12 lead ecg learning package

CET: 12 Lead ECG Assignment Learning Package

©WFA Clinical Education Team


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This document has been peer reviewed and moderated. Changes to content must not be made without the approval of the Clinical Education and Training Manager – and a documented moderation process. All teaching packages should be reviewed biannually, or externally moderated.

Moderation

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Date Details Authorised29/03/2005

Original Assignments Jacqui Eades

01/06/2012

Content Review Todd Mushet



›Introduction

This package is designed as either a learning or revision tool.

It incorporates features specific to the interpretation of a 12 lead Electrocardiograph (ECG). These include:

Lead systems Lead groups Axis & Axis Determination ECG indicators of myocardial Infarction Chamber enlargement (RVH/LVH/RAA/LAA) Bundle Branch Blocks (RBBB/LBBB/IVCD) & Hemiblocks

(LAH/LPH) ECG markers of Pulmonary disease Sundry causes of ECG change (pericarditis, pulmonary embolism

& cerebral injury)

The assignment can be done primarily through reading the texts and web sites in the recommended reading section. However referring to other journal articles, texts and web sites that you may have sourced through your own research may enhance your answers.

It is expected that the assignment will take up to 30 hours to complete. This will vary depending on how much research you do and the depth you choose to go into.



›Instructions

Answers should be entered in the spaces provided. Each answer should have a reference showing where you sourced the information from. For an example on how to format the reference refer to the references entered in the recommended reading section below. For a more detailed guide to formatting references refer to the Wellington Free Ambulance Services Assignment Guide. Copies are available on station, from the Training Department or under training on the intranet section of the Wellington Free Ambulance web site http://www.wfa.org.nz/.

Submitting the assignment can be done by sending it to the following address:

Clinical Education TeamWellington Free Ambulance ServicePO Box 601Wellington

Alternatively you can submit your assignment electronically via e-mail to [email protected] in MS word format. Please put the words Continuing Education Assignment in the subject line of the email.

The Clinical Education Team will be marking your assignment

Please do not hesitate to contact a Clinical Educator if you have any concerns regarding the assignment.


Important Note

Due to the extensive nature of this topic, this assignment has been divided into sections to enable students who have limited time or prefer to develop certain areas only. As such you may choose to do one or more components independently, with CE points allocated accordingly.

The final section; practice ECGs, does however require knowledge from each section, so this should only be challenged if you have completed all components of the assignment or have prior 12 lead ECG knowledge or interpretation experience.

mailto:[email protected]

http://www.wfa.org.nz/


›Grades

Grading will be A B or C the criteria for which follows;

A A comprehensive understanding of the subject matter is demonstrated and information is incorporated from a wide range of sources inclusive of recent research. Information is factual with few errors. Presentation is excellent

B A good understanding of the subject matter is demonstrated. Information from standard sources is incorporated. Information is factual with few errors. Presentation is good.

C Does not demonstrate understanding. Few facts are presented and not supported. Consistent errors in facts, and presentation is poor.

Continuing Education Points

Section 1: Lead systems 3 points

Section 2: ECG Indicators of myocardial Ischemia, Injury & Infarction 5 points

Section 3: Cardiac Vectors & Axis 3 points

Section 4: Chamber Enlargement (RAE/LAE/RVH/LVH) 3 points

Section 5: Bundle Branch Blocks & Hemiblocks 3 points

Section 6: ECG Changes for pulmonary disease and other miscellaneous conditions 3 points

Section 7: Practice ECGs 10 points



Total: 30 points

Section 8: Practice ECGs: Extra for Experts! 5 points

Total: 35

points

›Recommended Readings

1. Bledisloe, B.E. (1999). 12 Lead ECG Monitoring and Interpretation. Disease Findings. P. 1044-46.

2. Conover, M.B. (1996). Understanding Electrocardiology. (7th ed.). Mosby: St Louis.

3. Garcia, T.B, & Holtz, N.E. (2003). Introduction to 12 Lead ECG: The Art of Interpretation. Jones and Bartlett Publishers: Massachusetts.

4. Grauer, K. (1998). A Practical Guide to ECG Interpretation. (2nd ed.). Mosby: St. Louis.

5. Hampton, J.R. (2003). The ECG in Practice. (4th ed.). Churchill Livingston: London.

6. Hampton, J.R. (2003). The ECG made Easy. (6th ed.). Churchill Livingston: London.

7. Huzar, R.J. (2002). Basic Dysrhythmias: Interpretation and Management. (3rd ed.). Mosby: St Louis.



8. Magdic, K.S., & Saul, L.M. (1997). ECG Interpretation of Chamber Enlargement. Critical Care Nurse. 17:1: pp13-25.

9. Morton, P.G. (1996). ECG/Pacemaker: Using the 12 Lead to Detect Ischemia, Injury, and Infarction. Critical Care Nursing. 16:2: pp85-95.

