ALS Manual 2010.version 1

INFORMATION MANUAL
FOR
ALS TRAINING PROGRAMME
ALS Information Manual PAH 2010

1
CONTENTS
INTRODUCTION 6
1 PREREQUISITES 7
1.1 LEARNING GOALS 7
PRIOR TO WORKSHOP 8
1.2 LEARNING OUTCOMES / OBJECTIVES 8
1.3 THE RAPID RESPONSE TEAM 9
CRITERIA FOR CALLING THE RAPID RESPONSE TEAM
1.4 ROLES AND RESPONSIBILITIES OF THE ARREST TEAM AND ALS COMPETENT STAFF 10
MEMBER
2.0 AIRWAY MANAGEMENT 12

OXYGENATION, VENTILATION AND AIRWAY MANAGEMENT OVERVIEW 12
2.1 PHARYNGEAL AIRWAYS 12
Oropharyngeal Airways 12
Technique for insertion 12
Special considerations 13
The Nasopharyngeal Airway (Nasal Trumpet) 13
Technique for insertion 13
Special considerations 14
2.2 MANUAL RESUSCITATION BAGS (MRBs) 14
2.3 LARYNGEAL MASK AIRWAY 15
2.3.1 POTENTIAL PROBLEMS 16
2.4 TRACHEAL INTUBATION 17
2.4.1 Indications for Intubation 17
2.4.2 Intubation Technique 18
2.4.3 Cricoid Pressure 20
2.5 ENDOTRACHEAL SUCTION 21
2.6 MECHANICAL VENTILATION DURING CPR 21
2.7 AUTOMATIC TRANSPORT VENTILATION (ATV) 21
2.8 TRACHEOSTOMY PROBLEMS 22
REFERENCES 23
3.0 CARDIAC RHYTHMS 24

3.1 LETHAL ARRHYTHMIAS 25
3.1.1 VENTRICULAR FIBRILLATION 25
Delivery of a Precordial Thump 25
Treatment 25
Causes of Ventricular Fibrillation 26
3.1.2 VENTRICULAR TACHYCARDIA 27
Treatment 27
3.1.3 TORSADES DE POINTES 28
Treatment 28
Causes 28
3.1.4 ASYSTOLE 29
Treatment 29
3.1.5 VENTRICULAR STANDSTILL 30
Treatment 30
3.1.6 PULSELESS ELECTRICAL ACTIVITY (PEA) 31
Treatment 31
Causes 31
3.2 BRADYARRHYTHMIAS 32
Treatment 32
Causes 32
3.3 TACHYARRHYTHMIAS 33
Supra-Ventricular Tachyarrhythmia 33
Treatment 33
Causes 33
3.4 COMPLETE AV BLOCK / COMPLETE HEART BLOCK 34
Treatment 34
Causes 34
2
3.5 IDIOVENTRICULAR RHYTHM 36

Treatment 36
ASYMPTOMATIC 36
Causes 36
Rapid Idioventricular Rhythm 36
Treatment 37
3.6 PACED RHYTHM 38
SPECIAL NOTES 39
Recommended readings 39
4.0 DEFIBRILLATON 40
INTRODUCTION 40
4.1 TWO METHODS OF DEFIBRILLATION 40
EXTERNAL DEFIBRILLATION 40
INTERNAL DEFIBRILLATION 40
4.2 SAFETY PRINCIPLES OF DEFIBRILLATION 41
4.3 EMERGENCY DEFIBRILLATION 42
COMPLICATIONS OF DEFIBRILLATION 42
4.4 SYNCHRONIZED DEFIBRILLATION / CARDIOVERSION 43
INDICATIONS FOR CARDIOVERSON 43
SAFETY PRINCIPLES OF ELECTIVE CARDIOVERSION 43
POST PROCEDURE 44
4.5 Types of Defibrillator’s at PAH 44
5.0 CARDIAC PACING 45

Modes of Pacing 45
Indications for Emergency Cardiac Pacing 45
Routes for Temporary Pacing 45
5.1 EXTERNAL / TRANSCUTANEOUS PACING 46
Method 46
5.2 MODES OF PACING 47
5.2.1 DEMAND MODE 47
5.2.2 FIXED MODE 47
5.2.3 PACED RHYTHM 47
Characteristics of Paced Rhythm 47
5.3 SAFETY ASPECTS OF PACING 48
5.4 COMPLICATIONS OF PACING 48
5.5 TROUBLE SHOOTING PROBLEMS 49
5.5.1 FAILURE TO PACE 49
5.5.2 FAILURE TO CAPTURE 50
5.5.3 FAILURE TO SENSE 51
5.5.4 OVERSENSING 52
5.6 DOCUMENTATION OF PACING 53
6.0 PHARMACOLOGY 54
6.1 INTRAVENOUS DRUG ADMINISTRATION 54
6.2 ENDOTRACHEAL DRUG ADMINISTRATION 54
6.3 OXYGENATION 55
6.4 ADRENALINE 56
Action 56
Half-Life 56
Indications 56
Dose 56
Adverse Effects 56
Precautions 56
6.5 ATROPINE 57
Action 57
Half-Life 57
Indications 57
Dose 57
3
Adverse Effects 57
Precautions 57
6.6 LIGNOCAINE 58
Action 58
Half-Life 58
Indications 58
Dose 58
Adverse Effects 58
Precautions 58
6.7 AMIODARONE 59
Action 59
Half-Life 59
Indications 59
Dose 59
Infusion 59
Adverse Effects 59
Precautions 59
Drug Interactions 59
6.8 POTASSIUM 60
Action 60
Indications 60
Dose 60
Adverse Effects 60
Precautions 60
6.9 MAGNESIUM SULPHATE 61
Action 61
Indications 61
Dose 61
Adverse Effects 61
Precautions 61
6.10 SODIUM BICARBONATE 62
Action 62
Indications 62
Dose 62
Adverse Effects 62
Precautions 62
6.11 CALCIUM CHLORIDE 63
Action 63
Indications 63
Dose 63
Adverse Effects 63
Precautions 63
6.12 OTHER EMERGENCY DRUGS 64
6.12.1 ISOPRENALINE 64
Action 64
Indications 64
Dose 64
Adverse Effects 64
Precautions 64
6.12.2 ADENOSINE 65
Action 65
Half-Life 65
Indications 65
Dose 65
Adverse Effects 65
Precautions 65
6.12.3 SALBUTAMOL 66
Action 66
Indications 66
Dose 66
Adverse Effects 66
4
6.13 NEUROMUSCULAR BLOCKERS 67
6.13.1 SUXAMETHONIUM 67
Action 67
Half-Life 67
Indications 67
Dose 67
Adverse Effects 67
Precautions 67
6.13.2 VECURONIUM 68
Action 68
Half-Life 68
Indications 68
Dose 68
Adverse Effects 68
Precautions 68
ADULT ALS ALGORITHM FLOWCHART 69
7.0 ADULT ALS ALGORITHM 70

7.1 INITIAL MANAGEMENT OF CARDIAC ARREST 70
7.2 MANAGEMENT OF SPECIFIC ARRYTHMIAS 71
Ventricular Fibrillation / Pulseless Ventricular Tachycardia (VF/VT) 71
8.0 MANAGEMENT AFTER CARDIAC ARREST 73

8.1 POST ALS ALGORITHM 74
8.2 CRITICAL INCIDENT DEBRIEFING 75
9.0 SPECIAL CASES PREGNANCY 76

9.1 PHYSIOLOGICAL CHANGES IN PREGNANCY 76
9.2 CAUSES OF CARDIOPULMONARY ARREST IN PREGNANCY 77
9.3 FACTORS AFFECTING RESUSCITATION IN PREGNANCY 78
9.4 OTHER CONSIDERATIONS 79
PAEDIATRIC CARDIORESPIRATORY ARREST ALGORITHM FLOWCHART 80
REFERENCES AND FURTHER READINGS 81
5
INTRODUCTION
This information package is specifically designed for medical staff at Registrar and Senior House
Officer level and nursing staff currently employed in Critical Care areas of the Princess Alexandra
Hospital.
Nursing staff from the Coronary Care Unit, the Intensive Care Unit, the Cardiac-Surgical Unit, the
Cardiac Catheter Laboratory, the Anaesthetic and Post Anaesthetic Care Unit, Trauma HDU and the
Emergency Department are able to achieve the Advanced Life Support (ALS) Competency, after they
have acquired 12 months experience in their critical care specialty and met the required knowledge /
skill levels.
The contents of this package describe the knowledge and skills required for the achievement of the
ALS competency. Each section covers the basic material and knowledge required but readers are
expected to undertake further readings relevant to their experience and background, to reinforce their
knowledge. Each section has selected references for recommended readings.
This manual was originally compiled in November 1994:

Revised in:
• March 1996
• June 1999
• August 2000
• September 2001
• April 2003
• June 2004
• August 2006
• June 2008
• January 2010
6
1 PREREQUISITES
Prior to attending the Advanced Life Support workshop, it is mandatory that nursing staff have the
knowledge and skills to perform the following advanced clinical skills:
• Cardiac Arrest Procedure including competency in Basic Life Support – Semi Automatic External
Defibrillator
• Cardiac Monitoring, Recognition and Treatment of Arrhythmias
• Defibrillation – demonstrate safe and appropriate defibrillation technique
• External Cardiac Pacing – demonstrate safe and effective external pacing.
1.1 LEARNING GOALS
PRIOR TO WORKSHOP
(a) Cardiac Arrest Procedure

Staff should be familiar with the Cardiac Arrest Procedure at the PAH. They should have
achieved competency in Basic Life Support (BLS) including the use of the Semi Automatic
External Defibrillator (SAED). Refer to the Policy and Procedure Manual.
(b) Airway Management

Staff should demonstrate the ability to perform intubation (medical staff) or assist with
intubation and be able to manage an intubated patient.
Staff should demonstrate effective manual ventilation techniques and be familiar with the
portable ventilators available at the PAH. Refer to Section 2.
(c) Cardiac Monitoring

Staff should be familiar with how to operate cardiac monitors used at PAH.
Staff should be able to recognise the arrhythmias described in Section 3 and outline the
management of each arrhythmia.
(d) Defibrillation
Staff should demonstrate defibrillation technique, including the use of semiautomatic external
defibrillators and outline the safety principles of defibrillation described in Section 4.
(e) Emergency Drugs

State the use, dosage and adverse effects of Adrenaline/Epinephrine, Atropine, Lignocaine,
Amiodarone, Calcium, Magnesium, Potassium and Sodium Bicarbonate. Refer to Section 6.
7
1.2 LEARNING OUTCOMES / OBJECTIVES
Staff competent in Advanced Life Support will be able to:
(a) State the emergency response procedure used at the PAH to advise of a Code Blue situation.
(b) Outline the responsibilities of nursing, medical and allied health staff during a Code Blue
situation.
(c) State the location of emergency equipment – oxygen, suction, defibrillator / monitor,
cannulation and intubation equipment.
(d) Demonstrate effective Cardiopulmonary Resuscitation techniques (basic life support

measures).
(e) Demonstrate recognition of lethal arrhythmias and state the management of each arrhythmia
according to the Australian Resuscitation Council Algorithm.
(f) Demonstrate recognition of other potentially life-threatening arrhythmias and state the
management of these arrhythmias.
(g) Demonstrate safe defibrillation techniques and describe the safety precautions used.
(h) Explain the indications for, the correct dose and the adverse effects of the primary emergency
drugs – Adrenaline, Atropine, Lignocaine, Amiodarone, Magnesium, Calcium, Potassium and
Sodium Bicarbonate.
(i) Describe / demonstrate the steps required for intubation of the patient.
(j) Discuss the indications for External Cardiac Pacing of the patient.
(k) Demonstrate knowledge of the pacing functions of External Pacemakers.
(l) Describe the management of the patient following a Code Blue situation.
(m) Outline the variations in management for the paediatric and for the pregnant patient.
(o) Identify the need for critical incident stress debriefing (CISD) and avenues for instigating CISD
at PAH.
8
1.3 THE RAPID RESPONSE TEAM
A Rapid Response Team call system is in place at the PAH. The Rapid Response Team is summoned
to any person (patient, visitor, and staff) who is in respiratory or cardiac arrest or has observations that
meet any of the deteriorating patient calling criteria. If doubt exists about the presence of respirations
or pulse, or if the patient meets the deteriorating patient criteria, CALL THE RAPID RESPONSE
TEAM – DIAL 666 throughout the hospital.
CRITERIA FOR CALLING THE RAPID RESPONSE TEAM RAPID RESPONSE TEAM (RRT)
Acute Change In Physiology

Airway Noisy Laboured Breathing
Breathing Respiratory arrest
Respiratory Rate < 8 bpm
Respiratory > 36 bpm
Fall in SpO2 <90%
Circulation Cardiac arrest
Pulse Rate <40
Pulse Rate >140
Fall in systolic Blood Pressure <90 mmhg
Significant blood loss
Neurology Sudden Fall in level of consciousness
Fall in GCS>2 points
Repeated or prolonged seizures
Other Any patient you are seriously worried about that does not
fit into the above criteria particularly with changing
parameters
To initiate a Rapid Response Team (RRT) call, dial 666 state “code blue” exact location and treating
team (if known). Further information regarding RRT call criteria is available in the Princess
Alexandra Hospital Health Service District Procedure Manual
EXCEPTIONS (AT THE PRINCESS ALEXANDRA HOSPITAL)
• ICU, CCU, ED, OT where the respective Registrar or Consultant is present and states that
adequate personnel are already available.
9
The procedure for conducting BLS is outlined in the Princess Alexandra Hospital Health Service
District Procedure Manual (Procedure No. 80031/v7/10/2009)
1.4 ROLES AND RESPONSIBILITIES OF THE RAPID RESPONSE TEAM AND THE
ALS COMPETENT STAFF MEMBER
The composition and skill mix of the team will vary from time to time but it is imperative that the
Medical Registrar or ALS competent staff member assumes the role of the team coordinator.
Team Coordinator:
• Undertakes clinical management of the resuscitation

