EMS State of the Science Conference leads tonew thinking on prehospital resuscitation practices

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An editorial supplement to JEMS, sponsored byLaerdal Medical Corp. & Philips Medical Systems

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Reprinted with permission on Jems Communications. © 2004

14ACLS UpdateCurrent & future direction for the resuscitation of cardiacarrest patientsBy Clifton W. Callaway, MD, PhD, & David Hostler, PhD, NREMTP

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Forecast for ResuscitationAn editorial supplement to JEMSSponsored by Laerdal Medical Corp. & Philips Medical Systems

Publisher/General Manager Jeff BerendEditor A.J. HeightmanSenior Editor Keri LosavioEditorial Assistant Lisa A. BellSupplement Art Director Kristy D. EnlowProduction Manager Tim Francis

Cover Photo: Jonny LayefskyForecast for Resuscitation is an editorial supplement sponsored by Laerdal Medical Corp. & Philips Medical Systems and publishedby Jems Communications, 525 B Street, Suite 1900, San Diego, CA 92101-4495; 800/266-5367 (fed. ID #13-935377). Copyright 2004 ElsevierInc. No material may be reproduced or uploaded on computer network services without the expressed permissionof the publisher. Subscription information: To subscribe to a Jems Communications publication, visit www.jems.com.Advertising information: Rates are available on request. Contact Jems Communications Advertising Department at525 B Street, Suite 1900, San Diego, CA 92101-4495; 800/266-5367.

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6Highlights from the 2004 EMS State of theScience Conference, Dallas, February 20–21, 2004

Eagle Creek Report:Results of the 2-DayConsensus Conference onLeading Concerns in EMSBy A.J. Heightman, MPA, EMT-P

Close Up: Eagles Explainthe Rationale for ChangeInterviews with Joseph P. Ornato,MD, & Paul E. Pepe, MD, MPHBy David LaCombe, EMT-P

4From the EditorBy A.J. Heightman, MPA, EMT-P

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TThe U.S. Metropolitan Municipalities EMS

Medical Directors, whose members are ju-

risdictional EMS medical authorities from

the nation’s largest cities, meet each

February in Dallas at the annual EMS State

of the Science conference to review and

discuss research on EMS concepts, proce-

dures and equipment.

The group, representing EMS systems that serve 50 mil-lion Americans, also develops member consensus state-ments on what emerging science indicates are effective(and ineffective) medical procedures. The EMS medical di-rectors frequently return to their respective organizationsarmed with the research, scientific evidence and consensusnecessary to implement changes in their systems’ medicalprocedures.

This annual meeting is often referred to as the “Gatheringof Eagles” because a media representative, commenting onthe list of prominent EMS physicians participating in thegroup, once said, “Wow, that’s some gathering of eagles.”The group of medical directors then became known as theEagles Coalition.

The 2004 conference again brought together a stellar fac-ulty of EMS industry leaders to present cutting-edge infor-mation on EMS research, management issues and patientcare innovations, usually their own. This year’s program of-fered attendees the added opportunity to hear first-hand theresults of the coalition’s two-day retreat, dubbed EagleCreek, during which many of the metropolitan medical di-rectors, other respected cardiologists and American HeartAssociation representatives closely reviewed the latest re-sults of research on patient resuscitation.

After two intense days, the physicians walked away withseveral consensus opinions about where EMS clinical prac-tices are lagging behind the available science and where im-provements in patient resuscitation can occur in their ownsystems—in some cases, immediately.

The Eagles Coalition, spearheaded by EMS pioneer PaulE. Pepe, MD, MPH, agreed to allow JEMS to publish this spe-cial supplement, which is sponsored by Laerdal MedicalCorp. and Philips Medical Systems. The supplement reviewsthe status of advanced cardiac life support (ACLS) resuscita-tion in the United States and highlights important topicsfrom the 2004 EMS State of the Science Conference.

This supplement affords EMS administrators, medical di-rectors and field providers the opportunity to review someof the latest clinical research findings and proceduralchanges that these medical directors considered priorities tobe addressed as soon as possible to improve field care andpatient resuscitation practices in their jurisdictions.

However, readers must be cautioned that many of the rec-ommended changes may not be implemented quickly intheir own EMS systems because of the appropriate adminis-trative, political or medical reviews necessary to supportnew policies. Therefore, it is the intent of this supplement toserve as an important reference source to assist you in un-derstanding the rationale for changes on the horizon andprepare you to implement operational and proceduralchanges in the future.

The first part of this report takes a close look at some ofthe Eagles’ consensus recommendations and zeroes in onimportant facts that explain why certain changes shouldoccur in current clinical practice. EMS educator DavidLaCombe, director of education at the National EMSAcademy (operated by Acadian Ambulance Service) and anattendee at the 2004 EMS State of the Science conference,discusses important clinical information presented byJoseph P. Ornato, MD, medical director of the RichmondEMS Authority, and Paul E. Pepe, MD, MPH, medical directorfor the Dallas EMS system, to outline why targeted clinicalchanges will improve patient care and resuscitation resultsin the future.

The second part of this supplement presents an in-depthreview of some current ACLS procedures and much of theresearch validating the Eagles’ recommendations for proce-dural changes. Clifton Callaway, MD, PhD, an assistant pro-fessor at the University of Pittsburgh and an emergencyphysician at UPMC-Presbyterian Hospital, and David Hostler,PhD, NREMT-P, director of research at the University ofPittsburgh-affiliated Emergency Medicine Residency pro-gram, cite 43 references to illustrate key points in their arti-cle. (Visit myWebCE.com to earn CE units for this article.)

The combination of expert research, committed EMSmedical leadership and well-referenced content makes thisa must-read document explaining why changes must, andwill, occur in your EMS system in the near future. �

—A.J. Heightman

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A.J. Heightman, MPA, EMT-P, is the editor-in-chief of JEMS, a former regional EMS directorand EMS operations director. Contact him viae-mail at a.j.heightman@elsevier.com.

The Eagles Coalition at its 2004 Dallas conference.

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MMost of the EMS medical directors from the nation’s largest EMS systems attended the EMS State of the Science: A Gathering of Eagles

VI conference. The group presented clinical topics on key areas in EMS and results from its two-day clinical retreat (dubbed Eagle Creek)

to physicians, nurses, paramedics, educators and media representatives from throughout the United States. Discussions focused on the

group’s latest innovations and research-based changes that the medical directors plan to make in their systems to immediately improve

clinical care even while anticipating the next set of resuscitation guidelines, scheduled for release in 2005 by the American Heart

Association.

The U.S. Metropolitan Municipalities EMS Medical Directors (Eagles) coalition proactively involves staff and board members from the

AHA, National Association of EMS Physicians (NAEMSP) and American College of Emergency Physicians (ACEP) in its conferences and

research summit. It was clear the coalition will revisit any consensus recommendations whenever such groups as the AHA, NAEMSP

and ACEP publish new guidelines or position statements. In that respect, the Eagles worked hard, for example, to avoid making inter-

nal recommendations or changes that might conflict with future AHA recommendations and endorsed the AHA’s comprehensive

process in drafting, reviewing and publishing new guidelines.

After reviewing the current science and fellow colleagues’ successes during trial studies, the Eagles decided to implement a few sys-

tem changes immediately, believing that this proactive approach would save more lives, provide better care and predictably be com-

pliant with future guidelines, but on a timetable that’s months, if not years, ahead of the typical rollouts.

Although the medical directors presented more than 20 topics, the presentations on the resuscitation of cardiac arrest victims were

the most compelling. In the articles that follow, we present a synopsis of the Eagles Coalition recommendations and the bottom line on

why EMS systems need to make these types of changes in how they provide resuscitation.

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Highlightsfrom the 2004EMS State of theScience ConferenceDallas, February 20–21, 2004

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Eagle Creek Report:Results of the 2-DayConsensus Retreat onLeading Controversiesin EMSBy A.J. Heightman, MPA, EMT-PAs part of the EMS State of the ScienceConference, Paul E. Pepe, MD, MPH, re-ported on the two-day Eagles retreat con-ducted to review current research andestablish a working agenda on recom-mended changes or improvements for thegroup’s EMS systems. Some key agendapoints:

1. EMS systems need to revise clini-cal practice procedures to ensurethat cardiac compressions aren’tinterrupted unless absolutelynecessary. The results from auto-mated cardiac compression de-vices that deliver consistentcompressions are promising andcould aid in this area.

2. Research indicates that agonalgasping that often occurs soonafter the onset of sudden cardiacarrest may actually assist in betteroxygenating and enhancing ve-nous return than “assistedbreaths” in unresponsive patients.Also, uninterrupted cardiac com-pressions may prolong thatprocess, avoiding the need forearly ventilation support. In fact,interrupting compressions tobreathe for such gasping patientsmay diminish blood flow to thebrain and respiratory apparatus,thus limiting the duration and ef-fectiveness of the gasps.

