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Atrial Fibrillation and Atrial Flutter

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Chemical Cardioversion

Ibutilide 1 mg over 10 minutes
Avoid if EF<20% or QTc>480
must observe for 4 hours to make sure no QT prolongation
augments electrical cardioversion (NEJM 1999;340(24):1849

 

 

ashman beats from variable repolarization of the bundles Holiday heart=etoh generated a-fib, can also be from withdrawal. Usually spontaneously resolves.   P-ulmonary Embolism I-schemia R-espiratory A-trial myxoma, enlargement T-hyroid E-thanol S-epsis     A. flutter less likely to have atrial clots, but in one study of hospitalized patients, 21% had a clot, most likely due to coexistence of A. Fib in these pts. (Am J Cardio 1995 76:3)   If there is any doubt about A. Fib on ekg, get a strip with 50 mm/sec speed and use calipers to determine regularity.

decremental conduction

faster hit (a/v node) the less it conductsby slowing the flutter rate, you actually can wind up increasing the ventricular rate

Cardioversion

· Joglar et al, who showed an initial single shock success rate of 14% with 100J, 39% with 200J, and 95% with 360J in patients with AF for more than 48 hours · Use the steak sauce for best conduction · Lack of myocardial damage from DCC in AF at levels higher than 360. (Heart 1998, 80:3) and Resuscitation 1998;36:193-199. Latter article showed sig. increase in CK but CK-MB fraction and troponin not elevated · Start at 200J in stable patients, 360J in unstable patients. · Use Anterior-Posterior Shock, not Anterior-Lateral (Lancet 360:9342, 2002) When acute AF was excluded incidence of embolism with inadequate anticoagulation was 1.7-4.7% (Mayo Clin Proc Sept 2002, Vol 77)

Medications

Conversion

  • Ibutilide-1 mg over 10 minutes, may repeat in 10 minutes. Causes prolonged QT in 5-10% and TdP in 1-5%, give MgSO4 prophylaxis . Facilitates electrical conversion if used as a premedication (NEJM 340:24 June 1999 JB17) Monitor for four hours after use.
  • Dofetilide
  • Amiodarone-150 mg over then 10 min, then 1 mg/min x 6 hours then .5 mg/min or 3-5 mg/kg over 10 minutes then 5 mg/kg q 8 hrs divided as infusion (One MA says it works (Ann Intern Med 2003, 163:777)
  • Flecainide-300mg PO x 1 (In short cut review, more efficacious than Amiodarone Emerg Med J 2004; 21:199)
  • Propafenone-600 mg PO

Rate Control

  • Diltiazem .25 mg/kg over 2 minutes, may repeat at .35 mg/kg if inadequate response, the drip at 5-15 mg/hr or 60 mg PO. (give 1-3 cc of CaCl or 5-10 cc CaGluc if hypotension develops or as pretreatment for pt’s with borderline BP Calcium Pretreatment Moser et al. the use of calcium salts in the prevention and management of verapamil induced hypotension. Ann Pharmoacother 2000;34:622-9Haft et al. treatment of atrial arrythmias. Effectiveness of verapamil when proceeded by calcium infusion, Arch Intern Med 1986;146:1085-9   Barnett JC et al. Short term control of supraventricular tachycardia with verapamil infusion and calcium pretreatment. Chest 1990;97:1106-9   Miyagawa K, et al. Administration of intravenous calcium before verapamil to prevent hypotension in elderly patients with paroxysmal supraventricular tachycardia. J Cardiovas Pharmacol 1993;22:273-9   Weiss AT et a l. The use of calcium with verapamil in the management of SVT In J Cardiol 1983;4:275-84   Salerno DM, et al. Intravenous verapamil for treatment of multifocal atrial tachycardia with and without calcium pretreatment. Ann Internal Med 1987;107:623-8   Kuhn M et al. Low-dose calcium pretreatment to prevent verapamil-induced hypotension. AM Heart J 1992;124:231-2)   Recent RCT of dilt c 3.33 cc cacl preinfusion showed no difference, but no side effect. Only 5 pts with hypotension, only one pt with sx hypotension. One pt had increased HR and LOC in placebo group, recovered with Ca Alternatively, use infusion of Diltiazem 2.5 mg/min to maximum of 50 mg (Resuscitation 52:167, 2002)If pt is unstable, give in 5 mg aliquots every few minutes. Contraindicated in children < 1 y/o.
  • Magnesium 2-4 g over 10 minutes. Has effects of CCB and B-Blockers, but doesn’t effect the sinus node. (Clin Card 12:2, 1989 and J Am Coll Card 7:6, 1986) Head to head with amiodarone (Crit Care Med 1995;23 equal for rate control and more effective conversion) or diltiazem ( Internat J Cardiol 2001;79 287-291 randomized, prospective 46 pts, 2.5 G MG over 15 min or 25 mg dilt over 15 min Mag was equal for rate control and more effective for conversion to sinus)
  • another Blinded RCT (Ann Emerg Med 2005;45(4):347) Continue drip at 1-2 g/hr

