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Ibutilide 1 mg over 10 minutes
\nAvoid if EF<20% or QTc>480
\nmust observe for 4 hours to make sure no QT prolongation
\naugments electrical cardioversion (NEJM 1999;340(24):1849<\/p>\n
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ashman beats from variable repolarization of the bundles Holiday heart=etoh generated a-fib, can also be from withdrawal. Usually spontaneously resolves. \u00a0 P-ulmonary Embolism I-schemia R-espiratory A-trial myxoma, enlargement T-hyroid E-thanol S-epsis \u00a0 \u00a0 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) \u00a0 If there is any doubt about A. Fib on ekg, get a strip with 50 mm\/sec speed and use calipers to determine regularity.<\/p>\n
faster hit (a\/v node) the less it conductsby slowing the flutter rate, you actually can wind up increasing the ventricular rate<\/p>\n
\u00b7 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 \u00b7 Use the steak sauce for best conduction \u00b7 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 \u00b7 Start at 200J in stable patients, 360J in unstable patients. \u00b7 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)<\/p>\n
Author Dose Response Moran et al 1995 37mg\/kg bolus followed by infusion of 25mg\/kg\/hr 42 patients \u2013 60% conversion in magnesium group and 45% in amiodarone group. Brodsky, et al, 1994 2 grams over 6 minutes \u2013 then 1 gram per hour 10\/10 reduced HR to < 90 versus only 4 of 8 in placebo by 4 hours Tachyarrhythmia\u0092s Notes 10 Mel E. Herbert, MD, MBBS, BMedSci, FACEP, FAAEM Hays et al 1994 2 grams bolus minutes \u2013 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)<\/p>\n
dilt was better than amio and dig but, dig and amio seemed the same for rate control (Crit Care Med 2009;37(7):2174)<\/p>\n
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\u0094 Weigner et al Ann Intern Med 1997;126:615-620 \u00a0 \u00a0 Independent predictors of ischacmic stroke in non-valve atrial fibrillation<\/strong> Consistent predictors<\/strong><\/p>\n Inconsistent predictors<\/strong><\/p>\n Factors which decrease the risk of stroke<\/strong><\/p>\n *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 \u00a0 Practical guidelines for antithrombotic therapy in non-valvar atrial fibrillation<\/strong> Assess risk, and reassess regularly High risk (annual risk of cerebrovascular accident=8-12%)<\/strong><\/p>\n Moderate risk (annual risk of cerebrovascular accident=4%)<\/strong><\/p>\n Low risk (annual risk=1%)<\/strong><\/p>\n *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 \u00a0 \u00a0 \u00a0 From Michelle Lin: Atrial Fibrillation (AF) = 5x risk for CVA and increases with ageStroke risk stratification for patients with AF:\u0095 Prior CVA or TIA\u0095 HTN\u0095 Age \u2265 75\u0095 CHF\u0095 Poor LV function\u0095 DMCHADS2 stroke risk stratification scheme (Gage BF et al. JAMA 2001;285:2864\u009670.)\u0095 C = Congestive heart failure (1 pt)\u0095 H = Hypertension (1 pt)\u0095 A = Age \u2265 75 (1 pt)\u0095 D = DM (1 pt)\u0095 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 \u2264 35%DM Treatment Treatment TreatmentASA or Warfarin ASA or Warfarin (1 risk factor) WarfarinWarfarin (\u2265 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 \u00a0 \u00a0 \u00a0 \u00a0 \u00a0 \u00a0 \u00a0 \u00a0 LMWH is just as good as UFH in a-fib in a large RCT (Circulation 2004;109:997-1003)<\/p>\n rate control has more long term benefit than conversion and maintenance of sinus (NEJM 347:p. 1825, 2002 and NEJM 347:p. 1834, 2002) \u00a0 \u00a0 One study showed safe to withhold anticoagulation if less than 48 hours (Ann Intern Med 1997;126:615) \u00a0 Transient ST-depression with Rapid AF \u2013 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 \u201cpositive stress-test equivalent\u201d. 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 \u2013 in the absence of clinical predictors suggesting acute myocardial ischemia (e.g. chest pressure, dyspnea, diaphoresis, etc.), routine \u201crule-out ACS\u201d 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) \u00a0 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 \u2013 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.<\/p>\n\n
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Rate Control vs. Rhythm Control<\/h4>\n