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ACLS Study Guide

SIXTH EDITION

Barbara Aehlert, MSEd, BSPA, RN

Table of Contents

Cover image

Title page

Copyright

Preface to the sixth edition

Acknowledgments

About the author

1. Chain of survival and high-quality cardiopulmonary resuscitation

References

2. Teams

References

3. Patient assessment and resuscitation therapies

References
4. The patient with respiratory compromise

Case study 4.1

Case study 4.1 Answers

References

5. Bradycardias

Case study 5.1

Case study 5.2

Case study 5.1 Answers

Case study 5.2 Answers

References

6. Tachycardias

Case study 6.1

Case study 6.2

Case study 6.1 Answers

Case study 6.2 Answers

References

7. Cardiac arrest rhythms

Case study 7.1

 Case study 7.2

Case study 7.1 Answers

Case study 7.2 Answers

References

8. Acute coronary syndromes

Matching

Case study 8.1

Matching

Case study 8.1 Answers

References

9. Acute ischemic stroke

Case study 9.1

Case study 9.1 Answers

References

10. Posttest

Posttest Answers

Glossary
Index
Copyright
Elsevier
3251 Riverport Lane
St. Louis, Missouri 63043

ACLS STUDY GUIDE, SIXTH EDITION ISBN:

978-0-323-71191-3

Copyright © 2022 by Elsevier, Inc. All rights reserved.

Previous editions copyrighted 2017, 2012, 2007, 2002.

No part of this publication may be reproduced or transmitted in any

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www.elsevier.com/permissions.

This book and the individual contributions contained in it are

protected under copyright by the Publisher (other than as may be
noted herein).

Notices
Knowledge and best practice in this field are constantly changing.
As new research and experience broaden our understanding,
changes in research methods, professional practices, or medical
treatment may become necessary. Practitioners and researchers
must always rely on their own experience and knowledge in
evaluating and using any information, methods, compounds or
experiments described herein. Because of rapid advances in the
medical sciences, in particular, independent verification of
diagnoses and drug dosages should be made. To the fullest extent
of the law, no responsibility is assumed by Elsevier, authors,
editors or contributors for any injury and/or damage to persons or
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or from any use or operation of any methods, products,
instructions, or ideas contained in the material herein.

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Senior Content Strategist: Sandra Clarke

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Publishing Services Manager: Deepthi Unni
Project Manager: Janish Ashwin Paul
Printed in India

Last digit is the print number: 9 8 7 6 5 4 3 2 1

Preface to the sixth edition
I took my first Advanced Cardiac Life Support (ACLS) class many
years ago. I was terrified (and lost) throughout the entire course.
Although I spent weeks studying before the course, the information I
read seemed to be written in a foreign language. I could find no
resources to “translate” the information into something useful to me.
The course consisted of very long lectures by instructors who read
slides and offered little useful insight. The most memorable part of
the course was the “Patient Management” station in which each
course participant was evaluated one-on-one by an instructor. (For
those of you who have been around awhile, you are probably having
flashbacks of those days). I will never forget that experience.
Despite the time spent studying, I was a mental wreck as soon as
the door closed behind me. The instructor proceeded to
methodically strip away any self-confidence I might have had in
treating a patient who had a cardiac-related emergency. I answered
the questions asked of me until I was presented with a patient who
had symptomatic bradycardia. Atropine had not worked
(transcutaneous pacing was not a readily available option that many
years ago), and the next drug that was recommended at that time
was isoproterenol. I knew that I could not recall whether
isoproterenol was given in mcg/min (correct) or mg/min. I took a
“50/50” guess and said mg/min. Because that was the wrong
decision, I was told I had failed the course and would need to
schedule myself to attend another two-day class.
Before driving home, I sat outside for a few minutes,
contemplating what had happened and what I could have done to
change the outcome. On that day, I promised myself that I would
become an ACLS instructor someday and find a way to teach the
information in a more user-friendly atmosphere. I also promised
myself that I would be a part of teaching courses useful for
practicing healthcare professionals and delivered in an environment
where the participants looked forward to the class—instead of
dreading it.
As the years passed, I did become an ACLS instructor, and I loved
it. After each course, participants would often write on their course
evaluations that a study guide would have helped them prepare for
class. Those suggestions resulted in writing a few pages of
information and ultimately became a book—this book.
The ACLS Study Guide is designed for paramedic, nursing, and
medical students; electrocardiogram monitor technicians; nurses;
and other allied health personnel working in emergency
departments, critical care units, postanesthesia care units, operating
rooms, and telemetry units preparing for an ACLS course. This
edition is based on current science, treatment recommendations, and
guidelines cited in the reference section of relevant chapters.
Medicine is a dynamic field, and resuscitation guidelines change,
new medications and technology are being developed, and medical
research is ongoing. As a result, be sure to learn and follow local
protocols as defined by your medical advisors. The author and
publisher assume no responsibility or liability for loss or damage
resulting from using the information contained within.
I genuinely hope you find the information in the pages that follow
helpful and wish you success in your ACLS course and clinical
practice.

