ECG Differential Diagnoses: Instant Reviews

Published on 21/06/2015 by admin

Filed under Cardiovascular

Last modified 22/04/2025

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 1402 times

Chapter 24 ECG Differential Diagnoses Instant Reviews

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

Low-Voltage QRS Complexes

1. Artifactual or spurious, e.g., 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: dilated, hypertrophic, or restrictive types

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 paradoxical combination of relatively low limb lead voltage and prominent precordial voltage.

Wide QRS Complex (Normal Rate)

I. Intrinsic intraventricular conduction 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 conduction 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

IV. Ventricular preexcitation: Wolff-Parkinson-White pattern and variants

∗ Bundle branch block patterns may occur transiently. Note also that a spuriously wide QRS complex occurs if the ECG is unintentionally recorded at fast paper speeds (50 or 100 mm/sec).

Left Axis Deviation (QRS Axis of −30° or More Negative)

I. Left ventricular hypertrophy

II. Left anterior (hemiblock) fascicular block (strictly, −45° or more negative)

III. Inferior wall myocardial infarction (typically with QS waves in leads II, III, and aVF)

IV. Endocardial cushion defects (congenital), especially ostium primum atrial septal defects

Right Axis Deviation (QRS Axis of +90° or More Positive)

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

II. Normal variant, especially in children and young adults

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., pulmonary stenosis, secundum atrial septal defects, or primary pulmonary hypertension)

V. Lateral wall myocardial infarction

VI. Left posterior (hemiblock) fascicular block; note: need to exclude all other causes of right axis deviation and rigorously requires marked rightward axis (+110–120° or more)

QT(U) Prolongation (Long QT Syndromes)

I. Acquired long QT syndrome

A. Electrolyte abnormalities
1. Hypocalcemia
2. Hypokalemia
3. Hypomagnesemia
B. Drugs∗
1. Class IA or III antiarrhythmic agents (e.g., quinidine, procainamide, disopyramide, dofetilide, ibutilide, sotalol, dronedarone, and amiodarone)
2. Psychotropic agents (e.g., phenothiazines, tricyclic antidepressants, tetracyclic agents, atypical antipsychotic agents, haloperidol)
3. Many others: arsenic trioxide, chloroquine, methadone, certain antibiotics (e.g., erythromycin, levofloxacin, and pentamidine), etc.
C. Myocardial ischemia or infarction (especially, with deep T wave inversions)
D. Cerebrovascular injury (e.g., intracranial bleeds)
E. Bradyarrhythmias (especially high-grade atrioventricular heart block)
F. Systemic hypothermia
G. Miscellaneous conditions
1. Liquid protein diets
2. Starvation
3. Arsenic poisoning

II. Congenital (hereditary) long QT syndromes (LQTS)

A. Romano-Ward syndrome∗∗ (autosomal dominant disorders)
B. Jervell and Lange-Nielsen syndrome (autosomal recessive disorder associated with congenital deafness)

∗ For an excellent, updated review of drugs associated with the acquired long QT syndrome and torsades de pointes risk, see the Arizona Cert website: http://www.azcert.org/medical-pros/drug-lists/browse-drug-list.cfm.

∗∗ The Romano-Ward syndrome is the classic, general term used to designate a number of specific, inherited abnormalities in ion channel function (“channelopathies”) that are associated with prolongation of ventricular repolarization (long QT-U) and increased risk of torsades de pointes (see Chapter 16). These hereditary ion channel (potassium, sodium, or calcium) disorders can prolong and increase heterogeneity of ventricular repolarization.

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 or dextrocardia (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 (leads with negative delta waves)

∗ 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 side of chest

II. Myocardial injury

A. Posterior or lateral myocardial infarction
B. Duchenne muscular dystrophy

III. Ventricular enlargement

A. Right ventricular hypertrophy (usually with right QRS 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 or Takotsubo/stress or apical ballooning cardiomyopathy∗)
B. Acute myocardial infarction (MI)
C. Post-MI (ventricular aneurysm pattern)

II. Acute pericarditis

III. Normal variant (benign “early repolarization” and related patterns)

IV. Left ventricular hypertrophy/left bundle branch block (V1-V2 or V3 and other leads with QS or rS waves, only)

V. Brugada patterns (right bundle branch block patterns with ST elevations in right precordial leads)

VI. Myocardial injury (noncoronary injury or infarction)

A. Myocarditis (ECG may resemble myocardial infarction or pericarditis patterns)
B. Tumor invading the left ventricle
C. Trauma to the ventricles
D. Acute right ventricular ischemia (usually V1-V2/V3, e.g., with massive pulmonary embolism)

VII. Hypothermia (J waves/Osborn waves)

VIII. Hyperkalemia (usually localized to V1-V2)

∗ May exactly simulate ECG sequence of ST elevation MI.

