Recognition of the Deteriorating CHAPTER

Patient and Prevention of

Cardiorespiratory Arrest
3
problems) that is unnoticed by staff, or is recognised but
Learning outcomes treated poorly. The cardiac arrest rhythm in this group is
usually non-shockable (PEA or asystole) and the survival
To understand:
rate to hospital discharge is very low.
 The importance of early recognition of
the deteriorating patient Early recognition and effective treatment of the
 The causes of cardiorespiratory arrest in deteriorating patient might prevent cardiac arrest, death or
adults an unanticipated intensive care unit (ICU) admission.
Closer attention to patients who have a ‘false’ cardiac
 How to identify and treat patients at risk of arrest (i.e. a ‘cardiac arrest team’ call when the patient has
cardiorespiratory arrest using the Airway, not had a cardiac arrest) may also improve outcome,
Breathing, Circulation, Disability, Exposure because up to one third of these patients die during their
(ABCDE) approach in-hospital stay. Early recognition will also help to identify
individuals for whom cardiorespiratory resuscitation is not
appropriate or who do not wish to be resuscitated.
Introduction
Early recognition of the deteriorating patient and Prevention of in-hospital cardiac
prevention of cardiac arrest is the first link in the chain of
survival. Once cardiac arrest occurs, fewer than 20% of
arrest: the Chain of Prevention
patients having an in-hospital cardiac arrest will survive to The Chain of Prevention can assist hospitals in structuring
go home. Prevention of in-hospital cardiac arrest requires care processes to prevent and detect patient deterioration
staff education, monitoring of patients, recognition of and cardiac arrest. The five rings of the chain represent:
patient deterioration, a system to call for help, and an staff education; the monitoring of patients; the recognition
effective response. of patient deterioration; a system to call for help; and an
effective response (Figure 3.1):
Survivors from in-hospital cardiac arrest usually have a
witnessed and monitored ventricular fibrillation (VF) arrest, • Education: how to observe patients; interpretation of
primary myocardial ischaemia as the cause, and receive observed signs; the recognition of signs of
immediate and successful defibrillation. deterioration; and the use of the ABCDE
approach and simple skills to stabilise the patient
Most cardiorespiratory arrests in hospital are not sudden pending the arrival of more experienced help.
or unpredictable events: in approximately 80% of cases
there is deterioration in clinical signs during the few hours • Monitoring: patient assessment and the
before cardiac arrest. These patients often have slow and measurement and recording of vital signs, which may
progressive physiological deterioration, particularly include the use of electronic monitoring devices.
hypoxia and hypotension (i.e. Airway, Breathing, Circulation

Figure 3.1 Chain of Prevention

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Chapter 3 Recognition of the Deteriorating Patient and Prevention of Cardiorespiratory Arrest

Score 3 2 1 0 1 2 3
Pulse (min-1) ≤ 40 41 - 50 51 - 90 91 - 110 111 - 130 ≥ 131

Respiratory rate (min-1) ≤8 9 - 11 12 - 20 21 - 24 ≥ 25

Temperature (°C) ≤ 35.0 35.1 - 36.0 36.1 - 38.0 38.1 - 39.0 ≥ 39.1

Systolic BP (mmHg) ≤ 90 91 - 100 101 - 110 111 - 249 ≥ 250

Oxygen saturation (%) ≤ 91 92 - 93 94 - 95 ≥ 96

Inspired oxygen Air Any oxygen

therapy

AVPU Alert (A) Voice (V)

Pain (P)

Unresponsive (U)

TABLE 3.1 Example of early warning scoring (EWS) system*

* From Prytherch et al. ViEWS - Towards a national early warning score for detecting adult in-patient deterioration.
Resuscitation. 2010;81(8):932-7

• Recognition encompasses the tools available to observations, or the total EWS, indicates the level of
identify patients in need of additional monitoring or intervention required, e.g. increased frequency of vital
intervention, including suitably designed vital signs signs monitoring, or calling ward doctors or resuscitation
charts and sets of predetermined ‘calling criteria’ to teams to the patient. An example of an EWS system is
‘flag’ the need to escalate monitoring or to call for shown in Table 3.1.
more expert help.
Early warning scores are dynamic and change over time
• Call for help protocols for summoning a response to a and the frequency of observations should be increased to
deteriorating patient should be universally known and track improvement or deterioration in a patient’s condition.
understood, unambiguous and mandated. Doctors and If it is clear a patient is deteriorating help should be called
nurses often find it difficult to ask for help or escalate for early rather than waiting for the patient to reach a
treatment as they feel their clinical judgement may be specific score.
criticised. Hospitals should ensure all staff are
empowered to call for help. A structured communication The patient’s EWS is calculated based on Table 3.1. An
tool such as SBAR (Situation, Background, Assessment, increased score indicates an increased risk of deterioration
Recommendation) or RSVP (Reason, Story, Vital signs, and death. There should be a graded response to scores
Plan) should be used to call for help. according to local hospital protocols (Table 3.2).

