Download SAED Guide revised Jan 2008 - Grampians Region Health

DEFIBRILLATION AND THE
AUTOMATIC EXTERNAL DEFIBRILLATOR
A GUIDE FOR
EDUCATION & COMPETENCY
Compiled by: Pat Standen,
Grampians Regional Emergency and Critical Care Coordinator.
ACKNOWLEDGEMENTS
Sue Garner, Clinical Educator, Intensive Care/Coronary Care Unit, Ballarat Health
Services, Amber van Dreven, Clinical Educator, Emergency Department, Ballarat Health
Services and Geoff McCurdy, Director of Pharmacy, Ballarat Health Services for reviewing
the original document and providing their expert advice.
Thank you to Wendy Porteous, Clinical Educator – Emergency Department, Ballarat Health
Services for reviewing this 2007/08 version.
Ballarat Health Services and Rural Ambulance Victoria for so generously allowing their
clinical practice guidelines to be used as a guide.
For information regarding this Guide contact:
Pat Standen
Department of Human Resources
PO Box 712
Ballarat 3353
Email: [email protected]
Phone: 03 5333 6026
Version
1.0
1.1
Date
September 2005
January 2008
Major Changes
Page No
Basic Life Support Flowchart
AED Flowchart
Competency Assessment form
Basic Life Support Table
16
17
18
20
DISCLAIMER:
Care has been taken to confirm the accuracy of the information presented in this guide, however, the authors,
editors and publisher are not responsible for errors or omissions or for any consequences from application of the
information in the guide and make no warranty, express or implied, with respect to the contents of the
publication.
Every effort has been made to ensure the clinical information provided is in accordance with current
recommendations and practice. However, in view of ongoing research, changes in government regulations and
the flow of other information, the information is provided on the basis that all persons undertake responsibility
for assessing the relevance and accuracy of its content.
Defibrillation and the AED, A guide to education and competency
Revised Jan 2008-
Page 2 of 28
TABLE OF CONTENTS
Page
INTRODUCTION
4
SECTION 1
BRIEF REVIEW OF THE HEART
1.1 Anatomy
1.2 Coronary Arteries
1.3 The Conduction System
5
5
6
7
SECTION 2
2.1
ECG COMPLEX
2.2 ECG Grid Paper
9
10
SECTION 3
CARDIAC RHYTHMS AND DEFIBRILLATION
Examples of AEDs
3.1 Position of Pads
3.2 Pads
3.3 Rhythms:
Ventricular Tachycardia
Ventricular Fibrillation
3.4 Defibrillation Safety
3.5 Procedure
Basic Life Support Flowchart (example)
AED Flowchart (example)
Competency Assessment Form (example)
BASIC LIFE SUPPORT TABLE
11
11
11
12
12
13
14
15
16
17
18
20
SECTION 4
DRUG ADMINISTRATION
4.1 Mode of Administration
4.2 Key Drugs Used In Cardiac Arrest
21
21
23
REFERENCES
28
SUGGESTED FURTHER READING
28
Defibrillation and the AED, A guide to education and competency
Revised Jan 2008-
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INTRODUCTION
The purpose of this guide is to assist educators in the Grampians Region to design their
own Health Service specific package for Registered Nurses Division 1 required to use the
Automatic External Defibrillator (AED). There are a number of these devices available for
purchase; the aim of this guide is to provide generic information based on principles of
care.
It is the responsibility of each individual practitioner and Health Service to ensure
appropriate education for all equipment and that competency in the use of the equipment
is maintained.
The use and education around the AED should be undertaken in conjunction with Basic
Life Support (BLS) and Laryngeal Mask Airway (LMA) management.
Defibrillation and the AED, A guide to education and competency
Revised Jan 2008-
Page 4 of 28
SECTION 1
1.0
A BRIEF REVIEW OF THE HEART
1.1
Anatomy
Approximately the size of a person’s fist, the heart weighs between 250 and 300grams. It
sits within the mediastinum and extends from the second rib to the fifth intercostal space.
It assumes an oblique position in the thorax; approximately two-thirds of its mass is left
of the midsternal line with the balance projecting right. The broad superior portion is
approximately 9cms wide and is directed towards the right shoulder. The pointed apex is
directed towards the left hip and rests on the diaphragm.
The heart consists of four chambers, two atria and two ventricles. There is a valve through
which blood passes before leaving each chamber of the heart. The valves prevent the
backward flow of blood. These valves are actual flaps that are located on each end of the
two ventricles. They act as one-way inlets of blood on one side of a ventricle and one-way
outlets of blood on the other side of a ventricle. Each valve actually has three flaps, except
the mitral valve, which has two flaps. The four heart valves include the following:
 Tricuspid valve: located between the right atrium and the right ventricle
 Pulmonary valve: located between the right ventricle and the pulmonary artery
 Mitral valve: located between the left atrium and the left ventricle
 Aortic valve: located between the left ventricle and the aorta
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1.2
Coronary Arteries
Coronary arteries supply blood to the heart muscle. Like all other tissues in the body, the
heart muscle needs oxygen-rich blood to function.. The coronary arteries consist of two
main arteries: the right and left coronary arteries, and their two branches, the circumflex
artery and the left anterior descending artery.

