ACCCN's Critical Care Nursing

328 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


Inspiration Expiration
Intrapulmonary
pressure
+2
0
Pressure relative to atmospheric pressure (mm Hg) −2 Trans- Pulmonary
pulmonary
vein to
pressure
−4
left heart
−6
Intrapleural
pressure
Pulmonary
−8
artery from
plexus
right heart Capillary
Volume of breath
Volume (L) 0 Alveoli
0.5
5 seconds elapsed
FIGURE 13.4 Changes in intrapleural and intrapulmonary pressure during
4
inspiration and expiration.

the midline, are completely separate from each other. The
parietal pleura lines the inner surface of the chest wall
and is in close contact with the visceral pleura, which
covers the lungs. The pleural space, between these two
layers, contains a small amount of serous fluid, which FIGURE 13.5 Terminal ventilation and perfusion units of the lung. 5
normally limits friction during lung expansion.
The intra-pleural pressure in the pleural space under
normal circumstances is always negative with a range of
−4 to −10 cmH 2 O; this negative pressure keeps the lungs remarkably low (normal pulmonary artery pressure is
7
inflated. During inhalation the pressure becomes more only 25/8 mmHg; mean 15 mmHg). This low pressure
negative as both the lungs and the chest wall are elastic system ensures that the work of the right heart is as small
structures. These elastic fibres of the lung pull the visceral as feasible, while promoting efficient gas exchange in the
11
pleura inwards while the chest wall pulls the parietal lungs (see Figure 13.6).
pleura outward. The pressure difference between the alve-
olar pressure (0 cmH 2 O pressure in the lungs) and the Bronchial Circulation
intra-pleural pressure (−4 cmH 2 O) across the lung wall The bronchial circulation, part of the systemic circulation,
is termed the trans-pulmonary pressure (+4 cmH 2 O supplies oxygenated blood, nutrients and heat to the con-
[0 − (−4) = +4]), and is the force that hold the lungs ducting airways (to the level of the terminal bronchioles)
open (see Figure 13.4). and to the pleura. Drainage of this deoxygenated
3,4
blood is predominantly through the bronchial network,
Pulmonary Circulation although some capillaries drain into the pulmonary arte-
The circulatory system of the lung receives the entire rial circulation, contributing to venous admixture or
7
cardiac output but operates as a low pressure system, as right-to-left shunt (see Pathophysiology below for further
it only directs blood back to the left side of the heart discussion).
(unlike the systemic circulation which pumps blood to
different regions of the entire body). The pulmonary cir- CONTROL OF VENTILATION
culation involves oxygen-depleted blood being pumped Normal breathing occurs automatically and is a complex
by the right ventricle to the lungs via the pulmonary function not fully understood. It is coordinated by the
artery, with oxygen-rich blood returning to the left atrium respiratory centre, regulated by controllers in the brain,
via the pulmonary veins. Pulmonary blood vessels follow effectors in the muscles and sensors including chemore-
the path of the bronchioles, with the capillaries forming ceptors and mechanoreceptors. There are also protective
a dense network in the walls of the alveoli. As illustrated reflexes that respond to irritation of the respiratory tract
5
in Figure 13.5, the entire surface area of the alveolar wall such as coughing and sneezing.
is covered by these capillaries, where gas exchange occurs
as the capillaries are just large enough for a red blood cell Controller
to pass through.
In the brainstem, the medulla oblongata and the pons
Pulmonary vessels are short, thin and have relatively little regulate automatic ventilation while the cerebral cortex
smooth muscle. The pressure inside the vessels is regulates voluntary ventilation (see Figure 13.7). The

Respiratory Assessment and Monitoring 329

respiratory rhythmic centre in the medulla can be divided Effectors
into inspiratory and expiratory centres, with the follow- The diaphragm is the major muscle of inspiration, although
ing functions: 8
the external intercostal muscles are also involved. The
● The inspiratory centre (or dorsal respiratory group) accessory muscles of inspiration (scalenes, sternocleido-
triggers inspiration. masteoid muscles and the pectoralis minor of the thorax)
● The expiratory centre (or ventral respiratory group) are active only during exercise or strenuous breathing.
only functions during forced respiration and active Expiration is a passive act and only the internal intercostal
expiration. muscles are involved at rest. During exercise, the abdomi-
4
● The pneumotaxic and apneustic centre in the pons nal muscles also contribute to expiration. Inspiration is
adjusts the rate and pattern of breathing. triggered by stimulus from the medulla, causing the dia-
● The cerebral cortex provides conscious voluntary phragm to contract downwards, and the external intercos-
control over the respiratory muscles. This voluntary tal muscles to contract, lifting the thorax up and out. This
control cannot be maintained when PCO 2 and hydro- action lowers pressure within the alveoli (intra-alveolar
gen ion (H ) concentration become markedly ele- pressure) relative to atmospheric pressure. Air rushes into
+
vated; an example is the inability to hold your breath the lungs to equalise the pressure gradient. After contrac-
8
for very long. Emotional and autonomic activities tion has ceased, the ribs and diaphragm relax, the pressure
also often affect the pace and depth of breathing. gradient reverses, and air is passively expelled from the
lungs and return to their resting state due to elastic recoil.
Mean = 15 Mean = 100
Sensors
25 / 8 120 / 80
Artery Artery
A chemoreceptor is a sensor that responds to a change in
12 Pulmonary Systemic 30 the chemical composition of the blood; there are two
types: central and peripheral. Central chemoreceptors
25 / 0 120 / 0
account for 70% of the feedback controlling ventilation,
Cap RV LV Cap 20 and respond quickly to changes in the pH of cerebral
9
spinal fluid (CSF) (increase of PCO 2 in arterial blood).
RA LA If the PCO 2 in arterial blood remains high for a pro-
8 2 5 longed period, as in chronic obstructive pulmonary
10 disease (COPD), a compensatory change in HCO 3 occurs
and the pH in CSF returns to its near normal value.
7
Vein Vein Under these conditions a patient breathes due to hypoxic
drive; that is, low levels of O 2 are detected by peripheral
FIGURE 13.6 Comparison of pressure in the pulmonary and systemic cir- chemoreceptors and this triggers breathing. For this small
7
culations (mmHg). percentage of the population with COPD, care is required


Higher brain centers
(cerebral cortex-voluntary
control over breathing)
Other receptors (e.g. pain)
and emotional stimuli acting ±
through the hypothalamus

±
Respiratory centers
(medulla and pons)


Peripheral
chemoreceptors +
+
O 2 ↓,CO 2 ↑,H ↑ Stretch receptors
in lungs
+ −
Central
chemoreceptors
+
CO 2 ↑,H ↑ −
+ Irritant
FIGURE 13.7 Respiratory centres and reflex receptors
4
controls. (Elaine N. Marieb and Katja Hoehn, Receptors in
HUMAN ANATOMY & PHYSIOLOGY, 8th Ed. © muscles and joints
2010, p. 836. Reprinted by permission of
Pearson Education, Inc., Upper Saddle River,
New Jersey).

330 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

9
when administering oxygen so that the stimulus to blood. Other receptors include stretch receptors located
breathe is not compromised, as increases in PO 2 may in the lungs that inhibit inspiration and protect the lungs
reduce respiratory drive. Peripheral chemoreceptors from over-inflation (Hering–Breuer reflex), and in the
respond to low partial pressure of oxygen in arterial muscles and joints (see Figure 13.7).
blood (PaO 2 ) and contribute to maintaining ventilation,
functioning optimally when oxygen levels fall below PULMONARY VOLUMES AND CAPACITIES
70 mmHg. 7 In healthy individuals, the lungs are readily distensible
Central chemoreceptors located in the medulla respond or compliant; when exposed to high expanding pressures
to changes in hydrogen ion concentration in the CSF that or in disease states, compliance is increased or decreased.
surrounds these receptors. A change in the partial pres- A range of lung volumes and capacities are illustrated in
sure of carbon dioxide in arterial blood (PaCO 2 ) causes Figure 13.8. Tidal volume (TV) is the volume of air enter-
movement of CO 2 across the blood–brain barrier into ing the lungs during a single inspiration and is normally
the CSF and alters the hydrogen ion concentration. This equal to the volume leaving the lungs on expiration
increase in hydrogen ions stimulates ventilation. Central (around 500 mL). During inspiration, the TV of inspired
chemoreceptors do not however respond to changes in air is added to the 2400 mL of air already in the lungs.
PaO 2 levels. Opiates also have a negative influence on This volume of air that remains in the lungs after a normal
4
these chemoreceptors causing less sensitivity to changes expiration is the functional residual capacity (FRC),
in hydrogen ion concentration. Note also that hyperven- which:
7
tilation may reduce the level of PaCO 2 to a level that ● has an important role in keeping small alveoli open
could cause accidental unconsciousness if the breath is and avoiding atelectasis
held after hyperventilation. This phenomenon is well ● can be reduced during anaesthesia or neuromuscular
known amongst divers and is due to increasing levels of blockade, most likely due to loss of muscle tone 12
CO 2 as the primary trigger of breathing. If the CO 2 level ● if reduced, results in the smallest alveoli closing at the
is too low due to hyperventilation, the breathing reflex is end of the expiration (the ‘closing volume’).
not triggered until the level of oxygen has dropped below
what is necessary to maintain consciousness. The closing volume plus the residual volume is called the
‘closing capacity’. The closure of the smallest airways may
Peripheral chemoreceptors are located in the common occur because dependent areas of the lungs are com-
carotid arteries and in the arch of the aorta. These recep- pressed, although this is not the only mechanism as these
tors are sensitive to changes in PaO 2 and are the primary airways also close in the weightlessness of space. The
responders to hypoxaemia, stimulating the glossypharyn- closing volume is dependent on patient age; in a young
geal and vagus nerves and providing feedback to the healthy person it is 10% of vital capacity, while for an
medulla. Peripheral chemoreceptors also detect changes individual aged 65 years it increases to 40%, approximat-
in PaCO 2 and hydrogen ion concentration/pH in arterial ing total FRC. 11


6000

5500
5000
4500
Total amount of air in lungs (ml) 3500
4000


3000

2500
2000
1500
1000

500
0
Measure TLC V T FRC IC IRV ERV RV VC
Value (ml) 5800 500 2300 3500 3000 1100 1200 4600
6000 2400 3600 3100 1200 1300 4800
FIGURE 13.8 For lung volume measurements, all values are approximately 25% less in women. ERV, expiratory reserve volume; IC, inspiratory capacity;
10
IRV, inspiratory reserve volume; FRC, functional residual capacity; TLC, total lung capacity; RV, residual volume; VC, vital capacity; VT, tidal volume.

Respiratory Assessment and Monitoring 331

Alveolar Ventilation lungs through to the blood in the adjacent alveolar capil-
Minute volume (MV), often referred to during mechani- lary networks. Similarly, carbon dioxide diffuses from
cal ventilation, is TV multiplied by respiratory frequency capillaries to the alveoli and is then expired.
(e.g. 500 mL × 12 breaths per minute = 6000 mL MV). Oxygen Transport
Importantly, only the first 350 mL of inhaled air in each
breath reaches the alveolar exchange surface, with 150 mL In oxygenated blood transported by the pulmonary capil-
remaining in the conducting airways (called the ‘ana- laries, there is 20 mL of oxygen in each 100 mL of blood.
tomic dead space’). Alveolar ventilation is the amount of Oxygen is transported in two ways; dissolved in plasma
inhaled air that reaches the alveoli each minute (e.g. (about 0.3 mL; 1.5%) with the remainder bound to hae-
8
350 mL × 12 = 4200 mL of alveolar ventilation). 8 moglobin. The 1.5% of oxygen dissolved in the blood is
what constitutes PaO 2 and measured by arterial blood
4
WORK OF BREATHING gases. One gram of haemoglobin carries 1.34 mL oxygen,
and the level of saturation within the total circulating
In a resting state, energy requirements to breathe is haemoglobin can be measured clinically, commonly by
7
minimal (less than 5% of total O 2 consumption). pulse oximetry. The amount of oxygen actually bound to
However, changes in airway resistance and lung compli- haemoglobin compared with the amount of oxygen the
ance affect the work of breathing (WOB), resulting in haemoglobin can carry is commonly reported as SaO 2 .
13
increased oxygen consumption (VO 2 ). As noted earlier, Oxygen is attached to the haemoglobin molecule at four
the lungs are very distensible and expand during inspira- haem sites. As the majority of oxygen transport is via
tion. This expansion is called the elastic or compliance haemoglobin, if all four sites are occupied with oxygen
work and refers to the ease by which lungs expand under molecules the blood is determined to be ‘fully saturated’
pressure. Lung compliance is often monitored when (SaO 2 = 100%). 14
patients are mechanically ventilated, and is calculated by
dividing the change in lung volume by the change in trans- A large reserve of oxygen is available if required, without
3
pulmonary pressure. For the lung to expand, it must the need for any increase in respiratory or cardiac work-
overcome lung viscosity and chest wall tissue (called load. Oxygen extraction is the percentage of oxygen
‘tissue resistance work’). Finally, there is airway resistance extracted and utilised by the tissues. At rest, just 25% of
work – movement of air into the lungs via the airways. the total oxygen delivered to the tissue is extracted,
The work associated with resistance and compliance is although this amount does vary throughout the body,
easily overcome in healthy individuals but in pulmonary with some tissue beds extracting more and others taking
disease, both resistance and compliance work is less. Normally, the oxygen saturation of venous blood is
increased. 3,14 During exertion, when increased muscle 60–75%; values below this indicate that more oxygen
function heightens metabolic rate, oxygen demand rises than normal is being extracted by tissues. This can be due
to match consumption and avoid anaerobic metabolism, to a reduction in oxygen delivery to the tissues, or to an
8,9
and work of breathing is increased. The term ‘work of increase in the tissue consumption of oxygen.
breathing’ is often used in those who are critically ill, when Oxygen delivery (DO 2 ) and oxygen consumption (VO 2 )
basic respiratory processes are challenged and breathing are important aspects to consider in the management of
consumes a far greater proportion of total energy. a critically ill patient. Normal oxygen delivery in a healthy
person at rest is approximately 1000 mL/min. Normal
9
PRINCIPLES OF GAS TRANSPORT AND oxygen consumption is 200–250 mL/min, but this can
EXCHANGE IN ALVEOLI AND TISSUES increase significantly during episodes of sepsis, fever,
hypercatabolism and shivering. The difference between
14
Oxygen and carbon dioxide is transported in the blood- normal delivery and normal consumption highlights the
stream between the alveoli and the tissue cells by the large degree of oxygen reserve available to the body.
cardiac output. Delivery of oxygen to tissues and transfer
of carbon dioxide from the tissues to the capillary occurs Oxygen–Haemoglobin Dissociation Curve
by diffusion and is therefore dependent on the pressure
gradient between the capillary and the cell. Diffusion As blood is transported to the tissues and end-organs, the
involves molecules moving from areas of high concentra- affinity of haemoglobin and oxygen to combine decreases,
tion to low concentration. Other determinants of the rate relative to the surrounding arterial oxygen tension. This
of diffusion include the thickness of the alveolar mem- relationship is illustrated by the oxyhaemoglobin disso-
brane, the amount of surface area of the membrane avail- ciation curve (see Figure 13.9). As oxygen is offloaded at
able for gas transfer and the inherent solubility of the gas. the tissue level, carbon dioxide binds more readily with
Carbon dioxide diffuses about 20 times more rapidly haemoglobin, to be transported back to the lungs for
4
than oxygen because of the much higher solubility of removal.
7
carbon dioxide in blood. At the most distal ends of the In the upper part of the curve (within the lungs), relatively
conducting airways lies an extensive network of approxi- large changes in the PaO 2 cause only small changes in
mately 300 million alveoli. The surface area of the lungs haemoglobin saturation. Therefore, if the PaO 2 drops
2
if spread out flat is about 90 m – about 40 times greater from 100 to 60 mmHg (14–8 kPa), the saturation of hae-
4
than the surface of the skin. Gas exchange occurs through moglobin changes only 7% (from a normal 97%
the exceptionally thin alveolar membranes. Oxygen to 90%). The lower portion (steep component) of the
uptake takes place from the external environment via the oxygen–haemoglobin dissociation curve, when PaO 2 is

332 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 including haemoglobin. The dissolved carbon dioxide


%O 2 saturation 80 Curve before constitutes PaCO 2 and is measured by arterial blood
100
gases. The greater solubility of CO 2 when compared with
oxygen results in rapid diffusion across the capillary
shift
60
4
for elimination. Carbon dioxide, a byproduct of cellular
40 Curve shifts to right membranes, and therefore the gas can be easily removed
as pH CO 2 respiration, is produced at a rate of 200 mL/min, with
Increased 20 temperature only minor differences in normal concentrations in arte-
oxygen rial (480 mL/L) and venous (520 mL/L) blood. 9
release 0
to tissue 0 20 40 60 80 100
PO 2 (mmHg)
PO 2 in tissue Relationship Between Ventilation
and Perfusion
In the tissues, the oxygen–haemoglobin dissociation Gas exchange is the key function of the lungs, and the
curve shifts to the right. As pH decreases, PCO 2 unique anatomy of capillaries and alveoli facilitates this
increases, or as temperature rises, the curve (black) process. However, a number of physiological factors
shifts to the right (blue), resulting in an increased mean that the ventilation (V) to perfusion (Q) ratio is
release of oxygen. not matched in a 1 : 1 relationship. As normal alveolar
A ventilation is about 4 L/min and pulmonary capillary
perfusion is about 5 L/min, the normal ventilation to
7
perfusion ratio (V/Q) is 0.8. In addition, pressure in the
Increased pulmonary circulation is low relative to systemic pres-
uptake of 100 sure, and is influenced much more by gravity/hydrostatic
oxygen
in lungs 80 pressure. In the upright position, lung apices receive less
7
Curve shifts to left perfusion compared with the bases. In the supine posi-
60 as pH CO 2 tion, apical and basal perfusion is almost equal, but the
temperature
%O 2 saturation 40 Curve before greater perfusion than the anterior lung area. Ventilation
posterior (dependent) portion of the lungs receives
is also uneven throughout the lung, with the bases
20
shift
receiving more ventilation per unit volume than the
7
0
Pressure within the surrounding alveoli also influences
0 20 40 60 80 100 apices.
PO 2 (mmHg) blood flow through the pulmonary capillary network.
PO 2 in lungs The pressure gradients between the arterial and venous
ends of a capillary network normally determine blood
In the lungs, the oxygen–haemoglobin dissociation flow. However, alveolar pressure can be greater than
curve shifts to the left. As pH increases, PCO 2 venous and/or arterial pressure, and therefore influences
decreases, or as temperature falls, the curve (black) blood flow and gas exchange.
shifts to the left (blue), resulting in an increased ability For a patient in an upright position, in:
of haemoglobin to pick up oxygen.
B ● Zone 1 (upper area of the lungs): alveolar pressure is
generally greater than both arterial and venous capil-
FIGURE 13.9 Shift of the oxyhaemoglobin dissociation curve (A) to the lary pressure [P A >P a >P v ], and blood flow is reduced,
85
right and (B) to the left. leading to alveolar dead space (alveoli ventilated but
not adequately perfused).
between 60 and 40 mmHg (8–5 kPa) reflects however that
as haemoglobin is further de-saturated, larger amounts of ● Zone 2 (middle portion of the lungs): perfusion and
oxygen are released for tissue use, ensuring an adequate gas exchange is influenced more by pressure differ-
oxygen supply to peripheral tissues is maintained even ences between arterial and alveolar pressures than by
4
when oxygen delivery is reduced. Oxygen saturation still the usual difference between arterial and venous pres-
remains at 70–75%, leaving a significant amount of oxygen sures [P a >P A >P v ], with a normal V/Q ratio.
in reserve. The relationship between the two axes of this ● Zone 3 (lung bases): alveolar pressure is lower than
curve assumes normal values for haemoglobin, pH, tem- both arterial and venous pressures [P a >P v >P A ], and
perature, PaCO 2 and 2,3-DPG. Changes to any of these ventilation is reduced leading to intrapulmonary
values will shift the curve to the right or left and therefore shunting (alveoli perfused but not adequately venti-
7
reflect different values for PaO 2 and SaO 2 . 8 lated) (see Figure 13.10).
These physiological relationships are more complex in a
Carbon Dioxide Transport critically ill patient when ventilation and/or lung perfu-
Carbon dioxide is transported by blood in three forms: sion is further compromised by disease processes and
combined with water as carbonic acid (80–90%), dis- positive pressure ventilation, and the patient is in a
solved (5%), or attached to plasma proteins (5–10%), supine or semi-recumbent position. 7

Respiratory Assessment and Monitoring 333

Apex bicarbonate and pH returns to normal (i.e. the respiratory
Alveolus 11
Zone I alkalosis is compensated).
Capillary
Arteriole PA . Pa . Pv
Venule
PATHOPHYSIOLOGY
Three common pathophysiological concepts that influ-
Zone II ence respiratory function in critically ill patients are
Alveolus Pa . PA . Pv hypoxaemia, inflammation and oedema. The principles
for these phenomena are discussed below. Related pre-
Pulmonary Pulmonary senting disease states including respiratory failure, pneu-
artery vein
monia, acute lung injury, asthma and chronic obstructive
pulmonary disease are described in Chapter 14.
Alveolus
Zone III HYPOXAEMIA
Pa . Pv . PA
Hypoxaemia describes a decrease in the partial pressure
4
of oxygen in arterial blood (PaO 2 ) of less than 60 mmHg.
This state leads to less efficient anaerobic metabolism at
the tissue and end-organ level, and resulting compro-
mised cellular function. Hypoxia is abnormally low PO 2
in the tissues, and can be due to:
FIGURE 13.10 The effects of gravity and alveolar pressure on pulmonary
86
blood flow. Notice the three lung zones. ● ‘hypoxic’ hypoxia: low PaO 2 in arterial blood due to
pulmonary disease
ACID–BASE CONTROL: RESPIRATORY ● ‘circulatory’ hypoxia: reduction of tissue blood flow
due to shock or local obstruction
MECHANISMS ● ‘anaemic’ hypoxia: reduced ability of the blood to
The respiratory system plays a vital role in acid–base carry oxygen due to anaemia or carbon monoxide
balance. Changes in respiratory rate and depth can poisoning
produce changes in body pH by altering the amount of ● ‘histotoxic’ hypoxia: a cellular environment that does
carbonic acid (H 2 CO 3 ) in the blood. When dissolved, not support oxygen utilisation due to tissue poisoning
−
CO 2 forms bicarbonate ion (HCO 3 ), carbonic acid (e.g. cyanide poisoning). 7
2−
(H 2 CO 3 ) and carbonate ion (CO 3 ); these concentrations
affect the acid–base balance. In common with other acids, A hypoxic patient can show symptoms of fatigue and
carbonic acid partially dissociates when in solution, to shortness of breath if the hypoxia has developed gradu-
form CO 2 and water or bicarbonate and hydrogen ion: ally. If the patient has severe hypoxia with rapid onset,
they will have ashen skin and blue discolouration (cya-
CO 2 + H O ↔ H CO 3 ↔ HCO 3 + H . nosis) of the oral mucosa, lips, and nail beds. Confusion,
+
2
2
disorientation and anxiety are other symptoms. In later
The strength of the dissociation is defined by the 15
Henderson–Hasselbach equation that describes the rela- stages, unconsciousness, coma and death occur.
tionship between bicarbonate, CO 2 and pH, and explains Acute respiratory failure is a common patient presenta-
why an increase in dissolved CO 2 causes an increase in tion in ICU that is characterised by decreased gas exchange
−
16
the acidity of the plasma, while an increase in HCO 3 with resultant hypoxaemia. Two different mechanisms
causes the pH to rise (i.e. acidity falls): cause acute respiratory failure: Type I presents with low
PO 2 and normal PCO 2 ; Type II presents with low PO 2 and
( HCO 3 )
1
+
pH = 6 1 log high PCO 2 (see Chapter 14 for further discussion).
.
( CO 2 )
In general, impaired gas exchange results from alveolar
(6.1 = the dissociation constant in plasma). 11 hypoventilation, ventilation/perfusion mismatching and
intrapulmonary shunting, each resulting in hypoxaemia.
Respiratory acidosis is caused by CO 2 retention and
increases the denominator in the Henderson–Hasselbach Hypercapnia may also be present depending on the
17
equation resulting in a decreased pH level. This condition underlying pathophysiology.
occurs when a patient takes small breaths at a low respira- Alveolar hypoventilation occurs when the metabolic
tory rate (hypoventilation). In the acute state the body needs of the body are not met by the amount of oxygen
cannot compensate. If the patient develops chronic CO 2 in the alveoli. Hypoxaemia due to alveolar hypoventila-
retention over a long period, there will be a renal response tion is usually extrapulmonary (e.g. altered metabolism,
to the increase in CO 2 . The renal system retains bicarbon- interruption to neuromuscular control of breathing/
ate to return the pH to normal (i.e. respiratory acidosis ventilation) and associated with hypercapnia. 17
is compensated).
Ventilation/perfusion (V/Q) mismatch results when areas
Respiratory alkalosis occurs when a patient hyperventi- of lung that are perfused are not ventilated (no par-
lates with large, frequent breaths; CO 2 decreases in ticipation in gas exchange) because alveoli are collapsed
arterial blood and pH rises. If this condition is main- or infiltrated with fluid from inflammation or infection
tained (e.g. walking at high altitude), the kidney excretes (e.g. pulmonary oedema, pneumonia). This results in

