American

Heart
Association.
life is why-

ADVANCED CARDIOVASCULAR
LIFE SUPPORT

PROVIDER MANUAL

020'6 _ , , , . , HeM Assoa.11.,.,

PT\otad in me Lnted States of Arnenca: lnr99f'ICOIO<. lTD, 3210 l.....,.,atl\09 Way. Meoqune, Te•••. USA 7:;149
1$8"1 973-1-61669-500-2 lmemallOf\31 EOQlish llVE) ea.uoo 1~?805. PM! date J/16
Orvnal EngNh ecition
Acll<anced CM!ova..,._ lJle SlJl)pCXt "'°"oder,....,,..._.,
C 2016 Amer"""1 Heart AS&M>a!loo
 Acknowledgments
The Amencan Heart Association tllanks the following people
for thetr contnbutlons to tne devel()pfTlefll of this manual
Michael W. Donnino. MO: Kenneth Navarro. MEd. LP;
Kathenne Berg. MD; Steven C. ~s. MD. MHSc;
..kAte ender. PhD, Mary Fran Hazin6kl. RN MSN· Theresa
A. Hoadley, RN, PhD. TNS; Sa;J1e Johnoon. Ph.YmD, BCPS:
Venu "4enon. MD; Susan Monis, RN; Pe!J:lr D Panagos, MD:
MiCtiael Shuster MD; David Sla!t91)'. MD: and the AHA ACLS
Project Team.

=
. . . . To find out about any updates or corrections to this text. visit www.intemational.heart.org,
naV!gate to the page for this course, and click on " Updates.•

To access the Student Website for this course, go to www.heart.org/eccstudent and enter this code:
acls15

II
 -

Part 1
Introduction 1

Course Description and Goal

Course Objectives 1

Course Design 2
Course Prerequisites and Preparation 2
BLS Skills 3
ECG Rhythm Interpretation for Core ACLS Rhythms 3
Basic ACLS Drug and Pharmacology Knowledge 3
Course Materials 4
ACLS ProV1der Manual 4
Student Website 5
Pocket Reference Cards 7
?recourse Preparat100 Checklist 7

Requirements for Successful Course Completion 7

ACLS Provider M anual Abbreviations 8

Advanced Cardiovascular Life Support 10

Closing the Gaps 11

Quality Assessment, Review, and Translational Science 11
Part 2
Systems of Care 13
Introduction 13

Cardiopulmonary Resuscitation 13
Quality Improvement In Resuscitation Systems, Processes, and Outcomes 13
A Systems Approach 13
Measurement 16
Benchmarking and Feedback 17
Change 17
Summary 17
Acute Coronary Syndromes 17
Starts • on the Phone" With Activation of EMS 18
EMS Components 18
Hospital-Based Components 18
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 -

Contents

Acute Stroke 18
Regiooalozatton of Stroke Care 18
Community and Professional Education 18
EMS 18

Post-<:ardiac Arrest Care 19

Targeted Temperature Management 19
Hemodynamic and Ventilation Optimization 19
Immediate Coronary Reperlusion With PCt 20
Glycem1c Control 20
Neurotog1c Care and Prognostication 20

Educa tion, Implementation, and Teams 20

The Need for Teams 20
Cardiac Arrest Teams (In-Hosp ital) 20
Rapid Response System 21
Published Studies 22
lmplementaiion of a Rapid Response System 22
Part 3
Effective High-Pe rformance Team Dynamics 25
Introduction 25

Roles of the Leader and Members of a High-Perlonnance Team 25

Role of the Team Leader 25
Role o f the Team Member 26
Elements of Effective High·Perlormance Team Dynamics 26
Roles 26
What to Communicate 29
How to Communicate 31
Part 4
The Systematic Approach 33
Introduction 33

The Systematic Approach 33

Overview of the Systematic Approach 33

The BLS Assessment 34

Overview of the BLS Assessment 35
The Primary Assessment 38
Overview of the Pnmary Assessment 38
The Secondary Assessment 40
Overview of the Secondary Assessment 40
H's and rs 40

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 Contents

Diagnosing and Treating Underlying Causes 41

Introduction 41
Conditions and Management 41
Hypovotemia 41
Cardiac and Pulmonary Conditions 41
Drug Overdoses or Toxic Exposures 42
Part 5
The ACLS Cases 43

Overview of the Cases 43

Respiratory Arrest Case 44
Introduction 44
Case Drugs 44
Normal and Abnormal Breathing 44
ldent1flcatlon of Respuatory Problems by Severity 44
Respiratory Distress 44
Respiratory Failure 45
Respiratory Arrest 45
The BLS Assessment 46
Assess and Reassess the Patient 46
Ventilation and Pulse Check 46

The Primary Assessment 46

Airway Management in Respiratory Arresl 46
Ventilations 46

Management of Respiratory Arrest 47

Overview 47

Giving Supplementary Oxygen 47

Ma1nta1n Oxygen Salurat1on 47

Opening the Airway 47

Common Cause of Arrway Obstruction 47
Basic Airway Opening Techniques 47
Airway Management 48

Providing Basic Ventilation 49

Basic Airway Skills 49
Bag-Mask Ventilation 49

Basic Airway Adjuncts: Oropharyngea/ Airway 51

Introduction 51
Technique of OPA Insertion 51

Basic Airway Adjuncts: Nasopharyngeal Airway 53

Introduction 53
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 -

Contents

Technique of NPA Insertion 53

Suctioning 55
Introduction SS
Sof\ vs Rigid Catheters S5
Oropharyngeal Suct10,ing Procedure 56
EndotracheaJ Tube Sucboning Procedure S6

Providing Ventilation Wrth an Advanced Airway 56

Introduction 56
Ventllahon Rates 57
Laryngeal Mask Alrwirj 57
Laryngeal Tube 57
Esophageal-Tracheal Tube 57
Endotracheal Tube 58

Precautions for Trauma Patients 58

Summary 58

Acute Coronary Syndromes Case 59

Introduction S9
Rhythms for ACS 59
Drugs for ACS 59
Goals for ACS Pati ents 60
Pathophysmlogy of ACS 60

Managing ACS: The Acute Coronary Syndromes Algorithm 62

Overview of the Algorithm 62
Important Considerah,ns 63
Application of the ACS Algorithm 63
Identification of Chest Discomfort Suggestive of lschemia 63
Signs and Conditions 63
Starting Wrth Dispatch 64
EMS Assessment, Care, and Hospital Preparation 64
Introduction 64
Monitor and Support ABCs 64
Adm1mster Oxygen and Drugs 65
Obtain a 12-lead ECG 67
Immediate ED Assessment and Treatment 67
Introduction 67
The First 1O Minutes 68
Patient General Treatment 68
Classify Patients According to ST-Segment Deviation 69
C lassify Into 3 Groups Based on ST-Segment Deviation 69

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 Contents
J
STEM/ 69
Introduction 69
Early Reperfusion Therapy 70
Useol PCI 70
Use of F1bnnolytic Therapy 71
Adjunctive Treatments 71
Acute Stroke Case 73
Introduction 73
Potential Arrhythmias With Stroke 73
Drugs for Stroke 73
Approach to Stroke Care 74
Introduction 74
Goals o f Stroke Care 75
Cntical Time Penods 76
Application of the Suspected Stroke Algorithm 78

Identification of Signs of Possible Stroke 78

Warning Signs and Symptoms 78
Activate EMS System Immediately 78
Stroke Assessment Tools 78
Critical EMS Assessments and Actions 81
Introduction 81
Critical EMS Assessments and Actions 81
In-Hospital, Immediate General Assessment and Stabilization 82
Introduction 82
Immediate General A,;sessment and Stabilization 82

Immediate Neurologic Assessment by Stroke Team or Designee 83

OveNiew 83
Establish Symptom Onset 83
Neurologlc Examination 84

CT Scan: Hemorrhage or No Hemorrhage 84

Introduction 84
Decision Point: Hemorrhage or No Hemorrhage 84

Rbrinolytic Therapy 86
lntroduct1on 86
Evaluate tor F1brinolyt ic Therapy 86
Potential Adverse Effects 87
Patient Is a Candidate for Fibrinolytic Therapy 88
Extended IV rtPA Window 3 to 4.5 Hours 88
lntra-artenal rtPA 88

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 Contents

Endovascular Therapy 89
Introduction 89
lntra·artenal rtPA 89
Mechanical Clot D1srupbon/Stent Retnevers 89
Systems of Care 89

General Stroke Care 89

Introduction 89
Begin Stroke Pathway 90
Monitor Blood Glucose 90
Monitor for Compilcaaons of Stroke and F1bnnolyt1c Therapy 90
Hypertension M11nagernent 1n rtPA Candidates 90

Cardiac Arrest: VF/Pulseless VT Case 92

Introduction 92
Measurement 92
Benchmarking and Feedback 92
Change 93
Rhythms for VF/Pulseless VT 93
Drugs for VF/Pulseless VT 93

Managing VF/Pulseless VT: The Adult Cardiac Arrest Algorithm 93

Overview 93
VF/pVT (left Side) 93
Asystole/PEA (Right S 'Ce) 94
Summary 94

Application of the Adult Cardiac Arrest Algorithm: VF/pVT Pathway 95

lntroeuct1on 95
Minimal Interruption of Chest Compressions 95
Deliver 1 Shock 96
Purpose of DefibnllatJon 96
Principle of Early Defibnllation 97
Resume CPR 98
Rhythm Chee~ 99
Self-Adhesive Pads 99
Shock and Vasopressors 99
Rnythm Check 100
Shock and Ant1arrhyth mies 100
Cardiac Arrest Treatment Sequences 101
Phys1010g1c Mon1tonng During CPR 102
Treatment of VF/pVf In Hypothermia 104

Routes of Access for Dnrgs 104

Pnont•es 104
Intravenous Route 104
lntraosseous Route 105
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 Contents

Endotracheal Route 105

Fluid Adm1mstrahon 105

Vasopressors 105
Introduction 105
Vasopressors Used During Cardlac Arrest 106
Ep1nephnne 106

Antiarrhythmic Agen ts 106

Introduction 106
Amoodarone 106
Lldoca1ne 106
Magnesium Sulfate 107
Steroids in Cardiac Arrest 107
Respiratory or Cardiac Arrest Associated With Opioid Overdose 107

Extracorporeal CPR (for VF/Pulseless VT/Asystole/PEA) 109

Extracorporeal Membrane Oxygenation 109

Ultrasound (for VF/Pu/sel ess VT!Asystole/PEA) 109

Ultrasound Use In Cardiac Arrest 109

Cardiac Arrest: Pulseless Electrical Activity Case 110

lntroductlon 110
Rhythms for PEA 110
Drugs tor PEA 110

Description of PEA 110

Introduction 110
Historical Perspective 110

Managing PEA: The Adult Cardiac Arrest Algorithm 111

0vefVl0W 111
The PEA Pathway of the Cardiac Arrest Algonthm 111
Decision Point: Rhythm Check 111
Administer Ep1nephnne 111
Nonshockable Rhythm 111
Decision Point: Shockable Rhythm 113
Asystole and PEA Treatment Sequences 113
Identification and Correction of Underlying Cause 113

Cardiac Anest: Asystotc Case 114

Introduction 11 4
Rhythms for Asystole 114
Drugs for Asystole 114

Approach to A.systole 114

Introduction 114

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 Contents

Pauents With ONAR Orders 11 :i

Asystole as an End Point 115

Managing Asystole 115

Overview 115
Adult Cardiac Arrest AJgorrthm 115
ldentrticabon and Correcbon of Undec1ying Gause 116

Application of the Adult Cardiac Arrest Algorithm: Asystole Pathway 116

Introduction 116
Confirmed Asystole 116
Administer Epinephrine 116
Decision Point. Rhythm Check 116
Nonshockable Rhythm 116
Shockable Rhythm 116
Asystole and PEA Treatment Sequences 116
TCP Not Recommended 117
Routine Shock Administra11on Nol Recommended 117
When 1n Doubt 117

Terminaling Resuscita tive Efforts 117

Terminating In-Hospital Resuscitative Efforts 117
Terminating Out-of-Hospital Resuscitative Efforts 117
Duratoon of Resuscitative Efforts 118
Asystole: An Agonal Rhythm? 118
Ethical Cons1derat1ons 118
Transport of Patients 1n Cardiac Arrest 119

Bradycardia Case 120

Introduction 120
Rhythms for Bradyeard1a 120
Drugs for Bradycard1a 121

Description of Bradycardia 122

Def1m1tons 122
Symptomatic Bradycardia 122
Signs and Symptoms 122

Managing Bradycardla: The Bradycardia Algorithm 123

Ovef'Vlew ol the Algonthm 123

Application of the Bradycardia Algorithm 124

Introduction 124
ldent1f1cation of Bradycard1a 124
Pnmary Assessment 124
Are Signs or Symptoms Caused by Bradycard1a? 124
Decision Point Adequate Perfusion? 124
Treatment Sequence Summary 125
•
 Treatment Sequence. Alropone 125
Treatment Sequence: Pacing 126
Treatment Sequence· Epinephnne. Dopamine 126
Next AcllOllS 127
Transcutaneous Pacing 127
Introduction 127
lnd1cat1ons 127
PrecaU1100S 127
Technoque 127
Assess Response 10 Treatment t28
Bradycard1a With Escape Rhythms 128
Standby Pacing 128
Tachycardi a: Stable and Unstable 129
lntrodUCIJon 129
Rhythms for Un51abl~ Tachycardia 129
Drugs for Unstable Tachycardia 130
The Approach to Unstable Tachycardia 130
Introduction 130
Oef1n1t1ons 130
PothophySK>logy of Unstable Tachycardia 131
Signs and Symptoms 131
Rapid Recognition Is the Key to Management 131
Seventy 131
lndocattOnS for CardtOVetSIOn 131
Managing Unstable Tachycardia: The Tachycardia Algorithm 132
Introduction 132
Overview 132
Summary 133
Application of the Tachycardia Algorithm to the Unstable Patient 134
lntroductton 134
Assess Appropnateness for Clinical CondrtlOO 134
ldenl1fy and Treat the Underlying Cause 134
Dec1s1on Point. Is the Persistent Tachyarrhythm1a
Causing Significant Signs or Symptoms? 134
Perform Immediate Synchronized Cardioversion 135
Oetenm1ne the Width or the ORS Complex 135
Cardioversion 136
lntroduct on 136
Unsynchroruzed vs Synchronized ShockS 136
Potenual Problems With Synchrornzat10n 136
Recommendations 137

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 Contents

Energy Doses for Card loversion 137

Synchronized Cardioversl on Technique 137

Introduction 137
Technique 138
Stable Tachycardias 139
Rhythms for Stable Tachycardia 139
Drugs for Stable Tachycardia 139

Approach to Stable Tachycardia 139

Introduction 139
Oueshons to Oetermme Classdicatlon 140

Managing Stable Tachycardia: The Tachycardia Algorithm 140

lntroduchon 140
Overview 141

Application of the Tachycardia Algorithm to the Stable Patient 141

Introduction 141
Patient Assessment 141
BLS and ACLS Assessments 141
Dec1s10n Point: Stable or Unstable 141
IV Access and 12-Lead ECG 141
Decision Point Narrow or Wide 142
Wide-Complex Tachycardias 142
Narrow ORS, Regular Rhythm 143
Tachycardia Algorithm Advanced Management Steps 144

Immediate Post-Cardiac Arrest Care Case 145

Introduction 145
Rhythms for Post-Cardiac Arrest Care 145
Drugs for Post-Cardiac Arrest Care 145
Mulhple System Approach to Post-Cardiac Arrest Care 145
OveN1ew of Post-Cardiac Arrest Care 146

Managing Post-Cardiac Arrest Care: The Post-

Cardiac Arrest Care Algorithm 147

Application of the lmmedjate Post-Cardiac Arrest Care Algorithm 148

lntroduct1on 148
Opt1m1ze Ventilation and Oxygenation 148
Treal Hypotens1on (SBP Less Than 90 mm Hg) 150
STEMI Is Present or High Susp1c1on of AMI 151
Coronary ReperfusK>n 151
Following Commands 151
Targeted Temperature Management 151
Advanced Critical Care 152
Post-Cardiac Arrest Maintenance Therapy 152
• II
Appendix 155

Testing Checklists and Leaming Station Checklists 157

ACLS Pharmacology Summary Table 170
2015 Sci ence Summary Table 173
Glossary 175
Foundation Index 1n
Index 179

Note on Medication Doses

Emergency cardiovasculnr care is a dynamoc science. Ad•ances n ueatmoo1 and drug lllerapoes occur rapt<Jly
Readers should use the following sources to check for changes 1n recommended doses, 1nd1cat1ons, and contrmnd1·
catJOnS: the ECC Handbook , available as opttonal supplementary matenal, ond the pacJ<age insert product 1nf0<matt00
sheet for each drug a'ld meoical device

a1ii
Contents
 ·-------

life is -why.~ ~~~;_

I - -- "".: ..-;; :
At 111e Amercan Hearl Assoclal!OO ;ve want people 10 expeneoce more of 111c·s preclOl.IS moments Thats
v.try we·ve macle betttlf heart and bran heailll our llllSSiOn Its also why we remain committed to excep!JOOal
training- the act of bringing resuscltatoo science to life-through genuine partnersh p \"1th you Only through
our continued collabOraloo and dedication can we truly make a difference and save lives
Until there's a world free or heart disease and stroke. the American Heart Association will be there, w()l1(Jng
with you to make a healthier, longer hfe possible f()( everyone.

Why do we do what we do?

life is why.
Life Is Why 1s a ceJellratton at life Asunple yet powerful answer to the quesoon or wily we SlloulCf all
be healthy in heart and mind h also exola ns wily we do wtiat we do: Lifesaving work fa-ery day
Throughout your student manual, you wlll llnd inlormauon that correlates what you are learning 10 lh1s
class to Lile Is Why and the Importance ol card1ovascufar care. LoOk for the
Life Is Why icon (shown at right), and remember lhal what you are lea ming today
has an Impact on lhe mission al the American Hearl Association.
We encourage-you to discover youi Why and sha1e 11 v~tll others. Ask yourself, whai
are lhe moments. people. and experiences I hv~ lo(I What brings me 1oy, wonder
and happiness? Why am I parinenng with the AHA to help save lives? Why is
cardlovasculaJ care important to me? The answer to these questJOOs 1s your Why.

Please hnd on the back of this page a chance for you lo particloate 1n lite AHA's
m1ss1on and Lile Is Why campaign. Complete lhtS activity lly 11 llng in the blank
with the word that describes your Why.

V
Sha1e your "- - Is Why" with tre people you love. and ask them 10 Ll1scover ~ American
their Why. Heart
Associat ion ..
Talk about it. Share iL Post it. Live it. #lileiswhy #CPRSaveslives
life is why·

- -- -1 -- -- ---

D rl Bi ~ ~ rm m m
""
 is why.

O
~ American
Heart
Association.
life is why·

- ~ -- - - --
 Introduction

Course Description and Goal

The Advanced CardK>VaSCtJlar Life Support IACLS) Provider Course is des1gned for
healthcare providers whO e11her direct or participate 1n the management of cardiopulmo-
nary arresl or other cardiovascular emergenoes Through didactic 1ns1ruction and active
part1c1pat1on in simulated cases. students will enhance their skills 1n the recognition and
Intervention ol cardiopulmonary arrest. Immediate post-<:ardiac arres1. acute arrhythmia,
stroke, and acute coronary syndromes (ACS).

The goal of the ACLS Provider Course 1s to improve outcomes for adult patients of cardiac
arrest and other card1opulmoriary emergencies lhrough early recogmt>on Bl'ld mtervenuons
by high performance 1eams

Course Objectives

Upon successful oompletJOn of this course. s1uden1s should be able to

• Apply the Basic Ltfe Support tBLS). Pnmary, end Secondary Assessment sequences
for a systemattc evalua11on of adult patients
• Perform prompt, hlgh-qualtty BLS. including prioritizing early chest compressions and
integrating early automated external deflbrillator (AEDl use
• Recognize respiratory arrest
• Perform early management or respiratory arrest
• 01scuss early rec-09nition and management of ACS. 1nclud1ng appropriate d1spositon
• Discuss earty recogn1t1on and management of stroke. 1nclud1ng appropnate disposition
• Recognize bradyarrhythmlas and tachyarrhythmlas that may result 1n cardiac arrest or
complicate resuscitation outcome
• Perlorm early management of bradyarrhythm1as and tachyarrhythm1as that may result
1n cardiac arrest or oomphcate resuscitation outcome
• Recognize cardiac arres1
• Perlorm early management of cardiac arrest until terrrnnabon of resuscitation or trans·
fer of care. Including lmmedlale post-cardiac arrest care
• Evaluate resuscitative efforts during a cardiac arrest through continuous assessmem
of cordlopulmonary resuscitation (CPR) quality. mon1tonng the pa11enrs physiologic
response, and de11venng real·l•me feedback 10 1he team
• Model effective commun1cat1on as a member 0< leader of a high perlonmance team
• R9C09mze the impact of team dynamlCS on overall team perlormance
 Part 0
• Discuss how the use of a rapid response 1eam or m edical emergency team may
11nprove p atient ou1comes
Define systems of care

Course Design

To help you ach;eve th!'Se obtoctNes the ACLS Provider Course includes pract.C. learning
stations and a Megacode evaluation station

The pn .tice ,'eafTllflg stat""15 g.ve you an opportunity to actively partoe pate in a vanety of
le:lrning acw.t es. 1ncluo ng

• Simulated c11nica 1scenanos

CX>moosuanons by 1n&1ructors or llideo
• Discussion and role playing
• Prac11ce In effective high p erlormance tonm beh aviors
In these learning stations. you will practice P,sentlat sktlls both lnd1v1dually and as part o f
a high· performance team This course emphasizes effective team skills as a vital pan ol
the resusc1ta~ve e'lort You >'<ill have the opponun1ty to practice as a member and as a
leader of a high-performance team

Al 1he end of the course. ~ou will participate 1n a Megacode evaluation s tation to validate
your ach.evement of the course obpec;tives A simulated canl1ac arrest scenano will evnlu ·
a!e me follow•'lQ-
• Know!edge of core case ma:erial and Skills
• Know1~e of ~hrM
Understane11ng of arrhythmia 1nterpreta11on
• Uso of appropriate baste ACLS drug therapy
Perlormance as an et1ect1ve lead er of a h igh-performance team

Course Prerequisites and Preparation

The American Heart Association (AHA) ltmtts enrollment 1n the ACLS Provider Course to
heatlhcnre providers who <1irec1 or participate tn 1he resuscrtatJOO ol a patient either 1n or
out of hospi1a1. Part1c1pants who enter lhe cour!>A!I must have the basic knowledge El10
5k Us to parlJClpa:e actniely w1:h the 1nstruc:1or and othef Studerts

. . . Be•ore :ne co. rse P'._ •eao t"'! ACLS Provraer Manual. comple:e uie
c;:, 1•1andatory Preco ,, s.:·•·Asse<vr>MI moouieS on the Student Web$te
1www.heart.org/ eccstudent). 1den11fy .my gaps in your knowledge. and remed1 ·
ate those gaps by studying l he apphcable content In the ACLS Provider Manual or othor
supplememary resou rces. including the Studeni Websn e. A passing score ror the self
ass11ssment 1s 70%. an<I you may take 11 an unlimited number of t•mes 10 achieve a pas•
1nq core You w ill need to bring your Precourse Self-Assessmont certificate with you
to c lass.

The fo1low1ng knowledge and skills are required ror successtul course completion·
BLS skills
Elftttrocard1ogram lECGt rhythm 1n1erpreta1ion tor core ACLS rhythms
Kno"' 1dge of arway ~land adpJnc!S
Basic: ACLS d<UQ and pharmacok>gy knov.1odge
PriKtcat 3opjication of ACLS mythms and oiugs
Effe<.t1ve rugh-performanco team skills

:z
 Introduction

BLS Skills The foundatJOn of advanced "e suppon 1s $lrong BLS so<. Is You must pass the hlgh-qual·
course. Make sure that you are profic100t 111
1ty BLS Testing Station to complete the ACLS
BLS skills before attending the course

f;a Watc/1 the H1gh-Ouahty BLS Skills video found on the Student Websrte
~ (www.heart.org/eccstudent). Review the Htgh-Ouality BLS Skills Tesnng
Checklist located m the Append11t

ECG Rhythm The basic cardiac arrest and per1arrest algorithms require students to recognize these
Interpretation ECG itiy1hms
for Core ACLS • Sinus rhythm
Rhythms • Atnol fob<lll:Jtton 3lld flutt<r
• Bradyl:ardia
• Tachycardia
• Atnoventncular (AV) bloc~
• Asystole
• Pulseless electrical act1v1ty (PEA)
• Ventncular tacllycardia (VT)
• Ventncular fobnttatJOn f\/F)
f;a You "ii need to comP'ete the ACLS Precourse Sett·As.;e o.ment. which contains
=-:! ECG rhytllm odenLfic<rJOn. on the Student WeOSJte www.heart.org/eccstudentJ
At the end of the assessment you wot receive your score and feedback to help
you 1dent1fy areas of strength and weokness Remediate any gops 1n your knowledge
before entenng the course. During the course, you must be Obie to ldonuty and interpret
rhythms during practice as well as during the final Megacode evoluotlon station.

Basic ACLS Drug You ln\.St know the drugs anc doses us'>d m the ACLS algor•tnms You wiD also need to

=
and Pharmacology ilnOw "hen to use wl'llch ~ l>ased on the ctonoca SitualJOtl
Knowledge tml You w~ need to complete the ACLS Precourse Se<f-Asse<sment. v.tuch contall\S
pharrnaCOlogy ques11ons, on lhe Studen1 Websne fwww.henrt.org/e<:cstudent)
Al lhe end of the assessment, you will receive your score ond feedback to help
you Identify areas or strength and weakness. Remediate any gaps In your knowledge
before entering the course.

3
 Part 0

Course Materials

=
fii1 Course materials consist of the ACLS Provider Manual, Student Website
(www.heart.org/eccstudent), 2 Pocket Reference Cards, and Precourse
Preparation Che<:~hst. The icon on the left dlre<:ts you to additional supplementary
1nrormalion on the Stvden1 Website.

ACLS Provider The ACLS Provider Manual contains the basic tnformation ycu need for effectrve parhcipa·
Manual t1on m the course. This 1mponant matenal includes the systematJc appmach to a caidio-
pulmonary emergency. effective high-performance team commumcahon, and the ACLS
cases and algonthms. Please review this manual beforo attending the course. Bring it
w ith you for use and roferenc.o during the course.
The manual is organized into lhe following parts·

Part 1 Introduction
Part 2 Systems of Care

Part 3 Effective Hogh·Perfoonance Team Dynamics

Pa rt 4 The Systematic Approach

Part 5 I The ACLS Cases
Appendix Testing Checklists and Learning Station Checklists
ACLS Pharmacology Ba~c ACLS drugs, doses, lndlcat.ions and contraindlca·
Summary Table lions, and side effects
2015 Science H19hhght.s of 2015 science changes 1n the ACLS Provider
Summary Table Course

Glossary Alphabetical list of terms and their definitions

Foundation Index Pages where key sub)e<:ts can be found (eg, epinephrine.
card1overs1on, pacing)
Index

=
fiil The AHA requires lhat Student.s complete and pass lhe Precourse Sett-
Assessment found on the Student Webstte and pnnt their scores for subm1ssoon
to their ACLS Instructor The Precourse Sett-Assessment allows students to
understand gaps 1n Knowledge required 10 participate In and pass the course.
Supplementary topics loca•ed on the Student Web~te are useful but not essential for
Successful completion or the course.

4
 Introduction

Call-out Boxes
The ACLS Provider Manual contains imponant information presented 1n call-out boxes
that require the reader's attention. Please pay particular attention to the c all-out boxes,
listed below:

Crltlcal Conc.pts Pay particular attention to lhe Critical Concepts boxes

that appear in the ACLS Provider Manual. These
boxes contain the most im portant information that you
must know.

C•ut/on Caution boxes emphasize specific nsks associated

with interventions .

FYI 20111 Gulde/Ines FYI 2015 Guidelines boxes contain the new 2015
AHA Guidelines Update for CPR and Emergency
Cardiovascular Ql/8 (ECC) anformabon.

l'ound•tlon•I F•cts Foundational Fact s boxes contain basic Information

that will help you understand the topics covered in
the course.

Life Is Why Life Is Why boxes describe why taking this course matters.

Student Website
=
f1ii1 The ACLS Student Website (www.heart.org/ eccstudent) contains the following
sett-assessment and supplementary resources:

Resource D escription ' H ow to U se

M andatory The Precourse Self· Complete before the

Preco urse I Assessment evaluates a
Self -Assessment studenl's knowledge in 3
sections: rtlythm. phar·
macology, and prac tical
application
course to help evaluate
your proficiency and
deterrmne the need for
addrtional review and
practice before the course

(continued)

5
 P art 0
(continued)
Resource Deacrlptlon How t o Uae
ACLS Supplementary • Bask: AJrway Add1llonal Information to
Information Manogement
supplement ba$lc c;on·
• AOvanc:ed Alrway c;ep15 p.-esented in the
Management
ACLS course
• ACLS Cora Rhythm$
• Oef1bl'illato0n Some 1nlormato0n ia sup-
• Ac:c:.a for Medlc;ations plementaty; other.,_ -
• Acute Coroner; tor m. •nt-ted student
Syneromea (I( advanced provide<
• Human, Ethocal, and
Legal Oimenalonl of ECC
and ACLS
• Web-Based 5'11·
Assessment. Drugs Used
in AJgootlvns
High-Quality BLS video • Hogh quahty BLS
• Compressions
• \l....t~toOnS
• AEOU$8
ACS video • ST·megment ....,1lto0n
myoc;atdial infll'CtJOn
(STEMl)
• Chain of Survlval
• Supplementary oxygen
• 12· lead ECG
• Reperlusoon
• PIWCIJ18naous ooronaty
1ntervento0n
• F1br1nolytoc therapy
Stroke vid6o • Acute stroke
• CM n of Survival
• 8 o·a of StrOl<e Care
• F1br1nolytie therapy
Airway Management • Altwey ao,uncts
video • Advanc:ed llfWllYS
• Conlumato0n deviees

II
 Introduction l
Pocket Reference The Pocket Reference Cards are 2 stand-alone cards packaged with the ACLS Provider
Cards Manual. These cards can be earned In your pocket for quick reference on the following
topics:

Topic / Reference C•rds

Cardiac arrest, • Adult Cardiac Arrest Algorithms
arrhythmi as, and • Table with drugs and dosage reminders
t reatment • Adult Immediate Post-Cardiac Arrest Care Algorithm
• Adult Bradycardia With a Pulse Algonthm
• Adult Tachycardia With a Pulse Algorithm
A CS and stroke • Acute Coronary Syndromes Algonthm
• Flbnnolytlc Checklist for STEMI
• F1bnnolytic Contraindications for STEMI
• Adult Suspect ed Stroke Algon1hm
• Stroke Assessment-Cincinnati Prehospttal Stroke Scale
• Use of IV rtPA for Acute lschemlc Stroke
• Hypertension Management in Acute lschemlc Stroke

Precourse The Precourse Preparation Crecklost can be found on the Student Website
Preparation (www.heart.org/eccstudenl). Please review and checK the boxes after you have com-
Checklist pleted preparation for each section.

Requirements for Successful Course Completion

To successfully complete the ACLS Provider Course and obtain your course completion
card. you must

• Pass the Adult H1gh-Quahty BLS Skills Test

• Pass the Bag-Mask Ven~lat1on Skills Test. including oropharyngeal airway/
nasopharyngeaJ airway insertion
• Demonstrate competency in learning station skills
• Pass the Megacode Test
• Pass the open-resource exam with a minimum score of 84%

Life Is Why Saving Lives Is Why

Cardiac arrest remruns a leadrng cause of death. so the AHA trains m1lloons of people
each year to help save lives both 1n and oul of the hospital. This course is a key part of
that effort.

7
 P ar t 0
ACLS Provider Manual Abbreviations

ACE Mgl0te<1SIO-COl1\lel'llng _,zyme

ACLS Advanced cardiovascular Ille suppo11

ACS Acute cororwy ~

AED Automated t•ternal def t><dlator

AHF Acute heart failure

ANA
AMI Ac\lle myocardf41 infarction

aPTT Activated p;irt1al thromboplast1n 11me

AV Atrioventricufar

BLS BaSIC hie S<Jpporl . Check responsiveness , activate emergeo<:")

response sy~tam. check carot«I pulse. provide def>tl<dl4tlOl1

CARES cardiac Atro$t Registry 10 Enl\Gnee Soo!ivat

CCF CheSt compress'°" fraction
CPR Catdoclpu4mon:wy 191U10t.lt.on
CPSS Cinc•nnall Preho$pltal Stroke Scale

COi Continoou1 Quality 1mprovlm8f1t

CT Compuled tom igraohy

DNAR Do not attempt resuscitation

ECG E1eetrocard.og1 un
ED Emergency department
EMS Emergency medical sef'lllces
ET Endotracheal

FDA Food and DrtlQ Adm1n1sll<1hon

Fraction ol ln~tred OXYll""l

GI Gastro1ntuath10I

8
 Introduction

ICU Intensive care unit

INR International nonnalrzed ratio

10 lntraosseous

IV Intravenous

LV Left ventricle or left ventncu1ar

mA Milliamperes

MACE Major adverse cardiac events

MET Medical emergency team

Ml Myocardial 111farction

mm Hg M1lh'Tleters of mercury

NIH National Institutes of Health

NIHSS National Institutes of Health Stroke Scale

NINOS National Institute of Neurological Disorders and Stroke

NPA Nasopharyngeal airway

NSAID Nonsteroidal anb-111flammatory drug

NSTE-ACS Non-ST-segment elevation acute coronary syndromes

NSTEMI Non-ST-segment elevation myocardial infarction

OPA Oropharyngeal airway

Paco, Partial pressure ol carbon diOxide 111 attenai blood

PCI Percutaneous coronary intervention

PE Pulmonary embolism

PEA Pulseless electrical acbV11y

PETCO, Partial p<essure of end-tidal carbon dioxide

PT Prothromb1n lime
pVT Pulseless ventncular tachycardia

ROSC Return of spontaneous c1tculation

RRT Rapid response team

rtPA Recombinant trssue plasm1nogen actrvator

RV Right ventricle or right ventricular

II
 P a rt 0

SBP Systolic blood pressure

STEM I ST-segment elevation myocardial infarction

SVT Supraventncular tachycardia

TCP Transcutaneous pacing

TTM Targeted temperature management

UA Unstable angina

VF Ventricular fibrillation

VT Ventricular tachycardia

Advanced Cardiovascular Life Support

ACLS providers face an 1mponnnt challenge - tuneliomng as a team that Implements

and integrates both basic and advanced life support t o save a person's life. The 2015
AHA Guidelines Update for CPR and ECC reviewed evidence that shows that in both
the In-hospital and out-of-hospital settings, many cardiac arrest patients do not receive
high·Quality CPR. and the majority do not survive. One study of In-hospital cardiac arrest
showed that the Quality of CPR was inconsistent and did not always meet guidelines
recommendations.· Over the years. however. patient OU1comes alter c31diac arrest have
improved Table 1 shows the recent trends Ill SUl'\l1Val 111 both out-of-hospital and in-hospital
cardiac arrest in the United States.'

T•bl• 1. Recent Cardiac Arrest Survival Data

Out- of-Hospital In-H ospital

Cardiac Arrest Cardiac Arrest
---.,
Statistical
Update Bystander Survival Survival
Incidence. CPR Rate• lncidence,t Rate•
n (Ove<all}, (Overall), n (Adults),
% % %

2013
ft

• t ••

359400
'

40.1
.
:
I •

I .

9.5
e• 11 I

t • 11 I

209000 23.9
2012 382800 41.0 11.4 209000 23.1
Baseline 31 7.9 19
·5,,...,..a110 hosprt3l d scl\arge.
EJ1Crropo1a1ad mCfdenco ba~ on tho same 2011 Get With The Gu1dol nes·Resusc1tatlon s1ucty.

10
 Introduction J
To ana11·ze these findings. a "back-to-basics• evidence review refocused on the esseo-
11als of CPR, the links 1n the Cham of Survival, and the integration of BLS wrth ACLS.
Minimizing the Interval between stopping chest compressions and delivering a shock (ie.
minimizing the preshack pause) improves the chances of shock success· and patient
suMval • Expel'IS believe that high surviva1 rates lrom both out-of-hospital and in-haspital
sudden cardiac death are possible with strong systems of care.

High survival rates In studies are associated with several common elements·
• Tra nong al knowledgeable healthcare providers
Planned and practiced response
• Rapid recognition al sudden cardiac arrest
• Prompt provision of CPR
• Oetibnllat.on as early as poSSlble and w1th1n 3 to 5 minutes of collapse
• Organized post-cardiac arrest care
When trained persons Implement these elements ear1y. ACLS has the best chance of
produong a successful OU1come

Critical Conce pts Optimization of ACLS

ACLS 1s optimized when a team leader effectJvely integrates high-qualny CPR and
minimal Interruption of high-quality chest compressions with advanced Ille support
strategies (eg. defibnllation. med1ca11ons. advanced airway).

Critica l Conce pts Minimize Interruptions in Compressions

Studies have shown that a reduction 1n the interval between stopping compressJons and
shock delivery can Increase the predicted shock success. Interruptions 1n compressions
should be l1m1ted to cnt1cal 1ntervent1ons (rhythm analysis. Shock delivery. Intubation.
etc), and even then. these should be m1nim12ed to 10 seconds or fess

Closing the Gaps

Quality Assessment, Every emergency medical service (EMS) and hospital system should per1orm contlnu·
Review, and ous quahty improvement 10 assess its resuscltehon interventions and outcomes through
Translational Science a defined process of data co ectton and review There is now Wl<lespread consensus
that the best way to improve either community or 1n-hosp1tal survival from sudden car-
diac arresl IS to stan with the standard "quahty tmprovemen1 model" and then modify
1ha1 model according to the Chain of Survival metaphor. Each link 1n the chain comprises
s1ructural. process. arid outcome vanables that can be examined. measured. and record·
ed System managers can quickly 1dentJfy gaps that exist berween observed processes
and outcomes and local expectations or published "gold standards."

Life Is Why Life Is Why

At the Amencan Hean As1i0Claoon, we wan1 people to expenence more ol life's precle1.s
moments What you learn 1n this course can help build healthier. longer lives for every0<1e.

11
 Part 0
Referenc-e s
1. Abella BS. Alvarado JP. Myklebusl H. e1 al. Ouahly ol car-
diopulmonary resuscitation dunng in· hospital cardiac arrest
JAMA 2005;293{3)305-310.

2 Mozaffanan D. Bentam'" EJ. Go AS. el al: on behott of

tho Amencan Hearl AssoclatJon StahSllCS Commonee and
Slro!<e S1n11st1CS Svbeommntee. Heart d<sease and slroke
sta11st1cs- 2015 upda10: a report lrom the American Hean
Assoc1nuon. Qrcul1won. 2015:131(4te29-e322

3. Edelson DP, AbeQa 8S Kramer-Johansen J e· al Effects

of compression deplh ond P'&-Shock pauses pted.cl
dei1br11!Bt1on failure during ca1dlac arrest. Resusc1tat1011
2006.7 1(2): 137-145

4 Edelson DP. lrtzlngor B Arora v el al. lmpt0111ng in-oospnal

card.ac """51 process ano outcomes v.1th pe.-tormance
deboehng Arcll/nrem Med 2ooa.1G&10):1063-1069

12
 l

Systems of Care

Introduction A system Is a group of regularly lntemct1ng and interdependent components The system
provides the n~s for tl>o Chain and determines the strength of each lonk and the chain as
a .,,.tio;e By dt!'.nil.O'I tno system cs.-temiines :he u 1 ma:e outeo<r" ""° PfOV1(Je5 coaec-
t"e support and otgan1zatoon The idea wOtl< llow :o accompl;Sh tesusc iatoon success·
fully IS hoghly oepenoent on the system of care as a whole.

Cardiopulmonary Resuscitation

Quality lmprolfement CPR 1s a series of hfeS<lw1g actions that Improve the chance or survival after cardiac
in Resuscitation arrest. Ahhough the op11mal ~proach to CPR may vary, depending on the rescuer, the
Syatems, Processes, patient, and the avaolable resources. the fundamental Challenge remains how 10 achieve
and Outcomes early and effective CPR

A Systems Approach In thls P8ll we wil focus on 2 distinct systems of care. the system for pat•ents who arrest
onside of the hospital and tne one for tll0$e who arrest ou-.s>de o! •I \Ve will set onto con ·
text me bo idong block$ for a system of can. for cardiac arrest w'th consoderatoon ol the
setling. team. and available rosources as wen as continuous quality improvement (COil
from ire moment the patient becOmes unstable unti alter the paLent •s d<SCharged

Healthcare def very requ.r... °'ructure leg people. equipment. educat()rlJ and P<OC'lSS 1eg
poloc1es, protocols. proceaures), wh'Ch. wneo integrated. proouce a system (eg. proqrams.
organizations. cultures) lending to outcomes {eg. patient safety. quahty, satosfact1on) An
effecllve system of care comprises all of these elements-structure, process , system, and
patieOt outcomes- in a framework ot COi (Figure 1)

13
 Part 0

Taxonomy of Systems of Care: SPSO

Structure Process System Outcome

Pooplo Protocols Progrnma Satisfaction

Educ11t1on Pof1cios Or9anlznllon
Equipment Procedures Culture

Quality Safety

Continuous Quality Improvement

Integration, Collabor.ltlon, Measurement, Benchmarkmg, Feedback

Soccesstuf resusc11ato00 at:er cardcac arrest requ r"5 an 1ntegra1ed set of COO<d1nafed
a<;flOnS fl'P'8$e'1ted by me hni<S 1n the system-SP"'C fie Chains of Survival !Figure 2}

Effective re51.1sc1tation requires an integrated response known as a system of C8/'8.

Fundamental to a successful resusc1t:1t1on system of care os the c0Uec11ve approoatlOl'I
of the challenges and opportunities presented by tt>e Chain of Surv111aJ. Thus 1nd1voduals
and groups must work togettler. sharnig Ideas and 1nlormato0n, to evaluate and improve
their resuscitar.on system Leadersh p and accoontaboLty are important components of
this team Jpp<Oacil.

To improve care. readers must assess the performance ol each system component
Only whPn perfonnance •S evarualed can particopanls 1n a system effectively intervene to
1mp<ove care This prcicess of quality improvement consists of an oteratrve and cont1nu ·
ous cycle ot
• Sy.tematoc evaluation of teS1.1SC1tation care and OYtcome
• 6' cnmawng w.th sta~~ feedbaek
• Strategic e'lons to addreSS ioerotified deficoenoes
Whole the care tor an oostresusc1tatJOn patients. regattl ess of v.tlere the arres· ciccUIT9d
converges 1n tile hOSpttaJ generally on an 1ntens1ve care unit OCU) tile structure and
prcice .s etemoots before that convergence vary highly for the 2 patient popula1oons
Pahents with out-ol-hospital cardiac arres1 (OHCA} de~nd on their community tor sup
por1 Lay 1escuers are expected to recognize a patient's distress, call for help. and 1n1tlo1e
CPA and public-access def bnllat1on (PAD) until a team of professionally trained EMS
providers assumes respons1b<hty and transports the patient to an emeigency department
JEDI 1'1<1 or care ac cathetenzattOn 3b before the patoeot 1s traf\Sferred to an ICU for
cont nued caro

In cor •riw pat er.ts "' th 111-h()sp<:al cardoac arrest ( HCA) oepero on a system of llllCl<O-
priare sun.eillance ana preven:JOn ot carctoac arrest When they oo arrest, they~
on the smooth interact.on of the 1n~MU1oort's varoou• depanments and setvoces and on 1
mult1d1sc1plonary team of professional provlde<s, which Includes phys1c1ans, nu~. respl •
ratory thernp1sts, pharmacists. cou11selors. and olhers

14
 Systems of Care

IHCA

OHCA

Foundational Facts Medical Emergency Teams and Rapid Response Teams

• Many hosprtals have implemented the use or METs or RRTs. The purpose or these
teams is to improve patient outcomes by identifying and treating early clinical dete-
rioration (Figure 3). IHCA Is commonly preceded by physiologic changes. In recent
studies, nearly 80% of hospitalized patients with cardlorespiratory arrest had abnor-
m al vrtal signs documented for up to 8 hours bef&e the actual arrest. Many of these
changes can be recognized by monitoring routine Vttal s.gns.. lme<ventoon before
clinical detenoration or cardiac arrest may be possible.
• Consider this question: "Would you have done anything differently 1f you knew
15 minutes before the arrest that .. .?"

l'igure 3 . Management of hfe·mreatcn ng emerQOl'C!es reqv res tntogratJOn of multlCltSCiphnary 1ooms tha'
can involvo RRTs. cardiac arrest teams. and lntena.ve care speciallles to achieve survival of the patient..
Team eaoers t\Qvc an essen1.aj role in coordin:n.on ot care \o.t·fth team memberS and other spooo.lists.

15
 Part 0
The ciassoc reSUSClt31JOn Chain of Survival concept hnked the community to EMS and
EMS to hosprtals. wrth hospttal care as the des11nahon. 1 But patients wrth a catd1ac eme<·
gency may erter the system of care at one of many different points (Figure 4).

They can present anywhere, anytime-on the street or at home. yes, but also rn the hosp1·
tal's ED. inpatient bed. ICU, operating surte. cathetenzatton suite. or imaging department.
The system of care must be able to manage cardiac emergencies wherever they occur.

Bystander EMS
Witnessed Witnessed IHCA

Ptgure 4 . Pat cot's po1n1 of Em~ry. Abb<ov1QhOl"IS: EMS. emergency med.eat MtrVioes; IHCA. in hos~tal
cardiac arrP.st. SOC. sys!Cm of cara, AEHS. 11ct1va1e emergency response system DC, d.scharge

Measurement Continual efforts to improve resuscitation outcomes are 1mposs1ble w.1houl data capture
The COllec11on of resusotation prcocess measures 1s the underpming of a system of care's
qua11ty 1mp<0vement efforts Quality improvement relies on valid assessment of resusc1ta·
hon performance and outcome

Utste1n-style guidelines and templates have been prepared for reporting resuscitation
outcomes a fter t rauma and drowning.'

• The Utstein Guidelines' provide guidance for core performance measures, Including
- Rate of bystander CPR
- Time to defibrlllahon
- Time to advanced aimay management
- une to first adm1rnslration of resuscitation medication
Survival to hospital discharge
Monitors to meawre CPR performance are now widely available. • They provide rescuers
with invaluable real-time feedback on the quality of CPR delivered during resuscitative
efforts. data for debriefing after resuscitation. and retrospective Information for system·
wide CPR CQI programs. Without CPR measurement and subsequent understanding of
CPR performance. Improvement and opum1zed performance cannot CtCCur. Providing CPR
without mon~onng performance can be likened to ny1ng an airplane Without an altimeter.

Routinely ava able 'eedback on CPR perfonnance chatactenstJcs includes chest compres
s.on rate. depth. and reco1 • Currently, cenam impo<lant parameters {chest compression
fraction and preshock. penshock. and postshock pauses) can be reviewed only retrospec·
t1vely. whereas others (vent ilation rate, airway pressure. tidal volume, and Inflation
duration) connot be assessed adequately by current technology. Add111onally,

16
 Systems of Care

acoeterometers are insensrtJve to manress compresslO<l, and current devices often pnon-
bze the order of feedbaok by use of a ngld algorithm in a maMer tha1 may no1 be optimal
or real stic (eg, an accelerometer cannot measure dep1h 1f there is too much leaning, so
the device will pnoritize feedback to correc1 leaning before correcting depth), Mhough
some software (automated algorithms) and hardware (smart backboard , dual accelerom-
eters. relerence markers, and o thers) solutions curren tly exist, continued development of
optimal and widely available CPR monitoring is a key component to improved performance.

Life Is Why High-Quality CPR Is Why

Early recognition and CPR are crucial for &KVIV3l from cardiac arrest By learning high·
quality CPR. you'll have the abltrty to improve patient outcomes and save more fives.

Benchmarlcing and Data should be systematically reviewed and compared internally to pno r performance and
Feedback externally to similar systems. Existing registries can facilitate t his bench marking effort.
Examples mclude

• Cardiac Arrest ReglS1fY to Enhance Survival (CARES) for OHCA

• Get With The Guidelines - Aesusc1tat1on program for !HCA

Change Simply measuring and benchmarking care can posit ively influence outcome. How ever,
ongoing review and mterpretat1on are necessary to identify areas lor improvement,
such as
• Increased bystander CPA response rates
• Improved CPA performance
• Shortened time to defibriltatlO<l
• Citizen awareness
• Citizen and healthcare professional education and training

Summary Over the past 50 years, the modern-era BLS fundamentals of early recognition and
activation, early CPR, and earl y delibrillation have saved hundreds of thousands of
hves around the world. However. we still have a long road to travel if we are to fulfill the
potential offered by the Chain ol Survival. Survival disparities presented a generation ago
appear to persist. Fortunately we currently possess the knowledge and tools-repre-
sented by the Chain of SurvMll-to address many ol these care gaps, and future discov-
eries w II otter opportunities to improve rates of surv111al.

Acute Coronary Syndromes

- - --
The primary goals of therapy for patients with acute coronary syndromes (ACS) are to

1. Reduce the amount of myocardial necrosis t hat occurs In pattents with acute myo-
cardial infarction, thus preseivlng left ventricular function, preventing heart failure,
and limiting other cardiovascular complications
2. Prevent major adverse cardiac events: death. nonfatal myocardial infarction, and the
need for urgent revasculanzation
3, Treat acute, life-threatening comphcal1ons of ACS. such as ventricular fibnllatton (VF),
pulseless VT (pVT). un stable tachycardias, symptomatic brodycardias, pulmonary
edema, cardiogenic shock, and mechanical complications of acute myocardlal infarction

17
 Part 0
Starts "On the Prompt d1agnos1s and treatment otters the greatest potential benefit for myocardial sal·
Phone" With vage. Thus, it is imperative that healthcare providers recognize patients with potential ACS
Activation of EMS to lnlliate evaluahon, appropriate triage. and management as expeditiously as possible.

EMS Components • Prehosp1tal ECGs

• Notmcalion of the receiving facility of a patient with possible ST-segment elevation
myocardial infarcbon ('"STEMI alert1
• Activatl<lfl of the cardiac calhetenzatlOfl team to shorten reperlus1on time
• Continuous reV'ew and qua.1ty improvement

Hospital-Based • ED protocols
Components - Activation of the cardiac cathetenzation laboratory
- Admission to the coronary ICU
- Quality assurance. real·time feedback, and healthcare provider education
• Emergency physician
- Empowered to select the most appropriate repertusion strategy
- Empowered to activate the cardiac catheterization team as indicated
• Hospital leadership
- Must be involved 1n the pr~ss and committed to Sl.IPport rapid access to STEMI
reperfusion therapy

Acute Stroke

The healthcare system has ach eved significant improvements in stroke care through 1nte-
gra11on of pub 1c education. emergency d ispatch, prehospital detection and tnage. hosp1·
tal stroke system development. and stroke unit management. Not only have the rates of
appropriate f1bnnolytic therapy increased over the past 5 years. but overall stroke care has
also Improved, 1n part through the creation o r stroke centers.

Regionalizatlon of With the National lnslttute of Neurological Disorders and Stroke recombinant !Jssue plas·
Stroke Care m1nogen activator (ltPA) ttial.' the crucial need for local partnerships between academic
medical centers and community hospitals became clear. The time-sens.live nature or
stroke requ res such an approach. even 1n densely populated metropolitan centers.

Community and Commun.ty and professional education 1$ essential and has successfully increased the
Professional proportion of stroke patients treated w ith fobMOfytic therapy.
Education
• Patient education efforts are most effective when the message is clear and succinct.
• Educa11onal efforts need to couple the knowledge of the signs and symptoms of
stroke with action-acltvate the emergency response system.

EMS The Integration of EMS into regional stroke models is crucial tor improvement or patient
outcomes.•

• EMS response personnel trained In stroke recognition

• Stroke-prepared hospitals-primary stroke centers
• Access to stroke expertise via telemed1cine lrom the nearest stroke center

18
 Systems of Care

Post- Cardiac Arrest Care

The healthcare system should mplement a comprehensive. structured mulbd1sc1pilnary

system of care in a consistent manner for the treatment ol post-cardiac arrest pabents
Programs should address targeted lemperature management [lTM), hemodynamic and
ventilation optim1za11on. immediate coronary reperfusion with percutaneous coronary inter-
vention (PCI) for eligible patients. neurologic care and prognostication, and other struc-
tured 1ntervenbons.

Patients who achieve return of spontaneous circulation (ROSC) after cardiac arrest in any
setting have a complex e-0mbinat1on of pathophys1olog•c processes descnbed as post-
cardiac arrest syndrome. which includes postarrest brain 1n1ury, postarrest myocardial
dysfunction. systemic ischemia or reper1usion response, and persistent acute and chronic
pathology that may have precipitated the cardiac arrest Post~diac arrest syndrome
plays a S1Qnrticant rote 1n pauent mortalrty

lnd1v1dual hospitals with a high frequency of treating cardiac arrest patients show an
increased likelihood ol survival when these Interventions are provided."

Targeted Temperature The 2015 AHA Gutdelmes Update for CPR and ECC recommends that TIM 1nte<Venttons
Management be adm1n1stered to comatose roe. lacking meaningful response to vertJal commands) adult
patients with ROSC after cardiac arrest, by selecting and maintaining a constant tempera-
ture between 32°C and 36'C (89 6' F and 95.2 F) for at least 24 hours.

Hemodynamlc Although providers oh en use 100% oxygen while performing the inltlal resuscltauon. pro·
and Ventilation Vlders should trtrate 1nsp1red oxygen dunng the post~iac arrest phase to the lowest
Optimization level required to achieve an anenal oxygen saturatJon of 94 % or greatet, when feasible
This helps to avO<d any potential e-0mphcauons associated with o>eygen toxicity

Avoid excessive venl1lation of the patient because of potential adverse hemodynamic

effects when lntrathorac1c pressures are Increased and because of potential decreases
1n cerebral blood flow when partial pressure of carbon dioxide 1n artenal blood (Paco,)
decreases.

Healthcare providers may start ventllatoon rates at 1O/m1n, Normocarb1a (partial pressure
of end-tidal ca.rbon dioxide [PETco,j of 30 to 40 mm Hg or Paco, of 35 to 45 mm Hg) may
be a reasonable goal unless patient factors prompt more lnd1v1dualized lreatment. Other
Paco, targets may be tolerated for spec1f1c patients For example, a higher Paco, may
be permlSS!ble 1n patients With acute lung in1ury or high airway pressures Likewise. mild
hypocapn1a migh1 be useful as a temporary measure when treatmg cerebral edema. but
hyperventilation could cause cerebral vasoconstnct1on. Providers should note that when
a patient's temperalure is below normal, laboratory values reported for Paco, might be
higher than the actual values.

Healthcare providers should utrate fluid adm1nistrat:1on and vasoactJve or 1notroplc agents
as needed to opum1ze blood pressure, cardiac outpUt, and systemic perfuSIOl'l The opu-
mal post-cardiac arrest blood pressure remains unknown; however, a moon artenal pres-
sure of 65 mm Hg or greater is a reasonable goal.

19
 Part 0
Immediate Coronary After ROSC in patients 1n whom coronary artery occlusion is suspected, rescuers should
Reperfusion With P·C I transport the patient to a lac1llty capable of rellably providing coronary reperfusion (99,
PCI) and other goal-directed post-cardiac arrest care therapies. The decision to perform
PCI can be made irrespective of the presence ol coma or the dectsJon to induce hyoo-
themua because concurrent PCt and hypothem11a are feasible and safe and have good
outcomes

Glycemic Control Healthcare providers should not attempt to alter glucose concentrotion within a lower
range (80 to 110 mg/dl [4 4 to 6. 1 mmol/L]), because of the increased risk of hypoglyce-
mia The 2015 AHA Guidelines Update tor CPA and ECC does not recommend any spe·
cmc target range of glucose management m adull patJents with ROSC alter cardiac arrest.

Neurologlc Care and The goal of post-cardiac arresl management is 10 return patients to their prearrest lune·
Prognostication tional level. Reliable early prognostication of neurologic outcome is an essentral com·
ponent of post-cardiac arrest care, but the optimal timing Is important to consider. In
patients treated with TIM, prognostication using clinical examination Should be delayed
untol al least 72 hours after return to normolherrnia For those not treated With TIM, the
earliest tome os 72 hours aner cardiac arrest and potentoally tonger rf the residual effect of
sedation or paralysis confounds the clinical exam1natJOn.

Education, Implementation, and Teams

The Chain of Survrval is a metaphor used to organize and descnbe the integrated set of
bme-sensmve coordinated actions necessary to maxlmize survival from cardiac arrest The
use of evidence-based education and implementatJon strategies can opt1m1ze the hnks 1n
the choln.

The Need for Teams Mortahry from IHCA remaJns high. The average survival rate Is approximately 24%, despote
signrlicant advances on lreatmentS. Survrval ra1es are particularly poor tor arrest assoctated
w11h mythms 01her than VFipVT Non-VF/pvr mythms are present 1n more than 82% of
arrests 1n the hospital.••

Many ln· hosp1tal arrests are p1eceded by easily recognizable physiologic c hanges. many
or which are evident with routine monitoring of vital signs. tn recent studies, nearly 60%
of hospitalized patients with cardiorespiratory arrest had abnormal vital signs documented
for up 10 8 hours before the ac1ual arrest. ThlS fonding suggests tha1 there 1s a penod of
1ncreas1ng 1nstabillry before the arrest

Cardiac Arrest Teams Cardiac arrest teams are unlikely to prevent arrests because their locus has traditionally
{In-Hospital} been 10 respond only after the arrest has occurred. Unfortunately, the mortality rate is
more than 75% once the arrest occurs.'0

Over the past few years. hosp1tals have e~pancted the focus to include patient safety and
poevento0n of arrest. The best way to improve a pa11ent's chance of survival from a card10
respiratory arrest is to prevent 1t from happening

Poor-quality CPR should be considered a preventable harm.• In healthc are environments.

variab1hty in clinician performonce has affected the abdrty to reduce heatthcare·assoclated
compllcations.'' and a standardized approach h(IS been advocated to improve outcomes
and reduce preventable harms. Doing so requires a Significant cultural shift wrthm 1nstitu·
tJons Actions and rnterventlOOS need to be proactive wnh the goal of improving rates of
morbtdtty and mortalrty rather than reacting to a catastrophic event

20
 Systems of Care

Rapid assessment and Intervention for many abnormal phys1olog1c vanables can
decrease the number of arrests occurring on the hospital.

