Advanced ECG Interpretation

Advanced ECG Interpretation Self-directed Learning Package: Module 3 2018

Introduction This package is part three of three self-directed modules designed to provide an introduction to interpreting ECGs: Module One -Basic ECG Interpretation Module Two -Intermediate ECG interpretation Module Three - Advanced ECG interpretation This module is required to be completed and submitted to the Nurse Educator, Professional Nursing and Midwifery Services (ph. 4433 3759) This course complements the Clinical Competency Assessments which you can access on QHEPS. http://qheps.health.qld.gov.au/tville/cdsu/clinical-competency-ax/nmsc-ecg-12-leadrecording.pdf

Module Editor Version 1 July 2017 CNC Cardiac services, Townsville Hospital Copyright Statement Copyright Creative Commons BY-NC-ND Attribution – Non-Commercial – No Derivatives

© State of Queensland (Queensland Health) 2009. This document is licensed under a Government Information Licensing Framework Attribution Non-Commercial No Derivative License http://www.gilf.gov.au/restrictive-licence-template. Use of this material is limited according to agreed permissions and restrictions. For permissions beyond the scope of this license contact: Intellectual Property Officer, Queensland Health, GPO Box 48, Brisbane Q 4001, email IP_Officer@health.qld.gov.au, phone (07) 3234 1479.

Statement of Indemnity Material in this document cannot be reproduced in part or in whole without the express permission of Queensland Health and remains the intellectual property of Queensland Health. Queensland Health does not accept any responsibility for the use of this material outside the scope for which it has been designed and outlined in the appropriate Curriculum Document.

This program has been reviewed and endorsed by the Acute Cardiac Education Training Support (ACETS) Committee. We acknowledge the contributions to content of the previous Education for Practice in Queensland (EPiQ) Advisory Committee.

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Table of contents Overview of the Module ...................................................................................................................................... 4 Cardiac Axis: ....................................................................................................................................................... 4 Activity 1............................................................................................................................................................10 Activity 2............................................................................................................................................................11 Left Bundle Branch Block: ................................................................................................................................14 Activity 3............................................................................................................................................................17 Brugada Syndrome ...........................................................................................................................................17 Fascicular Blocks: .............................................................................................................................................19 Heart Blocks .....................................................................................................................................................25 First degree AV Block .......................................................................................................................................26 Second Degree Heart Block Mobitz Type 2 .....................................................................................................28 Third Degree AV Block .....................................................................................................................................29 Activity 5............................................................................................................................................................30 ST Elevation in Lead AVR ................................................................................................................................33 Wellens Sign .....................................................................................................................................................33 Left Ventricular Hypertrophy: ............................................................................................................................35 Right Ventricular Hypertrophy ..........................................................................................................................37 Electrolyte Imbalances......................................................................................................................................39 References .......................................................................................................................................................41

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Advanced ECG Interpretation Overview of the Module • • • • • •

Heart Blocks/Bundle branch blocks Complex ECGs- Triple vessel Disease, Left Main Disease, Brugada syndrome Cardiac Axis and why it is important Fascicular Blocks Ventricular Hypertrophy Electrolyte imbalances

Cardiac Axis:

The electrical signal recorded on the electrocardiogram (ECG) contains information relative to direction and magnitude of the various complexes. The average direction of any of the complexes can be determined.

See image below:

Figure 1.

The normal QRS electrical axis, as established in the frontal plane, is between -30 and 90º (directed downward or inferior and to the left) in adults [10]. An axis between -30º and -90º (directed superior and to the left) is termed left axis deviation. If the axis is between 90º and 180º (directed inferior and to the right), then right axis deviation is present. An axis between -90º and -180º (directed superior and to the right) is referred to as extreme right or left axis.

If the QRS is equiphasic in all leads with no dominant QRS deflection, it is indeterminate axis. The QRS axis moves leftward throughout childhood and adolescence, from a normal value of 30 to 190º at birth to 0 to 120º during ages 8 to 16 years. There is some disagreement among authors on the definitions (in degrees) of a normal, right, and left axis.

The QRS axis can be determined by examining all of the limb leads, but the easiest method involves looking at leads I, II, and aVF only. If the QRS complex is positive (upright) in both leads I and aVF, then the axis falls between -30 and 90º, and the axis is normal.

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Figure 2. ECG demonstrating normal cardiac axis

Left Axis Deviation If the QRS complex is positive in lead I but negative in lead aVF, then the axis is leftward (30 to -90º).

Figure 3. ECG demonstrating Left Axis deviation

Causes for left axis deviation include: ●Normal variation (physiologic, often with age) ●Mechanical shifts, such as expiration, high diaphragm (pregnancy, ascites, and abdominal tumour) ●Left ventricular hypertrophy

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●Left bundle branch block ●Left anterior fascicular block ●Congenital heart disease (primum atrial septal defect, endocardial cushion defect) ●Emphysema ●Hyperkalemia ●Ventricular ectopic rhythms ●Pre-excitation syndromes (Wolff-Parkinson-White) ●Inferior wall myocardial infarction.

