Chapter 23: ECG ABNORMALITIES

ACUTE ANTERIOR MYOCARDIAL INFARCTION

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

1. The left anterior descending artery supplies blood to the anterior and lateral left ventricle and ventricular septum.

2. Normal R-wave progression (increasing upward amplitude with R wave > S wave at V₃ or V₄) may be interrupted.

3. 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.

ACUTE INFERIOR MYOCARDIAL INFARCTION

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

1. 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.

2. Infarctions involving the SA node may produce sinus dysrhythmias including tachycardias, bradycardias, and sinus arrest.

3. Infarctions involving the AV node may produce AV blocks.

4. 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.

5. 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.

ACUTE RIGHT VENTRICULAR MYOCARDIAL INFARCTION

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

1. 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.

2. 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.

3. Obtain a right-sided ECG in any patient with inferior or posterior MI, and in any patient with a significant hypotensive response to nitrates.

ACUTE POSTERIOR MYOCARDIAL INFARCTION

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

1. 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).

2. 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).

3. 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.

4. 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.

LEFT MAIN LESION

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

1. 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.

2. Normal R-wave progression (increasing R-wave amplitude across the precordial leads) may be interrupted.

3. Risk of cardiogenic shock is high since so much of the left ventricle is served by the left main coronary artery.

4. A left main coronary thrombosis is also known as the “widowmaker lesion.”

5. Isolated ST segment elevation in lead aVR may also indicate acute myocardial ischemia from left main coronary artery disease.

SGARBOSSA CRITERIA FOR AMI IN SETTING OF LBBB

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)

Pearls

1. 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.

2. Score of greater than or equal to 3 gives a specificity for myocardial infarction of 90%.

3. The first and third criteria listed above may also be used in ECGs with wide QRS complexes resulting from a pacemaker or idioventricular rhythm.

SUBENDOCARDIAL ISCHEMIA

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

1. 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.

2. ST elevation in other leads suggests that the depression may represent reciprocal changes from acute injury rather than subendocardial ischemia.

3. 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.

4. Isolated ST depression in leads V₁ and V₂ may represent posterior ischemia.

HYPERACUTE T WAVES

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

1. Hyperacute T waves occur very early (within minutes) during myocardial injury and are transient.

2. 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.

3. Serial ECGs are useful in distinguishing transient hyperacute T waves from other causes of tall, peaked T waves.

WELLENS WAVES

ECG Findings (Two Classic Types)

• Biphasic T waves in anterior and/or lateral leads

• Deeply inverted, symmetrical T waves in the same leads

Pearls

1. These characteristic patterns of T-wave changes are closely associated with critical left anterior descending artery stenosis.

2. The changes are classically apparent on ECG after resolution of chest pain.

3. These changes are transient, and often are not associated with cardiac enzyme elevations.

4. Wellens waves are not associated with changes in R-wave progression.

5. Serial electrocardiograms may assist in differentiating Wellens waves from stable, nonspecific findings.

“CEREBRAL” T WAVES

ECG Findings

• Inverted, wide T waves are most notable in precordial leads (can be seen in any lead).

• QT interval prolongation.

Pearls

1. These are associated with acute cerebral disease, most notably an ischemic cerebrovascular event or subarachnoid hemorrhage.

2. They may be accompanied by ST segment changes, U waves, and/or any rhythm abnormality.

3. Differential diagnosis includes extensive myocardial ischemia.

4. Strongly suspect an intracranial etiology in a patient with altered mental status and these electrocardiographic findings.

EARLY REPOLARIZATION

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

1. 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

2. 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.

LEFT VENTRICULAR ANEURYSM

ECG Findings

• ST elevation in anterior contiguous leads

• Deep pathologic Q waves in anterior leads

Pearls

1. ST segment elevation which occurs in the setting of a myocardial infarction should resolve within days under normal circumstances.

2. Persistent ST-segment elevation occurring for weeks or longer after a myocardial infarction is suspicious for ventricular aneurysm.

3. Ventricular aneurysms may follow a large myocardial infarction in the anterior portion of the heart.

4. 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.

5. 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.

PERICARDITIS

ECG Findings

• Diffuse ST elevation in noncontiguous leads

• PR depression

• T-wave flattening or inversion

• PR elevation in lead aVR

Pearls

1. Pericarditis may produce inflammation of the epicardium. This is most often demonstrated on the ECG as a widespread injury pattern.