10. Taigman, M., & Canan, S. (1990). Cardiology Practicum: Reading Bundle Branch Blocks. Journal of Emergency Medical Services. May: pp41-44.

11. Tintinalli JE, Kelen GD, Stapezynski JS. (2000). Emergency Medicine – A Comprehensive Study Guide. (5th Edition). McGraw-Hill Companies Inc: United States of America

12. Victoria University of Melbourne. Paramedic Sciences. Graduate Certificate in Intensive Care Paramedics. Course Lecture Notes: HHP5620 Advanced Cardiac Care.

13. Wagner, G.S. (2001). Marriot’s Practical Electrocardiography. (10th ed.). Lippincott Williams & Wilkins: Philadelphia.

›Websites

www.12leadECG.com

http://sprojects.mmi.mcgill.ca/heart/egcyhome.html EKG world Encyclopedia.

http://bmj.bmjjournals.com/cgi/content/full/324/7334/415

http://www.ecglibrary.com/ecghome.html


http://www.ecglibrary.com/ecghome.html

http://bmj.bmjjournals.com/cgi/content/full/324/7334/415

http://sprojects.mmi.mcgill.ca/heart/egcyhome.html

http://www.12leadecg.com/

›Key Words

Axis Bundle Branch Blocks Cerebral injury Electrocardiograpgh (ECG) Electrical current/impulse Hemiblocks Lead Left atrial enlargement (LAE/LAA) Left Ventricular Hypertrophy (LVH) Myocardial Infarction (MI), injury & ischemia Pericarditis Pericardial effusion Pulmonary disease Pulmonary embolism (PE) Right atrial enlargement (RAE/RAA) Right Ventricular Hypertrophy (RVH) Waveform

© WFA Clinical Education Team

CET: 12 Lead ECG Learning Package

›Lead Systems

The electrical picture obtained from the heart is referred to as a ‘lead’ 1(7). Several leads are utilized to view the heart from different vantage points, each forming a different view of electrical activity and therefore a different ECG pattern1-3.

The 12 lead ECG is made up of lead systems that correspond to the plane from which they view the heart. The six limb leads view the heart from the vertical / frontal plane, giving information about current flow that is right, left, inferior or superior. The six limb leads are made up of three standard leads and three augmented leads. The six precordial leads lie immediately in front of the heart and view the heart from the horizontal / transverse plane, giving information about current flow that is right, left, anterior, or posterior1-9.

1. Name the three standard leads and the three augmented leads that make up the limb leads.

Standard Augmented

Answer:

Standard

Augmented

2. Name the six leads that make up the precordial leads.

Answer:



“Accurate placement of the precordial leads on the chest is crucial. Placing a lead as little as one intercostal space too high or too low can dramatically alter QRS morphology and amplitude2 (15)”.

3. Anatomical landmarks are utilized for identifying correct placement of the precordial leads on the chest. Describe these landmarks and provide a labelled diagram showing the location of each of the precordial leads.

V1 – V2 – V3 – V4 –

V5 – V6 –

Answer:

V1

V2

V3

V4

V5

V6



›Lead Groups

Leads are grouped according to the area of the heart visualized by one or more leads2.

4. Name the leads associated with each of the following groups:

Inferior wall leads: Septal wall leads: Anterior wall leads: Lateral wall leads:

Lateral precordial leads:

High lateral leads:

Answer:

Inferior wall leads

Septal wall leads

Anterior wall leads

Lateral wall leads

Lateral precordial leads

High lateral leads


NOTE: There is slight variation from text to text due to an overlap in precordial lead orientation, i.e. V2 is both a septal and anterior lead, while V4 is both an anterior and


›12 Lead Orientation Systems

Two basic formats are used to display the 12 standard leads of an ECG2(16):

Vertical Lead Orientation Format

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

Horizontal Lead Orientation Format

I II III

aVR aVL aVF

V1 V2 V3

V4 V5 V6

Today the vertical lead system is the most commonly used. Using a three-channel recorder these have the ability to simultaneously record lead groups in a vertical column. As shown previously, the standard limb leads (I, II, III) comprise the first lead group, followed by simultaneous vertical recording of the augmented leads (aVR, aVL, aVF) and then in two successive groups, the precordial leads (V1-V6)2.

The horizontal lead format was the most exclusively used system in the past and is still utilized in the community by a number of GP’s – hence the need to become familiarised with both systems! The horizontal lead orientation system is obtained on a single channel recorder. The advantage of this system is that a large amount of information can be regularly obtained. The disadvantage being that this information is obtained one lead at a time over a 40-60 second interval. This continuous stream of tracing then has to be analysed and the tracing segmented and mounted for official interpretation2.



5. Using the following tracings in the vertical lead format indicate the anatomical areas visualized by the leads that are shaded:

Answer:

A.

