Mini-Review Demon: Brief Chapter Reviews with Questions and Answers

Review

An electrocardiogram ( ECG or EKG ) is a graphical (voltage as a function of time) recording of some of the electrical activity generated by heart muscle cells. The electrical signals are detected by means of metal electrodes . For a standard 12-lead ECG the electrodes are placed on the patient’s chest wall and extremities. The electrodes function as sensors and are connected to an instrument termed the electrocardiograph . The heart’s low amplitude electrical signals, which are detected, amplified, and displayed the electrocardiograph (ECG machine), represent only those produced by the working (contracting) atrial and ventricular muscle fibers (myocytes). The analysis of these recordings, from basic science and applied clinical perspectives, defines the field of electrocardiography or electrocardiology . This major area of modern medicine, in turn, falls under the more general rubric of cardiac electrophysiology .

In highly simplified terms, the heart can be conceptualized as an electrically timed, biologic pump whose activity is modulated by the autonomic (parasympathetic and sympathetic divisions) nervous system and other regulatory control mechanisms. The initiation of cardiac contraction by electrical stimulation is a key event setting off the complex set of processes referred to as electromechanical coupling . A fundamental aspect of the contractile (pumping or squeezing) mechanism is the release (and then reuptake) of calcium ions inside the atrial and ventricular heart muscle cells (myocytes). This process is triggered by the spread of the electrical activation signal through the atria and then the ventricles.

Normally, the cardiac stimulus starts in pacemaker (automatically and repetitively firing) cells of the sinus node . This network of specialized pacemaker cells, also termed the sinoatrial (SA) node , located in the high right atrium near the opening of the superior vena cava. From the SA node, the electrical stimulus (signal) spreads downward and to the left, through the right and left atria, and reaches the atrioventricular (AV) node , located at the bottom of the interatrial septum and near the top of the interventricular septum. After a delay, the stimulus spreads through the AV junction (comprising the AV node and bundle of His ).

The bundle of His then subdivides into right and left bundle branches. The right bundle branch extends down the interventricular septum and into the right ventricle. From there the small Purkinje fibers rapidly distribute the stimulus outward into the main muscle mass of the right ventricle. Simultaneously, the left main bundle branch conveys the stimulus down the interventricular septum to the muscle mass of the left ventricle, also by way of the Purkinje fibers.

This recurring sequence of stimulation and recovery of the heart defines the normal physiologic processes cardiac electrical signaling. Disturbances of intrinsic pacemaker function (automaticity) and impulse propagation/recovery may result in cardiac arrhythmias and conduction disturbances.

Chapter 1: Questions

• 1.

  What is the normal (intrinsic) pacemaker of the human heart?

• 2.

  Identify the major components of the cardiac electrical signaling system.

  

• 3.

  What is the difference between an electrocardiogram and an electrocardiograph ?

• 4.

  True or false : The ECG may provide clues about certain life-threatening electrolyte abnormalities and drug toxicities.

• 5.

  True or false : The ECG directly records only the electrical activity of working heart muscle cells (myocytes), not that of the SA node pacemaker cells or of cells comprising the specialized conduction system (AV node and His–Purkinje system).

Chapter 1: Answers

• 1.

  The collection of cells composing the sinus or sinoatrial (SA) node, located in the high right atrium near the opening of the superior vena cava.

• 2.

  Click on accompanying figure for answers.

  

• 3.

  The standard ECG is a graphical representation of cardiac electrical activity generated by working (contractile) myocardial cells (myocytes), as recorded by electrodes placed at designated locations on the body surface (chest wall and extremities). The electrocardiograph is the device used to record the ECG.

• 4.

  True

• 5.

  True. However, you can often deduce the nature of disturbances involving the SA node, the AV junction, and the bundle branch system from their effects on the timing and/or morphology of the relevant ECG waveforms.

Review

The electrocardiogram (ECG), whether normal or abnormal, records two basic physiologic processes: depolarization (activation) and repolarization (recovery).

• 1.

  Depolarization: spread of stimulus through the heart muscle. This process produces the P wave from the atria and the QRS complex from the ventricles.

• 2.

