ACCCN's Critical Care Nursing

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Ventilation and Oxygenation
Management 15







Louise Rose
Gabrielle Hanlon



ventilation is complex, ranging from simple interven-
Learning objectives tions, such as nasal cannulae through to invasive mechan-
ical ventilation and extracorporeal support. Additionally,
After reading this chapter, you should be able to: the meaning of ventilator terminology is often unclear
● describe oxygen therapy, including low-flow and high flow and terms may be used interchangeably. Critical care
devices, complications associated with oxygen therapy, and nurses must have a strong knowledge of the underlying
management priorities principles of oxygenation and ventilation that will facili-
● state nursing priorities for airway management strategies tate an understanding of respiratory support devices,
including laryngeal masks, endotracheal tubes and associated monitoring priorities and risks.
tracheostomy tubes
● summarise current knowledge on the physiological OXYGEN THERAPY
benefits, indications for use, associated monitoring Oxygen is required for aerobic cellular metabolism and
priorities, complications, modes, settings and interfaces for ultimately for human survival, with some cells, such as
non-invasive ventilation those in the brain, being more sensitive to hypoxia than
● state the indications for use, associated monitoring others. Refer to Chapter 13 for discussion of oxygen deliv-
priorities, complications, classification framework, modes ery and consumption, the oxyhaemoglobin dissociation
and settings for invasive mechanical ventilation curve, hypoxaemia and tissue hypoxia; this material
● outline the weaning continuum and current evidence for provides rationales for clinical decisions regarding the
optimising safe and efficient weaning from mechanical administration of oxygen therapy or ventilation strate-
ventilation gies. Oxygen therapy should be considered for patients
● discuss ventilation management strategies for refractory with a significant reduction in arterial oxygen levels, irre-
hypoxaemia spective of diagnosis and especially if the patient is
● discuss ventilation management strategies for severe drowsy or unconscious.
airflow limitation
INDICATIONS
Indications for oxygen therapy include:

● cardiac and respiratory arrest
Key words ● type I respiratory failure
● type II respiratory failure
artificial airway ● chest pain, cardiac failure, myocardial infarction
oxygen therapy ● low blood pressure, cardiac output
mechanical ventilation ● increased metabolic demands
non-invasive ventilation ● carbon monoxide poisoning
weaning
COMPLICATIONS
Administration of oxygen, regardless of the delivery
device, has potential adverse effects. High concentrations
INTRODUCTION of oxygen cause nitrogen washout, resulting in absorp-
tion atelectasis.
Supporting oxygenation and ventilation are two of the
most common interventions in intensive care; in 2007–
2008, approximately 41% of patients in Australian and Hypoventilation and CO 2 Narcosis
New Zealand ICUs received invasive mechanical ventila- High-dose oxygen therapy may lead to hypoventilation,
1
tion and 8% received non-invasive ventilation (NIV). worsening hypercapnia and CO 2 narcosis due to inhibi-
The technology available for supporting oxygenation and tion of the hypoxic drive in a small proportion of patients 381

382 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E

with chronic obstructive pulmonary disease (COPD). ● patient factors: inspiratory flow rate, respiratory rate,
These patients require close monitoring of PaCO 2 levels tidal volume, respiratory pause
when oxygen therapy is instituted or increased. Although ● oxygen device factors: oxygen flow rate, volume of
COPD patients frequently may have a lower baseline mask/reservoir, air vent size, tightness of fit
SpO 2 (88–94% compared to 96–100% in patients with Normal inspiratory flow in a healthy adult ranges between
no lung pathology), treatment of hypoxia is still essential, 25 and 35 L/min. Patients with respiratory failure tend to
and oxygen should not be withheld or withdrawn while increase their flow demand from 50 up to 300 L/min.
hypoxia remains, even if hypercapnia worsens. 2,3
Patients in respiratory distress are characterised by high
respiratory rates and low tidal volumes that can signifi-
4,5
cantly decrease the FiO 2 available via an oxygen delivery
Practice tip device, depending on the type in use.
Oxygen should not be withheld or withdrawn while hypoxia All oxygen delivery devices use some type of reservoir to
remains, even if hypercapnia worsens. support oxygen delivery and prevent CO 2 rebreathing. In
the case of a face mask, the reservoir is the mask; for nasal
cannulae it is the patient’s pharynx. Patients with high
Oxygen Toxicity inspiratory flow and tidal volume will deplete the reser-
voir faster than it can be replenished, resulting in air
Administration of high concentrations of oxygen may entrainment and dilution of the oxygen concentration.
lead to oxygen toxicity; symptoms include non-productive
cough, substernal pain, reduced lung compliance, inter- VARIABLE FLOW DEVICES
stitial oedema, and pulmonary capillary haemorrhage. A range of low or variable flow oxygen delivery devices
These symptoms may be mistakenly attributed to the are available to meet a patient’s physiological needs.
underlying illness, especially in a sedated and ventilated These devices range from nasal cannulae and oxygen
patient. Many of the symptoms abate once the percentage masks with different features, through to bag–mask
or fraction of inspired oxygen (FiO 2 ) is reduced, although ventilation.
irreversible pulmonary fibrosis may occur (see Box 15.1).
The concentration and duration of oxygen exposure that Low-flow Nasal Cannulae
4
induces oxygen toxicity varies between patients; the Traditional low-flow nasal cannulae sit at the external
lowest possible FiO 2 should therefore be used to achieve nares and deliver 3–4 L/min of oxygen. Higher flows may
the target PaO 2 or SpO 2 .
cause discomfort and damage from the drying effect on
OXYGEN ADMINISTRATION DEVICES respiratory mucosa. They are generally well-tolerated by
the patient. Increased flow demand with respiratory dis-
Initial management of hypoxia in a spontaneously- tress dilutes the oxygen, reducing the FiO 2 to the alveoli.
breathing patient with an intact airway is low-flow oxygen Mouth-breathing and talking can also render nasal can-
via nasal cannulae (up to 6 L/min) or face mask (up to nulae ineffective.
15 L/min). Although oxygen devices have traditionally
had FiO 2 ascribed to specific flow rates, the FiO 2 delivered High-flow Nasal Cannulae
to the alveoli is influenced by: High-flow nasal cannulae (HFNC) have slightly larger
prongs that facilitate oxygen flow of up to 60 L/min
leading to less air entrainment effect than with other
5,6
oxygen delivery systems. HFNC generate low levels of
BOX 15.1 Signs and symptoms of oxygen end-expiratory pressure and can therefore reduce tachy-
7,8
toxicity pnoea and work of breathing. The high gas flow may
flush CO 2 from the anatomical dead space preventing
Central nervous system: CO 2 rebreathing and thereby decreasing PaCO 2 , although
● nausea and vomiting this is not well supported by the literature. 9,10 These
● anxiety systems are also generally well-tolerated by the patient,
● visual changes but must be used with heated humidification to avoid
● hallucinations drying the respiratory mucosa. HFNC are now used more
8
● tinnitus frequently in clinical practice to avoid more invasive ther-
● vertigo apies but there is limited high-quality evidence on their
● hiccups use in adults.
● seizures
Pulmonary:
● dry cough Practice tip
● substernal chest pain
● shortness of breath Patients using any type of nasal cannulae should avoid mouth-
● pulmonary oedema breathing and talking to minimise diluting oxygen delivery to
● pulmonary fibrosis the lungs.

Ventilation and Oxygenation Management 383

Oxygen Masks tilting their head slightly back and lifting the chin, or
Loose-fitting oxygen masks include simple (Hudson) face thrusting the jaw forward. The head-tilt/chin-lift mano-
15
masks, aerosol masks used in combination with heated euvre is not used if cervical spine injury is suspected.
humidification and nebuliser treatments, tracheostomy The jaw-thrust manoeuvre may require two hands to
16
masks and face tents. All are considered low-flow or maintain. If more prolonged support is required, an
variable-flow devices, with the delivered FiO 2 varying oro- or nasopharyngeal airway can be used that may also
with patient demand. Flow rates ≥5 L/min minimise CO 2 facilitate bag–mask ventilation.
rebreathing. The addition of ‘tusks’ to a Hudson mask
11
may increase the oxygen reservoir, but does not guaran- ORO- AND NASOPHARYNGEAL AIRWAYS
tee a consistent FiO 2 and has probably been superseded The Guedel oropharyngeal airway is available in various
by high-flow systems. 12 sizes (a medium-sized adult requires a size 4). The airway
Partial rebreather and non-rebreather masks have an is inserted into the patient’s mouth past the teeth, with
attached reservoir bag that enables delivery of higher the end facing up into the hard palate, then rotated 180
levels of FiO 2 . Both mask types have a one-way valve degrees, taking care to bring the tongue forward and
precluding expired gas entering the reservoir bag. A non- not push it back. Oropharyngeal airways are poorly toler-
rebreather mask has two one-way valves on the mask ated in conscious patients and may cause gagging and
14
13
preventing air entrainment. The maximum FiO 2 deliv- vomiting.
ery with non-rebreather masks is 0.85 with low flow A nasopharyngeal airway (see Figure 15.1) is inserted
demand, with a steep decline in FiO 2 concentration at through the nares into the oropharynx; it can be difficult
the alveoli level as the patient’s minute volume increases. to insert and require generous lubrication to minimise
Non-rebreather masks may perform worse than a Hudson trauma. This type of airway should not be used for
mask without a reservoir bag. 5 patients with a suspected head injury. As well as opening
Venturi Systems the airway, suction catheters can be passed to facilitate
secretion clearance. Once inserted these airways are better
Venturi systems use the Bernoulli Effect to entrain gas via tolerated than an oropharyngeal airway.
a side port; gas flow through a narrowing increases speed
and gains kinetic energy, resulting in an area of low pres- LARYNGEAL MASK AIRWAY
sure that entrains room air through the side port. An FiO 2
concentration can be selected by widening or narrowing AND ITS INTUBATION
the aperture in the Venturi device to a maximum FiO 2 of The classic laryngeal mask airway (cLMA) (see Figure
0.6. The FiO 2 concentration using a Venturi system is less 15.2) is positioned blindly into the pharynx to form a
affected by changes in respiratory pattern and demand low-pressure seal against the laryngeal inlet. It is easier
compared to other low-flow oxygen devices. 5 and quicker to insert than an endotracheal tube, and is
particularly useful for operators with limited airway skills;
Bag–Mask Ventilation the cLMA does not carry the same potentially fatal com-
Bag–mask ventilation (BMV) with a self-inflating bag plications such as oesophageal intubation although the
(and reservoir), non-return valve and mask delivers risk of aspiration remains. 17
assisted ventilation at an FiO 2 of 1. Addition of a positive Mechanical ventilation can be delivered with low-airway
end-expiratory pressure (PEEP) valve will improve oxy- pressures (less than 20 cmH 2 O) via a cLMA. This device
genation. Manual ventilation requires a good seal between is widely used in elective general anaesthesia, and can
15
the patient’s face and the mask; this may be difficult to be used in critical care as an alternative to bag–mask
achieve as a single operator. One person may be required ventilation or endotracheal intubation when initial
17
to hold the mask and lift the patient’s chin, while another attempts at intubation have failed. The ‘intubating’
18
squeezes the bag. Effective bag–mask ventilation is con- LMA is most commonly used when a difficult
firmed when the chest visibly rises as the bag is squeezed intubation is anticipated or encountered. This device
14
as well as improved oxygen saturations. BMV may cause has a handle and is more rigid, wider and curved than
gastric insufflation, increasing the risk of vomiting and the cLMA, enabling passage of a purpose-made endo-
subsequent aspiration. tracheal tube. 17

COMBITUBE
Practice tip
The combitube is more widely used in North America for
15
Transparent face masks are recommended for bag–mask venti- emergency situations than in Australia and the UK. It is
lation as they allow immediate recognition if a patient vomits. a dual-lumen, dual-cuff oesophageal-tracheal airway that
enables ventilation if inserted into either the oesophagus
or trachea. Inexperienced operators may find a combi-
AIRWAY SUPPORT tube more difficult to insert correctly than a cLMA.
19
Complications may occur in up to 40% of patients and
The most common cause of partial airway obstruction in include aspiration pneumonitis, pneumothorax, airway
an unconscious patient is loss of oropharyngeal muscle injuries and bleeding, oesophageal laceration and perfo-
tone, particularly of the tongue. This may be alleviated by ration and mediastinitis. 20

384 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E































FIGURE 15.1 Nasopharyngeal airways. 272
























FIGURE 15.2 Laryngeal mask airways. 272

INTUBATION

Endotracheal intubation is the ‘gold standard’ for airway
support, providing airway protection in the presence of
an airway oedema, absent gag, cough or swallow reflex.
Intubation facilitates delivery of mechanical ventilation
and pulmonary secretion clearance. 16

ENDOTRACHEAL TUBES
Endotracheal tubes (ETT) are available with internal
diameters ranging from 2–10 mm (common adult sizes 272
are 7–9 mm), and are up to 30 cm long. A longitudinal FIGURE 15.3 Endotracheal tube.
radio-opaque line allows visualisation of tube placement volumes, but are commonly high-volume, low-pressure
on a chest X-Ray. Markings at 1 cm intervals indicate (see Figure 15.3).
the length from the distal end. Tubes are available
with and without a distal cuff. Adults typically require a Endotracheal tubes may be reinforced with a wire coil
cuffed ETT to seal their trachea, facilitating positive pres- embedded within the plastic for the entire length of the
sure ventilation and preventing aspiration of oropharyn- tube to prevent kinking and occlusion. These tubes are
21
geal contents. Cuffs come in a range of profiles and more commonly used in the operating room. The wire

Ventilation and Oxygenation Management 385

coils can however be irreversibly compressed by a strong PROCEDURE
bite that occludes the airway. Reinforced tubes also The patient is preoxygenated to minimise desaturation
increase the risk of tracheal damage and therefore should during apnoea and laryngoscopy, commonly via bag
be replaced with a standard endotracheal tube on arrival and mask, although other methods such as non-invasive
in the ICU. Most endotracheal tubes have a ‘Murphy eye’, ventilation have been suggested. Intubation in ICU is
24
an oval-shaped hole in the side of the tube between the usually performed via laryngoscopy with insertion of an
cuff and the end of the tube that provides a patent aper- oral ETT. Intubation may be performed using a fibreoptic
ture if the distal opening is occluded. 22
bronchoscope when difficulty is encountered, or for nasal
intubation.
PREPARATION FOR INTUBATION
Adequate preparation of the patient, equipment and Oral vs Nasal Intubation
environment, as well as strong knowledge of emergency Oral intubation is preferred unless there are specific indi-
procedures is important to ensure safe and efficient intu- cations for nasal intubation. Oral intubation is easier to
bation. Up to 50% of patients undergoing endotracheal perform and allows use of a larger diameter tube. While
intubation in ICU will experience a complication; 28% nasal intubation provides better splinting for the ETT and
will have a serious complication, including hypoxaemia, facilitates oral hygiene, it can damage nasal structures,
circulatory collapse, cardiac arrhythmia, cardiac arrest, is contraindicated in skull fractures and increases
oesophageal intubation, aspiration and death. 23 the risk of maxillary sinusitis and ventilator-associated
pneumonia. 25
Patient Preparation Cricoid Pressure
If appropriate, and time permits, explain the procedure
to the patient and family. Prepare the patient with: Cricoid pressure (Sellick manoeuvre) was introduced in
the 1960s to prevent aspiration of gastric contents during
● reliable intravenous access established to allow rapid intubation. The oesophagus lies behind and in line with
fluid and drug administration the trachea. The cricoid cartilage, situated below the
● accurate blood pressure monitoring (preferably thyroid prominence, is a closed tracheal ring which, when
intra-arterial) compressed, closes the oesophagus while the trachea
● continuous oxygen saturation and ECG monitoring remains open. Cricoid pressure is performed by placing
● nasogastric tube (if in situ) should be aspirated and your thumb on one side of the patient’s trachea, middle
placed on free drainage finger on the other side and index finger directly on the
● positioned supine in the ‘sniff’ position cricoid. Although widely used over the last 50 years, its
26
efficacy is being questioned as technique is frequently
Equipment and Drugs poor, and there is wide anatomical variation in the exact
27
All equipment should be checked immediately prior to orientation of the oesophagus in relation to the trachea. 28
intubation, including
Backwards, Upwards, Rightward
● oxygen supply Pressure Manoeuvre
● suction supply, with a range of Yankaeur and Y-suction The backwards, upwards, rightward pressure (BURP)
catheters manoeuvre on the thyroid cartilage was introduced in the
● laryngoscope blades and holder are compatible, with mid-1990s to improve visualisation during difficult laryn-
a functioning light goscopy. The patient’s jaw is thrust forward, so their head
● appropriately-sized face mask is in the ‘sniffing’ position. Place your thumb and third
● manual ventilation (ambubag™) available and finger on either side of the thyroid cartilage and index
attached to oxygen supply finger on top. Pressure is applied in the sequence back-
● ETT cuff inflated in sterile water to ensure no leaks and wards (towards the spine), upwards (towards the head),
even inflation rightward (towards the patient’s right side). This is
● water-based lubricant of tube and cuff (while main- easier to perform following administration of muscle
taining sterility) relaxants. 29,30
● capnography (chemical CO 2 detectors are often used
in emergency situations) Cuff Management
● ventilator and circuit
● emergency/resuscitation trolley at bedside Endotracheal and tracheostomy tube cuffs prevent airway
● gloves, eye protection contamination by pharyngeal secretions and gastric con-
● drugs (sedative and muscle relaxant) tents and loss of tidal volume during mechanical ventila-
tion. The cuff does not secure the tube in the trachea.
Cuff inflation pressures should be maintained at 20–
30 cmH 2 O. 31,32 Cuff inflation pressures ≤20 cmH 2 O
Practice tip (15 mmHg) are associated with an increased risk of aspi-
ration and a 2.5-fold increase in ventilator-associated
During intubation, know who to call for help, and do not hesi- pneumonia (VAP). Conversely, tracheal wall damage
33
tate to do so. may occur if cuff pressure exceeds the capillary perfusion
pressure in the trachea (27–40 cmH 2 O/20–30 mmHg).

