Intermediate ECG Interpretation

Intermediate ECG Interpretation Self-directed Learning Package: Module 2 [Date]

Course Outline This package is part two 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) prior to the commencement of Module three.

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 June 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 Licence 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 licence 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 Electrocardiogram ........................................................................................................................... 4 Rhythm Interpretation ..................................................................................................................... 4 Arrhythmia Interpretation................................................................................................................. 4 Tachycardia .................................................................................................................................... 5 Narrow complex tachycardia ........................................................................................................... 5 Sinus tachycardia............................................................................................................................ 5 Supraventricular tachycardia ........................................................................................................... 6 Atrial flutter...................................................................................................................................... 6 Activity 1 ......................................................................................................................................... 7 Critical Point 1................................................................................................................................. 7 Atrial Fibrillation .............................................................................................................................. 8 Activity 2 ......................................................................................................................................... 8 Regular wide complex tachycardia .................................................................................................. 9 Ventricular tachycardia.................................................................................................................... 9 Ventricular fibrillation ..................................................................................................................... 10 Asystole ........................................................................................................................................ 10 Activity 3 ....................................................................................................................................... 11 General Considerations in Arrhythmia Management ..................................................................... 13 Critical Point 2............................................................................................................................... 13 Conclusion .................................................................................................................................... 13 Signs of Ischemia and Infarction ................................................................................................... 14 Which ECG leads are related to which Coronary Artery? .............................................................. 16 Left Anterior Descending............................................................................................................... 16 Right Coronary Artery ................................................................................................................... 17 Left Circumflex .............................................................................................................................. 18 Right Sided AMI ............................................................................................................................ 19 Posterior AMI ................................................................................................................................ 20 Arrhythmias Relative to the Location of Acute Myocardial Infarction ............................................. 21 Management of Unstable Angina and NSTEMI: ............................................................................ 22 Multiple Choice Questions ............................................................................................................ 25 Reference: .................................................................................................................................... 31

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Intermediate ECG Interpretation Electrocardiogram The interpretation of alterations in the ECG waveform is complex, with different physiological or pathophysiological changes producing identical or similar changes in waveform. The ECG is an important tool used by health professionals to diagnose and monitor a wide array of cardiac abnormalities, including arrhythmias and myocardial damage. The purpose of this module is for participants to learn or consolidate their ability to interpret abnormal electrocardiograms (ECG).

Rhythm Interpretation An arrhythmia describes any cardiac rhythm other than sinus rhythm. The framework for rhythm analysis that is utilised should be reflective of the components of a normal cardiac rhythm (sinus rhythm) and enable identification of any abnormalities present.

Arrhythmia Interpretation Arrhythmias occur when there is an alteration to the usual initiation or conduction of the hearts electrical impulses. It is helpful at this point to identify some of the terminology you will use to describe arrhythmias. Their site of origin is not the only method of classifying abnormalities; it is also done by the mechanism that is occurring for example in an adult:

Term

Definition

Tachycardia: Bradycardia Accelerated

Heart rate is greater than 100 beats per minute (bpm).

Heart rate is less than 60 bpm.

Heart rate exceeds the inherent rate of the pacemaker site, but is less than 100 bpm. For example the atrioventricular (AV) junctional pacemaker site’s inherent rate is 40-60bpm.

If the junctional rate is 75 bpm, it is called accelerated AV junctional rhythm, but not a tachycardia because the rate is less than 100 bpm.

Premature impulse(s) originating outside the SA node from irritable sites in the atria, AV junction and ventricles.

Impulse(s) originating from a source other than the sinoatrial node.

Protective late impulse(s) that occur after the next expected normal beat and arise from the secondary pacemakers located in the AV junction and/or ventricle. They take over pacing the heart rate when the sinus node slows or fails to fire.

Rapid, regular, repetitive incomplete contraction of the atria or ventricles.

Chaotic, uncoordinated quivering of atrial or ventricular musculature.

Delay or failure of conduction of electrical impulses through the AV junction.

Ectopic beats or rhythms

Escape beats or rhythms

Flutter Fibrillation AV Blocks

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Tachycardia Tachycardia is a heart rate of more than 100 beats per minute. The heart normally beats at a rate of 60 to 100 times per minute Tachycardia can be part of the body's normal response to anxiety, fever, rapid blood loss or strenuous exercise. It also can be caused by medical problems, such as an abnormally high level of thyroid hormones, as a result of a cardiac arrhythmia, lung problems, such as pneumonia or a blood clot in one of the lung's arteries. In other cases, tachycardia can be a side effect of some foods and drinks, including coffee, tea, alcohol and chocolate, tobacco, or medication.

