Sections View Full Chapter Figures Tables Videos Annotate Full Chapter Figures Tables Videos Supplementary Content + INTRODUCTION Download Section PDF Listen +++ ++ Second-Degree AV Block (Mobitz I, Wenckebach). The PR interval gradually increases until a P wave is not followed by a QRS and a beat is “dropped.” The process then recurs. P waves occur at regular intervals, though they may be hidden by T waves. (ECG contributor: James Paul Brewer, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) + PART 1: ST-T ABNORMALITIES Download Section PDF Listen +++ +++ ACUTE ANTERIOR MYOCARDIAL INFARCTION ++ FIGURE 23.1A Acute Anteroseptal Myocardial Infarction. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ ST segment elevation in the anterior precordial leads. V1-V4: Anteroseptal injury. V3-V4: Anterior injury. V3-V6: Anterolateral injury. Leads I and aVL may also be involved, especially if the circumflex artery is affected (high lateral injury). Reciprocal ST segment depressions are often present in the inferior leads (II, III, aVF). +++ Pearls ++ The left anterior descending artery supplies blood to the anterior and lateral left ventricle and ventricular septum. Normal R-wave progression (increasing upward amplitude with R wave > S wave at V3 or V4) may be interrupted. The development of pathologic Q waves in any of the V leads other than V1 strongly suggests that the injury has progressed to an infarction, as seen in this example. ++ FIGURE 23.1B Pathologic ST-segment elevation beyond 1 mm (double arrow) with pathologic Q waves (arrow) in lead V3. The ST segment demonstrates a convex upward, or “tombstone,” morphology. Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ACUTE INFERIOR MYOCARDIAL INFARCTION ++ FIGURE 23.2A Acute Inferior-Posterior Myocardial Infarction. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ ST segment elevation in inferior leads (II, III, aVF) ST segment depressions in the anterior leads (V1-V3) and possibly high lateral leads (I, aVL) +++ Pearls ++ The right coronary artery supplies blood to the right ventricle, the sinoatrial (SA) node, the inferior portions of the left ventricle, and usually to the posterior portion of the left ventricle and the atrioventricular (AV) node. Infarctions involving the SA node may produce sinus dysrhythmias including tachycardias, bradycardias, and sinus arrest. Infarctions involving the AV node may produce AV blocks. In the presence of acute inferior injury, a right-sided ECG should be obtained to look for right ventricular involvement. The administration of nitroglycerin in the presence of acute right ventricular infarction can precipitate profound hypotension, as these patients are preload-dependent. Since the right coronary artery so often supplies the posterior left ventricle, look for evidence of a posterior infarction (as present in the example) and consider obtaining an ECG with posterior leads. ++ FIGURE 23.2B ST-segment elevation is present in the inferior leads (II, III, aVF) (arrow), with reciprocal ST depression in the anterior leads (V2-V4) (arrowhead) and high lateral leads (I, aVL). Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ACUTE RIGHT VENTRICULAR MYOCARDIAL INFARCTION ++ FIGURE 23.3A Right Ventricular Myocardial Infarction. This ECG was obtained with right-sided lead placement. (ECG contributor: Thomas Bottoni, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ ST elevation in right-sided V leads (V4R, V5R). ST elevation greater in lead III than lead II suggests RV MI. ST elevation in the normally obtained V1 also strongly suggests RV MI. Often associated with inferior MI and/or posterior MI. +++ Pearls ++ The smaller muscle mass of the right ventricle produces a less intense injury pattern that is overwhelmed by the left ventricle in the normally obtained ECG. Placement of right-sided V leads, with V1-V6 in mirror-image locations on the right side of the chest, is important in detecting right ventricular injury. The heart with an injured right ventricle is very preload-dependent. Beware of lowering preload with nitrates in any patient with suspected RV MI as severe hypotension may occur. Treat hypotension with volume. Obtain a right-sided ECG in any patient with inferior or posterior MI, and in any patient with a significant hypotensive response to nitrates. ++ FIGURE 23.3B ST elevation in V4R and V5R (arrows), with the V4 and V5 leads placed in their mirror-image locations on the right side of the chest. Any ST elevation seen in the right-sided precordial leads is significant. Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ACUTE POSTERIOR MYOCARDIAL INFARCTION ++ FIGURE 23.4A Acute Posterior Myocardial Infarction. (ECG contributor: R. Jason Thurman, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ With acute injury pattern—ST segment depression in lead V1 and/or V2 with acute injury pattern With infarction pattern—Small S wave and large R wave greater than 4 ms duration in lead V1 or V2 with infarction With infarction pattern—R-wave/S-wave ratio greater than 1 in lead V1 or V2 with infarction +++ Pearls ++ The posterior portion of the left ventricle has no EKG electrodes directly overlying it and is the last portion of ventricle to depolarize. It receives its blood supply from either the right coronary artery (in 85% of individuals) or the circumflex artery (in 15% of individuals). V1 and V2 are primarily affected as the most anterior leads and indirectly assess the posterior left ventricle, though in an “inverted” orientation. Instead of observing downgoing Q waves and ST elevation, one expects to see large upgoing R waves and ST depression. By holding the EKG up to a backlight upside down and horizontally flipped, the more classic injury pattern can be observed by looking through the EKG paper (see Fig. 23.4C). Posterior involvement may be confirmed with posterior leads. V8 is located at inferior tip of left scapula; V9 is positioned between V8 and the spine at the same level. Frequently, an inferior MI is also present with a posterior MI, since the right coronary artery serves both areas. In the above example, there is subtle ST elevation in the lateral leads, indicating posterior-lateral injury. ++ FIGURE 23.4B This tracing demonstrates injury in the posterior LV, manifesting as acute ST depression in V2 (arrow). Graphic Jump LocationView Full Size||Download Slide (.ppt) ++ FIGURE 23.4C By inverting and rotating the EKG, the characteristic ST-elevation injury pattern is easily seen (arrow). This can be done in practice by flipping the EKG upside down and looking through the printed EKG with a backlight. Graphic Jump LocationView Full Size||Download Slide (.ppt) ++ FIGURE 23.4D The ST depression is subtle and downsloping. However, the R-wave amplitude approximates that of the S wave, and the R-wave duration is significant (>4 ms). This is actually an “inverted Q wave” from a posterior infarction that has evolved since the initial tracing. Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ LEFT MAIN LESION ++ FIGURE 23.5A Left Main Coronary Artery Lesion (Widowmaker). (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ ST segment elevation in the precordial leads (V2-V6) and high lateral leads (I, aVL). Reciprocal ST segment depressions in the inferior leads (II, III, aVF). ST segment elevation in AVR coupled with reciprocal ST depressions may indicate AMI from left main disease. +++ Pearls ++ The left main coronary artery branches into the left anterior descending artery and the circumflex artery. It supplies blood to the ventricular septum and the anterior and lateral aspects of the left ventricle, usually sparing the posterior and inferior portion, which is most often served by the right coronary artery. Normal R-wave progression (increasing R-wave amplitude across the precordial leads) may be interrupted. Risk of cardiogenic shock is high since so much of the left ventricle is served by the left main coronary artery. A left main coronary thrombosis is also known as the “widowmaker lesion.” Isolated ST segment elevation in lead aVR may also indicate acute myocardial ischemia from left main coronary artery disease. ++ FIGURE 23.5B Significant ST elevation is present in the precordial leads (V2-V6) and high lateral leads (I and aVL) (arrows). In this example, significant Q waves have appeared, signaling infarction (arrowhead). Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ SGARBOSSA CRITERIA FOR AMI IN SETTING OF LBBB ++ FIGURE 23.6A Acute Myocardial Infarction by Sgarbossa Criteria in the Setting of Underlying LBBB. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ ST elevation greater than or equal to 1 mm concordant with QRS deflection (score = 5) ST depression greater than or equal to 1 mm in leads V1, V2, V3 concordant with QRS deflection (score = 3) ST elevation greater than or equal to 5 mm discordant with QRS deflection (score = 2) ++ FIGURE 23.6B The ST elevation is greater than 5 mm discordant from the primary QRS deflection (arrow). Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ Pearls ++ These scored criteria may be used to diagnose acute myocardial infarction in the setting of a left bundle branch block (LBBB). However, most myocardial ischemia in the setting of LBBB does not produce these changes. An absence of these findings should not be used as evidence against acute coronary syndrome. Score of greater than or equal to 3 gives a specificity for myocardial infarction of 90%. The first and third criteria listed above may also be used in ECGs with wide QRS complexes resulting from a pacemaker or idioventricular rhythm. ++ FIGURE 23.6C The ST depression is greater than 1 mm concordant to the primary QRS deflection (arrow). Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ SUBENDOCARDIAL ISCHEMIA ++ FIGURE 23.7A Subendocardial Ischemia. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ ST segment depression greater than or equal to 1 mm in anatomically adjoining leads. ST segments may be horizontal or downsloping with acute ischemia. +++ Pearls ++ Some ST depression in the lateral precordial leads (V4-V6) is common at higher heart rates, and is commonly seen during exercise treadmill tests, but such depression should not be downsloping unless ischemia is also present. ST elevation in other leads suggests that the depression may represent reciprocal changes from acute injury rather than subendocardial ischemia. Downsloping ST depression may also be seen in left ventricular hypertrophy (LVH), but this depression should not be dynamic, and should be stable with serial ECGs. ST depression from ischemia will be dynamic, changing with time on serial ECGs. Isolated ST depression in leads V1 and V2 may represent posterior ischemia. ++ FIGURE 23.7B Downsloping ST segments depressed greater than 1 mm (arrow). These changes were dynamic over time. The patient sustained a nontransmural myocardial infarction. Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ HYPERACUTE T WAVES ++ FIGURE 23.8A Hyperacute T Waves. T waves in a patient with acute myocardial ischemia. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ T-wave amplitude/QRS amplitude greater than 75%. T waves greater than 5 mV in the limb leads. T waves greater than 10 mV in the precordial leads. T waves have asymmetric appearance. +++ Pearls ++ Hyperacute T waves occur very early (within minutes) during myocardial injury and are transient. The term “hyperacute T waves” is reserved for the early stages of myocardial infarction. “Prominent T waves” can also be seen with LVH, early repolarization, or with hyperkalemia. Serial ECGs are useful in distinguishing transient hyperacute T waves from other causes of tall, peaked T waves. ++ FIGURE 23.8B T-wave height is greater than 10 mm in V5 (double arrow) and is asymmetric. This height was transient and was significantly diminished in a tracing obtained 15 minutes later. Note also in the 12-lead ECG example above the presence of inferior ST elevation. Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ WELLENS WAVES ++ FIGURE 23.9A Wellens Waves. Wellens waves are present and are indicative of a high-grade LAD lesion. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings (Two Classic Types) ++ Biphasic T waves in anterior and/or lateral leads Deeply inverted, symmetrical T waves in the same leads +++ Pearls ++ These characteristic patterns of T-wave changes are closely associated with critical left anterior descending artery stenosis. The changes are classically apparent on ECG after resolution of chest pain. These changes are transient, and often are not associated with cardiac enzyme elevations. Wellens waves are not associated with changes in R-wave progression. Serial electrocardiograms may assist in differentiating Wellens waves from stable, nonspecific findings. ++ FIGURE 23.9B Biphasic T waves with the later segment inverted, as in V2 above (arrow), or deep symmetric inverted T waves, as in V5 above (arrowhead). These findings in the precordial leads, in the setting of suspected ACS, strongly suggest an underlying high-grade LAD lesion. Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ “CEREBRAL” T WAVES ++ FIGURE 23.10A Cerebral T Waves. This ECG was obtained on a patient with a severe acute hemorrhagic CVA. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ Inverted, wide T waves are most notable in precordial leads (can be seen in any lead). QT interval prolongation. +++ Pearls ++ These are associated with acute cerebral disease, most notably an ischemic cerebrovascular event or subarachnoid hemorrhage. They may be accompanied by ST segment changes, U waves, and/or any rhythm abnormality. Differential diagnosis includes extensive myocardial ischemia. Strongly suspect an intracranial etiology in a patient with altered mental status and these electrocardiographic findings. ++ FIGURE 23.10B Deep, symmetrical, inverted T waves (arrowhead) with a prolonged QT interval. Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ EARLY REPOLARIZATION ++ FIGURE 23.11A Early Repolarization. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ ST elevation, usually in the anterior leads. J-point elevation, but usually less than one-third the total height of the T wave. ST segment is “concave upward,” or “holds water,” or “is smiling at you.” J-point notch strongly suggests early repolarization, but is not always present. +++ Pearls ++ This is a normal variant and is especially common in young healthy males, but also may be present in other groups. However, any clinical suspicion for ongoing myocardial ischemia should prompt further investigation Q waves and reciprocal ST-segment depression in other leads should not accompany early repolarization. If present, they strongly suggest ischemia as the cause for the ST elevation. ++ FIGURE 23.11B ST elevation in precordial leads, with a concave-upward ST segment and a J-point notch (arrow). Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ LEFT VENTRICULAR ANEURYSM ++ FIGURE 23.12A Left Ventricular Aneurysm. This ECG was obtained on an asymptomatic patient with history of MI 2 years prior. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ ST elevation in anterior contiguous leads Deep pathologic Q waves in anterior leads +++ Pearls ++ ST segment elevation which occurs in the setting of a myocardial infarction should resolve within days under normal circumstances. Persistent ST-segment elevation occurring for weeks or longer after a myocardial infarction is suspicious for ventricular aneurysm. Ventricular aneurysms may follow a large myocardial infarction in the anterior portion of the heart. The aneurysm consists of scarred myocardium, which does not contract but bulges outward during systole; complications include congestive heart failure, myocardial rupture, arrhythmias, and thrombus formation. Suspect an LV aneurysm when these findings appear in the ECG of a patient who does not demonstrate symptoms suggesting ACS. However, one should also be vigilant for the presence of “silent” ACS. ++ FIGURE 23.12B Persistent ST elevations (arrow) and deep, pathologic Q waves (arrowhead) in an asymptomatic patient with a history of anterior myocardial infarction 2 years earlier. Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ PERICARDITIS ++ FIGURE 23.13A Acute Pericarditis. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ Diffuse ST elevation in noncontiguous leads PR depression T-wave flattening or inversion PR elevation in lead aVR +++ Pearls ++ Pericarditis may produce inflammation of the epicardium. This is most often demonstrated on the ECG as a widespread injury pattern. Pericarditis does not produce abnormal Q waves. The presence of abnormal Q waves must prompt consideration of acute or old coronary syndrome, including Dressler syndrome or postinfarct pericarditis. Pericarditis may be focal, resulting in regional rather than diffuse EKG changes. Benign early repolarization and myocarditis may also appear as ST elevation in many noncontiguous leads. ++ FIGURE 23.13B ST elevation in noncontiguous leads I and II (arrows) with PR depression (arrowhead). No pathologic Q waves or reciprocal changes are present. Graphic Jump LocationView Full Size||Download Slide (.ppt) + PART 2: CONDUCTION DISTURBANCES Download Section PDF Listen +++ +++ FIRST-DEGREE AV BLOCK ++ FIGURE 23.14A First-Degree AV Block. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ A PR interval greater than 200 ms (normal 120-200 ms) with no significant variation in PR intervals between beats. Each P wave is followed by a QRS complex. +++ Pearls ++ This type of heart block usually does not affect heart function and can be considered nonpathologic (especially in athletes or patients with higher vagal tone). First-degree block may also be due to heart disease (myocarditis, rheumatic fever) or drugs (digoxin, amiodarone, β-blockers, calcium channel blockers). ++ FIGURE 23.14B The PR interval is fixed (double arrows) and is longer than 0.2 seconds, or five small blocks. Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ TYPE 1 SECOND-DEGREE AV BLOCK (MOBITZ I, WENCKEBACH) ++ FIGURE 23.15A Second-Degree AV Block (Mobitz I, Wenckebach). (ECG contributor: James Paul Brewer, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ Progressive PR-interval prolongation throughout the cardiac cycle until a P wave occurs without a QRS complex (“dropped” beat). After the dropped QRS complex, the cycle continues again with the PR interval of the first beat in the cycle always shorter than the PR interval of the last beat in the previous cycle. P wave may be hidden by the preceding T wave. +++ Pearls ++ The number of P-QRS complexes prior to the “dropped” beat may vary. A clue to the diagnosis of Mobitz type I heart block can be found in the appearance of grouped QRS complexes. This type of block is normally asymptomatic, and may be seen in athletes. These patients have low risk of progression to complete heart block, and usually do not require a pacemaker. However, Mobitz type I heart block may be caused by inferior myocardial infarction or drugs (digoxin, amiodarone, β-blockers, calcium channel blockers). ++ FIGURE 23.15B The PR interval gradually increases (double arrows) until a P wave is not followed by a QRS and a beat is “dropped” (brackets). The process then recurs. P waves occur at regular intervals, though they may be hidden by T waves. Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ TYPE 2 SECOND-DEGREE AV BLOCK (MOBITZ II) ++ FIGURE 23.16A Type II Second-Degree AV Block (Mobitz II). (ECG contributor: Michael L. Juliano, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ The PR interval remains constant and does not increase (as seen with Mobitz type I) with each cardiac cycle prior to the “dropped” QRS complex. P-P interval is constant, and R-R interval is constant until the dropped beat. R-R interval encompassing the “dropped” QRS should be roughly equal to two P-P intervals. +++ Pearls ++ This type of heart block is associated with disease of the conduction system distal to the AV node. A pacemaker is usually indicated. Mobitz type II block can accompany myocardial infarction and has a high chance of progression to a complete heart block. ++ FIGURE 23.16B The PR interval is constant (double arrows) until the dropped beat (brackets). Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ THIRD-DEGREE (COMPLETE) AV BLOCK ++ FIGURE 23.17A Third-Degree AV Block (Complete Heart Block). (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ Atrial and ventricular electrical activities are entirely disassociated. The P-P and R-R intervals remain constant. P waves may be hidden in the QRS complex or may distort the shape of the T wave. The atrial rate is usually faster than the ventricular rate. +++ Pearls ++ Third-degree block is also called complete heart block because no impulses are conducted from the atria to the ventricles. AV rate and QRS morphology depend upon the location of the escape pacemaker. A node escape rate is typically 40 to 60 bpm, with a narrow QRS complex. Ventricular escape rate is usually 20 to 40 bpm, with a widened QRS complex. Complete heart block may be caused by myocardial infarction, conduction system disease, or drugs such as digoxin. Complete heart block may dramatically decrease cardiac output, cardiac pacing is often required. ++ FIGURE 23.17B The P-P interval is uniform (lower double arrows) and the R-R interval is uniform (upper double arrows), but the P waves and QRS complexes are disassociated. Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ QT INTERVAL PROLONGATION ++ FIGURE 23.18A Prolonged QT Interval. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ Normal QTc interval is less than 440 ms. QTc interval greater than 440 ms is considered prolonged. QTc interval greater than 550 ms is markedly prolonged. +++ Pearls ++ The QT interval is measured form the beginning of the QRS complex to the termination of the T wave (or U wave if present) and should be measured in the EKG lead with the longest-appearing QT interval that has a distinct T wave with a clear termination point. The QT interval will increase with bradycardia and decrease with tachycardia, thus it is important to use the corrected QT interval (QTc = QT/μR-R interval) for heart rates other than 60 (in which the QTc = QT). Prolonged QT intervals may be congenital. The vast majority are acquired, usually due to medications or electrolyte abnormalities (hypokalemia, hypomagnesemia, hypocalcemia, and hyperphosphatemia). Numerous medications may prolong the QT interval in therapeutic or toxic doses. Prolongation of the QT interval predisposes to torsades de pointes. Look carefully for prolonged QT intervals in patients who present with syncope. ++ FIGURE 23.18B QT Interval Prolongation. QT of 440 ms, QTc of 498 (double arrow). Note the QT interval is measured from the beginning of the QRS complex to the termination point of the T wave. Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ RIGHT BUNDLE BRANCH BLOCK ++ FIGURE 23.19A Right Bundle Branch Block. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ Wide QRS complex, at least 120 ms (three small blocks). QRS complex has sR’ or rsR’ in leads V1 and V2. Slurred S wave V6 and I. +++ Pearls ++ The signal exiting the AV node is carried rapidly to the LV through the intact left bundle, but is delayed into the right ventricle, where depolarization must propagate cell-to-cell. Since the RV myocardial mass is much smaller than that of the LV, this delay in depolarization is best seen in the leads overlying the right ventricle, leads V1 and V2. Acute right heart strain, as may occur with pulmonary embolism, may result in new onset right bundle branch block (RBBB). ++ FIGURE 23.19B rsR’ pattern in V1 (arrowheads), with T wave downgoing (arrow). QRS duration greater than 120 ms (double arrow). Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ LEFT BUNDLE BRANCH BLOCK ++ FIGURE 23.20A Left Bundle Branch Block. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ Wide QRS complex, at least 120 ms (three small blocks). T wave appears on the opposite side of the baseline from the QRS complex. The QRS precordial axis is normal or deviated to the left. QRS complex deflection is predominately downward in lead V1 and upward in lead V6. +++ Pearls ++ The signal exiting the AV node does not proceed through the left ventricular conduction system. It must propagate more slowly cell-to-cell through the myocardium, starting in the septum. Therefore, the QRS is wider and the bulk of the depolarization signal is deflected toward the far lateral aspect of the heart. Acute myocardial infarction may produce a new onset LBBB on ECG. Therefore, patients with new onset LBBB with a clinical presentation consistent with acute coronary syndrome should be treated as having an acute ST segment elevation myocardial infarction (STEMI). ++ FIGURE 23.20B The QRS is wider than 120 ms (double arrow). The T-wave deflection is in the opposite direction from the QRS deflection (arrowhead). Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ LEFT ANTERIOR FASCICULAR BLOCK ++ FIGURE 23.21A Left Anterior Fascicular Block. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ QRS complex widening, usually 90 to 120 ms Left axis deviation beyond minus 45 degrees with no other cause (such as inferior myocardial infarction) Small R wave and large S wave in the inferior leads Slurred S wave in V5 and V6 +++ Pearls ++ The signal exiting the AV node is carried rapidly to the inferior aspect of the LV and all of the RV through the intact left posterior fascicle and right bundle, where quick depolarization occurs. However, conduction to the high lateral and upper portions of the left ventricle is slower and must proceed cell-to-cell due to the blocked left anterior fascicle. Therefore, the latter portion of the QRS depolarizes toward the upper lateral myocardium, manifested as strong left axis deviation. Left anterior fascicular block is the most common intraventricular conduction disturbance associated with acute anterior myocardial infarction, with the left anterior descending artery usually involved. ++ FIGURE 23.21B Small R waves, large S waves in all inferior leads (arrows), with QRS axis deviated left beyond minus 45 degrees. Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ LEFT POSTERIOR FASCICULAR BLOCK ++ FIGURE 23.22A Left Posterior Fascicular Block. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ QRS complex widening to 90 to 120 ms. Right axis deviation must be beyond 100 degrees and must have no other cause (such as lateral myocardial infarction). Small R wave and large S wave in the high lateral leads, I and aVL. Slurred S wave in V5 and V6. This example also contains unrelated ST changes. +++ Pearls ++ The signal exiting the AV node is carried rapidly to the upper aspect of the LV and all of the RV through the intact left anterior fascicle and right bundle, where depolarization is rapid. However, conduction to the inferior portion of the left ventricle is slower and must proceed cell-to-cell due to the blocked left posterior fascicle. Therefore, the latter portion of the QRS depolarizes toward the inferior myocardium, manifesting as strong right axis deviation. Left posterior fascicular block may be associated with acute inferior myocardial infarction as well as with multiple cardiomyopathic conditions. ++ FIGURE 23.22B Small R waves and large S waves in leads I and aVL (arrows). Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ TRIFASCICULAR BLOCK ++ FIGURE 23.23A Trifascicular Block. (ECG contributor: R. Jason Thurman, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ RBBB with left anterior or posterior hemiblock and first-degree AV block Somewhat of a misnomer, not a true blocking of three fascicles: two fascicles blocked coupled with PR interval prolongation LBBB plus first-degree AV block sometimes referred to as trifascicular block as well, but again only two fascicles truly blocked in this scenario +++ Pearls ++ Trifascicular block may be a precursor to complete heart block: Pacemaker evaluation is warranted, especially if symptomatic, but incidence of progression to complete heart block is low. AV blocking agents can potentiate degree of block. Can be due to systemic diseases (Chagas disease) but usually indicative of primary advanced conduction system abnormalities secondary to coronary artery disease. ++ FIGURE 23.23B The QRS is wide with RBBB pattern (blue double arrow). Left posterior fascicular block is present (diagonal arrows) along with a prolonged PR interval and first-degree AV block (black double arrow). Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ASHMAN PHENOMENON ++ FIGURE 23.24A Ashman Phenomenon. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ Aberrant ventricular conduction, usually with RBBB pattern. Altered durations of the refractory period of the bundle branch or ventricular tissue are present, commonly due to atrial fibrillation, atrial ectopy, and atrial tachycardia +++ Pearls ++ After depolarization, tissue repolarizes during its refractory period. Refractory period changes with the preceding cardiac cycle, with longer R-R intervals producing longer refractory periods and shorter R-R intervals producing shorter refractory periods. A longer R-R interval lengthens the following refractory period. When an early or premature (ectopic) depolarization reaches the ventricular conduction system before it has completely repolarized, aberrant conduction may occur and be manifest on the ECG with a bundle branch block (BBB) pattern. Ashman phenomenon most commonly appears with an RBBB pattern, since the right bundle has a longer refractory period than the left bundle. Ashman phenomenon is often seen in atrial fibrillation, when a long R-R interval is followed by a much shorter R-R interval. In the setting of a premature atrial beat (as seen in this example), the earlier in the cycle the PAC occurs and the longer the preceding R-R interval is, the more likely aberrant conduction of the beat will occur. ++ FIGURE 23.24B After a relatively long R-R interval (double arrow), a PAC (diagonal arrow) is followed by an aberrantly conducted QRS with RBBB morphology (arrowhead). After a short pause (single arrow), the next beat is conducted normally as it has occurred outside of the refractory period set by the previous beat. Graphic Jump LocationView Full Size||Download Slide (.ppt) + PART 3: RHYTHM DISTURBANCES Download Section PDF Listen +++ +++ JUNCTIONAL RHYTHM ++ FIGURE 23.25A Junctional Rhythm with Retrograde P Waves. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ The QRS complex is narrow, with a rate typically between 40 and 60 bpm. P waves are absent, retrograde, very slow, or unrelated to the QRS complex. +++ Pearls ++ When the atria fail to initiate a cardiac rhythm, or when no pacing signal reaches the lower AV node, the AV node or His bundle usually picks up the pacemaking responsibility. P waves may be conducted retrograde and buried in the T wave as seen in this example. In the case of a complete AV block, the P waves have no relation to the QRS complex. If a BBB is also present, the QRS may be wide, and may be difficult to discern from a primary ventricular rhythm. ++ FIGURE 23.25B The QRS is narrow. P waves are not present before the QRS. In this example, the signal which originated in the His bundle is conducted retrograde through the AV node into the atria, and retrograde P waves are apparent in the ST segment (arrows). Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ VENTRICULAR RHYTHM ++ FIGURE 23.26A Ventricular Rhythm with Retrograde P Waves. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ The QRS complex is wider than 120 ms, with a rate typically between 20 and 40 bpm. The T wave is discordant relative to the QRS. +++ Pearls ++ When the atria and the AV node fail to initiate a cardiac rhythm, or when no pacing signal reaches the ventricle, the ventricular tissue usually picks up the pacemaking responsibility. P waves may also be conducted retrograde and buried in the T wave as seen in this example. In the case of a complete AV block, the P waves have no relation to the QRS complex. ++ FIGURE 23.26B Wide-complex (double arrow) regular QRS at a rate of approximately 50 bpm. Retrograde P waves are seen in this example (arrow). Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ PACED RHYTHM ++ FIGURE 23.27A Dual-Chamber Pacemaker, Paced Rhythm. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ Very narrow signal of no discernable width, immediately followed by a P wave (if an atrial lead) or a QRS complex (if a ventricular lead). The narrow pacer “spike” amplitude varies, and can be larger than the QRS or may be indiscernible. A QRS complex initiated by a pacer spike will be wide, with morphology similar to a PVC or idioventricular rhythm. The axis is unlike typical BBBs, because the signal usually originates low in the right ventricle. +++ Pearls ++ Pacemakers are designated by the “five letter” system. In this system, the letter “A” denotes atrium, “V” denotes ventricle, “D” denotes dual (both chambers), and “O” denotes neither. The first three letters are the most commonly used: First letter—designates chamber(s) paced Second letter—designates chamber(s) sensed Third letter—designates pacemaker response to sensed electrical activity: T: triggered—fires even when beat sensed, I: inhibitory—holds when beat sensed, D: dual—atrial triggered and ventricle inhibited Fourth letter—extra options: P: programmable, M: multiprogrammable, C: communicating, R: rate adaptation, O: none Fifth letter—cardioverting options: P: pacing, S: shocking, D: dual (P+S), O: none The two most common pacemaker malfunctions are failure to pace and failure to sense. Some ECG machines perceive small pacer spikes as artifact and do not reproduce them on the printed tracing. ++ FIGURE 23.27B Tiny pacer spikes (arrows) precede the P waves, and somewhat larger pacer spikes precede the QRS complexes (arrowheads). The QRS complexes are wide, with discordant T waves. Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ATRIAL FIBRILLATION ++ FIGURE 23.28A Atrial Fibrillation. (ECG contributor: R. Jason Thurman, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ Electrical activity in the atria is chaotic. The ECG baseline, representing the ongoing chaotic atrial activity, is unorganized. The resulting “rumbling” baseline may have large or indiscernibly small amplitude. The AV node has a refractory period, and therefore does not conduct every signal it receives from the atria. Thus, ventricles depolarize variably creating varying R-R intervals and an “irregularly irregular” pattern. +++ Pearls ++ Most “irregularly irregular” rhythms are due to atrial fibrillation, but other rhythms may produce similar findings. These include multifocal atrial tachycardia, atrial flutter with variable AV block, and frequent PJCs. Therapy is geared toward either rate control of the ventricles or rhythm control and cardioversion (chemically or electrically). Synchronized cardioversion may be indicated if a patient is unstable, but the risk of clot embolization must be carefully considered when planning nonemergent electrical cardioversion of atrial fibrillation. ++ FIGURE 23.28B R-to-R interval varies in an “irregularly irregular” pattern (double arrows). The baseline “rumble,” representing “F waves,” may be very fine or even indiscernible. Graphic Jump LocationView Full Size||Download Slide (.ppt) ++ FIGURE 23.28C The baseline “rumble” may be very coarse resembling atrial flutter waves. Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ATRIAL FLUTTER ++ FIGURE 23.29A Atrial Flutter. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ Electrical activity in the atria is ongoing and regular, self-propagating in a roughly circular movement. Flutter waves appear in a rapid sine wave or “sawtooth” pattern, usually in the inferior leads. Atrial activity in lead V1 often appears as rapid P waves at a rate approximating 300 bpm. +++ Pearls ++ The AV node’s refractory period prevents 1:1 conduction to the ventricles. Usually, conduction is blocked at a ratio of 1:2 to 1:4. The QRS complexes should appear with regular periodicity. However, AV conduction may be variable from beat-to-beat creating irregular R-to-R intervals. A conduction ratio of 2:1 is usually difficult to discern, because the two flutter peaks between QRS complexes may look like normal P and T waves. A ventricular rate of 140 to 160 bpm should prompt consideration of the possibility of atrial flutter with 2:1 block. Conditions that cause rapid repetitive tremors (such as Parkinson disease, rigors, shivering, or hepatic tremor) may mimic flutter waves on EKG (known as pseudoflutter). ++ FIGURE 23.29B Atrial flutter with 4:1 block. The flutter waves (arrows marking every other flutter wave) may be mistaken for P and T waves. Graphic Jump LocationView Full Size||Download Slide (.ppt) ++ FIGURE 23.29C The “sawtooth” pattern is most apparent in the inferior leads. Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ MULTIFOCAL ATRIAL TACHYCARDIA ++ FIGURE 23.30A Multifocal Atrial Tachycardia. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ Multiple P-wave morphologies with heart rate greater than 100 bpm A chaotic R-R interval Varying PR intervals +++ Pearls ++ Multiple atrial foci are capable of acting as pacemakers. When irritated by stretching, medications, or certain acute medical conditions, these foci compete in pacing the atria. The different atrial foci produce P waves of different morphologies. Since the atrial foci vary in distance to the AV node, PR intervals vary. Multifocal atrial tachycardia (MAT) usually results from exacerbation of another condition which produces distention or irritation of the atria. The most common cause of MAT is COPD exacerbation. Treatment of the underlying condition should correct the arrhythmia. ++ FIGURE 23.30B Multiple P morphologies (arrowheads), varying PR intervals (lower double arrows), and varying R-R intervals (upper double arrows) with heart rate greater than 100 bpm. Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ SUPRAVENTRICULAR TACHYCARDIA (SVT) ++ FIGURE 23.31A Supraventricular Tachycardia (AVNRT). (ECG contributor: R. Jason Thurman, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ Tachycardia, rate usually greater than 140 bpm Narrow QRS complex Absent, retrograde, or unusual P waves +++ Pearls ++ SVT occurs when the SA node rhythm is superseded by a faster rhythm, usually originating in the AV node. Three common types are: Atrial tachycardia—originates from an ectopic focus in the atrium. P waves may have an unusual morphology or may be hidden by the preceding T wave. AV nodal reentrant tachycardia (AVNRT) occurs when an electrical impulse continues around the AV node in a circular pattern causing rapid depolarizations of the ventricles. Since the AV node is the origin of the atrial depolarization, the P-wave deflection should be inverted if seen (eg, downgoing in II, III, aVF). AV reentrant tachycardia (AVRT) as seen with bypass tracts outside of the AV node (WPW). Instead of intranodal reentrant activity as seen with AVNRT, an accessory tract provides the reentrant pathway to propagate the tachycardia. Normal deflections seen in the ST segments are relatively wide based. When you see “tight little turns” in the ST segment, you should strongly consider the presence of retrograde P waves. ++ FIGURE 23.31B A narrow-complex tachycardia, with no clear P waves preceding the QRS. R-R intervals are regular (double arrows), differentiating this from fine atrial fibrillation. This rhythm converted to a normal sinus rhythm after the administration of IV adenosine. Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ SVT WITH ABERRANCY ++ FIGURE 23.32A Supraventricular Tachycardia with Aberrant Conduction, Underlying RBBB. (ECG contributor: Walter Clair, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ Tachycardia (usually >140 bpm) with a wide QRS complex No “capture” or “fusion” beats or AV dissociation as seen with ventricular tachycardia QRS morphology consistent with one of the BBB patterns +++ Pearls ++ When a person with a chronic wide-complex (aberrant) BBB enters an SVT, the ECG will display a wide-complex tachycardia. The rapid rate of an SVT may “outrun” the ventricular conducting system’s ability to repolarize quickly, producing a rate-related BBB. The signal then must propagate cell-to-cell, producing a wide-complex tachycardia. A typical bundle branch pattern usually results. An irregularly irregular or chaotic R-R interval, even if subtle, strongly suggests atrial fibrillation or flutter as the culprit SVT. In contrast, the R-R interval of ventricular tachycardia is almost never chaotic. Ventricular rates of 140 to 160 bpm should prompt consideration of atrial flutter with a 2:1 block. ++ FIGURE 23.32B Wide-complex tachycardia with a rate of 188 bpm. This patient has sudden onset of SVT with a known underlying RBBB. QRS complexes are wide (lower double arrows) and R-R intervals are regular (upper double arrows). Graphic Jump LocationView Full Size||Download Slide (.ppt) ++ FIGURE 23.32C Wide-complex tachycardia at approximately 150 bpm. The R-R interval is regular, except for one pause, when characteristic atrial flutter waves are apparent (arrowhead). Graphic Jump LocationView Full Size||Download Slide (.ppt) ++ FIGURE 23.32D Irregularity in the R-R interval, as seen most easily in the baseline (double arrows), strongly suggests the presence of rapidly conducted atrial fibrillation with aberrancy. Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ VENTRICULAR TACHYCARDIA ++ FIGURE 23.33A Ventricular Tachycardia with Capture Beat. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ Tachycardia (usually >120 bpm) with a wide QRS complex. AV dissociation is present; P waves may appear periodically in the T wave or baseline. “Capture” beats may occur if atrial depolarization occurs prior to the intrinsic firing of the ventricle. “Fusion” beats may occur if atrial depolarization passes through the AV node at the same time as the intrinsic ventricle depolarization, producing a QRS that appears to be different or narrower than the other VT QRS complexes. +++ Pearls ++ Findings more suggestive of VT versus aberrant SVT or antidromic WPW: ++ Apparent AV dissociation, capture, or fusion beats. An unusual QRS axis, between 180 and 270 degrees. Precordial concordance, in which QRS complexes in the precordium are all upgoing or all downgoing. A completely upgoing QRS in V1. Predominately downgoing QRS in V4, V5, and V6. ++ FIGURE 23.33B A wide-complex tachycardia. AV dissociation is apparent, as P waves occasionally appear superimposed in the ST segment or just prior to the QRS (arrows). A capture beat occurs following a lapse in the VT (arrowhead). Graphic Jump LocationView Full Size||Download Slide (.ppt) ++ FIGURE 23.33C Another example of ventricular tachycardia, featuring a fusion beat (arrowhead). (ECG contributor: Marc Mickiewicz, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ VENTRICULAR FLUTTER ++ FIGURE 23.34A Ventricular Flutter. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ Tachycardia with a wide monomorphic QRS complex. Ventricular rate may be very rapid (300 bpm). Sine wave appearance with regular large oscillations. +++ Pearls ++ Imagine an atrial flutter sawtooth with much larger amplitude. When you see a very rapid wide-complex tachycardia (>240 bpm), consider ventricular flutter or WPW with atrial fibrillation or flutter. WPW with atrial flutter may be indistinguishable from ventricular flutter. Ventricular flutter is treated as ventricular tachycardia and usually leads to ventricular fibrillation if not promptly corrected with antiarrhythmic medications or electrical cardioversion. Patients with such a rapid rate are almost always unstable. Emergent cardioversion is indicated. If the patient appears to be stable enough for chemical cardioversion, choose a medication which is safe to use with WPW, such as procainamide or amiodarone. ++ FIGURE 23.34B Very rapid, regular, wide-complex tachycardia with sine-wave appearance. The rate in this example is 330 bpm. Differential diagnosis includes WPW with atrial flutter. Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ TORSADES DE POINTES ++ FIGURE 23.35A Torsades de Pointes. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ Wide-complex tachycardia with QRS polymorphism. QRS morphology changes gradually throughout the tracing, appearing to rotate around the baseline to the opposite direction. +++ Pearls ++ The cyclic rotation of the QRS complex gives rise to the term torsades de pointes (French meaning “twisting of the points”). Common precipitating factors are etiologies which prolong the QT interval, such as medications, electrolyte abnormalities (hypocalcemia, hypomagnesemia, hypokalemia), and hereditary disorders. Torsades can also occur in the setting of myocardial ischemia without prolongation of the QT interval. Torsades is treated as a ventricular tachycardia, usually requiring defibrillation. Magnesium is used as an adjunct therapy to normal ACLS protocols. ++ FIGURE 23.35B Very rapid wide-complex tachycardia with sine-wave appearance and fluctuations in the amplitude of the QRS complexes consistent with torsades de pointes. Graphic Jump LocationView Full Size||Download Slide (.ppt) + PART 4: STRUCTURAL ABNORMALITIES Download Section PDF Listen +++ ++ FIGURE 23.36A Dextrocardia. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ DEXTROCARDIA +++ ECG Findings ++ P, QRS, and T are downgoing in lead I, a mirror image of normal. QRS deflections in V4 to V6 are small and downgoing. +++ Pearls ++ The orientation of the heart in the chest cavity is reversed with the predominant electrical activity moving left to right (as opposed to right to left). Normally placed precordial leads in a patient with dextrocardia are actually placed over the thinner right ventricle instead of the left ventricle. Reversing all EKG leads should produce an essentially normal EKG. A “reversed” lead I (‘downward’ QRS) and aVR (‘upward’ QRS) with normal-appearing V leads strongly suggests accidental limb lead reversal. ++ FIGURE 23.36B The P wave, QRS, and T wave are downgoing in lead I. Differential diagnosis includes limb lead reversal and dextrocardia. The 12-lead ECG above represents dextrocardia as evidenced in the abnormal precordial leads. Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ LEFT VENTRICULAR HYPERTROPHY ++ FIGURE 23.37A Left Ventricular Hypertrophy with Strain Pattern. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ Large S waves in anterior precordial leads Large R waves in lateral precordial leads R wave in aVL + S wave in V3 greater than 28 mm in males, greater than 20 mm in females S wave in V1 + R wave in V5 or V6 greater than 35 mm if age over 40, greater than 40 mm if age 30 to 40, greater than 60 mm if age 16 to 30 R wave in aVL greater than 11 mm T waves deflected opposite to QRS complex (strain pattern) +++ Pearls ++ The muscular left ventricle normally dominates the QRS morphology. LVH can produce related changes such as left atrial abnormality. It may also produce ST-T wave changes, particularly in opposite deflections of the T wave with respect to the main deflection of the QRS complex. These ST deflections, often referred to as “LVH with strain,” may be confused with ischemia. LVH is often a sign of disease states such as systemic hypertension or aortic stenosis. LVH may manifest on the ECG in many different ways. Several different systems for diagnosing LVH by ECG have been promoted. No one system is adequately sensitive and specific enough to warrant exclusion of all others. ++ FIGURE 23.37B The QRS deflections are very large. The R wave in V5 plus the S wave in V1 total approximately 75 mm (arrows). ST downsloping to inverted T waves in V4 and V5 (arrowheads) may also be seen, a finding often referred to as “LVH with strain.” Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ RIGHT VENTRICULAR HYPERTROPHY ++ FIGURE 23.38A Right Ventricular Hypertrophy. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ S-wave amplitude increases in lateral leads (V5, V6, I, aVL). R-wave amplitude increases in aVR, V1, V2, and may exceed the S-wave amplitude (especially in lead V1). Right axis deviation (> +90 degrees). T-wave inversions in relation to QRS complex. +++ Pearls ++ Hypertrophy of the right ventricle causes characteristic EKG changes as the predominant electrical signal of the left ventricle is overcome. As right ventricular hypertrophy (RVH) persists, right atrial enlargement (RAE) may occur as seen in the example (P-wave amplitude in V1 >1.5 mm). Congenital heart disease, pulmonic or mitral stenosis, and pulmonary hypertension are common causes of RVH. ++ FIGURE 23.38B The R-wave amplitude exceeds the S-wave amplitude (arrows) in lead V1. In addition, the P-wave upward deflection exceeds 1.5 mm, indicating concomitant right atrial enlargement. Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ LEFT ATRIAL HYPERTROPHY ++ FIGURE 23.39A Left Atrial Hypertrophy with LVH Present. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ Increased duration (width) of the P wave without affecting its upward amplitude (as commonly seen with right atrial abnormalities) Negative P-wave deflection in lead V1, with width and depth greater than 0.04 seconds (one small box) Wide P wave in lead II Notched P wave in II, III, or aVF with duration greater than or equal to 0.12 seconds (also known as P-mitrale) +++ Pearls ++ Normal P-wave morphology has an amplitude of less than 2.5 mV (2.5 vertical boxes) and a duration (width) of less than 120 ms (three small boxes). The left atrium depolarizes after the right atrium and therefore has the most effect on the second portion of the P wave. Causes of left atrial abnormality or P-mitrale include valvular heart disease (mitral and aortic), CAD, cardiomyopathy, hypertension, and LVH. ++ FIGURE 23.39B The P wave in V1 is downgoing. The downgoing segment is wider and deeper than one small block (double arrows). Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ RIGHT ATRIAL HYPERTROPHY ++ FIGURE 23.40A Right Atrial Hypertrophy. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ Increased amplitude of P wave without affecting duration (as commonly seen with left atrial abnormalities) Peaked P waves (>2.5 mm) in leads II, III, aVF (also known as P pulmonale) P-waves upward deflection greater than 1.5 mm in lead V1 or V2 +++ Pearls ++ Normal P-wave morphology has amplitude of less than 2.5 mV (2.5 small vertical boxes) and duration (width) of less than 120 ms (three small boxes). The right atrium depolarizes before the left atrium and therefore has the most effect on the first portion of the P wave. RAE is often associated with RVH, COPD, some congenital heart diseases, and pulmonary hypertension, and may be seen transiently in pulmonary embolus. ++ FIGURE 23.40B The P wave in lead II (an inferior lead) is greater than 2.5 mm in amplitude (double arrow). Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ HYPERTROPHIC CARDIOMYOPATHY ++ FIGURE 23.41A Hypertrophic Cardiomyopathy with Underlying Atrial Flutter with 2:1 Block. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ High-voltage QRS suggesting LVH Left atrial abnormality Prominent Q waves, especially in the lateral precordial leads Deep S waves in anterior precordial leads Poor R-wave progression across precordium Lateral T-wave inversions +++ Pearls ++ The ventricular myocardium hypertrophies abnormally, either concentrically or focally. Left ventricle outflow obstruction from the hypertrophy may lead to LVH without dilation. Hypertrophic cardiomyopathy (HCM) is also known as idiopathic hypertrophic subaortic stenosis (IHSS), hypertrophic obstructive cardiomyopathy (HOCM), and muscular subaortic stenosis (MSS). ECG changes are variable and usually do not include all listed above. Always consider this condition in young athletes with syncope or unusual dyspnea. HCM is associated with a systolic ejection murmur that diminishes with increases in preload (having the patient squat) and augments with decreases in preload (Valsalva maneuver). ++ FIGURE 23.41B Deep S-wave voltage (28 mm S in V2, large arrow), and narrow Q waves in V5 and V6 (arrowheads). This patient also has atrial flutter with 2:1 block. The additional P waves appear in the ST segments (small arrows). Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ BRUGADA SYNDROME ++ FIGURE 23.42A Brugada Syndrome. (ECG contributor: Michael L. Juliano, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ Incomplete or complete RBBB pattern in leads V1, V2, and sometimes V3 ST elevation of at least 1 mV in leads V1, V2, and sometimes V3 followed by T inversion (convex pattern) or upright T (concave, or “saddle back” pattern) +++ Pearls ++ This syndrome was first described in individuals who experienced sudden cardiac death with structurally normal hearts, but congenitally abnormal ion channels in myocyte cell membranes have been associated with the disease. Concern for spontaneous ventricular dysrhythmia is high. Consultation with a cardiologist is recommended for electrophysiological testing and intracardiac defibrillator placement. ++ FIGURE 23.42B RBBB pattern with ST elevation (type 1 Brugada syndrome). Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ WOLFF-PARKINSON-WHITE SYNDROME ++ FIGURE 23.43A Wolff-Parkinson-White Syndrome. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ Normal P waves Shortened PR interval Prolonged QRS interval Delta waves (slurring of the initial upstroke of R wave) +++ Pearls ++ Accessory tracts from the atria to the ventricles lead to depolarization of ventricles without using the AV node as the primary connecting route. Tachycardia associated with WPW may be mistaken for ventricular tachycardia. Suspect WPW if the QRS complex is wide and tachycardia is extreme (ventricular rate > 240). Do not treat this tachycardia with AV nodal blocking agents (calcium channel blockers, β-blockers, digoxin). This may lead to unopposed ventricular stimulation through the accessory tract and may worsen the tachycardia. Procainamide, amiodarone, and cardioversion are accepted methods for conversion of a tachycardia associated with WPW. Depolarization via the accessory pathway may produce “pseudo-Q waves” as shown in leads III and aVF in this example. ++ FIGURE 23.43B The PR interval is shortened (double arrow) and a delta wave (upsloping initial QRS segment) is seen (arrow, shaded area). Graphic Jump LocationView Full Size||Download Slide (.ppt) + PART 5: ECG ABNORMALITIES OF NONCARDIAC ORIGIN Download Section PDF Listen +++ +++ HYPOTHERMIA ++ FIGURE 23.44A Hypothermia with Osborne Waves (“J” Waves) Present. (ECG contributor: Michael L. Juliano, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ Sinus bradycardia or atrial fibrillation with slow ventricular response. PR, QRS, and QT intervals are typically prolonged. Osborne or “J” wave (a positive deflection of the terminal portion of the QRS complex). The J wave may be subtle or large and “humped.” +++ Pearls ++ The hypothermic patient’s rhythm slows, proceeding from sinus bradycardia to atrial fibrillation with slow response and may proceed to other arrhythmias including ventricular fibrillation and asystole. The amplitude of the “J” wave corresponds to the degree of hypothermia. Myocardial damage and EKG changes associated with hypothermia are not necessarily due to low temperature. They may be indirectly caused by systemic circulatory issues such as hypoperfusion. Defibrillation and many medications may be ineffective in the hypothermic patient. Rapid rewarming is indicated as an initial and critical resuscitative measure. ++ FIGURE 23.44B A large Osborn wave (J wave) (arrow) follows the QRS, and is distinct from the T wave (arrowhead). Graphic Jump LocationView Full Size||Download Slide (.ppt) ++ FIGURE 23.44C This is a more typical appearance of a J wave (arrow). Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ HYPERKALEMIA ++ FIGURE 23.45A Hyperkalemia (K 7.1). (ECG contributor: R. Jason Thurman, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ Findings are variable but tend to correlate with increasing serum potassium levels following the order below: ++ Peaked T waves, tented with a narrow base (may be >10 mm high in precordial leads and/or >6 mm in limb leads) QT interval shortening QRS complex widening PR interval prolongation Decreased P-wave amplitude As potassium levels approach and exceed 8.0 mEQ/L: Indiscernible P waves Sine wave appearance of QRS-T complex Left or right bundle branch pattern Ventricular tachycardia, fibrillation, or asystole ++ FIGURE 23.45B Peaked T waves (arrow), widened QRS (double arrow), and subtle flattening of the P waves are seen in this patient with a serum K of 7.1. Graphic Jump LocationView Full Size||Download Slide (.ppt) ++ FIGURE 23.46A Severe Hyperkalemia (K 8.5). (ECG contributor: Ben Heavrin, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ Pearls ++ As the QRS complex widens, it appears more “blunted” than expected when compared with an LBBB. Acute treatment for hyperkalemia includes insulin and glucose, sodium bicarbonate, and β-agonists in an attempt to drive potassium into the cell. Intravenous calcium may be used to stabilize the myocardium but has no effect on serum potassium levels. These are temporizing measures which must be followed by definitive treatment of the underlying problem, which may include the need for dialysis. ++ FIGURE 23.46B Wide, blunted QRS with near sine-wave appearance. No P waves visible. Serum K was 8.5 in this patient. These abnormalities resolved with rapid treatment. Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ HYPOKALEMIA ++ FIGURE 23.47A Hypokalemia. (ECG contributor: R. Jason Thurman, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ Flattened or inverted T waves Prominent U waves ST segment depression Conduction disturbances +++ Pearls ++ Hypokalemia can produce varied ECG changes associated with the repolarization phase of the cardiac cycle. Unlike hyperkalemia, in hypokalemia there is no direct correlation with the potassium level and the severity of ECG changes. However, more ECG changes may become apparent as the potassium level falls. Suspect hypomagnesemia if the ECG does not normalize after potassium replacement. ++ FIGURE 23.47B This EKG demonstrates multiple findings consistent with hypokalemia: flattened T waves (blue arrowhead), U waves (black arrowhead), prolonged QT (QU) intervals (double arrow), and ST-segment depression (arrow). This patient’s potassium level was 1.9. Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ PULMONARY EMBOLISM ++ FIGURE 23.48A Sinus Tachycardia and S1Q3T3 Pattern in a Patient with Acute Pulmonary Embolism. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ Sinus tachycardia, nonspecific ST-T changes Precordial T-wave inversions Prominent S wave in lead I, Q wave in lead III, and inverted T wave in III (S1/Q3/T3) Incomplete or complete RBBB, P pulmonale (lead II) May see right axis deviation +++ Pearls ++ No EKG pattern is diagnostic for pulmonary embolism. Small-to-moderate emboli may not affect the EKG. With large emboli, increased resistance to pulmonary arterial flow produces right ventricle overload and dilation. Increased right atrial pressures may produce “P pulmonale” (tall P waves >2.5 mm in lead II) or atrial dysrhythmias. ++ FIGURE 23.48B S wave is apparent in lead I (blue arrowhead), Q wave in lead III (black arrowhead), and inverted T wave in lead III (blue arrow). Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ PERICARDIAL EFFUSION ++ FIGURE 23.49A Pericardial Effusion with Electrical Alternans. (ECG contributor: Kevin E. Zawacki, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ Sinus tachycardia Low voltage of QRS complex (QRS averaging <5 mm height in limb leads, or <10 mm height in precordial leads) Electrical alternans (beat-to-beat change in electrical axis and/or amplitude of the QRS complex) +++ Pearls ++ A physiologically significant pericardial effusion compresses the heart, and affects the ability of the heart to fill properly. This typically results in a reflex sinus tachycardia to maintain cardiac output. Pericardial effusion may be caused by pericarditis, malignancy, uremia, trauma, iatrogenic injury (CVL placement), aortic dissection with retrograde involvement of the pericardium, and free wall rupture after a myocardial infarction. Initial treatment of physiologically significant pericardial effusion is with intravenous fluid bolus to increase preload. Pericardiocentesis should be reserved for hemodynamically threatening effusions due to a high associated morbidity. Surgical pericardial window may be necessary, especially in malignant effusions. Electrical alternans is an uncommon finding. Pericardial effusion should be suspected in the setting of a sinus tachycardia and low voltage. ++ FIGURE 23.49B Low voltage, sinus tachycardia, electrical alternans (arrowheads) demonstrate beat-to-beat alternating QRS electrical axis and/or amplitude. Electrical alternans is often best seen in the anterior precordial leads V3 and V4. Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ DIGOXIN EFFECT, TOXICITY ++ FIGURE 23.50A Digoxin Effect with Evidence of Toxicity. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ ST segment shortening and depression leading to a “scooped” appearance. QT interval shortening. PR interval prolongation. Decreased T-wave amplitude. Premature ventricular complexes are the most common dysrhythmia. Bradydysrhythmias, various heart blocks, especially with findings consistent with increased automaticity (atrial tachycardia with block, atrial fibrillation with slow ventricular response, accelerated junctional rhythms). Bidirectional ventricular tachycardia may rarely be seen (see Fig. 17.72). +++ Pearls ++ ECG changes associated with digoxin can be seen from therapeutic or toxic levels. ST-segment changes may be exaggerated by myocardial disease or tachycardia. An acute overdose of a digoxin is usually associated with hyperkalemia which may increase the height of the T wave. Avoid calcium for treatment of hyperkalemia in the setting of digoxin toxicity as this may potentiate some adverse effects of digoxin. A digoxin overdose can lead to almost any dysrhythmia, but it commonly blocks the transmission of impulses through the AV node leading to bradycardic rhythms and accelerated escape rhythms. ++ FIGURE 23.50B The “sagging” appearance of the ST segment (arrow) is characteristic of digoxin therapy, and is not a sign of toxicity. However, this patient also has a sign of chronic digoxin toxicity. Atrial fibrillation is present, but the R-to-R interval has become regular. Digoxin toxicity has produced a total AV block but has also excited the AV node, producing a relatively accelerated junctional escape rate. Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ TRICYCLIC ANTIDEPRESSANT EFFECT ++ FIGURE 23.51A Tricyclic Antidepressant Toxicity. (ECG contributor: Saralyn R. Williams, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ Tachycardia QRS complex widening QT prolongation Prominent terminal R wave in aVR or V1 Prominent S in Lead I +++ Pearls ++ Tricyclic antidepressants (TCAs) produce their effects by several mechanisms. Anticholinergic effects may induce tachycardia and sodium channel blockage may lead to QRS widening. The QRS widening seen in a TCA overdose has a nonspecific pattern and is typically unlike any BBB morphology. ECG effects are rate-dependent and become more pronounced with tachycardia and acidosis. ++ FIGURE 23.51B Prominent S wave in lead I (arrowhead) with prominent terminal R wave in aVR (arrow). The QRS complex is wide (double arrow), the QT interval is prolonged, and the patient is tachycardic. Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ LIMB LEAD REVERSAL ++ FIGURE 23.52A Limb Lead Reversal. (ECG contributor: Michael L. Juliano, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings (dependent on which leads are reversed) ++ Reversal of the left arm (LA) and right arm (RA) most common P, QRS, and T predominantly downgoing in lead I P, QRS, T upgoing in lead aVR Precordial leads unaffected Reversal of the leg leads (left leg [LL] and right leg [RL]) Does not commonly produce EKG changes because RL is used as a grounding electrode Reversal of LA-LL Transposition of leads I and II and leads aVF and aVL with reversal of lead III Reversal of RA-RL Transposition of aVR and aVL and inversion of lead II Incorrect precordial lead placement Isolated reversal of the usual R-wave progression from V1 to V6 +++ Pearls ++ If the ECG seems to have an unusual axis or appearance, especially when compared with a prior ECG on the same patient, consider a lead misplacement and repeat the tracing, confirming correct lead positions. A “reversed” lead I with normal-appearing V leads strongly suggests accidental limb lead reversal as opposed to dextrocardia. Dextrocardia features a “reversed” lead I, while QRS deflections in V4 to V6 appear small and downgoing. ++ FIGURE 23.52B The P wave, QRS, and T wave are inverted in lead I in this EKG. Normal-appearing V leads in the 12-lead ECG above suggest limb lead reversal rather than dextrocardia. The arm leads were indeed reversed, and correction produced a normal-appearing tracing. Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ LOW VOLTAGE ++ FIGURE 23.53A Low-Voltage EKG. (ECG contributor: James V. Ritchie, MD.) Graphic Jump LocationView Full Size||Download Slide (.ppt) +++ ECG Findings ++ QRS amplitude of less than or equal to 5 mV in all limb leads or a sum of all limb lead QRS amplitude less than or equal to 30 mV and/or QRS amplitude less than or equal to 10 mV in all precordial leads +++ Pearls ++ Differential diagnosis includes normal variant, low standardization of the ECG machine, pericardial or pleural effusion, obesity/anasarca, COPD/emphysema, cardiac infiltrate (tumor, amyloid), myocardial infarction, myocarditis, cardiomyopathy, adrenal insufficiency, or hypothyroidism. Always check the calibration markings at the left of the ECG to check for low standardization of the ECG machine as an etiology for the observed tracing. ++ FIGURE 23.53B QRS height is less than 5 mm in limb leads in this normally calibrated tracing. Graphic Jump LocationView Full Size||Download Slide (.ppt)