schematics show how progression of depolarization and repolarization produces parts of the QRS loop (and the entire ST-T loop), which are positive in lead V6. The S wave occurs because the terminal part of the QRS loop is located beyond the perpendicular line. When using this type of lead derivation, any precordial lead will only record forces moving in an anteroposterior (or posteroanterior) and in a left-to-right or right-to-left direction. Forces moving up or down will not be recorded. This contrasts with scalar concept of precordial leads which can, especially when misplaced, record forces moving in any direction. (From Lemberg and Castellanos.151 Reproduced with permission from the publisher and authors.)

' Figure 11-42: Planar projections of normal spatial VCG obtained with the Frank method. The ST-T loops are enlarged in the bottom view. In the horizontal plane, the QRS loop shows the expected, normal, counterclockwise (CCW) rotation (indicated by arrows). Although the narrow frontal plane QRS loop has clockwise (CW) rotation, in this plane either CCW, CW, or figure-eight rotations can be normal. In the right sagittal plane, the QRS loop displays its normal (CW) rotation. Enlargement of the ST-T loop clearly shows that its first half is inscribed more slowly. Therefore, the dashes (each representing 0.0025 s, or 25 ms) are closer together. Note that the rotation of the ST-T loop is similar to the rotation of the QRS loop in all planes. (From Lemberg and Castellanos.151 Reproduced with permission from the publisher and authors.)


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