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Damian Crump 2007.

Contents Arrhythmia Map ECG Component – normal range Sinus Node Arrhythmias

1 2 Sinus Rhythm. Sinus Bradycardia. Sinus Tachycardia. Sinus Arrhythmia. Sinus Arrest / Sinoatrial Exit Block. Sick Sinus Syndrome.

8 8 8 8 8 9

Atrial Arrhythmias

Premature Atrial Contractions (PAC). Atrial Flutter (& AF with AV Dissociation). Atrial Fibrillation. Atrial Flutter / Fibrillation. SVT / Paroxysmal Atrial Tachycardia. Differentiating SVT & Sinus Tach. Hypertensive SVT. Wide Complex Tachycardia. Wondering Atrial Pace Maker. Wolff Parkinson White syndrome. Atrial Fibrillation with underlying WPW.

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Junctional Arrhythmias

Premature Junctional Contractions (PJC). Junctional Escape Rhythm. Junctional Rhythm with AV Dissociation. Junctional Bi / Tri / Quadrigeminy. Accelerated Junctional Rhythm. Junctional Tachycardia.

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Premature Ventricular Contractions (PVC). Couplet / Triplet PVC‟s. Unsustained Ventricular Tachycardia. Sustained Ventricular Tachycardia. Ventricular Bi / Tri / Quadrigeminy. R on T Phenomenon. Idioventricular Rhythm / Agonal rhythm. Accelerated Idioventricular Rhythm (With sufficient / insufficient output). Ventricular Arrhythmia with AV Dissociation. Ventricular Tachycardia. Torsade De Pointes. Ventricular Fibrillation. Asystole.

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1st 0 AV Node Block. 2nd 0 AV Node Block Type I (Wenckebach). AV Node Block Ratio Definition. 2nd 0 AV Node Block Type II.

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Ventricular Arrhythmias

AV Node Blocks

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Differentiating Type I & Type II. AV Node Block Ratio List. 2nd 0 AV Node Block I & II Ratio 2:1 & Higher. 3rd 0 AV Node Block.

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AMI Phases. Abnormal T Waves (peaked / inverted T waves). ST Depression. ST Elevation. Pathological Q Waves (QR / QS Waves). Aspects of the Heart – Contiguous Leads. Aspects of the Heart - Ischaemia Diagrams. Aspects of the Heart - Table for diagnosis. Coronary Arteries involved in Specific AMI‟s.

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P Pulmonale. P Mitrale. Pericarditis. Hyperkalaemia. Hypokalaemia. Digoxin Toxicity. Cor Pulmonale. Pulmonary Embolism. EMD / Pseudo EMD. EMD (common rhythms involved). EMD Causes. Tricyclic Antidepressant Overdose Hypothermia

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Rhythm Analysis

7 Steps to Determine Arrhythmia. Various Arrhythmia Rates. Determine if Rhythm is Essentially Regular.

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Understanding ECG Leads

Standard, Augmented, V leads.

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Mechanisms of the Ectopic Pacemaker Sites

Enhanced Automaticity. Re-entry. Inherit Pacemaker Rates (SA, AV, BB, PN). Sympathetic / Parasympathetic Innovation.

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Ischaemic ECG Changes

Miscellaneous ECG Changes

Paced Rhythm Arrhythmia Aetiology

Nervous control of the Heart

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ARRHYTHMIA MAP Sinus node arrhythmias

1 2 3 4 5

1. Sinus bradycardia. 2. Sinus rhythm. 3. Sinus tachycardia. 4. Sinus arrhythmia. 5. Sinus arrest & sinoatrial exit block.

Atrial arrhythmias

6 7 8 9 10 11

1. Premature atrial contractions. 2. Wondering atrial pace maker. 3. SVT / atrial tachycardia. 4. Wide complex tachycardia. 5. Atrial flutter. 6. Atrial fibrillation.

