MEIDA ASTRIANI

Acute Coronary Syndrome

Worldwide Statistics
Each year:
> 4 million patients are admitted
with unstable angina and acute MI
> 900,000 patients undergo PTCA
with or without stent

Myocardial Ischemia
Spectrum of presentation
silent ischemia
exertion-induced angina
unstable angina
acute myocardial infarction

Ischemic Heart Disease

evaluation
Based on the patients
history / physical exam
electrocardiogram

Patients are categorized into 3

groups
non-cardiac chest pain
unstable angina
myocardial infarction

ACS

Acute Coronary Syndrome

The spectrum of clinical conditions
ranging from:
unstable angina
non-Q wave MI
Q-wave MI

characterized by the common

pathophysiology of a disrupted
atheroslerotic plaque

Risk stratification

Risk of death

Directed therapy

Patient evaluation in ACS

Acute Coronary Syndromes

Chest pain
suggestive of ischemia

Immediate assessment (<10 minutes)

Measure vital signs (automatic/standard BP cuff)
Measure oxygen saturation
Obtain IV access
Obtain 12-lead ECG (physician reviews)
Perform brief, targeted history and physical exam;
focus on eligibility for fibrinolytic therapy
Obtain initial serum cardiac marker levels
Evaluate initial electrolyte and coagulation studies
Request, review portable chest x-ray (<30 minutes)

Immediate general treatment

Oxygen at 4 L/min
Aspirin 160 to 325 mg
Nitroglycerin SL or spray
Morphine IV (if pain not relieved with
nitroglycerin)
Memory aid: MONA greets
all patients (Morphine, Oxygen,
Nitroglycerin, Aspirin)

Assess initial 12-lead ECG

EMS personnel can

perform immediate
assessment and treatment (MONA),
including initial 12-lead
ECG and review for
fibrinolytic therapy
indications and
contraindications.

Aspirin
Indications Administer to all patients
with ACS, particularly reperfusion
candidates
Give as soon as possible

Blocks formation of thromboxane A2,

which causes platelets to aggregate

Nitroglycerine
Indications
Chest pain of suspected cardiac origin
Unstable angina
Complications of AMI, including
congestive heart failure, left ventricular
failure
Hypertensive crisis or urgency with
chest pain

Nitroglycerin
Indications

Decreases pain of ischemia

Increases venous dilation
Decreases venous blood return to heart
Decreases preload and cardiac
oxygen consumption
Dilates coronary arteries
Increases cardiac collateral flow

Morphine Sulfate
Indications
Chest pain and anxiety associated with
AMI or cardiac ischemia
Acute cardiogenic pulmonary edema (if
blood pressure is adequate)

Morphine Sulfate
Indications
To reduce pain of ischemia
To reduce anxiety
To reduce extension of ischemia by
reducing
oxygen demands

Morphine Sulfate
Precautions (Watch Out!)
Administer slowly and titrate to effect
May compromise respiration; therefore
use with caution in acute pulmonary
edema
Causes hypotension in volume-depleted
patients

Acute Coronary Syndromes

ST elevation or new or
presumably new LBBB:
strongly suspicious for
injury
ST-elevation AMI

ST depression or dynamic
T-wave inversion:
strongly suspicious
for ischemia
High-risk unstable angina/
nonST-elevation AMI

Nondiagnostic ECG:
absence of changes
in ST segment or
T waves
Intermediate/low-risk
unstable angina

ST Elevation

27

Recognition
of AMI
Know what to look
for
ST elevation >1 mm
3 contiguous leads

J point plus
0.04 second

Know where to look

Refer to 2000 ECC
Handbook

PR baseline
ST-segment deviation
= 4.5 mm
28

ST Elevation
Baseline
Ischemiatall or inverted T wave (infarct),
ST segment may be depressed (angina)
Injuryelevated ST segment, T wave
may invert
Infarction (Acute)abnormal Q wave,
ST segment may be elevated and T wave
may be inverted
Infarction (Age Unknown)abnormal Q wave,
ST segment and T wave returned to normal
29