Rapid Response The w.de vanabtlity in incidence and location of catdiac arrest on the hosprtal suggests
System potenllal areas for standardization or quality and prevention of at least some cardiac
arrests. More than half of cardiac arrests in the hospital are the result of respiratory
failure or hypovolemic shock. and the ma1ority of these events are foreshadowed by
changes in physiology, sueh as tachypnea. taehycard1a. and hypo1enslon. As such. car·
doac arrest on the hosp,tal often represents the progression of physiologic instabdoty and a
failure to identify and stabilize the patient 1n a timely manner. This scenario 1s more com-
mon on the general wards, outside of critical care and procedural areas. where patient·
to-nurse ratios are higher and monitonng of patients less intense. In this setting. intermit-
tent manual vital sign mon1tonng with less frequent direct obseNation by clinicians may
increase the likelihood of delayed recogMoon.

Over the past decade. hospitals in several countries have designed systems to identify
and treat earty clinical deterioration in patients. The purpose of these rapid response sys·
tems is to improve patient outcomes by bl'inging critical care expertise to patients. The
rapid response system has several components:
• Event detecllon and response triggering arm
• A planned response arm. such as the RRT
• Duality monitoring
• Adm1n1strati11e support
Many rapid response systems allow activation by a nurse. physician, or family member
who is concerned that the patient os detenoratlng. Some rapid response systems use
specific physlologic criteria to determine when to call the team. These parameters may be
weighted. combined, and scored as pan of an earty warning sign system. The following
hst gives examples of such cnteria for adult patients:
• Threatened airway
• Respiratory rate less than 6/mln or more than 30/min
• Heart rate less than 40/min or greater than 140/m n
• Systohc blood pressure less than 90 mm Hg
• Symptomatic hypertension
• Unexpected decrease In level of consciousness
• Unexplained agitation
• Seizure
• Significant fall in unne oulput
• Subjective concern about the pat1en1

Medical Emergency Teams and Rapid Response Teams

RRTs. or METs. were estab41shed for early interventJOn in pattents whose conditions were
deteriorating. with the goal of preventing !HCA."" They can be composed of varying
combinations of physicians. nurses, and respiratory therapists. These teams are usually
summoned to patient bedsides when an acute deterioration is recognized by other hos-
pital staff. Monitoring and resuscitation equipment and drug therapies often accompany
the team.
The rapid response system is critically dependent on early identification and activation to
Immediately summon the team to the patient's bedside. These teams typically consist of
°'
healthcare providers with both the crit1C81 care emefgency care expenence and skills
to support immediate intervention for hfe-threaternng SltuattOOS. These teams are respon-
sible tw per1orm1ng a rapid patient assessment and Initiating appropriate treatment to
reverse physiologic deterioration and prevent a poor outcome.

21
 Part 0
Published Studies The ma,onty of pubhshed before-and-after studies of METS or rapid response systems
have reported a 17% to 65% drop 1n the rate of cardiac arrests after the intervention.
Other documented benefits of these systems include
• A decrease 111 unplanned emergency transfers 10 the ICU
• Decreased ICU and 101a1 h0sp1tal 'ength of stay
• Reductions in postoperalive morbidity and mortality rates
• Improved rates of survival from cardiac arrest
The recently published Medical Emergency Response Improvement Team (MEAll} tnal
ts the only randomized controtted tnal comparing hospitals wrth an MET with thOse with·
out one. The study did nol show a difference in the composne pmnary outcome (cardiac
arrest, uneKpected death, unplanned ICU adm1ss1on) between the 12 hospitals In which an
MET system was introduced and 11 hOsp.tals that had no MET system 1n place. Further
research 1s needed about the cri1Jcal details of implementation and the potential effective·
ness of METS 1n preventing cardiac arrest or improving other important patient outcomes.

Implementation of Implementing any type of rapid response syslem will require a sigmficanl cultural change
a Rapid Response 1n most hospitals. Those who design and manage the syslem must pay particular atten-
System tion to 'ssues that may prevent the syslem from bemg used effect1vely. Examples of such
issues are Insufficient resources. poor education, fear of calling the learn, fear of losing
control over patient care. and resistance from team members.

lmplementat,on of a rapid response system requires ongolllQ education, impeccable data

collectlOn and review, and feedback. Deve4opment and ma;ntenance of these programs
requires a long-term cultural and financial commitment from the hospital admrnrstration.
Hospital administrators and healthcare professionals need to reorient lherr approach to
emergency medical events and develop a culture of patient safely with a primary goal of
decreasing morbidity ond mortahly.

Life Is Why Education Is Why

Heart d sease is the No. 1 cause of death 1n the world - with more than 17 mo •On deaths
per year That's why the AHA is continuously transforming our training solutions as sci-
ence evolves, and driving awareness of how everyone can help save a life.

References lntemat.onal Lia"'°" Committee on Resusatat,on (American

1. Cummins RO, Ornato JP, Thies WH, Pepe PE. Improving sur·
vival rrorn sudden cardiac arrest: the "'chain of survJva1•· con..
cepc. A statement for health professionals ttOm tne Advanced
Cardiac Ufo Support Subcommittee and the EmBf90ncy
Cardiac Care Commrttee Amencan Hean Assoaa:oon.
Circulat>on. 1991;83(5): 1832· 1847.
Hean Associal!On. European ResuS<:1tat1on Council, Austranan
Resusclta11on Council, New Zealand Resuscitalion Council,
Heart and Stroke Foundation or Caneda, lnterAmericon Heart
FoundatlOf\, Resusclta11on Councils of Southern AtrlC8)
Qrculal.ot!. 2004 1 t~1 ):3385-3397
3. Cummins RO, Chambe11ain 0, Haz1nsld MF, et al.
Recommended gu1del nes f0< reviewing, rcponing, .lnd con 4

2. Jacobs I, Nadkarnl V, Bahr J, et al; lnlernahonal Liaison
Comm11tee on Resuscrta11on: Am<lrican Heart Association:
European Resusc1ta!IOf"I Covncu. Australt.an Resuscn.a.1100
Counc1t New Zealand ResuscJUtJon Counol; Heart
and StfOl<e Foundation of Canada, ln:erAmencan Heart
Foundation: Rosuscitahon Counc,ls of SoutMrn Afnca;
ILCOR Task Force on Cardiac Arrest and Cardlopu monary
Resusc1tal•on Outcomes Cardiac arrest and rordlopu monary
resuscitation outcome ropons update and slmph~cabon ot
lhe utst01n templates for resusc.tauon regJSt"6. a state-
ment for nea1hcMe P<O'essoona!s from a task force of the
ducting research on In-hospital resuseilalion: the ln·hospilal
· u1s1eln style." American Heart Assoelatoon. Circulaf1on.
1997.95(8'):2213-2239
4. Meaney PA. Bobrow BJ, Mancino ME. e1 al, CPR Ouallty
Summit lnvest19at0f'S, 1he Amencan H~rt Association
Emergency Caroiovaseular Caro Commlttoe, the Council on
Cardiopulmonary Cnileal Care Perloperntive Resuscitahon
Cardiopulmonary resuscilatJon quality (corrected] omproving
cam« resuscitabon outcomes bolh "'Side and oulStde the
tiosp.1a a consensus statement 'rom 1he Amencan Hean
Assoelatoon. C1rcuta11M. 2013:128(4):417-435.

22
5. The National lnstrtute of Neurolog.oel Disorders and Stroke
rt· PA Stroke S:udy Group. Tissue plasm nogen activator for
acute ischemie stroke N Engl J Med.
1995:333(24):1581-1587
6. Acker JE Ill, Pancoob /'M, Crocco TJ, et a , American Heart
Assoc1atioo. A'Tlencan Stro~e Assoc"311on Expert Panel
on Eme<geney Medocal Setvlces Systems Stroke Council.
lmjl!emen:at101 strategies lot ~medical ~Ices
WlttUn stroke syslems or c:ate a poloey s1a1emen1 from Ille
Amencan Hea1 Assoc•abOnfAmene;in Stroke Assoaa!IOO
Expen Panel ro Emergency Medtea' Serv-ces Sys1ems and
the Stroke Couricil. Strol<e 2007.38(11):3097-3115
7 Neomar RW. Nolan JP. Adrie C. er al. Post-caro1ac
arrest syndrome: epidemiology. pa1h0phys.ology. treat·
rnent. and prognosbcatlO<'I A consensus statement from
the lntematiorol Liaison Comm1llee on Rosusc1tation
(American Heart Association. Australian and New Zealand
Council on Resusc1tat1on. Europonn Resuscilahon Council.
Hean and Stroke Foundation or Conoda. lnlerAmerican
Heari Founda'.ion. Resuscrtatlon Council of Asia. and the
Resuscnaiion Council ol Southern Africa): the American Heart
Associa1ion Emergency Cardiovascular Core Committee:
the Council on Card1ovaccul~r Surgli)ty :i.nd Anesthesi:i: thP.
Council on C;.rdK>PUlmonnry. Penoperawe. and Cnt1cal Care:
the Council <>" C11111cal Caro ology and tM Stroke Coone•
Orculat10n. 2008, 118a31:24S2·2483
8. CaiT BG. KalVl JM Mercllant RM Kromer AA. Nelmar RW
lrrter-hospnal vanabol ty •n po$t-cardiac arrest monalny.
ReStJsettallOO. 2009;80(1):30·34
9. Gallaway C}.Y, Schmieker R. Kampmeyer M. et al. ReceiVing
hosprta cha.ractensbcs associa1ed with survival a'ter out-of..
1
hospital cardiac arrest Resusc1lelK>/1 2010:81(5):524-529
10. Go AS. Mozattanan 0. Roger VL, el al; Ameocan Heart
Association Statistics Committee. Siroke Sta11st1cs
Subcommittee. Heart d1seaso and siroko slatlshcs-2013
update: a rep:>r1 trom the Ameocan Heart Assoclat•on.
Circularion. 2013. 127(1):e6-o245
11. Gurses AP, Se.di KL, Vaidya v. et al. Systems amb1gu1ty 8J'ld
guideline compliance: a qualrtalive study of how intensive
care units follow ovidence-basoo guidelines to r9duce health·
care-associated 1nfec11ons. Oua/ Sa/ Health Care.
2008.17\5) 35 1-359
12.Proncvost PJ Bo-Linn GW Preventi'IQ patient rarms through
systems of c.>re. JAMA 2012:308(8)-769· 770.
13 Oev1la MA. Be<lomo R. Hilman K. el al. Findings of the r.rst
consensus con!erence on medical emergency t•ams Ctit
c.n Mttd 2006:34(9):2463-2478.
14. Pebet<!Y MA. Cretd<os M, Abe'la BS, et a.. lntemationa ualson
Cotnm•nee on Resuscna11011. Amer<;an Heart Assoc<atlO<'I.
Austra Ian Resusc1tat.on Counci, European Resuscitatoon
Counc,I, Hean Stroke Fouooation of Canada. lnlerArnencan
Heart Foundation, Rosuscl\ation Council of Southern
Africa. New Zealand Resuscrtation Counc•I, Amencan Heart
Assoc1at1on Emergency Cardiovascular Care Commiltoe,
American Heart Assoc.ation Council on Cardio~ulmonary
Porioperatlve Critical Care. lntord•sciptinary Wo1king Group
on Quality o f Caro and Outcomes Research. Recommended
guldohnes for monitoring, reponing, and conducting research
on med.oaf emergency team. outreach. and rapid response
systems· 4n Utstein~sryte scientmc statemenl ci :to(..!.::1.,.
t1hc staroment frotn the lnterna11onal uason Ccmm1ttee
on Resusc UltlO<'I (Arnencan Heart AssociatlO<'I. Austra .an
Resusc1tat100 Cooool, Eurooean 'lesuscrtation councal.
He3118nd Sttt><e founctanon of Canada lnter""'encan Heart
Foundatoo. Res"'5C tatlOO Council o! Southern Alrica. 3nd
the New Zea:anct Resusc•tation Coone.ii· the AinenCan Heart
AssociatlO<'I E.-gency Cardiovascular care Commttee; the
Council on Caroopu1monwy. Penoperat,.,,e. and Cntocal Care;
and the lnterd•sc pl1nary \\lorlong Group on Qu>lrty of Care
and Outcotnes Researcll. Circulation
~007:1 16(2 t ):2481 -2500.
23
Part 0
 Effective High-Performance Team Dynamics

Introduction Successful resuscitation attempts often requtre healthcare providers to simultaneously

perform a variety of Interventions. Although a CPR-trained bystander working alone can
resuscllate a patient wnhin the first moments after collapse, most attempts require the
concened efforts of multJple tealthcare providers. Effective teamwork divides lhe tasks
while multiplying the chances of a successful outcome.

Successful high-performance teams not only have medical expertise arid mastery of
resusc1tat10n skills, but they also demonstrate effective communication and team
dynamics. Part 3 of this manual discusses the importance of team roles, behaviors of
effective team leaders and IBMn members, and elements of effective high-performance
team dynamics.

During the course, you will ha·1e an opponumty to practice performing different rotes as a
membe< and as a leader of a simulated high-pertormance team

Foundational Facts Understanding Team Roles

Whether you are a team member or a team leader dunng a resusettat1on atlempt, you
should understand not only your role but also the roles of other members. This
awareness will help you anticl~ate

• What actions will be periormed next

• How to communicate and work as a member or as a leader of a high- pertormance
team

Roles of the Leader and Members of a High-Performance Team

Role of the The role of the team leader is multtfaceted The team leader
Team Leader • Organizes the group
• Monitors Individual perlormance of team members
• Backs up team members
• Models excellent team behavior
• Trains and coaches
• Fac1htates understanding
• Focuses on comprchenswe potlent care

25
 0
'

Part

Every h1gh-perlormance team ~s a leader 10 organize the efforts of the group The
team leader 1s responsible for making sure everything 1s done at the nght time in the nght
way by monitoring and 1n1egrat1ng Individual performance of team members. The role of
the team lender is s1mtlar to that of an orchestra conductor directing 1nd1vldual muslclans.
l.Jke a conductor. the team leader does not play the 1ns11Umems but instead knows hOw
each member of the orchestra fits Into the overall music

The role of the team leader also includes modeling excellent team behavior and leadership
sktlls for the team and other people involved or interested 1n the resuscltauon. The team
leader should serve as a teacher or guide to help train future team leaders and rmprove
learn effectiveness. Aller resusc 1tat1on, the team leader cari facilitate analyS1s, critique. and
practJce 1n preparation tor the next resuscrtat1on attempt

The team leader also helps learn membefs understand why they must perlorm certain
tasks in a specific way The team leader should be able to explain why •t 1s essential 10

• Push hard and fast 1n the center of the chest

• Ensure complete chest recoil
• M1n1m1ze 1nterrup11ons 1n chest compressions
• Avoid excessive ventilation
Whereas members of a h1gh- perlormance team should focus on their 1nd1vidual taskS. the
team leader must locus on comprehensrve patient care.

Role of the Team members must be proficient 1n performing the skills authorized by their scope of
Team Member praetice 11 lS essenttal to the success of the resusotat>on attempt that members of a
hlgh-perlormance team are

• Clear about role assignments

• Prepared to fulfill their role responsibiflltes
• Well practiced on resuscrtabon skills
• Knowledgeable about the algorithms
• Committed to success

Elements of Effective High-Performance Team Dynamics

Roles Clear Roles and Responsib11tt1es

Every member of the team should know his or her role and responsibilities. Just as d1tfer-
ent-shaped pieces make up a 1igsaw puzzle. each team member's role 1s unique and
critical to the effective performance of the team Figure 5A 1denbfies 6 team roles for
resusc1tat1on. When fewer than 6 people are present, these tasks must be priont1zed Wld
assigned to the healthcare providers present. Figure 58 shows how multiple providers
can take on h1gl1-priorlty tasks seamlessly as more team members get to the patient

26
 Effective Hlgh-Perlormance Team Dynamics J
Positions for 6-Person H igh-Pe rformance Teams•
Leodcrahlp Roles

...n--
· ~ - ...,..~.,,. • E-...ry f"MUSC'hation
. i;,.,s.,,- t.-m must have a
~w:r'"'

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Dcfibnll"lr:;r""Pf't 'i :vck•
ur 2 rrlif'!UtDS ~Of e.,rlll'lt 1 • M,1h~ t1MtiTIA"lf da:lli10l 'lli
!11911F>nffat.9-1B;..J 111 • Pn.>\11tl<J1:1 luud~to the
'' 1r4thP·f>fllTlas~
• A.Mu·~ !9$l.(J"61)11Jr~ " '
"(1111)!"W;I'~

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• lrn1~!1tJ'., IW100CCC$$
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0Pf"l'~lcat~

'l~t~ofiro'
l"IO,...,~~
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---
1111J wTll.Alo:t.
!IP~· !)fll l'lf!)O dJej

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· ~16tMall'Wllf • ~•1 -.:v.i· ~1~ f"{'Que,..cv ;:inn
t1.-1111rTJ ol 111turrupl.u<1$11

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.
lllljife' Jnl""i

• ...,,,.8'W#t adf.IT'li llfV ....~ tnc!.o 1· rflfi

TeYl'1 I ""'ll.1fC .-Id 1t'E f06t

A
,..
...... ......................
~-
-~ . . . Ol'hll• . . ..
....... -- ..,.,,..

i1CP •a ... Os

i!ffl'
Oehl.I >Ill'

nos

24ll s

B
l'lQu,.. s. A. SUggeS111<1 IOCaloons al taam -
1
end t""'1 ~ OuMQ eaoe ""'""11IOOS an<! diRca events. B, Pnonl'f "°""" .....,_,_
respons.. Tiws figure 1flvstra!es a potenLal searnie5.'I ,....,._ sonsmve. 1riteQr.t1od tearn-ba.SOO approach 10 resuscrtatJOn wl'l«e roles and '"terven-
uons are pnorlnzed and dittnbutod 3S more rtll$0Ul'Ce5 emve to tne pat1«11 Tamos (m seconds) may vary based on c1rcumstanees. ~ tlf'l'let,
and k>cal protocols. ·with 2 0t more rescuers. ono nooithcare provldef (HCP) ahoukJ assume Iha rolo or team lead-er.
27
 Part G
When roles are unclear. team performance suffers. Signs of unclear roles Include

• Performing the same task more than onco

• M1ss1ng essential tasks
• Team membe<s having multiple roles even 11 there are enough providers
To av0td inefficiencies. the team leader must clearty delegate tasJ<s Team members
should communicate when and 11 they can harldle additional respooSlb1l111es. The team
leader should encourage team members to part1c1pate In leadership and not simply 1ollow
directions blindly.

Team leader Clealfy define an team member roles 111 the Cl1nocal setting

Team members • Seek out and perform clearty defined tasks appropriate to
I your level of competence
• Ask for a new task or role 1f you are unable to perlorm your
assigned task because It is beyond your level of experience
or competence

• Assign tasks to team memllers who are unsure of their

responsibilities
D1stnbute assignments unevenly, leavmg some wrth too
much to do and others with too httle

Team members • Avoid taking assignments

I • Take assignments beyond your level o1 competence or

expertise

Knowing Your Limitations

Not only should everyone on the team know his or her own limitalions and capabilities,
bul Iha team leader should also be aware of them. This allows the team leader to evaluate
team resources and call for backup of team members when assistance Is needed. High·
perlonnance team membe<!I should anticipate srtuauons in whrch they might require assls·
tance and infonn the team leader

Dunng the stress of an attempted resuscrtatJon, do not practice or explore a new skill. If
you need extra help. request it early. It is not a sign of weakness or Incompetence to ask
for help; 11Is better to have more help than needed rather than not enough help, which
might negatively affect patient outcome.

Team leeder and Call for assistance eal1y rather than wa111ng un11I the patient
team members deteriorates to the point that help Is cntical
• Seek advice from more experienced personnel when the
patlem's condition worsens despite pnmary treatment

28
 Effective High-Perlonnance Team Dynamics

Don't
- - - --- ~- - - ~

Team leader and • Reject offers from Others to carry out an assigned task you
l e.am m embers are unable 10 complete, especially ii 1ask completion 1s
essential to treatment

Team members • Use or start an unfam11Jar treatment or therapy without seeking

advice from more expenenced personnel
• Take on too many assignments at a time when assistance Is
readily available

Constructive Interventions

Durnng a resuscttauon anempt, the leader or a member of a high-performance team may

need to intervene if an action that is about to occur may be inappropnate at the time.
Alth ough constructive intervention is necessary, 11 should be tact ful. Tenm leaders should
avoid confrontation with team members. Instead, eol\duet a debnefing afterward 11eon-
strucuve cntic1sm 1s needed.

Te am l oader • Ask that a d ifferent Intervention be started If It has a higher

priority

Te11m members • Suggest an alternative dn;g or dose In a confident manner

• Question a colleague who 1s about to make a mistake

I
Don't
Team loader • Fail to reassign a team member who 1s t1ylng to function
beyond his or her level or skill

Te11m members • lgllO(e a team membe< who is about to 8dm1mster a drug

inco<rectly

What to Knowledge Sharing

Communicate
Sharing information is a critical component of effective t eam perfom1ance. Team leaders
may become trapped on a specific treatment or diagnostic approaCh: thos common humaro
9fTOI 1s called a fixatron emJf Examples o' 3 common typeS of foomon em>rs are

• Evetythlng is OK."
"This and only this Is the correct path."
"Do anything but this."

When resusc1tatove efforts are ineffective, go back to the basics and talk ns a team. with
conversatJons llke. "Well, we've observed the following on the Pnmary Assessment.. .
Have we mJSSed something?"

Members of a high-performance team should inrorm the team leader of any changes In
the patient's condition to ensure that decisions are made with all available Information.

29
 part e

Team leader • Encourage an environment of information sharing and ask for

suggestions of uncertain of the n ext best Interventions
• Ask for good ideas lor dofferenbal dcagnoses
Ask of anything has been overlooked (eg, intravenous access
should have been obtained or d rugs should have been
administered)

Team members
I• Share in formation with o ther team members

Don't
Team le ader • Ignore others' suggestions for treatment
• Overlook or fad to examine clinical sign s that are relevant to
the trea tment

Team members • Ignore important Information to Improve your rote

Summanzmg and Reevaluating

An essen11a1 role o f the team lead er os monitoring and reevaluating

• The pa tient's status

• Interventions that have been performed
• Assessment findings
A good practice os for the team leader to summarize this 1nformatton out loud 1n a penod1e
update to the team. Review lhe status of the resusc1ta t1on a ttempt and announce the plan
for l he next few steps. Remember that the p atient 's cond1t1on can change. Remain flexible
to chonglng treatment p lans and revisiting the ln111a1 differential doagnos.s. Ask for in forma-
tion and summanes from the timer/ recorder as well

Team le ader • Draw conbnuous attention to decisions about d1fferent1al

diagnoses
• Review or maintain an ongoing record o f drugs and trea t-
ments administ ered and the patient's response

Team leader and • Clearly draw attention to significant changes In the patient's
team members chnieal coodlll<>n
• Increase momtonng (eg, frequency ol resplrations and blood
pressure) when the pat ient's condlllon d etenorates

Don't
Team leader • Fail to change a treatment strategy when new 1nforma11on
supports such a change
• Fail to inform amvrng personnel o f the current status and
plans for further action

30
 Effective High-Performance Team Dynamlca

How to Closed-Loop Communications

Communicate
When COITllTlUOICaWlg w tll l'llgll perlonnance team members. t~ •earn eader should use
closec:Hoop comrm.ncat.on by tak ng tlleSe steps:

1 The team leader gives a me5sage O<der. or as51gnment to a team member

2. By receiving a clear response and eye contact. the team leader confirms that the
team member heard and understood the message.

3. The team leader listens for confirmation of task performance from the team member
bef0<e aSS19ning another taSk

Team leader Assign another task after rece<V1ng oral conhrmauon that e
ta.. k has been completed. such as. "Now that the IV 1s 1n,
give 1 mg of ep1nephnne"
Team members • CloM the loop: lnfonn the team leader when a task beg ns
or ends, suc:h is. "The N is m•

Team leader • Gve more laSks to a team memoer w1U'lout asking °' recetv!ll9
coof1tmat1011 of a completed assignment
Team members • G1 ve drugs without vertJally confirming the Older with the
te;im leader
• Forget to Inform the team leader after giving the drug or per-
forming the procedure

Clear Messages

Clear messages consist of concise communocatJon spoken w.tn d1stmct1'e speech 1n a

contrOlled tone of voice All hea theare providers should dei•vlll' messages and orders 111
a calm and direct manner wotnout yelling or shouting. Unclear commun>eatJOn can lead to
unnecessary delays 1n treatment or to med1cauon errors.

Yet 1ng or shouting can 1mpa1r ettect•ve high-performance team 1n'.eractJOn. Only one po<·
son Should talk a1 any time

Team leader • Encourage team members to speak cle.lffy

Team members • Rel)83t the medication order

I • Question an order if the slightest doubt exl sts

Don't
Team leader • Mumble or speak 1n ncomplete sentences
• Give unc; ear messages and drugimedoeatJOn orders
• Veit scream or ShoU1

Teammemben • FMI petronozed by <fisunct and c:oncise messages

31
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-1oheQ· t1Q1r1 s 9vsr1 oT .19nn&m evonoqque ,l&1gelloo s no 15r1lsQOJ >how bns wrllo rloss 101
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.9vsr1 '(Srn e1edmem mse! ooli:ieqe

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'(116olono boole

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S:C
 The Systematic Approach

Introduction Healthcare providers use a systematic approach to assess and treat arrest and acutely Ill
or 1n1urecl pahents for optimal care. The goal ol 1he high-performance 1oam's Interventions
for a p3ttent 1n respiratory or cardiac arrest 1s to support and restore ettectrve oxygenauon.
venlllauon. and c1rculat1on with relum of rntact ne\Jrologic funcnon. An 1ntennediate goal of
resusc1tat10n IS return of spontaneous circulauon (AOSC). The actions used are guided by
the following systematic approaches:
• BLS Assessment
• Primary Assessment (A. B. C. D. and El
• Secondary Assessment (SAMPLE. H's and rs)

The Systematic Approach

Overview of A fte-r determinabon of scene safety, the systematic approach (Figure 61 hrst requires ACLS
the Systematic providers to determine the patient's level of consciousness. As you approach the patient,
Approach If the patient appeatS unconsc10Us
- Use the BLS Assessment for the initial evalunhon
- Alter completing all or the appropriate steps of the BLS Assessment, use the
Primary and Secondary Assessment s for more advanced evaluallon and treatment
• II the patient appears conscious
- Use the Pnmary Assessment for your initial evaluation
Before conducting these assessments, make sure the scene is safe.

33
 Part 0
The Systematic Approach

Initial Impression
(Provider visually
checks while
approaching patient)

(l Conscious Patient
Unconscious Patient
(appearance) (appearance)

• .... •
BLS Assessment Primary Assessment

• Secondary Assessment

The detaJ s of lne BLS Assessment and Primary and Secondary Assessments are
oesGf bed beloN

The BLS Asse11ment

Foundational Fac t• Starting CPR When You Are Not Sure About a Pulse
If you are unsure about the p<esen<:e of a pulse. begin cycles of compr8SSlons and ventt·
lotions. Unnecessary compressions are less harmful than railing to provide compressions
whrn needed Delaying or railing to start CPR in a patient without a pulse reduces the
c;h.1nce 01 survival

34
 The Systematic Approach

Overview of the The BLS Assessmen1 1s a systematic approach to BLS that any 1ralned healthcare pro-
BLS Assessment vider can perform. This approach stresses early CPR and early deflbnllaUoll II does not
include advanced 1nterventJons. such as advanced airway techniques or drug admonostra-
tion. By using the BLS Assessment, healthcare p1oviders may achieve their goal or sup-
porting or restoring etteclive oxygenation. vent ilation. and circulation until ROSC or Initia-
tion ol ACLS Interventions Perlorm1ng the actions on the BLS Assessment substantially
improves the patient's chance of survival and a gooo neurologte outcome.

Remember: Assess ... then perform appropnate action.

Caution Agonal Gasps

• Agonal gasps are not normal breathing. Agonal gasps may be present in the first m in-
utes alter sudden cardiac arrest.
• A patooot Who gasps usually looks like he is drawing air 1n very quickly The mouth
may be open and the 1aw ttead, or neck may move wrth gasps Gasps may appear
forceful or weak. Some time may pass between gasps because they usually happen at
a slow rate. The gasp may sound like a snort, snore. or groan. Gasping is not normal
breathing. It is a sign of cardiac arrest.

Although the BLS Assessment requires no advanced equipment. healthcare providers can
use any readtly avatlabte universal precaut ion supplies or adjuncts, such as a bag-mask
vent ilahon device. Whenever possible, place the pahent on a firm surface 1n a supine posi-
tion to max1m1ze the effectiveness of chest compreSStons. Table 2 os an overview of the
BLS Assessment. an<! Figures 7 tlirOoQl'I 11 tllustra!e the steps needed dunng 11\e BLS
Assessment. Before approaching the patient, ensure scene safety. A rapid scene survey
should be performed to determine Ir any reason exists not to in1t1ate CPR. such as a threat
to safety or the provider.

=
fiiii'll For more details. watch the Hogh-Qualrty BLS video on the Student Website
(www.heart.org/eccstudent)

38
 P a rt 0
Table 2 . The BLS A ssessment

Assess I Assessment Technique and Action :

Check • Tap and shout, "Are you OK?"

responsiveness

Shout for nearby help/ • Shout for near'by help

activate the emergency
response system and get
the AEO/delibrillator
• Activate the emergency response system
• Get an AED If one os available. or send
someone 10 activate the emergency
response system and get an AED or
def1brltlator

l''lJure 8. Shout fot ~ helplacwa•o the

""""1l"f1C responso sysl em/ge1 81' AEO

Chec k breathing • Check for absent or abnormal breathing

and pulse (no breathing or only gasping) by looking at
or scanning the chest for movement lor
about 5 to 1O seconds
Ideally, the pulse check is performed
simultaneously wUh the breathing
check to minimize delay in detection
of cardiac arres t and initiation of CPR
• Check pulse for 5 to 10 seconds
• If no pulse within 1O seconds, start CPR. Fl9ure 9. Choe:~ brnalhlng and pul'o
beg1nn1ng with chest compressions 11mui1aneous1y

• If there 1s a pulse. stan rescue breath ng

at 1 breath every 5 to 6 S<eCOnds Check
pulse about every 2 minutes

F1 gure 1o . Cl""'""1g a carotid ,,.,...

Defibrillotlon • If no pulse, check for a shockable rhythm

with on AED/defibrillator as soon as II
amves
• Provide shocks as indicated
• FollOw each shock 1mmed1atefy wnh CPR,
beg1nn1ng with compressions

36
 The Systematic Approach

Critical Concepts Minimizing Interruptions

ACLS providers must make overy offort to minimize any intotruptions in chest
c ompressions. Try to hm1t Interruptions in chest compressions (eg, def1brillation and
rhythm analysis) to no longer than 10 seconds, except In extreme circumstances, such
as removing the patient from a dangerous enVlronment. When you stop chest compres·
SIOOS blOod flow to the brain and heart stops. See Figure 12

Avoid:

• P,()j()O iged rhythm aflatySIS

• Fniqvent or ff'lilPP'0ll'l3te pu -. Checks
• Toking too long to give breaths to the patient
• Unnocessarily moving the patient

Comprualone

~~~~ ~, 1 1 ~1 1 1 1 1 1 1 1 1 1 1 ~--=-~
, 1 1 1 1 1 1 1 1~1 1 1 1 1
Coron..1ry perlusion pressure (CPP) is oortic relaxa11on (~d1astohc1 pressure minus nght
otr1ol relaxation ("diastolic") pressure Dunng CPR, CPP correlotos with both myocardial
blood flow and ROSC. In 1 human study. ROSC did not occur unless a CPP of 15 mm Hg
or gremer was achieved during CPR

Crltlclll Concepts Quality Compressions

• ComP<9S$ the chest at least 5 cm

-
• ComP<9S$ the chest at a rate of 100 to 120/min.
• Allow complete chest recall ofter each compression

Founda tional Facts Chest Compression Depth

Che!'\ compresSOlS are more tten too stiariow man 100 deep Howe.er research
sug<,je$!S that compres$1011 oepth greeter than 6 cm in adu ts may not l>e DPtJma1 for
~di from cardiac atT8S1 dlld may cause lnjUfleS If you ha•• a CPR Qual ty feedback
devic.... 1t 1s optimal to target your cornp<eSSIOll depth from 5 to 6 cm

37
 ---

p art 0

Foundational Facts Single Healthcare Provider May Tailor Response

• Single healthcare providers may tatlor the sequence o f rescue actions to the most
likely c ause o f arrest. For example, if a lone healthcare provider sees an adolescent
suddenly collapse, rt 1s reasonable to assume that the patient has su ffered a sudden
carchac arrest.
• A single rescuer should call for help (activate the eme<gency response system), get an
AED r11 nearby). return to the patient to attach the AED. and then proVJde CPA.
On the other hand. 11 hypoi<iil is the presumed cause of the cardiac arrest (such as 1n
a drowning pauent). the healthcare proVlder may g111e approxmately 2 minutes of CPR
before acuvat1ng the emergency response system

Critical Concepts High-Quality CPR

• Comp1ess the chest hard and fast.
• AllOw complete chest recoil after each compression.
• M1mmize interrupboflS in compresslOl'IS (1O seconds or less).
• AvOld excessrve ventdauon.
• Switch compressor about every 2 minutes or eart1er II fa11gued:

The Primary Assessment

Overview of For unconSCIOUS patients 1n arrest (card;ac or resp<ralory).

the Primary • Healthcare providers Should conduct the Pnmary Assessment after completing the
Assessment BLS Assessment.
For conscious pa!Jents who may need more advan ced assessment and management
techniques:

• Healthcare providers should conduct the Primary Assessment first.

In Ille Primary Assessment. you continue to assess and per1orm an actJon as appropriate
until transfer to the next level of care Many bmes. mem~ of a high- performance team
perlorrn assessments and actions 1n ACLS simultaneously

f:lemember: Assess ... then perform appropnate action.

Table 3 provides an overview of the Primary Assessment.

38

Ta ble 3 . The Primary Assessment
-
Assess
Airway
• Is the airway patent?
• Is an advanced airway
indicated?
• Is proper placement of air·
way device confirmed?
• Is tube secured and place-
ment reconfirmtKI frequently?
Breathing
• Are ventilation and oxygen·
ation adequate?
• Ate quan111awe waveform
capnography and oxyhemo·
globln saturation monitored?
Circulation
• Ar9 chest compressions
effective?
• What IS the cardiac rhythm?
• Is def/bnffation or carcf10ver-
sion Indicated?
• Has /V/10 access been
establtShed?
• Is ROSC present?
• Is the patient with a pulse
ur.stable?
• Ate medications ~ for
rhythm or blood pressure?
• Does the patient need vol-
ume /fluid} for resuscitation?
Oisab1lity
Exposure
PETCO, is the pan1al pressure of CO: on exhaled air a1 the end of the exhalation phase
The Systematic Approach
Action as Appropriate
• Maintain airway patency in unconscious patients by use of the head btt~ lrf\,
orophal)'T19eal airway, or nasopharyngeal airway
• Use advanced airway management If needed (eg. laryngeal mask airway, laryngeal
ttibe, esophageal-tracheal tube, endotracheal tube)
Healthcate pro'liders must weigh the benefit of advatteed airway placement against tJ:e
adverse effects of interrupting chest compressions. If bag-mask ventilation 1s adequate,
neailhcare providers may defer Insertion of an advanced airway untll the patient does
not respond to lflltJal CPR and defibnllatlOfl or unlJI spontaneous citculallOfl returns.
Advanced airway d&Vlces such as a laryngeal mask airway. laryngeal tube, or esopha·
geal-tracheal tube can be placed while chest compressions continue.
If USH'lg advanced airway devices:
• Confirm proper integration of CPR and ventilation
• Connrm proper placement of advanced airway devices by
- Physical euminatlon
- Ouantilawe waveform capnogrophy
• Secure the device to prevent dislodgment
• Monitor airway placement with continuous quantitative waveform capnograplty
• Give supplementary oxygen when Indicated
- For cardiac arrest patients. administer 100% oxygen
- For others, htrate oxygen administration to achieve oxygen saturation values ol
94% or greater by poise oximetry
• Monitor the adequacy of ventilallon and oxygenation by
- Clinical c riteria (chest nse and cyanosis)
- Ouanmauve waveform capnography
- Oxygen sa1ura11on
• Avoid exc,e ssive ventilation
• Monitor CPR quality
- Ouan11tat1ve waveform capnography (~PETCO, is less than 10 mm Hg, attempt
10 improve CPR quality)
- lntra·artenaJ pressure (11 relalcation phase [diastolic] pressure ls less than
20 mm Hg, attempt to Improve CPR quality)
• Attach monitor/defibrillator for antlythmlas or cardiac arrest rhythms (eg. ven-
tricular fibrillation [VF]. pulseless ventricular tachycardia [PVTJ. asystole, pulseless
electrical actJv11y [PEAD
• Provide defibrillatlo n/cardioversion
• Obtain IV/10 access
• Give appropriate drugs to manage rhythm and blood pressure
• Give IV/10 ftuids If needed
• Check glucose and temperature
• Check perfusion Issues
• Check for neurologic function
• Oulc kly assess for responsiveness, levels of consciousness, and pupil dilation
• AVPU: Alert, Voice, Painful. Unresponsive
• Remove clothing to perform a physical examination, looking for obvious signs
of trauma, bleeding, burns. unusual markings, or medico! alert bracelets
39
 -

Part 0
The Secondary Assessment

Overview of The Secondary Assessment involves the d1tferontlal diagnosis. Including a focused medl·
th e Secondary cal history and sean:1>1ng fly and treating underlying causes (H's and T'sl Gathenng a
Assessment focused htStory of the pa1>e<1t IS recommended Asil specific qoes!Jons related to the
patients pr'1sentation Consider using the melTlO')I aid SAMPLE:

S gns and symptoms

~ "'!! ~

M edicatoons l1""1udong ti'• ast do • "'"""'

Past medical hista<y (especially 1etat ng to !tilt current Illness)
Last meal consumed
Events
The answers to t hese quest ons can help you quickly rule In or rule out suspected diagno-
ses Look lor and treat the under1y1ng cause by considering the H's and rs to ensure you
are not 011erloolun9 a dangerous or likely po~"'bt11ty The H's and rs create a road map for
posSlble diagnoses and interventions for your patient.

H 's a nd T's Table 4 shOws the potential reversible causes of catd1ac arrest as welt as emetgeney
cardiopolmc nary cond tJOnS (H's nnd T's) The ACLS cases. provide ~tails on
these components

PEA tS associa1ed v. th ll13l1'f cond ~ Hflalthcate providets should memonze the ltSt
of common causes 10 1<eep from overtoo11.ng an oo,110US cause of PEA that mogti: be
reversed by appropriate 1re:nmen1

The most common causes of cardiac arrest are presented as H's and T's 1n the
1ao1e be4ow

Table 4 . The M ost Comm~n Cousos o f Cardiac Arrest

H '• I T..
Hypovolemta Tension pneumolhorax
Hypoxia T amponade (cardiac)
Hydrogen ion (acidosis) ToXlns
H'fPO- lhypet'ka,em a Thrombosis I pulmonary)
H ypothemla Tlvombos.s {Corooary)

Critical Concepts Common Underlying Causes of PEA

• Hypovo1~m1a and hypoxia are tho ;> most common underlying and potentially revors1ble
causes of PEA.
• Se sure 10 look for evtderice ot t'-9 ptObloms as you assess the patoont.

40
 The Systematic Approach

Diagnosing and Treating Underlying Causes

Introduction Patients 1n cardiac arrest (VFlpVT/ asystole/PEA) need rapid assessment and management.
Cardiac arrest may be caused by an underlying and potentially reversible problem. If you
can quickly identify a specific condition that has caused or 1s contributing to PEA and cor-
rect 1t, you may achieve ROSC. The Identific ation of the underlying cause is or paramount
importance 1n cases of PEA and asystole.

In the search for the underlying cause, do the following:

• Consider frequent causes of PEA by recalling the H's and rs

• Analyze the ECG tor clues to the underlying cause
• Recognize hypovolemia
• Recognize drug overdose/poisonings

Conditions and The H's and T's are a memory aid for the most common and poten11ally reversible causes
Management of perlarrest and cardiopulmonary arrest (Table 4).

Hypovolemia Hypovofemia. a common cause of PEA. initially produces the classic phys10logic response
of a rapid, narrow-complex tachycardoa (S111Us tachycardoa/ and typically produces
increased diastolic and decreased syst011c pressures. As toss ol blood volume conbnues,
blood pressure drops. eventually becoming undetectable, but the narrow ORS complexes
and rapid rate contmue Oe. PEA).

You should consider hypovolemla as a cause ol hypotension, which can deteriorate to

PEA. Providing prompt treatment can reverse the pulseless state by rapidly correcting
the hypovotemia. Common nontraumatic causes of hypovolemla include occult internal
hemOfrtiage and severe dehydration Consider volume infusion for PEA associated with a
narrow-comp4ex tachycardia

Cardiac and Acute coronary syndromes 1nvolVlng a large amount of heart muscle can present as PEA
Pulmonary That is. occlusion of the left main ()( proximal left antenor descending coronary artery can
Conditions present with cardiogenic shock rapidly progressing to cardiac arrest and PEA. However, in
patients with c ardiac arrest and without known pulmonary embolism (PE), routine fibrino-
lytlc treatment given dunng CPR shows no benefit and is not recommended.

Massive or saddle PE obstructs flow to the pulmonary vasculature and causes acute right
heart failure. In pabents with cardiac arrest due 10 presumed or known PE. it is reasonable
to administer fibrinolytlcs.

Pencard1al tarnponade may be a revers.ble condition. In the per1arrest period. volume !Illu-
sion 1n this cond1t1on may hep while definitive therapy is lni1iated. Tension pneumothorax
can be effectively treated once recognized.

Note thot cardiac tarnponade, tension pneumothorax, and massive PE cannot be treated
unless recognized. Bedside ultrasound, when performed by a skilled provider, may aid In
rapid tdenhlication of tamponade and PE. There 1s growing evidence that pneumothorax
can be Identified by using bedside u11rasound as well. Treatment f()( cardiac tamponade
may require pericardJocentesis. Tension pneumothorax reqwes needle aspiration and chest
rube placement. These procedures are beyond the scope of the ACLS Provider Course.

41
 Part 0
Drug Overdoses or Certain drug overdoses and toxic exposures may lead to peripheral vascular dilatation
Toxic Exposures and/or myocardial dysfunction with resultant hypotension. The approach to poisoned
patients should be aggressive because the toxic effects may progress rapidly and may be
of limited duration. In these situations, myocardial dysfunction and arrhythmias may be
reversible. Numerous case reports confirm the success of many specific limited interven-
tions with one thing In common: they buy time.

Treatments that can provide this level of support include

• Prolonged basic CPR in special resuscitation situations

• Extracorporeal CPR
• Intra-aortic balloon pumping
• Renal dialysis
• Intravenous lipid emulsion
• Specific drug antidotes (digoxin immune Fab, glucagon, bicarbonate)
• Transcutaneous pacing
• Correction of severe electrolyte disturbances (potassium. magnesium,
calcium, acidosis)
• Specific adjunctive agents

Remember, if the patient shows si gns of ROSC, post-cardiac arrest care should
be initiated.

42
 The ACLS Cases

Overview of the Cases

The ACLS Stmulated cases are designed to review tl'>e knOwledge and skills you need to
successfully participate in COLtSe events and pass the Megacode skills test Each case
contains th9 following topics:
• lntroductlOO
• Rhythms and drugs
• Descriptions or definitions of key concepts
• OveMew of algonthm
• Algorithm Rgure
• Application of the algorithm to the case
• Otner related top•CS
This part contains the following cases:
• Respiratory Arrest
• Acute Coronary Syndromes
- STEMI
• Acute Stroke
• Cardiac Arrest
- VF/Pulseless VT
- Asystole
- PEA
Bradycardla
• Tachycardia {Stable and Unstable)
• Immediate Post-Cardiac Arrest Care

43
 Part 0

Respiratory Arrest Case

Introduction This case reviews appropoate assessment. 1nteNentlOl'I, and management options 10< an
unconscious. unresponsive ~dult patient m respiratory arrest. Respirations are completely
absent or clearly lnadequare to maintain effective oxygenation and ventilation. A pulse 1s
present (Do not confuse agonal gasps wrth adequate resp1ratlOllS.) I he BLS ASsessment
and the Pnmary and Secondary Assessments are used even though the patten! is 1n
respiratory arrest and nol in cardiac arrest.

Case Drugs This case involves the following drugs:

• Oxygen
Systems 0< lac11itJes using rapid sequence 1ntubatJOn may consider add'rttonal drugs.

Normal and The average respiratory rate for an adult is about 12 to 16/mrn. N0<mal tidal volume of
Abnormal 8 to 1Omllkg mamtruns normal oxygenauon and elimination ot CO,.
Breathing Tacnypnea is a respiratory rate above 20/mln and brodypnea is a respiratory rate below
12/mm. A respiratory rate below 6/mm (hypovenblat1on) requires assisted venblation w1tll a
bag-mask device or advanced airway with 100% oxygen.
~~~~~~~~~~~~~~~~-

Identification of lden1Jfylng the seventy of a resp11atory problem will help you decide the most approp<1ate
Respiratory Problems 1nt81'Vent1ons. Be alert 10< signs of
by Severity • Respiratory distress
• Respiratory failure

Respiratory Distress Respiratory distress is a cltnical state characterized by abnormal respiratory rate (eg,
tachypnea) or effort. The respirate<y effO<t may be increased (eg. nasal flanng retractKlflS.
and use ol accessory muscles) 0< Inadequate (eg, hypoventilahon or bradypnea).

Respiratory distress ~n range from mild to severe. For example, a patient with mold
taehypnea and a mold increase 1n respiratory effort with changes rn rurway sounds is on
mild respiratory distress. A patient with marked tachypnea, slgrnf1cantly Increased resplfa·
tory effort. deterioration 1n skin color, and changes in mental status is 1n severe resplfatory
distress Severe resptratory distress can be an rndicauon of resplrate<y frulure.

Clrnocal signs of respiratory distress typically Include some or all of the following:
• Tachypnea
• Increased respiratory effort (eg, nasal nanng, retractions)
• Inadequate respiratory effort (eg , hypoventilation or bradypnea)
• Abnormal rurway sounds (eg, stridor, wheezing. grunting)
• Tachyc.~rd1a
• Pale, cool skin (note that soma causes of respiratory distress. like sepsis, may cause
the skin to get warm. red, and d1aphoret1c)
• Changes 1n level of consc1ousness/agotat1on
• Use of abdominal muscles 10 assist In breathing
These indicators may vary in severity.

Resplfa1ory dosttess 1s apparent wl'len a patient tnes to maintain adequate gas excl'lange
d espite aJrway o bstruction. reduced lung complmncA. o r lt1no tissuA <ii~easFt. A~ thA
patient 11res or as respiratory function or eHOrt or both deteria<ate. adequnte gas exchange
canoot be maintained When this happens. cltn1cal signs of respiratory failure develop
-- - - - -- -- -- - - -
 The ACLS Cases: Respiratory Arrest

Respiratory Failure Respiratory failure is a clinical state of inadequate oxygenation, ventilation, or both.
Respiratory !allure is often the end stage of respiratory distress. If !here as abnormal cen·
tral nervous system control of breathing or muscle weakness, the patient may show little
or no respiratory effort despite being in respiratory failure. In these situations, you may
need to identify respiratory failure based on clinical findings. Confirm the diagnosis with
objective measurements, such as pulse oximetry or blood gas analysis.

Suspect probable respiratory failure if some of the following signs are present:

• Marked tachypnea
• Bradypnea. apnea (late)
• Increased, decreased, or no respiratory effort
• Poor to absent distal air movement
• Tachycardia (early)
• Bradycardia (late)
• Cyanosis
• Stupor, coma (late)
Respiratory failure can result from upper or lower airway obstruction, lung tissue disease,
and disordered control of breathing (eg, apnea or shallow. stow respirations). When respi·
ratory effort is inadequate, respiratory failure can occur without typical signs of respiratory
distress. Respiratory failure is a clinical state that requires intervention to prevent deterio·
ration to cardiac arrest. Respiratory failure can occur with a rise an arterial carbon dioxide
levels (hypercapnia}, a drop in blood oxygenation (hypoxemia). or both.

Respiratory Arrest Respiratory arrest is the cessation (absence) of breathing. Respiratory arrest is usually
caused by an event such as drowning or head injury. For an adult in respiratory arrest,
providing a tidal volume of approximately 500 to 600 m l (6 to 7 mUkg) should suffice.
This is consistent with a tidal volume that produces visible chest rise.

Patients with airway obstruc tion or poor lung compliance m ay require high pressures to
be properly ventilated (to make the chest visibly rise). A pressure-relief valve on a resus-
cit ation bag-mask device may prevent the delivery of a sufficient tidal volume in these
patients. Ensure that the bag-mask device allows you to bypass the pressure-relief valve
and use high pressures. if necessary, t o achieve visible chest expansion,

Excessive ventilation is unnecessary and can cause gastric inflat>on and i1s resultant
compllcations, such as regurgit ation and aspiration. More important, excessive ventila-
tion can be harmful because it increases intrathoracic pressure, decreases venous return
to the heart, and diminishes cardiac output and survival. Healthcare providers should
avoid excessive ventilation (too many breaths or too large a volume) during respiratory
arrest and cardiac arrest.

4S
I
Part 0
The BLS Assessment
When evaluating a patient, proceed with the BLS Assessment after determining that the
scene is safe as described on " Part 4: The Systematic Approach."

Assess and The systematic approach is assessment, then action, for each step in the sequence.
Reassess the
Patient Remember: Assess .•. then perform appropriate action.
In this case, you assess and find that the patient has a pulse. so you do not use the AED
or begin chest compressions.

Ventilation and In the case of a patient in respiratory arrest with a pulse. deliver ventilations once every
Pulse Check 5 to 6 seconds with a bag- mask device or any advanced airway device. Recheck the
pulse about every 2 minutes. Take at least 5 seconds but no more than 1 D seconds for
a pulse check.

The Primary Assessment

Airway If bag-mask ventilation is adequate, providers may defer insertion of an advanced airway.
Management Healthcare providers should make the decision to place an advanced airway during the
in Respiratory Primary Assessment.
Arrest Advanced air11ay equipment includes the laryngeal mask airway, the laryngeal tube, the
esophageal-tracheal tube, and the endotracheal (El) tube. If It is within your scope of
practice, you may use advanced airway equipment in the course when appropriate and
available.

Ventilations ln this case, the patient 1s in respiratory arrest but continues to have a pulse. You should
ventilate the patient once every 5 to 6 seconds. Each breath should take 1 second and
achieve visible chest rise. Be careful to avoid excessive ventilation (too many breaths per
m inute or too large a volume per breath),

FYI 2015 Guidelines Correct Placement of ET Tube

The AHA recommends continuous waveform capnography in addition to clinical assess-
ment as the most reliable method of confirming and monitoring correct placement of an
ET tube.

48
 The ACLS Cases: Respiratory AnMt

Management of Respiratory Arrest

Overview Management of respiratory arrest includes both BLS and ACLS 1nterven1JOl\s These inter·
vent1ons may include

• Giving supplementary o>tygen

• Opofll19 !he a11Way
• Providing baSIC ven11lal100
• Using bask: airway ad1uncts (OPA and NPA)
• Sucootwlg

According to the 2015 AHA Guidelines Update for CPR and ECC. tor
patients wrth a perlusing rhythm, ventilations should be delivered once
every 5 to 6 seconds.

Critical Concepts Avoiding Excessive Vent ilation

When using any fO<'m of assisted vont1lat1on. you must avoid def1venng excessive venhla
lion (loo many breaths per minute or too large a volume per breath) Excessive ventda
tooo can be hatmful because t •ncreases imratnoracoe P<essute. decreases •eooos return
10 the llean, and 01m1n.shes cardiac output It may also cause gastnc onflation and pre
dispose the patient to vomiting and aspirat•Ol'I of gastric contents tn addition. hyper·
ventilation may cause cetebral vasocoostrlction, reducing blood llow to tlwl brain.

Giving Supplementary Oxygen

----·---
Maintain Oxygen Give oxyqen 10 patients with a~ute c111diac symptoms or respiratory d1stre!.!l
Saturation MonolO< oxygen saturauon and titrate supplementary oxygen to ma nlaln a satu·
1

ration or 94% or greater. For P3tlents In respiratory or cardiac arrest. stnv1ng for
100% oxygen w01Jtd be more approprlnte.

See the Stuoent Websl1e (www.heart.org/eccstudentl for detaJls on

use of oxygen on pat1e1ts not In respiratory or cardiac arrest.

Opening the Airway

-----
Common Cause Figure I 3 demoflstrates the anatomy of the Btrway The most convnon cause of upper
of Airway a rway obstruet100 •n the UOCOOSCIOUS/unmpons.ve pa1>ent is IOSs of tone 1n the throat
Obstruction muscles In this case, the tongue falls back and occludes the airway at the levol ol the
phatynK (Figure t 4A).

Basic Airway Basic nlrway opening techniques win ettecuvely reheve airway obstruction caused eit her
Opening by the tongue or from relaxation of muscles In the uppe< airway. The basic airway open
Techniques 1ng t e<:hrnque IS head ~it with ameoor d•sptacement of the mandible, ie head bit-chin lift
(Figure t 48).

tn the trauma patent w•lh suspected nee< ln1ury use a iaw thruSt wrthout head extension
1Fogutt I 4CI Because mainta.tw>g an open a ""ay and orovoel ng •en' lal!Otl as a pnonty
use a nead 1d1-ch1n lift manetl\er of the 1aw thrust does not open the airway ACLS provid-
ers SllOuld be aware that current BLS training courses leach the aw·thrust technique t o
hea11ncare prov1ders but not 10 lay rncuers
- --- ------- --- ----- - -- -- - - - - ---
 Part C)

Airway Proper airway posmoning may be all that tS required f0< patients who can breathe spon-
Management taneously. In patients who are unconscious wrth no cough or gag reflex. Insert an OPA or
NPA to maintain airway patency

II you frnd an unconsc1ous/unrespons1ve pa11ent whO was known 10 be choking and 1s

now unresponsive and In respiratory arrest. open the mouth wide and look for a foreign
Oob1ect. If you see one remove 1t with your fu">gers. If you do not see a lore19n ob1ect. begin
CPR. Each time you open the airway to give breaths. open tt>e mouth wide and took for
a foreign ob1ect. Remove rt wit h your fingers 1f present. If there 1s no foreign object,
resume CPA

Tongue

Vocal Fold
(Cords) - - - - - - - - -
Thyroid
Cartila9"
Cricoid
CartiJage~------""----":-

T- ----------!:-4~

Esophagu1 - - - - - - - -- -7- --'-;;i-.;..-- + ,

48
 The ACLS Cases: Resplratoty Airest J

A B c
Figure 14. Obstruction of the airway by the tongue and epiglottis. Whoo a patient is unfesponsive, the wngue can obstrvct the airway. nie head
ttlt-chln lifl relreves obstrvction I.I\ 0'1e unresponsive patient. A. The tongue is obstructing the airway. 8 , The head tilt-chin lift lifts the tongue. tobev
4

ing the obstruction. C, tf cclVical spine trauma Is suspected, hea1rhcafe pl'ovider'S shovld us.& th-e jaw 1hn.rs1 Without head e.xten~on.

Providing Basic Ventilation

Basic Airway Skills Basic airway skills used to ventilate a patient are

• Head tilt-chin lift

• Jaw thrust wlthOut head extension (suspect ed cervical spine trauma)
• Mouth-to-mouth ventilation
• Mouth-to-nose ventilation
• Mouth-to-barrier device (using a pocket mask) ventilation
• Bag-mask ventilation (Figures 15 and 16)

Bag-Mask A bag-mask ventilation device consists of a ventilation bag attached to a face mask.
Ventilation These devices have been a mainstay of emergency ventilation for decades. Bag-mask
devices are the most common method of providing positive-pressure ventilation. When
using a bag-mask device, deliver approximately 600 ml tidal volume sufficient to produce
chest rise over 1 second. Bag-mask ventilation is not the recommended method of venti·
lation for a single healthcare provider during CPR. (A single healthcare provider should use
a pocket m ask to give ventilation, if available.) It is easier for 2 trained and experienced
rescuers to provide bag-mask ventilation. One rescuer opens the airway and seals the
mask to the face while the other squeezes the bag, with both rescuers watching for visible
chest rise.

The 1,mlversal connections present on all airway devices aUow you to connect any ventila-
tion bag to numerous adjuncts. Valves and ports may include
• One-way valves to prevent the patient from rebreathmg exhaled air
• Oxygen ports for administering supplementary oxygen
• Medication ports for administering aerosolized and other medications
• Suction ports for clearing the airway
• Ports for quantitative sampling of end-tidal co,
You can attach other ad1unc1s to the patient end of the valve, including a pocket face

=
mask, laryngeal mask airway, laryngeal tube. esophageal-tracheal tube, and ET tube.

fiii1 See the Student Website (www.heart.org/ eccstudent) for more infonmation on
bag-mask ventilation.