Sincerely,
Barbara Aehlert
Acknowledgments
My sincerest thanks to Danielle Frazier for her development of this
text and a special thanks to all instructors who share the same
philosophy about teaching ACLS as I do.
About the author
Barbara Aehlert, MSEd, BSPA, RN, has been a registered nurse for
more than 40 years with clinical experience in medical/surgical
nursing, critical care nursing, prehospital education, and nursing
education. Barbara is an active CPR and ACLS instructor who enjoys
teaching dysrhythmia recognition and ACLS to nurses and
paramedics.
List of Tables
TABLE 1.1 Phases of Cardiac Arrest and Resuscitation
TABLE 2.1 Essential Resuscitation Team Roles and Responsibilities
TABLE 3.1 Primary Assessment
TABLE 3.2 Signs of Adequate and Inadequate Breathing
TABLE 3.3 Manual Airway Maneuvers
TABLE 3.4 Pharyngeal Airways
TABLE 3.5 Mouth-to-Mask Ventilation
TABLE 3.6 Oxygen Percentage Delivery by Device
TABLE 3.7 Leads and Heart Surfaces Viewed
TABLE 3.8 Electrocardiogram Components—Waveforms and
Complexes
TABLE 3.9 Electrocardiogram Components—Segments and Intervals
TABLE 3.10 Common Medications Used in Cardiovascular
Emergencies
TABLE 7.1 Adult Nontraumatic Out-of-Hospital Cardiac Arrest
Survival Rates (2017 data)a
TABLE 7.2 The Hs and Ts: Possible Reversible Causes of Cardiac
Arrest
TABLE 7.3 Components of Postcardiac Arrest Syndrome
TABLE 8.1 Possible Causes of Elevated Cardiac Troponin Values
Because of Myocardial Injury
TABLE 8.2 Diagnostic Criteria for Type 1 and Type 2 Myocardial
Infarction
TABLE 8.3 Relationships Among Ventricular Surfaces, Facing Leads,
and Coronary Arteries
TABLE 8.4 Nitroglycerin
TABLE 8.5 Morphine Sulfate
TABLE 8.6 Beta Blockers
TABLE 8.7 Calcium Channel Blockers
TABLE 8.8 Lipid Management
TABLE 8.9 Renin-Angiotensin-Aldosterone System Inhibitors
TABLE 8.10 Antiplatelet Medications
TABLE 8.11 Aspirin
TABLE 8.12 Anticoagulants
TABLE 9.1 Cerebral Vessels and Neurologic Deficits
TABLE 9.2 The 8 Ds of Stroke Care
TABLE 9.3 Immediate Diagnostic Studies for Suspected Stroke
List of Illustrations
Fig. 1.1 Heart disease is the leading cause of death for men and
women in the United States.
Fig. 1.2 A drone carrying an automated external defibrillator can
reduce the interval from patient collapse to defibrillation time.
Fig. 1.3 Waveform capnography during cardiac arrest. (A) End-tidal
carbon dioxide partial pressure (PETCO2) diagram showing a typical
ventilation cycle and CO2 waveform. The point that represents
PETCO2 is marked with an arrow. (B) PETCO2 recording during
cardiopulmonary resuscitation. This image demonstrates the use of
capnography during ongoing resuscitation. The chest compression
waveform is shown in red (top panel), and the PETCO2 waveform is
shown in blue (bottom panel). EtCO2, End-tidal CO2.
Fig. 1.4 Several defibrillators, such as the MRx-QCPR shown here,
are equipped with a chest compression pad that enables monitoring
of the quality of chest compressions and provides corrective
feedback to rescuers.
Fig. 1.5 This Zoll R Series Monitor defibrillator filters
cardiopulmonary resuscitation artifact, enabling the rescuer to
analyze a patient’s cardiac rhythm without interrupting chest
compressions.
Fig. 2.1 Rapid Response Systems can be useful in reducing the
incidence of cardiac arrest.
Fig. 2.2 Key elements of effective team performance include verbal
and nonverbal communication, situation awareness, decision
making, task management, and teamwork. The components are
intertwined with and related to each other, indicated by the arrows
between the elements.
Fig. 2.3 Each member of the team has an opportunity to engage in
honest dialogue during a debriefing.
Fig. 2.4 When conveying bad news, allow time for the shock to be
absorbed and as much time as necessary for questions and
discussion.
Fig. 2.5 Know how to recognize the warning signs of stress in
yourself and know how to deal with them.
Fig. 3.1 Colorimetric exhaled carbon dioxide detector.
Fig. 3.2 Using the head tilt–chin lift maneuver to open the airway.
Fig. 3.3 The jaw thrust maneuver is used to open the airway when
cervical spine injury is suspected.
Fig. 3.4 A rigid suction catheter is used to remove secretions from the
mouth and throat.
Fig. 3.5 A flexible suction catheter is used to remove secretions from
the lower airway.
Fig. 3.6 (A) Guedel airway. (B) Berman airway. (C) Oropharyngeal
airway in place.
Fig. 3.7 Select an oropharyngeal airway of appropriate size.
Fig. 3.8 An oropharyngeal airway that is too long may press the
epiglottis against the entrance of the larynx, which may result in a
complete airway obstruction.
Fig. 3.9 An oropharyngeal airway that is too short will not displace
the tongue, and it may advance out of the mouth.
Fig. 3.10 Open the patient’s mouth and insert the oropharyngeal
airway with the tip pointing toward the roof of the mouth.
Fig. 3.11 Nasopharyngeal airways.
Fig. 3.12 A nasopharyngeal airway of proper size extends from the
tip of the patient’s nose to the angle of the jaw or the earlobe.
Fig. 3.13 Nasopharyngeal airway insertion.
Fig. 3.14 Pocket mask.
Fig. 3.15 The E-C clamp technique for mouth-to-mask or bag-mask
ventilation.
Fig. 3.16 The thenar eminences of both hands of the rescuer hold the
face mask firmly in place.
Fig. 3.17 The rescuer’s fingers are positioned under the angle of the
patient’s mandible to perform a jaw lift.
p p j
Fig. 3.18 Bag-mask devices.
Fig. 3.19 Single-rescuer bag-mask ventilation using the E-C clamp.
Fig. 3.20 Low-flow nasal cannula.
Fig. 3.21 Simple face mask.
Fig. 3.22 (A) Partial rebreather mask. (B) Nonrebreather mask.
Fig. 3.23 Schematic drawing of the conducting system of the heart.
An impulse normally is generated in the sinoatrial node. It travels
through the atria to the atrioventricular node, down the bundle of
His and Purkinje fibers, and the ventricular myocardium. Recording
of the depolarizing and repolarizing currents in the heart with
electrodes on the surface of the body produces characteristic
waveforms.
Fig. 3.24 View of the standard limb leads and augmented leads.
Fig. 3.25 Chest (i.e., precordial) leads V1 through V6.
Fig. 3.26 Electrode locations for recording a right chest
electrocardiogram (ECG). Right chest leads are not part of a standard
12-lead ECG but are used when a right ventricular infarction is
suspected.
Fig. 3.27 Left posterior chest lead placement.
Fig. 3.28 Electrocardiogram strip showing the markings for
measuring amplitude and duration of waveforms, using a standard
recording speed of 25 mm/s.
Fig. 3.29 Components of the electrocardiogram recording.
Fig. 3.30 Apply adhesive pads to the patient’s bare chest per the
manufacturer’s instructions.
Fig. 3.31 Continue cardiopulmonary resuscitation (CPR) while the
defibrillator is readied for use.
Fig. 3.32 Attach the adhesive pads to the patient’s chest.
Fig. 3.33 Verify the presence of a shockable rhythm on the cardiac
monitor.
Fig. 3.34 Select an appropriate energy level using the manufacturer’s
recommended energy dose.
Fig. 3.35 Charge the defibrillator and clear everyone from the
patient.
Fig. 3.36 After ensuring that everyone is clear of the patient, press
the “Shock” control to defibrillate. Immediately resume CPR.
Fig. 3.37 Administer sedation if time and the patient’s condition
permit.
Fig. 3.38 Place adhesive pads in proper position on the patient’s bare
chest according to the defibrillator manufacturer’s instructions. Press
the “Sync” control on the defibrillator. Make sure the machine is
marking each QRS complex and that no artifact is present.
Fig. 3.39 Select the appropriate energy level on the defibrillator.
Fig. 3.40 Press the “Charge” button the defibrillator and recheck the
electrocardiogram rhythm.
Fig. 3.41 Call “Clear!” After confirming that the area is clear, depress
the “Shock” button until the energy is delivered.
Fig. 3.42 Reassess the rhythm and the patient.
Fig. 3.43 Apply adhesive pacing pads to the patient according to the
manufacturer’s recommendations.
Fig. 3.44 Turn the pacemaker on and set the pacing rate to the
desired number of ppm.
Fig. 3.45 After setting the rate, start the pacemaker and slowly
increase the current output until electrical capture is achieved.
Fig. 3.46 After achieving electrical capture, assess for mechanical
capture by palpating for a pulse.
Fig. 4.1 Respiratory complaints are common in patients of all ages.
