31
Electrocardiography

I. Overview of ECG leads and QRS morphology

An ECG lead consists of two poles (a positive pole and a negative pole). It captures the cardiac electrical potential spreading between these two poles (Figures 31.1, 31.2). If a wave spreads towards the negative pole then turns towards the positive pole, a negative deflection is initially seen, followed by a positive deflection. If the vector of the propagating wave is parallel to the line formed by the two poles, the amplitude of the deflection will be largest; if it is orthogonal, the deflection will be small and almost isoelectric. The electrodes that are positioned on the limbs and the precordium are the poles, whereas the axis formed between two poles is called a lead. Leads I, II, and III are bipolar leads that register the electrical spread between two limb poles. Limb leads aVR, aVL, and aVF register the electrical spread between a central pole and one limb pole; the central pole is the center of the two other limb poles (Figures 31.3, 31.4).

Precordial leads V₁–V₆ register the electrical spread between a central pole and one chest pole; the central pole is the center of all limb poles, located in the center of the chest (Figures 31.5, 31.6). The limb leads aVR, aVL, and aVF, and the precordial leads, are called unipolar leads because they mainly depend on the position of one pole.

Precordial leads V₅–V₆ and limb leads I and aVL point to the left and are left lateral leads, leads I and aVL being high lateral leads. Precordial leads V₁–V₂ are right-sided leads but also septal leads; they overlie the right heart but also the interventricular septum. V₁–V₃ are anteroseptal leads. Limb leads II, III, and aVF point inferiorly, and are thus inferior leads.

Schematic illustration of P–QRS–T complex. — **Figure 31.1** P–QRS–T complex. P wave represents the atrial depolarization and includes a part of the AV nodal conduction. PR interval consists of P wave and AV conduction. AV conduction consists of AV nodal conduction, His conduction, and infra-Hisian conduction (bundle branches before the myocardium); most of the AV conduction time is consumed by conduction through the AV node. The PR segment also includes the atrial repolarization; in normal states, the PR segment is isoelectric or slightly depressed < 0.8 mm (as a result of atrial repolarization).

QRS complex represents ventricular depolarization. ST–T segments represent ventricular repolarization. ST segment = phase 2 of the action potential or plateau phase of repolarization. T wave = phase 3 of the action potential. TP segment = phase 4 of the action potential. The normal U wave is a diastolic wave related to the mechanical stretch of the myocardium in phase 4 (diastole).

Normal calibration:

Height of one small box = 1 mm = 0.1 mV. One big box = 5 small boxes = 0.5 m

V.Width of one small box = 1 mm = 0.04 seconds. One big box = 5 small boxes = 0.2 seconds (sweep speed: 25 mm/s).

Watch for half-standardization, especially when comparing ECGs.

Schematic illustration of arrows show the spread of the electrical depolarization. — **Figure 31.2** Arrows show the spread of the electrical depolarization. Ventricular depolarization starts at the left-sided septum, then spreads to the whole septum from left to right (through the left bundle, *blue arrows 1*). It then spreads to each ventricle through the left and right bundles (*gray arrows 2*). The apex of each ventricle is depolarized first, followed by the lateral wall and the posterior basal region (apical-to-basal spread of depolarization bilaterally, *black arrows 3*). Note that *septal depolarization occurs from left to right.*

Schematic illustration of how the electrical depolarization spreads in the heart (frontal plane, bipolar limb leads). — **Figure 31.3** Illustration of how the electrical depolarization spreads in the heart (frontal plane, bipolar limb leads). The *blue arrows* represent the left-to-right septal depolarization. The *gray arrow* is the main axis of depolarization along the septum towards the LV and apex. The *black arrows* represent the late depolarization spreading towards the base. The QRS deflections that correspond to each one of these depolarizations are colored likewise.

The QRS complex in each lead represents how the electrical activity is spreading in relation to the lead. The **septal depolarization** (*blue*) **explains the normal small q wave** seen in normal individuals in lead I, other limb leads (sometimes), and left precordial leads. The basal depolarization explains the late “s” wave in those leads. The main deflection (big R or big S) is explained by the main depolarization spread. One can imagine how the amplitude of a deflection changes with a slight change in the way depolarization spreads.

**To grossly conceive how QRS appears in a lead (amplitude, positive vs. negative direction), contrast the sum vector of depolarization with the axis of the lead.**

Schematic illustration of how electrical depolarization spreads in the heart (frontal plane, unipolar limb leads).Start In order to catch cardiac activity, the axis of the lead should traverse near the heart; as such, no cardiac activity is detected when both poles are placed on the legs. — **Figure 31.4** Illustration of how electrical depolarization spreads in the heart (frontal plane, unipolar limb leads).

In order to catch cardiac activity, the axis of the lead should traverse near the heart; as such, no cardiac activity is detected when both poles are placed on the legs. The limb leads’ poles are best placed at the mid or distal portions of the limbs. If placed more proximally, on the torso, the amplitude of some QRS waveforms is magnified, especially with proximal positioning of left arm pole.

One can imagine a myriad of non-standard ECG leads. For telemetry monitoring, one bipolar lead consists of right chest pole and left shoulder pole (called middle chest lead MCL, with a recording somewhat similar to the unipolar V1). For long-term rhythm monitoring, a 2-pole patch is positioned on the left upper chest, parallel to the cardiac axis.

Schematic illustration of how electrical depolarization spreads in the heart (horizontal plane, unipolar precordial leads). — **Figure 31.5** Illustration of how electrical depolarization spreads in the heart (horizontal plane, unipolar precordial leads). **V₁ and V₂** overlie the **right** heart and the septum, whereas **V₄ through V₆** overlie the **apex and the LV**. The QRS complex starts as rS in leads V₁–V₃ and progresses to qRs in the left leads. The small r in V₁–V₂ and the small q past the transition zone (V₄–V₆) represent septal depolarization. At the transition zone (e.g., V₃ in this picture), the R wave represents septal depolarization and part of the main axis of depolarization. The amplitude of R or S in each lead depends on how parallel the sum vector of depolarization is to the axis of the lead.

Since leads V₁ and V₂ overlie the right heart, any abnormality that makes electrical forces go towards the right heart makes QRS positive in V₁ or V₂; this is the case in RBBB and RVH. Conversely, any abnormality that makes electrical forces go towards the left makes QRS positive in V₅ or V₆; this is the case in LBBB and LVH.

V₁ → 4th intercostal space, right sternal border. V₂ → 4th intercostal space, left sternal border. V₄ → 5th intercostal space, midclavicular level. V₃ → between V₂ and V₄. V₅ → 5th space, anterior axillary line. V₆ → 5th space, midaxillary line. V₇ → posterior axillary line, V₉ → paraspinal line; V₈ → between V₇ and V₉ (~ below the scapula)

Appendix 2 provides an illustration of cardiac depolarization and the QRS morphology in the limb and precordial leads in various disease states.

The electrical spread of ventricular depolarization (QRS) and ventricular repolarization (ST–T) is captured by the ECG leads. Ventricular repolarization (phases 2 and 3 of the action potential) has an opposite polarity to ventricular depolarization (phase 0 of the action potential), yet the T wave has the same polarity as QRS. In fact, ventricular depolarization spreads from the endocardium to the epicardium; however, the epicardium has a shorter action potential than the endocardium, and although it is activated later, repolarization starts earlier in the epicardium and spreads to the endocardium. Therefore, in normal individuals, the electrical vectors of repolarization and depolarization have the same direction. QRS and ST–T are concordant, with the ST segment being isoelectric as all myocardial cells reach the same phase 2 plateau level without any intramyocardial gradient.

In disease states where some myocardial areas are activated very late, such as bundle branch block or ventricular dilatation or hypertrophy, the late areas are repolarized very late as well, so that the difference in action potential duration between epicardium and endocardium is unable to restore the polarity of repolarization. For example, in LBBB, both the endocardium and epicardium that depolarize late repolarize late as well; in severe concentric LVH, the epicardium depolarizes so late that it repolarizes late as well. In these patients, the electrical vectors of depolarization and repolarization have opposite polarity and directions (QRS and ST–T are discordant), and different parts of the myocardium reach phase 2 (ST segment) at different times, which creates an oblique deviation of the ST segment. This is particularly true in patients with the most delayed depolarization (severe ventricular hypertrophy or enlargement, LBBB).

Schematic illustration of frontal view of the precordial leads. — **Figure 31.6** Frontal view of the precordial leads. Normally, R wave progressively increases in height between V₁ and V₃, V₁ and V₂ overlying the right heart. Occasionally, depending on the heart orientation, the electrode V₂ may be on the left of the septum, while V₃ may be on the right of the septum. R wave may be large in V₂ but becomes small again in V₃. This is more likely to happen if V₃ is placed at the same vertical level as V₂.

On the other hand, the length of the QT corresponds to how dispersed the repolarization is across various myocardial areas, regardless of which areas are repolarized first and last.

II. Stepwise approach to ECG interpretation

The following steps are followed in ECG interpretation:¹

Rhythm: look at QRS regularity and rate.
- Then look for P waves, and assess the P–QRS relationship.
- Determine if the rhythm is sinus (P [+] in I and II and [–] in aVR).
Determine QRS axis in the frontal plane (leads I, II, and aVF). Also assess R-wave progression in V₁–V₆ (normal vs. poor progression vs. early transition).