Tachycardia may be classified as ‘regular’ or ‘irregular’, and may have a ‘narrow’ or ‘wide’ complex

Narrow complex tachycardia A narrow complex tachycardia is usually one of these four rhythms: 1. Sinus tachycardia (ST) 2. Supraventricular tachycardia (SVT) 3. Atrial flutter.

4. Atrial fibrillation (Irregular narrow complex tachycardia)

Sinus tachycardia Sinus tachycardia is common, but usually reflects systemic illness or injury (such as sepsis, trauma or dehydration), rather than a primary cardiac condition. The electrical conduction through the heart is normal, albeit accelerated.

The ECG appearances of ST include: • regular rate, usually less than 120 bpm in an otherwise healthy person • normal appearance of P, QRS and T waves • QRS may be widened if an associated conduction defect is present—bundle branch block (BBB).

Figure 1: Sinus tachycardia

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Supraventricular tachycardia SVT includes several tachycardia’s arising from the AV node or above. The two most common forms are AV node re-entry tachycardia and tachycardia associated with accessory conduction pathways, such as Wolf-Parkinson-White syndrome (WPW)3.

In both forms, an alternative electrical pathway is present which allows repeated rapid conduction of atrial impulses to the ventricles and subsequent ventricular stimulation.

The ECG appearances of SVT are characterised by: • Hidden or absent P waves • Regular QRS complexes (ventricular rate)—typically 120–180 bpm • Normal QRS complexes in the absence of associated BBB (QRS may be widened in WPW with conduction along the accessory pathway) • Normal T waves.

Figure 2: Supraventricular tachycardia

Atrial flutter Atrial flutter is a common regular tachycardia more prevalent in older patients.

Atrial flutter is often misdiagnosed as SVT, but a rate of 150 bpm with narrow QRS complexes should alert one to the diagnosis. It may be present in association with atrial fibrillation.

The ECG appearances of atrial flutter are characterised by: • P waves (flutter waves) at a rate of 300 bpm (atrial rate). These are often described classically as ‘sawtooth’ in appearance.

• Regular QRS complexes (ventricular rate). However, the ventricular rate depends on conduction through the atrio-ventricular (AV) node. If every second P wave (atrial beat) is conducted, the QRS (ventricular) rate will be 150 (2:1 AV block). If every third P wave is conducted, the QRS rate will be 100 (3:1 AV block).

• Normal QRS complexes in the absence of associated BBB. • Normal T waves.

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Figure 3: Atrial flutter 2:1

Figure 4: Atrial flutter 4:1

Activity 1

Identify 5 causes of Atrial Flutter.

1.

2.

3.

4.

5.

Critical Point 1 With atrial flutter the atrial and ventricular rates are calculated using the 300 rule. For example, if the atrial rate is 300 and the ventricular rate is 100, then there is atrial flutter with 3:1 conduction. This is necessary as P waves can be buried in the QRS and T waves.

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Atrial Fibrillation An irregular tachycardia in a conscious patient is almost always atrial fibrillation (AF).

AF is the result of chaotic electrical current flow in the atria resulting in independent muscle fibre contraction (fibrillation), rather than a synchronous contraction of all muscle fibres. The sino-atrial (SA) node no longer acts as a pacemaker for the heart.

The ECG appearances of AF are characterised by: • variable ventricular rate (QRS complexes) •

absence of P waves

•

erratic baseline between QRS complexes

•

narrow QRS complexes in most cases, but these may be wide if an associated BBB is present (aberrant conduction)

•

normal T waves.

Figure 5: Atrial fibrillation

Activity 2

Identify 5 causes of Atrial Fibrillation.

1.

2.

3.

4.

5.

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Regular wide complex tachycardia Wide complex tachycardia should always be regarded as being ventricular tachycardia (VT) until proven otherwise.

The differential diagnosis includes any of the narrow complex regular tachycardia’s (ST, SVT, atrial flutter) with an associated interventricular conduction defect (BBB)

Ventricular tachycardia VT consists of at least three consecutive ventricular complexes with a rate of more than 100 bpm. Patients may or may not be conscious as a result of their VT. The ECG appearances of VT are characterised by: • no P waves • regular QRS complexes 120–200 bpm • wide QRS complexes > 120 ms • no identifiable T waves.

Figure 6: Ventricular tachycardia

Torsade de pointes, or polymorphic VT, is a variation of VT, where the amplitude of the waveform varies quickly over time, resulting in a twisted (torsade) appearance of the rhythm strip.

