Andrew Petrosoniak, MD PGY2 Emergency Medicine University of Toronto Canada  Tachyarrhythmias & Cardioversion
Objectives <ul><li>(Very) Briefly review pathophysiology of arrhythymias (4 slides!) </li></ul><ul><li>Cardioversion </li>...
Cardiac conduction system
Action Potentials
Tachyarrhythmias: mechanisms <ul><li>Automaticity </li></ul><ul><ul><li>Increase/decrease rate of spontaneous depolarizati...
Re-entry mechanism <ul><li>Necessary Conditions </li></ul><ul><li>Two paths </li></ul><ul><li>One path must be slower </li...
Now, the patient! <ul><li>IV, oxygen, monitor & defibrillator to bedside </li></ul><ul><li>Rhythm strip  </li></ul><ul><li...
Questions to ask when analyzing an ECG   <ul><li>Is the patient stable or unstable? </li></ul><ul><li>Is the QRS narrow or...
Questions to ask when analyzing an ECG   <ul><li>Is the patient stable or unstable? </li></ul><ul><li>Is the QRS narrow or...
<ul><li>Hypotension </li></ul><ul><li>Chest pain (suggestive of ischemia) </li></ul><ul><li>Shortness of breath </li></ul>...
UNSTABLE = SYNCHRONIZED CARDIOVERSION
Electrical Cardioversion  <ul><li>Electrical shock to heart ( synchronized  to QRS complex) </li></ul><ul><li>Cardiac cell...
Electrical Cardioversion <ul><li>Synchronization = Prevent R on T phenomenon </li></ul><ul><li>Press “Sync” on the machine...
<ul><li>Insufficient evidence to suggest either position is superior for effective cardioversion (AP vs. AL)  Emerg Med J ...
Narrow Complex QRS  Wide Complex QRS Irregular Regular Regular  Polymorphic VT (Am J Emerg Med 2010;28:159-165, AHA 2010 g...
Recap <ul><li>Re-entry mechanism: most common tachydysrhythmia </li></ul><ul><li>Every ECG = 4 Questions  </li></ul><ul><l...
Questions to ask when analyzing an ECG   <ul><li>Is the patient stable or unstable? </li></ul><ul><li>Is the QRS narrow or...
Narrow Complex Tachycardia Hemodynamically Unstable Hemodynamically Stable Irregular Regular Synchronized cardioversion Ap...
Narrow complex tachycardias REGULAR  IRREGULAR  <ul><li>Sinus Tachycardia </li></ul><ul><li>Paroxysmal supraventricular ta...
<ul><li>Case: 24 year old, healthy male  </li></ul><ul><li>Chief complaint: 1 hour of palpitations  </li></ul><ul><li>No c...
Narrow complex tachycardias REGULAR  <ul><li>Sinus Tachycardia  </li></ul><ul><li>Paroxysmal supraventricular tachycardia ...
Case: 24 year old, healthy male  Palpitations, stable hemodynamically ECG: regular, narrow complex tachycardia  What are t...
Regular narrow complex tachycardia Modified from Neumar et al. Circulation 2010; 122;S729-S767
<ul><li>Case: 24 year old, healthy male  </li></ul><ul><li>ECG: regular, narrow complex tachycardia </li></ul><ul><li>Mana...
62 M with palpitations and dyspnea PMHx: CHF, HTN
Narrow complex tachycardias REGULAR  <ul><li>Sinus Tachycardia  </li></ul><ul><li>Paroxysmal supraventricular tachycardia ...
Atrial Flutter: Management <ul><li>ACLS: classify unstable vs. stable </li></ul><ul><ul><li>Stable: rate control and only ...
<ul><li>Management </li></ul><ul><li>Further history: 7 days of palpitations </li></ul><ul><li>In ED, BP 130/65 P 150 98%1...
Case: 68 yr old female 1 day of palpitations, slight chest discomfort  PMHx: NSTEMI 10 yrs ago, high cholesterol, hyperten...
Narrow complex tachycardias IRREGULAR  <ul><li>Atrial fibrillation </li></ul><ul><li>Atrial flutter with variable block </...
Questions to ask when analyzing an ECG   <ul><li>Is the patient stable or unstable? </li></ul><ul><ul><li>Hypotension </li...
Management of Atrial Fibrillation in the ED <ul><li>Lack of strong evidence to guide ED management </li></ul><ul><li>Decis...
New Onset Atrial Fibrillation Hemodynamically Unstable Hemodynamically Stable Rate Control IV metoprolol or diltiazem > 48...
Rate control <ul><li>No accessory pathway </li></ul><ul><li>Diltiazem IV 0.25mg/kg over 2min  (Class I) </li></ul><ul><li>...