Beta Blockers
Indications (When & Why?)
To reduce myocardial ischemia and
damage in AMI patients with elevated
heart rates, blood pressure, or both
Blocks catecholamines from binding to
-adrenergic receptors
Reduces HR, BP, myocardial contractility
Decreases AV nodal conduction
Decreases incidence of primary VF

Heparin
Indications (When & Why?)
For use in ACS patients with Non Q wave
MI or unstable angina
Inhibits thrombin generation by factor
Xa inhibition and also inhibit thrombin
indirectly by formation of a complex
with antithrombin III

Glycoprotein IIb/IIIa Inhibitors

Indications (When & Why?)
Inhibit the integrin glycoprotein IIb/IIIa
receptor in the membrane of platelets,
inhibiting platelet aggregation
Indicated for Acute Coronary Syndromes
without ST segment elevation

Glycoprotein IIb/IIIa Inhibitors

Indications (When & Why?)
Abciximab (ReoPro)
Non Q wave MI or unstable angina with
planned PCI within 24 hours
Must use with heparin
Binds irreversibly with platelets
Platelet function recovery requires 48 hours

Glycoprotein IIb/IIIa Inhibitors

Indications (When & Why?)
Eptifibitide (Integrilin)
Non Q wave MI, unstable angina managed
medically, and unstable angina / Non Q
wave MI patients undergoing PCI
Platelet function recovers within 4 to 8 hours
after discontinuation

Glycoprotein IIb/IIIa Inhibitors

Indications (When & Why?)
Tirofiban (Aggrastat)
Non Q wave MI, unstable angina managed
medically, and unstable angina / Non Q
wave MI patients undergoing PCI
Platelet function recovers within 4 to 8 hours
after discontinuation

Fibrinolytics
Indications (When & Why?)
For AMI in adults
ST elevation or new or presumably new
LBBB; strongly suspicious for injury
Time of onset of symptoms < 12 hours

Fibrinolytics
Indications (When & Why?)
For Acute Ischemic Stroke
Sudden onset of focal neurologic deficits or
alterations in consciousness
Absence of subarachnoid or intracerebral
hemorrhage
Alteplase can be started in less than 3 hours
of symptom onset

ACE Inhibitors
Indications (When & Why?)
Reduce mortality & improve LV
dysfunction in post AMI patients
Help prevent adverse LV remodeling,
delay progression of heart failure, and
decrease sudden death & recurrent MI

ACE Inhibitors
Indications (When & Why?)
Suspected MI & ST elevation in 2 or
more anterior leads
Hypertension
Clinical signs of AMI with LV dysfunction
LV ejection fraction <40%

ACE Inhibitors
Indications (When & Why?)
Generally not started in the ED but
within first 24 hours after:
Fibrinolytic therapy has been completed
Blood pressure has stabilized

Acute Myocardial Infarction

Definition
Otherwise know as heart attack
An MI occurs when there is a diminished
blood supply to the heart which leads to
myocardial cell damage and ischemia.
Contractile function stops in the necrotic
areas of the heart.
Ischemia usually occurs due to blockage
of the coronary vessels.

 This blockage is often the result of

thrombus that is superimposed on an
ulcerated or unstable atherosclerotic
plaque formation in the coronary artery.
MIs are described by the area of
occurrence.
Anterior, Inferior, Lateral or Posterior.

Coronary artery events

Ischemia Outer most area, source of
arrhythmias, viable if no further infarction.
Injury Viable tissue found between
ischemic and infarcted areas.
Infarction/necrosis Center area, dead
not viable tissue that turn into scar.

MI Classifications
MIs can be subcategorized by anatomy
and clinical diagnostic information.
Anatomic
Transmural and Subendocardial
Diagnostic
ST elevations (STEMI) and non ST
elevations (NSTEMI).

