How to Use This Section This chapter includes criteria for the diagnosis of basic electrocardiographic waveforms and cardiac arrhythmias. It is intended for use as a reference and assumes a basic understanding of the electrocardiogram (ECG) *. Electrocardiographic interpretation
is a “stepwise” procedure, and the first steps are to study and characterize the cardiac rhythm. Step One (Rhythm) Categorize what you see in the 12-lead ECG or rhythm strip, using the three major parameters that allow for systematic analysis and subsequent diagnosis of the rhythm: *Several parts of this section on electrocardiography are based on the work of G. T. Evans, MD, who was the author of this chapter in the first edition of the book. Step Two (Morphology) Step 2 consists of examining and characterizing the morphology of the cardiac waveforms. STEP ONE: DIAGNOSIS OF THE CARDIAC RHYTHM A. Approach to Diagnosis of the Cardiac Rhythm Most electrocardiograph machines display 10 seconds of data in a standard tracing.
A rhythm is defined as three or more successive P waves or QRS complexes. Categorize the patterns seen in the tracing according to a systematic method. This method proceeds in three steps that lead to a diagnosis based on the most likely rhythm producing a particular pattern: Using the categorization above, refer to Tables 7–1 and 7–2 to select a specific diagnosis for the cardiac rhythm. AV =
atrioventricular; BBB = bundle branch blocks; IVCD = intraventricular conduction delay. AV = atrioventricular; BBB = bundle branch blocks; IVCD = intraventricular conduction delay; WPW = Wolff-Parkinson-White syndrome. B. Normal Heart Rate 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 VI, 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. Tachycardia Tachycardias are normally classified by whether the QRS complex is narrow or wide and whether the rhythm is regular or irregular. A narrow QRS tachycardia indicates normal activation of the ventricular tissue regardless of the tachycardia mechanism. Narrow QRS tachycardias are frequently grouped together as supraventricular tachycardia (SVT) and can be due to a number of mechanisms described in the
following text. This grouping also has clinical usefulness because SVTs are not usually life-threatening. In addition to QRS width, it is useful to consider the anatomic site from which the tachycardia arises: atrium, atrioventricular junction, ventricle, or utilization of an accessory pathway (Figure 7–1). Figure 7–1. Anatomic classification of tachycardias. ( Adapted with permission from Kusumoto FM: Arrhythmias. In : Cardiovascular Pathophysiology, FM Kusumoto [editor], Hayes Barton Press, 2004. ) Narrow QRS Tachycardia with a Regular Rhythm: Regular SVT 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 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. 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). MORPHOLOGY ALGORITHMS FOR IDENTIFYING VT 1. Method One: Quick Method for Diagnosis of VT (Requires Leads I, V1, and V2) This method derives from an analysis of typical waveforms of RBBB or LBBB as seen in leads I, V1, and V2. If the waveforms do not conform to either the common or uncommon
typical morphologic patterns, the diagnosis defaults to VT. Step One Determine the morphologic classification of the wide QRS complexes (RB type or LB type), using the criteria below. 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. 2. Method Two: The Brugada Algorithm for Diagnosis of VT (Requires all six precordial leads.) Brugada and coworkers reported on a
total of 554 patients with WC-TRR whose mechanism was diagnosed in the electrophysiology laboratory. Patients included 384 (69%) with VT and 170 (31%) with SVT with aberrant ventricular conduction. 3. Method Three: The Griffith Method for Diagnosis of VT (Requires Leads V1 and V6) This method derives from an analysis of typical
waveforms of RBBB or LBBB as seen in both leads V1 and V6. If the waveforms do not conform to the typical morphologic patterns, the diagnosis defaults to VT. 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. Wide QRS Tachycardia with an Irregular Rhythm 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. 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).