Rhythm control: Stable patients <ul><li>Consider cardioversion especially if younger, without hypertension or heart diseas...
BACK TO THE CASE  Case: 68 yr old female 1 day of palpitations, slight chest discomfort  Vitals: 150-170bpm, BP 108/45, 95...
Recap Narrow complex tachycardias <ul><li>Unstable vs. stable </li></ul><ul><li>Synchronized cardioversion if unstable </l...
Wide complex tachycardias
Approach to wide complex tachycardias Wide Complex Tachycardia Hemodynamically Unstable Hemodynamically Stable Irregular R...
<ul><li>Hypotension </li></ul><ul><li>Chest pain (suggestive of ischemia) </li></ul><ul><li>Shortness of breath </li></ul>...
Wide Complex Tachycardias Differential Diagnosis  Regular <ul><li>Monomorphic VT </li></ul><ul><li>SVT with aberrancy (BBB...
Wide Complex Tachycardias Ventricular Tachycardia vs. SVT
Wide Complex Tachycardias Regular wide complex tachycardia is ventricular tachycardia until proven otherwise
Wide Complex Tachycardias Management: Stable, regular WCT <ul><li>Consider adenosine ONLY if regular WCT </li></ul><ul><li...
Case 1: 33 M severe palpitations; healthy; BP 145/85 Case 2: 75 F chest pain; PMHx MI; BP 109/75
<ul><li>Impression: most likely SVT w/ aberrancy  </li></ul><ul><li>Management  </li></ul><ul><li>Consider Adenosine – ens...
FUSION BEAT CAPTURE BEATS Wide Complex Tachycardias ECG Findings Suggestive of VT AV DISSOCIATION
Wide Complex Tachycardias Accessory Pathways Orthodromic/Anterograde QRS typically normal More common Antidromic/Retrograd...
<ul><li>Why do accessory pathways matter? </li></ul>Wide Complex Tachycardias Accessory Pathways Wide complex, irregular t...
Wide Complex Tachycardias Accessory Pathways
Wide Complex Tachycardias Accessory Pathways <ul><li>When to suspect accessory pathway? </li></ul><ul><li>Rapid ventricula...
Recap Wide complex tachycardias <ul><li>Unstable vs. stable </li></ul><ul><li>Synchronized cardioversion if unstable </li>...
Objectives: recap <ul><li>(Very) Briefly review pathophysiology of arrhythymias (4 slides!) </li></ul><ul><li>Cardioversio...
References <ul><li>Rosen’s Emergency Medicine (7 th  edition) </li></ul><ul><li>Lilly LS. Pathophysiology of heart disease...
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Emergency lectures - Arrhythmias & cardioversion andrew petrosoniak

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  • Very nice summary of etiology, diagnosis and management of SVT!
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  • Impulse in sinus node travels down atrium to AV node Atrial depolarization = p wave on ECG AV node connects atrium &amp; ventricle AV node acts to slow fast atrial rates (PR interval = conduction traveling in AV node) Impulse then travels down Lt &amp; Rt bundle branches (QRS interval) After complete depolarization &amp; contraction, repolarization of ventricles occurs (manifests as T wave)
  • Important to understand which electrolytes/channels are involved in cardiac impulse conduction to understand how drugs will work Primary Pacemaker Cells No resting potential Generate regular, spontaneous action potentials Governed by slow Ca currents No fast Na channels (different from non-pacemaker cells) Phase 0 = Calcium enters cell to cause further depolarization Non-pacemaker cells Faster depolarization than pacemaker cells Involve fast Na channels At baseline (phase 4), outward going K keeps intracellular membrane potential very negative Then an AP from adjacent cell causes rapid depolarization at a threshold -70mV causing fast Na channels to open
  • Automaticity: if enhanced automaticity affects sinus node, then sinus tach occurs If pacemaker is another site, then other arrhythmias develop Examples include atrial tachycardia with digitalis toxicity (increases phase 4 depolarization in other myocardial cells while decreasing SA node impulse conduction) Re-entry Triggered Less common: problem at ion channel level that result in abnormal propagation of electrical activity that can lead to sustained rhythm (ectopic atrial rhythms or junctional rhythms) Result from after-depolarizations and dependent on heart rate for propagation
  • 3 Criteria are necessary for re-entry Two paths (or a circuit) Each path must have unequal responsiveness One path must be slower Re-entry can occur within a small local region of the heart or globally (atria/ventricles) For example, in normal tissue, a purkinje fiber could form two branches which could be a site for re-entry AV nodal reentry tachycardia (which occurs within the AV node): some people have different conduction velocities &amp; refractory periord within these AV node pathways which can lead to AV nodal re-entry = paroxysmal supraventricular tachycardia Impulses travel from atria to ventricles then back to atria through AV node; atrial rate is stimulated by reentrant impulses so there remains 1:1 atrial/ventricular rates AV reentry tachycardia:
  • These questions should be asked relatively in the above order Assessment of patient stability is paramount
  • These questions should be asked relatively in the above order Assessment of patient stability is paramount