Alternatively, systems incorporating calling criteria are

• Response to a deteriorating patient must be assured,
of specified speed and by staff with appropriate acute based on routine observations, which activate a response
or critical care skills, and experience. when one or more variables reach an extremely abnormal
value. It is not clear which of these two systems is better.
Some hospitals combine elements of both systems.
Recognising the deteriorating patient
Even when doctors are alerted to a patient’s abnormal
In general, the clinical signs of critical illness are similar
physiology, there is often delay in attending to the patient
whatever the underlying process because they reflect
or referring to higher levels of care.
failing respiratory, cardiovascular, and neurological
systems i.e. ABCDE problems (see below). Abnormal
physiology is common on general wards, yet the Response to critical illness
measurement and recording of important physiological
The traditional response to cardiac arrest is reactive: the
observations of acutely ill patients occurs less frequently
name ‘cardiac arrest team’ implies that it will be called
than is desirable. The assessment of very simple vital
only after cardiac arrest has occurred. In some hospitals
signs, such as respiratory rate, may help to predict
the cardiac arrest team has been replaced by other
cardiorespiratory arrest. To help early detection of critical
resuscitation teams (e.g. rapid response team, critical care
illness, many hospitals use early warning scores (EWS) or
outreach team, medical emergency team). These teams
calling criteria. Early warning scoring systems allocate
can be activated according to the patient’s EWS (see
points to measurements of routine vital signs on the basis
above) or according to specific calling criteria. For
of their derangement from an arbitrarily agreed ‘normal’
example, the medical emergency team (MET) responds
range. The weighted score of one or more vital sign

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12
 EWS Minimal Escalation
observation
frequency Recorder’s action Doctor’s action
3-5 4 hourly Inform nurse in charge

6 4 hourly Inform doctor Doctor to see within 1 h

7-8 1 hourly Inform doctor Doctor to see within 30 min and discuss

Consider continuous monitoring with senior doctor and/or outreach team

≥9 30 min Inform doctor Doctor to see within 15 min and discuss

Start continuous monitoring with senior doctor and ICU team

TABLE 3.2 Example escalation protocol based on early warning score (EWS)

not only to patients in cardiac arrest, but also to those with exist in many forms ranging from a single nurse to a
acute physiological deterioration. The MET usually 24-hour, seven days per week multiprofessional team. An
comprises medical and nursing staff from intensive care outreach team or system may reduce ward deaths,
and general medicine and responds to specific calling postoperative adverse events, ICU admissions and
criteria (Table 3.3). Any member of the healthcare team readmissions, and increase survival.
can initiate a MET call. Early involvement of the MET may
reduce cardiac arrests, deaths and unanticipated ICU All critically ill patients should be admitted to an area that
admissions, and may facilitate decisions about limitation of can provide the greatest supervision and the highest level
treatment (e.g. do-not-attempt-resuscitation [DNAR] of organ support and nursing care. This is usually in a
decisions). Medical emergency team interventions often critical care area, e.g. ICU, high dependency unit (HDU),
involve simple tasks such as starting oxygen therapy and or resuscitation room. These areas should be staffed by
intravenous fluids. The benefits of the MET system remain doctors and nurses experienced in advanced
to be proved. resuscitation and critical care skills.

MET calling criteria Hospital staffing tends to be at its lowest during the night
and at weekends. This influences patient monitoring,
Airway Threatened
treatment and outcomes. Admission to general wards in the
evening, or to hospital at weekends, is associated with
Breathing All respiratory arrests increased mortality. Studies have shown that in-hospital
Respiratory rate < 5 min-1 cardiac arrests occurring in the late afternoon, at night or at
Respiratory rate > 36 min-1 weekends are more often non-witnessed and have a lower
survival rate. Patients discharged at night from ICUs to
Circulation All cardiac arrests general wards have an increased risk of ICU readmission
Pulse rate < 40 min-1 and in-hospital death compared with those discharged
Pulse rate > 140 min-1 during the day and those discharged to HDUs.
Systolic BP < 90 mmHg

Causes of deterioration and

Neurology Sudden decrease in level of
consciousness cardiorespiratory arrest
Decrease in GCS of > 2 points Deterioration and cardiorespiratory arrest can be caused
Repeated or prolonged seizures by primary airway and/or breathing and/or cardiovascular
problems.
Other Any patient causing concern
who does not fit the above
criteria Airway obstruction
For a detailed review of airway management see Chapter 7.
TABLE 3.3 Medical emergency team (MET)
calling criteria
Causes
In the UK, a system of pre-emptive ward care known as Airway obstruction can be complete or partial. Complete
critical care outreach, has developed. Outreach services airway obstruction rapidly causes cardiac arrest. Partial

