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

Part III. OVERVIEW AND REVIEW

Chapter 24. ECG Differential Diagnoses

Instant reviews

This chapter presents 15 boxes that review selected aspects of ECG differential diagnosis for easy reference. For the most part, the boxes recap topics covered in this book. Some advanced topics are briefly mentioned, with additional discussion available in references cited in the Bibliography .

Wide QRS Complex

 

I.   

Intrinsic intraventricular delay (IVCD)[*]

 

A.   

Left bundle branch block and variants

 

B.   

Right bundle branch block and variants

 

C.   

Other (nonspecific) patterns of IVCD

 

II. 

Extrinsic (“toxic”) intraventricular delay

 

A.   

Hyperkalemia

 

B.   

Drugs: class I antiarrhythmic drugs and other sodium-channel blocking agents (e.g., tricyclic antidepressants and phenothiazines)

 

III. 

Ventricular beats: premature, escape, or paced

 

VI. 

Ventricular preexcitation: Wolff-Parkinson-White pattern and variants

*  Bundle branch block patterns may occur transiently. Note also that a spuriously wide-appearing QRS complex occurs if the ECG is unintentionally recorded at fast paper speeds (e.g., 50 mm/sec).

Low-Voltage QRS Complexes

 

1.   

Artifactual or spurious (especially unrecognized standardization of the ECG at half the usual gain, i.e., 5 mm/mV). Always check this first!

 

2.   

Adrenal insufficiency (Addison's disease)

 

3.   

Anasarca (generalized edema)

 

4.   

Cardiac infiltration or replacement (e.g., amyloid, tumor)

 

5.   

Cardiac transplantation, especially with acute or chronic rejection

 

6.   

Cardiomyopathies[*]

 

7.   

Chronic obstructive pulmonary disease

 

8.   

Constrictive pericarditis

 

9.   

Hypothyroidism/myxedema (usually with sinus bradycardia)

 

10. 

Left pneumothorax (mid-left chest leads)

 

11. 

Myocardial infarction, usually extensive

 

12. 

Myocarditis, acute or chronic

 

13. 

Normal variant

 

14. 

Obesity

 

15. 

Pericardial effusion/tamponade (latter usually with sinus tachycardia)

 

16. 

Pleural effusions

*  Dilated cardiomyopathies may be associated with a combination of relatively low limb-lead voltage and prominent precordial voltage. 

Right Axis Deviation

 

I.   

Spurious: left-right arm electrode reversal (look for negative P wave and negative QRS complex in lead I)

 

II. 

Normal variant

 

III. 

Dextrocardia

 

IV. 

Right ventricular overload

 

A.   

Acute (e.g., pulmonary embolus or severe asthmatic attack)

 

B.   

Chronic

 

1.   

Chronic obstructive pulmonary disease

 

2.   

Any cause of right ventricular hypertrophy (e.g., pulmonic stenosis or primary pulmonary hypertension)

 

V.   

Lateral wall myocardial infarction

 

VI. 

Left posterior fascicular block (exclude all other causes of right axis deviation)

QT Prolongation (Long QT Syndromes)

 

I.   

Acquired long QT syndromes

 

A.   

Electrolyte abnormalities

 

1.   

Hypocalcemia

 

2.   

Hypokalemia

 

3.   

Hypomagnesemia

 

B.   

Drugs

 

1.   

Class IA or III antiarrhythmic agents (e.g., amiodarone, disopyramide, dofetilide, ibutilide, procainamide, quinidine, and sotalol)

 

2.   

Psychotropic agents (e.g., phenothiazines, tricyclic antidepressants, tetracyclic agents, and haloperidol)

 

3.   

Others: astemizole, terfenadine, bepridil, certain antibiotics (e.g., erythromycin and pentamidine), probucol, cisapride, etc.

 

C.   

Myocardial ischemia or infarction (with deep T wave inversions)

 

D.   

Cerebrovascular injury

 

E.   

Bradyarrhythmias (especially high-grade AV heart block)

 

F.   

Systemic hypothermia

 

G.   

Miscellaneous conditions

 

1.   

Liquid protein diets

 

2.   

Starvation

 

3.   

Myocarditis

 

4.   

Arsenic poisoning

 

II. 

Congenital (hereditary) long QT syndromes

 

A.   

Romano-Ward syndrome (autosomal dominant)

 

B.   

Jervell and Lange-Nielsen syndrome (autosomal recessive with congenital deafness)

Q Waves

 

I.   

Physiologic or positional factors

 

A.   

Normal-variant septal Q waves

 

B.   

Normal-variant Q waves in leads V1, V2, aVL, III, and aVF

 

C.   

Left pneumothorax (acute loss of lateral R wave progression)

 

D.   

Dextrocardia (chronic loss of lateral R wave progression)

 

II. 

Myocardial injury or infiltration

 

A.   

Acute processes

 

1.   

