Thursday, May 20, 2021

Emergency medicine atrial fibrillation case file

Posted By: Medical Group - 5/20/2021 Post Author : Medical Group Post Date : Thursday, May 20, 2021 Post Time : 5/20/2021
Emergency medicine atrial fibrillation case file
Eugene C. Toy, MD, Barry C. Simon, MD, Terrence H. Liu, MD, MHP, Katrin Y. Takenaka, MD, Adam J. Rosh, MD, MS

Case 3
A 70-year-old man presents to the emergency department complaining of shortness of breath for the past 2 weeks. Previously, he could walk everywhere, but now he becomes fatigued after a short stroll through the grocery store. He also notes that he has felt his heart racing even when he is at rest. His past medical history is notable only for hypertension, for which he takes hydrochlorothiazide and amlodipine. On physical examination, he appears comfortable and speaks in full sentences without difficulty. His blood pressure is 130/90 mm Hg, heart rate is 144 beats per minute, respiratory rate is 18 breaths per minute, oxygen saturation is 98% on room air, and temperature is 37°C (98.6°F). His head and neck examination is unremarkable. His lungs are clear to auscultation. His heartbeat is irregular and rapid, without murmurs rubs or gallops. He has no extremity edema or jugular venous distension. His abdomen is soft and nontender, without masses. Labs show a normal CBC, normal electrolytes, BUN, creatinine, troponin, BNP, and thyroid stimulating hormone. A chest x-ray reveals a normal cardiac silhouette with no pulmonary edema. The ECG is shown below (Figure 3–1).

 What is the most likely diagnosis?
 What are some of the common contributing factors?
 What are some of the complications to this condition?


Figure 3–1. Electrocardiogram. (Reproduced with permission from Tintinalli JE, Kelen GD, Stapczynski
JS, eds. Emergency Medicine. 6th ed. New York, NY: McGraw-Hill; 2004:185.)

Atrial Fibrillation

Summary: A 70-year-old man presents with mild dyspnea on exertion and palpitations. The physical examination reveals a heartbeat that is irregular and rapid at a rate of 144 beats per minute.
  • Most likely diagnosis: Atrial fibrillation with rapid ventricular response
  • Common contributing factors: Increasing age, underlying cardiopulmonary disease (such as hypertension, heart failure, and COPD), hyperthyroidism, sepsis, pulmonary embolism, and electrolyte abnormalities
  • Complications: Early—diminished cardiac output. Late—thromboembolism and cardiomyopathy

  1. Know that atrial fibrillation is often a manifestation of serious underlying disease processes.
  2. Be able to recognize atrial fibrillation on ECG.
  3. Understand the approach to rate control versus rhythm control of atrial fibrillation.
  4. Understand the role of antithrombotic therapy in both the acute and chronic management of atrial fibrillation.

This individual is a 70-year-old man of fairly high function, who is brought into the emergency department because of dyspnea and palpitations. The initial approach should begin with ABCs and an assessment of any life-threatening concerns. Upon arrival, this patient should get an IV and be placed on cardiac and pulse oximetry monitors. The history and physical examination should focus on the patient’s cardiac and pulmonary status. His pulse and the rhythm on the cardiac monitor will both reveal an irregular tachycardia, which should prompt an immediate ECG. The ECG shows an irregularly irregular tachycardia consistent with the diagnosis of atrial fibrillation (AF) with rapid ventricular response (RVR).

In this patient with symptomatic AF with RVR, an early priority in management will be to slow the ventricular rate. For most patients with AF, the typical symptoms of palpitations and dyspnea can be alleviated through simple rate control. In rare cases, tachycardia and loss of the “atrial kick” can lead to diminished cardiac output, hypotension, or congestive heart failure. In those cases, if the arrhythmia is thought to be the primary cause of the patients’ instability, emergent electrical cardioversion is indicated. In the more stable patients, the decision of whether to convert the rhythm depends on a number of factors, including risk of thromboembolism, need for

diseases associated with atrial fibrillation

anticoagulation, and odds of recurrent AF. In all patients, a search for the underlying etiology should be undertaken because AF is often best managed by treating the underlying cause of the rhythm rather than the rhythm itself (Table 3–1).

