CARDIAC CONCERNS
| ATRIAL FIBRILLATION IN THE ED: IT’S NOT JUST DIGOXIN AND DILTIAZEM ANYMORE —Gary
F. Pollock, MD, Associate Residency Director, University of Pittsburgh School of Medicine, Pittsburgh, PA
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| Associated problems: mortality (roughly double that of age-matched controls); embolism and stroke; congestive
heart failure (CHF); leads to problems with anticoagulants; risk for adverse effects from drugs used to control heart
rate; chronic fatigue
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| Etiology: acute coronary syndrome (ACS) most prominent; ≤20% of patients with myocardial infarction (MI) or ischemia
develop atrial fibrillation (AF) close to event; in recent study, ≈15% of patients presenting to emergency
department (ED) with new-onset AF had ACS; other causes include pulmonary disease and pulmonary embolism
(PE), some drugs (eg, alcohol, cocaine, theophylline), and hyperthyroidism
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| Differential diagnosis: heart rate rises to 120 to 140 bpm; if rate slower (90-100 bpm), suspect use of rate-controlling
drugs or preexisting conduction system disease; if rate faster (160-170 bpm), suspect accessory pathway; may
also be due to blood loss, sepsis, or fever
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| Atrial flutter: in general, treatment similar to that of AF; however, flutter generally needs lower energy dose for
conversion; risk for embolic events, (eg, PE) lower, but patients with atrial flutter may drift in and out of AF
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| Management: first determine if patient stable, and reason for any instability; severe ischemia, loss of consciousness,
hypotension, or heart failure require emergency cardioversion, although relapse rate high
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 | Cardioversion: administer sedation and analgesia first if possible; apply pads firmly; most patients respond best to
anterior-posterior pad location, but change location to anterolateral if that proves ineffective; for unstable patients,
recommended starting energy level for monophasic defibrillator 200 to 360 Joules (biphasic defibrillators
may require less energy)
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| Factors associated with cardioversion failure: underlying disease, eg, hyperthyroidism or CHF, which keeps
heart from converting easily; dilated atria; long duration of AF; starting defibrillation with too little energy;
poor pad placement; anticipate failure (have backup plan)
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| Managing stable patients: rate control best approach; slowing heart rate increases diastolic filling time and improves
hemodynamic status; target heart rate 90 to 100 bpm
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| Pharmacologic treatment: mainstays calcium channel blockers, β-blockers, and digoxin; no large head-to-head comparisons
performed, so tailor choice to patient’s individual needs (stability, underlying illness, and comorbid
conditions)
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| Calcium channel blockers: usual first choice; rapid onset of action; response rate 90% to 100%; verapamil safe
choice for patients with stable blood pressure (BP); diltiazem also good; if patient rate-controlled on intravenous
(IV) dose of diltiazem, can switch to oral therapy; start with low dose and increase if needed; precautions and
contraindications—heart block or sick sinus syndrome; simultaneous infusion of β-blocker (combination could
produce heart block); presence of accessory pathway; calcium pretreatment—suggested as way of preventing hypotension;
supporting evidence “a little bit weakbut may work” (little downside other than risk for calcium chloride
extravasation); suggested dose half ampule calcium chloride or 1 ampule calcium gluconate, administered
over several minutes; may help patients with borderline BP; may also be given as rescue medication in patients
who develop hypotension
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| β-blockers: also have rapid onset and high response rate; choose over calcium channel blockers for patients with
MI or other ACS, hyperthyroidism, or other conditions associated with catecholamine excess; precautions and
contraindications—similar to those for calcium channel blockers; bronchospasm also risk with these agents; esmolol
expensive but good choice for unstable patients (short half-life allows it to wash out quickly in case of
problems); otherwise, other agents just as good
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| Digoxin: long history of safety and efficacy; works on vagus nerve, making it ineffective for patients with high
sympathetic tone; poor choice in emergency settings due to slow rate of onset (4-6 hr); not conversion agent;
has positive inotropic effect in patients with CHF, but otherwise second choice; precautions and
