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Download Management: Rhythm Control - Calgary Emergency Medicine
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Tachydysrhythmias Adam Davidson Bryan Young Thanks to McCrossin for donating his previous blood, sweat and tears! I think this is where I insert something funny.. I was drawing a blank, until… Kipper (as of Oct 15th): GAA: 5.00 Sav%: 0.826 That’s Funny!!! Tachydsyrhythmias Outline 1. 2. 3. 4. 5. 6. Introduction: Approach to tachydysrhythmias Narrow Complex AVNRT vs AVRT A fib + Ottawa Protocol Wide Complex If we have time: practice ECG’s Tachydysrhythmias Outline Predominant focus on: ECG recognition (just recognize the rhythms) Rhythm Management Some pathophysiology Easy approach to remembering diagnosis and treatment without killing anyone in the attempt for simplicity Special attention to RT’s, A fib, and WCT’s Tachydysrhythmias Introduction 5 Step Approach to dysrhythmia management 1. 2. 3. 4. 5. IV, O2, Monitor, Advanced airway and defibrillator to the bedside Are they stable or unstable? Is the QRS narrow or wide? Is the rhythm regular or irregular? Are there p-waves? Are they normal? ACLS Guidelines Tachydysrhythmias Narrow Complex, regular rhythm Wide Complex, Regular Rhythm Sinus Tach Ventricular tachycarida AVNRT SVT with BBB Orthodromic AVRT (WPW) Antidromic AVRT Atrial Flutter with consistent Wide Complex, Irregular AV block Rhythm Narrow Complex, Irregular Polymorphic ventricular rhythm tachycardia Torsades Atrial fibrillation Atrial fibrillation with BBB Atrial flutter with variable block WPW with atrial fibrillation Multi-focal atrial tachycardia Atrial flutter with variable AV block and BBB Tachydsyrhythmias Introduction Stable vs Unstable 1. 2. 3. 4. Chest pain: may not always indicate instability in young patients without CV risk factors. A consideration; but a relatively unreliable predictor of CV stability Altered mental status: look for other causes of AMS (e.g. pt with septic shock and a compensatory rapid Afib or sinus tach) Hypotension: Beware of young female with a normal SBP of 90 Pulmonary Edema: May be acute and secondary to decreased CO with tachyarrhythmia, or may be chronic Think of stability as a spectrum (not dichotomous) Narrow, Regular Sinus Tach AVNRT OAVRT A flutter P waves What’s normal? •Best seen in V1 •Upright in II •Negative in AVR Regular NCT Sinus Tachycardia Can be confused with SVT and A Flutter with 2:1 block Pearl: Maximal tachy response = 220 - patient’s age Monitor 1 Adenosine: 6mg IV push Flutter! Atrial re-entrant circuit surrounding tri-cuspid valve Very distinct pathway with little variation among individuals Time to complete circuit is ~200msec Leads to atrial rate of ~300/min Ventricular rate based on degree of AV block 2:1-150, 3:1-100, 4:1-75, 5:1-60 Treatment 60% occurs w/ some acute disease process Harder to chemically convert than A fib ACC recommend rate control followed by electrical cardioversion Cardioversion improved with incr AV block Require very low joules 10-20 joules often sufficient While poor evidence, follow same anti-coagulation rules as A fib Monitor 2 AVNRT + AVRT Accessory pathways w/in or outside of AV node Symptoms similar: Palpitations 98% Dizziness 78% Dyspnea 48% CHEST PAIN 38% (structurally normal hearts) STD/TWI in 25% and 57% respectively Still need to take seriously if RF for CAD or elderly AVNRT Etiology Idiopathic Often no precipitating cause Circus pathway w/in AV node Differ in conduction velocity and refractory period Usually triggered by a PAC Regular NCT AVNRT Diagnosis Trial of Adenosine ECG Findings Rate 120-220 P waves may be retrograde or may be buried in QRS Initiation of rhythm demonstrates a prolonged PR Negative T waves after AVNRT termination is very common (does not mean IHD) AVNRT Regular NCT AVNRT Management 1. 