• Co-ordinates personnel and delegates duties.
• Four tasks are assigned by the team leader at the start of the resuscitation:
1. airway and intubation management
2. chest compression
3. monitoring and defibrillation
4. intravenous access and blood sample collection
• Ensures that treatments proceed as per the ALS algorithms derived from the Australian
Resuscitation Council guidelines
• Assesses the need for additional personnel
• Ensures safety of patient and staff at all times
• Determines appropriateness of patient treatment in consultation with the appropriate clinicians
• Ensures that resuscitation documentation is completed
• Undertakes debriefing and staff counselling as necessary
Other medical staff:

• Provide assistance with the clinical management of the resuscitation under the direction of the team
coordinator
Ward nursing staff – Responsibilities:

• Ready the patient for BLS – SAED
• Summon help from ward staff – press yellow staff assist button
• Take the Ward Arrest Trolley, with the SAED, Drugs, portable suction and Manual Ventilation
Bag to the bedside
10
• Summon the Rapid Response Team – Dial 666
• Commence BLS procedures prior to the Rapid Response Team (RRT) arriving.
• Ensure that wall suction and oxygen is available
• Ensure that the Medical Records are at the bedside
• Inform the RRT of any ‘Biohazard Control Procedures’ that may be required
• Prepare and prime infusion line
• Maintain documentation of the sequence of events during the arrest
• Arrange for transport of urgent blood specimens
• Notify the patient’s clinical team
• Ensure Medical Officer notifies the patient’s relatives
• Co-ordinate care and debriefing of other patients and relatives at the scene
• A member of the ward staff must remain with the RRT throughout
Ancillary staff:
• Assist with patient transport
• Answer the ward telephone
• Be available to assist staff with any tasks as requested
11
2.0 AIRWAY MANAGEMENT
OXYGENATION, VENTILATION AND AIRWAY MANAGEMENT OVERVIEW
Maintaining the patient’s airway is the first priority and ventilation with 100% oxygen should be
commenced as soon as possible.
During cardiopulmonary arrest, placement of a tracheal tube is only to be performed by those trained
in tracheal intubation and advanced airway management. Maintenance of effective ventilation is
essential until a medical officer skilled in advanced airway management arrives. The principles of
basic life support airway maintenance should be observed initially:
i) Jaw thrust and chin lift (or lateral positioning of spontaneously breathing patient)
ii) Pharyngeal airway
iii) Laryngeal mask airway
iv) Manual resuscitation bag
v) Endotracheal intubation
2.1 PHARYNGEAL AIRWAYS
Oropharyngeal Airways
The oral pharyngeal (oropharyngeal) airway is a semi-curved, tubular device which when properly
positioned, holds the tongue forward of the posterior aspect of the pharynx. This prevents the tongue
from occluding the airway and allows ventilation to occur through the lumen of the tube and around
the airway.
The oropharyngeal airway is only needed in the patient with a depressed conscious state, impaired gag
reflex and loss of muscle tone, which results in airway obstruction. The chin-lift technique should be
used in conjunction with the airway if not contraindicated. Insertion of this device in a conscious or
semi-conscious patient, is likely to activate the gag reflex (when the back of the tongue or posterior
pharyngeal wall is touched) and precipitate vomiting.
Appropriate sizing of the device may be estimated at the bedside or in the field. Align the tube on the
side of the patient’s face and choose an airway that extends from the centre of the lips to the angle of
the mandible or to the bottom of the ear.
Technique for insertion:
There are two ways to position the oropharyngeal airway. The quickest method is to insert the device
upside down into the mouth. As soon as the distal end reaches the hard palate, the airway is gently
rotated 180o and slipped behind the tongue into the posterior pharynx.
The second technique for insertion of the oral pharyngeal airway requires a tongue blade. The tongue
is depressed and the airway is inserted right side up into the oral pharynx. With either technique, the
flange of the tube should sit comfortably on the lips if the device has been properly inserted.
12
Special considerations:
• Although the second technique (i.e. direct visualisation with the use of a tongue blade) may seem
intuitively easier, one must be sure that the airway is inserted deep enough so as to come to rest
behind the tongue. Unless careful attention is paid to doing this, it’s all too easy to stop short – in
which case the device may actually cause airway obstruction by pressing on the tongue and
pushing it back to occlude the airway.
• If the tube repeatedly comes out of the mouth, it is likely to be improperly seated (and compressing
the tongue into the posterior pharynx). This may further obstruct the airway. Don’t continue to
force the airway in. Remove it entirely and then try to insert it again.
• Although the lumen of the tube is adequate for ventilating the patient, it should not be used for
suctioning because the lumen is not large enough to allow passage of the suction catheter. The
suction catheter is instead inserted adjacent to the airway. Suction is then performed in the usual
manner.
• The head tilt/chin lift should not be attempted if a known or high suspicion of cervical spine injury
exists. Jaw thrust method can be used in this situation.
The Nasopharyngeal Airway
The nasopharyngeal airway is an extremely compliant rubber tube approximately 15cm in length. The
tube is designed so that its distal tip sits in the posterior pharynx while the proximal tip rests on the
external nares. The lumen of this device permits the passage of air into the lower respiratory tract.
Technique for insertion:
Correct sizing of a nasopharyngeal airway is achieved by measuring from the patient’s nare, to the tip
of the ear. It is important to size the tube prior to insertion to ensure a patent airway and to prevent
advancement into the oesophagus. The tube should be lubricated with 2% lignocaine gel prior to
insertion. The purpose of the lignocaine is two-fold. It anaesthetises the nasal mucosa in the posterior
pharynx (so as to minimise sensitivity of the gag reflex), and lubricates the tube to facilitate insertion.
Once inserted, a safety pin is attached to the end of the airway to prevent it migrating through the nare
and into the nasal passage. Care should be taken to ensure that pressure from the pin is not exerted
onto the nare.
The nasopharyngeal airway is then advanced into the nares by placing the bevel against the septum of
the nose and gently sliding the tube backward in line with the base of the ears. In that way the tube
passes parallel to the floor of the nasal cavity. When completely inserted, the distal end is seated in the
posterior pharynx.
Special considerations:
• Although in most cases proper insertion of the nasopharyngeal airway will result in correct
position of the distal end in the posterior pharynx, on occasion the tube may be too short or too
long. Be alert to the fact that if this happens, adequate ventilation may not be achieved.
• While most conscious or semi-conscious patients are able to tolerate this device, the gag reflex of
particularly sensitive individuals may still be activated.
13
• Forceful introduction of the airway into the nasal passage should be avoided, since this may cause
abrasions or lacerate the nasal mucosa and produce significant bleeding. Cautious use of nasal
airways in patients with deviated septum is warranted, to avoid nasal trauma and bleeding.
2.2 MANUAL RESUSCITATION BAGS (MRBs)
Manual Resuscitation Bag Ventilation
This is the preferred in-hospital technique for initial ventilation. It is recommended that 100% (15
litres) inspired oxygen is used as soon as possible during BLS and ALS.
When the patient resumes adequate spontaneous ventilation, oxygen administration should be
continued. Supplemental oxygen can be provided by any firmly fitting oxygen mask, but partial-
rebreathing or non-rebreathing systems deliver higher percentages of oxygen and are preferred.
Manual resuscitation bags (MRBs) are not designed to deliver oxygen to spontaneous breathing
patients. The one-way valve in the bag creates resistance that the patient must overcome to breathe in
oxygen rich gas. If the patient has adequate spontaneous respirations then oxygen administration by a
mask is more appropriate.
MRBs can be used to deliver intermittent positive pressure ventilation (IPPV) via a mask,
Endotracheal, Laryngeal Mask Airway or tracheostomy tube. MRBs consist of a self-inflating bag, a
non-rebreathing valve and a supplemental oxygen reservoir, which should always be attached during
CPR. The self-inflating bag allows breath delivery without a pressurised gas source, allowing the
initiation of IPPV when wall or portable oxygen is not immediately available.
Masks selected for resuscitation should be sized to provide an airtight seal for breath delivery. As a
general guide in female patients use a size 3-4, and for males, size 5-6 mask. Masks should be made of
transparent material to allow detection of regurgitation. An input oxygen flow rate of 15 litres per
minute should be secured from wall or cylinder oxygen.
Inexperienced operators may have difficulty providing a leak-proof seal to the face while ventilating
the patient and maintaining an open airway. Effective ventilation is best achieved when two rescuers
use these devices. One rescuer should hold the mask and one ventilate the patient by squeezing the
bag. This will promote more effective breath delivery as assessed by the adequacy of chest wall
movement.
Potential operators must be familiar with the methods of checking these devices as faulty operation
may cause barotrauma, hypoventilation or hypoxia. If there is a loose connection in the MRB, the self-
inflating bag can be compressed without gas being delivered to the patient. High pressure in the circuit
from jamming of the valves or too forceful manual ventilation can cause trauma to the patient’s lungs
and / or reduce venous return.
It is vital to know the detail of operating your MRB prior to a cardiac arrest situation. Make sure you
familiarise yourself with the breathing circuit utilised in your clinical area.
MRBs should always be available when transporting a ventilated patient post successful resuscitation,
to enable manual ventilation in the event of loss of pressurized gas supply.
14
• It is expected that to achieve Airway management competence, that the staff should be able
to assemble MRBs and understand the principle underlying the one-way valve mechanism.
• All staff should check their emergency equipment at the beginning of each shift and be
familiar with handling, assembling, operation and cleaning of departmental emergency
equipment.
Single rescuer bag mask ventilation Two rescuer bag mask ventilation
Bag Mask Ventilation

Images copyright: Kathy Mak June 2004
2.3 LARYNGEAL MASK AIRWAY (LMA)
The LMA is only used where intubating skills are not available or in the event of failed intubation.
The LMA is introduced into the pharynx and advanced until resistance is felt as the distal portion of the
tube locates in the hypopharynx. The cuff is then inflated, which seals the larynx, leaving the distal
opening of the tube just above the glottis, providing a clear airway. Please note that the airway is not fully
protected. The potential advantage of the LMA is that it can provide a clear and relatively secure airway
without the requirement for the skill of tracheal intubation. When correctly performed the insertion
technique is simple and non-traumatic. The LMA should only be used when the patient is:
• profoundly unconscious and unresponsive;

• without glossopharyngeal reflexes; and
• has an identified need for an artificial airway eg. cardiac arrest.2
The LMA may be inserted by those trained in its use. It is not a superior alternative to tracheal intubation.
Its use should be confined to those operators who do not possess intubation expertise and to patients in
whom immediate intubation is not possible for anatomical or other reasons.
The LMA provides a more secure and reliable means of ventilation than the facemask. It does not ensure
absolute protection against aspiration. Even when the LMA is inserted, a small proportion of patients
cannot be ventilated.
15
1 2
3 4
Laryngeal Mask Insertion

Images copyright: Janet Fong June 2004 (Adapted)
2.3.1 POTENTIAL PROBLEMS
Three problems may be anticipated during use of the LMA:
• difficulty with insertion

• air leak around the cuff during positive pressure ventilation
• pulmonary aspiration of gastric or pharyngeal contents.2
Difficulty with insertion in profoundly unconscious patients may be minimised by scrupulous attention to
use of the recommended technique. If a problem occurs, deflate the cuff, remove the LMA and try again
using another correctly prepared and deflated mask.2
Air leak around the cuff may occur in 10-15% of cases.2 In the majority the leak is small and acceptable,
provided the chest is seen to rise normally during inflation. If the leak is major, or the chest does not rise,
the cuff should be deflated and the mask repositioned.2
Aspiration of regurgitated gastric contents is possible with the LMA in situ. The incidence is small and
much less than occurs with the unprotected airway associated with other techniques. Regurgitation is
more likely to occur if the stomach has already been inflated by mouth-to-mouth, mouth to mask or
bag-valve-mask ventilation applied prior to insertion of the LMA.2 If regurgitation is suspected,
aspirate the hypopharynx prior to LMA insertion. Aspiration may also occur after mask removal.
Again, aspiration of the hypopharynx should be performed, preferably with the patient head down in
the lateral recovery position, before the cuff is deflated and the LMA removed.2
16
Preparation for use:
The LMA may be either disposable or reusable following autoclaving. The correct size is as follows:
SIZE 3 Small adult;
SIZE 4 Normal adult;
SIZE 5 Large adult.
If in doubt, choose a larger rather than smaller size.
Equipment:
1. 50 ml syringe (for cuff inflation)

2. Lubricant
3. Surgical or cotton tape
4. Bite block (rolled gauze)
Insertion and management of the airway can be achieved without items 2, 3, and 4 but they should be
available when possible. Fully deflate the cuff ensuing there are no folds near the tip of the LMA. Apply
lubricant only to the rear of the mask in the distal end of the tube (posterior surface).
2.4 TRACHEAL INTUBATION
Rationale
In the absence of an endotracheal tube (ETT), lung inflation pressures may be high enough to cause
gas to be forced into the stomach, resulting in gastric distension with subsequent risk of regurgitation
and aspiration of gastric contents into the lung.
2.4.1 Indications for intubation
As soon as practicable during the resuscitation (usually the second or third shock sequence or when
there is a medical officer present that is competent in intubation) the trachea should be intubated. The
advantages of endotracheal tube (ETT) placement include:
- Provides a definitive patent airway

- Isolates the airway reducing but not eliminating the risk of aspiration
- Allows the delivery of IPPV and high oxygen concentration
- Enables tracheal suctioning
- Provides a route for the administration of emergency drugs (Atropine, Lignocaine, Adrenaline,
Diazepam and Naloxone)
In addition, once an ETT is in place, ventilation need not be synchronised with chest compressions.
Rather, it should be performed asynchronously at 8-10 ventilations per minute.
In PULSELESS, witnessed and monitored Ventricular Tachycardia or Ventricular Fibrillation,

intubation should only be attempted after the initial sequence of 3 DC shocks has failed (or after
first shock with SAED if not witnessed and monitored).
In the difficult to intubate patient, the resuscitation team should be mindful that greater harm will be
caused by failure to ventilate than failure to intubate.
17
2.4.2 Intubation Technique
Prior to attempting intubation, all equipment should be quickly but thoroughly checked.
During endotracheal intubation the maximum interruption to ventilation should be 20 seconds.

Adequate ventilation and oxygenation must be provided between attempts.
Preoxygenate the patient with 100% oxygen prior to any intubation attempt.
Collect all necessary equipment:

- Suction source - occluding the suction tubing with suction turned on should result in a –ve 40
Kpa pressure change
- Yankauer suction device and suction catheter (size 12-14 G for adult sized ETTs)
- Laryngoscope - light source bright, bulb securely in position
- ETT - correctly sized for the patient; check cuff and valve integrity by inflating cuff with a
syringe filled with air – the inflated cuff should be concentric and not protrude over the tip of
the tube
- Introducer - ensure plastic coating intact; do not manipulate, allow MO to shape as required
- Bougie - long flexible introducer used as a guide for placement of ETT. Will be supplied by
ALS staff from CCU and ED
- Water soluble lubricant - apply on request from MO only
- Magill’s forceps - can be used to guide the position of the ETT into larynx or for removal of
foreign bodies
- 10ml syringe to inflate ETT cuff
- Tape to secure ETT
- End tidal CO2 detector (Oximax N-85)
Typical tracheal tube sizes are:

- Adult male 8.0 – 9.0
- Adult female 7.0 – 8.0
- Paediatric age + 4
4
Emergency intubation procedure:
• The patient should be positioned optimally to promote successful intubation. In an emergency

situation this can mean ensuring the patient is supine and placed at a height that allows the
operator optimal view of the vocal cords. A pillow or rolled towel underneath the shoulders (if
not contraindicated) may assist the view of the cords.
• Preoxygenate the patient with 100% oxygen
• The MO may request the application of Cricoid pressure (section 2.4.3)
• Laryngoscopy is performed. Direct laryngoscopy involves the use of a laryngoscope to view

the vocal cords, allowing placement of the ETT in the trachea.
In the emergency setting an introducer may be used to assist with placement of the tube through the
glottic opening. The introducer should not protrude beyond the end of the tube and is removed once
18
the ETT is placed in the trachea. The ETT should be positioned so that the cuff comes to rest beyond
the vocal cords and 2 cms above the carina.
• Inflate the cuff with the minimum amount of air required to obtain a seal.
• Ventilate the patient ensuring that the chest is rising and falling with each breath. Auscultate
the lung fields for the presence of breath sounds.
• Connection of the End-tidal CO2 detecting device between the ETT and manual ventilation
bag, verifying tube placement
• Secure the ETT using cotton tape. Note the position of the tube by recording the level of the
tube markings at the patient’s lips or teeth. For Example, 21 cm for a male, 23 cm for a female.
• A portable chest x-ray should also be performed after ROSC to confirm optimal ETT
placement.
Continual monitoring of oxygenation and ventilation is vital and is based on clinical assessment
including patient colour, chest wall movement and auscultating air entry.
End-tidal CO2 monitoring devices are used to assess tracheal tube placement. A failure to detect
carbon dioxide usually means that the tube is in the oesophagus. However, occasionally carbon dioxide
may not be detected in cardiac arrest patients with extremely low blood flow to the lungs or in those
with a large amount of dead space (eg. significant pulmonary embolism).
Oximax N-85 Portable bedside Capnograph Capnograph Tubing Connection

Images copyright: Nellcor 2006 (Adapted)
The Oximax N-85 Capnograph is a portable monitor that continuously monitors end tidal CO2 (mmHg),
respiratory rate, fractional inspired carbon dioxide, oxygen saturation and pulse rate. The monitor operates
on batteries or on AC power. Before using the monitor in the field, ensure that the battery pack is fully
charged.
Operation
Prior to start up:
• Slide open the FilterLine input connector shutter and connect the appropriate FilterLine
• Turn the monitor on by sliding the on/of switch to the on position. When turned on, the monitor
automatically performs a self test.
• Place the Filter Line between the Manual Resuscitation bag and the ETT.
• Monitor the end tidal CO2 (EtCO2) result displayed on the machine to ascertain ETT placement.
19
• EtCO2 monitoring should continue at all times while the patient is intubated to ensure the ETT is
not dislodged.
(Refer to Operators manual for further information)
Interpretation:
Successful placement of the ETT into the trachea will result in an EtCO2 measurement being obtained
(mmHg), as well as an appropriate waveform. If a failed intubation has occurred no EtCO2 will be
present and thus, a numerical value and waveform will be absent.
Pulse oximetry should be employed on return of spontaneous circulation (ROSC). A portable chest x-
ray should also be performed after ROSC to confirm optimal ETT placement.
NOTE: Paediatric tracheal tubes are uncuffed and require a small gas leak to be audible on
positive pressure ventilation. Paediatric resuscitation equipment is kept in Emergency
Department and Recovery.
2.4.3 CRICOID PRESSURE
Cricoid pressure or Sellick’s manoeuvre should be applied during a tracheal intubation sequence. The
Cricoid cartilage is a ring shape, not a ‘C’ shape like other tracheal rings. This shape allows
compression of the oesophagus between the Cricoid cartilage and the spine. Correctly applied, Cricoid
pressure prevents or controls passive gastric content regurgitation, minimizing the risks of pulmonary
acid aspiration. In addition it decreases gaseous filling of the stomach and may provide a clearer view
of the vocal cords during a difficult intubation.
Cricoid pressure should not be performed at any time where there is active vomiting or where there is
swelling of the front of the neck from recent trauma or if the anatomy is difficult to define. Cricoid
pressure should only be used when the patient is unconscious or drug paralysed, otherwise vomiting
may be stimulated.
Technique:
Firm symmetrical pressure is applied with the index finger and thumb on the anterolateral aspect of the
Cricoid cartilage, which is below the cricothyroid membrane. The effect is similar to applying
20
pressure against the bridge of one’s nose that causes discomfort, or pressure against one’s cricoid that
prevents swallowing. Pressure is not applied at the level of the Thyroid cartilage as this is ineffective,
distorts the entire larynx and makes ventilation and intubation more difficult. Cricoid pressure must
not be released until the medical officer performing the intubation requests its removal. This is usually
after cuff inflation of the ETT and correct tube placement has been confirmed by auscultation.
2.5 ENDOTRACHEAL SUCTION
To suction the tracheal airway, ensure the following:

• suction catheter to be no greater than half the diameter of the tracheal tube;
• suction pressure for adults to be between 100-150 mmHg (greater pressures may be needed,
depending on secretion consistency);
• suction time no greater than 10-15 seconds;
• pre and post oxygenation (100%);
• aseptic technique;
• observe patent response;
• observe hemodynamics, oxygenation/ventilation parameters.
2.6 MECHANICAL VENTILATION DURING CPR
Mechanical ventilators should not be used in the initial management of cardiac arrest in the
intubated patient. The patient should be manually ventilated with 100% oxygen. (ARC Policy
Statement 11.7)
Rationale: this gives the operator complete control of ventilation and helps discern a differential
diagnosis (eg. exclude tension pneumothorax and gas trapping).
In the event of insufficient available rescuers, a temporary alternative to this is to leave the patient
mechanically ventilated. This option should only be utilized until further assistance arrives.
• The oxygen setting should be increased to 100%, the pressure limit is increased to account for
increased peak inspiratory pressures generated with cardiac compressions, and the minute
ventilation should be appropriate for resuscitation (e.g. in the adult patient RR 12 bpm). This
allows the bedside nurse to commence cardiac compressions until assistance arrives.
2.7 AUTOMATIC TRANSPORT VENTILATION (ATV)
The use of ATV in ALS is usually reserved for post-arrest situations when the cardiac rhythm is stable
and supplementary ventilation support is required. ATVs can be used during CPR as outlined above.
ATVs deliver set minute ventilation (volume of each breath x number of breaths delivered per minute)
and provide information about the airway pressures generated with breath delivery. The ventilators
free one team member for other tasks in the post-resuscitation period.
21
The disadvantages of ATVs include the need for an oxygen source and in some models, a power
source. ATVs should not normally be used in children under five. This is due to difficulty maintaining
the subtle pressures and volumes required in young children. If mechanical ventilation is required for
young children it is preferable to have a pressure cycle ventilator, rather than a volume cycle
ventilator.
The Dräger Oxylog 2000 and Oxylog 3000 ventilator is used for ATV in the Emergency
Department and Intensive Care Unit.
2.8 TRACHEOSTOMY PROBLEMS
If called to see a patient with a tracheostomy problem, request senior assistance early. Consider
calling the ENT registrar and calling switchboard (via ‘666’) and requesting urgent airway assistance.
Accidental dislodgement of the tracheostomy

1. Apply 100% O2 via bag & mask to face and via the tracheostomy
a. N.B Following a laryngectomy oxygenation via the upper airway is not possible
2. If the patient’s breathing is adequate – call for senior assistance to replace the tracheostomy
3. If the patient’s breathing is inadequate – call a code blue
For suspected occlusion or malposition

1. Occlusion or malposition are suspected if the patient is in respiratory distress and there is an
inability to pass a suction catheter
2. Apply 100% O2 via bag & mask to face
3. Attempt to pass a suction catheter down tracheostomy and suction trachea – if you are unable
to pass a suction catheter, this is an emergency, call for urgent assistance
4. Being able to pass a suction catheter does not exclude a partial occlusion and if the patient is
hypoxic or in respiratory distress call a code blue
5. In the case of a partially / blocked tracheostomy removing an ‘inner cannula’ or deflating the
cuff (if either present) may improve the patients ability to ventilate adequately
Removing the tracheostomy is indicated if

1. Total occlusion unrelieved by the above measures resulting in hypoxia or respiratory distress
2. You suspect the tracheostomy is not in the trachea but in the subcutaneous tissues of the neck.
This is dangerous as attempts to ventilate the patient will be ineffective and result in
subcutaneous emphysema.
Apply 100% O2 via bag & mask to face
If you remove the tracheostomy you may need to occlude the stoma with an occlusive dressing
(eg Tegaderm) to achieve adequate bag-mask ventilation. In the case of a well established
tracheostomy a new tracheostomy may be inserted if required.
22
REFERENCES:
Australian Resuscitation Council Guidelines – Policy Statements (2006): Basic Life Support
Guidelines: 4 - Airway & 5 – Breathing.
Australian Resuscitation Council Guidelines – Policy Statements (2006): Advanced Life Support
Guidelines 11.1 – 11.
Fong, J. (2004) Laryngeal Mask. Department of Anaesthesia and Intensive Care, The Chinese
University of Hong Kong. Retrieved 4/12/2006
http://www.aic.cuhk.edu.hk/web8/Laryngeal%20mask.htm
Joynt, G.M. (2003) Airway management and acute upper airway obstruction. In Bersten, A.D
& Soni, N. editors. Intensive Care Manual (5th ed.). Butterworth Heinemann: Edinburgh: 283-296.
Mak, K (2004) Bag mask Ventilation. Department of Anaesthesia and Intensive Care, The
Chinese University of Hong Kong.
Retrieved 4/12/2006. http://www.aic.cuhk.edu.hk/web8/Copyright%20policy.htm
Morley, P.T. and Walker, T. (2006) Australian Resuscitation Council: Adult advanced life support
(ALS) guidelines 2006. Critical Care and Resuscitation. June. 8(2):129-131.
Pierce, L. (2007) Management of the mechanically ventilated patient. 2nd Edition. Saunders: St.
Louis.
American Heart Association (2005) Part 7.1: Adjuncts for Airway Control and Ventilation.
Circulation. Supplement. December 13. 112(24):IV-51 to IV-57.
23
3.0 CARDIAC RHYTHMS
The following section contains examples of some of the important cardiac rhythms and the
management of these rhythms. It is a mandatory requirement that ALS competent staff are able to
recognise and treat lethal arrhythmias. The management is based on the ARC Guidelines and
Algorithm (Guideline 11.2).
Section 3.1 contains the Lethal Arrhythmias:

• Ventricular Fibrillation
• Ventricular Tachycardia
• Asystole
• Ventricular Standstill
• Electro Mechanical Dissociation (EMD) / Pulseless Electrical Activity (PEA)
Section 3.2 contains some other important arrhythmias that may lead on to cardiac arrest:
• Bradyarrhythmias
• Tachyarrhythmias
• Complete Heart Block
• Idioventricular Rhythm
• Torsades de pointes
• Paced Rhythm
24
3.1 LETHAL ARRHYTHMIAS
3.1.1 VENTRICULAR FIBRILLATION
Comment: An erratic bizarre rhythm due to multiple foci in the ventricles rapidly discharging.
Results in ineffective ventricular contraction and no cardiac output.
Delivery of a Precordial Thump

A precordial thump is a single sharp blow to mid sternum of patient’s chest, delivered by the rescuer’s
fist. It should only be done in a monitored and witnessed VF / pulseless VT arrest within the first 15
seconds if a defibrillator is not immediately available.
It may also be done when cardiac arrest is caused by electrocution. It is contraindicated in recent
sternotomy – post op cardiac surgery or chest trauma, or if the patient has a pulse. (A.R.C., Manual of
Adult Advanced Life Support Skills)
Treatment:
ASSESS THE PATIENT - unconscious and pulseless

• Precordial Thump as described above if witnessed and monitored
DEFIBRILLATE IMMEDIATELY
Biphasic Defibrillator – Philips Heartstart XL
¾ DCCS 150J >150J >150J
Biphasic Defibrillator – Medtronic Lifepak 12/20
¾ DCCS 200J >200J >200J
• Check rhythm between defibrillation
• If using paddles, keep insitu on chest
• Commence CPR and obtain IV access
• IV Adrenaline 1mg - Flush with 30ml saline and continue CPR for 2 minutes to circulate drug
• Repeat DCCS 150j x 1 Biphasic Defibrillator – Philips Heartstart XL
• Repeat DCCS 200J x 1 Biphasic Defibrillator – Medtronic Lifepak 12/20
25
• Repeat IV Adrenaline 1mg every 3 minutes

If no response - Intubate and Ventilate with 100% oxygen
• Continue to repeat the single shock regime of DCCS @ 150J or 200J followed by 2 minutes of
CPR and drug therapy
• Consider Antiarrhythmic drugs: Amiodarone & Lignocaine
• Amiodarone 300mg diluted in 20ml Dextrose slowly over 2 minutes (Nursing staff must have
medical order to administer)
• Lignocaine 1 - 1.5mg/kg
• Find and treat the cause if possible
Causes
Predisposing Factors:
Myocardial Infarction
Acidosis
Metabolic disturbances
? Diabetic Ketoacidosis
Trauma
Thromboembolism
Hyperkalemia
Hypoxaemia
Hypothermia
Hypovolaemia
Drug overdose / Drug Toxicity
? Digitalis / ? Anti-arrhythmic Therapy
Electrocution
Trauma:
Complications of CPR or MVA
Tension Pneumothorax?
Pericardial Tamponade
Irreversible Causes:
Massive Myocardial Infarction
Ruptured Aortic Aneurysm
26
3.1.2 VENTRICULAR TACHYCARDIA
Comment: This is a rapid arrhythmia that results in reduced cardiac output. It can lead to
haemodynamic instability and loss of consciousness.
Treatment:
ASSESS THE PATIENT
• Assess Pulse, BP and LOC
If Asymptomatic
• 12 Lead ECG, notify Doctor, monitor and observe patient
If Symptomatic but conscious:
• Lie flat & give oxygen, monitor patient, 12 Lead ECG if possible
• Notify Doctors
• Consider IV Amiodarone 300mg bolus
• Consider IV Lignocaine 1-1.5mg/kg bolus (Nurses @ PAH trained in ALS can administer)
• Consider Amiodarone or Lignocaine infusion
• Consider Cardioversion
• Find and treat the cause
If SYMPTOMATIC - Unconscious, Pulseless

• Precordial Thump if appropriate
IMMEDIATE DEFIBRILLATION
• Treat the same as Ventricular Fibrillation
27
3.1.3 TORSADES DE POINTES
Comment: This arrhythmia is Polymorphic Ventricular Tachycardia where the QRS axis is
changing. The changing axis causes the QRS complexes to be tall and then short.
Torsades de Pointes literally means a "twisting of the points". The arrhythmia is often self-limiting,
occurring for 5-10 seconds at a time.
Treatment:
ASSESS THE PATIENT
• Stop all antiarrhythmic infusions
• Defibrillate if prolonged and patient is compromised
• Commence CPR if indicated
• Consider IV Magnesium Infusion
• Check the Biochemistry (K+, Ca++, Mg++)
• Check Thyroid Function (TFTs)
• Find and treat the cause
• MO may consider overdrive pacing
Causes: Antiarrhythmic drugs

Electrolyte Imbalances- Hypokalaemia
Hypocalcaemia
Hypomagnesmia
Severe Bradycardia
Hypothyroid
Head Trauma and Subarachnoid haemorrhage
Congenital Syndromes (prolonged QT interval)
Psychotropic Drugs (eg Thioridiazine, Tricyclics)
Corticosteroids
Diuretics
Organophosphate insecticides
Liquid protein diets
28
3.1.4 ASYSTOLE
Comment: No Rhythm, No Pulse, No Cardiac Output
Treatment:
• ASSESS THE PATIENT - pulseless and unconscious
• Check rhythm in other leads
• Commence CPR immediately
• Obtain IV access and give Adrenaline 1mg, repeat every 3 minutes
• Flush the IV line with at least 30ml saline and continue CPR for 2 minutes
• Intubate & Ventilate with 100% oxygen
• Find & Treat the cause if possible
• Consider IV Atropine 1mg bolus dose, to a maximum of 3mg
• Consider External Pacing
• Consider Sodium Bicarbonate 1 mmol/kg if documented metabolic acidosis or prolonged cardiac
arrest
Causes: Heart Disease (poor prognosis)

Myocardial Infarction
Drugs, Overdose, Hypothermia
Acidosis, Hyperkalaemia, Hypoxaemia, Hypovolaemia
Prolonged VF deteriorates into Asystole
May result from a massive parasympathetic discharge
29
3.1.5 VENTRICULAR STANDSTILL
Comment: Atrial activity (P waves present) but no ventricular activity, therefore there is no cardiac
output.
This rhythm can be intermittent if AV block is occurring but if it is sustained it must be treated as
Asystole.
Treatment:
ASSESS THE PATIENT - pulseless and unconscious
• Treat as Asystole
• IV Adrenaline 1mg, repeat 3-5 minutely
• Consider IV Atropine 1mg bolus dose to a maximum of 3mg
• Consider IV Isoprenaline 20mcg bolus
• Consider External Pacing
Causes: Heart disease
30
3.1.6 PULSELESS ELECTRICAL ACTIVITY (PEA)
Comment: This is a condition where there is electrical activity occurring in the heart, as evidenced
by any rhythm on the monitor. However, there is no associated mechanical activity. This means that no
ventricular response or contraction occurs. The patient has no cardiac output. Some texts refer to this
as Electromechanical Dissociation (EMD). PEA / EMD has a poor prognosis.
Patient is collapsed and unresponsive.
Treatment:
ASSESS THE PATIENT - pulseless and unresponsive
• IV Adrenaline 1mg, repeat every 3-5 minutes
Find and Treat the cause if possible
Causes:
Circulatory
Pericardial effusion with tamponade due to chest trauma,
Pericarditis,
Uremia or vigorous CPR
Ventricular rupture or Aortic rupture
Massive Pulmonary Embolism
Hypovolaemia due to:
• Acute blood loss
• G.I. bleed
• Dehydration
Hypotension due to:
Septic shock
• Cardiogenic shock
• Anaphylactic shock
• Neurogenic shock
Hypothermia
Respiratory
Intubation of the right main bronchus
Hypoxia
Tension Pneumothorax due to
• Trauma
• Asthma
• Mechanical ventilation
Metabolic
Persistent Acidosis
Diabetic Acidosis
Lactic Acidosis
Electrolyte Imbalance - hyperkalemia
Overdose of cardiac depressant drugs
31
3.2 BRADYARRHYTHMIAS
Comment: Sinus Bradycardia is normal for fit and healthy persons. It is the physiological response
to sleep.
Bradycardia causes problems when there is associated heart disease or heart failure, the heart rate
slows and the heart cannot pump efficiently to maintain cardiac output.
Treatment:
ASSESS THE PATIENT
• IF SYMPTOMATIC:
• Lie flat and give Oxygen
• IV Atropine 0.5mg bolus dose
• Observe for any increase in heart rate
• Notify the doctor
• Wait 3-5 minutes for effect of Atropine
• No response, repeat IV Atropine 0.5mg
• Give IV Atropine up to a maximum 3.0mg
• Consider IV Isoprenaline 20mcg
• Consider External Pacing if no response to drugs
• Find and Treat the cause
Causes: Acute Myocardial Infarction

Beta Blockers, Calcium Channel Blockers
Hypothermia
Acute Hypertension
Sick Sinus Syndrome
Vagal Stimulation
32
3.3 TACHYARRHYTHMIAS
Comment: Ventricular Tachyarrhythmias have already been discussed under the Lethal
Arrhythmias.
Supra-Ventricular Tachyarrhythmia:
Sinus Tachycardia
Atrial Fibrillation
Atrial Flutter
Paroxysmal Atrial Tachycardia
SVT's are not lethal arrhythmias as such, but they can compromise the patient's haemodynamic status
if they are prolonged. It is necessary to investigate and treat a tachycardia.
Treatment:
ASSESS THE PATIENT
If Stable:
• MO may attempt Vagal stimulation ( Carotid Sinus Massage)
• Consider drugs: IV Adenosine, Beta Blockers, Digoxin, Sotalol
If Unstable:
• Sedate the patient and prepare for cardioversion
• Usually cardioverted with 100 - 200Joules
Causes: Increased Sympathetic stimulation (fear, pain and exercise)

Heart Failure
Thyrotoxicosis
Digoxin Toxicity
Hypertensive Heart Disease
Valve Disease
Cardiomyopathy
33
3.4 COMPLETE AV BLOCK / COMPLETE HEART BLOCK
Comment: This rhythm shows atrial activity (P waves) occurring but it is not associated with the
ventricular response. The atrial impulse is not penetrating the AV node to activate the ventricles - there
is complete AV block.
The ventricles are activating themselves independently, either from a Junctional Pacemaker site or a
ventricular pacemaker site. Junctional escape rhythm has a narrow QRS complex with a rate between
40 -60bpm. The Ventricular escape rhythm has a wider QRS with a slower rate between 15 - 40bpm.
Treatment:
ASSESS THE PATIENT
If Asymptomatic:
• 12 Lead ECG
• Check electrolytes
• Monitor and observe patient (dizziness, nausea)
• Report to doctor
If Symptomatic but maintaining BP Systolic > 90:

• Lie flat and give oxygen
• Notify the doctor
• Consider IV Isoprenaline 20mcg
• Commence External Pacing or Isoprenaline Infusion
• Prepare for Transvenous Pacing Wire Insertion
If Symptomatic but BP Systolic < 90:

• Lie flat and give oxygen
• Give IV Adrenaline 0.1mg and flush line with a minimum of 30mls 0.9% NaCl
34
• Notify medical staff urgently
• Prepare IV fluids
• Commence External Pacing
• Prepare for insertion of Temporary Pacing Wire
• Commence CPR if patient becomes pulseless
Causes: Myocardial Infarction

Ischaemic AV Node
Degeneration of the conduction system (elderly)
Congenital
35
3.5 IDIOVENTRICULAR RHYTHM
Slow Idioventricular Rhythm
Comment: This ventricular rhythm is initiated by an ectopic focus in the ventricles because the
primary pacemaker sites have failed. It does not produce a cardiac output and therefore is a pulseless
electrical activity situation. The rate is slow between 15 - 40bpm and is indicative of a dying heart.
Treatment:
ASSESS THE PATIENT
Asymptomatic Symptomatic but Unconscious – no pulse

conscious
- 12 lead ECG - lie flat, give O2 - treat as PEA
- frequent observation as - obtain IV access - CPR
condition may deteriorate - Atropine 0.5 mgs IV - obtain IV access
- check electrolytes - notify MO - Adrenaline 1mg every
- notify MO 3-5 mins
consider external pacing
find & treat cause if possible
Causes: Massive Myocardial Infarction

End Stage Heart Failure
Hypovolaemia causing ischaemia
Massive Pulmonary Embolism
Cardiac Tamponade
Tension Pneumothorax
Rapid Idioventricular Rhythm
Comment: This rhythm is quite a common reperfusion arrhythmia following Myocardial Infarction
treated with Thrombolysis. It is usually non - sustained.
36
Treatment:
ASSESS THE PATIENT
If asymptomatic - monitor and observe patient
Document in the patient's notes the frequency
Not treated unless patient is symptomatic (dizziness, nausea, blackouts)
If symptomatic and increasing frequency may be treated with Lignocaine bolus
Please Note: Rapid Idioventricular Rhythm with rate > 100 is VT

and should be treated as Ventricular Tachycardia.
37
3.6 PACED RHYTHM
Comment: It is necessary for the achievement of the ALS competency that staff can recognise
paced rhythm. They must also demonstrate how to effectively externally pace a patient, how to achieve
capture and how to recognise that pacing is effective.
The above rhythm is recorded from a patient receiving external pacing.
Capture means that there is a pacing spike on the monitor followed immediately by a widened
QRS complex, indicating that the pacemaker is initiating ventricular depolarization.
With every paced beat on the monitor there should be associated mechanical activity, which is
evidenced by a palpable PULSE for each QRS complex.
Specific pacemaker functions and troubleshooting are discussed in Section 5.0 Cardiac Pacing.
38
SPECIAL NOTES:
• Defibrillation takes priority over drugs and CPR in the management of VF and pulseless VT.
• If there is no IV access available, then Adrenaline, Atropine and Lignocaine may be given via the
EndoTracheal Tube. The dose is increased to 2 - 3 times the normal IV dose.
• Minimise the interruptions to CPR between each DCCS and Intubation.
• If there is return of spontaneous circulation, protect the patient's airway and move to post arrest
management.
• Consider Calcium Chloride 10% for the treatment of overdose of Calcium Channel Blockers,
hypocalcaemia and hyperkalaemia.
• Consider Sodium Bicarbonate for the management of documented metabolic acidosis,
hyperkalaemia, prolonged cardiac arrest and overdose of tricyclic antidepressants.
Recommended readings:
Australian Resuscitation Council Guidelines- Policy statements, (2006) Section 11, Advanced
Cardiac Life Support
Conover, M.B. (2004), Pocket guide series, Electrocardiography 5th Ed. Mosby, St Louis.
Conover, M.B. (1996), Understanding Electrocardiography 7th Ed. Mosby, St Louis; Chapters
11,13, 15 & 16)
39
4.0 DEFIBRILLATION
INTRODUCTION
In defibrillation, electrical energy is used to simultaneously depolarize all myocardial cells. The
uniform depolarization of all cardiac cells facilitates the return of the normal electrical conduction
pathways, via the primary pacemaker of the heart - the Sinus Node. The purpose is to stop the cells
fibrillating and allow the normal conduction pathways to regain control. Restoration of sinus rhythm
should improve the cardiac output.
4.1 TWO METHODS OF DEFIBRILLATION:
EXTERNAL DEFIBRILLATION
a. Manual Defibrillation – requires the operator to be able to identify lethal arrhythmia and
deliver appropriate defibrillation to the patient. External defibrillation can be facilitated by the
use of hand held paddles or adhesive pads.
• Anterior - Anterior Method – This is the most effective pad/paddle placement for
emergency defibrillation as the electrical current flows directly through the left ventricle.
Place one pad/paddle to the right of the sternum directly under the clavicle in the 2nd to 3rd
intercostal space. Place the second pad/paddle to the lower left anterior chest wall, in about the
5th to 6th intercostal space in the midaxillary line, over the apex of the heart.
• Anterior - Posterior Method - This method is suited to atrial arrhythmias - Place one
pad/paddle anteriorly, either to the left or the right of the sternum under the clavicle. Place the
second pad/paddle posteriorly under the left scapula. If using hand held paddles, the patient
must be lying on their right side for this method. Adhesive pads allow the patient to be supine.
b. Semi Automatic External Defibrillation – does not require the operator to have the skills to
interpret ECG. The SAED uses computerised algorithm to detect arrhythmia and advises the
operator ‘to shock or not to shock’
INTERNAL DEFIBRILLATION
Internal defibrillators are available in Emergency Department, Recovery and Intensive Care. The chest
cavity needs to be opened / reopened (thoracotomy) and the paddles are placed indirect contact with
the heart. One paddle is placed over the right atrium and the second paddle over the apex of the heart.
Internal defibrillation requires 20 joules regardless of the type of defibrillator.
40
NOTE:
There are two different defibrillators available for use at the PAH (Refer to Section 4.4). It is the
responsibility of the staff member to be familiar with the machines used in their units.
4.2 SAFETY PRINCIPLES OF DEFIBRILLATION
IF USING PADDLES:
• Moist gel pads should always be used to prevent or minimize burning to the skin. Gel pads or gel
decrease the resistance between the electrode and the patient's skin. Paddles should be placed over
gel pads and should not extend out over the edges of the gel pads. Only use specific Defibrillator
Gel.
• Defibrillate from the left side of the patient, if possible to avoid self-injury.
• Isolate yourself and bystanders from any water or fluids before discharging.
• Charge the paddles only when insitu on the chest wall. An experienced and competent person
should control charging and discharging of the paddles to avoid injury to other persons.
• Apply 10 kg (25lbs) of pressure when discharging. Do not leave a gap between paddle and
chest wall, as it is a spark and arcing hazard.
• Call out loudly “I’M CLEAR, YOU’RE CLEAR” and visually check before discharging.
• Do not defibrillate over ECG electrodes, ECG leads, Pacing wires , Central lines or GTN
patches.
• Do not allow oxygen from Airviva to flow onto patient’s chest during defibrillation.(risk of
spark and fire hazard)
• Do not place paddles over female breasts.
• Do not allow the patient to be in contact with any metal items such as bed rails and
handcuffs for prisoners outside of the Security Unit.
Post defibrillation keep paddles insitu and check the rhythm.
• Where the rhythm is a witnessed VF/ pulseless VT arrest and a manual defibrillator is
available, up to 3 stacked shocks for the FIRST ATTEMPT can be given. Further attempts
at defibrillation should be single shocks followed by immediate CPR for 2 minutes.
3 Consecutive shocks are thought to reduce the transthoracic resistance to electrical current flow,
thereby improving the effectiveness of the shock. However, time is critical so only rapid re-charging of
manual defibrillators and shock delivery will result in reduced impedance.
If the patient is in the back of a moving ambulance and requires defibrillation, this can be performed
while the vehicle is in motion, by using self-adhesive defibrillation pads. During aero medical retrieval
permission should be sought from the pilot prior to defibrillation.
41
4.3 EMERGENCY DEFIBRILLATION
Emergency defibrillation is necessary when the patient's cardiac rhythm is rapid and / or erratic, and is
no longer sustaining effective cardiac output.
The two most important rhythms requiring immediate defibrillation are:
Ventricular Fibrillation
Pulseless Ventricular Tachycardia
Please Note:
Any Tachyarrhythmia that is prolonged and is compromising the patient, (loss of consciousness,
hypotension), needs to be defibrillated.
If the patient is still conscious, consider sedation and elective cardioversion
COMPLICATIONS OF DEFIBRILLATION
• Skin burns to the patient (common)
• Cardiac arrhythmias - Asystole or Ventricular Fibrillation
• Electrical Shock to persons in contact with patient or bed
Sparks, burns to others and fire hazard
• Cellular damage
• Pulmonary or cerebral embolism
42
4.4 SYNCHRONIZED DEFIBRILLATION/ CARDIOVERSION
Synchronized defibrillation means that the electrical shock will be triggered by the "R" wave of the
QRS complex, thus avoiding the vulnerable phase of the cycle the "T" wave. Defibrillating on the "T"
wave can cause Ventricular Tachycardia to become Ventricular Fibrillation.
Choose the monitor lead with the most prominent "R" wave and increase the size of the lead. Observe
the rhythm to ensure that the ‘synchronise marker’ is actually on the R wave. Because the machine is
waiting for the "R" wave to occur, there may be a slight delay in discharge after the discharge buttons
have been pressed. Remember to keep the discharge buttons depressed until discharge is delivered.
SAED will only synchronise in manual mode
INDICATIONS FOR CARDIOVERSION:
Any Atrial or Ventricular Tachyarrhythmia where the patient is compromised should be considered for
cardioversion:
Atrial Tachycardia
Paroxysmal SVT
Rapid Atrial Fibrillation
Rapid Atrial Flutter
Prolonged Ventricular Tachycardia
SAFETY PRINCIPLES OF ELECTIVE CARDIOVERSION:
• Informed consent must be obtained from the patient

• Fast the patient for 6 hours prior if possible
• Sedation by anaesthetist
• Check electrolytes and correct if necessary (potassium)
• Check Digoxin levels are normal, not toxic
• Check anticoagulation is therapeutic (INR or APTT)
• Emergency drugs and equipment should be available
• Lower voltages are used for Atrial arrhythmias
o Biphasic Defibrillators
50 – 75 Joules for Atrial Flutter
100 – 200 Joules for Atrial Fibrillation
43
• Ideally, an echocardiogram should be performed prior to defibrillation to check for any emboli in
the atria. Elective cardioversions require Warfarinisation prior to Cardioversion.
• Patient should have pulse oximetry monitoring during procedure
• Patient should be connected to the monitor on the defibrillator
• Press the "SYNCH" button and observe monitor for the highlighted marker on the "R" wave
• This marker must fall on every “R” wave. If the marker is not consistently falling on the “R” wave,
choose another monitoring lead.
• Observe all the safety principles previously outlined.
POST PROCEDURE:
• Patient's airway should be protected until patient is fully awake and alert.
• Perform ongoing patient assessment including 5 - 10 minutely recording of vital signs while the
patient recovers from the anaesthetic.
• Perform a 12 Lead ECG when the patient is awake and analyse for / report abnormalities.
• Document the amount of joules required to revert the dysrrhythmia, number of shocks required and
the drugs used during the procedure in the patient's progress notes. Additionally document post
procedure patient assessment.
4.5 Types of Defibrillators at PAH
Medtronic Lifepack 12 and 20
The Medtronic Life pack 12 Defibrillator uses Biphasic technology to deliver the electricity to the
patient. This means that the electricity is generated from both pads rather than one. 200J is used to
defibrillate the patient resulting in:
• More effective first shock, and
• Less damage to the myocardium.
Philips Heartstart XL
The Philips Heartstart Defibrillator also uses Biphasic technology to deliver the electricity the patient.
150J is used to defibrillate the patient.
Recommended readings:
Grauer, K. and Cavallaro, D. (1993) ACLS: Certification Preparation Vol 1 (3rd Ed) Chapter 1, Section
B, pp 7 -17.
Woods, S.L., Sivarajan Froehlicher, E.S.,Halfpenny, C.J and Underhill, S. (1995) Cardiac Nursing (3rd
Ed), Philadelphia:Lippincott.pp 608, 609, 612.
44
5.0 CARDIAC PACING
A pacemaker is an electronic stimulator used to send a specified electrical current to the myocardial
muscle. This causes depolarization of the myocardial cells and subsequent contraction of the
myocardium. Pacing is used to maintain heart rate and cardiac output.
A pacemaker can be external or internal.
Modes of Pacing
• External or Transcutaneous - used in an emergency
• Transvenous or Endocardial - Temporary or permanent pacing wire
• Epicardial - used prophylactically postoperative cardiac surgery
Indications for Emergency Cardiac Pacing
• Complete AV Block with slow ventricular rhythm where the patient is compromised – low blood
pressure, loss of consciousness
• Severe Bradycardia where Atropine has failed to improve the rate and the patient is compromised
• Sinus Arrest or Asystole
• Overdrive pacing for Tachyarrhythmias
Routes for Temporary Pacing
• External / Transcutaneous - emergency pacing is achieved by depolarizing the heart through

the chest by means of 2 large skin electrodes
• Transvenous / Endocardial - the pacing electrode is inserted through a large vein into the right
atrium, then into the base of the right ventricle
• Epicardial - pacing electrodes are attached to the epicardium during cardiac surgery
• Transthoracic (rarely used) - a pacing electrode is inserted during an emergency by threading it
through a transthoracic needle into the right ventricle
45
5.1 EXTERNAL / TRANSCUTANEOUS PACING
Transcutaneous pacemakers are a means of applying an external electrical stimulus to the heart to
initiate cardiac cell depolarization and subsequent contraction of the myocardium.
It is a quick, effective, non-invasive method of treating symptomatic bradyarrhythmias,

tachyarrhythmias and asystole, which are unresponsive to other therapy.
Method
• Two pacing pads are placed on the patient's chest, either anteriorly and posteriorly, or anteriorly
and anteriorly, depending on the machine. Follow the instructions on the packets.
• The pacing pads are then connected to the machine via the pacing cable.
• The ECG leads from the machine must also be attached to the patient, in order for the machine to
sense or detect the patient's intrinsic rhythm.
• The pacing mode usually selected is called "DEMAND" mode.
• The pacemaker rate must be set depending on the patient's requirements. Usually the rate is set
between 60 -80, but should be reduced if the patient's intrinsic rate increases.
• The output, in milliamps, must be set according to the patient's requirements. Usually between 40
– 100 milliamps, adjusted until capture is obtained and a paced rhythm is observed on the monitor
screen.
• Assess the patient for a cardiac output, pulse and blood pressure once capture is observed.
• Sedate the patient. External pacing is very uncomfortable! Sedate the patient with Midazolam or
Valium (muscle relaxant). Analgesia is also required
• External pacing should only be a temporary measure to support the patient's rhythm until a
temporary pacing wire can be inserted.
• Failure to capture -
- May be related to the placement of the pacing pads, so reposition the pads.
- May be due to the output / milliamps being too low, so increase the output.
- Check all connections and power source / batteries.
- Check that pacing function is "ON" and "START" button is on.
- Check the pacing mode is "DEMAND" mode.
46
5.2 MODES OF PACING
5.2.1 DEMAND MODE

Demand Mode pacing means that the pacemaker senses the patient's own rhythm, called the intrinsic
rhythm, and will only deliver a paced beat when the machine does not sense an intrinsic rhythm or
beat. It inhibits the paced beat if an intrinsic beat is detected.
Demand Mode pacing is called "Synchronized" pacing because it synchronizes paced beats with the
patient's own rhythm.
5.2.2 FIXED MODE

Fixed Mode is "Asynchronized" pacing. It paces the patient at the set rate and output regardless of
the patient's own intrinsic rhythm. It does not sense the patient's own rhythm.
Fixed Mode pacing can be dangerous if it delivers a paced beat during the relative refractory period of
repolarization of the patient's own rhythm, as it could trigger VF or VT.
This mode is rarely used except when the need is to overdrive pace a tachyarrhythmia.
5.2.3 PACED RHYTHM

Characteristics of Paced Rhythm
• Pacing Spike - represents the output delivered by the pacing generator. The size of the pacing
spike varies with temporary and permanent pacemakers
• Wide QRS Complex > 0.12 secs - should immediately follow the pacing spike
• P waves are not associated with each paced beat, unless the atria are being paced
• Pacing spikes should occur regularly and at the preset rate
• Pacing spikes should not occur if patient's own intrinsic rhythm is present (if the pacemaker is
set in ‘demand’ mode)
47
5.3 SAFETY ASPECTS OF PACING
• Avoid operator contact with the electrode's gel pad as an electric shock may result if the unit is
turned on
• Use only moist gel pads to ensure best electrical contact and to avoid burns.
• Replace pacing pads after 24 hours if external pacing is still required.
• Keep patient supine in bed and sedated while externally pacing.
• For the best contact and conduction, clean patient's skin and shave if necessary.
• External pacing should be short term, so prepare for the insertion of a temporary transvenous
pacing wire.
• If the same machine is used for pacing and defibrillation, the machine will automatically switch the
pacing function off when the charge button is pushed, therefore it will be necessary to re-start the
pacing function after defibrillation has been performed.
5.4 COMPLICATIONS OF PACING
• Pain and discomfort for the patient as the skeletal muscle contract from the pacing stimulus, give
muscle relaxants such as Diazepam and Midazolam.
• Skin irritation and burns from the pacing electrodes, especially with higher current levels. Ensure
that the gel pads are moist and avoid prolonged external pacing.
• Fixed mode pacing can lead to a pacing stimulus inducing R-on -T phenomenon.
48
5.5 TROUBLE SHOOTING PROBLEMS
5.5.1 FAILURE TO PACE
Failure to pace is also known as Non Pacing or Non delivery of a stimulus
No pacing spike is seen on the monitor or rhythm strip
This will most likely be caused by pulse generator failure or loss of circuit integrity (disconnected /
loose lead or poor pad contact)
Action
Commence CPR & ALS measures if patient is compromised while performing the following
troubleshooting measures
• Check that the pulse generator is turned on – this is not just turning on the cardiac monitor
capability. The external pacing capability must also be activated
• Check that the pulse generator has a power source (plugged into power source or charged battery)
• Check connections
• Check contact of the pacing electrodes
− If unsure of the integrity of the pacing pads, replace pads (pads should always be moist &
applied to a clean, dry, non-hairy surface)
− Reposition the pacing electrodes if necessary to ensure good contact
49
5.5.2 FAILURE TO CAPTURE
Failure to capture or Non capture is when there are pacing spikes but they are not followed by widened
QRS complex which indicates ventricular stimulation and pacing.
This can be especially important when the patient's underlying rhythm is very slow or insufficient to
maintain cardiac output.
Assess the patient
Commence CPR & ALS measures if patient is compromised while performing the following
troubleshooting measures
• Increase the milliamps / output
• Check contact of the pacing electrodes
− If unsure of the integrity of the pacing pads, replace pads (pads should always be moist &
applied to a clean, dry, non-hairy surface)
− Reposition the pacing electrodes if necessary to ensure good contact
50
5.5.3 FAILURE TO SENSE
Failure to sense or non sensing is when the pacemaker, in demand mode, delivers pacing spikes
regardless of the patient's own rhythm. If the pacing stimulus occurs in the relative refractory period of
repolarization, there is a risk of ventricular arrhythmias.
This problem can look like failure to capture at times when the pacing spike comes immediately
after the patient's own intrinsic beat and consequently does not depolarize the myocardium.
To differentiate between failure to capture and failure to sense, look at the patient's underlying rhythm.
• If the rhythm is very slow, below the pacemaker set rate and pacing spikes are occurring but not
capturing, then the primary problem is failure to capture, turn up the output and reposition the
pads.
• If the underlying rhythm is reasonable and producing a pulse with each intrinsic beat, but pacing
spikes are still occurring through the rhythm strip, the primary problem is failure to sense.
Assess the patient

• Check ECG electrodes & position
• Consider changing the monitoring lead + / - increase the size of the ECG
Consider turning the pacemaker rate down below the patient’s intrinsic rate, if the patient’s
intrinsic rhythm is sufficient to maintain a blood pressure (for example in the rhythm strip above)
51
5.5.4 OVERSENSING
Over sensing occurs when the pacemaker, in demand mode, interprets that baseline movement of the
ECG tracing is the patient's intrinsic rhythm, and therefore inhibits a response - no pacing occurs.
Patient movement, muscular tremor or electrical interference may cause the artefact. Remove the cause
of the interference.
Clinically, over sensing is rarely a problem when utilising external pacing.
Assess the patient

• Reposition / replace the ECG electrodes on clean, dry, hairless skin
• Sedate the patient if due to muscle tremor or patient movement
• Change the ECG lead
• Remove any electrical equipment that may be causing interference
52
5.6 DOCUMENTATION OF PACING
• Record the incidence that required external pacing in the patient's record
• Document the pacing rate, the required output (milliamps), the patient's condition whilst being
externally paced
• Chart all medications given, including required sedation
• Document the percentage of time patient required pacing
• Record the paced rhythm strip and the underlying rhythm if possible
• Be familiar with the different pacemakers available in your unit
Recommended Reading:
Hildage, S. (1995) External pacing. Nursing Standard. 8(9), pp54.
Moses, H.W., Moulton, K.P., Miller, B.D. & Schneider, J.A. (1995)
A Practical Guide to Cardiac Pacing. 4th Edition. Little, Brown & Co: Boston
53
6.0 PHARMACOLOGY
Only a few drugs are indicated during immediate management of a cardiac arrest, and there is
limited scientific evidence to support their use during Resuscitation. The administration of
medications is secondary to Cardiopulmonary Resuscitation and Defibrillation. While the listed
drugs have theoretical benefits in selected situation, no medication has been shown to improve
long term survival in humans after cardiac arrest. Priorities are defibrillation, oxygenation and
ventilation together with external cardiac compressions.
6.1 INTRAVENOUS DRUG ADMINISTRATION:
• Once the airway has been established, oxygenation commenced and cardiac compressions
commenced IV cannulation and IV access should be obtained.
• Following the administration of IV medications, the IV cannula should be flushed with at least
30mls of normal saline. This facilitates the circulation of the drug from the cubital fossa to the
right atrium of the heart.
• CPR should be continued for 2 minutes to circulate the drug. The patient's arm may be elevated to
assist venous return.
6.2 ENDOTRACHEAL DRUG ADMINISTRATION:
• Give 2 - 3 times the recommended IV dose of the drug when giving it via ETT.
• Dilute the drug to 10ml with normal saline
• Suction the airway prior to administering the drug if possible.
• Insert a suction catheter beyond the tip of the E.T. Tube and instil the medication rapidly via the
catheter using a syringe
• Give 2 - 5 ventilations to disperse the drug in the lungs.
• Wear protective eyewear and gloves if using an open system.
54
Most drugs can be given via the ETT if necessary but specifically in a cardiac arrest, if venous access
is not available then Adrenaline, Atropine, Lignocaine, Naloxone and Valium may be given via
the ETT.
REMEMBER: Sodium bicarbonate and Calcium must not be given via the endotracheal tube.
6.3 OXYGENATION
When available, high concentration oxygen should be given to all patients in a cardiac arrest. Oxygen
in sufficient concentration to provide arterial oxygen saturation of > 90%, should be given to all
patients after restoration of spontaneous circulation and during treatment of peri – arrest arrhythmias.
55
6.4 ADRENALINE
Adrenaline is the first drug used in a cardiac arrest of any aetiology: it is included in the ALS universal
algorithm for use after each 3 minutes of CPR.
Action • Adrenaline is a directly acting sympathomimetic amine with both

alpha (α) and Beta (ß) adrenergic activity. The dose used in
resuscitation stimulates the α1 and α2 receptors to produce
vasoconstriction. Vasoconstriction improves cerebral and myocardial
perfusion during a cardiac arrest.
• It facilitates defibrillation by improving myocardial blood flow during
CPR
• ß2 receptor stimulation dilates cerebral vessels therefore producing a
relative increase in cerebral blood flow.
• It increases myocardial excitability and is arrhythmogenic especially
when the myocardium is ischaemic and/ or hypoxic.
Half-Life • 2 minutes
Indications • Cardiac Arrest - Asystole and EMD / PEA
• Cardiac Arrest - VF and Pulseless VT if defibrillation fails
• Anaphylactic reactions
Dose Cardiac Arrest:
• 1mg IV (Minijet 10ml of 1:10,000 / 1ml Amp of 1:1000)
Repeat dose every 3 minutes during CPR
• Initial onset of effect 30 secs, max effect 3 - 5 mins
Anaphylactic Reactions
• 0.3 -0.5mg subcutaneously or IM,
• Repeat after 5 minutes up to 1mg
Adverse • Sinus Tachycardia, SVT, and Ventricular Arrhythmias
Effects
• Severe hypertension
• Tissue necrosis if extravasation occurs
• Cold extremities, cerebral haemorrhage, pulmonary oedema
Precautions • Only use in life threatening situations
• Do not mix with Sodium Bicarbonate as it inactivates Adrenaline
• Do not give as a purely positive inotrope to patients with coronary
insufficiency
56
6.5 ATROPINE
Action • Blocks the parasympathetic nerve stimulation of the heart (muscarinic

receptors), therefore increases SA and AV node rate and speeds the
conduction through the AV node.
Half Life • 2-3 hours, peak effect
Indications • Symptomatic Sinus Bradycardia < 60 (hypotension, chest pain,
nausea and dizziness)
• Asystole
Dose Bradycardia:
• Initial bolus dose of 0.5mg, followed by increments of 0.5mg up to a
maximum dose of 3.0mg
• Given as a rapid IV push or via the ETT
Asystole:
• Bolus dose of 1mg. Repeat up to max dose of 3.0mg
Adverse • Tachycardia, hypotension, hot skin, ataxia,
Effects • Ischaemic chest pain due to increased heart rate
• Anticholinergic effects - constipation, dry mouth, blurred vision,
urinary retention
• Confusion, convulsions, paradoxical bradycardia and ventricular
fibrillation.
Precautions • Atropine raises intraocular pressure in patients with glaucoma.
• Treat with Pilocarpine eye drops if necessary.
57
6.6 LIGNOCAINE
Limited studies of lignocaine are available to guide practice. The use of lignocaine in cardiac arrest
management is largely historical, with its role in prophylaxis of ventricular arrhythmias being
equivocal. The Australian Resuscitation Council advises that in the absence of Amiodarone,
Lignocaine is the antiarrhythmic therapy of choice in refractory ventricular arrhythmias. Nurses at
Princess Alexandra Hospital who have gained Advanced Life Support Competency are able to initiate
Lignocaine in the appropriate setting.
Action • Membrane stabilising agent inhibits the fast inward sodium

movement and thus decreases the maximum rate of depolarisation,
particularly in ischaemic tissue.
• Class 1b anti arrhythmic depresses excitability by blocking the fast
sodium channels and decreases automaticity in the conduction
system.
• Local anaesthetic action suppresses ventricular ectopy
Half-Life • 1 - 2 hours
Indications • VF / VT when defibrillation has failed to revert rhythm
• Prophylaxis in the setting of recurrent VF / VT
Dose • 1mg - 1.5mg / kg IV bolus dose during cardiac arrest if
defibrillation fails
• Infusion - 2gm in 500ml of 5% Dextrose
• Lignocaine infusion only when return of spontaneous circulation
• Commence at rate of 60ml / hour (4mg / min for 1 hour)
• Then reduce to rate of 45ml /hour (3mg /min for 1 hour)
• Then reduce to rate of 30ml / hour (2mg / min for 22 hours)
Adverse • CNS- drowsiness, confusion, agitation, twitching, fits, slurred
Effects
speech, blurred vision, numbness
• RESP- Respiratory depression, dyspnoea
• CVS - hypotension, bradycardia, heart block, asystole,
anaphylactic reactions
• Negative inotrope - hypotension, bradycardia
Precautions • Cautious use in Renal and Liver disease
58
6.7 AMIODARONE
Amiodarone has better evidenced based support than any other antiarrhythmic drug. It is useful for
both ventricular and atrial arrhythmias. Amiodarone is recommended after defibrillation and
adrenaline in cardiac arrest with persistent VF/VT. If there is a medical officer present, Amiodarone is
the preferred antiarrhythmic drug at PAH&HSD.
Action • Class III antiarrhythmic which prolongs the repolarisation.

• Prolongs the action potential and the refractory period of AV
node and ventricles, suppresses ectopic activity.
• Systemic and cardiovascular vasodilator
Half-Life • varies from 25 - 110 days
Indications • Treatment of Tachyarrhythmia’s, WPW, PSVT, SVT and VT
Cardiac Arrest
• used if defibrillation fails to revert VF / Pulseless VT
Dose • Loading dose 300mg
• A further 150mg could be considered.
Infusion • 15mg / kg over 24 hours
• Use glass bottles and Non PVC tubing
• Use 5% glucose/dextrose
Adverse • Hypotension, Bradycardia, Heart block
Effects • Rapid peripheral infusion can cause "red man" syndrome
Long term use
• Blurred vision, corneal damage
• Cardiac Failure, Cardiogenic shock
• Abnormal Liver and thyroid function tests
• Pulmonary fibrosis, pneumonitis, hair loss, Hot flushes,
insomnia, tremor, neuropathy
• Photosensitivity Æ slate blue skin pigmentation
Precautions • Incompatible with normal saline
• Cautious use in patients with heart failure, liver / thyroid
dysfunction
Drug • Warfarin causing inhibition of warfarin mechanism
Interactions
• Digoxin causing increased plasma concentrations
Other antiarrhythmics- Flecainide, Procainamide`, Quinidine, Beta
Blockers & Ca++ Channel blockers
59
6.8 POTASSIUM
Action • Essential for membrane stability, transmission of nerve impulses, cardiac,

skeletal and smooth muscle contraction. Important intracellular cation.
• Normal plasma levels 3.5 - 5mEq/l.
• Low serum potassium ⇒ Ventricular arrhythmias
Indications • Hypokalemia
• Persistent VF (due to documented or suspected Hypokalaemia
Dose • 5mmol IV (5mls)

• (Ampoules 10mmols / 750mg Potassium ions in 10ml)
Adverse • Hyperkalemia ⇒ Hypotension, bradycardia, flaccid paralysis, cardiac arrest

Effects
• Asystole
• Nausea, vomiting, diarrhoea
• Extravasation causes tissue necrosis
Precautions • Contraindicated in Renal failure, severe haemolytic reactions, crush

syndrome, severe burns, acute dehydration, digoxin toxicity and pregnancy
60
6.9 MAGNESIUM SULPHATE
Action • Essential for membrane stability, mimics the action of potassium.

