CARDIAC ELECTROPHYSIOLOGY

The electrocardiogram (ECG) is an essential diagnostic test. In many ways, it is an ideal diagnostic modality because it is noninvasive, is readily performed without discomfort or potential patient injury, is inexpensive, and its results are immediately available. Most important, it provides a diagnostic window of cardiovascular surveillance for a multitude of cardiac pathophysiologic problems, including valvular, myocardial, pericardial, and ischemic heart disease. The ECG’s diagnostic utility is critically dependent on its accurate interpretation. This chapter addresses the diagnostic possibilities encountered in routine ECG interpretation, including a broad collection of clinical examples. A clinical history, detailed interpretation, and diagnostic summary are included for each tracing. A detailed review of this chapter will provide comprehensive preparation for the Cardiovascular Medicine Subspecialty Board Examination.

BOARD PREPARATION

To receive a passing score on the Cardiovascular Medicine Subspecialty Board Examination, the examinee must also receive a passing score on the ECG subsection. To best prepare for the ECG section, familiarization with the scoring sheet is essential. The scoring sheet is sent to each examinee before the test date, with diagnoses grouped systematically for easy reference. In preparation, understanding and being able to recognize each diagnosis is a “foolproof” preemptive approach.

A RECOMMENDED APPROACH TO ELECTROCARDIOGRAM INTERPRETATION

To ensure accurate and consistent ECG interpretation, a systematic approach is required. ECG interpretation is not an exercise in pattern recognition. To the contrary, employing a methodical strategy based on a thorough knowledge of the cardiac conduction sequence, cardiac anatomy, cardiac physiology, and cardiac pathophysiology can be applied to all ECGs, regardless of the findings.

One systematic approach to each ECG is to ascertain the following in this recommended order:

Cardiac pathology is manifest differently on the surface ECG, depending on which lead is interrogated. Each lead provides an “electrical window of opportunity” and, by this virtue, offers a unique electrical perspective. The experienced electrocardiographer amalgamates these different windows into a mental three-dimensional electrical assessment, drawing accurate conclusions pertaining to conduction system and structural heart disease. For example, precordial lead V₁ predominantly overlies the right ventricle, explaining why right ventricular cardiac electrical events are best observed in this lead. Likewise, precordial lead V₆ overlies the left ventricle. This lead optimally represents left ventricular cardiac electrical events.

Assess the Standardization and Identify the Recorded Leads Accurately

Standard ECG graph paper consists of 1-mm × 1-mm boxes divided by narrow lines, which are separated by bold lines into larger, 5-mm × 5-mm boxes. At standard speed (25 mm/s), each small box in the horizontal axis represents 0.040 second (40 milliseconds) of time and each large box represents 0.200 second (200 milliseconds). At standard calibration (1 mV/10 mm), each vertical small box represents 0.1 mV and each vertical large box represents 0.5 mV. One must be very careful to inspect the standardization square wave (1 mV in amplitude) at the left of each ECG to determine the calibration of the ECG. ECGs with particularly high or low voltages are often recorded at half standard or twice standard, respectively. In these cases, the 1-mV square wave possesses an amplitude of either 5 or 20 mm. This distinction is important because it will affect the interpretation of all other voltage criteria. All further references to amplitude in this chapter are under the assumption of the default or preset standardization (1 mV/10 mm).

Determine the Atrial and Ventricular Rates and Rhythms

The first step in determining the rate and rhythm is to identify atrial activity. If P waves are present, it is important to measure the P wave to P wave interval (P–P interval). This determines the rate of atrial depolarization. To estimate quickly either an atrial or ventricular rate on a standard 12-lead ECG, one can count the number of 5-mm boxes in an interval and divide 300 by that number. For example, if there are four boxes between P waves, the rate is 300 divided by 4, or 75 complexes per minute.