386 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E

There are four methods described for assessing cuff Confirmation of Tube Position
inflation:
The correct position of the ETT distal end is 3–5 cm above
1. minimal occluding volume (MOV) the carina. A lip level of 20 cm for women and 22 cm for
2. minimal leak test (MLT) men should prevent endobronchial intubation, with the
3. cuff pressure measurement (CPM) proximal end fixed at either the centre or the side of the
40
4. palpation. mouth. Confirmation of the ETT position is required
immediately following intubation and at regular intervals
In Australia and New Zealand, CPM is the most common thereafter as movement of the tube can occur.
35
34
form of cuff pressure assessment, in contrast to the UK
36
and North America where CPM is used infrequently. Chest auscultation is the traditional method to confirm
Cuff pressure varies with head and body position, tube ETT position. Observation of chest expansion is, however,
37
position and airway pressures. The optimum frequency unreliable, as the chest may appear to rise with oesopha-
of cuff pressure monitoring is unclear; at a minimum it geal intubation. Conversely the chest may not rise with a
should be done post-intubation, on arrival in ICU and correctly positioned tube if the patient is obese or has a
once per nursing shift. A persistent cuff leak or pressures rigid chest wall. Patients with left main bronchus intuba-
41
of ≥30 cmH 2 O (22 mmHg) to generate a seal should be tion may exhibit bilateral breath sounds. End-tidal CO 2
reviewed and referred to medical staff. monitoring is the ‘gold standard’ method for confirming
ETT placement. Disposable devices that change colour in
If performing MOV and MLT, aspiration should be pre- the presence of CO 2 are inexpensive and easy to use, but
vented by semi-recumbent positioning, suctioning at the may be inaccurate during cardiopulmonary resuscitation,
back of the mouth (as far back as tolerated), aspiration or if contaminated. Capnography is the most reliable
of the nasogastric tube and discontinuation of feeds technique to identify ETT placement in both arrest and
before cuff deflation. non-arrest situations. Continuous end-tidal CO 2 moni-
18
toring during intubation is recommended as a minimum
standard by the College of Intensive Care Medicine of
Practice tip Australia and New Zealand. 42
If the pilot tube for the ETT is accidentally cut, cannulate the
tubing with a 23- or 24-gauge needle to reinflate the cuff and Practice tip
clamp the tubing. If using a clamp with serrations, place gauze
between the tube and the clamps to avoid further damage to Always ensure there is someone who is skilled at intubation
the pilot tube. immediately available when extubating a patient.


Endotracheal Tube Fixation TRACHEOSTOMY
The purpose of ETT fixation is to maintain the tube in Tracheostomy may be required for upper airway obstruc-
the correct position, prevent unintended extubation and tion, although it is most commonly performed for ICU
facilitate mechanical ventilation while maintaining skin patients who require prolonged mechanical ventilation.
38
integrity and oral hygiene. ETT fixation methods include: The advantages of tracheostomy over endotracheal intu-
● tying cotton tape around the tube, then around the bation include decreased risk of laryngeal damage and
patient’s neck subglottic stenosis, reduced airway resistance and dead-
● taping the tube to the patient’s face using medical space which decreases the work of breathing and there-
43
adhesive tape fore supports weaning, and improved patient tolerance
● commercial tubeholders of varying designs. enabling reduction of sedation. The optimum time to
perform tracheostomy remains contentious, and is often
39
There is no evidence supporting a preferred method influenced by a patient’s diagnosis. 44
with each having specific strengths and weaknesses. Two
nurses are required to prevent ETT dislodgement during PROCEDURE
fixation. Although there is also no evidence to recom-
mend a preferred frequency, ETT fixation is generally Tracheostomy can be performed using a surgical tech-
changed at least daily, to allow assessment of the underly- nique (ST) or percutaneous dilatational technique (PDT).
ing skin with particular attention to the tops of the ears PDT is contraindicated in patients with anatomical
38
and corners of the mouth and to facilitate oral hygiene. anomalies of the neck and serious bleeding disorders,
The ETT position in the mouth is alternated at this time. and should be undertaken with caution in patients who
are obese, have a cervical spine injury, coagulopathy, dif-
45
ficult airway or require high levels of ventilatory support.
PDT is more commonly performed than ST in Australian
Practice tip and New Zealand ICUs. 45
Adhesive devices may become dislodged as facial hair grows A variety of tracheostomy tubes are available that
under them. facilitate secretion clearance, communication and differ-
ing patient anatomy. Inner cannulas (re-usable or

Ventilation and Oxygenation Management 387

disposable) prevent secretion build up on the tracheos- for cardiac arrhythmias. Manual hyperinflation is dis-
tomy tube, while fenestrated and talking tracheostomies couraged due to the risk of barotrauma and lack of
facilitate communication, as do Passe Muir valves used benefit. Similarly, installation of saline is not supported
with the cuff deflated. due to increased risk of flushing pathogens into distal
lung regions. 60
TRACHEOSTOMY CARE
The aim of tracheostomy care is to keep the site free of METHODS
infection, and prevent tube blockage or dislodgement. The three methods of suctioning are:
The site is cleaned with normal saline and fixation devices
changed at least 12-hourly with two nurses to safely ● open suction: a suction catheter is passed under
46
perform tape changes. Velcro tapes are easier to change aseptic technique directly into the ETT/tracheostomy
47
and more comfortable than cotton tape. Lint-free or after disconnection from the ventilator circuit. Disad-
superabsorbent foam dressings may be placed under the vantages include loss of PEEP resulting in loss of alve-
flange to absorb secretions. Adequate humidification and olar recruitment and increased risk of transmission of
suctioning will usually prevent tube obstruction (see later infective organisms. A surgical mask and protective
61
in this chapter). The use of inner cannulae has obviated eyewear should be worn.
the need for frequent tracheostomy tube changes. Single ● semi-closed suction: a suction catheter is passed
lumen (no inner cannula) tracheostomy tubes should be through a swivel connector with a self-sealing rubber
changed every 7–10 days. 46 flange.
● closed suction: in-line system is attached between the
COMPLICATIONS OF ENDOTRACHEAL ETT/tracheostomy tube and the ventilator circuit
where the suction catheter is contained in an inte-
INTUBATION AND TRACHEOSTOMY grated plastic sleeve. Alveolar derecruitment occurs to
Tube blockage, tube dislodgement and aspiration are a lesser degree than with open suction.
major complications. Partial ETT or tracheostomy tube There is no difference between techniques in relation to
dislodgement can cause greater harm than complete development of ventilator-associated pneumonia (VAP)
removal because of delays in diagnosis and resultant aspi- and quantity of secretions removed.
ration or worsening gas exchange. Tube dislodgement is
most likely to occur when turning the patient, if the The diameter of the suction catheter should not be greater
patient is agitated or when nursing staff are distracted or than half the diameter of the airway, using the formula:
48
on breaks. While physical restraint may be considered suction catheter size [Fr] = (ET tube size [mm] − 1) × 2.
to prevent tube dislodgement, multiple studies noted The suction catheter should be inserted to the carina, then
patients were restrained at the time of self-extubation or withdrawn 2 cm before suction is applied to prevent
device removal. 49-54 Effective levels of analgesia and seda- damage to the carina. Suction should only last 15 seconds,
tion is therefore most appropriate in minimising the risk using continuous, rather than intermittent, suction. Use
of self-extubation. of ETTs or tracheostomy tubes with integrated subglottic
suction ports may assist in preventing VAP, especially when
Complications during and immediately after endotra- performed with other prevention strategies such as semi-
cheal intubation and tracheostomy include cardiovascu- recumbant positioning and good cuff seal management.
lar compromise, bleeding, injury to the tracheal wall,
damage to the vocal cords, pneumothorax, pneumome- ADVERSE EFFECTS
diastinum and subcutaneous emphysema. Late compli- Adverse effects of suction can include hypoxaemia, intro-
cations of tracheostomy include tracheal stenosis, duction of infective organisms, tracheal trauma, bradycar-
tracheomalacia and tracheo-oesophageal fistula and dia, hypertension and increased intracranial pressure.
infection. As noted earlier, damage to the trachea is exac- Tracheal suctioning causes discomfort, and should there-
55
erbated by high cuff pressures. PDT results in fewer fore be performed only when clinically indicated, such as
wound infections, decreased incidence of bleeding and audible presence of secretions and desaturation. 58
reduced mortality compared to ST. 56
TRACHEAL SUCTION EXTUBATION
Following successful weaning from mechanical venti-
Patients with an ETT or tracheostomy tube require tra-
cheal suction to remove pulmonary secretions that can lation (see later in this chapter), assessment of the patient
lead to atelectasis or airway obstruction and impair gas prior to extubation should include adequate gas exchange,
exchange. Suction should be performed as clinically respiratory rate and work of breathing on minimal
57
indicated, with assessment of visible or audible secre- support for prolonged periods, respiratory muscle
tions, rising inspiratory pressure, decreasing V T or strength, the ability to cough and clear secretions spon-
58
increased work of breathing. A sawtooth pattern on the taneously and a stable haemodynamic status and mental
62
flow-volume waveform may also indicate the need for status. Serious post-extubation complications of laryn-
63
suction (discussed later in this chapter). 59 gospasm and stridor cannot be reliably predicted, so
the ease/grade of intubation should be considered
Preoxygenation using a FiO 2 of 1 for 60 seconds prior to prior to extubation and provision made for immediate
performing suction minimises hypoxia and the potential re-intubation. 64

388 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E



TABLE 15.1 Physiological indications suggesting the need for mechanical ventilation

Parameter Normal values ARF CRF Associated signs and symptoms
Respiratory 12–20 ≥28 ≥30 Dyspnoea, increased activation of accessory
rate muscles and active expiration
pH 7.35–7.45 <7.30 7.35–7.40 Failure to adequately ventilate:
No compensatory changes May be normal due to Elevated PaCO 2 , acidic pH, headache,
metabolic compensation confusion or other mental status change,
PaCO 2 35–45 mmHg >50 mmHg and rising >50 mmHg and rising tachypnoea (RR >30), flushed skin
80–100 mmHg <65 mmHg and falling <50 mmHg and falling Failure to adequately oxygenate:
PaO 2
Hb/HCT elevated as Decreased PaO 2 and SpO 2 , tachycardia,
compensatory mechanism hyper- or hypotension, dyspnoea, gasping,
nasal flaring, use of accessory muscles,
anxiety, agitation and altered mental
status, cyanosis
−
− 22–28 mmol/L Within normal limits If chronic hypercapnia, then HCO 3 >28 mmol/L is a compensatory mechanism
HCO 3
If CRF is primarily failure to oxygenate then HCO 3 will be within normal limits
−
ARF = acute respiratory failure; CRF = chronic respiratory failure.
MECHANICAL VENTILATION
TABLE 15.2 Equation of motion
As stated in the introduction, 41% of patients in Austra-
lian and New Zealand ICUs received invasive mechanical
ventilation and 8% received non-invasive ventilation Equation: P T (P airway + P muscle ) = V T /Cr + V T /T I × R + PEEP T
1
(NIV) in 2007–08. The median duration of invasive Abbreviations: P T = total pressure: the sum of the
mechanical ventilation for these patients was 2.5 days. pressure in the proximal airway and
the pressure generated by the
In the most recent international study of mechanical- respiratory muscles
ventilation practices, reporting data from 4968 patients V T = tidal volume
in 349 ICUs and 23 countries found the median duration Cr = compliance
of ventilation to be 4 days (interquartile range 2–8 T I = inspiratory time
65
days). In this patient cohort the three most common R = resistance
PEEP T = total positive end expiratory
reasons for mechanical ventilation were postoperative pressure: alveolar pressure at the end
respiratory failure, coma and pneumonia. This interna- of expiration and is the sum of PEEP
tional report did not include data from Australia and applied by the ventilator and any
New Zealand. A study describing ventilation and weaning intrinsic (auto) PEEP.
practices of 55 ICUs in Australia and New Zealand in Notes: V T /Cr: describes the elastic properties the
2005 reported a similar profile for the most common respiratory system
indications for mechanical ventilation. 66 V T /T I : reflects flow in the system
V T /T I × R: resistance of the respiratory
system.
PRINCIPLES OF MECHANICAL VENTILATION
Mechanical ventilation describes the application of posi-
tive or negative pressure breaths using non-invasive or Compliance and Elastance
invasive techniques. Indications for initiation of mechan- Compliance refers to the ease with which lung units
ical ventilation are discussed below. Table 15.1 lists the distend. Elastance is the tendency of the lung units to
patient parameters typically observed in acute and chronic return to their original form once stretched. Compliance
respiratory failure that may be influential in the decision is defined as the change in volume that occurs due to a
to ventilate. During positive pressure ventilation, the type change in pressure.
of ventilation used most commonly in critical care, the
∆
ventilator delivers a flow of gas into the lungs during C = ∆ V/ P
inspiration using a pneumatic system. Expiration is
passive. Lung tissue and the surrounding thoracic structures
contribute to respiratory compliance. Normal compli-
The Equation of Motion ance for a mechanically ventilated patient ranges from
The equation of motion for the respiratory system is a 35–50 mL/cmH 2 O. 68
mathematical model that relates pressure volume and
flow during the delivery of a breath, with the pressure Resistance
required to deliver a volume of gas to the lungs deter- Resistance refers to the forces that oppose airflow. Resis-
mined by the elastic and resistive properties of the respi- tance in the airways is affected by the diameter and length
67
ratory system (see Table 15.2). of the airways, including the artificial airway, the gas flow

Ventilation and Oxygenation Management 389

rate and the density and viscosity of the inspired gas. 7. the resistance, compliance and dead space charac-
During mechanical ventilation, bronchospasm, airway teristics do not adversely affect spontaneous
oedema, endotracheal tube lumen size, increased secre- breathing modes
tions, and inappropriate setting of flow rates can influ- 8. the sterility of the inspired gas is not
ence airway resistance. Normal resistance for intubated compromised. 73
patients is 6 cmH 2 O/(L/sec). 68
Humidification is applied using either a heat–moisture
exchanger (HME) or a heated water bath reservoir device
VENTILATOR CIRCUITS in combination with a heated ventilator circuit.

Delivery of mechanical ventilation requires a ventilator
circuit to transport gas flow to the patient. To prevent Heat–moisture Exchanger
condensation from cooling of warm humidified gas, Heat–moisture exchangers conserve heat and moisture
inspired gas is heated via a wire inside the wall of the during expiration, and enable inspired gas to be heated
circuit in either the inspiratory limb alone or both the and humidified. Two types of HMEs exist: hygroscopic
69
inspiratory and expiratory limbs. Historically ventilator and hydrophobic. Hygroscopic HMEs absorb moisture
circuits were changed frequently (48–72 hours) to onto a chemically impregnated foam or paper material
70
decrease the risk of VAP. Current guidelines for preven- and have been shown to be more effective than hydro-
tion of VAP found evidence that the frequency of ventila- phobic HMEs. HMEs are placed distally to the circuit
74
tor circuit changes had no relationship to the incidence Y-piece in line with the endotracheal tube and increase
75
of VAP and therefore recommended routine circuit dead space by an amount equal to their internal volume.
changes were not necessary and circuits should only be HMEs should be changed every 24 hours or when soiled
changed when soiled or damaged. 71 with secretions and are usually reserved for short term
humidification.
HUMIDIFICATION Heated Humidification
Humidification techniques warm and moisten gas to
facilitate cilia action and mucus removal as well as to Generally, heated humidification (HH) is used for patients
prevent drying and irritation of respiratory mucosa and requiring greater than 24 hours of mechanical ventila-
solidification of secretions. During endotracheal intuba- tion. Various models of heater bases and circuits are on
tion and mechanical ventilation, the normal humidifica- the market and we recommend their use in accordance
tion processes of the nasopharynx are bypassed. This, in with manufacturer instructions. A recent systematic
combination with the use of dry medical gas at high flow review and meta-analysis reported no overall effect on
rates, means alternative methods of humidification are artificial airway occlusion, mortality, pneumonia, or
required. The best conditions for mucosal health and respiratory complications when HMEs were compared to
function over prolonged periods are when inspired gas is HHs, although it noted that PaCO 2 and minute ventila-
warmed to core body temperature and is fully saturated tion were increased and body temperature was lower with
76
with water. 72 the use of HMEs.
NON-INVASIVE VENTILATION
Absolute and Relative Humidity
Non-invasive ventilation (NIV) is an umbrella term
Absolute humidity refers to the amount of water vapour
in a given volume of gas at a given temperature. Absolute describing the delivery of mechanical ventilation without
humidity rises with increasing temperature; during the use of an invasive airway, via an interface such as an
mechanical ventilation gas is heated to increase the oronasal, nasal, or full face mask or helmet. NIV tech-
amount of water vapour it will hold. Relative humidity is niques include both negative and positive pressure
expressed as a percentage, and is the actual amount of ventilation, although in critical care positive pressure ven-
water vapour in a gas compared to the maximum amount tilation is primarily used.
this gas can hold (ratio of absolute to maximal humid-
ity). Ideal humidification is achieved when: TERMINOLOGY
Positive pressure NIV can be further categorised as non-
1. the inspired gas delivered into the trachea is at invasive positive pressure ventilation (NIPPV) or conti-
3
37°C with a water content of 30–43 g/m nuous positive airway pressure (CPAP). NIPPV is the
(relative humidity is 100% at 37°C in the provision of inspiratory pressure support (also referred to
bronchi) as inspiratory positive airway pressure [IPAP]) usually in
2. the set temperature remains constant without combination with positive end expiratory pressure (PEEP)
fluctuation (also referred to as expiratory positive airway pressure
3. humidification and temperature are unaffected by [EPAP]). CPAP does not actively assist inspiration but
a large or differing types of gas flow provides a constant positive airway pressure throughout
4. the device is simple to use inspiration and expiration. 77
5. the humidifier can be used with spontaneously
breathing and ventilated patients The terms Biphasic (or bilevel) positive airway pressure
6. safety alarms prevent overheating, overhydration (BiPAP®) and non-invasive pressure support ventilation
78
and electrocution (NIPSV) are also used to refer to NIPPV. The acronym

