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Core knowledge in critical care medicine 2016

Core Knowledge
in Critical
Care Medicine
Wolfgang Krüger
Andrew James Ludman

123


Core Knowledge in Critical Care Medicine



Wolfgang Krüger • Andrew James Ludman

Core Knowledge in Critical
Care Medicine


Wolfgang Krüger
Medizinische Universitätsklinik

Kantonsspital Aarau
Aarau
Switzerland

Andrew James Ludman
Department of Cardiology
The London Chest Hospital
London
UK

ISBN 978-3-642-54970-0
ISBN 978-3-642-54971-7
DOI 10.1007/978-3-642-54971-7
Springer Heidelberg New York Dordrecht London

(eBook)

Library of Congress Control Number: 2014944745
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Special thanks appertains to Dr. M. Morgan,
Christchurch Hospital, NZ, for his inspiring
suggestions and particularly his editorial
support.
I would like to thank my wife Manuela for
her understanding and support during the
writing of this book.
Wolfgang Krüger



Contents

1

Mechanical Ventilation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1.1 Acute Respiratory Failure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1.2 Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1.3 Ventilator Modes Nomenclature . . . . . . . . . . . . . . . . . . . . . . . . . . .
1.4 Volume-Controlled (VC) Versus Pressure-Controlled (PC)
Ventilation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1.5 Indications for Intubation and Mechanical Ventilation. . . . . . . . . .
1.6 Patient–Ventilator Interaction . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1.7 Basics of Respiratory Physiology
and Pathophysiological Issues . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1.8 Pressures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1.9 Ventilator-Induced Lung Injury (VILI). . . . . . . . . . . . . . . . . . . . . .
1.10 PEEP . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1.11 Cardiovascular Effects of Positive Pressure
Mechanical Ventilation (PPMV). . . . . . . . . . . . . . . . . . . . . . . . . . .
1.12 Conclusion for Overall Respirator Settings . . . . . . . . . . . . . . . . . .
1.13 Ventilation of Nonobstructive Acute Respiratory
Failure Patients Not Suffering from ALI/ARDS . . . . . . . . . . . . . .
1.13.1 Summary, Invasive Mechanical Ventilation, Initial
Settings in Non-ALI/ARDS Patients . . . . . . . . . . . . . . . .
1.13.2 Non-invasive Positive Pressure Ventilation (NIV)
in Non-ALI/ARDS Patients . . . . . . . . . . . . . . . . . . . . . . .
1.14 Mechanical Ventilation in COPD and Asthma . . . . . . . . . . . . . . . .
1.14.1 Respiratory Support in COPD Patients . . . . . . . . . . . . . . .
1.14.2 Respiratory Support in Asthma Patients . . . . . . . . . . . . . .
1.15 Ventilator-Associated Pneumonia (VAP) . . . . . . . . . . . . . . . . . . . .
1.16 Weaning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

1
1
3
4
5
7
9
10
15
18
23
26
36
36
39
40
41
45
48
51
53
61

vii


viii

2

3

Contents

Acute Respiratory Distress Syndrome (ARDS). . . . . . . . . . . . . . . . . . .
2.1
Definition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.2
Epidemiology and Prognosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.3
Aetiology. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.4
Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.5
Diagnosis and Clinical Features . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.6
Therapeutic Considerations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.6.1
Respiratory Support/Mechanical Ventilation . . . . . . . . . .
2.6.2
Optimal PEEP . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.6.3
Permissive Hypercapnia . . . . . . . . . . . . . . . . . . . . . . . . . .
2.6.4
Treating Triggers. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.6.5
Respiratory Modes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.6.6
Rescue Measures. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.6.7
Initial Ventilator Settings . . . . . . . . . . . . . . . . . . . . . . . . .
2.6.8
Conservative (Restrictive) Fluid Management . . . . . . . . .
2.6.9
Treatment of Acute Right Heart Dysfunction
(RV-D)/Acute RV Failure (RV-F)
(With the Focus on ARDS) . . . . . . . . . . . . . . . . . . . . . . . .
2.6.10 Extracorporeal Techniques . . . . . . . . . . . . . . . . . . . . . . . .
2.6.11 Miscellaneous . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