2. 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.

3. Pericarditis may be focal, resulting in regional rather than diffuse EKG changes.

4. Benign early repolarization and myocarditis may also appear as ST elevation in many noncontiguous leads.

FIRST-DEGREE AV BLOCK

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

1. 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).

2. First-degree block may also be due to heart disease (myocarditis, rheumatic fever) or drugs (digoxin, amiodarone, β-blockers, calcium channel blockers).

TYPE 1 SECOND-DEGREE AV BLOCK (MOBITZ I, WENCKEBACH)

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

1. The number of P-QRS complexes prior to the “dropped” beat may vary.

2. A clue to the diagnosis of Mobitz type I heart block can be found in the appearance of grouped QRS complexes.

3. This type of block is normally asymptomatic, and may be seen in athletes.

4. 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).

TYPE 2 SECOND-DEGREE AV BLOCK (MOBITZ II)

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

1. This type of heart block is associated with disease of the conduction system distal to the AV node. A pacemaker is usually indicated.

2. Mobitz type II block can accompany myocardial infarction and has a high chance of progression to a complete heart block.

THIRD-DEGREE (COMPLETE) AV BLOCK

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

1. Third-degree block is also called complete heart block because no impulses are conducted from the atria to the ventricles.

2. AV rate and QRS morphology depend upon the location of the escape pacemaker.

3. A node escape rate is typically 40 to 60 bpm, with a narrow QRS complex.

4. Ventricular escape rate is usually 20 to 40 bpm, with a widened QRS complex.

5. Complete heart block may be caused by myocardial infarction, conduction system disease, or drugs such as digoxin.

6. Complete heart block may dramatically decrease cardiac output, cardiac pacing is often required.

QT INTERVAL PROLONGATION

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

1. 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.

2. 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).

3. Prolonged QT intervals may be congenital. The vast majority are acquired, usually due to medications or electrolyte abnormalities (hypokalemia, hypomagnesemia, hypocalcemia, and hyperphosphatemia).

4. Numerous medications may prolong the QT interval in therapeutic or toxic doses.

5. Prolongation of the QT interval predisposes to torsades de pointes.

6. Look carefully for prolonged QT intervals in patients who present with syncope.

RIGHT BUNDLE BRANCH BLOCK

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

1. 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.

2. Acute right heart strain, as may occur with pulmonary embolism, may result in new onset right bundle branch block (RBBB).

LEFT BUNDLE BRANCH BLOCK

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

1. 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.

2. 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).

LEFT ANTERIOR FASCICULAR BLOCK

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

1. 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.

2. 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.

LEFT POSTERIOR FASCICULAR BLOCK

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

1. 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.

2. Left posterior fascicular block may be associated with acute inferior myocardial infarction as well as with multiple cardiomyopathic conditions.

TRIFASCICULAR BLOCK

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

1. 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.

2. AV blocking agents can potentiate degree of block.

3. Can be due to systemic diseases (Chagas disease) but usually indicative of primary advanced conduction system abnormalities secondary to coronary artery disease.

ASHMAN PHENOMENON

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

1. 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.

2. 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.

3. Ashman phenomenon most commonly appears with an RBBB pattern, since the right bundle has a longer refractory period than the left bundle.

4. Ashman phenomenon is often seen in atrial fibrillation, when a long R-R interval is followed by a much shorter R-R interval.

5. 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.

JUNCTIONAL RHYTHM

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

1. 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.

2. 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.

3. If a BBB is also present, the QRS may be wide, and may be difficult to discern from a primary ventricular rhythm.

VENTRICULAR RHYTHM

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

1. 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.

2. 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.

PACED RHYTHM

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

1. 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:

   1. First letter—designates chamber(s) paced

   2. Second letter—designates chamber(s) sensed

   3. 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

   4. Fourth letter—extra options: P: programmable, M: multiprogrammable, C: communicating, R: rate adaptation, O: none

   5. Fifth letter—cardioverting options: P: pacing, S: shocking, D: dual (P+S), O: none

2. The two most common pacemaker malfunctions are failure to pace and failure to sense.

3. Some ECG machines perceive small pacer spikes as artifact and do not reproduce them on the printed tracing.

ATRIAL FIBRILLATION

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

1. 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.