B.

C.

D.


A B.

C D

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

aVR V1 V4

II aVL V2 V5

III aVF V3 V6


›ECG Indicators of Ischaemia, Injury and Infarction

Myocardial ischemia occurs almost immediately after disruption of blood supply. Without oxygen the ischemic tissue remains capable of depolarising, however the process of repolarisation is affected10. Depolarisation normally occurs from endocardium to epicardium. Repolarisation proceeds from the epicardium to endocardium, reflected as a positive T wave. If subendocardial ischemia is present then the process of repolarisation remains unchanged. However if subepicardial ischemia is present, conduction is slowed in the epicardium. This prevents the epicardium from repolarising first and instead the process begins in the endocardium6.

During ischemic events the blood supply is sufficient to keep myocardial tissue alive, however it is insufficient to maintain membrane integrity so a difference in membrane potential is created. The flow of electrical current during electrical systole (recorded through the ST segment) and electrical diastole (the QT segment) is therefore also altered6.

These abnormalities of repolarisation are reflected on ECG11.

1. What are the ECG indicators of myocardial ischaemia?

Answer:

Although T wave inversion can indicate myocardial ischaemia, it is always inverted in aVR and in a healthy individual may also be inverted in other leads6,10.

2. In what leads is T wave inversion a normal variant?

Answer:



If myocardial ischaemia is allowed to progress untreated then myocardial injury will occur. Although the affected area is no longer able to contract, the injured area is still capable of partially or completely depolarising (depending on the time taken to restore oxygen supply). With myocardial injury the electrical current flows between the pathologically depolarised area and the areas normally depolarised, a current flow referred to as either a ‘current of injury’6(395) or an ‘injury current’9(1044). This results in the injured tissue remaining depolarised and emitting a negative charge into the surrounding fluid when the surrounding normal myocardium is positively charged. This current of injury is reflected on ECG9.

3. What are the defining ECG characteristics associated with myocardial injury?

Answer:

‘J-point elevation’ or ‘early repolarisation10 (88)’ is a form of ST elevation that can occur in healthy individuals (reported in 2% of young adults11). The ST can be raised by as much as 3-4mm.

4. Describe the differentiating characteristics that are associated with ST elevation as a normal variant and compare those with that indicative of myocardial injury. An example of each may be incorporated with your answer.

Answer:



If a zone of injury is not reversed then the injury will progress and death or infarction of the myocardial tissue will occur. This evolution of MI is seen on ECG in stages. The earliest stage is known as the hyperacute phase10.

5. Describe the ECG characteristics evident in this hyperacute phase and the developmental QRS – ST changes that subsequently occur; markers of MI.

Answer:

A Q wave is said to be present when the first deflection after the PR interval (that of the QRS complex) is negative. Small narrow q waves occur normally in certain leads and represent the flow of electrical forces towards the intraventricular septum2.

6. Name the leads in which these are normally visualized and the parameters that define these as a normal variant.

Answer:

7. Define the parameters of a Q wave that are indicative of myocardial infarction.

Answer:

8. Why is the Q wave diagnostic of MI and how does a Q wave develop?

Answer:



9. The term ‘reciprocal change10’ is associated with ECG findings of MI. Define this term and outline how it is depicted on ECG.

Answer:

Patterns of Ischemia, injury or infarction can be identified on ECG according to their anatomical location6,10.

10. Using the Table below list the ECG leads utilized to view each of the following anatomical regions of the heart and name the coronary artery responsible for blood supply to that region.

Answer:


Anatomical Area(Site of infarction)

Facing Leads Coronary Artery

Anterior wall: Septal

Anterior (localized)

Anteroseptal

Lateral

Anterolateral

Extensive Anterior

Inferior wall(diaphragmatic)

Posterior wall

Right Ventricular wall


Views of the R ventricular wall and the posterior wall are limited by the standard 12 lead ECG. Better vantage points can be achieved by relocating the chest leads2,9.

11: Describe the correct lead placement for each of these areas.

RV Wall:

Posterior Wall:

Answer:

Using the standard 12 Lead ECG, posterior wall injury/infarction can also be viewed indirectly by assessing what happens electrocardiographically in leads V1, V2 and V3 by applying the principle of reciprocal change or by applying the ‘mirror test’2(243).

11. Describe the QRS – T changes associated with posterior wall infarction as seen in the anterior leads and describe how to apply the mirror test. Outline other findings (i.e. reciprocal changes) that are indicative of PWMI.

Answer:

12. Describe the QRS – T changes associated with Right Ventricular wall infarction (RVI).

Answer:



Non – Q Wave infarctions account for approximately 30% - 40% of acute infarctions (up to 50%7 depending on text) . Although these patients have a smaller infarct size, better residual left ventricular function and lower in hospital mortality, long-term survivability is on par or less than that of Q wave infarctions. The incidence of post-infarction angina and the rate of recurrence are also reported as higher with this group6.