3. Regarding citizen CPR involve-ment: a) If dispatch instructionsneed to be given to an untrainedbystander, dispatchers shouldgive compression-only instruc-tions. (Rationale: It takes a tremen-dous amount of time to sendsomeone away from the phone toopen an airway and give the ven-tilation, and then have them re-turn to the phone to receiveadditional instructions on how tocompress the chest, particularlywhen the patient has just col-lapsed and may be gasping andhave an oxygen reserve in thenon-circulating bloodstream.) b)If a person is on scene and al-

ready performing bystander CPR,let them continue as trained;don’t confuse things by havingthem switch to compression-onlyCPR.

4. Research indicates that it may bebeneficial for dispatchers to in-struct the public to begin the re-suscitation of unwitnessed cardiacarrest victims with four cycles of100 compressions only, then fol-lowed by only a couple of breaths.The CPR sequence would thencontinue at a ratio of 100:2 or50:2. (Note: In a recent animalstudy comparing 15:2 vs. com-pression-only vs. 100:2, the 100:2compression to ventilationmethod was the most successful.)This latter recommendation(adding some breaths after fourminutes) is optional, but may bemost applicable in EMS systemswith prolonged response intervals.

5. Research indicates that it may bemore beneficial for the first re-sponding crews to perform aminute or two of CPR (chest com-pressions) before delivering theirfirst defibrillation “to prime thepatient’s pump” and there shouldbe virtually no time delay be-tween cessation of compressionsand countershock delivery.(Rationale: When the heart goesinto ventricular fibrillation, itscells have only about three to fourminutes of “fuel,” known asadenosine triphosphate (ATP).Shocking the patient after thistime period may get rid of theVFib, but typically results in asys-tole or pulseless electrical activity.“Priming” the heart by perform-ing effective compressions anddelivering oxygen to the cells al-lows the cells to build up or main-tain ATP levels before the initialshock is delivered. Compressionsshould be continued while the de-fibrillator is being readied forshock delivery because severalseconds of delay to shock may re-duce the chances of successful re-suscitation. In most EMS systems,the real time from collapse to ac-tual first responder arrival at thepatient’s side exceeds the four-

minute window, even with report-ed response intervals of four tofive minutes [typically time fromthe first call to dispatch to arrivalat the street address].)

6. The use of vasopressin in concertwith epinephrine appears to bepromising in the resuscitation ofcardiac arrest victims, but this re-quires more definitive study.

7. Current research indicates thatthere are detrimental effects tooverventilating cardiac arrest ormajor trauma patients and whattraditionally have been referred toas “normal ventilation rates” mayeven be excessive, particularly inconnection with hypovolemia orobstructive lung disease (e.g.,asthma, COPD).

8. For non-cardiac arrest patients,the initial administration of 12 mgadenosine in patients with SVTmay be more beneficial thanstarting with 6 mg. There is nosignificant downside, a potentialbenefit and less cost involved inthis approach.

To put the cardiac arrest recommenda-tions in perspective, let’s take a look at acase that could be handled in your EMSsystem today.

Case studyA 56-year-old man suddenly collapses ata busy restaurant. As waiters attempt todetermine if the victim is breathing, a by-stander urgently calls 9-1-1. Each passingsecond feels like an eternity for restaurantpatrons. Receiving pre-arrival instructionsfrom dispatch, the caller yells to the wait-ers to open the airway and determine ifthe patient is at all responsive or breath-ing. “He looks like he’s gasping for air,”says one waiter. “I can’t feel a pulse,” saysanother employee.

The trained dispatcher on the phonetells the caller, “I need you to start CPR. Isthere an AED in the area?”

“I don’t know,” replies the excited by-stander. “No one here knows CPR.”

The dispatcher spends a minute ex-plaining how to open the patient’s airwayand administer two rescue breaths.However, the patient had vomited priorto collapsing, so the bystander hesitatesbefore administering the breaths. Thecaller returns to the phone for additional

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instructions. He then directs an employeeto begin chest compressions and tells himhow to do it.

While compressions begin, sirens be-come increasingly louder, and an enginecompany arrives at the patient’s side fourminutes after the initial call is placed.Firefighters instruct the bystanders to stopchest compressions so they can begin anassessment. The initial survey reveals thatthe patient is unconscious, apneic andpulseless. Firefighters begin to connectthe bag-valve mask to oxygen and placeAED electrodes on the patient’s chest.After analyzing, a shock is advised. Thecrew delivers the shock, the body twitch-es and they wait for the next instruction.

The recorded voice of the AED playsthe familiar statement: “Analyzing ... Noshock advised. Begin CPR.” The BLS firstresponders then initiate two-person CPRwith a 5:1 compression/ventilation ratio aminute or more after their arrival.

Paramedics arrive moments later andinitiate ALS, including ECG monitoring,intubation, IV access, medication therapyand pacing. Despite their efforts, the pa-tient remains in asystole and is pro-nounced dead 30 minutes later in theemergency department.

Could anything have been done differ-ently to improve the outcome for this pa-tient? The answer is yes—many things.Let’s take a look at the scientific evidencethat proves that some changes are neededin our approach to resuscitation.

Physiology of cardiac arrestEach day in the United States, more than950 people experience sudden cardiac ar-rest. Resuscitation of those patients re-quires an understanding of the body’smetabolism of energy, how ventilationprocedures can affect coronary perfusionand how compromised blood flow affectsventilatory needs.

The critical source of energy musclesneed to contract is obtained from adeno-sine triphosphate (ATP). These moleculesare literally fuel for muscles (including theheart). Several research studies revealthat, during certain cardiac arrests, theheart consumes ATP at a rapid rate.Ordinarily, ATP levels would be continu-ously replenished. However, during car-diac arrest, the body’s ATP reservescannot be maintained.

The most common etiology of cardiac

arrest is ventricular fibrillation. As theheart continues to fibrillate, the myocardi-um (heart muscle) consumes its ATP rap-idly. Within about four minutes, ATPstores are significantly depleted, and the“coarse” ventricular fibrillation deterio-rates to fine fibrillation and eventuallyasystole (standstill). So, in essence, the fib-rillating heart is eating up fuel.

Though less effective after several min-utes of arrest, the provision of chest com-pressions to pulseless patients circulatesblood and oxygen, which may allow heartcells to replenish their ATP stores. Whensufficient myocardial ATP levels are re-stored, there’s increased potential for suc-cessful defibrillation to be followed by a

pulse and blood pressure. Clearly, moreimmediate initiation of CPR is better andhelps to maintain ATP levels even longer.Nevertheless, even immediate bystanderCPR by family members has some poten-tial downsides.

Unfortunately, time-motion studies andother careful observations reveal thatboth bystander and professional rescuersinterrupt chest compressions too fre-quently and for time periods that aremuch too long. Several researchers haveconcluded that frequent pauses betweenrounds of chest compressions actuallycontribute to failed resuscitation efforts.

Recent studies have also indicated thatthe highest probability of survival exists

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Muscles obtain energy from ATP. The provision of chest compressions topulseless patients circulates blood and oxygen, which may restore ATP toheart cells and improve the chances for successful defibrillation.

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among those patients who receive chestcompressions to restore ATP levels toshockable levels prior to any attempt todefibrillate. Conversely, survival rates falldramatically within a matter of seconds ifthere is too long a pause from the timecompressions are stopped until the mo-ment the shock is actually delivered.

The provision of CPR can be lifesaving,if applied correctly. However, in one study,researchers observed that EMS personnelperform CPR differently in the field thanin the classroom by administering com-pressions of inconsistent depth. It’s alsoclear to medical experts that manyrescuers are very prone to excessivelyventilating patients, causing increased in-trathoracic pressures that markedly de-crease coronary perfusion, hamperingresuscitation.

Clearly, there is much work to be doneto readjust our thought processes andadapt our operating procedures to con-duct more effective resuscitation efforts.However, modern EMS now has the bene-fit of prehospital research that can serveas the beacon to guide the way to im-proved patient care.

Close Up: Eagles Explainthe Rationale for ChangeBy David LaCombe, EMT-PAn audience of more than 400 physicians,nurses, EMTs, paramedics, media repre-sentatives and government leaders lis-tened with enthusiasm as Joseph P.Ornato, MD, and Paul E. Pepe, MD, MPH,presented evidence at the 2004 EMS Stateof the Science Conference that some ofour time-honored practices in resuscita-tion are in need of change. I interviewedOrnato and Pepe, two of the nation’s lead-ing medical researchers and members ofthe Eagles Coalition. They agreed to sharesome of the most important informationpresented about sudden cardiac arrest forthis special JEMS supplement.