The left coronary artery (LCA), divides into the left anterior descending artery and
the circumflex branch, and supplies blood to the ventricles and left atrium.
 The right coronary artery (RCA), divides into the right posterior descending artery
and a large marginal branch, supplies the ventricles, right atrium, and sinoatrial
node.
 The circumflex artery (Cx) branches off the left coronary artery and encircles the
heart muscle. This artery supplies blood to the back of the heart.
 The left anterior descending artery (LAD) branches off the left coronary artery and
supplies blood to the front of the heart
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Coronary
Artery:
Right
Left
Area and Structures Supplied:
Complications resulting from
occlusion:
Inferior wall of left ventricle
Sinus node (55% of individuals)
AV node (90% of individuals)
Bundle of His (90% of individuals)
Posterior inferior division of left bundle
(a portion)
Vagus nerve fibres
Right bundle branch (superior onethird)
Inferior AMI, Posterior AMI and/or
Right Ventricular AMI
Conduction blocks  First degree heart block
 Second degree Type I and
Type II heart block
 Third degree heart block
Bradyarrhythmias
Hypotension
Anterior wall of left ventricle (LAD)
Posterior wall of left ventricle (LCX)
Sinus node (45% of patients) (LCX)
AV node (10% of patients) (LCX)
Right bundle branch (inferior twothirds)
Anterior superior division of left
bundle branch
Posterior inferior division of left bundle
branch (a portion)
Anterior AMI
Heart failure
Tachy arrhythmias associated with
heart failure
Conduction blocks  Right bundle branch block
 Left anterior hemiblock
 Left posterior hemiblock
 First degree heart block
 Second degree Type II
 Third degree heart block
LAD: Left anterior descending artery
LCX: Left circumflex artery
1.3
Potential aneurysm formation
VT/VF
The Conduction system:
Defibrillation and the AED, A guide to education and competency
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The ability of the heart muscle to depolarise is intrinsic. About 1% of the cardiac muscle
fibres become auto-rhythmic: they repeatedly and rhythmically generate action potentials.
These auto-rhythmic fibres serve two functions; the pacemaker, setting the rhythm for
the entire heart and the conduction system, the route for depolarisation to occur.

Sinoatrial (SA) node – located in the right atrial wall inferior to the opening of the
inferior vena cava the normal pacemaker of the heart rate approx 70 – 80 per
minute (sinus rhythm). The wave of depolarisation spreads through the two atria
and ends up at the AV node.

Atrioventricular (AV) node – located in the septum between the two atria. The
impulse from the SA node is delayed for about 0.1 sec at the AV node to allow the
atria to complete their contraction. The impulse then travels rapidly through the AV
bundle (Bundle of His) and enters both the right and left bundle branches. The
pacemaker rate of the AV node is 40 – 50.

Bundle branches – right and left, course through the interventricular septum
towards the apex of the heart.