Then start analyzing each ECG segment:
Analyze P wave in leads II and V₁–V₂ (left or right atrial enlargement).
Analyze PR interval.
Analyze QRS width : if ≥ 120 ms, look at the QRS morphology in the right leads V₁–V₂ and the left leads V₅–V₆, and characterize it as RBBB (wide upright QRS on the right, V₁–V₂), LBBB (wide upright QRS on the left, V₅–V₆), non-specific conduction delay, or pre-excitation (WPW).

Look for LAFB features.

Analyze QRS amplitude : look for big R wave on the right (RVH) or big R wave on the left (LVH), and use the hypertrophy criteria.
Look for abnormal Q waves.
Analyze ST–T segments. Are they depressed or elevated? In which leads and which family?
- In case of ST depression, does the abnormality appear secondary to LVH/LBBB/RVH/RBBB and is it opposite to the QRS direction? Or does it appear ischemic?
- In case of ST elevation, does the abnormality appear secondary to LVH/LBBB and is it opposite to QRS direction? Is it concave upward without reciprocal changes or Q waves (this may suggest pericarditis or secondary ST elevation)? Is PR segment depressed?
Assess QT segment. Look for patterns of electrolyte abnormalities.

III. Rhythm and rate

A. Look at the rhythm strip and survey for the following:

Assess the regularity of QRS complexes. Then look for P waves and assess the P and QRS relationship, i.e., look for an association between P and QRS, and look for hidden P waves manifesting as notches over the QRS or the ST–T segment. P wave is often best seen in lead II, which is often parallel to the P-wave axis.

Examples of cardiac rhythms:
1. Sinus rhythm or tachycardia : one sinus-looking P wave before each QRS (Figure 31.7).
2. Atrial tachycardia, atrial flutter : one or more P waves are seen before each QRS with consistent P–QRS association. R–R intervals are equal or, if not equal, there is a consistent repetition of the same pattern of R–R intervals.
  - Example: 2:1 conduction, meaning that every second P wave gets conducted, so there is one QRS for every two P waves with regular P–P intervals and R–R intervals.
  - Or 4:1 or 1:1 conduction.
  - Or variable conduction (2:1, mixed with 3:1, 4:1). In this case, R–R intervals are irregular, but there is repetition of the same R–R intervals.
3. Atrial fibrillation : irregularly irregular rhythm or tachycardia (total chaos; no repetition of the same R–R intervals; Figure 31.8). Another irregularly irregular rhythm is MAT. Unlike AF, in MAT, polymorphic P waves are seen and conduct in a 1:1 fashion.
4. AVNRT/AVRT : regular, narrow complex tachycardia. P waves are not seen or are seen just after or within ST–T, with a 1:1 QRS–P association (Figure 31.9).
5. Ventricular tachycardia : wide complex tachycardia with no relation between P waves and QRS complexes (AV dissociation) and/or more QRS complexes than P waves (Figure 31.10).
6. Bradycardia with regular P waves and regular QRS complexes, unrelated to each other : complete AV block (Figures 31.11, 31.12).
7. Bradycardia without any P wave : sinus arrest with junctional escape rhythm, AF with complete AV block and junctional escape rhythm, or hyperkalemia.
Premature ventricular or atrial complexes (PVCs or PACs). PVC is wide with ST–T directed opposite to QRS. PAC is narrow, but may be wide in case of aberrancy (Figure 31.13).
Irregular rhythm with some pattern or regularity, meaning that R–R intervals are not all equal, but some of them are:
- Atrial tachycardia or atrial flutter with variable AV conduction (e.g., conduction changes from 2:1 to 3:1, then 2:1 again). The rhythm is irregular, but there is a pattern to it (Figure 31.14).
- PVCs or PACs (PVCs and PACs are usually followed by a pause).
- Sinus arrhythmia (P–P interval varies cyclically, PR distance remains constant).
Groups of beats separated by pauses:
- Second-degree AV block (Figure 31.15)
- Frequent PACs, PVCs, or non-conducted premature Ps, each followed by a pause (Figure 31.13)
Look for pacemaker spikes (small vertical lines before P or QRS or both P and QRS).

Schematic illustration of regular QRS rhythm with a P wave before each QRS complex: sinus tachycardia or atrial tachycardia. — **Figure 31.7** Regular QRS rhythm with a P wave before each QRS complex: sinus tachycardia or atrial tachycardia. Analyze P morphology in leads I, aVR, and II to determine if the rhythm is sinus or ectopic atrial.

Schematic illustration of irregular tachycardia with no repetition of any R–R pattern. — **Figure 31.8** Irregular tachycardia with no repetition of any R–R pattern. No clear P wave is seen; rather, waves that vary greatly in shape are seen. This is AF with fibrillatory atrial waves.

Schematic illustration of narrow complex tachycardia with a pseudo-r’ in lead V1 that represents a retrograde P wave (arrows). — **Figure 31.9** Narrow complex tachycardia with a pseudo-r’ in lead V₁ that represents a retrograde P wave (*arrows*). This is a narrow complex tachycardia with a very short interval between QRS and the retrograde P wave → AVNRT.

Image described by caption. — **Figure 31.10** Wide complex tachycardia: VT vs. SVT with bundle branch block. Look for P waves on top of the ST–T segments: one can identify deflections that have a consistent *morphology* and *timing* and that can be marched out. They occur after every third QRS. Since the number of QRS complexes > number of P waves, this is VT. The P waves are retrograde P waves.

Schematic illustration of bradycardia with regular P waves and regular QRS complexes, unrelated to each other. — **Figure 31.11** Bradycardia with regular P waves and regular QRS complexes, unrelated to each other. Some P waves fall on top of the ST–T segments and manifest as notches. This is a third-degree AV block. If P wave occasionally conducts, the QRS rhythm would have some irregularity.

Schematic illustration of severe bradycardia with regular P waves and regular QRS complexes, unrelated to each other: third-degree AV block. — **Figure 31.12** Severe bradycardia with regular P waves and regular QRS complexes, unrelated to each other: third-degree AV block.

Schematic illustration of irregularity with a pattern. — **Figure 31.13** Irregularity with a pattern. Wide premature complexes with ST–T changes opposite to QRS are seen; these occur in a trigeminal pattern. A wide premature beat is typically a PVC, but could be a PAC with bundle branch block (aberrancy). In this case, the premature beat falls after a normally occurring, non-premature P wave (*blue arrows)* with a shorter PR interval than the sinus beat: this is typical of a PVC. **A PVC does not affect the sinus P wave, which keeps marching through it, sometimes falling before it at a short PR interval.** A PAC, on the other hand, should be preceded by a non-sinus premature P wave that does not march out with the preceding sinus P waves; the premature P may fall prematurely into the preceding T wave and deform it. *A deformed T wave is a clue to a PAC.*

Schematic illustration of atrial flutter with variable conduction (3:1, 4:1). — **Figure 31.14** Atrial flutter with variable conduction (3:1, 4:1). The sawtooth flutter waves are marked by the *arrows*. R–R intervals are not equal, but there is some repetition of the same R–R intervals.

Schematic illustration of there are two groups of beats followed by pauses (asterisks), which raises the suspicion of second-degree AV block (e.g., Wenckebach). — **Figure 31.15** There are two groups of beats followed by pauses (*asterisks*), which raises the suspicion of second-degree AV block (e.g., Wenckebach). P2 is not conducted: this could be AV block or a very premature PAC that gets blocked. The fact that P2 is not premature rules out a blocked PAC. The clue to AV Wenckebach is the progressive PR prolongation, especially manifest when comparing P3R to P1R (P3R < P1R); also, the progressive R–R shortening before the block is a feature of Wenckebach.

B. Calculate the ventricular rate

The ventricular rate is equal to 300 divided by the number of big boxes between two QRS complexes. If the rhythm is irregular (e.g., AF), count the number of QRS complexes in 3 seconds (15 large boxes), then multiply this number by 20; or count the number of QRS complexes on the standard 12-lead ECG run (10 seconds) and multiply it by 6.

C. The rhythm is sinus if P wave is upright in leads I, II, and aVF and inverted in lead aVR, corresponding to a P-wave axis of 0–75°.

Also, a sinus P wave is typically biphasic (positive then negative) in V₁ and V₂, but sometimes entirely positive in V₁–V₂ or entirely negative in V₁. A sinus P wave is always upright in V₃–V₆.

A different P-wave morphology means ectopic atrial rhythm/tachycardia, accelerated junctional rhythm with retrograde P wave, or AVNRT/AVRT with retrograde P wave. A retrograde P wave is negative in the inferior leads II, III, and aVF and is usually seen shortly after the QRS. If P waves have three different morphologies, the rhythm is a wandering atrial pacemaker (rate < 100 bpm) or a wandering atrial tachycardia (rate > 100 bpm, also called MAT) and is irregular.