  • Any of the above 4 findings make a patient unstable But remember, especially with subjective findings such as chest pain or shortness of breath, there’s a continuum from stable to unstable Importantly, chest pain that doesn’t sound ischemic (e.g. in a 22 year old with chest discomfort in a narrow complex rhythm) may not require as emergent management as a 65 yr male with wide complex tachycardia, crushing/retrosternal chest pain Also, assess whether the shortness of breath is likely from pulmonary edema – as this a significant finding
  • Typically when we discuss cardioversion (electrical) it refers to “synchronized” where the electrical impulse from the machine is timed to the patient’s QRS complex. This is NOT something to be used if the patient doesn’t have a pulse If impulse is coming from SA node(sinus tachycardia) or increased automaticity like (MAT, junctional tachycardia) then cardioversion is not effective
  • R on T phenomenon: premature depolarization of the heart from electrical stimulus (in this case the defibrillation machine) which occurs prior to cells being full repolarized. Essentially, the QRS is stimulated to occur somewhere during the T wave and this often leads to ventricular fibrillation or ventricular tachycardia Machines vary, some automatically revert back to unsynchronized after a shock is given, while other models remain in “sync” mode – be aware which
  • Small, heterogenous studies performed in non-emergent settings examined pad placement. Also, all studies that I was able to find examined patients in atrial fibrillation Largest study, n=301 (Botto et al. Heart 1999) showed that AP was superior to AL – should be noted that 3-4J/kg were used (relatively high J) but these were in non-emergent patients Most recently, Kirchhof et al.(Lancet 2002) n=108, using monophasic cardioversion in atrial fibrillation pts, starting at 50J upto 360J showed that AP was superior to AL (96% vs. 78% of pts); when cardioversion was successful in either group, there was no difference between mean energy required (about 210J)
  • Of note, not included in the slide is specifically regarding wide complex A. Fib. This should be converted with synchronized cardioversion at probably 150J
  • These questions should be asked relatively in the above order Assessment of patient stability is paramount
  • Emphasize that PSVT is also considered AV nodal re-entry tachycardia (AVNRT) and can include AVRT (AV re-entry tachycardia)
  • Let’s start with a case. ECG: 180bpm narrow complex tachycardia What could this be? Regular, narrow complex (no visible P waves): A. flutter, PSVT Regardless, ACLS does present us with an approach to the narrow complex tachycardia
  • Based on the previous ECG – here’s a differential diagnosis
  • It is important to differentiate the various forms of re-entrant SVT (supraventricular tachycardias) Two types: based entirely in atrial myocardium (A. Fib) vs. AV node involvement Arrhythmias whereby the AV node is part of the circuit (either partially or fully) respond well to AV nodal blocking agents and often arrhythmias are terminated with these medications Vagal Maneuvers: Successful 25% of cases Adenosine Give in large IV, ideally in antecubital vein, rapid push then flush with 20ml NS Always have defibrillator in place or nearby in case patient has A. Fib w/ WPW then triggering rapid ventricular rates Will not work in Atrial flutter but it might slow ventricular rate enough to observe flutter waves CCB Terminate reentry PSVTs that depend on conduction through the AV node Studies have shown efficacy with both diltiazem and verapamil (ACLS 2010 guidelines)
  • What is happening right now on the ECG? Would you be concerned if you had just given adenosine? Discuss what to expect after adenosine! Demonstration post administration of adenosine during PSVT and the potential prolonged pause
  • Go through the sequence again: stable vs. unstable Narrow vs. Wide Regular or Irregular P waves? Dx: Atrial flutter with 2:1 and occasionally 3:1 block – atrial flutter can either be regular or irregular Pathophysiology: Reentrant circuit within the Right Atrium
  • Based on the previous ECG – here’s a differential diagnosis
  • Remember, its rare for patient to remain in chronic atrial flutter In the ED, diltiazem is favored for rate control though little evidence to support it over metoprolol; however, metoprolol is favored by cardiologists Amiodarone may convert patient thus only use if &lt;48hrs Recent Canadian study (Scheuremeyer et al. Ann Emerg 2011) included 122 patients retrospectively and studied management and 1yr outcomes after atrial flutter presentation to the ED; within the electrical cardioversion group 91% converted while only 27% converted chemically – obviously limitations since retrospective but does suggest further investigations are required and that its not unreasonable to begin with electrical cardioversion even if stable No pts in the study developed stroke
  • ECG: Atrial fibrillation with moderate-rapid ventricular response; several aberrantly conducted beats and possible ST depression in V4-V5 What is the management?