Epidemiology
MIs are the leading cause of death in the
United States, affecting one in five men
and one in six women.
450,000 people in the US die from
coronary disease each year.
Incidence rates increase with age as do
mortality rates due to infarction.

Epidemiology
The survival rate for those hospitalized
due to MI has reached approximately
95%.
This is the result of the advancements
made in modern medical technology.

Risk Factors
The presence of any risk factor is
associated with doubling the risk of an MI.
Non Modifiable
Age
Gender
Family history

Risk Factors
Modifiable

Smoking
Diabetes Control
Hypertension
Hyperlipidemia
Obesity
Physical Inactivity

Smoking
Tobacco use increases the risk of
coronary artery disease two to six times
more than non smokers.
Nicotine increases platelet thrombus
adhesion and vessel
inflammation.

Diabetes & Hypertension

Diabetes not only increases the rate of
atherosclerotic formation in vascular
vessels but also at an earlier age.
The constant stress of high blood
pressure has been associated with the
increased rate of plaque formation.
Shearing Stress and inflammation of
endothelial lining begins the process.

Hyperlipidemia
Elevated levels of cholesterol, LDLs or
triglycerides are associated with the
increased risk of coronary plaque
formation and MI.
Almost 50% of the U.S.
population has some
form of dyslipidemia.

Obesity and Physical Inactivity

Mortality rate from CAD is higher in those
who are obese.
Some evidence shows that those who
carry their weight in their abdomen have a
higher incidence of CAD
Physically inactive people have lower HDL
levels with higher LDL levels and an
increase in clot formation.

Pathophysiology
Ischemia develops when there is an
increased demand for oxygen or a
decreased supply of oxygen.
Ischemia can develop within 10 seconds
and if it lasts longer than 20 minutes,
irreversible cell and tissue death occurs.
Myocardial cell death begins at the
endocardium. The area most distal to the
arterial blood supply.

Pathophysiology
As vessel occlusion continues cell death
spreads to the myocardium and eventually
to the epicardium.
Severity of the MI depends on three
factors.
Level of occlusion
Length of time of occlusion
Presence or absence of collateral circulation

Signs and Symptoms

Signs and symptoms are unique to each
individual patient.
Ranging from no symptoms to sudden
cardiac arrest.

Chest Pain
The most common initial manifestation is
chest pain or discomfort.
This is not relieved by rest, position
change or nitrate administration.
Pain is described by heaviness, pressure,
fullness and crushing sensation.
Not everyone experiences this sensation.

Chest Pain

PQRST assessment for chest pain

P- Precipitating events
Q- Quality of pain
R- Radiation of pain
S- Severity of pain
T- Timing

Nausea and Vomiting

Not everyone will experience this.
Vomiting results as a reflex from severe
pain.
Vasovagal reflexes initiated from area of
ischemia.

Sympathetic Nervous System

Stimulation
During an MI increased catecholamines
are released.
This results in diaphoresis and
vasoconstriction of peripheral blood
vessels.
Cool Sweat with a temperature increase
during the first 24 hours.

Cardiovascular Changes
Urine output will decrease
Lung sounds will change to crackles
Jugular veins may become distended and
have obvious pulsations.

Within the first 10 minutes upon

arrival to the hospital:
Check vital signs and evaluate oxygen
saturation
Establish IV access
Obtain and review 12-lead ECG
Take a brief focused history and perform a
physical exam
Obtain blood samples to evaluate initial cardiac
markers, electrolytes and coagulation

Diagnostics
After collecting patient health history, a
series of EKGs should be taken to rule
out or confirm MI.
12 lead EKGs can help to distinguish
between ST-elevation MIs and Non-STelevation MIs.

Normal Sinus Rhythm

Angina
Stable
Chest pain caused by the build up of lactic
acid and irritation to the myocardial nerve
fibers.
Chest pain caused by the 4 Es.
Pain is usually relieved with rest, pain
meds and nitrates.