IV. QRS axis in the limb leads and normal QRS progression in the precordial leads

A. Determine the frontal QRS axis by looking at the net QRS voltage (upward minus downward deflection) in leads I, II, and aVF (see Figure 31.16)

The normal QRS axis is between –30° and +90°. To determine QRS axis, start by looking at leads I and aVF. If the net QRS is negative in lead aVF, the axis is < 0°; one must look at lead II to determine if the axis is < –30°, which defines left-axis deviation.

If the net QRS is negative in lead I and upright in lead aVF, right-axis deviation is present. Six causes (the first four are abnormal):
- RVH (including pulmonary embolism)
- Lung disease even without RVH
- Left posterior fascicular block (LPFB) (usually associated with right bundle-branch block [RBBB])
- Lateral MI: Q wave is seen in lead I. Instead of a Q wave, a diminutive small r wave (rS pattern) sometimes appears in leads I–aVL. In this case, the Q waves in leads V₅–V₆ and the frequently seen T-wave inversion in I–aVL allow the diagnosis (≠ RVH)
- Normal variant: vertical heart with a 90–100° axis in young individuals
- Arm electrodes misplacement: P wave will also be negative in lead I, and upright in lead aVR
If right-axis deviation is present, evaluate for RVH by looking for a tall R wave in V₁ ± V₂ (R wave > 7 mm or R wave > S wave) or a deep S wave in V₆.

Note that isolated RBBB does not lead to right-axis deviation (think of an associated RVH or LPFB when right axis accompanies RBBB).
If the net QRS is upright in lead I but negative in leads II and aVF, left-axis deviation is present. Four causes:
- LVH
- Left anterior fascicular block (LAFB)
- Left bundle branch block (LBBB)
- Inferior MI
The QRS axis progressively shifts more leftward with obesity, which pushes the diaphragm up, and with age, but does not normally exceed –30°. Conversely, thin individuals tend to have a more vertical heart. Inspiration and upright position make the heart more vertical and may explain a change in axis without intervening disease.
If the net QRS is negative in leads I and aVF, the axis is in the northwest quadrant (extreme right or left deviation). The northwest axis may occur in various right or left pathologies.

If QRS is equiphasic in all limb leads, the axis is perpendicular to the frontal plane and is called indeterminate. This may be a normal variant or may occur with right ventricular pathology. One variant, S₁S₂S₃, signifies that S ≥ R in leads I, II, and III, and implies an indeterminate axis (S = R) or northwest axis (S > R). It may be a normal variant when the axis is indeterminate.

B. Look at the normal QRS progression across V₁–V₆

Normally, QRS is negative in V₁–V₂ (rS) and becomes progressively positive in V₅–V₆ (Rs). Note: rS denotes small R, big S. Rs denotes big R, small S.

If QRS starts positive in V₁–V₂ ( early transition ), consider six causes, the first two being “Right problems”:
- RVH (which also leads to right-axis deviation).
- RBBB.
- Posterior wall infarction: large, and more importantly, wide R wave in V₁, reciprocal of a posterior Q wave. Often, Q waves are present in V₇–V₉ and in the inferior leads.
- WPW: short PR and delta wave are present.
  
  Figure 31.16 Start by looking at leads I and aVF. If QRS is negative in lead aVF, the axis is < 0°; one must look at lead II to determine if the axis is < –30°, which defines left-axis deviation. In all other cases, looking at leads I and aVF is enough to grossly define the type of axis deviation. Reproduced with permission of Scrub Hill Press from Hanna et al. (2009).¹
- Septal hypertrophic cardiomyopathy (thick septum, thicker than the lateral wall, projects as big R in V₁–V₂ and big Q in the lateral leads); or Duchenne muscular dystrophy (posterior wall fibrosis).
- However, the most common cause of early transition is a normal variant. It is more common in young individuals, where the heart is swung more anteriorly than older individuals. A low malposition of electrodes V₁–V₂ is also a common cause of early transition.
Poor precordial R-wave progression means that the R-wave height remains < 3 mm (=0.3 mV, three small boxes) in lead V₃, and more specifically ≤ 1.5 mm, with failure of the R/S height ratio to increase.

It may be an equivalent of Q wave and may signify an anterior MI, particularly if one of the following two features coexists: (i) T inversion in V₁–V₃; (ii) R wave in lead I < 4 mm. The small R wave in lead I suggests diminution from a lateral MI, although it may also be secondary to COPD. Conversely, the following two features argue against MI: (i) improvement of R-wave progression with lower placement of the chest electrodes; (ii) sudden R-wave transition in V₄ or V₅, which suggests a high misplacement of electrodes V₁–V₂ and a normal placement of electrodes V₃–V₆, as in patients with large breasts. In MI, R wave remains small in V₄–V₅ and transitions slowly, yet a slow transition does not necessarily imply MI. Reverse R progression, which means that R wave not only progresses poorly but gets smaller between V₁ and V₂ or V₂ and V₃, slightly increases the likelihood of MI.

However, poor R progression is most often related to the following causes, the first three being “left problems” (Figure 31.17):
- LAFB.
- LVH.
- LBBB.
- High misplacement of electrodes V₁–V₂ or low heart/low diaphragm position (thin and tall individuals); or heart swung posteriorly, away from V₁–V₂ (older subjects). Normal R-wave progression may be seen when the chest leads are placed one interspace lower.
- COPD, in which case the heart is pushed down and posteriorly, away from the precordium: COPD leads to poor R-wave progression with right-axis deviation. Poor R-wave progression with right-axis deviation may also be seen when anterior MI is associated with a high lateral MI. The overall size of the QRS allows the distinction between COPD and anterior MI (QRS voltage is often reduced in COPD). Also, in COPD, recording the chest leads one interspace lower often corrects R-wave progression, at least partially.

V. P wave: analyze P wave in leads II and V₁ for atrial enlargement, and analyze PR interval (see Figures 31.18, 31.19)

A. Lead V₁ (and/or V₂)

Left atrial enlargement = terminal negative P-wave deflection > 1 box wide (40 ms) and 1 box deep (0.1 mV).
Right atrial enlargement = initial positive P-wave deflection ≥ 1.5 small boxes high.

B. Lead II (and I, III)

P waves should be < 2.5 small boxes high (0.25 mV high) and < 3 small boxes wide (120 ms wide).

Left atrial enlargement = P wave ≥ 120 ms and notched

P may have a negative terminal deflection in leads III and aVF, i.e., left P-axis deviation. While an abnormal P-wave axis suggests ectopic atrial origin, in context, it may rather imply atrial enlargement.

Figure 31.17 Poor R-wave progression probably secondary to LVH with a sudden transition in V₅ (arrows). Sudden transition is a good indicator of the absence of anterior MI. The lack of T-wave inversion in the anterior leads and the normal-size R wave in lead I also make MI unlikely.

Figure 31.18 Normal and abnormal RA and LA deflections. Atrial depolarization starts from the sinus node, at the junction of SVC–RA, and spreads in a radial fashion to depolarize the RA, interatrial septum, and LA.

RA enlargement (RAE) is characterized by increased voltage of the first atrial deflection in lead II and in leads V₁–V₂. LA enlargement (LAE) is characterized by prolongation of P duration in lead II with a double hump, the second hump corresponding to LA depolarization. Depending on the severity of LAE and on the heart orientation, the P wave may peak high and relatively early in lead II, simulating RAE (e.g., vertical heart). Also, it may have a positive component in lead V₁. Thus, anatomical LAE may mimic RAE electrocardiographically; up to 30% of cases of electrocardiographic RAE are actually LAE.

Moreover, depending on the severity of RAE, the duration of P wave may be increased and a negative component may be seen in lead V₁. Thus, anatomical RAE may simulate LAE electrocardiographically.

P-wave amplitude normally increases during sinus tachycardia or exercise, while the P-wave duration decreases; this is due to a more synchronized RA and LA depolarization. Thus, RAE criteria are less valid in sinus tachycardia, but LAE criteria remain valid. In fact, an increase in P duration with exercise suggests left HF with LA volume overload unveiled by exercise.

RAE and LAE may be seen on ECG as a result of increased atrial pressure or atrial ischemia, even in the absence of true enlargement. RAE may be seen in patients with lung disease (vertical heart) even in the absence of true enlargement. Thus, the ECG terms RAE and LAE are better replaced with RA abnormality and LA abnormality, respectively.

Figure 31.19 Right atrial enlargement and left atrial enlargement. Reproduced with permission of Scrub Hill Press from Hanna et al. (2009).¹
Right atrial enlargement = P wave is peaked ≥ 0.25 mV

P axis may be rightward > +75°, and P may become flat in lead I and inverted in aVL. This could suggest a non-sinus P wave. However, in the presence of other signs of right heart pathology (i.e., right-axis deviation of QRS), the P wave is rather a sinus P wave with a right P-axis deviation.

C. Normal PR interval

Normal PR interval is 120–200 ms (3–5 small boxes; assess it in multiple leads and take the longest).

PR < 3 small boxes: pre-excitation (WPW pattern), but may just be a fast-conducting AV node. Look for delta waves.
PR > 5 small boxes: first-degree AV block.
PR interval includes AV conduction but also atrial repolarization. Atrial enlargement, atrial infarction, or sinus tachycardia with increased P-wave amplitude may depress the PR interval; also, atrial repolarization may prolong and extend over the ST segment, causing ST depression.