  Repolarization: return of stimulated muscle to the resting state. This process produces the atrial ST segment and T wave (which are normally not seen on the surface ECG) and the ventricular ST segment, T wave, and U wave. The latter is usually a very small (≤1 mm) deflection just after the T wave. In important pathologic states (e.g., hypokalemia and with certain drug toxicities) prominent U waves may occur. Very prominent U waves are noteworthy because they are associated with increased risk of cardiac arrest from torsades de pointes ventricular tachycardia (see Chapter 16 ).

The five alphabetically named ECG waveforms are the P wave, QRS complex, ST segment, T wave, and U wave, occurring sequentially. ECG interpretation requires careful assessment not only of these waveforms themselves but also of the times within and between them.

Intervals are the portions of the ECG that include at least one entire waveform.

Segments are the portions of the ECG bracketed by the end of one waveform and the beginning of another.

The ECG in sinus rhythm is divisible into four major sets of intervals, defined as follows:

• 1.

  PR interval : from the beginning of one P wave to the beginning of the next QRS complex.

• 2.

  QRS interval ( duration ): from the beginning of one QRS complex to the end of the same QRS.

• 3.

  QT and QTc intervals : from the beginning of one QRS to the end of the subsequent T wave. Note: the QT interval is routinely c orrected (adjusted) for the heart rate, and the designation QTc is used.

• 4.

  RR and PP intervals : from one point (sometimes called the R-point ) on a given QRS complex to the corresponding point on the next. The instantaneous heart rate (beats per min) = 60/RR interval (in sec). Note: in sinus rhythm with normal (1:1) AV conduction, the PP interval will be the same as the RR interval. However, as discussed in later sections, the PP interval may be different from the QRS interval in certain AV conduction disturbances and cardiac arrhythmias.

The ECG recording in sinus rhythm is also divisible into three major segments, defined as follows:

• 1.

  PR segment : from the end of one P wave to beginning of the subsequent QRS complex. Atrial repolarization, which begins in this segment, continues during the QRS and usually ends during the ST segment.

• 2.

  ST segment : from the end of one QRS to the beginning of the subsequent T wave. As noted previously, the ST-T complex (waveform) is often considered as the earliest component of ventricular repolarization.

• 3.

  TP segment: from the end of one T wave to the beginning of the next P wave. This interval, which represents electrical diastole (resting state), is important because it is used as the isoelectric baseline reference from which to assess PR and ST segment deviations.

These basic ECG events are recorded on special graph paper divided into grid-like boxes. Each small box is 1.0 mm ² . At the conventional recording (“sweep”) speed of 25 mm/sec, each millimeter horizontally represents 40 msec (0.04 sec). Each 200-msec (0.2-sec) interval is denoted by a thicker vertical line.

ECG recordings are also standardized such that a 1-mV signal usually produces a 10-mm deflection. Therefore, each millimeter vertically represents 0.1 mV. Each 5-mm (0.5-mV) interval is denoted by a thicker horizontal line. (Different voltage or temporal calibrations may be employed in special circumstances: e.g., 5 or 20/mV, or 50 or even 100 mm/sec.)

Chapter 2: Questions

• 1.

  What key electrophysiologic event occurs just before the sinus P wave appears?

• 2.

  To what fraction of a second does the smallest time division on the conventional ECG (recorded at a “sweep speed” of 25 mm/sec) correspond?

Chapter 2: Answers

• 1.

  Sinoatrial (SA) node depolarization, which is not recorded by the surface ECG. The P wave is generated by depolarization of atrial muscle, which is normally initiated by SA node depolarization.

• 2.

  40 msec (0.04 sec) = 1/25 of a second. This very short amount of time (“blink of an eye”) highlights the capability of the ECG to capture physiologically meaningful events and pathologic changes that occur within fractions of a second, contributing to the importance and uniqueness of this clinical test.

Review

Because the electrocardiogram (ECG) graph is calibrated (standardized), its components (features) can be quantified by their amplitude (magnitude) and sign (positive or negative voltage) and by their width (duration). For clinical purposes, with the standardization set at its usual value of 1 mV = 10 mm, the absolute amplitude of a given waveform is generally reported in millimeters, not millivolts.

As described in Chapter 3 , clinicians assess four basic sets of intervals:

• 1.

  RR (and PP) intervals . The atrial and ventricular heart rate s are inversely proportional to the PP and RR (QRS–QRS) intervals, respectively. The longer/shorter the interbeat interval, the slower/faster the rate.

