Sinus Rhythm

The sinus node is the primary pacemaker for the heart. Because the sinus node is located at the junction of the superior vena cava and the right atrium, in sinus rhythm the atria are activated from “right to left” and “high to low.” The P wave in sinus rhythm is upright in lead II and inverted in lead aVR. In lead V_I, the P wave is usually biphasic with a small initial positive deflection due to right atrial activation and a terminal negative deflection due to left atrial activation.

The normal sinus rate is usually between 60 and 100 bpm but can vary significantly. During sleep, when parasympathetic tone is high, sinus bradycardia (sinus rates <60 bpm) is a normal finding, and during conditions associated with increased sympathetic tone (exercise, stress), sinus tachycardia (sinus rates >100 bpm) is common. In children and young adults, sinus arrhythmia (sinus rates that vary by more than 10% during 10 seconds) due to respiration is frequently observed.

Ectopic Atrial Rhythm

In some situations, the atria are activated by an ectopic atrial focus rather than the sinus node. In this case, the P wave will have an abnormal shape depending on where the ectopic focus is located. For example, if the focus arises from the left atrium, the P wave is inverted in leads I and aVL. If the depolarization rate of the ectopic focus is between 60 and 100 bpm, the patient has an ectopic atrial rhythm. If the rate is <60 bpm, the rhythm is defined as an ectopic atrial bradycardia.

Atrial Flutter With 4:1 Atrioventricular Conduction

In atrial flutter, the atria are activated rapidly (usually 300 bpm) owing to a stable reentrant circuit. Most commonly, the reentrant circuit rotates counterclockwise around the tricuspid valve. Because the left atrium and interatrial septum are activated low-to-high, “sawtooth” flutter waves that are inverted in the inferior leads (II, III, and aVF) are usually observed. If every fourth atrial beat is conducted to the ventricles (owing to slow conduction in the atrioventricular [AV] node), a relatively normal ventricular rate of 75 bpm is observed.

Accelerated Junctional Rhythm

Premature QRS Activity

It is common to have isolated premature QRS activity that leads to mild irregularity of the heart rhythm. A premature narrow QRS complex is most often due to a normally conducted premature atrial complex (PAC) or more rarely a premature junctional complex (PJC). A premature wide QRS complex is usually due to a premature ventricular complex (PVC) or to a premature supraventricular complex (PAC or PJC) that conducts to the ventricle with aberrant conduction due to block in one of the bundle branches. Premature supraventricular complexes (with or without aberrant conduction) are commonly observed phenomena that are not associated with cardiac disease. Although PVCs are observed in normal individuals, they are usually associated with higher risk in patients with cardiac disease.

Narrow QRS Tachycardia with a Regular Rhythm: Regular SVT

1. Sinus Tachycardia: Under many physiologic conditions, the sinus node discharges at a rate >100 bpm (Figure 7–2). In sinus tachycardia, an upright P wave can be observed in II and aVF and an inverted P wave is observed in aVR. The PR interval is usually relatively normal, because conditions associated with sinus tachycardia (most commonly sympathetic activation) also cause more rapid AV conduction.
2. Atrial Tachycardia: Rarely, a single atrial site other than the sinus node fires rapidly. This leads to an abnormally shaped P wave. The specific shape of the P wave depends on the specific site of atrial tachycardia. The PR interval depends on how quickly atrioventricular conduction occurs. As the atrial tachycardia rate increases, the AV node conduction slows (decremental conduction) and the PR interval increases; decremental conduction properties of the AV node prevent rapid ventricular rates in the presence of rapid atrial rates.
3. Atrial Flutter: The mechanism for atrial flutter is described above. Most commonly atrioventricular conduction occurs with every other flutter wave (2:1 conduction), leading to a heart rate of approximately 150 bpm. In some situations, very rapid ventricular rates can be observed due to 1:1 conduction, or slower rates observed due to 3:1 conduction.
4. Junctional Tachycardia: The most common type of tachycardia to arise from tissue near the atrioventricular junction is AV nodal reentrant tachycardia (AVNRT). In AVNRT, two separate parallel pathways of conduction are present within junctional and perijunctional tissue. Usually, one of the pathways has relatively rapid conduction properties but a long refractory period (“fast pathway”), and the other has slow conduction and a short refractory period (“slow pathway”). In some cases, a premature atrial contraction can block one of the pathways (usually the fast pathway), conduct down the slow pathway, and activate the fast pathway retrogradely, initiating a reentrant circuit. In rare circumstances, a site within the AV node fires rapidly as a result of increased automaticity. Regardless of the mechanism, because the tachycardia originates within the AV junction, the atria and ventricles are activated simultaneously. Most commonly (in approximately 50% of cases), the P wave is buried in the QRS complex and is not seen. In approximately 40% of cases, the retrograde P wave is observed in the terminal portion of the QRS complex. The easiest place to see the retrograde P wave is in lead V₁, where a low-amplitude terminal positive deflection (pseudo-R′ wave) is seen (Figure 7–2). In addition, a terminal negative deflection (pseudo-S wave) is seen in the inferior leads (II, III, and aVF). Finally, in about 10% of cases, the P wave is observed in the initial portion of the QRS complex. The location of the P wave depends on the relative speeds of retrograde activation of the atria and anterograde activation of the ventricles via the His-Purkinje system.
5. Accessory Pathway–Mediated Tachycardia: Usually, the AV node and His bundle provide the only path for AV conduction. In approximately 1 in 1000 individuals, an additional AV connection called an accessory pathway is present. The presence of two parallel pathways (the accessory pathway and the AV node-His bundle) for AV conduction increases the likelihood that reentrant tachycardia will occur. The most common tachycardia is a reentrant narrow QRS tachycardia in which the ventricles are activated via the His-Purkinje system and the atria are activated via retrograde activation from the accessory pathway (Figure 7–3). This type of tachycardia is frequently called orthodromic atrioventricular reentrant tachycardia (AVRT) because conduction through the AV node and His-Purkinje fibers occurs normally ( ortho is Greek for straight or normal). Orthodromic AVRT is one cause of SVT; the QRS complexes are narrow and normal-appearing because the ventricles are activated via the AV node and His-Purkinje system, ventricular tissue, an accessory pathway, and atrial tissue. Because the ventricles and atria are activated sequentially, the P wave is most often observed within the ST segment (Figure 7–2). As discussed later, accessory pathways can also be associated with regular and irregular wide complex tachycardias.