Junctional arrhythmias

12 13 14 15

1. Premature junctional contractions. 2. Junctional escape rhythm. 3. Accelerated junctional rhythm. 4. Junctional tachycardia.

Ventricular arrhythmias

16 17 18 19 20 21

1. Premature ventricular contractions. 2. Idioventricular rhythm. 3. Accelerated idioventricular rhythm. 4. Ventricular tachycardia. 5. Ventricular fibrillation. 6. Asystole.

AV node blocks

22 23 24 25 26

1. First degree AV node block. 2. Second degree AV node block Type I (W). 3. Second degree AV node block Type II. 4. 2:1 & Higher AV node block (advanced block). 5. Third degree AV node block.

Paced rhythm

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Ischaemic changes

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1. T wave changes. 2. ST segment changes. 3. Pathological Q waves.

Miscellaneous ECG changes

31 32 33 34 35 36 37 38 39

1. P pulmonale. 2. P mitrale. 3. Pericarditis. 4. Hyperkalaemia. 5. Hypokalaemia. 6. Digoxin toxicity. 7. Cor pulmonale 8. Pulmonary embolism. 9. TCA overdose.

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ECG Components Normal Ranges

ECG Paper

P Waves A Normal P wave indicates that the electrical impulse was generated by the SA Node and the left and right atria have depolarized. An abnormal P wave indicates a conduction problem.

The onset of the P Wave is identified as the first positive deviation from the baseline. The end is identified when the P wave becomes isoelectric again.

P Wave Duration is half of the R-R Interval. This measurement is taken in the lead where the T waves are most prominent.

Corrected QT Interval (QTc). This is an average expected QT interval based on heart rate. The faster the HR, the shorter the QTc. The slower the HR, the Longer the QTc. (Huszar 2002, pp. 79-81).

Damian Crump 2007.

R-R Interval The time between two successive Ventricular depolarisations. Duration - The time measures from one R wave to the next. This is HR dependant, may be regular or irregular depending on underlying rhythm.

ST Segment

This is the earliest stage of ventricular repolarisation. A normal ST segment and T wave indicate normal repolarisation of the ventricles.

Onset - The end of the QRS complex or J Point. End - The onset of the T wave.

Duration < 0.20 seconds (1 large square). The ST Segment is heart rate dependant. The faster the HR, the shorter the Segment The slower the HR, the longer the Segment.

(Huszar 2002, pp. 83-85). 6

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PR Segment

A normal PR segment indicates that the impulse has traveled through the AV Junction and Bundle Branches without delay. A long PR segment indicates a conduction defect.

Onset - The end of the P wave. End - The onset of the QRS complex.

Duration - 0.02 - 0.10 seconds. (0.5 - 2.5 small squares)

TP Segment The interval between two successive PQRST cycles, in which electrical activity is absent. The TP Segment is the isoelectric line, used to determine ST elevation or depression. Onset & End - The end of the T wave, to the start of the P wave. (Huszar 2002, pp. 91-93).

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SINUS NODE ARRHYTHMIAS 1. Sinus Rhythm 60 – 100 b/m. 2. Sinus Bradycardia    

< 60 b/m. Presentation – dizziness, chest pain, dyspnoea, hypotension, ↓ GCS. May occur during AMI (especially inferior) as a protective mechanism, only treat if symptomatic. Bradyarrhythmia / Bizarre Arrhythmia Protocol – Atropine, Adrenaline, Fluid, Elevate legs. May require CPR with no output/EMD.

3. Sinus Tachycardia    

>100 b/m. Dizziness, chest pain, dyspnoea, hypotension, ↓ GCS. Valsalva manoeuvre. 1-2 sprays of GTN only (if rate related chest pain).

4. Sinus Arrhythmia    

Looks like irregular Sinus Rhythm. Cyclic ↑ and ↓ in SA Node rate (very difficult to see on a strip). Due to ↑ and ↓ in vagal tone on respiration. Normal phenomenon in kids, adolescents and the elderly. Can occur in heart disease, AMI and Digoxin toxicity – nil Rx.