334 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


From interruption to these vital cellular activities is a reduction
pulmonary Airway in organ or tissue function, which in turn compromises
artery Impaired system and body functions.
ventilation
Alveolus Changes to the oxyhaemoglobin dissociation curve also
occur in states related to hypoxia. The curve shifts to the
right when there is acidosis and/or raised levels of PCO 2
as commonly seen in respiratory failure. Although this
Alveolocapillary change may alter patient oxygen saturation readings, the
membrane To Hypoxaemia increased release of oxygen from haemoglobin to the
Normal V/Q pulmonary vein Low V/Q tissues has obvious benefits for tissue oxygenation and
cellular metabolism. 7

Blocked Impaired perfusion Compensatory Mechanisms to
ventiation Optimise Oxygenation
Alveolar
Collapsed dead space When PO 2 in the alveolus is reduced, hypoxic pulmonary
alveous
vasoconstriction occurs, with contraction of smooth
muscles in the small arterioles in the hypoxic region,
directing blood flow away from the hypoxic area of the
lung. Peripheral chemoreceptors also detect hypoxaemia
7
and initiate compensatory mechanisms to optimise cel-
Hypoxaemia Hypoxaemia lular oxygen delivery. Initial responses are increased respi-
Shunt (very low) V/Q High V/Q ratory rate and depth of breathing, resulting in increased
minute ventilation, and raised heart rate with possible
FIGURE 13.11 Ventilation perfusion mismatch.
18
vasoconstriction as the body attempts to maintain oxygen
delivery and uptake. This overall up-regulation cannot be
an overall reduction in blood oxygen levels, which can sustained indefinitely, particularly in a person who is
usually be countered by compensatory mechanisms. 1
critically ill, and compensatory mechanisms begin to fail
Intrapulmonary shunting is an extreme case of V/Q mis- with worsening hypoxaemia and cellular and organ dys-
match. Shunting occurs when blood passes alveoli that function. Unless the hypoxaemia is reversed and/or respi-
are not ventilated. There can be significant intrapulmo- ratory and cardiovascular support is provided, irreversible
nary shunting, and therefore overwhelming reductions in hypoxia and death will ensue.
18
PaO 2 . Carbon dioxide levels may still be normal but
depending on the onset and progression of the respira- INFLAMMATION
tory pathophysiology, compensatory mechanisms may Inflammatory processes can occur at a local level (e.g. as
not be able to maintain homeostasis 1,11 (see Figure 13.11). a result of inhalation injuries, aspiration or respiratory
infections) or are secondary to systemic events (e.g. sepsis,
Tissue Hypoxia trauma). Damage to the pulmonary endothelium and
There are few physiological changes with mild hypoxae- type I alveolar cells appear to play a key role in the inflam-
20
mia (when O 2 saturation remains at 90% despite a PaO 2 matory processes associated with ALI. Once triggered,
of 60 mmHg [8 kPa]), with only a slight impairment in inflammation results in platelet aggregation and comple-
mental state. If hypoxaemia deteriorates and the PaO 2 ment release. Platelet aggregation attracts neutrophils,
drops to 40–50 mmHg (5.3–6.7 kPa), severe hypoxia which release inflammatory mediators (e.g. proteolytic
of the tissues ensues. Hypoxia at the central nervous enzymes, oxygen free radicals, leukotrienes, prostaglan-
system level manifests with headaches and somnolence. dins, platelet-activating factor [PAF]). Neutrophils also
Compensatory mechanisms include catecholamine appear to play a key role in the perpetuation of ALI/
1
release, and a decrease in renal function results in sodium ARDS. As well as altering pulmonary capillary permea-
retention and proteinuria. 19 bility, resulting in haemorrhage and fluid leak into the
pulmonary interstitium and alveoli, mediators released
Different tissues vary in their vulnerability to hypoxia,
with the central nervous system and myocardium at most by neutrophils and some macrophages precipitate pul-
risk. Hypoxia in the cerebral cortex results in a loss of monary vasoconstriction. Resulting pulmonary hyperten-
function within 4–6 seconds, loss of conscious in 10–20 sion leads to diminished perfusion to some lung areas,
seconds and irreversible damage in 3–5 minutes. In an with dramatic alterations to both perfusion and ventila-
11
environment that lacks oxygen, cells function by anaero- tion leading to significant V/Q mismatches, and the sub-
bic metabolism and produce much less energy (adenos- sequent signs and symptoms typically seen in patients
ine triphosphate [ATP]) than with aerobic metabolism with pulmonary inflammation/oedema.
(2 versus 38 ATP molecules per glucose molecule), and
lactic acid increases. With less available energy, the effi- OEDEMA
+
+
ciency of cellular functions such as the Na /K pump, Pulmonary oedema also alters gas exchange, and
nerve conduction, enzyme activity and transmembrane results from abnormal accumulation of extravascular
receptor function diminishes. The overall effect of fluid in the lung. The two main reasons for this are:
19

Respiratory Assessment and Monitoring 335

‘increased pressure’ oedema, where there is an increase in treatment. Depending on a patient’s situation, assess-
hydrostatic or osmotic forces (e.g. left heart ventricular ment can be either brief or detailed.
dysfunction or volume overload); and ‘increased perme-
ability’ oedema, that results from increased membrane PATIENT HISTORY
permeability of the epithelium or endothelium in the History-taking determines a patient’s baseline respiratory
lung, allowing accumulation of fluid (also called ‘non- status on admission to ICU. If the patient is in distress
cardiogenic’). Resulting clinical syndromes are acute lung only a few questions may be asked but, if the patient is
injury (ALI) or acute respiratory distress (ARDS) (see able, a more comprehensive interview can be performed,
Chapter 14 for further discussion). focusing on four areas: the current problem, previous

Changes to Respiratory Function problems, symptoms and personal and family history.
Question a family member or close friend if a patient is
During the early exudative phase of ALI/ARDS, tachy- not able to provide their own history.
pnoea, signs of hypoxaemia (apprehension, restlessness)
and an increase in the use of accessory muscles are usually When introducing yourself, ask the patient’s name, seek
evident as a result of infiltration of fluids into the alveoli. eye contact and create a rapport with the patient and the
With impaired production of surfactant during the pro- family. Ensure that the patient is in a comfortable posi-
liferative phase, respiratory function deteriorates, and tion, ideally sitting up in the bed. Provide privacy so that
dyspnoea, agitation, fatigue and the emergence of fine the interview is confidential and the physical examina-
crackles on auscultation are common. 1,11 Airway resis- tion can be done while maintaining the patient’s dignity
tance is increased when oedema affects larger airways. and modesty. To minimise distress for a patient who is
Lung compliance is reduced as interstitial oedema inter- acutely breathless, the use of short closed questions is
feres with the elastic properties of the lungs, and patients preferable.
may be quite a challenge to adequately ventilate. Infiltra-
tion of type II alveolar cells into the epithelium may lead
21
to interstitial fibrosis on healing, causing chronic lung Practice tip
dysfunction.
History-taking is a nursing interview and an interactive experi-
Respiratory Dysfunction: Changes to ence, especially the initial interview where both the patient
Work of Breathing and the nurse learn a lot about each other. This knowledge
has a considerable influence on building rapport between the
If respiratory compromise is not reversed, there will be patient and the nurse.
significant increases to the work of breathing. Clinical
manifestations include tachypnoea, tachycardia, dys-
pnoea, low tidal volumes and diaphoresis. Hypercapnia Current Respiratory Problems
will ensue, which further compromises respiratory muscle
function and precipitates diaphragmatic fatigue. Oxygen Begin by asking why the patient is seeking care. If possi-
consumption during breathing can be so great that reserve ble, let the patient describe the respiratory problem in
capacity is reduced. If patients with preexisting COPD his or her own words. Be focused and listen actively.
(who may breathe close to the fatigue work level) experi- Ask for location, onset and duration of the respiratory
ence an acute exacerbation, this can easily tip them into symptoms.
a fatigued state. Early identification and management of
respiratory compromise before these stages improves Previous Respiratory Problems
patient outcomes. 19 Many respiratory disorders can be chronic and pulmo-
nary diseases may recur (e.g. tuberculosis), and new dis-
ASSESSMENT eases can complicate old ones. Ask about problems with
22
breathing and their chest, number of hospitalisations,
Respiratory insufficiency is a common reason for admis- treatments, and childhood respiratory diseases.
sion to a critical care unit, for either a potential or an
actual problem, so comprehensive and frequent respira- Symptoms
tory assessments are an essential practice role. This section Assess any presenting symptoms in relation to: onset and
outlines history, physical examination, bedside monitor- duration, pattern, severity, and episodic or continuous.
ing and diagnostic testing focused on a critically ill patient Also ask about the patient’s perception of their respira-
with respiratory dysfunction. tory problem, their opinion about its cause and if the
symptoms cause fatigue, anxiety or stress. Ask the patient
Assessment is a systematic process comprising history
taking of a patient’s present and previous illnesses, and specifically about: dyspnoea, cough, sputum production,
physical examination of their thorax, lungs and related haemoptysis, wheezing, chest pain or other pain, sleep
systems. History taking and physical examination can be disturbances and snoring.
done simultaneously if the patient is very ill. Related Dyspnoea (shortness of breath) is subjective and there-
diagnostic findings inform an accurate and comprehen- fore difficult to grade. The mechanism that underlies the
sive assessment. A thorough assessment, followed by sensation of dyspnoea is poorly understood but it is
22
accurate ongoing monitoring, enables early detection of extremely uncomfortable and frightening. Assess the
condition changes and assessment of the impact of severity of dyspnoea by asking about breathing in

336 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

relation to activities (e.g. breathlessness when dressing exposure to allergens and toxins in the work place is
or walking across a room). Ask the patient how many important information to collect because this can be
27
pillows they need to sleep as this may indicate the sever- associated with a decline in lung function. Ask about
ity of any orthopnoea. If the patient becomes short of the patient’s home situation and whether they live with
breath when lying flat (orthopnoea) it can be a symptom someone with an infection or disease such as influenza
of increased blood in the pulmonary circulation due to or tuberculosis. Ask about children who are close to the
left ventricular failure, pulmonary oedema, bronchitis, patient, as innocuous viral infections in small children
22
asthma or obstructive sleep apnoea. may account for severe disease in adults. Check also
A cough can be dry or wet, episodic or continuous and, whether there is a family history of cancer, heart or respi-
if exacerbated when the patient is lying flat, can imply ratory diseases.
heart failure. A cough can also be related to viral infec-
tions and allergies or it can indicate intra-thoracic disease. PHYSICAL EXAMINATION
Ask the patient if they wake during the night due to the The four activities of physical examination are inspection,
cough, how long the cough has been present and if it is palpation, percussion and auscultation. Percussion is
getting better or worse. rarely used by critical care nurses, so only the other three
Sputum production should be considered for amount, techniques are discussed here. Prior to commencing the
colour or the presence of blood. Yellow or green sputum examination, prepare the patient as best as is possible by
is typical in bacterial infection. Haemoptysis or sputum providing privacy, warmth, good light and quiet sur-
mixed with blood is a significant finding and can indicate roundings (this can be difficult to achieve in the critical
tuberculosis or lung cancer. Wheezing can indicate vocal care environment). Explain to the patient that the exami-
cord disorder or asthma. 22 nation is a standard procedure and that you will use your
eyes, hands and a stethoscope. Help the patient into a
Chest pain can result from multiple causes, therefore comfortable sitting position in the bed if possible and
appropriate assessment is essential. Chest pain that occurs have all the necessary equipment easily accessible.
during inspiration can be due to irritation or inflamma-
tion of the pleural surface. Pleural pain is experienced Inspection
mostly on one side of the chest, is knifelike in character
and occurs in pneumonia and spontaneous pneumotho- Inspection involves carefully observing the patient for
rax. The most significant chest pain occurs as a result of signs of respiratory problems. Focus on: patient position,
myocardial ischaemia, due to too little oxygen to the chest wall inspection, respiratory rate and rhythm, respi-
coronary blood vessels. This pain is termed angina pec- ratory effort, central or peripheral cyanosis and clubbing.
toris and can arise from chronic stable angina or acute Note what position appears preferable for the patient,
22
myocardial infarction (see Chapter 10 for further discus- whether they look comfortable in bed, having trouble
sion). Chest pain also occurs with fractured ribs. breathing, or appear anxious. Observe from head to toe.
Observe the patient’s chest wall symmetry during the
Sleep disturbance and snoring may be related to obstruc- respiratory cycle, anatomical structures, and the presence
tive sleep apnoea (OSA). If the patient complains about of scars. The most important sign of respiratory distress
drowsiness in the daytime, ask how many hours of con- is respiratory rate and rhythm. Count the rate for a one-
tinuous sleep they have at night, and whether they take minute period. Normal respiratory rate for adults is
a nap during the day. 12–15 per minute. Abnormal breathing patterns are
4
noted in Table 13.1. Observe respiratory effort, in particu-
Personal and Family History lar the use of accessory muscles, abdominal muscles,
Patient family history and environment can influence nasal flaring, body position and mouth-breathing.
pulmonary presentations. The focus of this questioning Inspect the lips, tongue and sublingual area for central
is on: tobacco use, allergies, recent travel, type of occupa- cyanosis (a late sign of hypoxia that is almost impossible
tion, home situation and family history. Use of tobacco, to detect in a patient with anaemia). Observe the extrem-
1
current or past, is important in evaluating pulmonary ities for oedema (can be a sign of heart failure), fingers
symptoms. Ask the patient to quantify the amount of and toes for peripheral cyanosis and clubbing of the nail-
cigarette packs per week and how many years they have beds. Peripheral cyanosis can appear with low blood flow
smoked. The majority of smokers have reduced lung to peripheral areas. Clubbing of finger or toe nailbeds can
function. Tobacco smoking is responsible for 80–90% of be idiopathic in nature or more commonly due to respi-
the risk of developing chronic obstructive pulmonary ratory and circulatory diseases (e.g. chronic hypoxia in
disease but only 10–15% of these patients will develop congenital heart disease). 14,22
23
clinically significant symptoms. Exposure to second-
hand smoke may also be of interest. There is Note also if the patient requires oxygen and observe the
evidence that exposure to secondhand smoke for an dose. If the patient is intubated and mechanically venti-
extended period is a major cause in developing chronic lated (monitoring is explained later in this chapter),
24
bronchitis. A history of recent travel increases the pos- ensure the airway is adequately secured. If the patient is
sibility of exposure to infectious diseases affecting the orally intubated, observe the mouth for the presence of
25
respiratory system. Recent long flights are also respon- lesions or pressure on the oral mucosa and lips;
sible for the possibility of deep venous thrombosis which and observe the size of the tube, the length at the lips or
26
can lead to pulmonary embolism. An occupation with teeth margin, and how it is secured. If the patient has a

Respiratory Assessment and Monitoring 337



TABLE 13.1 Description of different respiration patterns 14

Type Description Pattern Clinical indication
Normal 12 to 20 breaths/min and Normal breathing pattern
regular
Tachypnea >24 breaths/min and shallow May be a normal response to fever, anxiety,
or exercise
Can occur with respiratory insufficiency,
alkalosis, pneumonia, or pleurisy
Bradypnea <10 breaths/min and regular May be normal in well-conditioned athletes
Can occur with medication-induced
depression of the respiratory centre,
diabetic coma, neurologic damage
Hyperventilation Increased rate and increased Usually occurs with extreme exercise, fear,
depth or anxiety. Causes of hyperventilation
include disorders of the central nervous
system, an overdose of the drug
salicylate, or severe anxiety.
Kussmaul Rapid, deep, laboured A type of hyperventilation associated with
diabetic ketoacidosis


Hypoventilation Decreased rate, decreased Usually associated with overdose of
depth, irregular pattern narcotics or anaesthetics

Cheyne-Stokes Regular pattern characterised May result form severe congestive heart
respiration by alternating periods of failure, drug overdose, increased
deep, rapid breathing intracranial pressure, or renal failure
followed by periods of May be noted in elderly persons during
apnoea sleep, not related to any disease process
Biot’s respiration Irregular pattern characterised May be seen with meningitis or severe
by varying depth and rate brain damage
of respirations followed by
periods of apnoea
Ataxic Significant disorganisation A more extreme expression of Biot’s
with irregular and varying respirations indicating respiratory
depths of respiration compromise

Air trapping Increasing difficulty in getting In chronic obstructive pulmonary disease,
breath out air is trapped in the lungs during forced
expiration


tracheostomy, observe the stoma for signs of infection or 3–5 cm during normal deep inspiration (see Figure
1
pressure areas; and observe the type and size of tracheos- 13.13). Asymmetry can occur in pneumothorax, pneumo-
tomy tube, the length at the hub if it is a tracheostomy nia or other lung disorders where inspiration is affected.
with an adjustable flange, and the way in which it is
secured. Palpation of tracheal position is useful to detect a medi-
astinal shift; deviation of the trachea from midline may
Palpation indicate a pulmonary problem. With a large pneumotho-
Palpate the patient’s chest with warm hands, focusing on: rax or after pneumonectomy, the trachea may shift away
28
areas of tenderness, tracheal position, presence of subcu- from the affected side. The presence of subcutaneous
taneous emphysema and tactile fremitus. Assess for sym- emphysema indicates air in the subcutaneous tissue and
metry (left compared to right) and anterior and posterior most commonly occurs in the face, neck and chest after
surfaces (see Figure 13.12). Check the thorax for areas of blunt or penetrating trauma to the chest (e.g. stabbing,
tenderness or bony deformities, and note symmetry of gun shot, fractured ribs); facial fractures; tracheostomy;
chest movement during breathing. Use the palm of your upper respiratory tract surgery; and patients who are
hand to assess skin temperature of the skin, noting for mechanically ventilated. Subcutaneous emphysema feels
clammy, hot or cold skin. To test for chest wall symmetry like crackling under your fingers due to air pockets in the
29
on inspiration, place both hands with thumbs together tissue.
on the patient’s posterior thorax and ask the patient to Palpation is also used to assess for the presence of tactile
take a deep breath. Your thumbs should separate equally (vocal) fremitus, a normal palpable vibration. Place your

338 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





















A B
FIGURE 13.13 Assessment of thoracic expansion. (A) Exhalation;
(B) Inhalation. 1




Practice tip
Prior to performing palpation and auscultation of a patient’s
chest, warm your hands and stethoscope diaphragm before
placing them on their skin.




Practice tip

Prior to use, remember to use an alcohol wipe to clean the
earpieces on the stethoscope to protect you from infection.



Auscultation
Careful interpretation of breath sounds and integration
of this assessment data with other findings can provide
important information about lung disorders. Use the dia-
phragm of the stethoscope and ensure full contact with
the skin for optimal listening. For a spontaneously breath-
ing patient, ask them to breathe through their mouth
(nose breathing may alter the pitch of the breath sounds).
Auscultation is performed in a systematic way so as to
compare the symmetry of breath sounds (see Figure
13.12). Normal breath sounds reflect air movement
through the bronchi, and sounds change as air moves
FIGURE 13.12 Sequence of systematic movements for auscultation and
palpation of the anterior (A) and posterior (B) chest. Comparison of the from larger to smaller airways. Sounds also change when
right and left sides of the chest should be performed by moving from side air passes though fluid or narrowed airways. Breath
to side, beginning proximally and moving distally down the chest wall. sounds therefore differ depending on the area auscul-
Palpation and auscultation of the thorax is performed in a sequential tated; the three general types of normal breath sounds are
fashion.
84
bronchial, bronchiovesicular and vesicular breath sounds
(see Table 13.2).
hands on the patient’s chest and ask the patient to vocalise
repeatedly the term ‘ninety nine’. Fremitus is decreased
(that is, impaired transmission of sounds) in pleural effu-
sion and pneumothorax. Fremitus is increased over those Practice tip
regions of the lungs were transmission is increased (e.g.
22
pneumonia, consolidation). In mechanically ventilated When performing chest inspection and auscultation, check for
patients, fremitus can be detected over the lungs when symmetry between one side of the body with the other.
there are secretions in the airways.

Respiratory Assessment and Monitoring 339

no airflow through that area of the lung and also requires
TABLE 13.2 Normal breath sounds 1 immediate treatment. 22,31

Sound Characteristics
Vesicular Heard over most of lung field; low pitch; soft Practice tip
and short exhalation, and long inhalation.
Respiratory rate is an early warning sign for respiratory distress.
Bronchovesicular Heard over main bronchus area and over If a patient has a high respiratory rate it can be a sign of hypoxia
upper right posterior lung field; medium
pitch; exhalation equals inhalation. as they attempt to compensate for a low PO 2 .
Bronchial Heard only over trachea; high pitch; loud
and long exhalation.
Documentation and Charting
Document the findings of your respiratory assessment in
the patient’s chart; if this is the first respiratory assess-
TABLE 13.3 Description of abnormal breath sounds 1 ment, describe the patient’s respiratory history carefully.
Any abnormal findings including abnormal sounds and
Abnormal their characteristics should be described to enable subse-
Sound Description Condition quent re-assessment. 30
Absent No airflow to Pneumothorax
breath particular Pneumonectomy RESPIRATORY MONITORING
sounds portion of lung Emphysematous blebs
Pleural effusion A thorough and comprehensive assessment, with accurate
Lung mass ongoing monitoring, enables early detection of condition
Massive atelectasis changes and assessment of responses to treatment for a
Complete airway
obstruction critically ill patient. This section describes the main
aspects of bedside respiratory monitoring and the instru-
Diminished Little airflow to Emphysema ments used to assess the efficiency of a patient’s gas
breath particular Pleural effusion
sounds portion of lung Pleurisy transfer mechanisms, including pulse oximetry, capno-
Atelectasis graphy, airway pressures and ventilator waveforms and
Pulmonary fibrosis loops.
Displaced Bronchial sounds Atelectasis with secretions
bronchial heard in Lung mass with exudates PULSE OXIMETRY
sounds peripheral lung Pneumonia
fields Pleural effusion A pulse oximeter is a non-invasive device that measures
Pulmonary oedema the arterial oxygen saturation of haemoglobin in a
patient’s blood flow. The technology is commonly stan-
Crackles Short, discrete Pulmonary oedema
(rales) popping or Pneumonia dard in critical care units and other acute care areas.
crackling sounds Pulmonary fibrosis It is important to note that the device does not provide
Atelectasis information on the patient’s ventilatory state, but it can
Bronchiectasis determine their oxygen saturation and detect hypoxae-
32
Rhonchi Coarse, rumbling, Pneumonia mia. This prompt non-invasive detection of hypoxaemia
low-pitched Asthma enables identification of clinical deterioration and more
sounds Bronchitis rapid treatment to avoid associated complications. 33
Bronchospasm
Pulse oximetry works by emitting two wavelengths of
Wheezes High-pitched, Asthma
squeaking, Bronchospasm light: red and infrared, from a diode (positioned on one
whistling sounds side of the probe) to a photodetector (positioned on the
opposite side) through a pulsatile flow of blood. The
Pleural Creaking, leathery, Pleural effusion
friction loud, dry, coarse Pleurisy signal emitted is measured over five pulses, causing a
rub sounds slight delay when monitoring. Oxygenated blood absorbs
light differently from deoxygenated blood; the oximeter
measures the amount of light absorbed by the vascular
bed and calculates the saturation of oxygen in those
Identify and become familiar with normal breath sounds capillaries.
before beginning to listen and identify abnormal breath
sounds. Abnormal breath sounds are either continuous Measurement of indirect arterial oxygen saturation of the
or discontinuous. Continuous sounds include wheezes peripheral circulation via pulse oximetry is referred to as
and rhonchi, while discontinuous sounds include crack- SpO 2 (the letter ‘p’ denotes peripheral) and is displayed
les (see Table 13.3). Stridor is an abnormal loud high- digitally on the monitor as a percentage, along with heart
pitched breath sound caused by obstruction in the upper rate and a plethysmographic waveform. Interpreting this
airways as a result of a foreign body, tissue swelling or waveform is essential in distinguishing a true oximetry
vocal cord; this emergent condition requires immediate signal from one displaying dampening or artefact (see
30
attention. Absent or diminished breath sounds indicate Figure 13.14). The probe is commonly sited on a finger,