Figure 7–2. ECG appearance of different forms of regular SVTs. Arrows show the first four atrial deflections in each SVT. In sinus tachycardia, the P wave has a normal morphology, and the PR interval is normal. In atrial tachycardia, the P wave is abnormal (positive in V₁, and the PR interval is prolonged because of decremental conduction in the AV node). In atrial flutter , inverted “saw-tooth” waves are observed in lead III. In AVNRT, a pseudo-R wave due to retrograde atrial activation is observed in lead V₁. In AVRT , a retrograde P wave is observed in the ST segment because the atria and ventricles are activated sequentially. The P wave is usually located relatively close to the preceding QRS complex because the accessory pathway conducts rapidly.

Figure 7–3. Initiation of SVT in a patient with an accessory pathway. During sinus rhythm, the ventricles are activated via the accessory pathway and the AV node-His bundle. Because the accessory pathway conducts rapidly and inserts into regular ventricular myocardium, the PR interval is short and a delta wave is observed ( large arrows ). A premature atrial complex (PAC) blocks in the accessory pathway and travels only down the AV node-His bundle, leading to a narrow QRS complex. The atria are activated retrogradely by the accessory pathway ( small arrows ), and orthodromic AVRT is initiated. (Adapted with permission from Kusumoto FM: Cardiovascular disorders: Heart disease. In: Pathophysiology of Disease: An Introduction to Clinical Medicine, 7th ed. Hammer G, McPhee SJ [editors], McGraw-Hill, 2014.)

Narrow QRS Tachycardias with an Irregular Rhythm: Irregular SVT

1. Atrial Fibrillation: Atrial fibrillation is the most common abnormal fast heart rhythm observed (Figure 7–4). Atrial fibrillation is most commonly due to multiple chaotic wandering wavelets of reentry that cause irregular activation of the atria. Because the AV node is also activated irregularly, AV conduction is variable and an irregular ventricular rhythm is observed. In atrial fibrillation, the rhythm is often called “irregularly irregular” because there is no organized atrial activity. On the ECG, continuous fibrillatory low-amplitude waves with varying morphology are observed with no easily identifiable isoelectric period. The fibrillatory waves are usually best seen in leads V₁, V₂, II, III, and aVF.
2. Multifocal Atrial Tachycardia: In multifocal atrial tachycardia (often called MAT), several atrial sites beat due to abnormal automaticity. This leads to P waves of three or more different morphologies. The rhythm is usually irregular; the different sites fire at different rates. MAT can be distinguished from atrial fibrillation by discrete P waves and isoelectric periods between the T wave and the P wave. The most common cause of MAT is chronic obstructive pulmonary disease (approximately 60% of cases).
3. Atrial Flutter With Variable Block: Atrial flutter can sometimes present as an irregular rhythm because of variable AV block. In this case, although the ventricular rhythm is irregular, there are often relatively constant intervals between the QRS complexes. For example, if the atrial flutter rate is 300 bpm, the possible ventricular rates will be 300 bpm, 150 bpm, 100 bpm, or 75 bpm for 1:1, 2:1, 3:1, and 4:1 AV conduction, respectively.

Figure 7–4. ECG appearance of atrial fibrillation and multifocal atrial tachycardia (MAT). In atrial fibrillation, continuous chaotic activation of the atria results in continuous low-amplitude fibrillatory waves. In MAT, discrete P waves ( arrows ) and an isoelectric T–P segment are observed.

Wide QRS Complex Tachycardia With a Regular Rhythm

The most common cause of wide QRS complex tachycardia with a regular rhythm (WCT-RR) is sinus tachycardia with either right bundle branch block (RBBB) or left bundle branch block (LBBB). However, if a patient with structural heart disease presents with WCT-RR, one assumes a worst-case scenario and the presumptive diagnosis becomes ventricular tachycardia (VT). Most commonly, VT originates from a rapid reentrant circuit located at the border of infarcted and normal myocardium. Because the ventricles are not activated via the bundle branches or the Purkinje system, an abnormally wide QRS complex is observed. Any atrial or junctional tachycardias associated with aberrant conduction can also cause a WCT-RR. Finally, in very rare circumstances, patients with accessory pathways present with antidromic AVRT in which the ventricles are activated via the accessory pathway (leading to a wide and bizarre QRS complex) and the atria are activated retrogradely via the His bundle-AV node ( anti is Greek for against).

The ECG differentiation between regular SVTs with aberrant conduction (sinus tachycardia, atrial tachycardia, atrial flutter, junctional tachycardia, orthodromic AVRT) and VT can sometimes be difficult. Accurate diagnosis of VT is critical because this rhythm is frequently life-threatening. The two principal techniques for identifying VT are the presence of AV dissociation and abnormal QRS morphology.

1. Atrioventricular Dissociation: In AV dissociation, the atria and ventricles are not related in one-to-one fashion. AV dissociation can be due to several conditions:
   1. Atrioventricular conduction block.
   2. Slowing of the primary pacemaker, most commonly due to sinus bradycardia or sinus pauses with junctional escape rhythm.
   3. Acceleration of a subsidiary pacemaker, most commonly due to VT or much less commonly due to junctional tachycardia.

