In this chapter you will learn:
1
a simple method to incorporate everything you have learned into a step-by-step analysis of any EKG
2
that all good things must come to an end, and we bid you a reluctant and fond farewell!
And that is really all there is to it.
Well, perhaps not quite all. What we need now is a way to organize all of this information, a simple methodical approach that can be applied to each and every EKG. It is important that every EKG be approached in an orderly fashion, particularly while you are still new at this, so that nothing important is missed. As you read more and more cardiograms, what initially may seem forced and mechanical will pay big dividends and will soon seem like second nature.
Two admonitions:
1. Know your patient. It is true that EKGs can be read with fair accuracy in a little back room in seclusion, but the power of this amazing tool only really emerges when it is integrated into a total clinical assessment of your patient.
2. Read EKGs. Then, read some more. Read them wherever you can find them —in books, in papers, in patients’ charts, on bathroom walls—and read other books; this may be the only EKG book you will ever need, but it should not be the only one you will ever want to read. There are many outstanding textbooks, each with something special to offer.
There are as many approaches to reading EKGs as there are cardiologists. Everyone ultimately arrives at a method that works best for him or her. The following 9-Step Method is probably no better and no worse than most others.
The 9-Step Method for Reading EKGs
Before you start, make sure the standardization mark on the EKG paper is 10 mm high so that 10 mm = 1 mV. Also make sure that the paper speed is correct.
1. Heart rate. Determine the heart rate.
2. Intervals. Measure the length of the PR and QT intervals and the width of the QRS complexes.
3. Axis. Is the axis of the P waves, QRS complexes, and T waves normal, or is there axis deviation?
4. Rhythm. Always ask The Four Questions:
• Are there normal P waves present?
• Are the QRS complexes wide or narrow?
• What is the relationship between the P waves and QRS complexes?
• Is the rhythm regular or irregular?
5. Conduction blocks.
• Atrioventricular (AV) block. Apply the criteria in Chapter 4.
• Bundle branch block or hemiblock. Apply the criteria in Chapter 4.
6. Preexcitation. Apply the criteria in Chapter 5.
7. Enlargement and hypertrophy. Apply the criteria for both atrial enlargement and ventricular hypertrophy in Chapter 3.
8. Coronary artery disease. Look for Q waves and the ST-segment and T-wave changes described in Chapter 6. Remember that not all such changes reflect coronary artery disease; know your differential diagnoses.
9. Other conditions. Is there anything on the EKG that suggests one of the other cardiac or noncardiac conditions discussed in Chapter 7? Are you totally lost? Never hesitate to ask for assistance.
The following pages are memory joggers you can hang onto. In early editions of this book, I suggested you cut these pages out and stick them in that little black book of medical pearls that everyone seemed to tote around. But who carries a little black book anymore? Therefore—if you haven’t thought of this already—take a photo of these pages with your smartphone and file them away for easy access. On the other hand, now that I think about it some more, cut these pages out anyway; the exercise will do you good after sitting and staring bleary-eyed at this book for so long.
The final chapter contains some sample EKGs with which to test yourself. Some are easy; some not so much. And if you are still thinking, “Is this really all there is to it?” The answer—reminding you that information only becomes knowledge with wisdom and experience—is, “Yes!”
Review Charts
• The 12 Leads
• Anterior leads: V2, V3, and V4 Inferior leads: II, III, and AVF
• Left lateral leads: I, AVL, V5, and V6
Right leads: aVR and V1
The heart is composed of pacemaker cells, electrical conducting cells, and myocardial cells. Pacemaker cells depolarize spontaneously and initiate each wave of depolarization. The SA node is usually the dominant pacemaker. Electrical conducting cells carry current rapidly and efficiently to distant regions of the heart. Myocardial cells constitute the bulk of the heart. When a wave of depolarization reaches a myocardial cell, calcium is released within the cell (excitationcontraction coupling), causing it to contract.
The P wave represents atrial depolarization. It is small and usually positive in the left lateral and inferior leads. It is often biphasic in leads III and V1. Typically, it is most positive in lead II and most negative in lead aVR.
The QRS complex represents ventricular depolarization. It is usually predominantly positive in most lateral and inferior leads. Across the precordium, the R waves increase in size, progressing from V1 to V5. A small initial Q wave, representing septal depolarization, can often be seen in the left lateral and inferior leads.
The T wave represents ventricular repolarization. It is the most variable waveform, but it is usually positive in leads with tall R waves.
The PR interval represents the time from the start of atrial depolarization to the start of ventricular depolarization.
The PR segment is the time from the end of atrial depolarization to the start of ventricular depolarization.
The QRS interval represents the duration of the QRS complex.
The ST segment represents the time from the end of ventricular depolarization to the start of ventricular repolarization.
The QT interval represents the time from the start of ventricular depolarization to the end of ventricular repolarization.