Once the atrial activity and rate are identified, the P-wave frontal plane axis should be ascertained. A normal P-wave axis (i.e., -0 to 75 degrees) typically reflects a sinus node P-wave origin. A simple way of determining a normal P-wave axis is to confirm a positive P-wave vector in leads I, II, III, and aVF. An abnormal P-wave axis supports an ectopic or non–sinus node P-wave origin.

Several possible atrial and junctional rhythms are listed below. They are grouped by cardiac rhythm origin and subsequently subcategorized by atrial rate. Distinguishing features are italicized for emphasis.

Rhythms of Sinus Nodal and Atrial Origin

Normal Sinus Rhythm A normal sinus rhythm (NSR) is defined as a regular atrial depolarization rate between 60 and 100 per minute of sinus node origin, as demonstrated by a positive P-wave vector in leads I, II, III, and aVF.

Sinus Bradycardia Sinus bradycardia is characterized by a regular atrial depolarization rate <60 per minute of sinus node origin, as demonstrated by a positive P-wave vector in leads I, II, III, and aVF. (This is similar to NSR, except the rate is slower.)

Sinus Tachycardia Sinus tachycardia is characterized by a regular atrial depolarization rate ≥100 per minute of sinus node origin, as demonstrated by a positive P-wave vector in leads I, II, III, and aVF. (This is similar to NSR, except the rate is faster.)

Sinus Arrhythmia Sinus arrhythmia is characterized by an irregular atrial depolarization rate between 60 and 100 per minute of sinus node origin, as demonstrated by a positive P-wave vector in leads I, II, III, and aVF. (This is similar to NSR, except there is irregularity in the P–P interval >160 milliseconds.)

Sinus Arrest or Pause Sinus arrest or pause is characterized by a pause of >2.0 seconds without identifiable atrial activity. This may be caused by frank sinus arrest or may be simply a sinus pause secondary to:

First-degree SA block involves a fixed delay between the depolarizing SA node and the depolarization exiting the node and propagating as a P wave. Because the delay is fixed, this delay cannot be detected on the surface ECG.

Second-degree SA block has two varieties. In Type I (Wenckebach) SA block, there is a progressive delay between SA nodal depolarization and exit of the impulse to the atrium. This is manifest as a progressive shortening of the P–P interval until there is a pause, reflecting an SA node impulse that was blocked from exiting the node. In Type II SA block, there is a constant P–P interval with intermittent pauses. These pauses also represent an SA node impulse that was blocked from exiting the node. However, in this case, the duration of the pause is a multiple of the basic P–P interval.

Third-degree SA block demonstrates no P-wave activity, as no impulses exit the sinus node. On the surface ECG, this is indistinguishable from sinus arrest, in which there is no sinus node activity.

Sinus Node Reentrant Rhythm Sinus node reentrant rhythm is characterized by a reentrant circuit involving the sinus node and perisinus nodal tissues. Given the sinus origin, the P-wave morphology and axis are normal and indistinguishable from a normal sinus P wave. The rate is regular at a rate of 60 to 100 per minute. (This is very similar to NSR, except characterized by abrupt onset and termination.)

Sinus Node Reentrant Tachycardia Sinus node reentrant tachycardia is characterized by a reentrant circuit involving the sinus node and perisinus nodal tissues. Given the sinus origin, the P-wave morphology and axis are normal and indistinguishable from a normal sinus P wave. The rate is regular at a rate of ≥100 per minute. (This is very similar to sinus tachycardia, except characterized by abrupt onset and termination.)

Ectopic Atrial Rhythm Ectopic atrial rhythm is characterized by a regular atrial depolarization at a rate of 60 to 100 per minute from a single nonsinus origin, as reflected by an abnormal P-wave axis. The PR interval may be shortened, particularly in the presence of a low ectopic atrial origin, closer to the AV node with a reduced intra-atrial conduction time. In the presence of slowed atrial conduction, the PR interval may be normal or even prolonged.