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Chapter 3 Recognition of the Deteriorating Patient and Prevention of Cardiorespiratory Arrest

obstruction often precedes complete obstruction. Partial consciousness, regardless of cause. Take steps to
airway obstruction can cause cerebral or pulmonary safeguard the airway and prevent further complications
oedema, exhaustion, secondary apnoea, and hypoxic such as aspiration of gastric contents. This may involve
brain injury, and eventually cardiac arrest. nursing the patient on their side or with a head-up tilt.
Simple airway opening manoeuvres (head tilt/chin lift or
jaw thrust), insertion of an oropharyngeal or nasal airway,
Causes of airway obstruction elective tracheal intubation or tracheostomy may be
required. Consider insertion of a nasogastric tube to
• Central nervous system depression empty the stomach.
• Blood
• Vomitus Breathing problems
• Foreign body (e.g. tooth, food)
• Direct trauma to face or throat Causes
• Epiglottitis
Breathing inadequacy may be acute or chronic. It may be
• Pharyngeal swelling (e.g. infection, oedema)
continuous or intermittent, and severe enough to cause
• Laryngospasm
apnoea (respiratory arrest), which will rapidly cause
• Bronchospasm – causes narrowing of the cardiac arrest. Respiratory arrest often occurs because of
small airways in the lung a combination of factors; for example, in a patient with
• Bronchial secretions chronic respiratory inadequacy, a chest infection, muscle
• Blocked tracheostomy weakness, or fractured ribs can lead to exhaustion, further
depressing respiratory function. If breathing is insufficient
to oxygenate the blood adequately (hypoxaemia), a
Central nervous system depression may cause loss of cardiac arrest will occur eventually.
airway patency and protective reflexes. Causes include
head injury and intracerebral disease, hypercarbia, the Respiratory drive
depressant effect of metabolic disorders (e.g. diabetes
mellitus), and drugs, including alcohol, opioids and Central nervous system depression may decrease or abolish
general anaesthetic agents. Laryngospasm can occur with respiratory drive. The causes are the same as those for
upper airway stimulation in a semi-conscious patient airway obstruction from central nervous system depression.
whose airway reflexes remain intact.
Respiratory effort
In some people, the upper airway can become obstructed
when they sleep (obstructive sleep apnoea). This is more The main respiratory muscles are the diaphragm and
common in obese patients and obstruction can be intercostal muscles. The latter are innervated at the level of
worsened in the presence of other factors (e.g. sedative their respective ribs and may be paralysed by a spinal
drugs). cord lesion above this level. The innervation of the
diaphragm is at the level of the third, fourth and fifth
segment of the spinal cord. Spontaneous breathing cannot
Recognition
occur with severe cervical cord damage above this level.
Assess the patency of the airway in anyone at risk of
obstruction. A conscious patient will complain of difficulty Inadequate respiratory effort, caused by muscle weakness
in breathing, may be choking, and will be distressed. With or nerve damage, occurs with many diseases (e.g.
partial airway obstruction, efforts at breathing will be noisy. myasthenia gravis, Guillain-Barré syndrome, and multiple
Complete airway obstruction is silent and there is no air sclerosis). Chronic malnourishment and severe long-term
movement at the patient’s mouth. Any respiratory illness may also contribute to generalised weakness.
movements are usually strenuous. The accessory muscles
of respiration will be involved, causing a ‘see-saw’ or Breathing can also be impaired with restrictive chest wall
‘rocking-horse’ pattern of chest and abdominal movement: abnormalities such as kyphoscoliosis. Pain from fractured
the chest is drawn in and the abdomen expands on ribs or sternum will prevent deep breaths and coughing.
inspiration, and the opposite occurs on expiration.
Lung disorders
Treatment Lung function is impaired by a pneumothorax or
The priority is to ensure that the airway remains patent. haemothorax. A tension pneumothorax causes a rapid
Treat any problem that places the airway at risk; for failure of gas exchange, a reduction of venous return to
example, suck blood and gastric contents from the airway the heart, and a fall in cardiac output. Severe lung disease
and, unless contraindicated, turn the patient on their side. will impair gas exchange. Causes include infection,
Give oxygen as soon as possible to achieve an arterial aspiration, exacerbation of chronic obstructive pulmonary
blood oxygen saturation by pulse oximetry (SpO2) in the disease (COPD), asthma, pulmonary embolus, lung
range of 94 - 98%. Assume actual or impending airway contusion, acute respiratory distress syndrome (ARDS)
obstruction in anyone with a depressed level of and pulmonary oedema.

