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Cardioversion is a medical procedure by which an abnormally fast heart rate (tachycardia) or other cardiac arrhythmia is converted to a sinus rhythm using electricity or drugs.
Synchronized electrical cardioversion uses a therapeutic dose of electric current to the heart at a specific moment in the cardiac cycle, restoring the activity of the electrical conduction system of the heart. (Defibrillation uses a therapeutic dose of electric current to the heart at a random moment in the cardiac cycle, and is the most effective resuscitation measure for cardiac arrest associated with ventricular fibrillation and pulseless ventricular tachycardia. (2025). 9781451121186, Wolters Kluwer Health/Lippincott Williams & Wilkins. ISBN 9781451121186) Pharmacological cardioversion, also called chemical cardioversion, uses antiarrhythmia medication instead of an electrical shock.
Timing the shock to the R wave prevents the delivery of the shock during the vulnerable period (or relative refractory period) of the cardiac cycle, which could induce ventricular fibrillation. If the patient is conscious, various drugs are often used to help sedate the patient and make the procedure more tolerable. However, if the patient is hemodynamically unstable or unconscious, the shock is given immediately upon confirmation of the Heart arrhythmia. When synchronized electrical cardioversion is performed as an elective procedure, the shocks can be performed in conjunction with drug therapy until sinus rhythm is attained. After the procedure, the patient is monitored to ensure stability of the sinus rhythm.
Synchronized electrical cardioversion is used to treat hemodynamically unstable supraventricular (or narrow complex) , including atrial fibrillation and atrial flutter. It is also used in the emergent treatment of wide complex tachycardias, including ventricular tachycardia, when a pulse is present. Pulseless ventricular tachycardia and ventricular fibrillation are treated with unsynchronized shocks referred to as defibrillation. Electrical therapy is inappropriate for sinus tachycardia, which should always be a part of the differential diagnosis.
Class I agents are sodium (Na) channel blockers (which slow conduction by blocking the Na+ channel) and are divided into 3 subclasses a, b and c. Class Ia slows phase 0 depolarization in the ventricles and increases the absolute refractory period. Procainamide, quinidine and disopyramide are Class Ia agents. Class 1b drugs lengthen phase 3 repolarization. They include lidocaine, mexiletine and phenytoin. Class Ic greatly slow phase 0 depolarization in the ventricles (however unlike 1a have no effect on the refractory period). Flecainide, moricizine and propafenone are Class Ic agents.
Class II agents are beta blockers which inhibit SA and AV node depolarization and slow heart rate. They also decrease cardiac oxygen demand and can prevent cardiac remodeling. Not all beta blockers are the same; some are cardio selective (affecting only beta 1 receptors) while others are non-selective (affecting beta 1 and 2 receptors). Beta blockers that target the beta-1 receptor are called cardio selective because beta-1 is responsible for increasing heart rate; hence a beta blocker will slow the heart rate.
Class III agents (prolong repolarization by blocking outward K+ current): amiodarone and sotalol are effective class III agents. Ibutilide is another Class III agent but has a different mechanism of action (acts to promote influx of sodium through slow-sodium channels). It has been shown to be effective in acute cardioversion of recent-onset atrial fibrillation and atrial flutter.
Class IV drugs are calcium (Ca) channel blockers. They work by inhibiting the action potential of the SA and AV nodes.
If the patient is stable, adenosine may be used for restoration of sinus rhythm in patients with macro-reentrant supraventricular tachycardias. It causes a short-lived cessation of conduction through the atrio-ventricular node breaking the circus movement through the node and the macro-reentrant pathway restoring sinus rhythm.
Before starting the procedure, the patient's chest and back will be prepped for electrode placement. The skin should be free of any oily substances (e.g., lotions) and hair which may otherwise interfere with adhesion of the pads. Once this is complete, the medical team will adhere the pads to the patient using a rolling motion to ensure the absence of air pockets. (see details on pad placement below). The anesthesiology team will then administer a general anesthetic (e.g., propofol) in order to ensure patient comfort and amnesia during the procedure. Opioid analgesics (e.g., fentanyl) may be combined with propofol, although anesthesiology must weigh the benefits against adverse effects including apnea. Bite blocks and extremity restraints are then utilized to prevent self-injury during cardioversion. Once these medications are administered, the glabellar reflex or eyelash reflex may be used to determine the patient's level of consciousness.
The pads are connected to a machine that can interpret the patient's cardiac rate and rhythm and deliver a shock at the appropriate time. The machine should synchronize ('sync') with the R wave of the rhythm strip. Although uncommon, sometimes the machine will unintentionally sync to high amplitude T waves, so it is important to ensure that the machine is synced appropriately to R waves. Interpretation of the patient's rhythm is imperative when using cardioversion to restore sinus rhythm from less emergent arrhythmias where a pulse is present (e.g., atrial flutter, atrial fibrillation). However, if a patient is confirmed to be in pulseless ventricular tachycardia "v-tach" or ventricular fibrillation "v-fib", then a shock is delivered immediately upon connection of the pads. In this application, electrical cardioversion is more properly termed defibrillation.
Often a transesophageal echocardiogram (TEE) is used to assess for thrombus in the left atrial appendage (LAA). This imaging procedure involves inserting an ultrasound probe into the esophagus to obtain detailed images of heart structures, particularly the LAA, where clots commonly form during arrythmia. Detecting the absence of thrombus via TEE allows for safer immediate cardioversion without the need for prolonged anticoagulation beforehand.
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