Fig. 4.2 Depending on its cause, therapeutic interventions for
respiratory distress may include the administration of nebulized
medications.
Fig. 5.1 Sinus bradycardia with ST segment depression.
Fig. 5.2 Junctional escape rhythm with ST segment elevation.
Fig. 5.3 Ventricular escape rhythm.
Fig. 5.4 Sinus rhythm with a first-degree atrioventricular block, ST-
segment depression.
Fig. 5.5 Second-degree atrioventricular block type I.
Fig. 5.6 Second-degree atrioventricular block type II.
Fig. 5.7 A 2:1 atrioventricular block with narrow-QRS complexes.
Fig. 5.8 Third-degree atrioventricular block with ST segment
depression and inverted T waves.
 p
Fig. 5.9 Adult bradycardia with a pulse algorithm.
Fig. 5.10 Case Study 5.1, question 5.
Fig. 5.11 Case Study 5.2, question 4.
Fig. 5.12 Case Study 5.2, question 8.
Fig. 6.1 Sinus tachycardia.
Fig. 6.2 Basic mechanisms of supraventricular tachycardia. Typical
atrial flutter (Aflutter) is a reentrant circuit around the tricuspid
valve in the right atrium. Atrioventricular nodal reentrant
tachycardia (AVNRT) is reentry within the atrioventricular node
(AVN) and tissue around the node. Orthodromic AVNRT is a reentry
circuit that traverses down the AVN and up a bypass tract, leading to
a narrow QRS. In antidromic atrioventricular reentrant tachycardia
(AVRT), conduction is first down the bypass tract and then up the
AVN, leading to a wide QRS complex. Atrial tachycardia (AT) is an
ectopic focus of atrial activity at a faster rate than the sinoatrial node
(SN). Atrial fibrillation (AFib) is several simultaneous wavelets in the
atrium with variable conduction through the AVN. Multifocal atrial
tachycardia (MAT) involves at least three distinct ectopic atrial sites.
Fig. 6.3 Atrial tachycardia (AT) (a type of supraventricular
tachycardia) that ends spontaneously with the abrupt resumption of
sinus rhythm. AT that starts or ends suddenly is called paroxysmal
supraventricular tachycardia. The P′ waves of the tachycardia (rate:
about 150 beats/min) are superimposed on the preceding T waves.
Fig. 6.4 Atrioventricular nodal reentrant tachycardia.
Fig. 6.5 Normal and abnormal conduction pathways. (A) Conduction
during sinus rhythm in the normal heart spreads from the sinoatrial
(SA) node to the atrioventricular (AV) node and then down the
bundle branches. The jagged line indicates physiologic slowing of
conduction in the AV node. (B) With Wolff-Parkinson-White (WPW)
pattern, an abnormal accessory conduction pathway called a bypass
tract (BT) connects the atria and ventricles. With WPW, during sinus
rhythm, the electrical impulse is conducted quickly down the bypass
tract, preexciting the ventricles before the impulse arrives via the AV
node. Consequently, the PR interval is short and the QRS complex is
wide, with slurring at its onset (delta wave). (C) WPW predisposes
patients to develop an atrioventricular reentrant tachycardia (AVRT),
p p y
in which a premature atrial beat may spread down the normal
pathway to the ventricles, travel back up the bypass tract, and
recirculate down the AV node again. This reentrant loop can repeat
itself over and over, resulting in a tachycardia. Notice the normal
QRS complex and often negative P wave in lead II during this type
of tachycardia.
Fig. 6.6 This rhythm strip shows an example of intermittent
preexcitation. The first three beats show preexcitation. This is
followed by abrupt normalization of the QRS complex in the next
two beats. The preexcitation pattern returns for the final three beats.
Fig. 6.7 Nonsustained ventricular tachycardia.
Fig. 6.8 Monomorphic ventricular tachycardia.
Fig. 6.9 Multifocal atrial tachycardia. Note the rapidly occurring P
waves showing variable shapes and PR intervals. This fast, irregular
rhythm may be mistaken for atrial fibrillation. Arrows with numbers
(1–3) above show a segment with multiple consecutive different P
waves.
Fig. 6.10 Atrial flutter with ST-segment depression.
Fig. 6.11 Atrial fibrillation.
Fig. 6.12 Atrial fibrillation with a rapid ventricular response.
Fig. 6.13 When the QRS complexes of ventricular tachycardia (VT)
vary in shape and amplitude, the rhythm is termed polymorphic VT.
Fig. 6.14 Adult tachycardia with a pulse algorithm.
Fig. 6.15 Location of the carotid sinus.
Fig. 6.16 Passively raising the patient’s legs during the Valsalva
maneuver or carotid sinus massage is recommended and may
increase the probability of successful rhythm conversion.
Fig. 6.17 Case Study 6.1, question 3.
Fig. 6.18 Case Study 6.1, question 10.
Fig. 6.19 Case Study 6.2, question 3.
Fig. 6.20 Case Study 6.2, question 7.
Fig. 7.1 Monomorphic ventricular tachycardia.
Fig. 7.2 Ventricular tachydysrhythmias. (A) Rhythm strip showing
monomorphic ventricular tachycardia (VT). (B) Example of
polymorphic VT. (C) Example of ventricular fibrillation. All tracings
are from lead V1.
Fig. 7.3 Asystole.
Fig. 7.4 “P-wave” asystole.
Fig. 7.5 The rhythm shown is a sinus tachycardia; however, if no
pulse is associated with the rhythm, the clinical situation is termed
pulseless electrical activity.
Fig. 7.6 Out-of-hospital cardiac arrest.
Fig. 7.7 Adult cardiac arrest algorithm.
Fig. 7.8 Remember to clear everyone from the patient before the
delivery of each shock.
Fig. 7.9 Adult immediate postcardiac arrest care algorithm.
Fig. 8.1 Major coronary arteries and some of their branches.
Fig. 8.2 Possible locations of infarctions in the ventricular wall.
Fig. 8.3 These cross-sections of the left anterior descending coronary
artery show atherosclerosis with more pronounced luminal
narrowing at the left, the more proximal portion of this artery.
Atherosclerosis is generally worse at the origin of a coronary artery
and in the first few centimeters, where turbulent blood flow is
greater. This turbulent flow over many years promotes endothelial
injury that favors inflammation with insudation of lipids to promote
the formation of atheromas. With lifestyle modifications, this process
is reversible.
Fig. 8.4 Plaque disruption and myocardial infarction. (A) Plaque
disruption. The cap of the lipid-rich plaque has become torn, with
the formation of a thrombus, mostly inside the plaque. (B)
Myocardial infarction. This infarct is 6 days old. The center is yellow
and necrotic with a hemorrhagic red rim. The responsible arterial
occlusion is probably in the right coronary artery. The infarct is on
the posterior wall.
Fig. 8.5 Mechanisms of plaque disruption. Rupture of the fibrous cap
(upper left) causes two-thirds to three-fourths of fatal coronary
thrombosis. Superficial erosion (upper right) occurs in one-fifth to
one-fourth of all cases of fatal coronary thrombosis. Certain
populations, such as diabetic individuals and women, appear more
susceptible to superficial erosion as a mechanism of plaque
disruption and thrombosis. Erosion of a calcium nodule may also
cause plaque disruption and thrombosis (lower left). In addition, the
friable microvessels in the base of the atherosclerotic plaque may
rupture and cause intraplaque hemorrhage (lower right). The
consequent local generation of thrombin may stimulate smooth
muscle proliferation, migration, and collagen synthesis, promoting
fibrosis and plaque expansion on a subacute basis. Severe
intraplaque hemorrhage can also cause sudden lesion expansion by
a mass effect acutely.
Fig. 8.6 Model of microvascular angina in women. HTN,
Hypertension; PCOS, polycystic ovary syndrome.
Fig. 8.7 Progression of myocardial necrosis after coronary artery
occlusion. A transmural segment of myocardium that is dependent
on the occluded vessel for perfusion constitutes the area at risk
(outlined). Necrosis begins in the subendocardial region in the center
of the ischemic zone and, with time, expands to involve the entire
wall thickness. Note that a very narrow zone of myocardium
immediately beneath the endocardium is spared from necrosis
because it can be oxygenated by diffusion from the ventricle.
Fig. 8.8 Acute coronary syndrome (ACS). Symptomatic,
morphologic, electrocardiographic, and serologic findings in patients
with various kinds of ACS. Individuals with ACS usually complain
of chest pain. If the involved coronary artery is totally occluded by a
fresh thrombus (shown on the right), the patient’s electrocardiogram
(ECG) reveals ST-segment elevation, cardiac biomarkers
subsequently are elevated, and the patient is diagnosed with an ST-
