FV refractaria Desfibrilación doble secuencial

Dra. Manuela Brinkmann Bizama Urgencióloga

@manu_brinkmann

FV refractaria

• PCR en FV / TVp luego de 1 descarga

• 3 adrenalinas + 3 descargas + 300 mg Amiodarona

• 5 DESCARGAS! [10% OHCA]

Panchal et al 2018 Focused Update on ACLS

Circulation. 2018;138:e740–e749. DOI: 10.1161/CIR.0000000000000613 December 4, 2018 e741

CLINICAL STATEMENTS

AND GUIDELINES

writing group determined Classes of Recommenda-tion and Levels of Evidence according to the most recent recommendations of the American College of Cardiology/AHA Task Force on Clinical Practice Guide-lines4 (Table) by using the process detailed in “Part 2: Evidence Evaluation and Management of Conflicts of Interest” in the “2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.”5

This 2018 ACLS guidelines focused update in-cludes updates only to the recommendations for the use of antiarrhythmics during and immediately after adult ventricular fibrillation (VF) and pulseless ven-tricular tachycardia (pVT) cardiac arrest. All other rec-ommendations and algorithms published in “Part 7: Adult Advanced Cardiovascular Life Support” in the 2015 guidelines update6 and “Part 8: Adult Advanced Cardiovascular Life Support” in the “2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care”7 remain the official ACLS recommendations of the AHA ECC Science Subcommittee and writing groups. In addition, the “2017 American Heart Association Focused Update on Adult Basic Life Support and Car-diopulmonary Resuscitation Quality: An Update to the American Heart Association Guidelines for Cardio-pulmonary Resuscitation and Emergency Cardiovas-cular Care” contains updated AHA recommendations for CPR delivered to adult patients in cardiac arrest.8 Through this systematic evaluation process, several is-sues have been identified in related areas that may be the subject of future systematic reviews.

BACKGROUNDShock-refractory VF/pVT refers to VF or pVT that per-sists or recurs after ≥1 shocks. An antiarrhythmic drug alone is unlikely to pharmacologically convert VF/pVT to an organized perfusing rhythm. Rather, the primary objective of antiarrhythmic drug therapy in shock-refractory VF/pVT is to facilitate successful defibrilla-tion and to reduce the risk of recurrent arrhythmias. In concert with shock delivery, antiarrhythmics can facilitate the restoration and maintenance of a spon-taneous perfusing rhythm. Some antiarrhythmic drugs have been associated with increased rates of return of spontaneous circulation (ROSC) and hospital ad-mission, but none have yet been demonstrated to increase long-term survival or survival with good neu-rological outcome. Thus, establishing vascular access to enable drug administration should not compromise the performance of CPR or timely defibrillation, both of which are associated with improved survival after cardiac arrest. The optimal sequence of ACLS inter-ventions, including administration of antiarrhythmic

drugs during resuscitation, and the preferred manner and timing of drug administration in relation to shock delivery are still not known.

For the 2018 ILCOR systematic review, the ALS Task Force considered new evidence published since the 2015 CoSTR. The review did not specifically address the selection or use of second-line antiarrhythmic drugs or different antiarrhythmic medications given in combina-tion to patients who are unresponsive to the maximum therapeutic dose of the first administered drug, and limited data are available to direct such treatment. In addition, the optimal bundle of care for shock-refractory VF/pVT has not been identified.