VI. Height of QRS: LVH, RVH

Grossly, look at the height and the width of QRS in leads V₁, V₆ and I–aVL.

A. Look for LVH (see Figure 31.20)

LVH can be identified using any of the following criteria (assuming standard calibration):

In lead I, R wave > 14 mm, or R wave in lead I + S wave in lead III > 25 mm.
In lead aVL, R wave > 11 mm or > 13 mm in case of LAFB (very specific criterion).
S wave in V₃ + R wave in aVL ≥ 28 mm in men or ≥ 20 mm in women. This is Cornell criterion, the most sensitive and specific LVH criterion. Specificity is reduced if LAFB is additionally present.
In the precordial leads: big R on the left (V₅–V₆) and big S on the right (V₁–V₂) translate into:
- S wave in V₁ + R wave in V₅ or V₆ ≥ 35 mm
- Any S wave (V₁–V₃) + any R wave (V₄–V₆) ≥ 45 mm
- R wave in V₆ > R wave in V₅.
- R wave in V₅ or V₆ > 26 mm
Notes:
- LVH may be associated with delayed precordial QRS transition, as the vector of depolarization is turned leftward.
- LAFB shifts the electrical depolarization superiorly and posteriorly; thus, R wave is increased in the limb leads I and aVL, and S wave is deepened across the precordial leads. This reduces the specificity of Cornell and aVL criteria.

Schematic illustration of LVH with secondary ST–T depression in the left lateral leads, directed opposite to the QRS complex, called strain pattern. — **Figure 31.20** LVH with secondary ST–T depression in the left lateral leads, directed opposite to the QRS complex, called *strain pattern* (marked by the *circles*).

The following LVH criteria are met (as indicated by the arrows):

R aVL + S V₃ ≥ 28 mm (5.5 big boxes)

R aVL > 11 mm (>2.2 big boxes)

R in I ≥ 15 mm (3 boxes); R in I + S in III > 25 mm

S in V₁ + R in V₅ or V₆ ≥ 35 mm; R in V₅ > 26 mm

B. Look for RVH (Figure 31.21)

RVH is characterized by:

Right-axis deviation (net QRS [–] in lead I, [+] in lead aVF)

and
Big R wave in the right lead V₁ (≥7 mm), or big S wave in the left leads V₅–V₆ (≥7 mm)

Or big R > S in V₁, big S > R in V₆, or small S in V₁ ≤ 2 mm

Or R in V₁ + S in V₆ > 10.5 mm

In the absence of RBBB, a monophasic R wave in V₁ or a qR pattern in V₁ signifies severely increased RV pressure (higher than systemic pressure in the case of qR pattern).

RVH differential diagnosis and coexisting patterns

Posterior MI may lead to a prominent R wave in V₁. In posterior MI, R wave is not only high but is also wide > 1 mm (≠ RVH), T wave is positive in V₁–V₂ (vs. inverted in RVH), the axis is not right, and there are often Q waves in V₇–V₉ and in the inferior or lateral leads.
An incomplete RBBB pattern with RSR’ may be seen along with RVH. In fact, incomplete RBBB with right axis is frequently secondary to RVH, more specifically a volume overload pattern of RVH, with prolonged right bundle conduction related to the RV size rather than right bundle disease. RVH is definitely diagnosed if the axis is right and R’ > 10 mm. As RVH progresses, R’ becomes taller and a monophasic R may develop, particularly with pressure overload patterns.
Lung disease, such as COPD , is characterized by: (1) right-axis deviation in the frontal plane as the heart is pushed down and made more vertical; (2) deep S wave in all precordial leads, V₁ through V₆, as the heart rotates posteriorly; (3) reduced overall QRS voltage in all leads, especially limb leads, because of increased chest air; while dominant, S wave is not particularly deep in the precordial leads. This chronic lung disease pattern simulates an old anterolateral MI, wherein R is diminished across all precordial leads and in the lateral leads I and a VL (rS pattern throughout all those leads).

The presence of true RVH in conjunction with lung disease is characterized by one of the following: large R or small S in V₁ (≤2 mm), RSR’ pattern, or T-wave inversion in V₁–V₂. P pulmonale may be seen with lung disease even without RVH.

Additional notes

Right-axis deviation may be less evident in patients with an associated LVH or LAFB.
Higher voltage and more strain pattern is seen with pressure overload (pulmonary hypertension) than with volume overload (ASD). ASD is often only characterized by rSR’ pattern, and rarely leads to tall monophasic R waves.
Left atrial enlargement supports the diagnosis of LVH, and right atrial enlargement supports the diagnosis of RVH in cases of borderline voltage criteria. LVH with right atrial enlargement or RVH with left atrial enlargement suggests biventricular hypertrophy, unless MS is present (MS may lead to left atrial enlargement + RVH).

C. Biventricular enlargement

Biventricular enlargement is characterized by any one of the following:

Voltage criteria for both LVH and RVH. This usually implies tall R waves in V₅–V₆ (LVH) with a small S wave in V₁, or R > S in V₁ (R is not usually large in V₁, but is larger than S).
LVH with right-axis deviation.
LVH with right atrial or biatrial enlargement.
LVH with T inversion in V₁–V₂ (T going in the same direction as QRS). This T inversion can be secondary to RV strain or anterior ischemia.
Tall R wave and tall S wave in the mid-precordial leads V₃–V₄ (Katz–Wachtel sign).

Schematic illustration of QRS is (–) in lead I and (+) in lead aVF, implying a right-axis deviation. — **Figure 31.21** QRS is (–) in lead I and (+) in lead aVF, implying a right-axis deviation. The smallest net QRS is in leads I and aVR. QRS axis is thus between perpendicular to I (+90°) and aVR (+120°). Axis is ~ +105°. RVH is diagnosed by the fact that axis is right and R > S in V₁. In fact, there is a qR pattern in V₁ (S = 0) (*arrow*), signifying severely increased RV pressure. P pulmonale and secondary T inversion are also seen.

VII. Width of QRS. Conduction abnormalities: bundle brunch blocks

The normal QRS duration is < 110 ms. In complete bundle branch block, the QRS is wide (≥120 ms or 3 small boxes). In incomplete bundle branch block, the QRS is 110–119 ms.

Look at the QRS complex in lead V₁. Is the net QRS complex upright (i.e., positive)?

If yes, consider RBBB.
If no (negative QRS in lead V₁), consider LBBB. A conduction block makes the QRS vector look towards it: RBBB makes the QRS vector look towards the right, leading to an upright wide QRS in the right leads (Figures 31.22–31.26).

Schematic illustration of RBBB, the vector of depolarization spreads from the left septum to the right and left ventricles. — **Figure 31.22** In RBBB, the vector of depolarization spreads from the left septum to the right and left ventricles. RSR’ is seen in V₁, R being septal depolarization, S being LV depolarization, and R’ being the late RV depolarization. RS is seen in V₆, R being LV depolarization, and the wide S being the slow RV depolarization.

In LBBB, the vector of depolarization spreads from the right septum to the left septum and the left ventricle. The vector looks toward V₆ and away from V₁. Thus, in LBBB, QRS is positive in V₅–V₆ and widely negative in V₁. The septal q wave that is normally seen in the left lateral leads is lost, as the septum depolarizes from the right to the left. The presence of any q wave in leads V₅–V₆ or lead I is not typical of LBBB and suggests an old MI. Only rarely, a q wave may be seen in lead aVL.

**In both RBBB and LBBB, QRS starts narrow and normal, then widens later.**

A. RBBB

In RBBB, QRS has a slurred positivity in the right leads. Beside QRS ≥ 120 ms, both the following two criteria are required to make the diagnosis of RBBB:

rSR’, rsR’, or rsr’ pattern in the right leads V₁ and/or V₂. R’ is usually wider and taller than the initial R wave. A qR pattern may replace rSR’ in lead V₁ when the initial r wave is isoelectric. A single wide R wave, often notched, may be seen instead of rSR’.
A wide S wave in the left leads I and V₆. S wave must be wider than R wave or wider than 40 ms.

In addition, T-wave inversion in V₁–V₂ is common but not mandatory (T directed in an opposite direction to QRS).

Schematic illustration of rBBB. — **Figure 31.23** RBBB. rSR’ is seen in V₁, notched R wave is seen in V₂, and rsR’ and qR patterns are shown on the right (rsR’ means small R, small S, big R’). Any of those patterns is consistent with RBBB in V₁–V₂. S wave is wide and slurred in leads I, aVL, and V₅–V₆.

Schematic illustration of sinus tachycardia with RBBB (rSR’ in V1–V2, wide and slurred S in V5–V6 and I–aVL, arrows). — **Figure 31.24** Sinus tachycardia with RBBB (rSR’ in V₁–V₂, wide and slurred S in V₅–V₆ and I–aVL, *arrows*). Right-axis deviation (QRS [–] in lead I, [+] in lead aVF) signifies an associated RVH (most commonly) or LPFB. T-wave inversion in V₁–V₃ and II/III/aVF is secondary to RBBB and RVH. The patient is diagnosed with PE. Reproduced with permission of Scrub Hill Press from Hanna et al. (2009).¹

B. LBBB

In LBBB, QRS has a slurred positivity in the left leads. The first four criteria are required to make the diagnosis of LBBB:

Wide notched R wave in leads I, aVL, and V₅–V₆ (M-shaped or slurred, plateaued R wave).
QRS is negative in leads V₁, V₂, V₃ with an rS or QS pattern.

