BBPpda ECGJulia Mayerhofer11/13/2003en-us

ECG pocket

Clinical Reference Guide

© 2003 Ralph Haberl

Börm Bruckmeier Publishing

- Index

- Table of Contents

- Figures

- Quick Reference

- My Bookmarks

- About

- Help

1.

Basics

2.

The Normal ECG

3.

Hypertrophy of the Heart

4.

Bundle Branch Block

5.

Atrio-Ventricular Block

6.

Myocardial Ischemia

7.

Bradyarrhythmias

8.

Tachyarrhythmias

9.

Carditis, Cardiomyopathy

10.

Electrolyte Disturbances, Drugs

11.

Interferences and Artifacts

12.

FIGURES

13.

QUICK REFERENCE

1. Basics

- Conduction System
- ECG Waves and Intervals
- The ECG Leads
- Methods

2. The Normal ECG

- Characteristics of the Normal ECG
- Axis Determination
- Evaluation of the ECG
- Normal Pediatric ECG Values

3. Hypertrophy of the Heart

- Right Atrial Enlargement
- Left Atrial Enlargement
- Right Ventricular Hypertrophy
- Left Ventricular Hypertrophy

4. Bundle Branch Block

- General Description
- Left Anterior Fascicular Block
- Left Posterior Fascicular Block
- Incomplete Left Bundle Branch Block
- Complete Left Bundle Branch Block
- Functional Left Bundle Branch Block
- Incomplete Right Bundle Branch Block
- Complete Right Bundle Branch Block
- Bifascicular Block

5. Atrio-Ventricular Block

- General Description
- First Degree AV Block
- 2° AV Block Mobitz Type I (Wenckebach)
- 2° AV Block Mobitz Type II
- 3° AV Block

6. Myocardial Ischemia

- Ischemia in Coronary Artery Disease
- Myocardial Infarction
- Non-Q-Wave Myocardial Infarction
- Stress Testing

7. Bradyarrhythmias

- Escape Rhythms
- Junctional Escape Rhythms
- Sinoatrial Block
- Reflex Bradycardia
- Atrial Fibrillation with Bradycardia

8. Tachyarrhythmias

- General Description
- Sinus Tachycardia
- Atrial Fibrillation
- Atrial Flutter
- AV Nodal Reenty Tachycardia
- Wolff-Parkinson-White Syndrome
- Atrial Tachycardia
- Sick Sinus Syndrome
- Premature Atrial Contractions (PACs)
- Premature Ventricular Contractions (PVCs)
- Sustained Ventricular Tachycardia
- Ventricular Fibrillation
- Proarrhythmia
- Long QT Syndrome

9. Carditis, Cardiomyopathy

- Acute Pericarditis
- Low Voltage QRS
- Dilated Cardiomyopathy
- Hypertrophic Cardiomyopathy

10. Electrolyte Disturbances, Drugs

- Hypokalemia
- Hyperkalemia
- Hypercalcemia
- Hypocalcemia
- ECG Changes induced by Digitalis
- Betablockers,Ca++ Channel Blockers

11. Interferences and Artifacts

- Incorrect Polarization
- Further Disturbances and Artifacts

Legendes of Figures
Fig.1 Conduction System of the heart.

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Fig.2 ECG waves and intervals.

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Fig.3 Einthoven's triangle of the limb leads.

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Fig.4 Placement of the limb leads.

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Fig.5 Placement of the unipolar chest leads (left) and reflection of the heart seen in a cross section (right).

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Fig.6 Augmented leads.

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Fig.7 Infarct localization.

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Fig.8 Calculation of heart rate.

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Fig.9 Normal intervals of the ECG: P wave 100ms, PR interval 200ms, QRS complex 100ms.

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Fig.10 Normogram of QT interval. Mean value and tolerance range. Waves in seconds. RR: interval between two Rs.

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Fig.11 Axis: determination of the QRS net area.

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Fig.12 Cardiac axis and Lewis circle. For example the positive QRS deflection is transferred to leads I, II and III. If it is negative, the arrow points away from that lead. Lines through the head of the arrows and perpendicular to the leads cross in one point of the circle demonstrating the cardiac axis.

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Fig.13 Normal axis, intermediate range.

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Fig.14 Normal axis, vertical range.

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Fig.15 Normal axis, horizontal range.

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Fig.16 Left axis deviation.

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Fig.17 Normal axis, vertical range.

