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Originally Posted by DoctorDoom
Would you mind posting a link to a representative article? I'm just curious. Thanks.
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I have googled for about two hours on this one and have found some articles dating as far back as 1998. However those arent what I am looking for so I have not referenced them for you.
From what I heard during my last ACLS cert a few months ago AHA will revise in 2005 based on research showing poor survival rate to discharge (not admit) involving ALS. Much of this is prehospital.
From my searching I have seen survival rates of 3-10% prehospital to discharge. Interestingly one study I glanced at showed survival rates of witnessed codes inhospital by ACLS certified nurses to be about 1 in 4 as opposed to nurse that werent certified.
The following is from the 1999 Bethesda Conference:
http://www.acc.org/clinical/bethesda/beth31/task1.htm
"Pharmacologic Adjuncts to Defibrillation
The prognosis is ominous for a sizable proportion of patients with cardiac arrest in whom spontaneous circulation is not restored by the first few defibrillation shocks and in whom additional ACLS measures, such as endotracheal intubation, epinephrine and antiarrhythmic medications, are required.
Antiarrhythmic drugs. Antiarrhythmic drugs, including lidocaine, bretylium, magnesium and procainamide, have been classified as an "acceptable, probably helpful" treatment for cardiac arrest secondary to ventricular tachyarrhythmias unresponsive to three or more shocks under current ACLS guidelines. Although these drugs represent current clinical practice in the U.S., there is limited evidence supporting the benefit from use of these agents in treating cardiac arrest victims. Use of antiarrhythmic agents has not been universally embraced as an essential component of treatment algorithms for shock-refractory cardiac arrest.
Evidence supporting any clinical benefit from early administration of antiarrhythmic drugs in cardiac arrest is scarce. In early animal trials, either resuscitation of VF was not improved by the addition of procainamide or lidocaine, or any benefit was offset by worsened short-term survival attributed to the drugs' adverse circulatory depressant effects. Ironically, lidocaine, procainamide, quinidine, phenytoin and oral and higher doses of intravenous amiodarone (10 mg/kg body weight) have all been observed to increase the defibrillation threshold and, in theory, make it more difficult to resuscitate hearts from VF (50–55) .
In the only published case-controlled clinical trial in which shock-refractory victims of out-of-hospital VF were stratified according to those who did and those who did not receive lidocaine, no significant differences were observed in the return of an organized rhythm, admission to the hospital or survival to hospital discharge between the treatment groups (56) . A retrospective evaluation of antiarrhythmic drug use during a trial of active compression–decompression CPR found that lidocaine and bretylium were independently associated with a lower likelihood of survival to 1 h after cardiac arrest (57) . Another retrospective study comparing outcomes from a time when ambulances were or were not staffed by personnel who were authorized to give medications found that recipients of lidocaine were more likely to have a return of spontaneous circulation and to be admitted to the hospital, although no survival benefit was demonstrated (58) . In contrast, in a prospective, randomized trial comparing administration of lidocaine with standard doses of epinephrine in shock-refractory VF, not only was there absence of benefit, but survival actually worsened when such pharmacologic therapies served to delay defibrillation (59) .
The current recommended use of magnesium in torsade de pointes is supported only by case reports. Two recent prospective, double-blind, randomized trials of cardiac arrest in patients in the hospital and in the Emergency Department found no benefit from routine treatment with magnesium (60,61) . Finally, none of the reported randomized trials comparing bretylium with placebo or with lidocaine in victims of cardiac arrest demonstrated any significant differences in outcome between treatment groups (62) .
In most studies to date, intravenous amiodarone has been administered only after failure of other antiarrhythmic medications to terminate malignant ventricular tachyarrhythmias. When compared with additional lidocaine and epinephrine in dogs with shock-refractory VF pretreated with prophylactic lidocaine, intravenous amiodarone significantly improved the success of subsequent defibrillation (63) . The Amiodarone in out-of-hospital Resuscitation of REfractory Sustained ventricular Tachyarrhythmias trial (ARREST), a recently published randomized, prospective, double-blind, placebo-controlled trial, evaluated intravenous amiodarone in out-of-hospital cardiac arrest due to VF or pulseless ventricular tachycardia (64) . In 504 randomized patients, a significant improvement in admission to hospital was observed in recipients of intravenous amiodarone as compared with placebo (44% vs. 34%, p = 0.03). The trial was underpowered to detect differences in survival to hospital discharge between the two treatment groups, which tended to favor recipients of intravenous amiodarone. However, this is the only randomized, placebo-controlled clinical trial ever to show a significant benefit from antiarrhythmic drug therapy during CPR.
Conclusions. With the possible exception of intravenous amiodarone, available evidence is inconclusive concerning benefit of antiarrhythmic drugs in cardiac arrest. Most studies addressing this question have been unpowered either to demonstrate or necessarily exclude benefit from such treatment or to have employed a positive but equally unproven control (lidocaine) comparison. The dose and manner in which to administer antiarrhythmic medications during cardiac arrest and the optimal variables by which to measure benefit from treatment (e.g., return of spontaneous circulation, admission alive to the hospital, 24 h survival, discharge from the hospital, neurologic function at hospital discharge, one-year survival) also remain controversial."
Although I have personally seen Amiodarone control arrythmias I doubt it is as effective as AHA or ARREST study in Washington State claims it is.
Also there isnt much evidence supporting ET route for ACLS medications that I am aware of.
Being in your current postition you have better access to this information than I but I will make it my mission to find whatever current research that is out there that actually contradicts the Myths of ACLS-
ccrn
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