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Electrocardiogram Interpretation 

Electrocardiogram Interpretation
Electrocardiogram Interpretation

Mohamad Kenaan

, and Kim Eagle

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date: 18 September 2020

  1. A. Introduction. Although there is no absolute right order for interpreting electrocardiograms (EKGs), it is important to be systematic and follow the same method and sequence when interpreting every EKG. One common approach is to evaluate EKG findings in the following order: rhythm, rate, axis, intervals, hypertrophy, Q waves, and ST segment/T wave changes.

  2. B. Rhythm

    1. a. Rhythm interpretation requires examination of rate, QRS regularity, atrial and ventricular complex origin/relationship, and intervals.

    2. b. Normal sinus rhythm. Each sinus morphology P wave (atrial depolarization) is followed by a QRS complex (ventricular depolarization) with a heart rate between 60 and 100 beats/min. A “normal” P wave is positively deflected (or above the baseline) in leads I, II, and aVF and negatively deflected (below baseline) in aVR.

    3. c. Tachycardia is a heart rate greater than 100 beats/min (see Chapter 7).

    4. d. Bradycardia is a heart rate less than 60 beats/min.

      1. i. Sinus bradycardia. Sinus rhythm as described above with heart rate less than 60 beats/min.

      2. ii. Other forms of bradycardia (e.g., atrioventricular [AV] nodal block) are discussed later in this chapter (E. a. ii.).

  3. C. Rate

    1. a. Regular rhythm. In sinus rhythm, the easiest way to estimate the heart rate is to divide 300 by the number of large boxes (each large box is 0.2 second) between two successive QRS complexes. This method could be applied to both atrial and ventricular rates when regular, but not necessarily in sinus rhythm. A quick method is to follow the order shown in Table 5.1 for each large box that is crossed. For a more precise estimation of rate, 1500 is divided by the number of small boxes (0.04 second) between two QRS complexes.

    2. b. Irregular rhythm or marked bradycardia. Identify the 3-second markers at the top/bottom of and EKG tracing. Count the number of QRS complexes appearing within 6 seconds and then multiply by ten. Alternatively, for EKG tracings spanning 10 seconds, multiply the number of QRS complexes in the 10-second tracing by six to approximate the rate.

      Table 5.1 Using the EKG to Determine Heart Rate for Patients in Sinus Rhythm*

      Number of Large Boxes

      Corresponding Heart Rate


      300 beats/min


      150 beats/min


      100 beats/min


      75 beats/min


      60 beats/min

      * Divide 300 by the number of large boxes between two successive QRS complexes.

  4. D. Axis

    1. a. The QRS axis, typically measured in the frontal plane, is the net vector generated by ventricular depolarization. For clinical purposes, it is often only necessary to determine whether the axis is normal, shifted left, or shifted right. Left and right axis shifts suggest disease of the ventricular myocardium.

    2. b. Normal axis. A normal axis is between –30° and +90° when plotted using a hexaxial reference system. Anything more negative than –30° is called a leftward or superior axis (because the axis is moving left toward the 12-o’clock position), and anything more positive than +90° is a rightward axis.

    3. c. Determining axis. QRS axis is determined by examining the “net QRS voltage” in leads I and aVF, in addition to lead II, by subtracting the area of upward and downward deflection to decide whether the QRS voltage is positive, negative, or isoelectric. The QRS axis is then determined according to Table 5.2.

      Table 5.2 Determining QRS Axis

      QRS Axis

      NET QRS Voltage

      Lead I

      Lead aVF

      Lead II

      Normal axis (90o to –30o)







      Left axis (–30o to –90o)




      Right axis (100o to 180o)




      Extreme right axis (180o to –90o)




    4. d. Causes of axis deviation

      1. i. Left axis deviation (LAD). Left anterior fascicular block and inferior wall myocardial infarction account for most cases of LAD.