13. Define the term ‘non-Q wave’ infarct and compare it to that of a Q-wave infarct.

Answer:

Diagnosis of non-Q wave infarction is made through detection of elevated cardiac enzymes [Troponin I/T)]6. Suspicion of non-Q wave infarct can however be formed through clinical presentation and associated ECG changes.

14. Outline ECG changes associated with a non-Q wave infarction.

Answer:



IMPORTANT: Remember ST elevation is not only caused by MI. Differential considerations include the following:


CAUSES OF ST ELEVATION12

ElectrolytesLBBBEarly RepolarisationVentricular hypertrophyAneurysmTreatment (pericardiocentesis)Injury (AMI, contusion, pericarditis)Osborne waves (hypothermia)Non-occlusive vasospasm prinz-metal angina, cocaine Quick Mention: ATRIAL INFARCTION

This is extremely rare and there is very little mention of it in standard texts.

It can however be seen on ECG when there is significant PR depression (in at least 2 leads) with associated signs of infarction and without any criteria for pericarditis5(77-78).

Other listed criteria includes:

↑PR > 0.5mm in V5 &V6 with ↓PR in V1 & V2 ↑PR > 0.5mm in lead I with ↓PR in leads II & III ↓PR > 1.5mm in precordial leads and > 1.2 in leads I, II & III,

combined with atrial arrhythmias

P waves may also be abnormal in shape (W, M, notched, or irregular)6(420)


›Cardiac Vectors and Access

The millions of individual electrical impulses generated by depolarisation and repolarisation vary in intensity and direction and are referred to as cardiac vectors5,7. Such vectors when travelling in the same direction add to each other and when travelling in opposing directions cancel each other out. If travelling at an angle towards each other then they add or subtract energy and change directions when they meet5. Combined these millions of vectors form main vectors. The electrical activity of the main vectors is detected by the ECG and converted into waveforms5.

During depolarisation the series of cardiac vectors produced are graphically represented as the QRS complex. The initial vector represents depolarisation of the interventricular septum in a left to right direction (1). A sequence of vectors produced by endocardial to epicardial depolarisation then immediately follows as shown:(2) beginning in the right and left ventricles near the septum(3) continuing through the thin wall of the right ventricle and thick lateral wall of the left ventricle(4) ending in the lateral and posterior aspect of the left ventricle, near its base7(255).

The sum total of all these vectors creates a single large vector, this final vector is what’s known as the “mean QRS axis or, simply, the QRS axis7(255)” of the heart7.


Huzar, R.J. (2002). Basic Dysrhythmias: Interpretation and Management. (3rd ed.). Mosby: St Louis. P. 255.


›Lead Axis

Each view of the heart (lead) is provided by recording the difference in electrical potential between a positive and a negative pole3.

A single electrode on the body surface serves as a positive pole for each lead

The negative pole of each lead is provided by either a single recording electrode (bipolar lead, I, II, III) or a “central terminal” that averages the input from multiple recording electrodes3 (unipolar / V leads: V1-V6, aVR, aVF, aVL6).

The axis of a lead is created is by placing a hypothetical line between the two electrodes, i.e. between the positive and negative electrodes of a bipolar lead or between the positive electrode and a reference point of the unipolar lead6,7.

An electrical current, cardiac vector, flowing parallel to the axis of a lead produces a positive (upward) deflection if travelling towards the electrode (lead) or a negative (downward) deflection if travelling away from the electrode. The greater the magnitude of the vector is the larger the deflection (amplitude), the lesser the magnitude the lesser the deflection7.

When flow is perpendicular to the lead axis, no deflection is produced and when it is bi-directional, i.e. partly towards and partly away from the lead axis, a biphasic (partly positive, partly negative) deflection is evident. When the mean of a biphasic deflection is more parallel towards the lead axis the biphasic deflection is more positive. When orientation is closer to the perpendicular, the waveform is less positive.

FRONTAL PLANE LEADS

The axis of the standard limb leads, I, II and III forms an equilateral triangle, ‘Einthovens Triangle2(11)’,with each lead separated by 60º. This provides a triaxial reference system for viewing electrical activity3,7. The augmented leads (aV) fill the gap between the standard limb leads and create a hexaxial reference system3,7. The six leads of this system are separated by angles of 30 °, providing a perspective similar to a clock face3.



Lead I can be seen to be a lateral (leftward) lead that views the heart from a horizontal vantage point defined as 0° from the positive pole (-180° from the negative pole). Lead I and is used as a reference point. Leads II & III are inferior leads that view vantage points angulated at +60° / -120° & +120° / -60°, from the positive and negative poles respectively2,7. . Lead aVL is a lateral, leftward monitoring lead. Vantage point looks down at the heart from the patients left shoulder. It corresponds to an angle of -30° / +150°. Lead aVF is an inferior monitoring lead. It records from the left lower extremity. Vantage point looks up at the heart from the patient’s feet. It is perpendicular and corresponds to an angle of +90° / -90°.