segment elevation myocardial infarction (STEMI). In some cases,
initial ST elevation can lead to non–Q-wave myocardial infarction. If
the involved coronary artery is partially occluded by a fresh
thrombus (shown on the left), the patient’s ECG does not show ST-
segment elevation. If cardiac biomarkers are not elevated, the patient
is diagnosed with unstable angina (UA). If cardiac biomarkers
remain negative or are not elevated during hospitalization, the final
diagnosis remains unstable angina. If cardiac biomarkers are
elevated, the patient is diagnosed with a non–ST-segment elevation
 p g g
MI (NSTEMI). Most patients presenting with NSTEMI develop
NQMI, but a few may develop QwMI. Dx, Diagnosis; NQMI, non–Q-
wave myocardial infarction; QwMI, Q-wave myocardial infarction.
Fig. 8.9 Myocardial ischemia and myocardial infarction (MI) can
result from various coronary disease processes, including
vasospasm, increased myocardial demand in the setting of a fixed
coronary lesion, and erosion or rupture of vulnerable atherosclerotic
plaque leading to acute thrombus formation and subsequent
ischemia. All result in myocardial oxygen supply-demand mismatch
and can precipitate ischemic symptoms, and all processes, when
severe or prolonged, will lead to myocardial necrosis or infarction.
Nonthrombotically mediated events (bottom half, left side) typically
occur without ST-segment elevation (STE) on the electrocardiogram
(ECG) but can have elevated levels of cardiac biomarkers if the
ischemia is severe and prolonged, in which case they are classified as
having type 2 MI. The atherothrombotic lesion is the hallmark
pathobiologic event of an acute coronary syndrome (ACS). The
reduction in flow may be caused by a completely occlusive
thrombus (bottom half, right side) or by a subtotally occlusive
thrombus (bottom half, middle). Ischemic discomfort may occur
with or without STE on the ECG. Of patients with STE, Q-wave MI
ultimately develops in most, but not all, patients, depending on the
duration of ischemia and collateralization. Patients without STE have
either unstable angina or non–ST-segment elevation MI (NSTEMI), a
distinction that is ultimately made by the presence or absence of a
serum or plasma cardiac marker (e.g., cardiac troponin) detected in
the blood. Non–Q-wave MI eventually develops in most patients
with NSTEMI on the ECG; Q-wave MI may develop in a few. MI that
develops as the result of the atherothrombotic lesion of an ACS is
classified as type 1 MI.
Fig. 8.10 Total acute coronary occlusion leads to serial
electrocardiogram changes. The evolution is variable and may be
interrupted or altered by successful reperfusion. ST segment
elevation is an early and relatively specific indicator of the need for
acute reperfusion in patients with an acute coronary syndrome.
Fig. 8.11 Chest leads from a patient with acute anterior ST-segment
elevation myocardial infarction (STEMI). (A) In the earliest phase of
the infarction, tall, positive (hyperacute) T waves are seen in leads V2
to V5. (A) Several hours later, marked ST-segment elevations are
present in the same leads, and abnormal Q waves are seen in leads in
V1 and V2.
Fig. 8.12 Typical myocardial segments supplied by the right
coronary artery (RCA), left anterior descending artery (LAD), and
circumflex (Cx) coronary arteries. The coronary anatomy is shown
on the left with the corresponding wall segments in standard
echocardiographic views on the right. The arterial distribution varies
among patients. Some segments have variable coronary perfusion, as
indicated by the hatched regions.
Fig. 8.13 The surfaces of the heart and facing leads.
Fig. 8.14 Anterior wall infarction. Occlusion of the midportion of the
left anterior descending (LAD) artery results in an anterior
infarction. Proximal occlusion of the LAD may become an
anteroseptal infarction if the septal branch is involved or an
anterolateral infarction if the marginal branch is involved. If the
occlusion occurs proximal to both the septal and diagonal branches,
an extensive anterior infarction will result.
Fig. 8.15 Septal infarction.
Fig. 8.16 Anteroseptal infarction.
Fig. 8.17 Lateral wall infarction. Coronary artery anatomy shows (a)
blockage of the circumflex artery, (b) blockage of the proximal left
anterior descending artery, and (c) blockage of the diagonal artery.
Fig. 8.18 Lateral wall infarction. Lead I shows a small Q wave with
ST-segment elevation (STE). A larger Q wave with STE can be seen
in lead aVL. This patient had an anterior non–ST-elevation
myocardial infarction (NSTEMI) 4 days earlier with STE and T-wave
inversion in leads V2 through V6. A coronary arteriogram at that
time showed a blocked LAD artery distal to its first large septal
perforator. The STE evolved and the T waves in all of the chest leads
had become upright the day before this tracing was recorded. The
patient then had another episode of chest pain associated with the
appearance of signs of acute lateral infarction, as shown in this
tracing. A repeat coronary arteriogram showed a new blockage of
the obtuse marginal branch of the circumflex artery.
Fig. 8.19 Inferior wall infarction. Coronary anatomy shows a
dominant right coronary artery (RCA). A blockage at point “a”
results in an inferior infarction and right ventricular infarction. A
blockage at point “b” involves only the inferior wall, sparing the
right ventricle.
Fig. 8.20 Inferior wall infarction. Coronary anatomy shows a
dominant circumflex artery. A blockage at point “a” results in an
inferior infarction. A blockage at “b” may result in a lateral and
inferobasal infarction.
Fig. 8.21 ST elevation in leads II, III, and aVF suggest an inferior wall
injury pattern. Reciprocal ST depression is seen in leads I and aVL.
Fig. 8.22 Inferobasal (posterior) infarction. (A) Coronary anatomy
shows a dominant right coronary artery (RCA). Blockage of the RCA
commonly results in an inferior and inferobasal infarction. (B)
Coronary anatomy shows a dominant circumflex artery. Blockage of
a marginal branch is the cause of most isolated inferobasal
infarctions.
Fig. 8.23 Fifteen-lead electrocardiogram with inferior, lateral,
posterior, and right ventricular acute myocardial infarction (AMI).
The standard 12-lead ECG reveals the typical ST-segment elevation
(STE) in the inferior and lateral leads, as well as ST-segment
depression with prominent R wave in the right precordial leads.
Posterior AMI is indicated by both the right precordial ST-segment
depression with prominent R wave and the STE in posterior leads V8
and V9. Note that the degree of STE is less pronounced than that
seen in the inferior leads because of a relatively longer distance from
the posterior epicardium to surface leads. The right ventricular
infarction is noted in this case, using the simplified approach with
only RV4, which demonstrates STE of relatively small magnitude.
Fig. 8.24 Right ventricular infarction (RVI). At “a,” blockage of the
right coronary artery proximal to the right ventricular marginal
branch results in an inferior infarction and RVI. At “b,” blockage of
the right ventricular marginal branch results in an isolated RVI.
Fig. 8.25 The right-sided chest leads in a patient with acute inferior
ST-segment elevation myocardial infarction show ST segment
elevation in leads V4R and V5R, consistent with concomitant right
ventricular infarction.
Fig. 8.26 Acute coronary syndromes algorithm.
Fig. 8.27 Site of action of medications used in the treatment of acute
coronary syndromes. (A) Site of action of antiplatelet agents, such as
aspirin, thienopyridines, and glycoprotein IIb/IIIa inhibitors. (B)
Heparin bonds with antithrombin III and thrombin to create an
inactive complex. (C) Fibrinolytic agents convert plasminogen to
plasmin, an enzyme responsible for degradation of fibrin clots.
Fig. 8.28
Fig. 9.1 Circle of Willis.
Fig. 9.2 (A) Subarachnoid hemorrhage, intracerebral hemorrhage. (B)
Ischemic stroke.
Fig. 9.3 After an occlusive stroke, the penumbra is an interface
between a region of permanent tissue damage and an area that will
most likely survive. Rapid and appropriate treatment, with
reperfusion of the penumbra, may salvage this region and reduce the
neurologic deficits experienced by the patient.
Fig. 10.1
Fig. 10.2
Fig. 10.3
Fig. 10.4
Fig. 10.5
Fig. 10.6
Fig. 10.7
Chapter 1: Chain of survival and
high-quality cardiopulmonary
resuscitation