Myocardial ischemia or infarction

 

2.   

Myocarditis

 

3.   

Hyperkalemia

 

B.   

Chronic processes

 

1.   

Myocardial infarction

 

2.   

Idiopathic cardiomyopathy

 

3.   

Myocarditis

 

4.   

Amyloid

 

5.   

Tumor

 

6.   

Sarcoid

 

III. 

Ventricular hypertrophy or enlargement

 

A.   

Left ventricular hypertrophy (slow R wave progression[*])

 

B.   

Right ventricular hypertrophy (reversed R wave progression[†]) or slow R wave progression (particularly with chronic obstructive lung disease)

 

C.   

Hypertrophic cardiomyopathy (may simulate anterior, inferior, posterior, or lateral infarcts)

 

IV. 

Conduction abnormalities

 

A.   

Left bundle branch block (slow R wave progression[*])

 

B.   

Wolff-Parkinson-White patterns

*  Small or absent R waves are seen in the right to mid-precordial leads. 

†  The R wave amplitude decreases progressively from lead V1 to the mid-lateral precordial leads. 

Tall R Wave in Lead V1

 

I.   

Physiologic and positional factors

 

A.   

Misplacement of chest leads

 

B.   

Normal variants

 

C.   

Displacement of heart toward right chest

 

II. 

Myocardial injury

 

A.   

Posterior and/or lateral myocardial infarction

 

B.   

Duchenne's muscular dystrophy

 

III. 

Ventricular enlargement

 

A.   

Right ventricular hypertrophy (usually with right axis deviation)

 

B.   

Hypertrophic cardiomyopathy

 

IV. 

Altered ventricular depolarization

 

A.   

Right ventricular conduction abnormalities

 

B.   

Wolff-Parkinson-White patterns (caused by posterior or lateral wall preexcitation)

ST Segment Elevations

 

I.   

Myocardial ischemia/infarction

 

A.   

Noninfarction, transmural ischemia (Prinzmetal's angina pattern)

 

B.   

Acute myocardial infarction

 

C.   

Post–myocardial infarction (ventricular aneurysm pattern)

 

II. 

Acute pericarditis

 

III. 

Normal variant (“early repolarization” pattern)

 

IV. 

Left ventricular hypertrophy (LVH)/left bundle branch block (LBBB) (V1–V2 or V3 and other leads with QS or rS waves, only)

 

V.   

Brugada pattern (right bundle branch block (RBBB)–like pattern with ST elevations in right precordial leads)

 

VI. 

Other (rarer)

 

A.   

Myocardial injury (non-infarction)

 

1.   

Myocarditis (ECG may resemble myocardial infarction or pericarditis patterns)

 

2.   

Tumor invading the left ventricle

 

3.   

Trauma to the ventricles

 

B.   

Hypothermia (J waves/Osborn waves)

 

C.   

Hyperkalemia (usually localized to V1 and V2)

ST Segment Depressions

 

I.   

Myocardial ischemia or infarction

 

A.   

Acute subendocardial ischemia or non–Q wave myocardial infarction

 

B.   

Reciprocal change with acute transmural ischemia

 

II. 

Abnormal noncoronary patterns

 

A.   

Left or right ventricular hypertrophy (formerly called “strain” pattern)

 

B.   

Secondary ST-T changes

 

1.   

Left bundle branch block

 

2.   

Right bundle branch block

 

3.   

Wolff-Parkinson-White preexcitation pattern

 

C.   

Drugs (e.g., digitalis)

 

D.   

Metabolic conditions (e.g., hypokalemia)

 

E.   

Miscellaneous conditions (e.g., cardiomyopathy)

 

III. 

Physiologic and normal variants[*]

*  With physiologic and normal variants, the often-transient ST segment/J point depressions are usually less than 1 mm and are seen especially with exertion or hyperventilation. 

Prominent T Wave Inversions

 

I.   

Normal variants

 

A.   

“Juvenile” T wave pattern

 

B.   

Early repolarization variants

 

II. 

Myocardial ischemia/infarction

 

III. 

Cerebrovascular accident (especially intracranial bleeds) and related neurogenic patterns

 

IV. 

Left or right ventricular overload/dysfunction

 

A.   

Typical patterns (formerly referred to as “strain” patterns)

 

B.   

Apical hypertrophic cardiomyopathy (Yamaguchi syndrome)

 

C.   

Other cardiomyopathies

 

V.   

Idiopathic global T wave inversion syndrome

 

VI. 

Secondary T wave alterations: bundle branch blocks, Wolff-Parkinson-White patterns

 

VII. 

Intermittent left bundle branch block, preexcitation, or ventricular pacing (“memory T waves”)

Tall Positive T Waves

 

I.   

Nonischemic causes

 

A.   

Normal variants (early repolarization patterns)

 

B.   

Hyperkalemia

 

C.   

Cerebrovascular hemorrhage (more commonly, T wave inversions)

 

D.   