49
I Part 0

Figure 1e. E-C clamp teohnoque for holding ine mask while llft1n9 IJle jaw. Position
yowself at the patient's head. Ci~clc tho thumb and first finger around the top ot the mask
{forming a "C") while using the tMrd. fourth, and fihh fmgers (f0<m1ng an "E") 10 lift rhe jaw.

Figure 16. TwO-ffi$Cuer use of the bag-mask c:!cvioo. The rescuer at the pabent's head tilts
the pahfmt's liead and seals the mask aga1ns1 me pa11enrs tace. with the thumb and fifst
finger of each hand creating a "C," co provide a complete seal aroulld the ooges of me rl'lask.
TOO rescuer use.s the 1ema ning 3 fingers (the "'E") to hft the law (lh1S hokls the airway open).
The second rescuer slowly squeezes the ba9 (over 1 second) until the chest rises. Both
providers should obSO<Ve chest rise.

!50
Basic Airway Adjuncts: Oropharyngeal Airway

Introduction The OPA tS used 1n patients who are at nsk tor developing airway obstrtJCtl0<1 from the
tongue or from relaxed upper airway muscles This J -shaped device (Figure 17A) fits over
the tongue to hold it and the sott hypopharyngeal structures away from the posterior wall
of the pharynx.

The OPA IS used 1n unconsclOUs patJents 11 procedures to open the arrway (eg, head tih-
ch111 lift or law thrust) fail to provide and maintain a clear, unobstructed airway An OPA
shof.Jld not be used Ina conscious or semiconscious patient because it may st imulate
gagging and vomiting. The key assessment is to c heck whether the patient has an intac t
coug h and gag reflex. If so. do not use an OPA

The OPA may be used to keep the airway open during bag-mask ventilation when provid -
ers m ight unknow ingly push down on the c hin, blocking the airway. The OPA Is also used
during suctioning of the moulh and throat and in intubated patients to prevent them from
brt1111g and occluding the ET tube.

Te chnique of Step Action

OPA lnserllon
Clear the mouth and pharynx of secretions , blood. or vomit by using a rigid
pharyngeal suction tip ii possible
•
Select the proper size OPA. Place the CPA against the side of lhe lace (Figure
178). When !he ft~ or the OPA Is at the CO<"ner of the mou1h. the tip is at
the angle of the mandible. A property sized and inserted OPA results 1n proper

•
alignment with the glottic opening .

Insert the OPA so that 1t curves upward toward the hard palate as 1t enters
the mouth
As the OPA passes through the oral cavity and approaches lhe posterior
wall ol the pharynx, rotate it 1so•
Into the proper position (Figure 17C). The
OPA can also be inserted at a 90• angle to the mouth and then turned down
toward the poslenc)( pharynx as n tS advanced. In both methods, the goal is
to curve the device around the tongue so that the tongue is not inadvertently
pushed back into the pharynx rather than be-ing pulled forward by the OPA.

An alternative method is to insert the OPA straight In while using a tongue

depressor or S1m1lar device to hold the tongue forward as the OPA is
advanced.

After insertion of an OPA, m onitor the patient. Keep the head and jaw positioned properly
to maintain a patent airway Suction the airway as needed

Caution Be Aware of the Following When Using an OPA

• OPAs that are too large may obstruct the larynx or cause lrauma to the laryngeal
structures
• OPAs that are roo small or inserted 1mproper1y may push the base of the tongue
posteriorly and obstrtJCt the airway.
• Insert the OPA carefully to avoid soft 11ssue trauma to the lips and tongue
Remember to use the OPA only 1n the unresponsive patient with no cough or gag f9flex. If
the patient has a cough or gag reflex. the OPA may stimulate vomiting and laryngospasm

51
 Part 0

c
Flgure 17 O<opnaryngeal rurwo,a A, Orophary~ a.rway devlcn 8, OropharynQeaJ ol!way device
............,_,L C,~ """'Y device ._,OCI
52
 The ACLS Cases: Respiratory Arrest

Basic Airway Adjuncts: Nasopharyngeal Airway

Introduc tion The NPA Is used as an altem abve to an OPA 1n patients who need a baSlc airway manage-
ment ad1unct The NPA is a soft rubber or plastic uncuffed rube (Figure 1BA) that provides
a conduit for alrllow between the nares and th e pharynx .

Unli ke oral airways, NPAs may be used in conscious. semiconscious. or unconscious

patients (patien tswith an Intact cough and gag refle x). The NPA is indicated when lnser·
tion o f an OPA is technically drlflcult or dangerous. Examples include patients with a gag
refle x. tnsmus. massive trauma around the mouth, or w1nng of the jaws. The NPA may
also be used 1n patients who are neurotog1cally 1mpa1red with poor pharyngeal tone or
cootd1nat1on leading to upper airway obstruction

Technique of Action
NPA Insertion
Select the proper size NPA.

• Compare the outer c ircumference o f the N PA with the inner aperture of the
nares. The NPA should not be so large that 1t causes su stained blanching
o f the nostrils. Some providers use the diameter o f the patient 's smallest
finger as a guide to selecting the proper si ze.
• Tht length of the NPA should be the same as the d1Stance from the tJp of
the patient's nose to the earlobe (FigUlll 188).

Lubricate the airway Wflh a water-soluble lubncant or anesthetic Jelly

Insert the airway through the nosm. 1n a posterior direcbon petpendlcular to the
plane of the face. Pass 11 gently along !he floor of the nasopharynX (Agute 18C).

If you encounter resistance:

• Slightly rotate the tube to facilitate Insertion at the angle of the nasal pns·
sage and nasopharynx.
• Attempt placement through the oth er nost ril because patients h ave differ·
ent·slzed nasal passages.

Reevaluate frequently. Maintain head tilt by providing antenor d isplacement of the man·
d1bEe by using a chin llft or 1aw thrust Mucus. blood. vomrt. or the soft llssues o f the phar·
ynx can obstruct the NPA. which has a small 1ntemal diameter. Freqvent evaluatJOfl and
suc1ion1ng of the aiiway may be necessary ro ensure patency.

Caution Be Aware of the Follow ing When Using a n NPA

• Take c are to Insert the airway gently to a void compllcahons. The airway can irritate the
mucosa or lae-0rate adenoidal tissue and cmi se bleeding . with possible aspira tJon o f
c lots in to th e trachea. Suction may be necessary to rem ove blood or secretions.
• An Improperly sized NPA may en ter the esophagus. With active ventilation. suc h as
b ag-mask ventliabon, the NPA may cause gastric 1n1lation and poSS1ble hypoventilatlon.
• An NPA may cause laryngospasm and vomiting. even though rt 1s commonly tolerated
by semieonscoOUS pallents.
• Use caution 1n patients wrth faClal trauma because of the n sk of misplacement into the
crarual cavity through a lractured cnbnform plate

53
 P ar t G

c
l'ig\>re 18. N~ -ays A., Na.aphoryngeal iJJIWay devices 8 , ~ -•Y
device measun:'"ment C, Nasoph.ary1~ M"'W3y OlMCe mseneo

54
 The ACLS Cnel: RHpltatoty AtrNt

C•utlon Precautions for OPAs and NPAs

Take the following precautions when using an OPA or NPA
• Always check spontaneous resptratlons 1mmed1ately after ln5-0nlon of either an OPA or
an NPA.
• If r8',plratlons are absent 01 Inadequate. stan posrtrve l)<essure venblabons at once
with an appropriate device
• If 9d1uncts are unava•lal> e uM mouth-to-rpask bamer device ventilation.

Suctioning

Introduction Suctioning is an essential component of maintaining a patient's a rway. Providers should

sue tlon lhe airway lmmedtatety If there are copious secre11ons, blood, or vomit.

Sucllon dev>oes COllSISt of both portable and wall-mounted units

P~al>le sucooo devlc8$ are easy to :ranspon but may not provide adequate suet.on
po .. er A suctJOl1 tcwce o• - 80 to - t 20 rrvn Hg is generaOy l'l8C8$S.l{)'.
Wa · mounted SUCllOll"' ts lhOuld be capabje of ptOVIO ng an allflow of greater than
40 Limon at me end of the oo""ery tube and a vacuum of more than - 300 mm Hg
when the tube JS Clamped at futl suet on.
• Ad1ust the amount ol suclloo force for use on children and Intubated patients.

Soft vs Rigid Both sott ttex1ble and rigid suc11on1ng catheters are available
Catheters Solt fleJI 01e catheters may 0.: used n the mouth or nose Sott flex•ble catheters are avail·
al>le in sterile wrappers and can alSo l>e used le< ET tube ~P SUC:tJon•ng

Rtfll(J carheters (eg. Yanllauer) are used to suction ttie oropharynx These are bener tor
suctioll'ng thick secretions and panoculate maner

Cathetar I Use for

'IYP•
Sott • Asph a11on ot thin secretions from the oropharynx and nasopharynx
• Perlormng 1ntratracheal sucllonong
• Soctionng through an n-piace a rway .e NPA1to access me back
ot the p11<1ryn• tn a pa~ent v. th clenched teeth
• More el'ectove suctoononQ of the oropllarynx partJCulatty If mere IS
thiCk particulate matter

$5
 P a rt 0
Oropharyngeal Follow the steps below to per!orm orophatyngeal suctioning
Suctioning
Procedure Ac t ion
• Measure the cmheter before $UCt1on1ng and do not insert it any further than
the distance rrom the tip of the nose to the earlobe.
• Gently insert the suction catheter or devlC8 Into the oropharynx beyond the
tongue
• Apply suction by OCCiuding the Side oP8lllOO or 1118 catheter whde With·
dnlwing With a rotating or 1WtSt11g mot on.
• If using a ngid suctoo del.-.ce 1eg Yarn<auer sucoon), place lhe tip gently
into the oral cav•ty Advance by pushing the tongue down to reacn the oro·
pharynx ~ necessaty.

Endotracheal Patients with pulmonary secretions may require suclton1ng even ofter ET intubation Follow
1Ube Suctioning the steps below to perform Er tube suctioning
Procedure
Im

•
Ac tion
• Use s1£!nle ted'lntQUe to reduce the akellhood of &lfWay contamination

• Gently insert the catheter 11110 the ET tube Be sure the Side open.ng 1a not
occluded dunog 1nsertl()fl
• Insertion ot the catheter beyond the tip ol the ET tube is not recommended
because 11 may on1ure the ET mucosa or stimulate coughing or broncho·
spasm

• Apply suction by occluding the Side opening only wn11e withdrawing the
catheter with a rotating or tw>Sting mooon.
• Suction attempm should not exceed 10 seconds. To aVOtd hypoxemia
precede and follow auctioning attempts w~h a short period of adm1n1Stra ·
tion of 100% oxygen

Mo111tor the patient's hc.Jrl rate, pulse, oxygen saturation, and clm1cal
appearance during suct1011/ng. If bradycard1a develops, oxygen saturut1011
drops, or elm/ca/ appeJra11ce detenorates, mterrupt suctioning at once
Adn11n1ster high-flow OKygen until the heart rate returns to nonna/ and the
clu11cal cond1t1on 1mprovus. Assist vent1lat1on as needed.

Providing Ventilation With an Advanced Airway

Introduction Selec11on of an advanced airway device depends on the tra1n1ng, scope of practice, and
equipment of the providers on the h1gh-per1ormance team. Advanced airways include but
01() no1 hmi1ed to
• Laryngeal mask airway
• Laryngeal tube
• Esop113gea.·tracheal tut>e
• ET tube
Because a smai proportion ot patients cannot be venlllated with a laryngeal masl< a•rway,
providers who use this d4tvace Should have an alternative airway management strategy A
txlg·mask deVK:e can be this alternate st1ategy.
 The ACl.S Cases: Resplrataty Atrnt

This course w 'am ianze you W•tn tyi- of advanced aorwa~ ln$1tVCt()ll in rhe sJ<d!ed
placement of these a.rwa~ IS beyond the scope of tne ba~ ACLS Provider Cou<se To
be prohcil!llt on the use of ad\.1nr.ed airway delllCeS. you must h.lve adequate onmal tm•n
Ing and ongoing expenence ProvtOers who •nsett advanced airways must participate '" a
l)(OCe$S of COi to document ond minimize comphcat1ons

In 1h1s course, you will practice venl1latlng with an advancod airway 1n place and ln1egrot
1ng ve'1t1lat1on wJth chesl compressions

Ventilati on Rates
Ai ~ Ventilation D...w.g Ventilation During
rwa7 ces Cardiac An-est RNpir.rtot'y .an.st

Any advanced atrway Once every 6 seconds Once every 5 to 6 seconds

Laryngeal Mask The laryngeal mask auway is an advanced airway alternative to f. r mtubatton and prowdes
Airway comparable ventilal!On. It 1s acceptable to use the laryngeal mas~ a rway as an a11ema11ve
to an FT tube 'Of airway maoag<imont n ca.'diac arrest Only e•~>ei >eed proVJCJers snouicJ
Pf!fform laryngeai masi< a"" 1IY "' "' "'
fiii1 See the Studen• Wet>s<te 1www.heart.org/eccstudent lor more nfonnanon on
~ the laryngeal mask airw.iy

Laryngeal Tube Tt1!) advantages or lhe l!lryngool lube are similar lo those ol 1he esophageal-tracheal lube:
however. the laryngeal tube 1& more compact and less comphcnted to insert
Healthcare P<Ofess>anais tm oo 1n the use of me latyngeal tube may constOer 11 as an
a11e<1111trve 10 bag·mask •e<it>at()ll or e-
'fl!ubatJOn for l!Jt'Nay management on can:I ac
arr"61 Only e•pe!lellCe<J proviOet'S st>o.;ld per.arm .aryngeal l.;b8 insertion.

fiiil See the Laryngeal lntub ll• "' .;ecl()ll on

the Stud• nt W<Mls•te
~ (www.heart.org/eccstudentl lat more •nl0tmatlO<l OC1 lhts procedure.

Esophageal-Tracheal Thi! o•;ophageal·tracheal tube IS an advanced airway a1101notlve 10 ET 1ntubat1on Thts

JUbe 001/'ICOprovides adequale ••'l'lt•llltlOl1 comparable 10 an fl tub<> ti IS acceptable to U5e 1h8
e50Pl'11geaHractleal tube as an llltefl'llt••e to an ET 11.1be tor a"'"~ management n car·
d.ac arrest Only oro•id<-fs e•/)CfJ6fl(;fld .. Ill :s use st>ould per';,rm esoctiagearuactieal
tuo. inser.on
See the Student Wec>Me (www.heart.org/eccs tudent '°' mOfe 1nforma1.on on
the esophageal tracheal lube

57
: Port
-
0
Endotracheal Tube A t:•"el summruy of the basic steps for pecfoonmg ET 111tubat.on •S g ven here to famdlanze
the ACLS PfO\'lder who maf assi:.t w,tfl the procedure

• Prepare for 1ntubahon by a~blmg the necessary equipment

• Perform ET intubahon 1see the Student Website)
• Inflate cuff or cuffs on the tube
• Attach the vent1lat1on bag.
• Confirm correct placement by physical examination ond a confirmation device
Continuous waveform capnography 1s recornm~ed fin add•tton to ct•nical assess·
ment as lhe most reliable methOd of confirming and monitonng correct placement
o• an ET tube Hea:thcare p.ov~ may use eolonmctnc a'ld nonwavelorm cart>on
dioxide detectOl'S when waveform capnography •s not avallable
• Secure the tube n place
• Moonor for displacement
Only experienced providers shO<.Jld perform IT intubatlOn

fm See the Endotracheol Intubation section on the Studenl Website

~ (www.heart.org/eccstudent) for more 1nlormat10n on thlS procedure

Caution Use of Cricoid Pressure

• The 1out1ne use of cncOl\J piessure 1n cardiac arrest IS not recommended.
• Crtco1d pressure m nonauest p1111ents may offer some measure of protection to the
011way from aspirallon and gastric 1nsufflallon during bag mask ventilation. However, 11
also may impede ventilation and interfere with placement or a supraglo ttlc airway
or 1ntubat1on.

Precautions for Trauma Patients

Summary wri. ., piovid1ng aSS1stecl ventilation for patients with known or suspected ce<vical sp1no
trauma, avoid unnecessary spine movement. Excessive head ond neck movement 1n
patients with an unstable Ce<Vlcal spinal column can causo Irreversible injury to the spinal
cord or worsen a minor splnJI cord injury. Approximately 2% of patients wrth blunt trauma
serious enough to require spln;il 1ma91ng 1n the ED have a ap.naJ 1n1ury. This nsk IS tnpled
11 t~'l pa1 em has a head or facia! tniury Assume that any patient w11h multiple trauma.
he3d lnJU'Y or 'actal trauma has a spine lllfury. Be par1icularfy cautlOUS 1f a pallent has
~llMI ceMC8l spone '"fUIY E•ampies are patiems who have been involved in a high·
spe«i mo1or \ehtde colllSlor\, ha•e f.,, •en from a heoght. or -..ere injured wnlle drvmg

Follow these precautions 11 you suspect cervical spme trauma ·

• Opon 1he airway by using a )Ow thrust without head extension. Because mainta1n1ng a
patent airway and providing adequate venUlation are priorities. use a head t1lt-ch1n loll
maneuver 1f the jaw thrust IS not effective.
• Have anolher team member stab<11ze lhe head ,,, a neutral pos.tlOll dunng illrway
man pulatJo<1 Use manual spinal motion restnction rather than lmmobiia11tlon
dev1CU. Manua spin;.
managemerr and ma) . , . , .
'°'
zatLOn s safer C8t'lo...i :OI ars may comphcate airway
ierlere w.lh airway palency
• Spma 1mmoblhzation CkviCas are helpful dunng transpor1

SS
 The ACLS Cases: Acute Coronary Syndromea

Acute Coronary Syndromes Case

Introduction The ACLS provider must have the basic knowledge to assess and stabilize patients with
ACS. Patients in this case have signs and symptoms of ACS, Including possible AMI. You
will use the ACS Algorithm as the guide to clinical strategy.

The initial 12-lead ECG Is used 1n all ACS cases to classify patteots Into 1 of 3 ECG cat·
egO<les. each wrth drlferent strategies of cara and management needs. These 3 ECG cat·
agOC'1es are ST-segment elevatlOn suggesting ong01ng acute 1n1ury. ST-segment deprllS8K>ll
suggesting 1schem1a, and nond1agnost1c or normal ECG. These are outlined 1n the ACS
Algonthm, but STEM! with time-sensitive reperfusion strategies Is the focus of this course
(Figure 20).

Key components of this case are

• Identification, assessment, and triage of acute ischoemlc chest discomfort
• Initial treatment of possible ACS
• Emphasis on early repoerfusion of the pauent wtth ACSISTEMI

Rhythms for ACS Sudden carchac death and hypoteosive bradyarrtlythm1as may occur With acute 1schem1a
Providers will understand lo anticipate these rhythms and be prepared for 1mmed1ate
a ttempts al defibnllatJon and administration of drug or electrical therap y for symptomatic
bradyarrhythm1as.

Although 12-lead ECG interpretation Is beyond lhe scope o f the ACLS Provider Course,
some ACLS providers will have 12-lead ECG reading skills For them. this case sum ma·
nzes the identification and management of patients with STEMI

Drugs for ACS Drug therapy and treatment strategies continue to evOll;e rapidly 1n the field of ACS. ACLS
providers and instructors will need 10 monitor 1mportani changes The ACLS Pro\/lder
Course presents only basic knowledge focusing on eany treatment and the priority of
rapl d reperlusion, rehef of 1schem1c pain. and treatment o f early hfe·threatenlng comphca·
lion s. Repertuslon may Involve the use of fibrinolytic therapy or coronary angiography with
PCI (le. balloon ang1oplasty/stenhng). When used as the Initial reper1usion strategy for
STEMI, PCI IS called pnmary PCI.

Treatment of ACS involves the 1nittal use of drugs to relaeve 1schemtc discomfort. d1SS01ve
clots. and 1nh1bn thrornbln and platelets. These drugs are

• Oxygen
• Asp1nn
• N11rog1ycenn
• Opiates (eg, morphine)
• F1brinolytlc therapy (overview)
• Heparin (UFH, LWMH)
Addn10nal agents that are ad1unct1ve to 1n1tJal therapy a.nd will not be discussed In the
ACLS Provider Course are

!)·Blockers
• Adenos1ne diphosphate (AOP) antagonists (cloptdogrel, prasugrel, tJcagrelor)
Angioteosin-converting enzyme (ACE) inhibitors
• HMG· CoA reductase inhibitors (statin therapy)
• Glycoprotein lib/Illa inh10itors

59
 Part 0
Goals for ACS Patients

Foundational Facts OHCA Response

Half of the pauents who die of ACS do so before reaching the hospital. VF or pulseless
VT 1s the prectprtatmg rhythm In most of these deaths. VF is most hkely to develop dur·
1ng the first 4 hOurs after onset of symptoms

Communmes should develOp programs to respond to OHCA. Such programs should

focus on

Recognizing symptoms of ACS

• Activating the EMS system. wllh EMS advance not ificallon ot the receiving hospital
• Providing early CPR
• Providing early def1bnllat10n with AEDs available through public access defibnllatlon
programs and first responders
• Pro\lld1ng a eoo<01nated system of care among the EMS system. the ED. and
CardlOlogy

The pnmary goals are

• Identi fication of patients with STEM! and triage for early reperfusion therapy
• Rehef of ischemic chest discomfort
• Prevention of MACE. such as death. nonfatal Ml. and the need for urgent postlnfarc-
tJon revasculanzatlon
• Treatment of acute. l1!e-threaten1ng compti<:allQ(IS of ACS. such as VF/pulseless VT.
symptomatic bradycardll!S, and unstable tachycardias
ReperluS10n therapy opens an occluded coronary artery with e1lller mechanical means or
dnigs PCI, performed 1n the hean cathetenzation suite after coronary angiography. allows
balloon dilation and/or stent placement for an occluded coronary artery. " Clot-buster·
drugs are called fibrinolytics, a m ore accurat e term than thrombalytics.

Pathophysio/ogy Pauents wrth coronary atherosclerosis may develop a spectrum of clinical syndromes rep-
of ACS resenting varying degrees of coronary artery occlusion. These syndromes include non-ST
el.evatlon ACS (NSTE·ACS) and STEM!. Sudden card.ac death may occur With each ol
these syndromes. Figure 19 illustrates the pathoph)'S'ology of ACS
~~~~~~~~~~ -~~~~~~~~~~~

60
 The ACLS Cases: Acute Coronary Sync1rolMa

A Unstable plaque
Early plaque formation
B Plaque rupture
C Unstable angina
D Microemboli
E Occlusive thrombus

Plaque rupture/thrombus B c

NSTE-ACS

t
STEMI E
Resolution/ stable angina

l'lgure 19. Pathophygiology o! ACS

61
 ~-

p ar t G
Acute Coronary Syndromes Algorithm-2015 Update

Symi>tomo llU990stive of - "'infarction

2 i
EMS . u...ment INld' gire and ho1pltal preparation
• _Moortor.9UpPQr1 .AUf.;.S 130 prepued 10-om'Y1do CPR and de!lbrillath')n
•
• Obta:n J2·1S911:ECO t ST •a:iori
~tbl'-a.spu-1n and ooMlder.-oxygen nitrogtye«tn a.fld ~ 11 ~

- Nolrfy ~ hoipUll wr::r -:tan.slTI~ CJf ..-~ llOfe t11n. Of

Ul"'l:S«Mciirll~cOl'lllCt
• ~~tt'IOl.AO~ ~~to~toST£""1
• tt ~~ ~ vM fibrinot1w cneckksl

3
Concurrtnt ED ~ (• 10 minutes.) lmm.ofat• EO g,eneral b'eatm.nt
-e""Ch«k .. t.t llgtS;. f!"ali.;&'tt'd ·YOW' .aab..lratllon • 1io U.l ,.9()'4,. $tart ~ 111.c {J,,..,_ mrr.e
• Es1:0~
· ~'blef~~ tary~eum . .....
..........,._ ~.,.
a.•
• NoifW'I 1so to.3'25.mo. "' ,,..,, err• O'J

• J\ew....... ~.,~~cNcliil1
1-..(lOt'ltl'~
• Obe•it'I #'l!lilll tarCllilO "*1<-•...........,
. ""1>0',....,.
- "''"'"""""""""-'"""'
1rdt1a1 oloctrofyl& and 0099olotl(W'I t 1udles
• ObC111ii pc:irlallle CheSt ).·f"I'¥ (,30 lnlllU!es}
~~~~~+-~~~~~~~~~~~~~~

ECG -
5 _[
ST eievauon Ot ntw or
I
ST depreSSIOn or OYf!nmlc
11
Normal or
l
nood~nOlllC CNwlges in )
p~-L8B8
llOOngly--lot...,,.,
sr-.- "'ISTOlll
T·wa·,..~IOf'l. l~"J

~"""""'"
H~rl!M ,,...ST..,."t'tiott ACS
flllSIT-ACSI ___,}
.. ST segment cw T w•ve
Low-An~ 1tMicllidMM ACS

• S ten ~nc;t;v. ~liplea

'!lir1dlta ted
10 I
"-." '-, -
• Oo not delay f'900rl'u1Mon TroPOOWi elevated or hlgtt..rtak patient Consider admlulon to
.. ,,.....,.,.,"""'"""".,_ _.,,.
CoMldet utty .,,\'....,.. 1n.teoy It
_,__.,.,.5....._
eo c,... paiin unrt °' t0
~tebedf«
1 ,,-'
rme trom GnMt or ~
:.1 2
.. ,
,,.,,_ .,~
, _ ,_ _ f ............
~ $ , 2 hc\d1 • ~·OJ h6art taMure

8
'-
l~. ..... $ ttit1 adtunctive chentp14:1
ou. n11roglycenn, ~"'11'-,I • '- •ntle.tiecl
... AJ-IA/ACC NStE ACS Q.Jlaei•flt$

~ --=--~
~-!>Jc... ...__ ~
•.i:.<r::na: -
• Door tc bal oon lnn.Uon
(PCQ eoa1 of 90 mini.I,••
• Doot4to~~• {ftbrtnotplsl
go., of 30 mlnutet

Managing ACS: The Acute Coronary Syndromes Algorithm

Overview of The Acute Coronary Syndromes Algonthm (Figure 20) outlines the assessment and man·
the Algori thm agemem steps for a patient presenung with symptoms suggest111e or ACS The EMS
responder m the 001-ol-hospnaJ environment can begin Immediate assessments and
acuons. These Include 91v1ng oxygen, aspirin. nnrogrycenn, and morphine 1r needed, and
obtaining an lnlllal 12-lead ECG (Step 2). Based on lhe ECG findings. the EMS provider
may complete a f1bnnolytlc therapy checklist and notify the receiving ED or a potential
62
 The ACLS Cases: Acute Coronary Syndromes

AMl·STf;MI when appropriate (Step 3). If out·ol·hosprtal providers are unable to complete
ihese initial steps before the patient's amval at the hospital, the ED provider should imple-
ment thlS component or care
Subs equent treatment occurs on the patient's arrival at the hospital. ED petsonnel should
review the out·of·hospital 12-lead ECG if available. If not per1ormed. acquisition of the
12-lead ECG should be a prlonty. The goal is to analyze the 12-lead ECG as soon as pos·
Slble w1th1n 10 minutes of the pauent's amval In the ED (Step 4). Hospital personnel shoo Id
categonze pallents into 1 of 3 groups according to analysis of the ST segment or the
presence of left bundle branch block (LBBB) on the 12-lead ECG. Treatment recommen·
dations are specific to eac h group.
• STEMI
• NSTE·ACS
• Low·/intermed1ate-nsk ACS
The ACS Case will focus on the early reperfus1on of the STEMI patient, emphasizing initial
car& and rapid triage for reperfusion therapy

Important The ACS Atgonthm (Rgure 201 provides general guidelines that apply to the m1t1al tnage
Considerations of patJent s based on sy mptoms and the 12·1ead ECG. Healthcare personnel often obtain
serial cardiac markers (CK- MB. cardiac troponlns) In most patients that allow additional
nsk s tratification and treatment r&Commendations. Two impor1ant points for STEMI need
emphasis:
• The ECG ts central to the 1nrt1al risk and treatment strat1hca11on process.
• Healthcare personnel do not need evidence of elevated cardiac markers to make a
decision to administ er hbrlnoly!Jc therapy or perform diagnostic coronary angiography
with coronary int ervention (angioplasty/stenting) 1n STEMI patients

Application of the The steps m the algorithm guide assessment and treatment·
ACS Algorithm • ldent1ticat1on or chest discomfort suggestive of 1scherrua (Step 1)
• EMS assessment, care. transport, and hospital prearrivat notffication (Step 2)
• Immediate ED assessment and treatment (Step 3)
• Classfficatlon ol patients according to ST segment analysis (Steps 5, 9, and 11)
STEMI (Steps 5 through 8)

Identification of Chest Discomfort Suggestive of lschemia

Signs and You .should knOw hOw to identify chest discomfort suggesuve ol 1scherrna Conduet a prompt
Conditions and targeted evaluation of every pabent whOse Initial complaints suggest possible ACS.

The most common symptom of myocardial lsehem1a and infarction 1s retrosternal chest
dJSOonlfort. The pallent may perceive this d1scomtort more as pressure or tightness than
actual palll.

Symptoms suggestive of ACS may also include

• Uncomfortable pressure. lullness. squeezing, or pain 1n the center of the chest
lasting several minutes (usually more than a few minutes)
• Cl\est discomfort spreading to the sitoulders. neck, one or bOlh arms, or iaw
• Chest discomfort spreading into the back or between the shoulder blades
Chest discomfort with light-headedness, dizziness, fa1nt1ng. sweating, nausea.
or vomiting
• Unexplained. sudden shol1ness of breath. which may occur with or w1th0ut
chest dlSComfort

63
 Part 0
Consider the bkehhood that the presenting cond1t1on is ACS or one of its potenflally lethal
mimics Other life-threatening cood111ons that may cause a<:vte chest d1scomf011 ere a0<11<o
dissection. acute pulmonarf embolism (PE). acvts pencatdial effusion wtth tamponade
and tension pneumothorax

Foundational Facb STEMI Chain of Survival

Th" STFMI r.h:.1n nf S.1Nl\•l tFio1111t :>IJ ~t•bed by the AHA is Slffil ar to tne Cllaon of
Survival for sudden carcf•ac arr~t It Inks actions to be taken by pat.ems. lam ly mem-
tiets und hea11leare prolllCe'S to max.,,,ze STI:Mi reaJIJef'Y These hnks are
• Rnptd recognrtoOI' ~ reactoan to STEM! warning Signs
• Rapid EMS d•sparch and rapod EMS system tronspori and preamval not1ficat•on to the
receiving hospital
• Rup1d assessment and c>agnos1s 1n the ED (or cath lab)
Rupid treatment

,19ure 21 . The ST£MI CM111 d Survtvnl

Starting With All dispatchers and EMS providers must rece.ve training In ACS symptom recognition
Dispatch along with the potential complications Dlspalchcrs, when aulhonzed by medical con·
trol or pmtocol. should tell pat11mts with no history ol aspirin allergy or signs of active or
recent oastmir1test1nal iGll ol!!"d no to chew asporon (160 to 325 mg) while wa•t•ng for EMS
orOVlllers to arm e

EMS Assessment, Care, and Hos pital Preparation

Introducti on EMS nssessrnen• care. anc tiosp,1a1 prep;w-ation ate ouu ne<11n Step 2 EMS responders
may perform the lollow1ng assessments and octlOl'ls during the stab< izat1on tnage. and
transport of the patient to an appropriate foclllty
• Monitor and support arway. breath ng and c1rculat1on (ABCs)
• Adm1n.s1er aspmn and consldM oxygen 11 0 saturation is less than 90%,
n11roglycer1n. and morphine 11 d1$Comfort is unresponsive to nitrates.
• Oblnin a 12-lead ECG: 1nterprot or transmit !or lnterpretallon.
• Complete 3 ribrinotyt1c checklist If indicated
• Provide prearnval not1catl()(I 10 th<! reo M"'I racdrty rt ST eoevaoon

Monitor and Mondorong and support of ABCs 1ncluaes

Support ABCs • Monotonng vital siqns and anMc rhythm
• &mg ptepa/t'd !l> p<o•'ld<> CPR
• Using a det 1:>nltat0< 1 neeooo

••
 The ACLS Cases: Acute Coronary S}'ndromel

Administer Oxygen Providers should be familiar w ith the actiol'IS, 1nd1cations, cautions, and treatment of side
and Drugs effects.

Oxygen
High inspired-oxygen 1enS1011 """ tend to maximtZe artenaJ oxygen saturation and. 111 tum,
artanal oxygen content Thrs .... 111 help support oxygen detlvety (cardiac OU1put x artenal
oxygen content) wtien cardiac OU1put 1s limited This short-term oxygen therapy does not
produce o xygen toxicity.

EMS providers should administer oxygen 1f the patient 1s dyspneic, Is hypoxemic, has
obvious signs of heart !allure. has an arterial oxygen saturatlOn less than 90%. or the
oxygen saturation is unknown Providers Should titrate oxygen therapy to a nornnvasivety
m0<1ttored oxyhemogtobin saturation 90% or greater. Because ns usefulness has not been
established In nonnoxlc patients wrth suspected or confirmed ACS. providers may con-
sider wlthl1old1ng supplementary oxygen therapy In these patients.

Aspirin (Acetylsalicyhc Ac id)

A dose of 160 to 325 mg of non-enterlc-coated aspinn causes 1mmed1ate and near-total
inhtbmon of thromboxane A. production by 1nh1b111ng platelet cyciooxygenase (COX-1).
Platelets are one of the pnnc1paJ and earliest panic1pants 1n thrombus formation. This
rapid lnh1b111on also reduces c0<0nary reocctusoon and other recurrent events Indepen-
dently and after fibrinolytlc therapy.

If the pat1en1 has not taken aspirin and has no history of true aspinn allergy and no evi-
dence of recent GI bleeding. give the patJent asp<rln (160 to 325 mg) to chew In the lntbal
hours of an ACS. aspmn is absorbed better when chewed than when swallowed. pamcu-
larly 1f rroorphme has been given Use rectal asplnn supposrtones (300 mg) for patients
with nausea, vomiting, acuve peptic ulcer disease. or other disorders of the upper GI tract.
Nitroglycerin (G/yceryl Trmltrate)
Nitroglycerin effectively reduces ischemic chest discomfort. and 11 has beneficial hemody-
namic ettects The phys!Olog1c effects of nitrates cause reductlOO 'n LV and right ventricu-
lar (RV) l)<eload through periiit'eral artenal and venous d11at1on.

Give the patient 1 subhngual nitroglycerin tablet (or spray "dose"! every 3 to 5 minutes
for ongoing symptoms If it is permitted by medical control and no contraindications exist.
Heallhcare providers may repeat the dose twice (total of 3 doses). Administer nitroglycerin
only rt the patient remains hemodynamically stable: SBP is greater than 90 mm Hg or no
lower than 30 mm Hg below baseline ~f known) and the heart rate tS SO to 100/min.

N1troglycenn 1s a vetl0d1lator and needs to be used caut10USly or not at all in patients with
inadequate ventricular preload These situations include

• Inferior wall M l and RV Infarction. RV Infarc tion may complicate an Inferior wall Ml.
Patients with acute RV Infarction are very dependent on RV filling pressures to main-
tain cardiac output and blood pressure. If RV 1nlarct1on cannot be ruled out. providers
must use caution 1n adm1n1stenng nitrates to patients with inferlOI STEMI. II RV infarc-
tJOn is ccnfirrned by nght·slded precordial leads or clinical findings by an expenenced
provider. nrtroglycenn and other vasoddators (morphine) or volume-depleting drugs
(diuretics) are contralnd1Caled as well.
• Hypotonsion, bradycardla, or tachycardia. Avoid use of nltroglycenn in patients
with hypotension (SBP tess than 90 mm Hg), marked bradycardla (less than 50/mln).
or tachycardia.
• Recent phosphodiesterase inhibitor use. Avoid the use of nltroglycenn If rt ls sus-
pected or known that the pallent has taken S1tdenaf1I or vatdenaf1I within the previous
24 hours or tadalafil with n 48 hours. These agents are generally used for erectde dys-
function or In cases of pulmonary hypertension and in combination with nitrates may
cause severe hypotens1on refractory to vasopressor agents

65
 -

Part 8
Opiates (eg, Morphine)

Give an opiate (eg, morphine) for chest disoomfOl't unresponsive to sublingual or spray
nrtroglycenn 1t authorized by protocol or medical control. Morphine 1s Indicated In STEM!
wheo chest dJSCOmfot1 1s unrespoosive to nitrates Use morphltlfl with caution 1n NSTE-
ACS because of an assoc.atoon w~h increased mortality.

Morphine may be utilized 1n the management of ACS because rt

• Produces central nervous system analgesia, which reduces the adverse effects o l
neurohumoral actlvatlon, catecholamine release. and heightened myocard ial oxygen
demand
• Produces venod1lation. which reduces LV pteload and oxygen requotemems
Decreases systemic vascular reststance. thereby reducing LV aftetload
• Helps red1stnbute blood volume In patients wnh acute pulmonary edema
Remember, morphine 1s a venodllalor. Like n11roglycerin, use smaller doses and carelully
monitor physiologic response before administering additional dose$ In patients who may
be preload dependent. If hypotens1on develops. admJnlster fluids as a first hne of therapy.

Critical Concepts Pain Relief With Nitro glycerin

Reliel or pain with nitroglycenn Is neither specific nor a useful diagnostic tool to deter-
mine the etiology of symptoms 1n ED patle01s with chest oam or dlscomfoo. GI etJolo-
g 1es as well as other causes or chest discomfoo can -respond" to nitroglycenn adm1n1s-
trat1on Therefore, the response to nnrate therapy 1s not d1agnos1JC ot ACS

Caution Use of Nonsteroidal Anti-inflammatory Dru9s

Use of nonsterOldal anti-inflammatory drugs (NSAIDs) IS contraindicated (except for
asp1nn) and should be dlscontmued. Both nooselect1ve as well as COX·2 selective drugs
stoould no1 be administered dunng hosp1tahzat1on for STE.Ml because of the Increased
nsk ot mortality, re1nfarchon, hypertenS1on, hean tallu re, and myocardial rupture assoc1-
a ted wlt11 their use.

GG
 The ACLS Cases: Acute Coronary Syndromes

Obtain a EMS pro111de1S should obtmn a 12-lead ECG. The AHA recommends out-of-hospital
12-Lead ECG 12-lead ECG diagnoSt•C programs In urban and suburban EMS systems.

EMS Action Recommendation

12-Lead ECG if The AHA recommends routine use o f 12-lead out-of-hospi tal
a vallable ECGs for patients with signs and symptoms o f possible
ACS.
Preanivaf ho spital Preamval notJficatoon of the ED shortens the lime to treat-
notification for STEMI ment (10 to 60 minutes has been achieved in ciinocal Stud·
1es) and speeds reperlusion thetapy wrth fibr1nofytJCS or PCI
or both. which may reduce mortality and mimm1ze myocar·
dial in jury.

Flbrin olytic check list If If STEMI is identif ied on the 12-lead ECG, complete a fibrl·
appropriate nolyt1c cheokhst if appropriate.

=
liiin See the Student Website (www.heart.org/eccst udent ) for a sample
hbnnolybc checkhst

Immediate ED Assessment and Treatment

Introduction The high-performance team should Quickly evaluate the patient with pot ential ACS on the
patient's arnval in the ED. Within the first 10 minutes. obtain a 12-lead ECG (ii not already
performed before amval) and assess the p atient.

The 12·/ead ECG (example in Rgure 22) is at the center of the decision
pathway m the management of 1schem1c chest discomfort and 1s the only
means of identifying STEM/.
A targeted evaluation should be performed and focus on chest discomfort, signs and
symptoms o f heart failure, cardiac history, nsk factors for ACS, and historical features that
may preclude the use o f fibrlnolytics. For the patient with STEMI . the goals of reperfus;on
are to give fibnnolytlcs within 30 minutes o f arrival or perform PCI within 90 minutes of
arnvaJ

J.
.. l

'1 ~I•

----- - , ~I-~--

·-.. -

Figure 22. Antooor STEM! on• 12 lead ECG

67
 Part G
Figure 23 shows how to measure ST-segment deviation

Fl9ure 23. How to measure Sl-seqmen1 deviation. A. lnfenor Ml The ST segment has no IOW poern flt IS
covered or concave). B, Anlf!flO' Ml

The First 1 O Minutes Assessment and stabilization of the patient m the first 10 minutes should tnciude
the following:

• Check vital signs and evaluate oxygen saturation.

• Establish IV access.
• Take a brief focused history and perform a physical examination.
• Complete the fibnnolyuc checklist and check for contraindications. if indicated
• Obtain a blood sample 10 evaluate Initial cardiac marker levets. electrolytes. and
coagulatl<ln.
• Obtain and reVtew portable chest x-ray Oess than 30 minutes alter the patient's amval
1n the ED). This should riot delay fibnnolybc therapy for STEMI or activation of the PCI
team for STEMI

Nore. The results of cardiac markers, chesl x-ray, and laboratory studies should not
delay reperfusion t11erapy unless chnlcally necessary, eg, su spected aortic d issection
or coagulopathy.

Patient General Unless allergies or contraindications exist, 4 agents may be considered 1n patients with
Treatment 1schem1c-type chest discomfort

• Oxygen 1f hypoxemte 10 % less than 90%) or Signs of hean failure

• Asplnn
• N1troglycenn
• Opiate (eg, morphine if ongoing discomfort or no response to nitrates)
Because these agents may have been given out of hospital , administer initial or supple-
mentaty doses as indicated !See the discussion of these drugs 1n the previous section,
EMS Assessment. Care, and Hospital Preparation.)
68
 The ACLS cases: Acute Coronary~

Critical Concept. Oxygen, Aspirin, Nitrates, and Opiates

• Unless contraindica1ed. Initial therapy with oxygen rt needed, aspirin. mtra1es, and. 11
1nd1Cated, morphine 1s recommended for all patoents suspected of having 1schemic
chest d1scomlon.
• The major contraind1cat1on to nitroglycerin and morphine is hypotens1on. 1nclud1ng
hypotension from an RV infarction. The maior contraindications to aspirin are true aspi-
rin allergy and active or recent GI bleeding.

Classify Patients According to ST-Segment Deviation

Classify Into 3 Groups Review Uie Initial 12-lead ECG (Step 4) and classify pahents into 1 of the 3 following clim·
Based on ST-Segment cal groups (Steps 5, 9. and 11):
Deviation
General Group : Description
STEMI ST elevatton
NSTE-A CS ST depression or dynamic T-wave 1nve<sion
Low-/intennediate-risk ACS INormal or nondlagnostic ECG
• STEM/ 1s charactenzed by ST-segment elevation in 2 or more contiguous leads or
new LBBB. Threshold values tor ST-segment elevauon conslS1ent wrth STEMI are
J-polnt elevation greater than 2 mm (0.2 mV) In leads v, and v,· and 1 mm or more 1n
all other leads or by new or presumed new LBBB
·2 5 mm In men younger than 40 years; 1 5 mm in all women
• NSTE-ACS is characterized by 1schem1c ST-segment depression 0.5 mm (0.05 mV) or
greater or dynamic T-wave Inversion with pain or discomlort. Nonpersistent or Iran·
sient ST elevation 0.5 mm or greater for less than 20 minutes is also included in this
category.
• Low-lfntermediate-risk ACS 1s characterized by nonnaJ or nond1agnostic changes in
1he ST segment or T wa• e tttat are inconcluStve and require funhef nsk S11at1ficatron.
This classtfication includes patients wrth normal ECGs and Uiose with ST-segment
deviation In either direction of less Uian 0.5 mm (0.05 mV) or T-wave Inversion ~ mm
or 0 .2 mV. Serial cardiac studies and functional testing are appropriate. Note that
additional information (troponin) may place the patient into a higher nsk classification
af1er initial classification
The ECG ciasStflcallon of 1schem1c syndromes is not meant 10 be excluslve A small per·
centage of patients With normal ECGs may be found to have Ml. for example. If the 1nrllal
ECG 1s nond1agnosttc and clinical circumstances indicate (eg, ongoing chest dlscomfort),
repeat the ECG.

STEMI

Introduction Patleots w1U1 STEMI usually have complete occiUSAOn of an epicaldJal coronary artery

The mainstay of treatment for STEM/ 1s early reperfus1on therapy achieved

with primary PC/ or fibrirtolytics.

69
 Part G
Reperfusion therapy for STEMI 1s perhaps the most Important advancement 1n treatment
of cordlovascular disease •n recent years. Early f1bnnolytic therapy or direct catheter-
based reperfusion has been established as a standard of care ror patients wrth STEMI
who present within 12 hours or onset of symptoms with no contralnd1ca11ons. Reperluslon
therapy reduces mortality and saves heart mUSGle. the shorter the time to reperlUSK>O, the
greater the benefit. A 47% reduction tn mortality was noted when 6bnnolyuc therapy was
provided In the first hour atter onset of symptoms.

Critical Concep t• Delay of Therapy

• Routine consu1ta11on with a cardiologist or another physician should not delay d1agno-
S1s and treatment except 1n equivocal or uncertain cases. Consultation delays therapy
and is associated w1t11 1nc1eased hospital mortafny rates.
Potential delay dunng the in-hospnal evaJuatton period may occur rrom door to data
(ECG), from data to decision. and from decision to drug (or PCI). These 4 major
points of ln·hospital therapy are commonly referred to as the "4 D's,·
• All providers must focus on minimizing delays at each of these points Out-of -hospital
transpor1 11me const1Mes only 5% of delay to treatment time: ED evaluatJon consto·
lutes 25% to 33% ol thlS delay.

Early Reperfusion Rapidly Identify patients with STEMI and quickly screen them for Indications and controll1-
Therapy d1catlons to fibrlnolyt1c therapy by using a fibnnolytlc checklist 11 appropriate.

The first qualified phyS<Clan who encounters a patient with STEM! should Interpret or cori-
firm the 12-lead ECG. detem11ne !he nsll/beneflt of reperluSlon therapy. and direct admon·
IS'!ratton of fit>nnolytic therapy or acnvauon of the PCI team. Earty activation of PCI may
occur wtth established protocols. The following time rrames are recommended:

• For PC/, this goal for ED door-t~balloon Inflation time is 90 minutes. In patients
presenting to a non-PCl·Capable hospital, tome from first medical contact to device
should be Jess than 120 minutes when primary PCI 1s cons.dered
• If f1br1nolysls 1s the tntended reperiuSlon. an ED door-to-needle time (needle ume IS
the beginning of infusion of a fibnnolytlC agent) of 30 minutes is the medlCai system
goal that 1s conslde<ed the longest time acceptable. Systems should strove to achieve
the shon est time possible.
• Patients who are inellg1b le for fibrinolytlc therapy should be considered for transfer to
a PCI facility regardless of delay. The system should p repare for a door-to-departure
tome of 30 minutes when a transfer decision Is made.
Ad1uncttve treatments may also be indicated.

Use of PC/ The most commonly used form of PCI 1s coronary 1ntet11ention with stent placement.
O ptimally performed pnmary PC/ Is the preferred reperfusion strategy over fibnnofytic
administration Rescue PC/ is used early a fter f1brtnolytics In patients who may h ave per-
sistent occlusion of the infarct artery (failure to repertuse with fibnnolyttcs). aithoogh this
term tias been recently replaced and 111Cluded by the ~erm pharmacomvaSJVe strategy. PCt
has been shown to be supenor to fibnnolys15 1n the combined end points of death, stroke.
and reinfarction 1n many studies tor pat1en15 presentu.,g between 3 and I 2 hours after
onset However. these results have been achieved in experienced medical settings with
skilled providers (performing more than 75 PCls per year) at a skilled PCI facility (perform-
ong more than 200 PCls for STEM! with cardiac surgery capabilities)

70
 The ACLS Cases: Acute Coronary Syndromea

ConsideratJons for the use of PCI Include the following:

• PCI 1s the treatment of choice for the management of STEMI when 11 can be per-
formed effectively with a door-to-balloon trme of less lhan 90 minutes from first
medical contact by a skilled provider at a skllled PCt facility.
• Pnmary PCt may also be offered to patients presenting to no,...PCl-capable centers
If PCI can be initiated promptly within 120 minutes from first medical contact. The
TRANSFER AMI (Trial of Routine Angioplasty and Stenting After Fibrinolysis to
Enhance Reperfusion in Acute Myocardial lntarction) trial supports the transfer of
high-risk patients who receive f1brinolys1s in a non-PCI center within 12 hours of
symptom onset to a PCI center within 6 hours of fibnnolytic administration to receve
routine early coronary angiography and PCI if indicated.
• For patients admitted to a hospital without PCI capabi 1t•es. there may be some
benefit aSSOCtated wrth transfer for PCl versus admmistratoon of on-Sile fibnnoiytlCS
in terms of reinfarction, stroke. and a trend to lower mortality when PCI can be
performed within 120 minutes of first medical contact.
• PCI is also preferred In patients with contraindications to fibnnolytics and is indicated
In patients with cardiogemc shock or heart failure complicating Ml..

Use of Fibrlnolytic A fibnnolytoc agent or "clOt·buster• 1s administered to patients with J-point ST-segment
Therapy elevation greater than 2 mm (0.2 mV) 1n leads V, and v, and 1 mm or more 1n all other
leads or by new or presumed new LBBB (eg. leads Ill, aVF: leads v,. V,: leads t and alll)
without contraindications. Fibnn·spec11ic agents are effective "' acnievmg nonnal flow
In abOut 50% of patients given these drugs. Examples of f1br1n-speofic drugs are rtPA,
reteplase. and tenecteplase. Streptokmase was the f1rst fibnnotytoc used widely. but rt is
not fibrin specific.

Considerations for the use of ftbnnolytic therapy are as follows:

• In the absence ot contraindications and 1n the presence of a favorable risk-benefit
rauo. f1brinolytic therapy is one option for repertusion in patients w1th STEM! and
onset of symptoms within 12 hours of presentation with qual fy•ng ECG findings and
1f PCt ,5 not available within 90 minutes of first medical contact
• In the absence of contra ndica11ons. 1t is also reasonable to give librinolytrcs to
patients with onset of symptoms w1th1n the prior 12 hours and ECG findings
consistent wrth true postenor Ml. Experienced providers will recognize this as a con·
d1hon where ST-segment depression In the early precord1al leads is equivalent to
ST-segment elevation In others. When these changes are associated with other ECG
findings. it is suggestive of a "STEMI" on the posterior wall of the heart.
• F1bnnolytics are generally not recommended for patients presenting more than
12 hours after onset of symptoms. But they may be considered 1f 1schemic chest
discomfort continues with persistent ST-segment elevation.
• Do not give fibnnolytics to patients who present more than 24 hours after the onset
of symptoms or patients wrth ST-segment depression unress a true postenor Ml is
suspected.

Adjunctive Other drugs are useful when Indicated In addition to oxygen, subhngual or spray nitroglyc-
l'>'eatments erin, aspirin, morphine, and fibrlnolyt1c therapy. These include
• Unfractionated or low-molecular-weight hepann
• B1vahrud1n
• P2Y., inhibitors
• iv nitroglycerin
• ~·Blockers
• Glycoprotetn !lb/Illa inh•b1tors

71
 Part 0
IV mtroglycerln and heparin are commonly used earty In the management of pa tients with
STEM I. These agents are bnelly discussed below. Use o f b1valirudln, P2Y,, inhibitors.
!}-blockers. and glycoprote.n lib/Illa Inhibitors will not be reviewed Use o f these agents
requires add1t1onal risk s trati fication skills and a detailed knowledge o f the spectrum of
ACS and, 1n some instances. continuing knowledge o f the results of clinical trials

Heparin (Unfractionated or Low-Molecular-Weight)

Hepafln is routinely given as an ad1unct for PCI and fibrinolytlc therapy wllh f1bt1n-spec1flc
agenlS (rtPA. reteplase. tenecteplase) It •S also Indicated In other specific h19h·r1sk s1rua-
t1ons. such as LV mural thrombus, atrial f1br1llallon, and prophylaxis for venous thrombo·
embolism 1n patients with prolonged bed rest and heart failure complicating Ml If you use
these drugs, you must be fam1har with dosing schedules for specific clJnicaJ strat egies

The inappropriate dosing and monitoring of hepann therapy has caused

excess int1acerebral bleeding and ma1or hemorrhage in STEM/ partents.
Providers using hepann need to know the md1cat1ons. dosing. and use in
the specific ACS categones.

The dosing. use, and duration have been denved from use In clinical tnals.
Specific patients may requrre dose mod1f1cat1on. See the ECC Handbook
for weight-based dosing guide/mes, intervals of admmistrat1on. and ad1ust-
ment of low-molecular-we1ght hcpann m renal function. See the ACCIAHA
gwdelmes for detailed discussion m specific categories.

IV Nitroglycenn

Routrne use of IV nitroglycerin 1s not indicated and has not been Shown to sigrvhcanUy
reduce mortality in STEM! IV n1troglycer1n is 1nd1cated and used wldety in 1schemic
syndromes It LS preferred over topical or IOng· acLng forms beeause 1t can be titrated 1n
a patient with POtentlally unsiable hemodynamlCS and clinlCaJ cond1t100 Indications IOI'
Initiation of IV nrtroglycer1n 10 STEMI are

• Recwrent or cononu1ng Chest d1scomfo'1 unrasponSJVe to subhnguaJ or spray nitroglycenn

• Pulmonary edema complicaling STEM!
• Hype<1ension complicating STEM I
T1eatment goals using IV nitroglycerin are as follows.

Treatment Goal Management

Relief of ischemlc chest discomfort Titrate to effect
• Keep SBP greater than 90 mm Hg
• Limit drop In SBP to 30 mm Hg below
baseline In hypertensive patients
Improvement In pulmonary edema and • Titrate to e ffect
hypertension • Limit drop In SBP lo 10% of baseline In
normotenslve patients
• Limit drop In SBP to 30 mm Hg below
baseline fn hypertensive patlenls

72
 The ACLS Cases: Acute Strolre

----

Acute Stroke Case

Introduction The idenu'icatJOn and 1n ha ~t of patients wth acute stroKe iS within IM scope
of an ACLS proVldef. This case c:ov8'$ pnnc1pies of our-ol-nosp;ra care and tunaamenral
aspec;rs of 1ni1Ja11n-nospirat S<:Ute stroke care

Otlt·Of·hospltal acute stroke care lotuses on

• Rapid 1dent1f1cat10t1 and assessment ot pabents with stroke
• Rapid transport (with prearnval notifi<:abon) to a facility capable of providing acute
stroke care
In-hospital acute stroke care ltl(:tudes the
• Ab1lrty to rapidly determine patient ehg1b1l1ty for fibnnolyt1c therapy
• Administration of f1brinolyt1<: therapy to appropnate candidates, with ava1lab1hty of
neurolog1c medical supervision within target times
• Considerat10t1 of new treatment options like endovascular therapy
• IMlatJOn of the stroke pathway and pattent adm ssion to a strolte unit it available
The target wnes ana goals a,,. recommended by the N NOS ~!Ch tias rec:ommended
measi.ab e goais for the evaluattOO of atroKa palJe<lts These targets 0t goais should be
ac:l>oe';ed f0t at ieast 80% of 119t.ents w th acute strOl<e

Potential The ECG does nol take pnonty over obta 1"11ng a computed tomography tCT) scan No
A"hythmlas With arrhythmias are spec1!1c for stroke. but the ECG may identity evidence of a recent AMI or
Stroke arrhythmias such as atrial fibflllallon as a cause of an embohc stroke. Many patients wllh
stroke may demonstrate arrhythmias. but If the patient is hemodynomlcally stable, most
arrhythmias will not require treatment There Is general agreement to recommend cardmc
mon1tonng dunng the first 24 hours of evaiuauon in patients w1lh acute •schemoc stroke to
detect atnal hbnliatJOfl and ~entiaity t1fe-threaten1ng arrhythm as

Drugs for Stroke Thas case involves these drugs

• Approved fibnnolytic: agent (rtPAI
• Glucose (0.J
• Labetalol
• Nicard1p.ne
• Eralapnlat
• Aspino
• N1trop<Usside

73
 -
Part 0

Foundational F•ct• Major Types of Stroke

Stroke Is a general term It refers to acute neurotogic 1mpa1rment that lollows 1nterruptl()(I
In blOod supply to a specif<: are;i of the bran Although exped tl()US stroke care 1$ 1mpo<·
tant tor all patients. lh•S case emphasaes reperlUSIOfl therapy 'or acute 1SC'*'11C strok"

The 1?18/0f ~pes ot stro"e .ire

• 1scn<>mic: stro• e Accourts for 87% of a SllOl<es and is usually caused by ao occlo·
SIOn of an arter, to a reoon o! 11'9 brain 1F19ure 24~
• Hemon-nagic strol<e Accounts 'or 13% ot a4 stroo<es and occurs ""*'
a blOod ves..-.el
"' tne bra•n suddenly ruptures onto tile surround ng t•ssue F1bnnolytJC therapy rs con·
traindic:ated in thJS type of stroke AVOtd ant.coagulants

• lschemlc
• lntrocerebral
• Suborachnold

,,_ , . 24 . T.i>M ol stroke eq,iy...,..on _ , o4 "'""'"".,.. isct*"'C Wld po•Ol"..ally ollgoble tor tan-
nol\llC t,.,...opy • paIJen:s ou....ise qua 'Y nr.- percent ol Olrol<es are~ •"<I tlie """°'ty
gt t'*8 4'8 lf'tr~ The rraie-to-f~ lf"OOenCe flr.:JQ IS 1 25 lfl pet10n1 S~ tO 64 yelfS Cf aQlf,
t ~ '" lhel<!e 65 to 7~ 1 07 "'ttose 75 to 8' and 0 76 ... lhooe 85 - - ea~. l'llvt almOlt ''""'
thens-. ot first ~ stroo-:e com~ \Iii tn wn tes

Approach to Stroke Care

Introduction Each year 1n the Urnted Sta!es. about 795000 people have a new or recurrent stro<e
Strcke remains a eadlng c:ause of death •., the UMed States

Ea1y recogn.i.on of acute schemic: stroke •S •mportant because IV f brinolytc treatment

should be proVldeo as earf) as poss Dle gene<aJ y v.tth n 3 hours of onset of symptoms,
°' "•tlld\ 4 5 hours of onset of symptoms lor se ected pat.ents EndoliaJCUlar thernpy
may be given w11M 6 hours of onset of symptoms. but better outcomes are 8SSOCI·
ated "''h shoner tJmes to t·eatment. Most strokes occur at home and only hall of ocute
strOke patients use EMS fo1 transport 10 the hospnal. Stroke patients ohen deny OI try 10
ra11onallze their symptoms. Even h1gh-nsk patients, such as those with atrial f1bnllat1on 0<
hypenens1on. fall to recognze the signs of stroke. This delays activation of EMS ond treat·
rnont, resulting 1n increased morbidity and monallty.