2. Therapy is geared toward either rate control of the ventricles or rhythm control and cardioversion (chemically or electrically).

3. 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.

ATRIAL FLUTTER

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

1. 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.

2. 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.

3. Conditions that cause rapid repetitive tremors (such as Parkinson disease, rigors, shivering, or hepatic tremor) may mimic flutter waves on EKG (known as pseudoflutter).

MULTIFOCAL ATRIAL TACHYCARDIA

ECG Findings

• Multiple P-wave morphologies with heart rate greater than 100 bpm

• A chaotic R-R interval

• Varying PR intervals

Pearls

1. 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.

2. The different atrial foci produce P waves of different morphologies.

3. Since the atrial foci vary in distance to the AV node, PR intervals vary.

4. 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.

SUPRAVENTRICULAR TACHYCARDIA (SVT)

ECG Findings

• Tachycardia, rate usually greater than 140 bpm

• Narrow QRS complex

• Absent, retrograde, or unusual P waves

Pearls

1. SVT occurs when the SA node rhythm is superseded by a faster rhythm, usually originating in the AV node.

2. Three common types are:

   1. 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.

   2. 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).

   3. 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.

3. 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.

SVT WITH ABERRANCY

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

1. When a person with a chronic wide-complex (aberrant) BBB enters an SVT, the ECG will display a wide-complex tachycardia.

2. 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.

3. 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.

4. Ventricular rates of 140 to 160 bpm should prompt consideration of atrial flutter with a 2:1 block.

VENTRICULAR TACHYCARDIA

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:

1. Apparent AV dissociation, capture, or fusion beats.

2. An unusual QRS axis, between 180 and 270 degrees.

3. Precordial concordance, in which QRS complexes in the precordium are all upgoing or all downgoing.

4. A completely upgoing QRS in V₁.

5. Predominately downgoing QRS in V₄, V₅, and V₆.

VENTRICULAR FLUTTER

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

1. Imagine an atrial flutter sawtooth with much larger amplitude.

2. When you see a very rapid wide-complex tachycardia (>240 bpm), consider ventricular flutter or WPW with atrial fibrillation or flutter.

3. WPW with atrial flutter may be indistinguishable from ventricular flutter.

4. Ventricular flutter is treated as ventricular tachycardia and usually leads to ventricular fibrillation if not promptly corrected with antiarrhythmic medications or electrical cardioversion.

5. 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.

TORSADES DE POINTES

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

1. The cyclic rotation of the QRS complex gives rise to the term torsades de pointes (French meaning “twisting of the points”).

2. Common precipitating factors are etiologies which prolong the QT interval, such as medications, electrolyte abnormalities (hypocalcemia, hypomagnesemia, hypokalemia), and hereditary disorders.

3. Torsades can also occur in the setting of myocardial ischemia without prolongation of the QT interval.

4. Torsades is treated as a ventricular tachycardia, usually requiring defibrillation. Magnesium is used as an adjunct therapy to normal ACLS protocols.

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

1. 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).

2. Normally placed precordial leads in a patient with dextrocardia are actually placed over the thinner right ventricle instead of the left ventricle.

3. Reversing all EKG leads should produce an essentially normal EKG.

4. A “reversed” lead I (‘downward’ QRS) and aVR (‘upward’ QRS) with normal-appearing V leads strongly suggests accidental limb lead reversal.

LEFT VENTRICULAR HYPERTROPHY

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

1. The muscular left ventricle normally dominates the QRS morphology.

2. 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.

3. LVH is often a sign of disease states such as systemic hypertension or aortic stenosis.

4. 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.

RIGHT VENTRICULAR HYPERTROPHY

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

1. Hypertrophy of the right ventricle causes characteristic EKG changes as the predominant electrical signal of the left ventricle is overcome.

2. 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).

3. Congenital heart disease, pulmonic or mitral stenosis, and pulmonary hypertension are common causes of RVH.

LEFT ATRIAL HYPERTROPHY

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

1. 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).

2. The left atrium depolarizes after the right atrium and therefore has the most effect on the second portion of the P wave.

3. Causes of left atrial abnormality or P-mitrale include valvular heart disease (mitral and aortic), CAD, cardiomyopathy, hypertension, and LVH.

RIGHT ATRIAL HYPERTROPHY

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

1. 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).