Approach To:
Atrial Fibrillation

DYSPNEA: Difficult or labored breathing, shortness of breath, or a sensation of breathlessness

THROMBOEMBOLISM: The passage of a blood clot through the vascular system from one part of the body to another—for example, in the setting of AF, a clot forms in the heart and then embolizes through arterial circulation to the brain

CARDIOMYOPATHY: Damage to heart muscle as the result of a number of various insults causing diminished functionality, which can eventually lead to heart failure, arrhythmia, and sudden death

AF affects 1% of the general population and is the most common treatable arrhythmia seen in the emergency department. The prevalence of AF increases with age. In adults younger than 55 years old the prevalence is only 0.1%, whereas in adults greater than 80 years old the prevalence is greater than 10%. AF is more common in men than in women and more common in whites than in blacks. Among patients with AF, 80% have cardiovascular disease, most commonly hypertension, coronary artery disease (CAD), and cardiomyopathy. The remaining common underlying causes include pulmonary diseases such as pulmonary embolism, COPD, and obstructive sleep apnea and systemic diseases such as hyperthyroidism, obesity, and diabetes. The exception is lone AF, which is a term used to describe AF in patients younger than 60 years old who have no evidence of heart disease. However, increasingly
the term “lone AF” has been falling out of favor because it does not have a standardized, universally-accepted definition (see Table 3–1).

It is theorized that AF is caused by a complex interaction between triggers for AF and abnormal atrial myocardium that has multiple reentrant circuits or automatic foci outside the sinoatrial (SA) node. This interplay leads to rapid electrical activity in the atria, which produces disorganized and ineffective atrial contractions. The rapid atrial electrical activity is also conducted through the atrioventriular (AV) node leading to an irregular ventricular response. The ventricular rate, which is usually around 100 to 160, depends on the AV node’s ability to conduct the atrial depolarization and to recover from the previous conduction. On ECG, AF looks like an irregularly irregular, usually narrow-complex, tachcycardia without associated p waves.

AF has a number of clinical implications, most importantly cardiomyopathy and thromboembolization. Acutely, the loss of the “atrial kick” leads to a reduction in cardiac output (CO) by as much as 15%. Together with the rapid ventricular response shortening the diastolic filling time, CO may be significantly reduced, especially in those with already poor left ventricular function. This reduction in CO can result in hypotension and symptoms of heart failure including dyspnea and fatigue. Over the long term, AF causes progressive structural and elctrophysiologic changes in the atria that promote recurrent episodes of AF. Additionally, chronic low levels of tachycardia lead to global cardiomyopathy, which in turn predisposes to more AF. For this reason it is said that AF “begets” more AF.

In addition to heart failure and cardiomyopathy, another important clinical implication of AF is thromboembolization. The disorganized, ineffective atrial contractions caused by AF lead to blood stasis in the left atria, especially in the left atrial appendage. This stasis promotes the formation of a thrombus, which can then dislodge and embolize through the arterial circulation, causing problems such as stroke and limb ischemia. Patients with AF have two to threefold higher risk of stroke compared with the general population.

The management of AF is challenging because AF, rather than being a disease unto itself, is often a symptom of underlying cardiac, pulmonary, endocrine, or toxicological pathology. Successful management begins by initially addressing the patient’s overall clinical status, searching for treatable contributing factors, controlling the rate, and preventing thromboembolism (Figure 3–2).

In stable patients with AF, the treatment options include rate control and/or rhythm control, with or without anticoagulation. In the acute setting such as the emergency department, ventricular rate control is the single most important goal of therapy. Slowing the ventricular response to AF has a number of positive hemodynamic effects including increasing diastolic filling time, improving stroke volume and cardiac output, and stabilizing blood pressure. Drugs used to control the ventricular rate work by slowing conduction through the AV node (Table 3–2).

Algorithm for management of atrial fibrillation

Figure 3–2. Algorithm for management of atrial fibrillation.

There are two groups of patients with AF who should not receive rate controlling agents: (1) unstable patients in whom the instability is presumed to be caused by the rhythm, (2) patients with Wolff-Parkinson-White (WPW) syndrome (Figure 3–3). Patients who are hemodynamically unstable should get immediate electrical cardioversion to restore sinus rhythm. Patients with WPW should not receive any AV nodal blocking agents since they can lead to accelerated conduction down the accessory pathway and potentially induce ventricular fibrillation and cardiac arrest. Patients with WPW and AF should instead get either pharmacologic or electrical cardioversion depending on their hemodynamic stability.

In order to cardiovert AF, several issues must first be addressed: the need for anticoagulation and the timing and method of cardioversion. During AF, uncoordinated atrial contractions lead to intra-atrial thrombus formation. The longer the duration of AF, the greater is the likelihood of clot formation. Following cardioversion, the period of “atrial stunning” can also lead to thrombogenesis. Without anticoagulation 4% to 5% of patients will have a thromboembolic event in the first

therapies for rate control of atrial fibrillation

Abbreviations: AV = atrioventricular; LV = left ventricle; ED = emergency department; CHF = congestive heart failure;
NSR = normal sinus rhythm.