Atrial Enlargement
Look at the P wave in leads II and V1.
Right atrial enlargement is characterized by the following:
1. Increased amplitude of the first portion of the P wave
2. No change in the duration of the P wave
3. Possible right axis deviation of the P wave
Left atrial enlargement is characterized by the following:
1. Occasionally, increased amplitude of the terminal component of the P wave
2. More consistently, increased P wave duration
3. No significant axis deviation
Ventricular Hypertrophy
Look at the QRS complexes in all leads.
Right ventricular hypertrophy is characterized by the following:
1. Right axis deviation of greater than 100°
2. Ratio of R-wave amplitude to S-wave amplitude greater than 1 in V1 and less than 1 in V6
Left ventricular hypertrophy is characterized by many criteria. The more that are present, the greater the likelihood that left ventricular hypertrophy is present.
Precordial criteria include the following:
1. The R-wave amplitude in V5 or V6 plus the S-wave amplitude in V1 or V2 exceeds 35 mm.
2. The R-wave amplitude in V5 exceeds 26 mm.
3. The R-wave amplitude in V6 exceeds 18 mm.
4. The R-wave amplitude in V6 exceeds the R-wave amplitude in V5.
Limb lead criteria include the following:
1. The R-wave amplitude in aVL exceeds 11 mm.
2. The R-wave amplitude in aVF exceeds 20 mm.
3. The R-wave amplitude in I exceeds 13 mm.
4. The R-wave amplitude in I plus the S-wave amplitude in III exceeds 25 mm.
The most accurate single criterion: the R-wave amplitude in aVL plus the S-wave amplitude in V3 exceeds 20 for women and 28 for men.
The presence of repolarization abnormalities (asymmetric ST-segment depression and T-wave inversion) indicates clinically significant hypertrophy, is most often seen in those leads with tall R waves, and may herald ventricular dilatation and failure.
The five basic types of arrhythmias are as follows:
1. Arrhythmias of sinus origin
2. Ectopic rhythms
3. Reentrant rhythms
4. Conduction blocks
5. Preexcitation syndromes
Whenever you are interpreting the heart’s rhythm, ask The Four Questions:
1. Are normal P waves present?
2. Are the QRS complexes narrow (<0.12 seconds in duration) or wide (>0.12 seconds)?
3. What is the relationship between the P waves and the QRS complexes?
4. Is the rhythm regular or irregular?
The answers for normal sinus rhythm are the following:
1. Yes, P waves are present.
2. The QRS complexes are narrow.
3. There is one P wave for every QRS complex.
4. The rhythm is regular.
Why Arrhythmias Happen
Hypoxia
Ischemia and irritability
Sympathetic stimulation
Drugs
Electrolyte imbalances
Bradycardia
Stretch
Rhythms of Sinus Origin
Supraventricular Arrhythmias
Ventricular Arrhythmias
Differential Diagnosis of a Wide Complex Tachycardia
1. Ventricular tachycardia
2. SVT with aberrant conduction (e.g., with bundle branch block)
3. SVT in a patient with preexcitation
4. Paced rhythms
Distinguishing Ventricular Tachycardia From Supraventricular Tachycardia With Aberrant Conduction
|
Ventricular tachycardia |
Supraventricular tachycardias with aberrant conduction |
|
|
Clinical clues |
||
|
Clinical history |
Diseased heart |
Usually normal heart |
|
Carotid massage |
No response |
May terminate |
|
Cannon A waves |
May be present |
Not seen |
|
EKG clues |
||
|
AV dissociation |
May be seen |
Not seen |
|
Regularity |
Slightly irregular |
Very regular |
|
Fusion beats |
May be seen |
Not seen |
|
Initial QRS deflection |
May differ from normal QRS complex |
Same as normal QRS complex |
AV Blocks
AV block is diagnosed by examining the relationship of the P waves to the QRS complexes.
1. First degree: The PR interval is greater than 0.2 seconds; all beats are conducted through to the ventricles.
2. Second degree: Only some beats are conducted through to the ventricles.
a. Mobitz type I (Wenckebach): Progressive prolongation of the PR interval until a QRS is dropped.
b. Mobitz type II: All-or-nothing conduction in which QRS complexes are dropped without PR interval prolongation.
3. Third degree: No beats are conducted through to the ventricles. There is complete heart block with AV dissociation in which the atria and ventricles are driven by independent pacemakers.
Bundle Branch Blocks
Bundle branch block is diagnosed by looking at the width and configuration of the QRS complexes.