Community and professional education Is essential, and ll has been successful In 1ncreos
1ng the proportion of eligible stroke patients treated with fibnnolyt1c therapy. Heollhcore
providers. hospitals, and canmurnt1es must continue to develop systems to 1mp1ove the
effic•en<:y and effectiveness of stroke care

74
 The ACLS Cases: Acute Stroke

Foundational FllcU Stroke Chain of Survival

The goal of stroke care is to mln1m1ze brain iniury and maximize the patient's recovery.
The Stroke Chain of Survival (Figure 25) described by the AHA and the American Stroke
Association is similar to the Chain of Survival for sudden cardiac arrest. It links actions
to be taken by patients. family members. and healthcare providers to maximize stroke
recovery. These links are

• Rapid recogn1hon and reaction to stroke warning signs

• Rapid EMS dispatch
• Raptd EMS system transpon and prearnval notification to the rece1v1ng hospital
• Raptd diagnosrs and treatment 1n the hosp.ta!

Figlil'e 25. The $110~0 Choin o! SuNival.

Foundational Facts The 8 D's of Stroke Care

The 8 O's of Stroke Care highhght the ma)O( steps in diagnosis and treatment of stroke
and key points at which delays can occur.

• Detection : Rapid recognition of stroke symptoms

• Dispat ch: Early activation and dispatch of EMS.
• Delivery: Rapid EMS identification, management. and transport
• Door: Appropriate triage to st roke center
• Data: Rapid triage, evaluat on, and management within the ED
• Deci sion: Stroke expertise and therapy selection
• Drug/Device: Fibnnolytlc or endovascular therapy
• Disposition: Rapid adm ss.on to the stroKe unit or cntical care umt
For more information on these cnt1cal elements. see the Adult Suspected Stroke
Algorithm (Figure 26).

Goals of Stroke Care The Suspected Stroke Algorithm (Figure 26) emphasizes Important elements of out -of-
hosp1tal care for possible stroke patients. These actions include a stroke scale or screen
and rapid transpon to the hospital As with ACS, poor not1llca11on of the receiving hospital
speeds the care of the stroke patient upon amval.

75
 part e
The NINOS has establlShed cnt1cal 111-hOspital time goals for assessment and manage-
ment of pa11ents with suspected stroke This algonthm reviews the critical in-hospital time
penods for patient assessment and treatment:

1. Immediate general assessment by 1he stroke team, emergency physician. or another

expert within 10 mmutes of arnval; order urgent noncontrast CT scan

2. Neurolog1c assessment by the stroke team or deslgnee and CT scan performed with-
in 25 minutes of hospital arrival

3. Interpretation of the CT scan within 45 minutes of ED amval

4. lnit1at1on of fibnnolyt1c therapy 1n appropnate patients (those without contralnd ca-

tions) Within 1 hour o1 hosp.1a1 amval and 3 hours from symptom onset

5. Door-to-admission time of 3 hours

Foundational Fact• The National Institute of Neurological Disorders and Stroke

The NINOS is a branch of the National Institutes of Health (NIH). Its m1ssmn is to reduce
the burden of neuroiog c di sease by supporting and conducting research. NINOS
researchers have studied stroke and reviewed data leading to recommendations for
acute stroke care. The NINOS has set cn11cal tune goals lor assessment and manage-
ment of stroke patients based on experience obtained in large s1ud1es ol stroke patients.

Critical Time Periods Patients with acute ischemlc stroke have a time-dependent benefit rorfibrinolytic therapy
similar to that of patients with ST-segment elevation M l. but this time-dependent benefit is
much shorter.

The cntical lime penod for adm1nistrat1on of IV fibrinolyt•C therapy begins wrth the onset of
symptoms. Cnllcal time penods from hOsp.tal arrival are summanzed below:

Immediate general assessment 10 minutes

Immediate neurologlc assessment 25 minutes

Acquisition of CT of the head 25 minutes

Interpretation of the CT scan 45 minutes

Administration of fibrinolytic therapy, 60 minutes

timed from ED arrival

Administration of fibri nolytlc therapy, 3 hours, or 4.5 hours In

timed from onset of symptoms selected patients

Administration of endovascular therapy, 6 hours in select ed patients

limed from onset of symptoms

Admission to a monitored bed 3 hours

78
 The ACLS Cases: Acute Stroke

Adult Suspected Stroke Algorithm

ldenUfy tlgns and symptom• or poollbfe stroke

Activate Emer90ncy Retl)OnM

2
l
EMS • ._,_,,. Ind Ktlons
Crit~

PC'O" ABCs g~• 0"Y!l<N1 • . j

NINOS • Plt.-4.grm ~la • "Ill
Time
Ooels
- , ......... ""' d '-"""" - 'lll$t)'O""ll'
oilQf!' 'O 51re:•e L~ •
.,, ric:ieorta.i c::or'S4d' onci trmneJ:et •o C.,. tcan
""" glUt<lse • """"' •
EO
r
. ..
Anlvll 3
~
~ 10 Immediate genatat a:uea•,....nt and 1tablliz.ation
• Ar.t.usa ABCs. vital .s.gri~
• Ptov~ OKYQen cf hypoxt-'f'IC'
• 001 n IV access a.no pett"orm NllllOl't1tOlfy ~
•
•
. ' "°°5oe~ UBaJ i ll'\dlCa'
...,, flll.IOiOglC SCfet'tq
""'°
~~

• Ac. .... ~tea.m

..., -'CT~ or IJl11 o!U....
· :n 12.-.ECG
.......
lD
4

lmm•di•l• MUrotoglc assessment by atroke team or designee

• Review patl<1<11 h stcxy
• E1t8bl1oh I ,..,. of syflUltom 00 . .1or I"'' known normal
• ~Olm rieurok>gic exam1natt0t1 INIH" S''Ok.• Scale oc

_
~ N@'Jrologica Se al~!

CD

"""'"
... Ha•u ... - .

II

Probable 1c ut1 lachem jc stroke; conlldtr flbrlnotytic thefapy

• Cht1el\'°" t1br1noty11c excl,JStOns
Fl..f ...al N'\.rologtt e'am: are dt<ll t• far Oly 1mpmviog to normal?

• ... ..~

........
ED

10

Rov,.w rk ktl -rrts will> pauent ond lomlly. • 8'1qm ,.,.,... or

II acceptabl« h~rtJoge pathway
• G1vn rt.PA • At;tm1t to ~trm<e una Of
• No anti< ~l)Y ants or anhplawle1 treatment
24 houro
'°' ITTltifl9'ti11 care unit

F190.. 21. The Mull SUspecteo S1ro>o Aig<Yllhm

77
 Part 0
Application of the We will now c1scuss the steps 1n the aigonthm, as well as other related topics.
Suspected Stroke • ldenl1fication of signs and symptoms of possible stroke and activation of emergency
Algorithm response (Step t)
• Cnucal EMS assessments and actions (Step 2)
• Immediate general assessment and stabilization (Step 3)
Immediate neurolog1c assessment by the stroke team or designee (Step 4)
• CT scan: hemormage or no hemorrhage (Step 5)
• f,bnnolyt>c therapy nsk strat1ftca11on rf candidate (Steps 6. 8 and 10)
• General stroke care (Steps 11 and 12)

Identification of Signs of Possible Stroke

Warning Signs The signs and symptoms of a stroke may be subtle. They Include
and Symptoms • Sudden weakness or numbness of the face, arm,
or leg, especially on ~ side of the body
• Sudden confUS<on
• Trouble speaking or understanding
• Sudden trouble seeing 1n one or both eyes
• Sudden trouble walking
• Dizziness or loss of balance or coordination
• Sudden severe headache with no known cause

Activate Stroke patients and their famllles must be educated to activate EMS as soon as they
EMS System detect potennal signs or symptoms of stroke. Currently half of all stroke patients are dt1v-
Immediately en to the ED by family or fnends

EMS provides the safest and most efficient method ol em8'1190CY transport lo the rospi·
lat The advantages of EMS transport 1nctude lhe following

EMS personnel can Identify and transport a stroke patient to a hospital capable of
providing acute stroke care and notify the hospital ol the patient's impending arrival.
• Prearnval notification allows the hospital to prepare ro evaluate and manage lhe
patient efficiently.
Emergency medical dlspatche<s also play a cn1ical role 1n timely treatment of potenlial
stroKe by

• Jdenbfy1ng possible stroke pauents

• Providing hogh-pnorrty dispatch
• Instructing bystanders 1n lifesaving CPR skills or other supportive care
rl needed while EMS providers are on the way

Stroke Assessment The AHA recommends that all EMS personnel be trained to recognize stroke by using a
Tools validated. abbreviated out-Of·hospnaJ neurolog1c evaluation tool such as the C1ncmna11
Prehosp1taJ Stroke Scale (CPSS) (Table 5)

Cmcmnat1 Prehospttal Stroke Scale

The CPSS ldentJl1es srroke on the basis of 3 physical findings:

• Facial droop (have the pallenr smile or try to show teeth)
• Arm drift (have the patient close eyes and hold both arms out, with palms up)
• Abnormal speech (hove rhe patient say, "You can't reach an old dog new tricks')

78
 The ACLS Cases: Acute Stroke

By using the CPSS, medical personnel can evaluate the patient in less than 1 minute. The
presence of 1 finding on the GPSS has a sensitivity of 59% and a speci ficity of 89% when
scored by prehospital providers.

With standard training in stroke recognition, paramedics demonstrated a sensitivity of

61 % lo 66% for identifying patients with stroke. After receiving tralning in use of a stroke
assessment tool, paramedic sensitivity for identifying patients with stroke increased to
86% to97% .

Table !S. The Cincinnati Prehospital Stroke Scale

Test
Facial droop: Have the patient show
teeth or smile (Figure 27)
I Findings
'
Normal - both sides of face move eqvany
Abnormal- one side of face does not
move as well as the other side

Arm drift: Patient closes eyes and Normal - both arms move the same
extends both arms straight out. with or both arms do not move at all (other
palms up, for 10 seconds (Figure 28) findings, such as pronator drift, may be
helpfuQ

Abnormal- one arm does not move or

one arm drifts down compared with the
other

Abnormal speech: Have patient
say, "you can't teach an old dog new
tricks"
Normal - patient uses conrect words with
no slurring
Abnormal-patient slurs words, uses the
wrong words. or is unable to speak

Interpretation: If any 1 of these 3 signs is abnormal, the probability of a stroke is 72%.

The presence of all 3 findings indicates that the probability of stroke Is greater than 85%.

Modified from Kothari AU, Pancioli A, Liu T, Brott T, Broderick J . Cincinnati Prehospital
Stroke Scale: reproducibility and validity. Ann Emerg Med. I 999;33(4):373-378. With per-
mission from Elsevier.

79
 part e

Ftgure 27. Facial droop.

Figure 28. One-sided motor weakness (right arm).

80
[ The ACLS Cases: Acute Stroke

Critical EMS Assessments and Actions

Introduction Prehospital EMS providers m ust minimize the interval between the onset of symptoms and
patient arrival on the ED. Specific stroke therapy can be provided only in the appropriate
receiving hospital ED, so time in the field only delays (and may prevent) definitive therapy.
More extensive assessments and initiation of supportive therapies can continue en route
to the hospital or in the ED.

Critical EMS To provide the best outcome for the patten! w ith potential stroke, do the following:
Assessments and
Identify Signs Define and Recognize the Signs of Stroke (Step 11
Actions
Support ABCs Support the ABCs and provide supplementary oxygen to
hypoxemic (eg, oxygen saturation less than 94 %) stroke
patients or those patients with unknown oxygen saturation.

Perform stroke Perform a rapid out-of-hospital stroke assessment (CPSS,

assessment Table 5).

Establish t.i me Det ermine when the patient was last known to be normal or
at neurologic t)aseline. This represents time zero. If the patient
wakes from sleep with symptoms of stroke, time zero is the last
lime the patient was seen to be normal.

Triage to stroke Transport the patient rapidly and consider triage to a stroke
center center. Support cardiopulmonary function during transport. If
possible, bring a witness, family member, or caregiver w ith the
patient to confirm time of onset of stroke symptoms.

Alert hospital Provide prearrival notification to the receiving hospital.

Check glucose During transport, check blood glucose if protocols or medical

control allows.

The patient with acute s troke is at risk for respiratory compromise from aspiration, upper
aorway obstruction. hypoventilation, and (rarely) neurogenic pulmonary edema. The combi-
nation of poor perfusion and hypoxemia w ill exacerbate and extend ischemic brain injury.
and it has been associated with worse outcome from stroke.

Both out-o f-hospital and in-hospital medical personnel should provide supplementary
oxygen to hypoxemic (ie, oxygen saturation less than 94 %) stroke patients or patients for
whom oxygen saturation is unknown.

81
 Part G

Foundational Facts Stroke Centers and Stroke Units

Initial evidence indicates a favorable benefit from triage of stroke patients directly to
designated stroke centers. but the concept of routine out·of· hospital tnage of stroke
patients requires continued evaluatton.

Each receiving hospital should define its capability for treating pattents wilh acute
stroke and should communicate this information to the EMS system and the community.
Although not every hospital has the resources 10 safely administer fibrinolytics or endo-
vascular therapy, every hospital with an ED should have a written plan that describes
how patients with acute stroke will be managed In lhal lnslilution. The plan should
• Detail lhe roles of healthcare providers in lhe care of patients with acute stroke, includ-
ing identifying sources or neurologic expertise
• Define which patients to treat wrth fibrinolytics or endovascular therapy at that facility
• Describe when patient transfer to another hospital with a dedicated stroke unit is
appropriate
Patients with stroke should be admitted to a stroke unit when a stroke unit with a multi-
disciplinary team experienced in managing stroke is available within a reasonable trans-
port interval.

Studies have documented improvement in 1-year survival rate. functional outcomes, and
quality of ltte when patients hospitalized ror acute stroke receive care in a dedicated unit
with a specialized team.

In-Hospital, Immediate General Assessment and Stabilization

Introduction Once the patient arrives in the ED, a number of assessment s and management activities
must occur quickfy. Protocols should be used to minimize delay in definitive diagnosis and
therapy.

The goal of the stroke team, emergency physician, or other experts should
be to assess the patient with suspected stroke within 10 minutes of arrival
in the ED: ''time i:s orain" (Step 3).

ED providers should do the following:

Immediate General
Assessment and Step I Actions
Stabilization Assess ABCs Assess the ABCs and evaluate baseline vilal signs.

Provide oxygen Provide supplementary oxygen to hypoxemlc (eg , oxyhe-

moglobin saturation less than 94%) stroke patients or those
patients wilh unknown oxygen saturation.

Establish IV access Establish IV access and obtain blood samples tor baseline
and obtain blood blood count, coagulation studies, and blood glucose. Do not
samples let this delay obtaining a CT scan of the brain.

(continued)

82
 The ACLS Cases: Acute Stroke

(canunued)

Step Actions

Cheek glucose Promptly treat hypoglycemia.

Perform neurologic Perfonn a neurolog1c screernng assessment Use the NIH

assessment Stroke Scale (NIHSS) or a similar tool.

Activate the stroke Activate Iha stroke team or arrange consultation with a stroke
team expert based on predetermined protocols

Order CT brain Order an emefgenl CT scan of the brain Have 11 read promptly
scan by a qualtf1ed phys1c1an

Obtain 12- lead ECG Obtain a 12-lead ECG, which may identify a recent or ongoing
AMI or arrhythmias (eg, atrial fibrillation) as a cause of embollc
strok e. A small percentage of patients with acute stroke or
transient ISChemte attack have coexlst1ng myocardial ISCheml3
°' other aboormalrt1es. There is general agr&M'lent to recom-
mend cardiac monitoring during the first 24 ho<Jrs of evalu-
arion In patients w ith acute lschemic stroke to detect atrial
fibnllalion and potentlally life-threatening arrhythmias.

Life-threatening arrhythmias can follow or accompany stroke,

pancutarly 1ntracerebral hemon'hage. If the patient IS hemody-
narn.cally stable. treatment of non-l1fe-threaten1ng anhytlVnlaS
(bradycardoa, vr, and atnoventricular [AV] conducuon blocks)
may not be necessary.

Do not delay the C T scan to obtain the ECG.

Immediate Neurologic Assessment by Stroke Team or Designee

Overview The stroke ream. neurovascular consultant. or emergency physician does the following:

• Reviews the pal!ent's history. performs a general physical exam1nauon, and estab-
hshes time of symptom onset
• Perf()(ms a neurologc examrnatlO<l (eg NtHSS)

The goal for neurolog1c assessment is within 25 minutes of the patient's

arrival in the eO: "time IS brain"' (Step 4).
- - -- --- --- - -- ---
Establish Symptom EstabhSh1ng the 11me of symptom onset may require 1nterview1ng out·of-hosprtal providers.
Onse t wrtnesse5. and family memberS 10 determme the tirne the patient was last known to be
normal.
- - - - - - ----

83
 Part 0
Neurologic Assess the patient's neurologic status by using one of lhe more advanced stroke scales.
Examination Following 1s an e~ample·

National Institutes of Health Stroke Scale

The NIHSS uses 15 items to assess the responsave stroke patient. This is a
valldatad measure of stroke seventy based on a detailed neurolog1c exam1nat1on
A detailed d iscussion 1s beyond the scope o f the AC LS Pro vider Cours e.

CT Sean: Hemorrhage or No Hemorrhage

Introduction A critical decision point In tile assessment of the patient with acute stroke Is the perlor-
mance and interpretation or a noncon1rast CT scan to differentiat e ischemic lrom hemor-
rhagic stroke. Assessment also includes identifying other structural abnorrnahtles that may
be responsible for the patient's symptoms or that represent contra1nd1cat1on to fibr1nolyllc
thecapy The 1nrtJaJ nonconiras1 CT scan IS the most 1mponant test lor a pa!lent with acute
stroke
• If a CT scan IS no1 readily available, stabilize and promptly transfer the patient
to a fac1hty wllh this capability
• Do not give agpir1n. heparin, or rtPA until the CT scan has ruled out lnttacramal
hemorrhage

The CT scan should be completed within 25 minutes of the patient's amval

m the ED and should be read within 45 minutes from £0 arrival: '"time is
brain" (Step 5).

Decision Point: Add1tlonal 1rnagrng techniQUes such as CT per!USlon. CT angiography, or magnetic reso-
Hemorrllage or nance 1rnag•ng scans of patents with suspected stroke should be promptly interpreted
No Hemorrllage by a physician skilled 1n neuroimag1ng 1n1erpretatlon. Obtaining these studies should not
delay initiation or IV rtPA in eligible patients. The presence of hemorrtiage versus no hem-
orrhage determines the next steps In treatment (Figures 29A and BJ.

Yes, Hemorrhage Is Present

It hemorrhage is noted on the CT scan, the patient is not a candidate for f1bnnolyt1cs.
Consult a neurologist or neurosurgeon Consider transfer for appropriate care (Step 7).

No. Hemorrhage Is Not Present

It the CT scan shows no eVldence of hemo<Thage and no sign of other abnoonality (eg,
tumor, recent stroke), the patient may be a candidate for f1bnnoly!Jc therapy (Steps 6 and 8)

If hemorrhage Is no! present on the Initial CT scan and the patient is not a candidate for
hbrinolytics for other reasons, consider giving aspmn (Step 9) either rectally or orally alter
perlorming a swallowing screen (see below). Although aspmn is not a ume·crrtJcal inter-
ven1ion. rt IS appropnate to adm1n1ster aspmn 1n the ED rl the patient IS not a candldale
for f1b<1nolys1s. The pa11ent must be able to safely swallow before asptrln lS given orafly
Otherwise. use the supposnory lorm.

84
 The ACLS Cases: Acute Stroke

B
F19ure 29 . Oociusion 1n a cerebrat art9"V by a 1hrombus A. Atoa ot •ntarctlon surroundir'IQ lmm9dmte
srte and distal potbOn of ora1n tissue after occlusion. B, Afe:J of tSChOmtC penumbra (1SCh9mtC. bul not yet
infarcted (dead] b<ain tissue) surrounding areos of lnfarctoon This il!Chllll'hC penumbra 1s oh•• but dysfunc·
tlonal ~-of altered membrane potentials The dysfunc1oon IS poton11•l'Y ~....,blo Cwent stroke
ueatmenl tnes 10 k""P the area of permanent b<a«\ infarc11011 as sm•~ at poss.Ole by proventing ll>O areas ol
reversbe brain ISChemia in I.he penumbra from tran!,form1ng nto targor &red of 1rreversiokt brUl Lflfarct;on.
 Part 0
Fibrinolytic Therapy

Introduction Severol studies have shOwn a higher likelihood of good to excellent functional outcome
when rtPA is given to adul:s with acute 1schemic stroke within 3 hours of onset of symp-
toms. or wtthon 4.5 hours of onset of symptoms for se1ected patients But these results
are obtaoned when rtPA is grven by phyStaans m hospitals with a stroke protocol that
rigorously adheres to the ellg1b1hty cntena and therapeutic regimen of the NINOS protocol.
Evidence from prospective randomized studies 1n adults also documents a greater hkeh-
hood of benefit the earlier lreatment begins.

The AHA and stroke guidelines recommend g1v1ng IV rtPA to patients with acute ischemlc
stroke who meet the NINOS elig Dlhty critena 11 it IS given by
• PhyStC1ans using a clearty dehned 1nst1tutt0nal protocol
• A knowledgeable 1nterd1scipllnary team fam1har with stroke care
• An Institution with a commitment to comprehensive stroke care and rehabilitation
The superior outcomes repcrted tn both community and tertiar/ care hospitals 1n the
NINOS trials can be difficu t to replicate in hospitals with less expenence in. and institu-
tional commnment to, acute stroke care. There 1s strong evidef1ce to aVO<d all delays and
treat pahems as soon as possible. Failure to adhefe to protocol is associated with an
increased rate of complications, particularly nsk ol lntracranial hemorrhage.

Evaluate for If the CT scan 1s negative for hemorrhage, tho patient may be a candidate for fibrinolytic
Fibrinolytlc Therapy therapy. Immediately perform further ellgibrhty and risk stratification:

• If the CT scan shows no hemorrhage, the probabtlit:y of acute 1SChemic stroke

remains. Re'llew mclt/Slon and exc/uSIO() cntena for N f1brinolytlc therapy (Table 6) and
repeat the neurologic exam (NIHSS or Canadian Neurological Scale)
• It the patient's neurolog•c function is rapidly improving toward normal, fibnnolytics
may be unnecessary

Table e. Inclusion and Exc lusion Characteristics of Patients With lschemic Stroke
Who Could Be Treated With rtPA Within 3 Hours From Symptom Onset'

Inclusion Criteria

• Otagnos.s of ischem1c strOke causing measurable neurolog<: dehc11

• Onset of symptoms <3 hours before beginning treatment
• Age >18 years

Exclusion Criteria

• Significant head trauma or prior stroke in previOus 3 months

• Symptoms suggest subarachnoid hemormage
• Artenal puncture at noncompressible site 1n previous 7 days
• History of previous intracramal hemon'hage
- lntracranial neoplasm, arterlovenous malformation, or aneurysm
- Recent intracranial or lntrasptnal surgery
• Elevated blood pressure (systolic > 185 mm Hg or diastolic > 110 mm Hg)
• Active internal bleeding
• Acute bleeding diathes•s, including but not limned to
- Platelet count < 100000/mm'
- Heparin received within 48 hours, resulttng in aPTT greater than the upper limit of
normal
- Current use of anticoagulant with INR > 1.7 or PT > t 5 seconds

(conhnuedJ
ae
 The ACLS Cases: Acute Stroke

(conMued}

- Current use of direct th'Olllbin inhibitors or direct factor xa

inhibitors with elevated
sensitive laboratory tes:s (such as aPTT, JNR. platelet count, and ECT; TI: or
appropriate fact or Xa activity assays)
• Blood glucose concentration <50 mg/dl (2.7 mmof/L)
• CT demonstrates mult1lobar infarction (hypodenSlty > Y.. cerebral hemisphere)

Relative Exclusion Criteri•

Recent experience suggests that under some c1rcumstances- w1th careful consider-
ation and weighing o r risk to benetit - pat1ents may receive flbrlnolytic therapy aesphe
1 or more relative contraindications. Consider nsk to benefit or rtPA administration
carefully 1f any one of these reiat rve coo1ra1nd lcations is present:

• Only minor or rapidly 1mprov1ng stroke symptoms (clearing spontaneously)

• Pregnancy
• Seizure at onset with postlctal residual neurologlc im pairments
• MaJOf surgery or serious trauma within previous 14 days
• Recent gastrointestinal 0< unnary tract hemorrhage (within prevtOUS 21 days)
• Recent acute myocardial infarction (within previous 3 months)

Notes
• The checklist includes some US FDA-approved indications and contraindications for
admlnlstrauon of rtPA for acute ischemoe stroke. Recent AH/VASA guideline reviSIOOS
may d iffer slightly from FDA cnteria. A physician with experUse In acute stroke care
may modify this fist .
• Onset time is either witntssed or last known normal.
• In patients without recent use of oral anticoagulants or heparin, treatment with rtPA
can be Initiated before 8\ailab1lrty of coagulation study results bu1 should be d1scon-
ltnued If INR is > 1.7 or PT is elevated by local laboratory standards.
• In patients wrthoul histo,., of thrombocytopenia, trea1rnent w th rtPA can be initiated
before avaifabifrty of platelet count but should be discontinued if platelet count is
<100 000/ mm1 •

Abbrevla1100s aPIT. a<:tivatad par11al thromboplastln l me: CT. computed tomography: ECT ecadn clo tting
time: FDA. Food and Drug Adn'ln1Stott10<1: INR. lntoma1t0nal normalized ratio: PT, prothrombln '"'' '" rtPA.
moorrbNnt t<SSUe ~ acw.llor n. ll1<0mbo'I time
·Jauch EC. 5'1vlt' JL Adams HP Jr ti a Guiaet nes fOI !he early manaqemenl ol pat<M\ts -..im ac.rta osch·
erruc strokQ: ;i guidel.ne for oo:i U"Kare ptofesSioo.a s from the Amenc:.a.n Hoart ;\ssQC1a11001Amencar Stroke
1

Association. Srro<e 2013 ;44(3\:870-941.

Potential Adverse As wrth all drugs. fibrinolytics have potential adverse effects. At this point, weigh the
Effects patient s nsk for adverse events against the po1enoa1 benefit ancJ d iscuss wiU 1Ille paltent
and famtly.
• Confirm that no exclus101 cnteria are present (Table 6).
• Consider risks and bene'its.
• Be prepared to m onitor and treat any pot ential compllcatlons
The waior comp foeation of IV rtPA for stroke Is 1ntracran1al hemorrhage. Other bleeding
comphcat1ons may occur and may range from minor to major. Ang1oedema and transient
h ypotension may occur.

87
 Part 0

Patient Is a If the patient remains a cand•date lor fibnnolybc therapy (Step 8). dtSCUss the nsks and
Candidate for potential benefits with the oatient or family If available (Step 10). After this d1scuSS1on 11
Fibrlnolytic the patient or family memters decide to proceed with fibnnoly1 c therapy, give the patient
Therapy rt PA. Begin your 1nst1tution's stroke rt PA protocol, often called a "pathway of care.•

Do not administer anti=oagulants or antiplatelet treatment for 24 hours

after administration of rtPA, typtca//y until a follow-up CT scan at 24 hours
shows no intracrania/ hemorrhage.

Extended IV rtPA treatment ot caretutly selected pauents with acute 1schem1c strOke wtth IV rtPA between
Window 3 to 4 .5 3 and 4.5 hours after onset of symptoms has also been shown to improve clinical out·
Hours come. al1hough the degree of chnical benefit 1s smaller than that achieved with treatment
within 3 hours. Data supporting treatment in this time window come from a large, random-
ized trial (ECASS-3 [European Cooperative Acute Stroke St udy)) that specifically enrolled
patients between 3 and 4.5 hours after symptom onset, as well as a meta-analysis
of prior trials.

At present, use of IV rtPA v11thin the 3· to 4.5-hour window has not yet been approved
by the US Food and Drug Administration (FDA), although 11 is recommended by an AHN
American Stroke Association science advisory. Admnistrahon of IV rtPA to patients with
acu1e 1schemic stroke who meet the NINOS or ECASS-3 Illig bthty cntena (Table 7) is
recommended ii rtPA 1s administered by physicians in the setting of a clearly defined
protocol. a knowledgeable team. and Institutional commitment.
Table 7 . Additional Inclusion and Exc lusion Charac teristics o f Patients With A cute
lschem lc Stroke Who Co uld Be Treated With IV rtPA Wi thin 3 to 4.5 Hours From
Symptom Onset•

Inclusion Criteria

• Diagnosis of ischemte stroke causing measurable neurolog c deficit

• Onset of symptoms 3 ·o 4.5 hours before beginning treatment

Exclu&ion Criteria

• Age >80 years

• Severe stroke (NIHSS score >25}
• Taking an oral anticoagulant regardless of INR
• History of both diabetes and prior ischemic stroke

~"""' INR. lmernabOn,ll--!l41<1 '"10: NIHSS. NattOnal Inst.tut.. of He3l"JI Stro«e Scale r1PA.
recomb11•1nt t ssue p4asmnoget1 ac•va10<

"Del Zoppo GJ, Save< JL, Jaueh ~C. Adams HP Jr. Amoocan Heart Assoc1a1on Strol<o Council. Expanst0n
01 the t,me w10dow for lfea1mentof acu1A 1schemic stroite with mtraveoous 1.ssuo plasm nogen actJ·
va1or: a Sciance advisory from the American Hean Assocmbon/f\motteun Slroke Association, Stroko.
2009.4~8l:294o·2948.

Intra-arterial rtPA Improved outcome from use ol cerebral 1ntra-arter1al rtPA has been documented For
patients with acu1e 1schemlc stroke who are not candidates for standard tv flbnnolyS!S.
e0<1sidet intra-arterial fibnnolys•s 10 centers with the resoutWs and expertise to provide 11
w1thlt\ the first 6 hours after onset of symptoms. Intra-arterial adm1n1strat1on of rtPA is not
yet approved by the FDA

88
 The ACLS Cases: Acute Stroke

Endovascular Therapy

Introduction Substantial new high-quahty evidence regarding the cl n1cal efficacy of endovascular treat-
ments of acute ischemic stroke has recently become available. To this end, while IV rtPA
remains as the first-line treatment. the AHA now recommends endovasc ular therapy for
select patients with acUle 1schem1c stroke.

As with fibnnolytic therapy, patients must meet inclusion cnteria to be considered for
this treatment S11r11larty, bener clinical outcomes are associated wrth reduced bJnes from
symptom onset to reperlus1on. but these new treatment options offer the added benefit of
expanding the treatment window up to 6 hours from the onset of symptoms.

Intra-arterial rtPA Improved outcomes from use of cerebral rntra-arterial rtPA has been documented. For
patients with acute ischemic st roke who are not candidates for standard IV fibrinolysis,
consider intra-arterial fibrinotysis In centers wrlh the resources and expertise to provrde it
within the llrst 6 hours after onset of symptoms. Intra-arterial administration of rtPA has
not yet been approved by the FDA.

Mechanical Clot Mechanical clot disrupnon or retneval with a stent has been demonstrated to proV1de
Disruption/ Stent clinical benefit in selected patients wrth acute ischemic stroke.
Retrievers Patients should receive endovasculor therapy wtlh a stent retriever 11 they meet all the
following criteria:

• Prestroke m RS score of 0 to 1
• Acute 1schem1c stroke receiving Intravenous rtPA within 4.5 hours of onset
according to guidelines from professional medical soc1ettes
• Causative occiusion of the internal carotid artery or proximal MCA (M1)
• Age t 8 years or older
• NIHSS score of 6 or greater
• ASPECTS of 6 or greater
• Treatment can be initiated (groin puncture) within 6 hours of symptom onset

Systems of Care Recent c linical trials suggest that all patients eligible for endovascular therapy should be
considered tor this treatment in add1t1on to IV rtPA. Systems of care for acute ischemic
stroke need to be 1n place so that eligible patrents can be quickly transported to compre-
hensive stroke centers that offer these treatments.

General Stroke Care

Introduction The general care of all patients with stroke includes the following:

• Begin stroke pathway.

• Support airway. breathing, and circu1ahon.
• t.'on1tor blood glucose.
• Monitor blood pressure.
• Monrtor temperature.
• Perform ctysphagia screening
Monitor tor complications of stroke and fibrinolyt1c therapy.
• Transfer to general intensive cmo if Indicated.
 Part 0
Begin Stroke Pathway Admit patients to a stroke unit (1f available) for careful observation (Step 11 ), including
monitoring o f blood pressure and neurologic status. If neurologic status worsens, order an
emergent CT scan. Determine if cerebral edema or hemormage ls the cause; consult neu·
rosurgery as appropriate.

Additional stroke care includes support of the airway, oxygenation, ventilation. and nutri-
tion. Provide normal saline to maintain intravascular volume (eg, approximately 75 lo 100
ml.lh} if needed.

Monitor Blood Hyperglycemia is associated with worse clinical outcome in patients with acute isch-
Glucose emic stroke. But there is no direct evidence that active glucose control improves c linical
outcome. There is evidence that insulin treatment of hyperglycemia in other critically ill
patients improves survival rates. For this reason. consider giving IV or subcutaneous
msuhn to lower blood glucose in patients with acute ischemic stroke when the serum
glucose level is greater than 185 mg/dL

Monitor for Prophylaxis for seizures 1s not recommended. But treatment of acute seizures followed by
Complications administration of antlconvulsants to prevent further seizures is recommended. Monitor the
of Stroke ancl patient for signs of increased intracranial pressure. Continue to control blood pressure to
Fibrinolytic reduce the pot ential nsk of bleeding.
Therapy

Hypertension Although management of hypertension in stroke patient s 1s controversial, patients who

Management in rtPA are candidates for fibrinolytic therapy should have their blood pressure cont rolled to lower
Candidates the risk of intracerebral hemorrhage after adm1nistra1Jon of rtPA General guidelines for the
management of hypertension are outlined In Table 8.

If a patient is eligible for fibrinolytic therapy, blood pressure must be 185 mm Hg or less
systolic and 110 mm Hg or less diastolic to limit the risk of bleeding complications.
Because the maximum interval from onset of stroke until effective treatment of stroke with
rtPA is lim ited. most patients with sustained hypertension above these levels will not be
ellgibte for IV rtPA.

Table 8 . Potential Approaches to Arterial Hypertension in Acute lschemic Stroke

Patients Wllo Are Potential Candidates for Acute Ref)<lrfusion Therapy*

Patient otherwise eligible tor acute reperfusion therapy except that blood pressure 1s
>185/1 10 mm Hg:

• Labetalol 10-20 mg IV over 1-2 m inutes, may repeat • 1 time, or

• Nicardipine IV 5 mg/h. titrate up by 2.5 mg/h every 5-15 minutes. maximum 15 mg/h;
when desired blood pressure is reached, adjust to maintain proper blood pressure
limits.or
• Other agents (hydralazine. enalaprilat, etc) may be considered when appropriate
If blood pressure is not maintained at or below 185/11 O mm Hg, do not administer rtPA.

(continued)

90
 The ACLS Cases: Acute Stroke

/COntd'l<led}

Managemenl of bk>od Pf9Aol'I <Mng n i aft• t1PA or other aaite reperlUSIOf'I thetllP)':
• Monitor blood pressunl 8\'lfY 15 rTWllJles for 2 hotn from the Start of ttPA lherapy.
tMn every 30 monutes for 6 llOutS and then f1VetY hour tor 16 hours
If S)'$tolic blood pressure 180·230 mm Hg or cfiastolic blood pressure 105-120 mm Hg:
• Labetalol 10 mg IV followed by continuous IV infusion 2·8 mg/min, or
• N1cardipine IV 5 mg/h. 111r1te up lo desired effect by 2.5 mg/h every 5·15 minutes,
maximum 15 mg/h
If blood pressure not cont/Oled or dlastoltc blood pressure > 140 mm Hg. consider
sodium nitropruSSlde

"Jauch CC. Sa".,.JL. Adams, HP Jf .,c al G 10.lf*S tor the early m.an.aQef"l"lt ot pati.ar'lt& wirh :M:Ut• 1scn-
em1C stroke. a gUIO&line '°'
nMl1hcWtt prcl,.~lonOls ~ tne Amer.can Hean Associauoro.'Amenc.;an Stroli.•
Assooat•on Slrol.• 2013,44/3187C 947

The management of anenal hypi>tteoslOO 1n palients not undergoing reperfusion strate

g1es remains cha"eng•ng Data to guide recommendat>OnS for treatment are •nconclusive
or contlCIJng Many patoeots have SPOOtaneous declines n blood piessure dunng the f1~t
24 hours ~er onset o• stlOke Unt more def,,_. ve da!a are ava..acie the t>ene' n of 11&a1.ng
attenaJ hypettenslOfl in trie w.iing of acute ISCl>emc S'JOo<e s not "eil es~ IC!ns
lib Le.el of Evidenee C~ Patents v.flO have malignan: hypertension or olhet m«1ca1
1ndica11ons for aggressM! tre•tment of blood p<essUre should be treated accord ngly
(re111sed from the previous quidel1ne) '

,,
 P •rt 0

Cardiac ArTest: VFIPulseloss VT Case

Introduction Ths case focuses on the ar.sessnient ano actJOns used for a cardiac arres1 due to VF or
pu1se1ess VT that is refractory (unresponsive) to the first shock

In this case and dunng the course. you will have an opportunity to demonstrate effec
11ve high-performance team behaviors while perforrrnng the assessment and ac11on
s11111s Ounng the BLS Asses~ment, team members will perform continuous htgh -qualtty
CPR with effec11ve chest compressions and vent1latton. The team leader wiU conduct the
Pnmary Assessment. lncluchng rhylhm recogn.t1on (shockable versus nonshockable). deft·
br 1ation usmg a manual del1br~ta1or. resuscrtatton drugs. a discussion of IV/intraosseous
(10) access. and advanced airways

The success of any resusc1101ion nltempt 1s bwlt on a strong base of htgh-quahty CPR and
def1bnllat1on when required by 1he pouent's ECG rhylhm. To improve care. leaders must
assess the performance of each system component Only when performance is evaluated
can part101P3nt!ii m ~ :;ystom 0Hoct1voty 1ntetVcnc io tmprove care 1lvs process of quality
1mpro•emen1 consists of a~ 11erato\le ano conlJllUOUS cycle of
• Systemauc evaJuatoo of resusc11a1JOl'I caie and OUtcome
• ~ w:th SU.keholdo< feedbac<
• Strategoe e!!orls to adOfesa Identified defooenoes
Another charactenstic of h1~h-quahty CPR is m1nrnal 1nterrupuons tn chest compressions
Studies demonstrate that healthcare providers interrupt compressions far too often and fo1
100 long. In some cases spending 25% to 50% of a resuscitation attempt without dellver-
tng chest compressions

Chest compression frac11or (CCF) Is the proportion of time dunng cardiac arrest resusclto·
hon when chest compressoos are performed CCF should be as high as possible. at least
60'(> arid Idea ly greater th.In 80'1b Data suggest lower CCF is associated w1lh decreased
ROSC arid su,..,..,aJ to hosptal discharge

M easurement Quality 1mpro,ement rl!loes on val:d assessment of resuscrtatoo performance arid ootcome
• The Utste1n gu>dehnes provide guidance for core performance measures, 1nctuchng
- Ra1e of bystander CPR
- Time to de~bollatoOn
- Survival to hospital C1scilatge
• 11 is important to share 1nforma1ion among a.II links in the s~s1em of care. includ1no
- Dispatch reco<ds
- EMS pauent care repo11
- Hospnal records

Benchmarking and 0010. should be systematlceny reviewed and compared internally to prior performonce and
Feedback externally to similar systems Ex1s11ng registries can facilitate this benchmarking eff0t1
Examples include the
• CARES for OHCA
• Get w m Tt>e Gutdehnes0 RMuscitato0n program for IHCA

112
 The ACLS Cases: Cardiac A/Test: VF/Pulseless VT

Change Simply measuring and benchmarking care can pos111vely Influence outcome. However.
ongoing review and interpretation are neoessaiy to identify areas for improvement, such as
• Citizen awareness
• CrtJzen and healthcare protessJOOal education and training
• Increased bystander CPR response rates
• Improved CPR performance
• Shortened time to defibrillatlon

Rhythms for 'IF/ This case involves these ECG rhythms:

Pulseless 'IT • VF (example in Figure 30)
• VT
• ECG artifact that looks like VF
• New LBBB

Flgu,. 30. Example of ventncular fibrillation.

Drugs for 'IF/ This case Involves these drugs:

Pulseless 'IT • Epinephrine
• Norep1nephrine
• AmlOdarone
• Lldoca1ne
• Magnesium sulfate
• Dopamine
• Oxygen
• Other medications, depending on the cause of the VT/pulseless VT arrest

Managing VF/Pulseless VT: The Adult Cardiac Arrest Algorithm

011erview The Adult Cardiac Arrest Algorithm (Figure 31) is the most important algonthm lo know
for adult resuscitation. This alg0<ithm outlines all assessment and management steps for
the pulseless patient who does not initially respond to BLS interventions, 1nclud1ng a hrst
shock from an AED. The algorithm consists of the 2 pathways for a cardiac arrest:
• A shockable mythm (VF/pulseless VT) displayed on the left side of the atgonthm
• A nonshockable mythm (asystole/PEA) displayed on the nght side of the algorithm
Throughout the case discussion of the Cardiac Arrest Algorithm, we will refer to Steps 1
through t 2. These are the numbers assigned to the steps in the algorithm.
~~~~ ·~~~~~~~~~~~~~ ~~~

'IF/ p'IT (Left Side} Because many patients with sudden cardiac arrest demonstrate VF at some point on thetr
arrest, it is hkely that ACLS providers will frequently follow the left side of the Cardiac
Arrest Algorithm (Figure 31). Rapid treatment of VF according to this sequence is the best
approach to restoring spontaneous circulation.

Pulseless VT is onctuded 111 the algonthm because rt 1s treated as VF. VF and polseless VT
require CPR until a defibrillator 1s available. Both are treated with high-energy unsynchro-
nized shocks.

93
 - Part 0
-

Asystole/ PEA The right side of lhe algorithm outlines the sequence of actions to perform 1f the rhythm is
(Right Side} nonshockable. You will have an opportunity to practice this sequence In the Asystole and
PEA Cases.

Summary The VF/Pulseless VT Case gives you lhe opportunity to practice performing rapid treat-
ment of VF/pVT by ronow1ng the steps on the left Side of the Cardiac Arrest Algonlhm
(Steps 1 through 8).

Adult Cardiac Arrest Algorithm-2015 Update

• t>.:ro~•~5~.-ld
•.n: "CY'- •Xl-~ Wida..,..
~-'*~rec:ot
· ~f"ttnlL'lllKJle.in
OCIT'O"esoS~&.
• A.lltll.!~Y1!1111•1'lc:Jl"I
• R::ilit!e~Stole~f'I')'
2 Mirute9. °' 90Ulll!I 1r r.:1t•o\Md
• tt no aa,a11Ctd iuw:iy,
JO? <:tJ!f'!l)fQ$SIOn-Yen1111'10n
Vu No rato
2 • 01.13(1Ulltr""~w.:1vr.fnr-n

VFIpVT .. C:'VIOQ•aptvv
- lf~oo .-.10m1n•ly ~ttlnpt

_--. _
l.;;.1r1p-uY11tC'.PPriu;1iltv
• t!•r.i Mb:rl~' pr.....-e

lfl'9la.oJltcln~aMl.....-
ltollC-•~ ...20,.,,..""1.
~llO~CJIR

......,..........,_
009I! JI ,21>-200 I A.....,..,._...

• EnoolrachHilr~flf
SIJP'~aci'.:'.W'IC.9dVMty
• 'N:twetcrn ~(if
~ COCO"hm #-1
f"ONOrC::IUba~
· ~~~f'l--
7-'!'~f¥el)6~
f0bomta.JT"rf...,~

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."""'°"""""'..,_,,,
• !o.Df'uOI ~likled lnr:f'NIM on
r£roc, (lyp~l1t ".60 f'l'll"f'i tly!
I • ~pnr1i1'TeolJS arteilal !J•tl'll(llt
wa~ w1lf'I 61t!;,t-.::irlnri.il
tmnlt01'1!"1:1

• H1~en-.ol
• H•rpal'.>.::i
12 • H:fdr.oger IO'l f.cldOMI
• HHJOlt'r~•
• If no signs of "efum Of •H;~
Ooto5or7
spon't~ c-a.MllOI" •Tfn$IOl"'pr-~.u
•TarrClOl'llll'Ji@~
(ROSC1- go to 10 or 11
•T~<"'S
• "f'OSC. go 10 · ~p~
Po.t-C.....C"'-tC... _:.Tl~~

' igure 3 I . The Adun Caroac An 1 A.9oottYn

14
 The ACLS Cases: Cardiac Arrest: VFIPulseless VT

Application of the Adult Cardiac Arrest Algorithm: VF/ pVT Pathway

Introduction This case discusses the assessment and treatment of a patient with refractory VF or
pulseless VT. This algorithm assumes that healthcare providers have completed the BLS
Assessment, including activation of the emergency response system, pertorming CPR.
attaching the manual defibrillator, and delivering the first shock (Steps 1 through 4).

The ACLS high-performance team now intervenes and conducts the Primary Assessment.
In this case, the team assesses the patient and takes actions as needed. The team leader
coordinates the efforts of the high-pertormance team as they pertorm the steps listed on
the VF/pVT pathway on the left side of the Cardiac Arrest Algorithm.

Minimal Interruption A team member should continue to perform high-quality CPR uni I the defibrillator arrives
of Chest and is attached to the patient. The team leader assigns roles and responsibilities and
Compressions organizes interventions to minimize interruptions in chest compressions. This accomplish-
es the most critical interventions for VF or pulseless VT; CPR with minimal interruptions In
chest compressions and defibrillation during the first minutes of arrest.

The AHA does not recommend continued use of an AED (or the automatic mode) when
a manual defibrillator is available and the provider's skills are adequate for rhythm inter-
pretation. Rhythm analysis and shock administration with an AED may result in prolonged
interTUptions on chest compressions.

Figure 32 demonstrates the need to minimize interruptions in compressions. CPP is aortic

relaxation ("diastol1c") pressure minus right atnal relaxatJon {"diastolic") pressure. During
CPR, CPP correlates with both myocardial blood flow and ROSC. In 1 human study,
ROSC did not occur unless a CPP 15 mm Hg or greater was achieved during CPR.

Compressions +@q;;:1.1.1y1 Compressions iffil.1,,1!.l.l.hfl

0 0
~~~· ~1 1 1 ~1 ~1 1 1 1 ~1 ~1 1 1 0 ~1 ~1 1 1~ 1 1
_.. Adequat·e
~CPP Level

Figure 32. Relauonship at quality CPR to coronary perfusion pcossure (CPPJ demonstrating the need to minimize mt~rup1!oos in compresS10(lS.

95
 Part 0

Foundational Far.ts Resume CPR W!1ile Manual Defibrillator Is Charging

• Shortening the interval between the last compression and the shock by even a few
seconds can improve shock success (defibrillation and ROSC). Thus, i t Is reasonable
for healthcare providers to practice efficient coordination between CPR and defibrilla-
tion to minimize the hands-off interval between stopping compressions and adminis-
tering the shock.
• For example, after verifying a shockable mythm and initiating the charging sequence
on the defibrillator, another provider should resume chest compressions and continue
until the defibrillator is fully charged. The defibrillator operator should deliver the shoc k
as soon as the compressor removes his or her hands from the patient's chest and all
providers are "clear" of contact with the patient.
• Use ol a multimodal defibrillator in manual mode may reduce the duration of chest
compression interruption required for rhythm analysis compared with automatic mode
but could increase the frequency of inappropriate shock. Individuals who are not com-
fortable interpreting cardiac rhythms can continue to use an AEO.
• For an AED, follow the device's prompts or know your device-specific manufacturer's
recommendations.
• II is important that healthcare providers be knowledgeable of how their defibnllator
operates, and 1f possible, limit pauses on chest compressions to rhythm analysis and
shock dehvery.

Deliver 1 Shock Step 3 directs you to deliver 1 shock. The appropnate energy dose is determined by
the identity of the defibrillator-monophasic or biphasic. See the column on the right ol
the algorithm.

If you are using a monophasic defibrillator, give a single 360-J shock. Use the same
energy dose for subsequent shocks.

Biphasic defibrillators use a variety of waveforms, each of which is effective for terminat-
ing VF over a specific dose range. When using biphasic defibnllators, providers should
use the manufacturer's recommended energy dose (eg, initial dose of 120 to 200 J). Many
b iphasic defibrillator manufacturers display the effective energy dose range on the face or
the device. If you do not know the effective dose ran ge, deliver the maximal energy dose
fo r the first and all subsequent shocks.

II the initial shock terminat es VF but the arrhythmia recurs later in the resuscitation
attempt, deliver subsequent shocks at the previously successful energy level.

Immediately after the shock, resume CPR, beginning with chest compres-
s ions. Give 2 minutes of CPR.

Purpose of Defibrillation does not restart the heart. Defibrillation stuns the heart and briefly terminates
Defibrillation all electrical activity, including VF and pVT. If 1he heart is still viable, its normal pacemak-
ers may eventually resume electrical activity (return o f spontaneous mythm) that ultimately
results in a perfusing mythm (ROSC).

In the first minutes after successful defibrillation, however. any spontaneous rhythm is typi-
cally slow and may not create pulses or adequate perfusion. The patient needs CPR {begin-
ning w ith chest compressions) for several minuies unti I adequate heart function resumes.
Moreover. not all shocks will lead to successful defibrillallon. This Is why it is important to
resume high-quality CPR, beginning with chest compressions immediately after a shock.

96
 The ACLS Cases: Cardiac Arrest: VF/Pu/seless VT

Principle of Early The interval from collapse to def1brillation is one of the most important det emiinants of
Defibrillation sutVival from cardiac arrest. Early de~bnOatJ0111s cnt•cal for pauents with sudden cardiac
arrest for the following reasons;

• A common 1rnt1al rhythm 1n out -of hosprtal witnessed sudden cardiac arrest is VF.
Pulseless VT rapidly detenoral es to VF. When VF Is present, the heart quivers and
does not pump blood.
• Electncal def1brillation is the most effective way to treat VF (delivery of a shock to
stop the VF).
• The probability of successful del1brillation decreases quickly over time.
• VF deteriorates to a.systole ti not treated.
The earlier defibnllation occurs, the higher the survival rate. When VF is present, CPR can
provide a small amount of blood flow to the hean and brain but cannot directly restore an
organized rhythm. The hkehhood of restonng a perfus1ng rhythm is optimized with 1mmedi·
ate CPR and defibrillation wit hin a few minutes o f the initial arrest (Figure 33).
For every minute that passes between collapse and defibnllahon. the chance of survival
from a witnessed VF sudden cardiac arrest declines by 7% to 10% per minute if no
bystander CPR ts provided.' When bystanders perform CPR, t he dechne is more gradual
and averages 3% to 4% pe< minute. • CPR perfomied eany can double'-' or tnple6
survova from wrtnessed sudden cardiac arrest at most def1bnllat1on intervals.

Lay rescuer AEO programs increase the ltkelthood of early CPR and attempted defibnlla·
lion This helps shorten the time between collapse and def1bnllat1on for a greater number
of pabents with sudden cardiac arrest

100
90
80
70
l
~ 50
60

'#. 40
30
20
10
0
2 3 4 5 6 7 8 9 10
Time(m1n)

figure :J.3. Rela'.onshoP 0 0 - SUMVal from Y«!lnetAar ficnlla1.on S<Jdden cardiac ones• and r.me Imm
colaps<t 10 cter.bnlia:ion.

97
 Part 8

Foundational Facts Clearing for Defibrillation

To ensure safety during defibnllat1on. always announce the shock warning. State the
warning firmly and in a forceful voice before delivering each shock (this entire sequence
should take less than 5 seconds):

• "Clear. Shocking."
- Check to make sure you are c lear of contact with the patient, the stretcher, or other
equipment.
- Make a visual check lo ensure that no one is touching the patient or stretcher.
- Be sure oxygen •s not newing across the patient's chest.
• When pressing the shock button. the defibrillator operator should face the patient,
not the machine. This helps to ensure coordination with the chest compressor and to
verify that no one resumed contact with the patient.
You do not need to use these exact words. but you must warn others that you are about
to deliver shocks and that everyone must stand clear of the patient.

Resume CPR • Immediately resume CPR, beginning wrth chest compressions.

• Oo not perform a rhythm or pulse check at this point unless t he patient is showing
signs of life or advanced monitoring indicates ROSC.
• Establish IV/10 access.

The Guidelines recommend that healthcare providers tailor the sequence ol rescue actions
based on the presumed etiology of the arrest. Moreover. ACLS providers funct ioning with-
in a high-performance team can choose the optimal approach for minimizing interruptions
in chest compressions (thereby improving chest compression fraction). Use of different
protocols. such as 3 cycles of 200 continuous compressions with passive oxygen insuffla·
tion and airway adjuncts. compression-only CPR in the first few minutes after arrest, and
continuous chest compressions with asynchronous ventilation once every 6 seconds with
the use of a bag-mask device, are a few examples of optimizing CCF and high-quality
CPR. A default compression·to·ventilation ratio of 30:2 should be used by less-trained
healthcare providers or if 30:2 is the established protocol. Figure 34 shows the progres-
sion from lay rescuers to highly trained and proficient healthcare providers.

Multirescuer Coordinated CPR

30:2CPR

Hands-Only CPR

Figure 34. Progression from lay rescuers 10 highly ccamed healthcare orovd$1"$ for CPR delivery.

98
 The ACLS Cases: Cardiac Arrest: VF/ Pulselftn VT

Rhyt.hm Check Conduct a rhythm check after 2 minutes of CPR. Be careful to minimize interruptlOns In
chest compressions.
The pause m chest compressions to check the rhythm should not exceed
10seconds.
• If a nonshockable rhythm is present and the rhythm is organized, a team member
should try to palpate a pu se. If there Is any doubt about the P<0$00C0 of a pulse,
rnmedoatety resume CPR
Remember: Perform a pulse check-preferably during rhythm analys1s- only If an
organized rhythm is present.

• If the rhythm is organized and there 1s a palpable pulse. proceed to post-cardiac

arrest care.
• If the rhythm check revea s a nonshockable rhythm and there 1s no pulse. proceed
along the asystole/PEA pathway on the nght side of the Cardiac Arrest Algonthm
(Steps 9 through 11 ).
• If the rhythm check reveals a shockable rhythm. give 1 shock and resume CPR imme-
diately for 2 minutes after the shock (Step 6).

Self-Adhesive Pa ds The AHA recommends roU11ne use of self-adhesive pads Using conductJve materials (Qel
pads or self-adhesive pads) during the def1brollation attempt reduces transthoraclc imped·
ance, or the resistance that chest structures have on electrical current.

Shock a nd For persostem VF/polsetess VT. give 1 shock and resume CPR immediately for 2 minutes
Vasopressors after the shock.

Immediately after the shock, resume CPR, beginning with chest compres-
sions. Give 2 minutes of CPR.

When IV/10 access 1s avrutabte. give epinephrine dunng CPR after the second shOck
as follows·
• Epinephrine 1 mg IV/10 repeat every 3 to 5 minutes
Note: If add1t1onal team members are available. they should anticipate the need for dru~s
and prepare them on advance

Epinephrine hydrochtorode is used dunng resuSCltation pnmanly lor its ~adrenerg1c

effects. 1e. vasoconstnctoon . Vasoconstnct on increases cerebral and coronary blOod flow
dunng CPR by increasing mean arterial pressure and aortic diastolic pressure. In previous
studies. escalating and h1gh·dose epinephrine admlmstratron did not improve survival to
discharge or neurologic outcome after resuscitation from cardiac arrest.

No known vasopressor (ep1nephnne) inc.-eases survival from Vf/putseless VT. Because

these rned1cat1ons can improve aortic d1astoltc blood pressure. c0<0nary artery perluslOfl
pressure. and the rate of ROSC, the AHA continues to recommend their use.

FYI 2015 Guideline• Vasopressin

Vasopress1n has been removed lrom the 2015 AHA Gurdelines Update for CPR and ECC.

The 20 15 AHA Guide/mes Update for CPR and ECC states that •vasopressin offers
no advantage as a substitute for epinephrine on cardiac arrest." As such. 11 has been
removed from the 2015 updated Adutt Cardiac Arrest Algonthm.

99
 Part 0
Rhythm Check Conduct a rhythm check after 2 minutes of CPR. Be careful to minimize interruptions in
chest compressions.

Interruption in compressions to conduct a rhythm analysis should not

exceed 10 seconds.
• If a nonshockable rhythm is present and the rhythm is organized, a t eam member
should try to palpate a pulse. If there is any doubt about lhe presence of a pulse,
immediately resume CPR.
• If the rhythm check is organized and there is a palpable pulse. proceed to post-
cardiac arrest care.
• If the rhythm check reveals a nonshockable rhythm and there is no pulse, proceed
along the asystole/PEA pathway on the nght side of the Cardiac Arrest Algorithm
(Steps 9 through 11).
• If the rhythm check reveals a shockable rhythm. resume chest compressions if indi·
cated while the defibrillator 1s charging (Step 8). The team leader is responsible for
team safety while compressions are being performed and the defibrillator is charging.