QS pattern may also occur in leads III and aVF, simulating an inferior MI, but not in lead II.

QR pattern does not occur with LBBB and always implies an associated MI.
The septal q wave should be absent in the left leads I and V₅–V₆. A narrow q wave may be seen in aVL.
The ST segment and T wave should be directed opposite to QRS. Unlike LVH, RBBB, and RVH, secondary ST–T changes are mandatory in LBBB.
Two less usual features may be seen in LBBB and do not preclude the diagnosis of LBBB:
- q wave in aVL.
- RS pattern (rather than a plateaued R pattern) in leads V₅–V₆. This occurs in patients with delayed QRS transition, such as patients with enlarged LV or LV depolarization that spreads from apex to base; the frontal QRS axis is leftward in both of these cases.

An incomplete RBBB or LBBB, also called bundle branch delay, is characterized by a QRS of 110–119 ms with QRS features of the respective bundle branch block in V₁, V₆, and I. Similarly to a complete block, an incomplete block is accompanied by the secondary repolarization abnormalities.

Schematic illustration of LBBB. — **Figure 31.25** LBBB. In the lateral leads, there may be an “M-shaped” R wave (as seen here in I and V₅) or a broad slurred R wave (as seen in V₆), with delayed R-wave peak time > 60 ms, measured from QRS onset to the second R notch or the end of the R plateau. When the LV is enlarged or the depolarization is turned further leftward, the transition zone and the wide R wave may not be reached in lead V₆, and an RS pattern is seen in leads V₅–V₆. The wide, M-shaped R wave will still be seen in leads I-aVL and will also be seen more laterally in leads V₇–V₉. Reproduced with permission of Scrub Hill Press from Hanna et al. (2009).¹

Schematic illustration of LBBB (slurred R wave in the left leads: V5–V6 and I–aVL) (arrows). — **Figure 31.26** LBBB (slurred R wave in the left leads: V₅–V₆ and I–aVL) (*arrows*). ST depression in V₅–V₆, I, and aVL, and ST elevation in V₁–V₃, directed opposite to QRS, are secondary to LBBB (*circles*).

rSR’ or rSr’ patterns in V₁–V₂ may be normal variants if QRS is < 110 ms and r and r’ are small (r’ < 5 mm) and smaller than S wave, without right-axis deviation, right atrial enlargement, or T-wave inversion.
Posterior MI may simulate rSR’ in V₁. As opposed to RBBB, r is usually wide.
RVH may lead to rSR’ pattern in V₁ with incomplete or complete RBBB. In those cases, RVH is diagnosed if the axis is right, as determined by the net voltage of the initial, unblocked 80 ms of QRS in the limb leads, along with a suggestive clinical context or R’>10 mm in V₁. In fact, right axis in a RBBB is most commonly due to RVH, more so when RBBB is incomplete. Incomplete RBBB may reflect a prolonged depolarization of a large RV rather than a histological abnormality of the right bundle.

A wide QRS (“complete block” ≥ 120 ms) typically has either RBBB or LBBB pattern. A mildly widened QRS (110–119 ms) may be an incomplete block (RBBB or LBBB pattern), or a widened QRS accompanying LVH, RVH, or fascicular block.

However, a mildly or a definitely widened QRS may also signify:

Pre-excitation (WPW). In that case, the wide QRS starts with a “slur” (= delta wave = slow QRS upslope). This slur is riding the P wave (= short PR). Unlike bundle branch block, where QRS has a steep initial portion and a slow terminal portion, the QRS complex of WPW is widened at its initial uptake (Figure 31.27).
Hyperkalemia.
Drugs (class Ic antiarrhythmic drugs, tricyclics, phenothiazines).
Non-specific intraventricular conduction delay.

Schematic illustration of WPW with short PR segment and slurred R wave. — **Figure 31.27** WPW with short PR segment and slurred R wave. The upslope of R wave is slow (≠ LBBB).

VIII. Conduction abnormalities: fascicular blocks

The left bundle divides into the left anterior and the left posterior fascicles. In fascicular blocks, unlike bundle branch blocks, QRS must not be very wide and must be < 120 ms; usually, QRS is 80–100 ms wide (Figures 31.28, 31.29, 31.30).

A. Left anterior fascicular block (LAFB)

LAFB is defined as “an unexplained left-axis deviation” with QRS axis between –45° and –90°. In other words, LAFB manifests as left-axis deviation beyond –45° without LBBB or inferior MI.
A qR pattern is seen in lead I and particularly lead aVL, while rS pattern is typically seen in the inferior leads II, III, and aVF (net QRS is negative in the latter leads). Beside being positive in I and negative in aVF, the net QRS is larger in aVF than in I, which defines axis ≤ –45°.
Additional notes:
- LVH does not preclude LAFB diagnosis. In fact, LVH with left-axis deviation over –45° usually implies LVH + LAFB.
- Inferior MI makes LAFB diagnosis more difficult. Inferior MI may lead to a QS pattern in leads II, III, and aVF and a left axis over –45°, whether LAFB coexists or not. If LAFB coexists, R wave will peak in aVL earlier than in aVR.
- LAFB does not, by itself, produce QS waves in leads III and aVF and should not mimic inferior MI.
- While the ACC guidelines mandate the presence of a small septal q wave in lead aVL for the definition of LAFB, a study has suggested that up to 27% of patients with LAFB do not have a q wave in leads I and/or aVL. These may be patients who have a horizontal heart, in whom the septal depolarization is orthogonal to lead I ± aVL, or patients who have a degree of septal conduction block.
- LAFB is common with and without underlying heart disease and does not portend an independent prognostic significance. LAFB does not lead to secondary ST–T abnormalities.
Figure 31.28 In LAFB, the vector of depolarization spreads from the posterior fascicle superiorly and to the left in a counterclockwise fashion. The superior spread in the frontal plane explains the left-axis deviation and the fact that R wave peaks earlier in lead aVL (left) than aVR (right). Also, the R wave amplitude is increased in leads I and aVL. Unlike LBBB, septal depolarization is still left-to-right, hence the septal q wave in leads I and aVL is not usually lost. The q wave may be lost in lead I if the septal depolarization is orthogonal to lead I, but not usually in lead aVL.

The superior spread away from the precordial plane explains the deep S waves across all of the precordial leads V₁–V₆ and the delayed R-wave progression. The small “r” corresponds to the initial, inferiorly directed septal depolarization. Occasionally, if the leads are moved up, away from this initial depolarization, the initial “r” is lost, which produces a QS pattern in V₁–V₂ mimicking anterior MI. Moreover, a tiny initial q wave may appear before “r” in V₁–V₃ (qrS pattern), further mimicking MI. The resolution of Q wave by moving the leads one intercostal space down argues against MI.

In LPFB, the depolarization spreads left/up through the anterior fascicle then down and to the right. This initial upward spread explains the q waves in leads III and aVF, while the inferior spread explains the prominent R wave in those leads, the right-axis deviation, and the deep S wave in leads I and aVL. LAF, left anterior fascicle; LPF, left posterior fascicle.
Figure 31.29 LAFB + RBBB.
- QRS is wide > 120 ms with rSR’ in V₁ and a wide S in V₅–V₆ = RBBB.
- The net QRS is (–) in lead aVF and equiphasic in lead I, implying a left axis of ~ –90°. In the absence of LBBB, this is diagnostic of LAFB. Also, a q wave is seen in lead aVL, which is often necessary to define LAFB.
Reproduced with permission of Scrub Hill Press from Hanna et al. (2009).¹

B. LPFB

LPFB is uncommon and typically occurs in conjunction with RBBB.
LPFB is defined as “an unexplained right-axis deviation” (more than +90°) = right-axis deviation without RVH, COPD, or lateral MI (R wave in V₁ and S wave in V₆ are not large). A qR pattern is seen in the inferior leads III/aVF. LPFB does not lead to ST–T abnormalities.

C. Bifascicular and trifascicular blocks

A bifascicular block is a block in two of the three conduction fascicles (right bundle, left anterior fascicle, and left posterior fascicle). It can take one of the following forms: (i) LBBB; (ii) RBBB + LAFB = RBBB with left-axis deviation; (iii) RBBB + LPFB = RBBB with right-axis deviation (which could also be RBBB + RVH).

