Basic principles of electrocardiographic interpretation

INTRODUCTION — The electrocardiogram (ECG) is a graphical record of electric potentials generated by the working heart muscle fibers during each cardiac cycle. These low-amplitude potentials are detected on the surface of the body using electrodes attached to the extremities and chest wall, and are then amplified by the electrocardiograph machine and displayed on special graph paper and/or on display monitors. A variety of systems are available for storage of vast amounts of digital ECG data as part of electronic medical records.

This topic will review the basic aspects of ECG interpretation, including:

●The cardiac electrical cycle

●ECG waveforms and intervals

●ECG leads

●Genesis of the normal ECG

Each of these issues is discussed in greater detail in published reviews [1-3].

THE CARDIAC ELECTRICAL CYCLE — The initiating event for cardiac contraction is the spread of depolarizing electrical currents through the heart. These currents are produced by three types of cells: cardiac pacemaker cells, specialized conduction tissue, and the heart muscle itself. The surface ECG, however, only records the depolarization and repolarization potentials generated by the "working" atrial and ventricular myocardial fibers.

The depolarization stimulus for the heartbeat normally begins in the sinoatrial (SA) or sinus node, a collection of pacemaker cells with spontaneous automaticity (figure 1) (see "Normal sinus rhythm and sinus arrhythmia", section on 'Anatomy'). The initial phase of cardiac electrical activation consists of the spread of the depolarization wave through the right and left atria, resulting in atrial contraction. As the impulse reaches the base of the interatrial septum, it also stimulates pacemaker and specialized conduction tissues in the atrioventricular (AV) nodal and His-bundle areas. Together, these two regions constitute the AV junction.

The bundle of His splits into two main branches: the right and the left bundles. The main left bundle bifurcates into two primary subdivisions: a left anterior fascicle; and a left posterior fascicle. The bundle branches and fascicles rapidly transmit depolarization wavefronts to the myocardium by way of Purkinje fibers that penetrate the ventricular walls to excite the working ventricular myocardial cells. The depolarization wavefronts spread through the ventricular wall, from endocardium (inner layer) to epicardium (outer layer), triggering intracellular calcium release and myofilament contraction (electromechanical coupling).

ECG ELECTRODES AND LEADS — Electrodes are the sites at which an electrical potential is measured, while ECG leads record the difference in potentials between two electrodes.

Electrodes — Standard surface electrodes (right and left arm, right and left leg, and the six precordial electrodes) measure the electrical potential at a site.

In addition, a reference site, the central terminal of Wilson, is calculated from the average voltage of the limb leads. This idealized site is meant to represent a reference at the center of Einthoven's triangle where total current is zero. The central terminal is referred to as the reference or indifferent electrode. Unipolar ECG leads are derived from the difference between the measured voltage at a surface electrode and the calculated voltage at this central reference point.

ECG leads — The 12 conventional ECG leads record differences in electrical potentials, either between two surface electrodes (bipolar leads), or between a surface electrode and the central terminal of Wilson (unipolar leads).

ECG leads are divided into two groups: six extremity (limb) leads and six chest (precordial) leads. The extremity leads record potentials transmitted onto the frontal plane and the chest leads record potentials transmitted onto the horizontal plane (figure 2).

Limb leads — The six extremity, or limb, leads are further subdivided into three "bipolar" leads (I, II and III) and three "unipolar" leads (aVR, aVL and aVF). Each bipolar lead measures the difference in potential between electrodes at two extremities, with one electrode connected to the positive pole and the other to the negative pole of the voltmeter:

●Lead I records the difference between potential sensed by the electrode placed on the left arm (the positive pole) and one placed on the right arm (negative pole).

●Lead II records the difference between electrodes on the left leg (positive) and the right arm (negative).

●Lead III records the difference between electrodes on the left leg (positive) and the left arm (negative).

These were the leads of the original string galvanometer, the forerunner of the modern electrocardiograph introduced by the Dutch physiologist, Dr. Willem Einthoven at the beginning of the 20th century.

The "unipolar" limb leads, in comparison, measure the cardiac voltage (V) at one site relative to the central terminal, which has approximately zero potential. Thus:

●Lead aVR records right arm potentials

●Lead aVL records left arm potentials

●Lead aVF records left leg (foot) potentials.

The lower case "a" indicates that these potentials are augmented by 50 percent. The right leg electrode functions as a ground.

The spatial orientation and polarity of the six frontal plane leads is represented on the hexaxial diagram (figure 3). As examples, lead I is primarily a left-right lead, while aVF is an inferior-superior lead.