        1. 1. Left anterior fascicular block

          • a. Pathogenesis. The left bundle splits into anterior and posterior fascicles. The anterior fascicle runs superiorly; therefore, when the anterior fascicle is blocked, the muscle that it serves (anterior and lateral walls) must be depolarized from inferior forces. These “extra” inferior to superior forces rotate the axis leftward (i.e., superiorly).

          • b. Criteria for diagnosis

            • i. QRS axis: between –45o and –90o.

            • ii. QRS duration: 90–119 msec.

            • iii. A qR pattern in lead I and rS pattern in leads II, III, and aVF.

            • iv. Because lead aVL is located near the left anterior fascicle (at approximately –30°), a block in the left anterior fascicle causes initial forces to move away from lead aVL, producing the qR pattern and delay in peak time.

        2. 2. Inferior wall myocardial infarction

          • a. Pathogenesis. Dead tissue at the inferior aspect of the left ventricle does not conduct; therefore, more net forces move superiorly (or leftward).

          • b. Criteria for diagnosis. Look for abnormal Q waves in the inferior leads (i.e., leads II, III, and aVF) to make the diagnosis.

        3. 3. Posteroseptal accessory pathway. Look for negative delta waves in the inferior leads, a short PR interval (less than 0.12 sec in duration), and a tall R wave in lead V2.

        4. 4. Left ventricular hypertrophy.

        5. 5. Left bundle branch block (LBBB).

        6. 6. Chronic obstructive pulmonary disease (COPD). A lower diaphragm can move the right ventricle below the larger left ventricle and cause more superior forces. However, when accompanied by pulmonary hypertension, COPD often produces right axis deviation (RAD).

        7. 7. Congenital heart disease (e.g., primum-type atrial septal defect, ventricular septal defect, tricuspid atresia)

        8. 8. Hyperkalemia (severe or acute)

        9. 9. Pulmonary embolism can produce LAD, but more often produces RAD.

        10. 10. Normal variant

      2. ii. Right axis deviation (RAD)

        1. 1. Right ventricular hypertrophy. RAD is caused by right ventricular hypertrophy until proven otherwise.

        2. 2. Cor pulmonale (e.g., pulmonary embolus, acute bronchospasm, COPD even in absence of right ventricular hypertrophy, pneumothorax). Look for a shift of axis to the right of more than 30° when compared with a prior EKG.

        3. 3. Extensive lateral wall myocardial infarction. Look for Q waves in leads I and aVL.

        4. 4. Lateral wall accessory pathway. Look for a short PR interval.

        5. 5. Left posterior fascicular block criteria for diagnosis:

          • a. QRS axis: between 90o and 180o.

          • b. QRS duration: 90–119 msec.

          • c. Pattern: rS pattern in lead I and qR pattern in leads III and aVF.

        6. 6. Lead reversal. An inverted P wave in lead I to suggests arm lead reversal.

        7. 7. Congenital heart disease (e.g., secundum atrial septal defect, dextrocardia)

        8. 8. Normal variant (in young adults/children)

        9. 9. Pectus excavatum

      3. iii. Extreme RAD: consider ventricular tachycardia or ventricular pacing.

  5. E. Intervals

    1. a. PR interval. The PR interval is normally 0.12–0.2 second in duration (three to five small boxes) measured from the beginning of the P wave to the beginning of the QRS complex.

      1. i. A short PR interval is often caused by a high catecholamine state that makes the AV node conduct faster; however, always look for delta waves to rule out an accessory pathway that may cause preexcitation. Other causes include ectopic atrial/junctional rhythms originating near the AV node, so look for P waves with abnormal morphology in leads I, II, and aVF.

      2. ii. A prolonged PR interval is associated with increased vagal tone or more permanent disease within the conduction system.

        1. 1. First-degree AV nodal block. If each P wave is followed by a QRS complex at a longer than normal interval (>0.2 second or one large box), a first-degree AV nodal block is diagnosed.

        2. 2. Second-degree AV nodal block. In second-degree AV nodal block, some P waves are not followed by a QRS complex, producing varying degrees of bradycardia. The P-P interval is usually regular. EKGs often demonstrate a pattern of “grouped” or “clustered” beats.