Learning objectives

After completing this chapter, you should be able to:

1. Define cardiovascular collapse, cardiac arrest, sudden

cardiac death, and sudden cardiac arrest.
2. Discuss the phases of a cardiac arrest.
3. Describe the links in the Chain of Survival.
4. Discuss the elements of high-quality CPR.
5. Consider common barriers to effective CPR and possible
actions that can be taken to overcome them.
6. Explore the use of continuous end-tidal carbon dioxide
(EtCO2) monitoring during resuscitation efforts.
7. Examine the use of feedback devices during CPR.

LEARNING PLAN
 • Whether you are preparing for your first ACLS course or
your 10th, schedule time to study and review before the
course. Studying in half-hour intervals with 10-minute
breaks allows a reasonable period for both learning and
relaxation.
• Read this chapter before class. Take the time to highlight
essential concepts as you read.
• Develop and use flashcards, flowcharts, and mnemonics
to help enhance your retention of the information
presented.
• Complete the chapter quiz and review the quiz answers
provided.

KEY TERMS
Automated external defibrillator (AED) A machine with a
sophisticated computer system that analyzes a patient’s heart
rhythm using an algorithm to distinguish shockable rhythms
from nonshockable rhythms and provide visual and auditory
instructions to the rescuer to deliver an electrical shock if a
shock is indicated.
Cardiopulmonary (cardiac) arrest The absence of cardiac
mechanical activity, which is confirmed by the absence of a
detectable pulse, unresponsiveness, and apnea or agonal,
gasping breathing.
Cardiovascular collapse A sudden loss of effective blood flow that is
caused by cardiac and/or peripheral vascular factors that may
 reverse spontaneously (e.g., syncope) or require interventions
(e.g., cardiac arrest).
Chain of Survival The essential elements of a system of care that are
necessary to link the victim of sudden cardiac arrest with
survival.
Sudden cardiac death (SCD) A natural death of cardiac cause that is
preceded by an abrupt loss of consciousness within 1 hour of the
onset of an acute change in cardiovascular status; sudden
cardiac arrest is a term commonly applied to such an event
when the patient survives.

Introduction
Heart disease is the leading cause of death for both men and women
in the United States (Benjamin et al., 2019) (Fig. 1.1). As a result, the
likelihood of encountering a patient who requires basic life support
(BLS) or advanced cardiac life support (ACLS) care is high. ACLS is
an orderly approach to providing advanced emergency care to a
patient who is experiencing a cardiac-related problem. This chapter
discusses the phases of cardiac arrest, the Chain of Survival, the
elements of high-quality cardiac pulmonary resuscitation (CPR),
common barriers to effective CPR, techniques and adjuncts to
improve the quality of CPR, and monitoring the patient’s response
and rescuer performance during CPR.
 FIG. 1.1 Heart disease is the leading cause of
death for men and women in the United
States. Source: (From istock.com.)