contraindications—predisposition to digoxin toxicity, eg, renal failure
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| Other agents: magnesium—effective rate-controller in small trials (consider as adjunctive or second-line therapy);
amiodarone—good at conversion as well as rate control, but benefit over other agents questionable;
clonidine—option for some patients
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| ED work-up: electrocardiography (ECG; look for ischemic changes); chest x-ray (look for signs of CHF); other
tests according to clinical scenario; complete blood cell count, platelet count if thrombocytopenia suspected;
electrolytes, especially potassium; measure drug levels (especially theophylline and digoxin); baseline coagulation;
screening thyroid-stimulating hormone (TSH); consider toxicology screening (cocaine may cause AF)
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| Enzyme measurement: currently supported for patients >60 to 65 yr of age with chest pain, other signs or symptoms
of ischemia, CHF, hypotension, or ECG changes (these patients may also require admission); use clinical
judgment in other cases; no prospective trials
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| Work-up for PE: not indicated unless patient symptomatic or other reasons for suspicion exist
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| Conversion in ED: in United States, varies according to region
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| Issues to keep in mind: risk for thromboembolism and need for anticoagulation; best approach to conversion; risks
and potential complications, and ability to explain to patient and obtain informed consent; actual benefits
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| Anticoagulation: AF leads to stagnation of blood in atria, with potential buildup of clot; without anticoagulation,
chronic AF increases risk for stroke by ≈6% per year; cardioversion itself associated with ≈1.5% incidence of
thromboembolic events (as high as 7% in some studies); anticoagulation for 3 wk before cardioversion decreases
incidence to ≈1.2%; drawbacks of anticoagulation include delayed cardioversion and increased risk for bleeding
complications; prolonged AF associated with higher risk of staying in AF; current cut-off time to cardioversion
48 hr (rate of thromboembolism similar to that of keeping patients on anticoagulants for 4 wk, converting them,
and then resuming anticoagulants for another 3 wk, as long as patient at low risk for thromboembolism; not recommended
for high-risk patients, ie, those with hypertension or diabetes)
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| Transesophageal echocardiography (TEE): possible way to identify patients who qualify for immediate cardioversion;
in acute trials, patients still developed atrial clots, but course of anticoagulation shortened; however, difficult
to perform routine TEE in ED
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| Low molecular weight heparin: consider for outpatients; not widely studied (some trials ongoing); cost savings of
sending patient home may offset expense of drug
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| Recommendations: anticoagulate before conversion if AF has lasted >48 hr; if <48 hr and patient at low risk for
thromboembolic complications, consider “blind” cardioversion, or obtain TEE; if TEE positive, administer anticoagulants
and have patient return; if negative, convert patient and follow with short course of anticoagulants;
some cardiologists recommend anticoagulants for everyone before cardioversion
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| Candidates for cardioversion: unstable patients; those with AF lasting >2 days; patients already taking anticoagulants;
weigh risks of conversion against fact that >50% of patients convert spontaneously within 1 to 2 days (obtain
informed consent; consult patient’s cardiologist or primary care physician, if possible)
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| Methods of cardioversion: electricity (superior to any drug; 86% success in one study); drugs (success rate 50%-
70%, but 50% of patients convert spontaneously anyway)
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| Drugs: procainamide effective and relatively inexpensive, but may cause torsades de pointes; ibutilide works
quickly and has short half-life (6 hr), but associated with 8% incidence of torsades (minimize by correcting hypokalemia
and excluding patients with left ventricular dysfunction); 70% of patients require second dose; expensive;
amiodarone considered good for rate control, less so for conversion (efficacy 50%-60%, depending
on study); recommended dose 150 mg; cost recently decreased; may cause hypotension, but generally considered
safe
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| Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) study: compared total mortality with
