Explain the value of invasive hemodynamic monitoring, including a discussion of whether an acute, chronic, or complex-care patient is a candidate

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CHAPTER 137 Inpatient 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 advanced directives?

INTRODUCTION

Cardiopulmonary resuscitation is a time-dependent, team-based effort to reverse physiologic events that may culminate in a patient’s imminent death. Biblical and ancient Egyptian 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 3300 years 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 to academic hospitals with a prevalence of approximately 65 people per 100,000 nationally.

In-hospital cardiac arrest encompasses a spectrum of disorders from insufficient cardiac output to generate appreciable cerebral perfusion such as arrhythmia or shock to complete cessation of cardiac activity. Vital sign anomalies may often herald impending inpatient cardiac arrest by minutes to hours, but many cardiac arrests occur suddenly and without warning. Acute pulmonary arrest (very common in pediatric populations, often due to airway obstruction; but much less common in adults) may precede IHCA and may occur from sedative or opiate analgesic overdose.

This chapter focuses on (1) the techniques that are essential to successful cardiopulmonary resuscitation especially with attention to good neurologic recovery (as defined by the cerebral performance category of zero or one), and (2) decision making based on patient resuscitation status.

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

Advanced cardiac life support combines basic life support (BLS) measures with specific interventions, such as medication, defibrillation, transthoracic pacing, and advanced airway management.

While often considered adequate for institution credentialing purposes, completion of American Heart Association (AHA) courses fails to result in long-term meaningful skill performance. Health care providers’ capabilities to demonstrate appropriate technique for CCCM and capabilities to successfully navigate the steps of cardiopulmonary resuscitation begin to degrade just weeks following course completion. Therefore, for the whole medical team to respond concisely and in a coordinated fashion, clinicians must have extensive medical knowledge, training, drilling practice, continued education, and feedback.

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

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

PRACTICE POINT

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

PATHOPHYSIOLOGY Cardiopulmonary arrest heralds death and may be an expected outcome in many hospitalized patients. However, rarely is cardiopulmonary arrest the first manifestation of physiologic events that ultimately culminate in collapse: patients frequently have alteration in mental status or significant vital sign changes (pyrexia, hypotension, bradycardia, decrease in oxygen saturation, change in respiratory rate), often hours before developing cardiac arrest. Intervention during this prearrest period may prevent cardiac arrest altogether. Alternatively, health care personnel may identify patients who are at the end of life and may thus benefit from a meaningful discussion about limiting resuscitative measures, including offering “Do Not Resuscitate” or “Allow Natural Death” orders. Many patients are not well informed about the resuscitative process and may have inflated images of routine successful resuscitation shaped from popular culture embodied by television and film. Clinicians often perform cardiopulmonary resuscitation on patients without informed consent—a discussion of the relevant risks, benefits, and alternatives to therapy along with the clinicians’ recommendations. Thus the prearrest period may offer an unparalleled opportunity to give patients an active role in deciding whether resuscitation 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 minimal intervention early on to alter the course of catastrophe (Table 137-1). Intervention during impending cardiac arrest requires a detailed history of recent interventions ranging from invasive procedures to recent sedation or anesthesia.

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

Cause Intervention Hypoxia due to medication or anesthesia Supportive oxygen, reversal agents

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(naloxone for opiates, flumazenil for benzodiazepines)

Acidemia due to hypercapnic respiratory failure from medication or obstructive sleep apnea

Ventilation support (noninvasive or mechanical ventilation)

Pulmonary embolism Appropriate VTE prophylaxis (pharmacologic unless significant contraindication); high index of suspicion and timely treatment

Cardiac arrhythmia due to acute coronary syndrome

Appropriate early intervention including antiplatelet therapy, beta-blockers, anticoagulation and early percutaneous coronary intervention (PCI)

Hyperkalemia Calcium, sodium bicarbonate, insulin with dextrose, consideration of early hemodialysis; check for acid-base derangements

Hypokalemia Correction of magnesium (first) followed by potassium; check for acid-base derangements

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

Hypotension from severe sepsis Early massive volume resuscitation with consideration of inotropes

Anticipated end-of-life care Discussion of appropriate “Do Not Resuscitate” or “Allow Natural Death” orders and palliative care in appropriate patients

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

RAPID RESPONSE TEAMS AND THE PREARREST PERIOD Recognizing that early intervention in impending cardiopulmonary arrest may prevent the arrest 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 clinical instability but are not yet in extremis. Rapid response teams facilitate earlier communication 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 some centers, 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 early goal-directed therapy in patients with sepsis; and stroke teams in patients with neurological crises. Consistently, RRTs prompt discussion with patients and families about advanced directives (do not resuscitate orders or limitations of care), and reduce escalation of care in patients who do not desire such aggressive interventions and when the medical condition is expected to be immediately terminal.