5. Sinus Arrest / Sinoatrial Exit Block Sinus Arrest – Episodes of SA Node failure resulting in Asystole or Bradycardia of AV or Ventricular origin (the lower heart takes over when the SA Node fails). Sinoatrial Exit Block – Blocked conduction of impulses from the SA Node to the atria, resulting in Asystole or Bradycardia, as in Sinus Arrest.

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   

Very difficult to distinguish between the two. Not a problem if AV Node takes over. Treat under Brady Arrhythmia Protocol if symptomatic. Syncope may occur during sustained periods of Asystole – intermittent CPR.

(Huszar 2002, pp. 121-130).

Sinoatrial Exit Block

(Huszar 2002, pp. 125-129). 6. Sick Sinus Syndrome Sick sinus syndrome (SSS) is an umbrella term for a group of arrhythmias caused by a damaged SA node. It is more common in elderly patients and may be caused by degeneration or scarring to the conduction system, cardiomyopathy, atrial surgery and coronary artery disease. Post surgical causes are more likely in children. The arrhythmias this syndrome may manifest are primarily bradycardias and tachycardias of atrial origin. Bradycardias include sinus arrest, sinoatrial exit block and sinus bradycardia. Tachyarrhythmias include paroxysmal surpraventricular tachycardia and atrial fibrillation. Tachycardias that occur with SSS are characterised by a long period of asystole after the tachycardia. Bradycardia-tachycardia syndrome is a variant of SSS where atrial flutter and fibrillation alternate with sustained periods of asystole.

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Tachyarrhythmias are well controlled with medication, yet these meds may exacerbate associated bradyarrhythmias. A pacemaker may be implanted before medication to treat tachyarrhythmias is commenced (Adan & Crown 2003 pp. 1725-32).

ATRIAL ARRYTHMIAS 1. PAC‟s      

P waves ↑ if origin in top of atria, ↓ when occurring low in atria. Origin is elsewhere in the atria, other than the SA node. May be uni/multifocal. No problem when occurring in healthy people. In Heart Disease – may warn of re-entry development/more serious atrial tachyarrhythmias. If occurring frequently (every 2-3 sinus beats), check conduction ratio (pulse rate Vs. Monitored rate).

2. Atrial Flutter aF        

This is a Tachyarrhythmia (Palpitations, dizziness, SOB, chest pain). Atrial rate 240 – 360 b/m (mean 300 b/m). F waves (inverted ↓). Best seen in II, III, aVF. Essentially regular ventricular response (unlike af). Ventricular rate is usually 150 b/m,(due to a 2:1 AV node physiological block). This rate creates a clinical presentation much like SVT (dyspnoea, chest pain, hypotension, altered cons state). Loss of atrial kick → ↓ CO. Due to an atrial ectopic focus or re-entry circuit, commonly initiated by a PAC. Expressed as a ratio i.e 4:1 3:1 2:1.

Atrial Flutter with a Variable Block: Rhythm is still essentially regular, but the block ratio alternates (can be grossly irregular if the block ratio is all over the place). aF with dissociation may occur in rare circumstances when aF occurs with a 3rd 0 AV Block. i.e no constant ration can be determined.    

Rx same as for af (Cardioversion / Digoxin). Ablation of re-entry circuit is required. Adenosine will slow rhythm only, if it does revert, it will be short lived. Ventricular rate can be slowed with Verapamil.



Atrial Flutter / Fibrillation: intermittent af / aF.

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Atrial Flutter

5:1

5:1

2:1

3:1

3:1

3. Atrial Fibrillation af    

350 – 600 b/m (atrial rate). Origin – multiple atrial ectopic sites. Rapid, fine, inverted F waves with an irregular ventricular response. Absence of P waves.