  • Remember, ask these 4 questions This patient’s ECG is irregular narrow complex tachycardia; remember the differential diagnoses for this? (see next slide)
  • Majority of large trials were conducted in among cardiology clinic patients thus applicability of AFFIRM and AF-CHF studies are less relevant to ED management AFFIRM: over 4000 pts who were likely to have A Fib for prolonged period, and either &gt;65yrs or at least 1 risk factor for stroke/death (HTN, DM, CHF, previous stroke…etc); no difference in total mortality but rhythm control was assoc w/ incr risk of hopsitalization, adverse drug effects and VTE Recent Canadian study (Stiell et al. Ann Emerg Med 2011 demonstrates the variation in ED management of atrial fibrillation. Retrospective observational cohort study among 1068 patients who presented with clear hx of onset &lt;48hrs or &lt;7 days if anticoagulated significant variation in practice at Cdn academic EDs 55% of pts received IV rate control (varying from 37-65%) and metoprolol being most commonly used 59.4% of pts underwent cardioversion attempt with chemical cardioversion being used first in 55% of pts but significant variation among hospitals from 31-93% Most common drug used for cardioversion was procainamide followed by amiodarone
  • Suggested guidelines by CHEST Hemodynamically unstable as specified by European Resuscitation Guidelines, UK NICE guidelines &amp; Joint American-AF guidelines agree that instability includes sBP &lt;90mmHg, ventricular rates &gt;150bpm, ongoing chest pain or decreased LOC Consider heparin infusion simultaneous with cardioversion in the unstable patient
  • In patients to receive anti-arrhythmics, remains controversial whether rate control should be instituted beforehand. Cardiologists in Toronto suggest that before procainamide, should administer B-blocker since it may increase tachycardia before conversion
  • If patient becomes hypotensive, develops chest pain or the ventricular rate increases then electrical cardioversion should be initiated Otherwise, take further history to establish duration of symptoms, previous hx of A Fib, hx of cardioversion and hx of stroke Revisit options for cardioversion but highlight that practice is variable and some physicians would rate control only, and establish follow-up
  • Adenosine if flutter may actually enable flutter waves to appear and aid with the diagnosis Highlight drug side effects Amiodarone: Immediate side effects include hypotension, adverse reactions most notably include Torsades (if long QT) in the longer term, risk of pulmonary fibrosis Procainamide: can cause transient increase in heart rate (anti-cholinergic) and some advise pretreatment with AV nodal blocker prior; may act as proarrhythmic, can cause heart block and longer term liver dysfunction
  • Here’s a simplified approach to the WCT. Remember always assess whether the patient is stable or unstable
  • Regardless of the specific rhythm if the patient has a wide QRS and is unstable then electrical cardioversion should be used as suggested by ACLS This slide is just a reminder of what to consider in all patients with arrhythmias!
  • Paced rhythms should also be considered – though usually not tachycardic and a pacer spike usually present Other causes: for example, hyperkalemia or sodium channel blockade can widen QRS so the ECG must be kept in the context of the patient and their history
  • A key issue is the differentiation between VT and SVT w/ aberrancy Several criteria can be used (Wellens, Brugada and Griffith) however they are not intuitive and difficult to remember In general, the above characteristics can be assess
  • Emphasize that adenosine should NOT be given if at all the patient is unstable, the rhythm is irregular or polymorphic If the rhythm is SVT w/ aberrancy then adenosine, it will slow or convert the rhythm to sinus rhythm; if it’s VT then most likely no effect Also, remember that the guidelines suggest only one attempt with chemical cardioversion before proceeding to electrical cardioversion