ECG of Wolff-Parkinson

Figure 3–3. ECG of Wolff-Parkinson-White syndrome with atrial fibrillation.

month following cardioversion either from the dislodging of an existing clot or the formation of new clot caused by the “atrial stunning.” This risk increases with the duration of the AF and the underlying disease processes.

Many practitioners use the “48-hour rule” to guide anticoagulation: AF of less than 48 hours duration does not generally require acute anticoagulation except when the patient has mitral valve disease, severe left ventricle dysfunction, or prior history of embolic stroke. Several recent studies have shown that it is both safe and cost-effective for patients with an uncomplicated clinical status who present to the emergency department with AF for less than 48 hours to be cardioverted and discharged directly from the emergency room.

Conversely, patients presenting with AF of greater than 48 hours duration should be anticoagulated prior to cardioversion. The two main approaches for pre-cardioversion anticoagulation are warfarin (Coumadin) or the combination of heparin/enoxaparin (LMWH) plus a screening transesophageal echocardiography (TEE). The conventional approach is to give warfarin therapy with an INR goal of 2 to 3 for 3 to 4 weeks before cardioversion. The alternative approach is quicker and consists of doing a TEE and, if no clot is seen, administering heparin or enoxaparin and proceeding immediately to cardioversion (Table 3–3). In both approaches, warfarin therapy (with and INR of 2-3) must be continued for at least 3 to 4 weeks post-cardioversion in order to prevent new clot formation during the “atrial stunning window.” Both approaches reduce the risk of thromboembolism to less than 1% over 8 weeks.

The two methods of cardioversion are direct current (DC) cardioversion and pharmacologic cardioversion, with DC cardioversion being the more effective approach (see Tables 3–4 and 3–5). The risk of thromboembolism is similar, regardless of which method is chosen. The likelihood of a successful cardioversion for either method depends on the characteristics of the patient, the etiology of the AF, and, most importantly, the duration of the AF. New-onset AF will spontaneously convert in about 70% of cases, whereas cases of AF with a longer duration and

anticoagulation approaches for cardioversion

dc cardioversion

dilated atria may prove refractory to all attempts at cardioversion. The success rate for electrical cardioversion is between 75% and 93%, but only about 50% if the AF has been present for more than 5 years. The success rate of pharmacological cardioversion, regardless of the drug used, is between 50% and 70% for recent onset AF and about 30% for chronic AF.

Following cardioversion, 20% to 30% of patients will remain in normal sinus rhythm (NSR). The patients most likely to have recurrent AF are those with hypertension, an enlarged left atrium, heart failure, or AF for more than a year. It is generally thought that the risks of toxicity and proarrhythmic effects of antiarrhythmic therapy after cardioversion outweigh the benefits, especially in patients with no prior episodes of AF. However, in some patients who have persistent symptoms

drugs for pharmacologic cardioversion

Abbreviations: CAD = coronary artery disease; IV= intravenous; VT = ventricular tachycardia; LV = left ventricle; AF =
atrial fi brillation.

despite adequate rate control or who have an inability to attain adequate rate control, a rhythm control strategy may be chosen. Amiodarone and propafenone are commonly used agents to maintain sinus rhythm.

Dronedarone is a new drug approved in the United States to prevent recurrent AF. It is structurally similar to amiodarone but lacks an iodine moiety. Dronedarone has been shown to be better tolerated than amiodarone with fewer thyroid, dermatologic, neurologic and ocular side effects. The drawbacks to dronedarone are that it is less effective at decreasing recurrent AF compared with amiodarone, and that it is associated with increased mortality in NYHA class IV heart failure or recently decompensated heart failure.

An alternative therapy to maintaining sinus rhythm that has had increasing interest and investigation is radiofrequency catheter ablation. Ablation is recommended for a select patient populations with symptomatic AF and mild or no left atrial enlargement in whom a rhythm control strategy has been chosen, but who have failed treatment with one or more antiarrhythmic drugs. Given the shortcomings of chronic antiarrythmic therapy, in terms of side effects and recidivism rates, electrophysiologic interventions are likely to become more widespread.

Thromboembolic Risk Reduction
Patients with AF have a two- to threefold higher risk of stroke than the general population. The risk is the same for patients with paroxysmal, persistent or chronic AF. It was previously thought that the use of antiarrhythmic agents to maintain a sinus rhythm reduced this risk. The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) trial, which compared rhythm control to rate control plus warfarin in 4060 patients, showed the rate control plus warfarin group had a trend toward better survival, fewer hospitalizations, and better quality of life scores. Interestingly, the rhythm control patients who were not on warfarin experienced a significantly higher incidence of stroke. This data suggest that even patients with rare or intermittent AF may benefit from antithrombotic therapy.