          • a. Type I second-degree AV nodal block (Wenckebach) is characterized by progressive PR prolongation culminating with a nonconducted P wave. Other features include regular P-P interval with progressive shortening of the R-R interval.

          • b. Type II second-degree AV nodal block (Mobitz II) is characterized by constant PR intervals preceding a nonconducted P wave. In this case, the P-P intervals and the R-R intervals are usually regular.

        3. 3. Third-degree AV nodal block. The timing of P waves and QRS complexes is completely dissociated, with the atrial rate being faster than the ventricular rate. Both the P-P intervals and the R-R intervals are regular, although occasionally the P-P interval could slightly vary (a phenomenon called ventriculophasic variation).

    2. b. QRS interval. The QRS interval is normally less than 0.09 second in duration. Measurement is from the beginning of the Q wave to the end of the S wave.

      1. i. Interventricular conduction delay or incomplete bundle branch block is diagnosed when the QRS complex is 0.1–0.12 second in duration.

      2. ii. Bundle branch block is diagnosed when the QRS complex is greater than 0.12 second in duration (“widened”).

        1. 1. Pathogenesis. If the right bundle is blocked, depolarization must proceed down the left bundle and then slowly to the right from muscle fiber to muscle fiber. Muscle conducts slowly compared with the specialized bundles; therefore, the QRS complex will be wider than normal, and the late electrical forces will move to the right. Similarly, LBBB will also have a wide QRS complex, and the late forces will move to the left.

        2. 2. Diagnosis

          • a. Determining the direction of the late forces (Figure 5.1). Draw a line down the middle of the QRS complex in lead V1 (a rightward lead) and lead V6 (a leftward lead). The half of the QRS complex to the right of the line represents the “late” forces. Check if these are positive (above the horizontal) or negative (below the horizontal).

            Figure 5.1 Determining the direction of the late forces. (A) Right bundle branch block. The late forces are positive in lead V1 and negative in lead V6. (B) Left bundle branch block. The late forces are negative in lead V1 and positive in lead V6.

            Figure 5.1 Determining the direction of the late forces. (A) Right bundle branch block. The late forces are positive in lead V1 and negative in lead V6. (B) Left bundle branch block. The late forces are negative in lead V1 and positive in lead V6.

          • b. Interpretation

            • i. Right bundle branch block (RBBB). If the late forces of V1 are positive and those of V6 are negative, then the late forces are moving toward the right from the left, signifying RBBB. Diagnostic criteria for RBBB include:

              • 1. QRS duration: greater than or equal to 0.12 sec.

              • 2. rsR, rSR, or rsr pattern in in V1/V2 (second r wave should be wider than first r wave).

              • 3. S wave in I and V6 that is of greater duration than the R wave.

            • ii. LBBB. If the late forces of V6 are positive and those of V1 are negative, then the late forces are moving toward the left from the right, indicating LBBB. Diagnostic criteria for LBBB include:

              • 1. QRS duration: greater than or equal to 0.12 second.

              • 2. Broad slurred or notched R wave in I, aVL, V5, and V6.

              • 3. Absent Q wave in I, V5, and V6.

            • iii. Nonspecific interventricular bundle branch block is often diagnosed when V1 and V6 are both negative or both positive.

        3. c. QT interval. The QT interval varies according to the heart rate, lengthening as the heart rate decreases. Measurement is from the beginning of the QRS complex to the end of the T wave. The QT interval is corrected for heart rate by dividing the measured QT interval by the square root of the R-R interval [Bazett’s formula: QTc = QT/(square root of R-R interval)]. For QT measurement, post-premature contraction beats should be avoided. Note that Bazett’s formula can overestimate QTc in the setting of tachycardia. A QTc interval greater than 0.44 second in duration in men and greater than 0.46 second in women is considered abnormal. Numerous drugs (e.g., tricyclic antidepressants, type Ia antiarrhythmics, type III antiarrhythmics, macrolides, fluoroquinolones, antiemetics) and electrolyte abnormalities (hypokalemia, hypomagnesemia, hypocalcemia) are common causes of a prolonged QT interval. Other causes of QT prolongation include congenital long QT syndrome, stress cardiomyopathy, myocarditis, hypothermia, myxedema, and intracranial hemorrhage.