Ectopic Atrial Bradycardia Ectopic atrial bradycardia is characterized by a regular atrial depolarization at a rate of ≤60 per minute from a single nonsinus origin, as reflected by an abnormal P-wave axis. (This is similar to an ectopic atrial rhythm, except slower.)

Atrial Tachycardia Atrial tachycardia is characterized by a regular, automatic tachycardia from a single, ectopic atrial focus typically with an atrial rate of 180 to 240 per minute. The ventricular rate may be regular or irregular, depending on the AV conduction ratio. The P-wave axis is abnormal, given the ectopic atrial focus. (This is similar to an ectopic atrial rhythm, except faster.)

Wandering Atrial Pacemaker A wandering atrial pacemaker (WAP) has a rate of 60 to 100 per minute from multiple ectopic atrial foci, as evidenced by at least three different P-wave morphologies on the 12-lead ECG, possessing variable P–P, PR, and R–R intervals. Be careful not to confuse this dysrhythmia with atrial fibrillation (AF). Unlike AF, discrete P waves are identifiable.

Multifocal Atrial Tachycardia Multifocal atrial tachycardia (MAT) is characterized by a rate of >100 per minute with a P wave preceding each QRS complex from multiple atrial ectopic foci, as evidenced by at least three different P-wave morphologies on the 12-lead ECG possessing variable P–P, PR, and R–R intervals. The ventricular response is irregularly irregular, given the unpredictable timing of the atrial depolarization and variable AV conduction. Nonconducted atrial complexes during the ventricular absolute refractory period are also often present. Be careful not to confuse this dysrhythmia with AF. Unlike AF, discrete P waves are identifiable. (This is similar to WAP, but the atrial rate is faster.)

Atrial Fibrillation AF is characterized by a rapid, irregular, and disorganized atrial depolarization rate of 400 to 600 per minute devoid of identifiable discrete P waves, instead characterized by fibrillatory waves.

In the absence of fixed AV block, the ventricular response to AF is irregularly irregular. Be careful not to confuse this dysrhythmia with WAP or MAT. The key is the lack of identifiable P waves.

Atrial Flutter Atrial flutter (AFL) is characterized by a rapid, regular atrial depolarization rate of 250 to 350 per minute, representing an intra-atrial reentrant circuit. The atrial waves are termed “flutter waves” and often demonstrate a “saw-toothed” appearance, best seen in leads V₁, II, III, and aVF.

Although the atrial rate is regular, the ventricular response rate may be either regular or irregular, depending on the presence of fixed versus variable AV conduction. Common AV conduction ratios are 2:1 and 4:1.

Rhythms of Atrioventricular Nodal and Junctional Origin

Atrioventricular Nodal Reentrant Tachycardia Atrioventricular nodal reentrant tachycardia (AVNRT) is a micro-reentrant dysrhythmia that depends on the presence of two separate AV nodal pathways. Slowed conduction is present in one pathway and unidirectional conduction block is present in the second pathway. This is a regular rhythm with a typical ventricular rate of 140 to 200 per minute, with abrupt onset and termination. Its onset is often initiated by premature atrial complexes (PACs). Atrial activity typically consists of inverted or retrograde P waves occurring before, during, or after the QRS complex, best identified in lead V₁. The QRS complex may be conducted normally or aberrantly.

Atrioventricular Reentrant Tachycardia Atrioventricular reentrant tachycardia (AVRT) is a macro-reentrant circuit that consists of an AV nodal pathway and an accessory pathway. This dysrhythmia may conduct antegrade down the AV nodal pathway with retrograde conduction through the accessory pathway (orthodromic AVRT), or antegrade down the accessory pathway with retrograde conduction up the AV nodal pathway (antidromic AVRT). As opposed to AVNRT, the P wave is always present after the QRS complex. With antidromic AVRT, the QRS complex, by definition, is aberrantly conducted (wide).

