Author
Lemi Luu, MD
Staff Physician
Section of Emergency Medicine
Yale-New Haven Hospital
New Haven, Connecticut
Disclosure: Lemi Luu, MD, has disclosed no relevant financial relationships.
Editors
Catherine A. Lynch, MD
Clinical Instructor and Global Health Fellow
Attending Physician, Department of Emergency Medicine
Emory University School of Medicine, Emory Healthcare
Atlanta, Georgia
Disclosure: Catherine A. Lynch, MD, has disclosed no relevant financial relationships.
Editors (cont.)
Lars Grimm, MD, MHS
House Staff
Department of Internal Medicine
Duke University Medical Center
Durham, North Carolina
Disclosure: Lars Grimm, MD, MHS, has disclosed no relevant financial relationships.
Alan R. Morrison, MD, PhD
Cardiology Fellow
Yale-New Haven Hospital
New Haven, Connecticut
Disclosure: Alan R. Morrison, MD, PhD, has disclosed no relevant financial relationships.
Rapid heart palpitations with associated dyspnea develop suddenly in a 40-year-old man. His symptoms are acute and progressive when the paramedics arrive. He is placed on a single-lead electrocardiogram (ECG) that demonstrates the above rhythm (ECG tracing courtesy of ECG Wave-Maven).
Which of the following vital signs will delineate the diagnostic or treatment strategy?
A. Respiratory rate
B. Heart rate
C. Blood pressure
D. Temperature
Answer: C, Blood pressure.
The paramedics measure his blood pressure at 156/96 mm Hg, indicating hemodynamic stability. The paramedics give a medicine that leads to ECG results similar to those illustrated above. What drug was most likely administered prior to the man's arrival in the emergency department (ED)?
A. Atropine 1 mg
B. Adenosine 6 mg
C. Amiodarone 300 mg
D. Diltiazem 20 mg
Answer: B, Adenosine 6 mg.
After the administration of adenosine and a subsequent short pause, the patient's presenting rhythm resumes. On arrival to the ED, the patient continues to feel rapid, irregular heart palpitations, as shown in the ECG strip above. He does not have chest pain, diaphoresis, light-headedness, or recent illness. He has a history of untreated hypertension and 1 prior episode of a similar rapid heart rate about 4 years ago. At that time, he was started on an unknown medication and treated for 2 years before discontinuing it on his own. His family history is significant for a father who died of a myocardial infarction at 45 years of age. His medications include 81 mg of aspirin daily.
On physical examination, the man is afebrile and has a heart rate of 165 beats/min and a blood pressure of 138/79 mm Hg. He is in no acute distress. Findings on head and neck examination are unremarkable, and there is no jugular venous distention. His heart rate is rapid and irregular, with an audible S1 and S2. No murmurs, rubs, or gallops are heard. His lungs are clear to auscultation bilaterally. His abdomen is soft, nontender, and without masses. He has no peripheral edema.
The above chest x-ray was done. What is the interpretation of the x-ray?
A. Retrocardiac infiltrate consistent with pneumonia
B. Increased perihilar markings and cephalization consistent with congestive heart failure
C. Normal chest x-ray
D. Widened mediastinum indicating possible aortic dissection
Answer: C, Atrial fibrillation (AF).
An irregular heart rhythm (#1) with no discernible P waves is shown. Without close examination of an ECG, rapid AF may be hard to differentiate from a narrow supraventricular tachycardia, which has a more regular rhythm (#2). The 2 conditions can have similar symptoms of heart palpitations and shortness of breath. Patients with rapid AF are commonly given adenosine to either aid in the diagnosis or treat presumed supraventricular tachycardia. The irregularity of AF can be difficult to discern, but the underlying atrial rhythm may be accurately determined when conduction to the ventricles is transiently disrupted. Atrial flutter, which typically has sawtooth flutter waves (#3), can also be diagnosed with adenosine. ECG tracings courtesy of ECG Wave-Maven.
The conversion from a normal sinus rhythm to AF may be caused by a number of conditions, including hyperthyroidism, anemia, infection, ischemic heart disease, valvular disease, drug intoxication, or the use of stimulants. Increased stress and overconsumption of coffee are contributing factors in this patient.
After sinus tachycardia, AF is the next most common type of arrhythmia seen in the urgent care environment.[1] This map shows AF hospitalization rates for patients age 65 years and older from 2000-2006. The estimated cost of the treatment of AF in 2005 was $6.65 billion/year, including the costs of hospitalization, inpatient and outpatient physician care, and medications.[2] An estimated 2.66 million people will have AF in 2010. As many as 12 million people will have the condition by 2050.[3]
In a patient with heart palpitations and dyspnea, what piece of clinical history is critical in guiding the initial management?
A. Recent cardiac stress test
B. Length of time of current symptoms
C. Lack of chest pain during symptoms
D. History of prior hospitalization for these symptoms
Answer B, Length of time of current symptoms.
The first step in the treatment of newly diagnosed AF is to determine both the hemodynamic stability of the patient and the time of onset of symptoms. All patients with AF, rapid ventricular response, and hemodynamic instability should undergo synchronized cardioversion. A normal sinus rhythm can be accomplished in approximately 60% of patients with 100 J and more than 80% of patients will have a normal sinus rhythm with 200 J of monophasic synchronized cardioversion.[4] If biphasic synchronized cardioversion of 150 J is used, 200 J is recommended for AF. If initial cardioversion is unsuccessful, amiodarone or procainamide can be given intravenously to facilitate further cardioversion attempts.
