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Explain the value of invasive hemodynamic monitoring, including a discussion of whether an acute, chronic, or complex-care patient is a candidate for this type of assessment. For a complex-care patient, propose an evidence-based treatment plan regarding the hemodynamic information. What are the risk factors to take into consideration for this patient?

Then, based on the first letter of your last name, discuss the following invasive hemodynamic pressures to which you are assigned.

If your last name starts with F through I, provide the normal values and discuss the differential diagnoses for the alteration in normal readings for systemic vascular resistance.

Support your summary and recommendations plan with a minimum of two APRN approved scholarly resources.

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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


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.

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

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).


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.

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

Acidemia due to hypercapnic respiratory
failure from medication or obstructive sleep

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

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

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

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.

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.


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 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 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

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TABLE 137-2 Cardiac Arrest Etiology by Anatomic Location

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

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

Aortic dissection


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]).


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

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.


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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

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).

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


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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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

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.


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

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 seconds for computer rhythm analysis, during which time rescuers are not
performing CCCM. All hospitalized patients in cardiac arrest should have self-adhesive
defibrillator 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 to
compression depth, recoil quality, and compression rate.

Most defibrillators in clinical use employ a biphasic waveform, in which polarity
reverses during the shock. Biphasic devices appear to confer better neurological
outcomes. Defibrillators can deliver shocks that are synchronized to patients’ cardiac
rhythms to prevent administration of a shock during the critical repolarization phase
represented by the T-wave (resulting in the “R on T” phenomenon and concomitant risk for
precipitation refractory arrhythmias). Since ventricular fibrillation is a disorganized cardiac
rhythm where no discrete T-waves exist, defibrillators set to “synchronization mode” may
not delineate a safe period to deliver a shock and therefore may not fire at all. Most
defibrillators will not have synchronization enabled when turned on without a clinician
specifically enabling it. Nevertheless, clinicians must have good familiarity with the
location 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 to
deactivate synchronization prior to another attempt at defibrillation.

Rescuers should attempt to defibrillate a patient as soon as the code cart arrives and
the defibrillator is fully set up and ready to deliver a shock. Compressions should continue
unabated until the defibrillator is fully prepared, otherwise unnecessary hands-off intervals
will result in poorer patient outcomes. Early defibrillation is critical as soon as a shockable
rhythm is diagnosed or suspected clinically since the window for successful defibrillation
decreases as patients progress from the electrical phase of ventricular fibrillation into the
circulatory and metabolic phases. Chest compressions extend this window for a limited
period of time, maintaining patients’ responses to defibrillation.


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


The ideal technique for bag-valve-mask use involves three hands: two to properly seal
the 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-handed
squeeze, which provides the appropriate tidal volume (750 mL) for most adults in
cardiopulmonary collapse. Two-hand BVM squeeze may lead to hyperventilation and
auto-positive end-expiratory pressure. The rate of BVM ventilations should be 1
ventilation every 5 seconds.

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

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high intrathoracic pressures, decreased cerebral and coronary circulation, and decreased
survival. Since tissue perfusion (and by convention intact circulation) is a prerequisite to
oxygenation, hyperventilating a patient without attending to proper chest compressions
fails to bolster tissue oxygen levels. While carbon dioxide levels rise rapidly in circulatory
collapse, carbon dioxide can only be off-gassed via ventilation if venous blood flow is able
to enter the thorax and thereby the lungs. The single most effective treatment for the
combined respiratory and metabolic acidosis uniform in cardiopulmonary arrest is
resumption of physiologically normal circulation. Therefore, the proper route to achieve
rescuers’ intents is via high-quality chest compressions with supplemental oxygen
administered 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 in

During cardiopulmonary arrest, the upper airway musculature may become lax,
resulting in the tongue and jaw occluding the airway. Proper head positioning during
ventilations will help decrease the risk of airway obstruction, but frequently other
measures are required. Placement of either an oropharyngeal airway (in unconscious
patients) or nasopharyngeal airway (in conscious patients) requires little training and may
help 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 medical
personnel with considerable training and experience in advanced airways should attempt
to place an invasive a


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