USE OF ANTIARRHYTHMIC DRUGS DURING RESUSCITATION FROM ADULT VF/pVT CARDIAC ARREST2018 Evidence SummaryAmiodaroneIntravenous amiodarone is available in 2 approved for-mulations in the United States. One formulation con-tains the diluent polysorbate, which is a vasoactive sol-vent that can potentially cause hypotension. The other formulation contains captisol, which has no known va-soactive effects. In 2 out-of-hospital, blinded, random-ized controlled trials in adults with shock-refractory VF/pVT who received at least 3 shocks and epinephrine, paramedic administration of intravenous amiodarone improved survival to hospital admission. In 1 study, the ARREST trial (Amiodarone in the Out-of-Hospital Re-suscitation of Refractory Sustained Ventricular Tachyar-rhythmias),9 amiodarone (300 mg) in polysorbate im-proved survival to hospital admission compared with a polysorbate placebo. In another study, the ALIVE trial (Amiodarone Versus Lidocaine in Prehospital Ventricu-lar Fibrillation Evaluation),10 5 mg/kg amiodarone in polysorbate improved survival to hospital admission compared with 1.5 mg/kg lidocaine with polysorbate. Survival to hospital discharge and survival with favor-able neurological outcome were not improved by amio-darone, but neither study was powered for those out-comes.

In ROC-ALPS (Resuscitation Outcomes Consortium–Amiodarone, Lidocaine or Placebo Study), a large out-of-hospital randomized controlled trial that compared captisol-based amiodarone with lidocaine or placebo for patients with VF/pVT refractory after at least 1 shock, there was no overall statistically significant difference in survival with good neurological outcome or survival to hospital discharge.11 In this study, ROSC was higher in patients receiving lidocaine compared with those re-ceiving placebo but not for those receiving amiodarone compared with patients receiving placebo. Survival to hospital admission was higher in patients receiving ei-

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the cardiac catheterization laboratory followed byECMO then PCI was associated with greater survivalwith good neurologic function as compared with his-torical control subjects (50% vs. 8.2%; p< 0.0001) (34).A randomized feasibility trial of ECMO in patients withrefractory cardiac arrest was recently initiated in theUnited States (NCT03065647). In summary, there isconsiderable interest in the effectiveness of ECMO inhumans with refractory OHCA.

Another technique that is promulgated to supportpatients with cardiac arrest is IV administration ofmedication to improve blood pressure and flow to thecoronary and cerebral circulation so as to enhancethe likely restoration of circulation and to reduce braininjury. Increased coronary perfusion pressure andcerebral perfusion pressure during CPR may beoffset by increased myocardial work and reducedsubendocardial perfusion (35). Multiple large obser-vational studies from southeast Asia have suggestedthat early but not late use of epinephrine is associatedwith improved outcomes after OHCA (36–38). The onlyplacebo-controlled trial of epinephrine (also calledadrenalin) reported to date did not achieve itsmaximum expected enrollment but did observe thatepinephrine significantly increased restoration ofcirculation and survival to admission as comparedwith placebo (39). Pooled analyses of prior trialsconfirm that vasopressin has no significant benefitover epinephrine (40). In 2 small trials in Greece,epinephrine combined with vasopressin and multipledoses of corticosteroids increased the likelihood ofrestoration of circulation as compared with placebo(41,42). A large pragmatic trial comparing epinephrinewith placebo is currently enrolling patients with OHCAin England (ISRCTN73485024). In summary, thereis considerable interest in the effectiveness of IVvasopressors in humans with refractory cardiac arrest.

Importantly, implementation of ECMO in patientswith refractory cardiac arrest is likely to requirespecialized expertise, delay application of otherpotentially life-saving therapies (e.g., PCI), and incurlarge costs. Similarly, efforts to establish vascularaccess and administer a vasopressor may delayapplication of other potentially life-saving therapies.Clinical research resources are limited. The effective-ness of interventions must be demonstrated defini-tively if claims of their health benefit are to havescientific credibility (43). Thus, evidence-based prac-tice guidelines recommend use of ECMO in patientswith cardiac arrest only with a potentially reversibleetiology during a limited period of mechanicalcardiorespiratory support in settings where it can berapidly implemented (26). In addition, they notethat there is insufficient evidence to make a

recommendation about the optimal timing and fre-quency of epinephrine administration in cardiacarrest (44).

