Part 7: Adult Advanced Cardiovascular Life Support – ECC … · 2019-01-18 · AHA’s 2010 ACLS...

Part 7: Adult AdvancedCardiovascular LifeSupportWeb-based Integrated 2015 & 2018 American HeartAssociation Guidelines for CPR and ECC

Highlights

2018 Summary of Key Issues and MajorChanges

The review considered the use of Amiodarone,Lidocaine, Magnesium and Beta-blockers forantiarrhythmic therapy during and immediatelyafter adult ventricular fibrillation (VF) andpulseless ventricular tachycardia (pVT) cardiacarrest. As a result, the Adult writing group’srecommendations for CPR and ECC have beenupdated and now provide further clarity regardingthe application of antiarrhythmics during cardiacarrest. The recommendations are as follows:

Adult Recommendations

Use of antiarrhythmic drugs duringresuscitation from adult VF/pVT cardiacarrest

Amiodarone or lidocaine may beconsidered for VF/pVT that isunresponsive to defibrillation. These

Key Words: arrhythmia cardiac arrest drugs

ventricular arrhythmia ventricular fibrillation

COLLAPSEDEXPANDED

1

Resuscitation ScienceSearch Guidelines...CPR & ECC Guidelines

drugs may be particularly useful forpatients with witnessed arrest, forwhom time to drug administrationmay be shorter.The routine use of magnesium forcardiac arrest is not recommendedin adult patients. Magnesium may beconsidered for torsades de pointes(ie, polymorphic VT associated withlong-QT interval). The wording ofthis recommendation is consistentwith the AHA’s 2010 Guidelines.

Use of antiarrhythmic drugs immediatelyfollowing return of spontaneous circulation(ROSC) following adult cardiac arrest

There is insufficient evidence tosupport or refute the routine use of aβ- blocker early (within the first hour)after ROSC.There is insufficient evidence tosupport or refute the routine use oflidocaine early (within the first hour)after ROSC.

Antiarrhythmic Drugs Immediately AfterROSC Following Adult Cardiac Arrest: β-Blocker Recommendation

2018 (Updated): There is insufficient evidenceto support or refute the routine use of a β-blockerearly (within the first hour) after ROSC.

2015 (Old): There is inadequate evidence tosupport the routine use of a β-blocker aftercardiac arrest. However, the initiation orcontinuation of an oral or intravenous β-blockermay be considered early after hospitalization fromcardiac arrest due to VF/pVT (Class IIb, LOE C-LD).

Why: The 2018 CoSTR summary andsystematic review considered the use ofprophylactic antiarrhythmic drugs immediately(within the first hour) after ROSC. Although nonew studies were reviewed for this topic, detailed

evaluation of the literature led to the simplificationof the recommendation. There is no Class or LOElisted because the writing group agreed that therewas insufficient evidence to make anyrecommendation.

Antiarrhythmic Drugs Immediately AfterROSC Following Adult Cardiac Arrest:Lidocaine Recommendations

2018 (Updated): There is insufficient evidenceto support or refute the routine use of lidocaineearly (within the first hour) after ROSC. In theabsence of contraindications, the prophylactic useof lidocaine may be considered in specificcircumstances (such as during emergencymedical services transport) when treatment ofrecurrent VF/pVT might prove to be challenging(Class IIb, LOE C-LD).

2015 (Old): There is inadequate evidence tosupport the routine use of lidocaine after cardiacarrest. However, the initiation or continuation oflidocaine may be considered immediately afterROSC from cardiac arrest due to VF/pVT (ClassIIb, LOE C-LD).

Why: The 2018 CoSTR summary andsystematic review considered the use ofprophylactic antiarrhythmic drugs immediately(within the first hour) after ROSC. Although nonew studies were reviewed for this topic, thewriting group acknowledged that while there isinsufficient evidence to support the routine use oflidocaine, there are situations for whichrecurrence of VF/pVT would be logisticallychallenging to manage (eg, during emergencymedical services transport); in such situations,lidocaine administration may be considered.

Use of Antiarrhythmic Drugs DuringResuscitation From Adult VF/pVT CardiacArrest: Amiodarone and LidocaineRecommendation

2018 (Updated): Amiodarone or lidocaine maybe considered for VF/pVT that is unresponsive todefibrillation. These drugs may be particularlyuseful for patients with witnessed arrest, forwhom time to drug administration may be shorter(Class IIb, LOE B-R).

2015 (Old): Amiodarone may be considered forVF/pVT that is unresponsive to CPR,defibrillation, and a vasopressor therapy (ClassIIb, LOE B-R). Lidocaine may be considered asan alternative to amiodarone for VF/pVT that isunresponsive to CPR, defibrillation, andvasopressor therapy (Class IIb, LOE C-LD).

Why: The 2018 CoSTR summary andsystematic review considered the use ofamiodarone or lidocaine during VF/pVT cardiacarrest refractory after at least 1 shock. The writinggroup evaluated a new large, out-of-hospitalrandomized controlled trial that compared aCaptisol-based formulation of amiodarone withlidocaine or placebo for patients with refractoryVF/pVT. Although the available studies did notdemonstrate an improvement in survival tohospital discharge (or neurologically intactsurvival to discharge) associated with either drug,ROSC was higher in patients receiving lidocainecompared with placebo, and survival to hospitaladmission was higher with either drug comparedwith placebo. As a result, lidocaine is nowrecommended as an alternative to amiodaroneand has now been added to the ACLS CardiacArrest Algorithm for treatment of shock-refractoryVF/pVT (see the Figure 2 and ACLS CardiacArrest Algorithm Update section).

Use of Antiarrhythmic Drugs DuringResuscitation From Adult VF/pVT CardiacArrest: Magnesium Recommendations

2018 (Updated): The routine use of magnesiumfor cardiac arrest is not recommended in adultpatients (Class III: No Benefit, LOE C-LD).Magnesium may be considered for torsades de

pointes (ie, polymorphic VT associated with longQT interval) (Class IIb, LOE C-LD). The wordingof this recommendation is consistent with theAHA’s 2010 ACLS guidelines.

2015 (Old): The routine use of magnesium forVF/pVT is not recommended in adult patients(Class III: No Benefit, LOE B-R).

2010 (Old): When VF/pVT cardiac arrest isassociated with torsades de pointes, providersmay administer IV/IO bolus of magnesium sulfateat a dose of 1 to 2 g diluted in 10 mL D5W (ClassIIb, LOE C).

Why: The 2018 CoSTR summary andsystematic review considered the use ofmagnesium during resuscitation from cardiacarrest. No new studies were reviewed for thistopic, and only a handful of small, nonrandomizedstudies have been identified in past reviews. Thecurrent recommendation reaffirms thatmagnesium should not be routinely used forcardiac arrest and notes that it may beconsidered for the treatment of torsades depointes (ie, polymorphic VT associated with longQT interval).

2015 Summary of Key Issues and MajorChanges

Key issues and major changes in the 2015Guidelines Update recommendations foradvanced cardiac life support include thefollowing:

The combined use of vasopressin andepinephrine offers no advantage to usingstandard-dose epinephrine in cardiacarrest. Also, vasopressin does not offer anadvantage over the use of epinephrinealone. Therefore, to simplify the algorithm,vasopressin has been removed from theAdult Cardiac Arrest Algorithm–2015Update.Low end-tidal carbon dioxide (ETCO ) in2

intubated patients after 20 minutes of CPRis associated with a very low likelihood ofresuscitation. While this parameter shouldnot be used in isolation for decisionmaking, providers may consider lowETCO after 20 minutes of CPR incombination with other factors to helpdetermine when to terminate resuscitation.Steroids may provide some benefit whenbundled with vasopressin and epinephrinein treating IHCA. While routine use is notrecommended pending follow-up studies, itwould be reasonable for a provider toadminister the bundle for IHCA.When rapidly implemented, ECPR canprolong viability, as it may provide time totreat potentially reversible conditions orarrange for cardiac transplantation forpatients who are not resuscitated byconventional CPR.In cardiac arrest patients withnonshockable rhythm and who areotherwise receiving epinephrine, the earlyprovision of epinephrine is suggested.Studies about the use of lidocaine afterROSC are conflicting, and routine lidocaineuse is not recommended. However, theinitiation or continuation of lidocaine maybe considered immediately after ROSCfrom VF/pulseless ventricular tachycardia(pVT) cardiac arrest.One observational study suggests that ß-blocker use after cardiac arrest may beassociated with better outcomes than whenß-blockers are not used. Although thisobservational study is not strong-enoughevidence to recommend routine use, theinitiation or continuation of an oral orintravenous (IV) ß-blocker may beconsidered early after hospitalization fromcardiac arrest due to VF/pVT.

Vasopressors for Resuscitation: Vasopressin

2

2015 (Updated): Vasopressin in combinationwith epinephrine offers no advantage as asubstitute for standard-dose epinephrine incardiac arrest.

2010 (Old): One dose of vasopressin 40 unitsIV/ intraosseously may replace either the first orsecond dose of epinephrine in the treatment ofcardiac arrest.

Why: Both epinephrine and vasopressinadministration during cardiac arrest have beenshown to improve ROSC. Review of the availableevidence shows that efficacy of the 2 drugs issimilar and that there is no demonstrable benefitfrom administering both epinephrine andvasopressin as compared with epinephrine alone.In the interest of simplicity, vasopressin has beenremoved from the Adult Cardiac Arrest Algorithm.

Vasopressors for Resuscitation: Epinephrine

2015 (New): It may be reasonable to administerepinephrine as soon as feasible after the onset ofcardiac arrest due to an initial nonshockablerhythm.

Why: A very large observational study ofcardiac arrest with nonshockable rhythmcompared epinephrine given at 1 to 3 minuteswith epinephrine given at 3 later time intervals (4to 6, 7 to 9, and greater than 9 minutes). Thestudy found an association between earlyadministration of epinephrine and increasedROSC, survival to hospital discharge, andneurologically intact survival.

ETCO for Prediction of Failed Resuscitation

2015 (New): In intubated patients, failure toachieve an ETCO of greater than 10 mm Hg bywaveform capnography after 20 minutes of CPRmay be considered as one component of amultimodal approach to decide when to endresuscitative efforts but should not be used inisolation.

2

2

2

Why: Failure to achieve an ETCO of 10 mmHg by waveform capnography after 20 minutes ofresuscitation has been associated with anextremely poor chance of ROSC and survival.However, the studies to date are limited in thatthey have potential confounders and haveincluded relatively small numbers of patients, so itis inadvisable to rely solely on ETCO indetermining when to terminate resuscitation.

Extracorporeal CPR

2015 (New): ECPR may be considered amongselect cardiac arrest patients who have notresponded to initial conventional CPR, in settingswhere it can be rapidly implemented.

Why: Although no high-quality studies havecompared ECPR to conventional CPR, a numberof lower-quality studies suggest improved survivalwith good neurologic outcome for select patientpopulations. Because ECPR is resource intensiveand costly, it should be considered only when thepatient has a reasonably high likelihood of benefit—in cases where the patient has a potentiallyreversible illness or to support a patient whilewaiting for a cardiac transplant.