LaCombe: What was your initial reactionto the studies revealing that in manycases, providing CPR prior to defibrillationwould improve outcomes in patients without-of-hospital ventricular fibrillation?

Ornato: This is bigstuff. It’s starting to ex-plain why a lot of whatwe do is not giving usthe results we’ve hoped

for. It’s been a mystery, but it’s now be-coming fairly simple to understand theconcept that you have fuel, and you haveto replenish the fuel, and that’s what it’sall about. Simply put, the more you doCPR [compressions], the more you sweet-en the myocardial blood flow; the moremyocardial blood flow you get, the moreATP is produced and ventricular fibrilla-tion becomes more coarse—increasingthe likelihood that defibrillation will besuccessful if delivered within five secondsof an interruption of chest compressions.

LaCombe: During your presentation youshowed video of an echocardiographtaken during the resuscitation of a patientreceiving CPR with a ratio of 15 compres-sions to two ventilations. Could you de-scribe for our readers the significance ofwhat that echo revealed?

Ornato: As the sternum is compressedduring CPR, blood clears the right side ofthe heart immediately, but it has to getthrough the lungs before exiting the leftside of the heart. While a round of 15compressions is delivered, the coronaryperfusion pressure increases—drivingblood through the coronary arteries toperfuse the heart.

The coronary perfusion drops signifi-cantly when compressions are paused fortwo ventilations. Then the compressionsstart the pump again. It takes eight to 10beats before the blood starts to flowthrough the coronary arteries at a decentlevel. Of course, just as blood flow be-comes decent, you pause again for addi-tional ventilations, and the perfusiondrops all the way back down again. It’slike trying to climb to the top of the lad-der: Just as you start to make realprogress, you go all the way to the bottomand start all over again. That’s what we’redoing when we pause for more than asecond or two during CPR.

Every time we stop pushing on thechest, everything comes to a halt. Andwhen we start pushing, it takes a finitetime period, eight to 10 compressions onaverage, before reasonable flow and pres-sure resume again

LaCombe: Isn’t this what led to a conceptreferred to as the hands-off interval? Couldyou explain what this means?

Ornato: The term hands-off intervalrefers to the number of seconds it takes

from the last CPR chest compression towhen you fire the defibrillator. This cameto light from a study in which ventricularfibrillation was electrically induced in 20swine that were untreated for seven min-utes before CPR was started [Yu, et al:Circulation. 106:368–372, 2002]. The re-searchers experimented with varioushands-off intervals.

Interestingly, all the pigs that receiveddefibrillation within three seconds of in-terruption of chest compression survivedwith good pulses and blood pressure.However, resuscitation dropped to 80%with a 10-second interruption interval,and 40% percent with a 15-second inter-ruption interval. None of the swine sur-vived with 20 seconds or more ofinterrupted chest compression.

LaCombe: So, if interrupted chest com-pressions are one of the culprits for failedresuscitation, what other areas have beenidentified for which we need to changeour clinical approach to resuscitation?

Pepe: Everyone always talks about theABCs in resuscitation. But, in my opinion,

we don’t talk enoughabout the B part of theABCs. Obviously, breath-ing is lifesaving, but itcan also be detrimental

if we overventilate our pa-tients—something that’s easy to do in alow flow state like CPR. It comes down tounderstanding the unique physiology ofCPR and why we often don’t behave as ifwe understand the effects of positive pres-sure ventilation on resuscitation.

Ornato: I agree with Paul. It’s really im-portant to understand the physiology ofthe body and its preference to maintaincirculation through gasping in the firstminutes of cardiac arrest. For example,the case study that opens this article in-volves a victim who suddenly arrests in adiner. Bystanders note his gasping effort,which is a typical response of the body tomaintain oxygenation and circulate someblood.

Pepe: Think about a gasp. Right now,as you breathe normally, your tidal vol-ume is probably only around 400 or 500mL. A gasp, however, may suck in muchmore air than a normal breath. The initialpresence of gasping probably indicatesthat the body’s oxygenation is still suffi-cient to maintain the brain’s control over

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the respiratory effort and the respiratorymuscle contractions. Furthermore, thegasping effort enhances negative pressurein the thorax, significantly increasing ve-nous return to the heart.

LaCombe: So the presence of gasping inthe cardiac arrest patient probably meansthat rescuers have arrived only minutesafter the onset of the arrest. What impli-cation does this have for EMS?

Ornato: In the first five to six minutesof adult, non-traumatic cardiac arrest,providing artificial ventilation isn’t as crit-ical as we once thought, particularly forthe lay public. When rescuers exhale intothe lungs of a patient, they are blowing ina high volume of CO2 and only about 17%oxygen. Every time we release pressureon the sternum following a chest com-pression, the lungs passively suck in someroom air, which contains 21% oxygen atsea level. An adult can usually maintainoxygen saturation above 80–85% for thefirst five minutes after onset of a cardiacarrest. Thus, it now seems to be more im-portant to provide uninterrupted chestcompressions rather than to pause peri-odically for ventilations.

After the first five minutes, ventilationsare needed because the amount of passiveventilation generated by each compres-sion decreases as the “bellows effect” ofthe chest deteriorates when the di-aphragm starts to run out of ATP.

Pepe: Most importantly, patients losetheir ability to gasp after several minutesof low flow (CPR) conditions. The same istrue for the heart’s energy. In airport AEDresponse and coronary care unit research,it’s been shown that if we deliver thatcountershock within the first three to fourminutes, those patients will generallycome back without much of a problem.The problem generally occurs after fourto five minutes of a ventricular fibrillationevent. The heart begins to run out of ATP,and it becomes less susceptible to conver-sion to an organized rhythm with pulsesafter a countershock.

If you do the data dredging and break itdown to those cases in which the re-sponse time interval (call to scene arrival)was an average of four minutes or less,there isn’t much of a difference whether ashock is given immediately or deferreduntil CPR is performed for two to threeminutes. Where the differences show up

is when there’s an excess of four minutesfor EMS response. Two or three minutes ofCPR first in these instances makes defib-rillation more successful. The data arevery compelling.

A randomized, controlled trial done inOslo, Norway, showed a better survival tohospital discharge if they gave three min-utes of standard CPR before they went toshocks.

LaCombe: The Eagles group said com-pressions should be administered for 90seconds to three minutes for patientsdown for a long time. Some might say thatthree minutes is a lot.

Pepe: First of all, our recommendationwas not to do CPR for three minutes, thenhurry up and put the defibrillator on.Crews can still be starting an IV, setting upfor intubation and putting the defibrillatorpads on during that time period whilecompressions are being performed sothat they’re ready to shock when the timecomes.

Regarding the duration of pre-shockCPR, as a group, we left an option openfor our systems: If a medical directorwants their system to do 90 seconds, or ifanother medical director wants to have itbe three minutes, that’s fine. So we’re rec-ommending, as a group, that our systemsdo five to 10 cycles of chest compres-sion/ventilation sequences when a first re-sponder gets on the scene [consideringthe heart has been deprived of oxygen foran extended period of time—beyond fourminutes].

What’s the exception? When you getthere and the guy arrests right in front ofyou. No question—shock him. But if theperson has been down for an extendedtime period, prime the pump and do fiveto 10 cycles of CPR [before shocking thepatient] and with little time delay betweencessation of compressions and the shock.

LaCombe: What’s the latest on the use ofvasopressin in resuscitation?

Pepe: In our consensus group, wetalked about vasopressin. We agreed thatthere aren’t enough data out there to say“let’s switch over to vasopressin vs. epi-nephrine right now.” We may eventuallyend up combining vasopressin and epi-nephrine somehow in our treatment regi-men, but we don’t have the definitive datayet. Still, we believe there’s compelling

enough information to look at in futurestudies.

Ornato: This combo effect [of vaso-pressin and epinephrine together] reallyis intriguing. Our colleagues in Europehave some pretty compelling data indicat-ing that the epinephrine receptors be-come less responsive over time duringresuscitation. We’ve known that for morethan a decade now. The actual mecha-nism is not clear. That doesn’t seem tooccur to the same degree with the vaso-pressin receptors.

In animal models, you can show thatvasopressin will continue to have a vaso-constrictor effect much longer than epi-nephrine during ongoing resuscitation. Bygiving vasopressin, then giving epineph-rine on top of it, one plausible theory toexplain why administering both drugsback-to-back seems to be more effectivethan either alone is that the vasopressin iscausing vasoconstriction and a rise in thecoronary perfusion pressure that actuallydelivers more epinephrine to its receptors.We [also] need to consider the net clinicalbenefit, probably one of the most difficultthings that we all grapple with in medi-cine. When you have a therapy, whateverit is—drug, device or combination—thereis an outcome that’s positive. But at thesame time, in another group of patients, ithas a bad outcome. You’re in a medicaland an ethical dilemma by trying to figureout if you’re doing more good for morepeople, even though you’re causing a littlemore harm.