Right Axis Deviation

If the complexes are negative in lead I and positive in aVF, then the axis is rightward (90 to 180).

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Figure 4. ECG demonstrating Right Axis Deviation

The causes of right axis deviation include: ●Normal variation (vertical heart with an axis of 90º) ●Mechanical shifts, such as inspiration and emphysema ●Right ventricular hypertrophy ●Right bundle branch block ●Left posterior fascicular block ●Dextrocardia ●Ventricular ectopic rhythms ●Pre-excitation syndrome (Wolff-Parkinson-White) ●Lateral wall myocardial infarction ●Secundum atrial septal defect

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Extreme Axis If the complexes are negative in both I and aVF, then the axis is extreme or “No man’s land” (180 to -90º).

Figure 5. ECG demonstrating extreme axis

Figure 6. Visual representation of extreme axis

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Causes of extreme or “No Man’s Land” Axis includes: •

Ventricular Tachycardia

•

Occasionally Bi Fascicular Block

Accurate plotting of QRS axis involves the following steps:

Look at the QRS complexes in lead 1 and count the positive deflection and subtract the negative deflection from this. For example, if the QRS is five boxes positive and three boxes negative then the net result will be +2. Plot this number on a horizontal plane. (See below) In the same way look at the QRS of aVF and count the positive deflection and subtract the negative deflection from this. Plot the resulting number on the horizontal plane Draw a perpendicular line down from the mark on the lead 1 axis and a perpendicular line across from the mark on the aVF axis Draw a line from the centre of the axis wheel to the spot where these two perpendicular lines meet. This line is the mean QRS axis. (In the case of the figure below the axis is + 50 degrees and normal.)

Figure 7 Visual representation of accurately plotting an axis

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Activity 1

Plot the Axis of the ECG above and describe the Axis

Axis is: __________________________________________________________________________

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Activity 2

Plot the Axis of the ECG above and describe the Axis

Axis is: __________________________________________________________________________

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Bundle Branch Blocks Normal ventricular depolarization occurs after an impulse traverses the atrioventricular (AV) node and the bundle of His. This bundle of specialized conducting tissue splits into two main branches, the right and the left bundles, that rapidly transmit depolarization impulses to the right and left ventricular myocardium, respectively, via the Purkinje fibers. The main left bundle bifurcates into two primary subdivisions: a left anterior fascicle and a left posterior fascicle. Some patients have a third subdivision, a median fascicle. The depolarization wave fronts spread through the ventricular wall, from endocardium (inner layer) to epicardium (outer layer), triggering intracellular calcium release and myofilament contraction (electromechanical coupling).

Figure 8. Image showing Bundle Branch and fascicles

Right and left bundle branch blocks usually reflect intrinsic impairment of conduction in either the right or left bundle system, respectively (intraventricular conduction disturbances).

Bundle branch block can be chronic or intermittent. As an example, transient rate-related bundle branch blocks do not uncommonly occur when the heart rate exceeds some critical value (tachycardia- or acceleration-dependent).

Bundle branch block leads to prolongation of the QRS interval and sometimes to alterations in the QRS vector the degree of prolongation of the QRS interval depends upon the severity of the impairment. With complete bundle branch blocks, the QRS interval is classically stated to be greater than or equal to 120 ms (0.12 sec) in duration (three small boxes on electrocardiogram [ECG] paper); with incomplete blocks, the QRS interval is defined between 100ms and 120 ms

Right Bundle Branch Block Right bundle branch block (RBBB) delays activation of the right ventricle to the late phase of depolarization. As a result, the terminal QRS vector is oriented anteriorly and to the right.

This vector points toward the positive axis of the anterior-posterior lead V1 and away from the positive axis of left-right lead V6.

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Figure 9. Showing the altered direction of depolarisation in right Bundle Branch Block and the associated changes to morphology in V1 and V6

As a result the QRS takes an “M” pattern in V1 and a “W” pattern in V6

Figure 10. Images of V1 and V6 showing the MW pattern of Right Bundle Branch Block

Features of the QRS in RBBB include

•

QRS duration greater than or equal to 120 milliseconds in adults.

•

Sr', rsR', or rSR' in leads V1 or V2. The R' or r' deflection is usually wider than the initial R wave. In a minority of patients, a wide and often notched R wave pattern may be seen in lead V1 and/or V2.

•

S wave of greater duration than R wave or greater than 40 milliseconds in leads I and V6 in adults.

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•

Normal R peak time in leads V5 and V6 but greater than 50 milliseconds in lead V1 (associated with the R' wave).