Introduction

These Web-based Integrated Guidelinesincorporate all relevant recommendations from2010, 2015 and 2018. This 2018 American HeartAssociation (AHA) focused update on theadvanced cardiovascular life support (ACLS)guidelines for cardiopulmonary resuscitation(CPR) and emergency cardiovascular care (ECC)is based on the systematic review ofantiarrhythmic therapy and the resulting “2018International Consensus on CPR and ECCScience With Treatment Recommendations”(CoSTR) from the Advanced Life Support (ALS)Task Force of the International Liaison Committeeon Resuscitation (ILCOR). The draft ALS CoSTRwas posted online for public comment, and a

2

2

2

summary containing the final wording of theCoSTR has been published simultaneously withthis focused update. AHA guidelines and focusedupdates are developed in concert with the ILCORsystematic evidence review process. In 2015, theILCOR process transitioned to a continuous one,with systematic reviews performed as newpublished evidence warrants them or when theILCOR ALS Task Force prioritizes a topic. Oncethe ILCOR ALS Task Force develops a CoSTRstatement, AHA ACLS science experts review therelevant topics and update the AHA’s ACLSguidelines as needed, typically on an annualbasis. A description of the ILCOR continuousevidence review process is available in the 2017CoSTR summary. The ILCOR systematic reviewsuse the Grading of RecommendationsAssessment, Development, and Evaluationmethodology and its associated nomenclature todetermine the quality of evidence and strength ofrecommendations in the published CoSTRstatement. The expert writing group for this 2018ACLS guidelines focused update reviewed thestudies and analysis of the 2018 CoSTRsummary and carefully considered the ILCORconsensus recommendations in light of thestructure and resources of the out-of-hospital andin-hospital resuscitation systems and theproviders who use AHA guidelines. In addition,the writing group determined Classes ofRecommendation and Levels of Evidenceaccording to the most recent recommendations ofthe American College of Cardiology/AHA TaskForce on Clinical Practice Guidelines (Table) byusing the process detailed in “” in the “2015American Heart Association Guidelines Updatefor Cardiopulmonary Resuscitation andEmergency Cardiovascular Care.” This 2018ACLS guidelines focused update includesupdates only to the recommendations for the useof antiarrhythmics during and immediately afteradult ventricular fibrillation (VF) and pulselessventricular tachycardia (pVT) cardiac arrest. All

other recommendations and algorithms publishedin “” in the 2015 guidelines update and “” in the“2010 American Heart Association Guidelines forCardiopulmonary Resuscitation and EmergencyCardiovascular Care” remain the official ACLSrecommendations of the AHA ECC ScienceSubcommittee and writing groups. In addition, the“2017 American Heart Association FocusedUpdate on Adult Basic Life Support andCardiopulmonary Resuscitation Quality: AnUpdate to the American Heart AssociationGuidelines for Cardiopulmonary Resuscitationand Emergency Cardiovascular Care” containsupdated AHA recommendations for CPRdelivered to adult patients in cardiac arrest.Through this systematic evaluation process,several issues have been identified in relatedareas that may be the subject of future systematicreviews.

Adjuncts to CPR - Updated

Oxygen Dose During CPR - Updated

The 2015 ILCOR systematic review consideredinhaled oxygen delivery both during CPR andin the post–cardiac arrest period. This 2015Guidelines Update evaluates the optimalinspired concentration of oxygen during CPR.The immediate goals of CPR are to restore theenergy state of the heart so it can resumemechanical work and to maintain the energystate of the brain to minimize ischemic injury.Adequate oxygen delivery is necessary toachieve these goals. Oxygen delivery isdependent on both blood flow and arterialoxygen content. Because blood flow is typicallythe major limiting factor to oxygen deliveryduring CPR, it is theoretically important tomaximize the oxygen content of arterial bloodby maximizing inspired oxygen concentration.Maximal inspired oxygen can be achieved with

3

3.1 ALS 889

high-flow oxygen into a resuscitation bagdevice attached to a mask or an advancedairway.

2015 Evidence Summary

There were no adult human studies identifiedthat directly compared maximal inspiredoxygen with any other inspired oxygenconcentration. However, 1 observationalstudy of 145 OHCA patients evaluatedarterial Po2 measured during CPR andcardiac arrest outcomes. In this study, duringwhich all patients received maximal inspiredoxygen concentration, patients were dividedinto low, intermediate, and high arterial Po2ranges (less than 61, 61–300, and greaterthan 300 mmHg, respectively). The higherranges of arterial Po2 during CPR wereassociated with an increase in hospitaladmission rates (low, 18.8%; intermediate,50.6%; and high, 83.3%). However, therewas no statistical difference in overallneurologic survival (low, 3.1%; intermediate,13.3%; and high, 23.3%). Of note, this studydid not evaluate the provision of variouslevels of inspired oxygen, so differencesbetween groups likely reflect patient-leveldifferences in CPR quality and underlyingpathophysiology. This study did not find anyassociation between hyperoxia during CPRand poor outcome.

2015 Recommendation - Updated

When supplementary oxygen is available,it may be reasonable to use the maximalfeasible inspired oxygen concentrationduring CPR.

Evidence for detrimental effects of hyperoxiathat may exist in the immediate post–cardiacarrest period should not be extrapolated tothe low-flow state of CPR where oxygendelivery is unlikely to exceed demand or

3.1.1

3.1.2

2

cause an increase in tissue Po . Therefore,until further data are available, physiologyand expert consensus support providing themaximal inspired oxygen concentrationduring CPR.

Passive Oxygen Delivery During CPR

This topic was updated in 2015 and isdiscussed in .

Monitoring Physiologic Parameters DuringCPR - Updated

Monitoring both provider performance andpatient physiologic parameters during CPR isessential to optimizing CPR quality. The 2010Guidelines put a strong emphasis on CPRquality. In 2013, the AHA published aConsensus Statement focused on strategies toimprove CPR quality. In 2015, the ILCORACLS Task Force evaluated the availableclinical evidence to determine whether usingphysiologic feedback to guide CPR qualityimproved survival and neurologic outcome.


Animal and human studies indicate thatmonitoring physiologic parameters duringCPR provides valuable information about thepatient’s condition and response to therapy.Most important, end-tidal CO2 (etco2 ),coronary perfusion pressure, arterialrelaxation pressure, arterial blood pressure,and central venous oxygen saturationcorrelate with cardiac output and myocardialblood flow during CPR, and threshold valueshave been reported below which return ofspontaneous circulation (ROSC) is rarelyachieved. These parameters can bemonitored continuously, without interruptingchest compressions. An abrupt increase inany of these parameters is a sensitiveindicator of ROSC. There is evidence that

2

3.2

3.3ALS 656

3.3.1

these and other physiologic parameters canbe modified by interventions aimed atimproving CPR quality.

The 2015 ILCOR systematic review wasunable to identify any clinical trials that havestudied whether titrating resuscitative effortsto a single or combined set of physiologicparameters during CPR results in improvedsurvival or neurologic outcome.


Although no clinical study has examinedwhether titrating resuscitative efforts tophysiologic parameters during CPRimproves outcome, it may be reasonableto use physiologic parameters(quantitative waveform capnography,arterial relaxation diastolic pressure,arterial pressure monitoring, and centralvenous oxygen saturation) when feasibleto monitor and optimize CPR quality,guide vasopressor therapy, and detectROSC.

Previous guidelines specified physiologicparameter goals; however, because theprecise numerical targets for theseparameters during resuscitation have not asyet been established, these were notspecified in 2015.

Ultrasound During Cardiac Arrest -Updated

Bedside cardiac and noncardiac ultrasound arefrequently used as diagnostic and prognostictools for critically ill patients. Ultrasound maybe applied to patients receiving CPR to helpassess myocardial contractility and to helpidentify potentially treatable causes of cardiacarrest such as hypovolemia, pneumothorax,pulmonary thromboembolism, or pericardialtamponade. However, it is unclear whether

,

3.3.2

3.4ALS 658

important clinical outcomes are affected by theroutine use of ultrasound among patientsexperiencing cardiac arrest.


One limited study with a small sample sizewas identified that specifically addressed theutility of ultrasound during cardiac arrest.This study evaluated bedside cardiacultrasound use during ACLS among adultpatients in pulseless electrical activity arrestand found no difference in the incidence ofROSC when ultrasound was used.

2015 Recommendations - Updated

Ultrasound (cardiac or noncardiac) maybe considered during the management ofcardiac arrest, although its usefulnesshas not been well established.

If a qualified sonographer is present anduse of ultrasound does not interfere withthe standard cardiac arrest treatmentprotocol, then ultrasound may beconsidered as an adjunct to standardpatient evaluation.

Adjuncts for Airway Control and Ventilation -Updated

Overview of Airway Management

This section highlights recommendations forthe support of ventilation and oxygenationduring CPR and the peri-arrest period. Thepurpose of ventilation during CPR is tomaintain adequate oxygenation and sufficientelimination of carbon dioxide. However,research has not identified the optimal tidalvolume, respiratory rate, and inspired oxygenconcentration required during resuscitationfrom cardiac arrest.

3.4.1

3.4.2

4

4.1

Both ventilation and chest compressions arethought to be important for victims of prolongedventricular fibrillation (VF) cardiac arrest and forall victims with other presenting rhythms.Because both systemic and pulmonaryperfusion are substantially reduced duringCPR, normal ventilation-perfusion relationshipscan be maintained with a minute ventilation thatis much lower than normal. During CPR with anadvanced airway in place, a lower rate ofrescue breathing is needed to avoidhyperventilation.

Ventilation and Oxygen AdministrationDuring CPR

During low blood flow states such as CPR,oxygen delivery to the heart and brain is limitedby blood flow rather than by arterial oxygencontent. Therefore, rescue breaths are lessimportant than chest compressions during thefirst few minutes of resuscitation fromwitnessed VF cardiac arrest and could reduceCPR efficacy due to interruption in chestcompressions and the increase in intrathoracicpressure that accompanies positive-pressureventilation.

Thus, during the first few minutes ofwitnessed cardiac arrest a lone rescuershould not interrupt chest compressions forventilation. Advanced airway placement incardiac arrest should not delay initial CPRand defibrillation for VF cardiac arrest.

Bag-Mask Ventilation - Updated

Bag-mask ventilation is an acceptable methodof providing ventilation and oxygenation duringCPR but is a challenging skill that requirespractice for continuing competency. Allhealthcare providers should be familiar with theuse of the bag-mask device. Use of bag-maskventilation is not recommended for a loneprovider. When ventilations are performed by a

4.2

,

4.3

,

lone provider, mouth-to-mouth or mouth-to-mask are more efficient. When a secondprovider is available, bag-mask ventilation maybe used by a trained and experienced provider.But bag-mask ventilation is most effective whenperformed by 2 trained and experiencedproviders. One provider opens the airway andseals the mask to the face while the othersqueezes the bag. Bag-mask ventilation isparticularly helpful when placement of anadvanced airway is delayed or unsuccessful.The desirable components of a bag-maskdevice are listed in “.”

The provider should use an adult (1 to 2 L) bagand the provider should deliver approximately600 mL of tidal volume sufficient to producechest rise over 1 second.13 This volume ofventilation is adequate for oxygenation andminimizes the risk of gastric inflation. Theprovider should be sure to open the airwayadequately with a head tilt–chin lift, lifting thejaw against the mask and holding the maskagainst the face, creating a tight seal. DuringCPR give 2 breaths (each 1 second) during abrief (about 3 to 4 seconds) pause after every30 chest compressions.

Bag-mask ventilation can produce gastricinflation with complications, includingregurgitation, aspiration, and pneumonia.Gastric inflation can elevate the diaphragm,restrict lung movement, and decreaserespiratory system compliance.

Bag-Mask Ventilation Compared WithAny Advanced Airway During CPR -Updated

As stated above, bag-mask ventilation is acommonly used method for providingoxygenation and ventilation in patients withrespiratory insufficiency or arrest. Whencardiac arrest occurs, providers mustdetermine the best way to support ventilation

4.3.1

ALS 783

and oxygenation. Options include standardbag-mask ventilation versus the placementof an advanced airway (ie, endotracheal tube[ETT], supraglottic airway device [SGA]).Previous guidelines recommended thatprolonged interruptions in chestcompressions should be avoided duringtransitions from bag-mask ventilation to anadvanced airway device. In 2015, ILCORevaluated the evidence comparing the effectof bagmask ventilation versus advancedairway placement on overall survival andneurologic outcome from cardiac arrest.