LaCombe: What about the concerns youpresent about the overventilation ofpatients?

Pepe: We have found that field crewsare definitely, and inadvertently, over-ventilating their patients nationwide.Ventilation should not be “normalized”during CPR conditions—it’s different.

Why do we ventilate? Yes, to get oxygento the blood. But there’s a difference be-tween oxygenation and ventilation.They’re intertwined in terms of respira-tion, but there’s a key distinction. In oxy-genation—pulmonary oxygenation, nottissue oxygenation—we are attempting tosaturate red cells. Ventilation describeshow much CO2 we are clearing (e.g., hy-perventilation or hypoventilation).

Colloquially, hyperventilation oftenmeans “breathe fast.” However, by true

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definition, it means, “low CO2 level,” andhypoventilation means “high CO2 levels”in the arterial bloodstream.

When I use the term ventilation, I’mnot thinking about oxygenation, I’mthinking about how much CO2 I need toremove. One should separate these twothings [oxygenation and ventilation] interms of patient care.

When you breathe, there’s a mixture ofopenings and closures in the lungs. Inopen (normal) air spaces, blood is virtual-ly 100% saturated with oxygen. PO2 at sealevel is about 760 mmHg, take away 50 forwater vapor pressure and 21% of that drygas gets you about 150 mmHg for oxygen.So when the air enters your trachea, it’s at150 mmHg and then, displaced by CO2

coming out, it falls to 110 mmHg in thealveoli. But when the PO2 gets to about110 mmHg, the saturation of red cells isstill about 98–99%.

So for all intents and purposes, youdon’t need to put 100% oxygen into thoseinflated lung units; it’s not going tochange much. Breathing faster won’t domuch either. Likewise, faster rates and100% O2 won’t affect fully closed units.Lung inflation is the key. Particularly inpatients who aren’t breathing, you have toreinflate their closed lung zones. So youfirst need to inflate enough to get mostlung units closer to 100% saturation. Rateis not the important variable here.

But what’s an adequate tidal volume?

Normal breaths are about 5–7 mL/kg orabout 400–500 mL in average person. Butwhat we find is that air maldistributeswhen we provide positive pressure breaths.Unlike normal breaths that pull the di-aphragm down and pull the lung zonesopen in a specific architecture, positivepressure breaths “push” the lungs openand maldistribute to pathways of least re-sistance (less “dependent” lung zones).

The irony is that oxygenation does re-quire the “normal” number of breaths perminute if the tidal volume is adequate,and in CPR conditions, the need to re-move CO2 is extremely low and much lessthan normal.

First of all, when you use larger thannormal tidal volumes, more CO2 is clearedwith each breath. More importantly, inCPR conditions, flow is so low that totalbody oxygen metabolism falls off, andeven when it continues in some tissues,return of the CO2 produced by that me-tabolism to the lungs is impaired by thelow flow state. In turn, there’s little need toventilate frequently, at least until pulsesreturn. In fact, positive pressure breathsinhibit venous return to the heart and, themore often they are provided, the morethat cardiac output (whatever is left) falls.This effect is clinically negligible in mostnormovolemic persons with normal cir-culation. But with obstructive lung disease(e.g., asthma, COPD), hypovolemia (e.g.,little preload or venous return) and severe

circulatory compromise (e.g., CPR situa-tions), the detrimental effects of positivepressure breaths are exaggerated and caneven be lethal by inhibiting coronary flowaltogether. This may often be an under-appreciated cause of PEA and EMD.

This effect applies even to situationswith spontaneous circulation. During ananimal study involving moderate hemor-rhage, and maintaining 10–12 mL/kg tidalvolume, we switched ventilations from 12to six, back to 20, 30, back to six. We ob-served variables right before the switch,but were continuously monitoring coro-nary perfusion pressure. At a respiratoryrate of 12, the cardiac output was low (2.5L/min.). But switching rates from 12 to six,cardiac output popped up to 2.8 L/min.More importantly, coronary perfusionpressure rose significantly while oxygena-tion was maintained.

When ventilation rates were raisedback to 20 or 30, it pushed the coronarypressures way down. Then when the ratereturned to six, there was a nice reboundeffect with markedly improved coronaryperfusion and maintenance of oxygena-tion. So there was much better oxygena-tion of the tissues by using slower rates.This study also pointed out that the respi-ratory rate, not just the hemorrhage, was aconfounding variable that caused muchof the low BP.

But is this issue well recognized? Wewent through 16 different paramedic andresuscitation training textbooks andfound they are providing fairly nonspecif-ic guidelines about ventilatory rates andthe negative effects of even “normal”rates in severe shock conditions, let alonecommentary about the hazards of over-ventilation. We found some that recom-mended 15–20 breaths per minute, somesaying 24–28 and others 24–30. In fact,recent investigations found that, even ifpersonnel were instructed to give just 12breaths per minute, they were out in thefield still providing more than 20 perminute.

Tom Aufderheide and his colleagues inMilwaukee directly monitored how oftencrews were giving breaths during CPR.They found the average was 37 perminute. Despite direct demonstration of12 breaths per minute in follow-up class-es, paramedics subsequently still averaged22 per minute in the field. Whether it’s theEMS “adrenaline effect” or whatever,

Field crews are definitely, and inadvertently, overventilating their patientsnationwide. Ventilation should not be “normalized” during CPR conditions—it’s different.

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we may need to control how we ventilatebeyond just training people to provideslower breaths.

LaCombe: How does the overventilationof patients negatively affect care and out-come studies?

Pepe: In looking back at the data weobtained from a multitude of studies, ven-tilation was not controlled and, thus, thismay have been an unrecognized con-founding variable that resulted in bad out-comes or blunted the positive effect of thedrugs studied (e.g., high-dose epi, amio-darone, etc.).

It may very well be that such occultvariables as overzealous positive pressureventilation also led to negative studies onrapid sequence induction intubation (RSI)outcomes and traumatic circulatory arrestfor which many protocols still call forrapid [ventilation] rates to “compensatefor metabolic acidosis” or to “pump moreoxygen in.”

The low pCO2 that showed up in theRSI outcome studies may be a surrogatevariable for overzealous ventilations, toomany positive pressure breaths cutting offadequate cardiac output.

Many unproven interventions for re-suscitation may, in fact, work. Theyworked well in the lab. It just may be thatwe need to look more closely at overven-tilation in the future as a key variable thataffects studies and, most importantly, sur-vival rates.

Concluding remarksPepe: Corey Slovis, MD, from VanderbiltUniversity and the Nashville, Tenn., EMSsystem perhaps summed up this processof change best when he said, “As all ofthese data get presented, we need to becertain in our uncertainty. That is, someservices may choose to give epi everythree minutes, some every five [minutes].Some [may] switch to vasopressin, some[may] alternate epi and vasopressin, andothers may go to vasopressin, vaso-pressin, then epinephrine. We need to tellour crews, ‘This is what we think is thebest right now; there’s going to be new in-formation.’ And we need to get away fromwhat we’ve had in the past, which is a lotof dogma: ‘This is how you do CPR peri-od. You need to know how to do it thisway.’ We need to stress to our personnelthat ‘[prehospital medicine] is continuing

to evolve—even more rapidly than in thepast. It’s just going to continue to evolve.’”

Ornato: I’m convinced that the solu-tion, if there is one to having the next leapin better outcome for in- or out-of-hospi-tal resuscitation, is likely not going to beone drug or one device. If you look atwhat’s happening physiologically to thehuman body, multiple bad things are hap-pening at once.

It’s awfully naïve of us as a scientificand medical community to think that onesingle drug is going to fix all of thosephysiologic derangements until the heartgets started again. Once you’re beyondthe electrical phase and into what’s calledthe metabolic phase, it looks like youneed multiple things.

What’s so exciting is that we’re nowhaving circulatory squeeze devices thatseem to at least provide better perfusionand pressure. We’ve got some hints thatwe can tweak the pharmacology to per-haps distribute the blood flow more intel-ligently. We’ve got, I think, the ability tomore intelligently apply our ventilationtechniques. We’ve got better wave forms.We’ve got all these things. I think the realfascinating thing to watch is what hap-pens when you combine them all togeth-er, vs. the standard way that we’ve beendoing it with one little tweak here andthere. The combo is where we’re going towind up in the future. �

Joseph P. Ornato, MD, is professor and

chair of the Department of Emergency Medi-

cine at Virginia Commonwealth University/

Medical College of Virginia in Richmond, Va.