Purkinje fibres – because the left ventricle is larger than the right the Purkinje
network is greater on the left. Conduction occurs at the apex of the ventricular
myocardium first then travels upward. Approx O.20 secs after the atria contract the
ventricles contract. The pacemaker rate is approx 20 – 40.
Defibrillation and the AED, A guide to education and competency
Revised Jan 2008-
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SECTION 2
2.1
E.C.G. COMPLEX
 P WAVE The first wave represents depolarisation of the atria. The impulse usually comes from the
SA node, which is the chief pacemaker of the heart and is situated in the right atrium.
The general wave of depolarisation is downwards and towards the left hand side of the
body.
The P wave is generally not higher (amplitude) than 2-3mm and no longer than 0.10 –
0.11 of a second in duration. It is normally upright in Lead I, Lead II, aVF, V3 – V6. It
may be inverted in aVR, may be biphasic in V1 and V2, and may be occasionally inverted
in Leads I and II and aVL.
 PR INTERVAL –
This interval represents the time taken for the impulse to go through the atria, across the
AV node and junction and down the Bundle of His. It is measured from the beginning of
the P wave to the beginning of the QRS. Normal duration 0.12 – 0.20 seconds.
 QRS –
This complex follows the P wave, PR interval and represents the depolarisation of the
ventricles. Depolarisation comes through the AV node, then goes through the septum and
then through the left and right ventricles. The general wave is downwards and to the left
of the body.
The QRS is usually 0.04 – 0.10 of a second in duration and between 5mm and 125mm in
amplitude, depending on the lead.
 The Q wave is the first downward deflection preceding the R or S wave. If
there is no R wave it is termed a QS wave. The Q wave is normally less than 0.04
seconds in duration, and less than a ¼ of the R wave. Q waves in Lead III and
aVF may vary with inspiration.
 The R wave – first upward deflection of the QRS complex usually less than
0.01 second in duration. The R wave in V6 represents left ventricle activity. The
R wave in V1 represents right ventricle activity.
 The S wave – first downward deflection following R wave is rarely deeper than
6mm and may be absent. An S wave in V1 represents left ventricle activity. An S
wave in V6 represents right ventricle activity.
 ST SEGMENT –
This segment represents the refractory period of the ventricles. The point where the QRS
joins the ST segment is called the “J” point.
The ST segment duration varies with the cardiac rate and ranges from zero to 0.15
seconds. It is normally iso-electric (on the baseline) because positive and negative forces
are equal during this period.
 T WAVE –
This usually starts at the iso-electric line and varies in shape. It represents rapid
repolarisation of the ventricles. Its amplitude is usually from 5mm – 10mm. It can be
upright in Lead I, Lead II, V3 to V6 inverted in aVR and variable in other leads.
Following the T wave a U wave of low voltage is sometimes seen, it may represent the
slow repolarisation of the ventricles. It is usually difficult to see.
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 QT INTERVAL –
This interval measures the total time taken for depolarisation and repolarisation of the
ventricle. It is measured from start of the QRS to end of the T wave. Its duration varies
with age, sex and cardiac rate, but usually is about 0.35 – 0.42 seconds. As a general
rule – QT should be less then ½ of the R – R interval.
2.2
ECG GRID PAPER
Measurements of paper and the complex:
 P wave – 0.20 sec
 PR interval – 0.12 – 0.20 sec
 QRS interval – 0.07 – 0.10 sec
 ST segment – measurement not significant, elevation or depression is more
important
 QT segment – measurement depending on heart rate
Calculation of Heart Rate
Paper speed: 25mm/sec – therefore 5 large boxes = 25mm or 1 sec therefore 300boxes =
1 minute
If heart rate regular:
Measure the interval between the complexes (R R interval) and divide into 300
For example: 1 complex every large box = Rate 300bpm
1 complex every 2 large boxes = rate 150bpm
1 complex every 3 large boxes = rate 100bpm
1 complex every 4 large boxes = rate 75bpm
1 complex every 5 large boxes = rate 60bpm
OR –
If the heart rate irregular:
15 large boxes = 3 secs therefore 30 large boxes = 6 secs
Count the complexes in a 6 second interval and multiply by 10 to get the rate per minute.
Defibrillation and the AED, A guide to education and competency
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SECTION 3
3.0
CARDIAC RHYTHMS AND DEFIBRILLATION
REMEMBER: EARLY DEFIBRILLATION PROVIDES THE BEST CHANCE OF SURVIVAL
IN VF OR PULSELESS VT
Defibrillation refers to the current of electricity passing through the heart and it occurs at
a random point in the cardiac cycle (unsynchronised). Defibrillation produces simultaneous
depolarisation of the mass of myocardial cells and enables the resumption of organised
electrical activity. The amount of current, which will penetrate the chest wall, may vary.
Automatic External Defibrillators (AED) use 150j in a biphasic mode.
Examples of some of the automatic external defibrillators available:
Welch Allyn AED 10
http://www.welchallyn.com/products/en-us/x-11-ac-100-0000000001041.htm
Phillips HeartStart FR2
http://www.medical.philips.com/main/products/resuscitation/index2.html
3.1
Powerheart AED G3
http://www.powerheart.com/products/phaed_g3auto.htm
Zoll AED
http://www.zoll.com.au/products/aed_plus/literature/AED_Plus_Brochure.pdf
Position of Pads
The electrode position should be standard (you can refer to the instructions on your AED.
The apex pad is placed over the 6th intercostal space, anterior chest wall, mid axillary line.
The sternal pad is placed with its top in the 2nd intercostal space, just right of the sternum.
Defibrillation and the AED, A guide to education and competency
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3.2
The Pads
The standard defibrillation pads for AEDs are about the size of your hand and are made of
soft thin foam coated on one side with a gel. The gel side is covered with a peel off
backing which is removed prior to placement on the chest. The backing is removed from
one pad at a time and the gel side firmly placed onto the patient’s bare chest (ensure
moisture is wiped away and the entire pad smoothed on firmly). Good pad contact will
reduce the risk of skin burns and reduce resistance to the current. When a shock is
delivered, the electrical current generated by the biphasic AED moves first in one
direction, from one pad through the chest and heart to the other pad, and then reverses.
The gel on each pad helps to conduct the current efficiently.
3.3
Rhythms
There are four lethal rhythms
 Ventricular Tachycardia (VT)
 Ventricular Fibrillation (VF)
 Pulseless Electrical Activity (Electro-Mechanical Dissociation)
 Asystole
The two shockable rhythms, which the AED will recognise, are VT and VF. The AED reads
the ECG from the pads applied to the chest. Some AEDs have screens that show the
rhythms, some do not. The AED identifies the heart rhythms. The operator does not need
to be able to identify the hearts rhythm or whether there is a need for defibrillation. It is
however useful to have a basic knowledge of heart rhythms.
Ventricular Tachycardia
Rate – variable from 140 to 250 beats per minute
P wave – absent or obscured by the QRS
Ventricular rhythm – usually regular but can be slightly irregular.
QRS – complex wide and bizarre >0.12 seconds in duration.
Significance – The rapid rate of this arrhythmia reduces ventricular filling time. Cardiac
output may drop due to the dissociation of atrial and ventricular activity. Patient is at risk
of cardiovascular collapse.
If patient unconscious, no signs of life –
attach AED as soon as possible and follow the prompts
Causes include –
 Hypoxia
 Electrolyte disturbances
 Myocardial infarction
 R on T phenomenon
 Coronary artery disease
Treatment – Treat as soon as possible, this rhythm can be a precursor to VF. Treatment
may vary depending on whether there is a palpable pulse (often difficult to find) or patient
is conscious or unconscious.
 Amiodarone
 Lignocaine
 Potassium
 Magnesium
Think – Is there a pulse? Is the patient haemodynamically stable?
If it is a wide complex it is VT until proven otherwise.
Defibrillation and the AED, A guide to education and competency
Revised Jan 2008-
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Rhythm strip – Ventricular Tachycardia
(Diagnosis should be made from the rhythm strip or the viewer on the AED. An ECG is not
required to diagnose unconscious/pulseless VT)
ECG – Ventricular Tachycardia
Ventricular Fibrillation
Rate – undeterminable
P wave – cannot be determined
Ventricular rhythm – chaotic irregular
QRS – duration indiscernible
Significance – With VF the ventricles quiver rather than contract, they fail to pump blood
and cardiac output falls to zero. Course fibrillation indicates more electrical activity in the
ventricles than fine fibrillation. The fibrillation waves become finer as acidosis and
hypoxaemia develop.
Causes include –
 Myocardial infarction
 Untreated VT
 R on T phenomenon
 Electrolyte imbalance
 Acid base imbalance
 Electric shock
 Hypothermia
Treatment – Early defibrillation, direct current counter shock provides the best chance
of survival in patients with VF or pulseless VT.
Defibrillation and the AED, A guide to education and competency
Revised Jan 2008-
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Rhythm Strip – Ventricular Fibrillation
(Diagnosis should be made from the rhythm strip or the viewer on the AED. An ECG is not
required to diagnose VF)
ECG – Ventricular Fibrillation
3.4
Defibrillation Safety
Operators must be aware of the need for safety when using the AED.
Considerations include:
 The patient is unresponsive, not breathing and NO SIGNS OF LIFE
 The use of AED in children (below 8yrs/40kgs) requires special pads
 Adult pads cannot be cut down to a smaller size
 There should be no contact with patient (by anyone) during defibrillation
 Check pad area for jewellery, ECG electrodes, pacemaker (if pacemaker
present adjust pads) and medication patches
 Think about conductive surfaces (water, fluids, metal)
 Explosive environment (oxygen, gases, fumes)
 Do not operate in an unstable environment which may prevent the AED from
performing a valid assessment of the ECG signal (eg. Rapidly moving vehicle)
 Respond to all prompts within safety constraints.
 Make sure all personnel are clear of the patient during analysis and prior to
initiating a shock.
 Cellular phones, radios or other devices that emit electrical signals can
interfere with the analysis of the AED and their use should be discorouged
within 6 feet.
Defibrillation and the AED, A guide to education and competency
Revised Jan 2008-
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3.5