PRACTICE POINT

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

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

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

CARDIAC ARREST

Cardiac arrest may occur from multiple distinct mechanisms. True cardiac arrest (cardiac standstill) occurs either as a primary mechanism (from arrhythmias like ventricular fibrillation that prevent normal cardiac function) or as a secondary mechanism (from asystole or from an extended period of failed resuscitation and cardiac myocyte death). Most cardiopulmonary arrest episodes do not occur due to true cardiac standstill but rather from marked impairment in cardiac output resulting in systemic arterial hypotension, tissue hypoxia, and organ failure. Precardiac, intracardiac, or postcardiac mechanisms may independently or in combination result in cardiopulmonary arrest (Table 137-2).

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TABLE 137-2 Cardiac Arrest Etiology by Anatomic Location

Precardiac Intracardiac/intrapulmonary Postcardiac Hypovolemia Shock (septic, distributive) Pericardial Tamponade Pneumothorax Hypoxia

Pulmonary embolism Myocardial infarction Shock (cardiac) Cardiac arrhythmia (ventricular or atrial) Left ventricular rupture Hypertrophic cardiomyopathy

Aortic dissection Hemorrhage Postcardiac

SUBTYPES OF CARDIAC ARREST

Once appropriate resuscitation equipment has arrived, clinicians should immediately begin 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 that inhibit normal cardiac function. These can include ventricular fibrillation, ventricular tachycardia, AV nodal reentrant tachycardia, atrial fibrillation, and atrial flutter. While ventricular fibrillation has a very characteristic pattern, the other rhythms may be difficult to differentiate during an emergency and in the absence of 12-lead electrocardiography. In the setting of an unconscious patient in severe distress, who is obtunded or clinically severely unstable, all of these rhythms are considered pathologic and warrant immediate electrical shock.

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

PRACTICE POINT

Precise differentiation between ventricular fibrillation, ventricular tachycardia, AV nodal reentrant tachycardia, atrial fibrillation, and atrial flutter may not be practical when a patient 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 a cardiopulmonary arrest.

Ventricular fibrillation results from disorganized myocardial electrical activity, and the heart is unable to generate a contraction to produce cardiac output. Hospitalists should be able 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 the importance of rapid electrical therapy. During the first few minutes of ventricular fibrillation (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. This explains in part why successful defibrillation is so common on commercial airlines and in casinos where employees are trained to rapidly attach and initiate automated external defibrillators (AEDs). The acute and electrical phases can be extended when CCCM is initiated promptly, thus underscoring how critical CCCM is as an immediate therapy while definitive defibrillation equipment is located, attached, and initiated.

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

Unchecked, patients will eventually enter the “metabolic” phase of ventricular fibrillation starting around the tenth minute of cardiac arrest. In the absence of effective CCCM, irreversible brain damage occurs. While there remains a slim hope of successful cardiac resuscitation at this point, survival to hospital discharge rapidly becomes improbable.

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

Perhaps the most overwhelming change to resuscitation in recent years is the acknowledgment of severe ventricular stunning following electrical shock. For several minutes following defibrillation—and extending for a variable duration thereafter—the heart is mechanically dysfunctional and unable to generate an adequate cardiac output for organ perfusion or brain function. Consequently, it is absolutely critical to reinitiate CCCM for 1 to 2 minutes after defibrillation whether or not the shock is successful at aborting the ventricular arrhythmia.

PRACTICE POINT

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

Nonshockable rhythms

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

Bradycardia may be due to a primary arrhythmia (such as sick sinus syndrome or arterioventricular [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 immediate correction and treatment of the underlying cause. Atropine is a vagolytic that can potently reverse excessive vagally mediated bradycardia. However, with unpredictable effects and a narrow therapeutic window (too high or too low a dose of atropine can potentially paradoxically 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 setup of 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 exceptionally uncomfortable but should be used to bridge to transvenous pacing. Patients may require analgesia or sedation during transcutaneous pacing while awake.