There is inadequate evidence to show adifference in survival or favorableneurologic outcome with the use of bag-mask ventilation compared withendotracheal intubation or otheradvanced airway devices. The majorityof these retrospective observationalstudies demonstrated slightly worsesurvival with the use of an advancedairway when compared with bag-maskventilation. However, interpretation ofthese results is limited by significantconcerns of selection bias. Two additionalobservational studies showed nodifference in survival.

Airway Adjuncts

Cricoid Pressure

Cricoid pressure in nonarrest patients mayoffer some measure of protection to theairway from aspiration and gastric insufflationduring bag-mask ventilation. However, italso may impede ventilation and interferewith placement of a supraglottic airway orintubation. The role of cricoid pressureduring out-of-hospital cardiac arrest and in-

4.3.1.1

, ,

,

4.4

4.4.1

hospital cardiac arrest has not been studied.If cricoid pressure is used in specialcircumstances during cardiac arrest, thepressure should be adjusted, relaxed, orreleased if it impedes ventilation oradvanced airway placement.

The routine use of cricoid pressure incardiac arrest is not recommended.

Oropharyngeal Airways

Although studies have not specificallyconsidered the use of oropharyngeal airwaysin patients with cardiac arrest, airways mayaid in the delivery of adequate ventilationwith a bag-mask device by preventing thetongue from occluding the airway. Incorrectinsertion of an oropharyngeal airway candisplace the tongue into the hypopharynx,causing airway obstruction.

To facilitate delivery of ventilations with abag-mask device, oropharyngeal airwayscan be used in unconscious(unresponsive) patients with no cough orgag reflex and should be inserted only bypersons trained in their use.

Nasopharyngeal Airways

Nasopharyngeal airways are useful inpatients with airway obstruction or those atrisk for developing airway obstruction,particularly when conditions such as aclenched jaw prevent placement of an oralairway. Nasopharyngeal airways are bettertolerated than oral airways in patients whoare not deeply unconscious. Airway bleedingcan occur in up to 30% of patients followinginsertion of a nasopharyngeal airway. Twocase reports of inadvertent intracranialplacement of a nasopharyngeal airway inpatients with basilar skull fractures suggest

4.4.2

4.4.3

,

that nasopharyngeal airways should be usedwith caution in patients with severecraniofacial injury.

As with all adjunctive equipment, safe use ofthe nasopharyngeal airway requiresadequate training, practice, and retraining.No studies have specifically examined theuse of nasopharyngeal airways in cardiacarrest patients. To facilitate delivery ofventilations with a bag-mask device, thenasopharyngeal airway can be used inpatients with an obstructed airway.

In the presence of known or suspectedbasal skull fracture or severecoagulopathy, an oral airway is preferred.

Advanced Airways - Updated

Ventilation with a bag and mask or with a bagthrough an advanced airway (eg, endotrachealtube or supraglottic airway) is acceptableduring CPR. All healthcare providers should betrained in delivering effective oxygenation andventilation with a bag and mask. Because thereare times when ventilation with a bag-maskdevice is inadequate, ideally ACLS providersalso should be trained and experienced ininsertion of an advanced airway.

Providers must be aware of the risks andbenefits of insertion of an advanced airwayduring a resuscitation attempt. Such risks areaffected by the patient’s condition and theprovider’s expertise in airway control. Thereare no studies directly addressing the timing ofadvanced airway placement and outcomeduring resuscitation from cardiac arrest.Although insertion of an endotracheal tube canbe accomplished during ongoing chestcompressions, intubation frequently isassociated with interruption of compressionsfor many seconds.

4.5

The provider should weigh the need forminimally interrupted compressions against theneed for insertion of an endotracheal tube orsupraglottic airway. There is inadequateevidence to define the optimal timing ofadvanced airway placement in relation to otherinterventions during resuscitation from cardiacarrest. In a registry study of 25 006 in-hospitalcardiac arrests, earlier time to invasive airway(<5 minutes) was not associated with improvedROSC but was associated with improved 24-hour survival. In an urban out-of-hospitalsetting, intubation that was achieved in <12minutes was associated with better survivalthan intubation achieved in ≥13 minutes.

In out-of-hospital urban and rural settings,patients intubated during resuscitation had abetter survival rate than patients who were notintubated, whereas in an in-hospital setting,patients who required intubation during CPRhad a worse survival rate. A recent study foundthat delayed endotracheal intubation combinedwith passive oxygen delivery and minimallyinterrupted chest compressions was associatedwith improved neurologically intact survivalafter out-of-hospital cardiac arrest in patientswith adult witnessed VF/pulseless VT.

If advanced airway placement will interruptchest compressions, providers mayconsider deferring insertion of the airwayuntil the patient fails to respond to initialCPR and defibrillation attempts ordemonstrates ROSC.

For a patient with perfusing rhythm whorequires intubation, pulse oximetry andelectrocardiographic (ECG) status should bemonitored continuously during airwayplacement. Intubation attempts should beinterrupted to provide oxygenation andventilation as needed.

To use advanced airways effectively,healthcare providers must maintain theirknowledge and skills through frequent practice.It may be helpful for providers to master oneprimary method of airway control. Providersshould have a second (backup) strategy forairway management and ventilation if they areunable to establish the first-choice airwayadjunct. Bag-mask ventilation may serve asthat backup strategy.

Once an advanced airway is inserted, providersshould immediately perform a thoroughassessment to ensure that it is properlypositioned. This assessment should notinterrupt chest compressions. Assessment byphysical examination consists of visualizingchest expansion bilaterally and listening overthe epigastrium (breath sounds should not beheard) and the lung fields bilaterally (breathsounds should be equal and adequate). Adevice also should be used to confirm correctplacement (see the section “EndotrachealIntubation” below).

Providers should observe a persistentcapnographic waveform with ventilation toconfirm and monitor endotracheal tubeplacement in the field, in the transport vehicle,on arrival at the hospital, and after any patienttransfer to reduce the risk of unrecognized tubemisplacement or displacement.

The use of capnography to confirm and monitorcorrect placement of supraglottic airways hasnot been studied, and its utility will depend onairway design. However, effective ventilationthrough a supraglottic airway device shouldresult in a capnograph waveform during CPRand after ROSC.

Once an advanced airway is in place, the 2providers should no longer deliver cycles ofCPR (ie, compressions interrupted by pausesfor ventilation) unless ventilation is inadequate

when compressions are not paused. Insteadthe compressing provider should givecontinuous chest compressions at a rate of100/min to 120/min, without pauses forventilation. The provider delivering ventilationshould provide 1 breath every 6 seconds (10breaths per minute). Providers should avoiddelivering an excessive ventilation ratebecause doing so can compromise venousreturn and cardiac output during CPR. The 2providers should change compressor andventilator roles approximately every 2 minutesto prevent compressor fatigue and deteriorationin quality and rate of chest compressions.When multiple providers are present, theyshould rotate the compressor role about every2 minutes.

Advanced Airway Placement Choice -Updated

Advanced airway devices are frequentlyplaced by experienced providers during CPRif bag-mask ventilation is inadequate or as astepwise approach to airway management.Placement of an advanced airway may resultin interruption of chest compressions, andthe ideal timing of placement to maximizeoutcome has not been adequately studied.The use of an advanced airway device suchas an ETT or SGA and the effect ofventilation technique on overall survival andneurologic outcome was evaluated in 2015.


Endotracheal Intubation VersusBag-Mask Ventilation - Updated

There is no high-quality evidencefavoring the use of endotrachealintubation compared with bag-maskventilation or an advanced airwaydevice in relation to overall survival orfavorable neurologic

4.5.1

4.5.1.1

4.5.1.1.1

outcome. Evaluating retrospectivestudies that compare bag-maskventilation to endotracheal intubation ischallenging because patients with moresevere physiologic compromise willtypically receive more invasive care(including endotracheal intubation) thanpatients who are less compromised andmore likely to survive. Within thatcontext, a number of retrospectivestudies show an association of worseoutcome in those who were intubatedas compared with those receiving bag-mask ventilation. While the studies didattempt to control for confounders, biasstill may have been present, limiting theinterpretation of these investigations.These studies illustrate thatendotracheal intubation can beassociated with a number ofcomplications and that the procedurerequires skill and experience. Risks ofendotracheal intubation duringresuscitation include unrecognizedesophageal intubation and increasedhands-off time.

Supraglottic Airway Devices -Updated

Several retrospective studies compareda variety of supraglottic devices(laryngeal mask airway, laryngeal tube,Combitube, esophageal obturatorairway) to both bag-mask ventilationand endotracheal intubation. There isno high-quality evidence demonstratinga difference in survival rate or favorableneurologic outcome from use of an SGAcompared with bagmask ventilation orendotracheal intubation. Threeobservational studies demonstrated alower rate of both overall survival andfavorable neurologic outcome when

4.5.1.1.2

,

, , , ,

SGA use was compared with bag-maskventilation, , whereas anotherobservational study demonstratedsimilar survival rates.

In studies comparing SGA insertion toendotracheal intubation, no high-qualitystudies have demonstrated a differencein overall survival or favorableneurologic outcome. Severalretrospective observational studiesshow more favorable outcome with theuse of an SGA device, whereas otherstudies favor the use of endotrachealintubation.


Either a bag-mask device or anadvanced airway may be used foroxygenation and ventilation duringCPR in both the in-hospital and out-of-hospital setting.

For healthcare providers trained intheir use, either an SGA device or anETT may be used as the initialadvanced airway during CPR.

Recommendations for advanced airwayplacement presume that the provider hasthe initial training and skills as well as theongoing experience to insert the airwayand verify proper position with minimalinterruption in chest compressions. Bag-mask ventilation also requires skill andproficiency. The choice of bag-maskdevice versus advanced airwayinsertion, then, will be determined by theskill and experience of the provider.

Frequent experience or frequentretraining is recommended forproviders who perform endotrachealintubation.,

,

, , ,

, , ,

4.5.1.2

EMS systems that perform prehospitalintubation should provide a program ofongoing quality improvement tominimize complications.

Clinical Assessment of Tracheal TubePlacement - Updated

The 2015 ILCOR systematic reviewconsidered tracheal tube placement duringCPR. This section evaluates methods forconfirming correct tracheal tube placement.

Attempts at endotracheal intubation duringCPR have been associated withunrecognized tube misplacement ordisplacement as well as prolongedinterruptions in chest compression.Inadequate training, lack of experience,patient physiology (eg, low pulmonary bloodflow, gastric contents in the trachea, airwayobstruction), and patient movement maycontribute to tube misplacement. Aftercorrect tube placement, tube displacementor obstruction may develop. In addition toauscultation of the lungs and stomach,several methods (eg, waveformcapnography, CO2 detection devices,esophageal detector device, trachealultrasound, fiberoptic bronchoscopy) havebeen proposed to confirm successfultracheal intubation in adults during cardiacarrest.


The evidence regarding the use oftracheal detection devices during cardiacarrest is largely observational.Observational studies and 1 smallrandomized study of waveformcapnography to verify ETT position invictims of cardiac arrest report a specificityof 100% for correct tubeplacement. Although the sensitivity of

4.5.2ALS 469

4.5.2.1

waveform capnography for detectingtracheal tube placement immediately afterprehospital intubation was 100% in 1study, several other studies showed thatthe sensitivity of waveform capnographydecreases after a prolonged cardiacarrest. Differences in sensitivity can beexplained by the low pulmonary blood flowduring cardiac arrest, which will decreaseETCO2 concentration.

