The initial review of the 12-lead electrocardiogram (ECG) should encompass the following: heart rate and rhythm, P-QRS-T morphology, presence of ST segment, and PR-QRS-QT intervals (see the image below). Each ECG should be thoroughly analyzed ("read") in a systematic fashion to avoid overlooking important abnormalities. The following steps are important to consider:
- Rate: Normal versus tachycardia versus bradycardia
- Rhythm: Abnormal versus normal sinus
- Intervals: PR, QRS, QT
- Axis: Normal versus left deviation versus right deviation
- Chamber abnormality: Atrial enlargement, ventricular hypertrophy
- QRST duration: Q waves, poor R-wave progression, ST-segment depressions/elevations, or T-wave changes
Electrocardiogram waves, intervals, and segments.
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The ECG grid
In the image below, the ECG is recorded on standard paper with large boxes in heavy lines of 0.5 cm on the sides. On the horizontal axis, each large box represents 0.2 seconds at a typical paper speed of 25 mm per second, which is then divided into five smaller boxes that each represent 0.04 seconds. On the vertical axis, the large box consists of five subdivisions, each of which is 1 mm in height. In standard calibration, each 10 mm equals 1 mV. The normal heart rate ranges from 60 to 100 per minute; rates below 60 per minute and, occasionally, lower than 50 per minute are routinely seen in seasoned athletes.
On standard calibration, each large box has sides of 0.5 cm. On the horizontal axis, each large box represents 0.2 seconds, and each smaller box represents 0.04 seconds. On the vertical axis, each small box is 1 mm in height; 10 mm = 1 mV.
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Heart rate
When the cardiac rhythm is regular, the heart rate can be determined by the interval between two successive QRS complexes. On standard paper with the most common tracing settings, the heart rate is calculated by dividing the number of large boxes (5 mm or 0.2 seconds) between two successive QRS complexes into 300. For example, if the interval between two QRS complexes is two large boxes, then the rate is 150 beats per minute (bpm) (300 ÷ 2 = 150 bpm). See the following images.
Heart rates associated with each of the large boxes in the following order are 300, 150, 100, 75, 60, 50, 43, 37, 33 beats per minute (bpm).
Heart rate boxes.
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If the heart rate is irregular, count the number of QRS complexes on the ECG and multiply by 6 to obtain the average heart rate in bpm (the ECG displays a period of 10 seconds; thus, 6 × 10 seconds = 60 seconds [1 minute]).
The P wave
The P wave represents atrial depolarization. The normal P wave morphology is upright in leads I, II, and aVF, but it is inverted in lead aVR. The P wave is typically biphasic in lead V1 (positive-negative), but when the negative terminal component of the P wave exceeds 0.04 seconds in duration (equivalent to one small box), it is abnormal.
Left atrial enlargement should be suspected when the P wave duration is increased; it is associated with being more than one small box deep (>1 mm2) in lead V1 and a bifid P wave in lead II with a duration that is longer than 110 milliseconds. [27] Right atrial enlargement is associated with a peaked P wave taller than 2.5 mm in the inferior leads and more than 1.5 mm tall in leads V1 and V2. [28]
The PR interval
The PR interval incorporates the time from the depolarization of the sinus node to the onset of ventricular depolarization. The measurement starts from the beginning of the P wave to the first part of the QRS complex, with a normal duration between 0.12 to 0.20 seconds. [7]
The QRS complex
The QRS duration represents the time for ventricular depolarization. The duration is normally 0.06 to 0.10 seconds. Q waves are inscribed when the initial QRS vector is directed away from the positive electrode. The R wave is the first positive deflection of the QRS complex; its amplitude varies by age, race, and cardiac pathology, and it should increase across the precordium from leads V1 to V5. The negative deflection after the R wave is the S wave.
The ST segment
The ST segment is an interval between ventricular depolarization and ventricular repolarization. It is identified as the end of the QRS complex to the beginning of the T wave.
The end of the T wave to the beginning of the P wave is described as the TP segment, which is the zero potential or isoelectric point. The amount of elevation or depression in millimeters is relative to the TP segment.
The J point is located at the junction between the end of the QRS complex and the beginning of the ST segment. J-point elevation is known as an Osborne wave, which represents distortion of the earlierst phase of membrane repolarization, and it is associated with hypothermia.