  • These cases highlight the differences in regular WCT – most importantly look at the patient, their history and age. Case 1: This patient is much more likley to have SVT w/ aberrancy – in fact, an old ECG shows a RBBB Case 2: This patient shows evidence of AV dissociation since the P waves (red arrows) are at different intervals from the QRS
  • In case 2: suggest to avoid adenosine is based on the likelihood that it is VT rather than SVT w/ aberrancy
  • Fusion Beats: occurs when sinus &amp; ventricular beat occur at same time to produce “hybrid” beat Capture Beat: when SA node transiently captures ventricles during AV dissocation to produce a QRS of normal duration AV dissociation: P waves and QRS complexes occur at completely different rates
  • Of note, it’s possible even when HR &lt;200 so Hallmark Features Short PR: in antidromic accessory pathway, the PR interval is shortened since it doesn’t pass through the AV node Delta Wave: occurs in antidromic conduction and manifests as a slurred upstroke of QRS – since conduction is slightly delayed through the initial pathway 3. Widened QRS: Preexcitation does NOT equal accessory pathway. They are related however, since pre-excitation is ventricular depolarization that occurs earlier than expected if it had been conducted via AV node – usually this implies the existence of an accessory pathway
  • AV nodal blockers do NOT slow conduction through accessory pathways, and sometimes they can actually shorten refractory periods of them. As a result, this may speed up conduction from atrium to ventricles and eventually lead to ventricular fibrillation. This is especially important when the patient has Atrial Fibrillation and an accessory pathway Essentially in AF +WPW, AV blockade will send all atrial impulses, regardless of speed through the accessory pathway resulting in significant ventricular rates which eventually degenerate to V Fib arrest
  • ECG example of atrial fibrillation + WPW Wide complex Fast ventricular rate Upsloping (Delta Waves) Stahmer &amp; Cowan (Emerg Clin N Am 2006): AF + WPW typically varies in width and morphology (compared to polymorphic VT)
  • Regarding management AHA 2005 guidelines suggest amiodarone (the 2010 guidelines simply suggest rhythm control agents without further specifics) Several articles including one cited in the above slide, question the safety of amiodarone and instead advocate for procainamide; the authors cite concern over associated (not necessarily causation) between WPW + AF patients who underwent amiodarone treatment and subsequent development of ventricular fibrillation
  • Emergency lectures - Arrhythmias & cardioversion andrew petrosoniak

    1. 1. Andrew Petrosoniak, MD PGY2 Emergency Medicine University of Toronto Canada Tachyarrhythmias & Cardioversion
    2. 2. Objectives <ul><li>(Very) Briefly review pathophysiology of arrhythymias (4 slides!) </li></ul><ul><li>Cardioversion </li></ul><ul><li>Tachydysrhythmias </li></ul><ul><li>Special case of wide complex tachyardia </li></ul><ul><li>Example ECGs </li></ul>
    3. 3. Cardiac conduction system
    4. 4. Action Potentials
    5. 5. Tachyarrhythmias: mechanisms <ul><li>Automaticity </li></ul><ul><ul><li>Increase/decrease rate of spontaneous depolarization of cells above their threshold </li></ul></ul><ul><li>Re-entry </li></ul><ul><ul><li>Impulse traveling in a circular movement </li></ul></ul><ul><li>Triggered </li></ul>
    6. 6. Re-entry mechanism <ul><li>Necessary Conditions </li></ul><ul><li>Two paths </li></ul><ul><li>One path must be slower </li></ul><ul><li>Critical timing </li></ul>
    7. 7. Now, the patient! <ul><li>IV, oxygen, monitor & defibrillator to bedside </li></ul><ul><li>Rhythm strip </li></ul><ul><li>If possible obtain ECG </li></ul><ul><li>Ask yourself 4 questions every time </li></ul>
    8. 8. Questions to ask when analyzing an ECG <ul><li>Is the patient stable or unstable? </li></ul><ul><li>Is the QRS narrow or wide? </li></ul><ul><li>Is the rate regular or irregular? </li></ul><ul><li>Are P waves visible? </li></ul>
    9. 9. Questions to ask when analyzing an ECG <ul><li>Is the patient stable or unstable? </li></ul><ul><li>Is the QRS narrow or wide? </li></ul><ul><li>Is the rate regular or irregular? </li></ul><ul><li>Are P waves visible? </li></ul>