390 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E

BiPAP® is registered to Respironics (Murrayville, PA), a
company that produces a number of non-invasive venti- TABLE 15.3 Indications and contraindications for
lators including the BIPAP Vision, a NIV ventilator com- non-invasive ventilation 77
monly used in the ICU. The acronym NIPSV is primarily
used in European descriptions of NIPPV. Indications
Bedside observations Increased dyspnoea: moderate to severe
Tachypnoea:
>24 breaths per min [obstructive]
>30 breaths per min [restrictive]
Practice tip Signs of increased work of breathing,
accessory muscle use and abdominal
When other members of the ICU team use the term BiPAP/ paradox
BIPAP, clarify if they are referring to non-invasive or invasive Gas exchange Acute or acute-on-chronic ventilatory
ventilation. failure (best indication), PaCO 2
>45 mm Hg, pH <7.35
Hypoxaemia (use with caution), PaO 2 /
FIO 2 ratio <200
PHYSIOLOGICAL BENEFITS Contraindications
The efficacy of NIV in patients with acute respiratory Absolute Respiratory arrest
failure is, at least in part, related to avoidance of inspira- Unable to fit mask
tory muscle fatigue through the addition of inspiratory Relative Medically unstable: hypotensive shock,
positive pressure thus reducing inspiratory muscle work. uncontrolled cardiac ischaemia or
79
Application of positive pressure during inspiration arrhythmia, uncontrolled upper
gastrointestinal bleeding
increases transpulmonary pressure, inflates the lungs, Agitated, uncooperative
augments alveolar ventilation and unloads the inspira- Unable to protect airway
80
tory muscles. Augmentation of alveolar ventilation, Swallowing impairment
demonstrated by an increase in tidal volume, increases Excessive secretions not managed by
secretion clearance techniques
CO 2 elimination and reverses acidaemia. High levels of Multiple (i.e. two or more) organ failure
inspiratory pressure may also relieve dyspnoea. 81 Recent upper airway or upper
gastrointestinal surgery
The main physiological benefit in patients with conges-
tive heart failure (CHF) is attributed to the increase in PaCO 2 : partial pressure of carbon dioxide in arterial blood; PaO 2 : partial
functional residual capacity associated with the use of pressure of oxygen in arterial blood; PaO 2 /FIO 2 : ratio of partial pressure of
oxygen in arterial blood to fraction of inspired oxygen.
PEEP that reopens collapsed alveoli and improves oxy-
82
genation. Increased intrathoracic pressure associated
with the application of positive pressure also may improve
cardiac performance by reducing myocardial work and
oxygen consumption through reductions to ventricular (CHF). Three meta-analyses have shown a reduction in
preload and left ventricular afterload. 82-84 NIV also pre- intubation rates, hospital length of stay and mortality for
serves the ability to speak, swallow, cough and clear secre- COPD patients managed with NIPPV compared to stan-
89-91
tions, and decreases risks associated with endotracheal dard medical treatment. COPD patients most likely to
intubation. 85 respond favourably to NIPPV include those with an
unimpaired level of consciousness, moderate acidaemia,
INDICATIONS FOR NIV a respiratory rate of <30 breaths/minute and who dem-
onstrate an improvement in respiratory parameters within
The success of NIV treatment is dependent on appropri- two hours of commencing NIV. 79,92
86
ate patient selection. Table 15.3 outlines indications
and contraindications to NIV. Early use of NIV in combination with standard therapy
for patients with CHF has also been shown to reduce
Acute Respiratory Failure intubation rates and mortality when compared to stan-
93-95
Evidence supporting the role of NIV in patients with dard therapy alone. A recent meta-analysis found
CPAP reduced hospital mortality whereas NIPPV did not
hypoxaemic respiratory failure is limited and conflict- have an effect on mortality. Both NIV modes were
94
82
ing. For patients with community-acquired pneumonia, shown in this meta-analysis to reduce the need for intu-
NIV has been shown to reduce intubation rates, ICU bation. An early study comparing NIPPV to CPAP in
length of stay and 2-month mortality but only in the patients with CHF reported a higher incidence of myo-
87
subgroup of patients with COPD. Pneumonia also has cardial infarction. Based on this finding, practice guide-
96
been identified as a risk factor for NIV failure. 88 lines from the British Thoracic Society recommend NIPPV
should only be used for patients with CHF when CPAP
Acute Exacerbation of COPD and CHF has been unsuccessful. More recently several studies
97
Strong evidence exists to support the use of NIV for have found no difference in myocardial infarction rates
patients with acute exacerbation of chronic obstructive when comparing the two modes. 98-101 A recent large mul-
pulmonary disease (COPD) and congestive heart failure ticentre randomised controlled trial found NIV delivered

Ventilation and Oxygenation Management 391

by either CPAP or NIPPV resulted in symptomatic
improvements, but failed to demonstrate a mortality TABLE 15.4 Monitoring priorities for non-invasive
102
benefit. Practice surveys indicate CPAP may be the pre- ventilation 104
ferred method of NIV for patients with CHF in Australia
and internationally. 103,104 Priority Assessment
NIV in Weaning Patient comfort Restlessness
Mask tolerance
NIV may be used as an adjunct to weaning to reduce the Anxiety level
duration of invasive ventilation and associated complica- Dyspnoea score
105
tions. Patients are extubated directly to NIV and then Pain score
weaned to standard oxygen therapy. This use of NIV Conscious level Glasgow coma score
differs from its role in preventing reintubation in patients Work of breathing Chest wall motion
that develop, or who are at high risk of, postextubation Accessory muscle activation
106
respiratory failure. A recent systematic review and meta- Respiratory rate
analysis of 12 trials of NIV as a weaning adjunct found Gas exchange parameters
reductions in mortality, ICU and hospital lengths of stay, Continuous SpO 2
Arterial blood gas analysis
107
duration of ventilation and rates of VAP. Conversely the (Baseline and 1–2 hourly
largest study of NIV use in postextubation respiratory subsequently)
failure reported worsened survival rates hypothesised as Patient colour
108
a result of delayed reintubation. A subsequent meta- Haemodynamic status Continuous heart rate
analysis suggested NIV may have a role in preventing the Intermittent blood pressure
development of respiratory failure postextubation for Ventilator parameters Air leak around mask
those at risk, but should be used with caution once respi- Adequacy of pressure support
ratory failure has developed and should not delay the (V T , pH, PaCO 2 )
decision to reintubate. 106 Adequacy peak end expiratory
pressure (SpO 2, PaO 2 )
Other Indications SpO 2 : saturation of peripheral oxygen; V T : tidal volume; PaCO 2 : partial
Other indications for NIV include: pressure of carbon dioxide in arterial blood; PaO 2 : partial pressure of
oxygen in arterial blood.
● asthma 109
● neuromuscular disorders (e.g. muscular dystrophy,
amyotrophic lateral sclerosis) features, commencing with low pressure levels, holding
● severe obstructive sleep apnoea the mask gently in position prior to securing with the
● palliation. straps/headgear, and ensuring straps prevent major leaks
INTERFACES AND SETTINGS but are not so tight they increase discomfort. Once
NIV is commenced, the patient should be monitored
NIV requires an interface that connects the patient to for respiratory and haemodynamic stability, response
either a ventilator, portable compressor or flow generator to NIV treatment, ongoing tolerance, and presence of
with a CPAP valve. The selection of an appropriate inter- air leaks (Table 15.4). Arterial blood gas analysis should
face can influence NIV success or failure. Oronasal masks be performed at baseline and within the first one to
cover both the mouth and nose and are the preferred two hours of commencement. During the initiation
97
mask type for the management of acute respiratory and stabilisation period, patients should be monitored
110
failure. Nasal masks enable speech, eating and drink- using a nurse-to-patient ratio of 1 : 1 with ongoing
ing, and therefore are used more frequently for long-term coaching to promote NIV tolerance throughout the early
NIV use. An oronasal mask enables delivery of higher stabilisation period.
ventilation pressures with less leak and greater comfort
111
for the patient. Other interfaces include full-face
111
masks that seal around the perimeter of the face and
cover the eyes as well as the nose and mouth, nasal Practice tip
pillows, mouthpieces that are placed between the patient’s
lips, and helmets that cover the whole head and consist NIV tolerance may be promoted with a simple explanation of
of a transparent plastic hood attached to a soft neck the therapy, reassurance and constant monitoring for your
collar. 112,113 These alternative interfaces may increase patient. During initiation, allow them to take short breaks
patient tolerance by reducing pressure ulceration, air from the mask if they are in discomfort or experiencing
leaks and patient discomfort. 114 claustrophobia.

INITIATION AND MONITORING PRIORITIES
Successful initiation of NIV is dependent on patient
acceptance and tolerance. Patient acceptance of NIV may POTENTIAL COMPLICATIONS
be aided by a brief explanation of the procedure and Masks need to be tight-fitting to reduce air leaks; however,
its benefits. Strategies to enhance patient tolerance this contributes to pressure ulceration on the bridge of
include: use of an interface that fits the patient’s facial the nose or above the ears (due to mask straps/headgear).

392 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E

Air leaks may cause conjunctival irritation and the high
flow of dry medical gas results in nasal congestion, TABLE 15.5 Set ventilator parameters
oral or nasal dryness and insufflation of air into the
stomach. Claustrophobia associated with the NIV inter- Parameter Description
face may also lead to agitation reducing the efficacy
of NIV treatment due to poor coordination of respira- Fraction of inspired The fraction of inspired oxygen
delivered on inspiration to the
oxygen (FiO 2 )
79
tory cycling between the patient and NIV unit. patient.
More serious, yet infrequent, complications include
aspiration pneumonia, haemodynamic compromise Tidal volume (V T ) Volume (mL) of each breath.
associated with increased intrathoracic pressures and Set breath rate (f) The clinician determined set rate of
pneumothorax. 80 breaths delivered by the ventilator
(bpm).
DETECTING NIV FAILURE Inspiratory trigger or Mechanism by which the ventilator
senses the patient’s inspiratory effort.
sensitivity
Failure to respond to NIV within 1–2 hours of com- May be measured in terms of a
mencement is demonstrated by unchanged or worsening change in pressure or flow.
gas exchange, as well as ongoing or new onset of rapid Inspiratory pressure Clinician determined pressure that is
shallow breathing and increased haemodynamic instabil- (P insp , P high ) targeted during inspiration.
111
ity. A decreased level of consciousness may be indicative Inspiratory time (T insp ) The duration of inspiration (sec).
of imminent respiratory arrest.
Inspiratory : expiratory The ratio of the inspiratory time to
ratio (I : E) expiratory time.
INVASIVE MECHANICAL Flow (V) The speed gas travels during inspiration.
VENTILATION (L/min).

Critically ill patients with persistent respiratory insuffi- Pressure support (PS) The flow of gas that augments a
ciency (hypoxaemia and/or hypercapnia), due to drugs, patient’s spontaneously initiated
disease or other conditions, may require intubation and breath to a clinician-determined
pressure (cmH 2 O).
mechanical ventilation to support oxygenation and ven-
tilatory demands. 115,116 Clinical criteria for intubation and Positive end- Application of airway pressure above
ventilation should be based on individual patient assess- expiratory pressure atmospheric pressure at the end of
expiration (cmH 2O).
(PEEP)
ment and patient response to measures aimed at revers-
ing hypoxaemia. Rise time Time to achieve maximal flow at the
onset of inspiration for pressure-
targeted breaths.
INDICATIONS Expiratory sensitivity During a spontaneous breath, the
Indications for intubation and mechanical ventilation ventilator cycles from inspiration to
include: expiration once flow has decelerated
to percentage of initial peak flow.
● apnoea Minute volume (VE) Generally not set directly but is
● inability to protect airway; e.g. loss of gag/cough reflex; determined by V T and f settings. Tidal
decreased Glasgow Coma Scale (GCS) score volume multiplied by the respiratory
● clinical signs indicating respiratory distress; e.g. rate over one minute (L/min).
117
tachypnoea, activation of accessory and expiratory Airway pressure (P aw ) The pressure measured in cmH 2 O by the
118
muscles, abnormal chest wall movements, tachycar- ventilator in the proximal airway.
dia and hypertension Plateau pressure (P plat ) The pressure, measured in cmH 2 O,
● inability to sustain adequate oxygenation for meta- applied to the small airways and
bolic demands; e.g. cyanosis, SpO 2 <88%, with sup- alveoli. P plat is not set but can be
plemental FiO 2 ≥0.5 measured by performing an
● respiratory acidosis (e.g. acute decrease in pH <7.25) inspiratory hold manoevre.
● postoperative respiratory failure
● shock.

The goals of mechanical ventilation are to achieve and
maintain adequate pulmonary gas exchange, minimise synchrony during both inspiratory and expiratory breath
the risk of lung injury, reduce patient work of breathing phases. Parameters commonly manipulated during
and optimise patient comfort. mechanical ventilation are detailed in Table 15.5. Para-
meters often observed and documented are discussed
MECHANICAL VENTILATORS below.
Contemporary ventilators use sophisticated microproces-
sor controls with sensitive detection, response and Fraction of Inspired Oxygen
control of pressure and gas flow characteristics. These The fraction of inspired oxygen (FiO 2 ) is expressed as a
mechanical ventilators are more sensitive to patient ven- decimal, between 0.21 and 1, when supplemental oxygen
tilatory demands, enabling improved patient–ventilator is applied. Room air has an oxygen content of 0.21 (21%).

Ventilation and Oxygenation Management 393

Ventilation is commonly commenced on a high FiO 2 ‘auto-triggering’ is triggering by the ventilator in the
setting, but as noted earlier, consideration is given to absence of spontaneous inspiratory effort.
the risks of oxygen toxicity which include disruption
to the alveolar-capillary membrane and fibrosis of the Inspiratory Time and Inspiratory :
alveolar wall. 119 Expiratory Ratio
The total time available for each mandatory breath is
Tidal Volume determined by the set frequency. The total breath time
Tidal volume (V T ) is the volume, measured in mL, of comprises the inspiratory and expiratory time which can
each breath. The V T is calculated using the patient’s be expressed as a ratio (I : E). In normal spontaneous
ideal body weight using height and gender-specific breathing, expiratory time is approximately twice as long
120
tables to achieve 6–8 mL/kg (see Table 15.6). Strong as the inspiratory time (1 : 2 ratio). Gas flow also influ-
evidence indicates a mortality benefit for using 6 mL/ ences inspiratory time, with higher gas flows resulting in
kg in patients with acute respiratory distress syndrome decreased time to achieve the target V T . The I : E ratio can
121
(ARDS). Some evidence also indicates 6 mL/kg as be manipulated to create an inverse relationship (1 : 1,
a target for patients without ARDS or acute lung injury 2 : 1, 4 : 1) with the goal of increased mean airway pres-
(ALI). 122,123 While further studies are required, clinicians sure resulting in alveolar recruitment and improved oxy-
should consider aiming for 6–8 mL/kg in all ventilated genation. Inverse ratios are more frequently applied with
patients. pressure control ventilation as application in volume
control can result in increased risk of barotrauma due to
Respiratory Rate peak and plateau airway pressure variation. 128
Mandatory frequency or respiratory rate (f, RR) is set with
consideration of the patient’s own respiratory effort, Inspiratory Flow and Flow Pattern
anticipated ventilatory requirements and the effect on the The flow rate refers to the speed of gas and is measured
I : E ratio. Use of high doses of sedation with or without in litres per minute (L/min). Generally, inspiratory flow
neuromuscular blockade requires setting a mandatory is delivered at speeds of 30–60 L/min. Higher flow rates
rate that facilitates adequate gas exchange and meets oxy- cause gas to become more turbulent and result in
genation requirements. A lower frequency can be set for increased peak airway pressures. Lower flow rates result
a patient able to breathe spontaneously in modes such as in laminar flow, an increased inspiratory time, improved
synchronised intermittent mandatory ventilation (SIMV) distribution of gas, and lower peak airway pressures. 129
and assist control (A/C) (see below) to enable spontane- The flow of inspiratory gas can be delivered in three
ous triggering. Physiologically normal respiratory rates styles: constant or square wave, decelerating ramp and
are 12–20 breaths per minute. Patients with hypoxaemic sinusoidal pattern (see Figure 15.4). In a constant flow
respiratory failure generally breathe 20–30 breaths per pattern, the peak flow is achieved at the beginning of
minute. 124 inspiration and is held constant throughout the inspira-
tory phase. This may result in higher peak airway pres-
Triggering of Inspiration sures. Using a decelerating ramp, the gas flow is highest
Depending on the mode of ventilation, breaths are trig- at the beginning of inspiration and tapers throughout the
gered by the ventilator or patient in various sequences. A inspiratory phase. Sinusoidal gas flow resembles sponta-
breath may be triggered by the ventilator in response to neous ventilation.
time in modes with clinician-determined set frequency Pressure Support
such as CMV, and in A/C and SIMV in the absence of
spontaneous effort. Patient triggering requires the ventila- When triggered by the patient, the ventilator delivers flow
tor to sense the patient’s inspiratory effort. Most modern to achieve the clinician-determined set pressure support.
generation ventilators now use flow triggering, as evi- The flow is variable, depending on the patient demand.
dence indicates that flow triggering may be more respon- The V T achieved with pressure support is dependent on
125
sive to patient effort than pressure triggering. Pressure chest and lung compliance as well as airway and ventila-
triggering requires the patient to create a negative pres- tor resistance. Pressure support is generally set at
sure within the ventilator circuit for long enough to 5–20 cmH 2 O. Increasing the level of pressure support
enable the ventilator to sense the effort and commence will result in increased V T , and improvements in gas
flow of gas. Flow triggering requires a predetermined flow exchange if compliance and resistance remain constant.
of gas, usually 5–10 L/min, referred to as the bias (or
base) flow, that travels continuously through the ventila- Positive End Expiratory Pressure
tor circuit. When the patient makes an inspiratory effort, Positive end expiratory pressure (PEEP) is the pressure
they divert flow that is sensed by the ventilator. If the flow applied at the end of the expiratory cycle to prevent alveo-
diversion reaches a clinician-determined set value, a lar collapse. PEEP increases residual lung volume thereby
breath is initiated. 126 The flow trigger is usually set at recruiting collapsed alveoli, improving V/Q match and
1–3 L/min (1 L/min represents less patient effort and enhancing movement of fluid out of the alveoli. 130,131
3 L/min represents greater patient effort). Despite PEEP was originally introduced by Ashbaugh and col-
advances in ventilator technology, various studies leagues 132 in the 1960s as a technique for treating refrac-
continue to identify missed patient triggers that contri- tory hypoxaemia in patients with ARDS. Animal studies
bute to patient–ventilator asynchrony. 127 Conversely, suggest ventilator-associated lung injury (VALI) may be

394 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E



TABLE 15.6 ARDSnet tables for predicted body weight for females and males

Height
PBW and Tidal Volume for Females PBW and Tidal Volume for Males
Centimetres
PBW 4 mL 5 mL 6 mL 7 mL 8 mL (inches) PBW 4 mL 5 mL 6 mL 7 mL 8 mL
31.7 127 159 190 222 254 137 (54) 36.2 145 181 217 253 290
34 136 170 204 238 272 140 (55) 38.5 154 193 231 270 308
36.3 145 182 218 254 290 142 (56) 40.8 163 204 245 286 326
38.6 154 193 232 270 309 145 (57) 43.1 172 216 259 302 345
40.9 164 205 245 286 327 147.5 (58) 45.4 182 227 272 318 363
43.2 173 216 259 302 346 150 (59) 47.7 191 239 286 334 382
45.5 182 228 273 319 364 152.5 (60) 50 200 250 300 350 400
47.8 191 239 287 335 382 155 (61) 52.3 209 262 314 366 418
50.1 200 251 301 351 401 157.5 (62) 54.6 218 273 328 382 437
52.4 210 262 314 367 419 160 (63) 56.9 228 285 341 398 455
54.7 219 274 328 383 438 162.5 (64) 59.2 237 296 355 414 474
57 228 285 342 399 456 165 (65) 61.5 246 308 369 431 492
59.3 237 297 356 415 474 167.5 (66) 63.8 255 319 383 447 510
61.6 246 308 370 431 493 170 (67) 66.1 264 331 397 463 529
63.9 256 320 383 447 511 172.5 (68) 68.4 274 342 410 479 547
66.2 265 331 397 463 530 175 (69) 70.7 283 354 424 495 566
68.5 274 343 411 480 548 178 (70) 73 292 365 438 511 584
70.8 283 354 425 496 566 180 (71) 75.3 301 377 452 527 602
73.1 292 366 439 512 585 183 (72) 77.6 310 388 466 543 621
75.4 302 377 452 528 603 185.5 (73) 79.9 320 400 479 559 639
77.7 311 389 466 544 622 188 (74) 82.2 329 411 493 575 658
80 320 400 480 560 640 190.5 (75) 84.5 338 423 507 592 676
82.3 329 412 494 576 658 193 (76) 86.8 347 434 521 608 694
84.6 338 423 508 592 677 195.5 (77) 89.1 356 446 535 624 713
86.9 348 435 521 608 695 198 (78) 91.4 366 457 548 640 731
PBW = predicted body weight
The formulae when using height in centimetres is, for Females = 45.5 + 0.91 × (height in cm − 152.4), for Males = 50 + 0.91 × (height in cm − 152.3)
Further information available at http://www.ardsnet.org/node/77460
Adapted from information courtesy of ARDSnet.






prevented using PEEP by recruiting atelectic alveoli and 40 sec), 141,142 did not demonstrate a difference in hospi-
bronchioles and preventing cyclic opening and closing tal or 28-day 142 mortality.
141
of alveoli. 133-136 PEEP may be beneficial, however, only if
the lung has sufficient potential for recruitment which
130
occurs in collapsed, as opposed to consolidated, lung. Rise Time
The setting of optimal PEEP remains controversial. The rise time controls how quickly the ventilator reaches
Low PEEP levels have been shown to be associated the clinician-determined inspiratory pressure (P insp
with higher mortality for ARDS patients in a number for mandatory breaths and pressure support for sponta-
of studies. 137-140 Two recently published randomised, neous breaths). Reducing the rise time results in a higher
controlled trials comparing low tidal volume ventilation peak flow as the ventilator aims to achieve the inspiratory
and conventional PEEP to low tidal volume pressure within a shortened time frame. Reduced
ventilation and high PEEP, with and without additional rise times may be desired in patients with airflow
recruitment man oeuvres (40 cmH 2 O applied for limitation.