In this issue of JACC: Basic to Translational Science,Bartos et al. (45) use a 2-by-2 factorial design toevaluate the role of ECMO and IV epinephrine in a pigmodel of refractory VF. This was done to simulatepatients with out-of-hospital refractory VF receivingearly transport to the cardiac catheterization labora-tory and ECMO-facilitated coronary revascularizationcompared with routine CPR-based revascularizationwithout ECMO, and to control for concurrent use ofIV epinephrine. The primary outcome of 4-h survivalwas significantly improved with ECMO use (82% vs.31%; p ¼ 0.003). Return of spontaneous circulationfollowing CPR was also significantly improved withECMO use (100% vs. 44%; p ¼ 0.001). A total of 9of the 14 animals on ECMO (64%) met criteria fordecannulation at 4 h. There was no significant dif-ference in 4-h survival in pigs receiving epinephrineversus placebo (47% vs. 69%; p ¼ 0.47), although thestudy lacked power to detect small but importantdifferences in outcome. There was no significantinteraction between use of epinephrine and ECMO.

This study supports the role of ECMO in refractoryVF arrest, and challenges use of epinephrine in thesame population. Epinephrine significantly increasedaortic and coronary perfusion pressures and lacticacid levels. Although the latter decreased in allgroups following reperfusion, those not receivingECMO (i.e., CPR-only group) had substantial attritionof those with the highest lactic acid levels. Unfortu-nately, the study lacked power to compare post-reperfusion lactate levels.

Higher lactic acid levels are associated with worseoutcomes (33) perhaps because of reduced overallperfusion, reduced local perfusion caused by vaso-constriction, increased transport out of tissues, orenhanced glycolysis. Bartos et al. (45) observed thebest survival in animals in the Epi"/ECMOþ groupfollowed by the Epiþ/ECMOþ group. The Epiþ/ECMO" group fared the worst. ECMO may havesalvaged those with the highest lactic acid levels. It isunclear if epinephrine would have had the sameeffect in nonischemic refractory VF or other in cardiacarrest with a nonshockable rhythm.

A limitation of the excellent work by Bartos et al. (45)is that to simulate refractory VF, defibrillation was notadministered to the animals until 45 min from arrest,which is later than is common in patients. The successof defibrillation and survival may have been differentin animals receiving epinephrine versus placebo.

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Another limitation of this work is that it consideredECMObut not othermethods ofmechanical circulatorysupport. There is limited evidence of the effectivenessof intra-aortic balloon pumps in patients with cardio-vascular emergencies (46–48). In a pig model ofmyocardial infarction, early use of an axial-flow cath-eter combined with delayed reperfusion reducedinfarct size versus standard PCI (e.g., Impella,Abiomed Inc., Danvers, Massachusetts) (49). In a pigmodel of VF, Impella improved resuscitability versusstandard care (50). In a pig model of VF, balloon oc-clusion of the aorta but not IV epinephrine improvedresuscitability (51). Although these methods do notprovide oxygenation as does ECMO, they are markedlyeasier and faster to deploy than ECMO. Lack ofoxygenation may be offset by briefer time withreduced blood flow. Future studies should evaluatethese methods of mechanical circulatory support inanimals and humans with cardiac arrest.

Importantly, most trials that evaluated advancedcardiac life support interventions were completed

before the recent emphasis on high-quality CPR andpost-cardiac-arrest care. Over the last 2 decades therehave been significant advances in interventionalcardiology and management of patients with acutecoronary syndromes including novel drugs, andrapid revascularization strategies that have markedlyimproved survival in such patients (52). It is impera-tive to now refocus attention on development andevaluation of evidence-based therapies and systemsof care for patients with refractory OHCA that havenot achieved return of spontaneous circulation butmay still be salvageable. Given the benefit of ECMOand lack of benefit of IV epinephrine observed byBartos et al. (45), such efforts might focus on me-chanical circulatory support rather than IV vaso-pressor therapy.

ADDRESS FOR CORRESPONDENCE: Dr. GrahamNichol, University of Washington, Harborview Centerfor Prehospital Emergency Care, Box 359727, Seattle,Washington. E-mail: nichol@uw.edu.

RE F E RENCE S

1. Benjamin EJ, Blaha MJ, Chiuve SE, et al. Heartdisease and stroke statistics–2017 update: a reportfrom the American Heart Association. Circulation2017;135:e146–603.