He is also medical director of the Richmond

Ambulance Authority, the city’s prehospital

paramedic system. He graduated from Boston

University Medical School magna cum laude

and completed his training in internal medi-

cine at New York City’s Mount Sinai Hospital

and in cardiology at New York Hospital Cornell

University Medical Center. He is triple board

certified (internal medicine, cardiology, emer-

gency medicine). Ornato is an active re-

searcher in the field of cardiopulmonary

resuscitation. He serves as the American editor

of the journal Resuscitation and is on the edi-

torial board of the American Journal of

Emergency Medicine. He is past chair of the

American Heart Association’s National

Emergency Cardiac Care Committee and the

AHA Advanced Cardiac Life Support

Subcommittee. He’s the American Heart

Association’s national representative to the

National Heart, Lung and Blood Institute’s

National Heart Attack Alert Program’s

Coordinating Committee, and he chairs its

Science Base Subcommittee. Ornato is also

special consultant to the Circulatory System

Devices Panel of the Food and Drug Admini-

stration. He chaired the National Steering

Committee on the joint-sponsored National

Institutes of Health/American Heart Associ-

ation/Industry Public Access Defibrillation

International Randomized Clinical Trial and is

principal investigator on a $1.5 million Health

Resources and Services Administration

(HRSA) Bioterrorism Training grant.

Paul E. Pepe, MD, MPH, is chair of

emergency medicine and professor of medi-

cine, surgery, public health & allied health at

the University of Texas Southwestern Medical

Center and the Parkland Health & Hospital

System in Dallas. He is also medical director

for the Dallas Metropolitan Medical Response

System (MMRS), the inter-agency government

medical strike team (FBI, police, public health,

DHS) that responds to terrorist and weapons

of mass effect situations as well as emergency

public health crises in Dallas. Pepe co-authored

the original American Heart Association

Chain of Survival publication, which delineat-

ed the survival advantages of a systems ap-

proach in resuscitative care, and the National

Institutes of Health Chain of Recovery concept

for stroke management. His programs have re-

sulted in some of the highest survival rates

among U.S. metropolitan areas for both trau-

ma and cardiac arrest. Pepe also served for 14

years as physician director for the City of

Houston EMS System (1982–1996) and in the

late1990s was appointed EMS Medical Director

for the Commonwealth of Pennsylvania in the

administration of then-Governor Tom Ridge.

Pepe also heads the U.S. Metropolitan Urban

EMS Medical Directors’ Consortium, compris-

ing the designated, jurisdictional EMS (9-1-1

system) medical directors for most of the na-

tion’s 25–30 largest cities and medical direc-

tors for such major federal agencies as the U.S.

Secret Service and FBI.

David LaCombe, EMT-P, is director of

the National EMS Academy,

an educational partnership

between Acadian Ambul-

ance Service and South

Louisiana Community Col-

lege. He’s a frequent con-

tributor to JEMS and an advocate for the

improvement of leadership training for the

EMS profession.

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Delaying defibrillation to give CPRConclusion: Patients with VFib andambulance response intervals longerthan five minutes had better out-comes with three minutes of CPR firstbefore defibrillation was attempted.Performing CPR first prior to defibrilla-tion offered no advantage (or disad-vantage) in improving outcomes forpatients with ambulance responsetimes shorter than five minutes.Therefore, patients should get threeminutes of CPR before shocks.

Reference: Wik L, Hansen TB, Fylling F, et al:“Delaying defibrillation to give basic car-diopulmonary resuscitation to patients without-of-hospital ventricular fibrillation.” TheJournal of the American Medical Association(JAMA). 289(11):1389–1395, 2003.

Importance of continuous chestcompressions during CPRConclusion: Continuous chest com-pression CPR produces greater neuro-logically normal 24-hour survival thanstandard ABC CPR when performed ina clinically realistic fashion.

Reference: Kern KN, Hilwig RW, Berg RA, etal: “Importance of continuous chest com-pression during cardiopulmonary resuscita-tion: improved outcome during a simulatedsingle lay-rescuer scenario.” Circulation.105(5):645–649, 2002.

Lethal delays in chest compressionConclusion: Longer delays in chestcompressions with an automated ex-ternal defibrillator than occur with amanual defibrillation can worsen theoutcome from prolonged VFib.

Reference: Berg RA, Hilwig RW, Kern KB, etal: “Automated external defibrillation versusmanual defibrillation for prolonged ventricu-lar fibrillation: lethal delays of chest compres-sions before and after countershocks.” Annalsof Emergency Medicine. 42(4):458–467, 2003.

Chest compressions aloneConclusion: The outcome after CPRwith chest compressions alone is sim-ilar to that after chest compressionwith mouth-to-mouth ventilation.Chest compressions alone may bethe preferred approach for by-standers inexperienced in CPR or re-ceiving instructions over the phone.

Reference: 1) Ferreira D: “Cardiopul-monary resuscitation by chest compressionalone or with mouth-to-mouth ventilation.”Portuguese Journal of Cardiology.

19(7–8):839–840, 2000. 2) Hallstrom A, Cobb L,Johnson E, Copass M: “Cardiopulmonary re-suscitation by chest compression alone orwith mouth-to-mouth ventilation.” The NewEngland Journal of Medicine. 342(21):1546–1553, 2000.

Negative effects of overventilationConclusion: There is increasing evi-dence that current practices of res-cue breathing may be detrimentalin the resuscitative management ofsevere trauma, respiratory failureand cardiac arrest. This effect is mostpronounced in patients with hypo-volemia and obstructive lung dis-ease largely because highfrequencies of positive pressure ven-tilation can inhibit venous returnand, in turn, cardiac output.

Reference: Roppolo LP,Wigginton JG,Pepe PE: “Emergency ventilatory manage-ment as a detrimental factor in resuscitationpractices and clinical research efforts.”Intensive Care and Emergency Medicine.Vincent JL (ed). Springer-Verlag: Berlin, pp.139–151, 2004.

Hyperventilation-induced hypo-tension during resuscitationConclusion: Rescuers were observedto excessively ventilate patients dur-ing prehospital CPR. Subsequent ani-mal studies demonstrated that similarexcessive ventilation rates resulted insignificantly increased intrathoracicpressure and markedly decreasedcoronary perfusion pressures and sur-vival rates in both cardiac arrest andhemorrhagic models.

References: 1) Aufderheide TP, SigurdssonG, Pirallo RG, et al: Circulation.109(16):1960–1965, 2004.

2) Pepe PE, Raedler C, Lurie K,WiggintonJG: “Emergency ventilatory management inhemorrhagic states: elemental or detrimen-tal?” Journal of Trauma. 54:1048–1057, 2003.

Interrupted compressionsConclusion: Interruptions of com-pressions for rhythm analysis that ex-ceed 15 seconds before each shockcompromise the outcome of CPRand increase the severity of postre-suscitation myocardial dysfunction.

Reference: Yu T,Weil MH, Tang W, et al:“Adverse outcomes of interrupted precordialcompression during automated defibrilla-tion.” Circulation. 106:368–372. 2002.

The effects of biphasic waveformConclusion: High energy and aver-age current are associated with in-creased post-shock dysfunction,while low energy and high peak cur-rent maximize survival, in an experi-mental comparison of biphasicwaveforms designs. Maximum sur-vival and minimum myocardial dys-function were observed with the lowcapacitance 150-J waveform, whichdelivered higher peak current whileminimizing energy and average cur-rent. The effects of biphasic truncatedexponential waveform design on sur-vival and post-resuscitation myocar-dial function after prolonged VFibwere examined. The study examineda low-capacitance waveform typicalof low-energy application (100 uF,≤ 200 J) and a high-capacitancewaveform typical of high-energy ap-plication (200 uF, ≥ 200 J) in a longdowntime (seven minutes untreatedVF) swine model.

Reference: Tang W,Weil MH, Sun S, et al:”The effects of biphasic waveform design onpost-resuscitation myocardial function.”Journal of the American College ofCardiology. 43(7):1228–1235, 2004.

Effects of transthoracic impedance& body weight on defibrillationConclusions: Data from EMS systemsusing low-energy, non-escalatingAEDs were retrospectively analyzedwith regard to the influences oftransthoracic impedance and bodyweight on defibrillation and resuscita-tion. High-impedance and over-weight patients were defibrillated bythe biphasic waveform at high rates,with a fixed energy of 150 joules, andwithout energy escalation. Rapid de-fibrillation, rather than differences inpatient impedance, accounts for re-suscitation success.

References: 1) White RD, Blackwell TH,Russell JK, et al: “Transthoracic impedancedoes not affect defibrillation, resuscitation, orsurvival in patients with out-of-hospital car-diac arrest treated with a non-escalatingbiphasic waveform defibrillator.”Resuscitation. 2004; in press.