The type of antithrombotic therapy (either anticoagulation or antiplatelet therapy) used to prevent thromboembolism depends on the patient’s individual risk of having a thromboembolic event and his risk of bleeding on antithrombotic therapy. The most validated and clinically useful risk stratification model for determining stroke risk is the CHADS2 score (Table 3–6).

Anticoagulation therapy traditionally consists of warfarin with an INR goal between 2 and 3. Dabigatran is a new oral anticoagulation agent that was shown



aAnnual bleeding risk on dabigatran or warfarin therapy is about 2%-3%.

to be superior to warfarin in the recent RE-LY trial. Dabigatran reduces the rate of ischemic and hemorrhagic strokes, major bleeding, and overall mortality compared to warfarin. In addition to being more effective and safer, it does not require INR monitoring, is less susceptible to diet and drug interactions, and does not have warfarin’s narrow therapeutic window. However, the drawbacks to dabigatran are its higher cost, twice daily dosing, need for adjustment in patients with renal failure, lack of an antidote, and lack of long-term safety data. The dosage for dabigatran is 150 mg twice daily. The 110 mg twice daily dose is recommended for patients with increased risk of bleeding. However, the 110 mg capsule is currently not available in the United States.

Antiplatelet therapy consists of aspirin 75 to 325 mg daily, clopidogrel 75 mg daily, or both together. Aspirin has only a very small ability to reduce stroke risk. For patients with no risk factors for stroke, the current evidence shows that the risk of bleeding from aspirin likely exceeds the small benefit of decreased stroke risk. Aspirin, clopidogrel, and aspirin plus clopidogrel are all less effective in preventing stroke than warfarin. For patients who need anticoagulation but cannot take warfarin or dabigatran, the combination of clopidogrel plus aspirin is more effective than aspirin alone. However, this combination carries similar bleeding risks to formal anticoagulation (Table 3–7).


3.1 A 75-year-old man is found to have asymptomatic atrial fi brillation. Which of the following is the most common complication of his atrial fi brillation?
A. Sudden death
B. Stroke
C. Shock
D. Dyspnea

3.2 An 83-year-old woman with a history of hypertension presents to the emergency department with dyspnea, fatigue, and palpitations. Her blood pressure is 85/50 mm Hg and her heartbeat is 150 beats per minute and irregular. Which of the following is the best treatment for this patient?
A. Diltiazem
B. Metoprolol
C. Coumadin
D. DC cardioversion

3.3 A 62-year-old woman is seen in the emergency department for wrist pain after tripping and falling. She is found to have a distal radius fracture on x-ray, which is reduced and splinted. However, her heart rate is 80 beats per minute and irregular to palpation. On ECG, she is diagnosed with atrial fi brillation with a ventricular response of 114 beats per minute. She does not recall ever being told about this condition. Which of the following is the best initial treatment for this patient?
A. Diltiazem
B. DC cardioversion
C. Synthroid
D. Ibutilide


3.1 B. Stroke is two to three times more likely in patients with AF than in the general population.

3.2 D. Always cardiovert any unstable patient (congestive heart failure, chest pain, hypotension) with AF if the instability is felt to be rhythm related. AF with rapid ventricular response does not allow for ventricular filling, leading to ineffective cardiac output.

3.3 A. Diltiazem was the only rate-controlling agent listed, and is very useful in the initial management of AF with rapid ventricular response.


 Treatment of atrial fibrillation (AF) begins with searching for any underlying reversible causes of the arrhythmia.

 In an acute setting, the most important goal of therapy is ventricular rate control, typically through the use of AV nodal blocking drugs.

 Unstable patients with AF or Wolff-Parkinson-White tachyarrhythmia with AF should undergo immediate electrical cardioversion.

 Stable patients with AF for less than 48 hours can be cardioverted in the ED provided they have no prior history of thromboembolism, mitral valve disease, or LV dysfunction.

 Stable patients with AF of greater than 48 hours or unknown duration can be cardioverted in two ways: (1) anticoagulation for 3-4 weeks prior to, and following cardioversion, or (2) imaging by TEE and, if no intracardiac thrombus is seen, acute anticoagulation with heparin/LMWH, followed by cardioversion, and anticoagulation for 3-4 weeks.

 70% of new-onset AF will spontaneously convert to sinus rhythm.

 Patients with AF have a two to three times higher risk of stroke than the general population.

 The choice of antithrombotic therapy for long-term AF depends on an individual’s CHADS2 score and risk of bleeding.

 Anticoagulation with either warfarin (INR goal 2-3) or dabigatran reduces the risk of thromboembolism.


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