Criteria for Right Bundle Branch Block
1. QRS complex widened to greater than 0.12 seconds
2. RSR' in leads V1 and V2 (rabbit ears) or a tall, broad R wave; there is also ST-segment depression and T-wave inversion
3. Reciprocal changes in leads V5, V6, I, and aVL
Criteria for Left Bundle Branch Block
1. QRS complex widened to greater than 0.12 seconds.
2. Broad or notched R wave with prolonged upstroke in leads V5, V6, I, and aVL with ST-segment depression and T-wave inversion.
3. Reciprocal changes in V1 and V2.
4. Left axis deviation may be present.
Hemiblocks
Hemiblock is diagnosed by looking for left or right axis deviation.
Left Anterior Hemiblock
1. Normal QRS duration and no ST-segment or T-wave changes.
2. Left axis deviation greater than -30°.
3. No other cause of left axis deviation is present.
Left Posterior Hemiblock
1. Normal QRS duration and no ST-segment or T-wave changes
2. Right axis deviation
3. No other cause of right axis deviation is present.
Bifascicular Block
The features of a right bundle branch block combined with the left anterior hemiblock are as follows:
Right Bundle Branch Block
1. QRS wider than 0.12 seconds
2. RSR' in V1 and V2
Left Anterior Hemiblock
Left axis deviation
The features of a right bundle branch block combined with the left posterior hemiblock are as follows:
Right Bundle Branch Block
RS wider than 0.12 seconds
RSR' in V1 and V2
Left Posterior Hemiblock
• Right axis deviation
Preexcitation
Criteria for Wolff-Parkinson-White
1. PR interval less than 0.12 seconds
2. Wide QRS complexes
3. Delta wave seen in some leads
Criteria for Short PR Without a Delta Wave
1. PR interval less than 0.12 seconds
2. Normal QRS width
3. No delta wave
Arrhythmias seen with preexcitation include the following:
1. AV reciprocating tachycardia—narrow QRS complexes are more common than wide ones.
2. Atrial fibrillation—can be very rapid and can lead to ventricular fibrillation.
Myocardial Infarction
The diagnosis of a myocardial infarction is made by history, physical examination, serial cardiac enzyme determinations, and serial EKGs.
During an acute STEMI, the EKG may evolve through three stages:
1. The T wave peaks (A) and then inverts (B).
Inverted T waves can be normal in leads V1 through V3 in children and can persist into adulthood in some patients; an isolated inverted T wave in lead III is also a common normal variant.
2. The ST segment elevates (C).
Distinguishing ST Elevation of Ischemia from J Point Elevation: Criteria for Ischemia:
The ST elevation must be present in at least two contiguous leads
3. Q waves appear (D).
Ischemic Q waves are almost never isolated to a single lead.
Criteria for Significant Q Waves
1. The Q wave must be greater than 0.04 seconds in duration.
2. The depth of the Q wave must be at least one-third the height of the R wave in the same QRS complex.
3. aVR doesn’t count!
Criteria for Non-Q-Wave Infarctions
1. T-wave inversion
2. ST-segment depression persisting for more than 48 hours in the appropriate setting
Localizing the Infarct
Inferior infarction: leads II, III, and aVF
Often caused by occlusion of the right coronary artery or its descending branch.
• Reciprocal changes in anterior and left lateral leads. T-wave inversion in aVL is the most common reciprocal change and may appear before ST elevation and T-wave inversion in the inferior leads.
Lateral infarction: leads I, aVL, V5, and V6
Often caused by occlusion of the left circumflex artery
Reciprocal changes in inferior leads
Anterior infarction: any of the precordial leads (V1 through V6)
Often caused by occlusion of the left anterior descending artery
Reciprocal changes in inferior leads
Special T-wave changes
de Winter T waves—In a patient with chest pain, upsloping ST depression leading into a tall symmetric T wave can be the first sign of an anterior infarction.
Wellens waves—Biphasic T waves in V2 or V3 (sometimes V4) may predict an impending proximal LAD occlusion and an anterior infarction.
Posterior infarction: reciprocal changes in lead V1 (ST-segment depression, tall R wave that is often greater than the S wave in magnitude)
Often caused by occlusion of the right coronary artery
Usually seen in concert with inferior infarctions
Use posterior chest wall leads to confirm
Right ventricular infarction: ST elevation in lead V1, often ST depression in V2
Virtually always in concert with inferior infarction. Suspect right ventricular infarction if ST elevation in III is greater in magnitude than that in lead II.
• Confirm with right chest wall leads
|
Symptom or Syndrome |
ST-Segment Changes |
Cardiac Enzymes |
|
Stable angina* without infarction |
ST depression |
Normal* |
|
Unstable angina* without infarction |
ST depression |
Normal* |
|
STEMI |
ST elevation |
Elevated |
|
Non-STEMI |
ST depression |
Elevated |
|
Takotsubo cardiomyopathy |
ST elevation |
Elevated** |
|
Prinzmetal angina |
ST elevation |
Normal |
Note: Appearance of a new left bundle branch block may signify infarction and should be treated with the same urgency as a STEMI.