Myocardial ischemia diagnosed by ECG is an integral part of the acute coronary syndrome (ACS) treatment pathway and allows patient stratification into ST-segment elevation ACS (STE-ACS) and non-ST-segment elevation ACS (NSTE-ACS). [5, 29, 30] ST-segment wave changes may be in association with disease states such as acute ischemia, myocardial injury, pericarditis, and intraventricular conduction delays.
In the absence of left ventricular hypertrophy (LVH) and left bundle branch block (LBBB), new ST-segment elevation in upward convexity are signs of myocardial infarction (typically 60 msec following the J point in two contiguous leads [with cut-off points in leads V2-V3 of ≥0.2 mV in men ≥40 years, ≥0.25 mV in men ˂40 years, or ≥0.15 mV in women, and/or 0.1 mV in other leads for both men and women]). [31] New horizontal or down sloping ST depression that is 0.05 mV or more in two contiguous leads and/or T-wave inversion that is 0.1 mV or more in two contiguous leads, with a prominent R wave or an R/S ratio over 1, are also signs of myocardial infarction.
Coronary spasm may be associated with angina (Prinzmetal) and with transient ST-segment elevation in a coronary artery branch distribution that has the spasm.
Pericarditis is associated with ECG manifestations of diffuse upward concave ST-segment elevation with PR depressions.
See the following images.
ST depression.
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ST elevation.
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ST morphology.
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The QT interval
The QT interval measures the depolarization and repolarizationof the ventricles. QT prolongation is associated with development of ventricular arrhythmias and sudden death. [32] It is commonly caused by various medications or can be a manifestation of an underlying ion channelopathy.
The QT interval is dependent on the heart rate. A faster heart rate leads to a shorter QT interval, whereas a slower heart rate leads to a longer QT interval. A corrected QT interval (QTc) corrects for the variations in heart rate. QTcb is the QT interval divided by the square root of the RR interval in seconds when using the Bazett formula. The normal value of for QTcb in men is 0.44 seconds or less; in women, it is 0.46 seconds or less. [33]
The ECG axis
The QRS axis represents the major vector of ventricular activation, which is the overall direction of electrical activity. The electrical activity in healthy individuals starts at the sinoatrial node and spreads to the atrioventricular node down the Bundle of His, followed by conduction through the left and right bundle branches,and then to the Purkinje fibers to cause ventricular contraction. A positive deflection is when the direction of the overal electrical activity is toward that lead. Therefore, the cardiac axis may provide the overall direction of electrical activity when the ventricles depolarize. The normal cardiac axis is expected to lie between -30º and 90º, which means the overall direction of electrical activity is toward leads I, II, and III.
Electrocardiographic axis. Normal axis is between -30º and 90º; left axis deviation (LAD) is between -30º and - 90º; right axis deviation (RAD) is between 90º and 180º; extreme axis deviation (EAD) (left or right) is between -90º and -180º.
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The electrical axis can be estimated from the standard frontal leads. There are shortcut methods to determine the axis. For example, if the QRS complex is upright in both leads I and II, then the axis must fall somewhere between -30º and 90º and the axis is normal.
If the complexes are negative in lead I and positive in lead aVF, then the axis is rightward. If the complexes are positive in lead I but negative in lead II, then the axis is leftward. If the complexes are negative in both leads I and aVF, then the axis is extreme.
The causes of left axis deviation include normal variation, left ventricular hypertrophy, left anterior fascicular block, congenital heart disease with primum atrial septal defect or endocardial cushion defect, ventricular ectopic beats, and preexcitation syndromes. [34]
The causes of right axis deviation include normal variation, right ventricular hypertrophy, left posterior fascicular block, ventricular ectopic beats, preexcitation,and dextrocardia. [34]
R wave progression
The R wave should progress in size across leads V1 to V6. Normally, in lead V1, there is a small R wave with a deep S wave; the R-wave amplitude should increase in size with the transition zone, normally in leads V2 to V4. Poor or late R-wave progression consists of a transition zone in lead V5 or V6, and it can be a sign of a previous anterior myocardial infarction. [35]
R-wave progression.
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