Emergency Medical

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Rapid Heart Rate

A 40-year-old man presents to the emergency department with palpitations and shortness of breath that started a few minutes before his arrival. The patient states that he was closing his shop when his heart began to beat rapidly and he had difficulty catching his breath. His symptoms started suddenly and continued when paramedics arrived minutes later. They observed a rapid heart rate on the cardiac monitor and associated rhythm strips (see Images 1-2). He was subsequently given adenosine 0.6 mg en route to the hospital. The patient had a momentary period of asystole, but his rapid heart rate returned.

On his arrival to the emergency department, the patient continued to have the sensation that his heart was racing. He denies having any chest pain, nausea, vomiting, diaphoresis, light-headedness, or recent illness. He felt well before this episode. He denies having any symptoms of infection, such as fever, cough, vomiting, diarrhea, anorexia, or dysuria. He reports increased stress at work and is drinking as many as 4 cups of coffee a day. He reports no notable history of medical conditions except for a similar episode of a rapid heart rate about 4 years ago; for this, he was treated with an unknown drug for 2 years. His family history is significant for a father who died of a myocardial infarction at 45 years of age. The patient takes 1 baby aspirin daily. He denies using any over-the-counter or illicit drugs; however, he smokes 3 packs of cigarettes per week.

On physical examination, the patient is afebrile and has a heart rate of 165 bpm and a blood pressure of 138/79 mm Hg. He appears well and is in no acute distress. Findings on head and neck examination are unremarkable. He has no jugular venous distention. His heart rate is rapid and irregular, with an audible S1 and S2 and no gallops, rubs, or murmurs. His lungs are clear bilaterally. His abdomen is soft, nontender, and without any masses. He has no peripheral edema. Results of his laboratory workup, including a CBC, serum electrolyte and cardiac enzyme measurements, and a coagulation panel, are all normal. His chest radiograph is also normal.

An ECG is obtained (see Image 3). What is the diagnosis?


Atrial fibrillation (AF) with a rapid ventricular response: The ECG shows an irregular heart rhythm with no discernible P waves. Rapid atrial fibrillation (AF) may be hard to differentiate from a narrow supraventricular tachycardia (SVT) without close examination of an ECG. The two conditions can result in similar symptoms of heart palpitations and shortness of breath. Patients with rapid AF are not uncommonly given adenosine to treat presumed SVT, as in this case. Although this treatment is typically unsuccessful, the underlying atrial rhythm may be accurately determined when the heart rate briefly slows.

The conversion from a normal sinus rhythm to AF may be due to a number of conditions, including hyperthyroidism, anemia, infection, ischemic heart disease, valvular disease, drug intoxication, or use of stimulants. Increased stress and over consumption of coffee are likely to have been the instigating factors in this patient.

AF is a common arrhythmia characterized by chaotic atrial depolarizations without effective atrial contractions. This rhythm is often seen with increasing age, with a male predominance. This arrhythmia can result in decreased cardiac output and the formation of atrial thrombi. Many patients with AF are asymptomatic, and most have recurrent episodes without knowledge of them.

The American College of Cardiology established a classification system for AF that is based on its duration and etiology. The categories are paroxysmal AF, persistent AF, permanent AF, and lone AF. In paroxysmal AF, the episodes last less than 1 week. If they recur, the condition is considered recurrent paroxysmal AF. In persistent AF, the episodes last longer than 1 week. In permanent AF, the episode lasts longer than 1 year without any attempts for conversion or with attempts that fail. Finally, in lone AF, no underlying structural cardiac or pulmonary disease is found. Patients with lone AF have a low risk of mortality and thromboembolism and may have paroxysmal, persistent, or permanent AF.

The workup for AF involves careful history taking and physical examination, laboratory studies (including a CBC, serum electrolyte tests, toxicology screening, and thyroid function tests), ECG, chest radiography, and echocardiography.