Junctional Premature Complexes Junctional premature complexes are premature QRS complexes of AV nodal origin that may have resultant retrograde P waves (a negative P-wave vector in leads II, III, and aVF) occurring immediately before (with a short PR interval), during, or after the QRS complex.

AV Junctional Bradycardia AV junctional bradycardia is characterized by QRS complexes of AV nodal origin that occur at a regular rate of <60 per minute. These represent a subsidiary pacemaker and may have resultant retrograde P waves (negative P-wave vector in leads II, III, and aVF) that occur immediately before (with a short PR interval), during, or after the QRS complex.

Accelerated AV Junctional Rhythm Accelerated AV junctional rhythm is characterized by QRS complexes of AV nodal origin that occur at a regular rate of 60 to 100 per minute. These represent a subsidiary pacemaker and may have resultant retrograde P waves (negative P-wave vector in leads II, III, and aVF) that occur immediately before (with a short PR interval), during, or after the QRS complex. (This dysrhythmia is similar to AV junctional bradycardia, except faster.)

AV Junctional Tachycardia AV junctional tachycardia is characterized by QRS complexes of AV nodal origin that occur at a regular rate of typically 100 to 200 per minute. This dysrhythmia emanates from the AV junction and serves as a dominant cardiac pacemaker with an inappropriately rapid rate. Retrograde P waves may be identified (negative P-wave vector in leads II, III, and aVF) that occur immediately before (with a short PR interval), during, or after the QRS complex. (This dysrhythmia is similar to AV junctional rhythm, except faster.)

Rhythms of Ventricular Origin

Idioventricular Rhythm Idioventricular rhythm is a regular escape rhythm of ventricular origin that possesses a typically widened QRS complex (>100 milliseconds) at a rate of <60 per minute. This is often seen in cases of high-degree AV block, in which the ventricle serves as a subsidiary pacemaker.

Ventricular Parasystole Ventricular parasystole is an independent, automatic ventricular rhythm that emanates from a single ventricular focus characterized by a widened QRS complex with regular discharge and ventricular depolarization. Because the rhythm is independent and not suppressible, ventricular parasystole is characterized by varying coupling intervals and unchanged interectopic R—R intervals. Fusion complexes can be observed when the parasystolic focus discharges simultaneously with native ventricular depolarization. When the ventricle is absolutely refractory, the parasystolic focus is not recorded on the surface ECG, but its discharge remains unabated.

Accelerated Idioventricular Rhythm Accelerated idioventricular rhythm (AIVR) is a regular rhythm of ventricular origin that typically has a widened QRS complex at a rate of 60 to 100 per minute. It is often seen in cases of high-degree AV block, in which the ventricle serves as a subsidiary pacemaker plus in cases of coronary artery reperfusion. (AIVR is similar to idioventricular rhythm, except faster.)

Ventricular Tachycardia Ventricular tachycardia (VT) is a sustained cardiac rhythm of ventricular origin that occurs at a typical rate of 140 to 240 per minute. In differentiating this from supraventricular tachycardia with aberrant conduction, the following features suggest VT:

Polymorphic Ventricular Tachycardia Polymorphic VT is a paroxysmal form of VT with a nonconstant R—R interval, a ventricular rate of 200 to 300 per minute, QRS complexes of alternating polarity, and a changing QRS amplitude that often resembles a sine-wave pattern (torsades de pointes). It is often associated with a prolonged QT interval at arrhythmia initiation.

Ventricular Fibrillation Ventricular fibrillation (VF) is a terminal cardiac rhythm with chaotic ventricular activity that lacks organized ventricular depolarization.

Determine the P-Wave and QRS-Complex Axes

A normal P-wave axis varies from 0 to 75 degrees but is usually between 45 and 60 degrees. P waves with a normal axis are upright in leads I, II, III, and aVF and inverted in lead aVR. An abnormal P-wave axis should prompt the interpreter to consider non-sinus nodal rhythms, dextrocardia, or limb lead reversal, among other causes.