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 (“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 very transient ST segment/J point depressions are usually less than 1 mm and are seen especially with exertion or hyperventilation.

Deep T Wave Inversions

I. Normal variants

A. Juvenile T wave pattern
B. Early repolarization

II. Myocardial ischemia/infarction

III. Takotsubo (stress; apical ballooning) cardiomyopathy

IV. Cerebrovascular accident (especially intracranial bleeds) and related neurogenic patterns

V. Left or right ventricular overload

A. Typical patterns (formerly referred to as “strain” patterns)
B. Apical hypertrophic cardiomyopathy (Yamaguchi syndrome)

VI. Idiopathic global T wave inversion syndrome

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

VIII. 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 segment 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 Bradyarrhythmias

I. Sinus bradycardia and its variants, including sinoatrial block and wandering atrial pacemaker (WAP)

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) and ectopic atrial escape rhythms

IV. Atrial fibrillation or flutter with a slow ventricular response

V. Ventricular escape (idioventricular) rhythms

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

Major Tachyarrhythmias (Basic List, Excluding Artifact)

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 (e.g., multifocal atrial tachycardia [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 tachycardias

A. Ventricular tachycardia (three or more consecutive premature ventricular complexes at a rate of 100 beats/min)
B. Supraventricular tachycardia (including sinus or PSVT), or atrial fibrillation or flutter, with aberrant ventricular conduction usually caused by either of the following:
1. Bundle branch block (may be rate related)
2. Atrioventricular bypass tract (e.g., Wolff- Parkinson-White preexcitation pattern)

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

Wide QRS Complex Tachycardias (More Comprehensive Classification)

I. Artifact (e.g., tooth-brushing; parkinsonian tremor)

II. Ventricular tachycardia: monomorphic or polymorphic

III. Sinus tachycardia, PSVT, or atrial fibrillation/flutter, with aberrant ventricular conduction caused by:

A. Bundle branch block or other IVCD (may be rate-related)
B. Atrioventricular bypass tract (WPW or related preexcitation pattern) with antegrade (top to bottom) conduction over the bypass tract
C. Drug toxicity (usually class IC, such as flecainide)
D. Hyperkalemia

IV. Pacemaker-associated

A. Sinus or other supraventricular tachyarrhythmia with appropriate pacemaker tracking to upper rate limit
B. Pacemaker-mediated tachycardia (PMT)

IVCD, intraventricular conduction delay; PSVT paroxysmal supraventricular tachycardia, including atrial tachycardia (AT), AV nodal reentry (AVNRT), and AV reentrant tachycardia (AVRT), which involves conduction up (antidromic) or down (orthodromic) a bypass tract; WPW, Wolff-Parkinson-White.

Atrial Fibrillation: Major Causes and Contributors

1. Alcohol abuse (“holiday heart” syndrome)

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. Genetic factors

8. Hypertensive heart disease

9. Idiopathic (“lone” atrial fibrillation)

10. Obstructive sleep apnea (OSA)

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

12. Pericardial disease (usually chronic)

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

14. Pulmonary emboli

15. Sick sinus syndrome

16. Thyrotoxicosis (hyperthyroidism)

17. 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 tachycardia
4. Ventricular fibrillation

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

Cardiac Arrest: Three Basic ECG Patterns

I. Ventricular tachyarrhythmia

A. Ventricular fibrillation (or ventricular flutter)
B. Sustained ventricular tachycardia (monomorphic or polymorphic)

II. Ventricular asystole (standstill)

III. Pulseless electrical activity (electromechanical dissociation)

Related posts:

Key Concepts Supraventricular Arrhythmias, Part II: Atrial Flutter and Atrial Fibrillation ECG Basics: Waves, Intervals, and Segments Myocardial Infarction and Ischemia, II: Non–ST Segment Elevation and Non–Q Wave Syndromes Drug Effects, Electrolyte Abnormalities, and Metabolic Factors ECG Leads