2) White RD, Blackwell TH, Russell JK, et al:“Body weight does not affect defibrillation,resuscitation or survival in patients with out-of-hospital cardiac arrest treated with a non-es-calating biphasic waveform defibrillator.”Critical Care Medicine. 2004; in press.

Studies Every EMS System Should Review Before Revising Resuscitation Protocols

14 FORECAST FOR RESUSCITATION � JEMS

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ACLS UpdateCurrent & future direction for the resuscitation of cardiac arrest patients

By Clifton W. Callaway, MD, PhD, & David Hostler, PhD, NREMTP

Cardiopulmonary arrest occurs both suddenly as a consequence of heart disease

and as the endpoint of chronic diseases. Sudden cardiac death is more common

in males than females and affects African-Americans more than Caucasians or

Asian-Americans.1,2 Although sudden death can affect patients of all ages, most

studies cite the mean age for sudden cardiac arrest between 65 and 70 years.1,3

In the United States, currently 6–7% of patients survive after out-of-hospital car-

diac arrest (OOHCA).4

Basic treatment priorities include rapidrestoration of spontaneous circulation(ROSC) and minimizing damage to or-gans, primarily the brain. ROSC consistslargely of mechanical and electrical res-cue shocks. In contrast, brain injury in-volves primarily cellular and molecularevents that are treated with specific anddetailed intensive care.

Meaningful survival is unlikely withoutattention to both heart and brain.Unfortunately, the cause of cardiopul-monary arrest is frequently unknown,and treatment follows guidelines with aone-size-fits-all approach, preventingproviders from directing treatment to op-timize resuscitation.

A single EMS provider may work formany months without seeing a cardiacarrest victim survive, but overall about

one-third of OOHCA patients have ROSClong enough to be admitted to the hospi-tal (see Figure 1, p. 16). Of those patientsadmitted to the hospital after OOHCA,two-thirds die prior to discharge.5 Themost common reason for death amongpatients after ROSC is post-ischemicbrain injury. Failure to regain conscious-ness leads to withdrawal of care anddeath for as many as 44–68% of OOHCAvictims.3,6

Restarting the heartThere are two barriers between theOOHCA victim and a positive outcome:restarting the heart and regaining con-sciousness. Two activities are central torestarting the heart: 1) artificial circula-tion (chest compressions augmented byvasoactive medications and ventilations)

to circulate oxygenated blood to the heartand brain and 2) electrical rescue shocksto terminate ventricular fibrillation (VFib)or unstable tachydysrhythmias. Rescueshocks should be used only when appro-priate. It’s critical to keep these prioritiesin mind because patients cannot be re-vived without excellent and near continu-ous chest compressions.

The contribution and recommendeddivision of time for resuscitation activitiesis depicted in Figure 2 (p. 16). All other ac-tivities, including antidysrhythmic med-ications and advanced airway maneuvers,are designed to supplement the chestcompressions or rescue shocks and maynot be appropriate for all patients.

Optimal resuscitation requires mini-mal interruption in chest compressions.After initiating resuscitation, patient re-

assessment can be reduced to constantawareness of the electrocardiogram (ECG)and whether or not pulses are present.For example, there is no reason to stopcompressions for a pulse check if asystoleor ventricular fibrillation is noted on theECG during ventilations.

Airway & ventilationAgonal respirations may delay recogni-tion of a cardiac arrest victim by lay peo-ple and EMS providers who report that thepatient is having “labored breathing” or is“breathing funny” when they are actuallypulseless and need CPR.

Agonal gasping is associated with sur-vival, probably because it stops after oneto two minutes and, thus, is a great timemarker for recent collapse.7,8 Agonal res-

pirations should signal to the prehospitalprovider that the patient is pulseless andneeds immediate chest compressions.

Advanced airway management is oftennot required in the initial phase of resus-citation. Excellent BLS skills are effectivefor oxygenating patients and do notrequire long pauses in chest compres-sions during the critical early moments ofresuscitation.

During cardiac arrest, muscle tone fails,and the tongue and soft tissue occlude theupper airway. Consequently, the airway israrely patent during cardiac arrest.9 If un-corrected, this obstruction prevents oxy-genation and ventilation, preventingresuscitation.

Simple maneuvers can open thehuman airway. Extension of the neck

(head-tilt) and forward displacement ofthe mandible (chin-lift) straightens andopens the pharynx. Insertion of anoropharyngeal airway can move thetongue forward in the pharynx. Withthese steps, positive pressure ventilationcan be provided using mouth-to-mask orbag-valve-mask ventilation.

A positive pressure breath of 10–15mL/kg delivered over two seconds will fillthe lungs. Ventilation with as little as 400mL in adults (6–7 mL/kg) will causethe chest to rise and meets the currentguidelines for artificial ventilation withsupplemental oxygen for unprotected(non-intubated) patients.10

For CO2 to be present in exhaled air,blood must be flowing through thelungs.11 Therefore, capnometry (end-tidalCO2 measurement) can be used to assessthe quality of ventilations and confirmplacement of an endotracheal tube. CO2

levels measured by a capnometer may bevery low (<10 mmHg) at the onset of re-suscitation. Good quality chest compres-sions will cause CO2 levels to increase,and these levels may be used as feedbackto improve or modify chest compressions.

An abrupt increase in end-tidal CO2 lev-els, usually to levels >35 mmHg, accom-panies the ROSC and may be the firstindication of successful resuscitation.

Airway devices: The self-inflating bagattached to a face mask (bag-valve mask)is the most common ventilation deviceused, but the bag-valve mask (BVM) hasseveral pitfalls. For example, maintainingan airtight seal between the mask and theface of the patient is often difficult, partic-ularly when simultaneously performinghead-tilt, chin-lift maneuvers. Practice in-creases ventilation success by a singleprovider, but two providers achieve morereliable airway management. Two-provider ventilation is optimal becausewhile one provider squeezes the bag, thesecond provider can use two hands tomake a seal and position the head.

A second difficulty with BVM ventila-tion is that a significant amount of air en-ters the stomach if the patient is tooaggressively ventilated, increasing thelikelihood of vomiting.12,13 In consciouspatients, the esophagus prevents air entryinto the stomach unless upper airwaypressures exceed 15–20 cm H2O.14

However, during cardiac arrest,esophageal muscle tone declines, and air

16 FORECAST FOR RESUSCITATION � JEMS

Figure 1: Early death after cardiac arrest results from cardiopulmonary collapse.Death during the first few days after hospital admission is usually related to brain in-jury and failure to awaken.

Deliver ChestCompressions

Not Organized ECG?

No Pulse?

Shock IfCoarse VF

Treat Causes

Pace or Drugs Too Slow Rhythms

Shock Too Fast Rhythms

Treat Causes

Advanced Airway

Pressor Drugs Other Drugs

Figure 2: Prioritization of activities during cardiac resuscitation: Chest compressionsshould be interrupted only to provide rescue shocks when appropriate. All drugs,airway devices and other interventions are designed to augment either artificial cir-culation or defibrillation. None of these adjuncts should interrupt or detract from per-forming the two core activities.

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will enter the stomach with upper airwaypressures above 5–8 cm H2O.15 Rapidlysqueezing the bag during the excitementof the resuscitation situation can result inmuch higher upper airway pressures. Atypical adult resuscitation bag holds ap-proximately 1,600 mL of gas. Manyproviders squeeze the resuscitation bag ascompletely as possible in the belief theyare delivering better ventilation, althoughonly 400–600 mL of oxygen is requiredfor average-sized adults. In addition topromoting inflation of the stomach, over-enthusiastic ventilation also causes posi-tive pressure in the thorax of a patientwith an unprotected airway, which fur-ther impedes venous blood returning tothe heart.

A recent study examining both humansand animals suggests that hyperventila-tion during CPR is very common duringresuscitation of cardiac arrest victims.16

Endotracheal intubation can secure theairway definitively by protecting it fromemesis and maintaining a patent airway.However, laryngoscopy usually requiresan interruption in chest compressions,and simply inserting an endotrachealtube will not restart the heart. Therefore,endotracheal intubation must be consid-ered an adjunct to the initial resuscitation,and it should not delay or interrupt chestcompressions. Obviously, any patientwith coma after ROSC will require endo-tracheal intubation, but the interruption

in artificial circulation required for thisprocedure should be carefully considered.With a protected airway, tidal volumes of10 mL/kg at slower rates are preferred.

Alternative airway adjuncts, such asdouble-lumen, combination endotra-cheal-esophageal tubes (CombiTube) orLaryngeal Mask Airways (LMAs) can beused to manage the airway during resus-citation.17,18 The CombiTube and LMAhave an advantage in that they can be in-

serted blindly in seconds without laryn-goscopy, thereby minimizing interruptionof chest compressions.12 One reporteddisadvantage of these devices is the in-ability to deliver medications by the endo-tracheal route. However, it is unclearwhether endotracheal medications haveany significant beneficial effect duringcardiac arrest.

