1979
DOI: 10.1016/s0002-9149(79)80008-9
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Cardiac damage produced by direct current countershock applied to the heart

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Cited by 163 publications
(33 citation statements)
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“…If an initial low-energy shock fails to defibrillate, the usual clinical practice is to repeat shocks at progressively higher energies until successful, but the combination of multiple shocks and a longer duration of ventricular fibrillation and ischemia increases the chances of myocardial damage. '13 14 If transthoracic impedance could be accurately determined in advance of defibrillation or cardioversion, inappropriately low energies could be avoided in patients with known high transthoracic impedance. This would help reduce the number of shocks required and avoid unnecessary delays in restoring sinus rhythm.…”
mentioning
confidence: 99%
“…If an initial low-energy shock fails to defibrillate, the usual clinical practice is to repeat shocks at progressively higher energies until successful, but the combination of multiple shocks and a longer duration of ventricular fibrillation and ischemia increases the chances of myocardial damage. '13 14 If transthoracic impedance could be accurately determined in advance of defibrillation or cardioversion, inappropriately low energies could be avoided in patients with known high transthoracic impedance. This would help reduce the number of shocks required and avoid unnecessary delays in restoring sinus rhythm.…”
mentioning
confidence: 99%
“…The incidence of post-operative ventricular arrhythmias may range from 1.8% -13% (14). Ventricular fibrillation status and attempts for treatment by DC shock may injure the myocardium during reperfusion (15). Although there several anti-arrhythmic agents can be used to prevent postoperative arrhythmia after aortic declamping, there are reports that show amiodarone may be more effective in preventing post-operative arrhythmias (16).…”
Section: Discussionmentioning
confidence: 99%
“…Transient ECG changes consistent with myocyte damage have been reported after transthoracic countershocks 12 and appear to be corroborated by the release of myocardium-specific enzymes 13 and ultrastructural damage to cardiac myocytes. 10 These indirect markers of countershock-induced injury, however, have proven difficult to correlate with surprisingly variable effects on myocardial function.…”
Section: Countershock-induced Contractile Dysfunctionmentioning
confidence: 99%