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Fig.18 Right axis deviation.

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Fig.19 SIQIII pattern.

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Fig.20 SISIISIII pattern.

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Fig.21 Cardiac axis and special types of axis deviation.

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Fig.22 Normal ECG: sinus rhythm, PR interval 0.2 s, QRS complex 0.1 s, normal axis, horizontal range.

Normal R progression, isoelectric ST segment (up to 0.2 mV in V2 is normal), T wave is positive in all chest leads.

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List of Figures
Fig.1: Conduction system of the heart

Fig.2: ECG waves and intervals

Fig.3: Einthoven’s triangle of the limb leads (39)

Fig.4: Placement of the limb leads

Fig.5: Placement of the unipolar chest leads

Fig.6: Augmented leads

Fig.7: Infarct localization

Fig.8: Calculation of heart rate

Fig.9: Normal intervals of the ECG

Fig.10: Normogram of QT interval

Fig.11: Net area of the QRS Complex

Fig.12: Cardiac axis and Lewis circle

Fig.13: Normal axis, intermediate range

Fig.14: Normal axis, vertical range

Fig.15: Normal axis, horizontal range

Fig.16: Left axis deviation

Fig.17: Left axis deviation

Fig.18: Right axis deviation

Fig.19: SIQIII pattern

Fig.20: SISIISIII pattern

Fig.21: Cardiac axis etc.

Fig.22: Normal ECG

Fig.23: Normal ECG

Basics

Conduction System

Fig.1 Conduction System of the heart.

The SA node is the primary pacemaker of the heart. It generates a regular, electrical impulse with a frequency of 60-80 beats/min. The depolarization is then spread by way of atrial conduction pathways to the AV node . On passing the AV node, conduction is delayed. If the sinus node fails to function properly, the AV node can generate the impulse with a frequency of 40-60 beats/min. The depolarization then passes from the AV node through the bundle of His and on to the bundle branches . The left bundle branch divides into a left posterior and a left anterior fascicle.

ECG Waves and Intervals

The depolarization of the SA node cannot be seen in the ECG. Atrial depolarization is represented by P waves . The first phase of the P wave corresponds to depolarization of the right atrium; depolarization of the left atrium follows. Atrial repolarization cannot be seen because it coincides with the QRS complex . At the end of the P wave the atria are completely depolarized and the impulse spreads by way of the AV node to the bundle of His. The Q wave represents the depolarization of the septum and the impulse quickly continues by way of the Purkinje fibers to the ventricles. At the end of the QRS complex the ventricles are completely depolarized. Due to the electromechanical delay, ventricular contraction starts at the end of the QRS complex. The normal ST segment is isoelectric and begins at the end of the S wave. Ventricular repolarization produces the T wave . The significance of the U wave is unknown.

Fig.2 ECG waves and intervals.

The ECG Leads

The standard ECG consists of the following leads

1. Einthoven's extremity (limb) leads (I, II, III)
These are bipolar leads. The amplitude is positive if the depolarization moves towards the positive electrode marked with +.

Fig.3 Einthoven's triangle of the limb leads.

Fig.4 Placement of the limb leads.

2. Wilson's chest (precordial) leads (V 1 - V 6 )
These leads are unipolar. They measure the voltage of any one electrode relative to a constructed zero potential. The electrodes are placed as follows:

V1

fourth intercostal space to the right of the sternum

V2

fourth intercostal space to the left of the sternum

V3

midway between V_2 and V_4

V4

fifth intercostal space in the left midclavicular line

V5

fifth intercostal space in the left anterior axillary line

V6

fifth intercostal space in the left midaxillary line

Fig.5 Placement of the unipolar chest leads (left) and reflection of the heart seen in a cross section (right).

Caution
Placing the electrodes improperly, for example in the second intercostal space, may lead to an R reduction in the anterior leads and may, therefore, be misinterpreted as an old anterior myocardial infarction. If a right ventricular infarction is suspected, Vr4 on the right side of the chest is useful.

3. Goldberger's augmented leads (aVR, aVL, aVF)
The augmented leads are obtained by recording voltages from the limbs. Their amplitudes are higher. The "a" stands for "augmented".

Fig.6 Augmented leads.

Localization of a myocardial infarction
Particularly in the diagnosis of a myocardial infarction, the localization of the pathological event seen in the reflecting leads is important. Guidelines are summarized in the following figure.

Fig.7 Infarct localization.