Phases of cardiac arrest

Cardiovascular collapse is a sudden loss of effective blood flow that
is caused by cardiac factors, peripheral vascular factors, or both, that
may reverse spontaneously (e.g., syncope) or require interventions
(e.g., cardiac arrest) (Myerburg & Goldberger, 2019).
Cardiopulmonary (cardiac) arrest is the absence of cardiac
mechanical activity, which is confirmed by the absence of a
detectable pulse, unresponsiveness, and apnea or agonal, gasping
breathing. Gasping is abnormal breathing, is common during the
first few minutes of primary cardiac arrest, and is a sign of adequate
blood flow to the brainstem (Ewy, 2012). Respiratory efforts can
persist for 1 minute or longer after the onset of a cardiac arrest
(Myerburg & Goldberger, 2019).
 It is estimated that one of every 7.5 people in the United States will
die of sudden cardiac death (SCD) (Benjamin et al., 2019). SCD is a
natural death of cardiac cause that is preceded by an abrupt loss of
consciousness within 1 hour of the onset of an acute change in
cardiovascular status (Myerburg & Goldberger, 2019). After the heart
stops, reestablishing circulation as quickly as possible is critical
because survival decreases by about 10% per minute (Institute of
Medicine et al., 2015). The phrase sudden cardiac arrest is used when
the patient survives such an event. Four phases of cardiac arrest
have been described, each with unique physiology and treatment
strategies (Kilbaugh et al., 2020; Topijan et al., 2013) (Table 1.1).
TABLE 1.1
Phases of Cardiac Arrest and Resuscitation

Phase Interval Focus of Care

Prearrest Period before Identify, anticipate, and
the arrest manage factors that may
result in cardiac arrest (e.g.,
use of rapid response
teams to recognize and
treat patients at risk of
deterioration)
No flow Untreated Prompt initiation of BLS upon
cardiac recognition of the arrest by
arrest a bystander or healthcare
professional
Low flow Onset of CPR Delivery of high-quality chest
compressions to optimize
myocardial and cerebral
perfusion; consider ECMO
for selected patients if
conventional CPR is not
promptly successful
Postresuscitation Return of Identify and treat the cause of
spontaneo the arrest, optimize cardiac
us output and cerebral blood
circulation flow, support end-organ
perfusion and function
BLS, Basic life support; CPR, cardiopulmonary resuscitation; ECMO,
extracorporeal membrane oxygenation.

Chain of Survival
The Chain of Survival represents the essential elements of a system
of care that are necessary to link the victim of sudden cardiac arrest
with survival. Links of the Chain depict the interrelated steps
needed in an adult cardiac arrest both outside and inside the
hospital setting. Two separate chains exist because there are
differences in these systems of care. Time is critical when dealing
with a victim of sudden cardiac arrest; a weak or missing link in
either Chain of Survival can reduce the likelihood of a positive
outcome.

Out-of-hospital Chain of Survival

The links in the out-of-hospital Chain of Survival for adults include
early recognition, emergency response activation, and prevention;
delivery of high-quality CPR; rapid defibrillation; effective advanced
life support (ALS); postcardiac arrest care; and recovery.

Early recognition, emergency response activation, and

prevention
The first link in the out-of-hospital Chain of Survival is recognition
of the event and activation of the emergency medical services system
(EMSS). When a cardiac emergency occurs, the patient (or a family
member or bystander) must identify their signs and symptoms,
recognize that they are related to a heart condition, and seek medical
assistance in the hope of preventing cardiac arrest. Because delays in
seeking assistance and delays in the arrival of assistance affect
patient outcomes, prevention measures include increasing public
awareness in recognizing the signs and symptoms of acute coronary
syndromes and cardiac arrest (Berg et al., 2020).
Emergency dispatchers, who are located at public service access
points, are the link between the call for help and the arrival of
medical assistance. Dispatchers are trained to recognize the caller’s
description of a potential heart attack or cardiac arrest and to
provide real-time CPR instructions over the phone if necessary while
quickly sending appropriately trained and equipped emergency
medical services (EMS) personnel to the scene. Dispatcher-assisted
CPR is also referred to as dispatcher-assisted bystander CPR (DA-
CPR), just-in-time instruction, and telecommunicator CPR (TCPR).
Research has shown that the availability of DA-CPR is associated
with a greater than fivefold increase in the likelihood of bystander
CPR (Panchal et al., 2019).
To minimize the risk for transmission of coronavirus disease 2019
(COVID-19), dispatchers should query callers to determine if the
patient has signs or symptoms (e.g., fever, cough, shortness of
breath) or risk factors for COVID-19 (e.g., known infection in the
victim or any recent contacts, including family members). When
determining the patient’s address, dispatchers should determine if
the address been identified as a known COVID-19 location. When
CPR is indicated, dispatchers should provide lay rescuers with
information about the risk of exposure to COVID-19 and instructions
for providing compression-only CPR (Edelson et al., 2020). If there is
a suspicion for COVID-19 infection, dispatchers should alert
responding EMS personnel to enable the use of appropriate personal
protective equipment (PPE).
Bystander CPR can markedly improve cardiac arrest survival
rates, neurologic outcomes, and the resulting quality of life (Institute
of Medicine et al., 2015). Strategies, such as placing automated
external defibrillators (AEDs) in public locations, have been used to
increase bystander response to cardiac arrests. Despite such efforts,
barriers to bystander response persist and can be divided into four
categories: (1) an inability to recognize an out-of-hospital cardiac
arrest (OHCA) followed by delayed activation of EMS, (2) a lack of
adequate CPR training, (3) concerns about possible harm when
delivering CPR and possible subsequent liability, and (4)
psychologic factors, rescuer confusion, and health concerns (Institute
of Medicine et al., 2015).

ACLS Pearl
Performing CPR, providing positive pressure ventilation, and
inserting an advanced airway are examples of aerosol-generating
procedures that can expose healthcare workers and lay rescuers to
pathogens that cause acute respiratory infections (Tran et al.,
2012). The fear of contracting an infectious respiratory disease is
often a factor in a bystander’s reluctance to provide CPR. This fear
is increased when a lay rescuer or healthcare worker does not
have access to adequate PPE, increasing their exposure risk. Before
performing CPR, all rescuers should wear appropriate PPE to
limit exposure to airborne and droplet particles (Edelson et al.,
2020).

Bystanders may have difficulty recognizing the signs of cardiac

arrest. For example, abnormal breathing, such as gasping, can
continue for several minutes after a cardiac arrest and may be
confused with difficulty breathing (or even interpreted by some as
adequate breathing), resulting in miscommunication with
dispatchers and delays in the start of CPR (Berdowski et al., 2009).
Research shows that agonal breathing is common and present in
about 40% to 60% of OHCA victims (Panchal et al., 2020). Oxygen
depletion that accompanies cardiac arrest can result in anoxic
seizures. Bystanders may confuse the resulting brief seizure-like
activity (i.e., shaking) with seizures, resulting in delays in cardiac
arrest recognition by bystanders and actions taken by dispatchers
(Clawson et al., 2008; Institute of Medicine et al., 2015).
In some areas, public safety agencies are using mobile apps with
increasing frequency to summon nearby volunteers to the scene of a
cardiac arrest in a public location to provide bystander CPR until the
arrival of EMS providers. In addition to providing the victim’s
location, some apps also provide the location of nearby AEDs.

