Defibrillation and cardioversion is the technique of passing a short burst (about 5 ms) of direct electric current across the thorax to terminate tachyarrhythmias. The electric current simultaneously depolarizes all excitable cardiac tissue and terminates any areas of reentry by halting further propagation of the impulse around the reentry loop. This places all cardiac cells in the same depolarized state, and a dominant pacemaker (usually the sinus node) paces the heart in a regular manner.
Defibrillation or cardioversion uses the same type of equipment. A device stores a known quantity of electrical energy in a storage capacitor and, on command, discharges it through two paddles placed on the chest wall. Usually, a rhythm monitor and a synchronizer circuit are built into the device. Paddle placement can be either anterior-posterior or apex-right parasternal. While some authors found a lower energy requirement for conversion using anterior-posterior paddles, others have not. For emergencies, paddle placement probably does not matter.
To reduce transthorax electrical impedance and increase the amount of current passing through the heart, certain techniques are important at the paddle-chest wall interface. Electrode paste, gel, or saline pads are applied to the surface of the paddles. Firm pressure of 10 to 12.5 kg/cm 2 (20 to 25 lb/in.2) is used to achieve good electrical contact. Larger paddles or defibrillator pads, within reason, have a reduced impedance, but this does not appear to significantly influence the energy required for conversion.
Older devices had significant internal energy losses and delivered as little as 40 percent of the stored energy to the patient. This is not a problem with modern defibrillators, as they deliver very close to the stored amount.
Defibrillation should be done as soon as ventricular fibrillation is diagnosed. The longer ventricular fibrillation persists, the less likely it is that resuscitation will be successful. Current ACLS guidelines recommend 200 J for the first attempt, 200 to 300 J for the second attempt, and 360 J for subsequent defibrillations. Several studies have found that most patients can be defibrillated with 160 to 200 J. Recommendations for children are 2 J/kg (1 J/lb) in the initial attempt and 4 J/kg on subsequent attempts.
Synchronized cardioversion applies the electric current at a time during the cardiac cycle well away from the vulnerable period when there is little chance of inducing ventricular fibrillation—usually about 10 ms after the peak of the R wave. On most machines, the synchronizer circuit must be turned on each time an impulse is desired. Many devices also display by the monitor screen or a flashing light that the synchronizer circuit is detecting properly the QRS complex. Cable leads, rather than the paddles, should be used to monitor the cardiac rhythm to avoid any movement artifact that could be misinterpreted by the synchronizer circuit as the QRS complex.
Complications of defibrillation or cardioversion include the following:
1. Direct myocardial damage: unusual unless there are repeated shocks at high energy (more than 325 J).
2. Ventricular fibrillation: incidence is less than 5 percent with a synchronized discharge but probably greater in the presence of digoxin or quinidine toxicity, hypokalemia, or AMI. However, patients on maintenance digoxin therapy can be safely cardioverted using low energies (less than 50 J).
3. Systemic emboli: about 1.2 to 1.5 percent in patients with chronic atrial fibrillation.
4. ST segment changes: transient elevations or depressions, usually resolving within 5 min.
5. Bradycardias: more common in patients with inferior MIs and those requiring multiple defibrillations-cardioversions. Bradycardias are usually evident during the first 5 s after shock and may occasionally persist for longer than 20 s and require external or internal pacing.
6. Tachycardias: usually sinus tachycardia, occasionally atrial flutter or fibrillation, and usually resolving spontaneously within 5 min.
7. Atrial, junctional, or ventricular ectopy: usually transient and benign.
8. Pulmonary edema: uncommon but may occur in patients with mitral or aortic valvular disease or left ventricular failure.
9. Hypotension: rare, inexplicable, and may last for several hours before spontaneously resolving.
10. Muscle damage: elevated levels of creatine phosphokinase and lactate dehydrogenase are common, but other more specific indicators (CPK-MB and troponin) are rarely abnormal.
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