Variable/Prinzmetal/Spasm
Transient ischemia that occurs
unpredictably and almost always at rest.
Pain is caused by vasospasm of the
arteries.
ST segment elevations will be noted.

Unstable
Chest pain at rest or with exercise and
tends to last greater than 15 minutes.
This results in reversible myocardial
ischemia but is a sign that an infarct is
soon to come.
EKG will reveal ST segment depression
and T wave inversion.

STEMI

ST segment elevations
T wave changes
Q wave development
Enzyme elevations
Reciprocals

NSTEMI

ST segment depressions
T wave changes
No Q wave development
Mild enzyme elevations
No reciprocals

STEMI vs. NSTEMI

Phases of a STEMI
Hyperacute Phase
Occurs within the first few hours of MI onset.
Leads facing the infarcted surface: ST
segment elevation.
Leads facing the uninjured surface: ST
segment depression (reciprocals)
T waves become tall, widened and might be
taller than the R wave.

Phases of a STEMI
Fully Evolved Phase
Q wave development
ST elevation
T waves start to become inverted in leads
facing the injury.

Phases of a STEMI
Resolution phase
Weeks after there will be a gradual return of
ST segments to baseline.
T waves will gradually return to normal but are
the last to change back.

Serum Cardiac Markers

Myocardial cells produce certain proteins
and enzymes associated with cellular
functions.
When cell death occurs, these cellular
enzymes are released into the blood
stream.
CPK and troponin

CPK

Creatine Phosphokinase
Begin to rise 3 to 12 hours after acute MI.
Peak in 24 hours
Return to normal in 2 to 3 days

Troponin
Myocardial muscle protein released into
circulation after injury.
These are highly specific indicators of MI.
Troponin rises quickly like CK but will
continue to stay elevated for 2 weeks.
Myoglobin-lacks cardiac specificity.

Serum Cardiac Markers

Treatment Options
The immediate goal for any acute MI is to
restore normal coronary blood flow to
vessels and salvage myocardium.
There are a variety of medical and
medicinal therapies to treat an MI.

General Treatment for the MI

patient
MONA

Morphine
Oxygen
Nitroglycerin
Aspirin

Fibrinolytic Therapy
Indicated for patients with STEMI MIs.
Should be given within 12 hours of
symptom onset.
Fibrinolytics will break down clots found
within the vessles
Contraindications: post op surgical
patients, history of hemorrhagic stroke,
ulcer disease, pregnancy, ect.

Cardiac Catheterization
A diagnostic angiography which includes
angioplasty and possible stenting.
Performed by an interventional
cardiologist with a cardiac surgeon on
stand by.
Percutaneous procedure through the
femoral or brachial artery.

Cardiac Catheterization
Upon arrival to the cath lab all actue MI
patients will receive:
A bolus dose of plavix
IV Integrelin
Heparin dose either subcu or IV drip
Angiomax : a DTI may be substituted for
heparin and integrelin.

Coronary artery bypass graft

Surgical treatment where saphenous vein
is harvested from the lower leg and used
to bypass the occluded vessels.

Long Term Care

Smoking Cessation and lifestyle
modifications.
Aspirin, Beta Blockers and Clopidogrel will
be indefinite.
Lipid lowering medication along with diet
modifications.

HANDLING
SUDDEN CARDIAC ARREST

Sudden Cardiac Arrest vs

Heart Attack

Heart Attack (Myocardial infarction) occurs

when the coronary artery becomes blocked
and the blood supply to heart muscle is
interrupted.

If the blockage is not reversed in a matter

of hours, permanent damage occurs.

Sudden Cardiac Arrest vs

Heart Attack

Sudden Cardiac Arrest occurs when the heart

starts beating chaotically and is unable to
pump blood to the body (no pulse or breathing).

It is the result of an electrical malfunction of

the heart.