99
99
102
103
104
110
113
113
114
117
118
119
120
123
124

Shock . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.1
Definition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.2
Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.3
Aetiology. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.4
Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.4.1
General Pathophysiological Aspects and Remarks. . . . . .
3.4.2
Compensatory Mechanisms and Shock Stages. . . . . . . . .
3.5
Special Pathophysiology of. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.5.1
Cardiogenic Shock . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.5.2
Hypovolaemic Shock . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.5.3
Septic (Distributive–Vasodilative) Shock . . . . . . . . . . . . .
3.6
Diagnostic and Clinical Issues . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.7
Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.7.1
General Approach . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.7.2
Vasopressor Application/Use . . . . . . . . . . . . . . . . . . . . . .
3.7.3
Cardiogenic Shock . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.7.4
Haemorrhagic Shock. . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.7.5
Septic Shock . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

159
159
159
160
163
163
170
173
173
179
181
191
197
197
206
210
215
217
226

125
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129
129


Contents

ix

4

Sepsis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.1
Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.2
Pathophysiology and Pathogenesis of Sepsis . . . . . . . . . . . . . . . . .
4.3
Clinical and Diagnostic Issues . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.4
Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.4.1
Overview . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.4.2
Special Issues . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

273
275
276
286
290
290
292
296

5

Acute Kidney Injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.1
Definition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.2
Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.3
Aetiology. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.3.1
Pre-renal . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.3.2
Intrinsic, Intra-renal Causes . . . . . . . . . . . . . . . . . . . . . . .
5.3.3
Postrenal Reasons . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.3.4
Doubts about Our Traditional Concept . . . . . . . . . . . . . . .
5.4
Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.5
Diagnostic Remarks . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.6
Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.6.1
Optimalization of Haemodynamics, Fluids
and Vasopressive Agents. . . . . . . . . . . . . . . . . . . . . . . . . .
5.6.2
Loop Diuretics. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.6.3
Miscellaneous . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.6.4
Renal Replacement Therapy . . . . . . . . . . . . . . . . . . . . . . .
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

313
313
315
316
317
319
320
322
323
333
336

Nutrition in Critical Illness . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
6.1
Practical Aspects. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
6.1.1
Enteral Nutrition Versus Parenteral Nutrition . . . . . . . . . .
6.1.2
Timing of Initiation of Enteral Nutrition. . . . . . . . . . . . . .
6.1.3
Dosing of Enteral Nutrition. . . . . . . . . . . . . . . . . . . . . . . .
6.1.4
Protein Requirements . . . . . . . . . . . . . . . . . . . . . . . . . . . .
6.1.5
Special Formulas. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
6.1.6
Management of Aspiration Risk . . . . . . . . . . . . . . . . . . . .
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

375
378
378
379
379
381
382
382
383

Appendix: Analgesia and Sedation in the Critically Ill Patients . . . . . . . .
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

391
400

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

409

6

337
343
344
345
349


Chapter 1

Mechanical Ventilation

1.1 Acute Respiratory Failure
Acute respiratory failure (ARF) is defined as the inability of the respiratory system
to meet the oxygenation, ventilatory, or metabolic requirements of the patient [1].
Most authors divide respiratory failure based on the two gas exchange functions,
oxygenation and elimination of carbon dioxide. Either, “only” oxygen replenishment may be compromised or a joint disruption occurs [2, 3]:
I. Hypoxaemic respiratory failure
II. Hypercapnic respiratory failure
Hypoxaemic respiratory failure refers to the failure of the lungs to oxygenate
mixed venous blood sufficiently, PaO2 <60 mmHg- [4, 5], while hypercapnic respiratory failure indicates a blunted elimination of carbon dioxide resulting in respiratory acidaemia with a PaCO2 >50 mmHg in the presence of hypoxaemia [5–7].
Hypercapnic respiratory failure is called ventilatory failure as well [6], highlighting that the ventilatory part of the respiratory system – the “pump function” of the
respiratory apparatus – has failed, mainly due to ventilatory muscle fatigue, rather
than to the gas exchange element [5].
As such, hypercapnia is a hallmark of ventilatory failure [5, 8], and an acutely
decompensated ventilatory failure is characterized by a respiratory acidosis (pH
<7.35) in the presence of hypercapnia [5].
Accordingly, the majority of authors classify respiratory failure into two subtypes [7, 9, 10], although others may distinguish four types [11, 12]:
Type 1: Hypoxaemic respiratory failure
Shunting and a ventilation–perfusion mismatch (V/Q mismatch) are the most
common underlying pathophysiological mechanisms causing hypoxaemia [10, 13,
14]. While V/Q mismatch will easily respond to oxygen delivery (chronic
obstructive pulmonary disease is a typical example [11]), hypoxaemia due to
shunting will persist even if oxygen is supplied [11, 15]. Pulmonary shunting can
be interpreted as an extreme form of V/Q mismatch [15] which occurs in the
W. Krüger, A.J. Ludman, Core Knowledge in Critical Care Medicine,
DOI 10.1007/978-3-642-54971-7_1, © Springer-Verlag Berlin Heidelberg 2014