Asystole as a primary cause of cardiac arrest is uncommon. Asystole typically is the end result of another pathophysiologic process, such as sustained hypoxia or coronary thrombosis. As such, asystole is a fairly late finding. Fine ventricular fibrillation may appear electrocardiographically similar to asystole. Clinicians should always confirm suspected asystole by checking multiple defibrillator leads and increasing the electrical gain. Doing such should clarify if the rhythm is actually asystole (vs masked fine ventricular fibrillation).Whereas defibrillation is likely to benefit a patient in ventricular fibrillation (and is necessary to terminate the rhythm), shocking a patient in asystole may result in depleting the heart of any remaining adenosine triphosphate (ATP) and with it any chance of successful resuscitation. In general, if clinicians are not certain whether asystole or ventricular fibrillation is the underlying rhythm, defibrillation is favored due to the overwhelming benefit patients with ventricular fibrillation receive from defibrillation compared to the minimal excess risk posed to those already in asystole.

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

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

MANAGEMENT While 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 published basic and advanced cardiac life support guidelines every 5 years, becoming the de facto standard 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 remember even just weeks following life support course completion. Also discordantly, the single most effective stratagem in resuscitation—effective chest compressions—frequently is not taught well or performed well during or following courses, with a time-dependent loss of skill following course completion.

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

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

CHEST COMPRESSIONS (CLOSED CHEST CARDIAC MASSAGE)

When an apparently unconscious patient cannot be aroused, clinicians should assume that the patient might be in cardiopulmonary arrest and should institute chest compressions 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 allowing adequate 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. Current recommendations suggest a compression depth of at least 2 inches, but that measurement is very difficult to extrapolate in clinical terms during resuscitation. The best advice is for rescuers to push as deeply as possible with arms locked and with the rescuer’s shoulders directly over the patient’s sternum with the rescuer using his or her body weight and waist flexion to deliver the compression.

Because most patients go into cardiopulmonary arrest in hospital beds, achieving proper positioning may be difficult, particularly when a patient is obese or the rescuer’s arm 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 in appearance but will offer virtually no benefit to the patient.

Compressions must be done on a hard surface, something a hospital mattress does not 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 for ensuring adequate compression depth; however, these devices have technological limitations. Frequently the devices interpret total patient motion as compression depth when in fact a substantial amount of the compression is expended compressing the mattress and not the patient’s chest. Compression depth indirectly correlates with patient survival.

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 rate has a substantial effect on tissue perfusion. Target compression rate of at least 100 compressions per minute should be instituted, but interruptions in chest compressions during change of rescuers, intubation, or rhythm analysis all result in a markedly lower total number of compressions over time. Studies consistently show that compressions are almost uniformly lower than 100 per minute, underscoring the need for practice, simulation, and feedback for all rescuers on a regular basis following completion of chest compression training.

Good compressions require a high degree of physical ability, but frequent rescuer rotation must be balanced with the need for uninterrupted compressions. While automated solutions (such as mechanical compression devices) may eventually replace most rescuer-performed compressions in inpatients, current devices are unwieldy or have failed to 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 limit the 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 evidence suggests it is essential to resume chest compressions immediately following a defibrillation attempt independent of the rhythm due to left ventricular stunning associated with highly impaired cardiac output.

Lastly, the beneficial effects of chest compressions are lost within seconds of discontinuation. Chest compressions’ benefits appear to be additive to one another over time with subsequent compressions improving circulation and perfusion pressures; if compressions are widely spaced or stopped for any length of time, the benefits of the previous compressions’ vascular effects are lost. Defibrillation success also depends on short “hands off” intervals (time when no compressions occur) as the chances of successful defibrillation diminish within seconds. This latter finding suggests that there is very 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 the patient’s chest to rise back to its rest position. The mechanisms by which compressions exert their physiologic effect appear to be a combination of increased intrathoracic pressure leading to compression of the great vessels and direct pumping of the heart through reduction of the anterior-posterior diameter of the chest. The recoil phase is effectively “diastole,” and incomplete recoil of the chest thus results in impaired blood return to the great vessels and heart resulting in further impairment in circulation in an already desperate perfusion environment. If recoil is consistently poor, rescuers will be incapable of surmounting this critical phase of circulation with adequate or consistent depth of compressions. Compression rate much more than 140 per minute will reduce effective recoil and return of spontaneous circulation.

ELECTRICAL THERAPY

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

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

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

Automated external defibrillators utilize self-adhesive pads as well but require a period of up to 20 sec

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