Figure 7: Torsade de pointes

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Ventricular fibrillation VF is an asynchronous chaotic ventricular rhythm that follows no regular pattern and produces no cardiac output. The patient will be unconscious.

The ECG appearances of VF are characterised by: • irregular undulations • no clear-cut ventricular complexes • varying ECG amplitude

Figure 8: Ventricular fibrillation

Asystole Asystole is the term used to describe a lack of cardiac activity and contraction as a result of a lack of any detectable electrical activity. It is usually a prelude to death.

The ECG appearances of asystole are: • lack of any P, QRS or T waves • lack of any irregular undulations • a ‘flat line’ appearance.

Fine VF may be mistaken for asystole, so clinicians should check the rhythm in several ECG leads before concluding that asystole has occurred.

Figure 9: Asystole

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Activity 3 Using the systematic approach provided, interpret the following rhythms

Rhythm Strip: Lead 11

Rate Rhythm P waves Assess Intervals

PR

QRS

PR

QRS

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

PR

QRS

ST segment / T wave Interpretation

Rhythm Strip: Lead 11

Rate Rhythm P waves Assess Intervals

PR

QRS

ST segment / T wave Interpretation

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General Considerations in Arrhythmia Management The generic approach to managing an arrhythmia includes: • Establish cardiac monitoring if not already present and assess the arrhythmia • Monitor vital signs • Establish oxygen therapy (if appropriate) • Obtain a 12 lead ECG • Assess the patient’s condition for the presence or absence of adverse features • Obtain intravenous access.

• Perform a focussed history and physical examination, assessing for factors contributing to the arrhythmia.

• Correct reversible causes

Critical Point 2 Not all arrhythmias will result in the patient becoming compromised and require treatment. It is vital when a patient has a change of rhythm that you assess their response to the arrhythmia.

Conclusion The overall aim of arrhythmia management is to restore sinus rhythm and prevent recurrences. If it is not possible to revert the patient to sinus, then the aim is to ‘normalise’ the ventricular rate and increase cardiac output (CO). Remember that if you do not correct the underlying cause then the arrhythmia will be less likely to revert or will return. The patient’s haemodynamic status will dictate the urgency of management.

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Acute Coronary Syndrome Signs of Ischemia and Infarction The ECG features of ACS are variable and depend on the extent and acuity of the ischaemia. Common ECG patterns of ACS include ST segment elevation. This is the classical feature of acute myocardial infarction (AMI) or ST elevation myocardial infarction (STEMI). ST segment elevation occurs early in transmural infarction.

Figure 14: ST segment elevation

ST segment depression: this is the classical feature of acute angina and usually resolves with the patient’s symptoms. It may also be present acutely in non-ST elevation myocardial infarction (non-STEMI).

Figure 15: ST segment depression

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T wave inversion: this feature may be seen after the initial phases of an STEMI, as the only feature in a non-STEMI, or as an indicator of ischemia without infarction (angina).

Figure 16: T wave inversion

Q waves: pathological Q waves develop after the acute phase of myocardial infarction, as the ST segments and T waves return to normal.

Figure 17: Q waves

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Which ECG leads are related to which Coronary Artery?

Left Anterior Descending The left anterior descending artery (LAD) supplies the septum and the anterior surface of the heart which is represented by leads V1-V4. ST elevation in these leads is usually the caused by a lesion in the LAD and represents an Anterior AMI However if the diagonal branch of the LAD is also occluded this may lead to ST elevation in leads V5-V6 and /or leads I and AVL and represents an Anterolateral AMI.

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Right Coronary Artery The right coronary artery (RCA) supplies the inferior surface of the heart and is represented by leads I, II and AVF. ST elevation in these is often caused by a lesion in the RCA or less commonly the LCx and represents an Inferior AMI (see below). In the limb leads ST elevation needs to be + or > 1mm to be considered a myocardial infarction.

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Left Circumflex The left circumflex artery (LCx) is represented by leads V5-V6 and or leads I and AVL. ST elevation in this leads is usually caused by a lesion to the LCx or the diagonal branch of the LAD and represents a Lateral AMI.

