CRITICAL ILLNESS AND INTENSIVE CARE e II
 Muscular system: myasthenia gravis, muscular dystro-
Respiratory failure
Rakesh Bhandary
Abstract
Respiratory failure is a common clinical condition, and is associated with
a 90-day mortality of approximately 40%. This article discusses the
causes, pathophysiology, presentation and management of respiratory
failure with reference to the identification and modification of risk in
the perioperative period.
Keywords Failure; hypercarbia; hypoxaemia; respiratory; ventilatory
Definition
Respiratory failure occurs when the respiratory system is unable
to perform its basic function of gas exchange. Traditionally there
are two types either of that may be acute or chronic:
 Type I (hypoxaemic) respiratory failure, where the
arterial oxygen level (PaO2) is below 8.0 kPa, whilst
breathing room air. This is due to impaired gas diffusion
across the alveolar-capillary membrane, shunt or
ventilationeperfusion mismatch.
 Type II (hypercarbic) respiratory failure, where the PaO2
is below 8.0 kPa, with a raised PaCO2, more than or equal
to 6.5 kPa. These patients have ventilatory failure.
Distinction between acute and chronic respiratory failure
Acute type II respiratory failure develops over a minutes to days
and is reflected by a respiratory acidosis with a pH below 7.3.
Chronic type II failure develops over days to months. It is char-
acterized by renal compensation with a near normal pH and
raised serum HCO3 levels.
Causes of respiratory failure
Respiratory failure can be precipitated by pathology in any of the
components of the respiratory system, from the upper airway to
the musculoskeletal system:
 Airway obstruction: foreign body, tumour, broncho-
spasm, chronic bronchitis.
 Pulmonary parenchyma: pneumonia, acute respiratory
distress syndrome (ARDS), alveolar oedema, lobar
collapse, pulmonary haemorrhage, atelectasis, interstitial
lung disease.
 Pleural pathology: pneumothorax, significant pleural
effusion, haemothorax.
 Vascular: pulmonary embolism, chronic thrombo-embolic
pulmonary hypertension (CTEPH).
 Central nervous system: sedative drugs, opiates, any
condition causing coma, motor neurone disease.
 Peripheral nervous system: Guillain-Barre syndrome,
high spinal cord lesion, phrenic nerve lesion, poliomyelitis.
Rakesh Bhandary MBBS FRCA EDICM is a Consultant in Critical Care
Medicine and Anaesthesia at University Hospital of North Tees,
Stockton-on-Tees, UK. Conflicts of interest: none declared.
SURGERY 33:10
phies, residual neuromuscular blockade following anaes-
thesia, diaphragmatic splinting (e.g. morbid obesity or
abdominal pain).
 Skeletal system: flail rib fracture, kyphoscoliosis.
Pathophysiology of respiratory failure
As discussed, respiratory failure can be caused by an abnormality
in any component of the respiratory system. Furthermore, pa-
tients with hypoperfusion secondary to shock may present as
respiratory failure.
In health, ventilatory capacity (ability to breath without fa-
tigue) greatly exceeds ventilatory demand (amount of breathing
required to manage metabolic demand). Respiratory failure may
result from a reversion of this relationship.
The pathological processes involved in respiratory failure are:
 diffusion impairment
 ventilation/perfusion (V/Q) mismatch
 shunt
 alveolar hypoventilation.
The first three are involved predominantly in hypoxic respi-
ratory failure (unless the shunt is in excess of 60%), while
alveolar hypoventilation is responsible for hypercapnic respira-
tory failure.
Clinical presentation
A careful assessment including history, examination and in-
vestigations should aim to elucidate cause and severity. Baseline
respiratory reserve and relevant co-morbidities are important in
predicting likely therapeutic requirements (e.g. mechanical
ventilation).
It should be noted that many signs (e.g. confusion in the
elderly) are non-specific, but particular attention should be paid
to the features in Table 1.
Specific investigations
Arterial blood gas analysis in an unwell patient on room air is not
usually necessary and should be avoided. The concentration of
oxygen being administered should always be noted. The
magnitude of the oxygen requirement helps determine the
severity of the pathology.
A chest X-ray should help to determine aetiology and disease
severity, although the radiological picture may often lag behind
the evolution and resolution of the disease process. It may also
indicate the need for a therapeutic intervention such as
thoracocentesis.
Other investigations (e.g. CT Chest) may help clarify difficult
diagnoses (see Chest imaging in the intensive care unit on pages