Lead aVR is the most distant recording electrode. Viewpoint is from the right shoulder (-150° / +30°). It is recorded as a negative deflection2,7.


Huzar, R.J. (2002). Basic Dysrhythmias: Interpretation and Management. (3rd ed.).

Huzar, R.J. (2002). Basic Dysrhythmias: Interpretation and Management. (3rd ed.). Mosby: St Louis. P. 250.



NB: the positive pole and negative poles are not defined by + or – rather the positive pole is represented as that labelled by the lead. This is evident in the aV leads

Lead aVL, positive pole = -30°, negative pole = +150°, Lead aVF, positive pole = +90°, negative pole = -90°.Lead aVR, positive pole = -150, negative pole = +30°

This concept is important to understand if you wish to advance your axis calculation from a quadrant to isolating axis within 10° [This is not covered within


TRANSVERSE PLANE LEADS

The precordial leads (V1 – V6) view the transverse plane. The precordial lead axis is produced by connecting the central terminal of the hexaxial system (centre of the electrical field) to a recording electrode placed at the various positions on the anterior and left lateral chest wall. The angles between these leads are approximately the same as the frontal leads, separated by angles of 30°3 (with the exception of V3, refer diagram 7(250)).

Precordial leads provide a panoramic view of the electrical activity of the heart, progressing from the thinner right ventricle and across the thicker left ventricle. Electrically illustrated this is viewed as progression and regression of the R and S wave, a reflection of intact anterior forces.

1. R-wave progression and the zone of transition are assessed when viewing the precordial leads. Define these terms.

R-wave progression:

Transitional Zone:

Answer:

2. Outline causes of poor R wave progression.

Answer:

Early Transition is said to occur when the QRS complex becomes predominantly positive sooner than usual, i.e. between V1 and V2, and late when the R wave becomes more positive later than usual.© WFA Clinical Education Team

Huzar, R.J. (2002). Basic Dysrhythmias: Interpretation and Management. (3rd ed.).


Early transition, a shift to the right toward V1 is referred to as counter-clockwise rotation. Late transition, a shift in transition zone to the left, toward V6 and usually after V4, is referred to as clockwise rotation6,8.

3. List possible causes of early and late (delayed) transition.

Early transition: Late transition:

Answer:



›Axis Determination

A shift in axis can be caused by pathological process such as hypertrophy, infarction or conduction defects8. Determining QRS axis can therefore give an insight into pathology and help put the 12 lead and clinical picture together6.

For the purpose of simplicity, axis determination can be rapidly obtained by applying the 2 lead and quadrant approach2,7.

2 lead approach;

The mean QRS is calculated in the frontal plane using leads I and aVF. Lead I is a horizontal lead orientated toward 0°. Lead aVF is orientated perpendicular to lead I at +90°2.

Quadrant approach;

The hexaxial reference system is divided into four quadrants by the bisection of lead axis I and aVF. Each of the four quadrants are separated by 90°7.



4. Name the four quadrants illustrated?

I (0º to –90º)II (0º - +90º)III (+90º - +/- 180º)IV (-90º - +/- 180)

1.Answer:

I (0º to –90º)

II (0º - +90º)

III (+90º - +/- 180º)

IV (-90º - +/- 180

Under normal circumstances the heart lies in the left side of the chest and the mean orientation of the electrical axis follows in the same direction as the hearts anatomical location i.e. towards the left2

5. Where does the normal axis lie?

Answer:



Rapid determination of the QRS axis can be done by assessing the dominant direction of the QRS complex in leads I and aVF. Using a ‘thumbs up’ method for positive deflections and a ‘thumbs down’ for negative deflection, orientation towards normal, left, right or indeterminate quadrants can be easy assessed2.

Net QRS Deflection &

Thumb direction

Lead I (left thumb)

Lead aVF (right thumb)

Normal AxisPositive Up Positive Up

Right Axis Deviation

Negative Down Positive Up

Left Axis Deviation

Positive Up Negative Down

Indeterminate Axis

Negative Down Negative Down

NB: If the QRS complex is equiphasic / isoelectric (equally positive and negative) then a net deflection of zero is yielded, axis is therefore determined on the direction of the alternative lead i.e. If the complex in lead I is equiphasic and the complex in lead aVF is positive then the axis has shifted to the right. If the complex in aVF is equiphasic and the complex in lead I is positive then the axis has shifted to the left.