Precordial leads — The six standard chest, or precordial, leads are also unipolar recordings. They represent the voltage difference between the central terminal and electrodes placed in the following positions (figure 4):

●V1 – 4th intercostal space (ICS), just to the right of the sternum

●V2 – 4th ICS, just to the left of the sternum

●V3 – midway between V2 and V4

●V4 – 5th ICS in the mid-clavicular line

●V5 – anterior axillary line, same level as V4

●V6 – mid-axillary line, same level as V4 and V5

Inadvertent misplacement of chest leads is quite common and can lead to considerable diagnostic confusion.

The ECG leads are designed so that a positive (upright) deflection will be recorded in a lead if a wave of depolarization spreads toward the positive pole of that lead. A negative deflection will be recorded if the wave of depolarization spreads toward the negative pole of any lead (ie, away from the positive role). As an example, depolarization spreading to the left and posterior will produce a positive deflection in lead I (a left-right lead) and a negative deflection in lead V1 (an anterior-posterior lead). If, however, the mean orientation of the depolarization vector (or electrical axis) is at right angles to a given lead axis, a small biphasic (equally positive and negative) deflection will be recorded.

Together, the frontal and horizontal plane electrodes provide a three-dimensional report of cardiac electrical activity. Each lead can be likened to a different video camera angle "looking" at the same dynamic events — atrial and ventricular depolarization and repolarization — from different spatial orientations. The standard 12 lead ECG can be supplemented with additional leads under special circumstances. In special circumstances, additional precordial leads may provide information. For example, right chest leads V1R to V6R (where V1R corresponds to V2 and V2R to V1, etc) are routinely obtained in cases of suspected acute right ventricular infarction, associated with inferior ST elevation myocardial infarction. Leads V7 to V9 may be useful in detection of postero-lateral ST elevation myocardial infarction. (See "Right ventricular myocardial infarction".)

ECG WAVEFORMS AND INTERVALS — ECG waves are labeled alphabetically starting with the P wave, which represents atrial depolarization (figure 5). The QRS complex represents ventricular depolarization and the ST-T-U complex (ST segment, T wave and U wave) represents ventricular repolarization. The J point is the junction between the end of the QRS and beginning of the ST segment. (Atrial repolarization occurs during the PR segment and QRS complex but is usually of too low an amplitude to be detected, but may become apparent in conditions such as acute pericarditis or atrial infarction.)

The QRS-T waveforms on the surface ECG correspond in a general way to the different phases of simultaneously obtained ventricular action potentials, the intracellular recordings from single myocardial fibers (figure 6). (See "Cardiac excitability, mechanisms of arrhythmia, and action of antiarrhythmic drugs".):

●QRS onset corresponds to the rapid upstroke (phase 0) of the action potential.

●The isoelectric ST segment corresponds to phase 2 of the action potential (plateau phase), during which myocardial fibers normally achieve about the same potential.

●The T wave corresponds to phase 3 of the action potential (active repolarization).

●The isoelectric segment between the end of the T wave and the next depolarization corresponds to phase 4 of the action potential (recovery).

Factors that decrease the slope of phase 0 by, for example, impairing the influx of sodium tend to increase QRS duration (eg, severe hyperkalemia or drugs such as flecainide or propafenone). On the other hand, factors that prolong phases 2/3 (eg, hypocalcemia or drugs such as amiodarone, dofetilide, or sotalol) increase the QT(U) interval. In contrast, factors such as digitalis and hypercalcemia shorten ventricular repolarization (phase 2) and abbreviate the ST segment.

The ECG waves are recorded on special graph paper which is divided into 1 mm² grid-like boxes. With the usual paper speed of 25 mm/sec, 1 mm of paper width (ie, small box) represents a 0.04 sec (40 ms) interval, and 5 mm of paper width (ie, large box) represents a 0.20 sec (200 ms) interval. When using a standard calibration, 10 mm of paper height (two large boxes) is equal to 1 mV of signal amplitude.

ECG intervals — There are four major sets of ECG intervals: R-R (inversely related to the pulse or heart rate), PR, QRS, and QT/QTc (figure 5). The instantaneous heart rate (beats/min) can be readily computed from the interbeat (R-R) interval by dividing the number of large (0.20 sec) time units between consecutive R waves into 300 or, for more precise measurement, the number of small (0.04 sec) units into 1500.

