Although the cardiologist has an arsenal of sophisticated diagnostic tools at his disposal, the ECG retains its central role in many circumstances. As examples, the ECG is the most important test for interpretation of cardiac rhythm, conduction system abnormalities, and for the detection of myocardial ischemia. The ECG is also of great value in the evaluation of other types of cardiac abnormalities including valvular heart disease, cardiomyopathy, pericarditis, and hypertensive disease. Finally, the ECG can be used to monitor drug treatment (specifically antiarrhythmic therapy), and to detect metabolic disturbances.

A systematic approach to interpretation of the ECG is important in order to establish rhythm and other abnormalities. Pattern recognition can be useful, but only after certain salient features have been determined. This card provides the framework for a systematic analysis of the ECG.

ECG GRID – The ECG is a plot of voltage measured by the leads on the vertical axis against time on the horizontal axis. The electrodes are connected to a galvanometer that records a potential difference. The needle (or pen) of the ECG is deflected a given distance depending upon the voltage measured.

P wave – The P wave represents left and right atrial depolarization and is an initial low amplitude positive deflection preceding the QRS complex. The duration is generally 0.4 sec. Since right atrial depolarization precedes that of the left atrium, the P wave is often notched in the limb leads and may be biphasic in lead V1. The initial positive deflection in V1 is due to right atrial depolarization that is directed anteriorly, while the second negative deflection represents left atrial depolarization that is directed posteriorly.

Atrial repolarization occurs simultaneously with depolarization of the ventricular myocardium. Thus, the atrial "T wave" is hidden by the QRS complex and not observed on the routine ECG. However, when the heart rate is increased (eg, with sinus tachycardia), the PR interval is shortened; atrial repolarization (the atrial T wave) then can be observed at the very end of the QRS complex, altering the J point, and resulting in J point depression. This is a physiologic and normal change.

PR interval – The PR interval is measured from the beginning of the P wave to the first part of the QRS complex. It includes time for atrial depolarization (the P wave), conduction through the AV node, and conduction through the His-Purkinje system. The length of the PR interval changes with heart rate, but is normally 0.14-0.20 sec. The interval is shorter at faster heart rates due to sympathetically mediated enhancement of AV nodal conduction; it is longer when the rate is slowed as a consequence of slower AV nodal conduction resulting from withdrawal of sympathetic tone or an increase in vagal inputs.

QRS complex – The QRS complex represents the time for ventricular depolarization.

• An initial negative deflection is the Q wave due to septal depolarization.

• The first positive deflection is the R wave which represents depolarization of the left ventricular myocardium. Right ventricular depolarization is obscured because the left ventricular myocardial mass is much greater than that of the right ventricle.

• The negative deflection following the R wave is the S wave which represents terminal depolarization of the high lateral wall.

• If there is a second positive deflection it is known as an R'.

• Lower case letters (q, r, or s) are used for relatively small amplitude waves of less then 0.5 mV (less than 5 mm with standard calibration).

• An entirely negative QRS complex is called a QS wave.

The entire QRS duration normally lasts for 0.06 to 0.10 seconds (2 1/2 small boxes) and is not influenced by heart rate.

ST segment – The ST segment occurs after ventricular depolarization has ended and before repolarization has begun. It is a time of electrocardiographic silence. The initial part of the ST segment is termed the J point.

The ST segment is usually isoelectric (zero potential) and has a slight upward concavity. However, it may have other configurations depending upon associated disease states (eg, ischemia, acute myocardial infarction, or pericarditis). In these situations, ST segment may be horizontally depressed (below the isoelectric line), elevated in a concave or convex direction (above the isoelectric line), or downsloping.  In some normal cases the J point is depressed and the ST segment is rapidly upsloping, becoming isoelectric within 0.08 seconds after the end of the QRS complex.

T wave – The T wave represents the period of ventricular repolarization. Since the rate of repolarization is slower than depolarization, the T wave is broad, has a slow upstroke, and rapidly returns to the isoelectric line following its peak. Thus, the T wave is asymmetric and the amplitude is variable.

Since depolarization begins at the endocardial surface and spreads to the epicardium while repolarization begins at the epicardial surface and spreads to the endocardium, the direction or vector of ventricular depolarization is opposite to that of ventricular repolarization. Thus, the T wave direction or vector on the ECG normally is in the same direction as the QRS.