When the axis is normal a more precise method is achieved by assessing the relative ‘net deflection2 (126)’ of the QRS complex in these leads. This can be done by adding up the number of small boxes in the R wave (positive deflection) and subtracting the number of small boxes in the Q and S waves (negative deflections). Then by viewing leads I at 0° and aVF at +90° a rough estimate in degrees can be achieved;

If the net deflection of lead I is about the same as that of lead aVF, then the mean QRS should lie midway between these leads (or close to +45°)

If the net QRS of lead I is positive and clearly exceeds that of aVF, then the mean QRS should lie closer to lead I (i.e. between 0° and +40°, depending on how much greater the positive deflection in lead I is).

If the net QRS of aVF is positive and clearly exceeds that of lead I, then the mean QRS should lie closer to lead aVF (i.e. between +50° and +90°, depending on how much greater the positive deflection in aVF is).

Remember: the mean QRS axis is orientated most toward the lead with



the greatest net QRS deflection and furthest away from the lead with the greatest negative net deflection.

›Practising Axis

QUESTION 6: Using the following, calculate the quadrant for which each axis is found.


1.

2.

3.

4.

5.

6.

7.

8.

9.

10.


Answer:

1.

2.

3.

4.

5.

6.

7.

8.

9.

10.



›Chamber Enlargement

The terms enlargement, hypertrophy and dilation are used synonymously to describe what happens to the heart as a result of work overload. The term hypertrophy is used to describe an increase in muscle mass that develops when the cardiac muscle fibres are stretched and increase their size as a result of the heart being forced to contract against increased resistance. Dilation refers to expansion of size (not mass). As the heart adapts to an increased workload the chambers may stretch or dilate to accommodate the increase in blood volume. Hypertrophy and dilation frequently occur together as compensatory mechanisms to maximize cardiac output. The term enlargement therefore encompasses both13.

When evaluating the ECG for chamber enlargement there are three basic concepts that enable understanding of why certain ECG changes occur:

1. The chamber may take longer to depolarise, potentially causing an ECG waveform of prolonged duration.

2. The enlarged chamber may generate more current than normal, thereby producing greater voltage and an ECG waveform of increased amplitude.

3. A larger percentage of the total current may move through the expanded chamber, thus shifting the electrical axis of the ECG13(16).

ATRIAL ENLARGEMENT

Given a p-wave reflects atrial depolarisation, assessment of atrial enlargement is based on p-wave morphology. That said, factors other than atrial enlargement such as rhythm disturbance or


More muscle mass = more muscle cells, therefore more conduction


alterations of atrial conduction may also produce abnormality of p wave morphology. Due to this, various text use the term ‘abnormality’ in preference to enlargement because the reliability or specificity of ECG criteria is subject to error2,6,13.

Atrial depolarisation is best seen in two key leads, II and V1. Lead II is the best lead because its orientation is virtually parallel to the orientation of the electrical impulse as it travels from the SA Node to the AV Node. The p wave in lead II should therefore always be upright. Lead V1 is chosen for its anatomical location, as a septal and right-sided lead this is placed in close proximity to the right atrium and views electrical activity from the right atrium as coming towards it and electrical activity from the left atrium as moving away from it. The p wave in V1 may normally have either one or two components and may be positive, negative or biphasic2,6,13.

1. List the ECG criteria outlined for right and left atrial enlargement.

Right Atrial Enlargement / Abnormality (RAE/RAA):

Left Atrial Enlargement / Abnormality (LAE/LAA):

Answer:

Chambers can enlarge individually or in groups. If both atria are enlarged at the same time, this is known as Biatrial enlargement3,5,13.

2. What are the ECG indicators are suggestive of biatrial enlargement?

Answer:



VENTRICULAR ENLARGEMENT

3. Outline the rules applied for interpretation of right and left ventricular enlargement.

Rules for Right Ventricular Hypertrophy (RVH):

Rules for Left Ventricular Hypertrophy (LVH):

Answer:

It is also possible for both the left and right ventricles to be enlarged at the same time, this is referred to as Biventricular enlargement3,5.

4. What are the ECG indicators suggestive of biventricular enlargement?

Answer:



›Bundle branch blocks and Hemiblocks

The intraventricular conduction system is comprised of the right bundle branch (RBB) and the left bundle branch (LBB). Originating from the LBB are two fascicles, the left anterior fascicle (LAF) and the left posterior fascicle (LPF)5,6. A third division, the septal fascicle, sends out connecting branches between the LAF and the LPF6. The RBB and the left fascicles further divide into smaller and smaller branches to form a network of terminal branches, the ‘purkinje system’5(123).

The RBB is responsible for innervating part of the right septum and the right ventricle. The LAF innervates the superior and anterior aspects of the left ventricle, while the LPF innervates the inferior and posterior aspects of the left ventricle5.