Cardiac Electrical Conduction

The
heart
muscle
contracts
in response to electrical
stimulus generated by
the
hearts pacemaker Cells
with the result of a
pulse,
blood pressure, breathing

& other
circulation.

signs

of

Sudden Cardiac Arrest (SCA)

Ventricular Tachycardia

Sudden Cardiac Arrest (SCA)

Ventricular
Fibrillation
Causes :
Coronary artery disease
Acute coronary syndromes
Electrocution.
Drug toxicity and sensitivity
Asphyxia
Drowning
Blunt force trauma to the chest.

Incidence of Sudden Cardiac Death (SCD)

of

150 Sudden Cardiac Deaths per 100,000 persons

annually in industrialised world.
40% of SCDs occur in people with no prior history
heart disease.

SCD accounts for more than 50% of cardiac

mortality.

Autospies revealed 90% victims have CAD.

Risk Factors of Sudden Cardiac Death

(SCD)

Prior Episode of V.TACH

Low LVEF.

Previous Myocardial Infarction.

Coronary Artery Disease

Family History of SCD.

Cardiomyopathy

Congestive Heart Failure

Long QT Syndrome.

Right Ventricular Dysplasia.

Sudden Cardiac Arrest (SCA)

Treatment
Chain of Survival
Early access.
Early CPR.
Early defibrillation.
Early advanced life support.

Sudden Cardiac Arrest (SCA)

Chain of Survival
access

First link Early

Call for Help !

Patient evaluation
Determine if conscious or not, by
placing
one hand on patients forehead and
shaking shoulders gently with
another
hand.
In case of SCA patient will not
respond.

Sudden Cardiac Arrest (SCA)

Chain of Survival
CPR

Second link Early

Steps preceding Cardiopulmonary Resuscitation

(CPR)
Determine A,B,C of Basic Cardiac Life Support

(BCLS).
*

A for Airway.

B for Breathing.

C for Circulation.

Sudden Cardiac Arrest (SCA)

Chain of Survival
CPR
Airway
* Head tilt

* Finger
sweep.
* Jaw Thrust.

Second link Early

Sudden Cardiac Arrest (SCA)

Chain of Survival
CPR

Second link Early

Breathing

* Look Down the line of chest

to
to see it rise and fall.
* Listen at mouth and nose for
breathing sounds.
* Feel for expired air at
patients
mouth and nose.

Sudden Cardiac Arrest (SCA)

Chain of Survival
CPR
Circulation

* Feel - carotids

Second link Early

Sudden Cardiac Arrest (SCA)

Chain of Survival
CPR

Second link Early

Once SCA is confirmed

Patient should be placed on hard surface.

Start CPR.

Give 2 expired breaths, followed by 15

compressions.
Continue 2:15 cycles for CPR both for 1- & 2 rescuers

Compression rate -100 per minute

Sudden Cardiac Arrest (SCA)

Chain of Survival
CPR

Second link Early

Mouth to mouth ventilation

Remove any obvious obstruction.

Open airway.
Pinch victims nose.
Give mouth to mouth ventilation.
Repeat breaths.

Sudden Cardiac Arrest (SCA)

Chain of Survival
CPR

Second link Early

Cardiac compressions

Locate correct chest compression site,

2 - fingers above xiphoid.
Place heel of other hand on the lower
end
of breast bone.
Fingers off the chest wall.

Sudden Cardiac Arrest (SCA)

Chain of Survival
CPR

Second link Early

Sudden Cardiac Arrest (SCA)

Chain of Survival Third link Early
Defibrillation
AHA/ERC Standards & Guidelines
Over 10 years ago, AHA expanded its early defibrillation standard of care
to include
AEDs for in-hospital first responders (1990).

Resuscitation committees often inappropriately emphasize the arrival of

core team
rather than the delivery of the first shock.
Treatment goal VF
Defibrillation
defibrillation
within 3 min. NSR
anywhere in the hospital.