Figure 11. ECG demonstrating Right Bundle Branch Block Morphology

The QRS morphology in patients with RBBB will vary depending on the position on the heart within the thorax as well as with other cardiac conditions that alter conduction (e.g., prior anterior myocardial infarction).

Chronic RBBB is generally asymptomatic and does not require treatment. However, the presence of a RBBB in the setting of an acute myocardial infarction is associated with a significant increase in mortality

Left Bundle Branch Block:

Figure 12. Showing the blocking of the left bundle branch

Left bundle branch block (LBBB) is different in that it alters both early and late phases of ventricular depolarization. The late QRS vector is still directed to the left and posteriorly, since depolarization is delayed in the left ventricle. However, the normal early left-to-right pattern of septal activation is disrupted so that septal depolarization proceeds from right-toleft as well. As a result, LBBB generates wide, predominantly negative (QS) complexes in Clinical Education and Clinical Simulation Services

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lead V1 and entirely positive (wide R wave) complexes in lead V6. A pattern identical to that of LBBB, preceded by a sharp spike, is seen in most cases of electronic right ventricular pacing because of the relative delay in left ventricular activation.

LBBB may result following an acute myocardial insult such as myocardial ischemia, myocardial infarction, or myocarditis. It may also occur due to degenerative disease of the conduction system which increases with age.

Figure 13. Image showing the altered depolarisation of the ventricles associated with Left Bundle Branch Block and the associated altered QRS morphology changes in V6

As a result the QRS takes an “W” pattern in V1 and a “M” pattern in V6

Figure 14. ECG showing Left bundle branch block morphology

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ECG features of LBBB include:

●QRS duration greater than or equal to 120 ms in adults ●Broad notched or slurred R wave in leads I, aVL, V5, and V6 and an occasional RS pattern in V5 and V6 attributed to displaced transition of QRS complex. ●Absent q waves in leads I, V5, and V6, but in the lead aVL, a narrow q wave may be present in the absence of myocardial pathology. ●ST and T waves usually opposite in direction to QRS complex. ●Depressed ST segments and/or negative T waves in leads with negative QRS ("negative QRS-T" concordance) are generally abnormal, and may be a sign of underlying ischemia

Figure 15. ECG showing the WM pattern in leads V1 and V6 associated with Left Bundle Branch Block

With LBBB it should be noted that: Depressed ST segments and/or negative T waves in leads with negative QRS ("negative QRS-T" concordance) are generally abnormal, and may be a sign of underlying ischemia Ventricular rhythms and ventricular pacing, conditions in which the QRS complex has a similar morphology to LBBB, need to be excluded prior to making the diagnosis of LBBB.

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Activity 3 List 3 ways to exclude VT or Ventricular pacing as a cause of LBBB morphology 1.

2.

3.

Brugada Syndrome The vast majority of cases of sudden cardiac arrest (SCA) and sudden cardiac death (SCD) are caused by ventricular tachyarrhythmia’s, with most of these associated with structural heart disease, particularly coronary heart disease. SCA in normal hearts only occurs in 510 percent of cases. One of the identified causes is Brugada Syndrome which is an autosomal dominant genetic disorder with variable expression characterized by abnormal findings on the surface electrocardiogram (ECG) in conjunction with an increased risk of ventricular tachyarrhythmia’s and sudden cardiac death. Typically, the ECG findings consist of a pseudo-right bundle branch block and persistent ST segment elevation in leads V1 to V2 (see below), although isolated cases have described similar findings involving the inferior ECG leads. Patients with typical ECG features who have experienced sudden cardiac death or a sustained ventricular tachyarrhythmia, or who have one or more of the other associated clinical criteria, are said to have the Brugada syndrome, whereas patients with typical ECG features who are asymptomatic and have no other clinical criteria are said to have the Brugada pattern.

The Brugada ECG pattern is more common in men than in women, with estimates ranging from 2 to 9 times more likely in men. It is most common in the Asian population.

Causes:

A variety of factors may contribute to the electrocardiographic and clinical manifestations of Brugada syndrome including mutations in the cardiac sodium channel SCN genes, right ventricular abnormalities, autonomic tone, fever, and the use of cocaine and certain psychotropic drugs ECG Characteristics:

•

Pattern of RBBB in leads V1-V3 with a late broad R wave (frequently small) called an “epsilon” wave

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Figure 16. The Epsilon wave as seen in Brugada

• •

ST Elevation in leads V1-V3 which unrelated to ischemia, electrolyte imbalances or structural heart disease Normal QT interval

Figure 17. ECG demonstrating Brugada

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Fascicular Blocks: The term fascicular block or hemiblock is used to describe block in either division of the bundle branch including the left anterior fascicle or the posterior fascicle. The most useful leads for recognising fascicular block include leads I and AVF for the axis and leads I and III for typical pattern of the fascicular block.