Cardiac rates are usually reported in units of beats or cycles/min. The ventricular (and atrial) rates are normally identical and can be quickly calculated in two ways:

Method 1 (box counting): Count the number of large (200 msec) time boxes between two successive R waves, and divide the constant 300 by this number. If you want a more accurate measurement of the instantaneous rate, divide the constant 1,500 by the number of small (40 msec) time boxes between two successive R waves.

Method 2 (beat counting): Count the number of QRS complexes that occur every 10 sec (the amount of data recorded on each page of most contemporary 12-lead devices) and multiply this number by 6. This method provides a useful measure of the short-term average heart rate over a given period. (You can do the same calculation for the atrial rate when this is different from the ventricular rate, as in second- or third-degree AV blocks, or in atrial tachycardias with block.)

• 2.

  The PR interval, which normally ranges from 120 to 200 msec (0.12-0.2 sec).

• 3.

  The QRS interval (or QRS duration), which is normally 100 msec (0.10 sec) or less, when measured in any given lead by eye. By electronic (computer) measurement, the upper limit of QRS duration is slightly longer at about 110 msec (0.11 sec).

• 4.

  The QT interval, which normally varies inversely with heart rate, becoming shorter as the heart rate increases, and vice versa. A variety of formulas, some given in the text, have been proposed for computing a rate-corrected QT, or QTc , interval ; none is ideal.

Chapter 3: Questions

• 1.

  Abnormally slow conduction in the atrioventricular (AV) node is most likely to cause which of the following?

  • a.

    Prolongation of the PR interval

  • b.

    Prolongation of the QRS interval

  • c.

    Prolongation of the QT interval

  • d.

    All of the above

• 2.

  A block in the left bundle branch is most likely to cause which of the following?

  • a.

    Shortening of the PR interval

  • b.

    Prolongation of the QRS interval (duration)

  • c.

    Shortening of the QT interval

  • d.

    All of the above

• 3.

  Name four factors that may prolong the QT/QTc interval.

• 4.

  Which of the following events is/are never observed on a clinical 12-lead ECG?

  • a.

    Atrial depolarization

  • b.

    Atrial repolarization

  • c.

    His bundle depolarization

  • d.

    Ventricular depolarization

  • e.

    Ventricular repolarization

• 5.

  For this lead V ₁ recording, answer the following:

  
  • a.

    What is the heart rate?

  • b.

    How would you describe the component waves of this QRS over the phone?

  • c.

    What is the QRS duration?

Chapter 3: Answers

• 1.

  a. Prolong the PR interval.

• 2.

  b. Prolong the QRS interval (duration or width)

• 3.

  Drugs (such as ibutilide, sotalol, quinidine, procainamide, amiodarone), electrolyte abnormalities (hypocalcemia, hypokalemia), systemic hypothermia, evolving myocardial infarction with T wave inversions, etc. See Chapter 25 for a more extensive, but still not exhaustive list.

• 4.

  c. Depolarization of the His bundle is never seen on the surface ECG. This low-amplitude, high-frequency physiologic event occurs during the isoelectric part of the PR interval. His bundle activation, however, may be detectable using a special electrode system inside the heart during cardiac electrophysiologic (EP) procedures. (See Supplemental Extras, Intracardiac Recording .)

  Note: Evidence of atrial repolarization is usually not seen on the standard ECG, but its signature may become apparent with acute pericarditis, in which there is often PR segment elevation in lead aVR (corresponding to the ST segment of the P wave) and PR segment depression in the inferolateral leads (see Chapter 12 ). In addition, sometimes with sinus rhythm and complete heart block, atrial repolarization (the atrial ST segment and atrial T wave) may be seen (unobscured by the QRS), appearing as low amplitude and short duration deflections of the baseline occurring just after each P wave.

• 5.

  a. 100/min

  • b.

    RSR′ (communicated by phone or in person as “RSR-prime”) complex

  • c.

    About 130 to 140 msec (0.13-0.14 sec), which is abnormally wide, due in this case to right bundle branch block ( Chapter 8 ). In addition, left atrial abnormality is present ( Chapter 7 ), evidenced by a biphasic P wave in lead V1 with a prominent (at least 40 msec in duration) terminal component.