Schematic illustration of RBBB + LPFB. — **Figure 31.30** RBBB + LPFB. Since QRS is wide > 120 ms, look in V₁ and in V₆ to determine if the morphology fits more with LBBB or RBBB. In this case, QR morphology is seen in V₁ (*box*), with a wide slurred S wave in V₅–V₆ and I, aVL (*circles*): this is RBBB. The axis is right (net QRS is negative in I and positive in aVF). Exact axis: QRS is closest to equiphasic in lead II → axis perpendicular to +60° → +150°. The cause of right axis could be RVH or LPFB. Because there are no RVH criteria (R’ < S in V₁, S not larger than R in V₆), LPFB is the probable diagnosis. Reproduced with permission of Scrub Hill Press from Hanna et al. (2009).¹

A trifascicular block implies that all three fascicles have a conduction block. The block is incomplete in at least one fascicle, otherwise complete AV block would be present. Trifascicular block may manifest as:

Bifascicular block + increased PR interval: this is often a trifascicular block (may also be bifascicular block with first-degree AV block)
Alternating RBBB + LBBB, i.e., RBBB and LBBB alternate on the same ECG or on different ECGs obtained up to several years apart
RBBB with alternating LAFB and LPFB

D. Wide QRS 110–119 ms or ≥ 120 ms that does not fulfill the typical LBBB or RBBB morphology

For example, one bundle branch block morphology is seen in the precordial leads and the contralateral bundle branch block morphology is seen in the limb leads. This wide QRS may be:

A form of RBBB + LAFB
Non-specific intraventricular conduction delay, especially in a patient with cardiomyopathy
Pre-excitation, hyperkalemia, or drugs (class I antiarrhythmics, tricyclics)

Note that QRS notching with a normal QRS duration < 110 ms does not imply a conduction delay and is often normal. It is related to the way the vector of depolarization spreads around the lead.

IX. Low QRS voltage and electrical alternans

Low QRS voltage is defined as an absolute sum of R and S waves < 5 mm in every limb lead and < 10 mm in every precordial lead. Also, a decrease in voltage in the limbs and/or precordial leads in comparison to an old ECG may be indicative of disease, even if it does not fulfill the listed criteria. A patient with baseline LVH may have a relatively reduced QRS voltage without fulfilling the low-voltage definition.

A. Differential diagnosis of small QRS voltage

Pericardial effusion. Electrical alternans may also be seen.
Any “shield” around the heart: COPD, obesity, large pleural effusion, and notably hypothyroidism (“low” and “slow”).
Constrictive pericarditis; some restrictive infiltrative cardiomyopathies (such as amyloidosis and hemochromatosis, but not Fabry disease).

B. High QRS voltage in the precordial leads with low QRS voltage in the limb leads is relatively specific for a dilated LV with low EF

C. Electrical alternans is an every-other-beat alternation of two different but equally wide and equidistant QRS complexes

Electrical alternans may also involve the P and T waves, in which case it is called total alternans and is very specific for pericardial effusion (Figure 31.31).

QRS amplitude may vary with respiration, particularly in patients who are breathing heavily. In this case, the heart position, and more particularly the septal position, varies with respiration; this may be seen in tamponade, but also in severe COPD or any respiratory distress. This cyclic change of QRS morphology and axis is not electrical alternans and correlates more with pulsus paradoxus (“electrical paradoxus”). Conversely, electrical alternans implies every-other-beat alternation of two distinct QRS morphologies and corresponds to a swinging heart in a patient with pericardial efffusion. Electrical alternans may also be seen with:

Severe HF, where it is mechanically induced by an alternate change in cardiac contraction (like pulsus alternans).
SVT, especially AVRT or any fast SVT, wherein a slight variation in ventricular conduction occurs alternately.
Acute myocardial ischemia or PE, where again there is a conduction alternans.
Intermittent pre-excitation or intermittent conduction block, such as LAFB or bundle branch block, occurring in an alternating fashion. This is rather a mimic than a true electrical alternans.

A slight change in QRS morphology may normally be seen between the beats of an irregular rhythm, making the diagnosis of true electrical alternans more difficult (e.g., AF).

X. Assessment of ischemia and infarction: Q waves

Normally, a small Q wave (q) may be seen in all leads except the right precordial leads before the R/S transition zone, which usually corresponds to leads V₁, V₂, and V₃. An abnormal Q wave signifies an old MI, a recent MI, or an acute evolving STEMI (in the latter, concomitant ST elevation would be present in the same leads) (Figures 31.32–31.35).

Schematic illustration of wide Q wave (QS or QR) may be normally seen in lead III of a horizontal heart looking away from lead III. — **Figure 31.32** Wide Q wave (QS or QR) may be normally seen in lead III of a horizontal heart looking away from lead III. QS or QR pattern may normally be seen in lead aVL in a patient with a vertical heart that looks away from lead aVL.

Schematic illustration of examples of an abnormal Q wave. — **Figure 31.33** Examples of an abnormal Q wave. **(a)** ECG shows minimal ST elevation with narrow small q waves in leads V₃–V₄ and post-ischemic terminal T-wave inversion (not a Wellens syndrome since Q waves are present). **Q of any size, when seen in the precordial leads before the transition zone as part of a qrS complex, is abnormal and is almost 100% indicative of MI** (the rare exception being the tiny q wave sometimes seen with LAFB). This ECG is a late STEMI, at a time when Q waves/T inversion have appeared and ST elevation is resolving. **(b)** Small q waves in leads V₄–V₅ where QRS is still overall negative. Thus, these q waves occur before the transition zone and imply MI, even if very small.

Schematic illustration of inferior Q waves and anterolateral QS waves (QS waves are wide monophasic Q waves, arrows). — **Figure 31.34** Inferior Q waves and anterolateral QS waves (QS waves are wide monophasic Q waves, *arrows*). QS waves may be normal in leads V₁–V₂, but not in leads V₃–V₆.

Schematic illustration of QS pattern is seen in leads V1–V2, small R wave is seen in leads V3–V4. — **Figure 31.35** QS pattern is seen in leads V₁–V₂, small R wave is seen in leads V₃–V₄. As opposed to QS pattern extending to V₃ or beyond, QS pattern limited to V₁ or V₂ is not definitely an anterior MI. Only 20% of patients with a QS pattern in leads V₁–V₂, without other abnormalities on the ECG, have an anterior MI. The differential diagnosis of a QS pattern in leads V₁–V₂ is similar to the differential diagnosis of delayed R-wave progression.

Q wave is abnormal when it is:

≥ 0.03 seconds wide (~1 small box) and ≥ 0.1 mV deep (1 mm)

or
whenever any q wave is seen before the precordial transition zone, no matter how small it is (= any q wave in leads V₁–V₃ is abnormal when QRS is still overall negative in V₁–V₃).

The criterion Q wave > ¼ of the R-wave height is not, per se, specific for the diagnosis of MI.

A wide and tall R wave in leads V₁ or V₂ is a mirror image of a posterior Q wave and implies posterior MI (R ≥ 0.04 seconds in width and R > S in height). As opposed to RVH, R wave is not just tall but wide, T wave is upright rather than inverted, and Q waves are often present in the inferior or lateral leads, and in leads V₇–V₉.

Differential diagnosis of pathologic Q waves

A QRS that consists of only one deep negative deflection is, in fact, a monophasic deep Q wave. Since there is no intervening R wave, this negative wave is a Q wave rather than an S wave, but is sometimes called a QS wave.
QS in V₁–V₂ may represent an anterior MI in 20% of the cases, but often does not. Similarly to poor R-wave progression, it often results from LBBB, LAFB, LVH shifting the heart leftward and posteriorly, COPD pushing the heart down and posteriorly, or, frequently, low heart/low diaphragm with high lead placement away from the heart. Moving the precordial leads below the standard position may correct Q waves in many of the latter cases (COPD, low heart, LAFB). QS that extends to V₃ is often an anterior MI, while QS extending to V₄ is definitely an anterior MI. Importantly, as opposed to QS, qrS in V₁–V₃ always signifies anterior MI, regardless how small the q wave is (rarely, anterior qrS may be seen with LAFB). While infrequently suggestive of anterior MI, poor R-wave progression may be the only sequela of ~25% of anterior MIs.

Figure 31.36 In expiration, Q wave is wide and deep in leads III and aVF (arrows); no Q wave is seen in lead II at any time (Q wave in lead II makes inferior MI definite). During inspiration or upright position, the Q wave becomes smaller and narrower in both leads III and aVF, implying that this Q wave is most likely related to a horizontal heart position during expiration. This lessens the probability of inferior MI but does not rule it out.
Whereas QS or QR in the inferior leads III and aVF often signifies an MI, it may be a normal variant in obese/stocky individuals with horizontal hearts directed away from the inferior leads. A deep breath or standing up verticalizes the heart and minimizes these Q waves (Figure 31.36).

QS in leads III and aVF, but not in lead II and not QR, may also occur with LBBB and LVH, cases where the depolarization vector looks away from the inferior leads.

QR in leads III and aVF may be seen with RVH or PE, wherein the LV is pushed up and the RV expands down. The up-looking LV depolarization explains the inferior Q waves.