QT interval – The QT interval consists of the QRS complex which represents only a brief part of the interval, and the ST segment and T wave which are of longer duration. Thus, the QT interval is primarily a measure of membrane repolarization. It is more accurate to measure a JT interval that does not include the QRS complex and therefore excludes depolarization.

The time for ventricular repolarization and therefore the QT (or JT) interval is dependent upon the heart rate; it is shorter at faster heart rates and longer when the rate is slower. Thus, a QT interval that is corrected for heart rate (QTc) is often calculated as follows:

QTc = QT interval ÷ square root of the RR interval (in sec)

The normal value for the QTc is < or =0.44 sec.

U wave – A u wave may be seen in some leads, especially the right precordial leads V2 to V4. The exact cause of this wave is uncertain, although it has been suggested that it represents delayed repolarization of the His-Purkinje system. Alternatively, it may represent a mechanical event such as ventricular relaxation.

HEART RATE – If the cardiac rhythm is regular, the interval between successive QRS complexes can be determined from the ECG grid.

• If the interval between two successive complexes is one large box (representing 0.2 seconds), then the rate is 300 beats/minute (60 seconds/minute ÷ 0.2 seconds/beat =300). If the interval is two large boxes, the rate is 150 (60/0.4=150). This calculation may be carried on down the line.

• If the interval falls between the large boxes, one can extrapolate. Thus, if the interval between successive QRS complexes is between one and two large boxes (eg, a rate between 150 and 300), each of the five small boxes 0.04 seconds represents 30 beats/minute. If between two and three large boxes (eg, a rate between 100 and 150 beats/minute), each small box represents 10 beats/minute. Between three and four large boxes (eg, rate 75 to 100 beats/minute) each small box represents 5 beats/minute.

If the rhythm is irregular, the simplest way to determine the rate is by counting the number of complexes which occur in six seconds (30 large boxes) and multiply by ten.

A rate of 60 to 100 is considered normal. A rate less than 60 is a bradycardia, while a rate over 100 is a tachycardia.

AXIS – The electrical signal recorded on the ECG contains information relative to direction and magnitude of the various complexes. The average direction of any of the complexes can be determined.

The normal QRS electrical axis is between 0° and 90° (directed downward or inferior and to the left). An axis between 0° and -90° (directed upward or superior and to the left) is termed left axis deviation. If the axis between 90° and 180° (directed inferiorly and to the right), then right axis deviation is present. An axis between -90° and -180° (superior and to the right hence an extreme right or left axis) is referred to as an indeterminate axis. There is some disagreement among authors on the definitions (in degrees) of a normal, right, and left axis. 

• If the QRS complex is positive (upright) in both leads I and aVF, then the axis falls within quadrant 1 and the axis is normal.

• If the QRS complex is positive in lead I but negative (downgoing) in lead aVF, then the axis falls within quadrant 2 and the axis is leftward.

• If the complexes are negative in lead I and positive in aVF, then the axis is in quadrant 4 and it is a right axis.

• If the complexes are negative in both I and aVF, then the axis is in quadrant 3 or indeterminate.

Another method of axis determination is to find the lead in which the complex is most isoelectric; the axis is directed perpendicular to the lead in which the complex is isoelectric or the lead with the smallest deflection. As an example, if the QRS is isoelectric in lead 3 which is directed at 120°, then the electrical axis is either 30° or -150°.

A third method is to determine the frontal lead in which the QRS is of the greatest amplitude. The axis is parallel to this lead.

By combining the quadrant determined by analysis of leads 1 and aVF with the isoelectric lead information, one can accurately and rapidly determine the electrical axis.

The causes of right axis deviation include:

• Normal variation (vertical heart)

• Mechanical shifts, such as inspiration and emphysema

• Right ventricular hypertrophy

• Right bundle branch block

• Left posterior fascicular block

• Dextrocardia

• Ventricular ectopic rhythms

• Preexcitation syndrome

• Lateral wall myocardial infarction

Causes for left axis deviation include:

• Normal variation (physiologic, often with age)

• Mechanical shifts, such as expiration, high diaphragm (pregnancy, ascites, abdominal tumor)

• Left ventricular hypertrophy

• Left bundle branch block

• Left anterior fascicular block

• Congenital heart disease (atrial septal defect, endocardial cushion defect)

• Emphysema

• Hyperkalemia

• Ventricular ectopic rhythms

• Preexcitation syndromes

• Inferior wall myocardial infarction.