The most important reason to identify AV dissociation is in wide complex tachycardia for the differentiation of SVT with aberrancy from VT. In VT, the rapid ventricular rate is often associated with retrograde block within the His-Purkinje system (ventriculoatrial block). This leads to P waves (from sinus node depolarization) that are not associated in 1:1 fashion with the QRS complexes (Figure 7–5). The presence of AV dissociation makes VT the most likely diagnosis in a patient with a regular wide complex tachycardia. In some circumstances, AV dissociation can be identified by the presence of capture beats or fusion beats. Occasionally, a properly timed P wave conducts to the ventricles and a portion (fusion beat) or all (capture beat) of ventricular tissue is activated by the His-Purkinje tissue for one QRS complex. It is always easier to identify AV dissociation rather than AV association; T waves can often be confused with P waves. Always examine the entire ECG for unexpected deflections in the QRS complex, ST segment, and T waves that are dissociated P waves. The P waves are usually most obvious in the inferior leads (II, III, and aVF) or V₁.

Figure 7–5. Lead II from a wide complex tachycardia. The arrows mark P waves that are not associated with every QRS complex (AV dissociation). The QRS complexes marked with an (*) are slightly narrower owing to partial activation from the preceding P wave (fusion complex).

Step One

Determine the morphologic classification of the wide QRS complexes (RB type or LB type), using the criteria below.

1. Determination of the Morphologic Type of Wide QRS Complexes: Use lead V₁ only to determine the type of bundle branch block morphology of abnormally wide QRS complexes.
   1. RBBB- and RBB-type QRS complexes as seen in lead V₁: A wide QRS complex with a net positive area under the QRS curve is called the right bundle branch “type” of QRS. This does not mean that the QRS conforms exactly to the morphologic criteria for RBBB. Typical morphologies seen in RBBB are shown in the box at left below. Atypical morphologies at the right are most commonly seen in PVCs or during VT.
      
   2. LBBB- and LBB-type QRS complexes as seen in lead V ₁ : A wide QRS complex with a net negative area under the QRS curve is called a left bundle branch “type” of QRS. This does not mean that the QRS conforms exactly to the morphologic criteria for LBBB. Typical morphologies of LBBB are shown in the box at left below. Atypical morphologies at the right are most commonly seen in PVCs or during VT.
      

Step Two

Apply criteria for common and uncommon normal forms of either RBBB or LBBB, as described below. The waveforms may not be identical, but the morphologic descriptions must match. If the QRS complexes do not match, the rhythm is probably VT.

1. RBBB: Lead I must have a terminal broad S wave, but the R/S ratio may be <1.
   
   In lead V₁, the QRS complex is usually triphasic but sometimes is notched and monophasic. The latter must have notching on the ascending limb of the R wave, usually at the lower left.
   
2. LBBB: Lead I must have a monophasic, usually notched R wave and may not have Q waves or S waves.
   
   Both lead V₁ and lead V₂ must have a dominant S wave, usually with a small, narrow R wave. S descent must be rapid and smooth, without notching.
   

Step One

Determine the morphologic classification of the wide QRS complexes (RB type or LB type), using the criteria above.

Step Two

Apply criteria for normal forms of either RBBB or LBBB, as described below. A negative answer to any of the three questions is inconsistent with either RBBB or LBBB, and the diagnosis defaults to VT.

1. For QRS Complexes With RBBB Categorization:
   1. Is there an rSR′ morphology in lead V₁?
      
   2. Is there an RS complex in V₆ (may have a small septal Q wave)?
      
   3. Is the R/S ratio in lead V₆ > 1?
2. For QRS Complexes With LBBB Categorization:
   1. Is there an rS or QS complex in leads V₁ and V₂?
      
   2. Is the onset of the QRS to the nadir of the S wave in lead V₁ < 70 ms?
   3. Is there an R wave in lead V₆, without a Q wave?
      

Wide QRS Tachycardia with an Irregular Rhythm

1. Polymorphic Ventricular Tachycardia and Ventricular Fibrillation : In polymorphic ventricular tachycardia and ventricular fibrillation, the ventricles are often activated continuously in chaotic fashion by disorganized wavelets of activation that produce irregular QRS complexes with no isoelectric periods. Both ventricular fibrillation and polymorphic ventricular tachycardia are life-threatening conditions that require prompt defibrillation. The distinction between ventricular fibrillation and polymorphic ventricular tachycardia is simply based on the amplitude of the QRS complexes and has very little clinical utility. The most common cause of polymorphic ventricular tachycardia and ventricular fibrillation is myocardial ischemia due to coronary artery occlusion.
2. Torsade de Pointes: Torsade de pointes (“twisting of the points”) is a specific form of polymorphic VT that is often pause dependent, has a characteristic shifting morphology of the QRS complex, and occurs in the setting of a prolonged QT interval. Torsade de pointes is associated with drug-induced states, congenital long QT syndrome, and hypokalemia.
3. Atrial Fibrillation with Anterograde Accessory Pathway Activation: If a patient with an accessory pathway develops atrial fibrillation, the ventricles are activated by both the normal AV node-His bundle axis and the accessory pathway. Because the accessory pathway does not have decremental conduction properties, it allows very rapid activation of the ventricles. The combination of an irregular wide complex rhythm with very rapid rates (250–300 bpm) should arouse suspicion of this scenario, particularly in a young, otherwise healthy patient.
4. Bradycardia, or slow heart rates, can be due to failure of impulse formation (sinus node dysfunction) or blocked AV conduction.

Sinus Node Dysfunction

Sinus node dysfunction is manifested in a number of ECG findings. Most commonly, there is a sinus pause with a junctional escape beat. Alternatively, sinus bradycardia can be associated with sinus node dysfunction.