Note, however, that a wide Q in the inferior lead II almost always implies MI, and a QrS pattern, even when limited to leads III and aVF, usually implies MI and is not seen with obesity or conduction abnormalities. Also, the presence of a wide R wave in lead aVR increases the likelihood of a true inferior MI.
QS or QR may normally occur in lead aVL in patients with vertical hearts, or in cases of chest deformity or left pneumothorax. Severe septal hypertrophy (HCM) may produce deep/wide Q waves in the lateral leads (QR pattern in leads I, aVL, V₅–V₆), and sometimes the inferior leads, ± prominent R waves in the right precordial leads V₁–V₂ (all correspond to the septal forces).
The negative delta wave of pre-excitation may simulate a wide and pathologic Q wave. It may be seen in the inferior, lateral, or anterior leads.
Any cardiomyopathy, especially infiltrative cardiomyopathy (e.g., amyloidosis), may lead to Q waves as a result of fibrosis or myocardial replacement with the infiltrative process. Myocarditis occasionally leads to Q waves.
Takotsubo cardiomyopathy, which leads to anterior ST-segment elevation and T-wave inversion, may also lead to transient anterior Q waves.

XI. Assessment of ischemia: ST-segment depression and T-wave inversion

Abnormalities of the ST segment and T wave represent abnormalities of ventricular repolarization. The ST segment corresponds to the plateau phase of ventricular repolarization (phase 2), while the T wave corresponds to the phase of rapid ventricular repolarization (phase 3). ST-segment or T-wave changes may be secondary to abnormalities of depolarization, i.e., pre-excitation or abnormalities of QRS voltage or duration. On the other hand, ST-segment and T-wave abnormalities may be unrelated to any QRS abnormality, in which case they are called primary repolarization abnormalities. They are caused by ischemia, pericarditis, myocarditis, drugs (digoxin, antiarrhythmic drugs), and electrolyte abnormalities, particularly potassium abnormalities.²

ST-segment deviation is usually measured at its junction with the end of the QRS complex, i.e., the J point, and is referenced against the TP or PR segment.³ Some authors, however, prefer measuring the magnitude of the ST segment deviation 40–80 ms after the J point, when all myocardial fibers are expected to have reached the same level of membrane potential and to form an isoelectric ST segment; at the very onset of repolarization, small differences in membrane potential may normally be seen and may cause deviation of the J point and of the early portion of the ST segment.⁴ A diagnosis of ST-segment elevation myocardial infarction (STEMI) that mandates emergent reperfusion therapy requires ST-segment elevation equaling or exceeding the following cut-points, in at least two contiguous leads (using the standard of 1.0 mV = 10 mm):⁵

1 mm in all standard leads other than leads V₂–V₃.
2.5 mm in leads V₂ and V₃ in men younger than age 40, 2 mm in leads V₂ and V₃ in men older than age 40, and 1.5 mm in these leads in women.
0.5 mm in the posterior chest leads V₇–V₉. ST-segment elevation is attenuated in the posterior leads because of their greater distance from the heart, explaining the lower cut-point.

Concerning ST-segment depression, a depression of up to 0.5 mm in leads V₂ and V₃ and 1 mm in the other leads may be normal.³

While ST-segment deviation that falls below these cut-points may be a normal variant, any ST-segment elevation or depression (≥0.5 mm) may be abnormal, particularly when the clinical setting or the ST-segment morphology suggests ischemia, or when other ischemic signs such as T-wave abnormalities, Q waves, or reciprocal ST-segment changes are concomitantly present. Conversely, ST-segment elevation that exceeds these cut-points may not represent STEMI. In an analysis of chest pain patients manifesting ST-segment elevation, only 15% were eventually diagnosed with STEMI. Beside size, careful attention to the morphology of the ST segment and the associated features is critical.

In adults, the T wave is normally inverted in lead aVR; is upright or inverted in leads aVL, III, and V₁; and is upright in the remaining leads. The T wave is considered inverted when it is deeper than 1 mm and is considered flat when its peak amplitude is between 1 mm and –1 mm.³

A. Secondary ST-segment and/or T-wave abnormalities

In secondary ST-segment or T-wave abnormalities, QRS criteria for ventricular hypertrophy (LVH or RVH), bundle branch block (LBBB or RBBB), or pre-excitation are usually present, and the ST segment and T wave have all of the following morphologic features (Figure 31.37A):

The ST segment and T wave are directed opposite to the QRS: this is called discordance between the QRS complex and the ST–T abnormalities. In the case of RBBB, the ST and T are directed opposite to the terminal portion of the QRS, i.e., the part of the QRS deformed by the conduction abnormality.
The ST segment and T wave are both abnormal and deviate in the same direction, i.e., the ST segment is downsloping and the T wave is inverted in leads with an upright QRS complex, which gives the ST–T complex a “reverse checkmark” asymmetric morphology.
The ST and T abnormalities are not dynamic, i.e., they do not change in the course of several hours to several days.

Thus, in LVH or LBBB, since the QRS complex is upright in the left lateral leads I, aVL, V₅, and V₆, the ST segment is characteristically depressed and T wave inverted in these leads (Figure 31.38). In RVH or RBBB, T waves are characteristically inverted in the right precordial leads V₁–V₃. LBBB is always associated with secondary ST–T abnormalities, the absence of which suggests associated ischemia. LVH, RVH, and RBBB, on the other hand, are not always associated with ST–T abnormalities, but when present, they correlate with more severe hypertrophy or ventricular systolic dysfunction,⁶ and have been called strain pattern. In addition, while these morphologic features are consistent with secondary abnormalities, they do not rule out ischemia in a patient with angina.

There are some exceptions to these typical morphologic features:

In LVH/LBBB, the transition of QRS from negative to positive may occur in a different lead than the transition of T wave from positive to negative. Thus, in one lead, the QRS and T wave may both be upright, or the QRS and T wave may both be negative. This, however, is usually limited to one lead.
RVH and RBBB may be associated with isolated T-wave inversion without ST-segment depression in the precordial leads V₁–V₃. In fact, RBBB and RVH are usually associated with only mild degrees of ST-segment depression in comparison to their left counterparts (the R wave and myocardial mass are smaller with RVH/RBBB than LVH/LBBB).
LVH may be associated with symmetric T-wave inversion without ST-segment depression or with a horizontally depressed ST segment. This may be the case in up to one-third of ST–T abnormalities secondary to LVH and is seen in hypertrophic cardiomyopathy in leads V₃–V₆ (this pattern is classically seen with the apical variant but is common with any variant).⁷

B. Ischemic ST-segment depression and/or T-wave inversion

ST-segment depression or T-wave inversion that adopts any of the features shown in Figure 31.37B–E is consistent with ischemia:

The ST-segment depression or T-wave inversion is directed in the same direction as the QRS complex: this is called concordance between the QRS complex and the ST or T abnormality (Figure 31.37B).
The ST segment is depressed but the T wave is upright (Figure 31.37C).
The T wave has a positive–negative biphasic pattern (Figure 31.37D).
The T wave is symmetrically inverted and has a pointed configuration, while the ST segment is not deviated or is upwardly bowed (coved) or horizontally depressed (Figure 31.37E).
The magnitude of ST-segment depression progresses or regresses on serial tracings, or ST-segment depression progresses to T-wave abnormality during ischemia-free intervals (dynamic ST-segment depression).

Unlike ST-segment elevation, ST-segment depression does not localize ischemia. ⁸ However, the extent and the magnitude of ST-segment depression correlate with the extent and the severity of ischemia. In fact, ST-segment depression in eight or more leads, combined with ST-segment elevation in leads aVR and V₁ and occurring during ischemic pain, is associated with a 75% predictive accuracy of left main or three-vessel disease (Figure 31.39).^9,10 This finding may also be seen in cases of tight proximal left anterior descending stenosis.¹¹ It implies diffuse subendocardial ischemia, with reciprocal ST-segment elevation in the two leads that look away from the normal myocardial repolarization. ST-segment elevation that is more prominent in aVR than V₁ often implies critical left main coronary disease and often mandates urgent angiography.¹¹

Note: T-wave inversion and Wellens syndrome

Either the positive–negative biphasic T waves of the type shown in Figure 31.37D or the deeply inverted (≥5 mm) T waves that often follow them, when occurring in the precordial leads V₂ and V₃, with or without similar changes in V₁, V₄, V₅, are virtually pathognomonic for very recent severe ischemia or injury in the distribution of the left anterior descending artery (LAD) and characterize what is known as Wellens syndrome (Figure 31.40).^12–15 Wellens et al. showed that 75% of patients who developed these T-wave abnormalities and who were treated medically without angiographic investigation went on to develop extensive anterior wall myocardial infarction within a mean of 8.5 days.¹² In a later investigation of 1260 patients presenting with unstable angina, 180 patients (14%) had this characteristic T-wave pattern.¹³ All of the latter patients had stenosis of 50% or more in the LAD (proximal to the 2^nd septal branch), and 18% had total LAD occlusion. Thus, although medical management may provide symptomatic improvement at first, early coronary angiography and revascularization should be strongly considered in anyone with Wellens syndrome because it usually predicts impending anterior myocardial infarction.

Schematic illustration of ST-segment and T-wave morphologies in cases of (a) secondary abnormalities and (b–e) ischemic abnormalities. — **Figure 31.37** ST-segment and T-wave morphologies in cases of **(a)** secondary abnormalities and **(b–e)** ischemic abnormalities. Modified with permission of Scrub Hill Press from Hanna et al. (2009).