Although exhaled CO2 detection suggestscorrect tracheal tube placement, false-positive results (CO2 detection withesophageal intubation) can occur afteringestion of carbonated liquids.66 False-negative results (ie, absent exhaled CO2in the presence of tracheal intubation) canoccur in the setting of pulmonaryembolism, significant hypotension,contamination of the detector with gastriccontents, and severe airflowobstruction. The use of CO2 -detectingdevices to determine the correctplacement of other advanced airways (eg,Combitube, laryngeal mask airway) hasnot been studied, but, as with an ETT,effective ventilation should produce acapnography waveform during CPR andafter ROSC.

Colorimetric and nonwaveform CO2detectors can identify the presence ofexhaled CO2 from the respiratory tract,but there is no evidence that thesedevices are accurate for continuedmonitoring of ETT placement. Moreover,because a minimal threshold of CO2 mustbe reached to activate the detector andexhaled CO2 is low in cardiac arrest,proper placement of an ETT may not beconfirmed with this qualitativemethodology.

, ,

, ,

While observational studies and a smallrandomized controlled trial (RCT) ofesophageal detector devices report a lowfalse-positive rate for confirming trachealplacement, there is no evidence that thesedevices are accurate or practical for thecontinued monitoring of ETTplacement.

An ultrasound transducer can be placedtransversely on the anterior neck abovethe suprasternal notch to identifyendotracheal or esophageal intubation. Inaddition, ultrasound of the thoracic cavitycan identify pleural movement as lungsliding. Unlike capnography, confirmationof ETT placement via ultrasonography isnot dependent on adequate pulmonaryblood flow and CO2 in exhaled gas. Onesmall prospective study of experiencedclinicians compared tracheal ultrasound towaveform capnography and auscultationduring CPR and reported a positivepredictive value for ultrasound of 98.8%and negative predictive value of100%. The usefulness of tracheal andpleural ultrasonography, like fiberopticbronchoscopy, may be limited byabnormal anatomy, availability ofequipment, and operator experience.


Continuous waveform capnography isrecommended in addition to clinicalassessment as the most reliablemethod of confirming and monitoringcorrect placement of an ETT.

If continuous waveform capnometry isnot available, a nonwaveform CO2detector, esophageal detector device,or ultrasound used by an experiencedoperator is a reasonable alternative.

, , ,

4.5.2.2

Postintubation Airway Management

After inserting and confirming correctplacement of an endotracheal tube, theprovider should record the depth of the tubeas marked at the front teeth or gums andsecure it. There is significant potential forendotracheal tube movement with headflexion and extension and when the patientis moved from one location to another.Continuous monitoring of endotracheal tubeplacement with waveform capnography isrecommended as discussed above.

The endotracheal tube should be securedwith tape or a commercial device.

Devices and tape should be applied in amanner that avoids compression of the frontand sides of the neck, which may impairvenous return from the brain.

One out-of-hospital study and 2 studiesin an intensive-care setting, indicate thatbackboards, commercial devices forsecuring the endotracheal tube, and otherstrategies provide equivalent methods forpreventing inadvertent tube displacementwhen compared with traditional methodsof securing the tube (tape). These devicesmay be considered during patienttransport.

After tube confirmation and fixation, obtain achest x-ray (when feasible) to confirm thatthe end of the endotracheal tube is properlypositioned above the carina.

Ventilation After Advanced AirwayPlacement - Updated

The 2015 ILCOR systematic reviewaddressed the optimal ventilation rate duringcontinuous chest compressions amongadults in cardiac arrest with an advancedairway. The 2015 Guidelines Update for

4.5.3

,

4.5.4ALS 808

ACLS applies only to patients who havebeen intubated and are in cardiac arrest. Theeffect of tidal volume and any otherventilation parameters during CPR are notaddressed in this recommendation.

Except for respiratory rate, it is unknownwhether monitoring ventilatory parameters(eg, minute ventilation, peak pressure)during CPR can influence outcome.However, positive pressure ventilationincreases intrathoracic pressure and mayreduce venous return and cardiac output,especially in patients with hypovolemia orobstructive airway disease. Ventilation atinappropriately high respiratory rates(greater than 25 breaths/ min) is commonduring resuscitation from cardiacarrest. There is concern that excessiveventilation in the setting of cardiac arrestmay be associated with worse outcome.


No human clinical trials were foundaddressing whether a ventilation rate of 10breaths/min, compared with any otherventilation rate, changes survival withfavorable neurologic or functionaloutcome. Although there have been anumber of animal studies and 1 humanobservational study evaluating ventilationrates during CPR, the design and datafrom these studies did not allow for theassessment of the effect of a ventilationrate of 10 per minute compared with anyother rate for ROSC or other outcomes.


After placement of an advanced airway,it may be reasonable for the provider todeliver 1 breath every 6 seconds (10breaths/min) while continuous chestcompressions are being performed.

,

4.5.4.1

,

4.5.4.2

Automatic Transport Ventilators

In both out-of-hospital and in-hospitalsettings, automatic transport ventilators(ATVs) can be useful for ventilation ofadult patients in noncardiac arrest whohave an advanced airway in place.

There are very few studies evaluating theuse of ATVs attached to advanced airwaysduring ongoing resuscitative efforts.

During prolonged resuscitative efforts theuse of an ATV (pneumatically poweredand time- or pressure-cycled) may allowthe EMS team to perform other taskswhile providing adequate ventilation andoxygenation.,

Providers should always have a bag-maskdevice available for backup.

Suction Devices

Both portable and installed suction devicesshould be available for resuscitationemergencies. Portable units should provideadequate vacuum and flow for pharyngealsuction. The suction device should be fittedwith large-bore, nonkinking suction tubing andsemirigid pharyngeal tips. Several sterilesuction catheters of various sizes should beavailable for suctioning the lumen of theadvanced airway, along with a nonbreakablecollection bottle and sterile water for cleaningtubes and catheters. The installed suction unitshould be powerful enough to provide anairflow of >40 L/min at the end of the deliverytube and a vacuum of >300 mm Hg when thetube is clamped. The amount of suction shouldbe adjustable for use in children and intubatedpatients.

Management of Cardiac Arrest - Updated

Overview

4.5.5

4.6

5

5.1

This section details the general care of apatient in cardiac arrest and provides anoverview of the ACLS Adult Cardiac ArrestAlgorithms ( and ). Cardiac arrest can becaused by 4 rhythms: ventricular fibrillation(VF), pulseless ventricular tachycardia (VT),pulseless electric activity (PEA), and asystole.VF represents disorganized electric activity,whereas pulseless VT represents organizedelectric activity of the ventricular myocardium.Neither of these rhythms generates significantforward blood flow. PEA encompasses aheterogeneous group of organized electricrhythms that are associated with eitherabsence of mechanical ventricular activity ormechanical ventricular activity that isinsufficient to generate a clinically detectablepulse. Asystole (perhaps better described asventricular asystole) represents absence ofdetectable ventricular electric activity with orwithout atrial electric activity.

Survival from these cardiac arrest rhythmsrequires both basic life support (BLS) and asystem of advanced cardiovascular life support(ACLS) with integrated post–cardiac arrestcare. The foundation of successful ACLS is

Figure 1: Adult Cardiac ArrestAlgorithm―2018 Update

⇥

Figure 2: ACLS Cardiac Arrest CircularAlgorithm - 2018 Update

⇥

high-quality CPR, and, for VF/pulseless VT,attempted defibrillation within minutes ofcollapse. For victims of witnessed VF arrest,early CPR and rapid defibrillation cansignificantly increase the chance for survival tohospital discharge. In comparison, other ACLStherapies such as some medications andadvanced airways, although associated with anincreased rate of ROSC, have not been shownto increase the rate of survival to hospitaldischarge. The majority of clinical trialstesting these ACLS interventions, however,preceded the recently renewed emphasis onhigh-quality CPR and advances in post–cardiacarrest care (see “”). Therefore, it remains to bedetermined if improved rates of ROSCachieved with ACLS interventions might bettertranslate into improved long-term outcomeswhen combined with higher-quality CPR andpost–cardiac arrest interventions such astherapeutic hypothermia and earlypercutaneous coronary intervention (PCI).

The ACLS Adult Cardiac Arrest Algorithms ()are presented in the traditional box-and-lineformat and a new circular format. The 2 formatsare provided to facilitate learning andmemorization of the treatmentrecommendations discussed below. Overallthese algorithms have been simplified andredesigned to emphasize the importance ofhigh-quality CPR that is fundamental to themanagement of all cardiac arrest rhythms.Periodic pauses in CPR should be as brief aspossible and only as necessary to assessrhythm, shock VF/VT, perform a pulse checkwhen an organized rhythm is detected, or placean advanced airway. Monitoring and optimizingquality of CPR on the basis of eithermechanical parameters (chest compressionrate and depth, adequacy of relaxation, andminimization of pauses) or, when feasible,physiologic parameters (partial pressure of

, ,

2 2

end-tidal CO [PETCO ], arterial pressureduring the relaxation phase of chestcompressions, or central venous oxygensaturation [ScvO ]) are encouraged (see“Monitoring During CPR” below). In theabsence of an advanced airway, asynchronized compression–ventilation ratio of30:2 is recommended at a compression rate ofat least 100-120 per minute. After placement ofa supraglottic airway or an endotracheal tube,the provider performing chest compressionsshould deliver at least 100-120 compressionsper minute continuously without pauses forventilation. The provider delivering ventilationsshould give 1 breath every 6 seconds (10breaths per minute) and should be particularlycareful to avoid delivering an excessive numberof ventilations.

In addition to high-quality CPR, the onlyrhythm-specific therapy proven to increasesurvival to hospital discharge is defibrillation ofVF/pulseless VT. Therefore, this intervention isincluded as an integral part of the CPR cyclewhen the rhythm check reveals VF/pulselessVT. Other ACLS interventions during cardiacarrest may be associated with an increasedrate of ROSC but have not yet been proven toincrease survival to hospital discharge.Therefore, they are recommended asconsiderations and should be performedwithout compromising quality of CPR or timelydefibrillation. In other words, vascular access,drug delivery, and advanced airway placementshould not cause significant interruptions inchest compression or delay defibrillation. Thereis insufficient evidence to recommend aspecific timing or sequence (order) of drugadministration and advanced airway placementduring cardiac arrest. In most cases the timingand sequence of these secondary interventionswill depend on the number of providersparticipating in the resuscitation and their skilllevels. Timing and sequence will also be

2 2

2

affected by whether vascular access has beenestablished or an advanced airway placedbefore cardiac arrest.

Understanding the importance of diagnosingand treating the underlying cause isfundamental to management of all cardiacarrest rhythms. During management of cardiacarrest the provider should consider the H’s andT’s to identify and treat any factor that mayhave caused the arrest or may be complicatingthe resuscitative effort ().

It is common for the arrest rhythm to evolveduring the course of resuscitation. In suchcases management should shift smoothly tothe appropriate rhythm-based strategy. Inparticular, providers should be prepared todeliver a timely shock when a patient whopresented with asystole or PEA is found to bein VF/pulseless VT during a rhythm check.There is no evidence that the resuscitationstrategy for a new cardiac arrest rhythm shouldnecessarily be altered based on thecharacteristics of the previous rhythm.Medications administered during resuscitationshould be monitored and total doses tabulatedto avoid potential toxicity.

If the patient achieves ROSC, it is important tobegin post–cardiac arrest care immediately toavoid rearrest and optimize the patient’schance of long-term survival with goodneurologic function (see “”). Finally, the realityis that the majority of resuscitative efforts donot result in ROSC. Criteria for endingunsuccessful resuscitative efforts areaddressed in .