Methods

The paper usually moves at a speed of 50 mm/sec. with an amplification of 1 mV/cm. Thus, 1 cm on the paper corresponds to 200 ms = 0.2 s. Most ECGs in this booklet are recorded at a speed of 25 mm/sec; those recorded at a speed of 50 mm/sec are marked with a *. The heart rate is determined using the following formula:

Fig.8 Calculation of heart rate.

The Normal ECG

Characteristics of the Normal ECG

Recognizing a pathological ECG is half the battle. The normal intervals are shown in Fig.9

All ECG intervals should be measured in the lead showing the biggest aberration. The P wave and the QRS complex should not take longer than 100 ms, the PR interval not longer than 200 ms. The QT interval depends on the heart rate. A prolonged QT interval caused by a congenital long QT syndrome or secondary to drugs ( >> ), can cause severe cardiac arrhythmias. Fig.10 shows standard values for the QT interval depending on the heart rate including lower and upper limits. A prolongation of the PR interval is called a "first degree heart block, a prolonged QRS complex a "bundle branch block."

Axis Determination

The cardiac axis reflects the electrical axis of the average direction of the ventricular activation in the frontal plane as the depolarization wave spreads through the ventricles. The cardiac axis is derived from the QRS complex in leads I, II and III. A useful system for the determination of the cardiac axis is demonstrated in Fig.12.
The normal cardiac axis of an adolescent shows an angle of +30° to +90°, that of an adult of -30° to +60°. It is not the maximum amplitude of a single lead that is important when calculating the cardiac axis, but the mean QRS vector, including all positive and negative deflections.
Fig.11 Axis: determination of the QRS net area.

Fig.12 Cardiac axis and Lewis circle. For example the positive QRS deflection is transferred to leads I, II and III. If it is negative, the arrow points away from that lead. Lines through the head of the arrows and perpendicular to the leads cross in one point of the circle demonstrating the cardiac axis.

Fig.13 Normal axis, intermediate range.

Fig.14 Normal axis, vertical range.

Fig.15 Normal axis, horizontal range.

Fig.16 Left axis deviation.

Fig.17 Normal axis, vertical range.

Fig.18 Right axis deviation.

Fig.19 SIQIII pattern.

Fig.20 SISIISIII pattern.

Changes in the cardiac axis can be caused by muscular hypertrophy (normal axis vertical range due to hypertension, normal axis horizontal range due to right ventricular hypertrophy), by changes in the anatomic position of the heart and by disorders of conduction (for example bundle branch block, fascicular block, >> ). A left anterior fascicular block ( >> ) leads to a left axis deviation, a left posterior fascicular block to right axis deviation. Typical cardiac axes show aberrations in the frontal plane. Shifting and rotation of the heart in the sagittal and horizontal planes ( Fig.20 ) lead to S I Q III or S I S II S III patterns. Both of these axis deviations can be a sign of strain on the right ventricle.

Fig.21Cardiac axis and special types of axis deviation.

Evaluation of the ECG

A systematic method for reading and interpreting an ECG should be developed and the following features should be analyzed. Although some of them may require a more detailed knowledge of ECG, they are mentioned here in order to provide guidelines for complete ECG interpretation. The single steps of ECG analysis are as follows:
1. Rhythm
The regularity of the rhythm is determined by assessing the RR intervals . Tachycardia is an increased heart rate > 90 beats/min. In bradycardia the heart rate is less than 50 beats/min. Sinus rhythm is defined by regular positive P waves in I - III.
2. Atrioventricular conduction
In a normal AV conduction the time from the start of the P wave to the start of the QRS complex is < 200 ms. Therefore the PR interval is < 0.2 s. Otherwise it demonstrates an AV block.
3. Axis
The cardiac axis is assessed as mentioned above, using the pattern shown in Fig.12 .
4. QRS complex
A normal QRS complex duration is 100 ms. A QRS complex that takes > 100 ms is a sign of a bundle branch block. In the chest leads the R amplitude increases constantly from V1 to V 6 (the so-called R progression). A decrease in the R amplitude is possible in V 5 and V 6 due to a longer distance between those leads and the chest wall. While interpreting the QRS complex, special attention must be paid to significant Q waves and signs of cardiac hypertrophy.
5. ST segment
In a normal ECG the ST segment is isoelectric. An insignificant ST elevation may occur only in V 2 and V 3 (up to 0.2 mV). Changes in the ST segment may be found in myocardial ischemia.
6. T wave
The T waves in leads I - III and V1 - V 6 are always positive. A negative T wave in a chest lead is always pathologic with the following exception: T waves in V1 and III may be slightly negative.
7. QT interval
The next step is to assess the QT interval. By using the corrected QT interval ( QTc) a predisposition to cardiac arrhythmias can be recognized.
8. Presumption diagnosis
At the end of an ECG analysis a presumption diagnosis should be made keeping the clinical picture of the patient in mind. The following diagram shows an ECG evaluation sheet . This evaluation sheet is available as a plastic card, ECG Evaluation pocketcard . It can also be found in the appendix of this book or on the Internet under www.media4u.com . It can be copied or downloaded and used for your own ECG interpretations.