Note that the P-P interval in sinus rhythm with 1:1 atrioventricular (AV) conduction ("normal sinus rhythm") can also be measured and will be equal to the R-R interval. However, in certain circumstances, notably sinus rhythm with second or third degree AV block, the P-P and R-R intervals will not be the same. In the two arrhythmias characterized by continuous atrial activity, namely atrial flutter and atrial fibrillation, there are no true P-P intervals; but the atrial cycle lengths will be much shorter than the R-R intervals in such cases due to atrial depolarization rates ≥250/min. (See "ECG tutorial: Atrioventricular block" and "Electrocardiographic and electrophysiologic features of atrial flutter".)

The PR interval measures the time (normally 0.12 to 0.20 sec; 3 to 5 small boxes) between the onset of atrial and ventricular depolarization. This includes the physiologic delay primarily caused by slower conduction through in the tissue in the AV junction area.

The QRS interval (normally ≤0.10 sec = 2.5 small boxes measured by hand, or <110 ms by computer in adults) is a measure of the duration of ventricular depolarization. The QRS complex is subdivided into specific deflections or waves. If the initial QRS deflection of a given lead is negative, it is termed a Q wave. The first positive deflection is termed an R wave. A negative deflection after an R wave is called an S wave. Subsequent positive or negative waves are labeled R' or S', respectively. Lower case letters (q, r, or s) are used for relatively small amplitude waves of less than 0.5 mV (less than 5 mm with standard calibration). An entirely negative QRS complex is called a QS wave.

The QT interval begins with the onset of the QRS complex and ends at the end of the T-wave, subtends both ventricular depolarization and repolarization times, and varies inversely with the heart rate. A rate-related (or corrected) QT interval (QTc) based on the original Bazett formula is calculated as:

where the QT and R-R intervals are measured in seconds. The upper limit of the normal value for the QTc is approximately 0.44 to 0.45 sec (440 to 450 ms).

However, this formula has been critiqued because it tends to under-correct the QT at slower heart rates and over-correct it at faster ones. Therefore, a number of other formulas have been proposed, without formal consensus, for correcting the QT. For example, Hodges (linear) formula, which is now widely used, is given by:

Computer-based measurements should be checked by hand if they appear to be incorrect. If present, large U waves should be included in the QTc. Bazett, Hodges, and other QT interval correction formulas can be found elsewhere (calculator 1).

Another set of clinical questions relates to what the lower limits of the QTc are and if the QTc can be pathologically short. The lower bounds of the QTc have not been well-established. Values of 330 to 360 ms are sometimes cited. Pathologic shortening of the QTc only occurs in a limited number of clinical settings: hypercalcemia (where the T waves may be normal), digitalis effect (usually with "scooping" of the ST-T), and with the hereditary (congenital) short QT syndrome, which may be associated with increased risk of sudden cardiac arrest. (See "Diagnostic approach to hypercalcemia", section on 'Clinical clues' and "ECG tutorial: Miscellaneous diagnoses", section on 'Hypercalcemia' and "Digitalis (cardiac glycoside) poisoning", section on 'Electrocardiogram' and "Congenital long QT syndrome: Diagnosis", section on 'General ECG principles'.)

Note that digoxin effect does not imply toxicity, but that most patients with digoxin toxicity do show digoxin effect on their ECG.

GENESIS OF THE NORMAL ECG — The direction and magnitude of the ECG waveform reflect the sequential vectors of atrial and ventricular depolarization and repolarization.

P wave — The wave of atrial depolarization normally travels downward and toward the subject's left, reflecting the spread of the depolarization stimulus from the sinus node to the right and left atrial muscle and the AV junction. This downward and left-oriented vector points toward the positive pole of lead II and the negative pole of lead aVR (figure 7). As a result, the normal sinus P wave is positive (upright) in lead II and negative (downward) in lead aVR. In contrast, activation of the atria from an ectopic pacemaker in the lower part of either atrium or in the AV junction region may produce retrograde P waves moving upward and to the right. This will produce P waves that are negative in lead II and positive in lead aVR.

QRS complex — Normal ventricular depolarization can be divided into two major, sequential phases. Each phase can be represented by a mean vector (figure 8).

●The first phase is depolarization of the interventricular septum from left to right (vector 1).

●The second phase is simultaneous depolarization of the main mass of the right and left ventricles. This second phase is normally dominated by the more massive left ventricle so that vector 2 points leftward and posteriorly.