Open table in a

Table 1: 2010 - Treatable Causes of CardiacArrest: The H's and T's

Rhythm-Based Management of CardiacArrest

In most cases of witnessed and unwitnessedcardiac arrest the first provider should startCPR with chest compressions and the secondprovider should get or turn on the defibrillator,place the adhesive pads or paddles, and checkthe rhythm. Paddles and electrode pads shouldbe placed on the exposed chest in an anterior-lateral position. Acceptable alternative positionsare anterior-posterior, anterior-leftinfrascapular, and anterior-right infrascapular.Rhythm checks should be brief, and if anorganized rhythm is observed, a pulse checkshould be performed. If there is any doubtabout the presence of a pulse, chestcompressions should be resumed immediately.If a cardiac monitor is attached to the patient atthe time of arrest, the rhythm can be diagnosedbefore CPR is initiated.

VF/Pulseless VT

When a rhythm check by an automatedexternal defibrillator (AED) reveals VF/VT,the AED will typically prompt to charge,“clear” the victim for shock delivery, and thendeliver a shock, all of which should beperformed as quickly as possible. CPRshould be resumed immediately after shockdelivery (without a rhythm or pulse checkand beginning with chest compressions) andcontinue for 2 minutes before the nextrhythm check.

When a rhythm check by a manualdefibrillator reveals VF/VT, the first providershould resume CPR while the secondprovider charges the defibrillator. Once thedefibrillator is charged, CPR is paused to“clear” the patient for shock delivery. Afterthe patient is “clear,” the second providergives a single shock as quickly as possible

5.2

5.2.1

to minimize the interruption in chestcompressions (“hands-off interval”). The firstprovider resumes CPR immediately aftershock delivery (without a rhythm or pulsecheck and beginning with chestcompressions) and continues for 2 minutes.After 2 minutes of CPR the sequence isrepeated, beginning with a rhythm check.

The provider giving chest compressionsshould switch at every 2-minute cycle tominimize fatigue. CPR quality should bemonitored based on mechanical orphysiologic parameters (see “MonitoringDuring CPR” below).

Defibrillation Strategies for VentricularFibrillation or Pulseless VentricularTachycardia: Waveform Energy andFirst-Shock Success

Currently manufactured manual andautomated external defibrillators usebiphasic waveforms of 3 different designs:biphasic truncated exponential (BTE),rectilinear biphasic (RLB), and pulsedbiphasic waveforms; they deliver differentpeak currents at the same programmedenergy setting and may adjust their energyoutput in relation to patient impedance indiffering ways. These factors can makecomparisons of shock efficacy betweendevices from different manufacturerschallenging even when the sameprogrammed energy setting is used. Asubstantial body of evidence now existsfor the efficacy of BTE and RLBwaveforms, with a smaller body ofevidence for the pulsed waveform. Animpedance-compensated version of thepulsed biphasic waveform is now clinicallyavailable, but no clinical studies wereidentified to define its performancecharacteristics.

5.2.1.1

ALS 470


There is no evidence indicatingsuperiority of one biphasic waveform orenergy level for the termination ofventricular fibrillation (VF) with the firstshock (termination is defined asabsence of VF at 5 seconds aftershock). All published studies supportthe effectiveness (consistently in therange of 85%–98%) of biphasic shocksusing 200 J or less for the firstshock. Defibrillators using the RLBwaveform typically deliver more shockenergy than selected, based on patientimpedance. Thus, in the single study inwhich a manufacturer’s nonescalatingenergy device was programmed todeliver 150 J shocks, comparison withother devices was not possible becauseshock energy delivery in other devicesis adjusted for measured patientimpedance. For the RLB, a selectedenergy dose of 120 J typically providesnearly 150 J for most patients.


Defibrillators (using BTE, RLB, ormonophasic waveforms) arerecommended to treat atrial andventricular arrhythmias.

Based on their greater success inarrhythmia termination, defibrillatorsusing biphasic waveforms (BTE orRLB) are preferred to monophasicdefibrillators for treatment of bothatrial and ventricular arrhythmias.

In the absence of conclusiveevidence that 1 biphasic waveform issuperior to another in termination ofVF, it is reasonable to use themanufacturer’s recommended

5.2.1.1.1

5.2.1.1.2

energy dose for the first shock. If thisis not known, defibrillation at themaximal dose may be considered.

Defibrillation Strategies for VentricularFibrillation or Pulseless VentricularTachycardia: Energy Dose forSubsequent Shocks

The 2010 Guidelines regarding treatmentof VF/pulseless ventricular tachycardia(pVT) recommended that if the first shockdose did not terminate VF/pVT, the secondand subsequent doses should beequivalent, and higher doses may beconsidered. The evidence supportingenergy dose for subsequent shocks wasevaluated for the 2015 Guidelines Update.


Observational data indicate that anautomated external defibrillatoradministering a high peak current at 150J biphasic fixed energy can terminateinitial, as well as persistent or recurrentVF, with a high rate of conversion. Infact, the high conversion rate achievedwith all biphasic waveforms for the firstshock makes it difficult to study theenergy requirements for second andsubsequent shocks when the first shockis not successful. A 2007 studyattempted to determine if a fixed lowerenergy dose or escalating higher doseswere associated with better outcome inpatients requiring more than 1 shock.Although termination of VF at 5 secondsafter shock was higher in the escalatinghigher-energy group (82.5% versus71.2%), there were no significantdifferences in ROSC, survival todischarge, or survival with favorableneurologic outcome between the 2groups. In this study, only 1

5.2.1.2

5.2.1.2.1

manufacturer’s nonescalating energydevice, programmed to deliver 150-Jshocks, was used. Thus, it is notpossible to compare this 150-J shockwith that delivered by any other deviceset to deliver 150 J.

There is a decline in shock success withrepeated shocks. One nonrandomizedtrial that used a BTE waveform reporteda decline in shock success whenrepeated shocks at the same energywere administered. For the RLBwaveform, 1 observational studyreported an initial VF termination rate of87.8% at a selected energy setting of120 J and an 86.4% termination rate forpersistent VF. Recurrence of VF did notaffect ultimate shock success, ROSC,or discharge survival.


It is reasonable that selection of fixedversus escalating energy forsubsequent shocks be based on thespecific manufacturer’s instructions.

If using a manual defibrillatorcapable of escalating energies,higher energy for second andsubsequent shocks may beconsidered.

Defibrillation Strategies for VentricularFibrillation or Pulseless VentricularTachycardia: Single Shocks VersusStacked Shocks

The 2010 Guidelines recommended a 2-minute period of CPR after each shockinstead of immediate successive shocksfor persistent VF. The rationale for this isat least 3-fold: First, VF is terminated witha very high rate of success with biphasicwaveforms. Second, when VF is

5.2.1.2.2

5.2.1.3

terminated, a brief period of asystole orpulseless electrical activity (PEA) typicallyensues and a perfusing rhythm is unlikelyto be present immediately. Third, thisprovides for a period of uninterrupted CPRfollowing a shock before repeat rhythmanalysis. The evidence for single versusstacked shocks was reviewed again in2015.


One RCT that comprised 845 OHCApatients found no difference in 1-yearsurvival when a single shock protocolwith 2 minutes of CPR betweensuccessive shocks was comparedagainst a previous resuscitation protocolemploying 3 initial stacked shocks with1 minute of CPR between subsequentshocks (odds ratio, 1.64; 95%confidence interval, 0.53– 5.06). AnRCT published in 2010 showed nodifference in frequency of VF recurrencewhen comparing the 2 treatmentprotocols. In that study, increased timein recurrent VF was associated withdecreased favorable neurologic survivalunder either protocol.

There is evidence that resumption ofchest compressions immediately after ashock can induce recurrent VF, but thebenefit of CPR in providing myocardialblood flow is thought to outweigh thebenefit of immediate defibrillation for theVF. Another study of patients presentingin VF after a witnessed arrest concludedthat recurrence of VF within 30 secondsof a shock was not affected by thetiming of resumption of chestcompressions. Thus, the effect of chestcompressions on recurrent VF is notclear. It is likely that in the future,

5.2.1.3.1

algorithms that recognize recurrent VFduring chest compressions with highsensitivity and specificity will allow us todeliver a shock earlier in the CPR cycle,thereby reducing the length of time themyocardium is fibrillating and theduration of postshock CPR.


A single-shock strategy (as opposedto stacked shocks) is reasonable fordefibrillation.

Automatic Versus Manual Modes forMultimodal Defibrillators

Use of a multimodal defibrillator in manualmode may reduce the duration ofinterruption of CPR required for rhythmanalysis compared with automatic modebut could increase the frequency ofinappropriate shock.

Current evidence indicates that thebenefit of using a multimodaldefibrillator in manual instead ofautomatic mode during cardiac arrestis uncertain.

CPR Before Defibrillation

This topic now covered in .

VF Waveform Analysis to PredictDefibrillation Success

Retrospective analysis of VF waveforms inmultiple clinical studies suggests that it ispossible to predict the success ofdefibrillation from the fibrillation waveformwith varying reliability. No prospectivehuman studies have specifically evaluatedwhether treatment altered by predicting

5.2.1.3.2

5.2.1.4

,

5.2.1.5

5.2.1.6

,

success of defibrillation can improvesuccessful defibrillation, rate of ROSC, orsurvival from cardiac arrest.

The value of VF waveform analysis toguide management of defibrillation inadults with in-hospital and out-of-hospital cardiac arrest is uncertain.

PEA/Asystole

When a rhythm check by an AED reveals anonshockable rhythm, CPR should beresumed immediately, beginning with chestcompressions, and should continue for 2minutes before the rhythm check isrepeated. When a rhythm check using amanual defibrillator or cardiac monitorreveals an organized rhythm, a pulsecheck is performed. If a pulse is detected,post–cardiac arrest care should be initiatedimmediately (see ). If the rhythm is asystoleor the pulse is absent (eg, PEA), CPRshould be resumed immediately, beginningwith chest compressions, and shouldcontinue for 2 minutes before the rhythmcheck is repeated. The provider performingchest compressions should switch every 2minutes. CPR quality should be monitoredon the basis of mechanical or physiologicparameters (see “Monitoring During CPR”below).

Treating Potentially ReversibleCauses of PEA/Asystole

PEA is often caused by reversibleconditions and can be treated successfullyif those conditions are identified andcorrected. During each 2-minute period ofCPR the provider should recall the H’s andT’s to identify factors that may havecaused the arrest or may be complicatingthe resuscitative effort (see and “”). Giventhe potential association of PEA with

5.2.2

5.2.2.1

hypoxemia, placement of an advancedairway is theoretically more important thanduring VF/pulseless VT and might benecessary to achieve adequateoxygenation or ventilation. PEA caused bysevere volume loss or sepsis willpotentially benefit from administration ofempirical IV/IO crystalloid. A patient withPEA caused by severe blood loss willpotentially benefit from a bloodtransfusion.

When pulmonary embolism ispresumed or known to be the cause ofcardiac arrest, empirical fibrinolytictherapy can be considered.

Finally, if tension pneumothorax isclinically suspected as the cause of PEA,initial management includes needledecompression. If available,echocardiography can be used to guidemanagement of PEA because it providesuseful information about intravascularvolume status (assessing ventricularvolume), cardiac tamponade, masslesions (tumor, clot), left ventricularcontractility, and regional wall motion. See“” for management of toxicological causesof cardiac arrest.

Asystole is commonly the end-stagerhythm that follows prolonged VF or PEA,and for this reason the prognosis isgenerally much worse.

ROSC After PEA/Asystole

If the patient has ROSC, post–cardiacarrest care should be initiated (see ). Ofparticular importance is treatment ofhypoxemia and hypotension and earlydiagnosis and treatment of the underlyingcause of cardiac arrest.

5.2.2.2

Therapeutic hypothermia may beconsidered when the patient iscomatose.