    10. 10. <ul><li>Hypotension </li></ul><ul><li>Chest pain (suggestive of ischemia) </li></ul><ul><li>Shortness of breath </li></ul><ul><li>Decreased level of consciousness </li></ul>Stable vs. Unstable
    11. 11. UNSTABLE = SYNCHRONIZED CARDIOVERSION
    12. 12. Electrical Cardioversion <ul><li>Electrical shock to heart ( synchronized to QRS complex) </li></ul><ul><li>Cardiac cells depolarize and restarts electrical cardiac activity </li></ul><ul><li>SA node resumes pacemaker activity </li></ul><ul><li>Avoid shock during relative refractory period (may cause VF) </li></ul><ul><li>Effective if etiology of arrhythmia is reentry circuit </li></ul><ul><li>Not effective if impulse originates from SA node </li></ul>
    13. 13. Electrical Cardioversion <ul><li>Synchronization = Prevent R on T phenomenon </li></ul><ul><li>Press “Sync” on the machine </li></ul><ul><li>Be familiar with your machine; do you need to press sync after each shock? </li></ul>
    14. 14. <ul><li>Insufficient evidence to suggest either position is superior for effective cardioversion (AP vs. AL) Emerg Med J 2005 22(1):44-6 </li></ul><ul><li>Reasonable to try alternative position if unsuccessful with initial attempts Interact Cardiovasc Thorac Surg 2004 3:386-89 </li></ul>Electrical Cardioversion FRONT BACK Botto G L et al. Heart 1999;82:726-730
    15. 15. Narrow Complex QRS Wide Complex QRS Irregular Regular Regular Polymorphic VT (Am J Emerg Med 2010;28:159-165, AHA 2010 guidelines) Electrical Cardioversion 100 - 150J 50J 100J 200J **Double energy dose if unsuccessful Unsynchronized
    16. 16. Recap <ul><li>Re-entry mechanism: most common tachydysrhythmia </li></ul><ul><li>Every ECG = 4 Questions </li></ul><ul><li>Unstable = synchronized cardioversion </li></ul><ul><li>Atrial fibrillation requires most energy (>100J) </li></ul>
    17. 17. Questions to ask when analyzing an ECG <ul><li>Is the patient stable or unstable? </li></ul><ul><li>Is the QRS narrow or wide? </li></ul><ul><li>Is the rate regular or irregular? </li></ul><ul><li>Are P waves visible? </li></ul>
    18. 18. Narrow Complex Tachycardia Hemodynamically Unstable Hemodynamically Stable Irregular Regular Synchronized cardioversion Approach to narrow complex tachycardias
    19. 19. Narrow complex tachycardias REGULAR IRREGULAR <ul><li>Sinus Tachycardia </li></ul><ul><li>Paroxysmal supraventricular tachycardia (PSVT) </li></ul><ul><li>Atrial flutter with consistent conduction </li></ul><ul><li>Atrial Fibrillation </li></ul><ul><li>Atrial flutter with variable conduction </li></ul><ul><li>Multifocal atrial tachycardia </li></ul>
    20. 20. <ul><li>Case: 24 year old, healthy male </li></ul><ul><li>Chief complaint: 1 hour of palpitations </li></ul><ul><li>No chest pain or shortness of breath </li></ul><ul><li>HR 180, BP 145/85, RR 18, 98% (room air) </li></ul>
    21. 21. Narrow complex tachycardias REGULAR <ul><li>Sinus Tachycardia </li></ul><ul><li>Paroxysmal supraventricular tachycardia (PSVT) </li></ul><ul><li>Atrial flutter with consistent block </li></ul>
    22. 22. Case: 24 year old, healthy male Palpitations, stable hemodynamically ECG: regular, narrow complex tachycardia What are the management options?
    23. 23. Regular narrow complex tachycardia Modified from Neumar et al. Circulation 2010; 122;S729-S767
    24. 24. <ul><li>Case: 24 year old, healthy male </li></ul><ul><li>ECG: regular, narrow complex tachycardia </li></ul><ul><li>Management is initiated </li></ul><ul><li>What does this rhythm strip demonstrate? </li></ul>
    25. 25. 62 M with palpitations and dyspnea PMHx: CHF, HTN
    26. 26. Narrow complex tachycardias REGULAR <ul><li>Sinus Tachycardia </li></ul><ul><li>Paroxysmal supraventricular tachycardia (PSVT) </li></ul><ul><li>Atrial flutter with consistent block </li></ul>
    27. 27. Atrial Flutter: Management <ul><li>ACLS: classify unstable vs. stable </li></ul><ul><ul><li>Stable: rate control and only consider cardioversion if <48hrs </li></ul></ul><ul><ul><li>Rate control (no CHF): IV metoprolol or IV diltiazem </li></ul></ul><ul><ul><li>Rate control (with CHF): digoxin or amiodarone </li></ul></ul><ul><ul><li>Electrical Cardioversion if unstable </li></ul></ul><ul><li>Electrical cardioversion may be preferred method yet electrical dose is unclear (Ann Emerg Med 2011 Jan 21 Epub ahead of print) </li></ul>
