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CHAPTER 137Inpatient Cardiac Arrest and

Cardiopulmonary Resuscitation

John E. Moss, MD

Jason Persoff, MD, SFHM

Key Clinical Questions

What are the fundamental goals of cardiopulmonary resuscitation? Which components of resuscitation are considered vital to success? How can the common pitfalls of resuscitation be surmounted? What treatments should be instituted immediately upon successful resuscitation? How should outcomes in resuscitation shape the discussion of advanceddirectives?

INTRODUCTION

Cardiopulmonary resuscitation is a time-dependent, team-based effort to reversephysiologic events that may culminate in a patient’s imminent death. Biblical and ancientEgyptian hieroglyphic texts allude to mouth-to-mouth ventilation in divine contexts, but

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other texts indicate Jewish midwives used mouth-to-mouth resuscitation as early as 3300years ago to revive stillborn children.

In the United States an estimated 375,000 to 750,000 hospitalized patients suffer in-hospital cardiac arrest (IHCA) requiring advanced cardiac life support (ACLS) annually.The incidence of IHCA is estimated to be as high as 1% to2% of all patients admitted toacademic hospitals with a prevalence of approximately 65 people per 100,000 nationally.

In-hospital cardiac arrest encompasses a spectrum of disorders from insufficientcardiac output to generate appreciable cerebral perfusion such as arrhythmia or shock tocomplete cessation of cardiac activity. Vital sign anomalies may often herald impendinginpatient cardiac arrest by minutes to hours, but many cardiac arrests occur suddenly andwithout warning. Acute pulmonary arrest (very common in pediatric populations, often dueto airway obstruction; but much less common in adults) may precede IHCA and may occurfrom sedative or opiate analgesic overdose.

This chapter focuses on (1) the techniques that are essential to successfulcardiopulmonary resuscitation especially with attention to good neurologic recovery (asdefined by the cerebral performance category of zero or one), and (2) decision makingbased on patient resuscitation status.

TRIAGESince standardization of closed chest cardiac massage (CCCM)—that is, chestcompressions—was first described systematically in the medical literature in 1960, CCCMhas remained the only reliable means of reviving a patient in cardiopulmonary collapse. Itis an effective and powerful intervention that, when unnecessarily delayed, may lead topoor patient outcomes. In one study, survival dropped from 34% to 14% if CCCM wasdelayed even as little as 60 to120 seconds from the time the patient collapsed. Therefore,clinicians must recognize and respond to cardiac arrest immediately for resuscitationmeasures to be effective.

Advanced cardiac life support combines basic life support (BLS) measures withspecific interventions, such as medication, defibrillation, transthoracic pacing, andadvanced airway management.

While often considered adequate for institution credentialing purposes, completion ofAmerican Heart Association (AHA) courses fails to result in long-term meaningful skillperformance. Health care providers’ capabilities to demonstrate appropriate technique forCCCM and capabilities to successfully navigate the steps of cardiopulmonaryresuscitation begin to degrade just weeks following course completion. Therefore, for thewhole medical team to respond concisely and in a coordinated fashion, clinicians musthave extensive medical knowledge, training, drilling practice, continued education, andfeedback.

Many providers are reluctant to initiate CCCM without complete assurance that thepatient is truly in cardiopulmonary arrest (confirmed by vital signs or electrocardiographicrhythm), often leading to unnecessary delays in initiation of potentially lifesavingtreatment. Furthermore, fundamental pulse assessment, even in nonemergency situations,cannot reliably and accurately predict the presence or absence of a pulse. One studytasked providers to determine whether or not patients had palpable pulses during electivecardiopulmonary bypass surgery. Ultimately providers took around 20 seconds to assessthe pulse and were less than 70% accurate.

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Time spent gathering cardiac monitoring, attaching leads, and setting up equipmentcan further delay promptly needed interventions to prevent death. In fact, clinicians mayneed to initiate CCCM prior to confirming cardiopulmonary arrest. Prompt initiation ofCCCM for any patient who appears to be in extremis (ie, unarousable or clinically unstablewith suspicion of cardiopulmonary arrest) should occur until confirmatory evaluation,often by a multispecialty resuscitation team, offers a high degree of confidence thatCCCM can be discontinued. Providers should share a culture of support that accentuatesthat the greater harm to patients is in failing to initiate CCCM in contrast to the potentialharms of CCCM (rib fracture, pneumothorax, organ perforation).