Author Dose Response Moran et al 1995 37mg/kg bolus followed by infusion of 25mg/kg/hr 42 patients – 60% conversion in magnesium group and 45% in amiodarone group. Brodsky, et al, 1994 2 grams over 6 minutes – then 1 gram per hour 10/10 reduced HR to < 90 versus only 4 of 8 in placebo by 4 hours Tachyarrhythmia’s Notes 10 Mel E. Herbert, MD, MBBS, BMedSci, FACEP, FAAEM Hays et al 1994 2 grams bolus minutes – then 1 gram per hour By 30 minutes, there was no significant change in the ventricular rate in patients receiving placebo while the rate decreased an average of 16% within five minutes after initiation of magnesium sulfate (p<0.02). Gullestad, L., et al, 1993 1.2g given over five minutes, with the dose repeated after five minutes if there was no response, followed by infusion of 0.6g per hour The rate of conversion to sinus rhythm within four hours was 58% (15/26) in the magnesium group and 23% (7/31) in the verapamil group, and the frequency of a heart rate reduction to less than 100/min was 28% (6/26) and 48% (15/31), respectively. RCT (Annals of Emergency Medicine Volume 45, Issue 4 , April 2005, Pages 347-353) Meta-analysis of magnesium therapy for the acute management of rapid atrial fibrillation. (Am J Cardiol. 2007 Jun 15;99(12):1726-32)

  • Digoxin works only in sedentary folks, because when you add catecholamines to the mix, the vagal response is overcome. Load 0.5 mg then 0.125 mg QD

dilt was better than amio and dig but, dig and amio seemed the same for rate control (Crit Care Med 2009;37(7):2174)

Anticoagulation

Probably need to anticoagulate after cardioversion due to cardiac stunning, ie. atrial EMD. (Am Heart J 2002 Jul;144(1):11-22, Eur Heart J 2001 Mar;22(6):520-1) anticoagulation with intravenous heparin be initiated on admission for all patients with atrial fibrillation, even if the clinically estimated duration of atrial fibrillation is less than 48 hours, and the therapy with heparin be continued for at least 24 hours after conversion” Weigner et al Ann Intern Med 1997;126:615-620     Independent predictors of ischacmic stroke in non-valve atrial fibrillation Consistent predictors

  • Old age
  • Hypertension
  • Previous stroke or transient ischaemic attack
  • Left ventricular dysfunction*

Inconsistent predictors

  • Diabetes
  • Systolic blood pressure >160 mm Hg
  • Women, especially older than 75 years
  • Postmenopausal hormone replacement therapy
  • Coronary artery disease

Factors which decrease the risk of stroke

  • Moderate to severe mitral regurgitation
  • Regular alcohol use (>14 drinks in two weeks)

*Recent clinical congestive cardiac failure or moderate to severe systolic dysfunction on echocardiography In some analyses, systolic blood pressure >160 mm Hg remained an independent predictor after adjustment for hypertension   Practical guidelines for antithrombotic therapy in non-valvar atrial fibrillation Assess risk, and reassess regularly High risk (annual risk of cerebrovascular accident=8-12%)

  • All patients with previous transient ischaemic attack or cerebrovascular accident
  • All patients aged >75 with diabetes or hypertension
  • All patients with clinical evidence of valve disease, heart failure, thyroid disease, and impaired left ventricular function on echocardiography*
  • TreatmentGive warfarin (target INR 2-3) if no contraindications and possible in practice

Moderate risk (annual risk of cerebrovascular accident=4%)