1. Sinus Bradycardia: The normal range of sinus rates changes with age. In infants less than 12 months old, the mean heart rate is 140 bpm with a range of 100–190 bpm. In contrast, the normal range for adults is probably 50–90 bpm. Sinus rates less than 60 bpm are classified as sinus bradycardia, but it must be remembered that sinus rates of less than 60 bpm are commonly observed (sleep, athletes). Treatment of sinus bradycardia (usually with a pacemaker) is indicated only when it is associated with symptoms, not because of a specific heart rate.
2. Sinus Pauses: In some individuals, the sinus node abruptly stops firing, leading to sinus pauses. Usually an escape rhythm from an ectopic atrial focus or the junction prevents asystole. Sinus pauses up to 2 seconds are seen in normal adults. Patients with sinus pauses >3 seconds should be evaluated for the presence of sinus node dysfunction.
3. Junctional Rhythm: If the sinus node rate is very low, sustained junctional rhythm can sometimes be observed. In junctional rhythm, the QRS is not preceded by a P wave. A retrograde P wave can sometimes be seen in the initial portion or terminal portion of the QRS complex, but most commonly it is “buried” in the QRS complex. Normally, junctional rhythms are <60 bpm. Transient junctional rhythm can be observed in normal individuals during sleep, but sinus node dysfunction should be suspected if junctional rhythm is observed when a patient is awake.

In rare circumstances, accelerated junctional rhythms between 60 and 100 bpm are observed due to more rapid depolarization of AV nodal cells. If the junctional rate is faster than the sinus rate, the sinus node will be suppressed by retrograde atrial activation because of repetitive depolarization from the junction. Accelerated junctional rhythms can be present in digitalis toxicity, rheumatic fever, and after cardiac surgery.

AV Block

Because AV conduction normally occurs along a single axis, the AV node and His bundle, atrioventricular (AV) block most commonly is due to block at one of these two sites. Block within the His bundle is associated with a worse prognosis and should be suspected in any form of AV block associated with a wide QRS complex. Electrocardiographically, AV block is usually described as first-degree, second-degree, or third-degree AV block. In first-degree (1°) AV block, every P wave is conducted to the ventricles, but there is an abnormal delay between atrial activation and ventricular activation (PR interval >0.2 second). In 1° AV block, the ventricular rate is not slow unless sinus bradycardia is also present.

In second-degree (2°) AV block, some but not all P waves are conducted to the ventricles. This leads to an irregular ventricular rhythm. Second-degree AV block is usually subclassified as Mobitz type I block, Wenckebach block or Mobitz type II block. In type I 2° AV block, progressive prolongation of the PR interval is observed; in type II 2° AV block, the PR interval remains relatively constant before the blocked P wave. The importance of this distinction is this: type I 2° AV block usually indicates that conduction is blocked within the AV node, whereas type II AV block suggests that conduction is blocked within the His bundle (regardless of the width of the QRS complex). The simplest way to differentiate between type I and type II 2° AV block is to compare the PR intervals before and after the blocked P wave. In type I 2° AV block, the PR interval after the blocked P wave is shorter than the PR interval before the blocked P wave; in type II 2° AV block, the PR intervals are the same.

In third-degree (3°) or complete AV block, no P waves are conducted to the ventricles. The P-to-P and QRS-to-QRS intervals are constant and unrelated (AV dissociation). The QRS rate and morphology depend on the site of the subsidiary intrinsic pacemaker. If the block is within the AV node, a lower AV nodal pacemaker often takes over and the rate is 40–50 bpm with a normal-appearing QRS complex (junctional rhythm). If the block is within the His bundle, a ventricular pacemaker with a rate of 20–40 bpm and a wide QRS will be noted (ventricular escape rhythm).

Right Atrial Enlargement (RAE)

Diagnostic criteria include a positive component of the P wave in lead V₁ or V₂ ≥1.5 mm. Another criterion is a P-wave amplitude in lead II >2.5 mm.

Note: A tall, peaked P in lead II may represent RAE but is more commonly due to either chronic obstructive pulmonary disease (COPD) or increased sympathetic tone.

Clinical correlation: RAE is seen with right ventricular hypertrophy (RVH).

Left Atrial Enlargement (LAE)

The most sensitive lead for the diagnosis of LAE is lead V₁, but the criteria for lead II are more specific. Criteria include a terminal negative wave ≥1 mm deep and ≥40 ms wide (one small box by one small box in area) for lead V₁ and > 40 ms between the first (right) and second (left) atrial components of the P wave in lead II, or a P-wave duration >110 ms in lead II.

Clinical correlations: left ventricular hypertrophy (LVH), coronary artery disease, mitral valve disease, or cardiomyopathy.

Diagnostic Criteria

The diagnosis of uncomplicated complete RBBB is made when the following criteria are met:

1. Prolongation of the QRS duration to 120 ms or more.
2. An rsr′, rsR′, or rSR′ pattern in lead V₁ or V₂. The R′ is usually greater than the initial R wave. In a minority of cases, a wide and notched R pattern may be seen.
3. Leads V₆ and I show a QRS complex with a wide S wave (S duration is longer than the R duration or >40 ms in adults).

ST–T changes in RBBB

In uncomplicated RBBB, the ST–T segment is depressed and the T wave inverted in the right precordial leads with an R′ (usually only in lead V₁ but occasionally in V₂). The T wave is upright in leads I, V₅, and V₆.

Diagnostic Criteria

The diagnosis of uncomplicated complete LBBB is made when the following criteria are met:

1. Prolongation of the QRS duration to 120 ms or more.
2. There are broad and notched or slurred R waves in left-sided precordial leads V₅ and V₆, as well as in leads I and aVL. Occasionally, an RS pattern may occur in leads V₅ and V₆ in uncomplicated LBBB associated with posterior displacement of the left ventricle.
3. With the possible exception of lead aVL, Q waves are absent in the left-sided leads, specifically in leads V₅, V₆, and I.
4. The R peak time is prolonged to >60 ms in lead V₅ or V₆ but is normal in leads V₁ and V₂ when it can be determined.
5. In the right precordial leads V₁ and V₃, there are small initial r waves in the majority of cases, followed by wide and deep S waves. The transition zone in the precordial leads is displaced to the left. Wide QS complexes may be present in leads V₁ and V₂ and rarely in lead V₃.

ST–T Changes in LBBB

In uncomplicated LBBB, the ST segments are usually depressed and the T waves inverted in left precordial leads V₅ and V₆ as well as in leads I and aVL. Conversely, ST-segment elevations and positive T waves are recorded in leads V₁ and V₂. Only rarely is the T wave upright in the left precordial leads. As a general rule, ST–T changes in LBBB are usually in the direction opposite the direction of the QRS complex (inverted T waves and ST-segment depression if the QRS is upright).