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14
Recognition
Causes of ventricular fibrillation
A conscious patient will complain of shortness of breath
and be distressed. The history and examination will usually • Acute coronary syndromes (Chapter 4)
indicate the underlying cause. Hypoxaemia and • Hypertensive heart disease
hypercarbia can cause irritability, confusion, lethargy and • Valve disease
a decrease in the level of consciousness. Cyanosis may • Drugs (e.g. antiarrhythmic drugs, tricyclic
be visible but is a late sign. A fast respiratory rate antidepressants, digoxin)
(>25 min-1) is a useful, simple indicator of breathing • Inherited cardiac diseases (e.g. long QT syndromes)
problems. Pulse oximetry is an easy, non-invasive measure • Acidosis
of the adequacy of oxygenation (see Chapter 15). • Abnormal electrolyte concentration (e.g. potassium,
However, it is not a reliable indicator of ventilation and an magnesium, calcium)
arterial blood gas sample is necessary to obtain values for
• Hypothermia
arterial carbon dioxide tension (PaCO2) and pH. A rising
• Electrocution
PaCO2 and a decrease in pH are often late signs in a
patient with severe respiratory problems.
Secondary heart problems
Treatment
The heart is affected by changes elsewhere in the body.
Give oxygen to all acutely ill hypoxaemic patients and treat For example, cardiac arrest will occur rapidly following
the underlying cause. Give oxygen at 15 l min-1 using a asphyxia from airway obstruction or apnoea, tension
high-concentration reservoir mask. Once the patient is pneumothorax, or acute severe blood loss. Severe hypoxia
stable, change the oxygen mask and aim for a SpO2 in the and anaemia, hypothermia, oligaemia and severe septic
range of 94 - 98%. For example, suspect a tension shock will also impair cardiac function and this may lead
pneumothorax from a history of chest trauma and confirm to cardiac arrest.
by clinical signs and symptoms. If diagnosed,
decompress it immediately by inserting a large-bore (14 G) Recognition
cannula into the second intercostal space, in the mid-
clavicular line (needle thoracocentesis). The signs and symptoms of cardiac disease include chest
pain, shortness of breath, syncope, tachycardia,
Patients who are having difficulty breathing or are bradycardia, tachypnoea, hypotension, poor peripheral
becoming tired will need respiratory support. Non-invasive perfusion (prolonged capillary refill time), altered mental
ventilation using a face mask or a helmet can be useful state, and oliguria.
and prevent the need for tracheal intubation and
ventilation. For patients who cannot breathe adequately, Most sudden cardiac deaths (SCDs) occur in people with
sedation, tracheal intubation and controlled ventilation is pre-existing cardiac disease, which may have been
needed. unrecognised previously. Although the risk is greater for
patients with known severe cardiac disease, most SCDs
occur in people with unrecognised disease. Asymptomatic
Circulation problems
or silent cardiac disease may include hypertensive heart
disease, aortic valve disease, cardiomyopathy,
Causes myocarditis, and coronary disease.
Circulation problems may be caused by primary heart
disease or by heart abnormalities secondary to other Recognition of risk of sudden cardiac death out
problems. Most often, circulation problems in acutely ill of hospital
patients are due to hypovolaemia. The heart may stop
Coronary artery disease is the commonest cause of SCD.
suddenly or may produce an inadequate cardiac output
Non-ischaemic cardiomyopathy and valvular disease
for a period of time before stopping.
account for some other SCD events. A small percentage of
SCDs are caused by inherited abnormalities (e.g. long and
Primary heart problems short QT syndromes, Brugada syndrome, hypertrophic
cardiomyopathy, arrhythmogenic right ventricular
The commonest cause of sudden cardiac arrest is an
cardiomyopathy), and by congenital heart disease.
arrhythmia caused by either ischaemia or myocardial
infarction. Cardiac arrest can also be caused by an
In patients with a known diagnosis of cardiac disease,
arrhythmia due to other forms of heart disease, by heart
syncope (with or without prodrome - particularly recent or
block, electrocution and some drugs.
recurrent) is as an independent risk factor for increased risk
of death. Apparently healthy children and young adults who
Sudden cardiac arrest may also occur with cardiac failure,
have SCD may also have symptoms and signs (e.g.
cardiac tamponade, cardiac rupture, myocarditis and
syncope/pre-syncope, chest pain, palpitation, heart murmur)
hypertrophic cardiomyopathy.

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Chapter 3 Recognition of the Deteriorating Patient and Prevention of Cardiorespiratory Arrest

that should alert healthcare professionals to seek expert The ABCDE approach
help to prevent cardiac arrest. Features that indicate a
high probability of arrhythmic syncope include:
Underlying principles
• syncope in the supine position; The approach to all deteriorating or critically ill patients is
the same. The underlying principles are:
• syncope occurring during or after exercise (although
syncope after exercise is often vasovagal); 1. Use the Airway, Breathing, Circulation, Disability,
Exposure approach to assess and treat the patient.
• syncope with no or only brief prodromal symptoms;
2. Do a complete initial assessment and re-assess
• repeated episodes of unexplained syncope; regularly.