In summary the following leads represent the following surfaces • • • • •

V1-V2 – Anteroseptal V3-V4 – Anteroapical V5-V6 – Anterolateral I, aVL – Lateral II, III, aVF – Inferior

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Right Sided AMI The RV branch of the RCA supplies the right side of the heart. Any blockage to the RCA , usually in the setting of an inferior AMI will lead to a RV infraction. This will be represented

by ST elevation in lead V4R. It is recommended that all patients presenting with inferior AMI have a right sided ECG taken

Elevation in V4R only needs to be 0.5 mv of elevation to be considered elevated

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Posterior AMI The posterior wall of the heart is supplied by the RCA and occasionally the LCx. The posterior surface is represented by leads V7-9 (see below). Posterior infraction can be caused by a lesion to the RCA or the LCx (most commonly the RCA) and will represent ST elevation in leads V7-9. Another sign of Posterior AMI is ST depression in leads V1-V2 with a tall R wave. All patients presenting with an inferior AMI should have a Posterior ECG taken.

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Arrhythmias Relative to the Location of Acute Myocardial Infarction Inferior MIs occur with occlusion of the Right Coronary Artery (RCA). Because the RCA perfuses the Sinoatrial (SA) node (50% of the population) and also the proximal bundle of His and Atrioventricular (AV) node (90% of the population), conduction disturbances can occur.

These include: •

Sinus bradycardia;

•

Sinus arrest;

•

First, second and third degree heart block.

Septal MIs and Anterior MI’s occur with occlusion of the Left Anterior Descending (LAD) artery and septal branch of the LAD artery.

Possible conduction disturbances include: •

Sinus tachycardia (secondary to sympathetic stimulation);

•

Second and third degree heart block;

•

Bundle branch blocks (BBB);

•

Left anterior fascicular blocks (LAFB);

•

Left posterior fascicular blocks (LPFB).

Right Ventricular (RV) MIs occur with occlusion of the RCA, Posterior Descending Coronary Artery, and the Posterior Left Ventricular Artery.

Possible conduction disturbances include: •

Sinus bradycardia;

•

Sinus arrest;

•

Premature atrial complexes;

•

Atrial flutter;

•

Atrial fibrillation;

•

First, second and third degree heart block;

•

LPFB.

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Cardiac arrhythmias are extremely common in the early stages of Acute Coronary Syndromes (ACS). It has become evident with increasing coronary care experience, that most of these arrhythmias do not require treatment. In modern coronary care practice, arrhythmias during ACS are treated actively only when they are symptomatic, lifethreatening, or cause an increase in myocardial consumption.

Treatment of ACS Management of Unstable Angina and NSTEMI: Once the diagnosis of UA or an acute NSTEMI is made, the acute management of the patient involves the simultaneous achievement of several goals: •

Relief of ischeamic pain

Oxygen: Avoid if oxygen saturations >92% as has been shown to cause coronary artery spasm.

Nitroglycerin: GTN in the form of the spray should be administered in the form of a 400mcg sublingual spray followed by another spray 5 minutes later if pain is not relieved. Avoid in hypotension, right sided infarct or aortic stenosis.

Morphine: If pain not relieved by GTN administer intravenous dose of 2.5mg repeated at intervals of 5 minutes until pain is relieved.

•

Estimation of Risk:

Early risk stratification in patients with acute coronary syndrome (ACS) is essential to identify those patients at highest risk for further cardiac events who may benefit from a more aggressive therapeutic approach. This can be calculated using the Thrombolysis in Myocardial Infarction (TIMI) or GRACE score to assess the patient’s risk.

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TIMI Score: Age ≥65 years • • • • • •

Presence of at least three risk factors for coronary heart disease (hypertension, diabetes, dyslipidemia, smoking, or positive family history of early MI).

Prior coronary stenosis of ≥50 percent Presence of ST segment deviation on admission electrocardiogram At least two anginal episodes in prior 24 hours Elevated serum cardiac biomarkers Use of aspirin in prior seven days (which is probably a marker for more severe coronary disease)

Patients are considered to be at low risk with a score of 0 to 2, intermediate risk with a score of 3 to 4, and high risk with a score of 5 to 7 • •

Choice of a management strategy, i.e., an early invasive strategy such as PCI or CABG vs versus a conservative strategy with medical therapy Initiation of antithrombotic therapy (including antiplatelet and anticoagulant therapies) to prevent further thrombosis of or embolism from an ulcerated plaque

Antiplatelets Anti-platelet therapy including Aspirin and platelet P2Y receptor blockers such as Clopidogrel or Ticagrelor are indicated in all patients with NSTEMI. Anticoagulants Anticoagulants should be provided to all patients with NSTEMI as it has been shown to generate better patient outcomes. Anticoagulants can include a Heparin Infusion or S/C Enoxaparin.

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Beta blocker therapy to prevent recurrent ischemia and life-threatening ventricular arrhythmias.

All patients with unstable angina should be started on Beta Blockers within 24 hours.