480e484 of this issue on pages 00e00 of this issue).
Management of respiratory failure
A structured airwayebreathingecirculation approach should al-
ways be adopted in severely unwell patients. Many hospitals
have a ‘track & trigger’ system for identifying and appropriately
referring patients to critical care services.1
474 Ó 2015 Elsevier Ltd. All rights reserved.
 CRITICAL ILLNESS AND INTENSIVE CARE e II
Clinical features of respiratory system inadequacy
Hypoxaemia
Neurological features Anxiety
Altered mental status
Seizures
Confusion
Cardiovascular features Tachycardia
Arrhythmias
Bradycardia and hypotension (if severe)
Respiratory features Tachypnoea
Accessory muscle use
General features Cyanosis
Diaphoresis
Table 1
The management of respiratory failure includes general
measures and focussed support in the form of CPAP, NIV or
mechanical ventilation where appropriate.
Supplemental oxygen
Supplemental oxygen is always indicated in patients with acute
respiratory failure. O2 is most effective when the main abnor-
mality is V/Q mismatch. O2 can be administered via variable
performance device (e.g. Hudson’s mask, nasal cannulae) or
fixed performance devices (high flow mask with reservoir, high
flow nasal cannulae, Venturi mask). A sub-group of COPD pa-
tients with chronic CO2 retention lose the hypercapnoeic stim-
ulus to the respiratory centre. These patients are dependent on
hypoxic respiratory stimulus and require titrated oxygen therapy
rather than high flow oxygen.
Antibiotics
When possible, sputum and blood cultures should be obtained
prior to commencing antimicrobial therapy. Appropriate anti-
microbial agents should be commenced on an empirical basis.
The choice of antibiotic often depends on hospital or community
acquisition and patient factors (e.g. previous colonization, co-
morbidities). The spectrum of coverage should be narrowed as
soon as microbiological reports are available.
The Surviving Sepsis Campaign strongly recommends
commencing antibiotic therapy as soon as possible, and always
within an hour of diagnosis of severe sepsis and septic shock. A
strong relationship exists between the delay in effective antimi-
crobial initiation following onset of septic shock and in-hospital
mortality.2
Control of secretions
Many patients with respiratory failure produce large quantities of
bronchial secretions which are often infected. It is imperative
that sputum retention is avoided as it often results in sputum
plugging and hypoxia, segmental collapse and atelectasis, inad-
equate treatment of infection and superinfection.
SURGERY 33:10 475
Hypercarbia
Somnolence & lethargy
Asterixis
Restlessness
Slurred speech
Headache
Decreased conscious level
Peripheral vasodilatation
Tachycardia
Arrhythmias
Bounding pulses
Signs of airway obstruction or narrowing (e.g. stridor, wheezing)
Warm peripheries
Methods include:
 Humidification of inspired gases to avoid secretions from
becoming tenacious.
 Mucolytic agents, like cysteine analogues can reduce
sputum viscosity.
 Chest physiotherapy, either preventive or therapeutic,
conventionally uses postural drainage, percussion & vi-
bration or incentive spirometry to mobilize secretions and
expand collapsed lung segments.
Bronchodilators
Bronchodilator therapy is often useful to improve airflow and
reduce the work of breathing.
Commonly used bronchodilators include b2 agonists, anti-
cholinergics, and phosphodiesterase inhibitors. Steroids are often
used in patients with a background of COPD or asthma, to reduce
airway inflammation and hyper-reactivity of the bronchiae.
Respiratory support
If the above measures are ineffective and the patient is tiring,
respiratory support can be provided using humidified high flow
nasal oxygen, continuous positive airway pressure (CPAP), non-
invasive ventilation (NIV), mechanical ventilation and much less
commonly extracorporeal techniques like extracorporeal mem-
brane oxygenation (ECMO) and extracorporeal carbon dioxide
removal (ECCO2-R). These are complex, high-risk technologies,
and are described more extensively in the mechanical ventilation
article in this issue.
High flow nasal cannulae (HFNC)
HFNC system provides humidified, heated, high flow (up to 50 l/
min) oxygen through nasal cannulae Figure 1. It can provide
titrated oxygen concentration of 30%e100%. HFNC improves
mucociliary clearance and provides distending pressures similar
to CPAP in the lower airways, although this effect is unpredict-
able. It can be used in patients as the first line of respiratory
Ó 2015 Elsevier Ltd. All rights reserved.
 CRITICAL ILLNESS AND INTENSIVE CARE e II