  • All patients <65 with clinical risk factors: diabetes, hypertension, peripheral vascular disease, ischaemic heart disease
  • All patients >65 not in high risk group
  • Treatment Either warfarin (INR 2-3) or aspirin 75-300 mg daily. In view of insufficient clear cut evidence, treatment may be decided on individual cases. Referral and echocardiography may help

Low risk (annual risk=1%)

  • All patients aged <65 with no history of embolism, hypertension, diabetes, or other clinical risk factors
  • TreatmentGive aspirin 75-300 mg daily

*Echocardiogram not needed for routine risk assessment but refines clinical risk stratification in case of moderate or severe left ventricular dysfunction (see figure below) and valve disease. A large atrium per se is not an independent risk factor on multivariate analysis       From Michelle Lin: Atrial Fibrillation (AF) = 5x risk for CVA and increases with ageStroke risk stratification for patients with AF:• Prior CVA or TIA• HTN• Age ≥ 75• CHF• Poor LV function• DMCHADS2 stroke risk stratification scheme (Gage BF et al. JAMA 2001;285:2864–70.)• C = Congestive heart failure (1 pt)• H = Hypertension (1 pt)• A = Age ≥ 75 (1 pt)• D = DM (1 pt)• S2 = prior Stroke or TIA (2 pts)Deciding whether to anticoagulate with ASA or Warfarin:(AHA/ ACC/ European Soc of Cardiology 2006 revised guidelinesfor antithrombotic therapy based on stroke risk)Weak Risk Factors Moderate Risk Factors High Risk FactorsFemale gender Age > 75 Prior CVA, TIA, embolismAge 65-74 HTN Mitral stenosisCAD Heart failure Mechanical heart valveThyrotoxicosis LVEF ≤ 35%DM Treatment Treatment TreatmentASA or Warfarin ASA or Warfarin (1 risk factor) WarfarinWarfarin (≥ 2 risk factors)* Anticoagulation goal with Warfarin is INR 2-3* If age < 60 years and zero risk factors: No anticoagulation b/c low risk for CVA                 LMWH is just as good as UFH in a-fib in a large RCT (Circulation 2004;109:997-1003)