Review

The electrical currents produced during atrial and ventricular depolarization and repolarization are detected by electrodes placed on the extremities and chest wall.

Twelve leads are usually recorded in standard clinical electrocardiograms (ECGs):

• 1.

  The six limb ( extremity ) leads record voltages (electrical potentials) generated by the heart that are directed onto the frontal plane of the body. (This plane divides the body into front and back halves.) The six limb leads include three standard (bipolar) extremity leads (I, II, and III) and three augmented (unipolar) extremity leads (aVR, aVL, and aVF).

  • a.

    A standard bipolar lead records the difference between voltages from the heart detected at two extremities. The standard limb leads can be represented by Einthoven’s triangle. These three leads are related by the simple equation:

    $\text{II}=\text{I}+\text{III}$

    A unipolar lead records voltages at one point relative to an electrode with close to zero potential. The unipolar limb leads can also be represented by a triaxial diagram. They are related by the simple equation:

    $\text{aVR}=\text{aVL}+\text{aVF}=0$

  • b.

    The three standard limb leads and the three augmented limb leads can be mapped on the same diagram such that the axes of all six leads intersect at a common point, producing the familiar hexaxial lead diagram.

  • c.

    As a general rule, the P-QRS-T pattern in lead I resembles that in lead aVL. Leads aVR and II usually show reverse patterns. The ECG patterns in lead aVF usually resemble those in lead III.

• 2.

  The six chest ( precordial ) leads (V ₁ to V ₆ ) record voltages generated by the heart and directed onto the horizontal (transverse) plane of the body (dividing the body into an upper and a lower half). These leads are obtained by means of electrodes placed in specific anatomic locations across the anterior-lateral chest wall.

In addition to the 12 conventional leads, ECGs can be recorded in special ways. For example, monitor leads, in which electrodes are placed on the anterior chest and sometimes abdominal wall, are employed in cardiac and intensive care units (CCUs and ICUs). Continuous ECGs can be recorded with the classical Holter apparatus for a period of 24 hours or more in ambulatory patients who are suspected of having intermittent events not captured on the standard 12-lead ECG, or to assess the heart rate (e.g., in sinus rhythm or in atrial fibrillation) during daily activities or during sleep. Very sporadic symptoms are better correlated with ECG rhythm changes by using one of a variety of the available external event recorders for periods of up to 2 to 4 or more weeks or longer. Increasingly, commercial “wearable” devices are being marketed directly to the consumer for self-monitoring or physician-assisted analysis. Standard Holter monitors are being largely replaced by cardiac event recorders capable of ECG rhythm monitoring for extended time periods (weeks to months). These longer time periods are often needed to correlate with transient symptoms and also with transient asymptomatic arrhythmias (e.g., atrial fibrillation, ventricular tachycardia, or AV heart block) that can be detected with reasonable reliability (and then reviewed by qualified readers) by automated programs.

Review

The three basic “laws” of electrocardiography are as follows:

• 1.

  A positive (upward) deflection is seen in any lead if the depolarization wave spreads toward the positive pole of that lead.

• 2.

  A negative (downward) deflection is seen if the depolarization wave spreads toward the negative pole (or away from the positive pole) of any lead.

• 3.

  If the mean orientation of the depolarization path is directed at right angles (perpendicular) to any lead, a biphasic ( RS or QR ) deflection is seen.

Atrial depolarization starts in sinus node and spreads from left to right and downward (toward the AV node), toward the positive pole of lead II and away from the positive pole of lead aVR. Therefore, with normal sinus rhythm the P wave is always positive in lead II and negative in lead aVR.

Ventricular depolarization normally comprises two major, sequential phases:

• 1.

  The first phase is stimulation of the ventricular septum. The vector is directed in an anterior and rightward direction. This initial phase of ventricular activation, therefore, accounts for the physiologic small (septal) r wave observed in the right chest leads (e.g., V ₁ and V ₂ ) and the small (septal) q wave seen in the left chest leads (e.g., V ₅ and V ₆ ).

• 2.