When fascicular block occurs left ventricular activation occurs left ventricular activation proceeds from one fascicle rather than both simultaneously leading to alteration in the morphology of the QRS in leads I and III. Also because the left ventricle is depolarized in an abnormal direction an axis deviation always occurs from fascicular block. However, the width of the QRS is not significantly altered.

Figure 18 1. Left Anterior Fascicular Block 2. Left Posterior Fascicular Block

Blood Supply

The left anterior and median fascicles are supplied either by septal branches of the left anterior descending artery or by the atrioventricular (AV) nodal artery. The proximal part of the left posterior fascicle is supplied by the artery to the AV node and, at times, by septal branches of the left anterior descending artery. The distal portion has a dual blood supply from both anterior and posterior septal perforating arteries

Left Fascicular Block In left fascicular block the impulse is conducted down the posterior fascicle and begins depolarising the ventricle in an inferior and rightward direction. It then travels through the left ventricular free wall in a superior and leftward direction resulting in left axis deviation.

The initial rightward and inferior direction of conduction lead to a small Q wave in lead I and a small R wave in lead III. The subsequent leftward and superior force lead to a normal R wave in lead I and a deep S wave in lead III. Causes:

Left anterior fascicular block is an indication of the following •

As the left anterior fascicle is usually supplied by the LAD artery. Any new left anterior fascicular block is associated with LAD disease

•

The presence of Left anterior fascicular in normal hearts has been associated with the risk of the development of atrial fibrillation or heart failure

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•

It can also be associated with conduction disease progression linked with ageing.

Treatment:

There are usually no symptoms induced by an isolated block in one of the left bundle fascicles. Therapy should be considered only in patients with persistent bifascicular or trifascicular block. However, a new block may indicate other pathologies.

Left Anterior Fascicular Block ECG Features:

•

Left axis deviation

•

Small Q wave followed by a normal R wave in lead I

•

Small R wave followed by a deep S wave in lead III

•

QRS of not greater than 0.12 seconds

•

Increased QRS voltage in limb leads due to the loss of cancellation of forces in left ventricle

Figure 19. ECG demonstrating Left anterior fascicular block

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Left Posterior Block In posterior fascicular block or “posterior hemiblock” the impulse conducts through the fascicle and begins depolarising the ventricle in a superior and leftward direction. It then travels through the ventricular wall in an inferior or rightward direction. resulting in right axis deviation. The initial rightward and leftward conduction lead to a small R wave in lead I and a small Q in lead III. The forces then travel inferiorly and rightward causing a deep S wave in lead I and a tall R wave in lead III Causes:

Isolated left posterior fascicular block is an uncommon finding due to the fascile having a dual blood supply. However isolated left posterior fascicular block can be seen in: •

The setting of extensive arteriosclerotic cardiovascular disease associated with inferior AMI

•

Cardiomyopathy

Left Posterior Fascicular Block ECG Features:

•

Right Axis deviation > +90 degrees

•

Small R wave followed by a deep S wave in lead I and avL or an rS pattern in leads I and AVL

•

Small Q wave followed by a tall R wave in lead III

•

Normal QRS duration <0.12 secs

•

Increased QRS voltage due to loss of cancellation of QRS forces.

Figure 20. ECG demonstrating Left Posterior Block

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Bi-fascicular Block Bi-fascicular block is when two of the three major fascicles are blocked. If both the anterior and posterior fascicles are blocked then the patient will present with left bundle branch block.

The patient can also present with right bundle branch blocked and one of the anterior fascicles blocked

Figure 21. ECG demonstrating showing bifascicular block with right bundle branch block and left anterior fascicular block

For patients who present with presyncope or syncope and are noted to have bifascicular block on ECG, additional monitoring and evaluation are required, as intermittent trifascicular (i.e., complete) heart block may result in hemodynamic instability leading to their symptoms.

In such patients, we perform continuous ECG monitoring for 24 to 48 hours, usually in an inpatient setting, to monitor for high-grade atrioventricular (AV) block. Echocardiography should also be performed to assess for underlying structural heart disease

Figure 22. ECG demonstrating Bifascicular block, Right Bundle branch block and left posterior fascicular block Clinical Education and Clinical Simulation Services

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Management of patients with bifascicular block begins by looking for and correcting reversible causes of impaired conduction such as myocardial ischemia and drugs that may slow conduction or prolong the refractory period of fascicular tissue. If no reversible causes are present, treatment involves the avoidance of medications that impair AV nodal conduction (when possible) and evaluation for permanent pacemaker placement

Trifascicular block The term trifascicular block is most commonly used to describe bifascicular block associated with prolongation of the PR interval (i.e., first degree AV block). However, this description, though commonly used in clinical practice, is inaccurate as the conduction delay resulting in the PR interval prolongation does not usually occur in a fascicle, but in the AV node. True trifascicular block would involve block of the right bundle branch and both fascicles of the left bundle branch; this manifests as third degree (complete) heart block and is referred to as such. Sinus rhythm with alternating left/right bundle branch block or right bundle branch block (RBBB) with alternating fascicular blocks on a beat-to-beat basis is a very rare manifestation of trifascicular block, usually heralding complete AV block.