PRACTICE POINT

Providers should initiate closed chest cardiac massage to any patient who appears inextremis without awaiting 100% confirmation that the patient is in cardiopulmonaryarrest. Even delaying CCCM by as little as 30 seconds confers worse survivaloutcomes for patients in cardiopulmonary arrest.

PATHOPHYSIOLOGYCardiopulmonary arrest heralds death and may be an expected outcome in manyhospitalized patients. However, rarely is cardiopulmonary arrest the first manifestation ofphysiologic events that ultimately culminate in collapse: patients frequently havealteration in mental status or significant vital sign changes (pyrexia, hypotension,bradycardia, decrease in oxygen saturation, change in respiratory rate), often hours beforedeveloping cardiac arrest. Intervention during this prearrest period may prevent cardiacarrest altogether. Alternatively, health care personnel may identify patients who are at theend of life and may thus benefit from a meaningful discussion about limiting resuscitativemeasures, including offering “Do Not Resuscitate” or “Allow Natural Death” orders. Manypatients are not well informed about the resuscitative process and may have inflatedimages of routine successful resuscitation shaped from popular culture embodied bytelevision and film. Clinicians often perform cardiopulmonary resuscitation on patientswithout informed consent—a discussion of the relevant risks, benefits, and alternatives totherapy along with the clinicians’ recommendations. Thus the prearrest period may offeran unparalleled opportunity to give patients an active role in deciding whetherresuscitation is desired (see Chapter 215 [Communication Skills for End of Life Care]).

While no one specific condition results in cardiopulmonary collapse, many health-care-associated interventions predispose patients to arrest and often require minimalintervention early on to alter the course of catastrophe (Table 137-1). Intervention duringimpending cardiac arrest requires a detailed history of recent interventions ranging frominvasive procedures to recent sedation or anesthesia.

TABLE 137-1 Interventions to Specific Conditions that may Prevent Evolution toCardiopulmonary Arrest in Hospitalized Patients

Cause InterventionHypoxia due to medication or anesthesia Supportive oxygen, reversal agents

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(naloxone for opiates, flumazenil forbenzodiazepines)

Acidemia due to hypercapnic respiratoryfailure from medication or obstructive sleepapnea

Ventilation support (noninvasive ormechanical ventilation)

Pulmonary embolism Appropriate VTE prophylaxis(pharmacologic unless significantcontraindication); high index of suspicionand timely treatment

Cardiac arrhythmia due to acute coronarysyndrome

Appropriate early intervention includingantiplatelet therapy, beta-blockers,anticoagulation and early percutaneouscoronary intervention (PCI)

Hyperkalemia Calcium, sodium bicarbonate, insulin withdextrose, consideration of earlyhemodialysis; check for acid-basederangements

Hypokalemia Correction of magnesium (first) followed bypotassium; check for acid-basederangements

QT prolongation Attention to medications known to prolongthe QT interval (such as fluoroquinolones)and consideration of cardiac monitoring

Hypotension from severe sepsis Early massive volume resuscitation withconsideration of inotropes

Anticipated end-of-life care Discussion of appropriate “Do NotResuscitate” or “Allow Natural Death” ordersand palliative care in appropriate patients

Responses to inpatient emergencies require multiple individuals who take on specificroles and integrate as a team. For care to function effectively and seamlessly duringhealth care emergencies, each clinician must assume a narrowly focused essentialfunction or task (such as assessing a patient’s airway, recording data in a flowsheet, orensuring chest compressions are adequate) and perform the task with high quality tofacilitate the best possible patient outcome engendered by the team as a whole.

RAPID RESPONSE TEAMS AND THE PREARREST PERIODRecognizing that early intervention in impending cardiopulmonary arrest may prevent thearrest altogether, many hospitals have implemented rapid response teams (RRTs),consisting of any combination of critical care nurses, respiratory therapists, pharmacists,and/or physicians to attend to patients who exhibit one or more parameters of clinicalinstability but are not yet in extremis. Rapid response teams facilitate earliercommunication with and transfer of care to intensive care units under the care of critical

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care teams and (when available) intensivists, which appear to reduce mortality in somecenters, and need for crisis activation of cardiopulmonary arrest teams (ie, code teams).Additionally, RRTs have seen a marked expansion and elaboration in many disease states,such as improved identification of patients with sepsis and rapid implementation of earlygoal-directed therapy in patients with sepsis; and stroke teams in patients withneurological crises. Consistently, RRTs prompt discussion with patients and families aboutadvanced directives (do not resuscitate orders or limitations of care), and reduceescalation of care in patients who do not desire such aggressive interventions and whenthe medical condition is expected to be immediately terminal.