The patientís history should include the time of onset, the frequency of episodes, any associated symptoms, and any history of treatment for AF. Laboratory studies may be useful in determining possible etiologies of AF. The WBC count may help in finding an underlying infection, and the hemoglobin concentration may demonstrate anemia. Electrolyte levels, such as magnesium and potassium levels, may be abnormal, and an elevated creatinine value may indicate a renal insufficiency. Certain illicit drugs can cause a rapid heart rate; therefore, a toxicology screening may be useful when indicated. Hyperthyroidism can predispose patients to AF. For this reason, an evaluation of thyroid function with measurement of the patientís thyroid-stimulating hormone (TSH) level is warranted.

AF can be diagnosed when the ECG shows an irregular rhythm with the absence of P waves. In addition, examine the patient for any signs of left ventricular hypertrophy, bundle branch blocks, and atrioventricular (AV) nodal blocks, as well as for evidence of cardiac ischemia or previous myocardial infarction. Chest radiographs may be useful in evaluating the cardiac silhouette for cardiomegaly and the lung fields and vasculature for evidence of airspace disease or pulmonary edema. A transthoracic echocardiogram can be obtained to identify the size and motion of the atria, ventricles, and cardiac valves, and it can reveal pericardial disease. Transesophageal echocardiography is more sensitive than transthoracic echocardiography for diagnosing left atrial thrombus or left atrial appendage thrombus.

Rate control is important in patients who present with rapid AF of more than 72 hoursí duration, and beta blockers (metoprolol or atenolol) or calcium channel blockers (verapamil or diltiazem) are recommended in patients who do not have an accessory pathway. Digoxin and amiodarone are the drugs of choice for controlling rapid AF in patients with left ventricular failure and no accessory pathway; however, digoxin should be loaded over 24 hours. Therefore, it is unlikely to have a notable effect in the acute setting. If unable to achieve rate control with pharmacologic therapy, catheter-directed AV nodal ablation by a cardiologist may be considered. Anticoagulation treatment is also recommended for most patients with persistent AF, and it is typically achieved with warfarin (dosed to maintain an international normalized ratio [INR] of 2.0-3.0). In patients considered to be at low risk for thromboembolism or in patients who have a contraindication to the use of warfarin, aspirin can be given instead.

Conversion to a sinus rhythm may be achieved with pharmacologic agents or with synchronized external electrical cardioversion. Conversion should be done only when the risk of thromboembolism is limited, as in patients with an onset of symptoms more than 72 hours before presentation, in those who received anticoagulation for 3 weeks, or in those in whom transesophageal echocardiographic results rule out a left atrial thrombus.

After successful cardioversion, anticoagulation therapy should continue for at least 1 month to decrease the risk of thromboembolism, which may occur from the formation of a mural thrombus. After cardioversion is done and the patientís AF reverts to a sinus rhythm, use of daily outpatient antiarrhythmic drugs is not typically recommended, as these drugs have associated risks; therefore, they should be taken only when patients have persistent or frequently recurring symptoms.

Antiarrhythmic drugs that can be used to 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 convert 30-60% of cases of AF to a normal sinus rhythm. Electrical cardioversion has a higher success rate, converting 75-95% of AFs to normal sinus rhythms. Electrical cardioversion may be done in a nonemergency setting after 3 weeks of anticoagulation treatment to decrease the risk of thromboembolism, or it may be required on an emergency basis in a hemodynamically unstable patient. In this situation, AF often has an acute onset, and the benefits of cardioversion outweigh the risks of thromboembolism.

The role of cardioversion to manage AF in the emergency department is an emerging one. Patients who are at low risk, who are clinically stable, and who present to the emergency department with new-onset AF can be treated with chemical or electrical cardioversion and safely discharged, home with close follow-up, by a primary physician or cardiologist.

Images courtesy of ECG Wave-Maven: Self-Assessment Program for Students and Clinicians.


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Link to further Information on:

For more information on AF, see the eMedicine articles Atrial Fibrillation (within the Emergency Medicine specialty) and Atrial Fibrillation (within the Internal Medicine specialty).