Incomplete LBBB

The waveforms are similar to those in complete LBBB, but the QRS duration is <120 ms. Septal Q waves are absent in I and V₆. Incomplete LBBB is synonymous with LVH and commonly mimics a delta wave in leads V₅ and V₆.

Incomplete RBBB

The waveforms are similar to those in complete RBBB, but the QRS duration is <120 ms. This diagnosis suggests RVH. Occasionally, in a normal variant pattern, there is an rSr′ waveform in lead V₁. In this case, the r′ is usually smaller than the initial r wave; this pattern is not indicative of incomplete RBBB.

Intraventricular Conduction Delay or Defect

If the QRS duration is ≥120 ms but typical waveforms of either RBBB or LBBB are not present, there is an intraventricular conduction delay or defect (IVCD). This pattern is common in dilated cardiomyopathy. An IVCD with a QRS duration of ≥170 ms is highly predictive of dilated cardiomyopathy.

Diagnostic Criteria

1. Mean QRS axis from –45 degrees to –90 degrees (possibly –31 to –44 degrees).
2. A qR pattern in lead aVL, with the R peak time, that is, the onset of the Q wave to the peak of the R wave ≥45 ms (slightly more than one small box wide), as shown below.
   

Clinical correlations: hypertensive heart disease, coronary artery disease, or idiopathic conducting system disease.

Diagnostic Criteria

1. Mean QRS axis from +90 degrees to +180 degrees.
2. A qR complex in leads III and aVF, an rS complex in leads aVL and I, with a Q wave ≥40 ms in the inferior leads.

Clinical correlations: LPFB is a diagnosis of exclusion. It may be seen in the acute phase of inferior myocardial injury or infarction or may result from idiopathic conducting system disease.

The Mean QRS Axis in the Frontal Plane (Limb Leads)

Arzbaecher developed the hexaxial reference system that allowed for the display of the relationships among the six frontal plane (limb) leads, which is shown on the following diagram.

The normal range of the QRS axis in adults is –30 degrees to +90 degrees.

It is rarely important to precisely determine the degrees of the mean QRS. However, the recognition of abnormal axis deviations is critical because it leads to a presumption of disease. The mean QRS axis is derived from the net area under the QRS curves. The most efficient method of determining the mean QRS axis uses the method of Grant, which requires only leads I and II (see below). If the net area under the QRS curves in these leads is positive, the axis falls between –30 degrees and +90 degrees, which is the normal range of axis in adults. (The only exception to this rule is in RBBB, in which the first 60 ms of the QRS is used. Alternatively, one may use the maximal amplitude of the R and S waves in leads I and II to assess the axis in RBBB.) The following diagram shows abnormal axes.

Left Axis Deviation (LAD)

The four main causes of left axis deviation are as follows:

1. Left Anterior Fascicular Block (LAFB): See criteria above.
2. Inferior Myocardial Infarction: There is a pathologic Q wave ≥30 ms either in lead aVF or lead II in the absence of ventricular preexcitation.
3. Ventricular Preexcitation (WPW Pattern): LAD is seen with inferior paraseptal accessory pathway locations. This can mimic inferoposterior myocardial infarction. The classic definition of the Wolff-Parkinson-White (WPW) pattern includes a short PR interval (<120 ms); an initial slurring of the QRS complex, called a delta wave; and prolongation of the QRS complex to >120 ms. However, because this pattern may not always be present despite the presence of ventricular preexcitation, a more practical definition is an absent PR segment and an initial slurring of the QRS complex in any lead. The diagnosis of the WPW pattern usually requires sinus rhythm.
4. COPD: LAD is seen in 10% of patients with COPD.

Right Axis Deviation (RAD)

The four main causes of right axis deviation (RAD) are as follows:

1. Right Ventricular Hypertrophy: This is the most common cause. However, one must first exclude acute occlusion of the posterior descending coronary artery, causing LPFB, and exclude also items B and C below.
2. Extensive Lateral and Apical Myocardial Infarction: Criteria include QS or Qr patterns in leads I and aVL and in leads V_4–6.
3. Ventricular Preexcitation (WPW Pattern): RAD seen with left lateral accessory pathway locations. This can mimic lateral myocardial infarction.
4. Left Posterior Fascicular Block (LPFB): This is a diagnosis of exclusion (see criteria above).

Right Superior Axis Deviation

This category is rare. Causes include RVH, apical myocardial infarction, VT, and hyperkalemia. Right superior axis deviation may rarely be seen as an atypical form of LAFB.

Repolarization Abnormalities

Typical repolarization abnormalities in the presence of LVH are an ominous sign of end-organ damage. In repolarization abnormalities in LVH, the ST segment and T wave are directed opposite to the dominant QRS waveform in all leads. However, this directional rule does not apply either in the transitional lead (defined as a lead having an R-wave height equal to the S wave depth) or in the transitional zone (defined as leads adjacent to the transitional lead) or one lead to the left in the precordial leads.

Spectrum of Repolarization Abnormalities

The waveforms, as in the following illustration, usually seen in leads I, aVL, V₅, and V₆ but more specifically in leads with dominant R waves, represent hypothetical stages in the progression of LVH.

Diagnostic Criteria

Recommended criteria for the electrocardiographic diagnosis of RVH are as follows:

1. Right axis deviation (>90 degrees), or
2. An R/S ratio ≥1 in lead V₁ (absent posterior myocardial infarction [MI] or RBBB), or
3. An R wave >7 mm tall in V₁ (not the R′ of RBBB), or
4. An rsR′ complex in V₁ (R′ ≥10 mm), with a QRS duration of <0.12 s (incomplete RBBB), or
5. An S wave >7 mm deep in leads V₅ or V₆ (in the absence of a QRS axis more negative than +30 degrees), or
6. RBBB with RAD (axis derived from first 60 ms of the QRS). (Consider RVH in RBBB if the R/S ratio in lead I is <0.5.)