2. Slovis CM, Wrenn KD. The technique ofreversing ventricular fibrillation: improve the oddsof success with this five-phase approach. J Crit Illn1994;9:873–89.

3. Dumas F, Cariou A, Manzo-Silberman S, et al.Immediate percutaneous coronary intervention isassociated with better survival after out-of-hospital cardiac arrest: insights from the Procat(Parisian Region out of Hospital Cardiac Arrest)Registry. Circ Cardiovasc Interv 2010;3:200–7.

4. Hallstrom AP, Ornato JP, Weisfeldt M, et al.Public-access defibrillation and survival after out-of-hospital cardiac arrest. N Engl J Med 2004;351:637–46.

5. Sladjana A, Gordana P, Ana S. Emergencyresponse time after out-of-hospital cardiac arrest.Eur J Intern Med 2011;22:386–93.

6. Do HQ, Nielsen SL, Rasmussen LS. Responseinterval is important for survival until admissionafter prehospital cardiac arrest. Dan Med Bull2010;57:A4203.

7. Agarwal DA, Hess EP, Atkinson EJ, et al. Ven-tricular fibrillation in Rochester, Minnesota: expe-rience over 18 years. Resuscitation 2009;80:1253–8.

8. Vukmir RB. Survival from prehospital cardiacarrest is critically dependent upon response time.Resuscitation 2006;69:229–34.

9. Pons PT, Haukoos JS, Bludworth W, et al.Paramedic response time: does it affect pa-tient survival? Acad Emerg Med 2005;12:594–600.

10. Shy BD, Rea TD, Becker LJ, et al. Time tointubation and survival in prehospital cardiac ar-rest. Prehosp Emerg Care 2004;8:394–9.

11. Cheskes S, Schmicker RH, Verbeek PR, et al.The impact of peri-shock pause on survival fromout-of-hospital shockable cardiac arrest duringthe Resuscitation Outcomes Consortium PrimedTrial. Resuscitation 2014;85:336–42.

12. Cheskes S, Schmicker RH, Christenson J, et al.Perishock pause: an independent predictor ofsurvival from out-of-hospital shockable cardiacarrest. Circulation 2011;124:58–66.

13. Stiell IG, Brown SP, Christenson J, et al. What isthe role of chest compression depth during out-of-hospital cardiac arrest resuscitation? Crit CareMed 2012;40:1192–8.

14. Stiell IG, Brown SP, Nichol G, et al. What is theoptimal chest compression depth during out-of-hospital cardiac arrest resuscitation of adult pa-tients? Circulation 2014;130:1962–70.

15. Idris AH, Guffey D, Aufderheide TP, et al.Relationship between chest compression rates andoutcomes from cardiac arrest. Circulation 2012;125:3004–12.

16. Idris AH, Guffey D, Pepe PE, et al. Chestcompression rates and survival following out-of-hospital cardiac arrest. Crit Care Med 2015;43:840–8.

17. Christenson J, Andrusiek D, Everson-Stewart S,et al. Chest compression fraction determines sur-vival in patients with out-of-hospital ventricularfibrillation. Circulation 2009;120:1241–7.

18. Vaillancourt C, Everson-Stewart S,Christenson J, et al. The impact of increased chestcompression fraction on return of spontaneouscirculation for out-of-hospital cardiac arrest

patients not in ventricular fibrillation. Resuscita-tion 2011;82:1501–7.

19. Hypothermia after Cardiac Arrest Study Group.Mild therapeutic hypothermia to improve theneurologic outcome after cardiac arrest. N Engl JMed 2002;346:549–56.

20. Bernard SA, Gray TW, Buist MD, et al. Treat-ment of comatose survivors of out-of-hospitalcardiac arrest with induced hypothermia. N EnglJ Med 2002;346:557–63.

21. Nielsen N, Wetterslev J, Cronberg T, et al.Targeted temperature management at 33 degreesC versus 36 degrees C after cardiac arrest. N Engl JMed 2013;369:2197–206.