340 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

NORMAL SIGNAL ● Pulse oximeters are relatively reliable when the SaO 2
is 90% or above, however accuracy deteriorates when
33
the SaO 2 falls to 80% or less. When SpO 2 appear
abnormal, assess the ABGs.
● As satisfactory arterial perfusion of the monitoring
area is required, low cardiac output states, vasocon-
striction, peripheral vascular disease and hypothermia
MOTION ARTEFACT can cause inaccurate pulse signals and falsely low
oxygen saturation readings. In these cases, confirm
oxygen saturation with intermittent arterial blood gas
testing.
● As cardiac arrhythmias can impair perfusion and flow,
signal quality may be compromised (see Figure 13.14).
In these cases, use a more central probe (earlobe or
forehead) to improve signal quality.
● Motion artefact (see Figure 13.14) caused by patient
LOW PERFUSION movement or shivering, is a significant cause of erro-
36
neously low readings and false alarms. Keep the
patient warm (if not contraindicated) and encourage
them to minimise movement as this may be a
problem. Using an ear probe may also reduce motion
FIGURE 13.14 Common pulse oximetry waveforms. artefact.
● There is conflicting evidence as to whether nail varnish
36
or acrylic nails interfere with SpO 2 readings. Blue,
but can also be placed on the toe, earlobe or forehead. green and black nail varnishes may affect accuracy of
Change the probe position frequently to maintain ade- readings. To ensure accuracy, it is recommended that
quate perfusion of the site and skin integrity. 32 nail varnish and acrylic nails be removed if possible.
● Dark skin pigmentation can lead to falsely elevated
37
SpO 2 values especially at low saturation levels. A
target SpO 2 level for patients with dark skin should be
Practice tip 95% to account for any over-estimation caused by
pigmentation. 33
In cool environments, wrap the patient’s hand or foot that has
the sensor probe attached; this may improve saturation ● External light, especially fluorescent light and heat
readings. lamps, can lead to an over- or under-estimation of
35
SpO 2 . Covering the probe with an opaque barrier,
such as a washcloth, can prevent this problem.
● Dyshaemoglobins, particularly carboxyhaemoglobin
It is important to understand that pulse oximetry (SpO 2 )
measures peripheral arterial oxygen saturation (SaO 2 ) and methaemoglobin render SpO 2 monitoring unreli-
33
and that this differs from arterial oxygen tension (arterial able. The pulse oximetry sensor cannot differentiate
partial pressure of oxygen; PaO 2 ). Note that SaO 2 and between oxyhaemoglobin, carboxyhaemoglobin and
PaO 2 are physiologically related; this is illustrated by the methaemoglobin, and therefore provides a falsely
35
two axes of the oxyhaemoglobin dissociation curve (see elevated oxygen saturation reading.
Figure 13.9, and the previous Physiology section for more ● Injection of intravenous dyes may lead to a false
discussion). A fit healthy adult (with a normal haemoglo- underestimation of SpO 2 for up to 20 minutes after
bin level) breathing room air has a SpO 2 of 97–99%. 34 their administration (methylene blue, indocyanine
green, indigo carmine). 33

Practice tip
Practice tip
Place the pulse oximeter probe on the finger of the opposite
arm to where blood pressure is being taken, particularly if there Correlate the heart rate reading displayed in the pulse oximetry
is no arterial line and frequent non-invasive BP measurement is section of the monitor to the heart rate calculated by the ECG.
occurring. If they do not correlate, this may indicate that not all pulsations
are being detected and the pulse oximetry reading may not be
accurate.
Limitations of Pulse Oximetry
The limitations of pulse oximetry can be seen as follows: CAPNOGRAPHY
● Pulse oximetry in isolation does not provide all the Capnography monitors expired CO 2 during the respira-
necessary information on ventilation status and acid– tory cycle (also termed end-tidal CO 2 [PetCO 2 ] monitor-
base balance. Arterial blood gas testing is therefore ing) by infrared spectrometry. The percentage of CO 2
also needed to assess other parameters. 35 exhaled at end expiration is displayed on the monitor

Respiratory Assessment and Monitoring 341

Capnography is recommended as a standard component
of respiratory monitoring in intubated and mechanically
41
ventilated patients in the ICU, during transport of a
D
40 critically ill patient and during anaesthesia. 43
42
C
PCO 2 (mm Hg) 20 B VENTILATION MONITORING
Mechanical ventilation is a common intervention in ICU
for patients with respiratory failure or who require respi-
ratory support. Advances in ventilation technology have
led to an increased ability to monitor many ventilator
parameters. A detailed understanding of mechanical ven-
tilation principles and functions enables patient data to
A be interpreted accurately and managed appropriately.
0 Chapter 15 provides a detailed discussion of mechanical
ventilation, including ventilation monitoring, airway
pressures (peak airway pressure, plateau pressure and
Expiration Inspiration positive end-expiratory pressure) and waveforms and
Time loop displays.
FIGURE 13.15 Normal capnogram. A: end inspiration; B: expiratory
upstroke; C: expiratory plateau; D: end-tidal carbon dioxide tension BEDSIDE AND LABORATORY
39
(PetCO 2 ).
INVESTIGATIONS
1
in addition to the waveform, called a capnogram (see Bedside and laboratory investigations add to the informa-
Figure 13.15 and Chapter 15 for waveform analysis and tion available regarding a patient’s respiratory status and
further discussion of PetCO 2 monitoring). Continuous assist in the diagnosis and treatment. This section focuses
capnography detects subtle changes in a patient’s lung on the common investigations used to assess a patient’s
dynamics (i.e. changes to physiological shunting or alveo- respiratory status and their response to treatment: arterial
lar recruitment) and can be measured in both intubated blood gas analysis; blood testing; and sputum and tra-
and non-intubated patients. It can be used to estimate cheal aspirates.
PaCO 2 levels in patients with a normal ventilation-
perfusion ratio (usually 1–5 mmHg less than PaCO 2 ). ARTERIAL BLOOD GASES
However, levels are affected by conditions common in the
critically ill (e.g. low cardiac output states, elevated alveo- Arterial blood gases (ABGs) are one of the most com-
lar pressures, sepsis, hypo/hyperthermia, pulmonary monly performed laboratory tests in critical care, and
embolism), so use PetCO 2 to estimate PaCO 2 levels in accurate interpretation of ABG analysis is therefore an
38
these patients with caution. Investigate any sudden important clinical skill. ABG measurements enable rapid
changes in PetCO 2 levels with arterial blood gas analysis. assessment of oxygenation and ventilation and all ICUs
are recommended to have a blood gas analyser as a
Despite this limitation, PetCO 2 monitoring has many minimum standard. 41
uses in the care of a critically ill patient:
Blood for ABG analysis is sampled by arterial puncture,
● it is the best method of confirming correct ETT place- or more commonly in critically ill patients, from an arte-
ment and maintaining correct positioning of the ETT, rial catheter usually sited in the radial or femoral artery.
ensuring tube patency and detecting leaks or discon- Both techniques are invasive but only allow for intermit-
nection of the circuit tent analysis. The advantage of the arterial catheter is that
● monitoring ventilation status during weaning from it facilitates ABG sampling without repeated arterial
mechanical ventilation and after extubation punctures. Continuous blood gas monitoring is possible
● assessing the effectiveness of cardiopulmonary resus- using fibreoptic sensor in-line with the intra-arterial line
citation compressions and detecting return of sponta- but this practice is yet to have wide application in
neous circulation Australasia due to cost and accuracy concerns. 44,45
● monitoring ventilation continuously during sedation
and anaesthesia Sampling Technique
● assessing ventilation/perfusion status. 40
A correct sampling technique is essential for accurate
results. Approximately 1 mL of arterial blood is collected
anaerobically and aseptically using a premixed syringe
Practice tip containing dry heparin. If drawing the sample from an
intra-arterial line, a portion of blood is discarded to
The capnography monitoring line can fill with condensation, prevent dilution and contamination of the sample by
particularly if the patient has a humidified ventilator circuit. saline present in the flush line. The discard amount is
Regularly check for this and drain or replace the line as neces- twice the dead space volume to ensure clinically accurate
sary, as condensation can interfere with accuracy of readings. ABG and electrolyte measurement and to prevent unnec-
essary blood loss (dead space is defined as the priming
46

342 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 13.4 Arterial blood gas normal values TABLE 13.5 Steps for arterial blood gas interpretation

Blood gas Normal Step Interpretation
measurements Description value 1 Assess oxygenation. PaO 2 < 60 mmHg indicates
Temperature (T) Patient’s body 37°C hypoxaemia.
temperature. Analyser 2 Assess the pH level. <7.36 indicates acidosis, >7.44
defaults to 37°C if not indicates alkalosis.
entered.
3 Assess PaCO 2 level. <35 mmHg indicates respiratory
Haemoglobin Samples should be fully Females:
(Hb) mixed so should be 115–165 g/L acidosis; >45 mmHg indicates respiratory alkalosis.
constantly agitated until Males: 4 Assess HCO 3 level. <22 indicates metabolic acidosis; >32
−
analysed. 130–180 g/L indicates metabolic alkalosis.
Acid–Base status Overall acidity or alkalinity 7.36–7.44 5 Assess pH, CO 2 and HCO 3 . Is there an acid–base
−
(pH) of blood. (36– disturbance and is it fully compensated, partially
44 mmol/L) compensated or uncompensated?
Carbon dioxide Partial pressure of arterial 35–45 mmHg 6 Assess other ABG results. Are they within normal limits
(CO 2 ) CO 2 . A potential acid. (4.7–6 kPa) for the patient?
Oxygen (O 2 ) Partial pressure of O 2 . 80–100 mmHg
Varies with age. (10.7–13.3 kPa)
−
Bicarbonate Standardised HCO 3 (actual 22–32 mmol/L When assessing PaO 2 , hypoxaemia (<60 mmHg) will
−
−
(HCO 3 ) HCO 3 minus the be the most common abnormality, and supplemental
−
HCO 3 produced by oxygen will be required to maintain adequate tissue
respiratory dysfunction) oxygenation. Hyperoxia rarely occurs unless a patient is
estimates true metabolic
function. An alkali or receiving supplemental oxygen therapy. Oxygen can be
base. toxic to cells if delivered at high concentrations for a
48
prolonged period. The pH level is assessed to determine
Base Excess (BE) Measures acid–base −3 to
balance. The number of +3 mmol/L if it falls on the acidic or alkaline side of 7.4.
molecules of acid or On the pH scale of 1–14 (1 = the strongest acid, 14 = the
base required to return 1
litre of blood to the strongest alkali), a pH of 7.4 is the middle of the normal
normal pH (7.4). range. pH measures the acid–base balance of the blood
+
sample, where Hydrogen (H ) ions are the acid and
Oxygen Haemoglobin saturation by 94.5–98.2% −
saturation oxygen in arterial blood HCO 3 is the base or buffer. The body’s acid–base balance
48
(SaO 2 ) is affected by both the respiratory and metabolic systems.
Acidaemia is present with a pH of <7.36; alkalaemia is
present with a pH of >7.44.
volume from sampling port to catheter tip; this differs PaCO 2 is an indicator of the effectiveness of ventilation
depending on the arterial line set up that is used). Arte- in removing CO 2 . CO 2 is a potential acid as it combines
rial blood exerts its own pressure, which is sufficient to with H 2 O in the blood to form carbonic acid (H 2 CO 3 ).
fill the syringe to the required level; active negative pres- Retention of CO 2 (through hypoventilation) leads to
+
sure is to be avoided, as this causes frothing. Any excess increased H resulting in a lower pH, and similarly a
air will also cause inaccurate readings and is expelled loss of CO 2 (through hyperventilation) results in a
49
before the syringe is capped with a hub, which prevents higher pH. A PaCO 2 of >45 mmHg (6 kPa) indicates
further contamination with air. The sample is analysed alveolar hypoventilation, due to chronic obstructive
within 10 minutes if not packed in ice, or within 60 pulmonary disease, asthma, pulmonary oedema, airway
minutes if iced; delays cause degradation of the sample. obstruction, over sedation, narcosis, drug overdose,
Degradation also occurs if the sample is shaken; therefore pain, neurological deficit or permissive hypercapnia in
50
gently roll the syringe/collection tube between your mechanically ventilated patients. Conversely, a PaCO 2
fingers to mix the sample with the heparin and prevent of <35 mmHg (4.7 kPa) reflects alveolar hyperventila-
clotting. 47 tion, and can be due to hypoxia, pain, anxiety, preg-
nancy, permissive hypocapnia in mechanically ventilated
Arterial Blood Gas Analysis patients or as a compensatory mechanism for metabolic
acidosis. 50
ABG analysis includes the measurement of the partial
−
pressure of oxygen in arterial blood (PaO 2 ), the partial Bicarbonate (HCO 3 ) is regulated by the renal system and
−
pressure of carbon dioxide in arterial blood (PaCO 2 ), the indicates metabolic functioning. A HCO 3 of < 22 mmol/L
hydrogen ion concentration of the blood (pH), and the can be caused by renal failure, ketoacidosis, lactic acido-
−
–
chemical buffer, bicarbonate (HCO 3 ). Normal values for sis, diarrhoea, or cardiac arrest. A HCO 3 of >32 can be
ABG parameters are listed in Table 13.4. Use a systematic caused by severe vomiting, continuous nasogastric
approach when interpreting the results of ABG analysis suction, diuretics, corticosteroids, or excessive citrate
(see Table 13.5). administration from stored blood or renal replacement

Respiratory Assessment and Monitoring 343



TABLE 13.6 Arterial blood gas findings for acid–base disturbances

−
pH PaCO 2 (mmHg) HCO 3 (mmHg)
Respiratory acidosis
Uncompensated <7.36 >45 Within normal limits
Partially compensated <7.36 >45 >32
Fully compensated Within normal limits >45 >32
Respiratory alkalosis
Uncompensated >7.44 <35 Within normal limits
Partially compensated >7.44 <35 <22
Fully compensated Within normal limits <35 <22
Metabolic acidosis
Uncompensated <7.36 Within normal limits <22
Partially compensated <7.36 <35 <22
Fully compensated Within normal limits <35 <22
Metabolic alkalosis
Uncompensated >7.44 Within normal limits >32
Partially compensated >7.44 >45 >32
Fully compensated Within normal limits >45 >32



therapy. Base excess is an additional parameter mea- outside of normal limits but not enough to bring pH
50
sured as part of the ABG report and it reflects the excess back to within normal limits
(or deficit) of base to acid in the blood. A positive figure ● in a non-compensated state, the pH will be outside
indicates a base excess (more base than acid; i.e. alkalosis normal limits, and the primary disruption (either CO 2
−
if >+3); a negative figure indicates a base deficit (more or HCO 3 ) will also be outside normal limits while
acid than base i.e. acidosis if >−3). If the base excess is the remaining parameter has not compensated for this
+2 mmol/L, then removal of 2 mmol of base per litre of derangement and has stayed within normal limits.
blood is required to return the pH to 7.4. If the base
excess is −2 mmol/L (i.e. a base deficit), then 2 mmol of It can be difficult to differentiate the patient’s primary
base per litre of blood needs to be added to have a pH problem from their compensatory response. As a quick
of 7.4. Understanding this concept is useful as it can guide, if the CO 2 is moving in the opposite direction to
determine how much treatment is necessary to restore a pH, then the primary disruption is respiratory; if the
−
patient’s pH to normal. 49,51 HCO 3 is moving in the same direction as pH, the disrup-
tion is metabolic. Table 13.6 provides a guide to ABG
52
The final step of interpretation is to examine the pH, CO 2 findings for each acid–base disorder. Other parameters
−
and HCO 3 levels collectively to determine if the patient measured on the ABG sample, such as lactate, electrolytes,
has fully compensated or partially compensated the haemoglobin and glucose, are also considered in deter-
primary dysfunction, or is in an uncompensated state. mining patient status.
With the respiratory system regulating the acid (CO 2 ) and
−
the metabolic system regulating the base (HCO 3 ), resto- Oxygen Tension Derived Indices
ration of normal acid–base balance and homeostasis is
49
possible. The ability of the body to achieve this deter- The alveolar-arterial gradient is a marker of intrapul-
mines whether the imbalance is fully compensated (pH monary shunting (i.e. blood flowing past collapsed areas
returned to normal), partially compensated (pH outside of alveoli not involved in gas exchange). The index is
of normal limits) or uncompensated. To assess compen- calculated as PAO 2 − PaO 2 (PAO 2 is the partial pressure
−
sation, pH, CO 2 and HCO 3 are examined in the context of oxygen in the alveoli). PAO 2 is determined by a
of a patient’s clinical presentation: complex equation, the alveolar gas equation. PAO 2 and
PaO 2 are equal when perfusion and ventilation are
● in a fully compensated state, the pH is returned to perfectly matched. The gradient increases with age but
within normal limits, but the other two parameters a value of 5–15 is normal up until approximately middle
will be outside normal limits as the body has success- age. Despite questions about its clinical usefulness,
−
fully manipulated CO 2 and HCO 3 levels to restore pH particularly in the critically ill, it is used in clinical
53
● in a partially compensated state, the pH is not within practice as a trending tool to track intrapulmonary
normal limits, and the other parameters will also be shunting. Simply put, the larger the gradient between

344 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

PAO 2 and PaO 2 , the larger the degree of intrapulmonary administration of nebulised saline (isotonic or hyper-
58
shunting. 54 tonic) can assist in producing a sample. There is no
evidence to support this for mechanically ventilated
The PaO 2 /FiO 2 ratio was introduced as a simpler way of
estimating pulmonary shunting, even though it does not patients, but anecdotally nebulised normal saline may
formally measure alveolar partial pressure. It remains assist in moistening the airways and thinning secretions
widely used to define ALI or ARDS. A PaO 2 /FiO 2 ratio of to facilitate sputum production. Physiotherapy is often
59,60
<300 indicates ALI and a ratio of <200 indicates ARDS. useful in producing a sputum sample, as manual
For example, for a patient receiving an FiO 2 of 0.65 with hyperinflation and head downtilt during the physiother-
61,62
a PaO 2 of 90 mmHg (12 kPa), their PaO 2 /FiO 2 ratio is apy session has increased sputum production.
138.5, indicating an ARDS state. 55 Instilling normal saline in an endotracheal tube (ETT) to
facilitate clearance of tenacious sputum and obtain a tra-
BLOOD TESTS cheal aspirate remains a controversial issue. There is no
Investigation of haematology and biochemistry values for evidence that instillation facilitates secretion clearance,
a patient with respiratory dysfunction can aid their overall while there is some evidence that it is more uncomfort-
treatment. Full blood count (FBC), including a leukocyte able for a patient and increases the risk of contamination
differential count, can track a patient’s white cell count of the lower airway with bacteria. The practice is therefore
63
(WCC) if they have a confirmed or suspected infective not recommended.
process. When infections are severe, the FBC will show a Nasopharyngeal aspirates (NPA) or nasopharyngeal
dramatic rise in the number of immature neutrophils. swabs (NPS) may be necessary to diagnose viral respira-
Blood cultures can also be drawn to assist in diagnosis tory infections. The NPA is collected by inserting a fine
of bacterial or yeast infections and isolation of the caus- sterile suction catheter (8 or 10 F), attached to a sputum
ative organism. Viral studies may be conducted to aid trap and suction, through the nare and back to the naso-
diagnosis for respiratory infections of unknown origin. pharynx. Suction is applied while withdrawing the cath-
If the patient is suspected of having a pulmonary embo- eter slowly using a rotating motion. Flush the catheter
lism, a D-dimer test can determine the presence of a through to the sputum trap with sterile normal saline or
thrombus. Urea and electrolytes will also be routinely transport medium if available. A NPS is collected by
measured to monitor a patient’s renal function and acid– inserting a specially designed swab to the back of the
base status. 56 nasopharynx and rotating for 5–10 seconds, withdrawing
slowly then placing the swab into the plastic vial contain-
ing transport medium. 64
Practice tip
DIAGNOSTIC PROCEDURES
Monitoring lactate levels is important as this reflects the effec- Assessment and monitoring of the respiratory status of a
tiveness and efficiency of resuscitative therapies. A persistently critically ill patient commonly relies on diagnostic tests,
elevated lactate level is associated with higher morbidity and including various medical imaging tests and bronchos-
poorer patient outcomes.
copy. Data generated through diagnostic procedures are
used to determine the cause of illness, the severity of the
illness episode, relevant comorbidities and the patient’s
SPUTUM, TRACHEAL ASPIRATES AND response to treatment.
NASOPHARYNGEAL ASPIRATES
Colour, consistency and volume of sputum provides MEDICAL IMAGING
useful information in determining changes in a patient’s A range of imaging techniques may be available for sup-
respiratory status and progress. Regular cultures of tracheal porting care of a critically ill patient with a respiratory
sputum facilitates tracking of colonisation by opportunis- dysfunction, depending on the level of broader health
tic organisms, or the identification of the cause of an acute service resources available. This sub-section describes
chest infection or sepsis. Many ICUs have routine surveil- X-ray, ultrasound, computerised tomography, magnetic
lance monitoring (weekly or twice-weekly) of tracheal resonance imaging and ventilation/perfusion scan
aspirates in long-term mechanically-ventilated patients. techniques.
In spontaneously breathing patients, sputum specimens
can be provided into a sterile specimen receptacle. These Chest X-ray
specimens are best collected early in the morning and
assisting the patient to clean their teeth prior to sample Chest X-ray (CXR) is a common diagnostic tool used for
collection prevents secondary contamination. In an intu- respiratory examination of critically ill patients. Chest
bated patient, a sputum sample is collected by suctioning radiography allows basic information regarding abnor-
the artificial airway using a sputum trap between the malities in the chest to be obtained relatively quickly. The
suction catheter and suction tubing. Maintain a sterile image provides information about lung fields and other
technique so that the specimen is not contaminated. 57 thoracic structures as well as the placement of various
invasive lines and tubes. 65,66 In the critically ill ventilated
If obtaining an adequate sputum specimen in non- patient, serial chest X-rays also enable sequential assess-
intubated patients is difficult, there is evidence that ment of lung status in relation to therapy. 66

Respiratory Assessment and Monitoring 345



Trachea


Scapula Clavicle
Vertebrae

Aortic arch
Right main
bronchus Carina
Right hilum Left main
bronchus
Lung Left hilum



Rib Heart
Diaphragm
Gastric air
Costophrenic bubble
angle

Liver Stomach
FIGURE 13.16 Chest X-ray, PA view. Courtesy the University of Auckland Faculty of Medical and Health Sciences.