     

Rapid (uncontrolled) af: ventricular response >100 b/m. Slow af: ventricular response 200 b/m = 2:1 conduction ration with a physiological AV block. (This block will not be seen on the ECG, as P waves are buried in the rate). (Huszar 2002, pp. 133-150).

    

Origin – ectopic atrial / AV node site or re-entry circuit, usually initiated by a PAC. Not from the SA node, this is an ectopic atrial focus or re-entry circuit (usually located in top end of the AV node). Palpitations, dizziness, syncope, dyspnoea, chest pain, anxiety, confusion. ↓EDV / ↓ ejection fraction → ↓CO. Progression to a ventricular arrhythmia is possible, yet rare. Adenosine (ensure rhythm is regular & not af) (huszar 2002 pp. 140-143).

Differentiating SVT & Sinus tachycardia. Look at the rate – Sinus tachycardia: 100-150b/m with fluctuating HR ↓↑. SVT: >150b/m constant unfluctuating rate due to re-entry. Work out maximal HR (220 – age). ST= < MHR

SVT= >MHR.

Slow ECG record speed from 25mm/sec to 50mm/sec to identify P waves. Valsalva can slow rate to look for P waves. In hospital, Adenosine is used diagnostically to slow the rate to identify P waves & regularity/irregularity to differentiate SVT, ST, Rapid af, aF. PSVT occurs spontaneously with no other aetiology. A Sinus tachycardia is likely to have some other underlying pathology creating the ↑ physiological response.

SVT / Paroxysmal Atrial tachycardia

SVT with 2:1 physiological AV Block

Wide Complex Tachycardia

Damian Crump 2007.

(Huszar 2002, pp. 135-141). Hypertensive SVT case study: 80 y/o presenting with BP 220/110, dyspnoea +++, SVT 165 b/m, mild/subclinical APO. Is this: - APO with a simple sinus tachycardia. - APO → hypoxia → re-entry → SVT. - SVT → pulmonary hypertension → APO. In the elderly, due to atherosclerosis (uncompliant vessels), SVT can present with hypertension and side effects of this such as APO. This is not a straight forward „hypotensive SVT‟ & Adenosine is not the first line treatment. Begin by dropping BP (Rx APO) & administering Bronchodilators (Gerimix). If this is APO with a Sinus tachycardia, the rate should drop/alter as the BP decreases (SVT will have a constant rate, regardless of BP). There is no problem giving GTN as this is not a hypotensive SVT – no chance of knocking off preload. Apply O2, ↓hypoxia may resolve SVT/re-entry. Bronchodilators will not aggravate rate as 165 is most likely a maximal heart rate anyhow. Don‟t assume this is a rate related problem, especially in the elderly with other chronic disease processes. If BP drops and rate persists with dyspnoea ? Adenosine under consult. Always consult for Adenosine in these more complex cases. 5. Wide Complex Tachycardia         

SVT with aberrancy (2.5 – 3 small squares). If symptomatic Rx as VT. Wide complex Af with aberrancy is a possibility (may look regular due to rapid rate). Valsalva may slow rate to identify irregularity. Conscious VT Protocol – Lignocaine, Midazolam, Cardioversion. Lignocaine / Amiodarone won‟t hurt SVT. Adenosine won‟t fix, but won‟t hurt af, aF, VT. If Adenosine is given to af, it may mimic a 3rd 0 block, yet will be short acting. Adenosine is used in hospital to slow rate to differentiate between SVT/VT or uncontrolled af/VT (to look for P waves and regularity). Electricity is the best Rx (Syncronised Cardioversion).

6. Wandering Atrial Pacemaker  

Pace maker moves between SA and AV Nodes, producing varied shaped P waves or ↑ ↓ P waves. Multiple atrial pace makers may or may not involve the SA / AV nodes.