Medications for Arrest Rhythms

The primary goal of pharmacologic therapyduring cardiac arrest is to facilitate restorationand maintenance of a perfusing spontaneousrhythm. Toward this goal, ACLS drug therapyduring CPR is often associated with increasedrates of ROSC and hospital admission but notincreased rates of long-term survival with goodneurologic outcome. One study randomizedpatients to IV or no IV medications duringmanagement of adult out-of-hospital cardiacarrest. The study demonstrated higher rates ofROSC in the IV group (40% IV versus 25% noIV [odds ratio (OR) 1.99; 95% confidenceinterval (CI) 1.48 to 2.67]), but there was nostatistical difference in survival to hospitaldischarge (10.5% IV versus 9.2% no IV [OR1.16; 95% CI 0.74 to 1.82]) or survival withfavorable neurologic outcome (9.8% IV versus8.1% no IV [OR 1.24; 95% CI 0.77 to 1.98]).This study was not adequately powered todetect clinically important differences in long-term outcomes. Evidence from onenonrandomized trial found that the addition ofACLS interventions including IV drugs in apreviously optimized BLS system with rapiddefibrillation resulted in an increased rate ofROSC (18.0% with ACLS versus 12.9% beforeACLS, P<0.001) and hospital admission(14.6% with ACLS versus 10.9% before ACLS,P<0.001) but no statistical difference in survivalto hospital discharge (5.1% with ACLS versus5.0% before ACLS). Whether optimized high-quality CPR and advances in post–cardiacarrest care will enable the increased rates ofROSC with ACLS medications to be translatedinto increased long-term survival remains to bedetermined.

5.3

Ventricular Fibrillation (VF) or PulselessVentricular Tachycardia (pVT)

Treating Potentially ReversibleCauses of VF/pVT

The importance of diagnosing and treatingthe underlying cause of VF/pVT isfundamental to the management of allcardiac arrest rhythms. As always, theprovider should recall the H’s and T’s toidentify a factor that may have caused thearrest or may be complicating theresuscitative effort (see and “”). In thecase of refractory VF/pulseless VT, acutecoronary ischemia or myocardial infarctionshould be considered as a potentialetiology. Reperfusion strategies such ascoronary angiography and PCI duringCPR or emergency cardiopulmonarybypass have been demonstrated to befeasible in a number of case studies andcase series but have not been evaluatedfor their effectiveness in RCTs. Fibrinolytictherapy administered during CPR foracute coronary occlusion has not beenshown to improve outcome.

ROSC After VF/pVT

If the patient has ROSC, post–cardiacarrest care should be started. Ofparticular importance are treatment ofhypoxemia and hypotension, earlydiagnosis and treatment of ST-elevation myocardial infarction (STEMI)

and therapeutic hypothermia incomatose patients.

Antiarrhythmic Drugs During andImmediately After Cardiac Arrest -Updated

5.3.1

5.3.1.1

5.3.1.2

5.3.2

ALS 428

The 2015 ILCOR systematic reviewaddressed whether the administration ofantiarrhythmic drugs for cardiac arrest due torefractory VF or pVT results in betteroutcome.

Antiarrhythmic Drugs During andImmediately After Cardiac Arrest:Antiarrhythmic Therapy for RefractoryVF/pVT Arrest - Updated

Refractory VF/pVT refers to VF or pVTthat persists or recurs after 1 or moreshocks. It is unlikely that an antiarrhythmicdrug will itself pharmacologically convertVF/pVT to an organized perfusing rhythm.Rather, the principal objective ofantiarrhythmic drug therapy in shock-refractory VF/pVT is to facilitate therestoration and maintenance of aspontaneous perfusing rhythm in concertwith the shock termination of VF. Someantiarrhythmic drugs have beenassociated with increased rates of ROSCand hospital admission, but none have yetbeen proven to increase long-term survivalor survival with good neurologic outcome.Thus, establishing vascular access toenable drug administration should notcompromise the quality of CPR or timelydefibrillation, which are known to improvesurvival. The optimal sequence of ACLSinterventions, including administration ofantiarrhythmic drugs during resuscitationand the preferred manner and timing ofdrug administration in relation to shockdelivery, is not known. Previous ACLSguidelines addressed the use ofmagnesium in cardiac arrest withpolymorphic ventricular tachycardia (ie,torsades de pointes) or suspectedhypomagnesemia, and this has not beenreevaluated in the 2015 GuidelinesUpdate. These previous guidelinesrecommended defibrillation for termination

5.3.2.1

of polymorphic VT (ie, torsades depointes), followed by consideration ofintravenous magnesium sulfate whensecondary to a long QT interval.

The 2015 ILCOR systematic review didnot specifically address the selection oruse of second-line antiarrhythmicmedications in patients who areunresponsive to a maximum therapeuticdose of the first administered drug, andthere are limited data available to directsuch treatment.


Amiodarone - UpdatedIntravenous amiodarone is availablein 2 approved formulations in theUnited States, one containingpolysorbate 80, a vasoactive solventthat can provoke hypotension, andone containing captisol, which has novasoactive effects. In blinded RCTs inadults with refractory VF/pVT in theout-of-hospital setting, paramedicadministration of amiodarone inpolysorbate (300 mg or 5 mg/kg) afterat least 3 failed shocks andadministration of epinephrineimproved hospital admission rateswhen compared to placebo withpolysorbate or 1.5 mg/kg lidocainewith polysorbate. Survival to hospitaldischarge and survival with favorableneurologic outcome, however, wasnot improved by amiodaronecompared with placebo oramiodarone compared with lidocaine,although these studies were notpowered for survival or favorableneurologic outcome.

Lidocaine - Updated

5.3.2.1.1

5.3.2.1.1.1

5.3.2.1.1.2

Intravenous lidocaine is an alternativeantiarrhythmic drug of long-standingand widespread familiarity. Comparedwith no antiarrhythmic drug treatment,lidocaine did not consistentlyincrease ROSC and was notassociated with improvement insurvival to hospital discharge inobservational studies. In aprospective, blinded, randomizedclinical trial, lidocaine was lesseffective than amiodarone inimproving hospital admission ratesafter OHCA due to shock-refractoryVF/pVT, but there were no differencesbetween the 2 drugs in survival tohospital discharge.

Procainamide - UpdatedProcainamide is available only as aparenteral formulation in the UnitedStates. In conscious patients,procainamide can be given only as acontrolled infusion (20 mg/min)because of its hypotensive effectsand risk of QT prolongation, making itdifficult to use during cardiac arrest.Procainamide was recently studiedas a second-tier antiarrhythmic agentin patients with OHCA due to VF/pVTthat was refractory to lidocaine andepinephrine. In this study, the drugwas given as a rapid infusion of 500mg (repeated as needed up to 17mg/kg) during ongoing CPR. Anunadjusted analysis showed lowerrates of hospital admission andsurvival among the 176 procainamiderecipients as compared with 489nonrecipients. After adjustment forpatients’ clinical and resuscitationcharacteristics, no association wasfound between use of the drug andhospital admission or survival to

,

5.3.2.1.1.3

hospital discharge, although amodest survival benefit from the drugcould not be excluded.

Magnesium - UpdatedMagnesium acts as a vasodilator andis an important cofactor in regulatingsodium, potassium, and calcium flowacross cell membranes. In 3randomized clinical trials, magnesiumwas not found to increase rates ofROSC for cardiac arrest due to anypresenting rhythm, includingVF/pVT. In these RCTs and in 1additional randomized clinical trial,the use of magnesium in cardiacarrest for any rhythm presentation ofcardiac arrest or strictly for VFarrest did not improve survival tohospital discharge or neurologicoutcome.

Recommendations - Updated

Amiodarone or lidocaine may beconsidered for VF/pVT that isunresponsive to defibrillation. Thesedrugs maybe particularly useful forpatients with witnessed arrest, forwhom time to drug administrationmay be shorter.

The routine use of magnesium forcardiac arrest is not recommended inadult patients.

Magnesium may be considered fortorsades de pointes (ie, polymorphicVT associated with long QT interval)

No antiarrhythmic drug has yet beenshown to increase survival or neurologicoutcome after cardiac arrest due toVF/pVT. Accordingly, recommendationsfor the use of antiarrhythmicmedications in cardiac arrest are based

5.3.2.1.1.4

,

,

,

5.3.2.1.2

primarily on the potential for benefit onshort-term outcome until more definitivestudies are performed to address theireffect on survival and neurologicoutcome.

Antiarrhythmic Drugs During andImmediately After Cardiac Arrest:Antiarrhythmic Drugs AfterResuscitation - Updated

The 2015 ILCOR systematic reviewaddressed whether, after successfultermination of VF or pVT cardiac arrest,the prophylactic administration ofantiarrhythmic drugs for cardiac arrestresults in better outcome. The onlymedications studied in this context are β-adrenergic blocking drugs and lidocaine,and the evidence for their use is limited.


β-Adrenergic Blocking Drugs -Updatedβ-Adrenergic blocking drugs bluntheightened catecholamine activitythat can precipitate cardiacarrhythmias. The drugs also reduceischemic injury and may havemembrane-stabilizing effects. In 1observational study of oral orintravenous metoprolol or bisoprololduring hospitalization after cardiacarrest due to VF/pVT, recipients hada significantly higher adjustedsurvival rate than nonrecipients at 72hours after ROSC and at 6 months.Conversely, β-blockers can cause orworsen hemodynamic instability,exacerbate heart failure, and causebradyarrhythmias, making theirroutine administration after cardiacarrest potentially hazardous. There isno evidence addressing the use of β-

5.3.2.2

ALS 493

5.3.2.2.1

5.3.2.2.1.1

blockers after cardiac arrestprecipitated by rhythms other thanVF/pVT.

Lidocaine - UpdatedEarly studies in patients with acutemyocardial infarction found thatlidocaine suppressed prematureventricular complexes andnonsustained VT, rhythms that werebelieved to presage VF/pVT. Laterstudies noted a disconcertingassociation between lidocaine andhigher mortality after acutemyocardial infarction, possibly due toa higher incidence of asystole andbradyarrhythmias; the routine practiceof administering prophylacticlidocaine during acute myocardialinfarction was abandoned. The useof lidocaine was explored in amultivariate and propensity score–adjusted analysis of patientsresuscitated from out-of-hospitalVF/pVT arrest. In this observationalstudy of 1721 patients, multivariateanalysis found the prophylacticadministration of lidocaine beforehospitalization was associated with asignificantly lower rate of recurrentVF/ pVT and higher rates of hospitaladmission and survival to hospitaldischarge. However, in a propensityscore–adjusted analysis, rates ofhospital admission and survival tohospital discharge did not differbetween recipients of prophylacticlidocaine as compared withnonrecipients, although lidocaine wasassociated with less recurrentVF/pVT and there was no evidence ofharm. Thus, evidence supporting arole for prophylactic lidocaine after

5.3.2.2.1.2

,

VF/pVT arrest is weak at best, andnonexistent for cardiac arrest initiatedby other rhythms.

Recommendations - Updated

There is insufficient evidence tosupport or refute the routine use of aβ-blocker early (within the first hour)after ROSC.

There is insufficient evidence tosupport or refute the routine use oflidocaine early (within the first hour)after ROSC.

In the absence of contraindications,the prophylactic use of lidocaine maybe considered in specificcircumstances (such as duringemergency medical servicestransport) when treatment ofrecurrent VF/pVT might prove to bechallenging.

Available evidence suggests that theroutine use of atropine during PEA orasystole is unlikely to have atherapeutic benefit.

There is insufficient evidence torecommend for or against the routineinitiation or continuation of otherantiarrhythmic medications after ROSCfrom cardiac arrest.

Vasopressors in Cardiac Arrest -Updated

The 2015 ILCOR systematic reviewaddresses the use of the vasopressorsepinephrine and vasopressin during cardiacarrest. The new recommendations in this2015 Guidelines Update apply only to theuse of these vasopressors for this purpose.