• syncope in individuals with a family history of sudden 3. Treat life-threatening problems before moving to the
death or inherited cardiac condition. next part of assessment.

Assessment in a clinic specialising in the care of those at 4. Assess the effects of treatment.
risk for SCD is recommended in family members of young
victims of SCD or those with a known cardiac disorder 5. Recognise when you will need extra help. Call for
resulting in an increased risk of SCD. Specific and appropriate help early.
detailed guidance for the care of individuals with transient
loss of consciousness is available 6. Use all members of the team. This enables
(http://guidance.nice.org.uk/CG109). interventions, e.g. assessment, attaching monitors,
intravenous access, to be undertaken simultaneously.
Treatment
7. Communicate effectively - use the SBAR or RSVP
Treat the underlying cause of circulatory failure. In many approach (see Chapter 2).
sick patients, this means giving intravenous fluids to treat
hypovolaemia. Assess patients with chest pain for an acute 8. The aim of the initial treatment is to keep the patient
coronary syndrome (ACS). A comprehensive description of alive, and achieve some clinical improvement. This
the management of ACS is given in Chapter 4. will buy time for further treatment and making a
diagnosis.
Most patients with cardiac ischaemic pain will be more
comfortable sitting up. In some instances lying flat may
9. Remember - it can take a few minutes for treatments
provoke or worsen the pain. Consider using an anti-
to work.
emetic, especially if nausea is present.

Survivors of an episode of VF are likely to have a further First steps

episode unless preventative treatment is given. These
1. Ensure personal safety. Wear apron and gloves as
patients may need percutaneous coronary intervention,
appropriate.
coronary artery bypass grafting, or an implantable
defibrillator.
2. First look at the patient in general to see if the patient
appears unwell.
Treating the underlying cause should prevent many
secondary cardiac arrests; for example, early goal-
3. If the patient is awake, ask “How are you?”. If the
directed therapy to optimise vital organ perfusion
patient appears unconscious or has collapsed, shake
decreases the risk of death in severe sepsis.
him and ask “Are you alright?” If he responds
Cardiovascular support includes correction of underlying
normally he has a patent airway, is breathing and has
electrolyte or acid-base disturbances, and treatment to
brain perfusion. If he speaks only in short sentences,
achieve a desirable cardiac rate, rhythm and output.
he may have breathing problems. Failure of the
Advanced cardiovascular monitoring and
patient to respond is a clear marker of critical illness.
echocardiography may be indicated. Appropriate
manipulation of cardiac filling may require fluid therapy
4. This first rapid ‘Look, Listen and Feel” of the patient
and vasoactive drugs. Inotropic drugs and
should take about 30 s and will often indicate
vasoconstrictors may be indicated to support cardiac
a patient is critically ill and there is a need for urgent
output and blood pressure. In some situations, mechanical
help. Ask a colleague to ensure appropriate help is
circulatory support (e.g. intra-aortic balloon pump) or
coming.
consideration of heart transplantation will be necessary.

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16
5. If the patient is unconscious, unresponsive, and is not Breathing (B)
breathing normally (occasional gasps are not normal)
start CPR according to the guidance in Chapter 5. If During the immediate assessment of breathing, it is vital to
you are confident and trained to do so, feel for a pulse diagnose and treat immediately life-threatening conditions,
to determine if the patient has a respiratory arrest. If e.g. acute severe asthma, pulmonary oedema, tension
there are any doubts about the presence of a pulse pneumothorax, and massive haemothorax.
start CPR.
1 Look, listen and feel for the general signs of respiratory
6. Monitor the vital signs early. Attach a pulse oximeter, distress: sweating, central cyanosis, use of the
ECG monitor and a non-invasive blood pressure accessory muscles of respiration, and abdominal
monitor to all critically ill patients, as soon as breathing.
possible.
2. Count the respiratory rate. The normal rate is 12 - 20
7. Insert an intravenous cannula as soon as possible. breaths min-1. A high (> 25 min-1), or increasing,
Take bloods for investigation when inserting the respiratory rate is a marker of illness and a warning
intravenous cannula. that the patient may deteriorate suddenly.