In-unit X-rays of patients using portable equipment are ● Lobar collapse or atelectasis: The image reveals all or
inferior to those taken using a fixed camera in the radio- some of the following features: loss of lung volume,
logy department. Patient preparation is therefore impor- displacement of fissures and vascular markings, and
tant to optimise the quality of the film. Patients should diaphragmatic elevation on the affected side.
ideally be positioned sitting or semi-erect for this proce- ● Pneumothorax: Check for lack of pulmonary vascular
dure; images using a supine position are less effective at markings on the affected side so the lung field appears
revealing gravity-related abnormalities such as haemo- black; there will be mediastinal and possibly tracheal
thorax. Lateral view chest X-rays can also be taken to view shift away from the affected side in a tension
lesions in the thorax. Film plate location in relation to pneumothorax.
the patient’s thorax determine the view; posterior- ● Pleural effusion: Visualised in the dependent areas of
anterior (PA) has the plate against the patient’s anterior the pleural spaces; costophrenic angles are blunted by
thorax (see Figure 13.16) while the anterior-posterior fluid and there may be a shift of the mediastinum
(AP) view has the plate against the patient’s back surface. away from a large effusion; best visualised with the
For mobile X-rays, the AP view is used. Images from the patient upright, and will only be evident on an AP
AP view magnify thoracic structures and can be less dis- image with 200–400 mL of fluid in the pleural space.
tinct or even distorted, so interpret findings with caution, ● Pulmonary oedema: Lung fields, particularly central
particularly if comparing them with previous PA images. 67 and perihilar areas, appear white; Kerley B lines (small
horizontal lines no more than 2 cm long) may be
present in the lung periphery near the costophrenic
angles.
Practice tip ● Pulmonary embolism: Although not the optimal diag-
nostic tool, areas of infarction may be visualised
When preparing your patient for a chest X-ray, minimise the although these can be mistaken for collapse or
amount of monitoring leads and unnecessary equipment in the consolidation.
CXR field to optimise the image.
● Pneumoperitonium: Free air under the diaphragm
elevates the diaphragm. 66,68
Interpretation of the CXR follows a systematic process Ultrasound
designed to identify common pathophysiological pro-
cesses and location of lines and other items. Table 13.7 Ultrasound imaging (sonography) is a useful bedside diag-
69
provides a comprehensive guideline for viewing and nostic tool for a select group of critically ill patients and
interpreting a CXR. can add to the diagnostic information provided by chest
X-rays and computerised tomography (CT) scanning. The
Common abnormalities that can be detected by CXR technique uses high-frequency sound waves which when
include: probed on the body, reflect and scatter. The advantages are

346 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 13.7 Guide to normal CXR interpretation 65

Item Recommendation
Technical issues ● Check X-ray belongs to correct patient; note date and time of film.
● Ensure you are viewing the X-ray correctly (i.e. right and left markings correspond to thoracic structures).
● Determine whether X-ray was taken supine or erect, and whether PA or AP.
● Check X-ray was taken at full inspiration (posterior aspects of 9th/10th ribs and anterior aspects of 5th/6th ribs should
be visible above diaphragm).
● Note the penetration of the film: dark films are overpenetrated and may require a strong light to view; white films are
underpenetrated; good penetration will allow visualisation of the vertebrae behind the heart.
Bones ● Check along each rib from vertebral origin, looking for fractures.
● Ensure clavicles and scapulas are intact.
Mediastinum ● Check for presence of trachea and identify carina (approximately level of 5th–6th vertebrae).
● Check width of mediastinum: should not be more than 8 cm.
Apex ● Ensure blood vessels are visible in both apices, particularly looking to rule out pneumothoraces that present as clear
black shading on the X-ray. Erect X-rays are essential to facilitate visibility of pneumothoraces.
Hilum ● Check for prominence of vessels in this region: it generally indicates vascular abnormalities such as pulmonary
oedema or pulmonary hypertension, or congestive heart failure.
Heart ● Cardiac silhouette should be not more than 50% of the diameter of the thorax, with 3 of heart shadow to the right of
1
the vertebrae and 3 of shadow to the left of the vertebrae; this positioning helps to rule out a tension pneumothorax.
2
It should be noted that, post-cardiac surgery, if the mediastinum is left open the heart may appear wider than this;
also in AP films this may be the case due to the plate being further away from the heart.
Lung ● Identify the lobes of the lungs and determine if infiltrate or collapse is present in one or more of them. Lobes are
approximately located as follows:
● left upper lobe occupies upper half of lung;
● left lower lobe occupies lower half of lung;
● right lower lobe occupies costophrenic portion of lung;
● right middle lobe occupies cardiophrenic portion of lung;
● right upper lobe occupies upper portion of lung.
Diaphragm ● Check levels of diaphragm: right diaphragm will normally be 1–2 cm above the left diaphragm to accommodate the liver.
Gastric ● Check for pneumoperitoneum and dilated loops of bowel.
Catheters and lines ● Identify distal end of endotracheal tube and ensure above the carina (i.e. not in the right main bronchus).
● Trace nasogastric tube along length and ensure tip is in stomach, or below stomach if nasoenteric tube.
● Check position of intra-aortic balloon pump and ensure it is in the descending thoracic aorta.
● Trace all central catheters and ensure distal tip in correct location.
● Identify other lines (e.g. intercostal catheters, pacing wires) and note location.
PA = posterior-anterior; AP = anterior-posterior.


no need for transport of a critically ill patient outside the renal failure may preclude a patient from receiving con-
ICU, and it is radiation-free. Ultrasound is most useful for trast. CT scanning is useful in the detection and diagnosis
patients with fluid in the pleural space (i.e. pleural effu- of pulmonary, pleural and mediastinal disorders (e.g
sion, haemothorax or empyema), as it provides more pleural effusion, empyema, haemothorax, atelectasis,
73
70
detailed diagnostic information than chest X-rays alone; pneumonia, ARDS). CT pulmonary angiography (CTPA)
it estimates the volume of fluid present, the exact location produces a detailed view of blood vessels and is therefore
of the fluid, and provides a guide for aspirating a fluid- the most definitive method for diagnosing pulmonary
filled area or the placement of chest tubes. 71 embolism. 74
A significant limitation of CT scanning is that the patient
Computed Tomography is transported away from the ICU. Transport usually
Computed tomography (CT) is a diagnostic investigation requires at least two appropriately trained staff to accom-
that provides greater specificity in chest anatomy and pany the patient and involves added risk to the critically ill
pathophysiology than a plain CXR, as it uses multiple patient. Detailed planning by the health care team (includ-
beams in a circle around the body. These beams are ing imaging staff) includes ventilator support, monitoring
directed to a specific area of the body and provide detailed, requirements and maintenance of infusions during the
consecutive cross-sectional slices of the scanned regions. scanning period. See Chapter 6 for discussion of in-hospi-
CT scans can be performed with or without intravenous tal transfers, and Chapter 22 for inter-hospital transport.
72
contrast. Contrast improves diagnostic precision but is Portable CT scanners are available in some centres, but the
used with caution in patients with renal impairment; image quality is inferior to fixed CT scanners. 75

Respiratory Assessment and Monitoring 347

Magnetic Resonance Imaging Fiberoptic bronchoscopy is a relatively safe procedure,
Magnetic resonance imaging (MRI) uses radiofrequency even in critically ill patients, when performed by an expe-
waves and a strong magnetic field rather than X-rays to rienced operator. In mechanically ventilated patients,
provide clear and detailed pictures of internal organs and insertion of the bronchoscope into the artificial airway
76
soft tissues. These high-contrast images of soft tissue are can lead to decreases in tidal and minute volumes result-
81
clearer than those generated by X-ray or CT scans. The ing in decreased PaO 2 and increased PaCO 2 . Serious
strong magnetic field around the scanner means that fer- complications such as bleeding, bronchospasm, arrhyth-
82
romagnetic objects (metallic objects containing material mia, pneumothorax and pneumonia occur rarely.
that can be attracted by magnets, such as iron or steel) Patient preparation pre-procedure may include chest
can become potentially fatal projectiles. MRI scans may X-ray; haemoglobin and coagulation profile, particularly
therefore be unsuitable for patients with implanted pace- if a biopsy is to be performed; arterial blood gases as a
makers, defibrillators or neurostimulation devices; some baseline measurement; and fasting or have feeds ceased
types of intracranial aneurysm clips; and loose dental for 4–6 hours prior.
fillings. The magnetic force can either attract these items Diagnostic indications include further investigation of
and dislodge them from the body or interfere with their poor gas exchange; evaluation of haemoptysis; collection
76
functioning. The strong magnetic fields also have the of specimens (e.g. bronchoalveolar lavage, bronchial
potential to interfere with ventilators, infusion pumps washings, bronchial brushings, lung biopsy) to assist
and monitoring equipment. Similar to CT scans, an MRI in diagnosis of infection, interstitial lung disease, rejec-
requires transport of the critically ill patient. The benefits tion post-lung transplantation and malignancy; and
of the diagnostic data obtained from the MRI is balanced diagnosis of airway injury due to burns, aspiration or
against any potential risk to the patient. 77 chest trauma. Therapeutic indications include removal
of mucous plugs; removal of foreign bodies; treatment
Ventilation/Perfusion Scan of atelectasis; assistance during tracheostomy; airway
The ventilation/perfusion (V/Q) scan is indicated when dilatation and stenting for tracheobronchomalacia and
a mismatch of lung ventilation and perfusion is sus- tracheobronchial stenosis; and lung volume reduction
pected; the most common indication is for pulmonary for emphysema. 79,83
embolism. The ventilation scan is performed with the
patient inhaling a radioisotopic gas to demonstrate ven- SUMMARY
tilation of the lung, while the perfusion scan is performed
using an intravenous radioisotope that reveals distribu- This chapter provided a comprehensive overview of
tion of blood flow in the blood vessels of the lungs. assessment and monitoring of a patient with respiratory
78
These two scans are then compared, with mismatches in dysfunction, to produce relevant data for clinical decision
perfusion and ventilation identified. In larger centres, the making. Acute respiratory dysfunction is a major cause
V/Q scan has been superseded by the use of CT pulmo- for admission to a critical care unit. Whether a primary
nary angiogram (CTPA) for detection of pulmonary or a secondary condition, compromise of the respiratory
embolism. system can lead to a life-threatening situation for a
patient. This chapter outlines related respiratory physio-
logy, pathophysiology, assessment and respiratory moni-
BRONCHOSCOPY toring, bedside laboratory investigations and medical
Bronchoscopy is a bedside technique used for both diag- imaging points. Importantly:
nostic and therapeutic purposes. The bronchoscope can ● Critical care nurses are in a prime position at the
be either rigid or flexible; the most widely used type in beside to provide systematic and dynamic assess-
critical care is the flexible fibreoptic bronchoscope. A flex- ments of a patient’s respiratory status; this includes
ible fibreoptic bronchoscope allows direct visualisation history-taking of past and present respiratory prob-
of respiratory mucosa and thorough examination of the lems, and physical examination of the thorax and
upper airways and tracheobronchial tree. The scope is lungs using inspection, palpation and auscultation
passed into the trachea via the oropharynx or nares. In techniques.
mechanically-ventilated patients, the scope can be passed ● Monitoring a patient’s respiratory function includes
quickly and easily down the endotracheal (ETT) or tra- pulse oximetry, and capnography for a patient with
cheostomy tube (TT) allowing rapid access to the non-invasive or invasive mechanical ventilation; pulse
79
airways. Supplemental oxygen can be administered oximetry provides non-invasive measurement of arte-
during the bronchoscopy in non-intubated patients and rial oxygen saturation of haemoglobin, and is regarded
FiO 2 can be increased in intubated patients. Accurate con- as standard practice in ICU.
tinuous monitoring during the procedure includes con- ● Bedside and laboratory investigations add to available
tinuous pulse oximetry, electrocardiography, respiratory information regarding a patient’s respiratory status
rate, heart rate and blood pressure. Equipment for and assists in the diagnosis and treatment of a criti-
advanced airway management, suctioning, cardiac defi- cally ill patient; this includes arterial blood gas analy-
brillation and advanced life support medications is sis; blood testing; and sputum and tracheal aspirates.
immediately available. In intubated patients, one person ABG is a commonly performed laboratory test, and
80
is responsible for security of the airway as there is a risk ABG interpretation is an important clinical skill for
that it may become displaced during the procedure. critical care nurses.

348 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 several diagnostic tools used for respiratory perfusion scans are more sophisticated devices for
dysfunction in ICU; the chest X-ray is the most patients when high diagnostic skills are needed.
common. Interpretation of a CXR follows a systematic
process designed to identify common pathophysiolog- Careful patient assessment is essential, particularly for
ical processes and locate lines and other items. Bron- respiratory dysfunctions which can be immediately life-
choscopy is a useful bedside diagnostic and therapeutic threatening. Contemporary critical care practice involves
device. Computed tomography provides greater speci- comprehensive clinical assessment skills and use of a
ficity than an X-ray. Ultrasound imaging is a useful range of monitoring devices and diagnostic procedures.
diagnostic tool for patients with fluid in the pleural This challenges a critical care nurse to be adaptable and
space. Magnetic resonance imaging and ventilation/ willing to embrace new skills and knowledge.




Case study

Patricia, a 65-year-old female weighing 82 kg, is admitted to ICU hypoxaemia and uncompensated respiratory acidosis. With her
after a 3-day history of worsening dyspnoea, lethargy, fevers and increasing exhaustion and hypoxia, a decision was made to intu-
a cough productive of yellowish-creamy sputum. She is a non- bate and mechanically ventilate. Patricia’s oxygenation did not
smoker but has a history of mild asthma, and no allergies. Initial improve significantly once mechanically ventilated. Her next arte-
examination by her assigned ICU nurse revealed: rial blood gas on FiO 2 0.8 showed: pH = 7.36, PaCO 2 = 44 (5.9 kPa),
● temperature 38.6 °C PaO 2 = 59 (7.9 kPa), HCO 3 = 22; indicating a normalised acid–base
−
● heart rate 110 beats/min balance but continuing hypoxia. Capnography was commenced to
● blood pressure 110/60 mmHg track her PetCO 2 levels and they remained constant at between
● respiratory rate 36 breaths/min 38–42 mmHg (5–5.6 kPa). A bronchoscopy was performed to visu-
● pulse oximetry 89% on 15 L/min via a non-rebreather oxygen ally inspect and toilet the airway. Marked inflammation of the
mask airways and copious tenacious mucous plugs was evident. The
● use of accessory muscles and nasal flaring evident mucous plugs and sputum were removed and sent for MCS; a
● unable to speak in sentences and appears exhausted bronchoalveolar lavage was performed and sent for viral studies
● auscultation of lung sounds revealed coarse crackles and bron- and MCS; the airways were toileted; and the position of the endo-
chial breathing in the left lower lung area tracheal tube was confirmed.
● chest X-ray demonstrated shadowing of the left lower lobe
with associated loss of the costophrenic angle indicating Patricia’s oxygenation improved after the bronchoscopy. Over the
pleural effusion next 12 hours her oxygen requirements decreased. On day 2 of ICU
admission, MCS showed Streptococcus pneumoniae, therefore cef-
The medical officer ordered an arterial blood gas (after placement triaxone was continued and azithromycin was ceased. Patricia con-
of a radial arterial line); blood cultures to be collected to isolate an tinued to respond well to antibiotics, and subsequent chest X-rays
infective organism; and a sputum specimen for microculture and over the next 3 days showed resolution of her left sided pleural
sensitivity (MCS). Patricia was diagnosed with left lower lobe effusion without intervention and decreased shadowing of the left
Community Acquired Pneumonia (CAP). She was commenced on lower lobe. Patricia was weaned off mechanical ventilation on Day
a broad spectrum intravenous antibiotic regime of azithromycin 4 of ICU admission and was transferred to the respiratory ward on
500 mg twice daily and ceftriaxone 1 g twice daily. Day 5 on 2 L of oxygen and oral antibiotics. She was discharged
from hospital on Day 10.
Her arterial blood gas on admission to ICU showed: pH = 7.3,
−
PaCO 2 = 50 (6.7 kPa), PaO 2 = 52 (7 kPa), HCO 3 = 24, indicating




Research vignette

Hodgson CL, Tuxen DV, Holland AE, Keating JL. Comparison of fore- prospectively compared the accuracy of a forehead reflectance
head Max-Fast pulse oximetry sensor with finger sensor at high sensor (Max-Fast) with a conventional digital sensor in patients
positive end-expiratory pressure in adult patients with acute respi- with acute respiratory distress syndrome during a high positive end-
ratory distress syndrome. Anaesthesia and Intensive Care 2009; 37: expiratory pressure (PEEP) recruitment manoeuvre (stepwise
953–60. recruitment manoeuvre). Sixteen patients with early acute respira-
tory distress syndrome were enrolled to evaluate the blood oxygen
Abstract saturation during a stepwise recruitment manoeuvre. PEEP was
In the critical care setting it may be difficult to determine an accu- increased from baseline (range 10–18) to 40 cmH 2 O, then decreased
rate reading of oxygen saturation from digital sensors as a result of to an optimal level determined by individual titration. Forehead
poor peripheral perfusion. Limited evidence suggests that fore- and digital oxygen saturation and arterial blood gases were mea-
head sensors may be more accurate in these patients. We sured simultaneously before, during and after the stepwise

Respiratory Assessment and Monitoring 349



Research vignette, Continued
recruitment manoeuvre at five time points. Seventy-three samples For analysis, data from the arterial blood sample SaO 2 was consid-
were included for analysis from 16 patients. The SaO 2 values ranged ered the ‘gold standard’, and compared to the forehead and the
from 73–99.6%. The forehead sensor provided measurements that finger sensor SpO 2 values. Each patient was used as their own
deviated more from arterial measures than the finger sensor (mean control for the five different measures: baseline, SRM at maximum
absolute deviations 3.4%, 1.1% respectively, P = 0.02). The greater PEEP, end of SRM, 30 and 60 minutes after SRM. A repeated mea-
variability in forehead measures taken at maximum PEEP was sures T test was used to assess for systematic differences on each
reflected in the unusually large precision estimates of 4.24% associ- of the five measurement points. Bland-Altman analysis was used
ated with these measures. No absolute differences from arterial to illustrate differences between forehead or finger sensors and the
measures taken at any other time points were significantly differ- gold standard SaO 2 . This analysis is an alternative to correlation
ent. The finger sensor is as accurate as the forehead sensor in coefficients which can be misleading, as correlation measures the
detecting changes in arterial oxygen saturation in adults with strength of relation between two variables but not the agreement
acute respiratory distress syndrome and it may be better at levels between them. Bland-Altman analysis is based on graphic tech-
of high PEEP such as during recruitment manoeuvres. niques and simple calculations (see Further reading). This paper
presents easily comprehensible figures demonstrating the differ-
Critique ences between forehead and finger sensors, and arterial blood
Critical care nurses often have to manage different monitoring oxygen saturation.
equipment, and patient safety is reliant on the function and preci- The study authors examined for measurement bias (systematic
sion of devices. This study compared forehead and finger sensors measurement differences between finger or forehead sensor and
in pulse oximetry in the ICU. Pulse oximetry is standard equipment ‘gold standard’). A small but statistically significant difference was
for assessing respiratory status and finger sensors are the most noted when comparing finger sensor SpO 2 and SaO 2 ; however this
common probe to measure oxygen saturation SpO 2 in critically ill was less than 1% and not considered clinically significant. Of note,
adults. Use of forehead sensors is a new technique believed to be there was a significant difference between the forehead and finger
less vulnerable to peripheral vasoconstriction and motion artifact sensor at maximum PEEP (40 cmH 2O); the forehead sensor devi-
than the finger sensor. The authors described that comparisons ated more in measurement from the SaO 2 than the finger sensor.
between these two sensors were previously conducted in studies There was also drop-out of signal from one patient with the finger
during anaesthesia, mechanical ventilation and low cardiac index. sensor at maximum PEEP level; the authors discussed that this
In the present study the probes were tested in patients with ARDS indicates that the equipment may not be reliable under all circum-
while a stepwise recruitment manoeuvre (SRM) was performed. stances. When comparing forehead and finger sensor saturation at
The SRM using high PEEP may cause a reduced cardiac output (CO) more routine PEEP levels, the differences were within an accept-
and damped arterial waves due to the subsequent high intratho- able range. Patients with any compromise in heart rate, blood pres-
racic pressure. For this reason it was relevant to compare the finger sure, arrhythmia or SpO 2 (<85%) during SRM were withdrawn.
sensor that influenced arterial waves with a forehead sensor that There was no discussion whether some patients had any of these
would remain unaffected.
complications; the authors described that 7 samples were not
This single-site prospective consecutive study included 16 included in the analysis due to low reliability of signals at maximum
mechanically ventilated (MV) adult patients with early ARDS; ven- PEEP.
tilation was pressure-controlled with different levels of PEEP. All
patients had a radial arterial line with invasive blood pressure For the primary outcome measure, finger sensors were more accu-
monitoring, and a central venous catheter. Excluded patients were rate than the forehead sensors at high PEEP levels during SRM. The
those with pneumothorax, intercostal catheter with air leak, bro- study demonstrated that the hypothesis – the newer forehead
chospasm, acute pulmonary oedema, raised intracranial pressure, sensor could measure oxygen saturation better – was not sup-
arrhythmia or mean arterial pressure (MAP) below 60 mmHg. The ported. The study did have a small sample, and these findings
authors did not indicate that any next of kin declined participation therefore need to be evaluated in a larger trial. This study can be
for the patient, and there was no explanation as to why only 16 seen as a pilot study; a common and appropriate way of creating
patients were included in the study. The demographic data dem- evidence for a larger trial. Also note that these results only relate
onstrated a good mix of patients in the ICU of different age, gender, to a certain brand of equipment; this could have been discussed
and diagnosis, although there was no detail about the sampling further.
procedure. It was not clear whether measurements of SaO 2 and Overall, this small but well-conducted study is an important con-
SpO 2 were gathered by the same data collector. Each patient was tribution to understanding the precision and reliability of new
tested on five different occasions (73 measures in total; seven were equipment, and reflects clinical practice in ICU. This study comple-
excluded due to equipment failure). Post-hoc sample size calcula- ments information provided in this chapter, and highlights
tions indicated that with a probability of 85% the study would potential measurement bias with equipment. Nurses need to
detect a treatment difference at 5% significance level if the true be confident in clinical information provided by monitoring
difference between the means was 2%; this makes the study find- equipment, to ensure that the assessment and monitoring of a
ings trustworthy. patient is not compromised nor their safety threatened.

350 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



Learning activities
1. When assessing a patient, what do the findings of accessory 5. What indicates uncompensated respiratory acidosis in Patri-
muscle use and nasal flaring indicate? cia’s first ICU arterial blood gas?
2. Describe what coarse crackles and bronchial breathing sound 6. What are the pathophysiological mechanisms behind Patricia’s
like and the pathophysiological mechanisms behind these hypoxia?
added lung sounds. 7. What monitoring is necessary when performing a
3. Outline the correct sampling technique for drawing an arterial bronchoscopy?
blood gas.
4. In relation to the case study, using Patricia’s first ICU arterial
blood gas data as a guide, what are the key variables to note
when interpreting arterial blood gases?




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Respiratory Alterations
14 and Management







Maria Murphy
Sharon Wetzig
Judy Currey




1
required mechanical ventilation; a statistic of 41% in
2
Learning objectives 2008. Failure or inadequate function of the respiratory
system occurs as a result of direct or indirect pathophysio-
After reading this chapter, you should be able to: logical conditions. The process of mechanical ventilation
● describe the pathophysiological mechanisms of acute may also injure a patient’s lungs, further impacting func-
respiratory failure (ARF) and key principles of patient tioning of the respiratory system. Preventing or minimis-
management ing ventilator-associated lung injury is therefore also a
● differentiate between hypoxaemic (type I) and primary goal of patient care. Chapter 13 described the
hypercapnoeic (type II) respiratory failure relevant anatomy and physiology and assessment and
● outline the incidence of respiratory alterations in the monitoring practices for a patient with life-threatening
Australasian critical care context respiratory dysfunctions. This chapter describes the
● discuss the aetiology, pathophysiology, clinical incidence, pathophysiology, clinical manifestations and
management of common respiratory disorders that result
manifestations and management of common respiratory in acute respiratory failure, specifically pneumonia
disorders managed in intensive care, specifically (including discussion of respiratory epidemics), asthma,
pneumonia, respiratory epidemics, asthma, chronic chronic obstructive pulmonary disease (COPD), acute
obstructive pulmonary disease (COPD), acute lung injury lung injury (ALI), pneumothorax and lung transplanta-
(ALI) and pneumothorax tion. Discussion of oxygenation and ventilation strategies
● describe the evidence base for key components of nursing to support respiratory function during a critical illness is
and collaborative practice involved in the management of presented in Chapter 15.
patients with ARF in ICU
● outline the principles and immediate postoperative
management for lung transplant recipients. INCIDENCE OF RESPIRATORY
ALTERATIONS
Respiratory diseases are common and affect significant
numbers of the population in Australia, accounting for
3
Key words almost half of all hospital admissions. These diseases are
also the most common illness responsible for emergency
admission to hospital, the most common reason to visit
acute respiratory failure a general practitioner and represent the most commonly
acute respiratory distress syndrome reported long-term illnesses in children. Despite these
4
hypoxaemic respiratory failure findings, the incidence of respiratory alterations is diffi-
hypercapnoeic respiratory failure cult to quantify as the number of patients who require
influenza admission to hospital as a result of respiratory disease
oxygenation represent a small proportion of the total number affected.
ventilator-associated pneumonia Further, patients who require admission to ICU as a result
of respiratory disease represent only a fraction of all hos-
pital admissions. 5,6
7
INTRODUCTION Data presented in Table 14.1 illustrates the total number
of patients (adults and children) admitted to hospital as
The most common reason that patients require admis- a result of a range of respiratory diseases. While it is dif-
sion to an intensive care unit (ICU) is for support of their ficult to determine the number of patients in each diag-
respiratory system. Over the last decade, almost half of nostic group who required admission to ICU as part of
352 all patients admitted to ICU in Australia and New Zealand their management, ICU admissions account for around

Respiratory Alterations and Management 353

● increased metabolic oxygen requirements may be
TABLE 14.1 Incidence of respiratory alterations caused by severe sepsis
in Australia 2007–2008 7 ● decreased capacity for gas exchange may be caused by
impairment in either ventilation (e.g. pulmonary
Hospital admissions oedema, pneumonia, acute lung injury, COPD) or
pulmonary perfusion (e.g. pulmonary embolism), or
Disorder n % a combination of the two.
Adult Respiratory Distress Syndrome 202 0.06
Importantly, respiratory failure can be an acute or chronic
Asthma 37,641 10.40 condition. While acute respiratory failure (ARF) is char-
COPD (acute exacerbation) 56,249 15.54 acterised by life-threatening alterations in function, the
manifestations of chronic respiratory failure are more
Influenza and pneumonia 70,232 19.41
subtle and potentially more difficult to diagnose. Patients
Lung transplantation 91 0.03 with chronic respiratory failure often experience acute
Pneumothorax 3,177 0.88 exacerbations of their disease, also resulting in the need
for intensive respiratory support. 6
Pulmonary embolus 9,234 2.55
Pulmonary oedema 902 0.25 PATHOPHYSIOLOGY
Total 177,728 49.11 Respiratory failure occurs when the respiratory system
fails to achieve one or both of its essential gas exchange
functions: oxygenation or elimination of carbon dioxide,
5
4% of all overnight hospital admissions. Infective pro- and can be described either as type I (primarily a failure
cesses (influenza and pneumonia), COPD and asthma of oxygenation) or type II (primarily a failure of
6
represent the three largest groups of hospital admissions. ventilation).
Conditions such as adult respiratory distress syndrome
(ARDS), pneumothorax, pulmonary embolus and pul- Type I Respiratory Failure
monary oedema are relatively small. It should be noted, A patient with type I (‘hypoxaemic’) respiratory failure
however, that these conditions often evolve throughout presents with a low PaO 2 and a normal or low PaCO 2 .
the course of an illness and may not therefore be included Hypoxaemic respiratory failure may be caused by
6
as the reason for admission. Common respiratory-related a reduction in inspired oxygen pressure (e.g. such as
ICU presentations are discussed in the following extreme altitude), hypoventilation, impaired diffusion or
sections. ventilation-perfusion mismatch. Most major respiratory
alterations cause this type of failure, usually as a result of
RESPIRATORY FAILURE hypoventilation due to alveolar collapse or consolida-
tion, or a perfusion abnormality. 6
Respiratory failure occurs when there is a reduction in the
body’s ability to maintain either oxygenation or ventila- When there is mismatch between ventilation and perfu-
tion, or both. It may occur acutely, as observed in pneu- sion in the lungs, exchange of gases is impaired and
monia and ARDS or it may exist in chronic form, as hypoxaemia ensues (see Figure 14.1): 6
observed in asthma and COPD. Respiratory failure, and ● In some cases, there may be reduced ventilation to a
the disorders that cause it, are responsible for a high certain area of lung tissue (e.g. pulmonary oedema,
proportion of death and disability throughout the world. 6
pneumonia, atelectasis, ARDS). A severe form of
AETIOLOGY OF RESPIRATORY FAILURE mismatch known as intrapulmonary shunting occurs
when adequate perfusion exists but there are sections
For the respiratory system to function effectively, the rate of lung tissue that are not ventilated. In these alveoli,
and depth of breathing is controlled by the brain, the the oxygen content is similar to that of the mixed
chest wall must expand adequately, air needs to flow venous blood and the CO 2 is elevated.
easily through the airways and effective exchange of gases ● In other instances, ventilation may be adequate but
needs to occur at the alveolar level. Conditions that perfusion is impaired (e.g. pulmonary embolus). In
impact on one or more aspects of the normal physiologi- its severe form, this is known as dead space ventilation
cal functioning of the respiratory system can cause respi- as the lungs continue to be ventilated but there is no
ratory failure, for example: perfusion, and therefore no gas exchange. In this situ-
ation, the alveolar oxygen content is similar to that of
● decreased respiratory drive may be caused by brain 6
trauma, drug overdose or anaesthesia/sedation the inspired gas mixture and the CO 2 is minimal (see
● decreased respiratory muscle strength may be caused Chapter 13 for further discussion).
by Guillain–Barré syndrome, poliomyelitis, myasthe-
nia gravis or spinal cord injury Type II Respiratory Failure
● decreased chest wall expansion may be caused by Conversely, a patient with Type II respiratory
postoperative pain, rib fractures or a pneumothorax (‘hypercapnoeic/hypoxaemic’) failure presents with a
● increased airway resistance may be caused by asthma high PaCO 2 as well as a low PaO 2 . This failure is caused
or COPD by alveolar hypoventilation, where the respiratory effort