PRACTICE POINT

Rapid response teams facilitate earlier discussion of patient advanced directives andimprove communication between critical care team members, and more recentevidence reveals reduced mortality and reduced need for crisis activation ofcardiopulmonary arrest teams in many institutions with RRTs.

Hospitalists must foster a culture of safety where any provider (or patient or familymember) may initiate an RRT for any reason without fear of reprisal or judgment.Hospitalists should always thank other clinicians for calling RRTs and keeping thepatients’ safety of the utmost concern.

RESPIRATORY ARRESTRespiratory arrest from medications (anesthesia, benzodiazepines, or opiates) may lead tocardiac arrest through hypoxia and changes in the pH due to combined metabolic andrespiratory acidosis. Respiratory arrest is often masked for some time due to the ubiquityof oxygen administration in hospitalized patients, which may lead to a prolonged period ofhemoglobin oxygenation while ventilation may have already decreased or stopped.Overreliance on pulse oximetry as a sole source of interpreting ventilation effort may delayresponse to respiratory arrest until the patient is hypoxic and has developed profoundacidemia. Systemic hypoxia causes pulmonary artery constriction, right ventricular failure,and systemic hypotension from poor right heart output coupled with loss of vascular tonefrom hypoxia (circulatory shock).

CARDIAC ARREST

Cardiac arrest may occur from multiple distinct mechanisms. True cardiac arrest (cardiacstandstill) occurs either as a primary mechanism (from arrhythmias like ventricularfibrillation that prevent normal cardiac function) or as a secondary mechanism (fromasystole or from an extended period of failed resuscitation and cardiac myocyte death).Most cardiopulmonary arrest episodes do not occur due to true cardiac standstill butrather from marked impairment in cardiac output resulting in systemic arterialhypotension, tissue hypoxia, and organ failure. Precardiac, intracardiac, or postcardiacmechanisms may independently or in combination result in cardiopulmonary arrest (Table137-2).

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TABLE 137-2 Cardiac Arrest Etiology by Anatomic Location

Precardiac Intracardiac/intrapulmonary PostcardiacHypovolemiaShock (septic, distributive)Pericardial TamponadePneumothoraxHypoxia

Pulmonary embolismMyocardial infarctionShock (cardiac)Cardiac arrhythmia(ventricular or atrial)Left ventricular ruptureHypertrophic cardiomyopathy

Aortic dissectionHemorrhagePostcardiac

SUBTYPES OF CARDIAC ARREST

Once appropriate resuscitation equipment has arrived, clinicians should immediatelybegin to differentiate whether the cardiac arrest is due to a “shockable” or “nonshockable”cardiac rhythm.

Shockable rhythms

Transthoracic electrical shocks can terminate some pathological cardiac rhythms thatinhibit normal cardiac function. These can include ventricular fibrillation, ventriculartachycardia, AV nodal reentrant tachycardia, atrial fibrillation, and atrial flutter. Whileventricular fibrillation has a very characteristic pattern, the other rhythms may be difficultto differentiate during an emergency and in the absence of 12-lead electrocardiography. Inthe setting of an unconscious patient in severe distress, who is obtunded or clinicallyseverely unstable, all of these rhythms are considered pathologic and warrant immediateelectrical shock.

Despite recommendations by the International Liaison Committee of Resuscitation(ILCOR) (the subsection of the American Heart Association responsible for publication ofthe ACLS guidelines) that differentiation of the exact cardiac arrhythmia may dictate verydifferent types of cardiac intervention, ranging from dose (in joules) of electrical therapy tomedication selection, confirming an exact rhythm diagnosis may not be practical. Thus, itis reasonable to treat all of these rhythms similarly in a cardiopulmonary arrest in theevent of clinical uncertainty. Fundamentally similar to administration of CCCM, delays inelectrical therapy may significantly negatively impact patient outcomes with even minimaldelays. If a patient is not critically ill, then time allows for conscientious assessment ofcardiac rhythm via 12-lead electrocardiogram (ECG) with appropriately targeted therapiesfor the underlying arrhythmia. (see Chapter 132 [Supraventricular Tachyarrhythmias] andChapter 124 [Ventricular Arrythmias]).