  During the second and major phase of ventricular depolarization, the stimulus spreads simultaneously outward (from endocardium to epicardium) through the right and left ventricles. Because the mass of the left ventricle normally overbalances that of the right ventricle, the spread of depolarization through the left ventricle predominates on the normal electrocardiogram (ECG). This vectorial “shift to the left” produces a relatively tall R wave in the left chest leads (e.g., V ₅ and V ₆ ) after the small “septal” q wave. In right chest leads (V ₁ and V ₂ ), the same process of ventricular stimulation produces a relatively deep S wave after the small initial (“septal”) r wave.

Chest leads between these extreme positions show a relative increase in R wave amplitude and a decrease in S wave amplitude, referred to as normal R wave progression.

In the extremity (limb) leads the morphology of the QRS complex varies with the so-called electrical position (axis) of the heart. These still useful terms from the classic ECG literature are descriptive rather than anatomical.

• 1.

  When the heart vector is said to be “electrically horizontal,” leads I and aVL show a qR pattern.

• 2.

  When the heart vector is said to be “electrically vertical,” leads II, III, and aVF show a qR pattern.

The normal T wave vector generally follows the direction of the main deflection of the QRS complex in any lead. In the chest leads the T wave may normally be negative in leads V ₁ and V ₂ . In most adults the T wave becomes positive by lead V ₂ and remains positive in the left chest leads. In the extremity leads the T wave is always positive in lead II and negative in lead aVR. When the heart is “electrically horizontal,” the QRS complex and T wave are positive in leads I and aVL. When the heart is “electrically vertical,” the QRS complex and T wave are positive in leads II, III, and aVF.

Review

The term mean QRS axis describes the overall direction in which the QRS axis is oriented with respect to the frontal plane of the body. Therefore, the mean QRS axis is measured in reference to the six limb (frontal plane) leads. These leads can be arranged in the form of a hexaxial (six axes) diagram.

The mean QRS axis can usually be approximated by using one of the following rules:

• 1.

  The axis will be pointed midway between the positive poles of any two leads that show R waves of equal height.

• 2.

  The axis will be pointed at right angles (perpendicular) to any lead that shows a biphasic complex and toward other leads that show relatively tall R waves.

The normal mean QRS axis in adults lies between about −30° and +90 to +100°. An axis more negative than −30° is defined as left axis deviation (LAD). An axis more positive than +90 to 100° is defined as right axis deviation (RAD). Conceptually, LAD can be viewed as an extreme form of a horizontal electrical axis; RAD as an extreme form of a vertical electrical axis.

• 1.

  LAD can be readily recognized if lead II shows an RS complex in which the S wave is deeper than the R wave is tall. In addition, lead I will show a tall R wave and lead III a deep S wave. LAD is always seen in the electrocardiograms (ECGs) of patients with left anterior fascicular block (hemiblock) and may be seen in certain other pathologic conditions, such as left ventricular hypertrophy and inferior Q wave wall myocardial infarction. Sometimes it is seen in the ECGs of apparently healthy people.

• 2.

  RAD is present if the R wave in lead III is taller than the R wave in lead II . In addition, lead I shows an rS complex. RAD can be seen in several conditions, including left–right arms lead reversal; right ventricular overload syndromes, lateral wall myocardial infarction, chronic lung disease, and left posterior fascicular block (hemiblock) (see Chapter 25 ). In addition, RAD may be seen in the ECGs of normal people (especially younger adults and is the normal finding in neonates). It also occurs with dextrocardia.

More rarely the QRS complex is biphasic in all six limb leads. This makes the mean electrical axis indeterminate , but this finding is not associated with any specific abnormality.

The mean electrical axis of the P wave and T wave can be estimated in the same manner as the mean QRS axis. With sinus rhythm, the normal P wave is about +60° (positive P wave in lead II). Normally the T wave axis in the frontal plane is similar to the QRS axis. Therefore, the T waves normally are positive in leads with a predominantly positive QRS complex.

Chapter 6: Questions

• 1.

  Based on the six limb leads (I, II, III, aVR, aVL, and aVF) shown here, what is the approximate mean QRS axis?

  

• 2.

  Tracings (A), (B), and (C) are, in mixed order, leads I, II, and III from an ECG with a mean QRS axis of −30°. This information should allow you to sort out which lead is which.

  

• 3.

  All but which ONE of the following conditions may cause right axis deviation?

  • a.