A variant of RVH (type C loop) may produce a false-positive sign of an anterior myocardial infarction.

Repolarization Abnormalities

The morphology of repolarization abnormalities in RVH is identical to those in LVH, when a particular lead contains tall R waves reflecting the hypertrophied RV or LV. In RVH, these typically occur in leads V_1–2 or V₃ and in leads aVF and III. This morphology of repolarization abnormalities due to ventricular hypertrophy is illustrated earlier. In cases of RVH with massive dilation, all precordial leads may overlie the diseased RV and may exhibit repolarization abnormalities.

Low-Voltage Limb Leads Only

Defined as peak-to-peak QRS voltage <5 mm in all limb leads.

Low-Voltage Limb and Precordial Leads

Defined as peak-to-peak QRS voltage <5 mm in all limb leads and <10 mm in all precordial leads. Primary myocardial causes include multiple or massive infarctions; infiltrative diseases such as amyloidosis, sarcoidosis, or hemochromatosis; and myxedema. Extracardiac causes include pericardial effusion, COPD, pleural effusion, obesity, anasarca, and subcutaneous emphysema. When there is COPD, expect to see low voltage in the limb leads as well as in leads V₅ and V₆.

Poor R-Wave Progression

The term “poor R-wave progression” (PRWP) is a nonpreferred term because most physicians use this term to imply the presence of an anterior myocardial infarction, although it may not be present. Other causes of small R waves in the right precordial leads include LVH, LAFB, LBBB, cor pulmonale (with the type C loop of RVH), and COPD.

Reversed R-Wave Progression (RRWP)

Reversed R-wave progression is defined as a loss of R-wave height between leads V₁ and V₂ or between leads V₂ and V₃ or between leads V₃ and V₄. In the absence of LVH, this finding suggests anterior myocardial infarction or precordial lead reversal.

Etiology

Causes of tall R waves in the right precordial leads include the following:

1. Right Ventricular Hypertrophy: This is the most common cause. There is an R/S ratio ≥1 or an R-wave height >7 mm in lead V₁.
2. Posterior Myocardial Infarction: There is an R wave ≥6 mm in lead V₁ or ≥15 mm in lead V₂. One should distinguish the tall R wave of RVH from the tall R wave of posterior myocardial infarction in lead V₁. In RVH, there is a downsloping ST segment and an inverted T wave, usually with right axis deviation. In contrast, in posterior myocardial infarction, there is usually an upright, commonly tall T wave and, because posterior myocardial infarction is usually associated with concomitant inferior myocardial infarction, a left axis deviation.
3. Right Bundle Branch Block: The QRS duration is prolonged, and typical waveforms are present.
4. The WPW Pattern: Left-sided accessory pathway locations produce prominent R waves with an R/S ratio ≥1 in V₁, with an absent PR segment and initial slurring of the QRS complex, usually best seen in lead V₄.
5. Rare or Uncommon Causes: The normal variant pattern of early precordial QRS transition (not uncommon); the reciprocal effect of a deep Q wave in leads V_5–6 (very rare); Duchenne muscular dystrophy; dextrocardia (very rare); chronic constrictive pericarditis (very rare); and reversal of the right precordial leads.

Definitions

1. Myocardial Infarction: Pathologic changes in the QRS complex reflect ventricular activation away from the area of infarction.
2. Myocardial Injury: Injury always points outward from the surface that is injured.
   1. Epicardial injury: ST elevation in the distribution of an acutely occluded artery.
   2. Endocardial injury: Diffuse ST-segment depression, which is really reciprocal to the primary event, reflected as ST elevation in aVR.
3. Myocardial Ischemia: Diffuse ST-segment depression, usually with associated T-wave inversion. It usually reflects subendocardial injury, reciprocal to ST elevation in lead aVR. In ischemia, there may only be inverted T waves with a symmetric, sharp nadir.
4. Reciprocal Changes: Passive electrical reflections of a primary event viewed from either the other side of the heart, as in epicardial injury, or the other side of the ventricular wall, as in subendocardial injury.

Steps in the Diagnosis of Myocardial Infarction

The following pages contain a systematic method for the electrocardiographic diagnosis of myocardial injury or infarction, arranged in seven steps. Following the steps will achieve the diagnosis in most cases.

• Step 1: Identify the presence of myocardial injury by ST-segment deviations.
• Step 2: Identify areas of myocardial injury by assessing lead groupings.
• Step 3: Define the primary area of involvement and identify the culprit artery producing the injury.
• Step 4: Identify the location of the lesion in the artery to risk stratify the patient.
• Step 5: Identify any electrocardiographic signs of infarction found in the QRS complexes.
• Step 6: Determine the age of the infarction by assessing the location of the ST segment in leads with pathologic QRS abnormalities.
• Step 7: Combine all observations into a final diagnosis.

Primary Anterior Area

ST elevation in two contiguous V_1–4 leads defines a primary anterior area of involvement. The left anterior descending coronary artery (LAD) is the culprit artery. Lateral (I and aVL) and apical (V₅ and V₆) areas are contiguous to anterior (V_1–4), so ST elevation in these leads signifies more myocardium at risk and more adverse outcomes.

Primary Inferior Area

ST-segment elevation in two contiguous leads (II, aVF, or III) defines a primary inferior area of involvement. The right coronary artery (RCA) is usually the culprit artery. Apical (V₅ and V₆), posterior (V_1–3 or V_7–9), and right ventricular (V₄R) areas are contiguous to the inferior (II, aVF, and III) area, so ST elevation in these contiguous leads signifies more myocardium at risk and more adverse outcomes.

The Culprit Artery

In the GUSTO trial, 98% of patients with ST-segment elevation in any two contiguous V_1–4 leads, either alone or with associated changes in leads V_5–6 or I and aVL, had LAD obstruction. In patients with ST-segment elevation only in leads II, aVF, and III, there was RCA obstruction in 86%.

