Incidence

FAT accounts for 5–15% of patients undergoing electrophysiologic studies. The rates are higher in children (1) [A].

Prevalence

• FAT: 0.34% in asymptomatic individuals and 0.46% in symptomatic patients (1) [A]
• MAT in the hospitalized population has been estimated to be 0.05–0.32% (2) [A].

• Incessant AT may result in dilated cardiomyopathy, which may be reversible after the tachycardia has been terminated.
• Patients being hospitalized with MAT are usually elderly and may have high mortality as a consequence of underlying chronic obstructive pulmonary disease (COPD) (2) [A].

History

• Review for presence of a cardiac or pulmonary disease, recent heart surgery, and the arrhythmogenic effects of current medications.
• Review for previous episodes, management, and current duration of AT.
• FAT may resolve spontaneously. However, failure to perceive the FAT of incessant nature can lead to depression of myocardial function and tachycardia-induced cardiomyopathy. If the tachycardia is not treated aggressively, the myocardial function can continue to decline, resulting in an irreversible cardiomyopathy. This occurs in 80% of cases due to FAT of abnormal automaticity. Patients with faster rates may be at higher risk (1) [A].
• The MAT usually occurs in elderly and seriously ill patients. It may resolve within days following successful management of the underlying disease. If management of the underlying disease is not successful, onset of MAT implies a poor prognosis. MAT may be preceded by or progress to atrial fibrillation or atrial flutter in 50% of cases. The choice of pharmacologic agents may depend on the presence of coexisting medical diseases.

Signs/Physical Exam

• The pulse rate may not be reflective of the atrial rate because of variable AV node conduction.
• The heart rates seen in FAT vary based on the patient's age and catecholamine state. In case of chronic FAT the rate tends to vary from hour to hour influenced by a variety of physiologic factors modifying autonomic tone. Ventricular rate is usually regular.
• In MAT, the rhythm is irregular and the physical examination findings clinically resemble atrial fibrillation.
• Dyspnea, hypoxemia, rales, and crackles are signs of cardiac decompensation.

Labs/Studies

• Electrolytes, digoxin level
• The majority of FATs can be diagnosed from the ECG; however, differentiation from other forms of supraventricular tachycardia (SVT) may be difficult.
  • FAT presents on the ECG with P’ waves that generally show an abnormal axis and configuration, but remain similar in shape. When the focus arises from the left atrium, the P’ wave is negative in lead I; those with focus in the low right atrium show a negative P’ wave axis in the lead aVF with a positive wave in lead I. Occasionally, the focus is in an area close to the sinus node or in the high right atrium and the P’ wave axis is similar to sinus tachycardia. When the rhythm resembles sinus tachycardia, it can lead to a delay in diagnosis and institution of therapy.
  • The atrial rate during FAT is generally between 100 and 180 bpm. Each P’ wave is usually followed by a QRS complex, and the PR interval is typically not prolonged. Thus the P’P’ intervals do not vary by more than 50 ms unless an exit block from the focus of FAT is present.
  • AV block may be present during FAT and is due to decreased sympathetic tone or digitalis toxicity.
  • Tachycardia-induced ST segment depression and T wave inversion may occur and may persist for some time after the cessation of long-lasting FAT.
  • During MAT there are 3 distinct P’ waves of varying morphology in the same ECG lead; there is no dominant atrial pacemaker (difference from sinus rhythm with frequent premature atrial complexes and focal AT); AV conduction may be variable; and there is an isoelectric baseline with varying PP, PR, and RR intervals. Multiple P’ wave morphologies and variable P-R and R-R intervals may contribute to confusion of MAT and atrial fibrillation. The ventricular rate is usually 100–150 bpm but may be as high as 250 bpm.
• Ambulatory (Holter) monitoring is very helpful in establishing the FAT diagnosis.
• Exercise testing is frequently not useful because the sinus heart rate increases and the automatic focus is suppressed.

• A combination of benzodiazepines and opioids will decrease anxiety and modulate sympathetic tone.
• Anticholinergic agents may worsen AT.
• Consider medications that decrease automaticity and AV conduction without decreasing cardiac output.

Increased risk of cardiac complications

Depends on the surgical procedure. There is insufficient evidence to suggest that either general or regional anesthesia is more beneficial for patients with ATs.

• Standard ASA monitors including ECG with ST segment and T wave trends
• Arterial catheter for cases of expected blood pressure instability or need for frequent blood gas evaluation (COPD)
• Central venous catheter is optional, but if utilized, intracardiac stimulation should be minimized during catheter placement.
• Pulmonary artery catheter may be used in cases of cardiomyopathy.

• Increased risk of hemodynamic instability due to cardiac depression caused by intravenous or inhalational anesthetics
• Consider administration of higher doses of benzodiazepines and opioids to decrease sympathetic tone
• Dexmedetomidine, an alpha-2 agonist, may be useful in decreasing the sympathetic tone and the heart rate, but the loading dose may cause significant hypotension.
• Ketamine and pancuronium are relatively contraindicated.
• Minimize the length of laryngoscopy or avoid laryngoscopy with the use of a laryngeal mask airway or intravenous sedation.

• Neither propofol nor volatile agents have significant electrophysiologic effects and are adequate maintenance agents.
• Conservative fluid management in case of cardiomyopathy

• Balanced reversal of neuromuscular block, with slow administration
• Avoid sympathetic stimulation
• Complications:
  • Hemodynamic instability, coronary ischemia
  • Tachycardia-induced cardiomyopathy