Shock and Give 1 shock and resume CPR beginning with chest compressions for 2 minutes immedi-
Antiarrhythmics ately after the shock.

Healthcare providers may consider giving antiarrhythmic drugs. either before or after the
shock. Research 1s still lacking on the effect of antiarrhythmic drugs given during cardiac
arrest on survival to hOspital d ischarge. If administered, amiodarone is the first-line antiar·
rhythmic agent given in cardiac arrest because it has been chnically demonstrated that it
Improves the rate of ROSC and hosprtal admission 1n adults with refractory VF/putseless VT.

• Amiodarone 300 mg IV/10 bolus, then consider an additional 150 mg IV/10 once
- Amiodarone is considered a class Ill antiarrhythmic drug. but it possesses elec-
trophysiologic characteristics of the other classes. Amiodarone blocks sodium
channels at rapid pacing frequencies (class I effect) and exerts a noncompetitive
antisympathetlc action (class II effect). One of the main effects of prolonged amio-
darone administration is lengthening of the cardiac action potential (class Il l effect).
If amiodarone is not available. providers may administer lidocaine.

• Lidocaine 1 to 1.5 mg/kg IV/10 first dose, then 0.5 to 0.75 mg/kg IV/10 at 5· to
10-minute intervals, to a maximum dose of 3 mg/kg
- L1docaine suppresses automa!Jcity of conduction tissue in the heart, by incre3sing
the etecttical stimulation threshold of the ventricle, His-Purkinje system, and
spontaneous depolarization of the ventricles during d iastole by a direct action on
the tissues.
- Lidocaine blocks permeability o f the neuronal membrane to sodium Ions, whbh
result s in inhibition of depolarization and the blockade of conduction.
Providers should consider magnesium sulfate for torsades de pointes associated with a
long QT interval.

• Magnesium s ulfate for torsades de pointes, loading dose 1 to 2 g IV/10 diluted in

1O ml (eg, o.w. normal saline) given as IV/10 bolus, typically over 5 to 20 minutes
- Magnesium can be classified as a sodium/potassium pump agonist.
- Magnesium has several electrophysiofogical effects. including suppression of atrial
L • and T· type calcium channels, and ventricular after-depolarizations.
Rou11ne administration of magnesium sulfate in cardiac arrest is not recommended unless
torsades de pointes is present.

Search for and treat any treatable underlying cause of cardiac arrest. See the column on
the right of the algorithm. See Table 4 in Part 4 for more information on the H's and T's.

100
 The ACLS Cases: Cardiac Arr9st: VF/Pulseless VT

Cardiac Arres t The Adult Cardiac Arrest Circular Algonthm (Figure 35) S\Jmmanzes the 1ecommended
Treatment sequence ol CPR. rhythm checks, shocks. and delivery of drugs based on expor1 con-
Sequences sensus The op~mal number of cycles of CPR and shocks required bef0<e s1an1ng phar·
macologic therapy remaons un'<llOWn. Note that rhythm checks and ShOcks ille organized
around 5 cycles of COITIPfl!SS'OOS and •entlla:!JOM. or 2 monui..s d a provider is t•mtng
the arrest

Adult Cardiac Arrest Circul ar Algorithm-

2015 Update
• Pultl twrd •at li6aSt s ~ #'Id ! a
• ~"'"""
Mnrl.U ..,.,~ l'l ccrnpr~

Start CPR •· ·~~~

Rot.-.~......., 2 mn.ilm Of X101W t f#qAd
• O.v• O•YOM • tf no ad'Vanced oww.ly 30 7 tompr""°' w«lti:.J ')Qr"! , ..tJO
• AnJCh montorldofibn11.o1or • Ouowlt..trltNe ,.3'.:•form t..1pticJVr-..r1y
- H PtToor <10 mm Hg, attfN'npt to 1mpru-.·o <.:.fJn qu.-Mv
• fflffl.M.Vteriat preuur•
Ret um of SPOntaneous
- ff rebxauon pnMt lO•llslol>(;> µ01iuure • X> mm ~•u i.illl'nipl to
Circulutlon (ROSC) lrT!prove CPR qu&.ty
"°91-Cardiac
. . .~r AITfft c.... -8-w•orO._,_
• 8lphasic: M.Yk.IS~H --~ K"O wtol iii )\)le (If 120 200 A
,, l.l'lknown. use 11um 1\1..._ S.C-Oa.i Ure I
ITli.1.b &1.ltJt,,ocpj11•"fl O:..

Orug Therapy ~ De equvaldr1l. ut d '""fhft ~ m.11 bu I.Mt G><-lt'f...t

• Monol)hasic: 300 J
IVllO aoces~
EJ)loopllrfna evury 3·S m1nu1ea
AmlOda•ooo for refractory VFlpV1

C...-Advw.ced Alfwrty
Ou... • t.1rrv11 ••~' """c:oapnograpt ry

.
• Pl.M M'cJ tlOOO ~
• -"bn..P.~~~P\
~at!--~ .. ~ l'TW"Hgt
ft •<:!\"~ .. #1IWtW ~

•H~ • Trt'I .111pw.."""1U10r>i>

• HfPOJJa • TM"~ C#Ollo
• Hvd"'9'"' IOI\ <ac:>dooiol • Tm11•
•HtlJO-~ • Thn "'"""~~
·H- • T coroniv.
llAl'l.

,..,.,,.. 35. rhe AOutt C ttd 3C Arrest C1teui.ar A9Jt1Uvn 0o not delay shocfll Continue CPA whil.ft P'ffJ.loMIOQ t.VtU .xln'l~lrfll'ICJ 1Jn-o •''CJ t.fQtV!nQ
the def1btlll.ator 1n1ant..1pt the,1 conlpross,1on~ Ol'1ly lor tMtt minimum anlOunt oi lime required lot vent 111100 (unt1t advanced turw.l'( pl.lr e<h mythm
chock, and ac1un1 &hock dol1vOfY

101
 -
P art 0
Physiologic ~AHA recommenos using quantrta!Jve wa>eform capnography 1n intubated pa11en1S 10
Monitoring During mon110< CPR quality \Figure 36). opturnze chest comprOS$SIOOS, and detect ROSC dt.nng
CPR ct'lest compr~ !Figure 37). A.lhough plaeemem of invasive monitors duMg CPR os
no1 genurally warranted. physiologic paraniete<S such as m1ra ·artU<oal relaxation pressures
·(Figures 36A and B) and central venous oxygen salurahoo (S<.VO,}, wr.en available. may
also be helpful to< optomtZ1ng CPR and detect•ng ROSC.

Animal and human s1ud•es indicate that PE7CO,, CPP. and scvo,
morntonng provides valu-
able ontounatlO<'I on t>oth tl1e patoents condouon and tile response to the<apy Most mpo<·
tanl, P£1co,. CPP. and Sc.o, correlate with cardoac OU1put and myocardial blOod flow
d1.>ring CPR When chest compressrons 'ail to a<:holM! 1<)er1t1!.oo thrll$hold values . ROSC is
o'
rarely aci1'evo;d . Furthermore, an anrup< 1ncre~ In any tt-~'!MI paiam&t....s IS a sens.t»e
1ndcat0< of ROSC tnat canoe monnored w11h(x.t or.terrui>tang cnest compressions

Al:nough no ctncal stuoy II.is exarmned whetl>er l•lt&hng 1~1tative efforts to pnySi·
<>logic; para"leters improves outcome. n is reasonable to use these parameters. d availatlle
to optimize comprt:S$10tlS and guode vasopressor therapy during cardiac arrest ,

t:nd-Tidal CO,
The mmn determinant of Pt rco, dunng CPR 1s blood delivery to !he lungs Pers1stanlly low
Pnco, values loss Ilion 10 mm Hg during CPR 111 h11ubaled patients (f'lguro 360} suggesl
lhal ROSC Is unlikely If Pcrco.. abruplly increases to o norrnnl voluo of 35 to 40 mm Hg 1l
1s rtJa:.onuble to consider lh1s an indicator of ROSC
If 1he Pu..:o. •S less than 10 mm Hg dunng CPR. It IS reasonabl~ 10 1ry 10 1mpro1e
chest comp<ess1oos attd vasopressor the<apy

Coronary Perfusion Pressure or Arterial Relaxation Pressure

Increased CPP conetaies "'tn botn myocarooal blood flow llncl ROSC A tea90flable surro-
ga1t1 10< CPP during CPR :s artenaJ rEJ<batJOn i doast0bc1 pr.-sure. which can bt:t fTloasuted
by using an tr.t'8·arterial cart>eier

• lf trw unenaJ rtola><at10<' pressore IS ess 1nan 20 mm Hg 'IF"JUfe 3b0), :ot is reasonable to
try 10 omprove chest compressions and vasopressor the<apy

Cenrral Venous Oxygen Saturation

If o•ygi.n consumption, an~nal oxygen sa1urat100 . and hemoglobin are constant , cnanges
1n Scvo, reflect char>g&S in oxygen delivery due to chnngcs •fl card•<•c output 5cVO; can
bu measured cor11tnuousty by usmg oximetnc lipped ttmtral venous ca1hete<s placed 1n the
superlO< vtlflU cava or pulmonary artery N0<mal range is 60% to 80%
II lhe SCVO, o.s less than 30%. n 1s reasonat>:e lo try to improve chest compressl:>nS
and va.'IOpressor tt,<!fapy.

102
 The ACLS Cases: Cardiac Arrest: VF/Pulseless VT

¥E '°
E

Time

r'~ ~
·-·· ::···T~ ....... - -·. ··· ...
~ . ...
•
•'-~~~~--.11-~~~ ......
~~~~~~~~~~~~~~~~~~~~~~~~~

B
Pieure 36. Ptlysoologoc monnonnq <Ming CPR. A, Hogh.qoai.ty com""°""°"' are "'1ow<1 th•oogh wevolonn c:aiinogapny al'<! lntra-ar1ehal roax-
ahon pessure PETCO vaaues less than 10 mm Hg '" nh.1b.tted poit~1s or lnlfa anenat rtt<axahon ~ -.S chart 20 mm Hg lndate that
enfd 1ac ourpu1 Is tnttdequa1e ta acnieve ROSC In either of thOSe ca!W!'$ 11 is ~abte to consider trying to mpro..-e qoal ty of CPR by optim l'OQ
chest eornpcession parnmeters or g1\!1ng a vasuprAssor °' both B, lneffoctlve CPR C'..ompress1oos shown through intra anerial ret~xa t100 pre$'-lre
and wavefomi capt\Ography.

103
 Part 0
, n.,.11i. rV...... I
l 50
37 5
'~
,, 5
0
CPA ROSC

, lgura 37. Waveform capnogrophy dunng CPR with ROSC. This capnography tracing
displays PETCO, 1n millimeters of mercury on the vertical wus over time. This patient is
intubated and receiving CPR Note that the ventilation rate is approximately 10fm1n. Chest
compressions are given continuously al a rate slightly faster than 100/IT\il'I but are not vis·
1ble with this tracing. The initial PETCO. 1s less than 12.5 mm Hg dunng the first minute,
indicating very low blood flow. PETCO, increases to between 12.5 and 25 mm Hg dunng
the second and third minutes, consistent wit h the Increase in blood now with ongoing
resuscitation. ROSC occurs during the fourth minute. ROSC Is recognized by the abrupt
Increase in PCTco, (visible 1ust after the fourth vertical hne) to greater than 50 mm Hg,
which Is consistent with a substantial Improvement m blood flow.

Treatment of VF/ pVT Oef1bn latlOll is appropriate fat the cardiac arrest pallent m VF/pVT who has severe hypo-
in Hypothermia thermia and a body temperature of less than 30'C (less than 86 F}. tt the patient does not
respond to the initial shock 1t is reasonable to perform add1t1Qnal defibrillation attempts
according to the usual BLS guidelines while engaging 1n active rewarming. The hypother-
m1c patient may have a reduced rnte of drug metabolism, raising concern that drug levels
may accumulate to toxic levels with standard dosing regimens. Although the evidence
does not support the use of ant1arrhythmic drug therapy In hypotherm1c patients in cardiac
arrest. 11 1s reasonable to consider administration of a vasopressor according to the stan·
dard ACLS algorithm concurrent wrth rewarming strategies.

ACLS treatment of the patient with severe hypothermia in cardiac arrest in the hospital
should be armed at rapid core rewarming.

Fat patients 1n cardiac arrest with moderate hypothermia (30 C to 34°C [S6•F to 93.2' F]).
start CPR, attempt defibnliation, give med1cat 1ons spaced at longer Intervals. and. 11 1n
hospital. provide active core rewarming.

Routes of Access for Drugs

Priorities Pnont•es during cardiac arrest are hrgh-qualrty CPR and earty def1bn lat>On. lnsertKJO of
an advanced airway and drug adm1mstrat1on are of secondary importance. No drug given
dunng cardiac arrest has been studied adequately to show improved survival to hospital
discharge or improved neurolog1c lunct1on after cardiac arrest

H1storlcaliy 1n ACLS. providers have administered drugs either via the IV or ET route. ET
absorption of drugs is poor and optimal drug dosing is not known. For this reason, the IV
or 10 roul e 1s preferred.

lntra11enous Route A peripheral IV is preferred for drug and fluid adm10AstratJOn unless central line access rs
already available

Central line access is not necessnry dunng most resuscitation attempts. Central line access
may cause interruptions 1n CPR and complicallons during insertion, including vascular lac·
eratlon, hema1omas. and bleeding. Insertion of a cefltral line in n noncompressible vessel is
a relative (not absolute) contoai11dlcatlon 10 fibrinolytic therapy in patients with ACS.
104
 The ACLS Cases: Cardiac Arrest: VF/Pulse/en VT

EstabhSlling a per1pheral line does not require 111terruptJon of CPR. Drugs. however. typi·
cally require 1 10 2 m111utes to reach the central circulation when given by the peripneral
IV route.

If a drug is given by the peripheral venous route. administer 1t as follows:

• Give the drug b y bolus injection unless otherwise specified.
• Follow with a 20-ml bolus of IV lluid.
• Elevate the extremity for aboul 10 to 20 seconds to facilitate delivery of the drug to
thB central circulation.

lntraosseous Route Drugs and fluids during resuscna11on can be delivered safely and effectively via the 10
route 1f IV access is not available Important potnts about to access are

• 10 access can be established In all age groups.

• 10 access o ften can be achieved In 30 to 60 seconds.
• The 10 route of adm1nistra11on is preferred over the ET route and may be easier to
establish in cardiac arrest
• Atty ACLS drug or fluid that Is adm1n1stered IV can be given 10.
10 cannulabon provides access to a noncollapsible marrow venous plexus, which serves
as a rapid, safe. and reliable route for administration of drugs, crystallolds. co41otds, and
blood dunng resuscitation. The technique uses a ngid needle. preferably a specially
designed 10 or bone marrow needle from an 10 access kit.

=
fiiii11 For more information on 10 access, see the Access tor Med1ca t1ons section on
the Student Web srte (www.heart.org/eccstudent).

Endotracheal Route IV and 10 administration routes are preferred over the ET administration route. When
consideflng administration of drugs via the ET route during CPR, keep these concepts 1n
mind

• The optimal dose of l1lOS1 drugs given by the ET route is unknown

• The typical dose of drugs administered via the ET route is 2 10 2'h times the IV route.
• CPR will need to be stopped transiently so drug does not regurgitate up the ET tube.
Studies demonstrate that ep inephrine. vasopressin, and lidocaine are absorbed into the
circulatory system after administration via the ET route. When giving drugs via the ET
route. dilute the dose in 5 to 10 ml of sterile water or normal saline. Inject the drug directly
into the ET tube.

Fluid Administration Healthcare providers should Wate fluid adm1nistratton and vasoacwe or inotropoc agents
as needed to optimize blood pressure, cardiac output, and system•c perfusron. The opt1·
mal post-cardrac arrest blood pressure remains unknown; however, a mean arterial pres·
sure 65 mm Hg or greater is a reasonable goal

In hypovolem1c pal ients , the ECF volume 1s typ ically restored with normal saline or lacta ted
Ringer's solution. Avoid D,W because it will reduce serum sOdlum too rapidly. Serum elec·
trolytes should be appropriately monitored.

Vasopressors

Introduction White there Is evidence that the use or vasopressors favors 1n1t1a resuscitation with ROSC,
research 1s still tack1ng on the effect ot rhe routine use of vasopressors at any stage during
management o f cardiac arrest on the rates or survival to hospital discharge.

10!1
 Part 0
Vasopressors Vasopressors optimize cardiac output and blood pressure. The vasopressor used during
Used During cardiac arrest is
Cardiac Arrest • Epinephrine: 1 mg IV/10 (repeat every 3 to 5 m inutes)
11 IV/IO access cannot be established or is delayed, give epinephrine 2 to 2.5 mg diluted
in 5 to 10 m l of sterile water or normal saline and injected d irectly into the ET tube.
Remember, the ET route of drug administration results in variable and unpredictable drug
absorption and blood levels.

Epinephrine Although healthcare providers have used epinephrine for years in resuscitation, few studies
have been conducted to address the question of whether it improves outcome in humans.
Epinephrine administration improves ROSC and hosprtal admission rates: however, large
studies have not been conducted to evaluate whether survival Is improved. Because there
are no large studies to confirm longer-term outcome, we rely on the positive short-term
effects of increased ROSC and increased hospital admission to support the use in car-
diac arrest. No studies demonstrate improved rates of survival to hospital discharge or
neurolog1c outcome when comparing standard epinephrine doses with initial high-dose or
escalating-dose epinephrine. Therefore, the AHA does not recommend the routine use of
high-dose or escalating doses o l epinephrine.

Epinephrine is thought to stimulate adrenefgic receptors, producing vasoconstriction,

increasing blood pressure and heart rate. and improving perfusion pressure to the brain
and heart.

Repeat epinephrine 1 mg IV/10 every 3 to 5 m inutes during cardiac arrest.

Remember; follow each dose given by peripheral mjection with a 20-mL

flush of JV fluid and elevate the extremity above the level of the heart for
10 to 20 seconds.

Antiarrhythmic Agents

Introduction As with vasopressors, research is still lacking on the effect of routine antiarrhythmic
drug admimstrat1ofl during human cardiac arrest and survival to hosp~al discharge.
Amiodarone, however. has been shown to increase short-term survival to hospit al admis-
sion when compared w ith placebo or lidocaine.

Amiodarone • Consider amiodarone for treatment of VF or pulseless VT unresponsive to shock

delivery, CPR. and a vasopressor.
• Am1odarone is a complex drug that affects sodium, potassium, and calcium channels.
It also has ~-adrenergic and ~-adrenergic blocking properties.
• Dunng cardiac arrest, consider am1odarone 300 mg tV/10 push for the first dose. II
VF/pulsele$S VT persists, consider giving a second dose of 150 mg IV/10 in 3 to
5 minutes.

Lidocaine Lidocaine is an alternative antiarrhythmic of long-standing and widespread familiarity.

However, 11 has no proven short-term or long-term efficacy in cardiac arrest. Providers
may consider giving hdocaine when am1odarone is not available.
• The initial lldocalne dose is 1 to 1.5 mg/kg IV/10. Repeat ii indicated at 0.5 to 0.75
mg/kg IV/10 over 5- lo 10-minute Intervals to a maximum of 3 mg/kg.
• II no IV/10 access is available, the dose for ET administration 1s 2 to 4 mg/kg.
~~~~~~~~~-~~~~~~~-

106
 The ACLS Csses: Cardiac Arrest: VFIPulse/ess VT

Magnesium Suffate • IV magnesium may tenrunate or prevent recurrent torsades de pomtes in pauents whO
have a prolonged QT .ntetVa during normal sinus rhythm. When VF/pulseless VT car-
diac arrest 1s associated with torsades de pointes. give magnesium sulfate at a load-
ing dose of 1 to 2 g IV/10 diluted in 10 ml (eg, D W, normal saline) given over 5 to
20 minutes. If a prearrest 12-lead ECG 1s available for review. check the OT interval
for prolongation.
• Remember that pulseless VT is treated with an immediate high-energy shock, where-
as magnesium is an adjunctive agent used to prevent recurrent or treat persistent VT
associated with torsades de po1ntes
• Magnesium sulfate is also 1nd1cated for patients with known or suspected low serum
magnesium. such as patients w'th alcoholism or other conditions associated with
malnutntJon or hypomagnesem1c states. For patients 1n relractory VF/pulseless VT,
check the patient's history, 1f available, for one ol these cond t1ons that suggests the
presence of a reve<sible electrolyte abnormality.

Steroids In • The use of steroids 1n cardiac arrest has been assessed 1n bol/1 the out-of-hospital
Cardiac Arrest and in-hospital settings. In IHCA, steroids were combined with a vasopressor bundle
or cocktail or epinephrine and vasopressin.
• In an initial randomized controlled trial (RCl) 1nvolv1ng 100 IHCA patients. the use or
a comb1nahon of methylprednlsolone, vasopress1n, and epinephrine dunng cardiac
arrest and hydrocorusone after ROSC for those with shock sign1f1cantly 'mproved sur-
111va1 to hOsprtal d1SCharge compared with the use of only epmephnne and placebo.'
In a subsequent Study published 1n 2013," 136 in 268 pauents w'th IHCA. the same
comb<nahon of methytprednlsolone. vasopressin, and epinephrine dunng cardiac
arrest (and hydrocon.sone in those with post-ROSC shock), s19mf1cantly improved !he
survival to discharge with good neurologic outcome compared with only epinephrine
and placebo.
• The same 2 RCTs provided evidence !hat the use of methylprednisolone and vaso·
pr~ss1n in add1t1on to epinephrine improved ROSC rates compared with the use of
placebo and epinephrine alone.
• In OHCA. steroids have been evaluated on 1 RCT' and 1 observabonal study." In
these studies, stefoids were not bundled as they were 1n the IHCA but studied as
a soie treatment. When dexamethasone was 91ven dunng cardiac arrest. rt did not
improve survival to hospual d•SCharge or ROSC or survival to discharge. as compared
with placebo The observational study showed no benefit 1n survival to discharge
but did show an associauon of improved ROSC with hydrocort1sone compared with
no hydrocort1sone.
• In light of the data presented, no recommendation can be made on the routine use
of steroids alone in IHCA However, the combination of Intra-arrest vasopressin, epi·
nephrine, and methylprednlsolone and postarrest hydrocort1sone may be considered
for IHCA patients.
• For OHCA patients. use of steroids dunng CPR is of uncerta n beoefl.

Respiratory or • In the United States in 2013. 16 235 people died of prescr1pbon op101d toxicity, and
Cardiac Arrest an additional 8257 died of heroin overdose-"·• In the Unned States 1n 2012. opiotd
overdose became the leading cause of uninten11onal 1n1urious death 1n people aged
Associated With 25 to 60 years, accounting for more deaths than motor vehicle collisions.'' A majonty
Opioid Overdose of t11ese deaths are associated with pre~cription opio1ds. Statistics are similar
1n Canada."
• Isolated op101d toxicity is associated with central nervous system (CNS) and resp1rato·
ry depression that can progress to respiratory and cardiac arrest. Most opioid deaths
1nv01ve the coingest100 of mulbple drugs or med.cal and mental health eomorbtdi-
tms • In addrtlOO, methadone and pr0p0xyphene can cause torsades de pointes,
and card otoxicrty has been reported wrth other opioids Except 1n specific clinical
settings (eg, unintended op<old overdose dunng a medical procedure). rescuers can-
not be certain that the patient's clinical condition 1s due 10 oplo1d-1nduced CNS and
respiratory depression toxicity alone.

107
1

PartG

• Naloxone is a potent opioid receptor antagonist in the brain, spinal cord, and GI
system. Naloxone has an excellent safety profile and can rapidly reverse CNS and
respiratory depression in a patient with an opioid-associated resuscitative emergency.
Based on the rescuer's training and clinical circumstance, naloxone can be adminis·
tered intravenously,'""' intramuscularly,28 ·29·" intranasally.''"''"' or subcutaneously 37 ;
nebulized for inhalation'03• ; or instilled into the bronchial tree via ET tube. <o
• For patients with known or suspected opioid overdose who are in respiratory arrest,
healthcare providers shOuld give naloxone as soon as it is available. It may be given
at a dose of 2 mg IN or 0.4 mg IM/ IV, which may be repeated every 4 minutes if
necessary. Figure 38 shows the algorithm for opioid overdose. While this algorithm
was designed for lay rescuers, ACLS providers will follow the ACLS systematic
approach, which includes a pulse check.

Opioid-Associated Life-Threatening Emergency (Adult) Algorithm-

New 2015

Assess and activate.

Check for unresponsiveness anCca]..
for neartly help. Senctsomeone to
- call your local emergency pumber and get
AEO and naloxone. ObserveJod ireathing
vs no breathing or only gasping.

l
Begin CPR.
If victim ts unresponsive with no breathing
O< only gasping, begin CPR.• If alone,
perform CPR for about 2 minutes bef0<e
leaving to phone your local emergency
number and get naloxone and AED.

Administer naloxone.
Give""11oxone as §OOn as ~ls avlliiable.
2 mg tnttailasal'. or 0.4 mg intramuscular.
May repeat after 4 minutes.

_ !-
Doesthe

<
Stimulate and reassess.
person respond? Continue to check responsiveness and
any time, does the person breathing until advanced help arrives.
mov e purposefully. breathe If the person stops responding,
regulally, moan, 0< beg.n CPR and repeal naloxone.
otherwise respond?
\__
No

G
ntinue CPR and use AED
as soon as it is available.
ontinue until the person responds
O< until advanced holp arrives.

"CPR technique based on f&SCuet's level of training.

Cl ?01 S A111(.'flcan Hean: Assooatt0n

Figure 38. The Opioid-Assoc1atQcJ Life-Threatening (Adutl) Emergency Algori1hm.

108
 The ACLS Cases: Cardiac An-est: VF/Pulselesa VT

Extracorporeal CPA (for VF/Pulseless VT/Asystole/PEA)

Extracorporea/ Extracorporeal CPR (ECPR) refers to venoarterial extracor poreal membrane oxygenation
Membrane during cardiac arrest, including extracorporeal membrane oxygenation and cardiopulmonary
Oxygenation bypass. These techniques require adequate vascular access and specialized equipment.
The use of ECPR may allow providers additional time to treat reversible underlying causes of
cardiac arrest (eg, acute coronary artery occlusion. PE, refractory VF, profound hypothermia,
cardiac injury. myocardhis. cardiomyopathy. congestive heart failure, dn.ig intoxication) or
serve as a bridge for LV assist device implantation or cardiac transplantation.

While there are currently no data from RCTs on the use of ECPR for cardiac arrest. evi-
dence reviewed for the 2015 AHA Guidelines Update for CPR and ECC suggests a benefii
to survival and favorable neurologic outcome with the use of ECPR when compared with
conventional CPR in patients with refractory cardiac arrest.

In settings w here ECPR can be rapidly implemented, providers m ay consider its use
among select cardiac arrest patients with potentially· reversible causes of cardiac
arrest who have not responded to initial conventional CPR.

Ultrasound (for VF/Pulseless VT/ Asystole/ PEA)

Ultrasound Use in Ultrasound may be applied to patients receiving CPR to help assess myocardial contractil-
Cardiac Arrest ity and to help identify potentially treatable causes of cardiac arrest. such as hypovolemia,
pneumothorax, pulmonary thromboembofism, or pericardial tamponade. However. it is
unclear whether important clinical outcomes are affected by the routine use of ultrasound
among patients experiencing cardiac arrest. If a qualified sonographer is present and use
of ult rasound does not interfere with the standard cardiac arrest treatment protocol. then
ultrasound m ay be considered as an adjunct to standard patient evaluation.

109
 Part 0

Cardiac Arrest: Pulseless Electrical Activity Case

Introduction This case focuses on assessment and management of a cardiac arrest patient with PEA.
During the BLS Assessment, hogh-porformMce team members wlll demonstrate high·
quai.ty CPR woth effectove chest compressK>ns and ven11la1ton with a bag-mask dovlce In
the Pnmary Assessment, the team leader will recognize PEA ard implement the appropn-
at e onterventlOflS outlil'led on the Cardiac Arrest Algonthm. Because correction of an under·
lymg cause of PEA. 11 present and 1dent1fied. •s cntical to pauen; outcome, the team leader
woH verbahze the differenual d1agnos•s whole leading lhe high-performance team 1n the
search for and treatment of reversible causes

Rhythms for PEA You will need to recognize the following mythms:
• Rate-too fast or too slow
• Width of ORS complexes-wide versus narrow

Drugs for PEA This case involves these drugs:

• Ep1nephnne
• Other med cat100S. depending on the cause of the PEA arrest

Description of PEA

Introduction PEA encompasses a heterogeneous group of mythms that are organized or sem1organlzed
but lack a palpable pulse. PEA Includes
• td1oventncular mythms
• Ventncular escape rhythms
• Postdefibrillation idooventrlcular thythms
• Sinus rhythm
• Qthll(

Any organized' rhythm w1lh0ut a pul5" os defined as PEA. Even sinus mythm without a
detectable pulse <S called PEA Pufseless rhythms that are excluded by definition 1ndude
VF pVT. and asystole
•,.., O"Q.Y117~ rtiytt'm C<lflSISlS of OAS CC>rf'Oilt•..., it\'lt r.. ~im :1f n apoearatiCe from beat to ~ ( ~ . each has
a un form OKS coof.quraror ~izeo mytMts rNy ha'w'li!' n.vmw OT wide oqs. cootpeJtM, they may oco.# et
°'
'"'°'°or~· rates the; may be A'qUl."lr ~'reou J . Qfld 1~ tri.ly or may not produce a puls(i

Historical Previously, high-performance teams used the term electromechanical dissociation (EMO)
Perspective to describe pahents who displayed electricol activity on the cardiac monitor but lacked
apparent contt act1le function because of an undetectable pulse. That is. weak contractofe
function os present- detectable by 1nvas1ve monrtonng or echocardiography- but the car-
diac function 1s too weak to produce n pulse or ettect ove cardiac output. This Is the most
common initial condition present after successful defibfllfatoon. PEA also includes other
cond1t1ons where the heart s empty because of inadequa1e pre,oad. In this case, the con·
tractlle funct:Jon of the heart 1s adequate but there •S inadequate volume tor the ventrk:fe
to erect This may occur as a result ol severe hypovolemoa. or as a resuit of decreased
venous return from PE or pneumothorax

110
 The ACLS Cases: Cardiac Arrest: Pulseless Electrical Activity

Managing PEA: The Adult Cardiac Arrest Algorithm

Overview As described earlier, the Cardiac Arrest Algonthm consists of 2 cardiac arrest pathways
(Figure 39). The left side of the algorithm outlines treatment for a shockable rhythm r-F/
pVD. The right side of the algonthm (Steps 9 through 11 ) outlines treatment for a non -
shockable rhythm (asystole/PEA). Because of the similarity in causes and management,
the Cardiac Arrest Algorithm combines the asystole and PEA pathways, although we will
review these rhythms in separate cases. In both pathways. therapies are organized around
periods (2 minutes) of uninterrupted, high-quality CPR.

The ability to achieve a good resuscitation outcome with return of a pertusing rhythm and
spontaneous respirations depends on the ability of the high-performance team to provide
effective CPR and to identify and correct a cause of PEA if present.

Everyone on the high-pertormance team must carry out the steps outlined in the algorithm
and at the same time focus on the identification and treatment of reversible causes of
the arrest.

The PEA Pathway of In this case. the patient is in cardiac arrest. High-performance team members initiate
the Cardiac Arrest and pertorm high-quality CPR throughout the BLS Assessment and the Primary and
Algorithm Secondary Assessments. The team interrupts CPR for 10 seconds or less for rhythm
and pulse checks. This patient has an organized rhythm on the monitor but no p1.1fse. The
condition is P£A (Step 9). Chest compressions resume immediately. The team leader now
directs the team in the steps outlined in the PEA pathway of the Cardiac Arrest Algorithm
(Figure 39), beginning with Step 10.

IV/10 access is a priority over advanced airway management unless bag-mask ventila-
tion is Ineffective or the arrest is caused by hypoxia. All high-pertormance team members
must simultaneously conduct a search for an underlying and treatable cause of the PEA in
addition to performing their assigned roles.

Decision Point: Conduct a rhythm check and give 2 minutes of CPR after administration of the drugs.
Rhythm Check Be careful to minimize interruptions 1n chest compressions.

The pause in CPR to conduct a rhythm check should not exceed

10 seconds.

Administer • Give epinephrine as soon as IV/10 access becomes available.

Epinephrine - Epinephrine 1 mg IV/ 10- repeat every 3 to 5 minutes

Administer drugs during CPR. Do not stop CPR to administer drugs.

• Consider advanced airway and capnography.

Nonshockable • If no electrical activity is present (asystole). go back to Step 1O.

Rhythm • If organized electrical activity is present, try to palpate a pulse. Take at least
5 seconds but do not take more than 10 seconds to check for a pulse.
• If no pulse is present. or if there is any doubt about the presence of a pulse, immedi-
ately resume CPR for 2 minutes. starting with chest compressions. Go back to
Step 1o and repeat the sequence.
• If a palpable pulse is present and the rhythm is organized. begin post- cardiac
arrest care.

1t 1
 part e
Adult Cardiac Arrest Algorithm-2015 Updat e CPR Oualrty

• Pu~h hard (a1 least 5 c:m) and

fast {100-120/minl and allow
r.omple1e chest recoc.
Start CPR • M1nim1ze 1n;erruptions in
• Grve oxygen compresStOns
• A'A)l(f exces.5tve verril'iiion
\... • Attach monitor/defibnllal 0<
" Rotate compres~nr f"oletV
' m1nu1eci. or MOOP.1' if fangued.
• If no advanced airway
30:2 comproosiOI' v9"til<ll()I\
~--
Y•_•__ / Rhythm '-.,___N_
o_~ rn:io
2 t
c ; shockable7/ • Ouanhta1iv<> wa'ICform
9 CUl)llOg1achy
VF/;VT ) Asystole/ PEA - 1Pnc;o.<10 mm Hg. attempt
to impr~P. Cf>R qu:lf ty.
• l fltfa·artP.nal prP,SMJl'P.
- i relaxa11on phase (dlR·
3 stolic) ~Slife <?0 mm Hg
, , Shock ,1nt".mp1 to irt1flf'Ov-e C:PA
qu.1 ty
4
Shock Enorgy for Defibnllatioo
CPR 2min
• NltO access • B!ph:.t$1c: Maf"Ufac1"re1
racnmmendM..on (P.f!, if't;lfil'll
dose of 120·200 J): if unlCOO'Hn
use max.mum available.
Sooond and sutr•.•uqoonl doses
Rhythm No sr'O.Jld be CQt11vl)lfWlL Md hi~
~.Smay be r.~ed
shockable? • M ooophasi c: 300 J

t
Yes Drug Ther.py
5
Shock • Epinephrine fV110 dose:
1 ng every 3..S minutes
8 10 • Amiodarone tv/10 dose: Frst
CIO!:itr. 300 mg bolus. Second
CPR 2 min
• Epinephrine every 3 -5 rnln • 1vnoCPR
<l.Ccess2min ~ OtGe: 150 mg.

• Considef advo.ooed auway, • Epinephrine every 3-5 mm

capnograplly • Consld9' ad\ianeed airway,
• Erdotracheal lntub;;tion or
capnography
Sl.4)raglottic advanced alf'Way
• WavetOIT'\ capnography or
e«inomc1ty 10 confirm and
r Rhythm No Rhythm Yea mom~or FT tube plaeemot\L
• CMce advanced alrw::iy In p&aco.
shoe~ shockable?
give · breathevay6~

~ Yes (10 b:ea'lhslrmn) w1h C0011'11)1)\1$

8
7
f &hock
11
No
C~? compress~

Retum of Spo1118neous
Cir culation (ROSC')

• Pulre ono lllOOd,,.......

CPR 2min CPR 2 min • Abrvpt sustained 1nccease in
• Amiodarone • Treat reversible causes PHC01 (typically ~40 mm Hg)
• Tl'eai reversd>le causes • Spontaneous arterral presstXe
waves w lh lrH.rd-artenal
monitoring

No Yeo
Rhythm
• Hypoi/Olemi:l
~ockab le?
• H'f·poiui'l
12 • Hydmgeo l()n !acidosis)
• Hyµo.ll'lyperkalam.a
• If no signs of return of
spontaneoos Clrcula;bon
Go to5 or7 j • Hypoth0rrr1a
• TeMton nr-eur'OOlhorax
(ROSC), go to iO 0< 11 • Tamponade. card1:ic
• If ROSC, go to • T OlM'lS

Post-cardiac Arrest Care • Ttvombo$11'1. pulmonory

• Thrombosis. comn:iry

Figur e 39. The Adutt Cardiac Arrest Al~ori1hm,

112
 The ACLS Cases: C•rdlac AITest: Pulseless E/ectrlctll Activity

Decision Point: • If the rhythm check reveals a shockable rhythm, resume CPR with chest compres·
Shockable Rhythm s1ons while the defibr!llatcr Is charging If possible.
• Switch to the left side of the algonthm and perform steps according to the VF/pVT
sequence st arting with St~p 5 or 7.

Asystole and Figure 39 summanzes the recommended sequence of CPR, rhythm checks. and
PEA Treatment delivery of drugs for PEA and asystote based on ex.pert consensus.
Sequences

Identification Treatment of PEA IS not limited to the 1ntervent1ons outlined tn the algonthm Healthcare
and Correction of provide.-s should attempt to 1dent1fy and correct an underlying cause if present. Healthcare
Underlying Cause rvnvirl""' m11•t • tnp, think. Am a!lk, "Why did this person have this cardiac arrest at this
time?" It is essential to search for and treat reversible causes or asystole tor resuscda·
tlve efforts to be potentially successful. Use the H's and T's to recall conditions that could
have contnbuted to PEA.

Critical Concepts Commo n Underlying Causes of PEA

Hypovolemia and hypoxia are the 2 most common underlying and potentially reversible
causes or PEA. Be sure to look for evidence ot these problems as you assess
the patient.

113
 part e
Cardiac Arrest: Asystole Case

Introduction In this case, thepat1ent is 111 cardiac arrest. High-performance team members initiate
and perform high-quality CPR throughout the BLS Assessment and the Primary and
Secondary Assessments. The team interrupts CPR for 10 seconds or less for a rhythm
check. TIJis patient has no pulse and the rhythm on the monitor is asystole. Chest com-
pressions resume immediately. The team leader now d irects the team in the steps outlinec
in the asystole pathway of the Cardiac Arrest Algorithm (Figure 31 in the section Managing
VF/Pulseless VT: The Adult Cardiac Arrest Algorithm), beginning with Step 10.

/V/10 access is a priority oi•er advtmced airway management unless bag-mask ventilation
is ineffective or the arrest is caused by hypoxia. All high-performance team members must
simultaneously conduct a search for an underlying and treatable cause of the asystole in
addition to performing thei· assigned roles.

At the end of this case, the team w m discuss the criteria for terminating resuscitative
efforts; 1n some cases, we must recognize that the patient is dead and that 11would be
more appropriate to direct efforts to supporting the family.

Rhythms for Asystole You will need to recognize the following rhythms:
• Asystole (example in F.gure 40)
• Slow PEA terminating 1n bradyasystol1c rhythm

Figure 40. Example of asystole.

Drugs for Asystole This case involves these d1ugs:

• Epinephrine
• Other medications, depending on the cause of the asystole arrest

Approach to Asystole

Introduction Asystole is a cardiac arrest rhythm associated with no d iscernible electrical activity on the
ECG (also referred to as flat line). You should confirm that the flat line on the monitor is
indeed "true asystole" by v~lidatlng !hat the flat line is

• Nol another rhythm (eg, fine VF) masquerading as a flat line

• Not the result of an operator error

11 4
 The ACLS Cases: Cardiac Arrest: Asystole

Foundational Fact• Asystole and Technical Problems

Asystole is a specific diagnosis. but flat line is not. The term flat line is nonspecific ond
can result from several possible conditions, Including absence of cardiac electrical activ·
1ty. lead or other equipment fatlure, and operator error Some defibnllators and monitors
slgnal the operator when a lead or Other equipment failure occurs. Some of these prob·
lems are not applicable to all defibnllators

For a panent with cardiac arrest and asystole. qu1Ckly rule out any other causes of an
isoelectnc ECG. such as

• Loose leads or leads not connected to the patient or defibnllator/mon11or

• No power
• Signal gain (amplitude/signal strength) too low

Patients With During the BLS, Primary. and Secondary Assessments. you should be aware of reasons to
DHAR Orders stop 01 withhold resuscitative efforts. Some o t these are

• Rigor mort1s
• Indicators of do-not·at1empt-resusc1tatt0n (ONAR) status (eg, bracelet. anklet. written
ciocumentahon)
• Threat to safety of providers
Out-of-hospna providers need to be aware of EMS-spec1f1C pol1c1es and protocols appb·
cable to these situations. ln-hosp~al providers and h1gh·performat1C0 teams should be
aware of advance d"ectives or spec1f1c hmits to resuscitation attempts that are In place
That 1s. some patients may consent to CPR and defibrillauon but not 10 intubation or 1nva·
slve procedures. Many hospnals will record this in the medical record.

Asystole as an O ften. asystole represents the final mythm . Cardiac function has diminished until electrical
End Point and functional cardiac activity finally stop and the patient dies. Asystole Is also the final
rhythm of a patient initially 1n VF or pVT.

Prolonged efforts are unnecessary and futile unless special resuscitation situations e xist.
such as hypothermia and orug overdose. Consider stopping if ETCO. is less than 10 alter
20 minutes of CPR.

Managing Asystole
- ----
Overview The management of asystote conslStS of the following components:

• Implementing the steps in the Cardiac Arrest Algonthm

• Identifying and correcting underlying causes
• Terminating efforts as appropriate

Adult Cardiac Arrest As descnbed 1n the VF/Pulseless VT and PEA Cases. the Cardiac Arrest Algorithm con·
Algorithm s1sts of 2 pathways (Figures 31 and 39) The left s•de ct the algonthm outlines treatment
for a sl'lockable rhythm (VF/pulseless VT) The right side of the algornhm (Steps 9 through
11) oothnes treatment for a nonshocl<.able rhythm (asystole/PEA). In both pathways. there·
p.es a•e des gned around penods (2 minutes) of uninterrupted. high-quality CPR In this
case Ne will focus on the asystole component of the asystole/PEA pathway.

1 111
 Part 0
Identification Treatment of asystole ts not limited to the interventions outlined in the algorithm.
and Correction of Healthcare providers should attempt to Identify and correct an underlying cause If present.
Underlying Cause Healthcare providers must stop, think, and ask, "Why did this person have this cardiac
arrest at this time?" It 1s essential to search for and treat reversrble causes of asystole for
resuscitative efforts to be potentially successful. Use the H's and T's to recall conditions
that could have contributed to asystole

Application of the Adult Cardiac Arrest Algorithm: Asystole Pathway

Introduction In thiscase, you have a patient in cardiac arrest High-quality CPR IS pe(fom\ed through-
out the BLS, Primary, and Secondary Assessments. Interrupt CPR for 10 seconds or less
while you perform a rhythm check. You Interpret the rttythm on the monitor as asystole.
CPR beginning with chest compressions for 2 minutes resumes immediately. You now
conduct the steps outlined in the asystole pathway of the Cardiac Arrest Algorithm begin-
ning with Step 9. At the same time, you are searching for a possible underlying cause of
the asystole.

Confirmed Asystole Give pr1onty to IV/10 access. Do not interrupt CPR while establishing IV or 10 access.

Administer • Conlll'lue htgh-qualrty CPR. and as soon as IV/10 access is available. gtve ep1nephnne
Epinephrine as follows:
- Epinephrine 1 mg IV/10-repeat every 3 to 5 minutes

Administer drugs during CPA. Do not stop CPR to administer drugs.

• Consider advanced airway and capnography.

Decision Point: Check the rhythm alter 2 minutes of CPR.

Rhythm Check Interruption of chest compressions to conduct a rhythm check should not
exceed 10 seconds.

Nonshockable • If no electnca/ activity Is pre$enl (asystole). go back to Step 10 or 11.

Rhythm • If electncal activrty is present and organized. try to palpate a pulse.
• If no pulse is present or 11 there Is any doubt about the presence or a pulse" continue
CPR. starting With chest compressoos for 2 minutes. Go back to Step 1Oand repeat
the sequence.
• If a good pulse is present and the rflythm 1s organized, begrn post-<:ardiac arrest care.

Shockable Rhythm If the rttythm check reveals a shockable rhythm, prepare to deliver a shock (resuming
chest compressions dunng charging ti appropriate). Refer to the left side of the algorithm
and perform steps according to the VF/pVT sequence, starting with Step 5 or 7.

Asystole and The diagram in Figure 39 (the Cardiac Arrest Algorithm) summanzes the recommended
PEA Treatment sequence of CPR, rhythm checks, and delivery of drugs for PEA and asystole based on
Sequences expert consensus.

1tll
 The ACLS Cases: Cardiac Arrest: AS}'Sfole

TCP Hot Se•t!<al random11:ed coouoUed tnals fa.led to .>how benef1I trom anempted TCP tor asysto
Recommended 1e. The AHA does not recommend the use ot TCP tor patoents wrth asys1011c cartMc arrest

Routine Shock There is no e.ldence that anempMg to "def1bnlla1e· asystole is benef1c1a1. In one study.
Administration Not the group that received shocks had a trend toward "'°""'
outcome Given the importance
Recommended of m1nun1ztng onumuptooo of chest compressions. the<e is no 1us11foeatooo lor onterruptong
chest compressions to dehver a shock 10 pouents wolh 11Syslole.

When in Doubt If It is uoclear whether 1he rhythm Is tone VF or asystole. an lnrtlal attemp1 at det1bnlla11on
may be warranted Frne VF may be the result 01 a prolonged arrest Al this 11me the ben·
ef1t of OOlaff19 defiboilatoon to perlorm CPA before del or latJon ;s unclear EMS system
meoa1 ditectors may conSoder mpiementrog a protOCOI :nat a iows EMS responder'S to
prOl/IOe CPA wtllle prepanng for defO'olal.On ot Pllbents found by EMS petSorVlel to be on VF

Terminating Resuscitative Efforts

Terminating If healthcare providers cannot rapidly iden11fy an underlying cause and lhe patient does
In-Hospital not respond 10 lhe BLS and ACLS onten1entt0ns 1ermo~1000 of all resusotalrve efforts
Resuscitatilfe should be considered
Efforts The decision to terminate resuscrtative effons rests with the treatJng physician 1n the
hosp11nl and Is based on conslderahon of many factors. rnclud;ng

• Time tram COiiapse to CPR

• Trne from COiiapse to first def bnllaoon attempt
• Comortlod disease
• Preorresl slote
• ln11131 arrest rhythm
• Rospo11se to resuscltallve measures
• ETCO,. less than 10 a fter 20 minutes of CPR
None of these factors alone or 1n comb1nalt0n rs clearly pred1ct1ve of outcome Howeve<,
!he dur11t.on ot resosc!latrve efforts is an 1mport;int lactor assooaled with poor outcome
The chance that the patent v. $Ul'llNe to haspotal d schatge and be neul'Ologocalfy onlact
dirnont5hes as resuscrtat.on time 1naeases Stop the resusc•tat.or anernpt when you dete<-
m1ne with a high degree of certainty that the patient v.111 not respond to further ACLS and
ECPR is not indicated or not available

Terminating Com nue out·of hosprtal resusotatJVe efforts untJ one of the fo1tow1ng occurs
Out-of-Hospital • Al'St orat1on of effeclrve. spontaneous cuculattOn and ventilation
Resuscitatilfe • Transfer o f care to a senior emetgency med1c11t prol ess1onaJ
Efforts • The proS-Once of reliable criteria indicating lrreversrblo death
• Tho healthcare provider is unable to con11nue bOcause ot exhaustton or dangerous
environmental hazards or because con11nU11d rE>susc1tat1on places the lives of others
"' ,eopardy
• A va 'd ONAR order' IS presented
• Online au1noozation from the rredical tor1trol pflySICian or tti prior moo.cal protOCOI
tor terminat.on of resusotatJOn

1H
 P •rt 0
Duration of The linal Clec saon to stoo r~tat.ve el'OttS can never be es 5'1Tlp·e as an solaled trne
Resuscitative "''crval II ROSC o• any OU<a:IOI\ C>OCU1$ t may oe appropna:e 10 coroSIOer extending tile
Effort• resusotal .e Ertf0'1

E•P<."1S l'\ave developed cr..,1cal rul&li to 11ssist on declSIO(IS to t&rrrunate resuSCltatove

ettons 101 on hospital and out·ol·hO~p11ar airests You should lam1hat1ze yourself with lht
established policy 01 protocols for your hosp11UI or EMS system.

Conhr1uo out ol hospital resusc11at1ve effons untd one or tho fo lowing occurs
• At >I0<.11Kll1 of eftectove. spontaneous corcuiatlOf and vei1toldt1on
TP.-.ster of care to a senl()r emergency medocm profeSSIOnal
-,.,,. presenc:;;o o• re aOle cnte<oa ltldicatong otl'evet1510le oeat~
"" rescuer is uroat>1e :o COl'.!JflUe t>ecauSe ot e.s.haustlOI\ 0t dangerO<JS enwonmerital
nazaros 0< oecause con:inued resusc tatlOI\ piaces :ne I •es of otllerS on ,eoi>attty
• A v,lltd ONAA O<der •S oresenteo
• Onltnp auihonzatoon from the medical control ptoysieoan or by prior medocal protocol
for 1erm1nat1on of resuscitation
fl rnoy .il!iO be appropnale to consider other issues such as drug overdose and severe
prearrest hypotherrma (eg submersion in icy waler) when decoding whether to extend
resusc11~11ve effoos Special resuscotatoon onlervento<>ns and prolonged resusc1tatove effons
m.1y be lll<l>Cat..O f0< Dalients woth hypetherrma orug overdose OI Other potenlially <evfl
11>1& caul>llS of arrest

Asystole: An You wolf see asystole most frequently on 2 si1uations

Agonal Rhythm? • As a 1erm1na1 rhythm 1n a resoscotatJOO attempt that staneo with another rhythm
• As Iha f rst rhythm •Oe,,11f1ect 1n a pa11>nt woth unwitnessed or prolooged arrest
Per~slent asystOle represer1s e•tensM~ myocarooal 1schemoa and dan109e from proloogao
peroods ol tnad.,quat" c0<onary perfusJOn Prognosis IS poor un"'ss a special resuscotaton
c11cumstance 0< 1mmed1atery reversible cause is present Survival from asystole is better
10< on hosp<tal lhan for out-of-hosp tal arrests according 10 data from Gel With
The G\Jld~ Ml> -Aesusc1tation tom1e<ty me Naloonal R1391s1ry of CPR
(www.heart.org/ resusc1tatoon).

Eth/cal The hogh perl01mance team must ma~e a conscoentlOUS and competent elfon to give
Considerations pal>ents •a tna of CPA ano ACLS • P<Ovoded the pa• !'flt had not expressed a deoslon to
forego resuso1a1 •ll effons and the VICI m rs not ooVlOuSly Cle40 eg ngor mon s. dec:om
POSotoon hemos.:ct.on oecao 1a110n (see the ONAA d scuSSIOI" on me Student Website)
The fonat <leCISIOI\ to stop resusci:a• >e enons can neve< be as 5'1Tlple as an ISOiated tome
tntervar

See Human. Ethoeal and Lt>Qal D1mens1ons ot CPR on the Student Website
(www.heart.org/eccstudent)

11 8
 The ACLS Cases: Cardiac Arrest: Asystole

Transport of Patients Emergency medical response systems should not require field personnel to transpOl1
in Cardiac Arrest every patient 111 cardiac arrest back to a hosprtal or to an ED. TransportaLon wrth continu·
1ng CPR 1s 1ustrfoed If 1nterven110nS available on the ED cannot be performed in the ou1·
of·hospital setting and they SB indicated for special circumstances (1e, card1opulm0nary
bypass or extracorporeal circulation for patients with severe hypothermia).

After OHCA with ROSC, tronsoort the patient to an appropriate hospital with a com·
prehenslve post-cardiac arresl treatment syst em of care that includes acute coronary
interventions. neurologic care, crrtocal care. and hypothermia Transport the in-hospital
post-cardiac arrest pauent to an appropriate cnbcal care unit capable of providing com·
prehens1ve post-cardiac arrest care.

119
 P art 0

Bradycardia Case

Introduction This case discusses assessment and management of a patient with symptomatic Orady·
cardia (heart rate less than 50/min).