Airway (A) 3. Assess the depth of each breath, the pattern (rhythm)
of respiration and whether chest expansion is equal
Airway obstruction is an emergency. Get expert help on both sides.
immediately. Untreated, airway obstruction causes hypoxia
and risks damage to the brain, kidneys and heart, cardiac 4. Note any chest deformity (this may increase the risk of
arrest, and death. deterioration in the ability to breathe normally); look
for a raised jugular venous pulse (JVP) (e.g. in acute
1. Look for the signs of airway obstruction: severe asthma or a tension pneumothorax); note the
presence and patency of any chest drains; remember
• Airway obstruction causes paradoxical chest and that abdominal distension may limit diaphragmatic
abdominal movements (‘see-saw’ respirations) and movement, thereby worsening respiratory distress.
the use of the accessory muscles of respiration.
Central cyanosis is a late sign of airway obstruction. 5. Record the inspired oxygen concentration (%) and the
In complete airway obstruction, there are no breath SpO2 reading of the pulse oximeter. The pulse
sounds at the mouth or nose. In partial obstruction, air oximeter does not detect hypercapnia. If the patient is
entry is diminished and often noisy. receiving supplemental oxygen, the SpO2 may be
normal in the presence of a very high PaCO2.
• In the critically ill patient, depressed consciousness
often leads to airway obstruction. 6. Listen to the patient’s breath sounds a short distance
from his face: rattling airway noises indicate the
2. Treat airway obstruction as a medical emergency: presence of airway secretions, usually caused by the
inability of the patient to cough sufficiently or to take a
• Obtain expert help immediately. Untreated, airway deep breath. Stridor or wheeze suggests partial, but
obstruction causes hypoxaemia (low PaO2) with the significant, airway obstruction.
risk of hypoxic injury to the brain, kidneys and heart,
cardiac arrest, and even death. 7. Percuss the chest: hyper-resonance may suggest a
pneumothorax; dullness usually indicates
• In most cases, only simple methods of airway consolidation or pleural fluid.
clearance are required (e.g. airway opening
manoeuvres, airways suction, insertion of an 8. Auscultate the chest: bronchial breathing indicates
oropharyngeal or nasopharyngeal airway). Tracheal lung consolidation with patent airways; absent or
intubation may be required when these fail. reduced sounds suggest a pneumothorax or pleural
fluid or lung consolidation caused by complete
3. Give oxygen at high concentration: bronchial obstruction.

• Provide high-concentration oxygen using a mask with 9. Check the position of the trachea in the suprasternal
an oxygen reservoir. Ensure that the oxygen flow is notch: deviation to one side indicates mediastinal shift
sufficient (usually 15 l min-1) to prevent collapse of the (e.g. pneumothorax, lung fibrosis or pleural fluid).
reservoir during inspiration. If the patient’s trachea is
intubated, give high concentration oxygen with a self- 10. Feel the chest wall to detect surgical emphysema or
inflating bag.
crepitus (suggesting a pneumothorax until proven
otherwise).
• In acute respiratory failure, aim to maintain an oxygen
saturation of 94 - 98%. In patients at risk of
11. The specific treatment of respiratory disorders
hypercapnic respiratory failure (see below) aim for an
depends upon the cause. Nevertheless, all critically
oxygen saturation of 88 - 92%.

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Chapter 3 Recognition of the Deteriorating Patient and Prevention of Cardiorespiratory Arrest

ill patients should be given oxygen. In a subgroup of 5. Count the patient’s pulse rate (or preferably heart rate
patients with chronic obstructive pulmonary disease by listening to the heart with a stethoscope).
(COPD), high concentrations of oxygen may depress
breathing (i.e. they are at risk of hypercapnic 6. Palpate peripheral and central pulses, assessing for
respiratory failure - often referred to as type 2 presence, rate, quality, regularity and equality. Barely
respiratory failure). Nevertheless, these patients will palpable central pulses suggest a poor cardiac
also sustain end-organ damage or cardiac arrest if output, whilst a bounding pulse may indicate sepsis.
their blood oxygen tensions are allowed to decrease.
In this group, aim for a lower than normal PaO2 and 7. Measure the patient’s blood pressure. Even in shock,
oxygen saturation. Give oxygen via a Venturi 28% the blood pressure may be normal, because
mask (4 l min-1) or a 24% Venturi mask (4 l min-1) compensatory mechanisms increase peripheral
initially and reassess. Aim for target SpO2 range of resistance in response to reduced cardiac output. A
88 - 92% in most COPD patients, but evaluate the low diastolic blood pressure suggests arterial
target for each patient based on the patient’s arterial vasodilation (as in anaphylaxis or sepsis). A narrowed
blood gas measurements during previous pulse pressure (difference between systolic and
exacerbations (if available). Some patients with diastolic pressures; normally 35 - 45 mmHg) suggests
chronic lung disease carry an oxygen alert card (that arterial vasoconstriction (cardiogenic shock or
documents their target saturation) and their own hypovolaemia) and may occur with rapid
appropriate Venturi mask. tachyarrhythmia.