Delivery of high-quality cardiopulmonary resuscitation

After recognizing that an emergency exists, assess the scene to
ensure that it is safe to enter. If dispatch information indicates that
the patient has a possible respiratory infection, be sure to don
appropriate PPE before entering the scene. If the scene is safe,
quickly assess the patient for life-threatening conditions and
determine the nature of the emergency.
 CPR is a part of BLS. BLS includes the recognition of signs of
cardiac arrest, heart attack, stroke, and choking; the relief of choking;
CPR; and defibrillation with an AED. Provide BLS until advanced
medical help arrives, and the providers assume responsibility for the
patient’s care. Emergency interventions may include the following:

• Patient positioning
• CPR for victims of cardiac arrest
• Defibrillation with an AED
• Rescue breathing for victims of respiratory arrest
• Recognition and relief of choking
• Early administration of naloxone for opioid-associated
respiratory arrest

Rapid defibrillation
When an individual experiences a cardiac arrest, the likelihood of
successful resuscitation is affected by the speed with which CPR and
defibrillation are performed. The goal for providing the first shock
for sudden cardiac arrest resulting from ventricular fibrillation (VF)
or pulseless ventricular tachycardia (pVT) is within 2 minutes of
collapse (Institute of Medicine et al., 2015).
The American Heart Association has promoted the development
of AED programs to improve survival from sudden cardiac arrest
since 1995. An AED is a machine with a sophisticated computer
system that analyzes the patient’s heart rhythm. The AED uses an
algorithm to distinguish shockable rhythms from nonshockable
rhythms. If the AED detects a shockable rhythm, it provides visual
and auditory instructions to the rescuer to deliver an electrical shock.
Defibrillation performed by citizens (such as flight attendants, casino
security officers, athletic or golf club employees, and ushers at
sporting events) at the scene is called public access defibrillation.
Defibrillation is discussed in more detail in Chapter 3.
The use of an “ambulance drone” is an innovative approach being
used to reduce the interval from patient collapse to defibrillation
time (Institute of Medicine et al., 2015). This strategy uses a drone
equipped with a camera, microphone, two-way speakers, AED, and
a built-in global positioning system (GPS) (Fig. 1.2). The drone can
deliver the AED within 4.6 square miles, using GPS coordinates, in
less than 1 minute. Once the drone is at the scene, a “remote”
operator can provide instructions to those at the scene with the help
of the drone’s cameras and speakers.

FIG. 1.2 A drone carrying an automated external

defibrillator can reduce the interval from patient
collapse to defibrillation time. Source: (From
istock.com.)

Effective advanced life support

Outside the hospital, early advanced care is provided by paramedics
(and/or nurses) arriving on the scene. Prehospital providers work
quickly to stabilize the patient by providing ventilation support,
vascular access, and giving emergency medications, among other
interventions.

Postcardiac arrest care

Prehospital providers transport the patient for definitive care.
Initiate contact with the receiving hospital as early as possible when
transporting a patient with known or suspected COVID-19.
Some studies suggest the postarrest patient should be transported
to the closest most appropriate emergency department (ED) for
initial stabilization with subsequent transfer to a higher acuity care
facility for further care. Other studies suggest that postarrest patients
should be triaged in the field and transported directly to specialized
centers that offer invasive coronary care to ensure the best possible
outcome (Geller & Abella, 2018; Institute of Medicine et al., 2015).
Terms used to identify these specialized centers include cardiac
arrest centers (CACs), cardiac arrest receiving centers,
comprehensive cardiac centers, and cardiac resuscitation centers.
Current guidelines consider the transport of resuscitated patients
directly to specialized CACs to be reasonable when comprehensive
postcardiac arrest care is not available at local facilities (Berg et al.,
2020).

ACLS Pearl
If return of spontaneous circulation (ROSC) has not been achieved
after appropriate resuscitation efforts in the field for a patient with
known or suspected COVID-19, experts advise considering not
transferring the patient to the hospital because of the low
likelihood of patient survival, balanced against the added risk of
additional exposure to EMS and hospital providers (Edelson et al.,
2020).

Several progressive EMS systems are collaborating with hospital

systems to deliver evidence-based bundles of care designed to
improve the ROSC and survival to hospital discharge. Components
of the bundles of care vary; examples include implementation of a
high-quality DA-CPR program, use of defibrillators equipped with
feedback functions, minimally interrupted chest compressions,
passive ventilation, delayed advanced airway insertion, or use of
mechanical CPR devices, among many other possibilities. A bundle
of care approach that has resulted in improved ROSC rates
implemented by Palm Beach County Fire Rescue in Florida includes
passive ventilation, delayed positive pressure ventilation, use of an
impedance threshold device, a focus on continuous chest
compressions with an early transition to CPR using a mechanical
chest compression device, and patient transport with the head and
thorax in an elevated position to allow a drop in intracranial
pressure and a potential improvement in cerebral perfusion
(Scheppke, 2019).

Recovery
Recovery has been added to the Chain of Survival to acknowledge
the importance of supporting survivors and their caregivers during
short- and long-term rehabilitation after a cardiac arrest.

In-hospital Chain of Survival

The links in the in-hospital Chain of Survival for adults include early
recognition and prevention of cardiac arrest, prompt notification and
response when a cardiac arrest occurs, the performance of high-
quality CPR, prompt defibrillation, intraarrest and postcardiac arrest
care, and recovery (Panchal et al., 2020).

ACLS Pearl
Studies show that survival after in-hospital cardiac arrest is lower
during nights and weekends compared with daytime during
weekdays (Ofoma et al., 2018).

Early recognition and prevention

A cardiac arrest experienced by a hospitalized adult is often
preceded by signs and symptoms that suggest physiologic
deterioration, such as abnormal vital signs (Andersen et al., 2016;
Douw et al., 2015; Lyons et al., 2018). The concept of a Rapid
Response System emerged after recognizing that early detection and
treatment of the patient who demonstrates signs of clinical
deterioration may prevent cardiac arrest and improve patient
outcomes. Chapter 2 discusses these systems in more detail.

Notification and response

Every member of the hospital staff should know how to recognize a
cardiac arrest and know how to summon assistance when such an
event occurs. Prompt notification and activation of the code team
may include pressing a “code button” at the patient’s bedside,
calling a specific phone extension, or use of a “quick-dial button”
located on telephones within the facility. The type of emergency and
its location are stated when the operator is reached. Once the
operator is notified of the emergency, members of the code team
typically are activated using cell phones, pagers, and/or a hospital-
wide public address system.

Performance of high-quality cardiopulmonary resuscitation

Although cardiac arrests and the performance of CPR are relatively
uncommon in in-hospital environments (Kronick et al., 2015),
hospital staff must be able to perform high-quality CPR immediately
upon recognition of a cardiac arrest. Because training may not be
adequate to ensure optimal performance, strategies such as timely
access to equipment, visual reminders, regular testing, and point-of-
care feedback have been suggested as methods to improve the
translation of resuscitation guidelines into practice during cardiac
arrest (Morrison et al., 2013).