Treatment:

With patients in this rhythm again any medication which slows conduction through the AV node such as beta blockers, calcium channel blockers and digoxin should be avoided. Also pacing should be considered.

Figure 23. ECG showing Right Bundle branch block, left posterior hemiblock and first degree AV block commonly referred to as trifascicular block

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Activity 4 Identify the axis and the fascicle which is blocked in the ECG below

1) Axis:

2) Fascicle blocked:

.

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Heart Blocks

Atrioventricular (AV) block results from interruptions in the conduction of impulses between the atria and ventricles. The AV block can be total or partial or it may delay conduction. The block can occur at the AV node, the bundle of HIS or the bundle braces. At a normal sinus rate of 60-100 impulse per minute the clinical effect of the AV block will depend on how many impulses are blocked and how this effects the ventricular rate. As cardiac output is dependent on the HR a slow ventricular rate can lower cardiac output and consequently the blood pressure. This can in turn lead to light headedness, confusion and in some cases loss of consciousness.

Common Causes of AV Blocks

• • • •

•

Myocardial infarction in which cell death occurs. If the cells are part of the conduction system then they no longer conduct impulses and permanent AV block occurs.

Myocardial ischemia where cellular function is impaired and injured cells may conduct impulses more slowly on inconsistently. Normal conduction is normally restored when ischemia is relieved.

Excessive dosage or an exaggerated response to a medication. Common drugs which may cause AV block include Digoxin, Beta Blockers and Calcium Channel blockers.

Cardiac Surgery can cause AV block. Particularly surgery involving the mitral or tricuspid valve or closure of an atrial septal defect. If the injury involves tissues adjacent to the surgical site and the conduction system is not physically damaged then normal conduction may recover. However if a portion of the conduction system is severed then a permanent block will occur.

Radiofrequency ablation of conduction pathways can also cause temporary or permanent AV block

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First degree AV Block

Figure 24. ECG rhythm strip demonstrating First degree AV block

First degree AV block is when impulses from the atria are consistently delayed through the AV node. Conduction eventually occurs but it takes longer than normal.

Causes include:

Myocardial infarction Degenerative changes in the heart Medications including Digoxin, Beta blockers, Calcium Channel blockers The ECG appearances of first degree AV block are characterised by:

Rate between 60- 100 bpm Regular ventricular rate (QRS complexes) P waves present Increased P-R interval of > 0.2 seconds or 5 small squares Narrow QRS complexes Treatment:

In first degree AV block the cause of the arrhythmia should be treated rather than the arrhythmia itself. This includes reviewing the patientâ&#x20AC;&#x2122;s medication or monitoring for signs of ischaemia. As first-degree AV block can progress to more serious forms of forms of AV block it should be monitored.

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Second Degree Heart Block Mobitz Type 1

Figure 25. Rhythm strip showing second degree heart block Mobitz Type 1

This rhythm is also called “Wenckebach” and occurs when each successive impulse from the AV node is more delayed than the previous impulse. This pattern occurs until an impulse fails to be conducted to the ventricles. This cycle then repeats Causes include:

Inferior Wall AMI Rheumatic fever Increased vagal stimulation Medications including Digoxin, Beta blockers, Calcium Channel blockers The ECG appearances of Second Degree AV block Mobitz Type 1 are characterised by: Rate between 60- 100 bpm Irregular ventricular rate (QRS complexes) but a regular pattern of “longer longer drop “ P waves present Increasing P-R interval which increases until a an impulse is not conducted Narrow QRS complexes Treatment

If the patient is asymptomatic than no treatment is required. However for a symptomatic patient atropine will increase AV conduction and increase the heart rate. Causes of the arrhythmia need to be investigated and addressed including ischemia or medications. In some cases temporary pacing may need to be initiated to increase the heart rate. This rhythm can progress to more serious forms of forms of AV block it should be monitored

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Second Degree Heart Block Mobitz Type 2 Second Degree Heart Block Mobitz Type 2 is less common than Second Degree Heart Block Mobitz Type 1 although it is far more serious. It occurs when occasional impulses from the SA node fail to reach the ventricles. There is no lengthening of the PR interval as with Second Degree AV Block Mobitz Type 1. Instead the PR interval remains constant and there will be an occasional dropped beat.

Figure 26. Rhythm strip showing Second degree Heart block Mobitz type 2

Causes:

Second Degree Heart Block Mobitz Type 2 is usually caused by Anterior Wall MI Other causes include:

• •

Degenerative changes in the conduction system Severe coronary artery disease

This rhythm indicates a problem at the level of the Bundle of HIS or bundle branches.

Type 2 is more serious than Type 1 because the ventricular rate tends to be slower and the cardiac output diminished. It is likely to cause symptoms if the sinus rate is low and conduction rate is 2:1.

The ECG appearances of Second Degree AV Block Mobitz Type 2 are characterised by:

• • • • •

Rate between 30 - 100 bpm Atrial rate regular. Irregular ventricular rate (QRS complexes) due to dropped beats.

P waves present P-R interval remains constant apart from on non-conducted beats QRS normal but can be widened if bundle branch block present

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Third Degree AV Block

Figure 27. Visual representation of Third degree AV Block showing the intrinsic pacing rates of the SA and AV nodeâ&#x20AC;&#x2122;s and the ventricles.

Figure 28. Rhythm strip showing Third degree Heart block

Third Degree Heart block is also called complete heart block. This occurs when impulses from the atria are completely blocked at the AV node and cannot be conducted through to the ventricles. Acting independently the atria under the control of the SA node normally maintain a rhythm of 60-100 bpm. The absence of an impulse from the SA node the AV can generate impulses from 40-60 bpm. In the absence of any other impulse generation the HIS Purkinje system can generate impulses from 20-40 beats per minute. In order to maintain cardiac output, impulses need to be generated from below the AV node leading to a reduced heart rate.

The rhythm strip will look like a strip of P waves laid independently over a strip of QRS complexes with no relationship between the P waves or QRS complexes.

Complete heart block will not only reduce cardiac output and blood pressure through reduced heart rate but also through the loss of atrial kick which is the 30% of blood which is ejected into the ventricles during atrial contraction. Any exertion on the part of the patient can worsen symptoms.

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Causes:

Complete heart block is most commonly a congenital condition; however it can be caused by other pathologies including: • Surgical injury • Anterior or Inferior MI • Sensitivity to calcium channel blockers, beta blockers and digoxin The ECG appearances of Third Degree AV block are characterised by:

• • • • •

Atrial rate can vary between 60-100 bpm. Ventricular rate is between 20-40 bpm Atrial rate and ventricular rate are regular but no relationship between the two.

P waves present P-R interval varies with no regularity QRS complexes are widened >0.12 seconds due to impulses coming from the ventricles.

Treatment:

If the patient is symptomatic temporary medical treatment may be required including: • Atropine • Isoprenaline • Adrenaline External pacing may also be required.

Using the systematic approach provided, interpret the following rhythms

Activity 5

Rhythm Strip: Lead 11

Rate Rhythm P waves Assess Intervals ST segment / T wave Interpretation

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Rhythm Strip: Lead 11

Rate Rhythm P waves Assess Intervals ST segment / T wave Interpretation

Rate Rhythm P waves Assess Intervals ST segment / T wave Interpretation

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Rhythm Strip: Lead 11

Rate Rhythm P waves Assess Intervals ST segment / T wave Interpretation

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ST Elevation in Lead AVR ST-segment elevation in lead aVR that is greater than or equal to ST-elevation in lead V1 may be useful for diagnosing an acute left main coronary artery obstruction. In a report in which 16 such patients were compared to 46 with left anterior coronary artery obstruction and 24 with right coronary artery obstruction, the above finding distinguished left main coronary occlusion from an LAD occlusion with a sensitivity and specificity of 81 and 80 percent, respectively. In addition, mortality was associated with a greater degree of ST elevation in aVR. Diffuse ST segment depressions may be seen in other leads. ST elevation in lead Avr can also be a sign of triple vessel disease.

Figure 28. ECG demonstrating ST elevation in aVR with associated ST depression in Anterior, Lateral and Inferior leads

Wellens Sign Wellens sign is a characteristic pattern seen in patients with critical stenosis of the left anterior descending (LAD) artery and is a warning of impending acute anterior wall MI. Recognition of Wellens syndrome indicates the need for immediate cardiac catheterisation to intervene in LAD with angioplasty or stenting before an acute MI occurs. These patients normally present with a diagnosis of unstable angina and no or minimal cardiac enzyme elevation and exhibit the following ECG changes during pain free periods: 1) ST segments: either normal or slightly elevated usually in leads V2-4 2) T waves: often start upright but the terminal portion dips below the baseline in V2-V3.

There is often progressive symmetric deep T wave inversion in leads V1-4 3) R waves: there is no loss of R wave progression in leads V1-V4 because there has been no infarct yet.

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Figure 29. ECG showing Biphasic T waves in V2-V4 with upright R waves demonstrating Wellens sign/warning

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Left Ventricular Hypertrophy: Left ventricular hypertrophy (LVH) refers to an increase in the size of myocardial fibers in the main cardiac pumping chamber. Left ventricular hypertrophy (LVH) is an important finding since it usually reflects pressure and/or volume loads, or a hypertrophic cardiomyopathy variant LVH is not an acute condition. It takes weeks and usually months to years to develop.