354 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

Pure
shunt
V/Q = 0
52
Alveolar PCO 2 (mmHg) Decreasing V/Q Normal V/Q space


Pure
dead

Increasing V/Q
V/Q = ∞



0
45 150
Alveolar PO 2 (mmHg)
6
FIGURE 14.1 Ventilation-perfusion mismatches. Ventilation-perfusion (V/Q) ratio displays the normal balance (star) between alveolar ventilation and
vascular perfusion allowing for proper oxygenation. When ventilation is reduced, the V/Q ratio decreases, in the most extreme case resulting in pure shunt,
where V/Q = 0. When perfusion is reduced, the V/Q ratio increases, in the most extreme case resulting in pure dead space, where V/Q = infinite (∞).
(published with permission)




(or minute ventilation) is insufficient to allow adequate
exchange of oxygen and carbon dioxide. This may be Practice tip
caused by conditions that affect respiratory drive such as
neuromuscular diseases, chest wall abnormalities or Respiratory failure:
severe airways disease (e.g. asthma or COPD).
Type I (‘hypoxaemic’) = low PaO 2 and normal or low PaCO 2
CLINICAL MANIFESTATIONS Type II (‘hypercapnoeic’) = high PaCO 2 and low PaO 2
Patient presentations in acute respiratory failure can
be quite diverse and are dependent on the underlying
pathophysiological mechanism (e.g. hypercapnoea and/
or hypoxaemia), the specific aetiology and any comor-
bidities that may exist. Specific clinical manifestations
6
for the clinical disorders discussed in this chapter INDEPENDENT NURSING PRACTICE
are provided in each section. Dyspnoea is the most The primary survey (airway, breathing and circulation)
common symptom associated with ARF; this is often and immediate management form initial routine prac-
accompanied by an increased rate and reduced depth of tice. Frequent assessment and monitoring of respiratory
10
breathing and the use of accessory muscles. Patients may function, including a patient’s response to supplemental
also present with cyanosis, anxiety, confusion and/or oxygen and/or ventilatory support, is the focus. Patient
sleepiness. 4 comfort and compliance with the ventilation mode, ABG
A systematic approach to clinical assessment and analysis and pulse oximetry guide any titration of ventila-
management of patients with ARF is crucial, given the tion. The key goals of management are to treat the
large number of possible causes. Clinical investigations primary cause of respiratory failure, maintain adequate
to assess the cause of respiratory failure vary depending oxygenation and ventilation and prevent or minimise the
on the suspected underlying aetiology and the pro- potential complications of positive pressure mechanical
gression of disease. Continuous monitoring of oxygen ventilation.
saturation using pulse oximetry, arterial blood gas (ABG)
analysis and chest radiograph assessment are used in Maintaining Oxygenation and Ventilation
8
almost all cases of respiratory failure. Other more spe- The therapeutic aim is to titrate the fraction/percentage
cialised tests such as computed tomography (CT) of the of inspired oxygen (FiO 2 ) to achieve a PaO 2 of 65–
chest and microbiological cultures may be used in 70 mmHg and to maintain minute ventilation to achieve
6
9
specific circumstances. With ABG analysis, the measure- PaCO 2 within normal limits where possible. Oxygen is
ment of PaO 2 , PaCO 2 , Alveolar–arterial (A–a) PO 2 dif- not a drug, therefore it does not require prescription for
ference and the patient response to supplemental oxygen use. Nursing staff in ICU are therefore commonly respon-
are key elements in determining the cause of ARF (see sible for titration of oxygen therapy to maintain a specific
Chapter 13). PaO 2 or SpO 2 , and the alteration of respiratory rate and/

Respiratory Alterations and Management 355

or tidal volume to maintain a specified PaCO 2 . One method should be considered for all ventilated patients.
concern that often arises, particularly with patients who The approach may result in tolerance of higher PaCO 2
require high concentrations of oxygen, is the risk of than normal in patients presenting with acute lung
oxygen toxicity. The link between prolonged periods of injury or ARDS (see Chapter 15 for further
oxygen concentrations approaching 100% and oxidant discussion).
injuries in airways and lung parenchyma has been estab- Development of ventilator-associated respiratory muscle
lished, although mostly from animal research. Although weakness has been reported as a significant issue when
it remains unclear how these data apply to human popu- the respiratory muscles are rendered inactive through
lations, most consensus groups have argued that FiO 2 adjustment of ventilator settings and administration of
values less than 0.4 are safe for prolonged periods of time pharmacotherapy. While it is not yet possible to provide
and that FiO 2 values of greater than 0.8 should be avoided precise recommendations for interventions to avoid this,
6
if possible (see Chapter 15 for further discussion of clinicians are advised to select ventilator settings that
oxygenation). provide for some respiratory muscle use. 11
Ventilator-associated lung injury is also a concern when Prevention or minimisation of complications associated
managing patients with acute respiratory failure. A lung with positive pressure mechanical ventilation remains a
can be injured when it is stretched excessively as a major focus of nursing practice. These complications may
result of tidal volume settings that generate high pres- relate to the patient–ventilator interface (artificial airway
sures, often referred to as barotrauma or volutrauma. and ventilator circuitry), infectious complications such
The most common injury is that of alveolar rupture as ventilator-associated pneumonia (VAP) or complica-
6
and/or air in the pleural space (pneumothorax). An tions associated with sedation and/or immobility. Some
approach known as ‘lung protective ventilation’ aims common complications and the appropriate manage-
to minimise overdistension of the alveoli through careful ment strategies are briefly outlined in Table 14.2 6,12-14 and
monitoring of tidal volumes and airway pressures. This discussed further in Chapter 15.





TABLE 14.2 Complications of mechanical ventilation and associated management strategies

Patient–ventilator interface complications
Airway dislodgement/disconnection Endotracheal tube (ETT) or tracheostomy tube is secured to optimise ventilation and prevent
airway dislodgement or accidental extubation.
Circuit leaks Cuff pressure assessment
Circuit checks
Exhaled tidal volume measurement
Airway injury from inadequate heat/humidity Maintain humidification of the airway using either a heat-moisture exchanger or a water-bath
humidifier.
Obstructions from secretions Assess the need for suctioning regularly and suction as required.
Tracheal injury from the artificial airway Assessment of airway placement and cuff pressure (minimal occlusion method)
Infectious complications
Ventilator-associated pneumonia (VAP) Hand washing
Appropriate antibiotic therapy
Ventilator Care Bundle:
● Elevating head of bed to 30–45 degrees
● Daily sedation vacation and assessment of readiness to extubate
● Peptic ulcer disease prophylaxis
● Deep vein thrombosis prophylaxis
Minimising interruptions to ventilator circuit (e.g. closed suctioning technique)
Drainage of sub-glottic secretions
Aerosolised antibiotics for patients who are colonised
Weaning and discontinuation of ventilatory support as soon as possible
Nurse-led weaning protocols
Complications associated with immobility/sedation
Gastrointestinal dysfunction Prokinetic medication
Constipation – bowel therapy regimen
Muscle atrophy Passive limb movements, foot splints (see Chapter 6) and early activity/mobility (see Chapter 4)
Pressure ulcers Pressure-relieving mattresses, regular repositioning
Assessment of risks and management of any pressure ulcers by wound care specialists,
nutrition advice

356 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

COLLABORATIVE PRACTICE of medications will vary depending on the underlying
A patient with ARF requires extensive multidisciplinary cause of respiratory failure, these are discussed in each
collaboration between nurses, physiotherapists, specialist section respectively.
medical staff, speech and occupational therapists, dieti-
tians, social workers, radiologists and radiographers. SPECIAL CONSIDERATIONS
Patients may require additional oxygen delivery through Respiratory failure in patients who are pregnant, elderly
an adequate haemoglobin level for oxygen transportation or have comorbidities require specific attention to avoid
and a cardiac output sufficient to supply oxygenated clinical deterioration. Respiratory physiology and the
6
blood to the tissues. At times this may require blood respiratory tract itself are altered during pregnancy; this
transfusion and/or the use of vasoactive medications (see may result in exacerbation of preexisting respiratory
Chapters 11 and 20). disease or increased susceptibility to disease (see Chapter
26). Upper airway mucosal oedema may increase the
Chest physiotherapy is a routine activity for managing likelihood of upper respiratory tract infection. Lung func-
patients with ARF. This involves positioning, manual tion and lung volume are also altered, compensated by
hyperinflation, percussion and vibration and suctioning. an increase in respiratory drive and minute ventilation.
The evidence base for these techniques is limited, however, The impact of these alterations on chronic conditions
with a systematic review not demonstrating an improve- such as asthma/COPD and acute illness are explored
12
ment in mortality. Guidelines for physiotherapy assess- in the subsequent sections. The impact on the fetus of
ment have enabled identification of patient characteristics infection, hypoxia and drug therapy is an important
for treatments to be prescribed and modified on an indi- consideration. 6
13
vidual basis. Table 14.3 6,13,15 outlines a number of col-
laborative practice issues for patients with respiratory The elderly have ageing organs and systems and other
failure, particularly those who may require prolonged comorbidities that may exacerbate their respiratory dys-
mechanical ventilation. function. Drug metabolism and excretion is slowed, com-
16
plicating drug dosing and response. Metabolism of
Medications anaesthetic agents is slower due to the diminished physio-
logy of ageing organs. Common comorbidities may also
Medications commonly prescribed in respiratory failure be present, including obesity, heart disease, diabetes, and
include inhalation steroids and bronchodilators, intrave- renal impairment or muscle wasting. Pneumonia is a
nous steroids and bronchodilators, antibiotic therapy, common presentation in the elderly and is often exacer-
analgesia and sedation to maintain patient–ventilator bated by chronic lung conditions. 6
synchrony, but may also involve nitric oxide, glucocorti-
coid or surfactant administration. A patient’s condition, Comorbidities add to the complexity of managing a
comorbidities and the above-mentioned pharmacologi- patient’s primary condition and increase the risk of addi-
cal therapy may also be supported with inotropic and tional organ dysfunction or failure. Chronic respiratory
other resuscitation therapies (see Chapter 11). As the use conditions can have a significant impact on the severity




TABLE 14.3 Collaborative practices for patients with respiratory failure

Long-term patient management Best practice
Timing of tracheostomy insertion Where mechanical ventilation is expected to be 10 days or more, tracheostomy should be
performed as soon as identified. Early tracheostomy is associated with less nosocomial
pneumonia, reduced ventilation time and shorter ICU stay.
Weaning protocols Specific plan is patient dependent; better outcomes are achieved when there is an agreed and
well communicated weaning plan (see Chapter 15)
Nutrition Consider adequate nutrition for physiological needs – important to not overfeed as this increases
CO 2 production and need to have balance of vitamins and minerals
Swallow assessment Assess for dysphagia
Mobilisation Sitting out of bed, mobilising (see Chapter 4)
Communication Communication aids, speaking valves
Activities Activity plan/routine, entertainment (TV/Films), visitors, outings
Sleep Clustering cares, reducing stimuli to promote sleep (see Chapter 7)
Family support Importance of providing physical, emotional and/or spiritual support to family members (see
Chapter 8)
Tracheostomy follow-up Outreach team: follow-up care by nurses experienced in tracheostomy care can prevent
complications and improve outcomes
End-of-life decisions in ARF see Chapter 5

Respiratory Alterations and Management 357

of respiratory infections, while cardiovascular and renal prevent microorganisms entering the lungs, such as par-
disease impact on disease severity and the management of ticle filtration in the nostrils, sneezing and coughing to
many respiratory alterations. Other factors such as smoking expel irritants and mucus production to trap dust and
and alcohol use, living conditions and lifestyle impact infectious organisms and move particles out of the respi-
on the predisposition and clinical course of an illness. ratory system. Infection occurs when one or more of
these defences are not functioning adequately or when
Post-anaesthesia Respiratory Support an individual encounters a large amount of microorgan-
6
Short-term respiratory support may be required after isms at once and the defences are overwhelmed. An
major surgery, in cases of extended anaesthesia, preexist- invading pathogen provokes an immune response in the
ing comorbidities and/or diminished physical reserve lungs, resulting in the following pathophysiological
(e.g. elderly, patients with obstructive sleep apnoea). processes:
Most patients requiring ventilation in the early post- ● alteration in alveolar capillary permeability that leads
operative period have had cardiothoracic surgery, and so to an increase in protein-rich fluid in the alveoli; this
much of the available research relates to this patient impacts on gas exchange and causes the patient to
group (see also Chapter 12). breathe faster in an effort to increase oxygen uptake
Preoperative assessment and management is a key factor and remove CO 2
in preventing respiratory complications. This involves ● mucous production increases and mucous plugs may
optimising physical condition and nutritional status, develop which block off areas of the lung, further
planning the timing of surgery to reduce the likelihood reducing capacity for gas exchange
of preexisting respiratory infection and patient education ● consolidation occurs in the alveoli, filling with fluid
regarding the importance of respiratory support, includ- and debris; this occurs particularly with bacterial
ing postoperative mobilisation and physiotherapy. pneumonia where debris accumulates from the large
Patients with suspected or confirmed chronic conditions number of white blood cells involved in the immune
6
require a thorough diagnostic work-up prior to surgery to response.
determine the best management strategy in the post-
operative period. 17 AETIOLOGY
Pneumonia is caused by a variety of microorganisms,
The key focus in management of postoperative ventilation including bacteria, viruses, fungi and parasites. In many
is to limit ventilation time, as prolonged ventilation time cases, the causative organism may not be known and
is associated with poor outcome. Once a patient has current practice in many cases is to initiate antimicrobial
reached normothermia, is haemodynamically stable, treatment as soon as possible, based on symptoms and
responsive and has adequate analgesia, weaning of venti- patient history, rather than waiting for microorganism
lation is commenced. Rapid and/or nurse-led weaning culture results. The true incidence of pneumonia is not
19
protocols are often implemented to minimise delays in well known as many patients do not require hospitalisa-
the weaning process. Anaesthetic care in these patients tion. Different ages and characteristics of the patient are
includes use of short-acting or regional anaesthesia (e.g. often associated with different causative organisms. Viral
epidural analgesia) to minimise respiratory depression. 18
pneumonias, especially influenza, are most common in
young children, while adults are more likely to have
PNEUMONIA pneumonia caused by bacteria such as Streptococcus
pneumoniae and Haemophilus influenzae. Pneumonia is a
Pneumonia is infection of the lung. Depending on the
type and severity of the infection and the overall health particular concern among elderly adults as they experi-
of the person, it may result in ARF. Pneumonia can be ence an increase in the frequency and severity of
6
caused by most types of microorganisms, but is most pneumonia.
commonly a result of bacterial or viral infection. In criti- Table 14.4 outlines the principal diagnoses of patients
7
cal care the key distinctions in assessing and managing a hospitalised with pneumonia in Australia during 2007–
patient with pneumonia relate to the specific aetiology or 2008. This information reflects the high proportion of
causative organism. This section reviews the aetiology, viral pneumonia and the large number of cases where the
pathophysiology, clinical presentation and management causative organism may not be known.
of two types of pneumonia:
● community-acquired pneumonia (CAP) Community-acquired Pneumonia
● ventilator-associated pneumonia (VAP) Clinical assessment, especially patient history, is impor-
tant in distinguishing the aetiology and likely causative
The issue of epidemic or pandemic respiratory disease as
a result of viral infections is included in the following organism in patients with community-acquired pneumo-
Respiratory pandemics section. nia (CAP). Specific information regarding exposure to
animals, travel history, nursing home residency and any
occupational or unusual exposure may provide the key
PATHOPHYSIOLOGY to diagnosis. Personal habits such as smoking and
9
The normal human lung is sterile, unlike the gastrointes- alcohol consumption increase the risk of developing
tinal tract and upper respiratory tract which have resident pneumonia and should be explored. Many patients
bacteria. A number of defence mechanisms exist to admitted to hospital or ICU with CAP have

358 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

recommended systems that produce scores and assess
TABLE 14.4 Principal diagnoses of patients severity based on patient demographics, risk factors,
hospitalised with pneumonia in Australia comorbidities, clinical presentation and laboratory
6
during 2007–2008 results. Recent evaluation found no significant differ-
ences between these systems in their ability to predict
24
Hospitalisations mortality. The Australian CAP Collaboration team
devised and validated the SMART-COP scoring system for
Principal Diagnosis n % predicting the need for intensive respiratory or vasopres-
Pneumonia due to identified influenza 1668 2.4 sor support in patients with CAP. The acronym relates to
virus the factors: low Systolic blood pressure, Multilobar chest
Influenza, virus not identified 1429 2.0 radiography involvement, low Albumin level, high Respi-
ratory rate, Tachycardia, Confusion, poor Oxygenation
Viral pneumonia, not elsewhere classified 1899 2.7 25
and low arterial pH.
Pneumonia due to Streptococcus 1331 1.9
pneumoniae Hospital-acquired and Ventilator-associated
Pneumonia due to Haemophilus 1029 1.5 Pneumonia
influenzae
Hospital-acquired or nosocomial pneumonia is defined
Bacterial pneumonia, not elsewhere 3184 4.5
classified as pneumonia occurring more than 48 hours after hospi-
tal admission. It is the second-most common noso-
9
Pneumonia due to other infectious 292 0.4 comial infection and the leading cause of death from
organisms, not elsewhere classified
infection acquired in-hospital. Ventilator-associated
Pneumonia, organism unspecified 59,389 84.6 pneumonia (VAP) is a nosocomial pneumonia in patients
Total 70,232 100.0 who are mechanically ventilated. The incidence of VAP is
reported at 10–30% among patients who require mechan-
ical ventilation for greater than 48 hours. 26

Critically ill ventilated patients commonly experience
comorbidities, suggesting that those who are chronically chest colonisation as a result of translocation of bacteria
ill have an increased risk of developing ARF. The most from the mouth to the lungs via the endotracheal tube
common chronic illnesses involved are respiratory disease (ETT). This may lead to clinical signs of infection, or the
(including smoking history, COPD/asthma), congestive patient may remain colonised without an infective
cardiac failure and diabetes mellitus. 6,20 Table 14.5 process. The patient’s severity of disease, physiological
outlines aspects of the clinical history associated with reserve and comorbidity influence the development of
6
particular causative organisms in CAP. 6,9,21 infection. Most cases (58%) of VAP are associated with
infection involving gram-negative bacilli such as Pseudo-
20
The Australian CAP study collaboration examined epi- monas aeruginosa and Acinetobacter spp. A high number of
sodes of CAP in which all patients underwent detailed cases (20%) are associated with gram-positive Staphylo-
assessment for bacterial and viral pathogens. Aetiology coccus aureus. Many cases of VAP are associated with mul-
was identified in 46% of episodes, with the most frequent tiple organisms. As in CAP, the presence of comorbidities
6
causes being Streptococcus pneumoniae (14%), Mycoplasma and other risk factors influence the causative organism.
pneumoniae (9%) and respiratory viruses (15%). Mechan-
ical ventilation or vasopressor support was required in Diagnosis and treatment of VAP
11% of cases.
VAP can be difficult to diagnose, as clinical features can
Diagnosis of CAP be non-specific and other conditions may cause infiltrates
Routine screening of patients with suspected pneumonia on chest X-ray (CXR). However, it is often suspected when
there are new infiltrates observed on CXR or when clinical
continues to rely on microscopy and culture of lower signs of infection begin to develop, e.g. new onset of
respiratory tract specimens, blood cultures, detection of pyrexia, raised white blood cell counts, purulent sputum
antigens in urine and serology. Methods for detection of and a difficulty in maintaining adequate oxygenation.
6
antigens are now widely available for several pneumonia Specific risk factors associated with increased mortality in
pathogens, particularly S. pneumoniae, Legionella and VAP have been identified over the last decade. The most
22
some respiratory viruses. Culture of respiratory secre- widely-recognised risk factor is the provision of appropri-
tions may be limited due to difficulty in obtaining sputum ate antibiotic treatment, which has reduced mortality and
samples. For this reason, nasopharyngeal aspirates or the rate of complications. Timeliness of antibiotic admini-
swabs may be taken as part of the routine screening stration is an independent risk factor for mortality; mor-
for CAP. 23 tality was increased where administration of antibiotics
26
was delayed for more than 24 hours after diagnosis.
Severity assessment scoring When VAP is suspected there are two treatment strategies,
International guidelines recommend a severity-based although a systematic review did not demonstrate any
approach to management of CAP. CURB65, CRB65 and differences in mortality, length of ICU stay or length of
the Pneumonia Severity Index (PSI) are the most widely ventilation period: 19

Respiratory Alterations and Management 359



TABLE 14.5 Clinical history/comorbidities associated with particular causative organisms in CAP

Condition Causative organisms
Individual factors
Alcoholism Streptococcus pneumoniae (including penicillin-resistant), anaerobes,
gram-negative bacilli (possibly Klebsiella pneumoniae), tuberculosis
Poor dental hygiene Anaerobes
Elderly group B streptococci, Moraxella catarrhalis, H. influenzae, L. pneumophila,
gram-negative bacilli, C. pneumoniae and polymicrobial infections
Smoking (past or present) S. pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, Aspergillus
spp.
IV Drug use S. aureus, anerobes, M. tuberculosis, S. pneumoniae
Comorbidities
COPD S. pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, Aspergillus
spp.
Post influenza pneumonia S. pneumoniae, S. aureus, H. influenzae
Structural disease of lung (e.g., bronchiectasis, cystic fibrosis) P. aeruginosa, P. cepacia or Staphylococcus aureus
Sickle cell disease, asplenia Pneumococccus, H. influenzae
Previous antibiotic treatment and severe pulmonary comorbidity, P. aeruginosa
(e.g. bronchiectasis, cystic fibrosis, and severe COPD)
Malnutrition related diseases Gram-negative bacilli
Environmental exposure
Air conditioning Legionella pneumophila
Residence in nursing home S. pneumoniae, gram-negative bacilli, H. influenzae, S. aureus, Chlamydia
pneumoniae; consider M. tuberculosis. Consider anaerobes, but less
common.
Homeless population S. pneumoniae, S. aureus, H. influenzae, Cryptococcus gattii: caused by
inhalation of spores while sleeping, associated with red gum trees
(Australia, Southeast Asia, South America)
Suspected bioterrorism Anthrax, tularaemia, plague
Animal exposure
Bat exposure Histoplasma capsulatum
Bird exposure Chlamydia psittaci, Cryptococcus neoformans, H. capsulatum
Rabbit exposure Francisella tularensis
Exposure to farm animals or parturient cats Coxiella burnetii (Q fever)
Travel history
Travel to southwestern USA Coccidioidomycosis; hantavirus in selected areas
Travel to southeast Asia Severe acute respiratory syndrome (coronavirus), Mycobacterium
tuberculosis, melioidosis
Residence or travel to rural tropics Melioidosis (Burkholderia pseudomallei)
Travel to area of known epidemic Avian influenza (H5N1), Swine influenza (H1N1) and SARS (coronavirus)