STEP TWO: MORPHOLOGIC DIAGNOSIS OF THE CARDIAC WAVEFORMS
The Normal ECG: Two Basic QRST Patterns
The most common pattern is illustrated below and is usually seen in leads I or II and V6. There is a small “septal” Q wave <30 ms in duration. The T wave is upright. The normal ST segment, which is never normally isoelectric except sometimes at slow rates (<60 bpm), slopes upward into an upright T wave, whose proximal angle is more obtuse than the distal angle. The normal T wave is never symmetric.
The pattern seen in the right precordial leads, usually V1–3, is shown below. There is a dominant S wave. The J point—the junction between the end of the QRS complex and the ST segment—is usually slightly elevated, and the T wave is upright. The T wave in V1 may occasionally be inverted as a normal finding in up to 50% of young women and 25% of young men, but this finding is usually abnormal in adult males. V2 usually has the largest absolute QRS and T-wave magnitude of any of the 12 electrocardiographic leads.
B. Atrial Abnormalities
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.
C. Bundle Branch Block
The normal QRS duration in adults ranges from 67–114 ms (Glasgow cohort). If the QRS duration is ≥120 ms (three small boxes or more on the electrocardiographic paper), there is usually an abnormality of conduction of the ventricular impulse. The most common causes are either RBBB or LBBB (see below). However, other conditions may also prolong the QRS duration.
RBBB is defined by delayed terminal QRS forces that are directed to the right and anteriorly, producing broad terminal positive waves in leads V1 and aVR and a broad terminal negative wave in lead I.
LBBB is defined by delayed terminal QRS forces that are directed to the left and posteriorly, producing wide R waves in leads that face the left ventricular free wall and wide S waves in the right precordial leads.
Right Bundle Branch Block
Diagnostic Criteria
The diagnosis of uncomplicated complete RBBB is made when the following criteria are met:
- Prolongation of the QRS duration to 120 ms or more.
- 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.
- 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.
Left Bundle Branch Block
Diagnostic Criteria
The diagnosis of uncomplicated complete LBBB is made when the following criteria are met:
- Prolongation of the QRS duration to 120 ms or more.
- 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.
- With the possible exception of lead aVL, Q waves are absent in the left-sided leads, specifically in leads V5, V6, and I.
- 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.
- 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).
D. Incomplete Bundle Branch Blocks
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.
E. Fascicular Blocks (Hemiblocks)
1. Left Anterior Fascicular Block (LAFB)
Diagnostic Criteria
- Mean QRS axis from –45 degrees to –90 degrees (possibly –31 to –44 degrees).
- 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.
2. Left Posterior Fascicular Block (LPFB)
Diagnostic Criteria
- Mean QRS axis from +90 degrees to +180 degrees.
- 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.
F. Determination of the Mean QRS Axis
The mean electrical axis is the average direction of the activation or repolarization process during the cardiac cycle. Instantaneous and mean electrical axes may be determined for any deflection (P, QRS, ST–T) in the three planes (frontal, transverse, and sagittal). The determination of the electrical axis of a QRS complex is useful for the diagnosis of certain pathologic cardiac conditions.
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:
- Left Anterior Fascicular Block (LAFB): See criteria above.
- Inferior Myocardial Infarction: There is a pathologic Q wave ≥30 ms either in lead aVF or lead II in the absence of ventricular preexcitation.
- 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.
- 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:
- 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.
- Extensive Lateral and Apical Myocardial Infarction: Criteria include QS or Qr patterns in leads I and aVL and in leads V4–6.
- Ventricular Preexcitation (WPW Pattern): RAD seen with left lateral accessory pathway locations. This can mimic lateral myocardial infarction.
- 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.
G. Ventricular Hypertrophy
1. Left Ventricular Hypertrophy
The ECG is very insensitive as a screening tool for LVH, but electrocardiographic criteria are usually specific. Echocardiography is the major resource for this diagnosis.
The best electrocardiographic criterion for the diagnosis of LVH is the Cornell voltage, the sum of the R-wave amplitude in lead aVL and the S-wave depth in lead V3, adjusted for sex:
- RaVL + SV3 >20 mm (females), >25 mm (males). The R-wave height in aVL alone is a good place to start.