To ascertain th frontal-plane axis of the QRS complex, the QRS-complex vector is assessed in each of the limb leads. A recommended approach is to search for the limb lead in which the QRS complex is isoelectric (i.e., the area of positivity under the R wave is equal to the area of negativity above the Q and S waves). The QRS-complex frontal-plane axis will be perpendicular to the isoelectric lead, thus narrowing down the axis to one of two possibilities (90 degrees clockwise or 90 degrees counterclockwise of the isoelectric lead’s axis). Next, one examines a limb lead whose vector is close to one of the two possible axes. Based on whether the QRS is grossly positive or negative in that lead, one can deduce which of the two possible axes is correct.

An alternative approach is as follows:

Measure All Cardiac Intervals

PR Interval

A normal PR interval is between 120 and 200 milliseconds. This represents the interval between P-wave onset and QRS-complex onset. The PR interval represents intra-atrial and AV nodal conduction time. A short PR interval (<120 milliseconds) is suggestive of facile intra-atrial or AV conduction and may represent ventricular preexcitation. A prolonged PR interval (>200 milliseconds) reflects delayed intra-atrial or AV conduction. In the setting of a varying PR interval, conduction block or AV dissociation may be present.

R–R Interval

The R–R interval is inversely proportional to the rate of ventricular depolarization. If AV conduction is normal, the ventricular rate should equal the atrial rate.

Atrioventricular Block

First-Degree AV Block First-degree AV block occurs when the PR interval is prolonged (>200 milliseconds), and each P wave is followed by a QRS complex. Typically the PR interval is constant.

Second-Degree AV Block, Mobitz Type I (Wenckebach) Second-degree AV block, Mobitz Type I (Wenckebach) is characterized by progressive prolongation of the PR interval, terminating with a P wave followed by a nonconducted QRS complex. Normal antegrade conduction resumes with a repetitive progressive prolongation of the PR interval with each cardiac depolarization, resuming the cycle. This results in a “grouped beating” pattern. In its most common form, the R-R interval shortens from beat to beat (not including the interval in which a P wave is not conducted). This typically represents conduction block within the AV node, superior to the bundle of His.

Second-Degree AV Block, Mobitz Type II Second-degree AV block, Mobitz Type II is characterized by regular P waves followed by intermittent nonconducted QRS complexes in the absence of atrial premature complexes. The resulting R-R interval spanning the nonconducted complex is exactly double the conducted R-R intervals. This typically represents AV conduction block below the bundle of His and has a high propensity to progress to more advanced forms of AV block.

Note that when there is AV block with a ratio of 2:1, one cannot definitively distinguish between Mobitz Type I and Type II. Longer rhythm strips, maneuvers, and intracardiac recordings may be necessary. A widened QRS complex supports Mobitz Type II but lacks certainty.

Third-Degree AV Block (Complete Heart Block) Third-degree AV block (complete heart block) is characterized by independent atrial and ventricular activity with an atrial rate that is faster than the ventricular rate. PR intervals vary with dissociation of the P waves from the QRS complexes. Typically the ventricular rhythm is either a junctional (narrow complex) or ventricular (wide complex) rhythm. (Note this should be distinguished from AV dissociation, which is also characterized by independent atrial and ventricular activity, but the ventricular rate is faster than the atrial rate.)

QRS Complex Interval

The QRS complex interval is best measured in the limb leads from the onset of the R wave (or Q wave if present) to the offset of the S wave. A normal QRS duration is <100 milliseconds.