antiarrhythmic therapy plus rate control to that associated with rate control alone (all patients received warfarin
[Coumadin]); no differences found in major end points; led to questions about wisdom of correcting AF at all
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| Prehospital treatment: could cause problems if patient has accessory pathway or Wolff-Parkinson-White (WPW)
syndrome; in field, most patients do well with oxygen and basic monitoring, as long as transport time short (inappropriate
intervention could be harmful); if transport time longer, consider patient’s stability
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| Coexisting WPW: if patient has AF with irregular wide-complex tachycardia, giving atrioventricular (AV) node
blocker suppresses node, slows ventricular rate, and could result in ventricular fibrillation; AV nodal blockers contraindicated;
suspect WPW if patient has very fast ventricular rate (ECG shows irregular “wide, bizarre complexes”);
delta wave also sign of WPW; electricity first choice; procainamide also safe
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| Indications for admission: exclusion of serious conditions, eg, PE, MI; monitoring for complications; starting antiarrhythmic
therapy and anticoagulation
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| Candidates for discharge: younger patients with no significant disease; successful conversion in ED or rate easily
controlled, with good follow-up
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| WHICH PATIENTS WITH ACUTE PERICARDITIS CAN BE DISCHARGED ?—Jeffrey Manko, MD, Assistant
Professor of Emergency Medicine, and Associate Program Director, Emergency Medicine Residency,
New York University School of Medicine, New York, NY
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| Classic case: young patient with classic chest pain (retrosternal, pleuritic, worsens upon lying down; audible pericardial
friction rub; ECG shows diffuse ST elevations and PR segment depressions); rarely seen
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| Pericardial disease: pericardium double-layered sac with 15 to 50 mL fluid between layers; increased thickness
associated with inflammation produces symptoms
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| Causes: 85% to 90% of cases idiopathic; other causes include infection, post-MI, neoplasm, uremia, trauma, and
autoimmune disease; imposters — PE, MI
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| Complications: pericardial tamponade most important; could be mistaken for gastroesophageal reflux disease
(GERD), leading to avoidance of aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs), which is treatment
for pericardial tamponade
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| History: onset may be acute or gradual; key symptom pain radiating along trapezius ridge unilaterally or bilaterally
(phrenic nerve traverses pericardium and innervates trapezius); associated features include low-grade intermittent
fever, dyspnea, and dysphagia; consider history as whole
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| Physical examination: friction rub — present in 85% of patients with pericarditis (intensity varies from minute to
minute); if not heard on first attempt, listen again; tamponade—rare in people with idiopathic pericarditis; check
for jugular venous distention, hypotension, and pulsus paradoxus; suspect tamponade in patients with pericarditis
due to malignancy, uremia, or trauma, and treat emergently when found; not same as effusion (effusion may
cause tamponade by compressing heart, resulting in limited cardiac output)
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| ECG: characterized by diffuse ST elevations across limb leads and precordium; phase 1—ST elevation and PR depression;
phase 2—normal; phase 3—inverted T waves; phase 4—normal; if large effusion present, may
see electrical alternans or low-voltage QRS complexes due to insulating effect of effusion
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| Ruling out MI: ST elevations associated with pericarditis usually concave (with MI, they are dome-shaped and
convex); in MI ST elevations regional, in pericarditis diffuse; Q waves and conduction problems absent on
pericarditis ECG; with MI, T-wave inversions come off ST elevation while it is still elevated; PR depressions
uncommon in MI, and arrhythmias uncommon in pericarditis; ST segment/T wave ratio—distance from baseline
to ST segment from lead V6 over peak T wave amplitude; ratio >0.25 suggests pericarditis
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| Chest x-ray: helpful if something visible that rules out pericarditis; can identify pneumonia, pneumothorax, air in
mediastinum, and cardiomegaly
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| Echocardiography: enables simple effusion to be distinguished from tamponade
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| Laboratory tests: cardiac enzymes often elevated, especially troponins