PRACTICE POINT

Precise differentiation between ventricular fibrillation, ventricular tachycardia, AV nodalreentrant tachycardia, atrial fibrillation, and atrial flutter may not be practical when apatient is in severe distress, obtunded, or clinically severely unstable. Thus in the event

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of clinical uncertainty it is reasonable to treat all of these rhythms similarly during acardiopulmonary arrest.

Ventricular fibrillation results from disorganized myocardial electrical activity, and theheart is unable to generate a contraction to produce cardiac output. Hospitalists should beable to identify ventricular fibrillation confidently on rhythm strip (Figure 137-1).

Figure 137-1 Rhythm strip of a patient with ventricular fibrillation.

The characteristic physiologic phases of ventricular fibrillation arrest underscore theimportance of rapid electrical therapy. During the first few minutes of ventricularfibrillation (reflecting the combination of the “acute” and “electrical” phases of arrest,lasting up to 5-6 minutes), the myocardium is highly responsive to counter shock. Thisexplains in part why successful defibrillation is so common on commercial airlines and incasinos where employees are trained to rapidly attach and initiate automated externaldefibrillators (AEDs). The acute and electrical phases can be extended when CCCM isinitiated promptly, thus underscoring how critical CCCM is as an immediate therapy whiledefinitive defibrillation equipment is located, attached, and initiated.

In the absence of CCCM, patients will degenerate into the “circulatory” phase whereelectrical therapies are less effective due to progressive tissue hypoxia and myocytedeath. During this phase, CCCM may need to be performed for several minutes antecedentto successful defibrillation. However, during the initial moments of a pulseless arrest,immediate rhythm identification and defibrillation of shockable rhythm takes precedenceover CCCM.

Unchecked, patients will eventually enter the “metabolic” phase of ventricularfibrillation starting around the tenth minute of cardiac arrest. In the absence of effectiveCCCM, irreversible brain damage occurs. While there remains a slim hope of successfulcardiac resuscitation at this point, survival to hospital discharge rapidly becomesimprobable.

Ventricular tachycardia resulting in cardiopulmonary arrest fundamentally is identicalto ventricular fibrillation in treatment: CCCM and early electrical shock are indicated.

Perhaps the most overwhelming change to resuscitation in recent years is theacknowledgment of severe ventricular stunning following electrical shock. For severalminutes following defibrillation—and extending for a variable duration thereafter—theheart is mechanically dysfunctional and unable to generate an adequate cardiac outputfor organ perfusion or brain function. Consequently, it is absolutely critical to reinitiateCCCM for 1 to 2 minutes after defibrillation whether or not the shock is successful ataborting the ventricular arrhythmia.

PRACTICE POINT

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Even when defibrillation is successful, patients require at least 1 to 2 minutes of CCCMimmediately following the shock due to stunning of the left ventricle. Resumption of asinus rhythm does not equate to resumption of normal mechanical heart function.

Nonshockable rhythms

Nonshockable unstable or pulseless rhythms (characterized by bradycardia, asystole, andpulseless electrical activity [PEA]) constitute the majority of inpatient cardiac arrests.Deterioration in clinical status signified by deviations in mental status or marked changesin vital signs often foreshadows these types of cardiopulmonary arrests, and they may bepreventable.

Bradycardia may be due to a primary arrhythmia (such as sick sinus syndrome orarterioventricular [AV] block), or may be due to a secondary cause such as medications(particular AV nodal blocking agents) or excessive vagal tone (due pain or nausea).Bradycardia severe enough to cause hemodynamic instability warrants immediatecorrection and treatment of the underlying cause. Atropine is a vagolytic that can potentlyreverse excessive vagally mediated bradycardia. However, with unpredictable effects anda narrow therapeutic window (too high or too low a dose of atropine can potentiallyparadoxically worsen bradycardia), its use is confined to select patients and only for short-term use. Chronotropic agents such as dopamine can be administered if time allows setupof an intravenous drip.

Bradycardia may respond to transcutaneous pacing, but this must be instituted rapidly.In conscious bradycardic patients transcutaneous pacing may prove to be exceptionallyuncomfortable but should be used to bridge to transvenous pacing. Patients may requireanalgesia or sedation during transcutaneous pacing while awake.