2. Vagal Maneuvers Adenosine • • 3. Very short 1/2 life Rarely produces hypotension CCB (verapamil, diltiazem) • • • If adenosine isn’t effective Negative inotropes Cause vasodilatation AVRT WPW is the common form Characterized by accessory pathways that conduct without the refractory period characterized by the AV node (conduction impulses are not limited) Accessory pathways can conduct anterograde (most common), retrograde, or both Triggered by a PAC or PVC AVRT Orthodromic WPW First beat is sinus rhythm with a short PR and wide QRS Second beat shows an atrial premature beat which is blocked by the AP and therefore travels down the AV node After myocardial depolarization impulse is now conducted retrograde up the AP AVRT Management (orthodromic) 1. 2. Vagal Maneuvers Adenosine 3. 4. As effective as verapamil @ terminating OAVRT Ultra-short acting so preferred if rhythm is to be restored with DC cardioversion Caution! Rate Control: CCB or BB Procainamide Safest drug if OAVRT presenting as a wide complex tachycardia (ie if any chance rhythm is VT) Adenosine Adenosine MOA Dosing Hyperpolarization of the AV node thereby decreasing frequency of depolarization 6 mg IV over 1-2 seconds; if not effective in 1-2 minutes may repeat with 12 mg Extremely short 1/2 life Decrease dose with: Central Line, Tegretol, Heart Transplant 3mg starting dose! ACC Adensosine Recommendations Adenosine Side Effects Various side effects occur 40-60% Facial flushing (18%) Palpitations/Chest Pain Dyspnea (12%) Sense of “impending doom” Usually very short lived (~5-10sec) BUT….. Beware!! Adenosine incr atrial ectopy. Can induce atrial fibrillation in 12-15% of AVRT’s Can have severe consequences, especially if already given an AV nodal blocker Very high ventricular rates and possibility of V fib Need to be ready to defibrillate Studies show 0% in AVNRT AVRT vs AVNRT Invisible p waves: 100% specific AVNRT R’V1 or SII: 100% predictive of AVNRT Isolated retrograde p waves, RP interval > 100msec, STE in aVR: highly predictive of AVRT Pre-excitation on sinus ECG: likely AVRT AVRT vs AVNRT RP >100msec STE aVR SII Regular NCT Differential Diagnosis Sinus Tach A Flutter AVNRT OAVNRT Summary Trial of adenosine Help to make diagnosis Help to break the rhythm Warn pt of S/E Max sinus rate = 220 - pts age Cardiovert unstable patients (assuming not sinus tach) V1 is best lead to see p-waves Risk of A fib w/ Adenosine and AVRT Monitor 3 Narrow, Irregular Irregular NCT Multifocal Atrial Tachycardia Commonly Misdiagnosed as A Fib More than two foci of impulse formation Etiology Often associated with pulmonary disease and hypoxemia Management Often resolves when hypoxemia is corrected Fluids if hypotensive Caution Important distinction to make from A Fib because you do not cardiovert these patients Most of these pts have reactive airways (don’t give BB) A Fib Management Three part approach to management: 1. 2. 3. Appropriate control of ventricular rate Need for, proper timing of, and appropriate method for restoration of sinus rhythm Need for anticoagulation to prevent thrombo-embolism A fib Management: Rate control Initial management in stable patients, regardless of duration, is rate control Rates in A Fib: Mean resting rate in AF of recent onset is between 110-130 Rates may exceed 250 in WPW Rates greater than 150 in absence of WPW should raise suspicion of a hyperadrenergic state Goal: A controlled rate is between 60-80 bpm at rest, 90-115 during moderate exercise Atrial Fibrillation: Rate Control DRUG Loading Dose Onset Maintenance Diltiazem 0.25 mg/kg over 2 minutes Repeat 15 min later at 0.35 mg/kg IV bolus 2-7 min 5-15 mg/hour by infusion Metoprolol 2.5-5 mg IV up to max 15mg 5 min N/A Verapamil (avoid 5-10 mg IV 3-5 min N/A Propranolol 1 mg IV over 2 min; q5 min to max 5 mg 5 min Esmolol 0.5 mg/kg IV over 1 min 5 min combining with BB; risk of asystole) 50-200mcg/kg/min A fib: Rate Control A fib Management: Rate Control Options for rate control: 1. 