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    

Often irregularly irregular rhythm due to varying P-R Intervals (If the atrial pacemaker varies, it will take varying amounts of time for each impulse to reach the AV node to create a ventricular response. If WAP rate > 100 b/m = Multifocal Atrial Tachycardia (presents as Rapid af). Don‟t confuse with Sinus Rhythm with PAC‟s, there is no primary pace maker. Found in young people and athletes. Due to blocked vagal innovation to SA node during inhalation. Normal phenomenon – No Rx. (Huszar 2002, pp. 134-143).

Wondering Atrial Pacemaker

7. Wolff Parkinson White Syndrome WPW is a pre-excitation syndrome. It is caused by an abnormal congenital accessory pathway between the atria and ventricles. During sinus rhythm, the impulse from the SA node is transferred normally through the AV node at a slow rate, but is also conducted through the accessory pathway rapidly, with no pause (usually created by the AV node). This means part of the ventricles depolarise early, before the normal impulse is conducted through the AV node. This creates a Delta wave (ventricular pre-excitation). A tachyarrhythmia can be established via a circus movement tachycardia. The normal impulse is generated by the SA node, travels down the AV node, to the ventricles (antegrade conduction) and back up to the atria, via the accessory pathway (Retrograde conduction), then back down the normal pathway round and round creating a tachyarrhythmia (Obel & Camm 1999, p. 199).

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The circus movement is travelling Anticlockwise.

www.mayoclinic.org

WPW occurs in 0.2% of the population, 70% of these are men. Only a fraction of these people will develop a tachyarrhythmia. The patient will present with symptoms of SVT (hypotension, APO, Acute heart failure, dyspnoea, ↓ GCS, or VT cardiac arrest). The diagnosis of WPW is not usually made until the tachycardia is resolved. During the tachyarrhythmia, standard differential diagnosis should include SVT, aF, af, or VT (depending on presentation of wide or narrow/ regular or irregular tachycardia). A diagnosis of WPW can sometimes be made (during the tachycardia) when a Delta wave exists with paroxysmal tachycardia (this is unlikely) (Hemingway 2006). During Sinus rhythm, the following criteria apply to WPW.    

Short P-R Interval < 0.12 sec (3 small squares). A slurred up stroke in the QRS „Delta wave‟ in several leads (best seen in V4). The QRS is wide, due to the delta wave. Normal S wave (Obel & Camm 1999).

Exaggerated Delta wave with a short P-R interval.

This Delta wave / short P-R is magnified from the ECG below.

Wide QRS. (Lead I circled). Normal S wave.

www.rnceus.com

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Google images.

Contrasting conduction and ECG morphology between Sinus rhythm and WPW.

www.amc.edu

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www.cardiologiapertutti.org

Treatment Options: Narrow complex tachycardia → Adenosine / Cardioversion if syncopal. Wide Complex Tachycardia → VT until proven otherwise. Adenosine will terminate WPW tachycardia if the rhythm is regular (narrow complex or wide complex SVT with aberrancy).

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Another example of Delta waves & short P-R Google images.

WPW and Atrial fibrillation: af can occur in some patients with underlying WPW. This is a serious arrhythmia as VT/VF can result. As discussed above, the circus arrhythmia travels anticlockwise. When af occurs with underlying WPW, the circus movement tachyarrhythmia now moves clockwise (Vinolas, Rodriguez & Bayes de Luna 1999, p.203). Numerous Af atrial ectopic sites. Atrial rate 400/m.

Fast

Slow pathway. (normal conduction through AV node with a

Irregular Tachycardia

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The SA node is not the primary pace maker in af, there are numerous atrial ectopic foci. This means the rapid impulses generated in the atria travel freely and rapidly down the accessory WPW pathway, and create a 1:1 transmission. The af impulses also travel through the AV node, but due to the pause in transmission of the AV node, the ratio is much slower than 1:1. (normal af ratio without WPW is 3:1 due to physiological AV node pause). When the 1:1 ratio is established, the ventric...