Asystole as a primary cause of cardiac arrest is uncommon. Asystole typically is theend result of another pathophysiologic process, such as sustained hypoxia or coronarythrombosis. As such, asystole is a fairly late finding. Fine ventricular fibrillation mayappear electrocardiographically similar to asystole. Clinicians should always confirmsuspected asystole by checking multiple defibrillator leads and increasing the electricalgain. Doing such should clarify if the rhythm is actually asystole (vs masked fineventricular fibrillation).Whereas defibrillation is likely to benefit a patient in ventricularfibrillation (and is necessary to terminate the rhythm), shocking a patient in asystole mayresult in depleting the heart of any remaining adenosine triphosphate (ATP) and with itany chance of successful resuscitation. In general, if clinicians are not certain whetherasystole or ventricular fibrillation is the underlying rhythm, defibrillation is favored due tothe overwhelming benefit patients with ventricular fibrillation receive from defibrillationcompared to the minimal excess risk posed to those already in asystole.

Pulseless electrical activity represents a complex spectrum of disorders where patientsappear to have an electrocardiographic rhythm that would be anticipated sufficient togenerate a cardiac output, but clinical examination reveals no evidence of a palpablepulse. By definition, PEA is not a rhythm derangement, and therefore will not respond toany form of electrical shock. Pulseless electrical activity is a problem with either too littlecardiac preload (vasodilation, pulmonary embolism, or profound volume depletion),ineffective cardiac output (due to cardiac failure or stunning), or extrinsic compression ofthe heart muscle (tension pneumothorax, severe airway obstruction, or pericardial

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tamponade). While seeking a cause, clinicians must pursue concomitant treatment withCCCM in spite of the apparently normal-appearing cardiac rhythm. Clinicians should useepinephrine and intravenous fluids along with the goal to furnish targeted treatment of theapparent cause of PEA (intubation for hypoxia or respiratory distress, needledecompression or chest tube insertion for tension pneumothorax, pericardiocentesis fortamponade, intravenous calcium for hyperkalemia, etc).

MANAGEMENTWhile the approach to cardiac arrest has changed considerably over the past 5 decades,survival has improved little since initial reports on CCCM in 1960. ILCOR has publishedbasic and advanced cardiac life support guidelines every 5 years, becoming the de factostandard of care in the United States and internationally. Despite their evidence base,criticism exists that many find the guidelines to be too complex and difficult to remembereven just weeks following life support course completion. Also discordantly, the singlemost effective stratagem in resuscitation—effective chest compressions—frequently is nottaught well or performed well during or following courses, with a time-dependent loss ofskill following course completion.

While many clinicians learned that resuscitation begins with the “A-B-Cs,” evidence nowsuggests that establishing an airway and initiating rescue breathing (accomplished inmost hospitals via bag-valve-mask [BVM] ventilations) are not nearly as important asCCCM during the early phases of most adult inpatient cardiac arrests (Figure 137-2).Guidelines therefore now recommend focusing on “C-A-Bs,” emphasizing that restoringcirculation with compressions and early defibrillation are of critical importance. Certainly,in primary respiratory arrest (such as from medications) and in children (in whomrespiratory arrest is much more common than cardiac arrest), management of airway andrespiration must occur rapidly (Figure 137-2).

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Figure 137-2 Flow diagram of assessment and treatment during cardiac or pulmonaryarrest.

CHEST COMPRESSIONS (CLOSED CHEST CARDIAC MASSAGE)

When an apparently unconscious patient cannot be aroused, clinicians should assumethat the patient might be in cardiopulmonary arrest and should institute chestcompressions without delay. The mantra for quality chest compressions is to push hard,pump fast, and allow good chest recoil.

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PRACTICE POINT

Good chest compression technique requires pushing hard, pumping fast, and allowingadequate chest recoil.

Push hard

Many providers are concerned with pushing down on the sternum too hard; however,evidence does not support the assertion that pushing too hard occurs. Currentrecommendations suggest a compression depth of at least 2 inches, but thatmeasurement is very difficult to extrapolate in clinical terms during resuscitation. The bestadvice is for rescuers to push as deeply as possible with arms locked and with therescuer’s shoulders directly over the patient’s sternum with the rescuer using his or herbody weight and waist flexion to deliver the compression.

Because most patients go into cardiopulmonary arrest in hospital beds, achievingproper positioning may be difficult, particularly when a patient is obese or the rescuer’sarm length is short; a stool or other lift may prove critical for proper hand positioning.Compressing the chest solely with the force of the rescuer’s arms may be highly kinetic inappearance but will offer virtually no benefit to the patient.