5.3.2.2.2

5.3.3

In 2010 it was noted that, no placebo-controlled trials have shown thatadministration of any vasopressor agent atany stage during management of VF,pulseless VT, PEA, or asystole increases therate of neurologically intact survival tohospital discharge. There is evidence,however, that the use of vasopressor agentsis associated with an increased rate ofROSC.

Vasopressors in Cardiac Arrest:Standard-Dose Epinephrine - Updated

Epinephrine produces beneficial effects inpatients during cardiac arrest, primarilybecause of its α-adrenergic (ie,vasoconstrictor) effects. These α-adrenergic effects of epinephrine canincrease coronary perfusion pressure andcerebral perfusion pressure during CPR.The value and safety of the β-adrenergiceffects of epinephrine are controversialbecause they may increase myocardialwork and reduce subendocardialperfusion. The 2010 Guidelines stated thatit is reasonable to consider administeringa 1-mg dose of IV/IO epinephrine every 3to 5 minutes during adult cardiac arrest.


One trial assessed short-term andlonger-term outcomes when comparingstandard-dose epinephrine to placebo. Standard-dose epinephrine wasdefined as 1 mg given IV/ IO every 3 to5 minutes. For both survival todischarge and survival to discharge withgood neurologic outcome, there was nobenefit with standard-dose epinephrine;however, the study was stopped earlyand was therefore underpowered foranalysis of either of these outcomes

5.3.3.1

ALS 788

5.3.3.1.1

(enrolled approximately 500 patients asopposed to the target of 5000). Therewas, nevertheless, improved survival tohospital admission and improved ROSCwith the use of standard-doseepinephrine. Observational studies wereperformed that evaluated epinephrine,with conflicting results.


Standard-dose epinephrine (1 mgevery 3 to 5 minutes) may bereasonable for patients in cardiacarrest.

Vasopressors in Cardiac Arrest:Standard Dose Epinephrine VersusHigh-Dose Epinephrine - Updated

High doses of epinephrine are generallydefined as doses in the range of 0.1 to 0.2mg/kg. In theory, higher doses ofepinephrine may increase coronaryperfusion pressure, resulting in increasedROSC and survival from cardiac arrest.However, the adverse effects of higherdoses of epinephrine in the postarrestperiod may negate potential advantagesduring the intraarrest period. Multiple caseseries followed by randomized trials havebeen performed to evaluate the potentialbenefit of higher doses of epinephrine. Inthe 2010 Guidelines, the use of high-doseepinephrine was not recommended exceptin special circumstances, such as for β-blocker overdose, calcium channel blockeroverdose, or when titrated to real-timephysiologically monitored parameters. In2015, ILCOR evaluated the use of high-dose epinephrine compared with standarddoses.


,

5.3.3.1.2

5.3.3.2

ALS 778 ALS 778

5.3.3.2.1

A number of trials have comparedoutcomes from standard-doseepinephrine with those of high-doseepinephrine. These trials did notdemonstrate any benefit for high-doseepinephrine over standard-doseepinephrine for survival to dischargewith a good neurologic recovery (ie,Cerebral Performance Categoryscore), survival to discharge, orsurvival to hospital admission. Therewas, however, a demonstrated ROSCadvantage with highdose epinephrine.

2015 Recommendation—New

High-dose epinephrine is notrecommended for routine use incardiac arrest.

Vasopressors in Cardiac Arrest:Epinephrine Versus Vasopressin -Updated

Vasopressin is a nonadrenergic peripheralvasoconstrictor that also causescoronary and renal vasoconstriction.


A single RCT enrolling 336 patientscompared multiple doses of standard-dose epinephrine with multiple doses ofstandard dose vasopressin (40 units IV)in the emergency department afterOHCA. The trial had a number oflimitations but showed no benefit withthe use of vasopressin for ROSC orsurvival to discharge with or withoutgood neurologic outcome.

2015 Recommendation—Updated

Vasopressin offers no advantage asa substitute for epinephrine incardiac arrest.

,

,

5.3.3.2.2

5.3.3.3

ALS 659

,

5.3.3.3.1

5.3.3.3.2

The removal of vasopressin has beennoted in the Adult Cardiac ArrestAlgorithm above ().

Vasopressors in Cardiac Arrest:Epinephrine Versus Vasopressin inCombination With Epinephrine -Updated


A number of trials have comparedoutcomes from standard doseepinephrine to those using thecombination of epinephrine andvasopressin. These trials showed nobenefit with the use of theepinephrine/vasopressin combinationfor survival to hospital discharge withCerebral Performance Category scoreof 1 or 2 in 2402 patients, no benefit forsurvival to hospital discharge or hospitaladmission in 2438 patients, and nobenefit for ROSC.


Vasopressin in combination withepinephrine offers no advantage as asubstitute for standard-doseepinephrine in cardiac arrest.

The removal of vasopressin has beennoted in the Adult Cardiac ArrestAlgorithm above ().

Vasopressors in Cardiac Arrest:Timing of Administration ofEpinephrine - Updated

2015 Evidence Summary: IHCA

One large (n=25 905 patients)observational study of IHCA withnonshockable rhythms was identified, inwhich outcomes from early

5.3.3.4

ALS 789

5.3.3.4.1

5.3.3.4.2

5.3.3.5

ALS 784

5.3.3.5.1

administration of epinephrine (1 to 3minutes) were compared with outcomesfrom administration of epinephrine at 4to 6 minutes, 7 to 9 minutes, andgreater than 9 minutes. In this study, theearly administration of epinephrine innonshockable rhythms was associatedwith increased ROSC, survival tohospital discharge, and neurologicallyintact survival. No studies wereidentified specifically examining theeffect of timing of administration ofepinephrine after IHCA with shockablerhythms.

2015 Evidence Summary: OHCA

For nonshockable rhythms, 3 studiesshowed improved survival to hospitaldischarge with early administration ofepinephrine. A study of 209 577 OHCApatients showed improved 1-monthsurvival when outcomes fromadministration of epinephrine at lessthan 9 minutes of EMS-initiated CPRwere compared with those in whichepinephrine was administered at greaterthan 10 minutes. Another studyenrolling 212 228 OHCApatients showed improved survival todischarge with early epinephrine (lessthan 10 minutes after EMS-initiatedCPR) compared with no epinephrine. Asmaller study of 686 OHCApatients showed improved rates ofROSC with early epinephrine (less than10 minutes after 9-1-1 call) when thepresenting rhythm was pulselesselectrical activity. For shockablerhythms, there was no benefit with earlyadministration of epinephrine, but therewas a negative association ofoutcome with late administration. Whenneurologically intact survival to

5.3.3.5.2

, ,

discharge was assessed, however,there was variable benefit with earlyadministration of epinephrine for bothshockable and nonshockable rhythms.Later administration of epinephrine wasassociated with a worse outcome.ROSC was generally improved withearly administration of epinephrinein studies of more than 210 000patients. Design flaws in the majorityof these observational OHCA studies,however, included the use of a “noepinephrine” control arm as thecomparator (thus not allowing forestimates on the effect of timing), andthe lack of known timing of epinephrineadministration upon arrival in theemergency department. In addition, therelationship of timing of defibrillation totiming of epinephrine is unknown forstudies that included shockablerhythms.

2015 Recommendations—Updated

It may be reasonable to administerepinephrine as soon as feasible afterthe onset of cardiac arrest due to aninitial nonshockable rhythm.

There is insufficient evidence to make arecommendation as to the optimaltiming of epinephrine, particularly inrelation to defibrillation, when cardiacarrest is due to a shockable rhythm,because optimal timing may vary basedon patient factors and resuscitationconditions.

Steroids - Updated

The use of steroids in cardiac arrest hasbeen assessed in 2 clinical settings: IHCAand OHCA. In IHCA, steroids werecombined with a vasopressor bundle or

, ,

, , ,

5.3.3.5.3

5.3.4 ALS 433

cocktail of epinephrine and vasopressin.Because the results of IHCA and OHCAwere so different, these situations arediscussed separately.

2015 Evidence Summary: IHCA

In an initial RCT involving 100 IHCApatients at a single center, the use of acombination of methylprednisolone,vasopressin, and epinephrine duringcardiac arrest and hydrocortisone afterROSC for those with shock significantlyimproved survival to hospital dischargecompared with the use of only epinephrineand placebo. In a subsequent 3-centerstudy published in 2013, of 268 patientswith IHCA (the majority coming from thesame center as in the first study), thesame combination of methylprednisolone,vasopressin, and epinephrine duringcardiac arrest, and hydrocortisone forthose with post-ROSC shock, significantlyimproved survival to discharge with goodneurologic outcome compared with onlyepinephrine and placebo.

The same 2 RCTs provided evidence thatthe use of methylprednisolone andvasopressin in addition to epinephrineimproved ROSC compared with the use ofplacebo and epinephrine alone.

2015 Evidence Summary: OHCA

In OHCA, steroids have been evaluated in1 RCT and 1 observational study. In thesestudies, steroids were not bundled as theywere in the IHCA but studied as a soletreatment. When dexamethasone wasgiven during cardiac arrest, it did notimprove survival to hospital discharge orROSC as compared with placebo. Theobservational study showed no benefit insurvival to discharge but did show an

5.3.4.1

,

5.3.4.2

association of improved ROSC withhydrocortisone compared with nohydrocortisone.

2015 Recommendations—New

There are no data to recommend for oragainst the routine use of steroids alonefor IHCA patients.

In IHCA, the combination of intra-arrestvasopressin, epinephrine, andmethylprednisolone and post-arresthydrocortisone as described byMentzelopoulos et al may beconsidered; however, further studiesare needed before recommending theroutine use of this therapeutic strategy.

For patients with OHCA, use of steroidsduring CPR is of uncertain benefit.

Access for Parenteral Medications DuringCardiac Arrest

Timing of IV/IO Access

During cardiac arrest, provision of high-quality CPR and rapid defibrillation are ofprimary importance and drug administrationis of secondary importance. After beginningCPR and attempting defibrillation foridentified VF or pulseless VT, providers canestablish IV or IO access. This should beperformed without interrupting chestcompressions. The primary purpose of IV/IOaccess during cardiac arrest is to providedrug therapy. Two clinical studies reporteddata suggesting worsened survival for everyminute that antiarrhythmic drug delivery wasdelayed (measured from time of dispatch).However, this finding was potentially biasedby a concomitant delay in onset of otherACLS interventions. In one study the interval

5.3.4.3

5.4

5.4.1

,

from first shock to administration of anantiarrhythmic drug was a significantpredictor of survival. One animal studyreported lower CPP when delivery of avasopressor was delayed. Time to drugadministration was also a predictor of ROSCin a retrospective analysis of swine cardiacarrest. Thus, although time to drug treatmentappears to have importance, there isinsufficient evidence to specify exact timeparameters or the precise sequence withwhich drugs should be administered duringcardiac arrest.

Peripheral IV Drug Delivery

If a resuscitation drug is administered by aperipheral venous route, it should beadministered by bolus injection and followedwith a 20-mL bolus of IV fluid to facilitate thedrug flow from the extremity into the centralcirculation. Briefly elevating the extremityduring and after drug administrationtheoretically may also recruit the benefit ofgravity to facilitate delivery to the centralcirculation but has not been systematicallystudied.

IO Drug Delivery

IO cannulation provides access to anoncollapsible venous plexus, enabling drugdelivery similar to that achieved byperipheral venous access at comparabledoses. Two prospective trials in children andadults and 6 other studies suggest that IOaccess can be established efficiently; is safeand effective for fluid resuscitation, drugdelivery, and blood sampling for laboratoryevaluation; and is attainable in all agegroups. However, many of these studieswere conducted during normal perfusionstates or hypovolemic shock or in animalmodels of cardiac arrest. Although virtually

5.4.2

5.4.3

all ACLS drugs have been givenintraosseously in the clinical setting withoutknown ill effects, there is little information onthe efficacy and effectiveness of suchadministration in clinical cardiac arrest duringongoing CPR.