Patients with LVH from any cause are at increased risk for major cardiovascular complications, including congestive heart failure and cardiac arrhythmias Because of its association with hypertension, cardiomyopathy, aortic or mitral valve disease, and myocardial fibrosis, the finding of LVH on ECG has adverse prognostic implications related to heart failure and atrial and ventricular arrhythmogenesis.

• •

The two most important pressure overload states are systemic hypertension and aortic stenosis The major conditions associated with left ventricular volume overload are aortic or mitral valve regurgitation and dilated cardiomyopathy.

Other causes include:

• • •

Ventricular septal defects: cause both right and left ventricular volume overload Hypertrophic cardiomyopathy: is an example of an inherited condition in which LVH (usually with asymmetric septal hypertrophy) occurs in the absence of any apparent hemodynamic pressure or volume overload Athletes Heart: Is a physiologic type of hypertrophy with increase in wall thickness and left ventricular end-diastolic volume may occur in trained athletes

Left ventricular hypertrophy (LVH) and related changes can produce five major electrocardiogram findings:

• • • • •

Increased QRS voltage Increased QRS duration, Left axis deviation Repolarization (ST-T) changes Left atrial abnormality

Increased QRS voltage:

An increase in left ventricular mass predictably will augment the amplitude of voltage generated by these fibers. This effect will, in turn, increase the amplitude of positive forces (R waves) recorded over the left chest leads and negative forces (S waves) recorded over the right chest leads. LVH will also increase the amplitude of R waves in those limb leads that record the projection of these positive forces (typically I and aVL with a horizontal or leftward QRS axis)

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There are two criteria for increased QRS voltage •

Sum of S wave in V1 and R wave in V5 or V6 ≥3.5 mV (35 mm) and/or

•

R wave in aVL ≥1.1 mV (11 mm) (sometimes ≥1.3 mV [13 mm] is used)

Increased QRS duration:

An increase in LV mass is often associated with widening of the QRS duration. This change may be subtle or may be associated with incomplete, or eventually complete, left bundle branch block (LBBB). On the other hand, most patients with LBBB have underlying LVH. In addition, some causes of LVH can lead to LBBB by other mechanisms such as calcification or fibrosis of the proximal ventricular conduction system, which lies close to the valve ring, in calcific aortic stenosis.

Left axis deviation:

LVH is usually associated with a horizontal or frankly leftward (≥-30º) QRS axis in the frontal plane leads. However, LVH may occur with a vertical QRS axis (or even rightward axis), especially in young adults or patients with biventricular hypertrophy.

Repolarization abnormalities:

Severe LVH, especially due to a pressure load, is often associated with ST depressions and T wave inversions in leads with relatively tall R waves (see below). This pattern, formerly referred to as LV "strain" (but best referred to as "LVH with associated ST-T wave abnormalities"), may be due to primary alteration in 2repolarization of hypertrophied muscle or to relative subendocardial ischemia.

Figure 30. ECG Demonstrating Left Ventricular Hypertrophy

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Left atrial abnormality Most patients with LVH develop abnormalities in left atrial depolarization due to conduction delay or actual atrial enlargement. The two major markers of left atrial abnormality are increased duration of P waves (≥120 ms) and notching of the P wave in the limb leads and/or biphasic P waves with a prominent negative component (≥40 ms in duration and/or ≥1 mV in depth) in V1. Biphasic P waves with a very prominent negative component may be a subtle but important clue to major abnormalities such as severe mitral regurgitation or dilated cardiomyopathy

Figure 31. ECG demonstrating Left atrial enlargement or P mitrale

Treatment:

The regression of LVH is associated with a reduction in cardiovascular risk and improved cardiac function. The use of antihypertensive agents (including calcium channel blockers and ACE inhibitors), weight loss, or dietary sodium restriction decreases cardiac mass in patients with LVH

Right Ventricular Hypertrophy Right ventricular hypertrophy (RVH) can be caused by any condition which produces a significant load on the right ventricle such as pulmonary disease, congenital or acquired heart disease, particularly mitral valve disease.

As the right ventricle enlarges the right sided electrical forces becomes as large or larger than the forces in the left. The normal sequence of depolarisation is altered resulting in ECG changes in axis, QRS morphology and voltage, producing tall R waves in the right precordial leads (V1 and V2), and deep S waves in the left precordial leads (V5 and V6).

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Right axis deviation (axis >+90º-100º) is often present with RVH. There also may be associated right atrial overload and ST segment and T wave abnormalities in the right precordial leads reflecting subendocardial ischemia or repolarization abnormalities of the right ventricular myocardium.