support for hypoxaemic respiratory failure where CPAP is

contraindicated (e.g. upper GI surgery, risk of aspiration) or the
not tolerated.

Continuous positive airway pressure (CPAP)

CPAP provides a continuous positive pressure throughout the
breathing cycle and is analogous to positive end expiratory
pressure (PEEP). CPAP requires a facemask, nasal mask or a
hood (or helmet) as an interface Figure 2. It is used primarily for
patients with type I respiratory failure. CPAP improves oxygen-
ation by recruitment of collapsed alveoli, thus reducing shunt.
CPAP is particularly useful for post-surgical respiratory failure
due to basal collapse/consolidation, acute cardiogenic pulmo-
nary oedema and selected patients with chest trauma who
remain hypoxaemic despite adequate analgesia. CPAP can be
provided transiently outside the ICU with a simple CPAP circuit
as shown in Figure 1 or in the ICU with CPAP bellows, NIV
machine or ventilators with NIV mode. Figure 2 A simple CPAP system for use on wards and A&E in an emer-
gency. The PEEP depends on the flow of oxygen and there is no
requirement for a PEEP valve.
Non-invasive ventilation (NIV)
NIV provides mechanical respiratory support without tracheal
intubation. NIV delivers a bilevel positive airway pressure Table 3 outlines the indications for intubation and mechanical
(BiPAP). It can be delivered using modern ventilators on the ventilation.
ICU or portable NIV devices outside the ICU setting Figure 3.
The interface used is normally a facial or nasal mask. A hood Ventilation strategy
(or helmet) can be used, but it is less effective in terms of CO2 This is detailed in the mechanical ventilation article in this issue.
elimination.3 Current recommendations6,7 include:
Although it has been used for a wide range of indications,  Limit tidal volume (VT) to 6 ml/kg.
including postoperative avoidance of intubation, and post-
extubation support, NIV is most beneficial in the management
of selected patients with acute exacerbation of COPD,4 neuro-
muscular conditions or chest wall abnormalities and manage-
ment of immunocompromised patients with respiratory failure,
as the risk of ventilator associated pneumonia (VAP) is high in
this patient sub-category (Table 2).
While both NIV and CPAP have proven benefits in some
clinical situations, they do not alter the outcome when used in
respiratory failure secondary to ARDS or pneumonia. In these
situations, NIV and CPAP may simply delay necessary
intubation.5

Invasive mechanical ventilation

Mechanical ventilation requires endotracheal intubation or tra-
cheostomy, and sedation with or without muscle relaxants.

Figure 1 Nasal high flow system in use and the nasal cannulae e the Figure 3 A modern portable NIV machine with facemask interface. These
system allows delivery of heated humidified of high flow oxygen. The can be used to provide respiratory support in form of CPAP as well as
flowmeter has maximum flow rate of 70 l/min. BIPAP.

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 CRITICAL ILLNESS AND INTENSIVE CARE e II

Prerequisites, pros and cons of non-invasive ventilation

Prerequisites for C Conscious
CPAP/NIV C Airway self maintained
C Co-operative
C Can tolerate periods without NIV/CPAP for chest physiotherapy, suction, oral feeds etc.
C Can tolerate tight fitting facemask, nasal mask or helmet interface device
C Able to cough up secretions
Contraindications C Low GCS (<8/15)
C Inability to protect airway
C Inability to cough and expectorate effectively
C Copious respiratory secretions
C Recent facial or upper airway surgery
C Risk of aspiration (e.g. bowel obstruction)
C Uncooperative patient, confusion, agitation or coma
C Maxillofacial injuries
Advantages of C Avoidance of tracheal intubation and associated complications especially ventilator associated pneumonia (VAP)
NIV/CPAP C Avoidance of sedation
C Natural airway defence is maintained
C Spontaneous coughing is not impaired
C Ventilatory support can be provided intermittently, to allow normal eating, drinking and communication
C Facilitates early mobilization
Problems with C Necrosis of skin over nasal bridge and face
NIV/CPAP C Air swallowing is common
C Claustrophobia with face mask
C Aspiration of gastric contents
C Cardiovascular instability

Table 2

Indications for endotracheal intubation and mechanical ventilation

Airway control/establishing definitive airway C Inhalational burns
C Stridor/airway oedema
C Tumour causing airway obstruction
C Airway or facial trauma
C Cervical haematoma or oedema
Protection of lungs from aspiration C Bulbar dysfunction
C Decreased conscious level (GCS <8)
C Full stomach
Respiratory dysfunction C NIV/CPAP fails or is contraindicated (Table 2)
C Clinical deterioration
C Worsening blood gases despite optimal medical treatment
C Respiratory muscle fatigue
C Vital capacity (<15 ml/kg)
C Severe respiratory acidosis
Optimizing physiology C Controlling intracranial pressure
C Reducing oxygen consumption as in severe sepsis or anaemia (e.g. Jehovah’s witness)
Facilitating interventions C For surgical intervention
C To facilitate diagnostic intervention (e.g. MRI/CT in children, stereotactic brain biopsy)
C Post-cardiac arrest stabilization
C Therapeutic hypothermia
C Transferring critically ill patients

Table 3

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 CRITICAL ILLNESS AND INTENSIVE CARE e II