RHYTHM ANALYSIS – Interpreting the rhythm of the ECG is sometimes difficult. However, as for ECG interpretation in general, a systematic approach along with a knowledge of arrhythmias often leads to a correct diagnosis.

Step 1: Locate the P wave – The most important and first step in rhythm interpretation is the identification of P waves and an analysis of their morphology. There are several questions that should be addressed:

• Are P waves visible? Absence of P waves may occur secondary to atrial fibrillation. Alternatively, P waves may be present but not visible if they are simultaneous with and therefore buried within the QRS complex as in a junctional rhythm or AV nodal reentrant tachycardia. In addition, they may be located within the ST segment as with an AV reentrant tachycardia or ventricular tachycardia.

• What is the rate of the P waves? If the rate is less than 60, then a bradycardia is present. If the atrial or P wave rate is over 100, the a tachycardia is present. In general, sinus tachycardia occurs at rates of 100 to 180; atrial tachycardia, AV nodal reentrant tachycardia,or AV reentrant tachycardia occur at rates of 140 to 220; atrial rates of 260-320 are seen with atrial flutter.

• What is the morphology and axis of the P waves? The normal sinus P wave is generally upright in leads I, II, and aVF and may be biphasic in leads III and V1. A negative P wave in the inferior leads or lead I suggests an ectopic rhythm (low atrial or left atrial respectively)

Step 2: Establish the relationship between P waves and the QRS complex – The next step is to determine the relationship between the P waves and the QRS complexes, addressing the following questions:

• Are the P waves associated associated with QRS complexes in a 1:1 fashion? If not, are there more or less P waves than QRS complexes and what are the atrial and ventricular rates? If there are more P waves than QRS complexes, then some form of AV block is present. If there are more QRS complexes than P waves, then the rhythm is an accelerated ventricular or junctional rhythm.

• Do the P waves precede each QRS complex as is the case with most normal rhythms? What is the PR interval, and is this interval fixed?

• Do P waves occur after each QRS complex as occurs in ventricular rhythms with retrograde VA conduction, or in AV nodal reentrant or AV reentrant arrhythmias? The RP interval should be noted and it should be established if it is fixed or variable.

Often, establishing the relationship between the P wave and the QRS complex is the most important diagnostic step in rhythm interpretation (see Overall approach to rhythm analysis below). 

Step 3: Analyze the QRS morphology – If the QRS complexes are of normal duration (<0.12 sec) and morphology, then the rhythm is supraventricular. It is essential to analyze the QRS in all 12 leads to be sure that it is normal.

If the QRS is wide and bizarre, then the rhythm is either supraventricular with aberrant conduction or it is of ventricular origin. It may be possible to differentiate the two by careful inspection of the QRS morphology. 

Step 4: Search for other clues – Often the diagnosis of a rhythm disturbance can be made by clues provided by breaks in the rhythm or other irregularities in an otherwise regular rhythm. As an example, an increase in the degree of AV block as occurs with carotid sinus massage may unmask the flutter waves of atrial flutter. Capture beats and fusion beats may be the clues which help establish AV dissociation and a diagnoses of ventricular tachycardia.

The regularity of the QRS complexes should be established by asking the following questions:

• Do the QRS complexes occur with regular intervals or are they irregular?

• If the complexes are irregular, is there a pattern to the irregularity? Is the rhythm regularly irregular, or is there group beating (eg, a repeating pattern of irregularity)?

Step 5: Interpret the rhythm in the clinical setting – Often the clinical history, including drugs being taken, can be helpful in establishing a diagnosis. As an example, a regular wide complex rhythm in an elderly patient first occurring post MI is most likely ventricular tachycardia.  Similarly a narrow complex tachycardia of sudden onset in a young person is likely AV nodal or AV reentrant tachycardia.

However, the clinical presentation and associated hemodynamic findings do not necessarily correlate with the etiology of an abnormal rhythm. The presence of hemodynamic stability during a tachycardia, for example, does not imply a supraventricular etiology, nor does instability mean that the diagnoses is ventricular tachycardia.