Procedure
Collapsed patient
Remember chain of survival
To get help
to buy time
to restart heart
to stabilise
Sourced from: http://www.padprograms.com/images/chainofsurvival.jpg














Access emergency response system
Open the airway
Give 2 initial breaths if not breathing normally
Start chest compressions (30 compressions to 2 breaths)
Turn on AED
Attach pads to patient (taking care with positioning correctly)
Attach leads to AED (Remember, analysis of rhythm can take up to 20
seconds)
Respond to audible or visual prompts from AED
If shock advised ensure all personnel are clear (say aloud ‘STAND CLEAR’ and
visualise area to ensure no contact is being made with patient or bed).
Press shock button as indicated by AED
Continue to shock when prompted
Commence BLS
If shock not advised, check airway, breathing and circulation and continue BLS
Consider the rhythm may be asystole or Pulseless Electrical Activity (ElectroMechanical Dissociation), which means BLS, is vital to sustain life.
Defibrillation and the AED, A guide to education and competency
Revised Jan 2008-
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An Example of
Basic Life Support Flow Chart
Collapsed Patient/Victim
(Adapted from Ballarat Health Services Flowchart)
Check for DANGER
YES
Continual
observations until help
arrives
Responsive to
Talk & touch?
NO
Send for HELP
emergency buzzer
Dial <insert number>
Send for AED
AIRWAY
Look for obstruction
Clear-suction
Open-chin lift/head tilt
&/or jaw thrust
YES
NO
BREATHING?
Look - Listen Feel
Breathing adequately
Not breathing or not
breathing normally
YES
Recovery Position
continual observations
until help arrives
Deliver TWO BREATHS
 Open airway
 100% oxygen
attached
CIRCULATION
quickly re/assess
Are signs of life
present?
NO
Commence 30 chest
compressions followed
by 2 breaths