Rate Control vs. Rhythm Control

rate control has more long term benefit than conversion and maintenance of sinus (NEJM 347:p. 1825, 2002 and NEJM 347:p. 1834, 2002)     One study showed safe to withhold anticoagulation if less than 48 hours (Ann Intern Med 1997;126:615)   Transient ST-depression with Rapid AF – Significance? Transient ST-segment depression during rapid atrial fibrillation is a common finding in the ED. Frequently, patients without known CAD exhibit such ischemic ST-segment depression during an episode of rapid AF. Clinicians often consider this to be a “positive stress-test equivalent”. However, a recent study indicates that in patients without a history of cardiovascular disease, there is no strong association between transient ischemic type ST-segment depression during paroxysms of AF and underlying occult CAD, i.e., they are not consistently associated with with positive stress testing or occlusions on cardiac catheterization (1). Conversely, however, if the ST-segment depression persists after the rate is controlled, then there should be greater concern. It should also be noted that new onset AF is rarely the sole manifestation of acute MI – in the absence of clinical predictors suggesting acute myocardial ischemia (e.g. chest pressure, dyspnea, diaphoresis, etc.), routine “rule-out ACS” admission is not supported by the literature. References: (1) Androoulakis A, et al. Transient ST-Segment Depression During Paroxysms of Atrial Fibrillation in Otherwise Normal Individuals J Am Coll Cardiol 2007;50:1909-1911. (2) Friedman HZ, et al. Cardiac care unit admission criteria for suspected acute myocardial infarction in new-onset atrial fibrillation Am J Cardiol 1987;59:866-869. (3) Mulcahy B, et al. New-onset atrial fibrillation: when is admission medically justified? Acad Emerg Med 1996;3: 114-19. (emedhome)   Ottowa Stuff (CJEM 2010;12(3): 1. Assessment: Assessment focuses on the stability of the patient, previous episodes and duration since onset. The decision of whether cardioversion is appropriate is made by the emergency physician involved and is usually based on the clarity of the history of arrhythmia onset. There is no upper age limit for the application of aggressive rhythm control. Every effort is made to ensure that the time from symptom onset is less than 48 hours and if this cannot be verified then rhythm control is not pursued unless the patient is on warfarin and has had a therapeutic international normalized ratio (INR) level for at least 3 weeks. If the time from symptom onset is longer than 48 hours or of uncertain duration, then transesophageal echocardiography can be pursued to determine the safety of cardioversion.19 Patients are not routinely screened for elevation of troponin unless there is chest pain or ST and T wave changes. 2. Rate control: Rate control is often omitted as there is no compelling evidence that its use facilitates cardioversion. Physicians who choose to control heart rate before attempting cardioversion typically use intravenous diltiazem or metoprolol. 3. Pharmacologic cardioversion: Typically, emergency physicians at our institution attempt pharmacologic cardioversion before electrical cardioversion. Intravenous procainamide is the drug of choice in Ottawa for rhythm control, and we have previously de – scribed its use in detail.20 Pharmacologic cardioversion is generally not attempted if the patient is deemed to be unstable (cardiac ischemia, severe congestive heart failure or hypotension) or if records indicate resistance to this approach on previous visits. The standard protocol is 1 g of procainamide in 250 mL of dextrose and water as a controlled infusion over 1 hour, under continuous cardiac and blood pressure monitoring. The infusion is interrupted if blood pressure falls below 100 mm Hg; if a bolus of 250 mL of normal saline corrects the hypotension, the infusion is resumed. 4. Electrical cardioversion: If chemical cardioversion fails, most patients then undergo electrical cardioversion in the ED, supervised by the emergency physician. Typically, procedural sedation and analgesia using fentanyl and propofol is administered and biphasic waveform energy levels of 150-200 J are delivered (during the study period most patients received monophasic waveform defibrillation as biphasic defibrillation was not yet widespread). 5. Anticoagulation: Patients with a time from symptom onset that is clearly less than 48 hours or with therapeutic INR levels typically do not receive anticoagulation in the ED. Although controversial, current recommendations advise warfarin be administered for patients with transesophageal echocardiogram- guided cardioversion or with a CHADS2 score of 1 or greater (Table 1).5,19,21,22 The role of heparin is unclear and is rarely used for any patients at our institution. 6. Disposition: Patients who undergo successful cardioversion are typically discharged home within an hour without medication (that is, no new oral anticoagulants, rate control agents or rhythm control agents are prescribed or given). For first-time episodes, outpatient echocardiography and cardiology follow-up is usually recommended. Monitoring of the INR and appropriate physician follow-up is arranged for the few patients started on warfarin. 7. Patients not treated with cardioversion: Patients who are not treated with cardioversion in the ED have their rate controlled and are then discharged on oral anticoagulants and rate control medication. Monitoring of the INR and physician follow-up is also arranged for this group. Heparin is rarely given to these patients in our ED.

Maybe we should not be rushing to shock the <48 hour patients (JAMA. 2014;312(6):647-649. doi:10.1001/jama.2014.3824)

Nuotio I, Hartikainen JE, Grönberg T, Biancari F, Airaksinen KE. Time to cardioversion for acute atrial fibrillation and thromboembolic complications. JAMA. 2014 Aug 13;312(6):647-9. PMID: 25117135

  • This is an interesting research letter suggesting that we might be a little bit “button happy” with our defibs in the case of new onset AF. I’ve always been a big fan of DCC for new AF and assumed that the “within 48hrs” was a useful protection against stroke. This small research letter (with 5000 cardioversions) suggests the rate of thromboembolism might be as high as 1% in the first 30 days following unanticoagulated DCC. As it’s only a research letter there’s not much details in the way of methods but gives pause to think before you charge. Especially considering that rate control and anticoagulation seems to produce the same outcomes. Hat tip to @drjohnm for the link
  • This retrospective review challenges the widely accepted concept that patients with recent onset atrial fibrillation of less than 48 hours duration are safe for cardioversion without preceding anticoagulation. The authors report a 1.1% risk of thromboembolism after symptoms have been going for greater than 12 hours (vs 0.3% in the < 12 hour group). Before practice is completely changed, though, it should be noted that the rate of CVA after cardioversion in anticoagulated patients (3 weeks of therapeutic anticoagulation) may be as high as 0.8%. Additionally, this study suffers from the standard flaws of all retrospective studies. More research is needed to help answer this question and guide management.
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