2. The right atrium depolarizes before the left atrium and therefore has the most effect on the first portion of the P wave.

3. RAE is often associated with RVH, COPD, some congenital heart diseases, and pulmonary hypertension, and may be seen transiently in pulmonary embolus.

HYPERTROPHIC CARDIOMYOPATHY

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

1. The ventricular myocardium hypertrophies abnormally, either concentrically or focally. Left ventricle outflow obstruction from the hypertrophy may lead to LVH without dilation.

2. Hypertrophic cardiomyopathy (HCM) is also known as idiopathic hypertrophic subaortic stenosis (IHSS), hypertrophic obstructive cardiomyopathy (HOCM), and muscular subaortic stenosis (MSS).

3. ECG changes are variable and usually do not include all listed above.

4. Always consider this condition in young athletes with syncope or unusual dyspnea.

5. 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).

BRUGADA SYNDROME

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

1. 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.

2. Concern for spontaneous ventricular dysrhythmia is high.

3. Consultation with a cardiologist is recommended for electrophysiological testing and intracardiac defibrillator placement.

WOLFF-PARKINSON-WHITE SYNDROME

ECG Findings

• Normal P waves

• Shortened PR interval

• Prolonged QRS interval

• Delta waves (slurring of the initial upstroke of R wave)

Pearls

1. Accessory tracts from the atria to the ventricles lead to depolarization of ventricles without using the AV node as the primary connecting route.

2. 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).

3. 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.

4. Procainamide, amiodarone, and cardioversion are accepted methods for conversion of a tachycardia associated with WPW.

5. Depolarization via the accessory pathway may produce “pseudo-Q waves” as shown in leads III and aVF in this example.

HYPOTHERMIA

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

1. 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.

2. The amplitude of the “J” wave corresponds to the degree of hypothermia.

3. 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.

4. Defibrillation and many medications may be ineffective in the hypothermic patient. Rapid rewarming is indicated as an initial and critical resuscitative measure.

HYPERKALEMIA

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

Pearls

1. As the QRS complex widens, it appears more “blunted” than expected when compared with an LBBB.

2. 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.

HYPOKALEMIA

ECG Findings

• Flattened or inverted T waves

• Prominent U waves

• ST segment depression

• Conduction disturbances

Pearls

1. Hypokalemia can produce varied ECG changes associated with the repolarization phase of the cardiac cycle.

2. 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.

3. Suspect hypomagnesemia if the ECG does not normalize after potassium replacement.

PULMONARY EMBOLISM

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

1. No EKG pattern is diagnostic for pulmonary embolism. Small-to-moderate emboli may not affect the EKG.

2. With large emboli, increased resistance to pulmonary arterial flow produces right ventricle overload and dilation.

3. Increased right atrial pressures may produce “P pulmonale” (tall P waves >2.5 mm in lead II) or atrial dysrhythmias.

PERICARDIAL EFFUSION

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

1. 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.

2. 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.

3. 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.

4. Electrical alternans is an uncommon finding. Pericardial effusion should be suspected in the setting of a sinus tachycardia and low voltage.

DIGOXIN EFFECT, TOXICITY

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

1. ECG changes associated with digoxin can be seen from therapeutic or toxic levels.

2. ST-segment changes may be exaggerated by myocardial disease or tachycardia.

3. An acute overdose of a digoxin is usually associated with hyperkalemia which may increase the height of the T wave.

4. Avoid calcium for treatment of hyperkalemia in the setting of digoxin toxicity as this may potentiate some adverse effects of digoxin.

5. 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.

TRICYCLIC ANTIDEPRESSANT EFFECT

ECG Findings

• Tachycardia

• QRS complex widening

• QT prolongation

• Prominent terminal R wave in aVR or V₁

• Prominent S in Lead I

Pearls

1. Tricyclic antidepressants (TCAs) produce their effects by several mechanisms. Anticholinergic effects may induce tachycardia and sodium channel blockage may lead to QRS widening.

2. The QRS widening seen in a TCA overdose has a nonspecific pattern and is typically unlike any BBB morphology.

3. ECG effects are rate-dependent and become more pronounced with tachycardia and acidosis.

LIMB LEAD REVERSAL

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

1. 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.

2. 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.

LOW VOLTAGE

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

1. 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.

2. 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.