22. Nichol G, Thomas E, Callaway CW, et al.Regional variation in out-of-hospital cardiac arrestincidence and outcome. JAMA 2008;300:1423–31.

23. Daya MR, Schmicker RH, Zive DM, et al. Out-of-hospital cardiac arrest survival improving overtime: results from the Resuscitation OutcomesConsortium (ROC). Resuscitation 2015;91:108–15.

24. Wissenberg M, Lippert FK, Folke F, et al. As-sociation of national initiatives to improve cardiacarrest management with rates of bystanderintervention and patient survival after out-of-hospital cardiac arrest. JAMA 2013;310:1377–84.

25. OkuboM, Kiyohara K, Iwami T, et al. Nationwideand regional trends in survival fromout-of-hospitalcardiac arrest in Japan: a 10-year cohort study from2005 to 2014. Resuscitation 2017;115:120–8.

26. Brooks SC, Anderson ML, Bruder E, et al. Part6: alternative techniques and ancillary devices forcardiopulmonary resuscitation: 2015 AmericanHeart Association Guidelines update for cardio-pulmonary resuscitation and emergency cardio-vascular care. Circulation 2015;132:S436–43.

Hira and Nichol J A C C : B A S I C T O T R A N S L A T I O N A L S C I E N C E V O L . 2 , N O . 3 , 2 0 1 7

Management of Refractory VF J U N E 2 0 1 7 : 2 5 4 – 7256

FV refractaria

Fisiopato

infarto PCR en FV/TValt eléctrica

RCPPCR en FV/TV isquemia

Por qué sigue en FV

La isquemia persiste

perfusión insuficiente

accidente de placa

Panchal et al 2018 Focused Update on ACLS

Circulation. 2018;138:e740–e749. DOI: 10.1161/CIR.0000000000000613 December 4, 2018 e745

CLINICAL STATEMENTS

AND GUIDELINES

als supporting an initial IV/IO dose of 300 mg with a second IV/IO dose of 150 mg if required.10,11 Both the ROC-ALPS and ALIVE trials permitted dose reductions in lower-weight patients; however, higher cumulative bolus doses of amiodarone have not been studied in cardiac arrest. It is also important to note that the cap-tisol-based formulation of amiodarone is currently mar-keted only as a premixed infusion, not in concentrated form, making it impractical for rapid administration during cardiac arrest. The polysorbate-based formula-tion is currently available in concentrated form for rapid administration.

The writing group reaffirms that magnesium should not be used routinely during cardiac arrest management but may be considered for torsades de pointes (ie, polymorphic VT associated with long-QT interval). Unfortunately, these recommendations are based on low-quality evidence, representing a significant knowledge gap concerning the use of magnesium for VF/pVT. Future randomized studies are needed with rigorous evaluation of the impact of magnesium on survival and neurological outcomes to

determine the importance of magnesium administra-tion in this condition.

The writing group is aware of increased interest in and early studies of β-adrenergic–blocking drugs used during cardiac arrest.18,19 The question of the effective-ness of these drugs has been referred to ILCOR for future systematic review.

ANTIARRHYTHMIC DRUGS IMMEDIATELY AFTER ROSC FOLLOWING CARDIAC ARRESTThe 2018 ILCOR systematic review sought to deter-mine whether the prophylactic administration of an-tiarrhythmic drugs after successful termination of VF/pVT cardiac arrest results in better outcome. This pro-phylaxis includes continuation of an antiarrhythmic medication that was given during the course of re-suscitation or the initiation of an antiarrhythmic after ROSC to sustain rhythm stability after VF/pVT cardiac arrest. Although improved survival is the ultimate goal of such treatment, other shorter-term outcomes (even

Figure 2. Adult Cardiac Arrest Circular Algorithm—2018 Update. CPR indicates cardiopulmonary resuscitation; ET, endotracheal; IO, intraosseous; IV, intravenous; pVT, pulseless ventricular tachycardia; and VF, ventricular fibrillation.

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¿Qué hacer cuando la receta estándar

no es suficiente?