Sequence of Normal Ventricular Activation

Following activation of the AV Node, the first part of the ventricles to be depolarised is the left side of the septum. Septal innervation occurs in a left to right direction and upon reaching the ventricles spreads simultaneously in an outward direction across the ventricular conduction pathways of both the right and left ventricle2.Because of the much greater size and mass of the left ventricle (LV), left sided electrical activity dominates on the ECG. During normal conduction septal depolarization is depicted on the right-sided lead (V1) as a small, positive r wave, electrical flow from left to right (i.e. towards the electrode). Following activation of both ventricles, left ventricular conduction dominates and conduction in V1 is viewed as moving predominantly away from the electrode, i.e. towards the left. This is recorded as a relatively deep, negative S wave2.

In left sided leads, leads I and V6, the opposite is viewed. Septal activation is recorded as an initial negative wave (septal q wave) as the electrical current moves from left to right, away from the viewing electrode. As activation of the LV then dominates, electrical activity is seen as moving in a right to left direction, i.e. toward the viewing electrode, and is depicted as a relatively tall, positive R wave2.

SUMMARY:

Right sided leads are predominantly negative Left sided leads are predominantly positive

Normal QRS appearance or morphology is therefore viewed in the three



key leads as follows:

Because leads I and V6 are left-sided leads and Lead V1 is a right-sided lead these are the three key leads used for recognition of BBB’s2.

An intraventricular conduction problem is present when a delay or obstruction of impulse conduction occurs anywhere along the bundle branch pathway. The type of conduction delay or block is identified according to the site/level from which the impulse conduction is delayed or obstructed and as such is termed as either right bundle branch block (RBBB), left bundle branch block (LBBB); an intraventricular conduction defect (IVCD) or a hemiblock; left anterior hemiblock (LAH) or left posterior hemiblock (LPH). The terms complete or typical and incomplete or partial are also applied to BB blocks3.


Remember: if a BBB exists innervation to the portion of the heart that branch serves is done via a slower cell-to-cell route. A larger period of time is therefore required to depolarize that section; the time taken is thus greater than 0.12 seconds. This is reflected on ECG as a wide QRS with altered QRS morphology5.

As a rule if the QRS is wide consider BBB.

Additionally a regular rhythm that looks ugly = LBBB (although this can be confused for a paced or ventricular rhythm!)In comparison, Hemiblocks cause little or no widening of the QRS because the amount of slow cell-to-cell transmission of the depolarised wave is limited5.

Remember also to select the lead in which the QRS looks the widest: lead I, II, or III, some leads may be deceptively narrow or borderline14.

Grauer, K. (1998). A Practical Guide to ECG Interpretation. (2nd ed.). Mosby: St. Louis. P. 102.

Lead I = R wave or qR

Lead V1 = rS or S wave

Lead V6 = R or qR wave.


1. Describe the following types of blocks. In your description include the ECG findings used to identify the existence of each block.

A). Complete Right bundle branch block (RBBBB). Incomplete Right bundle branch block (RBBB):

C). Complete Left bundle branch block (LBBB):

D). Incomplete Left bundle branch block (LBBB):

E). Intraventricular conduction defect/delay (IVCD):

F). Left anterior hemiblock (LAH), also termed left anterior fascicle block (LAFB):

G). Left posterior hemiblock (LPH), also termed left posterior fascicle block (LPFB):

Answer:



2. Secondary ST-T wave changes are associated with BBB’s. Why do these occur and what are the expected ECG findings?

Answer:

3. Define the terms bivascicular and trifascicular and outline the associated ECG findings.

Answer:



›Pulmonary Disease

Pulmonary disorders can produce characteristic and profound changes to the ECG. Recognition and understanding of these changes enables the interpreter to discern and eliminate a cardiac origin12.

1. Outline the expected changes associated with CORD

Answer:

2. Outline the expected changes associated with Emphysema.

Answer:



›Pericarditis

Pericarditis can be difficult to diagnose and relies primarily on the history and physical exam in association with ECG findings2.

Cause of ECG change is likely to be due to:1. Inflammation spreading to the adjacent layer of the myocardium

(epicardium), causing ST-T wave abnormalities as seen with epicardial ischemia or injury. Because the whole of the epicardium is usually effected ST change is widespread.

2. Significant pericardial fluid (as with effusion) or a thickened (fibrotic)

pericardium dampens the cardiac impulses causing a generalized decrease in electrical waveform3,12.

The ECG findings alone are non-conclusive, predominantly due to the lack of change in some cases and the possibility of variable ST-T changes, intermediate return to baseline and the nature of pericarditis being either acute or chronic. Additionally texts vary and refer to typically no change, non-specific change or distinct stages (stage 1 & 23,12 or 4 stages2,11).

Differential diagnosis needs also to include consideration to MI and or early repolarisation.

