What Are the Risks for Developing Atrial Fibrillation?
Atrial fibrillation is the most common arrhythmia seen in the intensive care unit setting, particularly in the elderly.16, 17 Risk factors for developing atrial fibrillation include hypertension, coronary artery disease, diabetes, valvular heart disease, and heart failure. Atrial fibrillation can also occur in patients with structurally normal hearts. Reversible causes of atrial fibrillation include hypoxia, cardiac ischemia, infection, hyperthyroidism, electrolyte disturbances, drugs (such as theophylline and digitalis), alcohol, sleep deprivation, obesity, and increased sympathetic tone. One must always consider an acute pulmonary embolism as the cause of atrial fibrillation, and this arrhythmia may rarely be the only sign. Atrial fibrillation is frequently seen in the postoperative period following cardiac and noncardiac surgery. In one study the incidence of postoperative atrial fibrillation following noncardiac surgery was 4.1%.18 There is a 10% to 65% incidence of atrial fibrillation following open-heart surgery.19
How Is Atrial Fibrillation Classified?
According to the ACC/AHA/European Society of Cardiology (ESC) guidelines, atrial fibrillation is classified as paroxysmal, persistent, or permanent.20 Paroxysmal atrial fibrillation is defined as recurrent atrial fibrillation (two or more episodes) that terminates spontaneously within 7 days. Persistent atrial fibrillation applies to recurrent atrial fibrillation with a duration of longer than 7 days that is not self-terminating. Persistent atrial fibrillation can terminate spontaneously after 7 days or can be cardioverted, either electrically or pharmacologically. Atrial fibrillation is considered “long-standing persistent” if it is present for longer than 1 year. It is considered “permanent” if cardioversion has failed or has not been attempted. The term “lone” atrial fibrillation has been used to apply to patients younger than 60 years old without evidence of structural heart disease.
How Would You Evaluate a Patient with Atrial Fibrillation?
Atrial fibrillation may be symptomatic or asymptomatic. The patient should be questioned regarding symptoms of palpitations, shortness of breath, lightheadedness, fatigue, or chest pain. History should also include the presence or absence of known heart disease, other contributing diseases, family history of atrial fibrillation, current medications, and social history (particularly alcohol intake). However, the patient may be intubated and unable to give any history.
It is important to determine the duration of the atrial fibrillation to help guide management, as this is related to the need for anticoagulation and safety of cardioversion. In addition to a 12-lead ECG, a transthoracic echocardiogram is indicated to evaluate for valvular abnormalities, left atrial size, left ventricular systolic function, and wall thickness, which will help guide medical therapy. For atrial fibrillation of unknown duration or lasting longer than 48 hours with plans for cardioversion, a transesophageal echocardiogram is recommended to exclude left atrial appendage thrombus. Transesophageal echocardiography may also occasionally aid in the diagnosis of a large pulmonary embolism. If the patient has an implantable pacemaker or defibrillator, interrogation of the device may help determine the duration of the atrial arrhythmia. A chest x-ray can also be performed to exclude an infectious process.
What Are the ECG Findings of Atrial Fibrillation?
The ECG will not show P waves, but rather “fibrillatory” waves. The ventricular rate typically ranges from 100 to 170 bpm with irregular R-R intervals in the absence of AV nodal blocking drugs. If there is normal conduction through the AV node, the QRS complex will be narrow. A wide QRS complex during atrial fibrillation represents either a preexisting bundle branch block, a rate-related aberrancy, or conduction through an accessory pathway. Comparison with an old ECG is always helpful.
How Do You Treat Atrial Fibrillation?
Indications for immediate cardioversion include hemodynamic compromise (hypotension), pulmonary edema, cardiac ischemia, or WPW syndrome with very rapid conduction down the accessory pathway. Direct-current cardioversion is painful and requires the patient to be heavily sedated with a short-acting anesthetic. The external defibrillator should be synchronized to the QRS complex to prevent induction of ventricular fibrillation during electrical conversion of atrial fibrillation. The starting energy for conversion of atrial fibrillation is 100 joules, with energies up to 360 joules if initial attempts are unsuccessful. Intravenous ibutilide can also result in conversion to sinus rhythm, but it must be administered cautiously in a monitored setting by trained personnel because of the risk of hypotension and torsades de pointes.
If the patient is hemodynamically stable, the determination of rate vs rhythm control should be made along with decisions regarding anticoagulation and timing of conversion. Anticoagulation status and the need for transesophageal echocardiography have been previously discussed in the atrial flutter section, and this also pertains to atrial fibrillation. Anticoagulation should be continued for at least 4 weeks after cardioversion. The timing and duration of anticoagulation are detailed in the ACC/AHA/ESC guidelines and summarized in Table 32-4.20 Attempts at conversion to sinus rhythm are contraindicated if transesophageal echocardiography demonstrates the presence of left atrial thrombus. In this case, therapeutic anticoagulation should be continued for at least 4 weeks until the thrombus resolves. Repeat transesophageal echocardiography can be performed to document resolution of the thrombus prior to cardioversion. The risks and benefits of anticoagulation must always be taken into account when determining plans for rhythm vs rate control and whether or not cardioversion will be attempted. If a patient is not considered a candidate for even short-term anticoagulation, cardioversion should not be attempted.
Table 32-4.Recommendations for Antithrombotic Therapy to Prevent Ischemic Stroke and Systemic Embolism in Patients with AF Undergoing Cardioversion ||Download (.pdf) Table 32-4. Recommendations for Antithrombotic Therapy to Prevent Ischemic Stroke and Systemic Embolism in Patients with AF Undergoing Cardioversion
|Class I |
For patients with AF of 48-h duration or longer, or when the duration of AF is unknown, anticoagulation (INR 2.0-3.0) is recommended for at least 3 wk prior to and 4 wk after cardioversion, regardless of the method (electrical or pharmacologic) used to restore sinus rhythm (level of evidence: B).
For patients with AF of > 48-h duration requiring immediate cardioversion because of hemodynamic instability, heparin should be administered concurrently (unless contraindicated) by an initial intravenous bolus injection followed by a continuous infusion in a dose adjusted to prolong the activated partial thromboplastin time to 1.5-2 times the reference control value. Thereafter, oral anticoagulation (INR 2.0-3.0) should be provided for at least 4 wk, as for patients undergoing elective cardioversion. Limited data support subcutaneous administration of low-molecular-weight heparin in this indication (level of evidence: C).
For patients with AF of < 48-h duration associated with hemodynamic instability (angina pectoris, myocardial infarction, shock, or pulmonary edema), cardioversion should be performed immediately without delay for prior initiation of anticoagulation (level of evidence: C).
|Class IIa |
During the 48 h after onset of AF, the need for anticoagulation before and after cardioversion may be based on the patient's risk of thromboembolism (level of evidence: C).
As an alternative to anticoagulation prior to cardioversion of AF, it is reasonable to perform transesophageal echocardiography (TEE) in search of thrombus in the left atrium (LA) or left atrial appendage (LAA) (level of evidence: B).
2a. For patients with no identifiable thrombus, cardioversion is reasonable immediately after anticoagulation with unfractionated heparin (eg, initiated by intravenous bolus injection and an infusion continued at a dose adjusted to prolong the activated partial thromboplastin time to 1.5-2 times the control value until oral anticoagulation has been established with an oral vitamin K antagonist [eg, warfarin] as evidenced by an INR ≥ 2.0) (level of evidence: B). Thereafter, continuation of oral anticoagulation (INR 2.0-3.0) is reasonable for a total anticoagulation period of at least 4 wk, as for patients undergoing elective cardioversion (level of evidence: B). Limited data are available to support the subcutaneous administration of a low-molecular-weight heparin in this indication (level of evidence: C).
2b. For patients in whom thrombus is identified by TEE, oral anticoagulation (INR 2.0-3.0) is reasonable for at least 3 wk prior to and 4 wk after restoration of sinus rhythm, and a longer period of anticoagulation may be appropriate even after apparently successful cardioversion, because the risk of thromboembolism often remains elevated in such cases (level of evidence: C).
For patients with atrial flutter undergoing cardioversion, anticoagulation can be beneficial according to the recommendations as for patients with AF (level of evidence: C).
If rate control is elected, a β blocker, calcium channel blocker (verapamil or diltiazem), or digoxin can be utilized. To obtain adequate rate control, more than one agent may be required. Standard drugs and dosing regimens are outlined in Table 32-5.
Table 32-5.Intravenously and Orally Administered Pharmacologic Agents for Heart Rate Control in Patients with Atrial Fibrillation ||Download (.pdf) Table 32-5. Intravenously and Orally Administered Pharmacologic Agents for Heart Rate Control in Patients with Atrial Fibrillation
|Drug in the acute setting ||Loading dose ||Maintenance dose |
|Esmolol ||500 μg/kg IV over 1 min ||60-200 μg/kg/min IV |
|Metoprolol ||2.5-5 mg IV bolus over 2 min; up to 3 doses ||N/A |
|Propranolol ||0.15 mg/kg IV ||N/A |
|Diltiazem ||0.25 mg/kg IV over 2 min ||5-15 mg/h IV |
|Verapamil ||0.075-0.15 mg/kg IV over 2 min ||N/A |
|Digoxin ||0.25 mg IV q2h, up to 1.5 mg ||0.125-0.375 mg daily IV |
|Nonacute setting and chronic maintenance therapy || || |
|Metoprolol || ||25-100 mg PO bid |
|Propranolol || ||80-240 mg PO daily in divided doses |
|Diltiazem || ||120-360 mg PO daily in divided doses |
|Verapamil || ||120-360 mg PO daily in divided doses |
Digoxin is renally excreted and the dose should be adjusted based on the patient's creatinine clearance. Digoxin is less effective in states of increased sympathetic tone and therefore may not significantly slow the ventricular rate in a shock state. Calcium channel blockers have a negative inotropic effect and are therefore contraindicated in patients with decompensated congestive heart failure or severe left ventricular systolic dysfunction. β Blockers should be avoided in patients with asthma or severe chronic obstructive pulmonary disease.
Intravenous amiodarone can be used if pharmacologic cardioversion is desired. Pharmacologic cardioversion carries a similar risk of thromboembolism as electrical cardioversion. Therefore, a transesophageal echocardiogram should be performed to rule out intracardiac thrombus before initiating any antiarrhythmic drugs in the absence of an adequate duration of anticoagulation. The loading dose of amiodarone is a 150-mg bolus over 10 to 15 minutes followed by a continuous infusion of 1 mg/min for the first 6 hours, then 0.5 mg/min for the next 18 hours. Amiodarone may cause hypotension, requiring the dose to be decreased or the infusion to be discontinued. Amiodarone's potential side effects include hepatic, pulmonary, and thyroid toxicities. Baseline liver function and thyroid function tests should be performed. Pulmonary function tests would not be feasible in a critically ill patient, but a chest x-ray should be examined for any serious underlying pulmonary disease. Before beginning any antiarrhythmic medication, a cardiology or electrophysiology consultation should be considered.
Ventricular Arrhythmias: Wide Complex Tachycardias. A 75-year-old man with a known history of coronary artery disease, remote anterior wall MI, status post–coronary artery bypass surgery (3 vessels) in 2002, and recent stenting to a saphenous vein graft presents to the emergency department with shortness of breath, chest pain, and syncope while driving. He is admitted to the ICU. Vital signs on arrival included a blood pressure of 90/50 mm Hg and a heart rate of 160 bpm. Examination was remarkable for a laceration on his forehead, laterally displaced PMI with a tachycardic S1 and S2, clear lung fields, and normal neurologic examination. Head computed tomography scan was unremarkable. His ECG upon presentation is shown in Figure 32-20.
Twelve-lead electrocardiogram is consistent with monomorphic ventricular tachycardia (VT). This VT has a right bundle branch pattern in V1 and QS in V6, with a right superior axis, occurring in a patient with a prior anterior wall myocardial infarction.