FV refractaria Desfibrilación doble secuencial

x

Y si sólo tengo 1 DF

Cambio posición

Cuál es la evidencia

Escasa• No hay diferencia significativa en sobrevida ni outcome

neurológico

Clinical paper

Double sequential external defibrillation forrefractory ventricular fibrillation: The DOSEVF pilot randomized controlled trial

Sheldon Cheskes a,b,c,*, Paul Dorian d, Michael Feldman a,e, Shelley McLeod b,f,Damon C. Scales c,e,f, Ruxandra Pinto g , Linda Turner a, Laurie J. Morrison c,e,Ian R. Drennan h,i, P. Richard Verbeek a,e

aSunnybrook Centre for Prehospital Medicine, Toronto, Ontario, CanadabDepartment of Family and Community Medicine, Division of Emergency Medicine, University of Toronto, Toronto, Ontario, Canadac Li Ka Shing Knowledge Institute, St. Michaels Hospital, Toronto, Ontario, CanadadSt. Michaels Hospital, Toronto, Ontario, CanadaeDepartment of Medicine, Division of Emergency Medicine, University of Toronto, Toronto, Ontario, CanadafSchwartz/Reisman Emergency Medicine Institute, Sinai Health System, Toronto, Ontario, CanadagDepartment of Critical Care Medicine, Sunnybrook Health Sciences Centre, Toronto, Ontario, Canadah Institute of Medical Science, University of Toronto, Toronto, Ontario, CanadaiSunnybrook Research Institute, Toronto, Ontario, Canada

AbstractObjectives: The primary objective was to determine the feasibility and safety of a cluster randomized controlled trial (RCT) with crossover comparing

vector change defibrillation (VC) or double sequential external defibrillation (DSED) to standard defibrillation for patients experiencing refractory

ventricular fibrillation (VF). Secondary objectives were to assess the rates of VF termination (VFT) and return of spontaneous circulation (ROSC).

Methods: We conducted a pilot cluster RCT with crossover in four Canadian paramedic services including all treated adult OHCA patients who

presented in VF and received a minimum of three successive defibrillation attempts. Each EMS service was randomly assigned to provide standard

defibrillation, VC or DSED. Agencies crossed over to an alternate defibrillation strategy after six months.

Results: 152 patients were enrolled. With respect to feasibility, 89.5% of cases received the defibrillation strategy they were randomly allocated to, and

93.1% of cases received a VC or DSED shock prior to the sixth defibrillation attempt. There were no safety concerns reported. In the standard group,

66.6% of cases resulted in VFT, compared to 82.0% in VC and 76.3% in the DSED group. ROSC was achieved in 25.0%, 39.3% and 40.0% of standard,

VC and DSED groups, respectively.

Conclusions: Our findings suggest the DOSE-VF protocol is feasible and safe. Rates of VFT and ROSC were higher in the VC and DSED than standard

defibrillation. The results of this pilot trial will allow us to inform a multicenter cluster RCT with crossover to determine if alternate defibrillation strategies

for refractory VF may impact clinical outcomes.

Keywords: Cardiopulmonary resuscitation, Heart arrest, Resuscitation, Defibrillation, Double sequential external defibrillation, Prehospital care

* Corresponding author at: Sunnybrook Centre for Prehospital Medicine, 77 Brown’s Line, Suite 100, Toronto, ON M8W 3S2, Canada.E-mail address: Sheldon.Cheskes@sunnybrook.ca (S. Cheskes).

https://doi.org/10.1016/j.resuscitation.2020.02.010

Received 9 December 2019; Received in revised form 26 January 2020; Accepted 12 February 2020

0300-9572/© 2020 Elsevier B.V. All rights reserved.

R E S U S C I T A T I O N 1 5 0 ( 2 0 2 0 ) 1 7 8 !1 8 4

Available online at www.sciencedirect.com

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FV refractaria Desfibrilación doble secuencial

Dra. Manuela Brinkmann Bizama Urgencióloga

@manu_brinkmann