● Clinical Strategy: involves treatment of patients with the diagnosis and causative organism. Antibiotic
new antibiotics, based on patient risk factors and the therapy is then guided by specific protocols.
local microbiologic and resistance patterns. Therapy is
adjusted based on culture results and the patient’s
response to treatment. CLINICAL MANIFESTATIONS
● Invasive Strategy: involves collection and quantitative Symptoms for pneumonia are both respiratory and sys-
analysis of respiratory secretions from samples temic. Common characteristics include fever, sweats,
obtained by bronchoalveolar lavage (BAL) to confirm rigours, cough, sputum production, pleuritic chest pain,

360 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

dyspnoea, tachypnoea, pleural rub, inspiratory crackles impacts on patient outcome. In particular, the first dose
on auscultation, plus radiological evidence of infiltrates of antibiotics is required as soon as possible after the
or consolidation. Cough is the most common finding diagnosis of pneumonia has been made. Studies where
and is present in up to 80% of all patients with CAP. 6,9 the first dose of antibiotic therapy was delayed showed
32
an increase in mortality. Antibiotic cover for pneumonia
COLLABORATIVE PRACTICE depends on the causative organism and sensitivity to
6
Early recognition of pneumonia and timely administra- drugs (see Table 14.6 ). Review of antibiotic prescribing
tion of antibiotic therapy are key aspects for patient man- practices in Australia and New Zealand has shown that
agement. The most important aspect of management in prescription of antibiotics in pneumonia is consistent
33
VAP is prevention and this is a key emphasis in the care with current guidelines.
of all mechanically-ventilated patients. One approach in
encouraging the implementation of VAP prevention was SPECIAL CONSIDERATIONS
the combination of four aspects of patient management Pneumonia is a leading cause of maternal and fetal mor-
into one evidence based guideline, known as the Ventila- bidity and mortality. It also increases the likelihood of
tor Care Bundle: elevating the head of bed to 30–45 the complications of pneumonia, including requirement
degrees, daily sedation vacation and assessment of readi- for mechanical ventilation. Bacterial pneumonia is the
ness to extubate, peptic ulcer disease (PUD) prophylaxis most common type experienced in pregnancy although
27
and deep vein thrombosis (DVT) prophylaxis. Effective- diagnosis is often delayed as a result of the reluctance to
ness of this strategy and implementation issues have been obtain a chest X-ray. Management is similar to a non-
further evaluated, with some additional perspectives pregnant patient with antibiotic therapy adjusted to con-
offered. While it is apparent that daily spontaneous awak- sider the impact on the fetus. 6
ening and breathing trials are associated with early libera-
tion from mechanical ventilation and VAP reduction, the CAP is a major cause of morbidity and mortality in
strategies included for DVT and PUD prophylaxis do not elderly patients. Streptococcus pneumoniae is the most
directly affect VAP reduction. Semi-recumbent position- common causative organism, with an increase in drug-
ing has been associated with a significant reduction in resistance being reported more widely in the over-65 age
14
VAP but is difficult to maintain in ventilated patients. It group. Treatment of elderly patients with pneumonia is
has been suggested that other methods to reduce VAP, similar to younger patients, with emphasis on supportive
such as oral care and hygiene, chlorhexidine in the pos- care, prevention of sepsis and management of preexisting
terior pharynx and specialised endotracheal tubes (con- chronic conditions. Immunisation with pneumococcal
tinuous aspiration of sub-glottic secretions, silver-coated), and influenza vaccines is beneficial in the prevention of
should be considered for inclusion in a revised Ventilator pneumonia in elderly patients. 34
Bundle more specifically aimed at VAP prevention. 14
Development of VAP is attributed in part to aspiration of RESPIRATORY PANDEMICS
oral secretions that are colonised by a variety of bacteria. Serious outbreaks of respiratory infections that spread
Maintenance of oral hygiene is therefore a key element in rapidly on a global scale are termed pandemics. Their
the care of mechanically-ventilated patients. Oral mucosa spread is so rapid because the infection is usually associ-
6
and dental plaque may also be colonised with bacteria ated with emergence of a new virus where the majority
and the use of an oral antiseptic solution (e.g. Chlorhexi- of the population has no immunity. These infections are
dine) may further reduce the risk of developing VAP. 28 characterised by extremely rapid ‘transmission with con-
Supportive ventilation is a key focus for managing patients current outbreaks throughout the globe; the occurrence
with pneumonia. In some instances this may include of disease outside the usual seasonality, including during
increased oxygen delivery and positive end expiratory the summer months; high attack rates in all age groups,
pressure (PEEP) to maintain oxygenation and prevent with high levels of mortality particularly in healthy young
alveolar collapse. Chest physiotherapy assists in the adults; and multiple waves of disease immediately before
35
29
prevention of VAP and remains a key component of and after the main outbreak’. Several severe respiratory
management of all ventilated patients. However, its infections have progressed to become pandemics in
contribution towards improving mortality in patients recent years; these have been associated with the Corona-
30
with pneumonia is unclear. Upright positioning and virus and Influenza viruses. Prediction of the interval
early mobilisation are important elements of both between pandemics is difficult, but occurrence is likely to
prevention and management of pneumonia. The effec- continue and therefore requires that the health care com-
tiveness of additional strategies, such as use of beds with munity be well prepared.
a continuous lateral rotation or a vibration function to
31
assist in the removal of secretions is yet to be shown. SEVERE ACUTE RESPIRATORY SYNDROME
See Chapter 15 for further discussion.
In 2002–03 an outbreak of a novel Coronavirus occurred
in China and rapidly spread throughout the world. The
Medications infection was highly virulent with over 8000 cases
Antibiotic administration is fundamental to a patient’s reported and a mortality rate of 11%. The infection was
clinical progress. As noted earlier, the importance of accu- called Severe Acute Respiratory Syndrome (SARS) due to
rate and timely administration of antibiotics directly the severity of the disease, characterised by diffuse

Respiratory Alterations and Management 361



TABLE 14.6 Preferred antimicrobial agents in pneumonia 6

Type of infection Preferred agent(s)
Community-acquired pneumonia
Streptococcus pneumoniae PCN-susceptible: Penicillin G, amoxicillin, clindamycin, doxycycline, telithromycin
PCN-resistant: cefotaxime, ceftriaxone, vancomycin, and fluoroquinolone
Mycoplasma Doxycycline, macrolide
Chlamydophila pneumoniae Doxycycline, macrolide
Legionella Azithromycin, fluoroquinolone (including ciprofloxacin), erythromycin (rifampicin)
Haemophilus influenzae Second- or third-generation cephalosporin, clarithromycin, doxycycline, β-lactam/β-
lactamase inhibitor, trimethoprim/sulfamethoxazole, azithromycin, telithromycin
Moraxella catarrhalis Second- or third-generation cephalosporin, trimethoprim-sulfamethoxazole,
macrolide doxycycline, β-lactam–β-lactamase inhibitor
Neisseria meningitidis Penicillin
Streptococci (other than S. pneumoniae) Penicillin, first-generation cephalosporin
Anaerobes Clindamycin, β-lactam–β-lactamase inhibitor, β-lactam plus metronidazole
Staphylococcus aureus Methicillin-susceptible Oxacillin, nafcillin, cefazolin; all rifampin or gentamicin
Methicillin-resistant Vancomycin, rifampicin or gentamicin
Klebsiella pneumoniae and other Enterobacteriaceae Third-generation cephalosporin or cefepime (all aminoglycoside) carbapenem
(excluding Enterobacter spp.)
Hospital-acquired infections
Enterobacter spp. Carbapenem, β-lactam–β-lactamase inhibitor, cefepime, fluoroquinolone; all +
aminoglycoside in seriously ill patients
Pseudomonas aeruginosa Anti-pseudomonal β-lactam + aminoglycoside, carbapenem + aminoglycoside
Acinetobacter Aminoglycoside + piperacillin or a carbapenem




alveolar infiltrates, resulting in about 20% of patients Pandemics of influenza were observed a number of times
requiring respiratory support. The SARS outbreak pro- in the twentieth century, and were believed to have
voked a rapid and intense public health response coordi- involved viruses circulating in humans that originated
nated by the World Health Organization (WHO), from influenza A viruses in birds. The ‘Spanish influenza’
resulting in a cessation of disease transmission within ten pandemic of 1918–19 resulted in the death of over 50
months. 35 million people worldwide and remains unprecedented in
its severity. 35
INFLUENZA PANDEMICS The first reported infection of humans with avian influ-
Epidemics of influenza occur regularly and are associated enza viruses occurred in Hong Kong in 1997, with six
with high morbidity and mortality. Incidence is usually recorded fatalities. The increased virulence of this disease
highest in the young, while mortality is highest in the was observed in the acuity of those affected by the out-
elderly population. Those with preexisting respiratory break of the highly pathogenic avian influenza virus
conditions such as asthma or COPD experience particu- (H5N1) in 2004–2005. Most patients presented with
35
larly high morbidity and mortality. In contrast, when non-specific symptoms of fever, cough and shortness of
influenza occurs on a pandemic scale it has been shown breath. In many patients this progressed rapidly to ARF
to affect greater numbers of younger and otherwise requiring ventilation and other supportive measures. The
healthy people. majority of people affected (90%) were less than 40 years
of age with case fatality rates highest in the 10–19-year-
A feature of the influenza virus that explains why it con- old age group. 36
tinues to be associated with epidemic and pandemic
disease is its high frequency of antigenic variation. This The most recent influenza pandemic declared by WHO
occurs in two of the external glycoproteins and is referred occurred in 2009 when a novel H1N1 influenza A virus
to as antigenic drift or antigenic shift, depending on the emerged in Mexico and the USA. This virus contained
extent of the variation. The result of this is that new genes from avian, human and swine influenza virus and
37
viruses are introduced into the population, and due to affected millions of people worldwide. Patients typically
the absence of immunity to the virus, a pandemic of presented with nonspecific flu-like symptoms, however in
influenza results. 6 a quarter of patients this was accompanied by diarrhoea

362 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

35
and vomiting. The disease spread globally with millions for most hospitals and health services and to reduce the
of cases reported and resulted in over 16,000 deaths by risk of nosocomial influenza in hospitals. 40
March 2010. 38
ISOLATION PRECAUTIONS AND PERSONAL
Australia and New Zealand communities had a high pro-
portion of cases of H1N1 influenza-A infection, with 856 PROTECTIVE EQUIPMENT
patients being admitted to ICU; 15 times the incidence Key aspects of infection control in an epidemic or pan-
of influenza A in other recent years. Infants (aged 0–1 demic situation focus on limiting opportunities for noso-
years) and adults aged 25–64 years were at particular risk; comial spread and the protection of health care workers.
others at increased risk were pregnant women, adults Guidelines for institutional management of these infec-
with a BMI over 35 and indigenous Australian and New tions involve designing and implementing appropriate
Zealand populations. Australian and New Zealand Inten- isolation procedures and recommending appropriate
sive Care Society (ANZICS) investigators prepared a personal protective equipment (PPE). The impor-
report based on the Australian and New Zealand experi- tance of adequate PPE was highlighted particularly in
ence to assist those in the northern hemisphere to better the SARS epidemic where there was overrepresentation
prepare for their winter influenza season. 39 of health care workers who became patients infected
with the virus. 35
The emergence of novel swine-origin influenza A virus
was not anticipated and it is unlikely, given the limita- Specific infection control guidelines are usually devel-
tions of current knowledge, that future pandemics can be oped for individual institutions, based on government
predicted. The threat of pandemic disease from avian recommendations for management of staff, appropriate
influenza remains high with the rapid evolution of H5N1 PPE and isolation procedures. Table 14.7 summarises
41
viruses; however the direction this will take is unpredict- the recommendations from the Australian and New
42
able. Priorities for prevention and management of future Zealand governments.
influenza pandemics therefore involve development of In all settings, it is important to ensure that staff members
an international surveillance and response network for are familiar with respiratory protection devices. In areas
early detection and containment of the disease, local or situations where respirators (P2 or N-95 masks) are
preparation for controlling the spread of the infection used, a fit-testing program ensures understanding of how
and further development of vaccines and antiviral the devices work and maximal safety. During the SARS
agents. 38
epidemic, infection of staff members through inappropri-
Influenza Vaccinations ate or ineffective use of these masks occurred, and infec-
tion due to failure to wear adequate eye protection was
Influenza vaccines are formulated annually based on also reported. 43
current and recent viral strains. Success in protecting an
individual against influenza requires that the virus strains ACUTE LUNG INJURY
included in the vaccine are the same as those currently
circulating in the community. Vaccines are commonly Acute lung injury (ALI) is a generic term that encom-
effective in 70–90% in preventing influenza in healthy passes conditions causing physical injury to the lungs.
adults younger than 65 years of age. Efficacy appears Acute respiratory distress syndrome (ARDS) is a severe
lower in elderly persons. Health care workers are a key form of ALI as a result of bilateral and diffuse alveolar
target group for the influenza vaccine, at the very least to damage due to an acute insult, and is the predominant
reduce absenteeism over what is often the busiest period form of ALI observed in ICU. 6






TABLE 14.7 Recommendations for personal protective measures in respiratory pandemics

Section Protective measure
Staff management Assessment of staff at increased risk of complications from the specific infection should be
redeployed if possible
Monitoring health care workers for signs of illness and management with antivirals as a priority
Personal protection: basic measures Hand hygiene, social distancing, safe cough/sneeze etiquette, and good ventilation
Personal Protective Equipment Gloves
Gowns/aprons
Eye protection
Masks: a range of masks are available to provide respiratory protection to workers in medium to
high-risk situations. Two options are available:
● Surgical mask: designed to contain droplet spread from the wearer but offers a degree of
protection from external infection
● P2 or N-95 particulate masks: provide a higher degree of filtration or respiratory protection,
when appropriately worn and handled

Respiratory Alterations and Management 363

AETIOLOGY
ARDS is a characteristic inflammatory response of the TABLE 14.8 Direct and indirect causes of acute
lung to a wide variety of insults. Approximately 200,000 lung injury 9
patients are diagnosed annually in the USA with ARDS,
44
accounting for 10–15% of ICU admissions. Commonly Direct lung injury Indirect lung injury
associated clinical disorders can be separated into ● Pneumonia ● Sepsis
9
those that directly or indirectly injure the lung (see ● Aspiration of gastric contents ● Multiple trauma
Table 14.8). ● Pulmonary contusion ● Cardiopulmonary
● Fat, amniotic fluid, or air embolus bypass
The most common cause of indirect injury resulting in ● Near drowning ● Drug overdose
ALI/ARDS is sepsis, followed by severe trauma and hae- ● Inhalational injury (chemical or ● Acute pancreatitis
smoke)
modynamic shock states. Transfusion-related ALI (TRALI) ● Reperfusion pulmonary oedema ● Transfusion of blood
products
is not common but is observed in ICU. ARDS arising
from direct injury to the lung is most commonly seen in
patients with pneumonia. An individual’s risk of develop-
ing ARDS increases significantly when more than one
predisposing factor is present. 6 chest X-ray. The Murray Lung Injury Score was developed
as a method for clarifying and quantifying the existence
46
PATHOPHYSIOLOGY and severity of the disease. The American-European
Inflammatory damage to alveoli from inflammatory Consensus Conference on ARDS provided the following
mediators (released locally or systemically) causes a definition:
change in pulmonary capillary permeability, with result- ● acute onset of arterial hypoxaemia (PaO 2 :FiO 2 ratio
ing fluid and protein leakage into the alveolar space and < 200)
pulmonary infiltrates. Dilution and loss of surfactant ● bilateral infiltrates on radiography without evidence
causes diffuse alveolar collapse and a reduction in pul- of left atrial hypertension or congestive cardiac failure.
monary compliance and may also impair the defence
mechanisms of the lungs. Intrapulmonary shunt is con- The spectrum of disease was also acknowledged and the
45
firmed when hypoxaemia does not improve despite sup- term ALI was introduced to describe patients with a less
plemental oxygen administration. The characteristic severe but clinically similar form of respiratory failure
6
47
course of ARDS is described as having three phases: 6,45 (PaO 2 :FiO 2 ratio <300). It has been suggested that these
definitions require review as they include such a broad,
1. Oedematous phase: involves an early period of heterogenous group of patients that has limited investiga-
alveolar damage and pulmonary infiltrates result- tion of appropriate management strategies. This may also
ing in hypoxaemia. This phase is characterised by be because the interventions studied were ineffective, but
migration of neutrophils into the alveolar com- it is just as likely that the broadly inclusive definition of
partment, releasing a variety of substances includ- ARDS captures a heterogeneous group of patients that
ing proteases, gelatinases A and B, and reactive respond differently to current therapies. 48
nitrogen and oxygen species that damage the
alveoli. Further damage is caused by resident alveo- CLINICAL MANIFESTATIONS
lar macrophages and release of proinflammatory While no specific test exists to determine whether a
cytokines that amplify the inflammatory response patient has ARDS, it should be considered in any patient
in the lung. Significant ventilation–perfusion with a predisposing risk factor who develops severe
(intrapulmonary shunt) mismatch evolves causing hypoxaemia, reduced compliance and diffuse pulmonary
hypoxaemia. infiltrates on a chest X-ray. ARDS usually occurs 1–2
44
2. Proliferative phase: begins after 1–2 weeks as pul- days following onset of a presenting condition and is
monary infiltrates resolve and fibrosis and remod- characterised by rapid clinical deterioration. Common
elling occurs. This phase is characterised by reduced symptoms include severe dyspnoea, dry cough, cyano-
alveolar ventilation and pulmonary compliance sis, hypoxaemia requiring rapidly-escalating amounts of
and ventilation–perfusion mismatch. Reduced supplemental oxygen and persistent coarse crackles on
compliance (stiff lungs) causes further atelectasis auscultation. 6
in the mechanically ventilated patient as alveoli are
damaged by increased volume and/or pressure on Assessment
inspiration.
3. Fibrotic phase: the final phase where alveoli A patient with ARDS requires ongoing monitoring of
become fibrotic and the lung is left with oxygenation and ventilation through ABG analysis and
emphysema-like alterations. pulse oximetry and monitoring of PaCO 2 to assess per-
missive hypercapnia. Monitoring of ventilatory pressures
and volumes ensures that additional lung injury is pre-
DIAGNOSIS vented. As many patients with ARDS require cardiovascu-
A standardised definition of ARDS was first described in lar support, assessment of haemodynamics and peripheral
1988, with three clinical findings; hypoxia, decreased pul- perfusion is important to ensure oxygen delivery to cells
monary compliance and diffuse infiltrates observed on a is achieved. 6

364 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

COLLABORATIVE PRACTICE patient–ventilator synchrony, especially when non-
The key principles of management are treatment of the conventional modes of ventilation are used. Improve-
precipitating cause and providing supportive care during ments in oxygenation are usually observed and may be
the period of acute respiratory failure. 6,45 Mortality rates attributed to reduction in oxygen consumption and
from ARDS have decreased over time; this is not attrib- improved chest wall compliance. The use of NMBAs,
uted solely to the use of low tidal volume ventilation however, is also associated with an increased risk of
promoted by the ARDS Network group, but to other myopathy, so any benefits gained should be weighed
51
44
advances in critical care. Specific strategies include cau- against known risks.
tious fluid management, adequate nutrition, prevention Inhaled nitric oxide (iNO) therapy may be used to
of ventilator-associated pneumonia, prophylaxis for deep improve oxygenation through selective vasodilation of
venous thrombosis and gastric ulcers, weaning of seda- the pulmonary blood vessels, promoting improvement in
tion and mechanical ventilation as early as possible, and ventilation–perfusion matching. Despite the lack of evi-
physiotherapy and rehabilitation (similar to ARF man- dence regarding its effectiveness in improving outcomes
agement). Management involves a coordinated collab- of patients with ARDS, its use is reasonably widespread.
orative approach including supportive ventilation, patient Improvement in oxygenation should be observed within
positioning and medication administration. the first hour of treatment to support its ongoing use.
51
Some groups have reported the use of iNO to be harmful
Ventilation Strategies and recommend that it not be used, given the lack of
52
The key focus of ventilation in ARDS is the prevention of evidence demonstrating reduction in mortality. A similar
refractory hypoxaemia rather than reversing it after it effect, in terms of pulmonary vasodilation, has been
develops. The use of small tidal volumes and adequate achieved using inhaled prostacyclines and this remains
levels of PEEP, along with careful attention to fluid status under investigation as an alternative therapy. 51
and patient–ventilator synchrony, may be sufficient to A number of medications are currently being investigated
maintain oxygenation at an appropriate level while mini- to treat ARDS in acute and subacute exudative phases.
mising further damage from barotrauma and nosocomial These include agents that target the disrupted surfactant
pneumonia. 6,47 The use of rescue therapies is controversial system (exogenous surfactant therapy), oxidative stress
as none to date have reduced mortality when studied in and antioxidant activity (antioxidants), neutrophil
large heterogeneous populations of patients with ARDS. recruitment and activation, expression and release of
Some therapies however demonstrated improved oxygen- inflammatory mediators (corticosteroids), activation of
ation, which may be an important goal in many patients the coagulation cascade (immunomodulating agents and
who experience severe hypoxaemia. The key focus of statins), and microvascular injury and leak (beta 2 -
rescue ventilatory strategies is alveolar recruitment, includ- agonists). The use of low-dose corticosteroids has been
53
ing higher levels of PEEP, use of airway pressure release associated with improved outcomes for patients with
ventilation (APRV), high-frequency oscillatory ventilation ARDS, although its use remains controversial and
54
(HFOV) and high-frequency percussive ventilation further investigation is recommended.
(HFPC) (see Chapter 15). If hypoxaemia is severe, extra-
corporeal life support may also be considered. As there is
no evidence to support the use of one strategy over another, SPECIAL CONSIDERATIONS
the choice of therapy is often based on equipment avail- ALI and ARDS occur in pregnancy usually as a result of
ability and clinician expertise. An evidence based approach aspiration pneumonitis, sepsis or pneumonia. Manage-
is likely to involve lung-protective ventilation (volume ment of ventilation is similar to the non-pregnant patient,
and pressure limitation with modest PEEP) requiring per- although consideration of the impact on the fetus is
missive hypercapnia and permissive hypoxaemia. 49 important in medication usage and ventilatory manage-
ment. Elderly patients who develop ARDS are likely to
6
Prone Positioning experience an increased severity of disease, yet have a
Use of prone positioning in patients with ARDS was mortality rate comparable to other patients. Develop-
described almost 30 years ago as a means of improving ment of other organ dysfunction depends on the presence
oxygenation. This improvement is largely due to the of chronic conditions such as renal and cardiovascular
effect that the prone position has on chest wall and lung diseases. 55
compliance. The result is a more homogenous ventilation
of the lungs and improved ventilation–perfusion match- ASTHMA AND CHRONIC
ing. Investigation into the effectiveness of this as a OBSTRUCTIVE PULMONARY DISEASE
6
therapy in ARDS has noted improvement in oxygenation,
but no corresponding improvement in mortality. It is Asthma is defined as a respiratory condition where airflow
therefore recommended as a rescue therapy for the patient limitation may be fully or partially reversible either spon-
at risk of death from hypoxia, rather than as a routine taneously or with treatment. 56-58 COPD is a respiratory
treatment. See Chapter 15 for further discussion. condition defined by a largely fixed airflow limitation.
50
The partial airway responsiveness to therapy in COPD
Medications results in a clinical overlap between COPD, asthma and
A number of non-ventilatory strategies may form part of chronic bronchitis. A non-proportional Venn diagram
the treatment of patients with ARDS. Neuromuscular (see Figure 14.2), originally used by the American Tho-
59
blocking agents (NMBAs) are used to promote racic Society and now in the Australian and New Zealand