Thus, a right precordial lead like V1 will record this biphasic depolarization process with a small positive deflection (septal r wave) followed by a larger negative deflection (S wave). In contrast, a left precordial lead such as V6 will record the same sequence with a small negative deflection (septal q wave) followed by a relatively tall positive deflection (R wave). Intermediate precordial leads show a relative increase in R wave amplitude and a decrease in S wave amplitude progressing across the chest from right to left (waveform 1). This normal R wave progression in the precordial leads is a reflection of the progressively more leftward orientation of these leads. The precordial lead where the R wave and S wave are of about equal amplitude is referred to as the transition zone (usually lead V3 or V4).

QRS axis — The electrical axis describes the overall orientation of the QRS vector with reference to the six frontal plane leads. The QRS pattern in the extremity leads may vary considerably from one normal subject to another depending upon the electrical axis of the QRS complex.

The normal QRS axis in adults ranges from about -30° to + 100° (figure 3). An axis more negative than -30° is referred to as left axis deviation (LAD), while an axis more positive than +100° is referred to as right axis deviation (RAD).

Left axis deviation can occur as a normal variant, but is most commonly associated with a more pronounced leftward QRS vector due to left ventricular hypertrophy, a block in the anterior fascicle of the left bundle system (left anterior fascicular block or hemiblock) or inferior myocardial infarction. (See "Left anterior fascicular block".)

Right axis deviation can be a normal variant (particularly in children and young adults), a spurious finding due to reversal of the left and right arm electrodes, or represent an underlying condition such as right ventricular overload, lateral wall infarction of the left ventricle, dextrocardia, left pneumothorax, or left posterior fascicular block (see "Left posterior fascicular block"). The latter, a diagnosis of exclusion, is most commonly seen with right bundle branch block.

The QRS axis can be estimated as being at right angles to the positive pole of any extremity lead in which the positive and negative deflections are of roughly equal magnitude. With lead II, for example, the positive pole is at +60° (figure 3); as a result, the axis must be either -30° (borderline LAD) or +150° (RAD) if the QRS complex has positive and negative waves of roughly equal magnitude in that lead. These two possibilities can be readily distinguished by looking at another lead such as lead I (positive pole at +0°), which will be have a net positive deflection with LAD and negative deflection with RAD.

In general, you can usually determine whether the QRS electrical axis is normal, leftward or rightward from simple inspection of leads I and II (figure 9):

●Normal QRS axis – Net QRS area positive in I and II

●Left axis deviation – Net QRS positive in I, negative in II

●Right axis deviation – Net QRS negative in I, positive in II

T and U waves — In the normal ECG, the orientation of the mean T wave vector is roughly the same as the mean QRS vector. Since depolarization and repolarization are electrically opposite processes, this physiologic QRS-T wave vector concordance indicates that repolarization must normally proceed in the reverse direction from depolarization (ie, from epicardium to endocardium or from cardiac apex to base).

The normal U wave is a small rounded deflection (≤1 mm) following the T wave, which usually has the same polarity of the T wave. An abnormal increase in U wave amplitude is most commonly due to drugs (such as ibutilide, dofetilide, sotalol, quinidine, procainamide, or disopyramide) or hypokalemia. Very prominent U waves with prolonged ventricular repolarization (long QT interval) are associated with increased susceptibility to torsades de pointes, a type of polymorphic ventricular tachycardia. (See "Acquired long QT syndrome: Definitions, pathophysiology, and causes" and "Catecholaminergic polymorphic ventricular tachycardia".)

SUMMARY

●The electrocardiogram (ECG) is a graphical display (mapping) of electric potentials recorded on the body surface, which are generated by the atrial and ventricular heart muscle during each cardiac cycle. (See 'Introduction' above.)

●The conventional ECG is recorded using 12 leads, applied to the arms, legs, and chest, that represent the difference in electrical potentials in the frontal and horizontal planes of the body. (See 'ECG electrodes and leads' above.)

●ECG waves are labeled alphabetically starting with the P wave, which represents atrial depolarization. The QRS complex represents ventricular depolarization and the ST-T-U complex (ST segment, T wave and U wave) represents ventricular repolarization. The J point is the junction between the end of the QRS and beginning of the ST segment. (See 'ECG waveforms and intervals' above.)

●There are four major sets of ECG intervals: R-R (inversely related to the pulse or heart rate), PR, QRS, and QT/QTc. (See 'ECG waveforms and intervals' above.)

●The ECG can be conceptualized in terms of vectors (arrows with magnitude and direction) that represent the orientation and balance of cardiac depolarization and repolarization forces projected onto the ECG leads. (See 'Genesis of the normal ECG' above.)