  6. F. Hypertrophy

    1. a. Left ventricular hypertrophy (LVH). EKG criteria for the diagnosis of LVH are poorly sensitive but highly specific. Commonly used voltage criteria for diagnosis of LVH include:

      1. i. Stand-alone Sokolow-Lyon Criteria: R wave in lead aVL >11 mm (>13 mm if left anterior fascicular block is present). Avoid using in the setting of left anterior fascicular block.

      2. ii. Cornell Criteria: R wave in lead aVL + S wave in lead V3 >20 mm in women or >28 mm in men.

      3. iii. Sokolow-Lyon Criteria: S wave in lead V1 + R wave in lead V5 or V6 (whichever is larger) >35 mm.

      4. iv. Supportive findings for all criteria: include left axis deviation, QRS widening (>90 msec), left atrial enlargement, and secondary repolarization changes.

    2. b. Right ventricular hypertrophy. Criteria for the diagnosis of right ventricular hypertrophy are also highly specific but insensitive.

      1. i. Right axis deviation (RAD) greater than 110°

      2. ii. R:S wave ratio in lead V1 greater than or equal to 1

      3. iii. R wave in lead V1 greater than or equal to 7 mm

      4. iv. R:S wave ratio in lead V5 or V6 less than or equal to 1

    3. c. Left atrial abnormality was formerly called left atrial enlargement, but the name was changed because the EKG findings may actually represent dilation, increased atrial pressure, or hypertrophy.

      1. i. Lead II. Notched P waves with duration greater than 0.12 second indicate left atrial abnormality.

      2. ii. Lead V1. If the terminal portion of the P wave (the negative deflection that represents left atrial depolarization) is equal to or greater than one small box by one small box (0.04 sec by 1 mm), left atrial abnormality is diagnosed.

    4. d. Right atrial enlargement

      1. i. Lead II. P wave greater than 2.5 mm high indicates right atrial enlargement.

      2. ii. Lead V1. If the initial force of the P wave (the positive deflection that represents right atrial depolarization) is greater than 1.5 mm, right atrial abnormality is diagnosed.

  7. G. Q Waves Indicate Forces Are Moving Away from Their Respective Leads

    1. a. Normal Q waves. Sometimes small Q waves (less than 0.03 sec in duration and less than 1 mm in amplitude) are normal and expected. For example, the interventricular septum is depolarized left to right, so a small or “septal” Q wave is expected in lead V6 (reflecting forces moving away from this leftward lead).

    2. b. Pathologic Q waves signify that forces are moving away from the area more than would normally be expected. A pathologic Q wave indicates an old myocardial infarction and is only diagnosed when the Q wave is at least 0.03 second (close to one small box) in duration and greater than 1 mm or one-half of the height of the ensuing R wave.

      1. i. Inferior wall myocardial infarction. Leads II, III, and aVF evaluate the inferior surface of the left ventricle. Q waves in these leads denote an inferior wall myocardial infarction. However, an isolated Q wave in lead III of up to 0.3 second may be seen as a normal variant. (A handy way of remembering this is: “A small Q in III is free, unless accompanied by a Q in either II or aVF.”)

      2. ii. Posterior wall myocardial infarction. Sometimes an inferior wall infarction is accompanied by a posterior wall infarction, producing a large R wave in lead V1 (i.e., forces move away from the posterior wall anteriorly). Differential diagnoses for a large R wave in V1 include:

        1. 1. Posterior wall myocardial infarction

        2. 2. Posteroseptal accessory pathway

        3. 3. Right ventricular hypertrophy

        4. 4. RBBB

        5. 5. Duchenne’s muscular dystrophy

        6. 6. Limb lead reversal (common)

        7. 7. Dextrocardia (rare)

        8. 8. Normal variant (in young people)

      3. iii. Anterior wall myocardial infarction. Q waves in the precordial leads (V1–V6) imply an old anterior myocardial infarction.

