Clinical Electrocardiography: A Simplified Approach, 7th Edition (2006)


Chapter 22. How to Interpret an ECG

Part One of this book discussed the fundamentals of the normal ECG, and Part Two described the major abnormal patterns and arrhythmias. Drawing on those concepts and information, this chapter provides a systematic approach to ECG interpretation.


Accurate interpretation of ECGs requires thoroughness and care. Therefore you must develop a systematic method of reading ECGs that is applied in every case. Many of the most common mistakes are errors of omission, specifically the failure to note certain subtle but critical findings. For example, overlooking a short PR interval may cause you to miss the important Wolff-Parkinson-White pattern. Marked prolongation of the QT interval, a potential precursor of torsades de pointes (see Chapter 16 ) and sudden cardiac death (see Chapter 19 ), sometimes goes unnoticed. These and other common pitfalls in ECG diagnosis are reviewed in Chapter 23 .


On every ECG, 14 features should be analyzed. These features are listed in Box 22-1 and discussed in the following sections.

BOX 22-1 

14 Features to Analyze on Every ECG

Standardization (calibration) and technical quality

Heart rate


PR interval

P wave size

QRS width (interval)

QT interval

QRS voltage

Mean QRS electrical axis

R wave progression in chest leads

Abnormal Q waves

ST segments

T waves

U waves

Standardization and Technical Features

Make sure that the electrocardiograph has been properly calibrated so that the standardization mark is 10 mm tall (1 mV = 10 mm) (see Chapter 2 ).[*] Also check for limb lead reversal (see Chapter 23 ) and ECG artifacts (discussed later in this chapter).

*  In special cases, the ECG may be intentionally recorded at one-half standardization (1 mV = 5 mm) or two-times normal standardization (1 mV = 20 mm).
Heart Rate

Calculate the heart rate (see Chapter 2 ). If the rate is faster than 100 beats/min, a tachycardia is present. A rate slower than 60 beats/min means that a bradycardia is present.


The cardiac rhythm can almost always be described in one of the following four categories: (1) sinus rhythm (or a sinus variant such as sinus bradycardia or sinus tachycardia); (2) sinus rhythm with extra (ectopic) beats such as atrial premature beats (APBs) or ventricular premature beats (VPBs); (3) an entirely ectopic (nonsinus) mechanism such as atrial fibrillation or flutter, ventricular tachycardia, or an atrioventricular (AV) junctional escape rhythm; or (4) sinus rhythm or some ectopic rhythm (e.g., atrial fibrillation) with second- or third-degree heart block or other AV dissociation mechanism.

Sometimes, the ECG will show an abrupt change between two of these mechanisms, for example, paroxysmal atrial fibrillation spontaneously converting to sinus rhythm.

Be particularly careful not to overlook hidden P waves. These waves may be present, for example, in some cases of second- or third-degree AV block, atrial tachycardia (AT) with block, or blocked atrial premature beats (APBs). Also, whenever the ventricular rate is about 150 per minute, always consider the possibility of atrial flutter because the flutter waves may mimic the P waves of AT or sinus tachycardia.

PR Interval

The normal PR interval (measured from the beginning of the P wave to the beginning of the QRS complex) is 0.12 to 0.2 second. A uniformly prolonged PR interval is often referred to as first-degree AV block (see Chapter 17 ). A short PR interval with sinus rhythm and with a wide QRS complex and a delta wave is seen in the Wolff-Parkinson-White pattern. By contrast, a short PR interval with retrograde P waves (negative in lead II) generally indicates an ectopic (atrial or AV junctional) pacemaker.

P Wave Size

Normally, the P wave does not exceed 2.5 mm in amplitude and is less than 3 mm wide in all leads. Tall peaked P waves may be a sign of right atrial overload (P pulmonale). Wide P waves are seen with left atrial abnormality.

QRS Width (Interval)

Normally, the QRS width is 0.1 second (100 msec) or less in all leads. The differential diagnosis of a wide QRS complex is described in Chapter 24 .

QT Interval

A prolonged QT interval may be a clue to electrolyte disturbances (hypocalcemia or hypokalemia), drug effects (quinidine, procainamide, amiodarone, or sotalol), or myocardial ischemia (usually with prominent T wave inversions). Shortened QT intervals are seen with hypercalcemia and digitalis effect.