Earliest Findings

1. “Hyperacute” Changes: ST elevation with loss of normal ST-segment concavity, commonly with tall, peaked T waves.
   
2. Acute Injury: ST elevation, with the ST segment commonly appearing as if a thumb has been pushed up into it.
   

Evolutionary Changes

A patient who presents to the emergency department with chest pain and T-wave inversion in leads with pathologic Q waves is most likely to be in the evolutionary or completed phase of infarction. Successful revascularization usually causes prompt resolution of the acute signs of injury or infarction and results in the electrocardiographic signs of a fully evolved infarction. The tracing below shows QS complexes in lead V₂.

1. Development of Pathologic Q Waves (Infarction): Pathologic Q waves develop within the first hour after onset of symptoms in at least 30% of patients.
   
2. ST-Segment Elevation Decreases: T-wave inversion usually occurs in the second 24-hour period after infarction.
   
3. Fully Evolved Pattern: Pathologic Q waves, ST segment rounded upward, T waves inverted.
   

Earliest Findings

The earliest findings are of acute injury (ST-segment elevation). The J point may “climb up the back” of the R wave (a), or the ST segment may rise up into the T wave (b).

Evolutionary Changes

ST-segment elevation decreases and pathologic Q waves develop. T-wave inversion may occur in the first 12 hours of an inferior myocardial infarction—in contrast to that in anterior myocardial infarction.

Right Ventricular Injury or Infarction

With right ventricular injury, there is ST-segment elevation, best seen in lead V₄R. With right ventricular infarction, there is a QS complex.

For comparison, the normal morphology of the QRS complex in lead V₄R is shown below. The normal J point averages +0.2 mm.

Acute Pattern

Acute posterior injury or infarction is shown by ST-segment depression in V_1–3 and perhaps also V₄, usually with upright (often prominent) T waves.

Chronic Pattern

Chronic posterior injury or infarction is shown by pathologic R waves with prominent tall T waves in leads V_1–3.

Primary Anterior Process

Aside from an acute occlusion of the left main coronary artery, occlusion of the proximal LAD conveys the most adverse outcomes. Four electrocardiographic signs indicate proximal LAD occlusion:

1. ST elevation >1 mm in lead I, in lead aVL, or in both
2. New RBBB
3. New LAFB
4. New first-degree AV block

If the occlusion occurs in a more distal portion of the LAD (after the first diagonal branch and after the first septal perforator), ST-segment elevation is observed in the anterior leads, but the four criteria described above are not seen. In patients with occlusion of the left main coronary artery, diffuse endocardial injury leads to ST-segment elevation in aVR, because this is the only lead that “looks” directly at the ventricular endocardium, and diffuse ST-segment depression is observed in the anterior and inferior leads.

Primary Inferior Process

Nearly 50% of patients with inferior myocardial infarction have distinguishing features that may produce complications or adverse outcomes unless successfully managed:

1. Precordial ST-segment depression in V_1–3 (suggests concomitant posterior wall involvement);
2. Right ventricular injury or infarction (identifies a proximal RCA lesion);
3. AV block (implies a greater amount of involved myocardium);
4. The sum of ST-segment depressions in leads V_4–6 exceeds the sum of ST-segment depressions in leads V_1–3 (suggests multivessel disease).

Reciprocal Changes in the Setting of Acute Myocardial Infarction

ST depressions in leads remote from the primary site of injury are felt to be a purely reciprocal change. With successful reperfusion, the ST depressions usually resolve. If they persist, patients more likely have significant three-vessel disease and so-called ischemia at a distance. Mortality rates are higher in such patients.

Identify Electrocardiographic Signs of Infarction in the QRS Complexes

The 12-lead ECG shown below contains numbers corresponding to pathologic widths for Q waves and R waves for selected leads (see Table 7–4 for more complete criteria).

One can memorize the above criteria by mastering a simple scheme of numbers that represents the durations of pathological Q waves or R waves. Begin with lead V₁ and repeat the numbers in the box below in the following order. The numbers increase from “any” to 50.

• Any Q wave in lead V₁, for anterior MI
• Any Q wave in lead V₂, for anterior MI
• Any Q wave in lead V₃, for anterior MI
• 20 Q wave ≥ 20 ms in lead V₄, for anterior MI
• 30 Q wave ≥ 30 ms in lead V₅, for apical MI
• 30 Q wave ≥ 30 ms in lead V₆, for apical MI
• 30 Q wave ≥ 30 ms in lead I, for lateral MI
• 30 Q wave ≥ 30 ms in lead aVL, for lateral MI
• 30 Q wave ≥ 30 ms in lead II, for inferior MI
• 30 Q wave ≥ 30 ms in lead aVF, for inferior MI
• R40 R wave ≥ 40 ms in lead V₁, for posterior MI
• R50 R wave ≥ 50 ms in lead V₂, for posterior MI

Test Performance Characteristics for Electrocardiographic Criteria in the Diagnosis of Myocardial Infarction

Haisty and coworkers studied 1344 patients with normal hearts documented by coronary arteriography and 837 patients with documented myocardial infarction (366 inferior, 277 anterior, 63 posterior, and 131 inferior and anterior) (Table 7–4). (Patients with LVH, LAFB, LPFB, RVH, LBBB, RBBB, COPD, or WPW patterns were excluded from analysis because these conditions can give false-positive results for myocardial infarction.) Shown below are the sensitivity, specificity, and likelihood ratios for the best-performing infarct criteria. Notice that leads III and aVR are not listed: lead III may normally have a Q wave that is both wide and deep, and lead aVR commonly has a wide Q wave.

Mimics of Myocardial Infarction

Conditions that can produce pathologic Q waves, ST-segment elevation, or loss of R-wave height in the absence of infarction are set out in Table 7–5.

Determine the Age of the Infarction

An acute infarction manifests ST-segment elevation in a lead with a pathologic Q wave. The T waves may be either upright or inverted.

An old or age-indeterminate infarction manifests a pathologic Q wave, with or without slight ST-segment elevation or T-wave abnormalities.

Persistent ST-segment elevation ≥1 mm after a myocardial infarction is a sign of dyskinetic wall motion in the area of infarct. Half of these patients have ventricular aneurysms.

Combine Observations into a Final Diagnosis

There are two possibilities for the major electrocardiographic diagnosis: myocardial infarction or acute injury. If there are pathologic changes in the QRS complex, one should make a diagnosis of myocardial infarction—beginning with the primary area, followed by any contiguous areas—and state the age of the infarction. If there are no pathologic changes in the QRS complex, one should make a diagnosis of acute injury of the affected segments—beginning with the primary area and followed by any contiguous areas.

Normal U Waves

In many normal hearts, low-amplitude positive U waves <1.5 mm tall that range from 160–200 ms in duration are seen in leads V₂ or V₃. Leads V₂ and V₃ are close to the ventricular mass and small-amplitude signals may be best seen in these leads.

Cause: Bradycardias.

Abnormal U Waves

Abnormal U waves have increased amplitude or merge with abnormal T waves and produce T–U fusion. Criteria include an amplitude ≥1.5 mm or a U wave that is as tall as the T wave that immediately precedes it.

Causes: Hypokalemia, digitalis, antiarrhythmic drugs.

Inverted U Waves

These are best seen in leads V_4–6.

Causes: LVH, acute ischemia.

Table 7–9 summarizes various classes and morphologies of ST–T–U abnormalities as seen in lead V₄.

VARIOUS CLASSES AND MORPHOLOGIES OF ST–T–U ABNORMALITIES AS SEEN IN LEAD V₄.

Use of the QT Nomogram (Hodges Correction)

Measure the QT interval in either lead V₂ or V₃, where the end of the T wave can usually be clearly distinguished from the beginning of the U wave. If the rate is regular, use the mean rate of the QRS complexes. If the rate is irregular, calculate the rate from the immediately prior R–R cycle, because this cycle determines the subsequent QT interval. Use the numbers you have obtained to classify the QT interval using the nomogram below. Or remember that at heart rates of ≥40 bpm, an observed QT interval ≥480 ms is abnormal.

Prolonged QT Interval

The four major causes of a prolonged QT interval are as follows:

1. Electrolyte Abnormalities: Hypokalemia, hypocalcemia
2. Drugs: Associated with prolonged QT interval and torsades de pointes Antiarrhythmics:
   • Class Ia agents: Quinidine, procainamide, disopyramide
   • Class 1c agent: Flecainide
   • Class III agents: Amiodarone, N-acetylprocainamide, dofetilide, ibutilide, sotalol
   Anticonvulsants: Fosphenytoin, felbamate Antihistamines: Azelastine, clemastine Antiinfectives: Amantadine, clarithromycin, chloroquine, foscarnet, erythromycin, itraconazole, halofantrine, ketoconazole, mefloquine, moxifloxacin, pentamidine, quinine, trimethoprim-sulfamethoxazole Calcium channel blockers: Bepridil, israpidine, nicardipine Chemotherapeutic agents: Pentamadine, tamoxifen (perhaps anthracyclines) Diuretics: Indapamide, moexipril/HCTZ Hormones: Octreotide, vasopressin Immunosuppressant: Tacrolimus Migraine serotonin receptor agonists: Naratriptan, sumatriptan, zolmitriptan Muscle relaxant: Tizanidine Psychotropic agents: Amitriptyline, chlorpromazine, desipramine, doxepin, fluoxetine, haloperidol, imipramine, lithium pimozide, risperidone, thioridazine, quietiapine, venlafaxine, Sympathomimetics: Salmeterol Sedative/hypnotics: Chloral hydrate Toxins and poisons: Organophosphate insecticides Miscellaneous: Methadone, prednisone, probucol
   
3. Congenital Long QT Syndromes: Though rare, a congenital long QT syndrome should be considered in any young patient who presents with syncope or presyncope.
4. Miscellaneous Causes: Third-degree and sometimes second-degree AV block At the cessation of ventricular pacing LVH (usually minor degrees of lengthening) Myocardial infarction (in the evolutionary stages where there are marked repolarization abnormalities) Significant active myocardial ischemia Cerebrovascular accident (subarachnoid hemorrhage) Hypothermia

Short QT Interval

The five causes of a short QT interval are hypercalcemia, digitalis, thyrotoxicosis, increased sympathetic tone, and genetic abnormality.

Right-Left Arm Cable Reversal versus Mirror Image Dextrocardia

Misplacement of the Right Leg Cable

This error should not occur but it does occur nevertheless. It produces a “far field” signal when one of the bipolar leads (I, II, or III) records the signal between the left and right legs. The lead appears to have no signal except for a tiny deflection representing the QRS complex. There are usually no discernible P waves or T waves. RL–RA cable reversal is shown here.

Early Repolarization Normal Variant ST–T Abnormality

Hypothermia

Hypothermia is usually characterized on the ECG by a slow rate, a long QT, and muscle tremor artifact. An Osborn wave is typically present.

Acute Pericarditis: Stage I (With PR-Segment Abnormalities)

There is usually widespread ST-segment elevation with concomitant PR-segment depression in the same leads. The PR segment in aVR protrudes above the baseline like a knuckle, reflecting atrial injury.

Differentiating Pericarditis From Early Repolarization

Only lead V₆ is used. If the indicated amplitude ratio A/B is ≥25%, suspect pericarditis (shown on left side). If A/B <25%, suspect early repolarization (shown on right side).

Wolff-Parkinson-White Pattern

The WPW pattern is most commonly manifest as an absent PR segment and initial slurring of the QRS complex in any lead. The lead with the best sensitivity is V₄.

1. Left Lateral Accessory Pathway: This typical WPW pattern mimics lateral or posterior myocardial infarction.
   
2. Posteroseptal Accessory Pathway: This typical WPW pattern mimics inferoposterior myocardial infarction.
   

COPD Pattern, Lead II

The P-wave amplitude in the inferior leads is equal to that of the QRS complexes.