Defibrillation Electrical Current Stops VF

Sudden Cardiac Arrest (SCA)

Chain of Survival
Defibrillation

Third link Early

Defibrillation Electrode Placement

Anterior lateral

Sudden Cardiac Arrest (SCA)

Chain of Survival
Defibrillation

Third link Early

The Importance of TIME :

Guidelines 2000

For communities :
3-5 minutes, preferably less than 3
minutes.
For hospitals :
less than 3 minutes.

Sudden Cardiac Arrest (SCA)

Chain of Survival
Defibrillation

Third link Early

Safety First

Attach AED only to someone not

breathing and without a pulse or
signs
of circulation.
Make sure no one is touching the
victim.
Be sure the electrodes are firmly
adhered to victims chest.
Move oxygen away from the rescue

Sudden Cardiac Arrest (SCA)

Chain of Survival
Defibrillation

Third link Early

Types of AEDs
Semi Automatic : Analyses patients rhythm and
advises if
rhythm needs a shock. Operator has to press shock
button
to deliver the shock.

Fully Automatic : Analyses patients rhythm and

delivers
shock if required all by itself.

Sudden Cardiac Arrest (SCA)

Chain of Survival
Defibrillation

Third link Early

TYPES OF AEDs

Semi Automatic External Defibrillator :

Simple 2 Button Operation

ON/OFF
(Auto Analyze)
SHOCK

Sudden Cardiac Arrest (SCA)

Chain of Survival
Defibrillation

Third link Early

TYPES OF AEDs

Fully Automatic External Defibrillator :

Simple 1 Button Operation

ON/OFF

(Auto Analyze & Auto Shock if required)

Sudden Cardiac Arrest (SCA)

Chain of Survival Fourth link Early
ACLS
For advanced Cardiac Life support (ACLS) shift the
patient
to the nearest hospital.
Treat victim with medicine and advanced
therapies.

VF / Pulseless VT

VF / Pulseless VT
Epinephrine 1 mg IV push, repeat every 3 to 5 minutes
or
Vasopressin 40 U IV, single dose, 1 time only

Resume attempts to defibrillate

1 x 360 J (or equivalent biphasic) within 30 to 60 seconds

Consider antiarrhythmics:
Amiodarone (llb for persistent or recurrent VF/pulseless VT)
Lidocaine (Indeterminate for persistent or recurrent VF/pulseless VT)
Magnesium (llb if known hypomagnesemic state)
Procainamide (Indeterminate for persistent VF/pulseless VT;
llb for recurrent VF/pulseless VT)
Resume attempts to defibrillate

Epinephrine
Indications (When & Why?)
Increases:
Heart rate
Force of contraction
Conduction velocity

Peripheral vasoconstriction
Bronchial dilation

VF / Pulseless VT

Vasopressin
Indications (When & Why?)
Used to clamp down on vessels
Improves perfusion of heart, lungs, and
brain
No direct effects on heart

VF / Pulseless VT

Amiodarone
Indications (When & Why?)
Powerful antiarrhythmic with substantial
toxicity, especially in the long term
Has effects on sodium & potassium

VF / Pulseless VT

Lidocaine
Indications (When & Why?)
Depresses automaticity
Depresses excitability
Raises ventricular fibrillation threshold
Decreases ventricular irritability

VF / Pulseless VT

Magnesium Sulfate
Indications (When & Why?)
Cardiac arrest associated with torsades
de pointes or suspected
hypomagnesemic state
Refractory VF
VF with history of ETOH abuse
Life-threatening ventricular arrhythmias
due to digitalis toxicity, tricyclic
overdose
VF / Pulseless VT

Procainamide
Indications (When & Why?)
Recurrent VF
Depresses automaticity
Depresses excitability
Raises ventricular fibrillation threshold
Decreases ventricular irritability

VF / Pulseless VT

PEA

PEA

Review for most frequent causes

Tablets (drug OD, accidents)
Hypovolemia
Tamponade, cardiac
Hypoxia
Tension pneumothorax
Hydrogen ionacidosis
Thrombosis, coronary (ACS)
Hyper-/hypokalemia
Thrombosis, pulmonary (embolism)
Hypothermia