Artificial circulationIn the pulseless patient, circulation ofblood can be accomplished by mechani-cal compression of the heart and chest.The critical parameter for restoring spon-taneous circulation is the development ofadequate pressure in the coronary arter-ies. Coronary perfusion pressure (CPP) isessentially the difference between pres-sure in the aorta and pressure inside theheart chambers. With mechanical com-pression of the heart and chest during re-suscitation, the primary perfusion of theheart occurs during the relaxation phase(see Figure 3, right).

CPP is the best predictor of resuscita-tion success.19 In humans, return of circu-lation requires that CPP exceed 15–20mmHg. Below this level, it is rare for re-suscitation efforts to result in ROSC. It isimportant to realize that chest compres-sions are the only intervention that willgenerate coronary perfusion pressure.

Vasoactive medications, such as epi-nephrine and vasopressin, will augmentthe CPP developed by chest compres-sions. Airway adjuncts, other drugs andmonitors facilitate other aspects of the re-suscitation, but they don’t increase CPP.Without advanced monitors, it’s impossi-ble to directly measure CPP during resus-citation. However, increasing end-tidalCO2 and improvement in the ECG (eitherfrom asystole to VFib or PEA, or an in-crease in PEA rate) provide indirect evi-dence that CPP is adequate.

Don’t interrupt compressionsInterruptions of chest compressions mustbe avoided. Research in animals hasshown that stopping compressions formerely four seconds can reduce CPP tozero, negating any benefit of previouschest compressions. Much like priming apump, 10–20 chest compressions afterthe interruption may be necessary tobuild up adequate perfusion pressure.

Because CPP is so critical for resuscita-

tion, every other intervention in OOHCAshould be considered an adjunct to chestcompressions and, with the exception ofdefibrillation, should not cause chestcompressions to stop.

Current research is examining whetherprolonging the intervals between ventila-tions is beneficial (for example, increasingthe interval from two breaths every 15chest compressions to every 30 chestcompressions), but these changes are stillinvestigational.

Delivery of chest compressions is ofteninadequate, and uninterrupted chest com-pressions are critical for restoration of cir-culation.20–22 Many studies have shownthat medical providers at all levels oftraining perform inadequate chest com-pressions. Common mistakes include notcompressing the chest deeply enough orquickly enough to generate CPP. It hasalso been shown that as rescuers becomefatigued they become less effective. Theeffects of fatigue can be measured as early

CHEST COMPRESSIONSCOMPRESSIONSWITH PRESSORS

Aorta

COMPRESSION

Heart ChambersAorta

RELAXATION

Blood Flow

Heart

Figure 3: Chest compressions create a pres-sure gradient between the aorta and the in-side of the heart chambers. This gradient isthe coronary perfusion pressure (CPP) whichdrives blood flow. Chest compression (topleft) increases pressure in both aorta andheart chambers. During relaxation (topright), pressure persists in the aorta, drivingblood flow. During chest compressions with-out drugs, much of the blood in the aortaruns off into the body as well as into the heart(bottom left). Adding vasoactive drugs, suchas epinephrine or vasopressin, increases theeffectiveness of chest compressions by con-stricting the peripheral arteries, and shuntingblood to the heart (bottom right).

Endotracheal intubationmust be considered anadjunct to the initialresuscitation, & it shouldnot delay or interruptchest compressions.

as three minutes after beginning chestcompressions even though the rescuerdoes not yet “feel tired.” Therefore, rotat-ing the provider delivering chest com-pression after every two to three minutesshould increase the overall quality ofchest compressions.

Several mechanical devices have beendesigned to provide more consistent andcontinuous chest compressions.23

However, no device has gained wide-spread use because of weight and cost.Persistent interest in these devices high-lights the need for strategies to improvechest compression delivery.

ECG monitoringContinuous ECG monitoring is essentialduring resuscitation. ECG rhythms can becategorized as organized and not organ-ized. Organized rhythms are supraventric-ular rhythms (e.g., sinus rhythm, atrialfibrillation, supraventricular tachycardia)or ventricular tachycardia. Disorganizedrhythms include VFib and asystole.

Organized rhythms can support pump-ing of blood unless they are too slow(<30–40 complexes per minute) or toofast (>170–180 complexes per minute).Disorganized rhythms cannot support thepumping of blood under any circum-stances. Therefore, only two actions mustbe based on the ECG:

1. If the rhythm isn’t organized, per-form an intervention to make itorganized; and

2. If an organized rhythm is too fastor too slow, perform an interven-tion to correct the rate.

Transthoracic electrical (rescue) shocksare highly effective for converting VFibinto an organized rhythm when VFib is ofvery brief duration (less than one to twominutes). However, repeated unsuccessfulshocks may directly damage the my-ocardium. Further, rescue shocks aremore likely to fail when cardiac arrest haslasted more than a few minutes.

In the prehospital setting, only 9% ofrescue shocks restore an organized ECG ifthe collapse was not witnessed by theEMS provider.24 Resuscitation is less likelyafter rescue shocks that convert VFib toasystole.25

Optimal therapy should provide rescueshocks at the lowest effective energy,while minimizing the number of unsuc-cessful rescue shocks. Thus, it will be-

come important in the future to deter-mine when a rescue shock is likely to re-store electrical activity and when a shockwill harm the patient by causing an unre-coverable asystole.

Improving shock successSeveral parameters can improve rescueshock success. Studies show that increas-ing the pressure of paddles against thechest wall from 0.5 kg to 8 kg (1 to 17 lbs.)improves conduction of electricitythrough the chest by as much as 14%.26,27

This advantage of paddle use must beweighed against the increased safety andconvenience afforded by hands-free ad-hesive defibrillation pads.

In the past, multiple shocks would bedelivered in rapid succession to decreasechest impedance. However, repetitiveshocks decrease chest impedance by onlya small amount.26

Biphasic shocks have been shown to bemore efficacious than monophasicshocks, and biphasic rescue shocks ap-pear to cause less cardiac dysfunctionafter ROSC. Finally, VFib becomes lesscoarse as soon as chest compressionsstop, suggesting that the rescuer shouldstrive for the briefest delay from the lastchest compression to the rescue shock.

The need to prime thecardiac pumpDuring cardiac arrest, the appearance ofVFib and the response of VFib to rescueshocks vary over time, leading researchersto suggest a phased approach to treatingcardiac arrest. VFib encountered withinminutes of collapse usually appearscoarse and should be immediately defib-rillated. However, VFib lasting longer thanthree to four minutes usually appears lessorganized, and a few minutes of chestcompressions can improve rescue shocksuccess.

Two clinical studies have found that 90seconds to three minutes of chest com-pressions prior to delivery of the initial res-cue shock improved resuscitation rates forsubjects with VFib outside the hospital,particularly when rescuer response inter-vals are longer than four minutes.28,29 Thus,defibrillation should be provided immedi-ately for VFib shortly after a witnessed col-lapse, but a brief period of artificialcirculation should precede any shock de-livery to VFib that has lasted longer.

Providers should follow their localprotocols, but be aware that the most re-cent research questions the traditionalteaching that all VFib should receive a res-cue shock as soon as recognized. In thefuture, providers may distinguish between“fresh,” very coarse VFib that is more like-ly to convert with a rescue shock and“later,” fine VFib that will benefit from aperiod of chest compressions to prime thecardiac pump with oxygenated blood.

Asystole is the extreme example of adisorganized cardiac rhythm and may beimpossible to distinguish from very fineVFib. In general, the amplitude of VFib de-creases over time because of the cardiachypoxia and ischemia that develops dur-ing cardiac arrest. There’s no official cut-off between very fine VFib and asystole,and both rhythms are unresponsive torescue shocks. However, many patients inasystole will exhibit higher amplitudeVFib after a few minutes of chest com-pressions, indicating that patients can tra-verse the spectrum from coarse VFib toasystole in two directions. Increasing am-plitude and organization of VFib providesa marker of adequate chest compressions.

Particularly when supplemented by va-sopressors, chest compressions may re-store VFib to a point where rescue shockscan result in ROSC. Thus, treatment ofasystole is primarily to provide adequateperfusion to the heart.

An organized rhythm without pulses iscalled pulseless electrical activity (PEA).The absence of perfusion in the presenceof organized electrical activity may resultfrom damage to heart muscle (as in mas-sive myocardial infarction) or from uncou-pling of electrical and mechanical activity(as in prolonged circulatory arrest).