Attach AED / Manual
Defibrillator as soon
as available
CONTINUE CPR until
signs of life return
an advanced life support provider instructs
you to pause / stop
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AN EXAMPLE OF
AUTOMATIC EXTERNAL DEFIBRILLATOR (AED) FLOWCHART
(Adapted from Ballarat Health Services Flowchart)
Commence Basic Life Support
Send for help and
AED
Attach AED
Recovery position,
continual observation
until help arrives
Follow AED prompts
YES
Follow prompts
Visual sweep area call out
“stand clear” when all is clear
NO
YES
Shock
Advised?
Signs of life
present?
press the shock button
NO
Commence 2 mins of CPR
immediately
after delivery of shock
Continue to follow AED prompts
Defibrillation and the AED, A guide to education and competency
Revised Jan 2008-
Commence CPR
Page 17 of 28
EXAMPLE OF A COMPETENCY ASSESSMENT FORM (Based on Ballarat Health Services
Centre for Nursing and Health Education Competency Assessment Form, Cardiopulmonary
Resuscitation - CPR )
To successfully complete this assessment the participant must demonstrate/describe all starred
*criteria in correct sequence ,and without prompt.
Please tick appropriate column:
Code: D - Demonstrated ND - Not Demonstrated P - Prompt
Item
Competency Element
Performance Criteria
1.
D – Danger
2.
R - Response
3.
Response noted
*Check environment: for hazards to
self and victim
*Talk and Touch: Place hands on victims shoulders and give
verbal command
*Lateral Recovery position until help arrives, continual
observation
4.
No response
5.
A - Airway
6.
B -Breathing
7.
Patient breathing
adequately
Patient Not breathing
normally
D
P
*Send for Help & AED if available
note time
*Assess, clear and open victims airway:
Inspect oropharynx, if foreign material present lateral position
or head to side and suction
May remove visible material with finger if victim is >1yrs
Open airway: perform head tilt/chin lift &or jaw thrust
according to victims age & size
*Look, Listen & Feel for signs of breathing:
Look for rise and fall of chest, listen for respiratory effort,
feel for air escape.
Lateral Position : observe continuously until help arrives
* Administer 2 effective breaths :
1 inspiration per second, ensure chest rises with each inflation
C – Circulation/Compression
*Observe for signs of life: i.e. responsive, breathing
normally and moving
If the carotid pulse is palpated spend no longer than 10
seconds determining the presence of a pulse
Signs of life present
Lateral Position: apply oxygen, ensure adequate breathing &
observe continually until help arrives
9.
No signs of life present
*Commence chest compressions immediately
10.
Chest Compressions
11.
Compression Ventilation
ratio: Adults
*Adequate chest compressions
Hand position on lower half sternum (centre chest)
Depth 1/3rd of chest (adult 4-5cm)
Rate 100 min
* 30 compressions to 2 inflations 1 or 2 operators
pause for ventilation until airway secured (ETT or LMA)
12.
Automatic External
Defibrillator (AED)
8.
ND
* BLS until defibrillator arrives
*Attach AED immediately when available
turn defibrillator on
apply defibrillator pads
plug in connector and follow voice prompts
if a shock is indicated
*visual sweep the area, checking all staff are clear &
call out “stand clear” before pushing the shock button
* Immediately commence CPR for 2 mins after shock is
delivered
Follow prompts and deliver shocks as prompted & continue
CPR until signs of life are present
Defibrillation and the AED, A guide to education and competency
Revised Jan 2008-
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NA
Item
Competency Element
Performance Criteria
13.
Recovery Check
CPR is continued until signs of life are present: i.e.
coughing, breathing, moving, responsive
14.
Discuss Change
of Operator
“Change” with second person every two mins
after 5 cycles with 30:2 ratio
15.
Recovery
16.
Paediatric Considerations
Return of spontaneous circulation and respirations.
Place victim in lateral recovery position, apply oxygen &
observe until help arrives
Airway management
Infant: head neutral position. Support jaw with chin lift &
without applying pressure on soft tissue.
Child: manage as per adult
Breathing
Discuss/Describe CPR
technique when dealing
with a infant / child
D
ND
P
Infant /Child: inflations adequate to see chest
rise
Circulation
Compression Ventilation
ratio: Infant & child
Infant : check signs life ( If pulse palpated brachial or
femoral no longer 10secs)
Child: check for signs of life (if pulse palpated, carotid no
longer than 10secs)
Compressions
lower half sternum, 1/3rd depth chest, rate 100/min
Infant: 2 fingers, 1& 2 operators
small infant & two operators two thumbs
Child: one or two hands
30 compressions to 2 inflations 1 or 2 operators
15 compressions to 2 inflations 2 operators in hospital setting
(bag-valve-mask & oxygen)
17.
Documentation
Documentation of relevant information
Comment:_____________________________________________________________________
_____________________________________________________________________________
Result:
Achieved Competency 
Re-assess 
Participant Signature: _______________________________________________
Assessor Signature:
________________________________________________
Defibrillation and the AED, A guide to education and competency
Revised Jan 2008-
Page 19 of 28
NA
TABLE OF BASIC LIFE SUPPORT FOR ADULTS, CHILDREN AND INFANTS
(Adapted from Ballarat Health Services)
AIRWAY
NEONATE
(Birth to
28 days)
No head tilt, jaw
support, clear
nose & mouth
carefully
CHILD
1-8
YEARS
No head tilt, jaw
support
Clear nose and
mouth
Slight head tilt
( á amount
required
with age) and
jaw
support
ADULT
>8
YEARS
Full head tilt and
jaw
support
INFANT
<1
YEAR
ECC
COMP RATE
PER
MINUTE
COMP :
VENTILATIO
N RATE
ALS EAR
with ETT
OR LMA
Brachial or
Apical
Encircle the chest
with both hands.
The thumbs
compress the
sternum anteriorly
1/3 depth of
chest Approx
2cm
120
compressions
per minute
3:1
(1 or 2 resc)
1 inflation
every 2
seconds
Brachial
or Femoral
Compression with
2 fingers or 2
thumbs
1/3 depth of
chest Approx
2cm
100
compressions
per minute
15:2 ( 2 resc)
30:2 (1 resc)
~10
breaths per
minute
Carotid
Compression with
1 or 2 hands
1/3 depth of
chest Approx
2-3cm
100
compressions
per minute
15:2 ( 2 resc)
30:2 (1 resc)
~10
breaths per
minute
Carotid
Compression with
2 hands
1/3 depth of
chest
4-5cm
100
compressions
per minute
30:2
(1 or 2 resc)
8-10
breaths per
minute
PULSE
CHECK
METHOD OF
COMPRESSION
Pregnant Woman - tilt pelvis
to the left
Defibrillation and the AED, A guide to education and competency
Revised Jan 2008-
Page 20 of 28
SECTION 4
DRUG ADMINISTRATION
All drugs given in an arrest situation should be checked by two suitably qualified
personnel and ordered by a Medical Practitioner.
4.1
Modes of Administration
Intravenous:
 two large bore cannulae, inserted in the upper limbs. Lower limbs should be
avoided due to the impairment of venous return
 flush the IV line with at least 20mls of normal saline following
administration of drug. This will enhance the drug delivery
 where a central line access is available, this should be the preferred route of
administration.
Endotracheal tube:
 when other routes are not immediately available in an arrest situation, the
ETT is indicated for the administration of adrenaline, atropine, lignocaine and
naloxone.
 dose should be 2-3 times the normal IV dose and made up to 10 mls with
water for injection
 technique –
 suction the airway
 insert a clean suction catheter (cut off the ‘y’ connector to enable
the syringe to be fitted) beyond the tip of the ETT
 instil the medication and give at least two vigorous ventilations to
spread the solution over the area of mucosa.

ADRENALINE, ATROPINE, LIGNOCAINE AND NALOXONE MAY BE GIVEN VIA
THE ETT OTHER DRUGS MUST NOT BE GIVEN VIA THE ETT AS THEY MAY CAUSE
MUCOSAL INJURY AND BRONCHIAL DAMAGE.
Intraosseous:
 vascular access when cannulation of a vein is unsuccessful or not possible
 sites:
 up to 3years of age – proximal tibia (1-2cm inferomedial to tibial
tuberosity) or distal femur in the midline (approx 3cm above the
condyles)
 any age – medial malleolus of the tibia (just above the ankle)
 The distal femur and sternum should not be used.
Defibrillation and the AED, A guide to education and competency
Revised Jan 2008-
Page 21 of 28

recommended intravenous rates for drugs and fluids can be administered
via the intraosseous route and reach the central circulation in equivalent
times.
 any fluid or drug that can be administered intravenously can be
administered through the intraosseous route. Strong alkaline and hypertonic
solutions should be diluted before use.
 site may be resistive to flow, use a 3 way tap and syringe (infusion pump
may alarm occluded) and administer under pressure
 contra-indications
 Absolute
 osteogenesis imperfecta
 osteoperosis
 Relative
 limb is traumatised
 fracture
 infection
Defibrillation and the AED, A guide to education and competency
Revised Jan 2008-
Page 22 of 28
4.2
Key Drugs Used in a Cardiac Arrest
DRUG
ADRENALINE
*adrenaline and
sodium
bicarbonate are
incompatible
AMIODARONE
*incompatible
with saline
ACTION
 acts on 3 receptors in
the body – alpha, beta
1 and 2
 alpha causes
peripheral
vasoconstriction and
increases aortic root
pressure, this in turn
increases coronary
artery perfusion
 beta 1 increases
heart rate
 beta 2 causes
bronchodilation
INDICATION
 VF after initial
counter shocks
have failed
 Asystole and
EMD/PEA as initial
treatment
 anaphylaxis
STRENGTH
 1:10,000
1mg per 10ml
(minijet)

1:1000 1mg
per ml
(ampoule)



150mg in
3mls
Class 111
antiarrhythmic drug
that prolongs
conduction time. It
prolongs the action
potential and refractory
period in the atria, AV
node and ventricles
 Increases coronary
blood flow
 Reduces cardiac
oxygen requirements
 Suppresses ectopic
pacemaker
Treatment for
resistant
ventricular
arrhythmias (after
DCR and
adrenaline has
failed)
 Used in atrial
flutter/fibrillation/
Wolfe ParkinsonWhite syndrome
Defibrillation and the AED, A guide to education and competency
Revised Jan 2008
STANDARD DOSE
 IV 1mg bolus
every 3 to 5 minutes
in an arrest
 ETT instil 2 to 2.5
times the IV dose (2
to 2.5mg of 1:10,000
solution in 10mls)
 May be followed
by infusion to 20
microgram per
minute by dedicated
central line
ADVERSE EFFECT
 Tachyarrhythmia’s
 Severe hypertension
post resuscitation
 Tissue necrosis if
extravasation occurs
 Anxiety
 Fear
 Restlessness
 Tremor
 Dyspnoea
 Palpitations
 Coldness of extremities
 Pallor
 Sweating
 Nausea
 Vomiting





unstable rhythm
300mg may be
diluted in 20ml of
5%dextrose
administered over
30minutes and in
arrest cases given
over 1-2minutes
 can be repeated
once at half the dose
i.e. 150mg
 may be followed
by infusion 15mg per
kilogram over 24
hours
Page 23 of 28
Severe bradycardia
Ventricular arrhythmia
Severe hypotension
Thyroid and liver
dysfunction
 Peripheral neuropathy
 Reversible benign
yellowish-brown corneal
deposits
 Skin photosensitivity
 Contra indication in
pregnancy/lactation/brady
cardia/AV blocks/thyroid
disease
 Increased risk of R on T
DRUG
ATROPINE
ACTION
 Anticholinergic
(parasympathetic
blocking agent) The
blocked
parasympathetic
nervous system leads
to unopposed
sympathetic response
resulting in increased
heart rate and blood
pressure
 Stimulates
respiration inhibits
micturition
 Reduces
gastrointestinal motility
 Reduces the
production of sweat,
saliva and other
secretions
INDICATION
 Bradyarrhythmi
as with
haemodynamic
compromise,
increases heart
rate by blocking
the vagal stimulus
 To increase
heart rate of
patient with
bradyarrhythmias
 In asystole
resistant to
standard
treatment
STRENGTH
 1mg in
10mls
100microgram
per ml (minijet)
 600microgra
m ampoule
STANDARD DOSE
 bolus 1mg
to maximum of 3mg.
ADVERSE EFFECT
 Tachycardia (increasing
myocardial oxygen
demand)
 Hypertension
 Palpitations
 Arrhythmias
 Flushing and dryness of
skin
 Urinary retention
 Restlessness
 Confusion
 Excitement
POTASSIUM



10mmol
(0.75g) in
10mls



10mmol in
100mls for IV
infusion
Low serum
potassium
especially in
conjunction with
digoxin therapy
and
hypomagnesemia
may lead to life
threatening
ventricular
arrhythmias
an electrolyte
essential for membrane
stability
persistent VF in
the setting of
diuretic use
without potassium
supplement
 documented
hypocalcaemia
 digoxin toxicity
precipitated by
loss of potassium
 diabetic
ketoacidosis
Defibrillation and the AED, A guide to education and competency
Revised Jan 2008
5mmol IV, (dilute
if possible) in an
arrest situation
Page 24 of 28
sudden increase in
plasma potassium
concentration which may
lead to cardiac arrest and
death
 inappropriate use will
lead to hyperkalaemia
 extravasation may lead
to tissue necrosis
DRUG
ISOPRENALINE
For use when no
pacemaker facility
available
LIGNOCAINE
*2nd line
antiarrythmic –
use Ammiderone
first
Use lignocaine
only if ETT only
route of drug
administration
ACTION
 synthetic
sympathomimetic
related to adrenaline
 Potent beta
adrenoceptor stimulant
 Increases the heart
rate and stroke volume
and therefore cardiac
output
 Increases peripheral
vasodilatation resulting
in lower diastolic BP,
may slightly increase
the systolic BP
 Relaxes (bronchiol)
smooth muscle causing
bronchodilation
INDICATION
 Emergency
treatment for
bradyarrhythmias
associated with
circulatory
impairment, not
responding to IV
atropine or when
pacing is not
available
STRENGTH
 1mg in 5ml
ampoule
(1 in 5000)
STANDARD DOSE
 200mcg (1ml)
diluted in 10ml of
N/Saline (1ml =
20microgram)
 initial dose
20microgram IV
increments of
20microgram given
at 2 minute intervals
until adequate
perfusion is attained
or heart rate 90bpm
or arrhythmia
develops
 infusion: 1mg of
Isuprel added to
100ml of 5%
dextrose vial infusion
pump
ADVERSE EFFECT
 tachycardia
 hypotension
 palpitations
 anginal pain
 nervousness
 tremors
 vomiting
 flushing
 sweating
 dry mouth
 headache
 dizzyness
 weakness
















antiarrhythmic agent
for treatment of
ventricular arrhythmias
 class 1b
 acts on sodium
channel
 effective in
suppressing
arrhythmias associated
with depolarisation (eg.
Ischaemia, digoxin
toxicity)
 relatively ineffective
against arrhythmias
occurring in normally
polarised tissues
 half life 1 hour
treatment or
prophylaxis of
ventricular
arrhythmias and
tachycardia
associated with
acute myocardial
infarction and
following cardiac
arrest
 when
adrenaline and
DCR have failed
 increases
defibrillation
threshold
Defibrillation and the AED, A guide to education and competency
100mg per
10ml (minijet)
 1g ampoules
for infusion
(1gram in
10mls)
*2gram
ampoules
discontinued by
Astra
Revised Jan 2008
1mg per kg initial
dose consider
following with by
0.5mg per kg
 it is not
recommended to
commence an
infusion until return
of spontaneous
circulation.
Page 25 of 28
nervousness
dizzyness
blurred vision
tinnitus
tremor
drowsiness
muscle twitching
convulsion
nausea and vomiting
bradycardia
hypotension
respiratory and/or
cardiac arrest
DRUG
MAGNESIUM
 low serum
magnesium may
be caused by
diuretic use,
severe diarrhoea
and alcohol
abuse
 hypomagnese
mia causes
myocardial
hyperexcitability,
particularly in
the presence of
hypokalemia and
digoxin toxicity
hypomagnesemia
may be present in
up to 20% of
patients
hospitalised with
another
electrolyte
disorder
ACTION
 an essential
electrolyte
CALCIUM
CHLORIDE