Epinephrine 1 mg IV push,
repeat every 3 to 5 minutes

Atropine 1 mg IV (if PEA rate is slow),

repeat every 3 to 5 minutes as needed, to a total
dose of 0.04 mg/kg

Atropine Sulfate
Indications (When & Why?)
Should only be used for bradycardia
Relative or Absolute

Used to increase heart rate

Asystole

Asystole
Transcutaneous pacing:
If considered, perform immediately

Epinephrine 1 mg IV push,
repeat every 3 to 5 minutes
Atropine 1 mg IV,
repeat every 3 to 5 minutes
up to a total of 0.04 mg/kg
Asystole persists
Withhold or cease resuscitation efforts?
Consider quality of resuscitation?
Atypical clinical features present?
Support for cease-efforts protocols in place?

Cardiac
Emergencies and
CPR

Introduction
Basic Life Support needed for patient whose
breathing or heart has stopped
Ventilations are given to oxygenate blood
when breathing is inadequate or has stopped
If heart has stopped, chest compressions are
given to circulate blood to vital organs
Ventilation combined with chest
compressions is called cardiopulmonary
resuscitation (CPR)
CPR is commonly given to patients in cardiac
arrest as a result of heart attack

Circulatory System:
Emergencies
Any condition that affects respiration
Reduces ability to deliver oxygen

Severe bleeding
Shock

Stroke
Reduces blood flow to brain

Heart conditions
Reduce tissue oxygenation

Circulatory System:
Emergencies continued
Heart attack
Can lead to cardiac arrest

Ventricular fibrillation
Heart muscle flutters rather than
pumping blood

Cardiopulmonary
Resuscitation (CPR)
CPR helps keep patient alive by circulating
some oxygenated blood to vital organs
Ventilations move oxygen into lungs where
it is picked up by blood
Compressions on sternum increase
pressure inside chest, moving some blood
to brain/other tissues

Cardiopulmonary
Resuscitation (CPR) continued
Blood circulation resulting from chest
compressions not as strong as circulation
from heartbeat
Can help keep brain/other tissues alive
until normal heart rhythm restored

Cardiopulmonary
Resuscitation (CPR) continued
Often electric shock from AED is needed to
restore a heartbeatand CPR can keep
patient viable until then
CPR should be started as soon as possible
In some instances, the heart may start
again spontaneously with CPR

General Technique of
CPR
If unresponsive, not breathing, and no
pulse, start chest compressions
Find the correct hand position
Two hands for adults
One or 2 hands for child
Two fingers for infant

General Technique of CPR

continued
If alone, alternate 30 chest compressions
and 2 ventilations for any age patient
In two-rescuer CPR for infant/child,
alternate 15 compressions and 2
ventilations
Chest-encircling method in infant
Give each ventilation over 1 second
Follow local protocol regarding oxygen

Single-Rescuer CPR
1. Check patients responsiveness,
open airway, and determine that
patient is not breathing adequately
2. Give 2 ventilations, each lasting 1
second
3. Determine victim has no pulse

Single-Rescuer CPR
2. Give 2
ventilations, each
lasting 1 second
3. Determine victim
has no pulse

Put hand(s) in correct position for

chest compressions

Give 30 chest compressions at rate

of 100 per minute
Then give 2 ventilations

Continue CPR until:

Patient begins to move
AED brought to scene and ready to
use
Professional help arrives to take
over
You are too exhausted to continue

 If patient starts moving, check for

adequate breathing
If patient is breathing adequately,
put patient in recovery position and
monitor breathing
When AED arrives, start AED
sequence

Chest Compressions
Alert
Be careful with
your hand position
For adults/children,
keep your fingers
off patients chest
Do not give
compressions over
bottom tip of
breastbone

Chest Compressions
Alert
When
compressing,
keep elbows
straight and
hands in contact
with patients
chest at all times

Chest Compressions
Alert
Compress chest
hard and fast, but
let chest recoil
completely
between
compressions.
Minimize amount
of time used giving
ventilations
between sets of
compressions.