Compressions must be done on a hard surface, something a hospital mattress doesnot offer. As soon as possible, a backboard should be inserted behind the patient. Real-time feedback devices, such as accelerometers, may offer the best opportunity forensuring adequate compression depth; however, these devices have technologicallimitations. Frequently the devices interpret total patient motion as compression depthwhen in fact a substantial amount of the compression is expended compressing themattress and not the patient’s chest. Compression depth indirectly correlates with patientsurvival.

Pump fast

Since ideal chest compressions result in only one-third normal cardiac output, about 10%of normal cerebral blood flow, and <5% of normal cardiac blood flow, compression ratehas a substantial effect on tissue perfusion. Target compression rate of at least 100compressions per minute should be instituted, but interruptions in chest compressionsduring change of rescuers, intubation, or rhythm analysis all result in a markedly lowertotal number of compressions over time. Studies consistently show that compressions arealmost uniformly lower than 100 per minute, underscoring the need for practice,simulation, and feedback for all rescuers on a regular basis following completion of chestcompression training.

Good compressions require a high degree of physical ability, but frequent rescuerrotation must be balanced with the need for uninterrupted compressions. While automatedsolutions (such as mechanical compression devices) may eventually replace mostrescuer-performed compressions in inpatients, current devices are unwieldy or have failedto show noninferiority to manual chest compressions.

Some aspects of resuscitation are incompatible with ongoing chest compressions(such as rhythm analysis and, at times, intubation). In these situations, rescuers must limitthe duration of the interruption as return of spontaneous circulation and neurologically

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intact survival are directly tied to chest compression rate. Furthermore, current evidencesuggests it is essential to resume chest compressions immediately following adefibrillation attempt independent of the rhythm due to left ventricular stunningassociated with highly impaired cardiac output.

Lastly, the beneficial effects of chest compressions are lost within seconds ofdiscontinuation. Chest compressions’ benefits appear to be additive to one another overtime with subsequent compressions improving circulation and perfusion pressures; ifcompressions are widely spaced or stopped for any length of time, the benefits of theprevious compressions’ vascular effects are lost. Defibrillation success also depends onshort “hands off” intervals (time when no compressions occur) as the chances ofsuccessful defibrillation diminish within seconds. This latter finding suggests that there isvery little latitude for prolonged rhythm analysis during a cardiac arrest.

Good chest recoil

At the completion of a chest compression, rescuers must extend at the waist allowing thepatient’s chest to rise back to its rest position. The mechanisms by which compressionsexert their physiologic effect appear to be a combination of increased intrathoracicpressure leading to compression of the great vessels and direct pumping of the heartthrough reduction of the anterior-posterior diameter of the chest. The recoil phase iseffectively “diastole,” and incomplete recoil of the chest thus results in impaired bloodreturn to the great vessels and heart resulting in further impairment in circulation in analready desperate perfusion environment. If recoil is consistently poor, rescuers will beincapable of surmounting this critical phase of circulation with adequate or consistentdepth of compressions. Compression rate much more than 140 per minute will reduceeffective recoil and return of spontaneous circulation.

ELECTRICAL THERAPY

Defibrillation is used to depolarize all myocytes simultaneously in order to achieve auniform repolarization period whereby the sinoatrial node theoretically resumes thepacemaking role of the heart, thus restoring normal cardiac function. The standard dosefor defibrillation is 120 to 200 J for biphasic defibrillators (and 360 J for monophasicdefibrillators).

Caregivers will be unlikely to accurately determine the workings of a defibrillator in acrisis without copious practice beforehand. Automated external defibrillators areubiquitous even in nonhospital settings, but even their setup may prove to be puzzlingduring a crisis if providers have not practiced using them.

Most manual defibrillators have self-adhesive defibrillator pads that are applied to thesternum and back (or alternately to the sternum and left midaxillary line, about thelocation of the cardiac apex) to deliver shocks. The pads concomitantly offer a “quicklook” mode, displaying the patient’s cardiac rhythm independent of cardiac leads. Thismeans rescuers can simultaneously identify a patient’s cardiac rhythm while charging thepads, and then deliver a shock.

Automated external defibrillators utilize self-adhesive pads as well but require a periodof up to 20 seconds for computer rhythm analysis, during which time rescuers are notperforming CCCM. All hospitalized patients in cardiac arrest should have self-adhesivedefibrillator pads attached as these offer continuous monitoring and allow rescuers to

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deliver shocks or to pace the patient. Newer models also offer real-time feedback tocompression depth, recoil quality, and compression rate.