12. If the patient’s depth or rate of breathing is judged to 8. Auscultate the heart. Is there a murmur or pericardial
be inadequate, or absent, use bag-mask or pocket rub? Are the heart sounds difficult to hear? Does the
mask ventilation to improve oxygenation and audible heart rate correspond to the pulse rate?
ventilation, whilst calling immediately for expert help.
In cooperative patients who do not have airway
9. Look for other signs of a poor cardiac output, such as
obstruction consider the use of non-invasive
reduced conscious level and, if the patient has a
ventilation (NIV). In patients with an acute
urinary catheter, oliguria (urine volume < 0.5 ml kg-1 h-1).
exacerbation of COPD, the use of NIV is often helpful
and prevents the need for tracheal intubation and
10. Look thoroughly for external haemorrhage from
invasive ventilation.
wounds or drains or evidence of concealed
haemorrhage (e.g. thoracic, intra-peritoneal,
Circulation (C) retroperitoneal or into gut). Intra-thoracic, intra-
abdominal or pelvic blood loss may be significant,
In almost all medical and surgical emergencies, consider
even if drains are empty.
hypovolaemia to be the primary cause of shock, until
proven otherwise. Unless there are obvious signs of a
11. The specific treatment of cardiovascular collapse
cardiac cause, give intravenous fluid to any patient with
depends on the cause, but should be directed at fluid
cool peripheries and a fast heart rate. In surgical patients,
rapidly exclude haemorrhage (overt or hidden). replacement, haemorrhage control and restoration of
Remember that breathing problems, such as a tension tissue perfusion. Seek the signs of conditions that are
pneumothorax, can also compromise a patient’s immediately life threatening, e.g. cardiac tamponade,
circulatory state. This should have been treated earlier on massive or continuing haemorrhage, septicaemic
in the assessment. shock, and treat them urgently.

1. Look at the colour of the hands and digits: are they 12. Insert one or more large (14 or 16 G) intravenous
blue, pink, pale or mottled? cannulae. Use short, wide-bore cannulae,
because they enable the highest flow.
2. Assess the limb temperature by feeling the patient’s
hands: are they cool or warm? 13. Take blood from the cannula for routine
haematological, biochemical, coagulation and
3. Measure the capillary refill time (CRT). Apply microbiological investigations, and cross-matching,
cutaneous pressure for 5 s on a fingertip held at heart before infusing intravenous fluid.
level (or just above) with enough pressure to cause
blanching. Time how long it takes for the skin to return 14. Give a rapid fluid challenge (over 5 - 10 min) of 500 ml
to the colour of the surrounding skin after releasing of warmed crystalloid solution (e.g. Hartmann’s
the pressure. The normal value for CRT is usually solution or 0.9% sodium chloride) if the patient is
< 2 s. A prolonged CRT suggests poor peripheral normotensive. Give one litre, if the patient is
perfusion. Other factors (e.g. cold surroundings, poor hypotensive. Use smaller volumes (e.g. 250 ml) for
lighting, old age) can prolong CRT. patients with known cardiac failure or trauma and use
closer monitoring (listen to the chest for crackles after
4. Assess the state of the veins: they may be under-filled each bolus, consider a CVP line).
or collapsed when hypovolaemia is present.

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18
15. Reassess the heart rate and BP regularly (every glucose has been given. Repeat blood glucose
5 min), aiming for the patient‘s normal BP or, if this measurements to monitor the effects of treatment. If
is unknown, a target > 100 mmHg systolic. there is no improvement consider further doses of
10% glucose.
16. If the patient does not improve, repeat the fluid
challenge. 6. Nurse unconscious patients in the lateral position if
their airway is not protected.
17. If symptoms and signs of cardiac failure (dyspnoea,
increased heart rate, raised JVP, a third heart sound
Exposure (E)
and pulmonary crackles on auscultation) occur,
decrease the fluid infusion rate or stop the fluids To examine the patient properly full exposure of the body
altogether. Seek alternative means of improving tissue may be necessary. Respect the patient’s dignity and
perfusion (e.g. inotropes or vasopressors). minimise heat loss.

18. If the patient has primary chest pain and a suspected

Additional information
ACS, record a 12-lead ECG early, and treat initially
with aspirin, nitroglycerine, oxygen, and morphine. 1. Take a full clinical history from the patient, any
relatives or friends, and other staff.
19. Immediate general treatment for ACS includes:
2. Review the patient’s notes and charts:
• Aspirin 300 mg, orally, crushed or chewed, as soon as
possible. • Study both absolute and trended values of
vital signs.
• Nitroglycerine, as sublingual glyceryl trinitrate (tablet
or spray). • Check that important routine medications are
prescribed and being given.
• Oxygen, aiming at a SpO2 of 94 - 98%; do not give
supplementary oxygen if the patient’s SpO2 is within 3. Review the results of laboratory or radiological
this range when breathing air alone. investigations.