The cornerstones of managing bradycatdoa are 10

• D1tterentiate between signs and symptoms that are caused by the slow rate versus
those that are unrelated
• Correctly diagnose the presence and type of AV block
• Use atropine as the drvg intervention ol first choice
• Decode when to initiate transcutaneous pacing (TCP)
• Decide when to start epinephrine or dopamine to maintain heart rat e and blood pres·
sure
• Know when to call for expert consultation about complicated rhythm Interpretation,
drugs, or management decisions
In addition . you must know lhe techniques and cautions for using TCP.
~~~~ ~~~~-

Rhythms for This case lllVOlves these ECG rhythms:

Bradycardia • Sinus bradycatdia
• Fust -degree AV block
• Second-degree AV block
- Type I (Wencl<ebach/Mobttz I)
- Type II (Mobrtz II)
• Third-degree AV block
You should know the major AV blocks because Important treatment decisions are based
on the type of block presenl (figure 41). Complele AV block is generally the most Impor-
tant and clinically s1gnlflcani degree or block. Also, complete or third-degree AV block
is the degree of block most likely to cause cardiovascular collapse and require 1mmed1·
ate pacing. Recognition of a symptomatic bradycard1a due to AV block is a primary goal
Recognition of the type of AV block is a secondary goal.

120
 The ACLS Cases: Bradycardia

l'lgun 4 1. ExaMPles of AV block A. S ros bnlclyCa(l a wrtn boroenne !1$1-<legt!e AV bloc!< 8 . Seeond.(legtee AV blclcK r;pe I. C. Second·
deg<ec AV b<ock rype II D, Complete AV bloc<"'"~ o v0<1trM:ular escape pacema~er (w.c!e ORS 0. t2 to 0.14 second E, Tt.ro-deg,.. AV block
with .ti junction.al lt!1Cape paC(tmi.'lkcr (narrow OAS: lebS than 0.12 second•.
--- - -- --- - -- --- -- -- -------- ---- - -
Drugs for This case involves these drugs:
Bradycardia • Atropine
• Dopamine (infusion)
• Epinept\nne (infusion)

t2t
 Part G
Description of Bradycardia

Definitions Definit ons used 111 this case are as follows:

Term I Definition
Bradyarmythmia or Any rhythm disorder with a heart rate less than 60/min - eg,
brodycardia' third-degree AV block-or sinus bradycard1a. When bradycard1a
Is tile cause of symptoms. the rat& Is generally less than 50/min.
Symptomatic Signs and symptoms due to the slow heart rate
bradyarrtiythmia

·For the purposes of thl$ case. we will use the term bradycarclia 1nte<changeably wrth
bradyarrhyrhm;a unless spec1fically defined.

Symptomatic Sinus bradycard1a may have multiple causes. Some are physiologic and require no
Bradycardia assessment or therapy. For example, a welt-trained athlete may have a heart rate in the
range of 40 to 50/min or occasionally lower.

In contrast, some patients have heart rates in the normal sinus range. but these heart
rates are 1nappropnate or insuffic eot f0< them. This is called a luncoonal or relative bra·
dycardia For example. a heart rate of 70/min may be relawely too slow for a patient in
card 1ogen1c or septic shock.

This case will focus on the patient with a bradycardia and heart rate less than 50/min. Key
to the case management is the delerm1nat1on of symptoms or signs due to the decreased
heart rate. A symptom atic bradycard1a exists clinically when 3 crltena are present:

1. The heart rate is slow

2. The pa11ent has symptoms

3 . The symptoms are due to the slOw heart rate.

Signs and Symptoms You must perform a focused history and physical examination to identify the signs and
symptoms o f a bradycardia

Symptoms include chest discomfort or pain. shortness of brenth, decreased level of con-
sciousness weakness. fatigue, hght-headedness. dimness. and presyncope or syncope.

Signs include hypotenst0n. drop in blood pressure on standing (orthostatic hypotension).

d1aph0<eS1s, pulmonary coogest•on on phyS1c81 examination or chest x-ray. frank cooges-
t1ve heart fa ure or PE. and bradycard1a-related (escape) frequent premature ventricular
complexes or VT.

122
 The ACLS Cases: Bradyc•rdl•

Managing Bradycardia: The Bradycardia Algorithm

Overview of the The Adu t Bradycardia w,tn a Pu se Aigoothm \Figure 421 out nes the $leps le< assess-
Algorithm IN!<lt and management of a pat~t presen1J119 ....in symptomatic b<adycaro a"' th P<Jlse
lmp1emen1a1t0n of this a1gor11hm begins with the den11fica11Qn ol braoycard1a !Step 11. ~
hean rate 1s less than 501m1n First steps 111Clude the compooen1s of the BLS Assessment
and ine Pnmary Assessment such as suppott1ng c1rcu1a11on and a•rw11y management,
giving o•ygen 11 indicated. mQl'I tonng the rhythm and v11a signs estab11sti.ng IV access.
and obtaining a 12-lead ECG I ava able 1S1ep 21 In the d1ffe<.int.a1 d«19nosis. you deter·
mine I the patient has S1Q"5 or symptoms o! poor pet1"51on and ~ theSe are caused b)
the b<adyCaldia 1Step 3

The P"'Tl(lfy decis'°'1 pot111 in the algonthm s me detenninabon ol adequate perfuSIOll If

the patent has adequate perfusion, you ooserve and monitor f$tep J) If the patient has
poor por1us1on. you administer atropine (Step 5). If atropine IS Ineffective. prepare tor TCP
or conMder dopamine or epinephrine Infusion (Step 5) tr ondocllli.>d, you prepare for trons-
venous pacing, search for and treat contribu11ng causes, and seek expcn consultauon
(Step61

Tile treatment seQuence 1n the algonthm is determined by 1ne sevet1ty of the pa11enrs
condition You may need to implement multtple 'ntenient1ons simullaneousty If cardiac
arrest develOps. go to the Cardiac Atresl AJgonthm

Adult Bradyc ardla With a Pulse Algorithm

• ..
.
1'1."
~[ Q,.•V~ OC""I- ~ ~ -

p.,.....,.
bt..:lp .. 1t1, '"'11• C9WW19'
4

./IQIMy----7
• M ~.o'?

• Sigw o4 lhxi?

.· ..,.te._.
--~7 .......1
5

Altopine IV dOff'
r.1s.1 l':SMff 0 ~ 11111 ht•!ue
Rcpea1 fl\'"')' J !1 1111111111••
Milll11T'11rn l uw.1
I Dopamilne IV tnfu..on
1
USva! ""'"" ri 1•
2 2f)ft't'.Q •\Ip m II!•

....._...,..,
ilfal~. Pll'-11 fOIC'.lO"lllf

E-"'"'"'"'°"
2-10"" I~ n'W'U'le
irtlAIC"'t Titrill&IOJWil.-.1
1esi-

123
 Part 0
Application of the Bradycardia Algorithm

Introduction In tnis caw you have a patient presenting wtth symptoms of bfadyc;lld1a You conduct
appropriate assessmen: ard 111ter.entlO<lS as out. ned in the BralfyCDtUia Algonthm At the
same time yOU are search.-.g for and treatlllQ poss ble contnbut1ng toctors

Identification of ld..nt1fy wlll'thef tile b<adyeardia IS

Bradycardla • Prt:sent by defn tion. oe nean ra:e .ess than 5Qlrrun
• Inadequate for the pat ems condruon (functional or relative)

Primary Assessment Next. perlorm the Pnmary Assessment including the foUowmg

a Maintain patent airway.

II Assist breathing as needed; give oxygen in case of hypoxem1a· monitor o xygen

sntu<auon

Are Signs or
•II Monitor blood pressure and heart rate; obtain and review a t 2 lead ECG.
establish IV access.

Conduct a problem-focused history and physical examlnmion

treat possible contnbuting factors

Step 3 prompts you to consider rf

search for ond

the Signs or symptoms of poor perfusion are cuused by

Symptoms Caused by the brady..:~rd.a
Bradycardia? n., key clinical quesuons ate
• Are tnore ·senous• signs or symptoms?
• Ale the signs and symptoms related to the slow lleart rate?
look for lld•e<Se signs and symptoms of the br3dycardta
• Symptoms eg ct>est oscorr•on shortness of 0<eath. decreased le11el of con&elOVS·
ness. v...akness fatigue. light-headedness. d1wness. presyncope or syncope)
• S.gns reg hypotension congesb11e heart failure. 11enlncular arrtiythmias relaled 10 !he
bradycardia
Samet m.-. 1ne symptom s not due to the bradycatdia For example. hyl>Otensoon asso-
c1a1eo w1lh bradycardoa may be due to myocardial dysfuncllon rathor than the bradycar·
d1a Keep this on mind when you reassess the patienl's response to treatment

Critical Concepts Bradycardia

The key ctin1cnl queslion 1s whether tho b radycardlo Is causing the pa11on1's symp1orns
or some 0111or Illness Is couslng the bradycardia

Decision Point: You rnusl now decide 1f 1he pa1lent has adequate or poor perfusion
Adequate Perfusion? • If lhe patienl has adequate perfusion. observe and morntor lStep 4)
• If tne pat.en! has poor perfusion proceed to Step 5

1 24
 The ACLS Cases: Bflldycardia

Treatment Sequence If the patient has poor periusion secondary to bradycardia. the treatmenl sequence is as
Summary follows·

Give atropine as first-line treatment Atropine 0.5 mg IV- may repeal to a total
dose of 3 mg

II atropine is Ineffective

Tnw.ICV!ancou:. pacmg or Dopamine 2 to 20 mc!Jlkg per minule

(chronotrop1c or heart rate dose)

Epinephrine 2 to 10 mcg/min

The treatment sequence is de-enm1ned by lhe sevenly of the pabenfs clinical presentation.
F0< patients with symptomatte bradycard1a, move quickly lhrough this sequence. These
patients may be ·pr~ardtac arrest• and may need multiple Interventions simultaneously.

Avoid relying on atropine In type II second· degree or third-degree AV block or in palients

with third-degree AV block w11h a new wide ORS complex where the location of the block
IS likely to be in 1nfranodal hSSJe (such as in the bundle of His 0< more distal conduction
system).

These bradyorrhythm1as are not likely to be responsive to reversal of cholinerglc effects

by atropine and are preferably treated wit h TCP or f}·adrenerg1c support as temponzing
measures while the patient is ~repared for transvenous pacing Atropine administration
should not delay implementaton of eXlemal pacing 0< ~adrenergic 1nfuS100 f0< pabents
wi1h unpend1ng cardiac arrest
Although not a first-line agent for treatment of symptomatic bradycard1a, a f>-adrenergic
infusion (ie, dopamine, epineJj)rine) is an alternative when a bradyarrhythmia Is unrespon-
sive t o. or inappropriate for, treatment wrth atropine. or as a temporizing measure while
the pattent Is prepared for transvenous pacing

No known vasopress0< (ep1neohnne) increases survival from bradycardia. Because these

medications can improve aort•c diastolic blood pressure. coronary artery perfusion pres-
sure, and the rate of ROSC, the AHA continues to recommend their use.

Alternative drugs may atso be appropriate in special circumstances such as the overdose
of a !}-blocker 0< calctUm challllel blocker. Healthcare proVJders should not wa 1 for a
maximum dose of a1rop1ne 1f lhe patient 1s presenting wrth second-degree or third-degree
block; rather, they may move to a second-line treatment after 2 to 3 doses of atropine.

Treatment Sequence: In the absence of immediately reversible causes, atropine remains the first·line drug for
Atropine acute symptomatic bradycarcia. Atropine sulfate acts by revefSlng choJinerg1c·med1ated
decreases In the heart rate ard AV node conduction. Dopamine and ep1nephnne may be
successful as an alternat1Ve to TCP.

For bradycardia. give atropine 0.5 mg IV every 3 to 5 minutes to a total dose of 0.04 mg.I
kg (maximum total dose of 3 'T\Q). Atropine doses of less than 0.5 mg may paradoxically
result in further slowing of the hearl rate.

Use atropine cautiously 1n thf presence of acute coronary ischem1a or M l. An atrop1ne-

mediated Increase in heart ra:e may worsen 1schemia or Increase Infarct size.

Do not rely on atropine in MOb1tz type II second-degree or third degree AV block or 1n

patients with third·degree AV block with a new wide ORS complex

125
 Part 8
»-eatment Sequence: TCP may be useful for treatment of symptomatic bradycard1a TCP is ll0f\llW3Sive and can
Pacing be perlormeo by ACLS pro111ders

Healthcare prov,ders should consider 1mmed1ate pacing 1n unstable patients wrth h1gh-
degr~ heart block when IV access Is not available. It 1s reasonable tor healthcare providers
to initiate TCP in unstable patients who do not respond to atropine.

After Initiation o f pacing. confirm electncal and mechanical capture. Because heart rate 1s
a major determinant of myocardial oxygen consumptJon. set the pacing rate to the lowest
effective rate based on clinical assessment and symptom resolution Reassess the patJent
for symptom 1111provement and hemodynam1c stabihty. Give analgesics and sedatives for
pain contrOI. Note that many of these drugs may further decrease blood pressure and
affect the patient's menta, status Try to dent1fy and correct the cause of the bradycardia

Some hm1tations apply. TCP can be pa,nful and may not produce effective electncal and
mechanical capture. If symptoms are not caused by the bradycard1a, pacing may be Inef-
fective despite capture. Because TCP is painful and not as reliable as transvenous pacing,
it should be considered as an emergent bridge to transvenous pacing in patients with
s1gmf1cant sinus bradycardia or AV block.

If you chose TCP as the second hne treatment and rt IS also 'neffective (eg. inconsistent
capture). begin an •nfusion of dopamine or epinephnne and prepare for possible transve-
nous pacing by obtaining expert consultabon.

Foundational Facts Sedation and Pacing

Most conscious patients should be given sedation before pacing. If the patient is in car-
diovascular collapse or rapidly detenorahng. it may be necessary to start pacing without
p11or Sedation. parocularly of drugs for sedation are not Immediately available. The chnl
cian must evaluate the need for sedat,on on light of the patient's cond1t,on and need for
immediate pacing. A review of the drugs used tS beyond the scope of the ACLS Pr0111der
Course. The general approach could include the following.
• Give paren1eral benzod1azep1ne for anxiety and muscle contractions.
• Give a parenteral narcotic for analgesia.
• Use a chronotropic infusion once available.
• Obtain expert consulta11on for transvenous pacing

Treatment Sequence: Nthough P-adrenergic agonists with rate-accelerating effects are not f1rst-ll00 agents for
Epinephrine, treatment of symptomatic bradycardia. they are alternatives to TCP or 1n special circum-
Dopamine stances such as overdose with a P-blOcker or calcium channel blocker.

Because epinephrine and dopamine are vasoconstnctors. as well as chronotropes. health-

care providers must assess the patient's intravascular volume status and avoid hypovole-
mla when using these drugs.

Both ep1neph1ine and dopamine infusions may be used tor patients with symptomatic
bradycard1a, particularly it associated with hypotension. for whom atropine may be 1nap-
propnate or after atropine tails

Begin eponephnne nfus10n at a dose of 2 to 10 mcglm1n and !llrate to patient response.

Begin dopamine infusion at 2 to 20 mcglkg per minute and titrate to patJent response
At lower doses. dopamine has a more selective effect on onotropy and heart rate, at higher
doses (greater than 10 mcgtkg per minute). ot also has vasoconslrict1ve effects.

126
 The ACLS Cases: Brsdycardla

Next Actions Ahcf consideration ot the treatment sequence in Step 5. you may need to

• Prepare the patient tor transvenous pacing

• Treat the contnbullng causes of the bradycardia
Consider expert consunaton-but do not delay treatment rl the patient IS unstable or
potentially unstable

Transcutaneous Pacing

Introduction A vanety of devices can pace the heart by delivenng an electncal sbmulus. causong elec-
mcaf depolariza11on and subsequent cardiac contraction. TCP delivers pacing impulses
to the heart through the skin by use of cutaneous elec trodes. Most manufacturers have
added a pacing mode to manual defibrillators.

The ab4!1ty lo perlomi TCP is now often as close as the nearest defibnllator Providers
neOO 10 know the •nd1ca1Jons. tecilnoques and hazards for using TCP

Indications Indications for TCP ore os follows:

• Hemodynam1cally unstable bradycard1a (eg, hypolenst0n, acutely alteted mental status.

Slgns of ShOCk. 1schem1c chest dtSComfort. acute heart !allure [AHF] hypotenslon)
Unstable clinical condition hkely due to the bradycardia
Fo1 pacing readiness 1n the setting of AMI as follows
- Symptomatic sinus bradycardla
- Mob1tz type II second-degree AV block
- Th1rd-degrae AV block
- New ~ft. nght or alternating bundle branch block or blfasc>cUlar blo<:k
Bradycard1a with symptoma11c ventncular escape rhylhms

Precautions Precautions for TCP are as follows:

TCP 1s contraindicated in severe hypothermia and is not recommended for asystole.
• Conscious pa11ents require analgesia ror d1s;;omton unless delay for sedatKln wiU
cause/conrnbure to derenoral!on
• Do not assess the caroud pulse to confirm mechanical capture; etectncal stlmulallon
causes muscular 1erkmg that may mimic the carot1dl pulse.

Technique Perform TCP by folio\\ 1ng these steps

Action
Place pacing electrodes on the chest according to package instructions.
M Turn the pacer on .
Set the demand rate 10 apptoximately 60/m1n This rate can be adjusted up or
• down tbased on patient chn1ca response) ooce pacing IS established
Set the current milliamperes output 2 mA GllOve the dose at whlCh consistent
• capture Is observed (safety margin).

External pacemakers have either fixed rntes (asynchronous mode} or demand rates.

127
 Part 0
Assess Response to Rather than target a precise heart rate, the goal ot therapy 1s to ensure improvement 1n
Treatment chmcal status (ie, signs and symptoms related to the bradycardia). Signs o f hemodynam1c
1mpa1rment include hypotens1on, acutely altered mental status signs of shock . lschemic
chest discomfort, AHF. or other signs or shock related to the bradycard1a Start pacing
at a rate of about 60/mm. Once pacing 1s 1mt1ated adJust the rate based on the patient's
chmcal response. Most patients will improve wrth a rate of 60 to 70/mm 1f the symptoms
are pnmanly due to the bradycard1a

Consider giving atropine before pacing ln mildly symptomatic patients. Do not delay
pacing for unstable patients, particularly those with high-degree AV block. Atropine may
increase heart rate improve hemodynamics, and el1m1nate the need tor pacing . II atropine
1s ineffective or likely to be lneffecuve or 1f estabhshmem of IV access or alropine admm•s·
tratlOll •S delayed beg.n pacing as soon as n IS available.

Pauents with ACS should be paced at the lowest heart rate that allows clin•cal stability
Higher heart rates can worsen lschemia because heart rate is a major determinate of
myocardial oxygen demand. lschemla. In turn, can precipitate arrhythmias

An a1temauve to pacing 11 symptomallc bradycald1a IS unresponsive to atropine IS a

chronotropic drug 1nfu5'0ll IO s11mulate heart rate
Ep1nephnne; lmt1ate at 2 to 10 mcglm1n and tnrate to patient response
• Dopamine: Initiate at 2 10 20 mcg/kg per minute and titrate to patient response

Bradycardia With A bradyc3Id1a may lead to se<:onda!)' bradycard1a·dependent ventricular rhythms. When
Escape Rhythms the nean rate 'alls. an electrically unstable ventncular area may ·escape" suppresslOll by
higher and faster pacemakers (eg. sinus node). especially 1n the semng of acute iscnemia
These ventncular rhythms often fail 10 respond to drugs. Wrth severe bradycard1a, some
patients will develop wide-complex ventricular beats that can prec1p11ate VT or VF. Pacing
may Increase the heart rate and eliminate bradycard1a·dependenl ventricular rhythms.
However. an accelerated ldloventricular rhythm (sometimes called AIVR) may occur In the
setting ot 1nler1or wall Ml This rhythm 1s usually stable and does not require pacing .

Patients with ventncular escape rhythms may have normal myocardium with disturbed
conduction. After correction of etec1tolyte abnormalities or ac1dos1s, rapid pacing can
stimulate effective myocardial contractions until the conduction system recovers.

Standby Pacing Sever.it bradycard1c rhythms 1n ACS are caused by acute 1schemia of conduction tissue
and pacing centers. Pat1en1S who are d1n1cally stable may decornpeosate suddenly or
become unstable over minutes to hours from worsening conductlOll at:>normafitJes. These
bradycard1as may detenorate to complete AV block and cardiovascular collapse.

Place TCP electrodes 1n anticipation of clinical deterioration 1n patients w ith acute myocar·
dial 1schem1a or infarction associated with the following rhythms:

• Symptomatic sinus node dysfunction wrth severe and symptoma11c sinus bradycardia
• AsymptomabC Mobttz lype II second-degree AV block
• Asymptoma11c third-degree AV block
• Newly acquired left, right, or atternabng bundle branch block or b1fascicular block 1n
lhe setting of AMI

1 28
 The ACLS Cases: Tachycardia: Stable and Unstable

Tachycardia: Stable and Unstable

Introduction If you are the team leader 1n tNs case. you wiU conduct the assessment and management
of a patten! with a rapid, unstable heart rate. You must be able to classify the tachycardia
and Implement appropnate Interventions as outlined in the Tachycardia Algorithm. You will
be evaluated on your knowledge of the foctors involved on safe and effective synchronized
cardioverslon as well as your pertonmance of the procedure.

Rhythms for This case involves these ECG rhythms (examples in Figure 43):
Unstable • S•nus tachycardia
Tachycardia • Atrial fibrillation
• Atnal flutter
• Reentry supraventncular tachycardia (SVT)
• Monomorph1c VT
• Polymorphic VT
• Wide-complex tachycardia of uncertain type

D
1211
 Part G

F
flguN 43 . E.arnol"" ot toe~ye<lrd•llS A, Sinus tachycarda. B, Atrial f1brMlat1on. C, Attia nutter 0 , SUpraventrocular tachycardia E, Monomorpl>c
Vef'lrlcular taenycard.a F, Polymotpt1IC -tncular tachyca"11<J

Drugs for Unstable Otugs are generally not used to manage patients wnh unstable iachycardra. Immediate
Tachycardia card1overs100 .s recommended Consider adm1nlstenng sedative drugs 1n the conscious
patient. But do not delay Immediate cardlovers1on in the unstable patient

The Approach to Unstable Tachycardia

Introduction A tachyarrhythmia (rhythm with heart rate greater than 100/min) has many potential
causes and may be symptomatic or asymptomatic. The key to management of a patient
with any tachycardia is to determine whether pulses are present. If pulses are present,
determine whether the patient 1s stable or unstable and then provide treatment based on
patient condrtron and rhythm.

If the tachyarrhythmra is Slrus tachycatd1a, conduct a diligent search for the cause of the
tachycardia. Treatment and cooect1on ol this cause wilt improve the Slgns and symptoms.

Definitions Oefin111ons useo 1n this case are as follows'.

Tenn I DefiniUon
Tachyarrhythmia, tachycardia" Heart rate greater than 100/min

Symptomatic tachyarrhythmla Signs and symptoms due to the rapid heart rate

·For the purposes of this case, we will use the term tachycard;a interchangeably with
tachyarrhythm1a. Sinus tachycardia will be specifically indicated.

1 30
 The ACLS Cases: Tachycardia: Stable and Unstable

Pathophysiology Un$lab Je tachyc\\rtlia exis)S when lhe heart r~1e 1$ too fast tor the patient 's clinical condl-
of Unstable lton and the l'txcessrve heart ra1e causes symptoms or an unstable condition because the
Tachycardia hean IS

• Beaung so fast that cardiac output is reduced, this can cause pulmonary edema,
coronary 1schem1a, and hypotension wlih reduced blood flow to vital organs
(eg, brain, kidneys)
• Beating rneff11Cttvely so lhat coordmalton between the atnum and ventnctes 0< the
ventricies themselves reduces cardiac output

Signs and Unstable tachycardia leads to serious signs and symptoms that include
Symptoms • Hypotens1on
~utely a1iered mi;>ntal status
Signs of shock
• lschem1c chest d1scomlort
• AHF

Rapid Recognition The 2 keys to management of pat•ents With unstable tachycard111 are
Is the Key to
1. Rapid recognouon that the pattent is s1gnlfrcantty symptomat•C or even unstable
Management
2. Rapid recognition that lhe signs and symptoms are caused by the tachycardia
You must quickly determme whether the patient's ta<;hycardia is producmg hemody-
namic instabl/1ty and serious signs and symptoms or whether the signs and symp-
toms (eg, the pain and distross of an AMI) Dr& producing the tachycardia.
This determ1nallon can be dlff1Cult Many experts suggest 1ha1 when a heart rate Is less
than 150/min. 11 1s unlikely that symptoms of lns1abdrty are caused primanly by the tachy-
c;ird1a unless !here •s 1mpa1red ventncular function. A heart ra1e greater than 150/min 1s
usually an 1nappropnate response 10 physiologic stress (eg, fever. dehydration) or other
unde<ly1ng cond1t1ons.

Severity Assess f0< the presence 0< absence of signs and symptoms and tor their seventy
Frequent paherit assessment is indicated

Indications for Rapl d identification of sympl omat1c 1achycardla will help you determine whe1her you
Cardioversion should prepare for 1mmed1ate cardiovers1on For exampl e:

• Sinus tachycardra 1s a physiologic respanse to exttinS<c facto<s, such as fever. ane-

mia or hypotensron/shock. wt11ch create the need for a compensatOfY and phys1-
olog1cal increase in heart rote. There Is usually a high degree of sympathetic tone and
neurohormonal faclors tn lhese settings. Sinus tachycardia will not respond to cardlo-
version. In fnct, If a shock is delivered. the heart rate often increases.
If the paM01 with tachycard10 1s stable (le. no senous 519ns related to the tachycardia),
patients may awart expert consultation beCa1Jse treatment has the poteotlal for harm.
• Atnal nuner typically produces a heart rate of approx1ma1ely t 50/min (lower rates may
be present 1n patients who have received ant1arrhythm1c therapy). Atrial flutter at this
rate 1s o f ton stable 1n the patient w1thou1 heart or serious systemic disease.
• At rates greater than 1 SO/min. symptoms ore often present and cardK>verston 1s often
reauired ti the parent 1s unstable.
• If the pahent is seriously 111 or has underty1ng cardiovascular disease. symptoms may
be present at lower rates
You must know when cardiovers1on 1s ind1ca1ed. how to prepare the paltent for 11 (includ-
ing approprmte medication). and how to switch lhe def1brlllator/monitor to operate as
a card1over1er
131
 Part 0
Managing Unstable Tachycardia: The Tachycardia Algorithm

Introduction The Adu" Tachycardia \'Vith a Pulse Algon1hm simplifies initial managemenl of tachycard1a
The presence or absence or pulses IS considered key 10 managemenl of a patient with
any tachycardia. If pulses are present, determine whether lhe patient 1s S1able or unstable
and then pro111de treatment based on the patient's condrt1on and rhythm If o pulseless
tachycardia 1s present. then manage the patient according to lhe Cardiac Arrest Algonthm
(Figure 31 on tne section Managing VF/Pul~ess VT· The Adult Cardiac Anvst Algonthrn)

The ACLS provider should e11her be an expen or be able to obtain exper1 consultation.
Actions in 1he steps require advanced knowledge of ECG rhythm lnterpretallon and anti·
arrhythmic lherapy and are intended to be accomplished In the in-hospital selling wrth
expert consultauon available

Overview The Tachycardia Algorithm :Figure 44) outlines tr.e steps for assessment and management
of a patient presenting with symptomatic tachycardia with pulses. Implementation of this
algonthm begins with the identification of tachycardia with pulses (Step 1) If a tachycar·
dia and a pulse are present. perlorm assessment and management steps guided by the
BLS Assessment and the Pnmary and Secondary Assessments (Step 2) The key in this
assessment Is to decide of the tachycardia 1s slable or unstable.

If signs and symptoms persist despi1e provision of supplementary oxygen and support
°'
of airway and ctrculation and 1f significant Signs symptoms are due to lhe tachycardia
(Step 31. then the tachycan:lla is unstable and 1mmed1ate synctvonized cardioversion is
1od1cated (Step 4).

If the palient Is stable, you will evaluate the ECG, and determine If the ORS complex is
wide or narrow and regular or irregular (Step 5). The treatment of stable tachycardia Is pre-
sented on the next case (Slep 6).

A precise d1agnos1s of the rhythm (eg, reentry SVT, atrial fluner) may not be possible at
this bme.

Foundational Facts Serious or Significant Symptoms

Unstable Condition

intervention is determined by the presence of slgnificanl symptoms or by an unstable

cood1t>oo resulttng from Ille tachycardia.·

Senous symptoms and signs include

• Hypotenslon
• Acutely altered menlai status
• Signs of ShOCk
• lschemic cheS1 d1scomf01
• AHF
"VentncuiaT rates less lhan 150/min usually do not cause serious signs or symptoms.

132
 Adult Tachycardia With a Pul se Algorithm

Asseos ~·-- '"' dnQI CCJrldltJOn_

tiean rate tyl""-'lllY .:150lm"' '' t.lChyant>ythmla
~,
tn.toal reconmenood -
• Nanvw regu.ilr so 1 ~ J
2 • - . . _ 120-200 J
b1<>1....: « 200 J iliO!IOPIW
• Woereguar •OOJ
• Marr.a.n "°'""' ..,,.."1 -tnot1'W'9es
• Oxygen l•f l'lyP<»""""I
riecassary · Wlde~-
dose loo• synclvomedl
• Cardoac """"'°'
to dent ty mythm. monotor blood Adonosine IV do. .:
pressure and 0"""'''Y F""' dose: 6 mg rap1d IV push
IOilow wnh NS hush
Second dOW 12 mg d roqu-
Alll/1Jrrl>y1hmlc Infusion• (0<
3
PO<'lls1ent 4 Stobie Wide-ORS Tnchyc•rrll•
tachyarThytllmla c1u11lng: Procainamid.e IV do•e:
• HypolonSIOtl? Synctvonlzed canli9ve1'91on 20-50 mg/min un111 ~rihythml•
v.. • ConSIOer -.,, on
• Aco.lt"'Y ..,...., ,,.. ""51.Jtua?
· ~OIShXI<?
• Tf r9QIAIW ..,. 'A C()ll"l"~ ll - - hypo•"" ""-.°'
ORS duraoon .,.,.._ '
• - Ct"ftl dmCClmt;;ort
"""""* _,.....,. ll'IO.<nvn oose 1 • "'II • g QOl"'I
• ~ ,_, lalltn~
~""""""
A>O<I d prolonged OT °' Off
- ' 4 ""'rnn.
Amlodarone IV dose:
r.s1 dose 150 mg°""' 10 minutes
Rei-I as need..d l VT rwcut•
WldeOl\57 f o.'1c)w by maintenanr ... It' fu11Qn of
>0.12MCOnd rfll9lJlN ~ 1110111()1 !'Cit pnc

7 =t
( : 1v a¢ci>ao an<f 12 1eao rcG '' ••.,1a1>1e
• V'IJlll "**"'""'
• eo....oer ~trmc r!uooon
. eo.- expert c:onoulliltoQn
1 ""',,., 1or mt 6

l
SotlllollVdose:
'~
100 mg (1.5 mg;kg) o- 5 monutM
AVOKI 1f proiof1Qed OT

• ~~ t regular)
. ~&oc· . Of ~ Cf'WYl@li CJllxk.er
• Cic:ir'9lder •"pen cc:w-..iU1tcn

Summary Your assessment and management of this patient will be guided t>y the following key
questlOlls presented 1n the Tachycardia Atgonlhm

Ase symptoms present Of absent?

• ts the pa11ent stable 0< unstable?
• Is the ORS narrow or wide?
• ts the rhythm regular 0< rregular?
• Is the ORS monomorphoc Of pol)'ITIOIJ)lllC7
YOU/. Wl$wers to these quest.ons will Clelemwie !he ne~I approp<'.ate steps

133
 - -
Part 0
Application of the Tachycardia Algorithm to the Unstable Patient
Introduction
Assess
Appropriateness for
Clinical Condition
Identify and Treat Use 1he BLS. Primary, and Second.i1y A$sessments 10 guide your app<oach
the Underlying Ca use • Look f0< s;gns of increased w<><k ol breathing Ui!Chypnea, ll'ltercos1a1 re1ract1ons.
S<Jp<astemal retractions. paradO»c.11 abdominal breathing) and hypoxerma as deter
Decision Point:
Is the Persist ent
Tac hyarrhythmla
Ca using Significant
Signs or Symptoms?
134
In lh1s casa yO\J have a pat en1 w11h l.lChycard a and 11 PV se You COl'lducl lhe s1eps out
kned 1n the Tachycardia Alg:iothm 10 evaluale and manag.: lhe patient
• Tachycardia os defined as an ,mnythmoa w11h a fille greater than 100/ll1'n
• The ra1e takes on c J(llCa SIQn loean<:I! ut its Qrealcr e•tremes and IS mo<e kelY
annblr.abie to an arrtiytrvm.i rn!e 01 150/111lll or great•
• It JS uni •ely t'>a! 5Yfl1P::>ms OI •11!.tabil tf a<e callSed Ptll'Nrit by the tachyeatd..i when
me hean rate is ess m..n 150/tnlll un?C$$ tr1e<e JS impaireo ventricular lunctlOl'I
mined by pulse oxometry
• Give oxygen. 1l 1nd1cated, and 1110111101 oxygen saturatron.
• Obtain an ECG to identify the 1hythm
• Evaluate blood p<eSSUre
• EStat>llSh rv access
• lden'u-;y and treat rever..ble causes
If S)mptoms pe<SISt 00$plte S<JppO<t ol aoequak oxygenatlOl'I ano ven1 a1ao p<oceed 10
St!>P 3
Unstable Patients
• Healthcare provtOers should obt;i11• a 12-tead ECG ear1y on the assessment to belle<
define 1he rhythm
• I lowever. unstable patients roqulro Immediato c ardloversion.
• Do not delay Immediate card1over~lon lor acqulS1t1on of the 12-lead ECG If lhe pa11ent
unsUlble
Assess the pat•ent's degree of inst. 1b1 ''Y and determine of the U\Slab1hty JS rt1,ated to
lhc t,1cnycard a
Unsrable
I tM t>al<e<"l oemonstra:es '3t&·roJaled catdlOVascWar COMp<omlSe With SJgl1S and
.ymploms such as h~po1ens1on, acuu.ly a11ered m"°tal status. signs ol Shock. 1scnem1c
'I.est discomfort, AHF, or olher signs of shock suspected lo be due to a 1act1yarrhythm1a.
proceed to 1mmed1a1e synchronize<! card10-ers1011 (Step 4)
Se<ious signs and symptoms ate uflh~ely 11 t11e "en1ncu1ar rate JS ess than 1MJJmon 1n
pa!•en1s with a healthy heart Howover, '' 1he pat•en1 is seriously UI <>< has s1gnil1cant
underlying hean disease or olher cond1l ons. symp1oms may be present at a lower
he,1rt rate
St.1ble
I• tM pat•ent does net ha>e ~dto-rou•oo caroiovascttar con"prom.se. P<OCeeCI 10 Step 5
Too heJ thcare prov>0er has 1me to obl:w\ a 12· eao ECG evaluate tne rnylllm, dete«Tkne
100 "'idth of the ORS, and Clotermtnl lr6lllmen1 optlOl'IS Slable patients may await e•pt.'f'I
consu11a11011 because treatment ha•. 1tiu potent•al 101 hatm
 The ACLS Cnes: Tachycardia: Stable and Unstable

Foundational Facts Treatment Based on Type of Tachycardia

You may not always be able to dislinguish between supraventrlcul<lr and ventricular
rhythms. Most w1de·cornplex (broad-complex) tachycardias ore ventricular in origin
(especially if the patient has underlying heart disease or 1s older). II the p atient Is pulse-
less, treat the rhythm as VF and follow the cardiac Arrest Algorithm.

If the patten! has a wide-complex tachycard a and IS unstable. assume rt IS VT unt~

proven otherwise. The amount of energy required for card1overs1on of VT is delerm1ned
by the morphologic characteristics.

• II the patient is unstable but has a pulse with regular uniform wide-complex VT (mono-
morphic V7):
- Treat with synchronized card1oversion and an 1nrtial shock of 100 J (monophasic
waveform).
- Ir there 1s no response to the first shock, increasing the dose in a stepwise lashlon is
reasonable.·
• Arrhythmias with a polymorphic ORS appearance (polymorphic V7). such as torsades
de poontes. wll usually not pennll synchronizal!oo. If the patient has po/ymorphlc VT:
- Treat as VF wrth h1Qh--rgy unsynchronized shocks (eg. def1bn abOO doses).
If there 1s any doubt about whether an unstable pauent has monomorph1c or polymer·
phic VT, do not delay treatment for further rhythm analysis. Provide high ·energy, unsyn·
chronized shocks.

'No studies that addressed this 1SSue had been ldentifed at the tlflle that the manuscnpt
for the 2015 AHA Guidelines Update for CPR and ECC was 1n preparat10n. Thus, this
recommendation represents expert opinion.

Perform Immediate • If poss ble. establish IV access before card10version and adm.n1St0f sedation 1f the
Synchronized patient IS COOSCIOUS
Cardio11ersion • Do not delay card1overs1on ii the patient is e><tremely unstable.
Further information about cardioversion appears below.

If the patient with a regular narrow-complex SVT or a monomorph1c w ide-complex tachy-

cardia is not hypotensrve. healthcare providers may adnw11s1er adenosine whi'e prepanng
for synchronized card1oversion

If cardiac arrest develops, see the Cardiac Arrest Algorithm.

Detennlne the Width • II the width of the ORS complex is 0. 12 second 0< more, go to Step 6.
of the ORS Complex • II the wodth of the ORS oomplex is less than 0.12 second, go to Step 7.

135
 Part 0
Cardioversion

Introduction You must know when cardo0version 1s indicated and what type of shock to administer.
Before card1overs•on. establish IV access and sedate the responsive patient if possible.
but do not delay cardiovers1on 1n the unstable or detenorat1ng patient.

This section discusses the following Important concepts about card1 aversion:

• The difference between unsynchronized and synchronized shocks

• Potential challenges to dehvety of synchronized shocks
• Energy doses for spec fie rhY1hms
~~~~~~~~~~~- -~~~~~~ -~~~~~~~ ~~~~~~-

Unsynchronized vs Modem def1brillator/cardooverters are capable of delivering 2 types of shocks:

Synchronized Shocks • unsynchronized shocks
• Synchronized shocks
An unsynchronized shock simply means that the electrical shock will be delivered as soon
as the operator pushes the shock button to discharge the device. Thus, the shock may fall
randomly anywhe<e w1th1n the cardiac cycle. These shocks should use higher energy levels
than synchronized card1overs1on.

Synchronized caraioversion uses a sensor to deuver a shock that 1s synclV'001Zed with

a peak of the ORS complex (eg. the highest point of the R wave). When this option
(the ·sync" option) 1s engaged. the operator presses the shock button to deliver a
shock There will likely be a delay before the defibrillator/cardloverter delivers a shock
because the device will synchronize shock dehvery with the peak of the R wave in the
patient's ORS complex. This synchronization may require analysis of several complexes.
Syncnronizallon avoids the dehvery ol a shoek dunng cardiac repolarizahon (represented
on the surface ECG as the T wave), a penod of vulnerab1hty 1n wh1Ch a shoe~ can pre-
cipitate VF. Sync:hromzed card10vers100 uses a lower energy level than attempted deflbnl·
latlOf'I. Low-energy shock$ sllould always be delivered as synclvontZed shocks to avOld
precipitating VF.
- - --
Potential Problems In theory, synchronization is simple The operator pushes the sync control on the lace
With Synchronization of the defibnllator/cardiove~er. In practice. however, there are potential problems.
For example:

• It the R·wave peaks of a tachycardia are undifferentiated or of low amplrtude. the

monitor sensors may be unable to ldenhfy an A-wave peak and therefore will not
dehver the shock.
• Many caroioverters will not synchronize through the handhetd quick-look paddles.
An unwaiy practrtt0ner may uy to synchronize-unsuccessfully 1n that the machine
will not discharge -and may not recognize the problem.
• Synchronization can take extra time (eg, if 1t is necessary to attach electrodes or 1f the
operator is unfamiliar with the cqulpmen1).

136
 The ACLS Ceses: Tachycardia: Stable and Unstable

Recommendations When to Use Synchroniz ed Shocks

Synchronized shocks are recommended for patients With
• Unstable SVT
• Unstable atrial fibrillation
• Unstable atnal flutter
• Unstable regular monomorphlc tachycardia with pulses

When to Use Unsynchronized Shocks

Unsynchronized high-energy shocks are recommended
• For a pattent who 1s pulseless
• For a patient demonstrating clinical deterioration (on prearrest), such as those with
severe shock or polymorphic VT. when you think a delay on converting the rhythm will
result in cardiac arrest
• When you are unsure whether monomorphic or polymorphic VT 1s present tn the
unstable patient
Should the shock cause VF (occumng on only a ve<y small m1nonty of patients deSpte
the theoretical risk). immediately attempt def1brillation.
----
Energy Doses for Select the energy dose for the specific type of rhythm.
Cardlo11ersion
For unstable atrial fibrlltation:

• Monophasoc catdooversion: Deliver an initial 200-J synchronized shock.

• Biphasic cardioversion: Deliver an initial 120- to 200-J synchronized shock.
• In either case increase the energy dose in a stepwise fashion for any subsequent
cardioversion attempts.
A dose of 120 to 200 J is reasonable with a b1phaslc waveform. Escalate the second and
subsequent shock dose as needed.

Cardioversion of atnal nutter and SVT gene<ally require less energy. An Initial energy dose
of 50 to 100 J with a monophasic or biphasic waveform Is often sufficient.

Monomorphoc VT (regular form and rate) with a pulse responds wel to monophaSlc or
blphas1c waveform card1oversion (synchronized) shocks at an 1nit1al dose of 100 J. If there
1s no response to the first shock. increase the dose in a stepwise fashion. No studies were
Identified that addressed this issue. Thus. this recomroon<lat1on represents expert Opinion.

Synchronized Cardioversion Technique

Introduction Synctvonozed cardroversoon is the treatment of choice when a patient tias a symptomatic
(unstable) reentry SVT or VT with pulses. It is also recommended to treat unstable atnaJ
fibrillation and unstable atrial flutter.

Card oversion Is unlikely to be elfectove for treatment of junctoonal tachycardia or ectOpic

or multifocal atrial tachycardia because these rhythms have an automatic focus arising
from cells that are spontaneously depolarizing at a rapid rate. Delivery of a shock gener-
ally c;annot stop these rhythms and may actually increase the rate of the tachyarrhythmia.

In synchronized cardiovers1on, shocks are administered through adhesive electrodes

or handheld paddles. You will neet1 to place the def1bn/la1or/moflJlor in synchronized
(sync) mode. The sync mode is designed to deliver -rgy 1ust after the A wave of tile
ORS complex.

t37
 Part 8
Technique Fo11ow these steps to perform synchronized cardioversion. Modify the ste:is for your
spec1f1C device.

DI Action

• Sedate all conscious patients unless unstable or deteriorating rapidly.

I
Turn on the dehbrillator (monophasic or b1phaslc).

Attach monitor leads to the patient ("whrte to right, red to nbs, what's left
over to the tell shoulder; and ensure proper display of the patient's rhythm.
Position adhesive electrode (conductOI') pads on tile patient.

- Press the sync control button to engage the synchron•zabon mode•

• Look for markers on the A wave indicating sync mode.

At11ust monttor gain II necessary un111sync markers occur with each A wave.

Select the appropriate energy level.

Deliver monophas1c synchronized shocks in the following sequence:

II I In itial Dose•
Unstable atrial fibrillation 200J

Unstable monomorphic VT 100J

Other unstable SVT/atrial

SO to 1DOJ
flutter

Polymorphic VT (irregular form Treat as VF with high-erergy shock

and rate) and unstable (del1bn 1at1on doses)

·Biphasic waveforms using lower energy are acceptable If documented to

be clinically equivalent or supenor to reports of monophas1c S'10Ck success.
Extrapolation from elective cardioversion of atrial fibrillation supports an ini-
tial biphasic dose of 120 to 200 J with escalation as needed.

Consult the device manufacturer for specific recommendations.

Announce to team members: "CharglllQ defibnllator-stand c1ea~·

- Press the charge button

Clear the patient when the defibrillator is charged (See "Founda:ional Facts
• Clearing lor Deflbr1llation" In the VF!Pulseless VT Case.)

Ill Press the shock button(s).

Check the monitor II tachycardia persists, Increase the energy level (joules)
according to the Elec1r1ca1 C3rd1oversion Algorithm

ml(see Supplementary Materials on the ACLS Student Websile; www.

~ heart.org/eccstudentj.

Activate the sync mode after delivery of each synchronized shock. Most deflbril·
lators default back to tl1e unsynchronized mode after de/ivety of a synchronized
shock. This default allows an immediate shock if card1oversion produces VF.
138
 The ACLS Cases: Tachycardia: Stable and Unstable

Stable Tachycardias Thos case reviews assessment ond management of a stable patient (•e. no seflO<Js signs
related 10 the tachyca!d.a} with a mpd heart rate Paloents woth hean rmes greater than
100/m., have a tachyarrhythma or tachycanl•a In this case. we w 11 use the terms tachy
catd a and tachyanhythm.a onterthangeabl): Note that •nus taehycardra •s excluaed from
the treat'"""t aJgonlhm Sonus ~Cllycard•a 1s almost arways phystOk>gc . deveiopong 1n
response to a comprornose 1n stroke volume or a condition tnal requires an 1riaease on
cardiac oulput (eg, fever, hypevolemoa) Treatment involves 1dent111catoon and correction ol
thal un<leolylng problem

You mu l be able to classify the type of tachycardia (wodo or narrow· regular or irregular)
a"<! lfl'plemen: appropnate 1t1terven1ons as ou1Joned '" the Tacnycardoa AJgorrth'll.
~ 'hiS case you ..ib
• Porlorm 1n tiaJ assessmen• and mariagernent
• Treat regular narrow-complex rhythms (except sinus tachycardia) with vagal
manouvers and adenosine
If the rhythm does not conven, you will monitor the patient and transport or ob1aln export
coosul1<11ton If the patoent bec;ornes cilnocally unstable you will Pfopare for 1mmed1-
a1e unsynchronu:ed shock or "vnc;hronozed cardJOVerso<>n as doscu~ 1n the UnSlable
Tachyeatd•a Case

Rhythms for Stable Tachycardias can be claSS1f1ed on S-OVeral ways based on the appearance of tne ORS
Tachycardia complex, heart rate, and whether they are regular or onegular
• Narrow-ORS complex ISVT) tachycardias (ORS less than 0 12 secondt
in orde< of frequency
Sinus tachycasdoa
Atnal f•bnllatJon
Atr101 Outter
AV nodal reentry
• W•~RS complex tachycanloas !ORSO 12 second or more
Moo IOmO<Jlll!C VT
- Polymor'phc VT
SVT with aberrancy
• Regular or irregular tachycardias
loregular narrow-complex illchycardias are probably atrial lobrillatoon

Drugs for Stable

Tachycardia • Ad< ._,,,.,,
Several ilg')n!S are also used to provide analgesia and sedation C\Jnng electncal card•O-
vtlfsoon. These agents are no1 covered on the ACLS Provider Course .

Approach to Stable Tachycardia

Introduction In thtS calie, a stable tachycardia refers to a condition •n wt11ch the pat•ent has
• A hean rate greater than 100/min
• No 6'QO•lcant signs or ~ymptoms caused by the 1rcreased rate
• A" undet1y•ng card.a<: ~weal abnormal ry that geriera1es tht rnythm_ _ _ __

139
 Part 8
Questions to Classiflca11on of the tachycardia depends on the careful c linical evaluaalon of
Determine these ques11ons:
C/assffication • Are symptoms p<esenl or absent?
• Are symptoms due to ll'le tachycardia?
• Is the pa1>en1 stable 0< unstable?
• Is the ORS complex narrow or wrde?
• Is 1he rhythm regular or irregular?
• Is the ORS monomorphic or polymorphic?
• ts lhe rhythm sinus tachycardia?
The answers guide subsequent diagooss and lfll3tment

Foundational Facts Understanding Sinus Tachycardia

• Sinus tachycardia 1s a heart rme that is greater tl'lan 100/min and Is generated by sinus
node discharge. The heart rate 1n Sinus tachycardia does not exceed 220/min and Is age
related &nus tachycardia usually does not exceed 120 to 13Q.lm1n, and 11 has a gradual
onset and gradual terrmnation Reentry SVT has an abrupt onset and 1erm1natJoo
• Srnus 1achycard1a 1s caused by external influences on the heart, such as lever, ane-
mia. hypolension, blood loss. or exercise. These are systemic oondil1ons. 001 cardiac
cond1l1ons Sinus tachycardia Is a regular rhythm, although the rate may be slowed by
vagol maneuvers. Cardlovers1on is contralnd1caled.
• ~-Blockers may cause clrnlcal deterioration If the cardiac output falls when a compen-
satoty tacnycard1a 1s blocked Th1S is because cardiac output 1s determined by the
volume ol blood eiected by the ventncies with each con1raetion (Slfoke volume) and
the nean rate.
Cardiac output (CO) : Stroke volume (Sll.) • Heart rate

• It a condrllon such as a large AMI limits ventricular function (severe heart failure or car·
d1ogen1c shock). the heart compensates by Increasing the heart rate If you attempt to
reduce the heart rate In patients with a compensatory tachycardia. cardiac output wrll
fall and the patient's condi11on will lrkety de1enora1e
In sinus tachycardia, lhe goal is ro identify and treat the underlying systemic cause.

Managing Stable Tachycardia: The Tachycardia Algorithm

Introduction As noted rn the Unstable Tachycardia Case, the key to management ot a p atient with
any 1achycard1a 1s to determine whether pulses are present, and 11pulses are present, to
de1erm1ne wheth er the patient Is stable or unstable and thllll to provide treatment based
on pahenl condition and rhythm. If the patient rs pulseless. manage the patient according
10 the Cardiac Arrest Algonlhm (Figure 31 1n the section Managing VF/ Pulsetess VT· The
Adutt Cardiac Arrest Algonthm) II the pabent has pulses, manage the pat>ent aceotd1ng 10
the Tachycardia Algonthm (Figure 44).
- -- -- --- - - - - - - - - -- - - -- - - - - - - - - - ----- - --

140
 - TM ACLS Cases: Tachycardia; Stable and Unsta"'-

Overview 11 a tachycardia and a pulse am present, perform assessment and management steps
guided by the BLS Assessment and tile Primary and SecondaJY Assessments. Determine
1f significant symptoms or SigllS are present Md 1t these ~ymptoms and signs are due to
It. tactycardla. This w dr<ea yo to erti- th" srable ~lf'PS 5 th ough " ' or un table
(Step 4) section of the algontnm

• II s·gnillcant Slgns Of symptoms are due to the tachyo.ard1a thfln the tachycardia 1s
unslac#I and rnmed ate cardlO\lers.on s llldoeateo '"""' me Un .table Tachycard>a
Case)
• II the patient develops /)Useless VT. dehver unsynchrornzed hogh·energy ShOcks (def1
bnllahon enc<gy) ond follcw tho C<1rd13c Arrect Algorithm.
• If the patient has polymorohic VT. treat the rhythm as VF and aet1ver high-enetgy
unsynctiron1zec sho<.kS (re dill Dti atoon energy)
In thrs case. the patient Is stable, and you will manage according lo the stable section o r
I,.,. Tachycardia AlgontMI Fogxe 441 A precise. .clerl' feat on 01111<> rhythm eg reentry
SVT, atnal flutter) may not be posSlble at thrs time

Application of the Tachycardia Algorithm to the Stable Patient

Introduction In this case, a pa11ent fllls stable tachycatd1a wrlll a pulse Conduct the steps outlined 1n
the Tachycaraia Algonhm to eval •te and man..ge the patient

Patient Assess ment Step 1 dtrl!C1S yoo to asse~s the patient's condition Typically, a heart rate greater than
150lmin at rest is due to tach(<!fl'hythmias other than &I'<• tachyo.,.c:i.a

BLS and ACLS Us ng the BLS Primary. and Secondary Assessments to guide your approach, evaluate
As•essments th!' patoent and do the tollo\WIQ os necessary:
• Look tor signs of increased w0tk of b<ealh1ng and hypoxia as determined
by pulse oximetry.
• Give o•ygeo mon tn< o-cvgen '3turatoon
• Support the ouway. b<eatnrng and crrcuta11on
• Obtain an ECG to 1don11~1 the rhythm, check blood prossure
• !dent fy and treat re-.ersibie <1uses
tt symptoms pers1S1, proceed to Step 3
- - - - - - - - --
Decision Point: Unstable
Stable or Unstable It th<> patient is unstable w1:h signs 0t symp10C11l as a re- ~I of :Ile tachycardia lea hypo·
tension. aculely allered mental s101us. srgns of shock. 1schem1c chest d1scomfon, or
AHFl go to Step 4 1pe<fom1 rnmechate synchron1led cardlove!SIOn) Se" the Unstable
Tachycardia Case

Stable
ti the patl9flt is stable. go 10 Step 5

IV Access and If the pauent with tachycmd1a 1s stable (ie. no serious signs or symptoms related to the
12-Lead ECG 1¥.hycardia). you have torT"' •o evaluate the rhythm and decide on treatment options.
Estab11Sh rv access If not a ready obt.ined Obta<n a 12 •Nld ECG wt>t • a'a...ib. or
rhythm strip 10 dotermlne 1f the ORS IS narrow (less than 0. t 2 second) or wide (0 12 second
or morel

14 1
 P •rt 0
Decision Point: The path ot treatment is now determined by whether the ORS IS wide (Step 6) or narrow
Narrow or Wide {Step 7). and whethe< the rtiythm 1s regular or 1neguL~r If a monomorpllic wide complex
rhythm is present and the po11em 1s stable. expert consultation .s advised POiymorphic
w de-complex tachycardia ~d be treated w•th 1m~iate unsynchronized card1oversion

Foundational Facts Treating Tachycardia

• You may not always be abl" to d1sttngu1sh t>etween supraventrlcular {aberrant) and
ventricular wide-complex rhythms If you are unsure. be aware that most w1de-com-
µlcx llJ<• .10-complex) tamycaro u are vemncuiar on ong n
• If a pa11ent is pulseless. follow the Cardiac Arrest Algorithm.
• 11 a pat1ent beco'TleS un able oo not de'.ly treat.,,"'' tor funhe< rhythm ana1ys.s_ For
tabie pat>enlS v. th ~ "111>'"• tacnycaro.as. transpon and monotor or consu.1 an
exper1 . t>ocause treatment has tho potentaal for Mrm

Wide· Complex Wide-complex tachycardias are deloned as a ORS ol 0 t 2 second or more Consider
Tac.h ycardias e•o.A c:onsu.raoon.
The most common lorms of Irle-threatening wide-complex tachycardias I <ely to deteno
ratt to vF >re

• Monomorph1c VT
• Polymorphic VT
Detarm1ne 11 the rhythm 1s regular or 1negular
• A '119 :it w'de-comp/<!> taehycatdoa os presumed to be VT 01 SVT w th at>.otraney
• An ITTegu1ar w.oe-comp. •x tacilycardia may be atnat fioollation with abemlncy, pre-
exc1ted atnal flbnllation 1au1al f1b<ollation usmg an accessory pathway tor antegrade
rend,,, toon) °' polymorphic VT torsades de po.n1es These are advanced rhythms
requiring add1honal expe111se or expen consultation
II the rtiythrn Is l•kely VT or SVT 1n a stable p:itlent, 1re01t based on the algorithm for that
rhyth

If th<> rhythm etiology canno: be determined and is re<)ular "' .ts rate U1d monomorphoc
rucent e•"ldf>nce sugges:s th 1 rv ~ •elatrvdy sare ror ootto tr tm"nt and O•ag
nos•s IV ant<arrhythm1c druci may be effective. We recommend proca1nam1do, omroda
rone. or sotnlol. See the nghl column of the Tachycard•a Algorithm (Figure 44) for recom
mended doses

In the case ol irregular wlde-comple• taehycatd•a management fOCUSf"" on control of the

rao-.J ventricular ra1e trate ca trol) COl'\lersl()l'I of hemodynamocaily un,.ta!)le atrial f bolla·
tlOfl to sinus rhythm !rhythm contro~. or both Expen consultation s advised

Caution Drugs to Avoid in Patients With Irregular Wide-Complex

Tachycardia
Avoid AV nodal olockong agents sueh as adenos1ne. c<1lclum channel blockers digoxrn.
ano ross.bly !}·blockers m patoen:s "· •., P<&- • c.:a· oon 11= • t>rolla'.ion, because lllese
O<ugs may cause a paradoxical •ncrease 1n tile "'ntncutar response.

142
 The ACLS Cases: Tachycardia: Stable and Unstable

Narrow QRS, The therapy for narrow OAS with regular rhythm is
Regular Rhythm • Attempt vagal maneuvers
• Give adenosine
Vagal maneuvers and adenosine are the preferred initial interventions for term inating
narrow-complex tachycardias that are symptomaltc (but stable) and supraventncular in
origin (SVl). Vagal maneuvers alone (Valsalva maneuver or carotid sinus massage) w ill
terminat e about 25% of SVTs. Adenos1ne is required for the remainder.

If SVT does not respond to vagal maneuvers:

• Give adenosine 6 mg as a rapid IV push in a large (eg, antecubital) vein over 1 second.
Follow with a 20 m l saline flush and elevate lhe arm immediately.
• If SVT does not convert wrthin 1 to 2 minutes. give a second dose of adenosine 12 mg
rapid IV push following the same procedure above.
Adenosine increases AV block and wlll terminate approximately 90% of reentry arrhyth·
mias within 2 minutes. Adenosine will not terminate atrial flutter or atrial fibrillation but will
slow AV conduction, allow ing for identification of flutter or fibnllal!On waves.

Adenosine is safe and effective In pregnancy. Adenosine does, however, have several
important drug interactions. Larger doses may be required for patients with significant
blood levels of theophylline. caffeine, or theobromine. The initial dose should be reduced
to 3 mg in patients laking dipyridamole or carbamazepine. There have been recent case
reports of prolonged asystole after adenos1ne administration to paltents with transplanted
hearts or after central venous administration, so lower doses such as 3 mg may be
considered in these situations.

Adenosine may cause bronchospasm; therefore, adenos1ne should generally not be given
to patients with asthma or chronic obstructive pulmonary disease, particularly if patients
are actively bronchospastic.

If the rhythm converts with adenos1ne, 1t is probable reentry SVT. Observe for recurrence.
Treat recurrenc-e with adenosine or longer-acting AV nodal blocking agents such as the
non-dihydropyridine calcium channel blockers (verapamil and diltiazem) or !}-blockers.
Typically, you should obtain expert consultation if the tachycardia recurs.

If the rhythm does not convert wi th adenosine, tt Is possible atrial flutter, ectopic atria.I
tachycardia, or junctional tachycardia. Obtain expert consultation about diagnosis
and treatment.

Caution What to Avoid With AV Nodal Blocking Agents

AV nodal blocking drugs should not be used for pre-excited atrial fibrillation or flutter.
Treatment with an AV nodal blocking agent is unlikely to slow the ventricular tate and in
some instances may accelerate the ventricular response. Caution 1s advised when com·
bining AV nodal blocking agents that have a longer duration of action. such as calcium
channel blockers or 13-blockers, because their actions may overlap if given serially, which
can provoke prolound bradycardia.

143
 part e
Tachycardia Some ACLS providers may be familiar with the differential d iagnosis and therapy of
Algorithm: Advanced stable tachycardias that do not respond to inttlal treatment. The basic ACLS provider is
Management Steps expected to recognize a stable narrow·complex or wide-complex tachycardia and classi fy
the rhythm as regular or irregular. Regular narrow-complex tachycardias may be treated
inttially with vagal maneuvers and adenosine. If these are unsuccessful, the ACLS provider
should transport or seek expert consultation.

If ACLS providers have experience w ith the differential diagnosis and therapy of stable
tachycardias beyond Initial management, the Tachycardia Algorithm lists additional steps
and pharmacologic agents used in the treatment of these arrhythmias, both for rate
control and for termination of the arrhythmia.

If at any point you become uncertain or uncomfortable during the treat-

ment of a stable patient, seek expert consultation. The treatment of stable
patients may await expert consultation because treatment has the potential
for harm.

144
 The ACLS Cases: Immediate Post-Cardiac A1Test Can1

Immediate Post-Cardiac Arrest Care Case

Introduction There 1s increasing recognition that systematic post-cardiac arrest care after ROSC can
improve the likelihood of patient survival with good quality of life. Positive correlations
have been observed between the likelihood of survival and the number of cardiac arrest
cases treated at any individual hospital."" Studies show most deaths occur during the
first 24 hours after resuscitation from cardiac arrest.''" Post-<:ardiac arrest care has a
significant potential to reduce earty mortahty caused by hemodynamic instability and later
morbidity and mortality caused by mult1organ failure and brain in1ury."'''•

There is a growing body of research focused on the identification and optimization of

practices that improve outcomes of patients who achieve ROSC after cardiac arrest."
Mere restoration of blood pressure and gas exchange does not ensure survival and
functional recovery. Sigrnficant cardiovascular dysfunction can develop after ROSC that
requires active support of blood flow and ventilation. including intravascular volume
expansion, vasoactive and onotrop1c drugs. and invasive devices. Targeted temperature
management (TIM) and treatment of the underlying cause of cardiac arrest impact sur-
vival and neurologic outcome. Hemodynam1c optimization protocols have been introdu~ed
as part of a bundle of care to improve survival."·50 The data suggest that proactive man-
agement of post-<:ardiac arrest physiology can improve outcomes by ensuring organ oxy-
genation and perfusion and by avoiding and managing complications.

This case focuses on the management and optimization of cardiopulmonary function and
perfusion of vital organs after ROSC.

To ensure the success of post-cardiac arrest care, healthcare providers must

• Optimize the patient's hemodynamic and ventilation status
• Initiate TIM
• Provide immediate coronary reperfusion with PCI
• Provide neurologic care and prognostication and other structured interventions
In this case, you will have an opportunity to use the 12-lead ECG while using the assess-
ment and action skills typically performed after ROSC.