Most defibrillators in clinical use employ a biphasic waveform, in which polarityreverses during the shock. Biphasic devices appear to confer better neurologicaloutcomes. Defibrillators can deliver shocks that are synchronized to patients’ cardiacrhythms to prevent administration of a shock during the critical repolarization phaserepresented by the T-wave (resulting in the “R on T” phenomenon and concomitant risk forprecipitation refractory arrhythmias). Since ventricular fibrillation is a disorganized cardiacrhythm where no discrete T-waves exist, defibrillators set to “synchronization mode” maynot delineate a safe period to deliver a shock and therefore may not fire at all. Mostdefibrillators will not have synchronization enabled when turned on without a clinicianspecifically enabling it. Nevertheless, clinicians must have good familiarity with thelocation of the synchronization button along with all functions on their hospitals’defibrillators so that when a defibrillator fails to fire, clinicians know where and how todeactivate synchronization prior to another attempt at defibrillation.

Rescuers should attempt to defibrillate a patient as soon as the code cart arrives andthe defibrillator is fully set up and ready to deliver a shock. Compressions should continueunabated until the defibrillator is fully prepared, otherwise unnecessary hands-off intervalswill result in poorer patient outcomes. Early defibrillation is critical as soon as a shockablerhythm is diagnosed or suspected clinically since the window for successful defibrillationdecreases as patients progress from the electrical phase of ventricular fibrillation into thecirculatory and metabolic phases. Chest compressions extend this window for a limitedperiod of time, maintaining patients’ responses to defibrillation.

RESPIRATORY THERAPY

Positive pressure ventilation via BVM provides oxygenation and ventilation. The design ofthe BVM is such that a one-handed squeeze provides the appropriate tidal volume formost adults in cardiopulmonary collapse: roughly 750 mL. Often, however, rescuers willuse two hands to squeeze the bag, resulting in larger tidal volumes that may exceed 1000mL. Data suggest that rescuers often deliver BVM ventilations at rates well beyond therecommended 1 ventilation every 5 seconds, with at least one report where ventilation rateexceeded the chest compression rate.

PRACTICE POINT

The ideal technique for bag-valve-mask use involves three hands: two to properly sealthe mask over the patient’s mouth and nose while tilting the head back, and one hand(from a second rescuer) to squeeze the bag. The BVM is designed for a one-handedsqueeze, which provides the appropriate tidal volume (750 mL) for most adults incardiopulmonary collapse. Two-hand BVM squeeze may lead to hyperventilation andauto-positive end-expiratory pressure. The rate of BVM ventilations should be 1ventilation every 5 seconds.

Well-intentioned rescuers often believe that hyperventilation will result in improvedoxygenation, improved carbon dioxide levels, and improved acid-base balance, but in facthyperventilation sets off a cascade of pathophysiologic changes that culminate in very

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high intrathoracic pressures, decreased cerebral and coronary circulation, and decreasedsurvival. Since tissue perfusion (and by convention intact circulation) is a prerequisite tooxygenation, hyperventilating a patient without attending to proper chest compressionsfails to bolster tissue oxygen levels. While carbon dioxide levels rise rapidly in circulatorycollapse, carbon dioxide can only be off-gassed via ventilation if venous blood flow is ableto enter the thorax and thereby the lungs. The single most effective treatment for thecombined respiratory and metabolic acidosis uniform in cardiopulmonary arrest isresumption of physiologically normal circulation. Therefore, the proper route to achieverescuers’ intents is via high-quality chest compressions with supplemental oxygenadministered via BVM ventilations (if rescuers are competent in its use) or via passive“blow-by” oxygen administered from a nonrebreather mask (if rescuers’ skills are indoubt).

During cardiopulmonary arrest, the upper airway musculature may become lax,resulting in the tongue and jaw occluding the airway. Proper head positioning duringventilations will help decrease the risk of airway obstruction, but frequently othermeasures are required. Placement of either an oropharyngeal airway (in unconsciouspatients) or nasopharyngeal airway (in conscious patients) requires little training and mayhelp stabilize the upper airway sufficiently to provide effective BVM ventilations.Nevertheless, rescuers may need to obtain an advanced airway (via laryngeal mask,endotracheal tube, or tracheostomy) in order to properly ventilate the patient. Only medicalpersonnel with considerable training and experience in advanced airways should attemptto place an invasive a