- RaVL >9 mm (females), >11 mm (males). Alternatively, application of the following criteria will diagnose most cases of LVH.
- Sokolow-Lyon criteria: SV1 + RV5 or RV6 (whichever R wave is taller) >35 mm (in patients age >35).
- Romhilt-Estes criteria: Points are scored for QRS voltage (1 point), the presence of LAE (1 point), typical repolarization abnormalities in the absence of digitalis (1 point), and a few other findings. The combination of LAE (see above) and typical repolarization abnormalities (see below) (score ≥5 points) will suffice for the diagnosis of LVH even when voltage criteria are not met.
- RV6 > RV5 (usually occurs with dilated LV). First exclude anterior myocardial infarction and establish that the R waves in V5 are >7 mm tall and that in V6 they are >6 mm tall before using this criterion.
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.
2. Right Ventricular Hypertrophy (RVH)
The ECG is insensitive for the diagnosis of RVH. In 100 cases of RVH from one echocardiography laboratory, only 33% had RAD because of the confounding effects of LV disease. Published electrocardiographic criteria for RVH are listed below, all of which have ≥97% specificity.
With rare exceptions, right atrial enlargement is synonymous with RVH.
Diagnostic Criteria
Recommended criteria for the electrocardiographic diagnosis of RVH are as follows:
- Right axis deviation (>90 degrees), or
- An R/S ratio ≥1 in lead V1 (absent posterior myocardial infarction [MI] or RBBB), or
- An R wave >7 mm tall in V1 (not the R′ of RBBB), or
- An rsR′ complex in V1 (R′ ≥10 mm), with a QRS duration of <0.12 s (incomplete RBBB), or
- An S wave >7 mm deep in leads V5 or V6 (in the absence of a QRS axis more negative than +30 degrees), or
- 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 V1–2 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.
H. Low Voltage of the QRS Complex
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.
I. Progression of the R Wave in the Precordial Leads
The normal R-wave height increases from V1 to V5. The normal R-wave height in V5 is always taller than that in V6 because of the attenuating effect of the lungs. The normal R-wave height in lead V3 is usually >2 mm.
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.
Tall R Waves in the Right Precordial Leads
Etiology
Causes of tall R waves in the right precordial leads include the following:
- 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.
- 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.
- Right Bundle Branch Block: The QRS duration is prolonged, and typical waveforms are present.
- 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.
- 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 V5–6 (very rare); Duchenne muscular dystrophy; dextrocardia (very rare); chronic constrictive pericarditis (very rare); and reversal of the right precordial leads.
Myocardial Injury, Ischemia, and Infarction
Definitions
- Myocardial Infarction: Pathologic changes in the QRS complex reflect ventricular activation away from the area of infarction.
- Myocardial Injury: Injury always points outward from the surface that is injured.
- Epicardial injury: ST elevation in the distribution of an acutely occluded artery.
- Endocardial injury: Diffuse ST-segment depression, which is really reciprocal to the primary event, reflected as ST elevation in aVR.
- 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.
- 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.
Steps One and Two
Identify presence of and areas of myocardial injury.
The GUSTO study of patients with ST-segment elevation in two contiguous leads defined four affected areas as set out in Table 7–3.
Two other major areas of possible injury or infarction were not included in the GUSTO categorization because they do not produce ST elevation in two contiguous standard leads. These are:
- Posterior Injury: The most commonly used sign of posterior injury is ST depression in leads V1–3, but posterior injury may best be diagnosed by obtaining posterior leads V7, V8, and V9.
- Right Ventricular Injury: The most sensitive sign of right ventricular injury, ST-segment elevation ≥1 mm, is found in lead V4R. A very specific—but insensitive—sign of right ventricular injury or infarction is ST elevation in V1, with concomitant ST-segment depression in V2 in the setting of ST elevation in the inferior leads.
Step Three
Identify the primary area of involvement and the culprit artery.