QRS Voltage

Look for signs of right or left ventricular hypertrophy (see Chapter 6 ). Remember that thin-chested people, athletes, and young adults frequently show tall voltage without left ventricular hypertrophy (LVH). Do not forget about low voltage, which may result from pericardial effusion or pleural effusion, hypothyroidism, emphysema, obesity, myocardial disease, or other factors (see Chapter 24 ).

Mean QRS Electrical Axis

Estimate the mean QRS axis in the frontal plane. Decide by inspection whether the axis is normal (between -30° and +100°) or whether left or right axis deviation is present (see Fig. 5-13 ).

R Wave Progression in Chest Leads

Inspect leads V1 to V6 to see if the normal increase in the R/S ratio occurs as you move across the chest (see Chapter 4 ). The terms “poor” or preferably “slow” R wave progression (small or absent R waves in leads V1 to V3)[*] refer to a finding that may be a sign of anterior myocardial infarction (MI), but may also be seen in many other settings, including: altered lead placement, LVH, chronic lung disease, left bundle branch block, and many other conditions in the absence of infarction.

*  The term reversed R wave progression is used to describe abnormally tall R waves in lead V1 that progressively decrease in amplitude. This pattern may occur with a number of conditions, including right ventricular hypertrophy, posterior (or posterolateral) infarction, and dextrocardia.
Abnormal Q Waves

Prominent Q waves in leads II, III, and aVF may indicate inferior wall infarction. Prominent Q waves in the anterior leads (I, aVL, and V1 to V6) may indicate anterior wall infarction (see Chapter 8 ).

ST Segments

Look for abnormal ST segment elevations or depressions.

T Waves

Inspect the T waves. Normally, they are positive in leads with a positive QRS complex. They are also normally positive in leads V3 to V6 in adults, negative in lead aVR, and positive in lead II. The polarity of the T waves in the other extremity leads depends on the QRS electrical axis. (T waves may be normally negative in lead III even in the presence of a vertical QRS axis.)

U Waves

Look for prominent U waves. These waves may be a sign of hypokalemia or drug effect or toxicity (e.g., amiodarone, dofetilide, quinidine, sotalol).

Memory aid: Students looking for a mnemonic to help recall key features of the ECG can try using “IR-WAX.” I is for the four basic intervals (Heart rate, PR, QRS, QT); R is for rhythm (sinus or other),W is for the five alphabetic waves (P, QRS, ST, T and U), and AX is for electrical axis.


After you have analyzed the 14 ECG features, you should formulate an overall interpretation. The final ECG reading actually consists of three sections:



A list of notable findings



An interpretive summary that attempts to integrate or explain these findings



A comparison with prior ECGs, if available.

For example, the ECG might show a prolonged QT interval and prominent U waves. The interpretation could be “Repolarization abnormalities consistent with drug effect or toxicity or hypokalemia. Clinical correlation suggested.” Another ECG might show wide P waves, right axis deviation, and a tall R wave in lead V1 (see Fig. 23-1 ). The interpretation could be “Findings consistent with left atrial abnormality (enlargement) and right ventricular hypertrophy. This combination is highly suggestive of mitral stenosis.” In yet a third case, the interpretation might simply be “Within normal limits.”

You should also formulate a statement comparing the present ECG with previous ECGs (when available). The absence of a comparison ECG should be noted.

Thus the ECG report is analogous to a newspaper account that consists of the hard facts and then the editorial comment. Like the editorialist, the ECG interpreter may sometimes offer suggestions such as “Serial tracings advisable to evaluate possible evolving ischemic T wave changes.” Figure 22-1 illustrates this systematic approach to ECG interpretation.