If the QRS duration is between 100 and < 120 milliseconds, the morphology should be further inspected for features of one or more of the following:

If the QRS complex duration is >120 milliseconds, the morphology should be further inspected for the following features:

QT Interval

The QT interval demonstrates heart rate interdependence. The QT interval is directly proportional to the R-R interval. The QT interval shortens as heart rate increases. To account for this variability with heart rate, the corrected QT interval (QT_c) is calculated, in which the QT interval is divided by the square root of the R-R interval. Normative tables for heart rate and gender are available. A normal QT_c is typically <440 milliseconds. A less cumbersome approximation involves measuring the QT interval directly (typically in lead II). If this is >50% of the R-R interval, this supports QT-interval prolongation. In this circumstance, calculating a QT_c interval is appropriate.

Differential diagnosis of a prolonged QT interval includes the following:

Determine If Cardiac Chamber Enlargement or Hypertrophy Is Present

If a patient is in sinus rhythm, the atria can be evaluated by analyzing the P-wave morphology in leads II, V₁, and V₂. Given the superior right atrial location of the sinus node, right atrial depolarization precedes left atrial depolarization. Therefore, right atrial depolarization is best represented in the first half of the surface ECG P wave. In lead II, if a bimodal P wave is present, the first peak represents right atrial depolarization and the second peak represents left atrial depolarization. In leads V₁ and V₂, the P wave is typically biphasic. The early portion is upright, representing right atrial depolarization toward leads V₁ and V₂, with the negative latter half representing left atrial depolarization, away from these leads.

Right Atrial Abnormality

Delayed activation of the right atrium due to hypertrophy, dilation, or intrinsically slowed conduction can result in the summation of right and left atrial depolarization. This typically produces a tall peaked P wave (≥2.5 to 3 mm) in lead II.

Left Atrial Abnormality

Delayed activation of the left atrium due to hypertrophy, dilation, or intrinsically slowed conduction can result in a broadening (>110 milliseconds) and notching of the P wave in lead II, or a deeper inverted phase of the P wave in leads V₁ and V₂:

Right Ventricular Hypertrophy

In RVH, there is a dominance of the right ventricular forces, which produce prominent R waves in the right precordial leads and deeper S waves in the left precordial leads. RVH is suggested by one or more of the following:

Left Ventricular Hypertrophy

Several criteria have been described and validated for the diagnosis of left ventricular hypertrophy (LVH) by electrocardiography.

Combined or Biventricular Hypertrophy

Combined ventricular hypertrophy is suggested by any of the following:

Assess the P-Wave, QRS-Complex, and T-Wave Morphologies

Once the cardiac rate, rhythm, axes, intervals, and chambers have been assessed, one should proceed with the identification of various morphologies that suggest pathologic states. There have been virtually innumerable descriptions of various morphologic criteria for a broad spectrum of pathologic states, but here we discuss those that are most common and/or most important.

ECG Abnormalities and Corresponding Differential Diagnoses

Incorrect Lead Placement or Lead Fracture Incorrect lead placement or lead fracture is most commonly identified in the limb leads, with a negative P-wave vector in leads I and aVL and normal precordial R-wave progression.

Low Voltage Low voltage in limb leads is defined as a QRS-complex amplitude of <5 mm in each of the standard limb leads (I, II, and III). Low voltage of all leads is defined as low voltage in the limb leads plus a QRS-complex amplitude of <10 mm in each of the precordial leads.

Low voltage on the ECG may be of primary myocardial origin or secondary to high-impedance tissue conduction. Differential diagnosis possibilities include the following:

Q Waves Q waves represent an initial negative QRS-complex vector. Pathologic Q waves are present if they are ≥1 mm (0.1 mV) in depth and ≥40 milliseconds in duration.

Q waves are most commonly associated with a myocardial infarction. To diagnose a myocardial infarction, Q waves must be identified in two contiguous leads:

Contiguous regions on an ECG include the following:

Other etiologies of Q waves include:

ST-Segment Elevation ST-segment elevation refers to elevation of the segment between the terminal aspect of the QRS complex and the T-wave onset. This elevation is relative to the isoelectric comparative TP segment located between the end of the T wave and the start of the P wave.

Causes of ST-segment elevation include the following: