What is the treatment of supraventricular tachydys-rhythmias?

What is the treatment of supraventricular tachydys-rhythmias?

The most important initial step is to evaluate whether the patient with an underlying tachycardia is stable or unstable. Tachycardias in unstable patients require imme-diate electrical cardioversion, whereas stable tachycardias are usually treated with drugs and/or electric cardioversion until further evaluation and diagnostic measures can be performed. It is extremely important to treat all wide com-plex tachydysrhythmias as VT. Clinical or ECG criteria used to differentiate wide complex supraventricular tachy-cardias from VT are problematic. Administration of verapamil to a patient with VT may cause irreversible hemo-dynamic collapse. However, since adenosine has almost no effect on blood pressure, it can be tried in stable patients who are suspected of having a wide complex supraventric-ular tachycardia. Adenosine is an endogenous purine nucleoside that depresses sinus and AV nodal activity that is extremely short-acting (the serum half-life is less than 5 seconds) and produces few significant side-effects.

In narrow complex supraventricular tachycardias, vagal maneuvers should be performed or adenosine (0.1 mg/kg i.v. push) administered to help identify the exact underlying rhythm. Treatment also depends on the underlying cardiac function (preserved or impaired, ejection fraction (EF) <40%, congestive heart failure). Paroxysmal supraventricular tachy-cardias can be treated with calcium-channel blockers, β-blockers, digoxin, or amiodarone (the latter especially in the patient with impaired cardiac function). In junctional tachycardia or ectopic or multifocal atrial tachycardia, elec-trical cardioversion is not recommended.

If atrial fibrillation/flutter is suspected as the underlying rhythm, it is imperative to evaluate the patient before further management is initiated. If possible, the patient’s cardiac function should be assessed, a Wolff-Parkinson-White (WPW) syndrome ruled out, and the time of onset of atrial fibrillation determined (<48 hours or >48 hours). The goals are to treat unstable patients urgently to control the rate, convert the rhythm, and to provide anticoagulation. Patients with an onset of symptoms > 48 hours should be evaluated for thrombi in the atria using transesophageal echocardiography (TEE) before electric cardioversion is attempted. WPW patients are preferably treated with elec-tric cardioversion or amiodarone. In these patients, adeno-sine, β-blockers, calcium-channel blockers, and digoxin are contraindicated. These drugs can lead to an increased ven-tricular response or may precipitate VF by selectively blocking the AV node in patients with coexisting accessory conduction pathways. Once the diagnosis of atrial fibrilla-tion/flutter is confirmed, treatment usually consists of elec-tric cardioversion, β-blockers, calcium-channel blockers (e.g., diltiazem), or digoxin. Amiodarone is preferred in the unstable patient or the patient with impaired ventricular function (Table 1.1).