Approach to ECG Interpretation
Step 1: Rate – The normal range of heart rate is between 60 and 100 beats per minute.Bradycardia is present if the rate is less than 60 beats per minute andtachycardia is present if the rate is greater than 100 beats per minute.
Step 2: Rhythm – Locate the P waves. All leads should be examined for P waves. The absence of P waves may denote atrial fibrillation. Establish the relationship between P waves and the QRS complex. The number of P waves should equal the number of QRS complexes. If there are more QRS complexes than P waves, then the rhythm is an accelerated ventricular or junctional rhythm. If there are more P waves than QRS complexes, then AV block is present. If P waves occur after each QRS complex consider: junctional rhythms, ventricular rhythms with retrograde AV conduction, an AV nodal reentrant rhythm or AV reciprocating tachycardias.
Step 3: Axis – Determine normal axis, left axis deviation or right axis deviation. The easiest way to determine the axis is by examining leads I and II. If the QRS complex has a positive deflection in both leads I and II then the axis falls between -30° and 90°, which means that there is no axis deviation. If the QRS complex is positive in lead I but negative in lead II then there is left axis deviation and the axis falls between -30° to -90°. If the QRS complex is negative in lead I and positive in aVF, then there is right axis deviation that falls between 90° to 180°. If the QRS complexes are negative in both leads I and II, then the axis is extreme (180° to -90°).
Step 4: Intervals – Normal PR intervals are 120 milliseconds to 200 milliseconds (3 to 5 small squares). Short PR intervals suggests Wolff-Parkinson-White syndrome. Long PR intervals are seen in first degree AV block. Normal QRS intervals last 60 milliseconds to 100 milliseconds (1 ½ to 2 ½ small squares). Long QRS intervals represent bundle branch block, ventricular preexcitation, ventricular pacing, or ventricular tachycardia.
Step 5: P wave – the P wave may vary in morphology, amplitude and duration. If the P wave has an amplitude of more than 0.25 millivolts and a duration of more than 120 milliseconds, then atrial enlargement is a possibility.
Step 6: QRS complex – If Q waves are prominent, consider myocardial infarction. Wide QRS complexes denote bundle branch block or pre-excitation.
Step 7: ST segment-T wave – Is there ST elevation or depression? Are there T wave inversions? These abnormalities denote myocardial ischemia or infarction.
Step 8: Overall interpretation – This is a collation of all the information gathered from steps 1 to step 8.
PATHOPHYSIOLOGY OF THE CURRENT OF INJURY AND MYOCARDIAL ISCHEMIA
In the normal patient, the ST segment is isoelectric with a measurement of relatively zero millivolts. At this point, all of the myocardial cells are in the plateau phase of the action potential (Figure 1).
In ischemic myocytes, the electrical properties are altered so that the resting membrane potential in phase 4 becomes less negative, the duration of the action potential is shortened to less than 200 milliseconds, and the morphology of phase 2 is altered.1 As a result, a voltage gradient forms between the normal myocytes and the ischemic myocytes. These changes are recorded by the electrocardiogram as deviations of the ST segment from the isoelectric point.
The change in resting membrane potential causes a depression of the ST segment during the diastolic stage and contributes to the appearance of the ST segment elevation on the ECG. Likewise, in transmural ischemia, a shortened action potential occurs which causes an abnormal current flow during the systolic stage of the cardiac cycle. The ST vector is shifted towards the outer positive epicardial zones, producing ST elevations and tall T waves (see Figure 2).
The amplitude of acute ischemic ST elevation indicates the severity of the ischemia. If marked ST elevation or depression in multiple leads is observed, consider severe ischemia or ischemia affecting large regions of the myocardium. Likewise, during thrombolytic therapy, substantial resolution of ST elevation is a good predictor of vessel patency and good prognostic outcomes post-therapy.2-4 Note that these observations are not universal for severe ischemia or myocardial infarction and can occur with slight or even absent ST-T changes.
The following are the electrocardiographic manifestations of acute myocardial ischemia5:
- For ST elevation: New ST elevation at the J point in two contiguous leads with the cut-points: >0.1 millivolts (1 small square*) in all leads other than V2-V3. In leads V2-V3 the cut-points are greater than or equal to 0.2 millivolts (2 small squares) in men 40 years old and above; greater than or equal to 0.25 millivolts (2 ½ small squares) in men less than 40 years old; or greater than 0.15 millivolts ( 1 ½ small squares) in women.*make sure the ECG settings are at 1 millivolt = 10 mm
- For ST-depression and T wave changes: New horizontal or down-sloping ST depression greater than or equal to 0.05 millivolts (1/2 small square) in two contiguous leads and/or T wave inversion greater than or equal to 0.1 millivolts (1 small square) in two contiguous leads with prominent R wave or R/S ratio greater than 1.
The clinical findings of the patient should always be evaluated together with ECG findings to increase the specificity. False-positive and false-negative findings ensue if the ECG tracing is taken too literally; in fact, a study has shown that unnecessary catheterizations were performed in 14% of patients.6
Four major types of acute coronary syndromes lead to different myocardial ischemia ECG patterns:
- Classic angina – manifested by transient ST segment depressions without QRS changes.
- Transmural ischemia (Prinzmetal’s angina) – transient ST elevations or paradoxical T wave normalization.
- Non-ST elevation myocardial ischemia – manifested by ST depressions or T wave inversions without Q waves, with supporting laboratory evidence of infarction.
- ST elevation myocardial ischemia – manifested by ST elevations or hyperacute T waves, followed by T wave inversions often associated with evolution of pathologic Q waves.
After recognizing a pattern of myocardial ischemia, the health care provider can perform appropriate actions towards preserving the patient’s health. It is suggested that the health care provider practice ECG tracing interpretation routinely.
- Mirvis DM, Goldberger AL. Electrocardiography. In: Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine, 9th edition, Bonow RO, Mann DL, Zipes DP, Libby P (Eds), W.B. Saunders Company, Philadelphia 2011.
- Zeymer U, Schröder K, Tebbe U, et al. Non-invasive detection of early infarct vessel patency by resolution of ST segment elevation in patients with thrombolysis for acute myocardial infarction; results of the angiographic substudy of the Hirudin for Improvement of Thrombolysis (HIT)-4 trial. Eur Heart J 2001; 22:796.
- Schröder K, Wegscheider K, Zeymer U, et al. Extent of ST segment deviation in a single electrocardiogram lead 90 min after thrombolysis as a predictor of medium-term mortality in acute myocardial infarction. Lancet 2001; 358:1479
- Zeymer U, Schröder K, Wegscheider K, et al. ST resolution in a single electrocardiograpic lead: a simple and accurate predictor of cardiac mortality in patients with fibrinolytic therapy for acute ST-elevation myocardial infarction. Am Heart J 2005; 149:91.
- Thygesen K, Alpert JS, Jaffe AS, et al. Third universal definition of myocardial infarction. Circulation 2012; 126.
- Larson DM, Menssen KM, Sharkey SW, et al. “False positive” cardiac catheterization laboratory activation among patients with suspected ST-segment elevation myocardial infarction. JAMA 2007; 298:2754.