• Morphine (or diamorphine) titrated intravenously to 4. Consider which level of care is required by the patient
avoid sedation and respiratory depression. (e.g. ward, HDU, ICU).

Disability (D) 5. Make complete entries in the patient’s notes of your

findings, assessment and treatment. Where
Common causes of unconsciousness include profound necessary, hand over the patient to your colleagues.
hypoxia, hypercapnia, cerebral hypoperfusion, or the
recent administration of sedatives or analgesic drugs. 6. Record the patient’s response to therapy.

1. Review and treat the ABCs: exclude or treat hypoxia 7. Consider definitive treatment of the patient’s
and hypotension. underlying condition.

2. Check the patient’s drug chart for reversible drug-

induced causes of depressed consciousness. Give
an antagonist where appropriate (e.g. naloxone for Key learning points
opioid toxicity).
• Most patients who have an in-hospital cardiac
arrest have warning signs and symptoms before
3. Examine the pupils (size, equality and reaction to
the arrest.
light).
• Early recognition and treatment of the
4. Make a rapid initial assessment of the patient’s deteriorating patient will prevent some
conscious level using the AVPU method: Alert, cardiorespiratory arrests.
responds to Vocal stimuli, responds to Painful stimuli
or Unresponsive to all stimuli. Alternatively, use the • Use strategies such as early warning scoring
Glasgow Coma Scale score. (EWS) systems to identify patients at risk of
cardiorespiratory arrest.
5. Measure the blood glucose to exclude hypoglycaemia
using a rapid finger-prick bedside testing method. If • Airway, breathing and circulation problems can
the blood sugar is below 4.0 mmol l-1, give an initial cause cardiorespiratory arrest.
dose of 50 ml of 10% glucose solution intravenously. If
necessary, give further doses of intravenous 10% • Use the ABCDE approach to assess and treat
glucose every minute until the patient has fully critically ill patients.
regained consciousness, or a total of 250 ml of 10%

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19
Chapter 3 Recognition of the Deteriorating Patient and Prevention of Cardiorespiratory Arrest

Further reading
Armitage M, Eddleston J, Stokes T. Recognising and responding to acute
illness in adults in hospital: summary of NICE guidance.
BMJ 2007;335:258-9.

Deakin CD, Nolan JP, Soar J, et al. European Resuscitation Council

Guidelines for Resuscitation 2010. Section 4. Adult Advanced Life Support.
Resuscitation 2010;81:1305-52.

Deakin CD, Morrison LJ, Morley PT, et al. 2010 International Consensus on
Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Science with Treatment Recommendations. Part 8: Advanced Life Support.
Resuscitation 2010;81:e93-e169.

DeVita MA, Bellomo R, Hillman K, et al. Findings of the first consensus

conference on medical emergency teams.
Crit Care Med. 2006;34:2463-2478.

DeVita MA, Smith GB, Adam SK, et al. “Identifying the hospitalised patient
in crisis”— a consensus conference on the afferent limb of rapid response
systems. Resuscitation 2010;81:375-82.

Featherstone P, Chalmers T, Smith GB. RSVP: a system for communication

of deterioration in hospital patients. Br J Nurs 2008;17:860-4.

Luettel D, Beaumont K, Healey F. Recognising and responding

appropriately to early signs of deterioration in hospitalised patients.
London: National Patient Safety Agency; 2007.

Marshall S, Harrison J, Flanagan B. The teaching of a structured tool

improves the clarity and content of interprofessional clinical
communication. Qual Saf Health Care 2009;18:137-40.

Meaney PA, Nadkarni VM, Kern KB, Indik JH, Halperin HR, Berg RA.
Rhythms and outcomes of adult in-hospital cardiac arrest. Crit Care Med
2010;38:101-8.

National Confidential Enquiry into Patient Outcome and Death. An Acute

Problem? London: National Confidential Enquiry into Patient Outcome and
Death; 2005.

NICE clinical guideline 50 Acutely ill patients in hospital: recognition of and

response to acute illness in adults in hospital. London: National Institute for
Health and Clinical Excellence; 2007.

O’Driscoll BR, Howard LS, Davison AG. BTS guideline for emergency
oxygen use in adult patients. Thorax 2008;63 Suppl 6:vi1-68.

Smith GB. In-hospital cardiac arrest: Is it time for an in-hospital ‘chain of

prevention’? Resuscitation 2010:81:1209-11.

Soar J, Mancini ME, Bhanji F, et al. 2010 International Consensus on

Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Science with Treatment Recommendations. Part 12: Education,
Implementation, and Teams. Resuscitation 2010;81:e283-e325.

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