Problems with CPR

Technique
CPR often ineffective because of poor
technique
Compressions not delivered steadily and
constantly during resuscitation efforts
Often compressions are too shallow,
resulting in ineffective blood flow
Compressions may be given at too fast a
rate
Only good-quality CPR improves chances of
survival

Chest Compressions:
Bradycardia in Child
Infant or child being given rescue
breaths or oxygen may have a pulse
but still inadequate perfusion
If pulse < 60 beats/minute and infant
or child has signs of poor perfusion,
provide CPR

Two-Rescuer CPR for Adults

and Children
Minimizes time
between rescue
breaths and
compressions
CPR becomes more
effective

Can more quickly

set up AED
Reduces rescuer
fatigue

Two-Rescuer CPR
Performed in cycles of 30:2 for adult
(15:2 for infant or child)
One rescuer provides breaths, second
rescuer gives chest compressions
Rescuers switch positions every 2
minutes
Change done after full CPR cycle
Accomplish change in < 5 seconds

Two-Rescuer CPR
continued
If AED present, one rescuer gives
CPR while the other sets up unit
If unit advises CPR, rescuers give
CPR together
Third rescuer can apply cricoid
pressure

Two-Rescuer CPR
continued
If you are assisting another trained rescuer
who places an advanced airway:
Chest compressions given continually
No pauses for ventilations
Give ventilations at rate of 8 10
breaths/ minute

Transitioning from OneRescuer CPR to Two-Rescuer

CPR

Second rescuer moves into position on

other side to prepare to take over chest
compressions
First rescuer completes a cycle of
compressions and ventilations
While first rescuer pauses to check for a
pulse, second rescuer finds correct hand
position for compressions

Transitioning from OneRescuer CPR to Two-Rescuer

CPR

When first rescuer says, No pulse, continue

CPR, second rescuer begins chest
compressions and first rescuer then gives
only ventilations

Differences in Two-Rescuer
Training
If First Responder started CPR, arriving
second rescuer may have a higher level of
training
Rescuer with greater training determines
how CPR should best be continued

Skill:
CPR For Adult
or Child
(Two Rescuers)

Rescuer 1 checks ABCs. Rescuer 2

locates site for chest compressions.

If no pulse, rescuer 2 gives 30

compressions for adult (15 for child)
at rate of 100/minute.

Rescuer 1 gives 2 breaths.

Continue cycles of 30:2 for adults

(15:2 for child). After 5 cycles (~ 2
minutes) switch positions.

Adult or Child Two-Rescuer

CPR Continued
Continue CPR until:
Patient moves
AED brought to scene and ready to use
Advanced help arrives and takes over
If patient starts breathing and has pulse,
put in recovery position and monitor ABCs
If AED brought to scene, start AED
sequence

 Uses different hand position

Place thumbs of both hands on sternum
while fingers encircle chest
Compress breastbone with both thumbs
while squeezing chest with fingers
Same rate and depth as usual

Two-Rescuer CPR:
Infants

Skill:
CPR: Infants
Two Rescuers

Rescuer 1 checks
ABCs. Rescuer 2
locates site for
chest
compressions.

If no pulse, rescuer
2 gives 15 chest
compressions.

Rescuer 1 gives 2 breaths.

Infant Two-Rescuer CPR

Continued
Continue cycles of 15:2 for ~ 2 minutes
then switch roles
Continue CPR until:
Infant moves
Advanced help arrives and takes over
If infant starts breathing, hold in recovery
position and monitor ABCs

When Not to Perform

CPR
Presence of a Do-Not-Resuscitate (DNR)
order
Patient obviously dead (decapitation;
incineration; or clear signs of prolonged
death, such as rigor mortis and dependent
lividity)
Not safe to be on the scene and the
patient cannot be moved somewhere safe
A physician pronounces the patient dead