    28. 28. <ul><li>Management </li></ul><ul><li>Further history: 7 days of palpitations </li></ul><ul><li>In ED, BP 130/65 P 150 98%1L NP </li></ul><ul><li>Decision to rate control and arrange follow-up </li></ul>62 M with palpitations and dyspnea PMHx: CHF, HTN
    29. 29. Case: 68 yr old female 1 day of palpitations, slight chest discomfort PMHx: NSTEMI 10 yrs ago, high cholesterol, hypertension Vitals: 150-170bpm, BP 108/45, 95% 1L NP, RR 20
    30. 30. Narrow complex tachycardias IRREGULAR <ul><li>Atrial fibrillation </li></ul><ul><li>Atrial flutter with variable block </li></ul><ul><li>Multi focal atrial tachycardia </li></ul>
    31. 31. Questions to ask when analyzing an ECG <ul><li>Is the patient stable or unstable? </li></ul><ul><ul><li>Hypotension </li></ul></ul><ul><ul><li>Chest pain </li></ul></ul><ul><ul><li>Shortness of breath </li></ul></ul><ul><ul><li>Decreased LOC </li></ul></ul><ul><li>Is the QRS narrow or wide? </li></ul><ul><li>Is the rate regular or irregular? </li></ul><ul><li>Are P waves visible? </li></ul>
    32. 32. Management of Atrial Fibrillation in the ED <ul><li>Lack of strong evidence to guide ED management </li></ul><ul><li>Decision to cardiovert new onset A. Fib, varies significantly between institutions: 42-82% at 8 Canadian EDs (Ann Emerg Med 2011 57(1):13-21) </li></ul><ul><li>AFFIRM & AF-CHF only apply to outpatient population but suggests no difference between rate vs. rhythm control </li></ul><ul><li>Significant controversy exists between rate vs. rhythm control in acute AF </li></ul>
    33. 33. New Onset Atrial Fibrillation Hemodynamically Unstable Hemodynamically Stable Rate Control IV metoprolol or diltiazem > 48hrs <48hrs Anti-arrhythmics +/- electric cardioversion TEE or 3wks anti-coagulation then cardioversion Chest 2009; 135:849-859 Synchronized cardioversion
    34. 34. Rate control <ul><li>No accessory pathway </li></ul><ul><li>Diltiazem IV 0.25mg/kg over 2min (Class I) </li></ul><ul><li>Verapamil IV 0.075-0.15mg/kg over 2min (Class I) </li></ul><ul><li>Accessory Pathway </li></ul><ul><li>Amiodarone IV 150mg over 10min (Class IIa) </li></ul><ul><li>Heart Failure without accessory pathway </li></ul><ul><li>Digoxin IV 0.25mg q2h (Class I) </li></ul><ul><li>Amiodarone IV 150mg over 10min (Class IIa) </li></ul>ACC/AHA/ESC 2006 Atrial Fibrillation guidelines
    35. 35. Rhythm control: Stable patients <ul><li>Consider cardioversion especially if younger, without hypertension or heart disease ACC/AHA/ESC Atrial Fibrillation guidelines 2006 </li></ul><ul><li>Ottawa protocol: IV 1g procainamide (in 250ml D5W) over 1hr; 58% conversion rate CJEM 2010 12(3):181-91 </li></ul><ul><li>Amiodarone 3-5mg/kg IV over 15-20min </li></ul><ul><li>Ibutilide 0.015-0.02mg/kg IV over 10-15min </li></ul><ul><li>Electrical cardioversion: 80-90% conversion rates </li></ul><ul><li>Admit AF patients if: </li></ul><ul><ul><li>Unstable, MI, worse heart failure </li></ul></ul>
    36. 36. BACK TO THE CASE Case: 68 yr old female 1 day of palpitations, slight chest discomfort Vitals: 150-170bpm, BP 108/45, 95% 1L NP, RR 20 <ul><li>MANAGEMENT </li></ul><ul><li>if patient becomes unstable then synchronized cardioversion </li></ul><ul><li>Probably reasonable to rate control </li></ul><ul><li>Decide whether chemical or electrical cardioversion is appropriate </li></ul>
    37. 37. Recap Narrow complex tachycardias <ul><li>Unstable vs. stable </li></ul><ul><li>Synchronized cardioversion if unstable </li></ul><ul><li>If stable Adenosine first if stable </li></ul><ul><li>Rate control especially if unknown duration </li></ul><ul><li>Chemical cardioversion: consider amiodarone or procainamide </li></ul><ul><li>Electricity more effective than medication </li></ul>
    38. 38. Wide complex tachycardias
    39. 39. Approach to wide complex tachycardias Wide Complex Tachycardia Hemodynamically Unstable Hemodynamically Stable Irregular Regular Synchronized cardioversion