Respiratory Alterations and Management 365

70
risk factor for the development of COPD. Continued
Overlap of bronchitis, emphysema and asthma
within chronic obstructive pulmonary disease smoking accelerates the decline of respiratory function in
(COPD) susceptible individuals. 71,72 However, less than 15% of
smokers actually develop clinically-significant COPD 68,73,74
suggesting that other factors are also involved, including
Chronic environmental and occupational pollutants, genetic pre-
bronchitis Emphysema disposition, hyper-responsive airways and respiratory
infections. 68,75-79 Disease progression in susceptible indi-
viduals is most likely to be dependent on the synergistic
effects of these factors.
COPD
Ventilation abnormalities in COPD result from airway
inflammation, bronchoconstriction, increased mucus
Airflow secretion and oedema. Perfusion abnormalities arise
from hypoxic-induced vasoconstriction of the capillary
obstruction
beds. Pulmonary ventilation/perfusion (V/Q) abnormali-
ties, and hyperinflation contribute to increased pulmo-
nary vascular resistance (PVR), and respiratory muscle
fatigue. Increased PVR and hypoxaemia require the
80
heart’s right side heart to work harder, over time resulting
Asthma in hypertrophy, remodelling and cor pulmonale. 81,82 The
incidence of right ventricular hypertrophy approximates
40% for patients with moderate levels of COPD (i.e. FEV 1
This non-proportional Venn diagram shows the overlap of chronic 60
bronchitis, emphysema and asthma within COPD. Chronic <1000 mL). The left ventricle may also be compromised
bronchitis, airway narrowing and emphysema are independent by hyperinflation, which generates an increased work
effects of cigarette smoking, and may occur in various of afterload. Heart disease is therefore a frequent
83
combinations. Asthma is, by definition, associated with reversible concomitant condition with COPD 84-86 (see Chapter 11
airflow obstruction. Patients with asthma whose airflow obstruction
is completely reversible do not have COPD. In many cases it is for further discussion). Impaired ventilation and perfu-
impossible to differentiate patients with asthma whose airflow sion leads to hypoxaemia and mechanical dysfunctions,
obstruction does not remit completely from persons with chronic with the primary cause of adverse lung mechanics being
bronchitis and emphysema who have partially reversible airflow hyperinflation.
obstruction with airway hyperreactivity.
83
Hyperinflation has two components: static and dynamic.
FIGURE 14.2 Overlap between asthma, emphysema and bronchitis. Loss of elastic recoil (static hyperinflation) and incom-
60, p. S10
plete expiratory airflow (dynamic hyperinflation) leads to
expert guidelines 60,61 depict this overlap between condi- air trapping and a reduced inspiratory capacity. 87,88 The
tions. It is not uncommon for people with an obstructive effects of incomplete and prolonged expiration accounts
lung disease to share clinical characteristics for more than for increased work of breathing, dyspnoea and reduced
one respiratory condition, although the dominant clini- exercise tolerance experienced by people with COPD. 89-95
cal symptom is usually indicative of the underlying con- Severity of COPD promotes hyperinflation of the lungs,
62
dition. It is however important to differentiate between and hyperinflation is a catalyst for hypoventilation. 96
COPD and asthma as they have different management COPD is also a systemic condition that has an effect on
and illness trajectories. 56
the skeletal muscles, the intercostals and diaphragm. 97-99
PATHOPHYSIOLOGY Bloodflow is diverted from lower limb muscles to meet
the oxygen requirements of these respiratory muscles; a
Asthma is a complex syndrome influenced by genetic and phenomenon referred to as circulatory steal. Use of
82
environmental factors. Altered airway physiology and supplemental oxygen to hypoxaemic patients with
63
airway wall remodelling in asthma are consequences of COPD has been found to reduce dynamic hyperinflation,
inflammatory processes. While initial symptoms can dyspnoea and improve exercise tolerance; 88,97 reduce
64
occur at any age, most patients exhibit episodes of wheez- PVR; 76,86,100 reduce ventilatory requirements and circulat-
ing and obstruction before the age of six. 65,66 The increas- ing lactate levels. The systemic limitations that arise
101
ing incidence of disease burden in children may be with COPD are therefore profound and complex. These
102
attributable to a greater awareness and diagnosis of the inter-relationships are illustrated in Figure 14.3.
condition, with the overall differences in global preva-
lence now becoming less. 67 CLINICAL MANIFESTATIONS
In contrast, COPD is a systemic, permanent and progres- With asthma and COPD, a patient may present with
sive condition with a number of mechanisms involved in wheeze, cough and/or dyspnoea. History and physical
its development. Smoking is the cardinal risk factor and assessment are fundamental to determining the severity
continuation is the most significant determinant for of presentation. Presence of diminished or silent breath
disease progression. 60,68 The concept of ‘pack years’ is sounds, central cyanosis, an inability to speak, an altered
used to quantify smoking, and is independent of whether level of consciousness, an upright posture and diaphore-
69
58
an individual is a current or reformed smoker. A history sis indicate a life-threatening case. Chest pain or tight-
of more than 20 pack years of smoking is a significant ness may be present. Underestimation of severity is

366 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

Ventilatory Limitation
Increased Ventitatory Requirement
Increased Work of Breathing
Deconditioning
LV Dysfunction Reduced
Pulmonary
Conductance
O 2
CO 2
• •
QO 2
CO 2 O 2 VCO 2
MUSCLE SYSTEMIC PULMONARY LUNGS
(Lactic Acidosis) CIRCULATION CIRCULATION
• O 2 CO 2
QCO 2 CO 2 •
VO 2
O 2
RV Dysfunction
Loss of
Gas Exchanging
Surface Area
FIGURE 14.3 The systemic interrelationships in COPD. 102, p. 148

58
71
associated with higher mortality. Recent longitudinal differentiating asthma and COPD. The most commonly
datasets for Australia and New Zealand highlight a trend used criterion in Australia and New Zealand is airway
in reduced ICU admissions following an exacerbation of reversibility in response to bronchodilator therapy: <15%
asthma and an improved health outcome. Conversely, reflects COPD; >15% reflects asthma. 60,110
103
studies in patients with COPD identified poorer 12
month health outcomes following an ICU admission for COLLABORATIVE PRACTICE
hypercapnoeic respiratory failure. 104,105 Contemporary management of asthma follows an asthma
management plan, to minimise the acute exacerbation
ASSESSMENT AND DIAGNOSTICS and any subsequent respiratory arrest. Many presenta-
Communication with patients that builds trust, through tions will be managed in the emergency department (see
honesty and effective intervention, contributes consider- Chapter 22 for further discussion). For patients requiring
ably to the de-escalation of panic and fear in patients ventilatory support, a case series noted that patients were
presenting with hypoxaemia. Creating a calm and trust- better managed with noninvasive ventilation (NIV), as
ing environment is paramount for those struggling for mechanical ventilation was associated with significant
111
breath. Forward-planning for potential deterioration and mortality and morbidity from hyperinflation and aggra-
58
constant assessment of respiratory, cardiovascular and vation of bronchospasm. Contemporary management
neurological systems are fundamental in determining of COPD has advocated a care plan for patients in the
optimal clinical progress for these patients. Where pos- community setting. This has an effect on prompting
sible, diagnostic tests and procedures involve peak flow patients to recognise a change in their symptoms and
monitoring, spirometry, radiology and ABGs. 58 seek appropriate care. However, improving symptom rec-
112
ognition does not reduce health care utilisation.
The ‘gold standard’ for diagnosing COPD is spirome- Patients with COPD managed with NIV in a timely
try. 60,75,106 While there is no gold standard in the diagnosis manner have a reduced length of hospital stay, reduced
of asthma, spirometry is the lung function test of choice. need for endotracheal intubation and reduced mortality
104
In Australia, respiratory function tests are usually per- rate. There are published guidelines on the prevention,
113
formed according to standard principles. Values identification and management of asthma and COPD. 61
107
56
obtained are expressed at body temperature, ambient
pressure, saturated with water vapour (BTPS), in absolute Medications
units (L or L/sec) and as a percentage of predicted normal Administration of oxygen and beta-agonists (salbutamol)
values. The carbon monoxide pulmonary diffusing capac- are first-line therapies. Nebulised salbutamol is the pre-
ity (TLCO), may be measured using the single breath ferred route, with IV administration considered for patients
technique modified by Krogh. Diffusing capacity indi- not responding to nebulised medication. See Table 14.9
58
cates the available surface area for gas exchange, and is for key medications used in the treatment of asthma.
reduced with emphysema but can be normal with
108
asthma. The TLCO can be a directly measured value or PNEUMOTHORAX
as a percentage of predicted normal for age, sex, height
and weight. A number of reference tables of predicted Pneumothorax describes air that has escaped from a
normal values enable comparison with population defect in the pulmonary tree and is trapped in the poten-
109
norms. A continuing lack of consensus remains for tial space between the two pleura. A pneumothorax

Respiratory Alterations and Management 367



TABLE 14.9 Key medications in an acute episode of asthma 58

Type of drug Generic medication Action Nursing considerations
Beta-agonist salbutamol Produces relaxation of bronchial smooth MDI-one to two puffs (100–200 mcg) 4-hourly and
muscle by action at β 2 -receptors. PRN. Also continuous nebulisation via ultrasonic
neb and IV administration
Steroids hydrocortisone Starts effect 6–12 hours after Glucocorticoid dramatically reduces inflammation
administration. by its profound effects on concentration,
Increases β-responsiveness of distribution and function of peripheral
airway smooth muscle. leucocytes and a suppressive effect on
Decreases inflammatory response. inflammatory cytokines and chemokines.
Decreases mucus secretion.
methyl-prednisolone A synthetic adrenal steroid with similar
glucocorticoid activity, but considerably less
severe sodium and water retention effects than
those of hydrocortisone.
Xanthine aminophylline Bronchodilator Administration can be in oral or IV form. The half
Inhibits the inflammatory phase in life is variable dependent on age, liver and
asthma thyroid function. This is a drug now used with
Stimulates the medullary respiratory decreasing frequency
centre





normally resolves with treatment. A pneumothorax is COLLABORATIVE PRACTICE
termed persistent if the air leak lasts for more than five Insertion of a thoracic underwater seal drain allows the
days, while one reappearing on the same side after collapsed lung to re-expand. This is facilitated with mechan-
114
115
seven days is termed reoccurring. A pneumothorax can ical ventilation if required. If a haemothorax is present,
arise spontaneously, from disease or from traumatic suction on the underwater seal drain (20–60 mmHg) will
injury and can be life-threatening.
expedite drainage and re-expansion of the lung. 118
A tension pneumothorax involves significant and pro- No differences in short- and long-term health outcomes
gressive respiratory or haemodynamic compromise that were reported between insertion of an underwater seal
116
is quickly offset by decompression. A patient with a drainage system and simple aspiration of the air for
tension pneumothorax can present with symptoms patients with a spontaneous pneumothorax. Treat-
119
similar to asthma, i.e. ‘respiratory distress, wheeze, tachy- ments for pneumothorax where there is concomitant
cardia, tachypnoea, desaturation, hyper-expansion, agita- lung disease, e.g. cystic fibrosis, identified a paucity of

tion and decreased air entry.’ 117, p. 525 Fortunately, tension data to guide practice. 120
pneumothorax is a far less common condition, and the
patient is more likely to report additional chest pain. The Pain management and facilitation of respiratory care with
actual incidence of a tension pneumothorax is relatively oxygen therapy, non-invasive or invasive ventilation,
unexamined but it is more likely to occur in a ventilated positioning and deep-breathing and coughing, and the
patient where a pneumothorax has been missed on monitoring of the chest tube and drainage for presence
assessment. 117 of air-leak and serous drainage, are key to recovery without
121
development of further complications. Drainage system
connections need to be tight and supported to prevent
PATHOPHYSIOLOGY drag on the patient. Evidence is available for the develop-
121
If the pleural defect functions as a one-way valve, air ment of clinical practice guidelines on thoracostomy.
enters the pleural cavity on inspiration but is unable to Chapter 12 discusses chest tube management in more
exit on expiration, leading to increasing ipsilateral intra- detail.
pleural pressure. This causes further lung collapse, dia-
phragmatic depression, and (dependent on mediastinal Medications
distensibility) contralateral lung compression. 117 Management of pain associated with chest trauma is
guided by the presence of any comorbidities. Epidural or
CLINICAL MANIFESTATIONS intravenous opioids are the most effective pain manage-
121
ment strategies (see Table 14.10).
Severe presentations are identified by history and clinical
examination (respiratory distress, cyanosis, tachycardia, PULMONARY EMBOLISM
tracheal shift and unilateral movement of the chest). They
are also detected on CXR with a translucent appearance Deep vein thrombosis (DVT) and pulmonary embolism
118
of the air and absence of lung markings (see Chapter (PE) are two aspects of the disease process known as
13 for interpretation of CXR). venous thromboembolism (VTE). 122 Certain factors lead

368 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 14.10 Common medications prescribed with chest injury: pneumothorax

Type of drug Generic medication Route/actions Nursing considerations
Opioids Morphine IV. Sedative effect with respiratory depression,
Activates opioid receptors in the brain decreased cough reflex, bradycardia
and spinal cord. Histamine release may lead to flushing of face or
Depresses respiratory centre and hypotension, nausea and vomiting.
cough reflex. Reduces gastrointestinal motility.
Alters pain perception and CNS Reversed by naloxone.
modulation of painful stimuli.
Fentanyl Epidural and IV. Sedative effect with respiratory depression
A synthetic phenylpiperidine Can obscure the clinical course of patients with
derivative. head injury.
Pharmacological actions are similar to Slow IV injection reduces the risk of respiratory
those of morphine, but action is muscle rigidity.
more prompt and less prolonged, Use with caution in patients with renal and
and fentanyl appears to have less hepatic impairment, as action will be prolonged.
emetic activity. Respiratory depression can be reversed by
naloxone. Bradycardia can be reversed by
atropine.
Antibiotic Cephalosporin IV. Active against a wide range of gram-positive and
(1st generation) Bactericidal as a result of inhibition of gram-negative bacilli. Highly active against
for 24 hours bacterial cell wall synthesis. Staphylococcus aureus, including strains resistant
to penicillin.





addresses the risks and benefits of treatments for medical,
TABLE 14.11 Risk factors for venous surgical and oncology patients. Further, VTE guidelines
thromboembolism (VTE) 123 for patients with heparin-induced thrombocytopenia;
pregnancy and childbirth are outlined with a listing of
Primary hypercoaguable Secondary the publications to support the level of evidence for the
states (thrombophilia) hypercoagulable states clinical management guidelines.
Antithrombin III deficiency Immobility (including
Protein C deficiency long-haul aircraft travel) CLINICAL MANIFESTATIONS
Protein S deficiency Surgery Pulmonary artery obstruction causes release of vasoactive
Resistance to activated Trauma
protein C (inherited factor V Malignancy agents from accumulating platelets, with subsequent
Leiden mutation) Pregnancy and the puerperium raised pulmonary vascular resistance and acute pulmo-
Hyperhomocysteinaemia Obesity nary hypertension. The arterial obstruction causes severe
Lupus anticoagulant Smoking shunting and life-threatening hypoxaemia. Symptomatic
(antiphospholipid antibody) Oral contraceptive pill
Indwelling catheters in great patients present with dyspnoea (most common), pleu-
veins and the right heart ritic chest pain and haemoptysis. The physical signs of
Burns tachypnoea, fever, tachycardia and right ventricular dys-
Patients with limb paralysis function may also be present. If a massive PE has occurred,
(e.g. spinal injuries, stroke) the patient exhibits hypotension with pale, mottled skin
Heart failure
and peripheral and/or central cynanosis. 124
to higher incidence: immobilisation (due to long bone, ASSESSMENT AND DIAGNOSTICS
pelvic and spinal fractures) and closed head injury in Investigations to confirm VTE include compression
particular (see Table 14.11 for a list of risk factors). 123 ultrasonography for a suspected DVT, pathology test for
Most PE originate in the lower limbs, pelvic veins or elevated levels of D-dimer in plasma 125 and a ventilation-
inferior vena cava. Three predisposing risk factors for perfusion (V/Q) isotope scan, computed tomographic
thrombosis are venous stasis, vein wall injury and hyper- (CT) and pulmonary angiography (helical CT) scan
coagulability of blood. Clinical risk factors are immo- for PE. 122
bility, surgery, trauma, malignancy, pregnancy or
thrombophilia. PE may have no clinical consequence or
123
it may be catastrophic, causing sudden death, and is COLLABORATIVE PRACTICE
responsible for 10% of in-hospital deaths. 124 The morbid- Current and ongoing treatment modalities for PE are
ity and costs associated with VTE are also significant. An selected according to the patient’s individual circum-
evidence-based clinical practice guideline has been pub- stances. In general, options include medications and per-
lished to address this significant health issue 122 and cutaneously inserted vena caval filters. 126

Respiratory Alterations and Management 369

To prevent VTE, prophylactic interventions include hydra- cardiac death has the potential to significantly increase
tion and early mobilisation that, depending on the need the number of organs available for lung transplanta-
for patient admission are not always possible in the tion. 132 In 1985, 13 lung transplant procedures were
critical care setting. Mechanical measures of prophylaxis reported worldwide. 133 In subsequent years, the number
aim to reduce venous stasis via external compression. of recipients worldwide has steadily increased to be in
134
Commonly employed measures include knee- or thigh- excess of 2700 annually. Patients have received lung
length graduated compression stockings and/or inter- transplants in Australasia since the early 1990s. Lung
mittent pneumatic compression and/or venous foot transplantation can be either single or double, depend-
pumps. Clinical practice guidelines are published to ing on a patient’s underlying disease state. In the post-
support evidence-based care. 124 Two Cochrane systematic operative period, clinicians need to carefully balance
reviews have established that combined modalities fluid management to optimise respiratory function
reduce the incidence of DVT but the effect on PE remains without causing haemodynamic compromise or renal
unknown. 127,128 dysfunction. As severe pain, particularly for transverse
thoracotomy incisions, can compromise recovery signifi-
Medications cantly, effective analgesic regimens to facilitate physio-
therapy are critical.
Table 14.12 outlines the key medications recommended
and prescribed for patients with PE. Risk reductions for
DVT postsurgery have been reported following the use of INDICATIONS
prophylactic medications. 129 Studies continue to postu- The two generally-accepted criteria for lung transplanta-
late the efficacy of novel versus standard medication tion in patients with end-stage pulmonary or pulmonary
administration for VTE with only preliminary conclu- vascular disease are a poor prognosis (less than 50%
135
sions available. 130,131 chance of surviving 2 years) and poor quality of life. In
terms of quality of life, prospective lung transplant recipi-
LUNG TRANSPLANTATION ents usually struggle to perform activities of daily living,
may be oxygen-dependent and have New York Health
Transplantation is a life-saving and cost-effective form of Authority functional class III or IV symptoms. As a result,
treatment that enhances the quality of life for people most patients presenting for surgery are at risk of being
with chronic respiratory disease. Lung transplantation is debilitated and may be malnourished or overnourished,
facilitated by organ donation from patients with brain and therefore require specific interventions by health
death or donation after cardiac death. 132 Donation after team members.





TABLE 14.12 Medications for pulmonary embolism
Type of drug Generic medication Action Nursing Considerations
Opioid morphine Pain relief See Table 14.10
Anticoagulant unfractionated heparin A strongly acidic muco-polysaccharide with Prophylaxis and treatment of venous
rapid anticoagulant effects. thromboembolism, PE and disseminated
Inhibits thrombin and potentiates naturally intravascular coagulopathy.
occurring inhibitors of coagulation, To prevent clotting in extracorporeal blood
antifactor X (Xa) and antithrombin III. circuits (e.g. renal dialysis or intravascular
No effect on existing thrombi. catheters).
Standard heparin has a molecular weight of Prophylaxis of arterial thrombosis (e.g. after
5000–30,000 daltons. vascular surgery, interventional radiology
or after thrombolysis for an AMI).
Low-molecular-weight LMW heparin ranges from 1000 to 10,000 Administered subcutaneously.
(LMW) heparin daltons, resulting in distinct properties.
LMW-heparin binds less strongly to protein,
has enhanced bioavailability, interacts
less with platelets and yields a very
predictable dose response, eliminating
the need to monitor aPPT.
Acetyl salicylic acid aspirin Preventive: inhibits thromboxane A 2 The aspirin antiplatelet effect lasts 8–10
(platelet agonist), prevents formation of days (the life of a platelet in general);
thrombi and arterial vasoconstriction. aspirin should be stopped 1 week
before surgery.
Thrombolysis recombinant tissue- massive pulmonary embolism, where The risks of therapy include haemorrhage.
type plasminogen restoration of pulmonary arterial flow Safety and monitoring of the patient’s
activator (rt-PA) is urgently required due to right clinical state are paramount
alteplase, urokinase, ventricular failure
and streptokinase

370 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 14.13 Comparison of the four standard lung replacement techniques, including their common indicators 135












Heart-lung Bilateral sequential lung Single Lung Live donor lobar
Incision Midline sternotomy Transverse sternotomy, i.e. Lateral thoracotomy Transverse sternotomy, i.e.
horizontal ‘clam shell’ horizontal ‘clam shell’
Anastomoses Tracheal Left and right bronchial Bronchial Lobar bronchus to bronchus
Right atrial ’Double’ left atrial Left atrial Lobar vein to superior
Aortic Right and left pulmonary artery Pulmonary artery pulmonary vein
Lobar artery to main
pulmonary artery
Advantages Airway vascularity Access to pleural space Easiest procedure Increases donors
All indications No cardiac allograft Increases recipients Can be performed ‘electively’
Less cardiopulmonary bypass
Disadvantages Cardiac allograft Airway complications Airway complications Complex undertaking
Organ ‘consumption’ Postoperative pain severe Poor reserve Donor morbidity
Common Congenital heart disease with Cystic fibrosis Emphysema Cystic fibrosis
indications pulmonary hypertension Bullous emphysema COPD Pulmonary fibrosis
Heart and lung disease Primary pulmonary Pulmonary fibrosis Primary pulmonary
Primary pulmonary hypertension bronchiectasis Primary pulmonary hypertension
hypertension hypertension
Nursing Recipients may be Pain must be optimally Risk of pulmonary Complex ethical issues
considerations malnourished and managed to facilitate dynamic
debilitated. physiotherapy and timely hyperinflation in
Rarely performed due to use of recovery. obstructive
three organs. If native heart Postoperative management disorders.
from heart-lung recipient is requires careful optimisation Complex ventilatory
transplanted into another of haemodynamic, issues.
patient (’domino’), it is respiratory and renal Postoperative
judicious to have relatives in function. management
separate waiting rooms requires careful
during surgery (i.e. complex optimisation of
issues may arise). haemodynamic,
respiratory and
renal function.




DESCRIPTION CLINICAL MANIFESTATIONS
The four possible forms of lung transplantation, indica- Postoperative nursing and medical management common
tions for each form of surgery and salient nursing impli- to all forms of lung transplant recipients involves inten-
cations are outlined in Table 14.13. Currently, lung sive clinical monitoring similar to that for heart trans-
transplantation takes two main forms: bilateral sequen- plant recipients, with a focus on the stabilisation and
tial lung transplantation (BSLTx) and single-lung trans- optimisation of haemodynamic, respiratory and renal
plantation (SLTx). BSLTx is the most common form of status. Great skill by clinicians is required to manage this
lung transplantation and confers a survival advantage complex interplay. Respiratory dysfunction can develop
over and above SLTx. However the advantage of SLTx over due to severe allograft dysfunction secondary to ischaemia-
BSLTx is that twice as many people receive life-saving reperfusion injury, pulmonary oedema, hyperacute rejec-
surgery. For SLTx recipients with COPD, there is an tion and pulmonary venous or artery anastomotic
increase in the complexity of postoperative respiratory obstruction. Other major complications in the early post-
management, and for this reason some centres may operative period that affect respiratory management
perform BSLTx for patients with COPD. SLTx is also include severe pain, diaphragmatic dysfunction, acute
utilised for patients with idiopathic pulmonary fibrosis rejection and infection. Patients who receive a SLTx for
(IPF) and other forms of interstitial lung disease (ILD) COPD are at risk of developing pulmonary dynamic
who have a high waiting list mortality. 136 hyperinflation, requiring independent lung ventilation.

Respiratory Alterations and Management 371

due to infection or hemidiaphragm paralysis secondary
TABLE 14.14 Possible causes of low cardiac output in to phrenic nerve damage. Although BSLTx is usually per-
first week after lung transplantation formed without cardiopulmonary bypass, for those
patients who require cardiopulmonary bypass for surgery,
Cardiovascular it is recognised that there is a higher incidence of PGD
but management principles are essentially the same.
Hypovolaemia
Haemorrhage
Hypothermia
Acute myocardial infarction Nursing practice
Pulmonary venous or arterial anastomosis obstruction (embolism, Severity of allograft dysfunction is assessed by ABG analy-
clot, stitch, torsion) sis, respiratory function and patient comfort, chest X-ray,
Pulmonary embolism (thrombus or air)
Non-specific left ventricular dysfunction bronchoscopy and haemodynamic parameters. A careful
Arrhythmias balance in the management of haemodynamic, respira-
Coronary artery air embolism tory and renal status is vital in the first 12 hours, and their
Pulmonary optimisation should be achieved with inotropes (e.g.
adrenaline, noradrenaline) and limited and judicious use
Pulmonary dynamic inflation of native lung in single-lung of colloid fluids to ensure adequate end-organ perfusion
transplantation
Pneumothorax without causing pulmonary overload. Fluid management
Oversized pulmonary allograft should aim to keep filling pressures low to normal in
light of a recent retrospective review that found a high
Other
CVP (>7 mmHg) was associated with prolonged mechan-
141
Sepsis/infection (especially line or occult gut) ical ventilation and high mortality. Importantly, there
Sedatives was no evidence of renal complications associated with
Analgesics (especially epidural) 141
Transfusion reaction these low filling pressures. Fluid resuscitation should
Anaphylaxis include products to correct anaemia and preoperative low
Hyperacute rejection (rare) plasma protein levels. 142
For patients who have required intraoperative cardio-
pulmonary bypass, high doses of inotropes are often
Haemodynamic function can be compromised in the needed to overcome a transient relative hypovolaemia.
early postoperative phase due to cardiac and respiratory Additionally, gentle rewarming measures are needed to
problems; renal and gastrointestinal dysfunction is also re-establish normothermia in order to prevent haema-
prevalent. Long-term respiratory complications include tological and peripheral perfusion impairments associ-
airway anastomotic problems (stricture and dehiscence), ated with hypothermia. Slow rather than rapid rewarming,
suboptimal exercise performance, and chronic rejection and close monitoring of CI, CVP and PAWP should
manifesting as bronchiolitis obliterans syndrome. The minimise the development of pulmonary oedema at this
most important aspects of these complications are dis- time. For patients with allograft dysfunction accompa-
cussed below in relation to nursing practice, and Table nied by high pulmonary pressures, inhaled NO is useful
14.14 provides a summary. in decreasing high pulmonary pressures and intrapul-
monary shunting. 143,144 Ongoing nursing assessments of
Respiratory Dysfunction MAP, CI, PAP, PAWP, CVP and urine output guide and
Respiratory dysfunction within the first 24–48 hours evaluate haemodynamic therapeutic interventions (see
Chapter 9).
postoperatively is usually caused by primary graft
dysfunction (PGD), a syndrome characterised by non- To assess the causes and progress of allograft dysfunction,
specific alveolar damage, lung oedema and hypoxae- chest X-rays provide vital information about line place-
mia. 137 Primary graft dysfunction may be aggravated by ment, ETT position, lung expansion, lung size, position
factors associated with the donor (e.g. trauma, mechani- of the diaphragm and mediastinum and the presence of
cal ventilation, aspiration, pneumonia and hypotension), pneumothorax, oedema and atelectasis. 145 Allograft dys-
cold ischaemic storage, 137 inadequate preservation and function due to ischaemia-reperfusion injury appears on
disruption of pulmonary lymphatics. Clinical signs of chest X-rays as a rapidly-developing diffuse alveolar
PGD range from mild hypoxaemia with infiltrates on pattern of infiltration that is greater in the lower regions, 142
chest X-rays to severe ARDS requiring high-level ventila- most commonly seen on the first postoperative day but
138
tory support, pharmacological support and ECMO. may occur up to 72 hours following surgery. The presence
Australian researchers have shown a decrease in the sever- of rapidly worsening pulmonary infiltrates (especially if
ity and incidence of PGD following the implementation associated with low cardiac indices) should however
of an evidence-based guideline for managing patients’ prompt urgent echocardiography to assess cardiac func-
respiratory and haemodynamic status postoperatively. 139 tion and pulmonary venous anastamosis patency. Beyond
The guideline directs clinicians to minimise crystalloid 72 hours, alveolar and interstitial infiltration may indi-
fluids, use vasopressors as the first-line treatment to cate either acute rejection or an infective process. 146 This
maintain blood pressure if cardiac output is adequate information is combined with other respiratory and hae-
and use ARDSNet principles for ventilatory support. 139,140 modynamic data to inform appropriate collaborative
Respiratory dysfunction beyond 72 hours is likely to be interventions.