For rhythms that are too fast, the ven-tricles of the heart may not fill with bloodbetween contractions, resulting in theabsence of palpable pulses during ventric-ular tachycardia, supraventricular tachy-cardia or atrial fibrillation with rapidventricular response. These tachyarrhyth-mias should be corrected by immediateelectrical cardioversion.

Outside of these tachyarrhythmias, therate of complexes in PEA is related to thelevel of hypoxia in the heart and may beused to monitor resuscitation efforts. Withincreasing hypoxia/ischemia, the heart’senergy stores are depleted and the rate ofPEA will slow. If resuscitation is delivering

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oxygen and improving the energy state ofthe heart, the rate of PEA will accelerate.

Narrow complexes reaching rates of80–100 beats per minute often signal thereturn of pulses. Falling rates of complex-es in PEA reflect poor heart perfusion,resulting in ischemia of the cardiac con-duction system. Thus, the cornerstones ofPEA treatment consist of cardioversionwhen appropriate and providing adequateperfusion of the heart.

Drug therapyDrug therapy in cardiac arrest can be di-vided into three categories: vasopressor,antidysrhythmic and metabolic drugs.There’s good evidence that vasopressorsimprove the CPP developed by chest com-pressions, making resuscitation more like-ly. Antidysrhythmic drugs are effective forpreventing dysrhythmias and, therefore,have a role in stabilizing the heart afterdefibrillation or ROSC. The value of anti-dysrhythmic drugs for terminating VFibor reversing asystole is less clear.Metabolic drugs, such as bicarbonate, canbe used to reverse acidosis or other elec-trolyte problems when they are recog-nized. However, there are no data tosupport the routine use of these drugs forall patients.

Vasopressors used during resuscitationinclude epinephrine and vasopressin.

Both of these drugs can increase coronaryperfusion pressure via actions on alpha-adrenergic (epinephrine) or vasopressinreceptors30,31 (see Figure 4, above).Epinephrine is usually administered in 1mg (~0.015 mg/kg) increments. In labora-tory studies, the pressor effects of epi-nephrine during cardiac arrest are brief(~5 minute).

Vasopressin is usually administered as40 unit boluses (~0.5 units/kg) and pro-duces a longer lasting increase in coro-nary perfusion pressure (~10 minutes).

In clinical studies, resuscitation ratesand survival are identical overall for pa-tients resuscitated with vasopressin andstandard doses of epinephrine.30,31 Thesestudies found that vasopressin might besuperior for patients whose first ECGrhythm is asystole and for those subjectsrequiring multiple doses of vasopressors.At present, use of either epinephrine orvasopressin is justified in the setting ofcardiac arrest.

Future studies may examine whethercombinations of epinephrine and vaso-pressin are more effective than eitherdrug alone.

The role of antidysrhythmic drugs dur-ing cardiac arrest is uncertain.32,33

Atropine may relieve bradycardia, but isineffective if the bradycardia is caused byischemia or hypoxia. Only case reports

support the use of atropine for treatmentof asystole.

Lidocaine, procainamide and bretyliumhave a long history of use in the treatmentof VFib because these drugs are known tosuppress ventricular ectopy. Once VFib isestablished, however, lidocaine increasesthe electrical energy required to defibril-late by more than 50%, making rescueshocks less effective.34 Amiodarone,bretylium and procainamide don’t havethis effect. Consequently, administrationof amiodarone (5 mg/kg) is superior toplacebo and to lidocaine for restoration ofpulses in prehospital patients with VFibthat’s not terminated by three rescueshocks.35,36

Many antidysrhythmic drugs alsocause hypotension after bolus injection.That is counterproductive in OOHCA andcan reduce the effects of vasopressorsgiven to increase pressure. In summary,antidysrhythmic drugs are commonlyused during resuscitation, but only amio-darone use has supporting human data.

Other drugs, such as bicarbonate,aminophylline, calcium and magnesium,have been suggested as treatments forOOHCA. However, none of these medica-tions are supported by research and maynot be useful outside very specific situa-tions. Therefore, the pharmacological ap-proach to treatment of cardiac arrest isfairly simple. First, the vasopressors epi-nephrine and vasopressin are useful foraugmenting CPP generated by chest com-pressions. Other vasopressors could alsobe useful, but lack prospective data.Second, antidysrhythmic drugs are usefulfor maintaining organized rhythms, butnot for terminating VFib. Only amio-darone has clinical data supporting its useduring VFib that persists after rescueshocks. All other drug therapy should bebased on the clinical situation and the re-sponse of the patient.

Minimizing brain injuryManagement of the patient after ROSC af-fects ultimate outcome. Because two-thirds of patients admitted to the hospitalafter ROSC fail to emerge from coma, im-provements in treatment of anoxic braininjury are essential for meaningful im-provement in overall survival.

Brain injury continues to developduring the hours and days after resuscita-tion, and involves complex biochemical

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Figure 4: Vasopressin and epinephrine increase CPP produced by chest compres-sions in a laboratory model. CPP increases only after about 60 seconds of chestcompressions. The effect of vasopressin is greater and longer lasting than that of ep-inephrine. Blood flow will reoxygenate and restore the heart only when CPP hasbeen increased. Thus, when treating cardiac arrest, it is unreasonable to expect aphysiological response to a pressor drug until at least 60 seconds of chest com-pressions, and it is more likely that the state of the heart will be changed after120–180 seconds of drug-augmented chest compressions. (Unpublished laborato-ry data).

events.37 Unfortunately, no drug to datehas demonstrated reduction of brain in-jury in human trials. Data do suggest thatavoiding fever, hypotension and hyper-glycemia improves neurological recoveryafter cardiac arrest.38–40 These data areprompting efforts to provide systematicbrain-oriented intensive care for the pa-tients with ROSC who are admitted to thehospital.

Two human trials have found that in-duction of mild hypothermia (33–34° C)for 12–24 hours after resuscitation im-proves survival and neurological recov-ery.41,42 Laboratory studies suggest thatcooling should be accomplished as soonas possible and is probably ineffective ifstarted more than four to six hours afterresuscitation.

During resuscitation, many patientsspontaneously cool to between 35° C and35.5° C when peripheral blood equili-brates with core blood.41–43 Thus, only asmall amount of additional cooling is nec-essary to reach a therapeutic range. It’spossible that, in the future, prehospitalproviders may initiate cooling in resusci-tated patients using a combination oftechniques, including cold IV fluids andcooling blankets.

The brain is very sensitive to low bloodpressure after cardiac arrest, and lowblood pressures during the first two hoursafter resuscitation are associated withpoor neurological recovery.39 Compli-cating this fact, the heart is also stunnedby cardiac arrest, and resuscitated pa-tients usually require drugs to support cir-culation during the first hours and daysafter resuscitation. Providers should antic-

ipate that the initial high blood pressureobserved moments after restoration ofpulses will decline quickly, and prepare touse dopamine or other vasopressors tohelp maintain brain perfusion (see Figure5, below).

Final wordOut-of-hospital cardiac arrest should notbe approached with a one-size-fits-alltreatment plan. Just as with other dis-eases, OOHCA patients will respond dif-ferently to treatments depending on thecause of the collapse and the length oftime the patient has been without a pulse.

The importance of CPR and its deliveryis being rediscovered. Providers mustplace more emphasis on external chestcompressions and less on advanced air-way management.

In the near future, EMS providers maybe asked to determine if a patient requiresimmediate defibrillation or be likely tobenefit from CPR and medications priorto delivering defibrillation.

Finally, as our ability to resuscitate pa-tients improves, prehospital providers willhave to provide the next segment of careby aggressively supporting blood pressureand initiating hypothermia to improve theultimate outcome. �

Clifton Callaway, MD, PhD, is an assistant profes-sor at the University of Pittsburgh and an emer-gency physician at UPMC-Presbyterian Hospital.He conducts research and has published numer-ous articles on cardiac arrest resuscitation andreducing brain injury in post cardiac arrestpatients. Contact him via e-mail at callawaycw@upmc.edu.

Dave Hostler, PhD, NREMT-P, has been a fire-

fighter/paramedic for 17 years. He is the directorof research at the University of PittsburghAffiliated Emergency Medicine Residency and avolunteer firefighter at Laurel Gardens VFibC inRoss Township, Pa. Contact him via e-mail athostlerdp@upmc.edu.

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Figure 5: Medications given during resuscitation wear off shortly after the return ofspontaneous circulation. In this graph of mean arterial pressure, an experimentalanimal resuscitated from cardiac arrest shows a high pressure initially after a rescueshock produces ROSC. However, this initial hypertension rapidly dissipates. This rapiddecline is known as the “CRUMP” and will cause the patient to lose pulses again ifnot anticipated and countered with an infusion of some vasopressor. Note the in-crease in pressure produced by chest compressions (CPR) after administration of adrug. (Unpublished laboratory data).

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