Complications relating to mechanical ventilation

General problems Cardiovascular changes
C Complications associated with intubation or tracheostomy C Decreased venous return
C Disconnection or accidental extubation C Cardiovascular collapse
C Failure of gas delivery or power supply C Peripheral oedema
C Mechanical faults
Respiratory changes Others
C Maldistribution of inspired gases C Side effects of sedating agents and muscle relaxants
C Collapse of distal lung segments C Venous thromboembolism
C Decreased surfactant activity C Ileus
C Barotrauma C Hepatic dysfunction
C Ventilator associated lung injury C Fluid retention
C Ventilator associated pneumonia C Psychological trauma

Table 4

 Limit peak pressure to 35 cm/H2O.
 Accept higher than normal PaCO2 (6e8 kPa) e permissive
hypercapnea.
 Accept lower than usual PaO2 (>8 kPa), or SpO2 > 90%.
 Use higher levels of PEEP (5e15 cm/H2O) to improve
alveolar recruitment.
 Use ventilation modes which allow and support sponta-
neous respiratory effort.
Problems with mechanical ventilation
Invasive mechanical ventilation is associated with marked
physiological changes and is associated with a number of diverse
problems listed in Table 4.
Extracorporeal circulations used in respiratory failure
Extracorporeal circuits are used in specialist centres as rescue
therapies in severe respiratory failure, but a discussion of these is
outside the scope of this article.
Properative risk stratification and postoperative risk reduction
strategies
Postoperative pulmonary complications have a marked impact
on morbidity and mortality from anaesthesia and surgery. The
most important include atelectasis, hospital-acquired pneu-
monia, respiratory failure and exacerbation of pre-existing pul-
monary disorders. A systematic review in 2006 suggested
patient, intervention and laboratory investigation related factors
associated with increased risk of postoperative respiratory com-
plications for non-cardiothoracic surgeries.8 These are outlined
in Table 5.
Strategies to reduce postoperative respiratory complications
Preoperative interventions should include optimization of med-
ications to treat COPD, for example. Complex cases should be
thoroughly reviewed in a preoperative assessment clinic or by a
respiratory physician. The evidence regarding preoperative
smoking cessation is unclear. Cessation over the 24 hours prior

Risk factors for postoperative respiratory complications following non-cardiothoracic surgery

Patient-related risk factors Procedure-related factors Laboratory tests

C Advanced age (>60 yrs) C Open aortic aneurysm repair C Serum albumin <35 g/L
C ASA grade >2 C Thoracic surgery C Abnormal chest X-ray
C Congestive cardiac failure C Upper GI surgery C Blood urea >7.5 mmol/L
C Partial or total functional dependence C Abdominal surgery C Abnormal Spirometry (FEV1 < 60% of
C COPD C Neurosurgery predicted or <1.2 L, FEV1:FVC ratio <70%)
C Cigarette smoking C Vascular surgery
C Obstructive sleep apnoea C Emergency surgery
C Obesity C Prolonged surgery (>2.5 h)
C Alcohol use C General anaesthesia
C Diabetes C Blood transfusion (>4 units)
C Asthma
C HIV infection
C Impaired sensorium
C Poor exercise tolerance

Table 5

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 CRITICAL ILLNESS AND INTENSIVE CARE e II
to surgery improves oxygen delivery to the tissues and mito-
chondrial function. However, stopping in the 2 months prior may
actually increase risk through airway hyper-reactivity and
increased secretions.
Only a few interventions have been shown to clearly or
possibly reduce postoperative pulmonary complications. Lung
expansion interventions (for example, incentive spirometry, deep
breathing exercises, and continuous positive airway pressure)
reduce pulmonary risk. Selective, rather than routine, use of
nasogastric tubes after abdominal surgery and short-acting rather
than long-acting intraoperative neuromuscular blocking agents
may reduce risk. The evidence is conflicting or insufficient for
epidural analgesia, and laparoscopic (versus open) operations,
although laparoscopic operations reduce pain and pulmonary
compromise as measured by spirometry. Similarly, while
malnutrition is associated with increased pulmonary risk, routine
total enteral or parenteral nutrition does not reduce risk. Enteral
formulations designed to improve immune status (immunonu-
trition) may reduce the risk of postoperative pneumonia.
Ultimately early detection of complications through clinicians’
awareness of risk, appropriate monitoring and vigilance is critical
in improving outcomes in this important group of patients. A
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FURTHER READING
Brun-Buisson C, Minelli C, Bertolini G, et al. Epidemiology and outcome of
acute lung injury in European intensive care units. Results from ALIVE
study. Intensive Care Med 2004; 30: 51e61.
Zambon M, Vincent JL. Mortality rates for patients with acute lung injur-
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479 Ó 2015 Elsevier Ltd. All rights reserved.