    Reversal of left and right arm electrodes

  • b.

    Severe chronic obstructive pulmonary disease

  • c.

    Lateral wall myocardial infarction

  • d.

    Acute or chronic pulmonary embolism

  • e.

    Left anterior fascicular block (hemiblock)

• 4.

  What is the mean electrical axis here? ECG shows sinus tachycardia, PR = 190 msec and prominent P waves.

  

Review

When cardiac enlargement occurs, the total number of heart muscle fibers does not increase; rather, each individual fiber becomes larger ( hypertrophied ). With dilation, the heart muscle cells become longer (termed eccentric hypertrophy ). With enlargement due to of increased wall thickness, the cells become wider (termed concentric hypertrophy ). One predictable electrocardiogram (ECG) effect of cardiac hypertrophy is an increase in the voltage or duration of the P wave or of the QRS complex. Increased wall thickness and chamber dilation occur together. Chamber enlargement usually results from some type of chronic pressure or volume load on the heart muscle. Other causes of hypertrophy relate to genomic mutations, exemplified by hereditable hypertrophic cardiomyopathies.

Pathologic hypertrophic syndromes are often accompanied by fibrosis (scarring) and changes in myocardial geometry (remodeling), which may both worsen myocardial function and promote arrhythmogenesis (e.g., atrial fibrillation and sustained ventricular tachycardia).

Right atrial abnormality (RAA), or right atrial overload, may be associated with tall, peaked P waves exceeding 2.5 mm in height. These waves are usually best seen in leads II, III, aVF, and sometimes V ₁ or V ₂ .

Left atrial abnormality (LAA), with or without frank left atrial enlargement, is manifested by wide, sometimes notched P waves of 0.12 sec or more duration in one or more of the extremity leads. A biphasic P wave with a prominent wide negative deflection may be seen in lead V ₁ . A more contemporary and increasingly used diagnostic label, inferable from very broad P waves (>120 msec) with a distinctive morphology, is interatrial conduction delay (IACD). The most advanced manifestation of IACD is a broad, notched sinus P wave in lead II (and often III and aVF) that is initially positive and then negative. These abnormal P waves have been associated increased risk of atrial fibrillation.

The ECG diagnosis of biatrial abnormality (enlargement) is based on the presence of tall and broad P waves. Such prominent P waves may be a clue to severe valvular disease or cardiomyopathy.

Right ventricular hypertrophy , especially due to chronic pressure overload syndromes, may produce any or all of the following:

• 1.

  A tall R wave in lead V ₁ , equal to or larger than the S wave in that lead

• 2.

  Right axis deviation

• 3.

  T wave inversions in the right to middle chest leads (sometimes called a right ventricular “strain” pattern)

With left ventricular hypertrophy (LVH), any or all of the following may occur:

• 1.

  The sum of the depth of the S wave in lead V ₁ (S _V1 ) and the height of the R wave in either lead V ₅ or V ₆ (R _V5 or R _V6 ) exceeds 35 mm (3.5 mV), especially in middle-aged or older adults. However, high voltage in the chest leads is a common normal finding, particularly in athletic or thin young adults. Consequently, high voltage in the chest leads (S _V1 + R _V5 or R _V6 >35 mm) is not a specific LVH indicator.

• 2.

  Another proposed set of LVH criteria (the Cornell voltage indexes) are based by summing components of the QRS voltages in leads V ₃ and aVL: for men, S _V3 + R _aVL >28 mm; for women, S _V3 + R _aVL >20 mm.

• 3.

  Sometimes LVH produces tall R waves in lead aVL. An R wave of 11 to 13 mm (1.1-1.3 mV) or more in lead aVL is another sign of LVH. A tall R wave in lead aVL may be the only ECG sign of LVH, and the voltage in the chest leads may be normal. In other cases the chest voltages are abnormally high, with a normal R wave seen in lead aVL.

• 4.

  Just as RVH is sometimes associated with repolarization abnormalities due to ventricular overload, so ST-T changes are often seen in LVH. This LV overload-related repolarization abnormality (formerly called LV “strain”) is usually best seen in leads with tall R waves.

• 5.

