A 55-year-old woman with a past medical history of congestive heart failure, hypertension, hyperlipidemia, asthma, gastroesophageal reflux disease, and lupus anticoagulant syndrome presents to the emergency department (ED) with severe, progressive shortness of breath that has lasted for the past 12 hours, with associated chest pressure and wheezing. She denies having any leg swelling, chills, sore throat, coughing, or heartburn. Before reaching the ED, she used her albuterol inhaler without relief of symptoms and contacted emergency medical services (EMS). She has a 40-pack-year history of tobacco use, as well as a history of alcoholism (with her last consumption being 4 years before presentation) and remote marijuana use. Her medication regimen includes furosemide, fosinopril, isosorbide nitrate, pantoprazole, spironolactone, and enteric-coated aspirin, but she has a well-documented history of noncompliance.
On physical examination, the patient is afebrile, with a heart rate of 150 bpm, a blood pressure of 202/126 mm Hg, a respiratory rate of 26 breaths/min, and an oxygen saturation of 81% while breathing room air (which improved to 92% when she was given a non-rebreather face mask). In general, she has labored respirations and is unable to speak in full sentences. She has no jugular venous distention of the neck; however, her lung fields are remarkable for bilateral crackles. Her heart sounds include S1 and S2, but no murmurs, rubs, or gallops are noted. The patient has 1+ pitting edema of the lower extremities bilaterally. Incidentally, an atopic dyshidrotic eczematous rash of the skin is noted on the palmar and plantar surfaces of the patient’s hands and feet.
An arterial blood gas drawn while the patient is breathing room air reveals a pH of 7.27, with a partial oxygen pressure of 54 mm Hg and a partial carbon dioxide pressure of 63 mm Hg. The complete blood count (CBC), coagulation profile, serum electrolyte panel, and renal function test are unremarkable. An electrocardiogram (ECG) is performed (see Figure 1), and it shows a tachycardic rhythm of 152 bpm, with a left bundle branch block (which is noted to be pre-existing when compared with a previous ECG). A chest radiograph is performed, which reveals evidence of pulmonary edema.
stepowl said,
March 27, 2008 @ 8:44 am
The initial ECG (see Figure 1) reveals a tachycardic rhythm that is regular and consistent with clockwise typical atrial flutter with a 2:1 atrioventricular conduction block[1]; this is consistent with congestive heart failure. Atrial flutter is a relatively common atrial tachyarrhythmia and is the most significant of the atrial tachyarrhythmias, after sinus tachycardia and atrial fibrillation. Atrial flutter is defined by the presence of stable, uniform atrial activation, which is seen on ECG as flutter waves (most evident in lead II; see Figure 1), and has traditionally been characterized as a macroreentrant arrhythmia, with atrial rates ranging from 240 to 400 bpm[1] (though the rate is most commonly around 300 bpm). Depending on the ventricular rate, the rhythm can interfere with cardiac output, leading to heart failure or atrial thrombus formation. Thrombus places the patient at risk for possible systemic embolization and stroke. Atrial flutter usually includes an atrioventricular (AV) block, with the rhythm commonly conducted at a 2:1 or 4:1 ratio; less commonly, a ratio of 3:1 or 5:1 is seen.[1]
The pathophysiology of atrial flutter includes multiple reentrant or ectopic atrial waveforms reaching the AV node. There are 2 forms of atrial flutter, referred to as type I and type II. Type I, also called typical, common, or isthmus-dependent atrial flutter, involves a reentrant circuit that encircles the tricuspid annulus of the right atrium, with rates that average 240-340 bpm. The depolarizing impulse can travel in a “counterclockwise” fashion around the tricuspid annulus, resulting in negative flutter waves in the inferior leads, or it can travel in a “clockwise” fashion, resulting in positive flutter waves in the inferior leads. Type II atrial flutter, also known as atypical aflutter, is less common and remains uncharacterized except for unusually high rates of
340-440 beats/min.[1,2] The exact etiology of atrial flutter is unknown, but it has been found to occur in patients with a variety of conditions, such as heart failure, pericarditis, valvular disease, pulmonary embolism, chronic obstructive pulmonary disease, and hyperthyroidism, as well as following most types of cardiac surgery. It is estimated that 200,000 new cases of atrial flutter are diagnosed each year in the United States. The condition tends to be more common in elderly men and in patients with the above mentioned comorbidities; however, it can also occur in patients without identifiable risk factors.[1]
After addressing the need for immediate cardioversion in patients with atrial flutter who may be hemodynamically unstable,[1] the general goals for pharmacotherapy include ventricular rate control, conversion to a normal sinus rhythm (NSR), prevention of recurrent episodes, minimization of the risk of thromboembolic complications, and minimization of any adverse effects from pharmacologic therapy.[2] Ventricular rate control can alleviate the symptoms associated with a rapid ventricular response. Two classes of medications are routinely used: calcium channel blockers (eg. diltiazem) and beta-blockers (eg. metoprolol). Both classes of medications work by blocking conduction of the atrial tachydysrhythmia through the AV node. The potential for hypotension associated with the negative inotropic effects of these drugs should be considered when they are used to treat atrial flutter.
After controlling the ventricular rate, the safety of attempting restoration of an NSR must be established; addressing the need for anticoagulation therapy for the prevention of thromboembolic phenomenon should be the first consideration. The success rate of direct current (DC) synchronized cardioversion is >95% for returning the heart to an NSR; however, as with atrial fibrillation, the success rate of sinus rhythm maintenance after 1 year of DC cardioversion without the aid of antiarrhythmic pharmacotherapy varies from 20 to 50%. Atrial flutter generally requires less energy for conversion than atrial fibrillation; in many cases, conversion is achieved with as little as 50 joules. Pharmacologic cardioversion is an alternative to electrical cardioversion, and it offers several choices with regard to specific medications. Procainamide is effective in 0-13% of patients; flecainide, in approximately 10% of patients; and dofetilide, in approximately 70-80% of patients. Ibutilide can convert recent-onset atrial flutter to an NSR in 63% of patients with a single infusion. Large, single oral doses of type IC antiarrhythmic agents, such as propafenone
(450-600 mg) or flecainide (200-300 mg), have been shown to be effective in converting recent-onset atrial fibrillation to an NSR as well.[2] Oral amiodarone during the loading period (>1 mo) has been shown to convert 18% of cases of atrial fibrillation or flutter to an NSR. Intravenous amiodarone is also effective in converting an atrial flutter to an NSR, and it slows the ventricular rate in patients with a rapid ventricular response. A final option is atrial overdrive pacing, which can be performed invasively or through the use of a transesophageal electrode to pace the left atrium; this therapy has a success rate of approximately 50%.[2] A combination of DC cardioversion and antiarrhythmic therapy is most commonly used to effectively restore an NSR and maintain sinus rhythm.[1,2]
After the initial episode of atrial flutter has terminated and any underlying precipitating factors have been treated, some patients may not need any further intervention, except for avoidance of the precipitating factor (eg, alcohol, caffeine); however, as mentioned above, approximately 30% of patients remain in sinus rhythm at 1 year without antiarrhythmic therapy, requiring some sort of maintenance therapy. The guidelines regarding the use of antiarrhythmic agents in atrial flutter are similar to those for using antiarrhythmic agents in atrial fibrillation. In addition, radiofrequency ablation has a high success rate and low complication rate for treating atrial flutter, and in some cases, it may be a more favorable option when compared with lifelong antiarrhythmic drug therapy because of adverse reactions that can include fatal proarrhythmic events and organ toxicity. Antiarrhythmics used to treat atrial fibrillation have been shown to be effective in treating fibrillation or flutter during a 6- to 12-month follow-up; the specific characteristics and the adverse effects of each antiarrhythmic agent should be considered when selecting which pharmacologic agent to use. Generally speaking, class IC agents may be used in patients without structural
heart disease[3]; however, for patients with left ventricular hypertrophy with or without ischemia or conduction delay, class III agents (specifically, sotalol or amiodarone) are the drugs of choice. For patients with significant systolic dysfunction, dofetilide can be an effective option provided that there is no evidence of renal dysfunction.[1,2]
There is an increased risk of thromboembolic complications for patients who have been in atrial flutter for more than 48 hours, which may result from episodic atrial fibrillation leading to impaired left atrial appendage function and subsequent thrombus formation. The same anticoagulation strategy used in patients with atrial fibrillation may be applied to patients with atrial flutter.[2] Some reports have demonstrated thrombus in the left atrium appendage in as many as 43% of patients with atrial flutter, with postcardioversion thromboembolic events occurring in up to 7% of patients who were not anticoagulated. These events, if not occurring immediately after cardioversion, typically occur at about 3 days following cardioversion, with almost all cases occurring within 10 days after restoration of an NSR. Stunning of the left atrial appendage is thought to contribute to thrombogenicity and may play a role for as long as 4 weeks following cardioversion. This is believed to be the source of emboli in patients who have had a thromboembolic event after cardioversion despite no evidence of thrombus found on transesophageal electrocardiography (TEE). Anticoagulation is also recommended for at least 1 week after any ablation of an atrial flutter that persists for more than 48 hours. Adequate anticoagulation, as recommended by the American College of Chest Physicians, has been shown to decrease thromboembolic complications in patients with chronic atrial flutter and in patients undergoing cardioversion.[2]
The patient in this case was placed on noninvasive positive pressure ventilation for her pulmonary edema and treated with intravenous diltiazem for the rapid ventricular response to the underlying 2:1 atrial flutter rhythm. Administration of diltiazem resulted in conversion to a variable block that was mainly 4:1, resulting in a heart rate of around 80 bpm. Additional intravenous pharmacologic therapy with furosemide, nitroglycerin, and morphine sulfate was administered for her congestive heart failure. Heparin was administered as an anticoagulant for the atrial flutter. After several hours, the patient improved notably and was in no evident respiratory distress. The initial examination of cardiac enzymes was unremarkable, and she was admitted to a cardiac unit on a monitored floor for further management of her congestive heart failure, evaluation for possible myocardial ischemia, and workup for her atrial flutter. She continued to improve with intravenous diuretic therapy; on hospital day 2, she underwent a TEE that did not reveal structural heart disease or thrombus in the left atrium. She was DC cardioverted successfully (see ECG in Figure 2) and discharged on warfarin therapy with follow-up.