FIGURE 22-1  ECG for interpretation: (1) standardization—10 mm/mV; 25 mm/sec (electronic calibration); (2) heart rate—75 beats/min; (3) rhythm—normal sinus; (4) PR interval—0.16 sec; (5) P waves—normal size; (6) QRS width—0.08 sec (normal); (7) QT interval—0.4 sec (slightly prolonged for rate); (8) QRS voltage—normal; (9) mean QRS axis—about -30° (biphasic QRS complex in lead II with positive QRS complex in lead I); (10) R wave progression in chest leads—early precordial transition with relatively tall R wave in lead V2; (11) abnormal Q waves—leads II, III, and aVF; (12) ST segments—slightly elevated in leads II, III, aVF, V4, V5, and V6; slightly depressed in leads V1 and V2; (13) T waves—inverted in leads II, III, aVF, and V3 through V6; and (14) U waves—not prominent. Impression: This ECG is consistent with an inferolateral (or inferoposterolateral) wall myocardial infarction of indeterminate age, possibly recent or evolving. Comment: The relatively tall R wave in lead V2 could reflect loss of lateral potentials or actual posterior wall involvement.

Every ECG abnormality you identify should summon up a list of differential diagnostic possibilities (see Chapter 24 ). You should search for an explanation of every abnormality found. For example, if the ECG shows sinus tachycardia, you need to find the cause of the arrhythmia. Is it a result of anxiety, hyperthyroidism, congestive heart failure, hypovolemia, sympathomimetic drugs, alcohol withdrawal, or other causes? If you find ventricular tachycardia, what are the diagnostic possibilities? Is it due to MI or some promptly reversible cause such as hypoxemia, digitalis toxicity, toxic effects of another drug, hypokalemia, or hypomagnesemia? If you see signs of LVH, is the likely cause valvular heart disease, hypertensive heart disease, or cardiomyopathy? In this way, the interpretation of an ECG becomes an integral part of clinical diagnosis and patient care.



Computerized ECG systems are now widely used. These systems provide interpretation and storage of ECG records. The computer programs (software) for ECG analysis have become more sophisticated and accurate.

Despite these advances, computer ECG analyses have important limitations and not infrequently are subject to error. Diagnostic errors are most likely with arrhythmias or more complex abnormalities. Therefore computerized interpretations (including measurements of basic ECG intervals and electrical axes) must never be accepted without careful review.



The ECG, like any other electronic recording, is subject to numerous artifacts that may interfere with accurate interpretation. Some of the most common of these are described here.


Interference from alternating-current generators produces the characteristic pattern shown in Figure 22-2 . Notice the fine-tooth comb 60-hertz (Hz) artifacts. You can usually eliminate 60-Hz interference by switching the electrocardiograph plug to a different outlet or turning off other electrical appliances in the room.

FIGURE 22-2  Common ECG artifact produced by 60-Hz electrical interference.


Involuntary muscle tremor (e.g., parkinsonism) can produce undulations in the baseline that may be mistaken for atrial flutter or fibrillation ( Fig. 22-3 ).

FIGURE 22-3  Common ECG artifact produced by muscle tremor. A, Wavy baseline simulating atrial flutter. B, Same recording without the artifact, showing normal P waves.


Upward or downward movement of the baseline may produce spurious ST segment elevations or depressions ( Fig. 22-4 ).

FIGURE 22-4  Wandering baseline resulting from patient movement or loose electrode contact.


Poor electrode contact or patient movement ( Fig. 22-5 ) can produce artifactual deflections in the baseline that may obscure the underlying pattern or be mistaken for abnormal beats.

FIGURE 22-5  Deflections simulating ventricular premature beats, produced by patient movement. An artifact produced by 60-Hz interference is also present.


The electrocardiograph, as mentioned, should be standardized before each tracing so that a 1-mV pulse produces a square wave 10 mm high (see Fig. 2-5 ). Failure to standardize properly results in complexes that are either spuriously low or spuriously high. Furthermore, most electrocardiographs are equipped with half-standardization and double-standardization settings. Unintentional recording of an ECG on either of these settings also results in misleading low or high voltage.



The following 14 points should be evaluated on every ECG: standardization, heart rate, rhythm, PR interval, P wave size, QRS width (interval), QT interval, QRS voltage, mean QRS axis, R wave progression in chest leads, abnormal Q waves, ST segments, T waves, and U waves. Any ECG abnormality should be related to the clinical status of the patient.

Computer interpretations of ECGs are subject to error and must be carefully reviewed. The ECG can also be affected by numerous artifacts, including 60-Hz interference, patient movement, poor electrode contact, and muscle tremor.