  With LVH the mean QRS electrical axis is usually horizontal (i.e., in the direction of lead I). Actual left axis deviation (i.e., an axis −30° or more negative) may also be seen. In addition, the QRS complex may become wider. Not uncommonly, patients with LVH eventually develop an incomplete or complete left bundle branch block (LBBB) pattern. LVH is a common cause of an intraventricular conduction delay (IVCD) with features of LBBB.

• 6.

  Signs of LAA (broad P waves in the extremity leads or biphasic P waves in lead V ₁ , with a prominent negative, terminal wave) are often seen in patients with ECG evidence of LVH. Most conditions that lead to LVH ultimately produce left atrial overload as well.

The diagnosis of LVH should not be made solely on the basis of high voltage in the chest leads because high voltages may occur normally, particularly in young adults, athletes, and lean individuals (exemplifying the limited specificity of voltage criteria; see Chapter 24 ). In addition, enlargement of any of the four cardiac chambers can be present without diagnostic ECG changes (exemplifying the limitation of sensitivity). Echocardiography is considerably more sensitive and specific than ECG analysis in assessing chamber enlargement.

Review

Right bundle branch block (RBBB) produces the following characteristic patterns: an rSR′ with a prominent wide final R’ wave in lead V ₁ , a qRS with a wide, terminal S wave in lead V ₆ , and a QRS width of 120 msec (three small time boxes) or more. Incomplete RBBB shows the same chest lead patterns, but the QRS width is between 100 and 120 msec.

Left bundle branch block (LBBB) produces the following characteristic patterns: deep wide QS complex (or occasionally an rS complex with a wide S wave) in lead V ₁ , a prominent (often notched) R wave without a preceding q wave in lead V ₆ , and a QRS width of 120 msec or more. Incomplete LBBB shows the same chest lead patterns as LBBB, but the QRS width is between 100 and 120 msec.

Fascicular blocks (hemiblocks) can occur because the left bundle splits into two main subdivisions (fascicles): the left anterior fascicle and the left posterior fascicle. Conduction through either or both of these fascicular subdivisions can be blocked.

Left anterior fascicular block or hemiblock is characterized by a mean QRS axis of about −45° or more. (When the mean QRS axis is about −45°, left axis deviation is present and the height of the R wave in lead I [R _I ] is equal to the depth of the S wave in lead aVF [S _aVF ]. When the mean QRS axis is more negative than about −45°, S _aVF becomes larger than R _I .)

Left posterior fascicular block or hemiblock is characterized by marked right axis deviation (RAD). However, before the diagnosis of left posterior fascicular block is made, other more common causes of RAD must be excluded, including lead reversal (left/right arm electrodes), normal variants, right ventricular overload syndromes (including chronic lung disease), and lateral wall infarction (see Chapter 25 ).

“Bifascicular block” patterns indicate blockage of any two of the three fascicles. For example, RBBB with left anterior fascicular block (LAFB) produces an RBBB pattern with marked LAD. RBBB with left posterior fascicular block produces an RBBB pattern with RAD (provided other causes of RAD, especially right ventricular hypertrophy and lateral myocardial infarction, are excluded). Similarly, a complete LBBB may indicate blockage of both the anterior and posterior fascicles.

Bifascicular block patterns are potentially significant because they make ventricular conduction dependent on the single remaining fascicle. Additional damage to this third remaining fascicle may completely block AV conduction, producing complete heart block ( trifascicular block ). The term “trifascicular block,” however, is rarely used in clinical practice. Occasionally one can infer trifascicular block from a 12-lead electrocardiogram (ECG), without sustained or intermittent complete or advanced AV block, when patients display alternating bundle branch block (RBBB and LBBB), thus placing them at high risk of abrupt complete AV heart block.

Caution : a very common misconception is that bifascicular block patterns (especially RBBB and LAFB) in concert with a prolonged PR interval are diagnostic of trifascicular disease. This inference is often wrong because the long PR interval may represent a delay in the AV node, not in the infranodal part of the conduction system

The acute development of new bifascicular block, usually RBBB and LAFB (especially with a prolonged PR interval), during an acute anterior wall myocardial infarction ( 9, 10 ), may be an important warning signal of impending complete heart block and is considered by some a strong indication for a temporary pacemaker. However, chronic bifascicular blocks with normal sinus rhythm have a low rate of progression to complete heart block and are not indications by themselves for permanent pacemakers.