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| Treatment: if cause infectious, treat with antibiotics; pain and inflammation of viral pericarditis treated with
NSAIDs (help in 85%-90% of cases); first choice ibuprofen; avoid indomethacin if patient has coronary artery
disease (decreases coronary blood flow); high-dose aspirin better than ibuprofen if patient has history of MI; 0.6
mg colchicine bid may reduce recurrence of pericarditis more effectively than NSAIDs; combination therapy
may be best; “do not give steroids for pericarditis” (high frequency of recurrence); exceptions—patient has
rheumatologic disorder, or proves refractory to initial therapy
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| Treating tamponade: IV fluids (increase intravascular volume and cardiac output); if fluids ineffective, pericardiocentesis
under ultrasonographic guidance mandatory; buys time until cardiovascular surgeon can provide permanent
drainage; may also leave catheter in after draining fluid
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| Admission criteria: pericardial tamponade; large pericardial effusion; use of anticoagulants; trauma; immunocompromise;
high fever
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| Final recommendations: rule out catastrophic diagnoses (aortic dissection, MI, PE); obtain echocardiography to rule
out tamponade and visualize effusion; outpatient treatment with NSAIDs helps most patients; warn patient that resolution
will take time
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Suggested Reading
[No authors listed]: Atrial fibrillation. Finding the right treatment. 25: 1, 2007; Ali S et al: Evaluation and management
of atrial fibrillation. Cardiovasc Hematol Disord Drug Targets 6: 233, 2006; Bush D et al: Atrial fibrillation
among African Americans, Hispanics, and Caucasians: clinical features and outcomes from the AFFIRM trial. J Natl
Med Assoc 98: 330, 2006; Chan TC et al: Electrocardiographic manifestations: acute myopericarditis. J Emerg Med
17: 865, 1999; Demangone D: ECG manifestations: noncoronary heart disease. Emerg Med Clin North AM 24: 113,
2006; Imazio M et al: Management, risk factors, and outcomes in recurrent pericarditis. Am J Cardiol 96: 736, 2005;
Lange RA, Hillis LD: Clinical practice. Acute pericarditis. N Engl J Med 351:2195, 2004; Lange U et al: Current
aspects of colchicines therapy—classical indications and new therapeutic uses. Eur J Med Res 6: 150, 2001; Page
RL: Medical management of atrial fibrillation: future directions. Heart Rhythm 4: S91, 2007; Rheuban KS: Pericarditis.
Curr Treat Options Cardiovasc Med 7: 419, 2005; Seferovic PM et al: Management strategies in pericardial
emergencies. Herz 31: 891, 2006; Stevenson WG, Tedrow U: Management of atrial fibrillation in patients with
heart failure. Heart Rhythm 4: S28, 2007; Watson T et al: Modern management of atrial fibrillation. Clin Med 7: 28,
2007; Wyse DG: Anticoagulation in atrial fibrillation: a contemporary viewpoint. Heart Rhythm 4: S34, 2007.
Educational Objectives
| The goal of this program is to improve the management of atrial fibrillation and pericarditis. After hearing and assimilating
this program, the clinician will be better able to:
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| 1. Distinguish atrial fibrillation from other heart rhythm disturbances.
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| 2. Recognize the indications for cardioversion.
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| 3. Explain the basic emergency department work-up of a patient in atrial fibrillation.
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| 4. Diagnose pericarditis.
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| 5. Describe the electrocardiographic characteristics associated with pericarditis.
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Faculty Disclosure
In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty members to disclose
relevant financial relationships within the past 12 months that might create any personal conflicts of interest. Any
identified conflicts were resolved to ensure that this educational activity promotes quality in health care and not a proprietary
business or commercial interest. For this program, the faculty reported nothing to disclose.
Acknowledgements
Dr. Pollock spoke at the 2006 Annual Scientific Assembly, held April 25-28, 2006, in Pittsburgh, PA, and sponsored
by the Pennsylvania chapter of the American College of Emergency Physicians. Dr. Manko was recorded at Contemporary
Concepts in Clinical Emergency Medicine, held June 7-9, 2006, in New York City, and sponsored by the Department
of Emergency Medicine, New York University School of Medicine, and NYU Postgraduate Medical
School. The Audio-Digest Foundation thanks the speakers and the sponsors for their cooperation in the production of
this program.
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