Prompt defibrillation
It is estimated that about half of all in-hospital cardiac arrests
(IHCAs) occur outside the intensive care unit (ICU) (Morrison et al.,
2013). Because it can take several minutes for code team members to
arrive with a defibrillator, the strategic deployment of AEDs
throughout the facility can aid in achieving prompt defibrillation,
with the goal being the delivery of the first shock within 3 minutes of
patient collapse (Link et al., 2010).

Intraarrest and postcardiac arrest care

During the arrest, and under the direction of a team leader, the code
team works to stabilize the patient by continuing high-quality CPR,
performing defibrillation for pVT/VF, obtaining vascular access and
giving medications, performing advanced airway management
procedures when warranted, and providing ventilation support,
among other interventions.
If a ROSC is achieved, postcardiac arrest care, including advanced
monitoring and targeted temperature management, is provided by a
multidisciplinary team in an ICU. After a resuscitation effort, a
debriefing of the resuscitation team is recommended to discuss areas
such as psychomotor skill issues, cognitive issues, team issues,
family emotional issues, and professional staff emotional issues
(Kronick et al., 2015).

Recovery
The recovery link recognizes the importance of providing effective
support for the physical, cognitive, and emotional needs of cardiac
arrest survivors and their caregivers as the patient transitions from
hospital care to home and returns to their role and social function
(Berg et al., 2020; Panchal et al., 2020).

High-quality cardiopulmonary resuscitation

The terms high-quality CPR and high-performance CPR are often
used interchangeably. In its 2015 report, Strategies to Improve Cardiac
Arrest Survival: A Time to Act, the Institute of Medicine explained the
difference between these terms. “High-quality CPR is CPR that meets
performance standards along a number of fundamental measures
identified as clinically relevant in national and international
guidelines. High-performance CPR emphasizes the importance of
team-related factors (e.g., communication, collaboration, teamwork,
and leadership) in attaining high-quality CPR, as well as other
aspects of performance that affect patient outcomes. Although the
scientific literature is inconsistent in its use of these terms, the
committee believes this distinction is useful for highlighting the
different skillsets requisite to the performance of effective CPR.
Optimally, these two concepts will be employed in tandem by any
resuscitation team” (Institute of Medicine et al., 2015, pp. 208-209).

ACLS Pearl
Even when CPR is delivered following recommended
resuscitation guidelines, experts say that it provides only 10% to
30% of normal blood flow to the heart and 30% to 40% of normal
blood flow to the brain (Meaney et al., 2013).

After recognizing that CPR is indicated, the patient should be

positioned supine on a firm, flat surface when feasible, and chest
compressions should be started. If the patient cannot be placed in the
supine position, current guidelines note that it may be reasonable for
rescuers to provide CPR with the victim in the prone position,
particularly in hospitalized patients with an advanced airway in
place (Panchal et al., 2020).
High-quality CPR consists of several elements, which are shown in
Box 1.1. When chest compressions are stopped during cardiac arrest,
no blood flow is generated; this is referred to as no flow time. As a
result, cerebral and coronary perfusion pressures fall quickly and
dramatically, thereby reducing blood flow to the brain and heart.
Even after compressions are resumed, several chest compressions
are needed to restore coronary perfusion pressure. Research shows
that an increased chest compression fraction (CCF), which is the
proportion of time spent performing chest compressions during a
cardiac arrest, is predictive of improved survival. Although a 2013
consensus statement about CPR quality recommended a CCF of at
least 80% for optimal outcomes (Meaney et al., 2013), current
resuscitation guidelines note that in adult cardiac arrest, it may be
reasonable to perform CPR with a CCF of at least 60% (Panchal et al.,
2020). Interruptions during compression delivery resulting from
pauses during vascular access procedures, intubation, compression
provider switching, and pauses before the delivery of a shock can
significantly decrease CCF (Bhardwaj & Abella, 2015). In adult
patients in cardiac arrest with a shockable rhythm, research shows
that perishock pauses (i.e., pauses in chest compressions before and
after a defibrillatory shock) of 40 seconds or longer are associated
with decreased odds of survival as compared with pauses of 20
seconds or less in duration (Cheskes et al., 2011).

BOX 1.1

Elements of High-Quality
Cardiopulmonary Resuscitation

• Maximize the chest compression fraction (i.e., at least 60%) by

minimizing pauses in chest compressions (keep pauses to 10
seconds or less)
• Perform chest compressions at a rate of 100 to 120
compressions per minute
• Compress the adult chest at a depth of at least 2 inches (5 cm),
not to exceed 2.4 inches (6 cm)
• Avoid leaning on the chest between compressions to allow full
chest wall recoil
• To avoid fatigue, change chest compressors about every 2
minutes or earlier if warranted (change should take about 5
seconds)
• Avoid excessive ventilation

ACLS Pearl
Interruptions in chest compressions must be kept to a minimum to
maximize the amount of time that chest compressions generate
blood flow during a cardiac arrest. When pauses in CPR are
necessary (e.g., defibrillation, rotation of rescuers performing
chest compressions, placement of a backboard), keep them to less
than 10 seconds if possible. In some areas, when there is any pause
in CPR for a pulse check, the rescuer performing chest
compressions begins a 10-second countdown and resumes CPR
automatically unless it is announced that a pulse is detected
(Hopkins et al., 2016).

High-quality chest compressions require pushing hard and fast on

the victim’s chest, which means compressing the adult chest a depth
of at least 2 inches (5 cm), not to exceed 2.4 inches (6 cm) at a rate of
100 to 120 compressions per minute. During the compression
(systolic) phase of chest compression, the compressions must be of
sufficient depth to provide adequate stroke volume and cerebral
perfusion pressure (Benner et al., 2011). During the release (diastolic)
phase of chest compression, intrathoracic pressure is low, which
helps increase the return of venous blood into the chest. If
intrathoracic pressure is too high, venous return is inhibited.
During a cardiac arrest, be mindful of the rate and volume used
when ventilating the patient. Ventilating the patient too fast or with
too much volume is common during resuscitation efforts and results
in excessive intrathoracic pressure, which results in decreased
venous return into the chest, decreased coronary and cerebral
perfusion pressures, diminished cardiac output, and decreased rates
of survival (Meaney et al., 2013; O’Neill & Deakin, 2007).

ACLS Pearl
It is important to ventilate a patient in cardiac arrest with just
enough volume to see the patient’s chest rise gently.

Barriers to effective cardiopulmonary resuscitation

Several studies have shown that the quality of CPR during actual
resuscitation often falls short of established resuscitation guidelines
in both out-of-hospital and in-hospital settings. Research indicates
that compressions are often not continued for long-enough periods
during resuscitation attempts. Compressions administered are often
too slow, too fast, or too shallow and have excessively long pauses
around defibrillation attempts, and ventilations are too fast (Institute
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