Whereas hemodynamically unstable patients require emergent cardioversion and hospital admission, those who are hemodynamically stable should be evaluated for thrombus risk. Those who have had symptoms of AF for more than 72 hours have an increased incidence of atrial thrombus formation and will require anticoagulation as well as transesophageal echocardiography (TEE) to rule out any thrombus before undergoing cardioversion.
If the patient is hemodynamically stable with a rapid ventricular response, as shown by the ECG above, rate control should be initiated with beta-blockers or calcium channel blockers until a decision about the need for cardioversion is made. Intravenous digoxin or amiodarone can be effective for patients with low ejection fraction; however, amiodarone carries a risk for chemical cardioversion, which must be weighed against the thrombus risk. Digoxin is given over 24 hours and has little use in the urgent care setting.
Conversion to a sinus rhythm may be done with drugs or synchronized electrical cardioversion. Conversion should be done only when the thromboembolic risk is limited, such as in patients with <72 hours of symptoms, those who received therapeutic anticoagulation for at least 3 weeks, or in those with TEE results that rule out a left atrial thrombus.
Drugs that can convert AF to a normal sinus rhythm include ibutilide, flecainide, procainamide, and amiodarone. Each has different risks, success rates, and indications based on the duration of AF. As a group, antiarrhythmic drugs can accomplish conversion in 30%-60% of cases of AF. Electrical cardioversion has a higher success rate (89%-95%) with minimal short- and long-term complications, resulting in a shorter length of stay in the ED.[5,6]
The pursuit of a rhythm- vs rate-control strategy should be individualized based on the nature, frequency, and severity of symptoms; length of time in persistent AF; left atrial size; comorbidities; response to cardioversion; age; and patient preference. If conversion to a normal sinus rhythm is accomplished, medications can be started to reduce the duration and frequency of AF events. The American College of Cardiology, American Heart Association, and European Society of Cardiology have jointly developed guidelines for long-term antiarrhythmic maintenance treatment of a sinus rhythm.[7]
Radiofrequency ablation has been shown to treat paroxysmal AF and chronic AF because AF episodes often begin in the pulmonary vein circuits. Three-dimensional electroanatomic models like the one above can be used to facilitate placement of the ablation catheter and map ectopic foci in preparation for ablation. The indication for radiofrequency ablation is AF with lifestyle-impairing symptoms and intolerance of at least 1 antiarrhythmic agent.
Patients in AF who have a CHADS2 (Cardiac Failure, Hypertension, Age, Diabetes, Stroke [Doubled]) score greater than 1, as seen above, have an increased risk for stroke annually and require anticoagulation for stroke prevention. The risk is similar for those who are rhythm-controlled and those who are rate-controlled. Thus, anyone presenting with AF of any duration should be evaluated for stroke risk.
In patients who have a high risk for falls or bleeding but who are not candidates for warfarin therapy, data show that aspirin and clopidogrel combined decrease the thrombus risk, but this carries an increased bleeding risk. Therefore, those who are not candidates for warfarin therapy should be placed on aspirin alone.[7,8]
Because of the side effect profile of warfarin, alternative pharmacologic therapies are being evaluated. An oral thrombin inhibitor, dabigatran, was associated with significantly lower rates of stroke and systemic embolism compared with warfarin (P < .001), and lower doses of dabigatran (110 mg) maintained the same efficacy with statistically lower rates of hemorrhage compared with warfarin (P < .001).[9] By binding to the active site on thrombin (as seen above), dabigatran is able to inactivate fibrin-bound and unbound thrombin, leading to more predictable anticoagulation than occurs with unfractionated heparin.[10-12]
Closer examination of the patient's history revealed that he had intermittent symptoms for 4 days prior to presentation. Therefore, he was considered outside the 72-hour time period where he would be at low risk for thromboembolism. He underwent rate control with diltiazem, was started on heparin for anticoagulation, and was admitted for TEE to rule out atrial thrombus. On the following day, the patient underwent successful cardioversion to normal sinus rhythm. Because this was only his second episode of AF in 4 years and he had a CHADS2 score of 1, he was discharged and started on aspirin therapy. Rate control was accomplished with metoprolol because of his concomitant untreated hypertension.
Author
Lemi Luu, MD
Staff Physician
Section of Emergency Medicine
Yale-New Haven Hospital
New Haven, Connecticut
Disclosure: Lemi Luu, MD, has disclosed no relevant financial relationships.
Editors
Catherine A. Lynch, MD
Clinical Instructor and Global Health Fellow
Attending Physician, Department of Emergency Medicine
Emory University School of Medicine, Emory Healthcare
Atlanta, Georgia
Disclosure: Catherine A. Lynch, MD, has disclosed no relevant financial relationships.
Editors (cont.)
Lars Grimm, MD, MHS
House Staff
Department of Internal Medicine
Duke University Medical Center
Durham, North Carolina
Disclosure: Lars Grimm, MD, MHS, has disclosed no relevant financial relationships.
Alan R. Morrison, MD, PhD
Cardiology Fellow
Yale-New Haven Hospital
New Haven, Connecticut
Disclosure: Alan R. Morrison, MD, PhD, has disclosed no relevant financial relationships.
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The Cause of the EKG Pause
Acute Stroke
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