372 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










Native lung
( compliance)






Graft lung
( compliance)


FIGURE 14.4 Mechanism of pulmonary dynamic hyperinflation: distribu-
tion of inspiratory gas.


Commonly, ventilatory settings and respiratory weaning
are guided by pH rather than CO 2 levels. A modest degree
of hypercarbia is anticipated postoperatively and resolves
over time. Given that low-volume ventilation has a posi-
tive impact on lung recovery and long-term outcomes
in patients with adult respiratory distress syndrome
(ARDS), 147 it has now been recommended that SLTx and
BSLTx recipients receive similar settings to prevent baro-
trauma while providing adequate ventilation. 142 In SLTx FIGURE 14.5 Chest X-ray of patient with left single lung transplant for
recipients, ventilation perfusion mismatches can also be COPD who has developed PDH.
improved by inhaled NO and by positioning patients
regularly with the allograft uppermost. To ventilator
Allograft dysfunction can develop in SLTx recipients with To ventilator
a remaining native COPD lung who are ventilated via a
single-lumen ETT, due to gas trapping in the over-
distensible native lung, a condition known as pulmonary
dynamic hyperinflation (PDH) (see Figure 14.4). Any
condition that lowers the compliance of the allograft can
lead to PDH in these patients. Nurses need to be aware Tracheal cuff
of the patients who can potentially develop PDH and
to remain hypervigilant, as early signs and opportunities
to stabilise patients’ haemodynamic and respiratory R.U.L. bronchus
status quickly can be easily missed. Initial presentation
of PDH is usually a set of ABGs showing inadequate
ventilation (hypercarbia and hypoxaemia). However, this
pattern of ABG values must not be responded to with R. main bronchus L. main bronchus
increases in respiratory rate, tidal volume or PEEP, as
these actions will exacerbate the degree of native lung
hyperinflation; rather, minute ventilation must be Bronchial cuff
reduced. 148 FIGURE 14.6 Correct positioning of double-lumen endotracheal tube for
pulmonary dynamic hyperinflation.
Other common presenting cues of PDH include a hae-
modynamic profile of cardiac tamponade, tracheal devia-
tion, obvious hyperinflation of the native lung with or
without mediastinal shift on chest X-ray, decreased air physician is required to administer an anaesthetic, insert
entry to the allograft on auscultation and pneumothorax. a dual-lumen ETT, check the position of each lumen’s
The early stages of PDH in a patient with a left SLTx for position and cuff with an intubating bronchoscope.
COPD can be seen on the chest X-ray in Figure 14.5. Secure placement of the tube is paramount, to avoid
Immediate management of the condition requires slight movement of the position and consequent dis-
attempts to minimise hyperinflation with altered ventila- placement of correct cuff placement (see Figure 14.6 for
tory settings and bronchodilators. If this fails, a skilled correct positioning of a dual-lumen ETT).

Respiratory Alterations and Management 373

Independent lung ventilation is then established to reduce the postoperative pain experienced by recipients.
ensure that the native lung receives no PEEP and a Ideally, all lung transplant recipients should receive epi-
minimal tidal volume and rate (e.g. four breaths of dural analgesia; however, the insertion of an epidural
100 mL/min). 148 The allograft may require high levels of catheter at the time of surgery may be contraindicated
PEEP to provide adequate ABGs. Ongoing assessment of due to preoperative anticoagulation therapy. In these cir-
respiratory function determines the timing of weaning cumstances, epidural analgesia should be instituted as
from the dual-lumen ETT and independent lung ventila- soon as appropriate after surgery. Higher failure rates of
tion to a single-lumen ETT and standard ventilatory prac- transition from epidural to oral analgesia have been
tice. If PDH is not recognised until the patient has a reported in lung transplant recipients than in other tho-
150
cardiac arrest, the single-lumen ETT should be pushed racotomy patients, and in our experience it is not
into the bronchus of the transplanted lung in order to uncommon for BSLTx recipients to require opiate analge-
selectively ventilate the allograft until the patient’s condi- sia for a month after surgery in order to perform activities
tion is stable, when a dual-lumen ETT can be safely of daily living and physiotherapy.
inserted.
Patients with allograft dysfunction are always assessed Nursing practice
by doctors for the emergence of rejection and pulmonary Consultation with pain services to ensure that patients
infection via bronchoscopy (using transbronchial biopsy receive optimal analgesic regimens should be an integral
and bronchoalveolar lavage) in critical care. Evidence component of patients’ postoperative management (see
of rejection will be treated with changes in the Chapter 19). Paracetamol is beneficial in relieving mild
im munosuppression regimen and appropriate ventil- to moderate pain, and may be used as an adjunct to
151
atory and haemodynamic support. Many patients with centrally-acting analgesics for moderate to severe pain.
rejection in the immediate postoperative period may The use of non-steroidal antiinflammatory drugs should
not exhibit classic signs of rejection such as abrupt onset be avoided, due to their detrimental effects on renal and
of dyspnoea, cough and chest tightness while mechani- gastrointestinal function. 151
cally ventilated. Subtle changes in respiratory effort, The nursing management of intercostal chest tubes is
gas exchange and minute ventilation may be the only similar to that for cardiac surgical patients 152 (see Chapter
signs to alert the nurse to respiratory dysfunction sec- 12), with a few additional considerations. Recipients of
ondary to rejection or infection during mechanical SLTx have one apical and one basal chest tube, whereas
ventilation.
BSLTx recipients have four chest tubes: two apical and two
Classic clinical signs of pulmonary infections include a basal. Both BSLTx and HLTx recipients have one pleural
low-grade fever, increasing dyspnoea and sputum produc- space, so the amount and consistency of drainage from
tion, cough and infiltrates on a chest X-ray. Hypotension, basal tubes will vary depending on patient positioning.
a reduced cardiac index and subtle changes in respiratory Apical chest tubes are removed prior to basal tubes. Once
parameters during mechanical ventilation noted above lung expansion is optimal and any pneumothoraces have
may also be present. Pulmonary infections may be resolved, the apical tubes are removed. Basal chest tubes
acquired through nosocomial, community or donor are removed once drainage is considered minimal in
means, with recipient-colonised and opportunistic volume (approximately 250 mL/day) and serous in
in fections prevalent. Regardless of the means of acquisi- nature.
tion, all infections are treated promptly with specific anti-
biotic, antifungal or antiviral therapies. The risk of Haemodynamic Instability
developing CMV and Pneumocystis carinii in lung trans- As noted earlier, all lung transplant patients can experi-
plant recipients is somewhat higher than in heart trans- ence haemodynamic compromise and renal impairment
plant recipients, so prophylactic therapies for both postoperatively as a result of managing respiratory func-
infections are provided. Clinicians play an important role tion. Potential causes of a low cardiac output are outlined
in preventing the transmission of infection between in Table 14.14. Patients with pulmonary hypertension
patients and cross-contamination within patients. Metic- must be carefully managed in the early postoperative
ulous hand-washing between patients and between pro- period because of impaired cardiac output and changes
cedures, as well as minimising traffic into and out of in right ventricular dynamics. Prior to surgery, prolonged
patient care areas, are important measures in reducing periods of a high right ventricular afterload lead to right
infection rates. 149
ventricular thickening and stiffness, accompanied by
limited wall motion of the left ventricle. 153
Pain

All recipients of lung transplantation can experience Nursing practice
severe pain afterwards due to the incisions and chest During arousal from anaesthesia and patient activity, fluc-
drains. However, recipients of BSLTx in particular experi- tuations in oxygenation and systemic and pulmonary
ence extremely severe postoperative pain secondary to the pressures exacerbate haemodynamic instability. 154,155
transverse sternotomy (clam-shell incision) and presence When weaning from mechanical ventilation, as ventila-
of four chest tubes. The recent use of a minimally invasive tion pressures fall, increases in preload may precipitate
thoracotomy rather than transverse sternotomy for acute pulmonary oedema, even days after surgery. 154 Con-
patients with obstructive respiratory illnesses may also versely, if the patient is hypovolaemic at the time of

374 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

weaning, right ventricular outflow obstruction may to irritability, insomnia, profound depression, mania or
occur. 142 These potential events confirm that careful titra- psychosis. 135
tion of fluid and inotropic therapies, guided by frequent, Although LTx surgery offers recipients relief from short-
accurate monitoring of invasive haemodynamic param- ness of breath and increased exercise tolerance, many
eters, is required in patients with preoperative pulmonary patients have to continue managing other aspects of their
hypertension.
underlying disease (e.g. cystic fibrosis). Thus, the burden
Renal and Gut Dysfunction of living with a chronic illness remains. Conversely, some
recipients experience wellness for the first time in their
Reasons for renal dysfunction in LTx recipients in the life, and this can alter family and relationship dynamics.
early postoperative phase are similar to those for heart In circumstances where lung function deteriorates after
recipients. The situation is, however, compounded in initial success, patients and families experience feelings
lung recipients due to aminoglycoside and NSAID use of devastation and hopelessness. Counselling services are
preoperatively, the high number of patients with diabetes essential in both the preoperative and the postoperative
and a requirement for ‘dry’ lungs postoperatively. Fortu- phase. 135,158-166
nately, the use of interleukin-2 receptor antibody drugs
can assist in lowering the doses of calcineurin inhibitor Long-term Sequelae
agents to offer some early protection to the kidneys Long-term sequelae for lung transplant recipients include
without inducing acute rejection. 156
renal impairment, hypertension and increased risk
Nursing practice of malignancies, similar to those with heart trans-
plantations. Further information about long-term com-
Routine management of gut function is an important plications specific to lung transplantation, such as
aspect of nursing practice, including the prevention of bronchiolitis obliterans syndrome and other non-
constipation (see Chapter 19). For patients receiving pulmonary complications, is available. 135
surgery for cystic fibrosis, pancreatic enzyme supplements
are required postoperatively. As these patients are invari-
ably debilitated preoperatively, enteral feeds that do not SUMMARY
require pancreatic enzyme supplements should be com- Respiratory alterations, whether a primary disruption or
menced as soon as possible after surgery, as these supple- a secondary complication of comorbidity, are the primary
ments cannot be administered via enteral feeding tubes. reason for ICU admission. Vigilant assessment, monitor-
Further specific information on managing patients with ing and being responsive to a deteriorating state are
cystic fibrosis is available. 157 central to critical care nursing practice. Contemporary
approaches to respiratory support focus on preserving a
Psychosocial Care patient’s respiratory function, including NIV, using less
In the early postoperative period, corticosteroids, seda- controlled ventilation when appropriate and consider-
tives, sleep deprivation and persistent pain contribute to ation of weaning from mechanical ventilation at the earli-
acute organic brain syndrome 135 (see Chapter 7). Rejec- est opportunity. The current evidence base supports
tion episodes can be emotionally demanding, and the strategies to prevent VAP, using daily checklists or care
requirement for higher doses of corticosteroids can lead bundles.


Case study

Frances is a thirty-six-year-old female. She presented to her local Investigations revealed:
general practitioner (GP) with an 11-day history of cough, fever and ● U&E: Na 132 mmol/L, K 3.2 mmol/L, BGL 8.5 mmol/L, Cr
+
+
shakes, and a 5-day history of expectorating tenacious yellow– 99 µmol/L, eGFR >90, bHCG <0.5
9
9
green sputum, decreased appetite and mild right-sided chest pain ● FBE: Hb 130 g/L, WCC 12.89 x 10 /L, Neut 174 x 10 /L
with increasing dyspnoea and a hoarse voice. Her GP organised for ● INR: 1.8
the ambulance to transport Frances directly to the Emergency ● CXR: Right middle lobe pneumonia
Department (ED) of the nearest major public hospital. A peripheral ● Pending: Legionella urinary antigen, atypical serology and
intravenous line was inserted and the patient was continuously respiratory polymerase chain reaction (PCR) testing.
monitored during transportation to the hospital.
Upon arrival at the ED, Frances was assessed as a Triage Category Frances’ past history included hirsutism, polycystic ovaries (PCOS),
2 patient and a baseline assessment was determined: pre-eclampsia and depression. She had no known allergies. At the
● CNS: GCS 15, Temperature 38.6 °C time of presentation to the ED her regular medications were ser-
● CVS: HR 135/min, sinus tachycardia, BP 150/78 mmHg, brisk traline and spironolactone (for PCOS). She reported that she lived
capillary refill with her partner and that she had been at home on annual leave
● RESP: RR 40/min, shallow rapid breathing, appears tired. SpO 2 from her employment for the past three weeks. Further, she
95% while receiving oxygen at 6 L/minute via Hudson Mask, reported that she had not been exposed to any exotic pets or
improving to 98% with increased flow to 8 L/minute. undertaken recent overseas travel.

Respiratory Alterations and Management 375


Case study, Continued

An additional peripheral intravenous line was inserted in ED. The that there was no shunt. The plan was to reduce the PEEP to
clinical impression was pneumonia secondary to possible H1N1 reduce the shunting and by day 4 of ICU the hypoxaemia had
Influenza A (swine flu). The decision was made to transfer Frances resolved.
directly to ICU where an arterial line was promptly inserted for
monitoring, followed by an elective endotracheal intubation for On day 9 of ICU, following an additional 161 hours of intubation,
respiratory distress. She was administered morphine and mid- Frances was extubated again and received high flow oxygen via
azolam sedation. Ceftriaxone, azithromycin, vancomycin and osel- nasal prongs. During the next 3 hours Frances complained of dif-
tamivir were commenced. A central venous catheter was inserted ficulty breathing with no apparent increase in her work of breath-
for fluid administration and inotropic therapy if required. The aim ing or alterations in arterial blood gases. An audible stridor and
was to maintain a mean arterial blood pressure (MAP) > 70 mmHg. bovine cough developed despite administration of nebulised
Her first arterial blood gas showed a respiratory acidosis with meta- adrenaline, intravenous steroids and application of BiPAP. Frances
bolic compensation (FiO 2 1.0, PO 2 197 mmHg; PCO 2 42 mmHg; pH was re-intubated; a Grade 1 airway was evident with oedematous
7.33; BE-9; bicarbonate 22 mmol/L and SaO 2 99%). epiglottis and vocal cords sighted. On day 10 of ICU percutaneous
tracheostomy (size 8) was inserted.
By day 1 of her ICU stay, Streptococcus had been identified in the By day 12 of ICU, following an additional 81 hours of ventilation,
blood cultures. Legionella was not detected. Frances remained Frances was successfully breathing via a tracheostomy-shield and
under respiratory isolation precautions pending PCR results. Venti- oxygenation was adequate. Frances was transferred to the ward on
lation settings were FiO 2 0.3, rate 18, V T 500 mL, PEEP 5 cmH 2 O, day 15 of her admission following more than 24 hours of successful
pressure support 10 cmH 2 O. A noradrenaline infusion was com- breathing via a tracheostomy shield. Antibiotic therapy continued
mence to maintain a MAP >70mmHg. Ongoing enteral feeding and while on the ward and her tracheostomy was removed later that
prophylactic VTE management had commenced. day. Frances remained haemodynamically stable and her health
By day 2 of ICU, the PCR repeat testing again returned a negative continued to rapidly improve so that three days later Frances was
result and respiratory isolation precautions were ceased. Following discharged home to convalesce with her family.
39 hours of intubation, Frances was extubated and maintained an Frances attended a clinical review in the ambulatory care depart-
oxygen saturation greater than 96% with FiO 2 0.5 and humidifica- ment four weeks after her ICU discharge. Her recovery had pro-
tion. Within the next ten hours Frances was re-intubated as she was gressed to the point that she reported being able to walk two
visibly exhausted with an increased work of breathing, and an kilometres (her baseline tolerance was five kilometres). On exami-
increased respiratory rate from 24 to 35 breaths/minute. Further, a nation her lung fields were clear, her oxygen saturation was 98%
reduced GCS and increasing FiO 2 requirement (0.8) to maintain her on room air and her CXR was clear indicating full resolution of
oxygen saturation supported the need for assisted ventilation. the pneumonia. Her blood pressure remained elevated at
Prior to reintubation her ABG result was PO 2 55 mmHg, PCO 2 150/70 mmHg and she was advised to remain on amlodipine and
48 mmHg, pH 7.35, BE 0.9, HCO 3 26 mmol/L and SaO 2 98%.
−
consult her GP for further follow-up and repeat prescriptions.
On day 3 of ICU, Frances’ oxygenation began to deteriorate with Frances was discharged from the ambulatory care clinic following
changes in positioning. Blood-stained sputum was being suc- this clinical review, with ongoing care to be provided by her GP.
tioned via the ETT. A computed tomography angiogram (CTA) of Frances experienced pneumonia post an initial viral illness. Her
the pulmonary vasculature was undertaken and excluded pulmo- plan for the future was to include annual Influenza vaccination in
nary embolus as a cause for the hypoxaemia. It did show that that her health maintenance plan, and timely consultation with health-
there was bibasal and right upper lobe consolidation. There was care workers with any development of unusual respiratory
no evidence of goitre. An echocardiogram bubble study reported symptoms.







Research vignette
Tiruvoipati R, Lewis D, Haji K, Botha J. High-flow nasal oxygen vs Methods
high-flow face mask: A randomized crossover trial in extubated Patients were randomised to either protocol A (n = 25; HFFM fol-
patients. Journal of Critical Care 2010; 25(3): 463–8. lowed by HFNP) or protocol B (n = 25; HFNP followed by HFFM)
Abstract after a stabilization period of 30 minutes after extubation. The
Purpose primary objective was to compare the efficacy of HFNP to HFFM in
Oxygen delivery after extubation is critical to maintain adequate maintaining gas exchange as measured by arterial blood gas. Sec-
oxygenation and to avoid reintubation. The delivery of oxygen in ondary objective was to compare the relative effects on heart rate,
such situations is usually by high-flow face mask (HFFM). Yet, this blood pressure, respiratory rate, comfort, and tolerance.
may be uncomfortable for some patients. A recent advance in Results
oxygen delivery technology is high flow nasal prongs (HFNP). Patients in both protocols were comparable in terms of age, demo-
There are no randomised trials comparing these two modes. graphic, and physiologic variables including arterial blood gas,

Research vignette, Continued
blood pressure, heart rate, respiratory rate, Glasgow Coma Score, Certain limitations were apparent within the study. The recruit-
sedation, and Acute Physiology and Chronic Health Evaluation ment period of time for the study is unreported. It is not reported
(APACHE) III scores. There was no significant difference in gas whether random number generation was responsible for the cre-
exchange, respiratory rate, or haemodynamics. There was a signifi- ation of the randomisation sequence (n = 50) or whether this was
cant difference (P = 0.01) in tolerance, with nasal prongs being well undertaken by the recruiters. The researchers had identified their
tolerated. There was a trend (P= 0.09) toward better patient comfort study’s limitations. This could not be a double- or even single-
with HFNP. blind study as the patient participating and their nurse were aware
of which high-flow modality was being used. Further, it is
Conclusions 170
High-flow nasal prongs are as effective as HFFM in delivering thought, but remains unclear, what window of time with
oxygen to extubated patients who require high-flow oxygen. The one high-flow set up before change over to the alternative
tolerance of HFNP was significantly better than HFFM. strategy is a sufficient length of time to wash out one intervention
before measuring the clinical, self report and bedside observer
Critique patient data.
This article is a well-written and readable research study. It is also
the first to report a scientific comparison between these two often- There are a number of recognised factors that influence
employed oxygen-delivery modalities in clinical practice. The gas exchange such as skeletal muscle conditioning, haematologi-
article’s liberal use of tables and headings allows for ease of under- cal profile and diffusion capacity. Variability of these factors was
standing and the ability to locate specific information.
offset by the trial design as each participant was their own control
This clinical enquiry was a randomised controlled study. Each study in this study’s design. However, it was unclear whether patient
participant had a stabilisation period and following this, proceeded positioning was consistent within and between the study’s partici-
to be randomised to either protocol A or B. The stabilisation period pants. Patient positioning could influence the level of alertness,
became the control period for each participant and increased the airway clearance and gas exchange. It would need to be assumed
strength of the study design. The merit of this experimental design when interpreting these data that the temperature/humidity of the
is that extraneous variables are controlled for. Extraneous variables inspired gas with each intervention was consistent across the
may be antecedent or intervening. Examples of antecedent vari- sample. The function of airway mucosa and temperature of inspired
ables include age, gender, socioeconomic status and premorbid gas has been long established. 171
health status. These data provide a baseline to confirm similarity
between groups prior to assessment of an effect of the interven-
167
tion. Intervening variables may occur during the course of the The sample size was small (n = 44) and the risk of drawing conclu-
study and are unrelated to the clinical trial but may influence the sions based on a small sample size risks a Type II error. These results
dependent variables. For example a media report on the merit of support the researchers’ contention that a larger sample size is
clinical research may influence the public’s attitude to participation required. Power calculations to determine equivalence between
172
in a clinical trial. interventions exist. It is unclear how many bedside nursing staff
participated in this study and if any and/or regular staff in-service
The study was well conducted. The researchers were transparent education occurred to achieve inter-rater reliability of their reports
in their handling of data and reporting of all those initially recruited of the patients’ tolerance with these two high-flow modalities. Each
into this study via the CONSORT statement. The duration of ven- high-flow set up was trialled in 30-minute episodes. How fre-
168
tilation prior to extubation report wide confidence intervals. This quently the bedside nurse observed the patient’s tolerance of the
could suggest that a wide profile of patients were enrolled into this high-flow set up may have been variable. Interestingly the utility
study. Due to this trial being a prospective evaluation undertaken of nasal-delivered high flow oxygen therapy in generating a posi-
in the local setting it is possible to generalise the applicability of tive airway pressure has been examined and reported in healthy
findings across the population in Australia and New Zealand. subjects as proportional to rates of gas flow and reduced pressure
Outcome measures were a combination of quantifiable data such in mouth breathers in Australia and New Zealand in healthy sub-
173
as arterial blood gas analysis and vital signs in addition to subjec- jects and ICU patients albeit with small sample sizes. This study
174
tive measures i.e. the nurse’s report of the patient’s comfort and is important, as it is the first randomised trial that compares two
tolerance for the flow delivery system using the visual analogue popular high flow delivery systems and highlights that further gen-
scale (VAS). The VAS is a ubiquitous, valid and sensitive measure in eration of evidence is vital to support our clinical decision making
a range of age groups. 169 in everyday practice.




Learning activities
1. A patient has severe ARDS following aspiration pneumonia. 4. Describe and compare the differences between a simple, per-
Their FiO 2 is 1 and PaO 2 60 mmHg. Core temperature is 40°C sistent and reoccurring pneumothorax.
and the only medications are antibiotics. Any activity including 5. At the commencement of your shift you undertake a respira-
suctioning causes profound desaturation. What additional tory assessment of your patient. List the parameters that
measures could be implemented to minimise this effect? should be examined.
2. What is your understanding of ARDS?
3. List the interventions required for a nurse to safely care for a
patient with a provisional diagnosis of a novel infectious
disease.

Respiratory Alterations and Management 377

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