Management of Acute ST Elevation Myocardial Infarction: Management of a STEMI patient involves the aforementioned goals for NSTEMI as well as the following goals for treatment.

•

Initiation of reperfusion therapy with primary percutaneous coronary intervention (PCI) or fibrinolysis

•

PCI has demonstrated enhanced survival and a lower rate of intracranial hemorrhage and recurrent MI compared to fibrinolysis. However if the patient is unable to undergo a PCI within 120 minutes then fibrinolysis should be considered.

•

If PCI or fibrinolysis has been unsuccessful then CABG should be considered

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Multiple Choice Questions 1) Identify the rhythm

A) Atrial flutter B) Atrial fibrillation C) Supraventricular tachycardia D) Sinus Rhythm

2) Leads V1 and V2 represent which surface of the heart: A) The Anterior surface B) The Septum C) The Inferior surface D) The Lateral Surface

3) Leads V5, V6. I and aVF represent which surface of the heart: A) The Anterior surface B) The Septum C) The Inferior surface D) The Lateral Surface

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4) What surfaces of the heart is infarction occurring in this ECG?

A)

The Anterior surface

B)

The Septum

C)

The Lateral surface

D)

All of the above

5) In the above ECG, which surface of the heart is reciprocal ischaemia occurring?

A)

The Anterior surface

B)

The Septum

C)

The Inferior surface

D)

All of the above

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6) In what leads would you look for Right Sided Infarction A)

V7, V8, V9

B)

V4R

C)

V3, V4

D)

II, III, AVF

7) ST elevation of more than 1mm in a chest lead represents myocardial infarction A) True B) False

8) GTN can be administered to patients who are having a right sided infarct A) True B) False

9) Oxygen should be avoided in all patients experiencing cardiac chest pain unless their oxygen saturations are less than <90% A) True B) False

10) The Inferior surface of the heart is supplied by the Left Anterior descending artery A) True B) False

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11) Identify the rhythm

A)

Atrial flutter

B)

Atrial fibrillation

C)

Ventricular tachycardia

D)

Ventricular fibrillation

12) Identify the rhythm

A)

Atrial flutter

B)

Atrial fibrillation

C)

Sinus Rhythm

D)

Ventricular fibrillation

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13) What kind of STEMI is occurring in the below ECG?

A)

Inferior infarct

B)

Anterior Infarct

C)

Lateral Infarct

D)

Posterior Infarct

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14) Which type of STEMI is occurring in the below ECG?

A)

Inferior infarct with right sided involvement

B)

Anterior Infarct

C)

Inferior, Lateral Infarct with posterior involvement

D)

Posterior Infarct

15) When there is evidence of inferior ST elevation Right sided and posterior lead ECGâ&#x20AC;&#x2122;s should always be taken.

A) True B) False

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Reference: 1. Thompson P.L. Coronary Care Manual. Chatswood, NSW: Elsevier; 2011 2. Moser DK & Riegel B. Cardiac Nursing a Companion to Braunwald's Heart Disease.

St. Louis, Missouri: Saunders Elsevier; 2008.

3. Woods S, et al, editors. Cardiac Nursing. 6th ed. Philadelphia: Wolters Kluwer/ Lippincott Williams & Wilkins; 2010 4. Urden L, Stacy K, Lough M. Thelan's Critical Care Nursing: diagnosis and management. 6th ed. St Louis, Massachusetts: Elsevier; 2010.

5. Garcia T.B. 12-Lead ECG: The Art of Interpretation. 2nd ed.2013 6. Hampton J.R., The ECG Made Easy 8th ed., Churchhill Livingstone, Elsevier 2013.

7. Balady.G. J.,Bufalino. V.J., Gulati.M.,et.al,(2016).COCATS 4 Task Force 3: Training in Electrocardiography, Ambulatory Electrocardiography, and Exercise Testing.,Journal of the American College of Cardiology.,65(17).

8. Hollander, J.E & Chase M. (2012). Evaluation of chest pain in the emergency department. Up to Date. Literature review current through: Dec 2012. | This topic last updated: Apr 3, 2012.

9. Miller C & Granger C.B (2012). Evaluation of patients with chest pain at low or intermediate risk for acute coronary syndrome. Up to Date. Literature review current through: Dec 2012. | This topic last updated: Jul 17, 2012.

10. Reeder G.S. & Kennedy H.L (2012). Criteria for the diagnosis of acute myocardial infarction. Up to Date. Literature review current through: Dec 2012. | This topic last updated: Dec 12, 2012.

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