Ventilation and Oxygenation Management 395


Unbel Flow Wave Pattern Description
(Rectangular, Peak flow rate is delivered immedately at the
square) onset of inspiration, maintained throughout
the inspiratory phase, and abruptly terminated
at the onset of expiration.
Common default pattern with volume-targeted
modes.

Sinusoidal Inspiratory flow rate gradually accelerates to
peak flow and then tapers off.
Believed to mimic spontaneous inspiratory
patterns.
May increase PIP (peak inspiratory pressure).
Accelerating Flow gradually accelerates in a linear fashion
(ascending to the set peak flow rate.
ramp)

Decelerating Flow is at peak at onset of inspiration and
(descending gradually decelerates throughout inspiratory
ramp) phase.

Flow ceases and ventilator cycles to expiratory
phase when flow decays to a percentage of
peak flow, usually 25% but varies by ventilator
model. Terminal flow criteria may be adjustable
in some newer ventilators.

Rapid intial flow raises mean airway pressure
and may assist in alveolar recruitment.
May improve the distribution of gases when
there is inhomogeneity of alveolar ventilation.
Decreases dead space, increases arterial
oxygen tension, and reduces PIP.

FIGURE 15.4 Standard mechanical ventilator flow-wave patterns.
129

Expiratory Sensitivity
Expiratory sensitivity describes the percentage of decay in Practice tip
peak flow reached during the inspiratory phase that
signals the ventilator to cycle to expiration for spontane- The P insp setting reflects a different value on different ventila-
ous breaths. In some ventilator models this is pre- tors. P insp equals total pressure including PEEP on some ventila-
determined at 25%, whilst other ventilator models tors and inspiratory pressure above PEEP on others. Use the
allow clinician selection. Premature termination of a pressure–time scalar to confirm.
breath will increase inspiratory muscle workload
whereas delayed breath termination increases expiratory
muscle load. 143
VENTILATOR MODES
Peak Airway Pressure The mode of ventilation describes inspiratory phase vari-
Airway pressures vary across the respiratory cycle, and are ables; how the ventilator controls pressure, volume, and
measured by the ventilator’s airway pressure gauge. A flow during a breath; as well as describing how breaths
number of pressures are identifiable (e.g. peak inspira- are sequenced. All breaths have trigger, limit and cycle
tory, end-expiratory). The airway pressure (P aw ) is an inspiratory phase variables. 144 Each breath is triggered
important parameter in assessing respiratory compliance (started) either by the patient or by the ventilator. During
and patient–ventilator synchrony, and will vary depend- inspiration, the breath is limited to a set target of pres-
ing on V T , RR, ventilator flow pattern, dynamic compli- sure, volume, or flow. This target cannot be exceeded
ance and airway resistance. In pressure-targeted modes during each breath. At the end of inspiration, the cycling
the peak inspiratory pressure is equivalent to the P insp . In variable determines the end of the inspiratory phase.
volume-targeted modes the peak inspiratory pressure is Again this variable may be pressure, flow, volume, or
determined by the set V T and patient compliance and time. Gas delivery during each breath is described by the
resistance. control variable. There are five control variables: pressure,

396 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E

68
volume, flow, time and dual control (such as used in the effort is not acknowledged by the ventilator. CMV may
mode pressure regulated volume control [PRVC]). Breath also be called volume-controlled ventilation (VCV) or
sequencing refers to the sequence of mandatory and pressure-controlled ventilation (PCV) depending on the
spontaneous breath. A spontaneous breath is one during target (volume or pressure) variable. VCV requires clini-
which inspiration is both started (triggered) and stopped cian selection of the frequency, PEEP, FiO 2 , tidal volume,
(cycled) by the patient. Spontaneous breaths may be flow waveform, peak inspiratory flow and either the
assisted, as with pressure support, or unassisted. Manda- inspiratory time or I : E ratio. PCV requires clinician selec-
tory breaths are either triggered or cycled by the ventila- tion of rate, PEEP, FiO 2 , inspiratory pressure, as opposed
tor. 145 A complete mode description should include: (1) to tidal volume, and inspiratory time or I : E ratio depend-
the control variable; (2) the breath sequence; and (3) the ing on the ventilator type. Peak inspiratory flow and the
targeting scheme (limit variable). flow waveform are manipulated by the ventilator, to
achieve the clinician-selected inspiratory pressure within
Pressure Control vs Volume Control the set inspiratory time. The inability to breathe sponta-
Traditionally, clinicians have favoured volume control neously during CMV contributes to diaphragm muscle
due to the ability to regulate minute ventilation (VE) dysfunction and atrophy which may result in difficulty
154
and carbon dioxide (CO 2 ) elimination with straight- weaning from the ventilator.
forward manipulation of ventilation. 146 Volume control
provides consistent tidal volume delivery, independent Synchronised Intermittent
of the patient’s lung mechanics. A disadvantage of Mandatory Ventilation
volume control, however, is the lack of control over peak Synchronised intermittent mandatory ventilation (SIMV)
airway pressure that changes in response to altered com- delivers breaths at a set frequency (rate), and can be either
pliance and resistance. Elevated peak airway pressures pressure- or volume-targeted. Setting of the ventilator is
may cause alveolar overdistension, barotrauma and similar to setting VCV or PCV. The availability of patient
haemodynamic effects such as reduced venous return, triggering with SIMV facilitates provision of gas flow in
cardiac output, hypotension and thus decreased organ recognition of a patient’s spontaneous effort. SIMV uses
perfusion. 147 Clinicians need to carefully monitor ventila- a timing window to deliver mandatory breaths in syn-
tion to avoid injurious pressures. In volume control the chrony with patient inspiratory effort. Additional spon-
116
peak airway pressure is achieved at the end of inspira- taneous breaths occurring outside of the timing window
tion, and only for a short duration, therefore distribution may be assisted with pressure support to augment the
of gas may not be optimised and shearing stress can patient’s spontaneous effort to a pre-set pressure level.
occur. 148
Pressure control allows ventilator control over the peak Assist Control
inspiratory pressure and inspiratory time. Clinicians are In assist control (A/C,) the patient can trigger the ventila-
required to monitor minute ventilation and gas exchange tor, however, unlike SIMV, every patient-initiated breath
due to the lack of a guaranteed tidal volume and pos- is assisted to the same clinician-determined tidal volume
sible changes in respiratory compliance and resistance. (A/C [VC]) or inspiratory pressure (A/C [PC]). All breaths
The variable and decelerating inspiratory gas flow pattern are cycled by the ventilator irrespective of being patient-
of pressure control enables rapid alveolar filling and or ventilator-triggered. In the absence of spontaneous
more even gas distribution compared to the constant breathing, A/C resembles CMV.
flow pattern that may be used with volume control.
This decelerating flow pattern results in improved Pressure Support Ventilation
gas exchange, decreased work of breathing and preven- Pressure support ventilation (PSV) is a spontaneous
tion of overdistension in healthy alveoli. 149-152 During mode of ventilation in which the patient initiates and
pressure control, the set inspiratory pressure is achieved cycles all breaths, with support of the patient’s inspiratory
at the beginning of the inspiratory cycle and maintained effort by the ventilator using rapid acceleration of flow to
for the set inspiratory time. This promotes recruitment achieve a preset level of inspiratory pressure. Unlike CMV,
of alveoli with high opening pressures and long SIMV or A/C, there is no setting of ventilator breaths in
time-constants.
this mode. PSV is usually employed with positive end
expiratory pressure (PEEP) which maintains partial infla-
COMMONLY EMPLOYED MODES tion of alveoli during the expiratory phase to promote
OF VENTILATORS alveolar recruitment and oxygenation.
Contemporary ventilators now provide a range of modes
to facilitate mechanical ventilation. Modes of mechanical Continuous Positive Airway Pressure
ventilation are described in Table 15.7. Continuous positive airway pressure (CPAP) is one set
baseline positive pressure applied throughout the inspira-
Controlled Mandatory Ventilation tory and expiratory phase. In this spontaneous breathing
Controlled mandatory ventilation (CMV) is a mandatory mode, unlike PSV, no additional positive pressure is pro-
mode, and is the original and most basic mode of ventila- vided to the patient during inspiration. Due to nomen-
tion. 153 CMV delivers all breaths at a clinician-determined clature used on some ventilator models, PSV is frequently
set frequency (rate) and the patient’s spontaneous misrepresented as CPAP.

Ventilation and Oxygenation Management 397



TABLE 15.7 Ventilator modes

Mode Descriptor Clinical implications
Controlled All breaths are mandatory, no patient triggering is enabled. Patients with respiratory effort require sedation and
mechanical Also called volume controlled ventilation (volume neuromuscular blockade.
ventilation targeted) (VCV) and pressure controlled ventilation Potential for respiratory muscle atrophy due to disuse.
(CMV) (pressure targeted) (PCV)
Assist-control (A/C) Breaths may be either machine or patient triggered but all Activation of the diaphragm with patient triggering.
are cycled by the ventilator. Assist control may be Potential for respiratory alkalosis If tachypnoea
delivered as volume (AC-VC) or pressure (AC-PC) targeted. develops.
Synchronised Mandatory breaths are delivered using a set rate and Reduced need for sedation.
intermittent volume (SIMV-VC) or pressure (SIMV-PC). Mandatory Activation of the diaphragm with patient triggering.
mandatory breaths are synchronised with patient triggers within a
ventilation (IMV) timing window. Between mandatory breaths the patient
can breathe spontaneously.
Pressure support All breaths are patient triggered and cycled. Pressure Reduced need for sedation.
ventilation (PSV) applied by the ventilator during inspiration (pressure Facilitates ventilator weaning.
support) augments patient effort. Level of PS can be adjusted to achieve desired V T .
Sustains respiratory muscle tone and decreases WOB.
Continuous All breaths are patient triggered and cycled. Positive Requires intact respiratory drive and patient ability to
positive airway pressure is applied throughout inspiratory and expiratory maintain adequate tidal volumes.
pressure (CPAP) phases of the respiratory cycle.
Volume support Spontaneous mode with clinician preset target tidal volume Requires intact respiratory drive
(VS) delivery achieved with the lowest inspiratory pressure.
Pressure-regulated Mandatory rate and target tidal volume are set, and the Dual control of volume and pressure enables guarantee
volume control ventilator then delivers the breaths using the lowest of volume and pressure
(PRVC) achievable pressure.
Airway pressure Ventilator cycles between 2 preset pressure levels for Reduced need for sedation.
release defined time periods. I : E ratio is inverse often with a Activation of the diaphragm with patient triggering.
ventilation prolonged Inspiratory time (4 sec) and shortened Promotes alveolar recruitment. Considered a rescue
(APRV) expiratory time (0.8 sec). Patient can breathe mode in ALI/ARDS when used with extreme inverse
spontaneously at both pressure levels ratio.
Biphasic positive As with APRV, the ventilator cycles between 2 preset Reduced need for sedation.
airway pressure pressure levels for defined time periods and the patient Activation of the diaphragm with patient triggering.
(BiPAP/ BILEVEL/ can breathe spontaneously at both pressure levels. The Promotes alveolar recruitment.
Bivent) inspiratory time is generally shorter than, or the same
length, as the expiratory time.
Mandatory minute The patient’s spontaneous minute ventilation is monitored Guarantees minute ventilation for patients with
ventilation by the ventilator. When the minute ventilation falls below fluctuating respiratory drive and muscle innervation
(MMV) the clinician determined target, the ventilator increases such as patients awakening from anaesthesia and
the mandatory rate or size of tidal volumes to regain the those with Guillain–Barré.
desired minute ventilation.
Proportional assist Delivers positive pressure throughout inspiration in Requires intact respiratory drive.
ventilation proportion to patient generated effort, and dependent on Patients with high respiratory drive as the ventilator
(PAV) 269 the set levels of flow assist (offsets resistance) and volume may overassist and continue to apply support when
assist (offsets elastance). 268 the patient has stopped inspiration. 269
Proportional assist Clinician only sets a percentage of work for the ventilator. Requires intact respiratory drive.
ventilation The ventilator assesses total work of breathing by Decreases work of breathing and improves patient
(PAV+™) randomly measuring compliance and resistance every ventilator synchrony.
4–10 breaths. Potential for use as a weaning mode.
Adaptive support Automatic adaptation of respiratory rate and pressure levels Automatically sets all ventilator settings except PEEP
ventilation (ASV) based on a clinician-set desired percentage of minute and FiO 2 .
ventilation. 270 Potential for use as a weaning mode.
Volume assured The ventilator switches from pressure control to volume Enables maintenance of a preset minimum V T and
pressure support control, or pressure support to volume control during reduces work of breathing.
(VAPS) inspiration.

398 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E

Pressure-regulated Volume Control Neurally-adjusted Ventilatory Assist
Pressure-regulated volume control, available on the Servo Neurally-adjusted ventilatory assist (NAVA) is available
300 and Servo I (Maquet, Solna, Sweden), uses a ‘learning on the Servo-I ventilator (Maquet, Solna, Sweden) and
period’ to establish a patient’s compliance that guides uses the electrical activity of the diaphragm to control
regulation of pressure/volume. During the learning patient–ventilator interaction. 163 Electrical activity of the
period, four test breaths of increasing pressure are deliv- diaphragm, measured using an oesophageal catheter,
ered. The ventilator regulates inspiratory pressure based should result in optimal patient–ventilator synchrony
on the pressure/volume calculation of the previous breath as it represents the endpoint of neural output from the
and the clinician-determined target tidal volume. To respiratory centres and thus is the earliest signal of
maintain the target tidal volume during ongoing ventila- patient inspiratory trigger and expiratory cycling. Pres-
tion, the ventilator continues to adapt the inspiratory sure delivered to the airways (P aw ) is proportional
pressure in response to changing compliance and to inspiratory diaphragmatic electrical activity using a
resistance. clinician determined proportionality factor set on
the ventilator. 164 NAVA provides breath-by-breath assist
Airway Pressure Release Ventilation and in synchrony with, and in proportion to, respiratory
165
Although clinical data on NAVA is currently
Biphasic Positive Airway Pressure demand. 164,166-168 this mode shows promise for improving
limited,
Airway pressure release ventilation (APRV) and biphasic patient–ventilator synchrony.
positive airway pressure (BiPAP) are ventilator modes
that allow unrestricted spontaneous breathing inde- VENTILATOR GRAPHICS
pendent of ventilator cycling, using an active expiratory
valve that allows patients to exhale even in the inspi- Analysis of ventilator graphics provide clinicians with the
ratory phase. 147,148,155,156 Both modes are pressure-limited ability to assess patient–ventilator interaction, appropri-
and time-cycled. In the absence of spontaneous breath- ateness of ventilator settings and lung function.
ing, these modes resemble conventional pressure limited,
time-cycled ventilation. 157 In North America the acronym Scalars: Pressure/time, Flow/time,
BiPAP® is registered to Respironics non-invasive Volume/time
ventilators (Murrayville, PA). Therefore ventilator com- Many mechanical ventilators now offer integrated graphic
panies have developed brand names such as BiLevel displays as waveforms that plot one of three parameters,
(Puritan Bennett, Pleasanton, CA, GE Healthcare, pressure, flow or volume, on the vertical (y) axis against
Madison, WI) Bivent (Maquet, Solna, Sweden), DuoPaP time, measured in seconds, on the horizontal (x) axis
(Hamilton Medical, Rhäzüns, Switzerland), PCV+ referred to as scalars. Examination of scalars can assist
(Dräger Medical, Lübeck, Germany) or BiPhasic (Viasys, with assessment of patient–ventilator synchrony, patient
Conshocken, PA) to describe essentially equivalent triggering, appropriateness of inspiratory/expiratory
modes. Ambiguity exists in the criteria that distinguish times, presence of gas trapping, appropriateness and ade-
APRV and BiPAP. When applied with the same I : E quacy of flow, lung compliance and airway resistance and
ratio, no difference exists between the two modes. circuit leaks. 169,170
APRV as opposed to BiPAP, however, is more frequently
described with an extreme inverse ratio and advocated Pressure vs time scalar
as a method to improve oxygenation in refractory
hypoxemia. 158 The morphology of this waveform depends on the
breath target (volume or pressure) and the breath type
(mandatory or spontaneous). Pressure–time waveforms
171
Automatic Tube Compensation reflect airway pressure (P aw ) during inspiration and expira-
Automatic tube compensation (ATC) is active during tion and can be used to evaluate peak, plateau and end
spontaneous breaths and compensates for the work of inspiratory pressures as well as inspiratory and expiratory
breathing associated with artificial airway tube resistance times and appropriateness of flow (see Figure 15.5).
via closed-loop control of continuously calculated tra- Pressure–time scalars vary in appearance depending on
cheal pressure. 159,160 During spontaneous inspiration, a the control variable (volume vs pressure). In volume-
pressure gradient exists between the proximal and distal control breaths, the inspiratory waveform continues to
ends of the artificial airway due to resistance created by rise until peak airway pressure is achieved at the end of
the tube. A reduced pressure at the proximal end of the inspiration. In pressure control breaths, the inspiratory
tube means a patient needs to produce a greater inspira- waveform reaches its peak at the beginning of inspiration
tory force (greater negative pressure) to generate an ade- and remains at this elevation until cycling to expiration.
161
quate tidal volume. Higher flow rates generate larger Spontaneous triggering of ventilation can be identified by
pressure gradients and greater resistance. ATC requires examination of the pressure–time scalar at the beginning
the airway type and size to be entered into the of inspiration. A small negative deflection indicates
ventilator program as well as the percentage of automatic patient effort. When pressure-triggering is used, a breath
tube compensation (ATC) to be applied. It appears to is triggered when the pressure drops below baseline.
have most use in reducing the work of breathing for The depth of the deflection is proportional to patient
patients with high respiratory drive who require high effort required to trigger inspiration. A flow-
inspiratory flow. 162 triggered breath occurs when the flow rises above baseline,

Ventilation and Oxygenation Management 399

Pressure
(kPa)
C Peak pressure

.
.
‘Resistance pressure’ (R V)
D
E Plateau pressure
B
Gradient
.
Resistance V/C ‘Compliance pressure’ (V /C)
T
Pressure
.
.
(R V) A Flow- Pause F
phase phase
‘PEEP’
Time (s)
Inspiration time Expiration time
(V insp = const.)
FIGURE 15.5 Airway pressure vs time. (Courtesy Drägerwerk AG & Co., KGaA.)



although this is frequently accompanied by a small nega- of the expiratory flow waveform also enables evaluation
tive deflection in the pressure-time scalar. Patient inspira- of the effects of bronchodilator therapy as, if efficacious,
tory attempts that fail to trigger the ventilator can also be improvements should be seen in the return to baseline
identified as negative deflections in the pressure waveform of the expiratory flow waveform (see Figure 15.7). 173,175
without corresponding responses from the ventilator. 172 Patient–ventilator asynchrony can be detected in the flow
Appropriateness of flow can be detected from the waveform as abrupt decreases in expiratory flow in the
pressure–time scalar. If the flow is set too high or the rise expiratory limb and abrupt increases in flow in the inspi-
time too short this can be seen as a sharp peak in the ratory limb of the flow waveform. 172
waveform. Conversely if flow is inadequate or the rise
time too long, the incline of the inspiratory portion Volume vs time scalar
of the pressure waveform may be dampened. 169
The volume waveform originates from the functional
residual capacity (baseline), rises as inspiratory flow is
Flow vs time scalar delivered to reach the maximum inspiratory tidal volume,
The flow–time scalar presents the inspiratory phase above then returns to baseline during expiration. The volume
the horizontal axis and the expiratory phase below (see waveform is useful in troubleshooting circuit leaks (see
Figure 15.6). The shape of the inspiratory flow waveform Figure 15.8) as it will fail to return to baseline if a leak
is influenced by the selection of flow pattern (constant, in the circuit–patient interface is present.
decelerating, sinusoidal) in volume-control breaths or
the variable and decelerating flow waveform associated Loops: Pressure/volume, Flow/volume
with pressure-control breaths. The inspiratory flow wave- Most contemporary critical care ventilators allow for
form of spontaneous breaths, those triggered and cycled monitoring of pressure, flow and volume parameters
by the patient, is influenced by the presence or absence integrated into graphic loops enabling measurement
of pressure support and the expiratory sensitivity. 169 of airway resistance, chest wall and lung compliance.
Evaluation of the expiratory limb of the flow-time scalar
assists with detection of gas trapping as well as the Pressure–volume loops
patient’s response to bronchodilators. In the absence of The two parameters, P aw and V T are plotted against each
gas trapping, the expiratory limb drops sharply below other, with P aw on the x axis. For mandatory breaths, the
baseline then gradually returns to zero before the next loop is drawn counter clockwise (see Figure 15.9). Spon-
breath. Failure to return to baseline indicates gas trapping taneous (triggered and cycled) breaths are drawn in a
whereby the gas inspired is not totally expired. Gas trap- clockwise fashion. At the beginning of inspiration, the P aw
ping results in development of intrinsic or ‘auto-PEEP’. starts to rise with little change in V T . As P aw continues to
This can adversely affect a patient’s haemodynamic status rise, the V T increases exponentially as alveoli are recruited,
and cause patient–ventilator asynchrony. 173 Gas trapping resulting in a marked increase in the slope of the inspira-
may occur in patients with airflow limitation such as tory limb. This point represents alveolar recruitment and
those with COPD and asthma. Consequences of gas trap- is referred to as the lower inflection point, and may be
ping include dynamic hyperinflation, reduced respiratory used to guide PEEP selection. 176,177 The inspiratory limb
compliance and respiratory muscle fatigue. 174 Evaluation continues until peak inspiratory pressure and maximal V T

400 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E

Volume Volume-oriented Air Trapping



Inspiration Normal
patient
Time
Flow (L/min) }
Flow Time (sec)

Air Trapping
Auto-PEEP
Expiration
Time
FIGURE 15.7 Gas trapping.
271
Pressure
Tidal volume m/sec Inspiratory Expiratory Tidal volume m/sec




Time Leak


0 Time 0 volume
Time
Volume Pressure-oriented (sec) (sec)
FIGURE 15.8 Tidal volume vs time, with and without leak.



Volume
Time Expiration B

Flow






Time
Inspiration
A Pressure

Pressure FIGURE 15.9 Pressure-volume loop. (Courtesy Drägerwerk AG & Co.,
KGaA.)

are achieved. The bend in the inspiratory limb towards
the end of inspiration is referred to as the upper inflection
point, and denotes the point at which small volume
Time increases produce large pressure increases indicating
lung overdistension. 176 The expiratory limb represents
lung derecruitment and is also useful in guiding PEEP
Flow Pause Flow Pause selection. 178,179
phase phase phase phase
For patient-triggered mandatory breaths, the initial part
Inspiration Expiration of the loop occurs to the left of the y axis and flows in a
clockwise fashion, reflecting patient effort. The loop then
FIGURE 15.6 Pressure, flow, volume vs time. (Courtesy Drägerwerk AG & shifts to the right of the y axis and moves in a counter-
Co., KGaA.) clockwise fashion as the ventilator assumes the work
68
of breathing. P–V loops reflect dynamic compliance

Ventilation and Oxygenation Management 401

alveoli or failure to recruit. 140 Once the recruitment
800 manoeuvre is terminated, derecruitment may occur
rapidly. Serious adverse effects have been noted during
Volume (mL) 600 High Raw pulmonary pressures resulting in reductions in venous
the use of RMs due to increased intrathoracic and intra-
return and cardiac output, and cardiac arrest and increased
400
(Solid line)
184,188
risk of barotrauma.
200 High Frequency Oscillatory Ventilation
High frequency oscillatory ventilation (HFOV) requires a
specialised ventilator and manipulation of four variables:
10 20 30 40 50 mean airway pressure (cmH 2 O), frequency (Hz), inspira-
Pressure (cm H 2 O) tory time, and amplitude (or power [ΔP]). 189 Alveolar
overdistension is limited through the use of sub-deadspace
*Dashed line depicts normal Raw tidal volumes whereas cyclic collapse of alveoli is pre-
129
FIGURE 15.10 Pressure–volume loop representing resistance changes. vented by maintenance of high end-expiratory lung
pressures. 190,191 High frequency (between 3 and 15 Hz)
oscillations at extremely fast rates (300–420 breaths/
min) create pressure waves enabling CO 2 elimina-
tion. 133,192 Oxygenation is facilitated through application
between the lungs and the ventilator circuit. Decreased of a constant mean airway pressure via the bias flow (rate
compliance requires greater pressure to achieve V T and is of fresh gas). 192,193 In adults, recommendations for the
reflected in a flattened P–V loop. 180 The area between the initiation of HFOV state mean airway pressure should be
loops represents the resistance to inspiration and expira- set 5 cmH 2 O above the peak airway pressure achieved
tion, known as hysteresis. As resistance increases, less V T with conventional ventilation. 194 The recommended fre-
is delivered resulting in a shorter and wider loop; con- quency range is 3–10 Hz with 5 Hz conventionally used
versely, as resistance decreases, a longer, wider loop is to initiate HFOV. Inspiratory time is set at 33% and the
generated (see Figure 15.10). 181 amplitude setting is determined by adequate CO 2 elimi-
nation. 133 Increased CO 2 elimination is achieved by low-
Flow–volume loops ering the frequency and increasing the amplitude.
Flow–volume loops recorded during positive pressure Until recently, HFOV was considered a rescue mode for
ventilation depict inspiration above the baseline and adult patients with acute respiratory distress syndrome
expiration below it. These loops are useful in determining (ARDS) experiencing refractory hypoxaemia and failing
response to bronchodilators and examining changes in conventional ventilation. 195,196 HFOV has been evaluated
airway resistance. in patients in early-onset ARDS and has been found to
improve oxygenation and to be well tolerated. 197 While
MANAGEMENT OF REFRACTORY HYPOXAEMIA further studies are required, these data suggest HFOV can
Refractory hypoxaemia may require strategies in addition be implemented in early ARDS.
121
to conventional lung-protective mechanical ventilation.
These include recruitment manoeuvres, high frequency Extracorporeal Membrane Oxygenation
oscillatory ventilation, extracorporeal membrane oxygen- Extracorporeal membrane oxygenation (ECMO) improves
ation and nitric oxide. total body oxygenation using an external (extracorporeal)
oxygenator, while allowing intrinsic recovery of lung
Recruitment Manoeuvres pathophysiology. Indications for ECMO include acute
Recruitment manoeuvres (RMs) refer to brief application severe cardiac or respiratory failure such as severe ARDS
198
of high levels of PEEP to raise the transpulmonary pres- and refractory shock. Bleeding as a complication of
sure to levels higher than achieved during tidal ventila- anticoagulation is a major risk of ECMO, with cerebral
199
tion with the goals of opening collapsed alveoli, recruiting bleeds being the most catastrophic. Another serious
slow opening alveoli, preventing alveolar derecruitment, complication is limb ischaemia when the femoral artery
and reducing shearing stress. 182-184 The most common is used.
RM is elevation of PEEP to achieve a peak pressure of ECMO consists of three key components:
40 cmH 2 O for a sustained period of 40 sec, although
studies report peak pressure elevations ranging from 25– 1. a blood pump (either a simple roller or centrifugal
50 cmH 2 O for durations ranging from 20–40 sec. 185 The force pump)
best method in terms of pressure, duration and frequency 2. a membrane oxygenator (bubble, membrane or
have yet to be determined. 186 Recruitment manoeuvres in hollow fibre)
humans have not produced consistent results in clinical 3. a countercurrent heat exchanger, where the blood
studies, 184,187 with a recent systematic review demonstrat- is exposed to warmed water circulating within
ing no mortality benefit despite transient increases in metal tubes.
oxygenation. 185 Effective recruitment may be difficult to In addition, essential safety features include bubble detec-
assess with the potential for either overdistension of tors that detect gas in the arterial line and shut the pump

402 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E

off; arterial line filters between the heat exchanger and ● unstable pelvic fractures
arterial cannula, to trap air thrombi and emboli; pressure ● prone positioning
monitors placed before and after the oxygenator, that ● haemodynamic support devices (IABP, LVAD, ECMO)
measure the pressure within the circuit and detect rising ● femoral catheterisation for continuous renal replace-
circuit pressures commonly caused by thrombus or circuit ment therapy
or cannulae occlusion; and continuous venous oxygen ● large abdominal wounds
saturation and temperature monitoring. On commence- ● following femoral sheath removal.
ment of ECMO the circuit is primed with fresh blood. The As some degree of semirecumbent position is preferable
acid–base balance and blood gas of the primer is adjusted to supine positioning, patients with suspected or existing
to ensure that the pH is within the normal range (7.35– spinal injury, pelvic fractures or being managed
7.45) and PaO 2 is adequate. ECMO can be delivered via with prone positioning can have the head elevated by
veno-arterial access which requires cannulation of an tilting the whole bed. Patients with femoral cannulation
artery. This method bypasses the pulmonary circulation and large abdominal wounds can usually achieve
while providing cardiac support to the systemic circula- 25–30 degree positioning.
tion and achieves a higher PaO 2 with lower perfusion
rates. The alternative is veno-venous access, used for Clinical practice audits conducted internationally and in
patients in respiratory failure with adequate cardiac func- Australia and New Zealand indicate that compliance with
tion as there is no support of systemic circulation. Perfu- a 45 degree semirecumbent position rarely occurs, even
sion rates are higher, the mixed venous PO 2 is elevated when taking into consideration contraindications. 208-212
and the PaO 2 is lower. 199 Similarly, interventions to improve compliance failed to
demonstrate adherence to the 45 degree backrest position
Nitric Oxide that can be sustained by the patient over time. 213,214
Nitric oxide (NO) is an endothelial smooth muscle relax- Due to uncertainty over compliance with 45 degree
semirecumbency in the original trial conducted by
ant. Inhaled NO is effective in the dilation of pulmonary Drakulovic, and the lack of difference in VAP rates
204
arteries resulting in reduced pulmonary shunting and despite difficulty achieving compliance with semirecum-
reduced right ventricular afterload due to reduced pulmo- bency in the van Niewenhoven study, new studies are
207
nary artery tone. Pulmonary shunting refers to failure of required to confirm the equivalence or lack of inferiority
uptake of alveolar gas by the pulmonary vascular bed due of lower degrees of backrest elevation to the strict
to vascular constriction or interstitial oedema. Inhaled 45 degree semirecumbent position.
NO has a role in the management of pulmonary hyper-
tension and was previously thought to have a role in
management of refractory hypoxaemia for patients with
ARDS. However, the most recent systematic review and Practice tip
meta-analysis of NO in ARDS comprising 14 RCTs and
1303 participants reported no effect on overall mortality Backrest elevation is difficult to estimate accurately. Use an
despite a statistically significant improvement in oxygen- objective measurement device such as an inclinometer or
ation in the first 24 hours, and some risk of renal impair- protractor.
ment among adults. 200

POSITIONING
Regular repositioning of critically ill patients is essential Lateral Positioning
for lung recruitment, prevention of atelectasis and main- Patients with unilateral lung disease experience a mis-
tenance of skin integrity (see Chapter 6). match of ventilation to perfusion if the consolidated
(pneumonic) or atelectic lung is placed in the dependent
215
Head of Bed Elevation position. Continuous lateral rotational therapy is a
positioning therapy advocated for the prevention and
Supine positioning has been associated with aspiration
of abnormally-colonised oropharyngeal and gastric management of respiratory complications associated
216
contents 201-203 and increased incidence of VAP compared with immobility. The most recently reported multicen-
to a semirecumbent position, defined as backrest eleva- tre randomised controlled trial found a significant reduc-
204
tion at 45 degrees. Guidelines and care bundles for the tion in VAP and shorter durations of ventilation and ICU
217
prevention of VAP recommend semirecumbent position- stay. Continuous lateral rotation therapy requires a
ing for all mechanically-ventilated patients. 71,205,206 A special bed system enabling rotation of the upper part of
more recent trial has however questioned the feasibility the body to a maximum angle of 90 degrees.
of 45 degree semirecumbent positioning as this backrest
elevation was only achieved for 15% of study observa- Prone Positioning
207
tions. There was also no differences in VAP incidence Prone positioning has been shown to improve oxygen-
between the supine and semirecumbent group. Contra- ation and intrapulmonary shunt fraction when compared
indications to backrest elevation include:
218
with rotational turning during the first 72 hours of ALI
219
● suspected or existing spinal injury and in patients with multiorgan failure. Prone posi-
● intracranial hypertension (for 45 degree elevation) tioning may also decrease the risk of VAP due to

Ventilation and Oxygenation Management 403

improved bronchial secretion drainage, limitation of Current Recommendations
colonisation of distal lung, decreased atelectasis and No ventilation strategy is more lung-protective than the
increased alveolar recruitment but may increase spread timely and appropriate discontinuation of mechanical
of pathogens in the lung and may increase the risk of ventilation. Weaning refers to the transition from ventila-
aspiration. 220-223 229
tory support to spontaneous breathing. Evidence based
116
Prone positioning results in changes to the distribution consensus guidelines published for weaning in 2001
230
of ventilation and pulmonary blood flow. Pleural pres- and 2007 emphasise the importance of preventing
sures are lower in non-dependent regions and higher in unnecessary delays in the weaning process, early recogni-
dependent regions due to gravitational forces, the weight tion of a patient’s ability for spontaneous breathing and
of the overlying lung and mismatch between the local the use of a systematic method to identify the potential
physical structures of the lung and chest wall. 224 The for extubation.
weight of the overlying lung increases in ARDS due to
parenchymal oedema and fluid within the alveoli. 225 This Weaning Predictors
gradient in pleural pressures means transpulmonary pres- Clinician judgement regarding prediction of weaning
sure is higher in non-dependent lung regions, compared readiness is known to be imperfect, with unnecessary
to dependent regions. 225 Perfusion also increases from prolongation of ventilation or high rates of reintuba-
231
previously nondependent to dependent lung regions tion as resultant consequences, both of which are associ-
resulting in optimal matching of ventilation and perfu- ated with adverse outcomes. 232,233 An evidence based
sion to promote gas exchange. review evaluating over 50 objective physiological mea-
Pleural pressure in the dependent dorsal regions in the surements for determining readiness for weaning and
supine position can result in airway closure, atelectasis extubation found most had only a modest relationship
and hypoxaemia. 224 The difference in pleural pressures with weaning outcome; no single factor or combination
234
from non-dependent and dependent lung regions is of factors demonstrating superior accuracy. Of all pre-
greater in the supine compared to the prone position. In dictors studied, the respiratory frequency to tidal volume
235
the supine position, the heart and abdominal contents ratio (f/V T ) appears to be most accurate. However inclu-
also compress lung bases and decrease FRC, whereas in sion of the f/V T as part of a weaning protocol was found
prone positioning, the weight of these structures are lifted in one randomised study to increase, as opposed to
236
from the lung. decrease, the duration of weaning. At present, consen-
sus guidelines do not recommend routine inclusion of
230
The benefits of prone positioning continue to be debated. weaning predictors.
Although oxygenation improves in 70–80% of patients
turned from supine to prone, 226 a mortality benefit Weaning Methods
has not been shown in all trials. The most recent sys-
tematic review and meta-analysis 227 confirms a reduction Various studies have attempted to identify the best
in mortality in patients with severe baseline hypox- weaning method. Two of the most frequently-cited studies
aemia (PaO 2 /FiO 2 ratio <100 mmHg), but reported this have produced conflicting results. Brochard and col-
237
benefit was not present in patients with less-severe leagues compared PSV, T piece trial and SIMV, and
hypoxaemia. Other benefits of prone positioning dem- concluded that PSV reduced the duration of mechanical
onstrated were improved oxygenation and decreased ventilation compared with the other methods. Esteban
238
rates of VAP. Adverse events related to prone position- and colleagues compared PSV, T piece trials, CPAP and
ing were increased risk of decubitus ulcer formation, progressive reduction of SIMV support, and found a once-
endotracheal obstruction and accidental line or tube daily T piece trial led to extubation three times more
dislodgement. quickly than SIMV and nearly twice as quickly as PSV.
Failure to produce consistent results favouring a single
Implementing prone positioning requires forward plan- weaning style suggests it is not the mode that is important
ning to ensure eye care and protection, mouth care, but rather the application of a systematic process. 239
wound dressings, and tracheal suction are attended to
before positioning the patient prone. Intravenous lines, Spontaneous breathing trials
electrocardiogram leads, urinary catheter drainage, chest Spontaneous breathing trials (SBTs) incorporate a focused
drains and ostomy bags need to be secured and reposi- assessment of a patient’s capacity to breathe prior to extu-
tioned appropriately once the patient is positioned. 228 bation 240 and are recommended as the major diagnostic
Prone positioning can be achieved by manual handling test to determine extubation readiness. SBTs can be
230
of the patient, requiring up to five staff, although conducted using either a T piece or low levels of pressure
commercial devices are available that facilitate the turning support and should need to last only 30 minutes. 242
241
and positioning of the patient. 228
This method of weaning is uncommon in the ANZ setting,
in contrast to international findings. 65,66
WEANING FROM THE VENTILATOR
Weaning traditionally occurs via clinician-directed adjust- Protocols
ments to the level of support provided by the ventilator, Implementation of various organisational strategies
culminating in a spontaneous breathing trial comprising such as weaning teams and non-physician-led weaning
either low level pressure support or a T piece trial. protocols may assist in the timely recognition of weaning

404 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E

and extubation readiness. 243-247 Recently, coupling of a difficulty. 260 These patients are most likely to benefit from
sedation and weaning protocol was found to result an individualised and structured approach to weaning
in a three-day reduction in the duration of ventilation using progressive lengthening of tracheostomy trials with
compared to standard care in four North American supportive ventilation in between in combination with
hospitals. 248 A recent systematic review and meta-analysis early physical therapy.
of 11 weaning protocol trials including 1971 patients
demonstrated a reduction in the duration of mechani-
cal ventilation. 249 However, the authors cautioned that
the effect of weaning protocols may vary according Practice tip
to the ICU organisational characteristics such as
an intensivist-led ICU model, high levels of physician Tachypnoea and decreased tidal volumes during weaning are
staffing, structured ward rounds, collaborative discus- clear indicators that a patient is not ready for extubation.
sion and more frequent medical review; all character-
istics reported for ICUs in Australia and New
Zealand. 250,251 Complications of Mechanical Ventilation
Physiological complications associated with mechanical
Automated weaning ventilation include ventilator-associated lung injury
Automated computerised systems potentially enable (VALI) and nosocomial infection (VAP). 116,122 VALI occurs
more efficient weaning by providing improved adapta- through alveolar over-distension and cyclic opening
tion of ventilatory support through continuous monitor- and closing of alveoli resulting in diffuse alveolar
ing and real-time intervention. 252 One such system, damage, increased permeability, pulmonary oedema,
SmartCare™/PS, monitors three respiratory parameters, cell contraction and cytokine production. 122,130,136,261-263
frequency, V T and end-tidal carbon dioxide (ETCO 2 ) con- VAP substantially increases the duration of ICU stay
centration, every two or five minutes and periodically and is associated with an attributable mortality of
adapts pressure support (PS). 252,253 SmartCare/PS estab- 5.8–8.5%. 264-266 Additional complications associated
lishes a respiratory status diagnosis, based on evaluation with mechanical ventilation are listed in Table 15.8.
of the three parameters, and may either decrease or Complications can occur due to inappropriate applica-
increase PS, or leave it unchanged to maintain the patient tion of mechanical ventilation. This may result in extra-
in a defined ‘respiratory zone of comfort’. 254,255 Once alveolar gas causing pneumothoraces or subcutaneous
SmartCare/PS has successfully minimised the level of PS, emphysema due to high peak inspiratory pressures, and
a one-hour observation period occurs. For patients who alveolar stretch and oedema formation as the result of
remain within the respiratory zone of comfort through- large tidal volumes. 68
out the observation period, SmartCare/PS recommends
to ‘consider separation’, indicating the patient’s respira- SUMMARY
tory status now suggests the patient will tolerate
extubation. Support of oxygenation and ventilation during critical
illness are key activities for nurses in ICU. Oxygen therapy
SmartCare/PS substantially reduced the duration of ven- promotes aerobic metabolism but has adverse effects that
tilation and ICU length of stay when compared to need to be considered. Various oxygen delivery devices
physician-controlled weaning using local guidelines in provide low or variable flows of oxygen.
five European ICUs. 256 These effects were not confirmed
when the SmartCare/PS system was compared to weaning Strong evidence supports the use of NIV for COPD and
managed by experienced critical care nurses in a single CHF, but caution is required when used for other
Australian setting. 257 diagnoses such as pneumonia. NIV success is dependent
on patient tolerance, with common complications
including pressure ulcers, conjunctival irritations, nasal
The difficult-to-wean patient congestion, insufflation of air into the stomach and
International reports indicate patients that require claustrophobia.
mechanical ventilation for ≥21 days account for less than
10% of all mechanically-ventilated patients, but occupy Airway support can be provided with oro- or nasopharyn-
40% of ICU bed days and accrue 50% of ICU costs. 258,259 geal airways, laryngeal mask airways and endotracheal
A recommendation from the National Association for intubation; oral intubation is the preferred method. For
Medical Direction of Respiratory Care (NAMDRC) states a patient with an ETT, the key points for practice are:
that prolonged mechanical ventilation should be defined ● ETT placement should be confirmed with end-tidal
as ‘≥21 consecutive days of ventilation required for ≥6 CO 2 monitoring
230
hours per day’. Prolonged weaning has been defined as ● the aim of endotracheal cuff management is to prevent
greater than 7 days of weaning after the first SBT or more airway contamination and enable positive pressure
230
than three SBTs. Little evidence defines the optimal ventilation
method for managing the difficult-to-wean patient. One ● closed suctioning reduces alveolar derecruitment
trial found no difference in weaning duration or success compared to opening suctioning
when comparing tracheostomy trials to low-level pressure ● instillation of normal saline is not recommended
support in patients with COPD experiencing weaning during routine tracheal suctioning.

Ventilation and Oxygenation Management 405



TABLE 15.8 Complications of mechanical ventilation

Item Complication
Barotrauma ● pneumothorax
● pneumomediastinum
● pneumopericardium
● pulmonary interstitial emphysema
● subcutaneous emphysema
Volutrauma Shearing stress, endothelial and epithelial cell injury, fluid retention and pulmonary oedema, perivascular and
alveolar haemorrhage, alveolar rupture
Biotrauma Activation of systemic and local inflammatory mechanisms
Ventilation/perfusion Alveolar distension causes compression of the adjacent pulmonary capillaries resulting in dead space ventilation
mismatch
↓ cardiac ouput Resulting in hypotension, ↓ cerebral perfusion pressure (CPP), ↓ renal and hepatic blood flow
↑ right ventricular afterload Due to ↑ intrathoracic pressure
May result in ↓ left ventricular compliance and preload
↓ urine output Due to ↓ glomerular filtration rate, ↑ sodium reabsorption and activation of the renin-angiotensin-aldosterone
system
Fluid retention Due to above renal factors as well as ↑ antidiuretic hormone and ↓ atrial natriuretic peptide
Impaired hepatic function Due to ↑ pressure in the portal vein, ↓ portal venous blood flow, ↓ hepatic vein blood flow
↑ intracranial pressure Due to ↓ cerebral venous outflow
Oxygen toxicity Alterations to lung parenchyma similar to those found in ARDS
Pulmonary emboli and Due to immobility
deep vein thrombosis
Ileus, diarrhoea Due to alterations in gastric motility
Gastrointestinal Gastritis and ulceration may occur due to stress, anxiety and critical illness
haemorrhage
ICU-acquired weakness Neuropathies and myopathies develop in association with critical illness, corticosteroids and neuromuscular
blockade
Psychological issues Delirium, anxiety, depression, agitation and post-traumatic stress disorder may be experienced by critically ill
ventilated patients in the acute and recovery phases




The optimal timing of tracheostomy remains uncertain, ● contemporary ventilators now provide a range of
however, tracheostomy should be considered for patients modes to facilitate mechanical ventilation
experiencing weaning difficulty. ● analysis of ventilator graphics provides clinicians with
The goals of mechanical ventilation are to promote gas the ability to assess patient–ventilator interaction,
exchange, minimise lung injury, reduce work of breathing appropriateness of ventilator settings and lung
and promote patient comfort: function
● semirecumbent positioning at 45 degree elevation
● despite its life-saving potential, mechanical ventila- has been shown to reduce VAP but compliance is
tion carries the risk of serious physical and psychologi- poor
cal complications ● recruitment manoeuvres, HFOV, ECMO and prone
● humidification of dry medical gas is required during positioning are strategies that may facilitate manage-
mechanical ventilation to prevent drying of secretions, ment of refractory hypoxaemia
mucous plugging and airway occlusion ● timely recognition of a patients readiness for weaning
● the pressure required to deliver a volume of gas and extubation is imperative. Strategies such as
into the lungs is determined by elastic and resistive weaning protocols, teams and automatic weaning are
forces all aimed at optimising this process.

406 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E



Case study
Mr Smith was a 51-year-old man admitted to ICU with septic shock decreased over the next two days, enabling weaning of the FiO 2 to
due to gangrene in his groin. His comorbidities included insulin- 0.35 whilst PEEP remained at 15 cmH 2 O. PEEP was then decreased
dependent diabetes, hypertension and obesity; his admission by 2.5 cmH 2 O twice a day during which time his PaO 2 and SpO 2
weight was 140 kg. Prior to ICU admission, he received 8 L of fluid remained stable.
resuscitation, but remained oliguric and required 25 mcg/min nor- On day 6, his PEEP was down to 7.5 cmH 2 O and CXR was much
adrenaline to maintain a MAP ≥65 mmHg.
improved. Sedation was halved during the morning multidisci-
On admission to ICU, his arterial blood gas was: pH 7.24, PaCO 2 plinary round however he continued to require high dose opiates
−
37 mmHg, PaO 2 79 mmHg, SpO 2 95%, HCO 3 15.6 mmol/L. He was for his wound pain. During the next few hours, his spontaneous
ventilated with SIMV-VC, FiO 2 0.7, PEEP 5 cmH 2O, f 14, V T 600 mL, rate increased and the mandatory breath rate was decreased to 8.
with PIP of 38 cmH 2 O, a spontaneous rate of 8 and V T of 300 mL. At 1700h he became agitated and intolerant of mandatory ventila-
His supine CXR showed small lung fields and diffuse bilateral infil- tor breaths. Rather than increase the sedation, the ventilator mode
trates suggestive of fluid overload. He required large doses of was changed to PSV (PS 15 cmH 2 O/PEEP 7.5 cmH 2 O) which was
sedation to tolerate SIMV and frequently reached the set peak well tolerated. His gas exchange remained stable overnight, and
inspiratory pressure limit. Mr Smith’s head-of-bed was raised as far the following morning sedation was turned off and analgesia
as his groin wound would allow (about 20 degrees) and the whole decreased.
bed tilted to further raise his head. Subsequently, PEEP was
increased to 10 cmH 2 O; and FiO 2 decreased to 0.5 and he was Over the next few days his limb and cough strength gradually
switched to PSV (PS 14, PEEP 10 cmH 2 O). This was well tolerated improved. His mobility was limited due to the groin wound and
and sedation was decreased. RRT, so he was changed to intermittent RRT to facilitate periods of
mobilisation. On day 10 Mr Smith’s ventilator settings were FiO 2
On day 2, during hyperbaric oxygen therapy and despite heavy 0.35, PS 12, PEEP 7.5 cmH 2 O, his spontaneous rate was 18 and V T
sedation, Mr Smith developed agitation, ventilator dyssynchrony 600. His CXR was much improved, gas exchange was good and he
and desaturation (PaO 2 60 mmHg, SpO 2 86% on FiO 2 1). Tracheal could cough spontaneously with minimal sputum. He remained on
suction yielded thin white sputum, but no improvement to oxy- intermittent RRT, but had a normal pH. He was cooperative and had
genation. PEEP was increased to 15 cmH 2O and muscle relaxants reasonable limb strength. He was extubated during the morning
administered. The ventilator mode was changed from SIMV-VC to multidisciplinary round. His gas exchange was good whilst awake,
SIMV-PC resulting in reduced mean airway pressures and improved but he ‘snored’ and had transient drops in SpO 2/PaO 2 and elevated
oxygenation. PaCO 2 when asleep and therefore required NIV overnight.
Mr Smith’s metabolic acidosis continued with deteriorating On day 13 Mr Smith was discharged to the respiratory ward where
renal function and worsening CXR. Renal replacement therapy he could have nocturnal CPAP, and was subsequently diagnosed as
(RRT) was commenced on day 3. His cumulative fluid balance having sleep apnoea.








Research vignette

Blackwood B, Alderdice F, Burns K, Cardwell C, Lavery G, O’Halloran Review methods
P. Use of weaning protocols for reducing duration of mechanical We included randomised and quasi-randomised controlled trials of
ventilation in critically ill adult patients: Cochrane systematic weaning from mechanical ventilation with and without protocols
review and meta-analysis. British Medical Journal 2011; 342: c7237. in critically ill adults.
Abstract Data selection
Objective Three authors independently assessed trial quality and extracted
To investigate the effects of weaning protocols on the total dura- data. A priori subgroup and sensitivity analyses were performed.
tion of mechanical ventilation, mortality, adverse events, quality of We contacted study authors for additional information.
life, weaning duration, and length of stay in the intensive care unit
and hospital. Results
Eleven trials that included 1971 patients met the inclusion criteria.
Design Compared with usual care, the geometric mean duration of
Systematic review.
mechanical ventilation in the weaning protocol group was reduced
Data sources by 25% (95% confidence interval 9% to 39%, P = 0.006; 10 trials);
Cochrane Central Register of Controlled Trials, Medline, Embase, the duration of weaning was reduced by 78% (31% to 93%,
CINAHL, LILACS, ISI Web of Science, ISI Conference Proceedings, P = 0.009; six trials); and stay in the intensive care unit length
Cambridge Scientific Abstracts, and reference lists of articles. We by 10% (2% to 19%, P = 0.02; eight trials). There was significant
did not apply language restrictions. heterogeneity among studies for total duration of mechanical

Ventilation and Oxygenation Management 407



Research vignette, Continued
ventilation I = 76%, P < 0.01) and duration of weaning I = 97%, delays in the recognition of weaning/extubation readiness and
2
2
P < 0.01), which could not be explained by subgroup analyses variation in practice thereby improving weaning outcomes.
based on type of unit or type of approach.
This well-conducted systematic review demonstrated discordant
Conclusion results in 11 trials of protocolised weaning (that included auto-
There is evidence of a reduction in the duration of mechanical mated weaning) when compared to usual care despite an overall
ventilation, weaning, and stay in the intensive care unit when stan- benefit of weaning protocols. The authors postulate this may be
dardised weaning protocols are used, but there is significant het- due to variability in organisational environments in the usual care
erogeneity among studies and an insufficient number of studies arm of trials such as the type of ICU [open vs closed], levels of
to investigate the source of this heterogeneity. Some studies physician and nurse staffing, frequency and structure of ward
suggest that organisational context could influence outcomes, but rounds, patient case-mix, and extent of collaborative interdisciplin-
this could not be evaluated as it was outside the scope of this ary discussion. Unfortunately these contextual elements are fre-
review. quently not sufficiently measured or defined in descriptions of
usual care. Critical care clinicians and administrators need to be
Critique aware of these contextual differences when considering the intro-
Weaning protocols generally include two components: (1) a daily duction of behavioural interventions such as weaning and seda-
assessment of weaning readiness using a list of objective criteria; tion protocols. This is of particular importance in Australia and New
and (2) a spontaneous breathing trial during which the patient is Zealand, as the majority of weaning protocol studies that demon-
evaluated for extubation readiness, and/or an algorithm detailing strate statistically and clinically significant reductions in the dura-
stepwise reductions in ventilatory support prior to extubation tion of mechanical ventilation have been conducted in North
assessment. The aim of this standardised approach is to reduce American ICUs where a very different organisational model exists.






Learning activities
1. What is the rationale for using oxygen therapy in patients with 8. Identify the clinical applications of pressure-volume and flow-
COPD and low SpO 2 ? volume loops.
2. Why is it important to consider the patient’s respiratory rate 9. What are the potential risks of mechanical ventilation as well
and tidal volume when using a low flow (variable flow) oxygen as those related to premature discontinuation of ventilation?
delivery device? Activities 10–15 relate to the case study:
3. How should ETT placement be confirmed? 10. What were the rationales for switching from SIMV-VC to
4. Describe assessment priorities and interventions before and SIMV-PC for Mr Smith on day 2?
after extubation. 11. What is the current research evidence on the benefits and dis-
5. What are the indications and relative and absolute contraindi- advantages of volume versus pressure ventilation?
cations for NIV? 12. Why was semirecumbent positioning a priority for Mr Smith?
6. Familiarise yourself with the ventilators in your unit. Confirm 13. Why do you think FiO 2 was weaned before PEEP?
you have a thorough understanding of the function and 14. What is the current research evidence for the use, benefits and
purpose of all ventilator settings. disadvantages of muscle relaxants in the critically ill?
7. Ensure you have a clear understanding of ventilator mode 15. Why was NIV beneficial for Mr Smith?
terminology.




ONLINE RESOURCES NHS Institute for Innovation and Improvement, http://www.institute.nhs.uk/
safer_care/general/human_factors.html
American Association for Respiratory Care, http://www.aarc.org/resources/ Thoracic Society of Australia and New Zealand, http://www.thoracic.org.au/
Anaesthesia UK, http://www.frca.co.uk/default.aspx Vent World, http://www.ventworld.com/
Australian and New Zealand Intensive Care Society, www.anzics.com.au/
safety-quality?start=2
ARDS network, http://www.ardsnet.org/ FURTHER READING
Canadian Society of Respiratory Therapists, Respiratory Resource, http://www.
respiratoryresource.ca/ Canadian Critical Care Trials Group/Canadian Critical Care Society Noninvasive
College of Intensive Care Medicine of Australia and New Zealand, www.cicm.org.au/ Ventilation Guidelines Group. Clinical practice guidelines for the use of non-
policydocs.php invasive positive-pressure ventilation and noninvasive continuous positive
Covidien education resources, http://www.nellcor.com/educ/OnlineEd.aspx airway pressure in the acute care setting. CMAJ 2011; 183(3): E195–214.
Critical Care Medicine Tutorials, http://www.ccmtutorials.com/ Esan A, Hess DR, Raoof S, George L, Sessler CN. Severe hypoxemic respiratory
Fisher and Paykel Resource Centre, http://www.fphcare.com/respiratory-acute- failure. Part 1: ventilatory strategies. Chest 2010: 137(6): 1203–16.
care/resource-library.html Lacherade JC, De Jonghe B, Guezennec P, Debbat K, Hayon J et al. Intermittent
Intensive Care Coordination and Monitoring Unit, http://intensivecare.hsnet. subglottic secretion drainage and ventilator-associated pneumonia: a multi-
nsw.gov.au/ center trial. Am J Respir Crit Care Med 2010; 182(7): 910–17.

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Neurological Assessment


16 and Monitoring





Di Chamberlain
Leila Kuzmiuk





INTRODUCTION
Learning objectives
The nervous system is the major controlling, regulatory
and communicating system in the body. It accounts for a
After reading this chapter, you should be able to:
● describe the anatomy and physiology of the nervous mere 3% of the total body weight, yet it is the most
system complex organ system. It is the centre of all mental activ-
● differentiate between the central and peripheral nervous ity, including thought, learning and memory. Together
with the endocrine and immune systems, the nervous
systems system is responsible for regulating and maintaining
● describe the techniques used for neurological assessment homeostasis. Through its receptors, the nervous system
● identify the distinction between normal and abnormal keeps in touch with the environment, both external and
findings internal. Diseases of the nervous system are common in
● state the determinants of intracranial pressure and describe the critical care unit, both as primary processes and as
compensatory mechanisms used to prevent large changes complications of multiple organ failure in the critically
in intracranial pressure when there are changes in brain, ill patient. An understanding of basic neurophysiology is
blood and cerebrospinal fluid volumes important if these disorders are to be recognised and
● explain the importance and process of continuous treated. This chapter provides an overview of the anatomy
neurological assessment in the brain-injured patient and physiology, describes common pathophysiological
● relate the procedures of selected neurodiagnostic tests to processes, and details the management of alterations in
nursing implications for patient care the nervous system.

NEUROLOGICAL ANATOMY
AND PHYSIOLOGY

COMPONENTS OF THE NERVOUS SYSTEM
The central nervous system (CNS) consists of the spinal
cord and the brain and is responsible for integrating, pro-
cessing and coordinating sensory data and motor com-
Key words mands (see Figure 16.1). The CNS is linked to all parts of
1
the body by the PNS which transmits signals to and from
central nervous system the CNS. The human PNS is composed of 43 pairs of spinal
peripheral nervous system nerves that issue in orderly sequence from the spinal cord,
intracranial pressure and 12 pairs of cranial nerves that emerge from the base
efferent neuron of the brain. All branch and diversify prolifically as they
afferent neuron distribute to the tissues and organs of the body. The periph-
autonomic nervous system eral nerves carry input to the CNS via their sensory afferent
sympathetic nervous system fibres and deliver output from the CNS via the efferent
fibres. Specific physiology of the CNS and PNS is discussed
parasympathetic nervous system in detail later in the chapter. First, however, neuron cell
Glasgow Coma Scale anatomy and physiology is examined.
neurological assessment
post traumatic amnesia Neurons
decorticate (flexor) Neurons are specialised cells in the nervous system; each
decerebrate (extensor) is comprised of a dendrite, cell body (soma) and axon.
2
414 Each neuron is a cell that uses biochemical reactions to

Neurological Assessment and Monitoring 415

Brain
CENTRAL Higher-order functions
NERVOUS such as memory, learning
and intelligence
Cranial nerves SYSTEM
Information
Spinal cord processing
Spinal nerves Sensory Motor
information commands
with with
afferent efferent
division division
includes
PERIPHERAL
NERVOUS
SYSTEM
Somatic Autonomic
nervous nervous system
system

Parasympathetic Sympathetic
division division

Special sensory Somatic sensory
receptors receptors monitor
provide sensations skeletal muscles, Smooth
of smell, taste joints, skin surface; Skeletal muscle
vision, balance and provide position sense muscle
hearing and touch, pressure,
pain and temperature Cardiac
sensations muscle
Glands
Visceral sensory receptors monitor
internal organs, including those of
cardiovascular, respiratory, digestive,
urinary and reproductive systems
RECEPTORS EFFECTORS
FIGURE 16.1 The functional divisions of the nervous system. 1


receive, process and transmit information. Most synaptic neurotransmitter synthesised in the cell body, along with
contacts between neurons are either axodendritic (excit- enzymes and lysosomes. The movement of materials
atory) or axosomatic (inhibitory). A neuron’s dendritic between the cell body and synaptic knobs is called axo-
tree is connected to many neighbouring neurons and plasmic transport. Some materials travel slowly, at rates
receives positive or negative charges from other neurons. of a few millimetres per day. This transport mechanism
The input is then passed to the soma (cell body). The is known as the ‘slow stream.’ Vesicles containing neu-
primary role of the soma and the enclosed nucleus is to rotransmitter move much more rapidly, travelling in the
perform the continuous maintenance required to keep ‘fast stream’ at 5–10 mm per hour which increases syn-
the neuron functional. Most neurons lack centrioles, aptic activity. Axoplasmic transport occurs in both direc-
important organelles involved in the organisation of the tions. The flow of materials from the cell body to the
cytoskeleton and the movement of chromosomes during synaptic knob is anterograde flow. At the same time,
mitosis. As a result, typical CNS neurons cannot divide other substances are being transported towards the cell
and cannot be replaced if lost to injury or disease. The body in retrograde flow (’retro’ meaning backward). If
fuel source for the neuron is glucose; insulin is not debris or unusual chemicals appear in the synaptic knob,
required for cellular uptake in the CNS. retrograde flow soon delivers them to the cell body. The
arriving materials may then alter the activity of the cell
A myelin sheath, consisting of a lipid-protein casing,
covers the neuron and provides protection to the axon by turning appropriate genes on or off. Retrograde flow
and speeds the transmission of impulses along nerve cells is the means of transport for viruses, pathogenic bacteria,
from node to node. (see Figure 16.2b). Myelin is not a heavy metals and toxins to the CNS, with resulting
3
continuous layer but has gaps called nodes of Ranvier disease such as tetanus, viral encephalitis and lead intoxi-
(see Figure 16.2a). cation. Defective anterograde transport seems to be
involved in certain neuropathies, including critical illness
Each synaptic knob contains mitochondria, portions of neuropathies. 4
the endoplasmic reticulum, and thousands of vesicles
filled with neurotransmitter molecules. Breakdown Synapses
products of neurotransmitter released at the synapse are The human brain contains at least 100 billion neurons,
reabsorbed and reassembled at the synaptic knob. The each with the ability to influence many other cells.
synaptic knob also receives a continuous supply of Although there are many kinds of synapses within the

416 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E

Dendrite

Nucleolus




Axon
hillock Nucleus


Initial segment Nissl bodies
Free nerve
endings in skin Oligodendroglial
Schwann cell cell myelin Axon
myelin CNS Myelin
sheath
Node of Ranvier PNS

Afferent cell body Nucleus of
in dorsal root ganglion Schwann
cell
Nucleolus
Nucleus Schwann cell myelin

Nissl
bodies PNS
CNS
Oligodendroglial
cell myelin




Synaptic Neuromuscular
A terminals B Muscle fibre junction
FIGURE 16.2 (A) Afferent and (B) efferent neurons, showing the soma or cell body, dendrites and axon. Arrows indicate the direction for conduction of
action potentials. 3



brain, they can be divided into two general classes: elec- Neurotransmitters
trical synapses and chemical synapses. Electrical synapses A neurotransmitter is a chemical messenger used by
permit direct, passive flow of electrical current from one neurons to communicate in one direction with other
neuron to another in the form of an action potential; they neurons. Unidirectional transmission is required for mul-
are described in Table 16.1. The current flows through gap tineuronal pathways, for example to and from the brain.
junctions, which are specialised membrane channels that Neurons communicate with each other by recognising
connect the two cells. Chemical synapses, in contrast, specific neuroreceptors.
enable cell-to-cell communication via the secretion of
neurotransmitters; the chemical agents released by the Chemically, there are four classes of neurotransmitters:
presynaptic neurons produce secondary current flow in 1. acetylcholine (ACh): the dominant neurotransmit-
postsynaptic neurons by activating specific receptor ter in the peripheral nervous system, released at
molecules (see Figure 16.3). neuromuscular junctions and synapses of the para-
5
Myelin increases conduction velocity. Demyelination of sympathetic division
peripheral nerves, as occurs in the Guillain–Barré syn- 2. biogenic amines: serotonin, histamine, and the
drome, slows conduction and may result in conduction catecholamines dopamine and noradrenaline
block, which manifests clinically as weakness. Con- 3. excitatory amino acids: glutamate and aspartate,
sequently, chronically demyelinated axons become and the inhibitory amino acids gamma-
vulnerable, with axon loss being a major cause of dis- aminobutyric acid (GABA), glycine and taurine
ability. In time, remyelination may occur, requiring the 4. neuropeptides: over 50 of which are known, amino
generation of myelin-competent oligodendrocytes but acid neurotransmitters being the most numerous.
most often does not fully recapitulate developmental In 2009, it was discovered that there is also more than
myelination. one neurotransmitter per synapse; these are called

Neurological Assessment and Monitoring 417



TABLE 16.1 Generation of action potentials (nervous tissue)

STEP 1: Depolarisation
● A graded depolarisation brings an area of excitable membrane to
threshold (−60 mV). +30 DEPOLARISATION 3 REPOLARISATION
STEP 2: Activation of sodium channels and rapid depolarisation
● The voltage-regulated sodium channels open (sodium channel
activation).
● Sodium ions, driven by electrical attraction and the chemical gradient, 0
flood into the cell.
● The transmembrane potential goes from −60 mV, the threshold level,
towards +30 mV. 2
STEP 3: Repolarisation: Inactivation of sodium channels and activation of
potassium channels −40
● The voltage-regulated sodium channels close (sodium channel Threshold
inactivation occurs) at +30 mV. Transmembrane potential (mV) −60
● The voltage-regulated potassium channels are now open, and
potassium ions diffuse out of the cell. −70 1
● Repolarisation begins. 4
STEP 4: Return to normal permeability Resting
● The voltage-regulated sodium channels regain their normal properties potential
in 0.4–1.0 msec. The membrane is now capable of generating another
action potential if a larger than normal stimulus is provided. ABSOLUTE RELATIVE
● The voltage-regulated potassium channels begin closing at −70 mV. REFRACTORY REFRACTORY
Because they do not all close at the same time, potassium loss PERIOD PERIOD
continues, and a temporary hyperpolarisation to approximately
−90 mV occurs. Time (msec)
● At the end of the relative refractory period, all voltage-regulated
channels have closed, and the membrane is back to its resting state.




co-transmitters. For example, neuropeptide Y (NPY) and CENTRAL NERVOUS SYSTEM
adenosine triphosphate (ATP) are co-transmitters of The CNS is composed of the brain and spinal cord (see
noradrenaline, which are released together and mediate Figure 16.4). The primary purpose is to acquire, coordi-
5
their function by activation of α- and β-adrenoceptors, nate and disseminate information about the body and its
and regulate renovascular resistance. Similarly, recep- environment. This section describes the anatomy and
6
tors are an important control point for the effectiveness physiology of the brain and spinal cord.
of synapses. Neurotransmitters are the common deno-
minator between the nervous, endocrine and immune
systems. Many neurotransmitters are endocrine ana- Brain
logues and acetylcholine, the main parasympathetic The brain is divided into three regions: forebrain, mid-
neurotransmitter, interacts with immune cells such as brain and hindbrain, as described in Table 16.3. The
macrophages through the anti-inflammatory cholinergic forebrain, which consists of two hemispheres and is
pathway. 7 covered by the cerebral cortex, contains central masses of
grey matter, the basal ganglia, the neural tube and the
Neuroglia diencephalon with its adult derivatives: the thalamus and
1
Neuroglia are the non-neuronal cells of the nervous hypothalamus. Midbrain structures include two pairs of
system and are 10–50 times more prevalent than the dorsal enlargements, the superior and inferior colliculi.
number of neurons. They are divided into macroglia The medulla, pons and midbrain compose the brain-
1
1
(astrocytes, oligodendroglia and Schwann cells) and stem. The hindbrain includes the medulla oblongata, the
microglia, and are described in Table 16.2. They not only pons and its dorsal outgrowth, the cerebellum.
provide physical support but also respond to injury, regu- Nervous tissue has a high rate of metabolism. Although
late the ionic and chemical composition of the extra- the brain constitutes only 3% of the body’s weight, it
cellular milieu, participate in the blood–brain and receives approximately 15% of the resting cardiac output
1
blood–retina barriers, form the myelin insulation of and consumes 20% of its oxygen. Despite its substantial
nervous pathways, guide neuronal migration during energy requirements, the brain can neither store oxygen
8
development, and exchange metabolites with neurons. nor effectively engage in anaerobic metabolism. An inter-
The CNS has a greater variety of neuroglia. Unlike ruption in the blood or oxygen supply to the brain rapidly
neurons, neuroglia continue to multiply throughout life. leads to clinically observable signs and symptoms. Without
Because of their capacity to reproduce, most tumours of oxygen, brain cells continue to function for approximately
the nervous system are tumours of neuroglial tissue and 10 seconds. Glucose is virtually the sole energy substrate
10
not of nervous tissue itself. 9 for the brain, and it is entirely oxidised. The brain can

418 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E





Myelin 2



An action potential invades
the presynaptic terminal



1 Transmitter is synthesised 3 Depolarisation of presynaptic
and then stored in vesicles terminal causes opening of
2+
voltage-gated Ca channels





4 Influx of Ca 2+
through channels




Synaptic
vesicle
2+
5 Ca causes vesicles to fuse
with presynaptic membrane
Transmitter
molecules
10 Retrieval of vesicular Ca 2+
membrane from plasma
membrane 6 Transmitter is released
into synaptic cleft via
exocytosis
Across
dendrite


Transmitter
molecules




Transmitter Postsynaptic
Ions receptor current flow
7 Transmitter binds tp
9 Postsynaptic current causes 8 Opening or closing of receptor molecules in
excitatory or inhibitory postsynaptic channels postsynaptic membrane
postsynaptic potential that
changes the excitability of
the postsynaptic cell

FIGURE 16.3 Sequence of events involved in transmission at a typical chemical synapse.
82
be seen as an almost exclusive glucose-processing machine, makes up about 80% of the human brain. The cerebral
producing water (H 2 O) and carbon dioxide (CO 2 ). cortex varies in thickness from 2 mm to 4 mm, being
Glucose also provides the carbon backbone for regenera- thinnest in the primary sensory areas and thickest in the
tion of the neuronal pool of glutamate. This process results motor and association areas. It contains the cell bodies
from close astrocyte–neuron cooperation. 11 and dendrites of neurons or grey matter which receive,
integrate, store and transmit information. Conscious
Cerebral cortex deliberation and voluntary actions also arise from the
The forebrain contains the cerebral cortex and the sub- cerebral cortex. White matter lies beneath the cerebral
cortical structures rostral (sideways) to the diencepha- cortex and is composed of myelinated nerve fibres. The
lon. The cortex, or outermost surface of the cerebrum, cortex is involved in the processing of both sensory

Neurological Assessment and Monitoring 419



TABLE 16.2 Neuroglia, their location and role as supporting nervous tissue

Type Location Main Function
Astrocytes CNS: The largest and most numerous ● Astrocytes are considered as important as
neuroglial cells in the brain and spinal the neuron in communication and brain
cord. regulation.
● They regulate communication, extracellular
ionic and chemical environments between
neurons.
● They respond to injury and have an
important role in cerebral oedema.





Ependymal cells CNS: Line the ventricular system of the ● Transport of CSF and brain homeostasis.
brain and central cord of the spinal ● Phagocytotic defence against pathogens.
canal. ● Store glycogen for brain tissue.











Microglia CNS: Located within the brain ● Wander between the peripheral immune
parenchyma behind the blood–brain system and the CNS as a defence to
barrier. infection.
● Displace synaptic input in injured neurons.









Oligodendrocytes CNS: Spiral around an axon to form a ● Responsible for the formation of myelin
multilayered lipoprotein coat in both sheaths surrounding axons.
the white and grey matter in the brain ● Oligodendrocytes wrap themselves around
and spinal cord. numerous axons at once.
PNS: Schwann cells are the supporting ● Schwann cells wrap themselves around
cells of the PNS. peripheral nerve axon.
● Unlike oligodendrocytes, a single Schwann
cell makes up a single segment of an axon’s
myelin sheath.





CSF = cerebral spinal fluid; CNS = central nervous system; PNS = peripheral nervous system.


information from the body and the delivery of motor The majority of the remaining cortical area is known as
commands. These occur in specific areas of the brain and the association cortex, where the processing of extensive
12
can be mapped. Topographically, the cerebral cortex is and sophisticated neural information is performed. The
divided into areas of specialised functions, including the association areas are also sites of long-term memory, and
primary sensory areas for vision (occipital cortex), they control human functions such as language acqui-
hearing (temporal cortex), somatic sensation (postcen- sition, speech, musical ability, mathematical ability,
tral gyrus), and primary motor area (precentral gyrus). complex motor skills, abstract thought, symbolic thought,
1
As shown in Figure 16.5, these well-defined areas com- and other cognitive functions. Association areas intercon-
prise only a small fraction of the surface of the cerebral nect and integrate information from the primary sensory
cortex. and motor areas via intra-hemispheric connections. The

420 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E

White
Cerebrum Grey matter
matter
Diencephalon Sympathetic chain
Ventral
root Sympathetic
Midbrain
chain ganglion
Pons
Dorsal root
Cerebellum ganglion
C1 Dorsal
2 Medulla root
3 Layers of
Cervical 4 dura mater
nerves 5 Spinal cord
6
7
8 Cervical
T1 enlargement
2
3 Vertebra
4
5 Spinal
nerve
6
Thoracic 7
nerves
8
9
10

11
Lumbar
12 enlargement

L1
Cauda
Lumbar 2 equina
nerves
3
4
5
S1
Sacral 2
nerves 3
4
5
Coccygeal Coc 1
nerves
82
FIGURE 16.4 The subdivisions and components of the central nervous system.


parietal–temporal–occipital association cortex integrates these functions may be lateralised to one side of the
neural information contributed by visual, auditory, and brain.
somatic sensory experiences. The prefrontal association
cortex is extremely important as the coordinator of The cerebral cortex receives sensory information from
emotionally motivated behaviours, by virtue of its con- many different sensory organs and processes the informa-
nections with the limbic system. In addition, the prefron- tion. The two hemispheres receive the information from
tal cortex receives neural input from the other association the opposite sides of the body. Sensory information is
areas and regulates motivated behaviours by direct input relayed to the cortex by the thalamus. Parts of the cortex
to the premotor area, which serves as the association area that receive this information are called primary sensory
of the motor cortex. Sensory and motor functions are areas and cross at various points in the sensory pathway,
controlled by cortical structures in the contralateral hemi- because the cerebral cortex operates on a contralateral
13
sphere. Particular cognitive functions or components of basis. The discriminative touch system crosses high, in

Neurological Assessment and Monitoring 421



TABLE 16.3 Organisation of the brain

Division Description Functions
Forebrain
Cerebrum Largest and uppermost portion of Cortex (outer layer) is the site of conscious thought, memory,
the brain. Divided into two reasoning and abstract mental functions, all localised within
hemispheres, each subdivided specific lobes.
into the frontal, parietal, temporal
and occipital lobes.



Diencephalon Between the cerebrum and the Thalamus sorts and redirects sensory input; hypothalamus
brainstem. Contains the thalamus controls visceral, autonomic, endocrine and emotional
and hypothalamus. function, and the pituitary gland. Contains some of the centres
for coordinated parasympathetic and sympathetic stimulation,
temperature regulation, appetite regulation, regulation of
water balance by antidiuretic hormone (ADH), and regulation
of certain rhythmic psychobiological activities (e.g. sleep).
Brain stem Anterior region below the Connects cerebrum and diencephalon with spinal cord.
cerebrum: the medulla, pons, and
midbrain compose the brainstem.
Midbrain
Midbrain Below the centre of the cerebrum. Has reflex centres concerned with vision and hearing; connects
cerebrum with lower portions of the brain. It contains sensory
and motor pathways and serves as the centre for auditory and
visual reflexes.




Basal ganglia or corpus striatum The mass of grey matter in the An important role in planning and coordinating motor
midbrain beneath the cerebral movements and posture. Complex neural connections link the
hemispheres. Borders the lateral basal ganglia to the cerebral cortex. The major effect of these
ventricles and lies in proximity to structures is to inhibit unwanted muscular activity; disorders
the internal capsule. of the basal ganglia result in exaggerated, uncontrolled
movements.


Pons Anterior to the cerebellum. Connects cerebellum with other portions of the brain; contains
motor and sensory pathways; helps to regulate respiration;
axons from the cerebellum, basal ganglia, thalamus and
hypothalamus; portions of the pons also control the heart,
respiration and blood pressure. Cranial nerves V–VIII connect
the brain in the pons.

Hindbrain Contains a portion of the pons,
the medulla oblongata and the
cerebellum.
Reticular activation system (RAS) The reticular formation networks Activity of the cerebral cortex is dependent on both specific
run through the brainstem core, sensory input and non-specific activating impulses from the
known as the tegmentum. RAS, and is critical to the existence of the conscious state,
states of alertness and arousal.

422 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E



TABLE 16.3, Continued

Division Description Functions
Medulla oblongata Between the pons and the spinal The medulla oblongata contains motor fibres from the brain to
cord. the spinal cord and sensory fibres from the spinal cord to the
brain. Most of these fibres cross at this level. Cranial nerves
IX–XII connect to the brain in the medulla, which has centres
for control of vital functions, such as respiration and the heart
rate.


Cerebellum Below the posterior portion of the Coordinates voluntary muscles; maintains balance and muscle
cerebellum. Divided into two tone; has both excitatory and inhibitory actions. It also
hemispheres. controls fine movement, balance, position sense and
integration of sensory input.










Central Primary sensory
Primary motor cortex sulcus cortex
(precentral gyrus) (postcentral gyrus)

Somatic motor association
area (premotor cortex) PARIETAL LOBE


Parieto-occipital sulcus

FRONTAL LOBE Somatic sensory
association area

Prefrontal cortex Visual association area
OCCIPITAL LOBE
Gustatory cortex
Visual cortex

Insula Auditory association area
Lateral sulcus
Auditory cortex
Olfactory cortex
TEMPORAL LOBE
Frontal eye field
Speech centre A
4
6
1
General interpretive
area 40 39
44 41 42

16
17

Prefrontal
cortex B C
FIGURE 16.5 (A) Major anatomical landmarks on the surface of the left cerebral hemisphere. The lateral sulcus has been pulled apart to expose the insula.
(B) The left hemisphere generally contains the general interpretive area and the speech centre. The prefrontal cortex of each hemisphere is involved with
conscious intellectual functions. (C) Regions of the cerebral cortex as determined by histological analysis. Several of the 47 regions described by Brodmann
are shown for comparison with the results of functional mapping. 1

Neurological Assessment and Monitoring 423

18
the medulla. The pain system crosses low, in the spinal nicotinic acetylcholine receptors). White matter at the
cord. The proprioceptive sensory system that guards anterior of the midbrain conducts impulses between the
balance and position goes to the cerebellum, which works higher centres of the cerebrum and the lower centres of
ipsilaterally and therefore doesn’t cross. Almost every the pons, medulla, cerebellum and spinal cord. The mid-
region of the body is represented by a corresponding brain contains the autonomic reflex centres for pupillary
region in both the primary motor cortex and the somatic accommodations to light, which constrict the pupil and
sensory cortex. 14 accommodate the lens. The fibres travel in cranial nerve
The homunculus (see Figure 16.6) visualises the connec- III, so damage to that nerve will also produce a dilated
tion between different areas of the body and areas in pupil. It also contains the ventral tegmental area, packed
15
brain hemispheres. The body on the right side is the with dopamine-releasing neurons that synapse deep
motor homunculus and on the left the sensory homun- within the forebrain and seem to be involved in pleasure:
culus. Representations of parts of the body that exhibit amphetamines and cocaine bind to the same receptors
fine motor control and sensory capabilities occupy a that it activates, and this may account at least in part for
greater amount of space than those that exhibit less their addictive qualities.
precise motor or sensory functions. The medulla oblongata lies between the pons and the
spinal cord and looks like a swollen tip to the spinal cord.
Basal ganglia and cerebellum Running down the ventral aspect of the medulla are the
The basal ganglia, consisting of the caudate, putamen, pyramids, which contain corticospinal fibres. The func-
globus pallidus, substantia nigra, subthalamic nucleus, tion of the medulla oblongata is to control automatic
and related nuclei in the brainstem, play an important functions (e.g. breathing and heart rate) and to relay
role in movement, as evidenced by the hypokinetic/rigid nerve messages from the brain to the spinal cord. Process-
and hyperkinetic disorders seen with lesions of various ing of interaural time differences for sound localisation
components. However, their role in the initiation and occurs in the olivary nuclei. The neurons controlling
control of movement cannot be isolated from the motor breathing have mu (µ) receptors, the receptors to which
activities of the cortex and brainstem centres discussed opiates bind. This accounts for the suppressive effect of
previously. Procedural memories for motor and other opiates on breathing. Impairment of any of the vital func-
unconscious skills depend on the integrity of the premo- tions or reflexes involving these cranial nerves suggests
16
tor cortex, basal ganglia and cerebellum. The cerebel- medullary damage. 19
lum plays a more obvious role in coordinating movements
by giving feedback to the motor cortex, as well as by The pons varolii is the part of the brainstem that lies
providing important influences on eye movements between the medulla oblongata and the mesencephalon.
through brainstem connections, and on postural activity It contains pneumotaxic and apneustic respiratory centres
through projections down the spinal cord. and fibre tracts connecting higher and lower centres,
including the cerebellum. The pons seems to serve as a
Brainstem relay station, carrying signals from various parts of the
The brainstem is composed of the midbrain, the pons cerebral cortex to the cerebellum. Nerve impulses coming
from the eyes, ears and touch receptors are sent on to the
1
and the medulla oblongata. These structures connect the cerebellum. The pons also participates in the reflexes that
cerebrum and diencephalon with the spinal cord. Brain- regulate breathing. Table 16.4 contains a description of
stem centres are organised into medial, lateral and amin- the cranial nerves including their type of tract, their func-
ergic systems. Collectively, these integrate vestibular, tion and location of origin.
visual and somatosensory inputs for the control of eye
movements and, through projections to the spinal cord, Hypothalamus and limbic system
provide for postural adjustments. For example, these The hypothalamus, the cingulate gyrus of the cortex,
centres keep the images on matching regions of the the amygdala and hippocampus in the temporal lobes,
retinas when the head moves by causing conjugate eye and the septum and interconnecting nerve fibre tracts
movements in the opposite direction to which the head among these areas comprise the limbic system. The
is turned. This is the basis for the ‘doll’s eyes’ test in neu- hypothalamus and limbic systems, which are closely
rological assessment, in which the head is rapidly turned linked to homeostasis, act to regulate endocrine secre-
and the eyes move conjugately in the opposite direction, tion and the autonomic nervous system, and to influence
demonstrating the integrity of much of the brainstem. behaviour through emotions and drives. The hypothala-
1
The sequence of sleep states is governed by a group of mus integrates information from the forebrain, brain-
brainstem nuclei that project widely throughout the brain stem, spinal cord and various endocrine systems. This
and spinal cord. 17 area of the brain also contains some of the centres for
The midbrain, inferior to the centre of the cerebrum, coordinated parasympathetic and sympathetic stimula-
forms the superior part of the brainstem. It contains the tion, as well as those for temperature regulation, appetite
reticular formation (which collects input from higher regulation, regulation of water balance by antidiuretic
brain centres and passes it on to motor neurons), the hormone (ADH), and regulation of certain rhythmic
substantia nigra (which regulates body movements; psychobiological activities (e.g. sleep). The release of
damage to the substantia nigra causes Parkinson’s stored serotonin from axon terminals in the diencepha-
disease) and the ventral tegmental area (which contains lon, medulla, thalamus, and a small forebrain area
dopamine-releasing neurons that are activated by (DMTF), results in inactivation of the RAS and

424 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E


Knee Hip Trunk Shoulder Arm

Leg
Elbow Wrist Hand Fingers
Head
Hip
Neck
Trunk
Arm
Elbow
Forearm
Thumb
Hand
Fingers
Neck
Thumb
Eye Brow
Eye
Nose
Face
Face
Lips Midline Toes Lips
Genitals
Teeth Jaw
Gums
Jaw Tongue

Tongue Pharynx
Pharynx Larynx
Abdomen




Somatosensory cortex Motor cortex












Left Right
FIGURE 16.6 Somatosensory and motor homunculi. Note that the size of each region of the homunculi is related to its importance in sensory or motor
15
function, resulting in a distorted-appearing map.



activation of the DMTF. DMTF activity results in the of the brain is biochemically isolated from the general
four stages of sleep. The hypothalamus contains a pleth- circulation by the blood–brain barrier.
ora of neurotransmitters. These are found in the termi-
nals of axons that originate from neurons outside the Cerebral Spinal Fluid
hypothalamus, but most are synthesised within the hypo- Cerebral spinal fluid (CSF) is an ultrafiltrate of blood
thalamus itself. The list of putative neurotransmitters plasma composed of 99% water with other constituents,
includes the ‘classic’ transmitters ACh, GABA, glutamate, making it close to the composition of the brain extra-
serotonin, dopamine and noradrenaline, as well as liter- cellular fluid. Approximately 500 mL CSF is secreted
1
ally dozens of peptides that have been identified in each day, but only approximately 150 mL is in the ven-
recent years. 20 tricular system at any one time, meaning that the CSF
is continuously being absorbed. The CSF produced in
PROTECTION AND SUPPORT OF THE BRAIN the ventricles must flow through the interventricular
The brain occupies the cranial cavity and is covered by foramen, the third ventricle, the cerebral aqueduct and
21
membranes, fluid and the bones of the skull. The delicate the fourth ventricle to exit from the neural tube. Three
tissues of the brain are protected from mechanical forces openings, or foramina, allow the CSF to pass into the
1
by (a) the bones of the cranium, (b) the cranial meninges, subarachnoid space (see Figure 16.7). Approximately
and (c) cerebrospinal fluid. In addition, the neural tissue 30% of the CSF passes down into the subarachnoid

Neurological Assessment and Monitoring 425



TABLE 16.4 The cranial nerves, their location and functions

Cranial nerve Tract(s) Function Location of origin
I. Olfactory Sensory Sense of smell Diencephalon
II. Optic Sensory Vision Diencephalon
III. Oculomotor Parasympathetic Muscles that move the eye and lid, pupillary constriction, lens Midbrain
accommodation
Motor Elevation of upper eyelid and four of six extraocular movements
IV. Trochlear Motor Downward, inward movement of the eye (superior oblique) Midbrain
V. Trigeminal Motor Muscles of mastication and opening jaw Pons
Sensory Tactile sensation to the cornea, nasal and oral mucosa, and facial skin
VI. Abducens Motor Lateral deviation of eye (lateral rectus) Pons
VII. Facial Parasympathetic Secretory for salivation and tears Pons
Motor Movement of the forehead, eyelids, cheeks, lips, ears, nose and neck to
produce facial expression and close eyes
Sensory Tactile sensation to parts of the external ear, auditory canal and
external tympanic membrane
Taste sensation to the anterior two-thirds of the tongue
VIII. Vestibulocochlear Sensory Vestibular branch: Equilibrium Pons
Cochlear branch: Hearing
IX. Glossopharyngeal Parasympathetic Salivation Medulla
Motor Voluntary muscles for swallowing and phonation
Sensory Sensation to pharynx, soft palate and posterior one-third of tongue
Stimulation elicits gag reflex
X. Vagus Parasympathetic Autonomic activity of viscera of thorax and abdomen Medulla
Motor Voluntary swallowing and phonation
Involuntary activity of visceral muscles of the heart, lungs and digestive
tract
Sensory Sensation to the auditory canal and viscera of the thorax and abdomen
XI. Spinal accessory Motor Sternocleidomastoid and trapezius muscle movements Medulla
XII. Hyoglossal Motor Tongue movements Medulla







space that surrounds the spinal cord, mainly on its dorsal junctions, collectively referred to as the blood–brain
1
surface, and moves back up to the cranial cavity along barrier (BBB). In particular, small non-charged, lipid-
its ventral surface. Reabsorption of CSF into the vascular soluble molecules can cross the BBB with ease. Experi-
system occurs, through a pressure gradient. The normal mental and clinical evidence suggests that the BBB
CSF pressure is approximately 10 mmHg in the lateral maintains the chemical environment for neuronal func-
22
recumbent position, although it may be as low as tion and protects the brain from harmful substances.
5 mmHg or as high as 15 mmHg in healthy persons. Substances in the blood that gain rapid entry to the
The microstructure of the arachnoid villi is such that brain include glucose, the important source of energy,
if the CSF pressure falls below approximately 3 mmHg certain ions that maintain a proper medium for electrical
the passageways collapse, and reverse flow is blocked. activity, and oxygen for cellular respiration. Small fat-
Arachnoid villi function as one-way valves, permitting soluble molecules, like ethanol, pass through the BBB.
CSF outflow into the blood but not allowing blood to Some water-soluble molecules pass into the brain carried
pass into the arachnoid spaces. The pressure in the CSF by special proteins in the plasma membrane of the endo-
manifests as normal ICP. thelial cells. Excluded molecules include proteins, toxins,
most antibiotics, and monoamines (e.g. neurotransmit-
ters). Some of these unwanted molecules are actively
Blood–Brain–Cerebral Spinal Fluid Barrier transported out of the endothelial cells. When injured
The CNS is richly supplied with blood vessels that bring (by force or infection or oxidative processes), the perme-
oxygen and nutrients to the cells there. However, many ability of the BBB is disrupted, allowing a proliferation
substances cannot easily be exchanged between blood of various chemicals and molecules – even bacteria –
and brain because the endothelial cells of the vessels into the brain parenchyma, with at times devastating
and the astrocytes of the CNS form extremely tight consequences.

426 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E


Extension of choroid Cranium
plexus into lateral ventricle Dura mater
Choroid plexus Arachnoid (endosteal
of third ventricle granulations layer)

Fluid
movement
Superior
sagittal sinus
Arachnoid
granulation
Dura mater
(meningeal
layer)
Cerebral Subarachnoid Arachnoid Subdural
cortex space space
Pia
mater
Superior
sagittal
Mesencephalic sinus
aqueduct
Lateral aperture B
Choroid plexus of
fourth ventricle Spinal
Median aperture cord
Arachnoid Central canal
Subarachnoid space

Dura mater






Filum
terminale


A

FIGURE 16.7 Circulation of the cerebrospinal fluid: (A) sagittal section indicating the sites of formation and routes of circulation of cerebrospinal fluid
(arrows); (B) orientation of the arachnoid granulations. 1


Cerebral Circulation do not have valves, so the blood flows freely by gravity.
1
The brain must maintain a constant flow of blood in The face and scalp veins can flow into the brain venous
order for brain activity to occur. The arterial blood flow sinuses; therefore, infection can easily be spread into the
to the brain consists of approximately 20% of the cardiac dural venous sinuses and then enter the brain. Patient
output (see Figure 16.8). Normal cerebral blood flow is position can prevent or promote venous drainage from
5
750 mL/min. The brain autoregulates blood flow over a the brain. Head turning and tilting may kink the jugular
wide range of blood pressure by vasodilation or vasocon- vein and decrease or stop venous flow from the brain,
striction of the arteries. In response to decreased arterial which will then raise the pressure inside the cranial vault.
1
flow, the circle of Willis can act as a protective mechanism Cerebral blood flow (CBF) is the cerebral perfusion pres-
by shunting blood from one side to the other or from the sure (CPP) divided by cerebrovascular resistance (CVR).
anterior to posterior portions of the brain. This compen- CVR is the amount of resistance created by the cerebral
satory mechanism delays neurological deterioration in vessels, and it is controlled by the autoregulatory mecha-
patients.
nisms of the brain. Specifically, vasoconstriction (and
The cerebral veins drain into large venous sinuses and vasospasm) will increase CVR, and vasodilation will
1
then into the right and left internal jugular veins (see decrease CVR. It is influenced by the inflow pressure
23
Figure 16.9). The venous sinuses are found within the (systole), outflow pressure (venous pressure), cross-
folds of the dura mater. The veins and sinuses of the brain sectional diameter of cerebral blood vessels, and

Neurological Assessment and Monitoring 427

Anterior
Anterior cerebral artery
cerebral
artery
Middle
cerebral
artery
Internal
carotid Portion of
artery temporal
lobe
removed
Basilar
artery Posterior
inferior Middle
Anterior cerebellar cerebral
inferior artery Posterior artery
cerebellar cerebral artery
artery Vertebral B
artery



Anterior
communicating Posterior
artery
communicating
artery
Posterior
cerebral artery Anterior
(to midbrain) cerebral
C Posterior artery
Basilar artery cerebral
(to pons) artery

A
Lenticulostriate
arteries



Anterior
cerebral
artery


Middle
cerebral
artery Anterior
Internal communicating
carotid artery
D artery
FIGURE 16.8 The major arteries of the brain: (A) ventral view: the enlargement of the boxed area showing the circle of Willis; (B) lateral and (C) midsagittal
82
views showing anterior, middle and posterior cerebral arteries; (D) idealised frontal section showing course of middle cerebral artery.


1
intracranial pressure (ICP). CVR is similar to systemic hypertension. CBF is affected by extrinsic and intrinsic
1
vascular resistance; but, due to the lack of valves in the factors. Extrinsic factors include systemic blood pressure,
venous system of the brain, cerebral venous pressure also cardiac output, blood viscosity and vascular tone. The
influences the CVR. An important characteristic of the body responds to these demands with changes in blood
cerebral circulation is its ability to autoregulate, that is, flow. Aerobic metabolism is critically dependent on
the ability to maintain constant cerebral blood flow oxygen in order to process glucose for normal energy
despite variations in perfusion pressure (see Table 16.5). production, and the brain does not store energy. There-
This is important in protecting the brain from both isch- fore, without a constant source of oxygen and energy, its
aemia during hypotension and haemorrhage during supply from CBF can be exhausted within 3 minutes.