  8. H. ST/T Wave Changes

    1. a. ST Elevation: Myocardial injury in the setting of acute coronary syndrome (STEMI) is the most concerning and life-threatening cause of ST elevations. However, other conditions can be associated with ST elevations. Some of these causes can be remembered using: ST-ELEVATION:

      • MNEMONIC: Conditions Associated with ST Elevations (“ST ELEVATION”)

        ST elevation myocardial infarction → convex ST elevations and T wave inversion

        Takotsubo/stress cardiomyopathy

        Early repolarization changes → normal variant with concave ST elevations and upright T waves


        Electrolyte abnormalities (hyperkalemia)

        Ventricular aneurysm → ST elevations with deep Q waves without symptoms of cardiac ischemia

        Arrhythmias (Brugada syndrome)


        Inflammation/pericarditis → diffuse ST elevations with PR depression but without reciprocal ST depressions

        Osborne or J waves (hypothermia)

        Normal coronaries with vasospasm (Prinzmetal’s angina)

    2. b. ST depression causes include but are not limited to myocardial ischemia (non–ST elevation acute coronary syndrome, demand ischemia), secondary repolarization changes in the setting of ventricular hypertrophy or bundle branch block, medications (digoxin), electrolyte abnormalities (hypokalemia), pseudo-depressions (flutter waves in atrial flutter), central nervous system injury.

    3. c. T wave inversions may indicate myocardial ischemia but are nonspecific for this diagnosis. Several other causes of T wave inversions exist (e.g., cardiomyopathies, myocarditis, electrolyte abnormalities, hyperventilation, postprandial).

    4. d. Terminology. Clinicians often refer to ST depression and elevation as ischemia and infarct, respectively, rather than simply “injury.” This is because ST depression is caused by injury to the subendocardial (inner) region that is often the result of supply/demand mismatch, nonocclusive thrombus, or occlusive thrombus in a vessel supplying well-collateralized territory. ST elevation, in contrast, implies transmural injury that usually occurs as a result of complete coronary occlusion from thrombus during an infarction.

  9. I. Classic Electrocardiogram Changes in Selected Conditions

    1. a. Electrolyte abnormalities

      1. i. Hypokalemia: Long QT, prominent U waves, ST depressions, and T wave inversions.

      2. ii. Hyperkalemia: Peaked T waves, widened QRS, PR prolongation, sine wave.

      3. iii. Hypercalcemia: Short QT interval (due to short ST segment), Possible PR prolongation.

      4. iv. Hypocalcemia: Long QT interval.

    2. b. CNS disorders/injury can present with large upright or deeply inverted T waves, prolonged QT interval, prominent U waves. Can mimic myocardial infarction with ST elevations.

    3. c. Thyroid disorders

      1. i. Hyperthyroidism: sinus tachycardia, atrial fibrillation, PR prolongation, increased QRS amplitude.

      2. ii. Hypothyroidism: sinus bradycardia, low-voltage QRS, T wave inversions.

    4. d. Cardiac amyloidosis: Low-voltage, conduction abnormalities; pathologic abnormalities that mimic ischemia or old myocardial infarction.

Suggested Further Readings

Bacharova L, Schocken D, Estes EH, Strauss D. The role of ECG in the diagnosis of left ventricular hypertrophy. Curr Cardiol Rev 2014;10:257–61.Find this resource:

Beitland S, Platou ES, Sunde K. Drug-induced long QT syndrome and fatal arrhythmias in the intensive care unit. Acta Anaesthesiol Scand 2014;58:266–72.Find this resource:

de Bruyne MC, Kors JA, Hoes AW, et al. Diagnostic interpretation of electrocardiograms in population-based research: computer program research physicians, or cardiologists? J Clin Epidemiol 1997;50:947–52. (Classic Article.)Find this resource: