SLCEP ALS e Book PDF

Advanced life support
Course manual 2023
Sri Lanka College of Emergency Physicians

43A, Dharmapala Mawatha Madiwela, Kotte 10100
Web: www.slcep.lk
Email: info@slcep.lk
List of contributors
1 Dr Inuka Wijegunawardana Consultant Emergency Physician
2 Dr A. G. Thanuja Darshani Consultant Emergency Physician
3 Dr Senitha Liyanage Consultant Emergency Physician
4 Dr Indika Lanarolle Consultant Emergency Physician
5 Dr Senaka Herath Registrar in Emergency Medicine
6 Dr Iresha Rathnayake Registrar in Emergency Medicine
7 Dr Damindi Wanniarachachi Registrar in Emergency Medicine

Contents
Chapter 1 Advanced Life support in Perspective 01
Chapter 2 Recognizing Deterioration and Preventing Cardiac 07

Arrest
Chapter 3 Basic Life Support (BLS) 17
Chapter 4 Advanced Life Support(ALS) Algorithm 27
Chapter 5 Airway Management & Ventilation 30
Chapter 6 Rhythm Recognition and Defibrillation 35
Chapter 7 Reversible Causes in Cardiac Arrest 43
Chapter 8 Post Resuscitation Care 46
Chapter 9 Resuscitation in Special Circumstances 57

Chapter
Advanced Life Support
1 in Perspective
In the year 2019, ischemic heart disease emerged as the leading global cause of death,
particularly prevalent in lower-middle-income countries like Sri Lanka. Meanwhile,
sudden cardiac arrest (SCA) ranked as the third leading cause of death in Europe. The
World Health Organization's 2020 data revealed that coronary heart disease accounted
for 26,304 deaths in Sri Lanka, constituting 22.66% of the total mortality rate. Notably,
coronary artery disease (CAD) was responsible for 34% of deaths in a Sri Lankan
autopsy study, a significantly higher percentage than the 17% recorded in the US and
UK.
Extensive efforts have been made to comprehend the underlying factors and causes of
cardiac arrest, along with variations in its occurrence both within and across countries.
While the determinants of survival following out-of-hospital cardiac arrest (OHCA) and
in-hospital cardiac arrest (IHCA) are well-documented, there still exists substantial
divergence in terms of incidence and outcomes.
Unfortunately, as of the latest available information, updated statistics specific to out-

of-hospital and in-hospital cardiac arrest data in Sri Lanka remain unavailable.
Therefore, data from authoritative sources such as the European Resuscitation Council
(ERC) and Australian guidelines have been used to shed light on these critical aspects.
Out of Hospital Cardiac Arrest (OHCA)

The annual occurrence of out-of-hospital cardiac arrest (OHCA) in the UK stands at
around 55 cases per 100,000 residents. Notably, the majority of these cardiac arrests
(72%) transpire in either private residences or workplaces (15%). Approximately two-
thirds of these incidents are witnessed by bystanders or ambulance personnel. Among
those who undergo resuscitation attempts, approximately 25-30% initially experience a
return of spontaneous circulation (ROSC), yet only about 8% ultimately survive to be
discharged from the hospital.
The initial rhythm observed during these events is shockable (ventricular

fibrillation/pulseless ventricular tachycardia (VF/pVT)) in approximately one-quarter of
cases, while the remaining cases present with non-shockable rhythms, including
asystole (about 50%) and pulseless electrical activity (PEA) (about 25%).
01
Chapter 1 Advanced life support in perspective
A study conducted in Victoria (Australia), covering a 7-year analysis period from 2006
to 2012, recorded 48,291 cases of Out of Hospital Cardiac Arrests (OHCAs). Of these
cases, resuscitation was attempted in 15,362 instances (45%). During this period, the
overall
survival rate to hospital discharge for cases where resuscitation was attempted was
12%, with a higher rate of 30% among patients presenting with a shockable rhythm.
It's important to note that the majority of cardiac arrests affect adults (98%), with
one-third (33%) of them falling in the age group of 15-64 years. Approximately 8 out
of 10 OHCA cases are attributed to cardiac causes. The rate of bystander
cardiopulmonary resuscitation (CPR) varies significantly between and within
countries, averaging at 58%, but ranging from 13% to 83%. The use of public access
defibrillators is reported to be relatively low, being employed in less than 1 in 10
OHCA cases.
Significant health disparities are evident in the incidence of cardiac arrest, the
provision of bystander CPR, and the availability of public access defibrillators.
Deprived areas and regions with a higher proportion of residents from minority
ethnic backgrounds experience a greater incidence of cardiac arrest, lower rates of
bystander CPR, and reduced access to public access defibrillators. Shockable rhythms
are initially detected in approximately 1 in 4 OHCA cases (22-25%), and ROSC is
achieved in around 30% of attempted resuscitations. Survival rates upon hospital
discharge average at 8%, although they vary from 0% to 18%.
In Hospital Cardiac Arrest (IHCA)

In Europe, the annual occurrence of in-hospital cardiac arrest (IHCA) falls within a
range of 1.5 to 2.8 cases per 1,000 hospital admissions. Several factors influence
survival rates, including the initial cardiac rhythm, the location of the arrest, the level
of monitoring during the incident (including whether it was witnessed), and individual
patient factors such as age and underlying health conditions. The typical age of
individuals experiencing IHCA is around 70 years. The majority of cardiac arrests
(85%) take place in hospital wards and involve patients who were initially admitted
for medical reasons.
Among the recorded cases, approximately 16.9% were shockable cardiac rhythm
(ventricular fibrillation/pulseless ventricular tachycardia VF/VT), while 72.3%
presented with non-shockable rhythms (asystole or pulseless electrical activity).
Survival rates to hospital discharge associated with these two types of rhythms were
49.0% and 10.5%, respectively. However, when considering statistics from the UK
spanning the years 2011 to 2013, the overall survival rate to hospital discharge was
calculated at 18.4%.
02
When a hospital's resuscitation team is involved in the treatment of IHCA cases,

return of spontaneous circulation (ROSC) is achieved in approximately half of the
cases (53%). Furthermore, a quarter of patients (23.6%) who receive treatment from
the hospital's resuscitation team go on to survive and are discharged from the
hospital. In European nations where the practice of withdrawing life-sustaining
treatment is common, more than four out of five patients (83%) who survive to
hospital discharge achieve a favourable neurological outcome.
Post-resuscitation care
Among patients admitted to critical care and necessitating invasive mechanical
ventilation, one in every ten individuals had experienced a cardiac arrest before their
admission. The typical duration of their stay in critical care units ranges from 4 to 6
days, with a subsequent hospital stay averaging between 14 to 21 days.
It's notable that among those admitted to critical care units, one in ten who
experienced out-of-hospital cardiac arrest (OHCA) and one in twenty-five who
experienced in-hospital cardiac arrest (IHCA) ultimately become organ donors for
transplantation.
Regarding survival rates, approximately half of those admitted to critical care

following OHCA manage to survive and are discharged from the hospital, while one-
third of those admitted following IHCA achieve the same outcome. Among the
survivors, two-thirds are able to return home after their hospital stay.
Post-cardiac arrest rehabilitation

Significant disparities exist in the availability of rehabilitation services and
psychological support for individuals who have experienced a cardiac arrest. A
substantial number of patients do not have the opportunity to access post-cardiac
arrest rehabilitation
03
The Chain of Survival
The interventions that contribute to a successful outcome after a cardiac arrest can
be conceptualised as a chain – the Chain of Survival. The chain is only as strong as its
weakest link; all four links of the Chain of Survival must be strong.
They are:
• early recognition and call for help
• early CPR
• early defibrillation
• post-resuscitation care
Early recognition and call for help
Cardiac arrest is defined as the sudden cessation of spontaneous respiration and

circulation.
a) Cardiac arrest is confirmed by the absence of signs of life (SOL)

b) Absent Carotid pulse
c) Unresponsive patient, not having normal breathing is in cardiac arrest
Within hospital settings, the timely identification of critically ill patients at risk of
cardiac arrest, along with the activation of the resuscitation team or medical
emergency team (MET), is essential for initiating preventative treatment. Hospitals
should implement a track-and-trigger early warning score system (EWS) to promptly
recognize patients who are critically ill or prone to clinical deterioration. This EWS
should include a predetermined, graded response tailored to the patient's score. The
selection of the system should take into account local considerations and align with
national guidelines.
04
Furthermore, it is imperative that all healthcare staff are authorized to request

assistance and are proficient in utilizing structured communication tools such as SBAR
or other appropriate methods to ensure effective and efficient communication.
SBAR:
▪ Situation
▪ Background
▪ Assessment
▪ Recommendation
It is recommended that a standardized number, such as 2222, be universally adopted

for calling the resuscitation team or medical emergency team (MET) in all European
hospitals.
In cases of out-of-hospital cardiac arrest (OHCA), prompt recognition of the

significance of chest pain is crucial. This awareness should prompt the victim or a
bystander to contact the Emergency Medical Services (EMS) to ensure the victim
receives timely treatment that can potentially prevent cardiac arrest. Access to the
EMS in cases of OHCA is of utmost importance, and in most countries, this is achieved
through a single telephone number, such as 112 or 999
Early CPR
Administering chest compressions and ventilation plays a crucial role in slowing down
the deterioration of both the brain and the heart.
In the event of a cardiac arrest, bystander CPR significantly extends the window for
successful resuscitation and substantially increases the likelihood of survival,
especially in cases of ventricular fibrillation (VF) cardiac arrest, where the chances of
survival can be tripled. Performing chest-compression-only CPR is more effective than
not providing any CPR at all.
Following an in-hospital cardiac arrest (IHCA), it is imperative to initiate chest

compressions and ventilation without delay. However, these actions should not
hinder attempts to defibrillate patients experiencing ventricular fibrillation (VF) or
pulseless ventricular tachycardia (pVT). It is essential to minimize interruptions in
chest compressions, allowing only very brief pauses during defibrillation attempts and
rhythm checks.
Early defibrillation
Several factors related to the patient and the CPR influence the outcome of out-of-
hospital cardiac arrest (OHCA). Community initiatives that involve lay bystander CPR
and the utilization of automated external defibrillators (AEDs) have shown significant
improvements in OHCA outcomes.
05
The critical components of OHCA CPR involve chest compressions and early
defibrillation. Prompt defibrillation remains the definitive treatment for ventricular
fibrillation (VF), emphasizing the need for the implementation of Public Access
Defibrillation programs with AEDs in many regions
Within hospital systems, there should be a focus on recognizing cardiac arrest
promptly, initiating CPR without delay, and administering defibrillation rapidly, ideally
within a time frame of less than three minutes when indicated. All hospital staff
should possess the ability to swiftly identify cardiac arrest, call for assistance,
commence CPR, and apply defibrillation, either by attaching an AED and following its
prompts or by using a manual defibrillator.
Post-resuscitation care
The return of spontaneous circulation (ROSC) marks a crucial stage in the continuum
of resuscitation. However, the ultimate objective is to restore the patient to a state of
normal cerebral function, a stable cardiac rhythm, and proper hemodynamic
function. This paves the way for the patient to leave the hospital in a reasonably
healthy condition with minimal risk of experiencing another cardiac arrest. The
quality of care during the post-resuscitation period plays a significant role in
determining the patient's ultimate outcome.
The post-resuscitation phase begins at the point where ROSC is achieved, and it is
incumbent upon the Advanced Life Support (ALS) provider to deliver exceptional post-
resuscitation care until the patient is safely transferred to an appropriate high-care
unit. In cases of out-of-hospital cardiac arrest (OHCA), patients who achieve ROSC
should be promptly transferred to a designated care center, such as a cardiac arrest
center, to optimize their chances of a successful recovery.
06
Chapter
Recognizing Deterioration
2 and Preventing Cardiac Arrest
Early recognition of the deteriorating patient and prevention of cardiac arrest is the
first loop of chain of survival. Steps of this loop include staff education, monitoring
of patients, recognition of patient deterioration, a system to call for help and
effective response .
Most cardiorespiratory arrest in hospital are not sudden or unpredictable event
most of the cases there is deterioration in clinical signs during the hours before
cardiac arrest. Early recognition and effective treatment of the deteriorating patient
might prevent cardiac arrest death or unanticipated ICU admission.
07
Chapter 2 Recognizing deterioration and preventing cardiac arrest
Prevention of in hospital cardiac arrest

The chain of prevention
How to observe patient, interpretation of observed signs,

recognition of sign of deterioration, the use of ABCDE approach,
Education simple skills to stabilise the patient until expert help, role in rapid
response team in the hospital
Recording of vital signs which may include the use of electronic

Monitoring monitoring and /or documentation device
Recognition Suitably design vital chart, sets of predetermined calling criteria
summoning a response to a deteriorating patient should be

universally known and understood, unambiguous and mandated. A A
Call for Help structured communication tool such as ISBAR (Identify, Situation,
Background, Assessment, Recommendation) or RSVP (Reason, Story,
Vital signs, Plan) should be used to call for help
Response By staff with appropriate acute or critical care skills
Recognizing the deteriorating patient
In general, the clinical signs of critical illness are similar whatever the underlying
process because they reflect failing respiratory, cardiovascular, and neurological
systems so call ABCDE problems. The assessment of very simple vital signs, such as
respiratory rate, may help to predict cardiorespiratory arrest To help early detection of
critical illness, health institutions use track and trigger or early warning scores (EWS) or
calling criteria. Early warning scoring systems allocate points to the measurements of
routine vital signs on the basis of their derangement from an arbitrarily agreed 'normal
range. The weighted score of one or more vital sign observations or the total EWS,
indicates the level of intervention required.
08
Early warning scores are dynamic and change over time and the frequency of
observations should be increased to track improvement. Alternatively, systems
incorporate calling criteria based on routine observations, which activate a response
when one or more variables reach an abnormal value. Recent research suggests that
EWS or systems where multiple factors can trigger a response may be better
discriminators of outcomes than calling criteria.
09
Response criteria- any observation in purple area, cardiac

Emergency call or respiratory arrest
Action -place emergency call
BLS/ALS
Clinical review Response criteria -any observation in red area

Action -senor medical officer review within 30 minutes
Response – any observation is in an orange area

Junior medical review Actions- junior medical officer review
Increase frequency of observation
Response - any observation is in a yellow area

Increase surveillance Action inform senor nurse
10
ABCDE approach
The approach to all deteriorating or critically ill patients .The steps of ABCDE approach
are:
1.Use the Airway, Breathing, Circulation, Disability, Exposure approach

to assess and treat the patient.
2.complete initial assessment and re-assess regularly
3.Treat life-threatening problems as soon as detected.
4. Assess the effects of treatment
5.Call for appropriate help early.
6. Communicate effectively using communication tool e.g. the SBAR approach
11
Initial approach
1. Ensure personal and patient safety. Wear appropriate PPE
2. Check whether patient is awake or not , If the patient appears unconscious or has
collapsed, shake him and ask "Are you alright?" If he responds normally, he has a
patent airway, is breathing and has brain perfusion.
3. If no response, “Look, Listen and Feel" of the patient which should take no longer
than 30 seconds.
4. If the patient is unconscious, unresponsive, and is not breathing normally start CPR
according to the guidance in chapter 4. If you are confident and trained to do so, feel
for a pulse to determine if the patient has a cardiac arrest. If there are any doubts
about the presence of a pulse start CPR.
5. If the patient is not in cardiac arrest start the ABCDE approach.
Examination Intervention Goal

ABCDE
A
APPROACH
Stridor /noises Suctions
Secretions Airway opening
Airway Oedema mauver -chin lift, jaw
Diminish air entry thrust, head tilt Patent air way
See-saw breathing. OPA/NPA
Front of neck access
High flow oxygen
1 Look, listen and feel for the
general signs of respiratory
distress:
2 use of the accessory muscles of
respiration. Oxygen therapy
3 Abdominal breathing. Nasal prong
Simple face mask Sufficient
B 4 Count the respiratory rate. The NRBM oxygenation
normal rate is 12-20 breaths min'. BVM and
Breathing A high (> 25 min ), or increasing, NIV ventilation
respiratory rate is a marker of Invasive ventilation
illness
5 the pattern (rhythm) of
respiration
12
6 Assess chest expansion is equal on both

sides.
7 Record the inspired oxygen
concentration FiO2(%) and the SpO,
8 Listen to the patient's breath sounds -
rattling airway noises indicate the
presence of airway secretions Oxygen
Stridor or wheeze suggests partial, but therapy
significant, airway obstruction. Nasal prong
B Simple face Sufficient
Breathing 9 Percuss the chest: hyper-resonance may mask oxygenation
suggest a pneumothorax; dullness usually NRBM and
indicates consolidation or pleural fluid BVM ventilation
NIV
10 Auscultate the chest: Invasive
bronchial breathing ventilation
lung consolidation with patent airways;
absent or reduced sounds
a pneumothorax or pleural fluid or lung
consolidation
11 Check the position of the trachea in the

suprasternal notch: deviation to one side
indicates mediastinal shift
12 Feel the chest wall to detect surgical

emphysema or crepitus (suggesting a
pneumothorax
13
Look at the colour of the hands

and digits: are they blue, pink,
pale or mottled?
Assess the limb temperature by

feeling the patient's hands: are
they cool or warm? Control catastrophic
bleeding if indicated
Measure the capillary refill time
(CRT). Apply cutaneous Large 2 bore cannulas
pressure for 5 s on a fingertip 14-16G
held at heart level (or just
above) with enough pressure to Take blood from the
cause blanching cannula for blood gas
Measure the patient's blood analysis, routine
pressure. response to reduced haematological,
cardiac output. A low diastolic biochemical,
blood pressure suggests arterial coagulation and Stabilisation
vasodilation (as in anaphylaxis microbiological of circulation
C or sepsis). A narrowed pulse investigations, and
Circulation pressure suggests arterial cross- matching, before
vasoconstriction (cardiogenic infusing intravenous
shock or hypovolaemia fluid.
Auscultate the heart. S1 S2 Assess fluid status

,Gallop rhythm , Is there a Passive leg raising
murmur or pericardial rub? Fluid responsiveness
Features of heart
Look thoroughly for external failure
haemorrhage from wounds or
drains or evidence of concealed
haemorrhage (e.g. thoracic, Seek measures
intra-peritoneal, retroperitoneal improving tissue
or into gut) Intra-thoracic, perfusion (e.g.
intraabdominal or pelvic inotropes or
vasopressors).
Seek the signs of conditions
that are immediately life
threatening, e.g. cardiac
tamponade, massive or
continuing haemorrhage, 14
septicaemic shock
Assess causes for

unconsciousness include
profound hypoxia, hypercapnia, Recognise neurologic
hypotension deficits e.gaphasia and
hypoglycaemia, other signs of stroke
intoxication
Nurse unconscious
1Review and treat the ABCs patients in the lateral
exclude or treat hypoxia and position if their airway
hypotension is not protected
If the blood sugar is

3. Examine the pupils (size, below 4.0 mmol I, give
equality and reaction to light). an initial dose of 50 ml
of 10% glucose
4 Make a rapid initial assessment solution intravenously.
of the patient's conscious level If necessary, give
using the AVPU method: Alert, further doses of
responds to Vocal stimuli, intravenous 10%
responds to Painful stimuli or glucose every minute Evaluation of
D Unresponsive to all stimuli. until the patient has neurological
Disability Alternatively, use the Glasgow fully regained status
Coma Scale score. consciousness, or a
total of 250 ml of 10%
Measure the blood glucose to glucose has been
exclude hypoglycaemia using a given. Repeat blood
rapid finger-prick bedside testing glucose measurements
method to monitor the effects
of treatment.
6. Consider other causes of
reduced levels consciousness like Antidote if indicated
electrolyte disorders or
metabolic disorders
(hyponatremia ,elevated plasma
ammonia in patients with liver
disease)
15
To examine the patient

properly full exposure of the
body may be necessary.
Assess the patient from head
E Temperature control – Revealing other
to toe.
Exposure passive and active symptoms and
Respect the patient's dignity, thermoregulatio
minimise heat loss and n
measure the body
temperature.
See any rashes
See any injuries from head to
toe
Signs of DVT , cellulitis etc
S.A.M.P.L.E history
S SIGN AND SYMPTOMS
A ALLERGIES
M MEDICATIONS
P PAST MEDICAL HISTORY
L LAST MEAL
E EVENT
16
Chapter
Basic life support
3
ADULT BASIC LIFE SUPPORT
The sequence of steps for the initial assessment and treatment of the unresponsive
victim are as below. If the patient is unresponsive with abnormal or absent
breathing, it is reasonable for the emergency dispatcher to assume that the patient
is in cardiac arrest
D - Danger
R - Response
S - Send /Shout for Help
A - Airway
DRS ABCD B - Breathing
C - CPR
D - Defibrillation
SEQUENCE DESCRIPTION
Danger
▪ Make sure you, the victim and any
Make sure it is safe to help
bystanders are safe
▪ Wear PPE (gloves, apron, mask) if
available
▪ Look out for blood spills, sharps,
electric wire unsteady beds,
trolley.. etc
17
Chapter 3 Basic life support
Gently tap his shoulders and ask

loudly: “Are you alright?"
Responsiveness
Check the victim for a response
If he responds-- leave him in the
position in which you find him,
provided there is no further danger.
• Try to find out what is wrong with
him.
• Get help if needed.
• Reassess regularly
If NO Response- Position the victim

on their back and check for
breathing
• Activate ERS.
Shout for help
activate Emergency Response System(ERS) • Shout “Emergency! Emergency!
Bring the resuscitation trolley and
defibrillator!”
• Health care provider (HCW) can

look for no breathing (or only
gasping) almost simultaneously
before activating the ERS.
18
Airway
Open the airway Head tilt chin lift
Place your hand on the forehead.
Gently tilt the head back and with
your fingertips under the point of
the victim's chin, lift the chin to open
the airway
Jaw thrust – if suspect cervical

injury
Use index and middle fingers to
physically push the posterior aspects
of the mandible upwards while your
thumbs push down on the chin to
open the mouth.
19
Look, listen and feel for breathing

for no more than 10 seconds
Breathing • Determine absent or abnormal
Assess for normal breathing breathing almost simultaneously
while opening the airway by looking
at the chest, neck and face
- In the first few minutes after
cardiac arrest, a victim may be barely
breathing, or taking infrequent, slow
and noisy gasps (abnormal
breathing).
- Do not confuse this with normal
breathing.
- Treat absence of breath or
presence of abnormal breathing as a
sign of cardiac arrest.
• Chest compression should be
started with the absence of breath
or presence of abnormal breathing.
If you have any doubt whether or
not breathing is normal, act as if
they are not breathing normally and
prepare to start CPR.
Send someone to get an AED if

SEND FOR AED available
If you are alone, do not leave the
victim and start CPR
20
Start chest compressions
Location: Lower half of the sternum/centre

of the chest
• Kneel by the side of the victim.

Circulation
• Place the heel of one hand in the centre of
Start chest compression the victim’s chest (centre of the chest).
• Place the heel of your other hand on top of
the first hand.
• Interlock the fingers of your hands and
ensure that pressure is not applied over the
victim's ribs.
• Keep your arms straight.
• Do not apply any pressure over the upper

abdomen or the bottom end of the bony
sternum (breastbone).
• Position your shoulders vertically above
the victim's chest and press down.
High quality chest compression:

• Middle of chest, lower half of sternum
• Depth: 5 - 6cm
• Rate : 100to 120/min
• 30 compressions: 2 ventilations
• Full recoil after each compression.
Each ventilation in 1 second
• Minimize interruption
Delivery of rescue breaths, shocks,
ventilations and rhythm analysis
lead to pauses in chest compression
- Pre-and post-shock pauses of less
than 10s
21
Bag-valve-mask (BVM) ventilation

• Position yourself directly above the
RESCUE BREATH victim’s head.
(compression to ventilation ratio 30:2) • Place the mask on the victim’s face,
using the bridge of the nose as a guide
for correct position.
• Use the E-C clamp technique to hold
the mask in place while you lift the jaw
to hold the airway open:
- perform head tilt.
- use the thumb and index finger of one
hand to make a “C” on the side of the
mask, pressing the edges of the mask to
the face. - use remaining fingers to tilt
angles of the jaw (3 fingers form an “E”).
• Squeeze the bag to give breaths (1
second each) while watching for chest
rise.
Mouth to mask ventilation

• Position yourself at the victim’s side.
• Place the mask on the victim’s face and
seal the mask against the face.
• Place index finger and thumb along the
edge of the mask, remaining fingers
along the bony margin of the jaw and
perform head tilt-chin lift to open the
airway.
• While you lift the jaw, press firmly and
completely around the outside edge of
the mask to seal the mask against face.
• Deliver air over 1 second, look for
victim’s chest rise.
22
Mouth to mouth rescue breath

• Pinch the soft part of the nose,
RESCUE BREATH
using the index finger and thumb.
(compression to ventilation ratio 30:2)
• Allow the mouth to open, but
maintain chin lift.
• Take a normal breath and place
your lips around the mouth, making
sure that you have a good seal.
• Blow steadily into the mouth while
watching for the chest to rise, taking
about 1 second as in normal
breathing; this is an effective rescue
breath.
• Maintaining head tilt and chin lift,
takAe your mouth away from the
victim and watch for the chAest to fall
as air comes out.
• Take another normal breath and
blow into the victim’s mouth once
more to achieve a total of two
effective rescue breaths. Do not
interrupt compressions by more than
10 seconds. Then return your hands
without delay to the correct position
on the chest/sternum and give a
further 30 chest compressions.
During delivery of rescue breath:
• Avoid hyperventilation
• The ventilation is over 1 second till
there is a visible chest rise.
23
If you are untrained, or unable to give

rescue breathes, give chest-
Compression-Only CPR
compression-only CPR (continuous
compressions at a rate of 100-120 min-
1)
When AED Arrives As soon as the AED arrives switch it on

and attach the electrode pads to the
victim’s bare chest
Switch on the AED and attach the electrode
• If more than one rescuer is present,
pads
CPR should be continued whilst the
electrode pads are being attached to
the chest
Follow the spoken and visual directions
given by the AED
• If a shock is advised, ensure that
neither you nor anyone else is touching
the victim
• Push the shock button as directed
•Then immediately resume CPR and
continue as directed by the AED
If NO SHOCK IS ADVISED Continue CPR
24
If no AED is available, OR whilst waiting

for one to arrive, continue CPR
Do not interrupt resuscitation until:
• A health professional tells you to
stop OR
IF NO AED IS AVAILABLE • the victim is definitely waking up,
Continue CPR moving, opening eyes, and
breathing normally OR
• You become exhausted
It is rare for CPR alone to restart the

heart. Unless you are certain that the
victim has recovered continue CPR
Signs that the victim has recovered
• Waking-up
• Moving
• Opening eyes
• Breathing normally
25
• If you are certain that the victim is

breathing normally but still
unresponsive, place them in the
recovery position
IF UNRESPONSIVE BUT BREATHING
• Be prepared to restart CPR
NORMALLY
immediately if the victim becomes
unresponsive, with absent or abnormal
breathing
Be prepared to restart CPR immediately if Recovery Position

the victim deteriorates or breathing normally • Remove the victim’s glasses, if
stops worn.
• Kneel beside the victim and make sure
that both his legs are straight.
• Place the arm nearest to you at right
angles to his body, elbow bent with the
hand palm-up.
• Bring the far arm across the chest, and
hold the back of the hand against the
victim’s cheek nearest to you.
• With your other hand, grasp the far leg
just above the knee and pull it up,
keeping the foot on the ground.
• Keeping his hand pressed against his
cheek, pull on the far leg to roll the
victim towards you on to his side.
• Adjust the upper leg so that both the
hip and knees are bent at right angles.
• Tilt the head back to make sure that
the airway remains open.
If necessary, adjust the hand under the
cheek to keep the head tilted and facing
downwards to allow liquid material to
drain from the mouth.
• Check breathing regularly.
Signs that the victim has recovered
▪ Waking up
▪ Moving
▪ Open eye
26
▪ Normal breathing
Chapter
Advanced Life Support
4 (ALS) Algorithm
To perform effective advanced life support 5 factors should be fulfilled
1. Patent airway and adequate ventilation.

2. High quality minimally interrupted chest compressions.
3. Rhythm recognition and safe defibrillation if indicated.
4. Reversal of probable causes.
5. Administration of required medications.
Each of these factors have discussed in different chapters under particular topics in
this manual.
Here we are going to discuss the management of advanced life support in where all
these factors should be done together with proper coordination and timing. To
perform this, we have to follow a methodical order, which we called “advanced life
support (ALS) algorithm” (see the figure).
Immediately after the confirmation of a cardiac arrest, effective chest compressions

and delivery of rescue breaths (with BMV device) should be started and maintained
at a ratio of 30:2 (See BLS chapter). Help should be requested as early as possible
from other staff or resuscitation team depending on the setup.
Patient should be attached to the defibrillator with electrodes immediately and lead
(II) and sensitivity (×1 or ×2) should be selected on machine without interrupting the
chest compressions. When you ready to assess the rhythm, ask chest compressor to
“STOP”. Recognize the rhythm as shockable or non-shockable without delay and ask
compressor to “START” chest compressions again immediately. (Here a new
compressor can start chest compressions)
If the rhythm is shockable (VF or VT) select the energy level (150J – 200J biphasic for
the first shock and maximal energy for subsequent shocks) and safe defibrillation
should be done with minimal interruption to the chest compressions (See the
rhythm recognition and defibrillation chapter).
27
Chapter 4 Advanced Life Support (ALS) Algorithm
In safe defibrillation, give safety commands verbally and also check them visibly
before charge the defibrillator and take off the paddles. Recommended safety
commands before charging are, “O2 free flow away”, “continue chest compressions”
and “everyone else stand clear”. Then charge the defibrillator and apply gel to the
patient’s chest while chest compression is continuing.
Ask chest compressor to “STOP” just before you take off the charged paddles.
Charged paddles should be taken one at a time (usually more distantly placed paddle
first) and take the other after you keep the first paddle on patient’s chest. After
keeping both paddles on chest with a good contact, release the charged energy by
pressing the shock button on both paddles simultaneously. As soon as you deliver the
shock ask chest compressor to “START” the compression again. Chest compression
should be continued for next 2 minutes.
If the rhythm is non-shockable (PEA or asystole) ask chest compressor to “START”
immediately and continue for next 2 minutes. Iv adrenaline 1:10000 1mg should be
administered immediately after start of chest compressions if the rhythm is non-
shockable.
During 2-minute cycle of chest compressions two things should be done.
1. Improve the quality of ALS – e.g. Assess ETCO2 and adjust the quality of chest
compression, insert definitive airway (supraglottic or endotracheal tube) if
indicated.
2. Check for reversible causes (4Hs and 4Ts) and treat appropriately (See the
reversible causes chapter).
3.
At the end of 2 minutes rhythm should be assessed again and defibrillation should be
delivered if indicated according to above mentioned sequalae. Then restart the CPR
and continue for another 2 minutes as mentioned above.
If the rhythm is shockable continuously, iv adrenaline 1:10000 1mg and iv
amiodarone 300mg should be administered after the 3rd shock.
Thereafter iv adrenaline should be repeated in both shockable and non-shockable
arrests in every 3 – 5 minutes (every other cycle) until ROSC achieve or decide to
terminate the resuscitation.
During the rhythm assessment, central pulse should also be checked. If pulse present
or if other signs of life (purposeful movements, breathing, eye opening or sudden rise
in ETCO2) returned, chest compressions should be discontinued and immediate post
resuscitation care should be started.
Rescue breaths should be continued if spontaneous breathing is absent or ineffective.
28
Chapter 4 Advanced Life Support (ALS) Algorithm
Unresponsive with absent or abnormal breathing
Call for help /

Resuscitation team
CPR 30:2
Attach defibrillator
Assess rhythm
Shockable Non – shockable

(VF/ Pulseless (Asystole/ PEA)
VT) Assess for signs of life
1 Shock ROSC
Immediately
resume CPR for 2
Post resuscitation
minutes
care
Give high quality chest compressions and Identify and reverse reversible causes
• Give high flow O2 • Hypovolaemia
• Waveform capnography • Hypoxia
• Continuous chest compressions if advanced airway • Hyper/ hypokalaemia/ metabolic
• Minimize interruptions to compressions • Hypo/ hyperthermia
• Intravenous or intraosseous access • Thrombosis (coronary or pulmonary)
• Give adrenaline every 3 – 5 minutes • Tension pneumothorax
• Give amiodarone after 3 shocks • Tamponade – cardiac
• Identify and treat reversible causes • Toxins
Consider ultrasound imagine to identify reversible causes.
Consider After ROSC

• Coronary angiography/ percutaneous coronary • Use an ABCDE approach
intervention • Aim for SpO2 of 94% - 98% and normal PaCO2
• Mechanical chest compressions to facilitate transfer/ • 12 lead ECG
treatment • Identify and treat cause 29
• Extracorporeal CPR • Targeted temperature management
Chapter
Airway Management and
5 Ventilation
Basic airway management and Ventilation
Objectives
• Identification of a threatened airway

• Basic airway management
• Use of simple devices for ventilation
• Definitive airway devices
The 1st step is to identifying and managing potentially life-threatening airway.
Initial assessment and frequent assessment of airway patency and adequacy of

ventilation are essential.
Therefore talk to the patient and stimulate verbal response to make sure that the
patient’s airway is patent, ventilation is intact and brain perfusion is sufficient.
If the patient is unresponsive look for chest and abdominal movements, look, Listen,
Feel for breaths while maintaining head tilt and chin lift at the mouth and nose.
Signs of airway obstruction
• Agitation
• Cyanosis (late finding)
• Use of accessary muscles for ventilation
• Desaturation (detected in pulse oxymetry)
• Abnormal sounds eg: snoring ,gurgling, and stridor which implies partial
airway obstruction of pharynx or larynx, hoarseness implies functional
laryngeal obstruction .
30
Chapter 5 Airway management & ventilation
Airway maintenance techniques

▪ Basic airway manures to open the airway
▪ Triple maneuver is practiced by health care providers. It includes, Head tilt, Chin lift
, Jaw thrust
Head tilt
Place one hand on patient’s forehead and tilt the head back gently.
Chin lift
In a head tilted patient, keep the fingertips of the other hand under mandible and
gently lifting upward to bring the chin anterior.
31
Jaw thrust
To relieve the obstructed airway by the tongue, soft palate, and epiglottis, bring the
mandible forward by keeping the index and other fingers behind the angle of
mandible then apply upward and forward pressure to lift the mandible. Thumbs
slightly open the mouth by the downward movement of the chin
After each manure look listen and feel for cleared airway. If it is not achieved look for
another cause for obstruction
In patients with suspected cervical injury, maintaining the head ,neck, chest and
lumbar region in neutral position is important to prevent spinal injury. Establish a
clear upper airway by using jaw thrust or chin lift along with manual inline
stabilization. But in life threatening airway obstruction little head tilt is allowed as the
airway takes priority over concerns about a potential cervical spine injury
32
Adjuncts to basic airway techniques
To maintain a patent airway during CPR nasopharyngeal and oropharyngeal airways are
important. They are helpful to overcome backward displacement of soft palate and
tongue in unconscious patients.
1)Oropharyngeal airway
Oral airways are inserted into the mouth behind the tongue. The preferred technique
is to insert oral airway is tip pointed the roof of the mouth .the tip of the appropriately
sized airway should reach the angle of the mandibular ramus.
Rotate the airway 180 degrees as you advanced it into posterior pharynx. In case of
trauma oropharyngeal airway is inserted, maintaining the curved part facing the palate
under direct visualization.
2) Nasopharyngeal airway
It is tolerated than the oropharyngeal airways by the patients who are not deeply
unconscious.
33
Oxygen
During CPR and airway management, use a self-inflated bag with a reservoir system
or using a demand valve system and giving maximum possible inspired oxygen
concentration should be given.
Advanced airway adjuncts
1. Laryngeal mask airway ( LMA)
Supraglottic device which sits tightly over the top of the larynx.
Can be used as an alternative to endotracheal intubation.
2. Endotracheal intubation
Intubation should be carried out by the most experienced personnel & chest
compression should not be interrupted for more than 10 seconds. If ventilation is
adequate with supraglottic airway endotracheal intubation can be delayed.
3. Cricothyroidotomy
Very occasionally, ventilation with a bag mask or other means may not possible and
requires an emergency surgical access to trachea from the anterior neck below the
level of obstruction. Surgical cricothyroidotomy is considered gold standard for
emergency neck rescue.
There are various small portable ventilators to deliver the breaths during
resuscitation. During basic mechanical ventilation during advanced life support,
hyperventilation should be avoided.
Initial suggested settings are
➢ Delivery of tidal volume 6ml/kg ideal body weight
➢ Respiratory rate of 10bpm
These settings should be reassessed according to the patients’ blood gas values.
34
Chapter
Rhythm Recognition and Safe
6 Defibrillation
During a cardiac arrest, recognition of the underlying cardiac rhythm is very

important. The pathway which we need to follow is depend on the rhythm itself.
Therefore, patient should be connected to the defibrillator or cardiac monitor as
early as possible.
You have to familiar with the defibrillator in your unit. There can be slight variations
in knobology in each defibrillator depending on the manufacturer. Switch on the
defibrillator first. Patient can be connected to the defibrillator either with electrodes
or with self-adhesive pads (see the figure).
Select appropriate lead and sensitivity on defibrillator. If electrodes are used to

detect the rhythm select the lead II, if pads are used select paddle mode. Select ×1
or ×2 sensitivity (See the figure). Now you are ready to read the cardiac rhythm.
35
Chapter 6 Rhythm Recognition and Safe Defibrillation
Chest compressions make artefactual waves on monitor. Therefore, ask chest

compressor to “STOP” to analyze the rhythm. As soon as you recognize the rhythm
ask to “START” the compressions again.
Lead
Sensitivity /
gain
Types of rhythms in cardiac arrest

Rhythms can be either shockable or non-shockable.
Shockable rhythms
1. Ventricular fibrillation (VF)

2. Ventricular tachycardia – pulseless (pVT)
Non-shockable rhythms
1. Asystole
2. Pulseless electrical activity (PEA)
36
Shockable rhythms
Ventricular fibrillation
▪ Bizarre irregular waveform

▪ No recognisable QRS complexes
Ventricular tachycardia
▪ Monomorphic VT
▪ Broad complexes
▪ Rapid rate
▪ Constant QRS morphology
Polymorphic VT
▪ Torsade de pointes
37
Non-shockable rhythms
Asystole
▪ Absent ventricular (QRS) activity

▪ Atrial activity (P waves) may or may not present
▪ Rarely a straight line
Pulseless electrical activity
▪ Clinical features of cardiac arrest

▪ ECG normally associated with an output
38
If the rhythm is shockable, then your next immediate management should be the
defibrillation. Defibrillation is a hazardous procedure unless you have taken necessary
safety precautions and actions. Follow the below steps to deliver a safe and effective
defibrillation without unnecessary interruptions to chest compressions.
▪ Select energy level (1): 150 – 200J for the first shock and 270J (or maximum) for
subsequent shocks.
▪ Give safety commands: “Free flow O2 away”, “continue chest compressions”,
“everyone else stand clear” – check this visibly also.
▪ Press the charge (2) button on defibrillator.
▪ Apply gel adequately.
▪ Give a command “STOP” to chest compressor.
▪ Take more distant paddle first and keep on the chest.
▪ Take the next paddle and keep on the chest.
▪ Apply an adequate weight on paddles for a good contact.
▪ Press the discharge (3) button
▪ Take off the paddles and give a command to “START” CPR.
▪ Keep the paddles on the machine.
1. Energy
selection
2. Charge
3. Shock
39
Paddles should be positioned in a way that energy travels across the heart. Standard
paddle positions are
▪ Apical: 5th intercostal space in mid axillary line and

▪ Right sub-clavicular: Below the right clavicle adjacent to the right sternal border
Alternative paddle positions also can be used depending on the situations. Bi-axillary
position (for patient with more chest hair or for patient with chest injuries), antero-
posterior position (for younger children) are few examples.
40
Synchronized Electrical Cardioversion

Synchronized electrical cardioversion is a treatment modality for tachyarrhythmias.
This is the treatment of choice for following tachyarrhythmias in non-arrested
patients with adverse clinical features, i.e. syncope, angina, shock or severe heart
failure.
1. Supraventricular tachycardia (atrioventricular nodal reentrant tachycardia [AVNRT]
and atrioventricular reentrant tachycardia [AVRT])
2. Atrial fibrillation
3. Atrial flutter (types I and II)
4. Ventricular tachycardia with pulse
This can be used for stable patients also, when the tachyarrhythmia is persistent
despite pharmacological treatments.
Following tachyarrhythmias are resistant and may get worse with electrical
cardioversion
1. Dysrhythmias due to enhanced automaticity, such as in digitalis toxicity and
catecholamine-induced arrhythmia
2. Multifocal atrial tachycardia
Even though the same device is used for both defibrillation and synchronized
cardioversion they have few differences.
▪ Defibrillation is used to convert shockable rhythms in cardiac arrested patient to

perfusable cardiac rhythms, while synchronized cardioversion is used to convert
tachyarrhythmias in non-arrested patient to sinus rhythm.
▪ For cardioversion, synchronized mode should be selected. This will detect the R
wave on cardiogram and deliver the shock avoiding the relative refractory period in
the T wave (R on T phenomenon). This will minimize the risk of inducing VF. In
defibrillation since the patient is on cardiac arrest no such synchronization is
needed.
▪ Since synchronized cardioversion is used for conscious patient, appropriate
analgesia and sedation should be given prior to the procedure. This can be either
general anaesthesia or conscious sedation. Prior information to the patient
regarding the procedure and possible discomfort feeling also advisable.
Defibrillation is attempted in arrested patients in where analgesia and sedation are
not indicated.
▪ For the first attempt in defibrillation lower energy can be used (150J – 200J).
Maximum energy is recommended for subsequent shocks. In synchronized
cardioversion energy levels depend on the type of tachyarrhythmia. For narrow
complex tachyarrhythmia 70J – 120J (except atrial fibrillation) and for broad
complex tachyarrhythmias 120J – 150J. For atrial fibrillation maximal possible
energy is recommended.
41
Following are the steps in synchronized electrical cardioversion
▪ Inform the procedure and possible discomfort feeling to the patient or bystander.
▪ Give an appropriate analgesia (eg. fentanyl) and sedation (eg. Midazolam).
▪ Attach the patient to cardiac monitor.
▪ Switch on the defibrillator.
▪ Select the synchronized mode on defibrillator.
▪ Select the relevant energy level; 70J – 120J for narrow complex tachyarrhythmias
(except atrial fibrillation), 120J – 150J for broad complex tachyarrhythmias,
maximal possible energy for atrial fibrillation.
▪ Apply adequate amount of gel on patient’s chest.
▪ Keep the paddles on patient’s chest (same positions as for defibrillation).
▪ Give safety commands to avoid free flow O2 and anyone touching the patient
▪ Charge the defibrillator by pressing the No.2 button on paddle.
▪ Press the discharge buttons (No. 3) on both paddles and keep until the energy
deliver to the patient. (This may take slightly longer period than defibrillation)
▪ Check the rhythm and vital clinical signs of patient and confirm the success of
cardioversion.
42
Chapter
Reversible Causes in Cardiac
7 Arrest
Hypoxia
▪ Ensure adequate oxygenation &ventilation

▪ Check for hypoxia (paO2<10kpas)
▪ Give 100% oxygen using bag valve mask & check device correctly connected
▪ Insert a supraglottic airway or tracheal tube if trained to do so
▪ Check chest movement & air entry
Hypovolaemia
▪ Look for hemmorage ,occult bleeding or fluid loss which represents reduction of
intravascular volume.
▪ Severe vasodilatation will give rise to relative hypovolaemia eg; in sepsis ,
anaphylaxis , spinal cord injury etc.
▪ During cardiopulmonary resuscitation,depending on the suspecting cause the
volume replacement should be done. In case of hemorrhage initially crystalloids
can be given aiming early blood transfusion & vasopressor support.
43
Chapter 7 Reversible Causes in Cardiac Arrest
Hypo/hyperkalemia
▪ Check for hypo/hyperkalemia and electrolyte abnormalities in ABG /VBG

▪ In the presence of hyperkalemia during cardiac arrest give 10 ml of calcium
chloride 10% IV by rapid bolus injection.
▪ If cardiac arrest is refractory consider repeating the dose.
▪ Give 10 units soluble insulin and 25 g glucose IV by rapid injection.
▪ Give 50 mmol sodium bicarbonate IV by rapid injection.
▪ Dialysis is considered for refractory hyperkalemic cardiac arrest.
▪ In hypokalemic during cardiac arrest, the cause should be treated. Rapid infusion
of potassium replacement is required in imminent cardiac arrest with 2mmol/min
for 10 minutes followed by 10 mmol over 5-10 minutes. Repletion of magnesium
will facilitate more rapid correction of hypokalemia.
Hypothermia
▪ Accidental hypothermia is involuntary drop of core temperature less than 350 C

▪ Tympanic thermometers can be used to check in those who are spontaneously
breathing & oesophageal thermometer can be used in intubated patients.
▪ In hypothermic cardiac arrest continuous CPR should be given during transfer.
▪ If ventricular fibrillation persists after three shocks further attempts should be
delayed until core temperature is above 30 0 C.
▪ Withhold adrenaline if the core temperature is < 30 0 C & increase adrenaline
administration intervals to 6-10 minute if the core temperature is > 30 0 C.
▪ Rewarming plays a major role.
44
Chapter 7 Reversible Causes in Cardiac Arrest
Thrombosis ( pulmonary or coronary)
▪ Acute coronary syndrome is the commonest manifestation of thrombosis leading

to cardiac arrest.
▪ Diagnosis & treatment will be usually done after ROSC is achieved.
▪ Pulmonary embolism is the commonest cause of thromboembolic or mechanical
circulatory obstruction leading to cardiac arrest.
▪ Commonly presents as pulseless electrical activity.
▪ Fibrinolysis should be considered. If fibrinolysis was done consider performing
cardiopulmonary resuscitation for at least 60-90 minutes before termination
attempts.
For cardiac tamponade

▪ Consider focused cardiac ultrasound
For tension pneumothorax

▪ Check for tracheal deviation, bilateral air entry , chest movement & airway
pressure
▪ Consider focused chest ultrasound
for toxins
• check drug chart & clinical notes
45
Chapter
Post Resuscitation Care
8
CONTENTS
▪ The post cardiac arrest syndrome
▪ Optimizing organ dysfunction
▪ The post cardiac arrest algorithm
▪ Prognostication
Introduction
The return of a spontaneous circulation (ROSC) is an important step in the

continuum of resuscitation. However, the next goals following ROSC are to return
the patient to a state of normal cerebral function, to establish and maintain a stable
cardiac rhythm and normal haemodynamic function
The quality of treatment provided in this post-resuscitation phase - the final ring in
the Chain of Survival - significantly influences the patient's ultimate outcome. The
post-resuscitation phase starts at the location where ROSC is achieved but, once
stabilised, the patient needs transfer to the most appropriate high-care area (e.g.
intensive care unit (ICU), coronary care unit (CCU)) for continued monitoring and
treatment. This may include preparation for transport to other facilities.
The post-cardiac arrest syndrome
The post-cardiac arrest syndrome comprises:

1. post-cardiac arrest brain injury
2. post-cardiac arrest myocardial dysfunction
3. systemic ischaemia/reperfusion response
4. persistent precipitating pathology.
46
Chapter 8 Post resuscitation care
Post cardiac arrest brain injury
The severity of brain injury will vary with the duration and cause of cardiac arrest. It
may not occur at all if the cardiac arrest is brief. Post-cardiac arrest brain injury
manifests as coma, seizures, myoclonus, varying degrees of neurocognitive
dysfunction and brain death.
Post-cardiac arrest brain injury may be exacerbated by microcirculatory failure,

impaired autoregulation, hypotension, hypercarbia, hypoxaemia, hyperoxaemia,
pyrexia, hypoglycaemia, hyperglycaemia and seizures.
post-cardiac arrest myocardial dysfunction

Significant myocardial dysfunction is common after cardiac arrest, but typically starts
to recover by 2-3 days, although full recovery may take significantly longer.
Systemic ischaemia/reperfusion response

systemic ischaemia/reperfusion response of cardiac arrest activates immune and
coagulation pathways contributing to multiple organ failure and increasing the risk of
infection. Thus, the post- cardiac arrest syndrome has many features in common with
sepsis, including intravascular volume depletion, vasodilation, endothelial injury and
abnormalities of the microcirculation.
Persistent precipitating pathology

The severity of this syndrome will vary with the duration and cause of cardiac arrest.
47
Airway and Breathing

Maintain SpO2 94-98%
Advanced airway
Waveform capnography
Ventilate lung to normocapnia
Circulation
12 lead ECG
IV Access
Aim for SBP >100
Restore nomovolemia
Intra arterial blood pressure monitoring
Consider vasopressor / inotrope to maintain SBP
Control temperature
Constant temperature 32 C-36 C
Sedation- control shivering
Likely cardiac arrest
No Yes
Consider CTPA/CT brain
ST elevation on 2 lead ECG
Treat non cardiac cause of

cardiac arrest
YES/NO
Coronary angiography
+/- PCI
48
CTPA/CT brain Cause for cardiac

Treat for non cardiac cause arrest identified
of cardiac arrest NO
Admit to ICU/CCU
ICU management
▪ Temperature control-constant temperature for 4 hours , prevent fever for at least
72 hours
▪ Maintain nomoxia and normocarbia ; protective ventilation
▪ Optimise hemodynamic [ MAP, lactate, ScVO2 CO/CI urine output ]
▪ Echocardiography
▪ Maintain normoglycemia
▪ Diagnose/treat seizure [EEG. Sedation, anticonvulsant ]
▪ Delayed prognostication for at least 72 hours
Figure
▪ CTPA - computed tomographic pulmonary angiogram
▪ CI - Cardiac index
▪ CO - cardiac out put
▪ ScVO2 - central venous oxygen saturation
▪ PCI - percutaneous coronary intervention
49
Continued resuscitation
In the immediate post-resuscitation phase, pending transfer to an appropriate high-
care area, treat the patient by following the ABCDE approach described in the post-
resuscitation care algorithm
Airway and breathing

Patients who have had a brief period of cardiac arrest and have responded
immediately to appropriate treatment (e.g. witnessed ventricular fibrillation (VF)
reverting to sinus rhythm after early defibrillation) may achieve an immediate return
of normal cerebral function. These patients do not require tracheal intubation and
ventilation, but should be given oxygen by face mask to maintain a normal arterial
oxygen saturation.
Hypoxaemia and hypercarbia both increase the likelihood of a further cardiac arrest
and may contribute to secondary brain injury. Several animal studies indicate that
hyperoxaemia causes oxidative stress and harms post-ischaemic neurones.
Observational studies, using data from intensive care registries, have produced
conflicting results: some have shown an association between hyperoxaemia and a
poor outcome while others have not.
A study of air versus supplemental oxygen in ST-elevation myocardial infarction

showed that supplemental oxygen therapy increased myocardial injury, recurrent
myocardial infarction and major cardiac arrhythmia and was associated with larger
infarct size. Based on this evidence, as soon as arterial blood oxygen saturation can
be monitored reliably (by blood gas analysis and/or pulse oximetry (SpO2)), titrate
the inspired oxygen concentration to maintain the arterial blood oxygen saturation in
the range of 94-98%.
Following measures are important to consider

▪ Tracheal intubation, sedation and controlled ventilation in any patient with
obtunded cerebral function.
▪ To maintain normoxia and normocarbia
▪ Examine chest wall to ensure no chest injury – e.g. fracture of ribs following CPR
/pneumothorax , flail segment, listen for evidence of pulmonary edema or
pulmonary aspiration of gastric content.
▪ Insert a gastric tube which will decompress the stomach. Prevent splinting of
gastric content and enable drainage of gastric contents.
If the intubated patient regains consciousness soon after ROSC, and is cooperative
and breathing normally, consider immediate extubation: coughing on the tracheal
tube will increase the patient's plasma catecholamine concentrations significantly,
which may provoke arrhythmias and/or hypertension. Ensure that a rigid sucker is
available. If immediate or early extubation is not possible, sedate the patient to
ensure the tracheal tube is tolerated, and provide ventilatory support. 50
Circulation
Cardiac rhythm and haemodynamic function are likely to be unstable following a

cardiac arrest. Continuous monitoring of the ECG is essential. Seek evidence of poor
cardiac function. Record the pulse and blood pressure and assess peripheral
perfusion: warm, pink digits with a rapid capillary refill usually imply adequate
perfusion. Grossly distended neck veins when the patient is semi-upright may
indicate right ventricular failure, but in rare cases could indicate pericardial
tamponade. Left ventricular failure may be indicated by fine inspiratory crackles
heard on auscultation of the lungs, and the production of pink frothy sputum. Try to
optimise right and left heart filling pressures: measurement of central venous
pressure will guide this. If the facility for direct continuous arterial blood pressure
monitoring is available (e.g. in the emergency department) insert an arterial cannula
to enable reliable monitoring during transfer. Once in a high-care area, the use of
non-invasive cardiac output monitoring devices may be valuable. nfusion of fluids
may be required to increase right heart filling pressures or conversely, diuretics and
vasodilators may be needed to treat left ventricular failure.
Record a 12-lead ECG as soon as possible. Acute ST-segment elevation or new left
bundle branch block in a patient with a typical history of acute myocardial infarction
is an indication for reperfusion therapy. This is usually achieved by percutaneous
coronary intervention if not ready available [ time delay > 120 minute ] consider
thrombolytic therapy which is not a contraindication following prolong CPR
Disability and exposure
Although cardiac arrest is frequently caused by primary cardiac disease, other

precipitating conditions must be evaluated and excluded e.g. massive blood loss,
respiratory failure, pulmonary embolism, intra cerebral haemorrhage. Assess the
other body systems rapidly so that further resuscitation can be targeted at the
patient's needs. To examine the patient properly full exposure of the body may be
necessary.
Assess neurological function rapidly and record the Glasgow Coma Scale score . The
maximum score possible is 15; the minimum score possible is 3.
Consider the need for targeted temperature management (TTM) in any patient that
remains comatose after initial resuscitation from cardiac arrest.When TTM is
considered an appropriate treatment, it should started as soon as possible - do not
wait until the patient is in the ICU before commencing cooling interventions.
51
Further Assessment
From Those involved in caring for the patient immediately
before the cardiac arrest may be able to help (e.g. emergency
medical personnel, primary/community care physician, and
relative
History Check available medical document. Pre hospital note
Make a note of any delay before the start of resuscitation, and
the duration of the resuscitation; this may have prognostic
significance.
SPO2
Respiratory rate
Arterial and central venous blood pressure
Monitoring Capnography
Core temperature
Urine output.
Arterial blood gas

12 lead ECG
CXR
Investigation FBC
Renal function
Troponin I
Electrolytes -K+ Ca
CT scan
Patient transfer
▪ Senior members of the admitting team and those involved in the transportation
phase. Continue all established monitoring during the transfer and secure all
cannulae, catheters, tubes and drains.
▪ Make a full re-assessment immediately before the patient is transferred.
▪ Ensure that portable suction apparatus, an oxygen supply and a
defibrillator/monitor accompany the patient and transfer team.
▪ The transfer team should comprise individuals capable of monitoring the patient
and responding appropriately to any change in patient condition, including a
further cardiac arrest.
▪ If transport is over a distance or long duration spare equipment and human
resources will need to be considered and planned for.
52
The decision to transfer a patient to another hospital must be made by a responsible

clinician in conjunction with colleagues from relevant specialties in both the referring
and receiving facilities. Pre- departure check lists may be used to help to ensure that
all necessary preparations have been completed.
Optimising organ function

The extent of secondary organ injury after ROSC depends on the ability to minimise
the harmful consequences of post- cardiac-arrest syndrome. There are opportunities
to limit the insult to organs following cardiac arrest.
Heart and cardiovascular system

Post-resuscitation myocardial dysfunction causes haemodynamic instability, which
manifests as hypotension, low cardiac index and arrhythmias. Perform early
echocardiography in all patients in order to detect and quantify the degree of
myocardial dysfunction. Post-resuscitation myocardial dysfunction often requires
inotropic support, at least transiently. Although dobutamine is the most established
treatment in the setting of myocardial dysfunction, the systematic inflammatory
response that occurs frequently in post-cardiac arrest patients causes vasoplegia and
severe vasodilation Thus, noradrenaline, with or without dobutamine. and fluid is
usually the most effective treatment. If treatment with fluid ,inotrope and vasoactive
drugs is insufficient to support the circulation consider insertion of intra aortic
balloon pump. Target systolic blood pressure 100 mmHg is usually required. Risk of
cardiac arrythmia need to be addressed during post resuscitation phase. Give
potassium to maintain serum potassium concentration between 4-4.5 mmol/l
Brain: optimising neurological recovery
Cerebral perfusion
Immediately after ROSC there is a period of cerebral hyperaemia. Autoregulation of
cerebral blood flow is impaired for some time after cardiac arrest, which means that
cerebral perfusion varies with cerebral perfusion pressure instead of being linked to
neuronal activity. As discussed above, following ROSC, maintain mean arterial
pressure near the patient's normal level.
53
Sedation
Although it has been common practice to sedate and ventilate patients for at least
24 h after ROSC, there are no data to support a defined period of ventilation,
sedation and neuromuscular blockade after cardiac arrest. Patients need to be well
sedated during treatment with targeted temperature management, and the
duration of sedation and ventilation is therefore influenced by this treatment. There
are no data to indicate whether or not the choice of sedation influences outcome,
but a combination of opioids and hypnotics is usually used Short-acting drugs (e.g.
propofol, alfentanil, remifentanil) will enable earlier neurological assessment.
Adequate sedation will reduce oxygen consumption. During hypothermia, optimal
sedation can reduce or prevent shivering, which enables the target temperature to
be achieved more rapidly
Control of seizures
Seizures are common after cardiac arrest and occur in approximately one-third of
patients who remain comatose after ROSC. Myoclonus is most common and occurs
in 18- 25%, the remainder having focal or generalized tonic-clonic seizures or a
combination of seizure types. Use intermittent electroencephalography (EEG) to
detect epileptic activity in patients with clinical seizure manifestations. With
ongoing sedation, Patients with electrographic status epilepticus may or may not
have clinically detectable seizure manifestations that may be masked by sedative
agent. Whether systematic detection and treatment of electrographic epileptic
activity improves patient outcome is not known. However seizure activity, including
status epilepticus, are related to a poor prognosis but individual patients may
survive with good outcome
Glucose control
There is a strong association between high blood glucose after resuscitation from
cardiac arrest and poor neurological outcome. However, severe hypoglycaemia is
associated with increased mortality in critically ill patients, and comatose patients
are at particular risk from unrecognised hypoglycaemia. Based on the available data
and expert consensus, following ROSC, maintain blood glucose at ≤10 mmol L¹ and
avoid hypoglycaemia (< 4.0 mmol L¹)
Temperature control
A period of hyperthermia (hyperpyrexia) is common in the first 48 h after cardiac
arrest. Several studies document an association between post-cardiac-arrest
pyrexia and poor outcome. Although the effect of elevated temperature on
outcome is not proved, treat any hyperthermia occurring after cardiac arrest with
antipyretics and/or active cooling.
54
Targeted temperature management [TTM]

Animal and human data indicate that mild induced hypothermia is neuroprotective
and improves outcome after a period of global cerebral hypoxia-ischaemia. Cooling
suppresses many of the pathways leading to delayed cell death, including apoptosis
(programmed cell death). Hypothermia decreases the cerebral metabolic rate for
oxygen (CMRO₂) by about 6% for each 1ºC reduction in core temperature and this
may reduce the release of excitatory amino acids and free radicals. Hypothermia
blocks the intracellular consequences of excitotoxin exposure (high calcium and
glutamate concentrations) and reduces the inflammatory response associated with
the post-cardiac arrest syndrome.
The term target temperature management or temperature control is now preferred

over the previous term therapeutic hypothermia. Maintain a constant target
temperature between 32-36 Celsius is recommended for TTM.
The practical application of TTM is divided into three phase.

➢ Induction
➢ Maintenance
➢ Rewarming
Methods of induction and maintenance

▪ Application of ice packs /towels
▪ Cooling blanket or pad
▪ Cold saline – 4 Celsius
▪ Intravascular heat exchange
▪ ECMO
Prognostication
The prognostication of post comatose post cardiac arrest patient is very complex
should be undertaken by experience clinicians and is out side the scope of ALS
Hypoxic-ischaemic brain injury is common after resuscitation from cardiac arrest. Two
thirds of those dying after admission to ICU following out-of-hospital cardiac arrest
die from neurological injury. Most of these deaths are due to active withdrawal of life
sustaining treatment (WLST) based on prognostication of a poor neurological
outcome. For this reason, when dealing with patients who are comatose after
resuscitation from cardiac arrest minimising the risk of a falsely pessimistic prediction
is essential.
55
Ideally, when predicting a poor outcome, these tests should have 100% specificity or
zero false positive rate (FPR) (i.e. no individuals should have a 'good' long-term
outcome if predicted to have a poor outcome). However, most prognostication
studies include so few patients that it is very difficult to be completely confident in
the results. Moreover, many studies are confounded by self-fulfilling prophecy, which
is a bias occurring when the treating physicians are not blinded to the results of the
outcome predictor and use it to make a decision on WLST. Finally, both TTM itself and
sedatives or neuromuscular blocking drugs used to maintain it may potentially
interfere with prognostication tests, especially those based on clinical examination.
Prognostication of the comatose post-cardiac arrest patient should be multimodal

and should be delayed sufficiently to enable full clearance of sedatives and any
neurological recovery to occur. in most cases, prognostication is not reliable until
after 72 h from cardiac arrest.
The tests are categorised:
▪ Clinical examination - GCS score, pupillary response to light, corneal reflex,

presence of seizures
▪ Neurophysiological studies- somatosensory evoked potentials (SSEPs) and
electroencephalography (EEG)
▪ Biochemical markers - neuron-specific enolase (NSE) is the most commonly used
▪ Imaging studies- brain CT and magnetic resonance imaging (MRI)
Rehabilitation
Although neurological outcome is considered to be good for the majority of cardiac

arrest survivors, cognitive and emotional problems and fatigue are common. Long-
term cognitive impairments are present in half of survivors. Memory is most
frequently affected, followed by problems in attention and executive functioning
(planning and organisation). The cognitive impairments can be severe, but are mostly
mild These patients may benefit from a formal program of rehabilitation, but such an
approach is currently rare.
Organ donation
Post cardiac arrest patient who do not survive will be a potential organ donors. All
patient who have established circulation after CPR and who subsequently progress to
death to be evaluated for organ donation.
56
Chapter
Resuscitation in Special
9 Circumstances
1. Anaphylaxis
2. Asthma
3. Cardiac arrests in pregnancy
4. Drowning
5. Traumatic cardiac arrest
Anaphylaxis
it’s a life-threatening allergic reaction with rapid onset and may leads to death.
Diagnostic Criteria (ANY of the two)
1. Acute onset (minutes to hours) of skin, mucosal tissue or both (hives, itching, flushing,
swollen lips tongue-uvula) with at least one of the following:
A. Respiratory Involvement (dyspnea, bronchospasms, stridor, reduced peak expiratory

flow, hypoxemia)
B. Hypotension or features of end-organ dysfunction (collapse, syncope, incontinence).
C. Severe gastrointestinal symptoms (crampy abdominal pain, repetitive vomiting)
2. Acute onset of hypotension or bronchospasms or laryngeal involvement after exposure
to a known or highly probable allergen even in the absence of typical skin involvement.
Initial Management
▪ Remove allergen (if still present)
▪ Lay patient flat. DO NOT ALLOW to stand or walk. Patients with severe difficulty in
breathing may prefer to sit with legs outstretched.
▪ IM Adrenaline 0.5 mg (1:1000 0.5ml) to the middle 1/3rd of the anterolateral
thigh. Use a 22-25G needle, 1 ml syringe. Adrenaline can be repeated after 5
minutes.
▪ Consider IV Infusion of adrenaline if more than 2 doses of adrenaline are
ineffective.
▪ For IV infusion mix 1 ml pr 1:1000 Adrenaline with 1000ml of normal saline and
start infusion at 5ml/kg/hr (0.1 microgram/kg/hr). IV Infusion 1:1000 adrenaline 1
mg mixed with 100ml normal saline infused as 0.5 ml/kg/hr through only an
infusion pump. If infusion pump is not available use a standard IV infusion set (
1ml : 20 drops) at 2 drops per second.. Titrate dose to response.
57
Chapter 9 Resuscitation in Special Circumstances
Adrenaline (epinephrine) dose chart
Volume (mL) of
Age Adrenaline injector devices
Weight (kg) adrenaline
(years) (for use instead of ampoules)
1:1,000 ampoules
~<1 <7.5 0.1 mL Not available
~1-2 10 0.1 mL 7.5-20 kg (~<5yrs)

~2-3 15 0.15 mL 150 microgram device
~4-6 20 0.2 mL
~7-10 30 0.3 mL >20 kg (~>5yrs)
300 microgram device
~10-12 40 0.4 mL
>12 and >50 kg (~12 years)

>50 0.5 mL
adults 300 microgram or 500 microgram device
If the patient is UNRESPONSIVE AND NOT BREATHING, Manage as Overwhelming

Anaphylaxis
▪ Strat CPR
▪ Give IV Adrenaline 1 mg boluses every 2-3 minutes. Follow Advanced life support
algorithm.
▪ Start aggressive fluid resuscitation (20 ml/kg normal saline under pressure).
▪ Attempt prolonged resuscitation.
▪ IM Adrenaline is unlikely to work.
Subsequent Management
▪ ABCDE approach
▪ Start high flow oxygen (6-8 L/min) and support airway if needed.
▪ If features of upper airway obstruction are seen nebulize with 5 ml of 1:1000
Adrenaline. Advanced airway interventions maybe needed.
▪ If persistent bronchospasms,
➢ consider bronchodilators and steroids after Adrenaline
➢ Nebulized Salbutamol 5mg or MDI Salbutamol (100μg) 8-12 puffs through
a spacer device.
➢ Oral prednisolone 1mg/kg (maximum dose 50 mg) or IV Hydrocortisone 5
mg/kg (maximum dose 200mg)
58
▪ If hypotensive
➢ initiate 20 ml/kg normal saline bolus through a 14 or 16 gauge cannula.
➢ For cardiogenic shock (patients on beta blockers) IV Glucagon 1-2 mg
(20-30 micrograms/kg upto 1 mg in children). May use a 1-2mg/hr
infusion for adults.
➢ IV Adrenaline infusion Ensure a dedicated line, infusion pump, trained
staff and adequate supervision.
➢ IV Metaraminol 92-10 mg) or IV Vasopressin (10-40 units) may be
considered. (under specialist supervision only).
▪ Antihistamines have no role in treating or preventing respiratory or

cardiovascular symptoms of anaphylaxis.
▪ Do not use sedating oral antihistamines.
▪ Do not use IM promethazine (may cause myonecrosis and hypotension).
▪ The patient should remain supine for at least 1 hour after IM Adrenaline dose.
▪ The patient should be observed for minimum of 4 hours after the last dose of
adrenaline.
▪ Admit all patients with high risk factors:

➢ Severe protracted anaphylaxis
➢ History of severe protracted anaphylaxis
➢ Presence of a concomitant illness
➢ Lives alone, far from medical facility or presented during after-hours.
59
Asthma
Acute severe and near fatal asthma patient are high risk of go into cardiac arrest if
no proper assessment and resuscitation happened.
Following circumstance will be predicted clinical deterioration in asthma patient

▪ History of near-fatal asthma requiring intubation and mechanical ventilation
▪ Hospitalisation or emergency care for asthma in the past year
▪ Low or no use of inhaled corticosteroids
▪ Increasing use of and dependence on beta-2 agonists
▪ Anxiety, depressive disorders and/or poor compliance with therapy
▪ Food allergy in a patient with asthma
Initial assessment and treatment of asthma will prevent cardiorespiratory arrest

Use the ABCDE approach to assess severity and guide treatment.
Asthma severity
Near fatal asthma Raised PCO2 and /or mechanical

ventilation with raised inflation pressure
Life threatening asthma Clinical signs Measurement

Altered conscious PEF<33%
level Spo2 <92%
Exhaustion PaO2 <60mmHg
Arrhythmias Normal PaCO2
Hypotension
Cyanosis
Silent chest
Poor expiratory
effort
Acute severe asthma Respiratory rate >25
Heart rate >110/min
Inability to complete sentence in one
breath
PEF 33-50 %
60
Wheezing is a common physical finding but severity does not correlate with the
degree of airway obstruction. The absence of wheezing may indicate critical airway
obstruction or inability to move air, whereas increased wheezing may indicate a
positive response to bronchodilator therapy.
Oxygen saturation of arterial blood (SpO,) may not reflect progressive alveolar
hypoventilation, particularly if oxygen is being given. Spo, may initially decrease
during therapy because beta-agonists cause both bronchodilation and vasodilation,
initially increasing intrapulmonary shunting.
The patient with acute severe asthma requires aggressive medical management to
prevent deterioration.
Use a concentration of inspired oxygen that will achieve an SpO2 of 94-98%High-flow
oxygen by mask is sometimes necessary.
Salbutamol (5 mg delivered by oxygen driven nebuliser) is the main therapy for acute
asthma. Repeated doses every 15-30 min, or continuous doses (5-10 mg h¹- requires
a special nebuliser), may be needed. If a nebuliser is not immediately available beta-2
agonists can be temporarily administered by repeating activations of a metered dose
inhaler via a large volume spacer device.
The use of supplemental oxygen delivery via nasal prongs or open ended oxygen
tubing tucked under/into the nebuliser mask may assist in maintaining the high flow
oxygen when using nebulisers.
Add nebulised ipratropium bromide (500 mcg 4-6 haurly) to beta-2 agonist treatment
for patients with acute severe or life-threatening asthma or those with a poor initial
response to beta-2 agonist therapy
Give steroids (prednisolone 40-50 mg orally or hydrocortisone 100 mg IV 6-hourly)

early. Oral formulations have a longer half-life but the IV route is easier to give in near
fatal asthma.
Give a single dose of IV magnesium sulfate (2 g IV over 20 min) to patients with acute
severe asthma who have not had a good initial response to inhaled bronchodilator
therapy.
Nebulised magnesium sulphate may be an option for add-on therapy in severe

exacerbations of asthma, particularly if IV access is not established. Nebulised
magnesium sulfate may produce benefits for adults in the treatment of acute asthma
when not responding to bronchodilators alone
Consider intravenous salbutamol (250 mcg IV slowly) only when inhaled therapy is
not possible (e.g. a patient receiving bag-mask ventilation).
61
Following expert/senior advice, consider aminophylline in severe or near-fatal asthma

only.
Consider tracheal intubation and controlled ventilation if despite efforts to optimise

drug therapy. If following condition are observed
➢ Deteriorating peak flow
➢ Decreasing conscious level, or coma
➢ Persisting or worsening hypoxaemia deteriorating respiratory acidosis
➢ Severe agitation, confusion and fighting against the oxygen mask (clinical signs of
hypoxaemia)
➢ Progressive exhaustion
➢ Respiratory or cardiac arrest
The role of non-invasive ventilation (NIV) in patients with severe acute asthma is
uncertain. NIV should be considered only in an ICU, Emergency Department or
equivalent clinical setting where monitoring and resources available ,Consider if
starting to tire or signs of respiratory failure.
For NIV following factors need to be considered

➢ The patient will need to be able to cooperate
➢ Do not sedate patient
➢ Consider if intubation is not imminently required, Should not delay intubation if
required
➢ If no improvement, consider intubating and mechanical ventilation
NIV enhances ventilation by unloading fatigued ventilatory muscles NIV has the
advantage that it can be applied Intermittently for short periods, which may be
sufficient to reverse the ventilatory failure NIV has been demonstrated to decrease
rates of ventilator failure, need for sedation
NIV should be avoided if the patient is agitated or vomiting or has profuse secretions,
reduced level of consciousness or haemodynamic instability
Cardiorespiratory arrest associated with asthma
Follow standard BLS and ALS protocols. Ventilation will be difficult because of
increased airway resistance; try to avoid gastric inflation
Intubate the trachea early. There is a significant risk of gastric inflation and
hypoventilation of the lungs when attempting to ventilate a severe asthmatic without
a tracheal tube.
62
The recommended respiratory rate (10 breaths min) and tidal volume required for a
normal chest rise during CPR should not cause dynamic hyperinflation of the lungs
(gas trapping).
If dynamic hyperinflation of the lungs is suspected during CPR, compression of the

chest wall and/or a period of apnoea (disconnection of tracheal tube) may relieve
gas- trapping. Although this procedure is supported by limited evidence, it is unlikely
to be harmful in an otherwise desperate situation.
Dynamic hyperinflation increases transthoracic impedance, but modern impedance-

compensated biphasic defibrillation waveforms are no less effective in patients with
higher impedance. As with standard ALS defibrillation protocols, consider increasing
defibrillation energy if the first shock is unsuccessful and a manual defibrillator is
available.
Look for all potential reversible causes using the 4 Hs and 4 Ts approach. Suspicion of
Hypoxia, Hypovolaemia and Tension Pneumothorax, and Hyperkalaemia/
Hypokalaemia metabolic disorders will be high.
Tension pneumothorax can be difficult to diagnose in cardiac arrest. It may be

indicated by unilateral expansion of the chest wall, shifting of the trachea, and
subcutaneous emphysema. Pleural ultrasound in skilled hands is faster and more
sensitive than chest X-ray for the detection of pneumothorax. Early needle
decompression (thoracocentesis) followed by chest drain insertion is needed. Needle
decompression may fail due to inadequate needle length In the ventilated patient,
thoracostomy (a surgical hole in the chest wall and pleura) may be quicker to perform
and more effective for decompressing the che
Always consider bilateral pneumothoraces in asthma- related cardiac arrest.
Extracorporeal life support (ECLS) can provide both organ perfusion and gas exchange
in cases of otherwise refractory respiratory and circulatory failure. Cases of successful
treatment of asthma-related cardiac arrest in adults using ECLS have been reported.
63
Cardiac arrest in pregnancy

The maternal cardiac arrest is a cardiac arrest that occurs at any stage in pregnancy
and upto 6 weeks after birth.
Following physiological differences should be considered during a maternal cardiac

arrest.
➢ Aortocaval compression – This significantly reduces cardiac output from 20 weeks
of gestation onwards and the efficacy of chest compressions during resuscitation.
➢ Changes in lung function – E.g. diaphragmatic splinting, increased oxygen
consumption. These make pregnant women become hypoxic more readily and
make ventilation more difficult.
➢ Soft tissue swelling, large breast – These make airway more prone to obstruct and
make intubation more difficult.
➢ High intra abdominal pressure and malfunctioning lower oesophageal sphincter –
These increase the risk of aspiration.
Maternal cardiac arrest resuscitation should follow the regular resuscitation

guidelines using the standard ABCDE approach, with some modifications for maternal
physiology, in particular relief of aortocaval compression.
Following are the modifications which should be done in maternal cardiac arrest
▪ Call for expert help early (including obstetrician and neonatologist)

▪ Manual displacement of the uterus to the left is effective in relieving aortocaval
compression in women above 20 weeks’ gestation or where the uterus is palpable
at or above the level of the umbilicus. If feasible add a left lateral tilt – the chest
should remain on supported on a firm surface (e.g. in operating room). Aim for a
tilt between 15 to 30 degrees. Even a small amount of tilt may be beneficial.
▪ Intubation in an unconscious woman with a cuffed endotracheal tube should be
performed immediately by an experienced person. Supplemental high flow oxygen
should be administered as soon as possible to counteract rapid deoxygenation. Bag
and mask ventilation or insertion of a simple supraglottic airway should be
undertaken until intubation can be achieved.
▪ If the airway is clear and there is no breathing, chest compressions should be

commenced immediately. Use the satndard hand position for chest compressions
on the lower half of the sternum if feasible. Rate and the depth are same as for
non-pregnant adult person.
64
▪ Two wide-bore cannulae (minimum 16 gauge) should be inserted as soon as

possible. If peripheral venous access is not possible, early consideration of central
venous access, intraosseous access or venous cutdown should be considered.
There should be an aggressive approach to volume replacement, although
caution should be exercised in the context of pre-eclampsia or eclampsia.
Abdominal ultrasound by a skilled operator can assist in the diagnosis of
concealed haemorrhage.
▪ The same defibrillation energy levels should be used as in a non pregnant woman.
Place defibrillator pads in the standard position as far as possible and use
standard shock energies. Remove fetal monitors prior to defibrillation.
Defibrillation with self adhesive pads is preferred. Increase paddle pressure if
using paddles.
▪ There should be no alteration in algorithm drugs or doses used in the

resuscitation.
▪ Common, reversible causes of maternal cardio pulmonary arrest should be

considered throughout the resuscitation process.
▪ Peri-mortem caesarean section (PMCS) – In women over 20 weeks of gestation, if

there is no response to correctly performed CPR within 4 minutes of maternal
collapse or if resuscitation is continued beyond this, then PMCS should be
undertaken to assist maternal resuscitation. Ideally, this should be achieved
within 5 minutes of the collapse. PMCS should not be delayed by moving the
woman. It should be performed where maternal collapse has occurred and
resuscitation is taking place. The operator should use the incision, which will
facilitate the most rapid access. This may be a midline vertical incision or a
suprapubic transverse incision. Scalpel and umbilical cord clamps (or alternative
ligatures) should be available on the resuscitation trolley in all areas where
maternal collapse may occur, including the accident andemergency department.
▪ Consider extracoporeal CPR (ECPR) as a rescue therapy if ALS measures are failing
.
▪ Resuscitation efforts should be continued until a decision is taken by the
consultant obstetrician and consultant anaesthetist to discontinue resuscitation
efforts. This decision should be made inconsensus with the cardiac arrest team.
65
66
Cardiac arrest associated with Drowning
Definition of drowning -
The international Liaison Committee on Resuscitation (ILCOR) defines drowning as a
“process resulting in primary respiratory impairment from submersion / immersion
in a liquid medium. (Liquid / air interface is present at the entrance of the victim’s
airway, preventing the victim from breathing air). The victim may live or die after
this process, but whatever the outcome, he or she has been involved in a drowning
incident”
Management of cardiac arrest following drowning

Bystander CPR is particularly important in a drowning incident in order to provide
immediate resuscitation for survival and to acquire a better neurological outcome.
▪ Get the victim away from the water safely and as fast as possible.
▪ Open the airway and check for signs of life.
▪ Cervical spine (C spine) immobilization is not routinely needed as injuries to the
C-spine is uncommon in drowning victims unless there are clinical signs of injury
or a concerning mechanism.
▪ Ventilation is generally considered the most important initial treatment for
victims in cardiac arrest or respiratory arrest as these are typically due to
hypoxemia.
▪ If rescue team is highly trained with appropriate equipment, rescue breathing
can be started in open water; as this is challenging, for most of the
circumstances, rescue breathing should be started as soon as the rescuer
reaches shallow water or a stable surface.
▪ Give five initial rescue breaths with supplemented oxygen if available.
▪ If no response to initial ventilations, start chest compressions
▪ If copious amount of foam presents obstructing the airway, continue rescue
breaths / ventilation until definitive airway is achieved.
▪ Administer automated external defibrillator (AED) when appropriate. However
before applying AED pads, patient’s wet clothes need to be removed and the
chest, neck and upper abdomen need to be dried.
▪ Attempts at rewarming hypothermic patients should be initiated, either by
passive or active means as available.
▪ As hypothermia is common in drowned patients; giving IV drugs and
defibrillation should be done considering the victim’s body core temperature as
discussed under “reversible causes of cardiac arrest / hypothermia”.
67
Traumatic cardiac arrest
Causes of cardiac arrest in trauma are hypovolemia, hypoxia to a lesser extend

hypothermia secondary to massive bleeding and resuscitative measures. Identifying
and treat the cause is again the most important step in traumatic cardiac arrest.
If the patient is in cardiac arrest, promptly start on basic life support and proceed
with advanced life support when the help is available.
Correct
▪ Hypovolemia – control external bleeding, splint the fractures, apply pelvic
binders, IV or IO fluids /blood
▪ Hypoxia - Basic and advanced airway management, Give oxygen
▪ Tension pneumothorax – decompress the chest
▪ Cardiac tamponade – decompress the pericardium
If there is penetrating chest trauma, cardiac tamponade and tension pneumothorax

could be the cause of cardiac arrest. Point of care ultrasound examination is an aid
of diagnosis in this situation.
Cardiac tamponade – modification to cardiopulmonary resuscitation

Decompress the pericardium by resuscitative thoracotomy (RT) or ultrasound guided
pericardiocentesis should be done.
Resuscitative thoracotomy is successful when following prerequisites are fulfilled.

four E’s)
▪ Expertise - team should be trained health care practitioners.
▪ Equipment
▪ Environment – Ideal place to perform is operating theater. But can perform out if
there is adequate physical access to patient.
▪ Elapsed time – the time from loss of vital signs to start performing RT should not
be longer than 15 minutes.
Tension pneumothorax – modification to cardiopulmonary resuscitation

Decompress the chest immediately by open thoracostomy when pneumothorax is
suspected in the presence of peri arrest or arrest.
Following successful resusitation transport to a hospital if pre hospital and in

hospital patients need damage control or definitive surgery or interventional
radiological management.
68
"On this final page, we encourage
you to embrace your newly acquired
Advanced Life Support skills with
confidence and compassion, knowing
that your expertise can truly make a
life-saving difference in the world”
Sri Lanka College of Emergency Physicians
43A, Dharmapala Mawatha Madiwela, Kotte 10100
Web: www.slcep.lk
Email: info@slcep.lk

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Advanced life support

Course manual 2023

Sri Lanka College of Emergency Physicians

1 Dr Inuka Wijegunawardana Consultant Emergency Physician

2 Dr A. G. Thanuja Darshani Consultant Emergency Physician

3 Dr Senitha Liyanage Consultant Emergency Physician

4 Dr Indika Lanarolle Consultant Emergency Physician

5 Dr Senaka Herath Registrar in Emergency Medicine

6 Dr Iresha Rathnayake Registrar in Emergency Medicine

7 Dr Damindi Wanniarachachi Registrar in Emergency Medicine

Chapter 2 Recognizing Deterioration and Preventing Cardiac 07

Chapter 4 Advanced Life Support(ALS) Algorithm 27

Chapter 5 Airway Management & Ventilation 30

Chapter 6 Rhythm Recognition and Defibrillation 35

Chapter 7 Reversible Causes in Cardiac Arrest 43

Chapter 8 Post Resuscitation Care 46

Chapter 9 Resuscitation in Special Circumstances 57

Unfortunately, as of the latest available information, updated statistics specific to out-

Out of Hospital Cardiac Arrest (OHCA)

The initial rhythm observed during these events is shockable (ventricular

In Hospital Cardiac Arrest (IHCA)

When a hospital's resuscitation team is involved in the treatment of IHCA cases,

Regarding survival rates, approximately half of those admitted to critical care

Post-cardiac arrest rehabilitation

The Chain of Survival

Early recognition and call for help

Cardiac arrest is defined as the sudden cessation of spontaneous respiration and

a) Cardiac arrest is confirmed by the absence of signs of life (SOL)

Furthermore, it is imperative that all healthcare staff are authorized to request

It is recommended that a standardized number, such as 2222, be universally adopted

In cases of out-of-hospital cardiac arrest (OHCA), prompt recognition of the

Following an in-hospital cardiac arrest (IHCA), it is imperative to initiate chest

Prevention of in hospital cardiac arrest

How to observe patient, interpretation of observed signs,

Recording of vital signs which may include the use of electronic

Recognition Suitably design vital chart, sets of predetermined calling criteria

summoning a response to a deteriorating patient should be

Response By staff with appropriate acute or critical care skills

Recognizing the deteriorating patient

Response criteria- any observation in purple area, cardiac

Clinical review Response criteria -any observation in red area

Response – any observation is in an orange area

Response - any observation is in a yellow area

1.Use the Airway, Breathing, Circulation, Disability, Exposure approach

2.complete initial assessment and re-assess regularly

3.Treat life-threatening problems as soon as detected.

4. Assess the effects of treatment

5.Call for appropriate help early.

6. Communicate effectively using communication tool e.g. the SBAR approach

5. If the patient is not in cardiac arrest start the ABCDE approach.

Examination Intervention Goal

6 Assess chest expansion is equal on both

11 Check the position of the trachea in the

12 Feel the chest wall to detect surgical

Look at the colour of the hands

Assess the limb temperature by

Auscultate the heart. S1 S2 Assess fluid status

Assess causes for