Patient D is a man, 68 years of age, who presents to the emergency department late one evening complaining of increasing shortness of breath, dizziness, and the sensation of his "heart racing." On admission, his heart rate is 160 bpm, blood pressure 100/50 mm Hg, respirations 26 breaths per minute, and oxygen saturation 88% on room air. Patient D says that his symptoms started abruptly earlier that day and have steadily become worse. He reports a history of long-standing hypertension, coronary artery disease, and a recent percutaneous transluminal angioplasty with placement of two stents.

Comments and rationale: Symptoms such as those Patient D presents are common indications of acute onset atrial fibrillation with rapid ventricular response. His past medical history is positive for risk factors for the development of atrial fibrillation. These include a positive cardiac history, with hypertension and coronary artery disease, as well as increasing age.

A 12-lead ECG is obtained. It shows a narrow QRS complex tachycardia with an irregularly irregular rhythm. A diagnosis of atrial fibrillation with rapid ventricular response is made. Oxygen via nasal cannula at 2 liters is started. Patient D is attached to continuous telemetry, oxygen saturation, and noninvasive blood pressure monitoring. Telemetry monitoring shows a variable heart rate ranging from 120 to 160 bpm. At lower rates, fibrillatory waves are present. Crackles are present in the bases of both lungs. Peripheral pulses are diminished and irregular. Patient D's skin is cool but dry. A peripheral IV access is established. After determining that Patient D has no known allergies to medications, 20 mg of diltiazem is prescribed to be given by IV push.

Comments and rationale: ECG characteristics associated with atrial fibrillation with rapid ventricular rate include a QRS complex within normal limits (sometimes called "narrow complex") and an irregularly irregular ventricular rhythm. Sinus P waves are absent. At rapid rates, the irregular rhythm and absence of P waves may be difficult to determine. Fibrillatory waves are present but are often not seen at rapid rates. Because of the variable filling time associated with atrial fibrillation, pulse pressure may be intermittent and some beats may not perfuse well to the periphery. Loss of normal atrial contraction coupled with tachycardic heart rates may precipitate signs of heart failure, such as dyspnea, rales, and hypotension. Patient D is symptomatic with his atrial fibrillation but not dangerously unstable (with rapidly falling blood pressure, rapidly increasing signs of heart failure, or increasing chest pain). Therefore, the initial goal of treatment is to slow his heart rate. Diltiazem, a calcium channel blocker, slows conduction through the AV node and prolongs the AV node refractory period, thus slowing the ventricular rate in atrial fibrillation. It has a rapid onset of action. Because IV diltiazem administration is associated with development of bradycardia, heart block, increased signs of congestive heart failure, and hypotension, the patient should be continuously monitored during and after its administration. If the diagnosis of atrial fibrillation with rapid ventricular response cannot be made, adenosine may be used to establish a diagnosis. Oxygen by nasal cannula is used to increase oxygen saturation and decrease the subjective sensation of dyspnea.

In response to the IV diltiazem, Patient D's heart rate initially slowed to a rate of 110 to 120 bpm but rapidly returned to a high rate. After 15 minutes, another bolus was ordered, followed by a continuous infusion of diltiazem at 5 mg/hour. The orders indicated that the drip could be titrated up to a maximum of 15 mg/hour to achieve the desired rate (as long as Patient D's blood pressure remained within ordered parameters). Additional laboratory and diagnostic tests are ordered to rule out or identify any precipitating causes for the arrhythmia. The tests included a complete blood count, serum electrolytes, thyroid function studies, renal and liver function studies, and cardiac enzymes. A portable chest x-ray is performed. Patient D is questioned about his use of over-the-counter medications, alcoholic beverages, illicit drugs, and dietary supplements or herbal medicines. He is then transferred to an inpatient telemetry unit for further monitoring and clinical management.

Comments and rationale: A diltiazem bolus may be repeated after 15 minutes if the desired rate control is not achieved from the initial bolus. The patient should be monitored for the development of side effects, such as hypotension and bradyarrhythmias. Following a bolus, a continuous infusion may then be started to achieve rate control. Blood pressure, ECG, and oxygen saturation monitoring should be done continuously during continuous intravenous infusion. Signs, such as falling blood pressure, decreasing oxygen saturation, and failure to control rate, should be noted and handled immediately. If intolerable side effects develop, the diltiazem will be discontinued and another medication prescribed. If side effects do not develop but rate control is not achieved, additional medications may be prescribed. Other medications used for rate control include procainamide, esmolol, metoprolol, and propranolol. Patients receiving multiple antiarrhythmics should be monitored closely as combination therapy may result in a cumulative effect on heart rate and rhythm, blood pressure, and the patient's risk of developing congestive heart failure. To effectively manage atrial fibrillation, any underlying or precipitating causes should be identified and corrected. Precipitating causes may include anemia, consumption of alcohol, use of cocaine or other similar substance, hyperthyroidism, and electrolyte imbalances (especially potassium and magnesium). Atrial arrhythmias may also develop during acute stages of myocardial infarction.

Patient D is transferred to an appropriate inpatient unit. Continuous ECG, blood pressure, and oxygen saturation monitoring are maintained. After one to two hours on the diltiazem drip, the patient's heart rate drops and stabilizes at 80 to 90 bpm. Fibrillatory waves and an irregularly irregular ventricular response are clearly present on ECG. His laboratory data comes back showing normal serum electrolytes, renal function studies, thyroid function tests, and liver function tests. His hematocrit and hemoglobin are within normal limits. His cardiac enzymes and troponin are negative for myocardial infarction. His chest x-ray shows some congestion in his lower lobes consistent with mild congestive heart failure. Intravenous furosemide is ordered at a low dose to relieve the pulmonary congestion. Patient D's vital signs improve. His blood pressure increases to 118/70 mm Hg, his respiratory rate slows to 18 breaths per minute, and he reports a decreased sensation of dyspnea and palpitations. After he stabilizes, the process of weaning the IV drip and starting the patient on oral diltiazem is initiated. Low-dose oral diltiazem is effective in maintaining rate control for Patient D when his activity is limited; however, when his activity level is increased, he begins to experience increasing episodes of an uncontrolled rate. The dose is increased, and rate control during activity improves. Evaluation of Patient D's medical therapy shows his heart rate controlled at 70 to 80 bpm, his blood pressure is stable, and his symptoms relieved. Because of the high risk of thromboembolic events and serious consequences of CVA, Patient D is started on anticoagulation therapy. It is determined that he is at high risk for a CVA, and a heparin drip is started. Oral anticoagulation with warfarin also begins at this time. Routine monitoring of his partial thromboplastin time and PT/INR is ordered.

Comments and rationale: Once rate control is achieved and maintained, the patient's vital signs are stable, and other signs (e.g., signs of congestive heart failure, angina) have resolved, the patient may be changed to an oral dose for maintenance therapy. Short periods of a rapid rate may still occur, especially with exertion. If these episodes are intermittent and nonsustained, they may be effectively managed by adjusting the medication dose or adding additional antiarrhythmic medications. Rate control is considered successful if it alleviates troublesome symptoms, relieves dyspnea, increases activity tolerance, and improves the patient's ability to perform activities of daily living. Anticoagulation is indicated for persons who remain in atrial fibrillation. Because the atria never fully contract in atrial fibrillation, stasis of blood can occur, which may lead to the development of clots. To prevent thromboembolic events such as CVA, anticoagulation should be started. For high-risk patients, warfarin is the drug of choice. In an inpatient setting, intravenous heparin may be used to provide adequate anticoagulation until warfarin reaches a therapeutic serum level.

With careful questioning, it is determined that Patient D's subjective symptoms of atrial fibrillation actually began a week or more prior to his admission. Patient D admits to feeling some palpitations and shortness of breath intermittently but did not seek medical care until the symptoms became severe. Current assessment of Patient D's status shows normal breath sounds with absence of rales, the chest x-ray shows resolution of pulmonary congestion, vital signs are stable, and he is able to participate in activities of daily living and ambulate without trouble. It is decided to send Patient D home on oral medication to maintain rate control, on warfarin for anticoagulation, and monitoring his status over the next several weeks to evaluate the effectiveness of this therapy.

Comments and rationale: Options for long-term management of the patient with atrial fibrillation include restoration of normal sinus rhythm through pharmacologic or electrical cardioversion or rate control through use of oral antiarrhythmic medications. For patients known (or suspected) to be in atrial fibrillation for more than 48 hours, national standards recommend adequate anticoagulation for three weeks prior to either pharmacologic or electrical cardioversion. Or, a transesophageal echo may be performed to rule out a left atrial thrombus. If no thrombus exists, the patient may be safely cardioverted. For patients whose symptoms are controlled by rate control, oral therapy/antiarrhythmics coupled with oral anticoagulation often is sufficient treatment. If the patient develops recurrent episodes of rapid atrial fibrillation, or experiences troublesome symptoms at home despite optimal antiarrhythmic therapy, he/she may benefit from restoration of normal sinus rhythm by more aggressive methods.

Patient D receives verbal and written instructions on how to take his warfarin and his antiarrhythmic medications. Appointments with the outpatient laboratory for PT/INR monitoring are set up, and a follow-up appointment with his physician is scheduled. Patient D is instructed on signs and symptoms to report to the doctor, including signs of bleeding and recurrence of his signs of rapid atrial fibrillation. Indications that medical therapy is effective in managing his atrial fibrillation include: ability to perform normal activities without symptoms of fatigue, dyspnea, dizziness, or palpitations; vital signs within desired parameters; absence of annoying or problematic side effects from medications; and absence of signs of thromboembolic events.

Patient W is a woman, 58 years of age, who is admitted to the unit with bradycardia and near syncope. She says that this morning she had been grocery shopping, became very dizzy, and nearly passed out. On admission assessment, her blood pressure is 116/74 mm Hg, and her heart rate is 48 bpm and irregular. Her respirations are even and easy at a rate of 20 breaths per minute. Her oxygen saturation on room air is 99%. Peripheral pulses are slightly diminished. Lung fields are clear to auscultation. Patient W is placed on continuous telemetry monitoring, and a 12-lead ECG is obtained. The ECG shows that her underlying rhythm is atrial fibrillation with a slow ventricular response. Patient W says that she has had atrial fibrillation for several months. Initially, her heart rate had been controlled on oral antiarrhythmic medications. However, over the last month, she has been experiencing increasing episodes of palpitations and a rapid heart rate. Her medication had been increased, but she developed hypotension and a slow heart rate on the increased dose. A few days prior to her admission, her oral antiarrhythmic medication was changed. On the new medication, she has not had any prolonged episodes of a rapid heart rate but experienced some "dizzy spells."

Comments and rationale: Lack of adequate rate control coupled with development of serious side effects such as bradycardia, hypotension, and syncope with multiple oral agents are indications that oral antiarrhythmic therapy is not effective in managing the patient's atrial fibrillation. Other options include pharmacologic cardioversion, electrical cardioversion, radiofrequency ablation with or without pacemaker insertion, or continuation of oral medications with insertion of a demand pacemaker to treat symptomatic bradycardia.

Laboratory tests are ordered, including a complete blood count, serum electrolytes, renal and hepatic function tests, chest x-ray, urinalysis, and PT/INR. A peripheral IV access is established. Continuous telemetry monitoring is maintained, and Patient W's vital signs are monitored every four hours. Her heart rate remains between 48 and 52 bpm. Patient W's oral antiarrhythmic medication is discontinued. Analysis of Patient W's ECG shows that her QTc is 580 msec. The therapeutic options of electrical cardioversion, radiofrequency ablation, and continued oral antiarrhythmic therapy with insertion of a demand pacemaker are discussed with the patient. The patient expresses reluctance to undergo pacemaker insertion at this time. With the patient's agreement, she is scheduled for electrical cardioversion. Patient W expresses the understanding that pacemaker insertion or ablation with pacemaker insertion might still be required if cardioversion is unsuccessful or if she becomes symptomatic on therapy to maintain sinus rhythm following successful cardioversion.

Comments and rationale: Laboratory tests such as a complete blood count and serum electrolytes are ordered to rule out any abnormal findings (e.g., anemia, hypokalemia, hypomagnesemia) that may make management of atrial fibrillation more difficult. Due to Patient W's continued bradycardia, her oral antiarrhythmic medication is discontinued. Her QTc interval is significantly prolonged. Because Patient W has developed bradycardia and a prolonged QTc interval, she is not a candidate for pharmacologic cardioversion.

Patient W's complete blood count, renal and hepatic function studies, and urinalysis come back within normal limits. Her serum electrolytes show hypokalemia but a normal serum magnesium level. IV potassium replacement is given, and a repeat potassium level returns within normal limits. Patient W's INR comes back at 2.7. Her usual warfarin dose is continued. A review of her outpatient laboratory results shows that her INR has been maintained between 2.6 and 3.1 for more than six weeks.

Comments and rationale: Hypokalemia may contribute to the continuation of atrial fibrillation. It should be corrected prior to electrical cardioversion or other intervention. Because of the risk of thromboembolic complications caused by left atrial thrombi for persons with atrial fibrillation of more than 48 hours duration, anticoagulation with warfarin is indicated. National standards require anticoagulation for at least three weeks prior to cardioversion. The therapeutic target for warfarin is an INR of 2.0–3.0.

Patient W is kept NPO for six hours prior to the cardioversion. She is taken to the preoperative area prior to the procedure and sedated with IV medications. Continuous ECG, blood pressure, and oxygen saturation monitoring is initiated. The cardioverter/defibrillator is set for a low-energy, synchronized shock. The initial shock is ineffective in restoring sinus rhythm. A second, slightly higher energy shock is effective. ECG monitoring shows Patient W is now in normal sinus rhythm at a rate of 62 bpm. Her vital signs are monitored closely until she wakes up from the sedation. Patient W is returned to her room. Continuous telemetry monitoring is continued.

Comments and rationale: Electrical cardioversion is a painful procedure; sedation or general anesthesia is required. Because of the risks associated with sedation/anesthesia, and the risk that the patient may go into ventricular fibrillation from an electrical shock, cardioversion should be performed in a setting where emergency equipment for intubation and management of cardiac arrest is readily available.

Patient W remains in normal sinus rhythm at an acceptable rate in the immediate period postcardioversion. Her blood pressure is stable, and her dizzy spells do not recur. She is discharged on a low-dose oral antiarrhythmic and warfarin. Patient W is instructed to notify a physician if she experiences palpitations, dizziness, or near-fainting spells.

Comments and rationale: Oral antiarrhythmic therapy is generally required to maintain normal sinus rhythm following successful cardioversion. Although Patient W had been unable to take higher dose oral antiarrhythmics, she was able to tolerate low-dose therapy. It is likely that Patient W will experience short episodes of atrial fibrillation. However, therapy is considered successful if these episodes are brief, do not cause debilitating symptoms, and resolve without additional treatment. National standards recommend that anticoagulation therapy be continued for at least four weeks following cardioversion.