2. Beta-Blockers Good for sympathetic states (thyrotoxicosis, postop) Caution in patients with asthma, COPD Diltiazem Beta-Blockers (metoprolol, propranolol, esmolol) CCB (verapamil, diltiazem) Faster onset than BB Caution with CHF (can give with parenteral calcium to decrease risk of hypotension) An oral rate control agent should be used if AF persists and discharge is considered The Biggies!! A fib Management: Rate vs Rhythm 1. Major Trials: RACE 2. NEJM 2002; 347(23): AFFIRM NEJM 2002; 347(23):1825-33 A fib RACE Management: Rate vs Rhythm RACE Comparison b/w rate control and rhythm control in chronic AFib Outcome Measures Death, HF, embolism, bleeding Inclusion 522 patients with previous failure to convert following electrical cardioversion (average age 69) Methods Rhythm control with sotalol, if failure after 6 months flecainide, if recurrence in 6 months amiodarone A fib Management: Rate vs Rhythm AFFIRM Comparison between rate vs rhythm control Outcome Measures: Primary: Mortality Secondary: Death, disabling stroke, anoxic encephalopathy, major bleeding, or cardiac arrest Inclusion Criteria: >/= 65 yrs old Other RF of stroke or death Previous history of A Fib for at least 6 hours in the past 6 months A fib Management: RACE Rate vs Rhythm and AFFIRM Results: Equal rates of embolization (primarily in patients who stopped warfarin or with subtherapeutic INR) Recurrent episodes of AF detected in 90% of patients with rhythm control 90% or recurrences asymptomatic 17% or asymptomatic recurrences last up to 48 hours More drug S/E in rhythm control arm A fib Management: Rate vs Rhythm What do we take away from RACE and AFFIRM results? Results show slightly better outcomes with rate control in a specific patient population Rate control and rhythm control with appropriate anticoagulation are acceptable approaches to management depending on clinical scenario Side effects of antiarrhythmics are not benign A fib Management: Major Rate vs Rhythm Trials to date have not included: Younger patients with lone AF (15% of patients with AF) Pts with highly symptomatic AF Pts with significant CHF Pts with contraindications for anticoagulation or rate control Pts with new onset AF Rates of recurrence of AF will vary depending on patient risk factors NCT: AF Rate vs Rhythm Favours Rate Control Persistent AF Recurrent AF Less Symptomatic > 65 yrs HTN No Hx of CHF Structural disease on echo (LAE) Previous antiarrhythmic drug failure Patient preference Favours Rhythm Control Paroxysmal AF First episode of AF More symptomatic < 65 yrs No HTN Hx of CHF No previous antiarrhythmic drug failure Patient preference Afib and CHF A fib and CHF Multicentre RCT w/ 1376 pt’s EF <35%, Sx of CHF, Hx of A fib Primary Endpoint: Time to death from CV causes Pt’s in A fib for longer than 12mo excluded Rhythm Control: medical +/- D/C cardioversion with long term med (usually amio) Rate Control: BB/CCB +/- Dig A fib and CHF Rhythm Control group had more hospitalizations. Otherwise no differences in primary and all secondary endpoints Overall annual mortality for pt’s w/ CHF and hx of A fib 10% !!! Study changes common held belief that A fib is an independent predictor of worse outcome in CHF A fib Management: Rhythm Control Who are you more likely to want to cardiovert? First Episode of AF Low risk for recurrence Persistent symptoms with rate control* Unstable patients A fib Management: Rhythm Control When would we expect trouble or less success with cardioversion? AF duration > 1 year Increased LA dimension on echo (>5cm) Paroxysmal AF of short duration which tends to resolve spontaneously and always recurs Patients with underlying medical conditions: CHF Hyperthyroidism COPD Electrolyte changes/ dig toxicity Of note Age alone is NOT a predictor or cardioversion success or higher complication rate Exercise caution in cardioverting patients with AV node dysfunction A fib Management: Rhythm Control Chemical Cardioversion Lower Success rate Slower conversion Proarrhythmic (may be following discharge) Longer ED stay Indications: Failed Electrical Patient Preference Electrical Cardioversion Higher success rate (75-93%) Faster conversion No risk of drugs Better ED flow Painful Narcotics +/- sedatives A fib Management: Electrical Rhythm control Cardioversion Safe if patient in AF for less than 48 hours Syncronized, AP position is better Monophasic 200 