Note: with early repolarisation there is an absence of symptoms and ECG change is localized to one, or at the most, two areas of the heart.With MI Q waves are usually associated with ST elevation and the ST elevation is localized to 2 or more corresponding leads, it’s not diffuse as seen with pericarditis.Additionally Hx and clinical picture should be consistent with pericarditis8.

3. Outline the possible ECG changes associated with pericarditis.

Answer:



›Pericardial Effusion

Most patients with pericarditis will also have a pericardial effusion3,4,12. ECG abnormalities evident are associated with “the “insulating” effect of pericardial fluid, which attenuates electrical signals of myocardial origin, and the pendular motion of the heart within the fluid-filled pericardial space11(393)”.

4. What is the triad of ECG criteria diagnostic of pericardial effusion.

Answer:

Note: The ST-T changes of early repolarisation mimic those of pericarditis, therefore making differentiating between the two a common problem.

Diagnosis can be assisted by measuring the ST segment / T wave amplitude ratio in leads V5, V6 or I. Using the end of the PR segment as baseline (0mV), measure the amplitude (height) of the ST at onset and in that same lead measure the amplitude of the T wave peak. If the ratio of the ST amplitude to the T wave amplitude is below 0.25mV, early repolarisation is most likely. If the ratio is above 0.25 the acute pericarditis is likely 11(393).

Remember: 1mm (height) = 0.1mV (amplitude)

Example: If the ST is 2mm (0.2mV) and the T wave is 5mm (0.5mV) then the ratio is 0.3, which meets the criteria for pericarditis.



›Pulmonary Embolism

ECG findings in the acute phase of Pulmonary Embolism (PE) are believed to be the result of right ventricular failure and acute right atrial and ventricular dilation. These occur secondary to pulmonary hypertension, which is caused by mechanical obstruction of a central or peripheral pulmonary artery6. This acute development of right heart strain is termed ‘cor-pulmonae3(214)’ and while it can be caused by other events the most common cause is PE3.

Since PE is under diagnosed in most clinical settings and it is estimated “that only one of every three of death-dealing pulmonary embolism is diagnosed while the patient is still alive6(433)”, early recognition or at least suspicion of PE is essential for increasing diagnosis and reducing mortality. While in many cases the ECG can remain unchanged or findings are non-specific and transient there are still changes or patterns that are clearly reflective of PE that can raise a high degree of suspicion and prompt further investigation. According to one study, 82% of patients with minor to massive PE had a combination of typical ECG change. In addition, patients with two thirds or more obstruction all had evidence of the commonly noted ECG change6(433). Other texts however argue that in the setting of PE most ECG’s are normal2,4, with the notable exception of Sinus Tachycardia in the present of sudden onset of SOB2-6.

NOTE: The described ECG patterns of acute PE can resemble those of MI, therefore if anterior or inferior wall MI is suspected consideration should be made towards the possibility of acute PE, particularly if the patient presents with severe dyspnoea. (Although dyspnoea presents with AMI the degree is much more pronounce if caused by a PE)2,6.

5. Outline the ECG findings associated with suspicion of acute PE

Answer:



›Cerebral Injury

Ischemic and hemorrhagic cerebral events, such as that of a major stroke, subarachnoid hemorrhage or traumatic brain injury (TBI) lead to repolarisation abnormalities.

6. Outline the ECG findings associated with suspicion of cerebral injury

Answer:



›Practice ECGs

A simple, systematic approach to descriptive analysis of 12 leads can be achieved by applying the mnemonic AHI AHI2(23).

RAteRHythm Intervals (PRI, QRS, QT)

Axis Hypertrophy Infarct (Q,R,S,T)

Q waves R-wave progression ST segment changes T-wave change

While you may prefer to use your own methodology, Grauer introduces this as a simple way of incorporating all the necessary components for descriptive analysis and interpretation of 12 leads. Once routinely applied, use of this or similar methods avoids under analysis or missing essential components that help with correct ECG interpretation.

Using the attached ECG’s (and your choice of approach) give a descriptive analysis of each of the essential components and outline your overall interpretation

The following is a guideline for formatting answers.

ECG 1:

RateRhythm/regularityP wavePRIQRS QTST segmentT waveAxis

TransitionHypertrophyInterpretation: Include underlying rhythm,



hypertrophy, ischemia/ infarction and any other findings.




PRACTICE ECG. 1



PRACTICE ECG. 2



PRACTICE ECG. 3



PRACTICE ECG. 4



PRACTICE ECG. 5



PRACTICE ECG. 6



PRACTICE ECG. 7



PRACTICE ECG. 8



PRACTICE ECG. 9



PRACTICE ECG 10



PRACTICE ECG 11



PRACTICE ECG. 12



PACTICE ECG. 13



PRACTICE ECG.14



PRACTICE ECG 15



PRACTICE ECG 1



PRACTICE ECG 2



PRACTICE ECG 3



PRACTICE ECG 4



PRACTICE ECG 5

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