*seldom indicated
Essential for normal
muscle and nerve
activity
 It transiently
increases myocardial
excitability and
contractility and
peripheral resistance
INDICATION
 torsades de
pointes
 arrhythmias
associated with
digoxin toxicity
and hypokalemia
 ventricular
arrhythmias
where
conventional
measures have
failed
 cardiac arrest
(from refractory
VT and VF) when
other measures
have failed
STRENGTH
 10mmol
(2.47gms) in
5ml ampoules
(10mmol of
magnesium)


Treatment of
arrhythmias or
hypotension
associated with
hyperkalemia,
hypocalcaemia,
overdose of
calcium channel
blocking drugs
Defibrillation and the AED, A guide to education and competency
STANDARD DOSE
 cardiac arrest
(resistant VF)
recommended dose
5mmol bolus IV,
ADVERSE EFFECT
 excessive use may lead
to muscle weakness,
paralysis and respiratory
failure
 flushing
 sweating
 hypotension
 sinus bradycardia
 flaccid paralysis
 circulatory collapse
1 gram in
10ml (10%)
7mmol calcium
chloride



10 to 20mls of 10%
calcium gluconate

5mmol =
2.5mls of 50%
magnesium
sulphate
or
5mls of 20%
magnesium
chloride
Revised Jan 2008
1gram in
10mls (10%)
calciulm
gluconate
5 to 10 mls of
10% calcium chloride
Or
Page 26 of 28
it may increase
myocardial and cerebral
injury by mediating cell
death/extravasation
produces tissue necrosis
DRUG
SODIUM
BICARBONATE
Not commonly
used, need
Arterial Blood Gas
results
ACTION
 alkalinising solution
which combines with
hydrogen ions to
produce CO2 and H2O
 theoretically it
reverses the metabolic
acidosis associated with
tissue hypoxia in cardiac
arrest
INDICATION
 treatment of
documented
metabolic acidosis
 protracted
arrest (greater
than 15minutes)
 forced alkaline
diuresis in acute
poisoning from
weakly acidic
drugs
(barbiturates, iron
salts or
salicylates)
resulting in
decreased renal
absorption
 widened QRS in
tricyclic overdose,
the sodium ion
reverses the
tricyclic-induced
block of the cell
membrane of the
sodium channel
Defibrillation and the AED, A guide to education and competency
STRENGTH
 50mmol in
50ml (minijet)
 100mmol in
100mls
Revised Jan 2008
STANDARD DOSE
 initial bolus of
1mmol per kg given
over 2 to 3 minutes,
then as guided by
arterial blood gases
Page 27 of 28
ADVERSE EFFECT
 alkalosis with skeletal
muscle and cardiac
irritability
 apathy and mental
confusion
 cellulitis and ulceration
due to extravasation
 (high dose)
hypokalaemia
 sodium overload
 paradoxical CNS acidosis
 potassium shift
intracellularly, lowering
serum potassium
 large sodium load,
particularly dangerous in
renal failure and severe
cardiac failure
 rebound respiratory
acidosis
REFERENCES
Australian Resuscitation Council Guidelines, http://www.resus.org.au/
Defibrillation and AED Use, Agilent Technologies
Defibrillation Training Course (Workbook), Surf Life Saving Australia (The life of the beach)
Version 2, December 2003
Smart, J. Ed. Paediatric Handbook 6th Edition 2000 Royal Children’s Hospital, Melbourne,
Blackwell Science Asia Pty Ltd
The Royal Melbourne Hospital, Emergency Department, Advanced Cardiac Life Support
Learning Package 2000
Tortora, G.T and Grabowski, S.R. 1996 Principles of Anatomy and Physiology 8 th Ed. Sydney:
Harper Collins.
http://medlib.med.utah.edu/kw/ecg/image_index/index.html#Vtachy
http://medlib.med.utah.edu/kw/ecg/index.html
http://www.cc.utah.edu/~mda9899/CPRTable.html
SUGGESTED FURTHER READING:
Finn, J.C. and Jacobs, I.G. 2003 Cardiac arrest resuscitation policies and practices: a survey
of Australian hospitals. Medical Journal of Australia (MJA) 179: 470-474
Jacobs, I., et al 2003 Energy Levels for Biphasic Defibrillation, An Advisory Statement from
the Australian Resuscitation Council.
Kenward, G., Castle, N. and Hodgetts, T.J. 2002 Should ward nurses be using automatic
external defibrillators as first responders to improve the outcome from cardiac arrest?
Asystematic review of the primary research. Resuscitation vol 52, issue 1, pp31-37
Liddle, R., Davies, C.S., Colquhoun, M. and Handley, A.J. 2003 ABC of Resuscitation: The
automatic external defibrillator. British Medical Journal (BMJ) 327:1216-1218
Resuscitation Council UK, The use of Automated External Defibrillators
http://www.resus.org.uk/pages/aed.pdf
Royal College of Nursing Australia 2006 Position Statement: The Role of Nurses in the
Management of Cardiorespiratory Arrest
http://www.rcna.org.au/UserFiles/role_of_nurses_in_the_management_of_cardio_respiratory
_arrest_revised_2006.pdf
Woolard, M., Whitfield, R,. Smith, A., Colquhoun, M., Newcombe, R.G., Vetter, N. and
Chamberlain, D. 2004 Skill acquisition and retention in automated external defibrillator (AED)
use and CPR by lay responders: a prospective study Resuscitation vol 60, pp 17-28.
Defibrillation and the AED, A guide to education and competency
Revised Jan 2008
Page 28 of 28