    40. 40. <ul><li>Hypotension </li></ul><ul><li>Chest pain (suggestive of ischemia) </li></ul><ul><li>Shortness of breath </li></ul><ul><li>Decreased level of consciousness </li></ul>Wide Complex Tachycardia Stable vs. Unstable Unstable = Immediate Synchronized Cardioversion
    41. 41. Wide Complex Tachycardias Differential Diagnosis Regular <ul><li>Monomorphic VT </li></ul><ul><li>SVT with aberrancy (BBB) </li></ul><ul><li>Antidromic Wolf Parkinson White syndrome </li></ul><ul><li>Electrolyte abnormalities or overdoses </li></ul>Irregular <ul><li>Polymorphic VT (including Torsades) </li></ul><ul><li>A. Fib with aberrancy (BBB) </li></ul><ul><li>A. Fib + accessory pathway </li></ul>
    42. 42. Wide Complex Tachycardias Ventricular Tachycardia vs. SVT
    43. 43. Wide Complex Tachycardias Regular wide complex tachycardia is ventricular tachycardia until proven otherwise
    44. 44. Wide Complex Tachycardias Management: Stable, regular WCT <ul><li>Consider adenosine ONLY if regular WCT </li></ul><ul><li>Procainamide (Class IIa) </li></ul><ul><li>Amiodarone (Class IIb) </li></ul><ul><li>Electrical cardioversion </li></ul><ul><li>ACLS guidelines 2010 </li></ul><ul><li>*** If ONE anti-arrhythmic fails then proceed to electrical cardioversion*** </li></ul>
    45. 45. Case 1: 33 M severe palpitations; healthy; BP 145/85 Case 2: 75 F chest pain; PMHx MI; BP 109/75
    46. 46. <ul><li>Impression: most likely SVT w/ aberrancy </li></ul><ul><li>Management </li></ul><ul><li>Consider Adenosine – ensure regular rhythm </li></ul><ul><li>Other options: Amiodarone, Procainamide, Electrical cardioversion </li></ul><ul><li>Impression: most likely VT </li></ul><ul><li>Management : </li></ul><ul><li>Avoid adenosine </li></ul><ul><li>Amiodarone or Procainamide or Electrical cardioversion </li></ul><ul><li>Concern about hemodynamic stability </li></ul>Case 2: 75 F chest pain; PMHx MI; BP 109/75 Case 1: 33 M severe palpitations; healthy; BP 145/85
    47. 47. FUSION BEAT CAPTURE BEATS Wide Complex Tachycardias ECG Findings Suggestive of VT AV DISSOCIATION
    48. 48. Wide Complex Tachycardias Accessory Pathways Orthodromic/Anterograde QRS typically normal More common Antidromic/Retrograde QRS typically wide Less common
    49. 49. <ul><li>Why do accessory pathways matter? </li></ul>Wide Complex Tachycardias Accessory Pathways Wide complex, irregular tachycardia can degenerate to ventricular fibrillation with AV nodal blockade Calcium Channel Blockers Beta Blockers Adenosine
    50. 50. Wide Complex Tachycardias Accessory Pathways
    51. 51. Wide Complex Tachycardias Accessory Pathways <ul><li>When to suspect accessory pathway? </li></ul><ul><li>Rapid ventricular response (>200bpm) </li></ul><ul><li>Wide, irregular QRS complexes </li></ul><ul><li>Bizarre QRS morphology </li></ul><ul><li>History of accessory pathway dysrhythmia </li></ul><ul><li>Management </li></ul><ul><li>Unstable = Synchronized cardioversion </li></ul><ul><li>Check previous ECG for PR interval & Delta wave </li></ul><ul><li>Always have defibrillator available with infusions </li></ul><ul><li>Amiodarone (AHA 2005 guidelines) </li></ul><ul><li>Procainamide (Intern Emerg Med 2010;5:421-426) </li></ul>
    52. 52. Recap Wide complex tachycardias <ul><li>Unstable vs. stable </li></ul><ul><li>Synchronized cardioversion if unstable </li></ul><ul><li>ONLY try adenosine if convinced it is regular WCT </li></ul><ul><li>Assume VT if cardiovascular history or >50yrs </li></ul><ul><li>No AV nodal blocker if irregular WCT </li></ul>
    53. 53. Objectives: recap <ul><li>(Very) Briefly review pathophysiology of arrhythymias (4 slides!) </li></ul><ul><li>Cardioversion </li></ul><ul><li>Tachydysrhythmias </li></ul><ul><li>Special case of wide complex tachyardia </li></ul><ul><li>Example ECGs </li></ul>
    54. 54. References <ul><li>Rosen’s Emergency Medicine (7 th edition) </li></ul><ul><li>Lilly LS. Pathophysiology of heart disease. 2003 </li></ul><ul><li>Cvphysiology.com </li></ul><ul><li>Simplified approach to tachyarrhythmias (EMRap.com) </li></ul><ul><li>EMCrit.org </li></ul><ul><li>References listed in presentation </li></ul>
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