Primary Anterior Area
ST elevation in two contiguous V1–4 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 (V1–4), 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 (V1–3 or V7–9), 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 V1–4 leads, either alone or with associated changes in leads V5–6 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%.
Primary Anterior Process
Acute occlusion of the LAD produces a sequence of changes in the anterior leads (V1–4).
Earliest Findings
- “Hyperacute” Changes: ST elevation with loss of normal ST-segment concavity, commonly with tall, peaked T waves.
- 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.
- Development of Pathologic Q Waves (Infarction): Pathologic Q waves develop within the first hour after onset of symptoms in at least 30% of patients.
- ST-Segment Elevation Decreases: T-wave inversion usually occurs in the second 24-hour period after infarction.
- Fully Evolved Pattern: Pathologic Q waves, ST segment rounded upward, T waves inverted.
Primary Inferior Process
A primary inferior process usually develops after acute occlusion of the RCA, producing changes in the inferior leads (II, III, and aVF).
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.
Posterior Injury or Infarction
Posterior injury or infarction is commonly due to acute occlusion of the left circumflex coronary artery, producing changes in the posterior leads (V7, V8, V9) or reciprocal ST-segment depression in leads V1–3.
Acute Pattern
Acute posterior injury or infarction is shown by ST-segment depression in V1–3 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 V1–3.
Step Four
Identify the location of the lesion within the artery to risk stratify the patient.
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:
- ST elevation >1 mm in lead I, in lead aVL, or in both
- New RBBB
- New LAFB
- 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:
- Precordial ST-segment depression in V1–3 (suggests concomitant posterior wall involvement);
- Right ventricular injury or infarction (identifies a proximal RCA lesion);
- AV block (implies a greater amount of involved myocardium);
- The sum of ST-segment depressions in leads V4–6 exceeds the sum of ST-segment depressions in leads V1–3 (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.
Step Five
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).
Notched R = a notch that begins within the first 40 ms of the R wave; Q = Q wave; R/Q = ratio of R-wave height to Q-wave depth; R = R wave; R/S ratio = ratio of R-wave height to S-wave depth; RV2 ≤ RV1 = R-wave height in V 2 less than or equal to that in V 1 ; S = S wave. ( Reproduced, with permission, from Haisty WK Jr et al. Performance of the automated complete Selvester QRS scoring system in normal subjects and patients with single and multiple myocardial infarctions . J Am Coll Cardiol 1992;19:341. )
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.
COPD = chronic obstructive pulmonary disease; LAFB = left anterior fascicular block; LBBB = left bundle branch block; LVH = left ventricular hypertrophy; RBBB = right bundle branch block; RVH = right ventricular hypertrophy.
Step Six
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.
Step Seven
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.
ST Segments
Table 7–6 summarizes major causes of ST-segment elevations. Table 7–7 summarizes major causes of ST-segment depressions or T-wave inversions. The various classes and morphologies of ST–T waves as seen in lead V2 are shown in Table 7–8.
M. U Waves
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 V4–6.
Causes: LVH, acute ischemia.
Table 7–9 summarizes various classes and morphologies of ST–T–U abnormalities as seen in lead V4.
QT Interval
A prolonged QT interval conveys adverse outcomes. The QT interval is inversely related to the heart rate. QT interval corrections for heart rate often use Bazett’s formula, defined as the observed QT interval divided by the square root of the R–R interval in seconds. A corrected QT interval of ≥440 ms is abnormal.
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:
- Electrolyte Abnormalities: Hypokalemia, hypocalcemia
- 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
- Congenital Long QT Syndromes: Though rare, a congenital long QT syndrome should be considered in any young patient who presents with syncope or presyncope.
- 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.
O. Miscellaneous Abnormalities
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.
- Left Lateral Accessory Pathway: This typical WPW pattern mimics lateral or posterior myocardial infarction.
- 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.
BASIC ELECTROCARDIOGRAPHY is a sample topic from the Guide to Diagnostic Tests.
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