P Pulmonale

Right ventricular enlargement can also be associated with the ECG sign P Pulmonale which is a sign of right atrial enlargement. Characteristics of P Pulmonale include P wave amplitude of: • 2.5 mm in the inferior leads (II, III and AVF) • 1.5 mm in V1 and V2

Figure 32. ECG representing P Pulmonale or Right Atrial enlargement

ECG criteria for the diagnosis of Right Ventricular Hypertrophy include:

•

Right axis deviation (>+90)

•

R in V1 >6 mm

•

R in V1 + S in V5 or V6 >10.5 mm

•

R/S ratio in V1 >1

•

S/R ratio in V6 >1

•

Incomplete right bundle branch block

•

ST-T wave abnormalities ("strain") in inferior leads

•

Right atrial hypertrophy/overload (“P Pulmonale”)

•

S>R in leads I, II, III

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Figure 33. ECG representing Right Ventricular Hypertrophy

Electrolyte Imbalances Hypokalemia

As potassium levels drop to below <3mmmol/l the ST segment become progressively more depressed, the T waves flatten and the U waves begin to become more prominent. The P wave and the PR interval can also widen.

Hypokalemia promotes atrial and ventricular ectopy and lead to the development of ventricular tachycardia, torsades de pointes and ventricular fibrillation.

Figure 34. ECG changes demonstrated by Hypokalaemia compared to normokalaemia

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Hyperkalemia

When the potassium level rises above >5.5 ECG changes the T wave and QRS complex are produced. The T waves become tall and peaked with a narrow base and the QT shortens. As the potassium level raises the QRS complex widens and ST elevation may occur. First degree AV block can also occur. In severe hyperkalaemia, the P waves flatten and eventually disappears pear whilst the QRS becomes broad and bizarre with a sine wave appearance. Hypocalcaemia is when the calcium is less <6.1 mmol and cause ECG changes including prolongation of the QT interval and the ST segment. The T is wave is unchanged. Arrhythmias are uncommon in hypocalcaemia

Figure 35. demonstrating how ECG changes with increased potassium levels

Hypocalacaemia

Hypocalcaemia is when the calcium is less <6.1 mmol and cause ECG changes including prolongation of the QT interval and the ST segment. The T is wave is unchanged.

Arrhythmias are uncommon in hypocalcaemia Hypercalcaemia

Hypercalcaemia is when the serum calcium is greater than >12mmol/l shortens the QT interval and shortens the ST segment to the point where it practically disappears. P waves and T waves are usually unchanged. Arrhythmias are uncommon in hypercalcaemia

Figure 36. ECG changes which occur with Hyper/hypocalcaemia

Magnesium Imbalances:

Magnesium imbalances do not produce specific ECG changes. However, Hypomagnesia can contribute to arrhythmias such as digitalis toxicity, ischemia, digitalis toxicity or hypokalaemia. Severe Hypermagnesia has been associated with AV block and intraventricular conduction disturbances.

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References Australian Resuscitation Council. (2016). Advanced Life Support: ARC Advanced Life Support Level 2 (6th Ed.). East Melbourne: Australian Resuscitation Council.

Goldberger, A. (2015, Sept 08). Basic approach to delayed intraventricular conduction.

Retrieved from Up-to-date: https://www-uptodatecom.tsproxy.slq.qld.gov.au/contents/basic-approach-to-delayed-intraventricularconduction?source=search_result&search=right%20bundle%20branch%20block&s electedTitle=2~133 Luna, A., Goldwasser, D., Fiol, M., & Bayes-Genis, A. (2011). Surface electrocardiography. In V. Fuster, R. Walsh, & A. Harrington (Eds.), Hursts: The Heart (13th ed., pp. 307-370). New York: McGraw-Hill.

McLaughlin, M. (Ed.). (2014). Cardiovascular care made incredibly easy. Philadelphia: Wolter Kluwer.

Prutkin. (2016, May 06). ECG tutorial: Chamber enlargement and hypertrophy. Retrieved from Up-to-date: https://www-uptodate-com.tsproxy.slq.qld.gov.au/contents/ecgtutorial-chamber-enlargement-andhypertrophy?source=search_result&search=right%20ventricular%20hypertrophy&s electedTitle=1~99 Rasmussen, P. (2012). Assessment made incredibly easy! Philadelphia: Wolters Kluwer Health Lippincott and Williams.

Sauer, W. (2015, November 19). Left anterior fascicular block. Retrieved from Up-to-date: https://www-uptodate-com.tsproxy.slq.qld.gov.au/contents/left-anterior-fascicularblock?source=search_result&search=fascicular%20block&selectedTitle=1~38 Soto, C. (2017). ECG: Essentials of Electrocardiography. Boston: Cengage Learning Inc. Thompson, P. (2011). Coronary Care Manual. Sydney: Elsevier.

Woodruff, D. (2017). Critical care nursing made incredibly easy (4th Ed.). Philadelphia: Wolters Kluwer.

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