Schematic illustration of an example of left ventricular hypertrophy with typical secondary ST–T abnormalities in leads I, II, aVL, V4–V6. — **Figure 31.38** Example of left ventricular hypertrophy with typical secondary ST–T abnormalities in leads I, II, aVL, V₄–V₆. The QRS complex is upright in these leads while the ST segment and T wave are directed in the opposite direction, i.e., the QRS and the ST–T complexes are discordant. Reproduced with permission of the Cleveland Clinic Foundation from Hanna and Glancy (2011).²

Schematic illustration of electrocardiogram of a patient with angina at rest and elevated cardiac biomarkers. — **Figure 31.39** Electrocardiogram of a patient with angina at rest and elevated cardiac biomarkers. ST-segment depression in nine leads with elevation in leads aVR and V₁ suggested subendocardial ischemia related to three-vessel or left main coronary artery disease. He had severe left main and three-vessel disease on coronary arteriography. Reproduced with permission of the Cleveland Clinic Foundation from Hanna and Glancy (2011).²

Schematic illustration of examples of Wellens-type T-wave abnormalities. — **Figure 31.40** Examples of Wellens-type T-wave abnormalities. **(a)** Wellens-type biphasic T wave in leads V₂ and V₃ *(arrows)* and deep T-wave inversion in lead V₄, with a straight or convex ST segment. **(b)** Wellens-type deep T-wave inversion in leads V₂–V₄. Each patient had a 90% proximal left anterior descending stenosis at coronary arteriography. Reproduced with permission of the Cleveland Clinic Foundation from Hanna and Glancy (2011).²

Wellens syndrome is characterized by two patterns of T-wave changes. In 75% of the cases, T waves are deeply (≥5 mm) and symmetrically inverted in leads V₂ through V₄. In 25% of the cases, the T wave has a characteristic positive–negative biphasic morphology in leads V₂ through V₄ (Figure 31.37D).¹² In both patterns, the ST segment is straight or convex, but is not significantly elevated (<1 mm); the downslope of the T wave is sharp (60–90°); and the QT interval is often prolonged. This abnormality is characteristically seen hours to days after the ischemic chest pain resolves. In fact, the ischemic episode is usually associated with transient ST-segment elevation or depression that progresses to the T-wave abnormality after the pain subsides.¹³ In Wellens’ original description, only 12% of patients had small increases in the creatine kinase level. Therefore, the ECG may be the only indication of an impending large anterior infarction in a chest-pain-free patient.¹⁴

No Q wave is seen and the ST segment is not significantly elevated. The same T-wave morphology may be seen with Q-wave MI or STEMI, but is not called Wellens syndrome in those instances. Rather, it is part of the ECG progression of Q-wave MI (Figure 31.33).

T waves that are symmetrically but less deeply inverted than Wellens-type T waves may still represent ischemia. However, this finding is less specific for ischemia and is associated with better outcomes than Wellens syndrome or ST-segment deviation, particularly when the T wave is less than 3 mm deep.¹⁶ In fact, one prospective cohort study found that isolated mild T-wave inversion in patients presenting with ACS is associated with a favorable long-term outcome, similar to patients with no ECG changes.¹⁷ Similarly to Wellens syndrome, U-wave inversion in leads V₁–V₃, a subtle finding, often implies anterior ischemia.

Biphasic T waves may be seen in the precordial leads outside Wellens syndrome (Figure 31.41).

Schematic illustration of non-Wellens biphasic T waves. — **Figure 31.41** Non-Wellens biphasic T waves. **(a)** Biphasic T wave in leads V₂–V₃, not absolutely typical of Wellens syndrome as the ST segment is concave and T-wave downslope is not very steep. However, this patient had 95% proximal LAD stenosis. **(b)** Normal variant T-wave inversion in an asymptomatic young black male, with prominent, early repolarization-type ST elevation (seen here in leads V₄–V₅, but may be seen in V₂–V₃). **(c)** Biphasic T wave in lead V₄ in a patient with LVH; T wave is transitioning to an inverted pattern in lead V₄, while ST segment is transitioning to depression in lead V₆. This early T-wave transition gives a biphasic shape in lead V₄. **(d)** Normal variant biphasic T wave in leads V₄–V₅ in a 50-year-old white man with negative cardiac markers and normal coronary angiography. This pattern was transient; ECGs performed the same day, before and after this ECG, were normal. Unlike Wellens, the ST segment is not straight and the downslope of the T wave is not very steep. A pattern of biphasic T waves may also be seen in pericarditis before T waves fully invert.

C. Frequently missed diagnoses manifesting as ST-segment depression or T-wave inversion

1. True posterior ST-segment elevation myocardial infarction (STEMI)

When accompanied by inferior STEMI, posterior infarction is easily recognized, but it can be difficult to diagnose when it occurs alone, the so-called true posterior STEMI. ST-segment depression that is most prominent in leads V₁ through V₃ often indicates posterior STEMI rather than non-ST-segment elevation ischemia and indicates the need for emergent revascularization. In fact, in the setting of posterior infarction, leads V1–V3 predominate as the areas of maximum depression, whereas greater ST-segment depression in the lateral precordial leads (V4 through V6) or inferior leads (II, III, aVF) is more indicative of non-occlusive and non-regional subendocardial ischemia (Figure 31.42A–B).^10,18–20 In most or all of the cases of posterior infarction, the posterior chest leads V₇–V₉ reveal ST-segment elevation.²¹ One study has found that ST-segment depression in the anterior precordial leads is as sensitive as ST-segment elevation in leads V₇ through V₉ in identifying posterior myocardial infarction (sensitivity 80%),²² while other studies revealed that ST-segment deviation on the standard 12-lead ECG has a lower sensitivity (~60%) in identifying posterior infarction.^20,23 The posterior leads are far from the myocardium, which explains how ST elevation may be minimized and missed in these leads; to improve the sensitivity, 0.5 mm of ST elevation is considered significant in those leads (ACC guidelines).³

Tall and wide (≥0.04 s) R waves in leads V₁ or V_2, particularly when associated with upright T waves, suggest posterior infarction and may further corroborate this diagnosis, but this finding may take up to 24 hours to manifest and is only seen in about 50% of patients with posterior infarction.²³

Studies have shown that ST-segment elevation on the standard 12-lead ECG is found in fewer than 50% of patients with acute left circumflex occlusion and inferoposterior infarction,²⁰ yet these are cases of “missed” STEMI that indeed benefit from emergent angiography and reperfusion. In addition, studies of non-ST-segment elevation ACS consistently identify patients who have acute vessel occlusion (~15–20% of cases),²⁰ yet their initial angiography is usually delayed for hours or days after the initial presentation.²⁴ Recognizing that ST-segment depression that is greatest in leads V₁, V₂, or V₃ represents posterior infarction helps identify a portion of the missed STEMIs in a timely fashion. In addition, in cases of anterior ST-segment depression and in cases of chest pain with non-diagnostic ECG, the recording of ST elevation in leads V₇–V₉ is highly sensitive for detecting a true posterior injury.

2. Acute pulmonary embolism

An anterior ischemic pattern of symmetric T-wave inversion in the precordial leads V₁ through V₄ may also be a sign of acute or chronic right ventricular strain, particularly acute PE. Sinus tachycardia is usually present, but other ECG signs of pulmonary embolism, such as RVH and RBBB, may be absent. In fact, T-wave inversion in leads V₁–V₄ is noted in 19% of patients with non-massive PE and in 85% of patients with massive PE, and is the most sensitive and specific ECG finding in massive PE.²⁵ In addition, acute PE may be associated with T-wave inversion in leads III and aVF,²⁶ and changes of concomitant anterior and inferior ischemia should always raise the suspicion of this diagnosis.²⁷ Rapid regression of these changes on serial tracings favors PE rather than MI.

Schematic illustration of examples of posterior infarction. — **Figure 31.42** Examples of posterior infarction. **(a)** ST-segment depression in the precordial leads V₁–V₄, with a maximal depression in lead V₃, in a patient with severe ongoing chest pain for the preceding 3 hours. This suggests a true posterior ST-segment elevation myocardial infarction. There is also a subtle ST-segment elevation in lead III, which further points to the diagnosis of inferoposterior infarction. Emergency coronary arteriography shows a totally occluded mid-left circumflex coronary artery.

**(b)** The ST segment is depressed in leads V₁–V₆ and leads II, III, aVF, with a maximal depression in leads V₂ and V₃. In addition, tall R waves are seen in leads V₁ and V₂ and Q waves are seen in the lateral leads I and aVL. In a patient with severe persistent chest pain, this suggests a posterolateral infarct. Coronary arteriography shows a totally occluded second obtuse marginal branch.

**(c)** In both A and B, ST elevation and wide Q waves are seen in the posterior leads V₇–V₉. ST elevation is barely 1 mm, as the posterior leads are further away from the heart than the anterior leads, which makes posterior ST changes subtle (0.5 mm of ST elevation in those leads is significant). ST elevation appears pronounced when compared to the size of the QRS.

Reproduced with permission of the Cleveland Clinic Foundation from Hanna and Glancy (2011).²

Tags: Practical Cardiovascular Medicine

Nov 27, 2022 | Posted by admin in CARDIOLOGY | Comments Off