Fig.22 Normal ECG: sinus rhythm, PR interval 0.2 s, QRS complex 0.1 s, normal axis, horizontal range/ Normal R progression, isoelectric ST segment (up to 0.2 mV in V2 is normal), T wave is positive in all chest leads.

Fig.23 Normal ECG. Normal cardiac axis, intermediate range (+60° to +90°)

Normal Pediatric ECG Values

>> click to view table

Quick Reference

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Hypertrophy of the Heart

Bundle Branch Blocks

AV Blocks

Myocardial Ischemia

Bradyarrhythmias

Sinoatrial Block

Tachyarrhythmias

Electrolyte Disturbances, Drug

Hypertrophy of the Heart

Right Atrial Enlargement
P-pulmonale: elevated, peaked P wave > 0.2 mV, particularly in II, III and aVF.

Left Atrial Enlargement
P-mitrale: widening of the P wave > 0.1 s, particularly in I, II and V 1 - V 3 . In V 1 often a biphasic P wave with a marked negative deflection.

Right Ventricular Hypertrophy
Sokolow index: R in V 2 + S in V 5 > 1.05 mV, normal axis/vertical range or right axis deviation, sometimes RBBB-like ECG.

Left Ventricular Hypertrophy
Sokolow-Index: S in V2 + R in V5 > 3,5 mV, normal axis/horizontal range - left axis deviation.

Bundle Branch Blocks

Left Anterior Fascicular Block
No widening of the QRS, but left axis deviation.

Left Posterior Fascicular Block
No widening of the QRS, but right axis deviation.

Incomplete Left Bundle Branch Block
Widening of the QRS > 0.10 s, but < 0.12 s, often R-reduction over the anterior wall.

Complete LBBB
Widening of the QRS > 0.12 s, delay of terminal deflection in V 6 > 0.05 s, frequently R-loss over the anterior wall, left precordial repolarization disturbances and ST-elevation.
Incomplete RBBB
Widening of the QRS complex > 0.10 s, but < 0.12 s, delay in terminal deflection of > 0.03 s in V 1 , often R prime (R') in V 1 .
Complete RBBB
Widening of the QRS > 0.12 s, delay in terminal deflection in V 1 > 0.03 s, frequently rSr' complex in V 1 , repolarization disturbances in V 1 -V_3.

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Please read!

This book is based on information from sources believed to be reliable, and every effort has been made to make the book as complete and accurate as possible and to describe generally accepted practices based on information available as of the printing date, but its accuracy and completeness cannot be guaranteed. Despite the best efforts of author and publisher, the book may contain errors, and the reader should use the book only as a general guide and not as the ultimate source of information about the subject matter. This book is not intended to reprint all of the information available to the author or publisher on the subject, but rather to simplify, complement and supplement other available sources. The reader is encouraged to read all available material and to consult other references to learn as much as possible about the subject. This book is sold without warranties of any kind, expressed or implied, and the publisher and author disclaim any liability, loss or damage caused by the content of this book. If you do not wish to be bound by the foregoing cautions and conditions , you may return this book to the publisher for a full refund.

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© 2003

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All rights reserved. This publication is protected by copyright. No part of may be reproduced, stored in a retrieval system, or transmitted in any form or by any means - electronic, mechanical, photocopying, recording or otherwise, without the prior written permission of the publisher (Börm Bruckmeier Publishing LLC, www.media4u.com), exept for download to your personal digital assistant and one (1) copy of the Software for backup purposes, and except for brief quotations embodied in critical articels and reviews. For information write Börm Bruckmeier Publishing LLC, www.media4u.com

Data conversion/ Realisation of Electronic Version: Julia Mayerhofer

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