* Stable and unstable angina are distinguished by the clinical history.
**Patients often have to undergo cardiac catheterization to distinguish this from infarction.
The ST Segment
Causes of ST-segment elevation:
1. An evolving STEMI
2. Prinzmetal angina
3. J point elevation/early repolarization
4. Takotsubo cardiomyopathy
5. Acute pericarditis
6. Acute myocarditis
7. Pulmonary embolism
8. Brugada pattern
9. Hypothermia
10. Ventricular aneurysm
11. CNS catastrophes
12. Postcardioversion
13. Left bundle branch block (uncommonly)
14. Left ventricular hypertrophy (uncommonly)
15. Paced rhythms
Causes of ST-segment depression:
1. Angina without infarction
2. Non-STEMI
3. During supraventricular tachycardias
4. Typically seen with bundle branch blocks
5. Hypokalemia
ST depression is also one indicator of a positive stress test.
Miscellaneous EKG Changes
Electrolyte Disturbances
Hyperkalemia: The great imitator; evolution of peaked T waves, PR prolongation and P-wave flattening, and QRS widening. Ultimately, the QRS complexes and T waves merge to form a sine wave (a rightward axis in a patient with wide QRS complexes suggests possible hyperkalemia as the cause); conduction blocks can develop; ultimately, asystole and ventricular fibrillation may occur.
Hypokalemia: ST depression, T-wave flattening, U waves; may cause supraventricular and ventricular tachycardias; when severe can prolong the QT interval.
Hypocalcemia: Prolonged QT interval.
Hypercalcemia: Shortened QT interval.
Hypomagnesemia: Prolonged QT interval.
Hypothermia
Osborn waves, prolonged intervals, sinus bradycardia, slow junctional rhythm, and atrial fibrillation. Beware of muscle tremor artifact.
Drugs
• Digitalis: Therapeutic levels associated with ST-segment and T-wave changes in leads with tall R waves; toxic levels associated with tachyarrhythmias and conduction blocks. PAT with block is most characteristic.
• Drugs that can prolong the QT interval: sotalol, quinidine, procainamide, disopyramide, amiodarone, dofetilide, dronedarone, tricyclic antidepressants, macrolides, quinolones, psychotropic drugs including selective serotonin reuptake inhibitors, various antifungal medications, some nonsedating antihistamines, and others. Grapefruit juice inhibits cytochrome P450 and can cause higher serum drug levels and QT prolongation.
Causes of a Prolonged QT Interval
Hypocalcemia
Hypomagnesemia
Hypokalemia (severe)
Congenital disorders
Medications
Hypothermia
Causes of Shortened QT Interval
Hypercalcemia Hyperkalemia
Other Cardiac Disorders
Pericarditis: Diffuse ST-segment and T-wave changes; no Q waves; PR depression. A large effusion can cause low voltage and electrical alternans.
Hypertrophic cardiomyopathy: Ventricular hypertrophy, left axis deviation, deep, narrow Q waves laterally and inferiorly.
Myocarditis: Conduction blocks.
Atrial septal defect: first-degree AV block, atrial tachyarrhythmias, incomplete right bundle branch block, and right axis deviation; crochetage (small notch in QRS of the inferior leads)
Pulmonary Disorders
• Chronic obstructive pulmonary disease: Low voltage, right axis deviation, and poor R-wave progression. Chronic cor pulmonale can produce P pulmonale and right ventricular hypertrophy with repolarization abnormalities.
Acute pulmonary embolism: Right ventricular hypertrophy with strain (although not acutely), right bundle branch block, and S1Q3 (T3); T-wave inversion in right precordial leads. Sinus tachycardia and atrial fibrillation are the most common arrhythmias.
Central Nervous System Disease
Diffuse T-wave inversion, with T waves typically wide and deep;
U waves
Causes of Lethal Arrhythmias and Sudden Death
Ischemia
Hypertrophic cardiomyopathy
Long QT syndrome
Wolff-Parkinson-White
Viral myocarditis
Infiltrative diseases of the myocardium
Valvular heart disease
Drug abuse (notably stimulants)
Commotio cordis (trauma to the heart)
Anomalous origin of the coronary arteries
Brugada
Arrhythmogenic right ventricular cardiomyopathy
The Athlete’s Heart
• Normal findings can include sinus bradycardia, nonspecific ST- segment and T-wave changes, left and right ventricular hypertrophy, incomplete right bundle branch block, first-degree or Wenckebach AV block, and occasional supraventricular arrhythmias, notched QRS complex in lead V1
Findings that require further evaluation: T-wave inversion beyond lead V2 in white athletes and beyond V4 in African American or Caribbean athletes; T-wave inversion in the lateral leads; ST-segment depression in any lead; findings consistent with congenital heart disorders