J; Biphasic 50-150 J (biphasic better) May need to do it more than once Propofol for sedation may actually increase success of conversion NPO Guidelines: 6 hrs for solids; 2hrs for fluids (Am Soc Anesth) NPO is a consideration for depth but not a contraindication (ACEP; Can Consensus Guidelines) Atrial Fibrillation Recurrence post DC cardioversion Majority in first week, up to 50% first month J Am Coll Cardiol 98; 31(1):167 A fib Management: Rhythm control Chemical Cardioversion Ibutilide (Level A evidence) Flecainide (Level A evidence) Propafenone (Level A evidence) Procainamide (Level B evidence) Sotalol (Level B evidence) Chronic oral Amiodarone (Level B evidence) Can be used to pretreat patients prior to electrical CV NOT used for unstable patients How long does it take? Are patients safe for D/C? A fib: Rhythm Control A fib Management: Rhythm Control Ibutilide (Class III) Conversion time 1 hour Dose: 1 mg IV over 10 min Success rate: 32-51% Side effects: Prolonged QT w/ arrythmias 3.2% Propafenone (Class Ic) Conversion time 2 hours Dose: 600mg PO (no IV form) Success rate: 50-55% Side effects: Arrhythmia 5%, lung effects similar to BB IA-Recommendations Management: Rhythm Control Procainamide (Class Ia) Conversion time less than 1 hr Dose: 1g IV infusion over 1 hour Success: fewer studies but Ottawa Protocol showed 52% Side Effects: hypotension, incr QTc, useful for acute onset Amiodarone (Class III) Conversion time: long Dose: 400mg PO tid Success: 35% Side Effects: bradycardia, incr QTc (less than Ibutilide), Vtach II-Recommendations Ottawa Procainamide Protocol Procainamide 1g in 250cc D5W Infused over 1hr Procainamide +/- Cardioversion A fib Management: Anticoagulation peri-cardioversion Risk Factors for thromboembolism AF > 48h Valvular heart disease Significant LV dysfunction Previous thromboembolism Hyperthyroidism ASD (even if repaired) One series of patients with symptomatic AF < 48 demonstrated 0.8% incidence of embolism 12-24 hrs post CV. All were elderly F with no prior hx of AF Ann Int Med 1997; 126(8): 615-620 A fib Management: Anticoagulation peri-cardioversion ACUTE trial: 13.8 % of patients who had AF > 48 h were found to have thrombus on TEE JACC 2001; 37(3): 691-702 Can use TEE in patients you don’t want to wait on for 3 weeks A fib Management: AF Anticoagulation Pericardioversion < 48 h Consider LMWH single dose in patients without RF Consider long-term anticoagulation in pts with RF AF > 48 & patients with RF for thromboembolism TEE negative: UFH or LMWH; then warfarin x 1 month TEE positive: LMWH + Warfarin 3/52, cardioversion, then warfarin x 1 month post cardioversion A fib Management: Anticoagulation CHADS2: CHF Hypertension Age >75 DM Previous Stroke or TIA (2 points) Patients with intermittant AF have same risk as patients with persistent AF JAMA, 2001 CHADS2 CHADS2 Anti-Coagulation Score: 0: ASA 1: ASA or Warfarin (take individual factors into account 2-6: Warfarin unless contra-indicated A fib Disposition Admit if Structural heart disease Embolic event Those at high risk for thromboembolism Those with failure of rate control in ED Patients in heart failure Low risk No comorbid disease No ischemic changes < 60 years old No chest pain* Irregular NCT Atrial Fibrillation and Pregnancy Etiology Structural Heart Disease Hyperthyroidism Management Rate Control Rhythm Control BB, CCB, Digoxin DC cardioversion if unstable Anticoagulation UFH or LMWH during 1st trimester and after 36 wks Warfarin or heparin during second trimester Irregular NCT Atrial BB Fibrillation and MI should be given whenever possible If BB contraindicated then give digoxin or amiodarone to slow the rate DC cardioversion if unstable Avoid class procainamide Give heparin Irregular NCT Atrial Flutter with variable AV block Similar treatment as with atrial fibrillation Irregular NCT Differential Diagnosis A Fib A Flutter with variable AV block MAT Summary Unstable A Fib = cardioversion AV nodal blockers are first therapy in A fib Unstable chronic A Fib is a B&%$# to deal with in elderly patients MAT is not a destabilizing rhythm Be cautious attributing symptoms to Afib in rates <150 My brain is seriously killing me. On a lighter note…. Choose One! Malibu Gets Owned Fat Kid Amusement Park Halloween Prank Gone Bad Monitor 4 Wide, Regular Regular WCT Antidromic AVRT First sinus beat has a short PR and a wide QRS (normal) When an atrial premature beat is triggered the AV node is refractory and therefore the impulse is blocked The ‘path of least resistance’ in this case becomes the AP and a wide complex tachycardia ensues High risk of Vfib, may be difficult to differentiate from VTach Anti Dromic AVRT Management (antidromic) 1. IV Procainamide • 2. Even if it doesn’t acutely terminate the tachycardia, it often helps slow the rate and improve hemodynamic stability Second line (consider only if absolutely certain of diagnosis) • • • IV Beta Blockers (Sotalol, Propranolol, Metoprolol) IV Ca Channel Blockers IV Adenosine Antiarrhythmics AVRT Treatment: Amiodarone ACLS Guidelines for management of WPW recommend Amiodarone Extreme caution for amiodarone in many other articles: AJEM 2007;25:576-583 JAMA 2007; 298(11):312-22 CJEM 2005; 7(4):262-5 Risk of accelerated ventricular rates Antiarrhythmics Treatment: Procainamide Blocks fast inward Na current and outward K current Shown to prolong refractory period of atrial, ventricular, and AP tissue as well as slow antegrade and retrograde conduction in the accessory pathway Strong potential for hypotension with rapid administration therefore requires a slow rate of infusion and slow onset of action (40-60 minutes) Dose: 20 mg/min until arrhythmia is suppressed, hypotension ensues, QRS prolonged > 50%, or a total of 17 mg/kg has been given (1.2 g for a 70 kg patient) Maintenance: 1-4 mg/min diluted in NS (reduce if patient is in renal failure) Other Indications Stable VT, Afib rate control, AVNRT, Afib and WPW Monitor 5 Regular WCT Ventricular Tachycardia Monomorphic VT Treatment: 1. 2. Unstable: Cardioversion Stable: Procainamide is first choice, if they drop their pressure then cardioversion • Safer in pregnancy • Safer if diagnosis is wrong (ie WPW) Amiodarone • • • • Falling out of favour 30-50% effective Better evidence for Procainamide Go to Amio if procainamide doesn’t work • Circ 2006 Ventricular Arrhythmia Guidelines Regular WCT Ventricular Tachycardia Diagnosis Fusion Beats AV Dissociation Capture Beats Extreme RAD Regular WCT Ventricular Tachycardia Diagnosis Fusion Beats AV Dissociation Capture Beats Regular WCT Ventricular Tachycardia Diagnosis Fusion Beats AV Dissociation Capture Beats Regular WCT Ventricular Tachycardia PVC is the most common inciting event R on T phenomenon high risk of VT Approach: Pulse absent: treat as VF Stable or Unstable: Cardioversion Differentiate between Mono vs Polymorphic Regular WCT Unknown WCT Brugada Criteria Proposed to distinguish between regular, monomorphic WCT caused by SVT and VT Regular WCT Unknown WCT Brugada Criteria Original Study: Other studies: Sn: 99%, Sp: 97% Sn: 79-92% Sp: 43-70% Follow up studies have not duplicated the sensitivity and specificity claimed in the original study Non-agreement between EM physicians in 22% of cases Regular WCT Unknown WCT Brugada Criteria Morphology associated with the fourth criterion with RBBB appearing complex Regular WCT Unknown WCT Brugada Criteria Morphology associated with the fourth criterion with LBBB appearing complex WCT R R P Regular RR and RP intervals, STE in aVR, RP> 100msec Baseline Regular WCT Differential Diagnosis VT SVT with BBB Antidromic WPW Summary Assume VT when in doubt Cardiovert early Stable patients can still have VT Procainamide is probably best antiarrhythmic in this group Brugada is unreliable Rx of SVT with VT Tx is safe and often effective Most likely VT if underlying heart disease Monitor 6 Irregular, Wide Irregular WCT Torsades Etiology (prolonged QT) Antiarrhythmics Ibutilide Procainamide Sotalol Amiodarone Antimicrobials Macrolides Fluroquinolones Psychotropics Diuretics Hypothermia Congenital prolonged QT K and Mg disturbances Jervell and