Left ventricular hypertrophy

 

E.   

Right precordial leads, usually in conjunction with left precordial ST depressions and T wave inversions

 

F.   

Left precordial leads, particularly in association with “diastolic overload” conditions (e.g., aortic or mitral regurgitation)

 

G.   

Left bundle branch block (right precordial leads)

 

H.   

Acute pericarditis (occasionally)

 

II. 

Ischemic causes

 

A.   

Hyperacute phase of myocardial infarction

 

B.   

Acute transient transmural ischemia (Prinzmetal's angina)

 

C.   

Chronic (evolving) phase of myocardial infarction (tall positive T waves reciprocal to primary deep T wave inversions)

Major Bradycardias

 

I.   

Sinus bradycardia and its variants, including sinoatrial block

 

II. 

Atrioventricular (AV) heart block[*] or dissociation

 

A.   

Second- or third-degree AV block

 

B.   

Isorhythmic AV dissociation and related variants

 

III. 

Junctional (AV nodal) escape rhythms

 

IV. 

Atrial fibrillation or flutter with a slow ventricular response

 

V.   

Ventricular escape rhythms (idioventricular rhythms)

*  AV heart block may occur with sinus rhythm or other rhythms (e.g., atrial fibrillation or flutter). 

Major Tachycardias

 

I.   

Narrow QRS complex

 

A.   

Sinus tachycardia

 

B.   

Paroxysmal supraventricular tachycardias (PSVTs),[*] a class of arrhythmias with three major mechanisms:

 

1.   

Atrial tachycardias, including single-focus or multifocal (MAT) variants

 

2.   

AV nodal reentrant tachycardia (AVNRT)

 

3.   

AV reentrant tachycardia (AVRT) involving a bypass tract

 

C.   

Atrial flutter

 

D.   

Atrial fibrillation

 

II. 

Wide QRS complex

 

A.   

Ventricular tachycardia (three or more consecutive premature ventricular beats at a rate ≥ 100 beats/min)

 

B.   

Supraventricular tachycardia or atrial fibrillation or flutter, with aberrant ventricular conduction usually caused by either of the following:

 

1.   

Bundle branch block patterns

 

2.   

Atrioventricular bypass tract (Wolff-Parkinson-White preexcitation patterns)

*  Nonparoxysmal supraventricular tachycardias may also occur, including certain types of junctional tachycardia, as well as incessant tachycardias caused by increased atrial automaticity or a slowly conducting bypass tract. 

Atrial Fibrillation: Causes and Contributors

 

1.   

Alcohol abuse (“holiday heart”)

 

2.   

Autonomic factors

 

a.   

Sympathetic (occurring during exercise or stress)

 

b.   

Vagotonic (occurring during sleep)

 

3.   

Cardiothoracic surgery

 

4.   

Cardiomyopathies or myocarditis

 

5.   

Congenital heart disease

 

6.   

Coronary artery disease

 

7.   

Hypertensive heart disease

 

8.   

Idiopathic (“lone” atrial fibrillation)

 

9.   

Obstructive sleep apnea

 

10. 

Paroxysmal supraventricular tachycardias or the Wolff-Parkinson-White preexcitation syndrome

 

11. 

Pericardial disease (usually chronic)

 

12. 

Pulmonary disease (e.g., chronic obstructive pulmonary disease)

 

13. 

Pulmonary emboli

 

14. 

Sick sinus syndrome (brady-tachy variants)

 

15. 

Thyrotoxicosis (hyperthyroidism)

 

16. 

Valvular heart disease (particularly mitral valve disease)

Digitalis Toxicity: Major Arrhythmias

 

I.   

Bradycardias

 

A.   

Sinus bradycardia, including sinoatrial block

 

B.   

Junctional (nodal) escape rhythms[*]

 

C.   

Atrioventricular (AV) heart block,[*] including the following:

 

1.   

Mobitz type I (Wenckebach) AV block

 

2.   

Complete heart block[*]

 

II. 

Tachycardias

 

A.   

Accelerated junctional rhythms and nonparoxysmal junctional tachycardia

 

B.   

Atrial tachycardia with block

 

C.   

Ventricular ectopy

 

1.   

Ventricular premature beats

 

2.   

Monomorphic ventricular tachycardia

 

3.   

Bidirectional ventricular tachycardia

 

4.   

Ventricular fibrillation

*  Junctional rhythms may occur with underlying atrial fibrillation leading to slow or regularized ventricular response. AV dissociation without complete heart block may also occur. 

Cardiac Arrest: Three Basic ECG Patterns

 

1.   

Ventricular tachyarrhythmia

 

a.   

Ventricular fibrillation (or ventricular flutter)

 

b.   

Sustained ventricular tachycardia (monomorphic or polymorphic)

 

2.   

Ventricular asystole (standstill)

 

3.   

Pulseless electrical activity (electromechanical dissociation)