• Electrolyte, intracellular cation that slows the rate of the SA node and prolongs
the conduction time, depresses skeletal, smooth and cardiac muscle activity.
Indications • Hypokalemia, hypomagnesaemia

• Torsades de Pointes
• Cardiac arrest due to digoxin toxicity
• Management of VF / Pulseless VT when defibrillation and a vasopressor has
failed
• Control seizures in toxaemia of pregnancy, epilepsy
• Orally has laxative effect
Dose Cardiac Arrest

• 5mmol IV slowly, repeat once if necessary
Infusion
• 40mmol in 100ml of 5% Dextrose over 4 hours
Adverse • Hypermagnesemia - flushing, sweats, thirst, hypotension, areflexia, muscle

Effects
weakness, flaccid paralysis
• Respiratory Failure
• Complete Heart Block, circulatory collapse
Precautions • Cautious use in existing heart block, Renal disease, Digitalised patients
• Low serum Magnesium is due to diuretics, alcohol, severe diarrhoea
• Increases myocardial excitability and prone to ventricular arrhythmias especially
if hypokalemic or digoxin
61
6.10 SODIUM BICARBONATE
Action • Alkalising solution binds with Hydrogen ions to form carbonic acid.
• Acid Base Balance: H + HCO3 ⇔ H2CO3 ⇔ H2O + CO2
In most arrests early oxygenation, ventilation and cardiac compressions negate
the use of Sodium Bicarbonate.
Indications • Documented metabolic acidosis
• Hyperkalemia
• Prolonged cardiac arrest > 15 minutes
• Overdose of Tricyclic antidepressants
Dose • 1mmol / kg IV over 2-3 minutes
Adverse • NaHCO3 is no longer initial therapy because of the risk of alkalosis,
Effects
hypernatraemia & hyperosmolality
• Alkalosis Intracellular acidosis may develop and worsen when CO2 is released
from the Sodium bicarbonate freely enters the cells.
• Sodium bicarbonate and Adrenaline or calcium when mixed together may
inactivate each other, precipitates and blocks the IV line
• Sodium Bicarbonate should not be given via the ETT as it causes mucosal
damage.
Precautions • Overdose causes Metabolic Alkalosis
62
6.11 CALCIUM CHLORIDE
Action • Calcium is essential for normal muscle and nerve activity.

• It transiently increases myocardia excitability and contractility and peripheral
resistance.
Indications • Hypocalcaemia
• Hyperkalemia
• Treatment of overdose of Calcium Channel blockers
Dose • 5-10ml of 10% Calcium Chloride (Minijet 10ml with 6.8mmol / 10%) IV
Adverse • Hypotension due to peripheral vasodilation
Effects
• Fainting, bradycardia, tingling sensation
• Cardiac arrhythmias, cardiac arrest
Precautions • Extravasation causes tissue necrosis

• May aggravate Digoxin toxicity
63
6.12 OTHER EMERGENCY DRUGS
6.12.1 ISOPRENALINE
Action • Positive Inotrope, chronotrope and dronotrope.

• Increases cardiac contractility, increases heart rate and conductivity
• Synthetic sympathomimetic amine, acts on Beta adrenergic receptors
• No alpha effects therefore peripheral vasodilation occurs
• Increases ventricular irritability
Indications • Treatment of symptomatic bradycardias such as 2nd Degree and 3rd Degree AV
Heart Blocks
Dose Initial Dose

• 0.02mg / 20mcg (1ml), followed by subsequent doses of 20mcg
• To make bolus dose – 1mg in 5ml Ampoule Isoprenaline (fridge) draw up 1ml /
200mcg in a 10ml syringe.
• Add normal saline (9mls) to make a concentration of 20mcg / ml
Infusion
• 2mg in 100ml 5% Dextrose, rate of 0.5 – 5mcg / min
• Initial effect 30 secs, duration 3 – 8 minutes, max effect 2 – 5 minutes
Do not use if injection is brown or precipitation is present
Side Effects • Tachycardia, Angina, Nausea, Ventricular Tachycardia

Precautions • Hypovolaemic shock, Tachycardia due to Digoxin Toxicity
• Should never be mixed with Sodium bicarbonate
• Should not be given with Adrenaline
64
6.12.2 ADENOSINE
Action • Depresses the AV Node and Sinus Node activity

• Used to assist in the diagnosis of rapid arrhythmias, slows conduction through the
AV node, therefore slows SVT's but not VT
Half Life • 10 - 30 seconds

Indications • SVTs including Wolff Parkinson White Syndrome
• To aid in the diagnosis of a rapid, broad complex rhythm.
Dosage • 6mg rapid IV bolus dose

• 12mg rapid IV bolus dose after 1-2 minutes, repeat if necessary
Adverse • Dyspnoea
Effects
• Facial Flushing
• Transient arrhythmias
Precautions • Contraindicated in patients with AV blocks, Sick Sinus Syndrome and Asthma
• Dipyridamole potentiates effects of Adenosine
• Theophylline and caffeine antagonise effects
65
6.12.3 SALBUTAMOL
Action • Predominantly a Beta 2 stimulant, resulting in the production of cAMP. Its effect
on bronchial dilation is greater than its effect on cardiac Beta 1 receptors.
However, it does not cause a significant effect in cardiac output.
Indications • To relieve bronchospasm

• To treat heart failure
• To stimulate the intracellular transport of potassium in a familial periodic paralysis
Dose • As a continuous infusion 500mcg in 100ml of 5% Dextrose (5mcg / ml) in doses of

5 - 20mcg per minute
Adverse • Tachycardia, hypertension

Effects
• Hypotension
• Tremor and muscle cramps
66
6.13 NEUROMUSCULAR BLOCKERS
6.13.1 SUXAMETHONIUM
Action • Neuromuscular blocker depolarises skeletal muscle cells.

• Acts like acetylcholine by blocking impulse transmission and causing paralysis.
• Effective within 30 seconds, effects reversed by endogenous plasma
pseudocholinesterase enzyme.
• Brief period of muscular excitability (fasciculations or muscle twitching)
followed by flaccid paralysis.
• Short acting skeletal muscle relaxant
Half-Life • 4 - 6 minutes
Indications • Emergency Intubation
Dose • 0.3 - 1.1mg / kg (100 -200mg IV bolus)
• Not recommended for continuous IV infusion
Adverse • Painful muscle fasciculations (reduced if given thiopentone)
Effects
• Cardiac Arrhythmias, bradycardias secondary to potassium release
• Increased intracranial pressure
• Transient increase in intraocular pressure
• Malignant Hyperthermia
Precautions • Causes potassium to be released from the cells
• Cautious use in patients with burns, crush injury, spinal cord injury, renal failure
and head injuries
• Can cause prolonged apnoea in patients with low levels of pseudocholinesterase
• Contraindicated in patients with history of Malignant Hyperthermia or
pseudocholinesterase disorders
NOTE: Neuromuscular blockers (NMB) DO NOT provide sedation or analgesic effects,

therefore administration of NMBs should be preceded by appropriate analgesic / sedative
agents.
67
6.13.2 VECURONIUM
Action • Non Depolarising skeletal muscle relaxant

• Acts by competing for cholinergic receptors at the motor end plate.
Half-Life • 60-80 minutes
Indications • To induce skeletal muscle relaxation, to facilitate mechanical ventilation and
surgery
Dose • Initial bolus dose of 0.1mg / kg provides relaxation suitable for ideal intubation
within 2.5 - 3 minutes. Muscle relaxation (to 25% recovery) will last for 20 – 40
minutes
Adverse • Subsequent doses of 0.04 – 0.06 mg / kg produces complete neuromuscular
Effects
blockade with duration of effect as above.
• Not suitable for emergency intubations
• Low occurrence of adverse effects, although anaphylaxis
has been reported
Precautions • Myasthenia Gravis
• Electrolyte imbalance, renal / hepatic dysfunction may prolong effect
NOTE: Neuromuscular blockers (NMB) DO NOT provide sedation or analgesic effects,

therefore administration of NMBs should be preceded by appropriate analgesic / sedative
agents.
Other Non Depolarising Agents: Pancuronium & Atracurium
Recommended Readings:
Australian Resuscitation Council Guidelines - Policy Statements. (2006) Section 11.6, Medications
in Adult Cardiac Arrest.
Opie, L., ( 1997) Drugs for the Heart. (4th edition), WB Saunders, Philadelphia.
The American Heart Association in Collaboration with the International Liaison Committee on
Resuscitation; International Guidelines: Resuscitation, 2000.
MIMS Annual. MIMS Australia.
68
Adult Cardiorespiratory Arrest
PAH
BLS Algorithm
Precordial if appropriate
Thump
For witnessed /
monitored arrest
Attach Defib - monitor
Assess rhythm/pulse
Shockable Non-Shockable
VF / Pulseless VT PEA / Asystole
During CPR
IF NOT ALREADY DONE
Check electrode/paddle position & contact

Attempt/verify/secure IV access
Defibrillation2 Give adrenaline 1mg & repeat every 3 minutes
1st attempt up to CORRECT REVERSIBLE CAUSES

• Hypoxaemia
• Hypovolaemia
3 stacked shocks • Hypo/Hyperthermia
Further attempts should be • Hypo/Hyperkalaemia & other metabolic
disorders
single shocks • Tamponade
3 • Tension pneumothorax
Manual Biphasic 150J (Phillips XL) • Toxins / Poisons / Drugs
200 J (Lifepak 12/20) • Thrombosis
- pulmonary / coronary
CONSIDER
Advanced airway
Antiarrhythmic
Amiodarone 300 mg
Immediate CPR Lignocaine 1-1.5 mg/kg. Immediate CPR
2 minutes Magnesium 5 mmol 2 Minutes
Electrolytes
Potassium 5 mmol
Buffer
NaHCO3 1 mmol/kg
Atropine (1-3 mg) + Pacing
(for asystole & severe bradycardia)
1. Flowchart modifications are based on March 2006 ARC guidelines for witnessed arrest
2. If arrest is neither witnessed nor monitored use single shocks for all defibrillation attempts
3. Optimum biphasic energy on Heartstart XL & Lifepak defibrillators recommended by suppliers
69
7.0 ADULT ALS ALGORITHM
The Australian Resuscitation Council Advanced Life Support Flow Chart describes the management of
cardiac arrests. It illustrates the sequence of actions to be undertaken once equipment and drugs are
available.
The ALS algorithm is based on the following considerations.

• The importance of early defibrillation to survival from sudden cardiac arrest.
• Ventricular Fibrillation is the most common primary rhythm; a vast majority of survivors from
sudden cardiac arrest are from this group.
• There is a group of potentially reversible causes which, if left untreated, may precipitate
recurrence of cardiac arrest or prevent the return of spontaneous circulation.
• Cardiac compressions and ventilation is essential between defibrillation sequences or in non
shockable rhythms
7.1 Initial Management of Cardiac arrest
If there is no defibrillator immediately available the patient should receive basic life support measures
– Cardiopulmonary resuscitation. If a defibrillator is available defibrillation is attempted before BLS if
the rhythm is VF/VT.
If there is any delay in rhythm diagnosis and the patient is unconscious and pulseless a ‘blind’ shock of
150 joules (Philips XL biphasic) or 200 joules (Medtronic Lifepak biphasic) can be given by a manual
defibrillator.
As part of the BLS process at Princess Alexandra Hospital staff utilise the SAED. Therefore patients
in general ward areas will already be attached to the SAED and if required defibrillation may already
have occurred by the time members of the cardiac arrest team arrive. Rhythm analysis from the SAED
is 98% accurate.
70
7.2 Management of Specific Arrhythmias
Ventricular Fibrillation/ Pulseless Ventricular Tachycardia (VF/VT)
The essence of treatment of VF is repeated efforts at electrical defibrillation with two minute of CPR
between each shock.
If using a Biphasic Defibrillator: The manufacturer’s advice regarding joule levels should be adhered
to. There are three types of biphasic defibrillators utilised at PAH. It is therefore important that staff
are aware of the advised joules.
External
Phillips Heartstream and XL
• Initial and all subsequent shocks are 150 joules
Lifepak 20 and Lifepak 12
• Initial and subsequent chocks are 200 joules
Internal
• all shocks are 20 joules.
NOTE:
• 80% of successful defibrillations occur with one of the initial defibrillations.
• A 3 stacked – shock strategy is recommended in cases where the occurrence of the cardiac
arrest (VF/VT) is witnessed and a manual defibrillator is immediately available. Interruption to
CPR should be minimised and resumed after the third shock as indicated. If further shocks are
indicated a single shock strategy is recommended.
• Between each shock, in a set of three, the defibrillator is recharged leaving the paddles or
defibrillator electrodes on the chest.
• If the first set of three shocks fails then the patient should be intubated and ventilated with
100% oxygen: adrenaline should be given to improve cerebral and myocardial perfusion.
• During CPR for a patient with an advanced airway in place it is reasonable to ventilate the
lungs at a rate of 8 to 10 ventilations per minutes without pausing during chest compressions to
deliver ventilations.
71
• CPR should be given for two minutes after the third shock (manual defibrillator) or after single
shocks have been delivered. During this period, techniques of ALS are applied and potential
causes of the arrest are sought. CPR should only be interrupted for endotracheal intubation (20
secs), defibrillation and other assessments such as rhythm analysis.
• If further shocks do not revert the rhythm then administration of antiarrhythmic therapy should
be considered. Due to the supporting evidence, amiodarone is the antiarrhythmic first line
drug of choice. However, ALS trained nurses at PAH can administer lignocaine if there is no
medical officer present.
72
8.0 MANAGEMENT AFTER CARDIAC ARREST
The decision to cease CPR should be made by the Medical Officer attending the arrest or the patient’s
consultant on an individual patient basis, when continuation would be of no benefit considering the
patient’s medical condition.
After attempted resuscitation, care will be very much determined by the underlying cause of the initial
arrest.
• Intubated patients will be transferred to the Intensive Care Unit
• If cardiac monitoring required, patient will be transferred to the Coronary Care Unit
• Patients not requiring ICU or CCU monitoring can be managed on the ward.
• Consider and treat the cause of the initial arrest.
- Hypotension
- Hypovolemia / haemorrhage
- Hypoxia
- Shock
- Myocardial Infarction
- Cardiac Tamponade
- Pulmonary Oedema
- Pneumothorax
- Pulmonary Embolism
- Electrolyte Imbalance (K+, Ca++)
- Drug Overdose
- Poisoning
- Acidosis
73
8.1 POST ALS ALGORITHM
MONITOR
Secure and clear ETT / Guedels, suction PRN, Chest

Airway
X-Ray
Assess depth, rate, colour, ABG’s manual /
Breathing
mechanical ventilation
SBP > 100 – consider GTN, Nitroprusside; Check
electrolytes
Circulation
SBP < 90 – consider volume expansion, Dopamine,
Adrenaline
Available at bedside until patient admitted to Critical
Defibrillation
Care Unit
External pacing Transcutaneous then transvenous if required
Explain events to family, allow visit, arrange

Family support
chaplain, social worker
Team leader to debrief group. Evaluate performance
Group support & recommend individual follow up via Critical
Incident Policy
Ensure summary record of events, interventions &
Hospital documentation outcomes are documented in patient notes & CPR
audit tool
All instruments & equipment should be cleaned &

Instruments
replaced, ready for use according to hospital policy
74
8.2 Critical Incident Debriefing
As soon as possible after the resuscitation, debriefing should occur with all team members present.
The team leader is responsible for calling the team together as close to the resuscitation location as
possible.
Key points of discussion should include:
• Management of the arrest. The cause and treatments instituted.
• Allow members to suggest recommendations for future arrests.
• Team members should be encouraged to share feelings, anxieties, anger and possible guilt.
• Team members need to know that they can contact the team coordinator if questions arise later
and especially if they are not coping with the situation.
• If the situation is particularly distressing for staff, contact should be made with the staff
counsellor for psychological debriefing. (Refer to Critical Incident Stress Debriefing Policy in
Occupational Health and Safety Policy and Procedure Manual).
75
9.0 SPECIAL CASES PREGNANCY
9.1 Physiological Changes in Pregnancy
Extent of physiological changes will depend on stage of gestation, prior to second trimester changes
are minimal. Beyond 20 weeks an emergency caesarean section, may be considered in order to
improve foetal and maternal outcomes.
Respiratory
¾ Tidal volume is increased by 40 %
¾ Respiratory rate is unchanged
¾ Respiratory alkalosis, is the norm at full term
¾ Oxygen consumption increases 15 to 20 %, in weeks 16 to 40
¾ Breathing changes from abdominal to thoracic, as pregnancy progresses
Cardiovascular
¾ Pulse rate is increased to 85 - 90 beats / minute
¾ Blood pressure falls by 5 - 15 mm Hg in second trimester
¾ Plasma volume is increased
¾ Cardiac output peaks at 24 - 28 weeks gestation at 30 to 50 % above non-pregnant levels
¾ Aortocaval compression syndrome
Other changes:
¾ Gastric emptying is delayed
¾ Risk of eclampsia
76
9.2 Causes of Cardiopulmonary Arrest in Pregnancy
Specific Causes:
These are conditions, which are more commonly occurring causes for a pregnant patient who has
arrested.
¾ Pulmonary embolism
¾ Arrest as a complication of pre-eclampsia
¾ Amniotic fluid embolism
¾ Hypovolaemia from obstetric related haemorrhage E.g. abruptio placenta, placenta praevia
¾ Disseminated intravascular coagulopathy (DIC) related to haemorrhage
Treatment priorities remain the same as in patients who are not pregnant, although resuscitation
and stabilisation should be modified to account for anatomical and physiological changes.
77
9.3 Factors Affecting Resuscitation in Pregnancy
A - Airway
Increased tendency to develop arterial hypoxaemia
• This is due to increased total oxygen consumption and increased intrapulmonary shunting
Predisposition to pulmonary aspiration syndrome
• This is resultant from increased gastric acidity and delayed gastric emptying. The increased risk of
regurgitation and aspiration of gastric contents warrants early tracheal intubation in
cardiopulmonary arrest
B - Breathing
Physiological hyperventilation
• This is a respiratory alkalosis with a PaCO2 at full term falling to 30 mm Hg. A Pa CO2 of 40 mm
Hg indicates inadequate or impaired respiration
C - Circulation
Aortocaval compression syndrome
• The enlarged uterus compresses the great vessels, impairing the venous return, can result in a drop
in cardiac output of up to 40%
Application to CPR
• CPR cannot be performed with the pregnant woman on their back. In their 2nd and 3rd trimesters,
pregnant women should be positioned on their left lateral side as much as possible (achieved with a
small wedge or pillow under right hip)
An expanded blood volume
This is associated with the physiological anaemia of pregnancy. Maternal blood volume and cardiac
output increase up to 50 % above non-pregnant levels
78
9.4 Other Considerations
Chest compressions
• Compression rate should be 100 / minute
• Higher rates appear to generate greater blood flow and improved coronary perfusion
Defibrillation
• Elective cardioversion and emergency defibrillation has been successfully carried out in pregnant
patients
• Transthoracic defibrillation should proceed as for defibrillation in every other adult case
• Minimise risk by carefully placing pads and paddles
• Death of the mother and foetus will certainly follow unsuccessful defibrillation.
Caesarean [Post mortem - Delivery]

• Delivery of the foetus (may only be considered < 5 minutes following the loss of vital signs) will
be considered in the emergency situation only if the foetus is greater than 20 weeks gestation
• The age of the foetus will be considered if the option of a caesarean is being explored
• Some literature indicates that early caesarean delivery can result in rapid improvement of the
maternal status
Trans-abdominal foetal heart monitoring

• Transabdominal foetal heart monitoring should be used to assess the foetal status. In lieu of this
equipment being available Doppler ultrasound, ultrasound, or a high quality stethoscope should be
used
79
80
REFERENCES AND FURTHER READING
• Cummins RO, Chamberlain D, Hazinski MF, Nadkarni V, Klocck W, Kramer E, Becker L,

Robertson C. Koster R, Zaritsky A, Bossaert L, Ornato JP, Callahan V, Allen M, Steen P,
Connolly B, Sanders A, Idris A, Cobbe S. Recommended guidelines for reviewing, reporting and
conducting research on in-hospital resuscitation: The in-hospital 'Utstein Style'. Circulation. 1997;
April 15; 95(8): 2213-2238.
• Billi JE. The educational direction of the ACLS training program. Annals of Emergency
Medicine. 1993; 22(2): 484-488.
• Pepe PE. ACLS systems and training programs: Do they make a difference? Respiratory Care.
1995; April 40 (4): 427-436.
• Cummins RO, Ornator JP, Thies WH, Pepe PE. Improving survival from sudden cardiac arrest.
The:"chain of survival" concept. Circulation. 1991; 83: 1832-1847.
• Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care:2000.

Part I: Introduction to the International Guidelines 2000 for CPR and ECC: A Consensus on
Science. Circulation. Aug 22, 102 (suppl I): 1-12

Part 6: Section 7. Principles and Practice of ALS. Circulation. Aug 22, 102 (suppl I): 136-140.

Part 6: Section 3. Adjuncts for Oxygenation, Ventilation, and Airway Control. Circulation. Aug
22, 102 (suppl I): 95-105.
• Joanna Briggs Institute Acute Care Practice Manual. March 2001.Tracheal suction literature
review. D14-3.
• Australian Resuscitation Council. 1999. Precordial Thump. Australian Resuscitation Council.

Policy Statement: 11.2.2.
81

Part 6: Section 2. Defibrillation. Circulation. Aug 22, 102 (suppl I): 90-95.
• Australian Resuscitation Council. 2006. Section 11-Adult Advanced Life Support. Protocols for
Adult Advanced Life Support. Australian Resuscitation Council. Policy Statement: 11.2.1.
• United Kingdom Resuscitation Council ALS Policy Statement 2000

Part 6: Section 7C: A Guide to the International ACLS Algorithms. Circulation. Aug 22, 102
(suppl I): 142-158.

Part 8: Section 1. Life-Threatening Electrolyte Abnormalities. Circulation. Aug 22, 102 (suppl I):
217-223

Part 8: Section 2. Toxicology in ECC. Circulation. Aug 22, 102 (suppl I): 223-229.

Part 8: Section3. Special Challenges in ECC. Circulation. Aug 22, 102 (suppl I): 29-250.

Part 6: Section 8. Postresuscitation Care. Circulation. Aug 22, 102 (suppl I): 166-172.
• Australian Resuscitation Council. 2002. Section 11-Medications in Advanced Life Support.

Australian Resuscitation Council. Policy Statement: 11.4.

Part 6: Section 5. Pharmacology I: Agents for Arrhythmias. Circulation. Aug 22, 102 (suppl I):
112-129.
82

Part 6: Section 6. Pharmacology II: Agents to Optimise Cardiac Output and Blood Pressure.
Circulation. Aug 22, 102 (suppl I): 129-136.

Part 6: Section 1. Introduction to ACLS 2000: Overview of Recommended Changes in ACLS
From the Guidelines 2000 Conference. Circulation. Aug 22, 102 (suppl I): 86-90.
• Australian Resuscitation Council. 2002. Section 11-Medications in Advanced Life Support.

Australian Resuscitation Council. Policy Statement: 11.4.
• Resuscitation Council. UK . 2000. ALS Course Provider Manual 2000. 4th Ed. Resuscitation
Council. UK.
83

ALS Manual 2010.version 1

Caricato da

Informazioni sul documento

Descrizione originale:

Titolo originale

Copyright

Formati disponibili

Condividi questo documento

Condividi o incorpora il documento

Opzioni di condivisione

Hai trovato utile questo documento?

Questo contenuto è inappropriato?

Copyright:

Formati disponibili

ALS Manual 2010.version 1

Caricato da

Copyright:

Formati disponibili

INFORMATION MANUAL

ALS TRAINING PROGRAMME

ALS Information Manual PAH 2010

2.0 AIRWAY MANAGEMENT 12

3.0 CARDIAC RHYTHMS 24

3.5 IDIOVENTRICULAR RHYTHM 36

5.0 CARDIAC PACING 45

ADULT ALS ALGORITHM FLOWCHART 69

7.0 ADULT ALS ALGORITHM 70

8.0 MANAGEMENT AFTER CARDIAC ARREST 73

9.0 SPECIAL CASES PREGNANCY 76

PAEDIATRIC CARDIORESPIRATORY ARREST ALGORITHM FLOWCHART 80

REFERENCES AND FURTHER READINGS 81

This manual was originally compiled in November 1994:

• Cardiac Monitoring, Recognition and Treatment of Arrhythmias

• Defibrillation – demonstrate safe and appropriate defibrillation technique

• External Cardiac Pacing – demonstrate safe and effective external pacing.

1.1 LEARNING GOALS

(a) Cardiac Arrest Procedure

(b) Airway Management

(c) Cardiac Monitoring

(e) Emergency Drugs

1.2 LEARNING OUTCOMES / OBJECTIVES

Staff competent in Advanced Life Support will be able to:

(d) Demonstrate effective Cardiopulmonary Resuscitation techniques (basic life support

(k) Demonstrate knowledge of the pacing functions of External Pacemakers.

1.3 THE RAPID RESPONSE TEAM

Acute Change In Physiology

EXCEPTIONS (AT THE PRINCESS ALEXANDRA HOSPITAL)

• Undertakes clinical management of the resuscitation

• Assesses the need for additional personnel

• Ensures safety of patient and staff at all times

• Determines appropriateness of patient treatment in consultation with the appropriate clinicians

• Ensures that resuscitation documentation is completed

• Undertakes debriefing and staff counselling as necessary

Other medical staff:

Ward nursing staff – Responsibilities:

• Summon the Rapid Response Team – Dial 666

• Ensure that wall suction and oxygen is available

• Ensure that the Medical Records are at the bedside

• Prepare and prime infusion line

• Maintain documentation of the sequence of events during the arrest

• Arrange for transport of urgent blood specimens

• Notify the patient’s clinical team

• Ensure Medical Officer notifies the patient’s relatives

• Assist with patient transport

• Answer the ward telephone

• Be available to assist staff with any tasks as requested

2.0 AIRWAY MANAGEMENT

OXYGENATION, VENTILATION AND AIRWAY MANAGEMENT OVERVIEW

2.1 PHARYNGEAL AIRWAYS

Technique for insertion:

The Nasopharyngeal Airway

Technique for insertion:

2.2 MANUAL RESUSCITATION BAGS (MRBs)

Manual Resuscitation Bag Ventilation

Bag Mask Ventilation

2.3 LARYNGEAL MASK AIRWAY (LMA)

• profoundly unconscious and unresponsive;

Laryngeal Mask Insertion

2.3.1 POTENTIAL PROBLEMS

Three problems may be anticipated during use of the LMA: