Case review

Rescue 18 and Engine 3 respond to a reported unconscious person on a basketball court in a city park. En route, the mobile data terminal in both vehicles flashes a message that CPR is in progress. The engine arrives first, takes over CPR from bystanders, and delivers a countershock from the AED.

The rescue arrives, verifies effective compressions and bag-mask ventilation, and begins advanced life support procedures. Paramedic Martin inserts an intraosseous line into the patient’s right tibia. Paramedic Erikson, who has assumed the position of code commander, requests the administration of epinephrine.

Shortly after the epinephrine administration, the team leader informs Erikson that the next shock is due in 15 seconds. Erikson begins charging the defibrillator. At the mark, Erikson clears the team, verifies the presence of ventricular fibrillation, and delivers the shock.

After switching chest compressors, the team settles into their third CPR cycle. While CPR is ongoing, Erikson notices that the ECG monitor appears to display an organized rhythm. At the two-minute mark, Erikson and Martin both verify the presence of a femoral pulse. The patient remains comatose and does not respond to Erikson’s commands. Martin successfully intubates the patient’s trachea as the team prepares to move the patient to the ambulance.

Transport to the hospital was uneventful. On arrival in the emergency department, the patient had a blood pressure of 110/70, a pulse of 98, and an end-tidal carbon dioxide reading of 45 mm Hg. The medics complete their paperwork and return to their station.

During the next shift, Erikson and Martin transport a different patient to the same hospital and ask about the cardiac arrest survivor. An ED nurse informs the pair that the patient rearrested before they could get him to the catheterization lab and they could not restore a pulse.

Study review

Researchers in King County, Washington retrospectively examined whether lidocaine improved various patient outcome measures when administered to patients who achieved ROSC after suffering an out-of-hospital cardiac arrest.[1] The study included all patients over the age of 18 years who suffered a bystander- or EMS-witnessed, cardiac-related, out-of-hospital cardiac arrest during a 17-year period from 1992-2008.

During the study period, emergency medical dispatchers sent automated external defibrillator (AED) equipped and EMT-trained firefighters simultaneously with paramedics. All EMS responders provided care consistent with American Heart Association resuscitation guidelines current at the time.

Patients selected for the study had ventricular fibrillation or pulseless ventricular tachycardia as the initial arrest rhythm. If the shockable rhythm persisted after the first shock, paramedics generally administered a lidocaine bolus as the first-line antiarrhythmic. However, because the study period spanned several revisions of the AHA cardiac arrest treatment guidelines, some patients received bretylium or procainamide as the bolus antiarrhythmic. Amiodarone was not used in this system except during a brief investigation during the 1990s.

In order to qualify for the study, each patient had to achieve a transient or sustained return of spontaneous circulation (ROSC) during the resuscitation. The transient ROSC period had to last long enough for the paramedic to record a blood pressure or identify other evidence of adequate perfusion. In either case, paramedics had the option of administering lidocaine either as a bolus or a drip to try to prevent rearrests.

The researchers identified three outcome measures for this study. The first was the frequency of rearrest before arrival at the emergency department. The second was whether the patient lived long enough to be admitted to the hospital. The final outcome measure was whether the patient lived long enough for discharge from the hospital. Although many investigations into cardiac arrest include some measure of neurological outcome in the survivors discharged from the hospital, this study did not include that variable as an outcome measure because the information was not uniformly available over the study period.

One thousand seven hundred and twenty one (1721) patients met all of the eligibility criteria for this study. The overwhelming majority (75%) received a lidocaine bolus or a drip during the ROSC period. Both groups (those who received prophylactic lidocaine and those who did not) had similar clinical characteristics (EMS response interval, receipt of early CPR, age, and gender).

Compared to those who did not receive prophylactic lidocaine, patients who did

Experienced significantly fewer rearrest episodes (first outcome variable);

Were more likely to survive long enough to be admitted to the hospital (second outcome variable); and

Were more likely to survive long enough to be discharged from the hospital (third outcome variable).

In a retrospective analysis such as this, researchers cannot control any of the variables that can alter the outcome of the study. However, researchers can use an analysis technique called logistic regression to study the independent effects of each of those variables. Compared to those who did not receive lidocaine, patients who received lidocaine during the immediate post-arrest period were

Three times less likely to rearrest because of a shockable rhythm;

Two times less likely to rearrest because of a nonshockable rhythm;

Almost twice as likely to be admitted to the hospital alive; and

One and one-half times more likely to survive to hospital discharge.

What this means for you

Almost a decade before publication of the first paper on modern CPR, clinicians in Maryland demonstrated the effective use of lidocaine in a prolonged resuscitation attempt of a patient who developed ventricular fibrillation during cardiac catheterization.[2] That same decade, researchers successfully used lidocaine in the resuscitation of canine cardiac arrest presenting in ventricular fibrillation.[3] The authors pointed out, however, that cardiac massage appeared to be an important component of lidocaine’s action. Later, researchers demonstrated the effectiveness of lidocaine in humans for the treatment of ventricular fibrillation that developed in an operating room.[4]

Lidocaine quickly became the antiarrhythmic most often administered during resuscitation attempts following cardiac arrest. Lidocaine, when used in combination with epinephrine, improved defibrillation success compared to epinephrine alone; however, the drug combination had a higher incidence of refibrillation.[5] Since refibrillation is associated with reduced survival,[6] any medication that reduces rearrest frequency without harmful effects has profound clinical significance.

In this study, lidocaine administered after achieving ROSC resulted in a lower frequency of rearrest from a shockable rhythm and a reduced need for additional shocks after achieving ROSC. This suggests that lidocaine may indeed have an antiarrhythmic effect during the post-cardiac arrest period similar to the effects seen with AMI patients in previous decades.[7-10]

Limitations

This study was retrospective and therefore can only establish an association between prophylactic lidocaine administration and improved outcome measures following out-of-hospital VF/pVT arrest. This study was not designed to prove, nor do the authors attempt to claim, that one variable causes the other.

This study only addressed the issue of whether lidocaine might be beneficial when administered during the post-cardiac arrest phase. The authors do not attempt to draw any conclusions on whether lidocaine (or any other antiarrhythmic) administered during the resuscitation attempt would improve outcome.

Patients in this study who received prophylactic lidocaine achieved ROSC significantly sooner after EMS dispatch and had higher systolic blood pressures at ROSC than those who did not receive prophylactic lidocaine. The prophylactic lidocaine obviously had nothing to do with these two variables, but could explain why the prophylactic lidocaine group had better outcomes.

Summary

This study suggests that lidocaine administered during the post-cardiac arrest phase may reduce the incidence of refibrillation in adult victims of witnessed out-of-hospital cardiac arrest presumed to be of cardiac nature. One must be careful not to conclude that the drug is the causative agent for the improved outcomes. The latest American Heart Association guidelines note that there is insufficient evidence to recommend or to refute the prophylactic administration of any antiarrhythmic during the post-cardiac arrest phase.[11] More research is needed to definitively determine the value of lidocaine administration during the post-cardiac period.

References

Kudenchuk, P. J., Newell, C., White, L., Fahrenbruch, C., Rea, T., & Eisenberg, M. (2013). Prophylactic lidocaine for post resuscitation care of patients with out-of-hospital ventricular fibrillation cardiac arrest. Resuscitation, 84(11), 1512-1518. doi:10.1016/j.resuscitation.2013.05.022 Southworth, J. L., McKusisk, V. A., Peirce, C. II., & Rawson, F. L. Jr. (1950). Ventricular fibrillation precipitated by cardiac catheterization: Complete recovery of the patient after forty-five minutes. Journal of the American Medical Association, 143(8), 717-720. doi:10.1001/jama.1950.02910430009003. Carden, N. L., & Steinhaus, J. E. (1956). Lidocaine in cardiac resuscitation from ventricular fibrillation. Circulation Research, 4(6), 680-683. doi:10.1161/01.RES.4.6.680 Degerli, I. U. (1972). The treatment of sixteen cases of cardiac arrest. Resuscitation, 1(3), 247-253. doi:10.1016/0300-9572(72)90054-8 Duncan, T. D., McClusky, D. M., & Porter, J. K. (1982). Use of drugs during cardiopulmonary resuscitation: A review of the literature. Journal of the National Medical Association, 74(12), 1218–1222. van Alem, A. P., Post, J., & Koster, R. W. (2003). VF recurrence: Characteristics and patient outcome in out-of-hospital cardiac arrest. Resuscitation, 59(2), 181–188. doi:10.1016/S0300-9572(03)00208-9 Koster, R. W., & Dunning, A. J. (1985). Intramuscular lidocaine for prevention of lethal arrhythmias in the prehospital phase of acute myocardial infarction. New England Journal of Medicine, 313(18), 1105–1110. doi:10.1056/NEJM198510313131801 Lie, K. I., Liem, K. L., Louridtz, W. J., Janse, M. J., Willebrands, A. F., & Durrer, D. (1978). Efficacy of lidocaine in preventing primary ventricular fibrillation within 1 hour after a 300 mg intramuscular injection. American Journal of Cardiology, 42(3), 486–488. doi:10.1016/0002-9149(78)90945-1 Lie, K. I., Wellens, H. J., van Capelle, F. J., & Durrer, D. (1974). Lidocaine in the prevention of primary ventricular fibrillation. New England Journal of Medicine, 291(25), 1324–1326. doi:10.1056/NEJM197412192912504 Valentine, P. A., Frew, J. L., Mashford, M. L., & Sloman, J. G. (1974). Lidocaine in the prevention of sudden death in the pre-hospital phase of acute infarction. New England Journal of Medicine, 291(25), 1327-1331. doi:10.1056/NEJM197412192912505 Peberdy, M. A., Callaway, C. W., Neumar, R. W., Geocadin, R. G., Zimmerman, J. L., Donnino, M., Gabrielli, A., Silvers, S. M., Zaritsky, A. L., Merchant, R., Vanden Hoek, T. L., & Kronick, S. L. (2010). Part 9: Post– cardiac arrest care: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation 122(suppl 3), S768 –S786. doi:10.1161/CIRCULATIONAHA.110.971002

The author has no financial interest, arrangement, or direct affiliation with any corporation that has a direct interest in the subject matter of this presentation, including manufacturer(s) of any products or provider(s) of services mentioned.

Send correspondence concerning this article to Kenneth W. Navarro, The University of Texas Southwestern School of Health Professions, 5323 Harry Hines Blvd, MC 9134, Dallas, Texas 75390-9134. E-mail: kenneth.navarro@utsouthwestern.edu