Rhythms for You will need to recognize the foftowlng rhythms:

Post-Cardiac • Rate-too fast or too slow
Arrest Care • Width of QRS complexes- wide versus narrow
~~~~~~~~~~~~~~-

Drugs for This case involves these drugs:

Post-Cardiac • Epinephrine infusion
Arrest Care • Dopamine infuston
• Norepinephrine infusions

Multiple System A comprehensive. structured, multidisciplinary system of care should be implemented •n

Approach to a consistent manner for the treatment of post-<:ardiac arrest patients. Programs should
Post-Cardiac include TTM. optimization of hemodynamics and gas exchange, immediate coronary
Arrest Care reperfusion when indicated for restoration of coronary blood flow with PCI. neurotogic
diagnosis, critical care management, and prognostication.

Clinicians should treat the precipitatmg cause of cardiac arrest after ROSC and initiate or
request studies that will further aid in evaluation of the patient. It is essential to identify and
treat any cardiac, electrolyte, toxicologic, pulmonary. and neurologic precipitants of arrest.

145
 part e
Overview of Providers should ensure an adequate airway and support breathing immediately after
Post-Cardiac ROSC. Unconscious patients usually require an advanced airway for mechanical support
Arrest Care of breathing. Providers should also elevat e the head of the bed 30° if tolerated to reduce
the incidence of cerebral edema, aspiration. and ventilatory-associated pneumonia.
Proper placement of an advanced airway, particularly during patient transport, should be
monitored by waveform capnography as descnbed in the 2015 AHA Guidelines Update
tor CPA and ECC. Oxygenation of the patient should be monrtored continuously with
pulse oximetry.

Although 100% oxygen may have been used during initial resuscitation. providers should
titrate inspired oxygen to the lowest level required to achieve an arterial oxygen satura-
tion of 94 % to 99% to avoid potential oxygen toxicity. Hyperventilation is common after
cardiac arrest and should be avoided because of the potential for adverse hemodynamic
effects . Hypervent1lallon increases intrathoracic pressure, which decreases preload
and lowers cardiac output. The decrease in Paco, seen with hyperventilation can also
decrease cerebral blood flow directly. Ventilation should be started at 1O/min and titrated
to achieve a PElCO, of 35 to 40 mm Hg or a Paco., of 40 to 45 mm Hg.

Healthcare providers should frequently reassess vital signs and monitor for recurrent car-
diac arrhythmias by using continuous ECG monitoring. If the patient is hypotensive (SBP
less than 90 mm Hg), fluid boluses can be administered . If TTM is indicated. cold fluids
may be helpful for Initial induction of hypothermia. If the patient's volume status is ade-
quate, infusions of vasoactlve agents may be initiated and titrated to achieve a minimum
SBP of 90 mm Hg or greater or a mean artenal pressure of 65 mm Hg or more. Some
advocate higher mean arterial pressures to promot e cerebral blood flow.

Brain injury and cardiovascular instability are the major factors that determine survival
after cardiac arrest.''' Because TIM is currently the only intervention demonstrated to
improve neurologic recovery, it should be considered for any patient who is comatose and
unresponsive to verbal commands after ROSC. The patient should be transported to a
location that reliably provides this therapy in addition to coronary reperfusion (eg, PCI) and
other goal-directed postarrest care therapies.

Clinicians should treat the precipitating cause of cardiac arrest after ROSC and initiate or
request studies that w ill further aid in evaluation of the patient. It is essential to identify
and treat any cardiac, electrolyte. toxicologic, pulmonary. and neurologic precipitants of
arrest. Overall, the most common cause of cardiac arrest is cardiovascular disease and
associated coronary ischemia.'" " Therefore. a 12-lead ECG should be obtained as soon
as possible to detect ST elevation or LBBB. Coronary angiography should be performed
emergently (rather than later in the hospital stay or not at all) for OHCA patients with sus-
pected cardiac etiology of arrest and ST elevation on ECG. When there 1s high suspicion
of AMI. local protocols lor treatment of AMI and coronary reperfusion should be activated.
Coronary angiography. if indicated, can be beneficial in post-cardiac arrest patients
regar<:lfess of whether they are awake or comatose. Even 1n the absence of ST elevation,
emergent coronary angiography is reasonable for patients who are comatose after OHCA
of suspected cardiac origin. Concurrent PCI and TTM are safe, with good outcomes
reported for some comatose patients who have undergone PCI.

Critical care facifit1es that treat patients after cardiac arrest shOuld use a comprehensive
care plan that includes acute cardiovascular interventions, use of TTM, standardized med-
ical goal-directed therapies, and advanced neurologic monitoring and care. Neurolog1c
prognosis may be difficult to determine during the first 72 hours after resuscitation. This
should be the earliest time to prognosticate a poor neurologic outcome in patients not
treated with TTM. For those treated with TTM, providers should wait 72 hours after the
patient returns to normotherm1a before prognosticating by using clinical examination
where sedation or paralysis can be a confounder. Many initially comatose survivors of
146
 The ACLS Cases: Immediate Post-Cardiac Arrest CanJ

cardiac arrest have the potential for full recovery.""· Therefore. rt rs important to place
patients In a hospital crrtlcal care unrt where expert care and neurolOglC evaluation can be
pertormed and where appropnate l estlng to aid prognosrs 1s performed In a timely manner.

Managing Post-Cardiac Arrest Care: The Post-Cardiac Arrest Care Algorithm

The Adult Immediate Post-Ca'liiac Arrest Cate Algomhm (figure 45) outhnes ah the s1eps
'°'1mmed•ate 3SSeSSlllent and management of post-ca((l1ac arrest pa11eo1s w1t/l ROSC .
Ounng thlS case. team members will ronbnue to maintain good veot•lalron and oxygen-
ation w th a oog-mask device or advanced airway. Thtoughout the case d•SCuSSlon ol
0

the Post-Gardr;ic Arrest Care AJ901ithm. we will refet to Steps 1 through 8. These are the
numbers assigned 10 lhe steps In the algonthm.

Use lhe H's and T's to recall cond1t1ons that could have contnbuted 10 1he cardiac airest
See column on the right ol th& algonthm and " Part 4. The Syst&matrc Approach" for more
rnformatlon on the H's and T's. including cllnrcal clues and suggested treatments

Adu lt Immediate Post- Cardiac Arrest Care Algorithm - 2015 Update

Return of spontaneous circulation (ROSC) Doua/Oota1l1

!
Ventilation/oxygenation:
AvOld excesStve ventilation
2
Stari al 10 b<Mth!llm1n and
OptirniZe ventilation and oxygenation ~ 111ra1e 10 1a1~1 P1 rr.(l ol
35-40 mm Hg
• Ma1nt11 n o n saturation ~~ \\then fe3.Slble, hlrate Fio,
• C0!1$0C..- advanced a rway aria waveform capnography 10 m1n1mum necessary to
• Do tl"(JI hypert1ont I.a.ta ac111eve Spo ;o9.l %
rv bolus:
3 Approx.malely 1·' L
"""""' sar.,., "' 18ctdtoo
. • fV1()
'Treat hypotenst00 ~BP <90 mm Hg)
OOIUs-
R•ng«•
Eptnephnne IV 1nfus1on;
o 1-0 5 Inell''<I per mnr.e
• v~ nfu"'°"'
i'" 70-kg adult 7 ·35 l1lCil
• co...ld!!< treatab'• """""' per mtnU!OI
Dopamine IV lnluaion:
5 10 mcqlkg per mrnu10

4 12-Lead ECG: Norep1nepflrine

Yeo STEM! IV infusion:
Coronary re~rfuslon or O1·05 mcglkg per m1nu1~
high suspicion (rn 70-kg adult 7-35 mcQ

[ o! AMI per mrnule)

7 • Hypo11olemlu
• Hypoxl.1
lnlllole targeled • Hydrogen ion (ocl<Jos1s)

•
temperature management • Hypo-/hyperkolom1a
• Hypothermtil
• Ten9•0ll pnoumothoro.1t
Tarnpo00de. cnrdloc

Advanc ed critical eare

____,,) l • To 1uns
• Thrombosis. pu1mon11.y
• Thrombos.s. coronary

14 7
 Part 0
Application of the Immediate Post-Cardiac Arrest Care Algorithm

Introduct ion This case discusses the assessment and treatment of a patient who had cardiac arrest
and was resuscitated with the use of the BLS Assessment and the ACLS Primary and
Secondary Assessments During rhythm check 1n the ACLS Primary Assessment, the
patient's rhythm was organl1ed and a pulse was detected (Step 12. Cardiac Arrest
Algorithm (Figure 3 1J). The team leader will coordinate the efforts of the high-performance
posH;ard1ac arrest care team as they perf0<m the steps of the Post-Cardiac Arrest
Care Algonthm

Optimiz e Ventilation Step 2 directs you to ensure an adequate airway and support breain1ng Immediately after
and Oxygenation ROSC. An unconsclOUslunresponsM! patient will require an advanc8d airway for mechanical
support of breathing
Use continuous waveform ca.pnography to confirm and monitor CO<rect placement of
the ET tube (Figures 46 and 47)
• Use the lowest inspired oxygen concentration 1ha1 will maint&1n arterial oxyhemoglo-
bm saturation 94% or greater When lltration of insptred oxygen 1s not feasible (eg. 1n
an out-of-hospital sett ng). II IS reasonable to emp1ncally use 100% oxygen until the
patient amves at the ED
• Avoid excessrve vent1lat10n of the patient (do not venlllate 100 fast or too much}.
ProVKler.; may begin vent1lal10nS at t O/m1n and tttrale to achieve a Pnco, of 35 to
40 mm Hg 0< a Paco, of 40 10 45 mm Hg
To avOtd hypox1a 1n adults Mth ROSC after cardl8C atrest and d appropnate equipment
1s available, providers may use the highest avwlable oxygen concentration unul the arte·
naJ oxyhemoglobln saturatoo 0< the part'31 pressure of artenal oxygen can be measured
Deaease the fractlOll of 1nspored oxygen (FIO,) wnen oxyhemogk>btn satura1l00 is 100%,
provided the oxyhemoglob<n saturation can be maintained fO< 94 % or greater

Because an oxygen saturation of 100% rr1ay correspond to a Pao, between app<0x1mately

80 and 500 mm Hg . m general 11 1s appropr1a1e to wean Fio, for a saturation of 100%.
provided the patient can mam1111n oxyhemogl0b1n saturatJOn of 94 % 0< greater.

Critical Concepts Waveform Capnography

In add1110fl to mon1tonng ET lube pos1t10n. quantttat1ve waveform capnography allows
healthcare personnel Jo mon1t0< CPR quality, optimize chest compreSS1ons, and detect
ROSC during chest compressjons or when a rhythm check reveals an organized rhythm

Caution Things to Avoid During Ventilation

• When securing an advanced airway, avoid using ties 1hat pass c1ri:umferent1ally around
the patient's neck. thereby obstructing venous return lrom the brain
• Excessive ventilation may potentially lead to adverse hemodynamlc effects when Intra-
thoracic pressures are increased and because of potential decreases In cerebral blood
flow when Poco, decreases.

148
 -
The ACLS Cases: Immediate Post-Cardfac An'Ht Cere

l'oundatlonal Facts Waveform Capnography

• En<H1dal CO, is the concentralton of carbon dioxide 1n exhaled air at the end of exp1·
ration. It is typically expressed as a pan1al pressure in m111imetn of mercury (PETCO,)
Because CO, is a trace gas 1n atmospheric air, co, detected by capnography in
exhaled air is produced in the body and delivered to the lungs by circulating blood.
• Cardiac output is the ma1or determinant of CO, delivery to the lungs. II ventilation Is
relatively constant, PETCO, correlates well with cardiac oul put during CPR.
• Providers should observe a persistent capnograph1c waveform with ventilation to
confirm and monitor ET tube plaoernent in the field, ui the tranSpot1 vehicle, on arrival
at the hospital, and after any pataeot transfer to reduce the nsk of urvecognized tube
misplacement 0< displacement.
• Although capnography to confirm and monrt0< correct placemeot of supraglOttic air·
ways (eg, laryngeal mask a rway. laryngeal tube, or esophageal-tracheal tube) has not
been studied, effective ventilation through a supraglothc airway device should result 1n
a copnography waveform during CPR and after ROSC .

...
~
~
""
Ttma
A

..,
~ ...
~
""

...
fE '°
E
..
• Time
c
f lgure • • · Wa.ef0<m capnogtaphy A. Nonnal range a' 35 to 4!> mm Hg B, 20 mm Ilg C, O mm Hg.

149
 P a rt 0

60

Time

ftgore 47. Wavefomi capnography w11h t'n ET showtng nOfm.al (adequate) venti'ahon pattern PETCO 35 to 40 mm Hg

Treat Hypotension Box 3 directs you to treat hypotenslon when SBP 1s less than 90 mm Hg. Providers
(SBP Less Than should obtain IV access 1f not already established Verify the patency of any IV lines ECG
90mm Hg} morutonng should continue after ROSC. during transport. and lhroughOut ICU care until
deemed chrucaJy not necessary Al this stage. consider treating any reverS1ble causes that
might have precipitated the card ac arrest but perS1st after ROSC.

When IV 1s established, treat hypotenSlon as follows:

• IV bolus 1-2 L normal saline or lactated Ringers

• Norepinephrine 0. 1--0.5 mcg/kg per minute ~n 70-kg adult: 7-35 mcg per minute) IV
1nfus1on titrated to achieve a mh11mum SBP of greater than 90 mm Hg or a mean arte-
nal pressvre of greater than 65 mm Hg
• Epinephrine 0. 1-0.5 mcg/kg per minute (10 70-kg advlt: 7-35 mcg per minute) IV lnfu·
s1on titrated to achieve a minimum SBP ol greater than 90 mm Hg or a mean arterial
pressure of greater than 65 mm Hg
• Dopamine 5- 1O mcg/kg per minute IV infusion ti trated to achieve a minimum SBP of
greater than 90 mm Hg or a mean arterial pressure of greater tnan 65 mm Hg

150
 The ACLS Cases: Immediate Post-Cardiac AtTest Care

Norepinephrlne (levanerenol) 1s a naturally occumng potent vasoconstnc1or and onotroptc

agent 11 may be elfectove for management of patients with ~""ere hypotension (eg SBP
ess 1t1;in 70 mm Hg) and a IOw 101a1peftplleral rl!Slslance who do not respond to Jess
po1en1 adrenergoc drugs such as dopamine, phenytepht1nP or methoxam1ne.
Epinephrine can be used In patlOOts who are not 1n cardiac arrosl but who require 1no1roplc
or vasopressor suppon

Dopamine hydrochloride is a catecholam1no-l1ke agent and a cl\emocal precursor of nor·

epuiephrone that stimulates the hean through both n and ~ adrone<gic receptors

STEM/ Is Present Both on· and ou1-of-llC)Spital mooica personnel Should obtam a t :l· Nld ECG as soon as
or High Suspicion possible after ROSC lo ~Illy tho$C paloents with STEM! 0< a high SU$l)IQOl'I of AMI
of AMI Once s~h pat.ents ti.he t>aen ident hed l\Osprtal personnel ShOuld a11ompt COt011afY
reperfuSIOf"l (Step 5)

EMS Pt>fSO<lnel should 1ranspon these patoents to a lac11tty that rehably provides thrs
therapy !Step 5)
~~~~~~ ~~~~~--

Coronary Aggressive treatment of STEM including coronary reperl~ wt•h PCI should beg1t1 1f
Repertusion aftllt ROSC regarOless of coma ()( rrM In tne C3S(! Of out -of hOSprtal STEMI
(lt!t(;lt(j
P<OVICk! advance not '.c.:itoon tn r«l!lWlg fadf;t.oes

Following Step 4 dorects yoo 10 e"3ITll<le the p;.itient s abo ty to IOl'ow verbal commanus
Commands If the pa1oen1 does not fOllOw commands. the hlgh-per10<mance 183m Should consider
omprementing rrM (Step 7). If the paloent is able 10 tollOw verbal commands move 10
Step8

Targeted To prote<.t ine t>ra.n and other~ tile hlgh-perlonnance t>1am should start TTM"'
Temperature patlllfllS v.ho remain comat~ (lack of meaningful response 10 •ert>al commands! 'Mlh
Management ROSC after catd'3C arrest

For rTM h"ailhcare providers Y>ol.lkt select and maintain a cons1.1n1 target lemper.lture
be!Wet>n 32 C and 36 C for a perlOd of m least 24 hOur~ Although the op11mal method
of ach1ev1ng the target 1empern1ure 1s unknown. any comb1n:i11on ot ropkt Infusion of Ice
cold. 1«01on1c. non-glucose-con1a1n1ng fluid (30 ml.Jl<g). endovil'ICular catheters. surface
coot1"!j devices. or simple ""'1.ica 1nll!fVen1tons (eg. •Ce bags1 appear.; to be safe
and ef'ectl\'e

Spec t c featU<tlS of the patoef11 may f;ivor se er::tion of one temperature over another for
rTM Hoghet temperatures mtqhl be preferred 1n paloenls 10< whom IOwer temperatures
convey some nSk (eg. hle001nq). and lower remperatures m1qhl be preferred when pat•enls
have c11n1cJI features 1ha1 are wor!lf'ned al higher temperntures (eq seizures. cerebral
edema) Of note, there are essentlally no p;;menls for whom J~mperolure control some-
where 1n the range between 32"C and 36' C is contralndlcnled I herofom. all pahents 111
whom Intensive care 1s continued Ole e11g1ble.

In the pruhospilal setting. rcx.t1ne cooling of pa11en1s aher ROSC wolh rapid mfus1011 of
cold IV fluids snould not be done Cununl evidence indocales lh31 there •S no direct out
come benefit from these 1n1etVenhons and lhat the IV fluid adm1111s1r.1t1on 1n the prehos·
p110I Si!ltlng may increase pulmonary edema and rearre$1 Whether d•Herenl methods or
devices for temperature con1rol outside of the hospttol are benof Cini Is unknown.

115 1
 P •rt 0

Foundational Facts Targeted Temperature M anagem ent

• ITM 1s the only intervention de01oi1struted to improve neurologlc recovery alte<
cardiac arrest
• The op11mal duration of TIM Is at It.JS! 24 hours Comparat<Ye studies of the duration
of ITM have not been oertom!OO in adults but hypotnermta lor up 10 72 hours was
"''" <J SJfL>ly 1n newborns
• H.oattncar11 providers snould montor tile putiont score temperature durWlg rTM by usng
an esopnageal tnennomtter. bbddor CL1thl:ter In nonanu:>c palients or a pulmonary
atte<y catneter rt one is placed tor othe< 1ndoeat1011S Axiltaly and ora tempera!...,.. are
na<leQuate for measurement ot core tempermu<e ChangeS
TTM snould not affect the dcc•SIOO to perlorm PCI. bocause concurrent PCI and nypo-
thermia are reported to bl> f• 1bl• and -.f..

Advanced After coronary reperfusion .nterventt0ns or '" Cl1>6'1 where the post-card1dC arrest patient
Critical Care has no ECG evidence or susp1e>on ot Ml the hoqh-perlormMCe team Should transfer the
patient to nn ICU

Post-Cardiac There is no evidence :o support con• nuod proj)hylactic adlTldl&Straton of ant.wmythmoc

A/Test Maintenance medocatons once tne patl("lt achlevvs ROSC
Therapy

Life Is Why Science Is Why

Cvcloovascucar d<SeaseS ClaolTI mote ~ves tnan nll lomis OI cancer comblnod This uns&l11111Q
statistic droves the AHA's comm1tmoot to bonll science to Joie by advancing resusc1tatt0n
knowledQe and researcil 1n new way,

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 Part 0
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anest ...- ~y P'l~ l!B.lt·
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anest Rew=t.Jt""1 :>oo9 f!Ol4t .1 t8 J24
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1!J5
Adult High-Quality BLS American
Skills Testing Checklist Heart
Association.
life is why-

Date of Test _ _ _ _ _ _ _ _ _ _ __

Hospital Scenario: "You are working in a hospital or clinic, and you see a person who has suddenly collapsed in the
hallway. You check that the scene is safe and then approach the patient. Demonstrat e what you would do next."
Prehospital Scenario: "You arrive on the scene for a suspected cardiac arrest. No bystander CPR has been provided.
You approach the scene and ensure that it is safe. Demonstrate what you would do next."

Assessment and Activation

D Checks responsiveness D Shouts for help/Activates emergency response system/Sends for AED
D Checks breathing D Checks pulse

Once student shouts for help, instructor says, "Here's the barrier device. I am going to get the AED. "
-·······················-··---------------
Cycle 1 of CPR {30:2) 'CPR feedback devices preferred for accuracy
~~~~~~ .................................................
....
Adult Compressions Adult Breaths
D Performs high-quality compressions·: D Gives 2 breaths with a barrier device:
• Hand placement on lower half of sternum • Each breath given over 1 second
• 30 compressions in no less than 15 and no more • Visible chest rise with each breath
than 18 seconds • Resumes compressions In less than
• Compresses at least 5 cm 10 secoods
• Complete recoil after each compression

r --······--- ------ - ---------------------·-

Cycle 2 of CPR (repeats steps in Cycle 1) Only check box if step is successfully pertonned
D Compressions D Breaths D Resumes compressions in less than 1O seconds

Rescuer 2 says, "Here is the AED. /'// take over compressions, and you use the AED. •·
r
AED (follows prompts of AED)
D Powers on AED 0 Correctly attaches pads 0 Clears for analysls D Clears to safely deliver a shock
0 Safely delivers a shoek

r
Resumes Compressions
D Ensures compressions are resumed Immediately after shock delivery
• Student directs instructor to resume compressions or
• Second student resumes compressions

STOP TEST

... . -.. .,. ,. .---1

Instructor Notes - - -
• Place a ./ in the box next to each step the student completes successfully.
• If the student does net complete all steps successfully (as indicated by at least 1 blank check bOx). the student must receive

---·~·-·~ ..,~---·
Test Results Circle PASS or NA to 1nd1cate pass or needs remediation. PASS NA

Instructor Initials Instructor Number Date - - -- -- - --

C} 2016 American H1wr1 Associa.tion

15 7
 V
~ American
Airway Management Heart
Skills Testing Checklist Association.
life is why·
Student Name _ _ __ __ _ _ _ _ _ __ __ _ _ _ _ _ _ _~ Date ot Test _ _ _ _ _ _ _ __

. ./ if done
Critical Pertonnance Steps correctly

BLS Assessment and Interventions

Checks for responsiveness
• Taps and shouts, "Are you OK?" I
Activates the emergency response system
• Shouts for nearby help/Activates the emergency response system and gets the AED
or
• Directs second rescuer t o activate the emergency response system and get the AED

Checks breathing
• Scans chest for movemen t (5·1Oseconds)

Checks pulse (5-10 seconds)

Breathing and pulse check can be done simultaneously
Notes that pulse is present and does not init iate chest compressions or attach AED
I--
Inserts oropharyngeal or nasopharyngeal airway I
Administers oxygen
~ ------------------------~
Performs effective bag-mask ventilation for 1 minute
• Gives proper ventilation rate (once every 5·6 seconds)
• Gives proper vent ilation speed (over 1 second)
• Gives proper ventilation volume (-half a bag)
STOP TEST

Test Results Circle PASS or NR to indicate pass or needs remediation: PASS NR

Instructor Initials _ _ _ Instructor Number Date

Instructor Notes
• Place a ./ in the box next to each step the student completes successfully.
• If the student does not complete all steps successfully (as indicated by at least 1 blank check box), the student must receive
remediation. Make a note here of which skills require remediation (refer to Instructor Manual for information about remediation).

Test Results Circle PASS or NR to indicate pass or needs remediation: PASS NR

Instructor Initials _ _ _ Instructor Number Date _ _ _ __

o 2016 Amehean Hoort Associmlon

158
 American
Megacode Testing Checklist: Scenarios 1/3/8 Heart
Bradycardia ' Pulseless VT ' PEA ' PCAC Association.
lffe is why·

Student Nam e - - - - - - -- - - - - Date of Test _ _ _ _ __

Critical Perfonnance Steps .I if done

correctly
Team Leader

Ensures high·quality CPR at all times

-------------~
Assigns team member roles

Ensures that team members perform well

Bradycanlia Management

Starts oxygen if needed, places monitor. starts IV

Places monitor leads in proper position

Recognizes symptomatic bradycard1a

Administers correct dose of atropine

Prepares for second-line treatment

Pulseless VT Management

Recognizes pVT

Clears before analyze and shock

tmmedlately resumes CPR after shocks

Appropnate airway management

Appropriate cycles of drug-<hythm check/shock-CPR

Rec0gnizes PEA __J

- - - - - --
Verbalizes potential reversible causes of PEA (H's and T's)
- - - -
Administers appropriate drug(s) and doses
- - - - -
Immediately resumes CPR after rhythm checks

Post-Cardiac Arrest Care

I identifies ROSC
! Ensures BP and 12· 1ead ECG are performed, O, saturation is monitored , verbalizes need for
endotracheal intubation and waveform capnography, and orders laboratory tests

Considers targeted temperature management

STOP TEST

~est Results Circle PASS or NR to indicate pass or needs remediation: PASS NR

Instructor Initials Instructor Number Date _ _ _ __

Learning Station Competency

0 Cardiac Arrest 0 Bradycardia
4' 20 16 American Heart ASSOCial on
n Tachycardia 0 Immediate Post-Cardiac Arrest Care n Megacode Practice J
159
 ,- American
Megacode Testing Checklist: Scenarios 2/5
Bradycardia -+ VF -+ Asystole -+ PCAC V Heart
Association.
life 1s why-

done
,/ If
correctly

Assigns team member roles

Ensures that team members perform well

Bradycanlia Management

Starts oxygen if needed, places monitor, starts IV

Places monitor leads in proper position

Recognizes symptomatic bradycardia

. Administers correct dose of atropine

Prepares for second-line treatment

I
VF Management

Recognizes VF

Clears betore analyze and shock

Immediately resumes CPR after shocks

-------------~
Appropriate airway management

Appropriate cycles of drug-rhythm check/shock-CPR

Administers appropriate drug(s) and doses

Asystole Management

Recognizes asystole
Verbalizes potential reversible causes ot asystole (H's and T's)

Administers appropriate drug(s) and doses

..
Identifies ROSC

Ensures BP and 12-lead ECG are performed, O, saturation is monitored, verbalizes need for
endotracheal intubation and wavetorm capnography, and orders laboratory tests
Considers targeted temperature management
1
STOP TEST

~t Results Circle PASS or NR to indicate pass or needs remediahon_:_ _ __

l Instructor lnltlals _ __ Instructor Number Date _ ---P-A-S-

S -~
I Learning Station Competency
D Cardiac Arrest D Bradycardia D Tachycardia I' Immediate Post-Cardiac Arrest Care D Megacode Practice
0 2016 Amenc:ln Hearl AssociatiCt'I

160
 ,_ American
Megacode Testing Checklist: Scenarios 4/7 /1 O
Tachycardia -+ VF -+ PEA -+ PCAC V Heart
Association .
life is why-

Date of T e s t - - - - - - - - -
./ if done
Critical Performance Steps COITectly

Ensures high-quality CPR at all times

Assigns team member roles

Ensures that team members perform well

Tachycardia Management

Starts oxygen if needed, places monitor, starts IV

Places monttor leads in proper posrtion

I--
Recognizes unstable tachycardia

Recognizes symptoms due to tachycardia

Recognizes VF

Clears before analyze and shock

Immediately resumes CPR after shocks

-------------- - -
Appropr iate airway management

Appropriate cycles of drug-rhythm check/shock-CPR

Administers appropriate drug(s) and doses

PEA Management

Recognizes PEA

Verbalizes potential reversible causes of PEA (H's and T's)

Administers appropriate drug(s) and doses

--------------------4--------~

..
Identifies ROSC
Ensures BP and 12-lead ECG are performed, O, saturation is monitored, verbalizes need for
endotracheal int ubation and waveform capnography. and orders laboratory tests
-------~

Considers targeted temperature m anagement

STOP TEST

Test Results Circle PASS or NR to 1nd1cate pass or needs remed1at1on: PASS NR

Instructor Initials Instructor Number __ Date _ _ _ _ __

I Learning Station Competency

LJ:J Cardiac Arrest D Bradycardia O Tachycordia D Immediate Post -Cardiac Arrest Care D Megacode Practice
l
C 2016 Amenca.n Heart Assocaatlon

161
 •
~ A merican
Megacode Testing Checklist: Scenarios 6/11 Heart
Association .
Bradycardia ' VF ' PEA ' PCAC
lif e is why·

Ensures high-quality CPR at all times

Assigns team member roles

Ensures that team members perform well

Bradycardia Management
Starts oxygen if needed, places momtor, starts IV

Places monitor leads In proper position

~~~~~~~~~~~~~~~~~~~~~~

Recognizes symptomatic bradycardia

Administers correct dose of atropine

Prepares for second-line treatment

VF Management
Recognizes VF

Clears before analyze and shock

·-~~~~~~~~~~~~~~~~~~~~~~--.~~~~~---j

Immediately resumes CPR after shocks

Appropriate airway management

------------------------,~--------,
Appropriate cycles of drug- rhythm check/shock-CPR

Administers appropriate drug(s) and doses

Recognizes PEA

Verbalizes potential reversible causes o f PEA (H's and T's)

Adminls ters appropriate drug(s) and doses

- -- ---- - - ---- - -
Immediately resumes CPR after rhythm checks

Ensures BP and 12-lead ECG are pertormed, o,

saturation 1s monitored, verbalizes need for
endotracheal intubation and waveform capnography, and orders laboratory tests

I Considers targeted temperature management - - - - - --

STOP TEST

Test Results Circle PASS or NR to indicate pass or needs remediation: PASS NR

~ructor Initials Instructor Number - - - - - -- Date _ _ _ __ _

I l earning Station Competency - - -==-- -

C. Cardiac Arrest D Bradycardia D Tachycardia 0 Immediate Post-Cardiac Arrest Care lJ Megacode Practice
0 201G: Amencan Heart Associa:ion

162
 V
~ American
Megacode Testing Checklist: Scenario 9 Heart
Tachycardia -+ PEA -+ VF -+ PCAC Association.
life is why ·

Date of Test

./ If done
Critical Perfonnance Steps
correctly

Ensures high-quality CPR at all times

Assigns team member roles

Ensures that team members perform well

l
Tachycardia Management

Starts oxygen if needed. places monitor, starts IV

1
Places monitor leads In proper position

Recognizes tachycardia (specific diagnosis)

Recognizes no symptoms due to tachycardia

Considers appropriate initial drug therapy

PEA Management

Recognizes PEA

Verbalizes potential reversible causes of PEA (H's and T's}

Administers appropriate drug(s) and doses

Immediately resumes CPR after rhythm check and pulse checks

VF Management

Recognizes VF

Clears before analyze and shock

Immediately resumes CPR after shocks

Appropriate airway management

Appropriate cycles of drug-rhythm check/shock-CPR

Administers appropriate drug(s) and doses

l
Post-Cardiac Arrest Care

Identifies ROSC

-
Ensures BP and 12-lead ECG are performed, O, saturation is monitored, verbalizes need for
endotracheal int ubation and waveform capnography. and orders laboratory tests

Considers targeted temperature management

STOP TEST

Test Results Circle PASS or NR to indicate pass or needs remediation: PASS NR

Instructor Initials _ _ __ Instructor Number o

__at_e_ :.:.:.- - -_-:__ _ ---~
Learning Station Competency
O Cardiac Arrest O Bradycardia 0 Tachycardia LJ Immediate Post-Cardiac Arrest Care 0 Megacode Practice

C 2016 Ao'!Cric~ Hean Associaton

163
 V
~ American
Megacode Testing Checklist: Scenario 12 Heart
Bradycardia ' VF ' Asystole/PEA ' PCAC Associat ion.
life 1s why·
Student Name _ _ Date of Test

Critical Performance Steps

Team Leader
Ensures high-quality CPR at all times

Assigns team member roles

Ensures that team members perform well

Bradycardia Management
Starts oxygen if needed, places m onitor, starts IV

Places monitor leads in proper position

Recognizes symptomatic bradycardia

Administers correct dose of atropine I

Prepares for second-line treatment

VF Management
Recognizes VF

Clears before analyze and shock

Immediately resumes CPR after shocks

Appropriate airway management

Appropriate cycles of drug-rhythm check/shock-CPR

Ensures BP and 12-lead ECG are performed. 0 2 saturation is monitored. verbalizes need for
endotracheal intubation and waveform capnography, and orders laboratory tests

~onsiders targeted temperature management

- - - -
STOP TEST
~t Results Circle PASS or NR to indicate p-ass
_ o_r_n_ee-ds remedr-a-tio_n_: _ _
PASS NR

~tructor lnihals _ _ _ Instructor Number _ _ __ Date _ _ _ __

I Learning Station Competency

l_g_Cardiac Arrest D Bradycardia D Tachycardia lJ Immediate Post-Cardiac Arrest Care LJ Megacode Prac~
@?016Amorican Hean A~•(l.l-On

164
 Cardiac Arrest VF/ Pulseless VT Learning Station Checklist

Adult Cardiac Arrest Algorithm-2015 Update

f' ' f'W>Nfdial-~CmllW>d
..... lasl j100., 20i"'"'f
aro allow~· theet ~~
Start CPR 0 .• AMiirwrlz•
___
lt'lll!lfNC)flOnl .,,
cor>pr9SSIOf1S
• Give oxygen·
• Attach moMor/defibnlalor 0 • Rotate~""""
2 mn.lies. Of' IOOMll' ff f.d~
• If no ad..ancect ..,ay,
u :!.comp!MSOt•¥ef'l.._Gn

VF/ pVT
v••
9
r
No

Asygtole/PEA
I
• o~~··..etotm
-~·
r. Pr.:::o: c_ 10 nwft Hg. .,.""""
to~CPR_,
• ~arena P""3l.ft
- H ,,,._,.,,, .,._ [<M
3
, Shock u - · _ . ·.20 IMl Hg
attemp1toim~CrR
quai1ty
~ t ••

CPR 2 min • Biphasic: M...lnu1~.i1 0t

• IV/10 access
!llCO!MlOO®toOn ftg 1n,1 .~
dose of l?()-2'0() Jt It t.tr11\00 Nn

Sec:aidano.._..,.._
4,l5e rnaJlJITU'1 . . . . . . . .

- "'"°"""'....... -
d;)ses. 'TWy at~
· ~ ~J

. ........,.... rvno-
· rig~3·5rnt11 h

10 • AmiodatonelVllO-•nt
dose 300 mg """" Socnn<l

1v110C:~~2 min ~
c1o5e· 1so mo
CPR 2mln
• Epinephrine every 3·5 min • Advanced Airwnv
• Consld« advanced airway, • Epinephrine every 3-5 min
capnography • CooS!dot advenoed airwoy, • Endotrac:heal UllUOOh(WI ()II
capnoQtaphy svpragtotUc aovnneect •lf'Vl'llY
• Wa\-efetrn caonc>Q<aplly.,

r No
-Rhythm
~ .....
eaooornet~ to cor1tolfM . . ,
monrtof" El IU06 P'IC ~
• Orce aa.~ _...,. "'plle""
shocbble? !t>'! l Of"'1ll -v
6 IOCOnll
1·0_.,,,,._..,._
v..

"lb ·----
cnes:COl•C)l.-O•

~ Shock o
7

8 r-:;
• Aorupl sust\Wlied Wt9ll1'* in
CPR 2 min CPR 2 min Prn:o. (typoc;ll'Y ,•o '""'HO>
• Amlodarone • Treat reversible cau1fn:I • Spootat1eou$ anenJI 1,i••u1•
• Troa1 reversible causes waves with lntn\·l rlHl.tl

. . r;;i
monitoring

111
shoc:Qbl<t? -
v..
- -i
0•111m
: :=--
...._.. ... -..
12

• Kno~ot......,,al
. . , . , , , _ araJlanon
CR()SCl. go IO 10 or 1 1
Goto5or7 ·H-· --
•tt,~
• Ten5iCJll"!~8•
·T~i;...a..c:
• T"""'5
• If AOSC. go to • T'WomllOs& ~
Post..(;;irdoac - Care • Ttwom:t>0515 COl'O'lo1t"t

16!1
 Cardiac Arrest Asystole/PEA Learning Station Checklist

Adult Cardiac Arrest Algorithm-2015 Update

• l'ushhanSIOl,....,~cmJ"""
0 ano
'""' 3llOW
100 12Qi"""l
conllllot• ,,,.., -
D . :::;:rvptiona lt1

• ~exceseM"VMl.il1flOrl

• ROlat• oomprfl'MOt ....err

D 2 trW'lXa. Ol IOOnilf rt t.J!..-,,_,
• ~ 00 aa-...anced W\llrllY
:1):2 oomoi....o • '""'~
No
. """
o.---......
9 caoi icq ao '
- ' P£rOo, <'0 nm Hg. ..,.....,.
!O -.,..,...,. CPfl _,.,
• act-~.a! ptll'S!iLn

- l'f '9'ai.altun QhrA 4Cb

3 5t0i1CI pronure 20 mm ~
, Sr...ck •-erv to ompc.,.. Cl>fl
qua.My
4

CPR 2 min
.. .
• IV/10 access • 8iphasic: Manut¥.tumr
recomrrienc:t.lbOn ~tig. ,,,,, 1t

---"""""
dose Of l20-200 J). It Uf''kt'llJWf'
L.:..e rT"aXifT1Uf"'I 9\1"-aifotH

.,._
Rhythm
shockabi.?

l
... ~-.wd oe ....-.._ rd tqw
doses rvf'/ O"" C0'1Sldlnd
• MonopNooc: 3liO J

:J
• f;pillej)ln • IVl'I 0 -
1"'!jewr;J~
II 10 ~ • AmoodsonelVllO - fnl
dOSe: JOO mg boll.- s..w..
CPR2every
• Epinephrine mlo3·5 min • IV/10 CPR2mln
access ~ dOSe: 150 mg

• Consider advancod airway. • Epinephrine every 3-1> min

oapnogrophy • Consider lldvanoed airway.
• Endouact...I mtubl'l1.oon Of
copoography
$.ipragloruc QIC.hd. ic"ll(J '"'*' '•
Rhylhm
shock.ole?
... _ t_ • \\a-.~ tapncqaphy 0t
~tOcor'"'"lll'lt.I
- a """'p1oc;...-
. ;,.e
o-oce--""'°"e
'l'M
'· _,,....
- ,.._,. 6- ~
_..,,._..
..
cnest. COi l iC> i$O •

~
7

I
lbock
lt!ft!t!f:; ~
• NSQaldblood~
CPR 2m~
• Amlodarone
• Abn.1p1 s.ustalrwtd •r<,...~
Pt:1c0i (t)'pic.31.y "•Orum HQ•
•O

• Treat reversible cau.es • Spontaneous al"lerlal PfMttl'•

wa1Jes with int,..·srtflllfl,,I
mof"ll!.Otlng

R...enible ea...
D
•tt;~
• H "°"'"
12 •H_ o o n _
• " 1'00 .....,"tl@"lo lliemlt
• •no99"ol~cl Gol050<7 • H .-pc;:--nu
~arcuwoon •T9"1SO'o-~a.·
!AO$C). go 10 10 Cf , 1
• II AOSC. go to . ,,..,.,._ ,,.....,.,.,,
•Ta-oor..oe~
• Tcit.~

Pos~ -Care
• T>Yombos<s. """"'""'

1111
 Bradycarclia Learning Station Checklist

Adult Bradycardia With a Pulse Algorithm

Assess approp ntneness tor clinical condition.

Hean rate typically <50/min ifbradyarrhytllmia.

l
Identify and treat underlying caus:e~~~~~~~~
Maintain pa te nt-aiMay; assist treathing as necessary Q
• Oxygen (if hypoxem•c)
• Cardiac monitor to lctenufy rhythm: monitor blood pressure and oximetry
• IV access 0
• 12·Lead ECG if available: don't delay therapy

Pcn:.1.ctcnt
bradyarmythmia causing:
• Hypotensbn?
Monitor and observe • Acutely at.e<ed mental status1
• Signs of shock?
• lschemic chest discomfort?
• Acute heart failure?

sO Yea
Ooses/ Deta1ls
Atropine
Atropine IV dose:
If atropine, neffectlve: First dose: 0.5 mg bolus.
• Transcutaneous pacfng Repeat every 3-5 m1mrtes.
or Maximum: 3 mg.
• Oopanine lnfUsion
Dopamine IV infusion:
or Usual infusion rate is
• Epinephrine infusion
2- 20 mcg/kg per minute.
Trtrate to patient response:
60
,,-,----
taper slowly.
\ Epinephrine IV Infusion:
Consider.
2-10 mcg per minute
• Expert consu1tation Infusion. irtrate to patient
• Transvenous pacing response.
C 2015 American Hean Assoc1a11on

167
 Tachycardia Learning Station Checklist

Adult Tachycardia With a Pulse Algorithm

10
Assess appropiia'leness for c linical conditio l). Doses/Details
Heart rate typic ally ~1 50/mirrrt tac/lyarrhythmia.
Synchronized cardioversion:

!
Initial recommended doses;
• Narrow regular. 50-1 00 J
• Narrow trregular: 120-200 J
btphas1c or 200 J monophasic
Identify and treat underly fng cause
• Wtdo regular: 100 J
• Maintain patent 9)rway: assist breathing as necessary 0 • Wide irregular: defibril!ation
• Oxygen (if hypoxemic) dose ~ior synchronized)
• Cardiac monitor to identify rhythm; monitor blood
Adenosina IV dose:
i:ressure and ox1metry O First dose: 6 mg rapid IV push.

30 ~1
follow with NS nush.
Second dose: 12 mg if required.

Antiarrhythmlc Infusions for

Persistent Stable Wide-QRS Tachycardia
tachy arrhythmia causing: .,('S
Procainamide IV dose:
• Hypotens100? SynchronJz ed cerdioversion 20-50 mg/min unltl arrhythmia
Yes • Consider sedation
• Acutely altered mental status? suppressed, hypotens1on ensues,
• Signs of shock? • If regutaf narrow complex. ORS duration iricreases >50 %. 01
• lschemic chest discomfort? consider adenosine maximum dose 17 mg/kg given.
• Acute heart failure? Maintenance infusion: 1·4 mg/min,
Avoid 1f prolonged QT or CHF,
No Amiod arone IV dose:
IV access_and 12-lead ECG
if.-available First dose: 150 mg over 1Ominutes.
Wide ORS? Yea Repeat as needed rt VT recurs
• Cons1deradenos ne only if
~0. 12
second Follow by maintenance infusion of
regular ard-monomorphic
1 mg/min for first 6 hours.
• Cons;der antlarrhythmic intusioo
• Consider expert consultation Sotalol IV dose:
No 100 mg ( 1.5 mg/kg) over 5 minutes.
Avoid 1f prolonged OT.

• IV access aocf 12-leacfECG ifava1labJe

• Vagaf..maneuvers
• Adenos1ne (if regu ar)
• ~-Blocker or calcium channet-b focke<
• Consider expert consultation
c 201 S Amei-ct1n Heart Associa1 -0n

168
Immediate Post-Cardiac Arrest Care Learning Station Checklist

Adult Immediate Post-Cardiac Arrest Care Algorithm-2015 Update

C Return of spontaneous circulation (ROSC)

- Optimize ventilation and oxygenation ,

• Maintain oxygen safuratioo ~94 %
• Consider advanced aui.'\•ay and waveform capnography
'4t• Do not hyperventilate

l
Treat hypotensfon (SBP <90 mm Hg)
• tVilO bolus
• Vasopressor infusion
• Consider treatable causes

12-Lead ECG:
Yea STEMI
Coronary reperfusion or
high suspicion
of A M I

Ho
10
Initiate targeted Follow
temperature management commands?

Yes
so
C 201 ~American Hearl AssoclatlOll c Advaneed critical care
~--'-"
)

• • !-

VenUlation/oxygenation:
Avoid excessive ventilation. Start at
10 breaths/min and titrate to iarget
Pri oo, ot 35-40 mm Hg.
When feasible, titrate F10, to
minimum neces.sary to achieve
Spo, ~94 %. • Hypovolemia
• Hypox1a
IV bolus: • Hydrogen ion (acidosis)
Approximately 1-2 L • Hypo-lhyperka!omia
normal saline or lactated Ringer's • Hypothe.-mia
Epinephrine IV infusion: • Tension pncumothorax
0.1-0.5 mcg/kg per m:nule (in 70-kg • Tamponado, ca:d~ac
adult: 7-35 mcg per minute) • Tox.ins
• Thrombosis. pulmonary
Dopamine IV infusion: • Thrombosis. coronary
5-1 O mcglkg per minute

t&9
 ACLS Pharmacology Summary Table
Drug Indications
Adenosine • First drug for most forms of
stable narrow-complex SVT.
Effective in terminating those
due to reentry involving AV
node or sinus node
• May consider for unstable
narrow-complex reentry
tachycardia while preparations
are made for cardioversion
• Regular and monomorphic
wide-complex tachycardia,
thought to be or previously
defined to be reentry SVT
• Does not convert atrial fibrilla-
tion, atrial flutter. or VT
• Diagnostic maneuver: stable
narrow-complex SVT
Amiodarone Because its use is associated
with tox1c1ty, amiodarone 1s
indicated for use in patients
with life-threatening arrhythmias
when administered with appro-
priate monitoring:
• VF/pulseless VT unresponsive
to shock delivery, CPR, and a
vasopressor
• Recurrent, hemodynamically
unstable VT
With expert consultation, amiod-
arone may be used for treatment
of some atnal and ventricular
arrhythmias
170
Prec_a~ion~/
Contraind1cat1ons
• Contraindicated in poison/
drug-induced tachycardia
or second- or third-degree
heart block
• Transient side effects
Include flushing, chest pain
or tightness, brief periods
of asystole or bradycardia,
ventricular ectopy
• Less effective (larger doses
may be required) in patients
taking theophylllne or
caffeine
• Reduce initial dose to 3 mg
in patients receiving dlpyri·
damole or carbamazepine,
in heart transplant patients,
or if given by central venous
access
• II administered for irregular,
polymorphic wide-complex
tachycardia/VT, may cause
deterioration (including
hypotension)
• Transient periods of sinus
bradycardia and ventncular
ectopy are common after
termination of SVT
• Safe and effective in
pregnancy
Caution: Multiple complex
drug interactions
• Rapid infusion may lead to
hypotension
• With multiple dosing, cumu-
lative doses >2.2 g over 24
hours are associated with
significant hypotension in
clinical trials
• Do not administer with other
drugs that prolong OT
interval (eg, procainamide)
• Terminal elimination 1s
extremely long (half-life lasts
up to 40 days)
Adult Dosage
IV Rapid Push
• Place patient in mild reverse
Trendelenburg position before
administration of drug
• Initial bolus of 6 mg given rap-
idly over 1 to 3 seconds fol·
lowed by NS bolus or 20 ml;
then elevate the extremity
• A second dose (12 mg) can
be given In 1 to 2 minutes if
needed
Injection Technique
• Record rhythm strip during
administration
• Draw up adenosine dose ard
flush in 2 separate syringes
• Attach both syringes to the
IV injection port closest to
patient
• Clamp IV tubing above
injection port
• Push IV adenosine as quick.y
as possible (1 to 3 seconds;
• While maintaining pressure on
adenosine plunger, push NS
flush as rapidly as possible
after adenosine
• Unclamp IV tubing
VF/pVT Cardiac Arrest
Unresponsive to CPR, Shock,
and Vasopressor
• First dose: 300 mg IV/10
push
• Second dose (if needed):
150 mg IV/10 push
Life-Threatening Arrhythmias
M aximum cumulative dose:
2.2 g IV over 24 hours. May be
administered as follows:
• Rapid infusion: 150 mg IV
over first 10 minutes (15 mg
per minute). May repeat rapid
infusion (150 mg IV) every
10 minutes as needed
• Slow infusion: 360 mg IV
over 6 hours (1 mg per
minute)
• Maintenance infusion:
540 mg IV over 1B hours
(0.5 mg per minute)
(continued)
(continued)
• Flrst drug for symptomatic
sinus bradycard1a
Can be given • May be benefrclal In presence
via endotra- of AV nodal block. Not likely
chea/ tube to be effective for type II
second-degree or third·
degree AV block o r a b lock
in nonnodal tissue
• RO\Jtlne use during PEA or
asystole 1s unlikely to have a
therapeubc benefit
• OrganophOsphate (eg, nerve
agent) poisoning· extremely
large doses may be needed
Dopamine • Second·ltne drug for
IV 1nfus1Dn symptomatrc bradycard1a
(after atropme)
• Use for hypotens1on (SBP ~70
to 100 mm Hg) with Slgns and
symptoms of shock
Epinephrine • Cardi ac arrest VF, pulseless
Can be g1Ven VT, esystole, PEA
via endotra- • Symptomatic bradycardfa:
cheal tube Can be considered after
atropine as an alternative
Available in
infusion to dopamine
1:10 ()()() and
1:1()()() C()ll- • Severe hypotenslon: Can be
used when pacing and atro·
centra tions
pine fad, when hypotension
accompanies bl11dycardia,
or with phosphodiesterase
enzyme Inhibitor
• Anaphylaxis., severe allergic
l'l!actions: Combine with large
fluid volume. corticosteroids,
antihistamines
• Use with caution In pres·
ence of myocardial lschemia
and hypoxia. Increases
myocardial oxygen demand
• Avoid In hypothermlc
bradycardia
• May not be effective for
lnfranodal (type II) AV block
and new third-degree block
wrth wide ORS compiexes.
Qn these patients. may
cause paradoxical slowing.
Be prepared to pace or give
catecholamines)
• Doses of al/Opine <0.5 mg
may result in paradoxical
slowing of hean rate
• Correct hypovolem1a with
volume replacement before
1nt11a11ng d0pam1ne
• use with cautlOO 1n
cardoOgeOIC shock With
accompanying CHF
• May cause tachyarrhylh·
m1as. exoess1Ve vasocon·
s1r1Coon
• Do not mix with sodium
bicatbonate
• RalSll1g blood pressure and
lncreasuig hean rate may
cause myocardial lschemla.
angina, and increased
myocardial oxygen demand
• Hrgh doses do not Improve
survival or neurologlc out·
come and may contnbule to
pos1resuscitation myocardial
dysfunction
• Higher doses mey be
required to treat poison/
drug-Induced shock
Bredycardia
(With or Without ACS)
• 0.5 mg IV f/Very 3 to 5 minutes
os needed, not io exceed
total dose of 0.04 mglkg (total
3mg)
• Use shorter dosing Interval
(3 minutes) and higher doses
In severe clinical c:ond1tions
Organophosphate Poisoning
Extremely large doses (2 to
4 mg or higher) may be needed
IV AdmlnlstratJon
• Usual 111fus1on rate Is 2 to
20 mcglkg per minute
• Titrate to pauent response;
taper slowty
Cardiac Arrest
• IV/10 dose: 1 mg {10 ml of
1· 1O 000 solution) adminls·
lered every 3 to 5 minutes
dunng resuscitation. Follow
each dose with 20 ml Hush.
elevate arm for 1O<lo
20 seconds afler dose
I • Higher dose: Higher doses
(up to 0.2 mg/kg) may be
used for specific Indications
(f.l·blocker or calcium channel
blocker overdose)
• Continuous Infusion: Initial
rate: 0.1 to 0.5 mcglkg per
minute (for 70-kg pati.e nt 7 to
35 mcg per minute); btrate to
response
• Endotracheal route: 2 to
2.5 mg diluted in 10 ml NS
Profound Bradycardia or
Hypotonaion
2 to 10 mcg per minute infusion;
tl\rale lo patient response
(continued)
17f
 (continued)

Drug
. .
lnd1cat1ons
I Precautlont/
C o ntran
1 di cations Adult Dosilge
I
Lidoc:aine • Alternative to am1odarone in • Contraindication: Cordloc Arrest From ~F/pVT
Can be given cardiac arrest from VF/pVf Prophylactic use 1n AMI is • Initial dose: 1 to t.5 mg/kg
via endotra- • Stable monomorph1c vr
wrth contr;11nd1cated IV/IQ
chea! tube preserved ventncular function • Reduce maintenance dose • For refractory VF, may give
• Stable polymorphic vrwith (not loading dose) In additional 0.5 to 0.75 mg/kg IV
normal baseline OT interval presence of 1mpa1red liver push. repeat In 5 to 10 min-
and preserved LV function function or LV dysfunction utes. maximum 3 doses or
when lschemia is treated • 01scont1nue 1nfuS10n total or 3 mg/kg
ano electrolyte balance is immediately 11 signs of
Per'fUlrtng Arthythmta
corrected toxicity develop
• Can be used for stable
For stable vr. Wide-complex
tachycardia or uncertain type.
polymorphic vr
with baseline
significant ectopy:
• OT-tnterval prolongation If
torsades suspected • Doses ranging from 0 5 to
0. 75 mg/kg and up to 1 to
t .5 mg/kg may be used
• Repeat 0 5 to 0.75 mg/kg
every 5 to 10 minutes; maxi-
mum total dose· 3 mg/kg
Mo1ntenanoe tnfusJOn
1 to 4 mg per minute (30 to 50
mcg/kg per minute)

M agnesium • Recommended for use 1n car-
Sulf ate dlllC arrest only If torsades de
pointes or suspected hypo-
magnesem1a 1s present
• Ufe-lhreaternng ventncular
antiythmias due to digitalis
toXJcrty
• Routine administration in
hospitalized patients with AMI
is not recommenoed
• Occaslonal fall in blood Cllrdiac: Arrest
pmssure with rapid admln- (Oue t o H ypom~..ernia or
IStration Torsades de Polntest
• Use wrth ceutJon If renal 1 to2g(2to4rnlofa50%
la•ture rs present solutlOll diluted Ill I0 ml (eg,
O.W. normal saline) given IV/IO)
Toraadea de Po1ntu
With o Pulse or AM I Wllh
Hypomagnesemia
• Loading dose of 1 10 2 g mixed
in 50 to 100 ml of d•uem (eg.
o_w. normal saline) over 5 to
60 minutas rv
• Follow with 0.5 to 1 g per
hour IV (titrat e 10 control
torsades)

172
 2015 Science Summary Table
Topic 2010 2015
Systematic Approach: • 1·2-3· 4 • Check responsiveness
BLS Assessment • Check responsiveness: - Tap and shout
(name change) • Shout for nearby help/activat e emergency
- Tap and shout
- Scan chest for movement response system/get AED
• Activate the emergency response system • Check breathing and pulse
and get an AED (simult aneously)
• Circulation: Check the carottd pulse. • Dehbrillation: If indicated, deliver a shock
If you cannot detect a pulse 1vithin with an AED or defibrillator
1o seconds, start CPR, begirning with
chest compressions, Immediately
• Defibrillation: If ind icated. delver a shock
with an AED or defibrillator

Syst ematic: Approach: • Airway • Airway

Primary Assessment • Breathing • Breathing
(name change)
• Circulation • Circulation
• Differential diagnosis (H's and T's) • Disability
• Exposure

Systematic Approach: • NA • SAMPLE

Secondary Assessment • H's and T's
(new)
BLS: High-Quality CPR • A rate of at least 1OD chest compressions • A rate of 100 to 120 chest compressions
per minute per minute
• A compression depth of at least 5 c m in • A compression depth of at least 5 cm in
adults adults'
• Allowing complete chest recoil after each • Allowing complete chest recoil after each
compression compression
• Minimizing Interruptions in ccmpressions • Minimizing int erruptions in compressions
(1O seconds or less) (1D seconds or less)
• Avoiding excessive ventilation • Avoiding excessive ventilation
• Switching providers about every • Chest compression fraction of at least
2 minutes to avoid fatigue 60% but ideally greater than 80%
• Switch compressor about every
2 minutes or sooner if fatigued
• Use of audio and visual feedback devices
to monitor CPR quality

'When a feedback device is available,

adjust to a maximum depth of 6 cm in
I adolescents and adults.
(continuedj

113
 (continued)

Topic I 2010 20 15

ACLS: Immediate • Consider therapeutic hypothermia (32'C • Consider targeted temperature

Post-Cardiac Arrest to 34'C for 12 to 24 hours) to optimize management to optimize survival
Care survival and neurologic recovery in and neurologic recovery in comatose
comatose patients patients-cool to 32• c to 36' C for at
least 24 hours
• Out-of-hospital cooling of patients with
rapid infusion of cold IV f luids after ROSC
is not recommended

ACLS: M anaging the • For cardiac arrest with an advanced • For cardiac arrest with an advanced
A irway airway in place, ventilate once every 6 to alrway in place, ventilate once every 6
8 seconds seconds

ACLS: Bradycardia • Dopamine dosing: 2 to 10 mcg/kg per • Dopamine dosing: 2 to 20 mcg/kg per
minut e minute

ACLS: A CS • NSTEMI • NSTE· ACS

• Titrate 0 2 saturation to ~94 % • Titrat e 0 2 sat uration to ;,90%

Topic 2015
ACLS: Cardiac Arrest • Removed vasopressin from the Cardiac Arrest Algorithm
• Administer epinephrine as soJn as feasible after the onset of cardiac arrest due to an
initial nonshockable rhythm
• Added Opioid-Associated Life-Threatening Emergency {Adult) Algorit hm
• Healthcare providers tailor the sequence of rescue actions based on the presumed
etiology of the arrest. Moreo•er. ACLS providers functioning within a high-performance
team can choose the optimal approach for m inimizing interruptions 1n chest
compressions (thereby impro1ing chest compression fraction [CCF]). Use of different
protocols, such as 3 cycles of 200 continuous compressions with passive oxygen
insufflation and airway adjuncts , compression-only CPR in ttie first few minutes after
arrest, and continuous chest compressions with asynchronous ventilation once every 6
seconds w ith the use of a bag-mask device, are a few examples of optimizing CCF and
high-quality CPR. A default cJmpression-to-ventilation ratio of 30:2 should be used by
less-trained healthcare provioers or if 30:2 is the established protocol.
• Consider using ultrasound dcring arrest to detect underlying causes (eg. PE)
• Extracorporeal CPR may be considered among select cardiac arrest pat ients who
have not responded to initial ~onventional CPR, 1n setlings where it can be rapidly
implemented
• Consider admirnstenng intravenous lipid emulsion, concomitant with standard
resusci tative care, to patients who have premonitory neurotoxicity or cardiac arrest due
to local anesthetic toxicity or other forms of drug toxicity and who are failing standard
resuscitative measures

ACLS: Stroke • Endovascular therapy (treatment window up to 6 hours)

174
 Glossary

Acute Having a sudden onset and short course

Acute myocardial infarction The early critical stage of necrosis of heart muscle tissue caused by blockage of a
(AMI) coronary artery
Advanced cardiovascular life Emergency medical procedures in which basic life support efforts of CPR are
s upport (ACLS) supplemented with drug administration, IV fluids, etc

Asystole Absence of electrical and mechanical activity in the heart

Atrial fibrillation In atrial fibrillation the atria .. quiver" chaotically and the ventricles beat irregularly

Atrial flutter Rapid, irregular atrial contractions due to an abnormality of atrial excitation
Atrioventricular (AV) block A delay in the normal flow o f electrical impulses that cause the heart to beat
Automated external A portable device used to restart a heart that has stopped
defibrillator (AED)

Basic life support (BLS) Emergency treatment of a victim of cardrac or respiratory arrest through cardiopul-
monary resuscitation and emergency cardiovascutar care

Bradycardia Slow heartbeat, whether physiologically or pathologically

1

Capnography The measurement and graphic display of CO, levels in the airways, which can be
performed by Infrared spectroscopy

Cardiac arrest Temporary or permanent cessation of the heartbeat

Cardiopulmonary A basrc emergency procedure for life support, consisting of mainly manual external
resuscitation (CPR) cardiac massage and some artificial respiration

Coronary syndrome A group of clinical symptoms compatible with acute myocardial lschemia. Also
called coronary heart disease.

Coronary thrombosis The blocking of the coronary artery of the heart by a lhrombus

Electrocardiogram (ECG) I A test that provides a typical record of normal heart action
Endotracheal (El) intubation The passage of a tube through the nose or mouth into the trachea for mainlenance
of the airway

Esophageal-tracheal tube A double-lumen tube with inftalable balloon cuffs that seal off the hypopharynx from
the oropharynx and esophagus; used for airway management

Hydrogen ion (acidosis) The accumulation of acid and hydrogen ions or depletion of the alkaline reserve
(bicarbonate content) In the blood and body tissues, decreasing lhe pH

Hyperkalemia An abnormally high concentration of potassium Ions in the blood. Also called
hyperpotassemia.
Hypoglycemia An abnormally low concentration of glucose in the blood

Hypokalemia An abnormally low concentration of potassium ions in the blood. Also called
hypopotassemia.

Hypothermia
I A potentially fatal condition that occurs when body temperature falls below 95°F
(35"C)

Hypovolemia A decrease in the volume of circulating blood

Hypoxia A deficiency of oxygen reaching the tissues of the body

175
 lntraosseous (10)
Intravenous (IV)
Moderate hypothennia
Nasopharyngeat
Perlusion
Prophylaxis
Pulmonary edema (PE)
Pulseless electrical activity
(PEA)
Recombinant tissue
plasminogen activator (rtPAJ
Severe hypothermia
Sinus rhythm
Supraglottic
Synchronized cardioversion
Syncope
Tachycardia
Tamponade (cardiac)
Tension pneumothorax
Thrombus
Ventricular fibrillation (VF}
Ventricular tachycardia (VT)
I A rapid heartbeat that ong1nates In one of the lower chambers (ventricles) of the hean
176
I Within a bone
Within a vein
When the l)tltlent's body temperature 1s between 86'F and 93 2°F
Pertaining to the nose and phatynx
The passage or Hulet (such as blood) through a sp&Qfi c organ or area of the body
(well as the heart)
Prevention of or protection agrunSt disease
A cond1toon In whlCll ftuld ocwmulatos In the lungs
Continued electrical rhythrmc11y of the heart 1n the absence of effective mechamcal
luriction
A ciot -d1ssotv1ng subslance produced naturally by cells In the walls of blood vessels
When the patient's body temperature iS <86 F
The rhythm of the lleat1 produced by Impulses lrom the Slnoatnal node
Situated or occumng above the glottos
Uses a sensor to delrver a Shock that 1s synchroruzed with a peak in the ORS complex
A loss of consc>OUSness over a shOn perk>d or time. caused by a temporary lack of
oxygen 1n the brain
Increased heartbeat. usually 2 100/min
A cond1Uon caused by accumulation ol fluid between Iha heart and the pericardium,
resulting 1n e~cess pressure on the hean This Impairs the heart's ability to pump
sutt1c 1ent blood.
Pneumothorax resulting from a wound In the c hest wall Which acts as a valve that
perm its air to entar the pleural cavity but prevents Its escape
A blood clot ronned within a blood vessel
Very rapid uncoordinated fluttering contractions ol the ventricles
 Foundation Index

AmlOdarone 106
Antlarrhy1hm1C drugs 106 Oropharyngeal suct1on1ng procedure 56
Aspinn 65 0)(}'gen 47
Asystole 114
Atrioventricular block 120 Pulseless electrical activity (PEA) 110
Atropine 125

Bag-mask device 49 Recombinant tissue plasminogen activator

(rt PA)
86
Bradycardla 120
Refractory VF 95
Reteplase 71
Defibnlla11on 96
Dopamine 126. 150

StreptOl<Jnase 71
Endorracheal tube suct>anlng p<ocedure 56
Epinephrine 99

Tachycardia 129
Tenecteplase 71
Transcutaneous pacing (TCP) 126
Head tilt-<:hln lift 47

Ventricular tachycardia (VT) 135

IV/10 access 104

Yankauet 55

Magnesium sulfate 107

Morphine 66

177
Al>t>reviataons used. 8·10 Acute coronary syooromes (ACS}. 17·18. 59-72
ABCDE ill Primary Assessment, 33. 34. 38-39 algonthm on. 59. 62-72
Accelerated ldiOVentriCUlar mythm (ANR). 128 bradycaldJa on. 59, 128
ACE 1nh1b<tO<S in acute cornnary syndromes, 59 changes in 2015 Guidelines 0<1. 174
AceiytsnflcyllC l\Cld commun;ty fMPO'IS6 to, 60
1n acute coronary syndromes. 59, 62, 64, 65. 68. 69 drug the<apy in, 59-60; adiunctove. 71 -72; atgomhm on. 62;
in stroke. 77, 84 In emergency deportment, 67, 68, 69; fibnnolytlc (see
Acidosis FlbrinOlytlc therapy, In acute coronary sylldromes), In
Card1acArrestAlgorithm on.94.10l. 11 2, 165· 166 prehospitol care. &5-66; 1n ST·segment etevatlon, 70,
Post-Cardiac Arrest Care Algorithm on, 147, 169 71-72: 11me to trea tment in, 62, 67, 70, 71
ACLS. See Advanced cardiovascular Ille support emergency departmenl care In. 62, 67-69
ACLS casGS, 43·152 emergency medical services in, 18. 62. 64-67
on acute coronary syndromes. 59· 72 goals or therapy on. 17
on acute sttoke. 73-91 pathophysiology or. 60-61
on asysrole. 114-119 percuianeous coronary uiterven~ons on. 70-71: as pnmary
on btadycarcfia. 120-128 therapy, 59 60. 70; as rescue therapy, 70, time 10
oveMew of. 43 rreatment tn, 62. 67, 70, 71
on posr-cardlac arrest care, 145-152 pulseless electrical act1v11y In. 41
on pulseless electrical actrvrty, 110·113 signs and symptoms In, 63-64
on respiratory arrest. 44-58 Student Webslle vodoo on, 6
on stable tachycardia, 139·144 transcutaneous pacing in. 128
on unstable tachycardia, 129- 138 Acute Coronary Syndromes Algonthm, 59. 62-72
on VF/pulseless VT, 92·109 Acut e myocardial Infarction (AMI). 59
ACLS Provider Course. 1-10 post-c>rciiac arresr care 1n. 146. 147, 151 , 169
al>bteWlllOns used on, 8-1O Acute stroke. 18, 73-91 Seoealso Stroke
ACLS casGS 1n, 43· 152 Adenosine Ill tachycard•a 139 142, 1~3. 144 170
completion N!qu1rements in. 7 algoo!hm 0<1, 133. 168
descnptl0<1 of, 1 i}-Adrenetg1c blocke<s
design ot, 2 In acute coronary synd<0mes. 59, 71. 72
goal of, 1 In tachycardia, 133, 140, 142. 143, 168
materials used in, 4-7 Advanced cardiovascular life support (ACLS). 10- 11
objectives of, 1·2 optlm1Zat ion ot, 11
P<eo'BQuistte knowledge and skills required for, 2·3; provider course on \See ACLS Provider Course)
p<ecourse self-assessment of. 2, 3, 4 5 summary of 2015 Guidelines 0<1, 174
Student Webs11e resoun;es for (see Srudenr Webslle) AED. See Auromated exterll\31 defibrillator
ACLS Provider Manval. 4-5 Agonal gasps. 35
abb<evla110<1S used on. 8-10 AHA Gwdelmes Update tor CPR and ECG (2015}
call·0\11 boxes in. 5 on e1<1racorporeat CPR, 109
Pocket Reference Cards on, 7 on 91ycem1c c0<11ro4. 20
Precoorse Prepararaon Checklist tn, 7 on h1gh-quahry CPR, I 0
ACLS Student Website. See Student Website on tachycardia rreatment, 135

179
 Index

on targeled 1emperature management 19 BLS Assessment in, 33, 34·38 (see also BLS Assessment)
on vasopressin 99 Pnmary Assessment In, 33. 34, 38-39 (see also Pr1mary
on wavefonn capnography, 146 Assessment)
Airway assessmen1 and management Secondary Assessmen1 In, 33. 34, 40-42 (see also
In acu1e coronary syndromes, 64 Secondary Assessment)
anatomy o f airway In, 47, 48 Asystole, 3. 111, 114· 11 9
In asystole, 94, 166 as agonal rhythm, 118
In brndycard1a, 123, 124, 167 CardiacAnestAlgorlthmon, 94, 115-11 7, 166
Cardiac Arrest Algorithm on. 94. 101, 112. 165· 166 common causes of. 41
1n cervical spme lrauma. 49. 58 drug therapy in, 114, 116, t66
changes 1n 2015 Guidelines. 174 durallon of resuscitation efforts ir1. 115, 118
orophatyngeaJ BlfWllY 111, 51 ·52 elhCaJ - ill, 118
111 pos1-catdl3C arrest care. 146, 147, 148, 149, 169 Megacode evalua1100 ol skills ,n, 162, 164
1n Pnmary Assessment, 39 rhythms in, 114
1n pulseless electncal activity. 94 . 166 tennlnatlon o f resusertauon efforts in, 114, 117
In respira1ory arrest, 45, 46, 47-58 transport o f patients In, 119
skills testing checklisl on, 158 treatment sequence in, 11 3, 116
In stroke, 8 1, 82 Atherosclerosis, acute coronary syndromes in, 60·61
Studenl Website video on, 6 Atnal fibrillation and llutter, 3, 170
In tachycardia with pulse. 133. 168 stable tachycardia in, 139, 141, 142, 143
team member responsible for. 27 unstable tachycardia in, 129, 131. 137. 138
m ventncular fiootlallon/pulseless VT. t O1, 112. 165 Atnoventncular block 3
Algonltvns b<adycardia 1n, 120. 125, 126, 128
Acute Coronary Synd'O<Tles Algonthm, 59. 62·72 firsHlegree, 120, 121
6radycard1a With Pulse Algonthm, 123·127. 167 second-degree. 120, 121, 12s. 127, 128
Cardiac Arrest Algorithm, 165-166. In asystole, 94, 115-117. th1rd·degree, 120, 121, 125, 127, 128
166; In pulseless electrical activity, 94. 111· 113. 166; in transcutaneous pacing in, 126, 128
venlricu lar fibtitlation/pulseless VT, 93· 104, 165 Attioventricular nodal blocking drugs, precautions in use of,
Post-Cardiac Arrest Care Algonthm on, 147 • t 52, 169 142, 143
Suspected Stroi<e Algorithm, 75. 77·91 Alrioventncular nodal reentry tachycardia, 139
Tachycardia Wrth Pulse AJgoolhm, 133. t 68: in stable Atropine. 171
patient. 140-144: 1n unstable patient, 132·135 1n asystole/pulseless electncal activrty, 111
Amet1can Stroke AssocialJOC'I, 75, 88 JO b<adycard18, 121, 123, 171, aJgontlvn on, 123 t 67,
Am•odarone. 170 and transcutaneoos paCJng, 128; in treatment
CardiacArrestAJgonthmon.94.101 112.165-166 sequence, t 25
1n tachycard•a with pulse, 106. 133. 142, 168 Automated external def1bntlator (AED), 36
In venmcular fibnllauon/pulseless VT, 94, 100, 101 165, 170 In opioid overdose, 108
Angina, unstable, 61, 69 skills tesbng checklist on use of, 157
Angiotens1n-convertlng enzyme inhibitors, 1n acu1e coronary team member responsible for, 27
syndromes. 59 in ventricular tibrillatlon/pulseless VT, 95, 96. 97
Anttarrhythmlc drugs
In tachycardia with pulse, 133, 1<12. 168 Bag-mask ventilation
1nventncular hbollatJOn/pulselessVT. 100, IQ.l t06·108 1n asystole, t t 4
An~·1nflammato.y drugs, nonsteroodal, contraindic;auons m '"resporale><y arrest. 45, 46. 49-50, 51
ACS.66 skills testing checkkst on. 158
Ann dnfl 1n stroke, 78, 80 m ventncular f1oollauontpulseless VT. 98
Aspinn Basic !rte suppon (BlS)
In acute coronary synoromes. 59, 62. 64 65. 68, 69 prerequ1s1te skills required, 3
In stroke. 77. 84 skdls lest1ng checklist on. 157-t 58
Assessmeni . systematic, 33-42 Studenl Website video o n, 3. 6, 35
180
 lndu

SU1TVN1ty ol 2015 Guidel""'5 on, 173 '" Pnmary Assessment. 39

Sy$tem&'IC asseumenl "' 33 34 ·38 "' reeporatOfY arrest. 44
Benchmall<s on c~ perlotmance and outeome 17. 92 ., slllb'e tachyca"O;;i, , ~ 1
~Blocke<s '" stroke. 8 t, 82
1n &c\111 coronary syndromes. 59. 71, 72 1n unstable lachycan:fia, 13-1
In tac/lyc<irdin t33, t40, 142, t43, t68 Bundle branch blocl<
B1phaSlc del1brlll;)tors, 96 acuie coronary syndromes 1n, 62. 63. 69. 71
Card•OC Arrest Algonthm on, 94 101, t 12. 165-166 po5t~rd1ac arrest care 1n, 146
81Yahrudln In acu1e coronary syndromes. 71. 72 transculaneous pacing '"· 127. 128
Blood pressure ventricular fobnllatlonlpulseless VT "'· 93
1n hypertension. 72, 90-9t
In hypolet1$00n (see Hypotenslon) Colcoum Channel blockers in 1achycardoa, 133, t42, 143. t68
post-<:llfd•ac arrest, 19, 147, 150-151. 169 Canadian N~ical Scale. 77
1n sirOl<e. 90·9t Capnoqrephy
BLS. See B4slC Me support Cord1ac Arrest Algorithm on. 94 , 101, t 12. 165-1 66
BLS Assessment 33. 34-38. 148 1n po<t-eardiac arrest care. 146. 147 148. 149, 169
n asy10t~ 114 115. 116 "' Primary Assessmef'.l. 39
l"ll)rad~ 123 "' reptalOtY an-es1 46
II\~ tleCtnc;aj ac!lv ty, t 10 on ven1ncu1ar f;bnllatJon.pulseess VT, 9' t01 102, 103-1()(
t65
In 1119P'8tory - · · 46
skills teslll\g checki.st on. t 57· 158 C8tbon doOxode
1n stable tachycardia, 141 11t1er"'I partial pressure 1n pos1-eattt1ac arrest care, 19,
summory o l 20 IS Guklehnes on, 173 t46, 148
1n unstable tachycardia, t32, 134 end-tidal pressure. 149; Cardiac Arrest Algonthm on. 94,
Jn vent!lcular llbrlllatlontpulsetess VT, 92 t01 , 112. 165-166; in post-cardiac arrest care. 19, 146,
Bradycard•a. 3. 59. 120-128 147 148, 169; inven1ncular l1br1llalton/pulseless VT. 94
1n acu1e coronatY syndrome. 59. t28 t01 102. 103. 104
algonthm on, t23-127 167 Catdiac arrest
changes 1n 20 t 5 GuodellneS. 174 ~gasps IO, 35
def•Mton of, 122 asystOle on, 94. 114-1 19
drug thetapy 111. 120. 121 171. algomnm on 123. 167, CllCOld ~ 111, 58
Mro01yconn precaUtJOnS 1n. 65. and transcutaneous drug lhefapy '"· 171, 172
pacor10. 128. in treatmern sequence. 125. 126 e•trllC0!1)()t9al CPR 1n, 109
escape mytllmS in. 128 1n hoeptal settJng 1see Hosp<taJ settJng catdlaC arrest on)
tunchonaJ or ....,.t,ve. t22, t24 "' opoocf o-.erdose. 107-108
leMnlng StatoOl'I c:heC;ldt5: on. 167 Olll -Ol-hospltal ise8 Out-of-h()spotal cardoac at1'9S1j
MegacodetvllluatoOl'lofsklllstn, t59-160.162 t64 and post-cardiac atreSI care(.- Post-cardiac - 1 catel
perluslOn assessment in. t 24 with pulseless eiectncal actMty, 94 1 IO- t t3
In resp.ro1ory ra11ure, 45 In relractory VFNr. 92-109
rhylhms Included In, 120 revors1blecausesof, 40-42, 109, 113.116, 147, 169;
sig ns and symptoms in. 122, 124 otgonthm on, 94, 101. 112, 165-166
iranscutanoous pacing..,, 120. 123, 125. 126. 127-128, 167 11ngle rescuer In, 38
iransvenous pac.ng ""· 123. 126. 127. 167 summaiy ot 2015 GUldehnes, 174
treat"*1t yquonce ... 12s-121 IUIV<VaJ rates "'· 10-' 1 20. 97
BtadycardllWtnPulaeAlgor.:hm 123- t27, 167 S)'\temsot care in, 14-15 16
,..,,, approach to. 15 20-22
~"
Bre.>thlng-1. 36 t58 transport o ! pa:tients "'· 119
on acule corotl8IY syndromes, 64 ultrasound In. 109
agonal gasps on, 35 CardoacArresl Algonlhm. 165-166
1n bradyeardia. t 24 1nosys1ole.94.11 5-t17, 166
181
 Index

1npUl$elesse1ec1nca1aet,.,ty 94 , tll-113. 166 Chain of S..rv1va1 11 14, 15, 16. 17. 20

1n ventncular hbnlla1<>1'1/pulseless VT, 93-104 185 •n acute CO<Onary syndromes. 64
Cardiac Arrest Registry to Enhance S..Mllal tCARESI. 17 92 on llCU18 SlrOke, 75
Cardiac OIJ1put t40. 149 Chest COITIP<85$10f'1 fracllOrl (CCf). 92. 98
Cardiac la/TlpOnade See Tamponade, catd.ac ClleSI compteSSIOOS
QwdlopUmonary bypasa l'l •entncular f•l:>nllatJol\ pulseless VT. 109 on asystOle, 114 , 116, 117, 166
CardlQpUlmonaty resuac11<1tion (CPR1, 13-17 Card<ac Arrest Algot'1lvn on. 94 101, 1t2,185· 166
1n acu!e coronary 1yn0romes. 60 62 64 c:otonaty perfusion pressure 111. 37
on asyslO'e. 114, 116. 117, 118. 166 deplh of. 37
on BLS Assessmoot, 35. 157 in tugh-quai,ty CPR, 37, 38
GardiacArreslAlgO<'olhmon.94, 101, 112.165-166 meaS<Jrement of. 16-17
chest compresslOl\s 1n (see Chest cO<'OpressKllls} m1n1m1zlng 1n1emJpt1onsin. 11,37, 38, 92. 95. 101. 118,
coronary perluSloo pressure in. 37 t85·166
e><VacOrpO<'e31, t 09 in pul&eless efectncal actMty, 166
high-quality. tO. 11. 37. 38. 173 rate or. 37
mon1rT1121ng1n1errup1.ons1n. 11 , 37 38.9295,116, 185-166 ratlO to venl•lallOl'I. 94 98. 112. 185-166
In Opioid CMlf'dose, 108 on team 81>Pf03Ch, 27
petfonnance and outcome measures in. 1&-17 on •tntncular fil)() JatJO<Vpulseless VT, 92, 95, 101 165. 111
ill Pnmaty Asles$m«ll , 39 cyCIM of CPR 98 101, al'Cl dnJg therllP), 99. 100. 111<1
pulse ¢1lec"5 11, 3A 36 ~&'so Puse cllecl(SI manual Cle'on.la!or use, 96. and rhythm Cheel<S, 99
ll'l~electncal actrvoty 111 112. 113.166 Che$t pein aocl d<SCOIT?fon
quality impro...-nent in 16·17, 20 111 acute c:otonaty syndromes. 63-64 nitrogiycenn 111, 65. 66,
on resporat°'Y arrest , 46, 47, 48 49 72. opoates on, 66
on Slngle rescuer. 38 In bradycardia 122, 123, 124, 167
1n stroke. 78 d1ttoreni1a1 diagnosis of, 64
summary ot 20 15 Gu1def1rnis on. 173 1n tachycardia. 132, 133, 134, 168
systems approach to. 13·16 Cincinnati Prehospltal Stroke Scale (CPSS), 78-79
team approach 10, 25 ·32 C1rcula11on
tetm•Ml•on of. t l 7 In ncute coronary syndromes, 64
dunng lranspotl ol paben~ . 119 in braoycatd•a 124
in •enlncutar f•bnlla1'°"' pulseless VT, 92 94 97. 165: cycles in Pnmary Assessment. 39
ol, 98, 101, and Otug tnetap) 99 100. 104 105. and rotum ol spontaneous (see Rerum ol soorianeous
llypo"*"1<a 10.: .,.., lay l'llSC\*, 98. and manual Ort:uiationj
de'CnllatO<' U5e 96, l1'WWl!lZlng r.:enupoons in. 95. 111StrOl<e, 81 , 82
101, pflySIOlogoemon.tomgduong 102·1().! rh)1tvn Cleanng 10( def DnlallOl'I, 98
check$ l'l. 99 100: 111 treatment seciuence. 98. 101 OoMd-loop communoca11()(\ ' " resuscrtatJOn 111111'1, 31
CardlOVt!f'SIO<I Communication"' resuscttatlOO teams. 29-32
synchionized. 136- 138, Tachycardia Wrtn Pulse Algonthm clllntyot, 31
on, 133. 168, In unstable tachycardia, 132, 133, 134, CIOSed· loop, 31
135, 136 138 con&1ruct111e Interventions in. 29
In unstoble tochycordla, 131, 134. 136-138: algorithm on, knowledge sharing In, 29-30
133: lndlcntions IOf, 131 137, synchronized shocks In, mutuol respect In, 32
132, 133, 13A 135, 136 138 requests lor OSSIStance 1n. 28-29
unsyncllrorozed , 136 137, 138 aummanz1ng llnd reevaluating in 30
CARES (Can:! ac Anwl ~try 10 Ennance Sur,,,.a,~. 17. 92 Computed lornogtllllhy 111 slrol<e 73. n 83 8"
carotid pulse 36 er tena 10<' fibnnolytic therapy., 8" 86
111 ltan9cut.lneou$ pacing. 127 timeto 76, 84
C8mtod $jrlU$ massage, 143 Consoousneu le-.el of 33. 34 38
Cathetenza:.on 10<' airv.D}' llUC'...c>nong 55 Construtt~e 111t""'9rltJOns . , resuscdabon teem, 29
Cervical spone 1rauma. 47 H . 58 Cortw1ta1cn with e•pen
182
 1n bradycareia, a1gon1hm on. 123, 167 1n un•1oble tacl!ycartfoa. 130
1n18ci'lycaldta 131, 132, 134. 142. 143, 144 algonthmon. In .i,n1rlculat hbnllatoon and taehycan:J1a {SM Ventncular
133. 168 t1bn1tatl()ll and taehycarcfoa. drug 1herapy on)
Coot1nuous quaJ ty mprovemen1. 13· 14
Coronary perfusoon pressure ,, CPR, 37, 95 102 E·C Clamp teehnoque on bag-mask ventllanon 50
Coronary syndromes acule See Acu1e coronary syndromes eci.ma pUlmonary. n•troglycem "'· 72
Coronary 1hlOmb05ls Edoeation, commun.ty and pro!essional on slrOke. 18. 74
CanliacArT851Algon1hmon.94 101. 112. 165-166 Electrocaroo0graphy <ECG>
Pos1-Cardiac Anest Cate Algonthm on • 47. 169 1n acute coronaty syndromes. 59 63. 69. algo<'lthm on. 62.
Conoeostl!fOld 1tierapy'" C<lldtac arrest. 101 in emt'fgency depar1ment. 67-68. on prehoepotal care.
Cough reflex. 51, 53 67 nsk class1focatoon based on 62. 63
Cnco1d pressure. 58 1n nsystole, 11 4, 115
on brodycardoa 121, 123. 167
De~bnllatJon, 36 flat line In, t14 . 115
1n as~101 e, 116. 117, 166 on post-card•ac arrest care. 146. 147, 169
with automa1ed ex1ernal def1bnlla1or (see Automated pre<equlsite inte<p<elabon slulls required. 3
ex1ema1 def bnlla10t) 1n stab<e tachycaldoa. t41
CatdiacArT851Algonthmon.~ 101.112 165-166 '"llro• .. 73. 83
in pyiSeiess eieC1nCal ICtrv•ty 112, 113 166 ., ""'~ tachycatdia. , 29-130. 132. t 33 134
in •entncuiar fbnnat.on ~VT. 92, 94 165: Wl1ll '"....,1ncUa< hbnllai.on.pO'seless VT. 92, 93
automated external def bnllator. 95. 96. 97. bophaslc EJect~d1SSOOaoon.110

94 101, Cte3Mg Watl'111lg .... 98. and drug therapy. 99• Embolism. pulmonary '11 . See alsD P1*nonary
100. eatty. importance of 97. and hypothemua. 104 thromboembol•sm
monophas1c 94 101, purpose of. 96, self-adhesive Emergency c1epartmen1 assessment and treatment
pads In, 99: shock dcllve<y 1n, 96: treatment sequence In ocute coronary syndromes, 18. 62. 67-69
In. 101 In stroke. 82·83
Dexame1hasone In cordloc orres1. 107 Eml!fYency medical services, 1 1
D1goxin In 1aehyoer<M. 142 In ocuto coronary syndromes, 18. 60. 62. 63. 64·67
O.sab<l1ty assessmen1 39 1naay1tole. 115, 117, 118, 119
Dispatchers '" acute coronary syndromes. 6d on Chain of Survival, 15. 16
Do llOI anempt retu9ClllllOll iONAR). 115. 117, 116 d•spetcr.t '"· 64
Dopamne. 171 QUal;ty ompt011ement in. 1 1
inbrallyeardo& 121 128 171 174 aJgOnttmon.123 167; ., 1•r00<•. 1e 1• 1s. n 78. a1
inuaatmenl~ 125.126 In '9ntr>eular fbnAatonioUse.ess VT 92
'"post-catdlac - Qre 145, 147, 150. 151, 169 e.-tracheel intuba:oi
Drug o..etdOSe. 42 125 ~t of tube plaeenU!l\ton. 46. 58 148. 149
oplOld 107 108 CardoacArrestAlgonthmon.94. 101. 1t2. t65·166

Drug therapy, 170 172 In post-cardiac arrest care. 148

In acute coronary syndromes {see Acu1e coronary 1n rosplro10<)' orrost. 46. 56, 58

syndromes, drug therapy In) suc toon•ng proco<lure In, 56

In asyS1ole, 114, 11 6. 166 111 ventricular hbrlllation/pulsetess VT. 94, IOI, t 65: drug
In bradycardla {see Bradycorc11a, dr1>9 therapy in) administration In, 105. 106
1npost-eardlacarrestcare. 19, 145.147 150·151 169 Epinephrine 171
prerequisite l<nOY<iedge reqwed. 3 1n asvstole, 116. 166
on pul-etectnc:alac:W1y. 110. 111, 112, 166 ,,, bl'ed1arooa 121 123. 128. 111, algomtvn on. 123. 167.
in trutmenuequence 125 126
.., respiratory 811'8Sl "'
... ~ taehyCaRloa. 133 139 142, •43 14.: C.0..C-Algor:mm on. 9-' 101 112 1M-1e6

"' Sl:rOt\9 i s . Stroo-e. druQ 1IWal>y in1 endc:rac:'-1 aQmnistraoon of. '05. 106
,, taChycarQoa"' th pulM. 133 t68 on post-c<ardiae atTesl care 1.-:5. 1 ~7, 150, 151, 169
team member rwpo<'ISIOI• for. 27 "' pulseleeS eiectncaJ actMty 1 11 • 112. 166
183
 I n d • 11

m ventricular flbnllat10111pulseless VT. 94. 99, 101 , 105. 106. Hereon 0.,1,dose. 107
107 165 HMG·CoA reductase 111hlbltors, 59
Escape ltlyt/lmS In b<adycardia. 128 Hospotat setMg
EsophageaHracheal tube, in respora10ty arrest, 46. 57 cardiac arrest'"· 10. early wamng s.gns ot, 20. 21 . 1UM<al
EllUcal ~ 1n asystole 118 rat• in. 10. 20; systems of care 111, 14, 15. 16, team
European Coopera~.e Acute Stroke 571.ldy iECAS.5-31 86 IPPI08Ch 10. 15. 20-22
Expert consultat.on See Consu tal.on w,th exoen strol.a care in, 73
Exposure. '" Pnmary Assessmenl. 39 Hypercapnoa .n resperal0ty tailt.re d5
Exlracorporeal membrane o<ygenaloen. 109 Hyperglycemia on s1-e, 90
HypeO<.alem<a
Facial droop In stroke, 78, 79, 80 Cord,acArresiAlgonthmon, 94, 101, 11 2, 165·166
F1bnlla1ton Post-Cardiac Arrest Care Algonlhm on, 147, 169
altial (see Atnol f1bnlla11on and flutter) HypertenslOO
ventncular (see Ven1r<cular l1bnlla1lon and tachycardia) n11roglycenn in, 72
Flbnnolytic ltwlrapy slrokt and f1bnnotyt1c the.-apy m. 90-91
1n acute coronary syndromes, 59. 60: rescue PCI afte<. 70, Hypoglycemia post-cardiac arrest. 20
in ST·segm<"Ot ~at.on, 70, 71, ~me 10 treatment 1n, Hypok.IJ..moa
62, 67, 70, 71 Caro.a.: Anesi Algontnm on, 94 101, 112. 165-166
""acute stre«e. 73. 74, 77, 8&-88 aa•erse e"ects ot, PCKt-Cardiac Anest Cate Algontnm on. 147, 169
87: compilCatonl ot 90. contraindJCat<>OS to. Hyporneonesernia 107, 172
84. exeluSIOn u.t- on. 8&-87. 88 hypertension Hypo191l$10M
managemen1 '"· 90-91, oncluSlon cmena on, 86. 88. '"bflldycardia . 122, 123. 124 128. 167
mtra-anenat admt.•~tratoon of, 88: nsks and benefrts of, dNg thetai>y '"· 171
87. tirne 10 treatment"' 74 76, 86, 88 1n hyl)OvOlemia, 41
Fixation errors 1n resusc1111t1on team, 29 n11roglyc00n precautions in, 65
Flat line In ECG, 11 4, 11 5 l)OSt-cntdlac arrest, 147, 150- 151, 169
Fluid admlnlstrahon 1n 1achycord1a, 132, 133, 134, 166
In post-card•oc arrest care. 19, 146, 147, 150, 151 Hypothermia
1n ventncular l1br1Uat1on/pulse1ess VT, 105, 106 bradyca!dia and transcutaneoos pacing In, 127
Flutter, atnal See Aimil ftbnllauon and ftuner Cafd,ac Anest AJgootrvn on, 94 101. 112. 165-168
Fe<etgn body a""'ay obstn.tllOf'l, 48 dehbnllal>On in, 10.:
Polt-Catd•ac Ar<est CateAJgor-Jirn on, 147 169
Gag re!l8JI. 5 I , 53 H~povoiemla 40. 41
Gasps, agonal. 35 A)'$10le. ?EA Jll, ~ 1
GetW1thThe~·R-.SC.taton 17, 92.118 CatOtac Am::>t Aigofltlvn on. 94 101, 112. 165· 166
Glucose blood le¥els llu>d adm1111Stralo0n '"· 105
., hypogPycem.. 20 Pos1-Catd•ac Arrest Care AJgontllm on. 147, 169
1n post-cardiac arrest care, 20 pulse''"' e•ec1ncal actMTy in, 40. 41, 113
1n stroke. 8 1. 83, 90 HyPoxemla
Glyce.yl tnnltrate, 65 In msp1rotory failure, 45
Glycoprotein tlbltllo l11h1bllors, 59, 71 72 tachycardia wllh pulse in, 133, 168
Hypexla, 40, 41
Head !flt-chin lltt maneuver. 47, 49 Card1acA1res1AJgonlhmon,94, 101 112.165-166
Heart failure. acute P06t-Catdiac Arrest Care AJgonttvn on. 147, 169
In bradycatdia 123, 167
~ ....:1t1Ca' 8ClMty "'· 40. 113
on tachycartha. I~, I 33 I 34 168 Stal>ie~.n . 141
Hemamage
cerebrovascular Slroi<e on, 1~ 77, 84 . 86 IO<oventriculw rt>ytnm, acce.erated. -2a
on ,_,,, "-"PY. 72 lmmoC>olllltoen .n CeMCal spone trmr>a. 58
Hepann. on acute coronary syno<ornes 59 71 , 72 tnfam'°"
184
 lndelt

-•.85
myoc:anl>al ~ Myocardai l5Chemia and mfarcoon1
acute. 59 posH:arO.ac atT1ISl care m t 46 147, 151, 169
asystoi. "'· 118
nsufln In "Yl*ll yc......a and stro.<e 90 drug therapy ,,, S!HiO. 62. 172
nttaosseout (IC>i ec:cess Metrocardo<>graphy '" 59 62. 69
m asys1oi., 114 116, 166 inf""°' wall, 65
1n pos1-card1ac 81T9St ca111. 169 non-ST-segment elevation. 60, 61. 62. 69
In pulseless etec::tncal activ11y, 111, 112. 166 path0Physo010gy in, 60-6 1
1n ventncular l·bnllabon/pulseless VT. 105 right venlncular, 65, 69
ntrav"noos (IV) access sogns and symptoms 1n, 63-64
inasys101e, 114, 116. 166 ST·seyment depressu1111, 59, 62 69, 71
in bradycardoa, 123, 167 ST-segmenl elevation m (5" ST-segment elevation
1n post-cardiac arrest ca'!!, 147, 150, 169 myocardial Infarction)
1n putseless elec:tncal actMty. 111 . 11 2 166 tnchycard•a In, 140
1n s1roke. 77. 82 tronacutaneous pacing 1n, 127
1n 1achycon:l1a w11h pulse. 133. 134, 168
1n venrncuter f1brlllabon/putseiess VT. H)4·105. 165 Naloxone 111 opod overdose, 108
SC.,.,,,.. Nasopllaryngeal a.rwa:y. 48. 53·55
e«ebrOvateular. stroi<e "" 74 n. 84 , 65. 86-88. 89 Nat()t\111111$1 'ute of N«imiogcal ~and Sll'Ol<e "·NOS1
myoc.wo.al (see Myoc;anllal ISChema and infan;tJonJ 18 73 ~6. 86
Natonal I0$~1utes of Heaith $lll)i(8 Scale NIHSSI. n 84
Jaw-1/Vusl ma-.- on trauma and resp.ra:ory arrest. 47. 49, 58 NeutOloQIC assessment 39
1n card•<IC arresl, 20. 146-147
Knowledge eha11ng 1n resusc.1ahon 1eam, 29-30 1n slroke. 76. 77, 83-84
Nloord1p1ne In stroke. 90. 91
Labe1a1011n stroke, 90. 9 1 Nl1roglycenn 1n acute coronary syndromes, 59, 65, 66. 71 72
Laryngeal maSk airway. 46, 57 otgol'llhm on. 62
l.alyngealtube, 46.57 .... emergency department, 68 69
Lay rescuers on ventncular frtnlabOfl/pulse<ess VT 98 precautions "' 65 69
Leadet'Ship alu ts on '1lSU$CJla!JOO learn, 2S-32 on prehosp<tal care. 65. 66
Megacode 1es1ong cheel<llSt on. 159-164 NonsterOldaJ antHnflammatory drugs contraindoe:at.ons 1n
l.JdOCalne. 172 ACS.66
on ventncuiar f1bnllabOfl/pUlseless VT. 100, 105, 106. 172 Non-ST-$99ment elevation myocardoal 1r1tarction (NSTEMI).
u1e is Wily. 11 22. 152 60, 69
aigon1hm on. 62
Magieslum aurlate. 112 pethOpllyslOlogy of 60 61
lf'lt~depo•nles. •00.101, 112 N~ot1post-can:t.acanes1care 145, t 47, 150.
Medical Emergency Response Improvement Team (MERfl) Ina! 151, 169
22
Med1col emergency 1eams. 15, 21-22 Opiatea 1n acute coronary syndromes. 59. 66, 69
Megaoode 1es11ng checklists. 159- 164 Opioid Assoc1aled Life-Threatening Emergency Atgorl1hm, I 08
Mental s1atu1 01tern1ion Opioid overdose, 107-108
'" bradycardia, 123. 167 Orqaoophosphale poisoning, 171
ln iachyc:.rdla 132. 133. 134. 168 0rophel)'nge318Jrway. AB, 51-52. 55
Me!llyiP<.oo.olone on c:arOiaC arrest. 107 Orophalynoeal suctJonmg. 56
Mot>U 1ypea o1 a1noventnculilf bl<X:k 120. 125. 121 128 0..1 -ot-hOSl)llal cattliac arrest
Monopnasoc: Otof'°"'8tors. 96 c:ommi.nty response to, 60
CatO<DCAmlstAlgonthmon.94 101 112.165- 166 ineldenee and S<JM\'& rates"'· 10
MO<Ph•ne '"acute coronary syTidromes 59 62. 66. 69 systems ol care m. 14 15 16
Myocatd1al 111C1>em1a and mtarcuon Oxygen
acce4ereted l(lo0ventrocular my!llm 1n, 128 '*'lral venous saturaoo11 1n CPR 102
1as
 I n d • 11

fracoon of onsprcd, in post-cardiac arrest care, 147 Post-Card•ac Arrest Care Algonthm on. 147, t69
148 t69 PrecoUf&e Preparntoon Checld1s1. 7
Oxygeo therapy 39 Precoutse Self·Assessment, 2. 3. 4 5
m acule coronary syndromes. 59 62 64 65. 68. 69 Prerequ1$.t8 knOwtedge ano skJlls reQUlred for Provid'!< Courte.
rn~l8 123 167 2·3
m post~.ac arrest care. 19, 146 147 148. 169 pruc:ourse 9lf-assessment of, 2, 3. 4 5
on respratO<Y atrest , 47 Pnmaty AslMlment 33. ~ 38-39 148
on stroke. 77 81 , 82 1n ai.ystore. 114 115. 116
on tachycardia W•th pu'se, 132, 133, 134, 141, 168 1n t>radycatd<a 123
on respo1at01Y arrest, 46
Pacing 1n stable tacnycard1a, 141
transcUlaneous 1n nsystole, lack of benefits m. 117. on summmy of 20t5 Guidelines on. 173
b<adycardJa 120. t 23. 125. 126. 127-128. 167 '" unstal>le tachycardia, 132. 134
tr1msvenous.1n b<adycard•n 123. 126. 127 167 rn ven1ncular fib<lllauon/pulseless VT. 95
PEA See Pulsetess electncal act1v1ty lPEAl Procalnamkle 1n tacnycardia with pulse. 133, 142, 168
Penumb<a •schemic. 85 Pro-.de< Course , HO. See also AU.S Provider Course
Pe<cUtaneous eo<onury •nttt\lentions IPCQ Pulmonary ~ n•trOglycenn on. 72
"'acute coronary sync1tom411, 10-;1 as p<vnary therapy. PulmonDI)' uvomooemooLsm. 40. 41
59 60 70. as rescue the<ap~ 70: ome to treatment "" Catdcac: Arrest Algon1lvn on. 94 101 112, 165· 166
62. 67. 70. 7t Post-Cardiac Airest Cale Algor;1!Tm on, 147 169
on post-catOlae arraat care. 19, 20 146. 151 !'\he checl<S. 34 36 148
PerfUSIOll 114 116
'" 8$)'atole
'" b<adycard<a, 124 1n pu~ e1ectncaJ acbvrty. 111
and repe<fuslO<I therapy (!60 Aepertus>0n therapy) In respiratory arrest, 46
Pharmacomvasive strotegy 1n acute coronary syndromes. 70 1n stable tachycardla, 140
Pharmacology. See Drug therapy 1n unstable tachycardia. 132
Phosphodoeste<ase lnh•b1tor use. nrtroglycerln precautions In, 65 rn ventncular f1b<1llation/pulseless VT. 99, 100
Plaque in atherosclerosis. lormotlon and rup!ure of, 61 Pul sol~ss electrical activity (lf'EA). 3. 110·11 3
Plasminogen aetivaror. recombrn.int tissue. See Recombmant Can.l1ac Arrest Algomhm on. 94. 11 1-113. 166
tissue ptasm1009en ac11vator common causes of, 40-42. 113
PneumothOta>t tens.on S.. T-.on pneumotnorax drug tllet'ilCll m. 110. 111 112. 166
Poel<et Aefen!f>Ce Catds. 7 ~oncal delcnDt>on of, 1' 0
Post-<atO<ac am1i.t care. • 9-20 1.:5. 152 l.legacooe e.a>.1;mon of s.olls ir. 159-161, 163. 1&a
ao-.anced c;r,•Ql care 111. 152, 169 "'~ oncludea Ill, 110
aJgontlVn on, 147· 152. 169 tr98111*\t seQUenCe Ill, 113. '16
capnograptry " " 146, 147, 148, 149, 169 Pul-•entncutanachyca!dia.92- 109159, 165
changes on 2015 G<li0et1nes. 174 P2Y •nhobotors on aeute coronary synd~. 71, 72
drugthe<apyon, 19 145, 147, 150-151, 169
1mmedJa1e. 145· 152 ORS complex In tachycardia, 135. 139, 140. 142· 143
learning station checklist on. 169 algonthm on, 133, 168
Megacode evaluollon ol skJllS in, 159. 164 Quality improvement, 11, 20
multlp~ system opproach 10, 145 continuous. 13·14
return or spootaneous c1rcula~on In, 42. 145. 146. 147. 150. Mle8$ur8S In, 16-17
151, 169 1n ~tncutar f.bnllaoon/puJseless VT, 92-93
rhythms m, 145
t<trgeted tempe<ature ~ton 1see Targeieo R'1Pld respo<IM t&a."'5 15, 21 ·22
temperature management on pos:~ atrest care I Recombln:it>t UUue ptasrr..ogen actvator 1rtPAJ. 18
Post-Garo...: Atrest Cate AiOO" ttwn, 1~7·152, 169 ., na.:e coroNlr)' synoromes 71 . 72
Po-.assun ..,,.,, """'5 on ~IJO!<•. 34 86-88. aJgOrrtnm on. 77. hyper!nntllOll
Ganliac; Anesi Algo,.tnm on. 9-' 10~ . 112, 165-166 management .,, 90-'91 ; tntra·anenat admtnostratoon of.
 Index

88, 89, time to treatment on. 88 Sell-assessment

Refractory Vf/ pulseless VT. 92· 109 on course prereqUtsrte skllls. 2. 3. 4 5
ReglONlhzation of stroke care. 18 on resusc1tauon team sl<ilts. 28·29
Reperlus.on 11\erapy Sliock
on acuie CO<OnafY syndromes. 59-60. 62, 69·71 '" bradycartlla. 123. 167
111 pos1~1ae arrest eare. 20. 147. 151. 169 on lachycaidoa. 132. 133. 134. 168
Respect In resuscitation team, 32 Stnote rescuer. 38
Respiratory arrest, 44-58 1n respiratory arrest. 49
airway assessment and management in, 45, 46, 47·58 S•nus bradycard1a. 120. 121, 127
BLS Assessment on. 46 Sinus rhythm, 110
In opioid overdose. 107-108 Sinus tachycardia. 130. 139. 140, 141
oxygen theropy In, 4 7 card1overs1on in, 131
Primary Assessment In, 46 In hypovolemia, 41
slngle rescuer in. 49 Soh flexible catheters for airway suctioning. 55
1n trauma, 47. 58 Sotalot on tachycardia w11h pulse, 133, 142, 168
Respiratory dJStress. 44 Speech dlSOrders on stroke 78. 79
Respiratory fo•lute, 44, 45 Spinal 1njunes cervical. 47, 49, 58
Respratory rate 44 ST·segment depression myocardial 1nfan:t100. S9 62. 69 71
Responsiveness assessment. 36. 158 ST-segment elevation myocardial infarcoon. 59. 60. 69-72
1n Opje)ld overdose, 108 algonthm on. 62
In post-cardiac arrest care, 1S1 , 169 Chain of Survival In, 64
In resp<ratory arrest. 47: and nasopharyngeal airway, 53; emergency department caie In, 67-69
and oropharyngeal airway. 51 emergency medical services in, 64 -67
Reteplase on acute coronary syndromes. 71 , 72 hbrinolytlc therapy in, 70, 71
Return of spontaneous circulation (ROSC), 19 , 33 polhophys1ology of. 60, 61
In asystole/pulseless electncal activity. 112, 118, 166 p~r~utaneous coronary interventions In. 70-71
Cardiac Arrest Algorithm on. 94. 101, 112, 16S·166 posH:ardiac arrest care on. 151. 169
coronary perfusion pressure In. 37 Stable tachycardia, 139- 144. See also Tachycardia, stable
post-<:ardlac arrest care in, 42, 145. 1•6. 147, 150. 151 169 Standby pacing, 128
1n ventr1culatf1bnlla11onlpulseless VT. 96. 101 , 102 103, Steroid therapy In cardiac arrest, 107
104, 106 StreptOl<lnase in acute coronary syndromes. 71
Rewarm<ng tec:hnlQUeS on hypotllermJa. 104 Stroke 18. 73· 91
Rigid catheters for airway suct1orung, 55 aJgOrrthm on. 75. 77-91
Roles and re$p00Slbtltbes on 11!SUSC11allon team, 25-28 arrhythmias 1n, 73
assessment tools 1n, 78-79, 84
Safety concerns In BLS Assessment. 33 Chain of Survoval 1n, 75
SAMPLE mn«nanlc on Secorldary Assessment, 33, 40 changes In 2015 Gu1dehnes. 174
Scene safety, 33 community and professional education on. 18, 74
Secondary Assessment. 33, 34. 40-42, 148 cnt1ca1 elements In, 75
in asystole. 11 4 . 11 s. 116 drug therapy 1n, 73: adverse effects of, 87; algomhm
In stable tochycard1a. 141 on, 77; complications of. 90: contraindications 10.
summary of 20 1S Guidelines on, 173 84; exclusion critena on, 86-87. 88: tibnnolytlc (see
on unstable tachycardia. 132, 134 Flbrinolytlc therapy, in acute stroke); hypertension
Sedauon management on. 90·91; 1nciuS10n cn1erla on. 86.
on bradycard•a and transcutaneOUS pacing. 126 88. lntra-artenal adm1nisttallon of, 88. 89. risks and
post-<:rudlac an9SI care and nwrolog1c assessmen1 on. beneftts of. 87: brT1e to treatment 1n 7J 76. 86. 88
20. 147 emergency depanmem care in. 82-83
In tachycatdla and c:ardioverSIOn. 133, 135. 136, 138. 139. 168 emergency medical seMCeS in. 18. 74 75 , 77. 78 . 81
Seizures on sttOke, 90 endoVascular therapy on, 76. 89
Self-adhesive pads lt1 defibnllauon, 99 gooeral care 1n, 77, 89-91
187
 Ind e a

goals of care In, 75-76 Secondary Assessmenl)

hemormag1e, 74. 71, 84. 86 Systems ol care, t 3-22
in-hospital care In, 73 In acute coronary syndromes, 17- t 8
ISChemc. 74 77, 85. Clot d•SIUPtlOO Ot retneval in. 89; 1n acute stroKe, 18
hbtlnolf!JC therlll>'f 111, 74 , 77 8-1 . 86-88 time to cardoQPl.llmonafY tl!SUSCltallon "'· 13-17
ueatrnent 1n. 88 ponts of eniry 111. 16
neurologic _,,.,,t "'· 77 83-8-1 tome to. 76 83 "'pos:-earo.ac res1 care. 19-20
"~research on. 73. 7b 86 l)Ublished stud-es on. 22
out-of-hospr'.al care on, 73 rapod response Ill, 21-22
regionasz.itoen ol care 111, 18 "'stro<e 89
77, 78-80. 83
Sogl'IS rd symptoms 111, :axonomy of. 14
Student Websote vodeo on, G team approach 1n. 20-21
systems of care 1n. 18, 89
team approach 1n, 82 . 83 Tachycardia, 3
nme to treatment 1n. 73, 74, 7b, 77, 81, 82; cn11cal nme deflnrtlon or, 130
periods In, 76 learning station checklist on, 168
transport of patients In, 78. 81 , 82 Megacode evaluahon of skills In. 161, 163
Stroke AJg0t1thm. 75, 77 ·91 narrow-complex, 41, 143. 144
Student Website. 3. 5· 6 n1trog1yceron precautions in, 65
on acute coronary syndrome, 6 1n resplratO<Y failure 45
on airway manage<oont. 6 Sinus. 130. 139 140. 141; car00ver.;ion 1n, 131;
on bag-masl< vent•tahon, 49 "' hypovolemla. 41
BLS video on . 3. 6. 35 stable 139- 144: advanced management 111, 144. algonthm
on cardoevers>on. 138 on, 140- 144; ctaSSfficatlOO ol. 140. d•fferentiated from
on DNAA on:lers, 118 unstable tachycardia. 141. drug thenlpy •n, 133. 139,
on endotracheal 1ntublt1on. 58 142, 143. 14.I mylhms .,, 139, signs and symptoms in.
on esophageal·treche<ll tube, 57 141, vagalmaneuve<slfl, 143, 144
on ethical 1$SU0S 1n CPR. t t 8 supraventnculat (see Suprnventnculat 1achyca<d1al
on hepann tllerapy, 72 unstable. 129· 138. 141, 142, 3lgonlhm on. 132· 135,
on ontraosseous a<:cess. 105 cardooversl0f1 1n lsee Cardooversl0f1. in un&table
on ~I n1~ba!JQll, 57 taehvclW'CllA ; d !!erent.ated from stable t.-ichyCarOIA ,
on laryngea I ~ •Mly, 57 141, drug therapy "'· 130: P11riophysdogy of. 131
on oxygen l/l<'tapy. 4 r raped recognit.on of, 131. r'1ytlVnS "'· 129· 130. 132,
on PTecourse s.rt-Assessment ~ 3. 4 5 sevemyof. 131, signsandsymotomu'I 131 , 132, 134
oo S1Jl:>o<e. 6 'entncutar. 92· 109 !See lllSO \letltncular hbnllatoen
Sucooneng o1airways111 r.-poratO<Y arregt 55·56 and taehycara•a)
SupraventncuCar taehycard.a 139. 1•2 Wlde-oompleK, 129. 133. 135. 142 144, 168
cardioverslon 1n. 137, 138 Tachycardia With Pulse Algonthm. 133, 168
differentiated from VT, 135 142 In s1able patient, 140-144
reentry, 129. 140 In unstable patient 132-135
vagal maneuvers In, 143 Tachypnea, 44
Suspected Stroke AJg0tlthm, 7!>, 77 91 Tamponode, cardiac, 40, 41
Synchronized cardloverslon, 136 138 Cardiac Arrest Algorithm on. 94, 10 1, t 12. 165 166
Tachycardia With Putse Algonthm on. 133. 168 Post-Cardoac Arrest Care AJgonthm on. 147 169
"'unstabl<! t.-ichyeattlia, 132, 133. 134 135. 136-138 Targeted temperature management 'n post-cardiac atreSt care.
Systema11c approxh. 33 -42 145. 151-152 174
BLS Assessment 1n, 33. 34 ·38lsH11/'SO BLS Assessmentl AHA Guow nes on 19
Pnmary "-8menl Ill 33. 34 38 ·39 ISM /l/$0 aigonthm on. 147, 169
Pnmaty~tl neurologc rec:overr 111, 20. 146
Secondary Assessmetlt 11'1, 33 34 40-42 j$ee al$O Team approach. 20-22, 25-32
188
 onasystOle 114 115.118
on carc«te amist. 15. 20-22
communication 1n, 29-32
constructive interventions 1n, 29
knowledge sharing •fl. 29-30
mede&I emergency teams 1n 15. 21 ·22
Megacode evaluation ofskifis 1n, 159-164
mon.tonng summarwng 8fl<l reevalua:mg 1n, 30
.....,..., l'es()eCt 1n. 32
lflposl~arrestca<e 147, 148. 151.152
1n pulseless electncal act1v1ty, I I 0, t 11
rapid response teams 1n. 15, 21 22
requests lor assistance"'· 28·29
rolos and responS<b<1111es 1n, 25·28
~H-awater>ess of limlta\JOl1s and copabltmes 1n. 28-29
"'strOl<e 82. 83
on unstable tacllycan!.a 129. 138
1n vemncular f.bnllal.JO<OpulSeleas VT. 98, 1()()
Tempe<ature
in hypothermia !see Hypothennial
latgeted mar.agement of (see Tatgeted temperature
management In post-<:ardlac orrest care)
Tenec1eplase In acute coror.ary syndromes 71. 72
Tension pneumothorax, 40 t 1
Cardiac ~I AJoonthnl on. 9~ 101, 112, 165- 160
Pos1-Car0iac Atres1 CaJe Algo<1thm on. t47, t69
TtvomOoly\c ttoerapy See Fbnnolyt c t,,_apy
nvomooe..
cerebral. 85
coronary (see Coronary thrombosis)
pulmonary (see Pulmonary thromboembol•sml
Tissue plasm>nogen aclovator recombinant. See Recombinant
ussue ptasm1nogen ac1Jva1or
Tongue, aorv.~ obstruct.on from 4 7 •9 51
Tcnactes o. poot11es magr--.m s.ttate in 100. 10; 172
Toxic conci.trons. 40, 42
CardlacArrestAlgonthmon,94, 10 1.112 165·166
on opootd overdose. 107-108
in organophosphate poisoning 111
Posl -Cardiac Anrest Care Algonthm on. 147, 169
Tracheal 1ntubal1on. See EnCIOttacheal tntubatlon
Transcu1-S paorig
in asv-toie. lacl< of ~ts in. 1 1 7
1n brlldyeatdla. 120, 123. 125. 126. 127·128, 167
TRANSFER AMI tnal. 71
Transpott of palleflts
1n card•ac arrest, 1 19
In post -cardiac arrest care. 146
s,ponal 1mmobolaatlon "" 58
"' strOl<e. 7 8. 8' . 82
Transvenous paong.,, bracfycard'8 123. 126. 121 167
Trauma. _..u, 47 49 58
Ullrasound. in cardiac arresl. 109
Unconscious pattent, 33, 34
paot-cardtae arrest care 1n 146, 148
Pnmary Assessment of, 38. 39
resi>ralory arrest •n 47, 48. 51
Unst8l>le angona. 61 69
Unstable p;r cent. leam app<0aeh ro 15
Uns1nbl• tnchycard1e, 129· 138 See also Tachycardia unsrot>le
Unsynchronized shocks, 136. 137, 138
Utst•n Guidellnes. 16. 92
Vagal maneuvers in tachycardia 133. 143. 144, 168
Valsa ••maneuver. 143
Yasopt-
endoltacheal edmonostratlOfl o! 105
updated gwdet•ne. on use of. 99
in vent~ f1t)(l lall0fl/putse1Ms VT. 107
Vnsopressor drugs
In bradycardia, t 25
1n past-cardiac arrest care. 147
on \l9fltncu!ar f.t)(l lallonlpu'-8M VT. 99 104. 105-106
Ventdatoo tec11niQueS
bag-mask vent•llltoon on (see Bag-mask ven111ation)
Catd.ac:Atrest.Algof'•hmon 94 101 112 165-166
compteSSIOfl·ventdatlOfl ratJO 1n 94 98. 112 1~166
in post-cardiac arrest care, 19, 147 148, 169
In Primary Assessment. 39
1n r95j).-atory arrest. 45, 46. 49 and advanced 111rway. 56·
58. excessrve ven11iatl0fl'" 45. 46. 47 rate of llreathl
1n. 46. 57
lfl ventncular fibnlatlOl\iput5~ VT. 95. 98. 101
Ventrcullr ft:nla!JOJ'I a"<l tacll)'CatU<a 3. 92.109
Card«lC Arrest Algofltnm 1n 93-104 165
cordloversion 1n, 135, 137, t38
drug therapy 1n. 93. 104-108. 172: algorithm on. 94,
t65, arrtJarrllythmoes '"· 100 106-108, hypothemuo
offecbng, 104. routes of access lot'. 104·105. steroids
In. 107; In treatment sOQoonce. 101, 104. vasoll(essora
'"· 99. 10$-106
e•trec;orporEaJ CPR in. 109
•fl hypothermoa 104
manual de'ibnllators 1n, 95: blphaslc. 94 101. Caldrac
Arrest Algornnrn on. 94 101 c1eanng warning"'· 98.
ard drug therapy, 99 100, monopllaSlC, 94. 101. sell ·
adhesive pads of. 99. shock delivery 1n, 96
lvlegacode evaluauon ot sk•lls •n. t59·164
mooomoophoe VT 129 13S 137 138. 139. 142
189
 Ind ea

ph)'SIOlogic mon.tonng •n. 102 ·11).S

polymorpl11c VT. 129, 135. 137, 138. 139. 141, 142
pulS&less VT, 141, 159, 165
quallty Improvement In, 92·93
refractO<Y. 92·109
SUIV•Val rate In, 97
team response to, 98. 100
t.me to derillnAauon a-10 CPR In, 9 7
ueaunem secuence 111, 101
U-!raSOund "'· 109

Website resources See Student Webslle

Wenckebach att1oventricular block. 120

Yonkauer catheters, 55

190