It is reasonable for providers to establishIO access if IV access is not readilyavailable.

Commercially available kits can facilitate IOaccess in adults.

Central IV Drug Delivery

The appropriately trained provider mayconsider placement of a central line(internal jugular or subclavian) duringcardiac arrest, unless there arecontraindications.

The primary advantage of a central line isthat peak drug concentrations are higher anddrug circulation times shorter compared withdrugs administered through a peripheral IVcatheter. In addition, a central line extendinginto the superior vena cava can be used tomonitor ScvO2 and estimate CPP duringCPR, both of which are predictive of ROSC.However, central line placement caninterrupt CPR. Central venouscatheterization is a relative (but not absolute)contraindication for fibrinolytic therapy inpatients with acute coronary syndromes.

Endotracheal Drug Delivery

One study in children, 5 studies in adults,and multiple animal studies have shown thatlidocaine, epinephrine, atropine, naloxone,and vasopressin are absorbed via thetrachea. There are no data regardingendotracheal administration of amiodarone.Administration of resuscitation drugs into thetrachea results in lower blood concentrations

5.4.4

,

5.4.5

,

than when the same dose is givenintravascularly. Furthermore, the results ofrecent animal studies suggest that thelower epinephrine concentrations achievedwhen the drug is delivered endotracheallymay produce transient β-adrenergic effects,resulting in vasodilation. These effects canbe detrimental, causing hypotension, lowerCPP and flow, and reduced potential forROSC. Thus, although endotrachealadministration of some resuscitation drugs ispossible, IV or IO drug administration ispreferred because it will provide morepredictable drug delivery and pharmacologiceffect.

In one nonrandomized cohort study of out-of-hospital cardiac arrest in adults using arandomized control, IV administration ofatropine and epinephrine was associatedwith a higher rate of ROSC and survival tohospital admission than administration by theendotracheal route. Five percent of thosewho received IV drugs survived to hospitaldischarge, but no patient survived in thegroup receiving drugs by the endotrachealroute.

If IV or IO access cannot be established,epinephrine, vasopressin, and lidocainemay be administered by the endotrachealroute during cardiac arrest.

The optimal endotracheal dose of mostdrugs is unknown, but typically the dosegiven by the endotracheal route is 2 to 2½times the recommended IV dose. In 2 animalCPR studies the equipotent epinephrinedose given endotracheally wasapproximately 3 to 10 times higher than theIV dose. Providers should dilute therecommended dose in 5 to 10 mL of sterilewater or normal saline and inject the drugdirectly into the endotracheal tube. Studies

,

,

with epinephrine and lidocaine showed thatdilution with sterile water instead of 0.9%saline may achieve better drug absorption.

Prognostication During CPR:End-TidalCO2 - Updated

The 2015 ILCOR systematic review consideredone intraarrest modality, ETCO measurement,in prognosticating outcome from cardiac arrest.This section focuses on whether a specificETCO threshold can reliably predict ROSCand survival or inform a decision to terminateresuscitation efforts. The potential value ofusing ETCO as a physiologic monitor tooptimize resuscitation efforts is discussedelsewhere (See Monitoring PhysiologicParameters During CPR, earlier in this Part).

ETCO is the partial pressure of exhaledcarbon dioxide at the end of expiration and isdetermined by CO production, alveolarventilation, and pulmonary blood flow. It is mostreliably measured using waveformcapnography, where the visualization of theactual CO waveform during ventilationensures accuracy of the measurement. Duringlow-flow states with relatively fixed minuteventilation, pulmonary blood flow is the primarydeterminant of ETCO . During cardiac arrest,ETCO levels reflect the cardiac outputgenerated by chest compression. Low ETCOvalues may reflect inadequate cardiac output,but ETCO levels can also be low as a result ofbronchospasm, mucous plugging of the ETT,kinking of the ETT, alveolar fluid in the ETT,hyperventilation, sampling of an SGA, or anairway with an air leak. It is particularlyimportant to recognize that all of theprognostication studies reviewed in this sectionincluded only intubated patients. Innonintubated patients (those with bag-maskventilation or SGA), ETCO may not

5.5ALS 459 ALS 459

2

2

2

2

2

2

2

2

2

2

2

consistently reflect the true value, making themeasurement less reliable as a prognosticationtool.


Studies on the predictive capacity of ETCOamong intubated patients during cardiacarrest resuscitation are observational, andnone have investigated survival with intactneurologic outcome. An ETCO less than 10mmHg immediately after intubation and 20minutes after the initial resuscitation isassociated with extremely poor chances forROSC and survival.

A prospective observational study of 127IHCA patients found that an ETCO lessthan 10 mmHg at any point during theresuscitation was predictive of mortality, andonly 1 patient with an ETCO value less than10 mmHg survived to discharge. In thatsame study, an ETCO greater than 20mmHg after 20 minutes of resuscitation wasassociated with improved survival todischarge. Another prospectiveobservational study of 150 OHCA patientsreported no survival to hospital admissionwhen the ETCO was less than 10 mmHgafter 20 minutes of resuscitation. Althoughthese results suggest that ETCO can be avaluable tool to predict futility during CPR,potential confounding reasons for a lowETCO as listed above and the relativelysmall numbers of patients in these studiessuggest that the ETCO should not be usedalone as an indication to terminateresuscitative efforts. However, the failure toachieve an ETCO greater than 10 mmHgdespite optimized resuscitation efforts maybe a valuable component of a multimodalapproach to deciding when to terminateresuscitation.

5.5.1

2

2

, , , ,

2

2

2

2

2

2

2

2

There are no studies that assess theprognostic value of ETCO measurementssampled from an SGA or bag-mask airway inpredicting outcomes from a cardiac arrest.

2015 Recommendations—New

In intubated patients, failure to achieve anETCO2 of greater than 10 mm Hg bywaveform capnography after 20 minutesof CPR may be considered as onecomponent of a multimodal approach todecide when to end resuscitative efforts,but it should not be used in isolation.

The above recommendation is made withrespect to ETCO in patients who areintubated, because the studies examinedincluded only those who were intubated.

In nonintubated patients, a specificETCO2 cutoff value at any time duringCPR should not be used as an indicationto end resuscitative efforts.

Overview of Extracorporeal CPR - Updated

The 2015 ILCOR systematic review comparedthe use of ECPR (or ECMO) techniques foradult patients with IHCA and OHCA toconventional (manual or mechanical) CPR, inregard to ROSC, survival, and good neurologicoutcome. The recommendations in this updateapply only to the use of ECPR in this context.

ECPR refers to venoarterial extracorporealmembrane oxygenation during cardiac arrest,including extracorporeal membraneoxygenation and cardiopulmonary bypass.These techniques require adequate vascularaccess and specialized equipment. The use ofECPR may allow providers additional time totreat reversible underlying causes of cardiacarrest (eg, acute coronary artery occlusion,pulmonary embolism, refractory VF, profound

2

5.5.2

2

5.6 ALS 723

hypothermia, cardiac injury, myocarditis,cardiomyopathy, congestive heart failure, drugintoxication etc) or serve as a bridge for leftventricular assist device implantation or cardiactransplantation.


All of the literature reviewed in the 2015ILCOR systematic review comparing ECPRto conventional CPR was in the form ofreviews, case reports, and observationalstudies. The low-quality evidence suggests abenefit in regard to survival and favorableneurologic outcome with the use of ECPRwhen compared with conventional CPR.There are currently no data from RCTs tosupport the use of ECPR for cardiac arrest inany setting.

One propensity-matched prospectiveobservational study enrolling 172 patientswith IHCA reported greater likelihood ofROSC and improved survival at hospitaldischarge, 30-day follow-up, and 1-yearfollow-up with the use of ECPR amongpatients who received more than 10 minutesof CPR. However, this study showed nodifference in neurologic outcomes.

A single retrospective, observational studyenrolling 120 patients with witnessed IHCAwho underwent more than 10 minutes ofCPR reported a modest benefit over historiccontrols with the use of ECPR overcontinued conventional CPR in both survivaland neurologic outcome at discharge and 6-month follow-up.

A single propensity-matched, retrospective,observational study enrolling 118 patientswith IHCA who underwent more than 10minutes of CPR and then ECPR aftercardiac arrest of cardiac origin showed nosurvival or neurologic benefit over

5.6.1

conventional CPR at the time of hospitaldischarge, 30-day follow-up, or 1-year follow-up.

One post hoc analysis of data from aprospective, observational cohort of 162patients with OHCA who did not achieveROSC with more than 20 minutes ofconventional CPR, including propensityscore matching, showed that ECPR wasassociated with a higher rate ofneurologically intact survival than continuedconventional CPR at 3-month follow-up.

A single prospective, observational studyenrolling 454 patients with OHCA who weretreated with ECPR if they did not achieveROSC with more than 15 minutes ofconventional CPR after hospital arrivaldemonstrated improved neurologicoutcomes at 1-month and 6-month follow-up.

The key articles reviewed in the 2015 ILCORsystematic review comparing ECPR toconventional CPR feature some variability intheir inclusion and exclusion criteria (), whichmay affect the generalizability of their resultsand could explain some of theinconsistencies in outcomes betweenstudies.


There is insufficient evidence torecommend the routine use of ECPR forpatients with cardiac arrest. In settingswhere it can be rapidly implemented,ECPR may be considered for select

Open table in a

Table 2: 2015 - Inclusion and ExclusionCriteria for Key Extracorporeal CPR Articles

5.6.2

cardiac arrest patients for whom thesuspected etiology of the cardiac arrestis potentially reversible during a limitedperiod of mechanical cardiorespiratorysupport.

Interventions Not Recommended forRoutine Use During Cardiac Arrest

Atropine

Atropine sulfate reverses cholinergic-mediated decreases in heart rate andatrioventricular nodal conduction. Noprospective controlled clinical trials haveexamined the use of atropine in asystole orbradycardic PEA cardiac arrest. Lower-levelclinical studies provide conflicting evidenceof the benefit of routine use of atropine incardiac arrest. There is no evidence thatatropine has detrimental effects duringbradycardic or asystolic cardiac arrest.

Available evidence suggests that routineuse of atropine during PEA or asystole isunlikely to have a therapeutic benefit.

Sodium Bicarbonate

Tissue acidosis and resulting acidemiaduring cardiac arrest and resuscitation aredynamic processes resulting from no bloodflow during arrest and low blood flow duringCPR. These processes are affected by theduration of cardiac arrest, level of blood flow,and arterial oxygen content during CPR.Restoration of oxygen content withappropriate ventilation with oxygen, supportof some tissue perfusion and some cardiacoutput with high-quality chest compressions,then rapid ROSC are the mainstays ofrestoring acid-base balance during cardiacarrest.

5.7

5.7.1

,

5.7.2

,

Two studies demonstrated increasedROSC, hospital admission, and survival tohospital discharge associated with use ofbicarbonate. However, the majority of studiesshowed no benefit or found a relationshipwith poor outcome.

There are few data to support therapy withbuffers during cardiac arrest. There is noevidence that bicarbonate improves thelikelihood of defibrillation or survival rates inanimals with VF cardiac arrest. A widevariety of adverse effects have been linkedto administration of bicarbonate duringcardiac arrest. Bicarbonate may compromiseCPP by reducing systemic vascularresistance. It can create extracellularalkalosis that will shift the oxyhemoglobinsaturation curve and inhibit oxygen release.It can produce hypernatremia and theref

,

,

Part 7: Adult Advanced Cardiovascular Life Support – ECC … · 2019-01-18 · AHA’s 2010 ACLS...

Documents

Transcript of Part 7: Adult Advanced Cardiovascular Life Support – ECC … · 2019-01-18 · AHA’s 2010 ACLS...