Lange Nielsen Romano-Ward Idopathic Electrolyte abnormalities Anorexia Irregular WCT Polymorphic VT Management Shock, then check the QT Prolonged QT - MgSO4 (any other antiarrhythmic may be harmful) QT normal - Any antiarrhythmic you want (keep in mind these rhythms may be a consequence of ischemia) Hemodynamically Stable MgSO4 2-4g IV bolus repeated in 2-4 minutes (careful in renal failure) Irregular WCT Differential Diagnosis PMVT Summary Torsades WPW with AF AF with BBB The most tricky of the 4 groups Using antiarrhythmics (amio, procainamide, and lidocaine) may cause harm in patients with torsades Using AV nodal agents in WPW with AF may cause harm (risk V Fib) If in doubt: Electricity and check QT after rhythm converted Old ECG’s very helpful!! Irregular WCT WPW & AF Management Concern is that by giving these patients beta-blockers we could potentially promote conduction down the accessory pathway Increased conduction down the accessory pathway can put these patients at risk of developing V Tach and ultimately V Fib Irregular WCT WPW & AF Diagnosis AF occurs in up to 40% of patients with WPW Thought to be the most common cause of cardiac death in patients with WPW because the rhythm can degenerate in V Fib Irregular WCT WPW & AF Diagnosis A. B. Consider WPW AF in patients with 1. Irregular rhythm 2. Rapid ventricular response (one that is too fast to be conducted down AV node) 3. Wide, bizarre QRS complex signifying conduction down an accessory pathway 4. May see an occasional QRS representing conduction down the AV node Other clues: patient is young (<50), or has a history of palpitations, rapid heart rate, or syncope Irregular WCT AF and WPW Treatment options: 1. 2. Contraindicated • Procainamide 30 mg/min; max dose 17 mg/kg Ibutilide 1 mg over 10 min; repeat once after 10 min AV nodal blocking agents (BB, CCB, Dig, Adenosine) Avoid • Amiodarone? ACLS Amiodarone Recommendations But… Irregular WCT WPW & AF Management Tijunelis and Herbert published a literature review on the use of amiodarone in WPW patients with AF No evidence showing benefit. Several case studies showing harm (pro-arrhythmic); therefore, best to use DC cardioversion or procainamide in these patients for rhythm control Can J Emerg Med 2005;7(4):262-5 Antiarrhythmics WPW & AF- Drugs of Choice Procainamide Fewer effects on QTc First line for WCT of unknown rhythm Dose: 15-18mg/kg infused over 25-30 minutes or 200mg q5min up to 1 g Avoid if hypotense, incr QTc Ibutilide More hemodynamically stable than procainamide Short 1/2 life (4 hours); rapid onset (20 min) Doesn’t interact with most of the meds used for rate control No dosing concerns for hepatic or renal function Considered relatively safe in elderly Dose: 1 mg over 10 minutes (undiluted), if first dose is unsuccessful then a second dose can be administered after 10 minutes; dose is 0.01 mg/kg if less than 60 kg Avoid if incr QTc, structural heart disease, sinus node disease Summary AVNRT/AVRT Adenosine very useful but be wary of A fib w/ accessory tracts Chest pain, dyspnea common sx even in young healthy people STD/TWI common, but still need to consider ischemia in elderly/at risk Afib/WPW Safest bet is always D/C cardioversion AV nodal blockers bad, bad, bad! Ibutilide or Procainamide are the drugs of choice WCT When in doubt treat as VT 1st line med for WCT- Procainamide Afib Consider rhythm control for young, new Afib with no underlying structural heart disease, or symptomatic with rate control CHF no longer means rhythm control Not every patient needs Warfarin Consider adding Ca when giving Diltiazem Ibutilide, Propafenone, Procainamide likely more effective than Amiodarone Thank You! Case Examples: 1. 45 y/o male with new onset A Fib, distinct onset 8 hours ago. 2. 80 y/o F with CHF, Afib x 30 years with acute decompensation. In AF with ventricular rate of 150, hypotensive 3. 72 y/o male with symptomatic A Fib and having and MI. How does your management plan differ? 4. 66 y/o male with unstable AF (HR 125) 5. 34 y/o F pregnant female, hemodynamically stable (HR 170)