1


1  Mechanical Ventilation

2

s­ etting of alveolar hypoventilation or alveolar collapse related to atelectasis and/or
alveolar flooding from infection, blood or fluid [16]. Typical examples are cardiogenic pulmonary oedema, non-cardiogenic pulmonary oedema (ARDS), pneumonia, lung haemorrhage, and atelectasis [5, 11, 17]. Other conditions which
may produce hypoxaemic respiratory failure include alveolar hypoventilation
due to high altitude (low FiO2), diffusion abnormalities and low mixed venous
oxygen content subsequent to increased peripheral uptake [10, 13, 14].
Type 2: Ventilatory, hypercapnic respiratory failure
Type 2 respiratory failure is attributed to alveolar hypoventilation as found in (a)
central nervous system disturbance, e.g. anaesthesia, head injury, drug
overdose;(b) neuromuscular diseases, e.g. myasthenia gravis, Guillain–Barre
syndrome, spinal cord diseases, myopathies;(c) elevated breathing workload,
e.g. COPD, asthma, pulmonary fibrosis; and (d) increased dead space, e.g. pulmonary embolism, hypovolaemia, poor cardiac output, alveolar distension and/
or increased CO2 production as in fever, sepsis or burns trauma [10, 11].
Respiratory acidosis in the setting of chronic ventilatory failure must be considered a potentially life-threatening situation, and early mechanically ventilatory
support is warranted [5].
Some authors additionally discriminate two further types:
Type 3: Perioperative ventilatory failure
This is actually a subtype of type 1 and is especially common in the postoperative phase. The main pathophysiology is atelectasis resulting from decreased
functional residual capacity (FRC), anaesthesia, upper abdominal incision, airway secretions, supine position, obesity and ascites [11].
Type 4: Respiratory failure in conditions of shock
Hypoperfusion may affect respiration attributed to either increased demand or
compromised delivery, leading to ARF [11, 12]. In addition, the central respiratory drive may be blunted [11].
Accordingly, a wide variety of etiological conditions may cause ARF, often not
directly affecting the lung tissue [7].
Causes of type I respiratory failure include [5, 17]:









ARDS
Acute asthma
Pulmonary fibrosis
Pneumonia
Pulmonary embolism
Pneumothorax
Pulmonary oedema
COPD

Conditions such as pneumothorax, asthma or particularly COPD may present
initially as type I respiratory failure but become complicated by developing hypercapnia, related to worsening ventilation–perfusion mismatch and/or increasing
work of breathing resulting in exhaustion of the respiratory muscles [5]. The latter
is referred to as ventilatory failure [5, 6] (see above).


1.2 Epidemiology

3

Causes of type II respiratory failure include [5, 17]:









COPD
Kyphoscoliosis
Obstructive sleep apnoea
Acute severe asthma
Abdominal distension (ascites, blood, peritonitis, pancreatitis, etc.)
Morbid obesity resulting in obesity hypoventilation syndrome
Chest wall trauma, e.g. flail chest or pneumothorax
Central nervous system with depression of central respiratory drive
–Coma
– Raised intracranial pressure
– Drugs, i.e. opioids, sedative

• Neuromuscular diseases
– Peripheral nervous system, e.g. Guillain–Barre syndrome, critical illness
polyneuropathy
– Neuromuscular junction, i.e. myasthenia gravis, muscle relaxants, organophosphate poisoning
– Myopathy, e.g. muscular dystrophy
– Cervical cord lesion, e.g. trauma, tumour, etc.

1.2 Epidemiology
A review by Esteban [18] revealed that the indications for positive pressure mechanical ventilation (PPMV) include:





Acute respiratory failure 66 %
Coma 15 %
Acute exacerbation of COPD 13 %
Neuromuscular disorders 5 %

This was largely confirmed in other surveys [19, 20], however all of these studies
were also performed by Esteban and colleagues. Acute respiratory failure may be
caused by a number of different disease entities such as pneumonia, postoperative
conditions, acute heart failure, ARDS and sepsis being the most frequent ones
(between 10 and 18 % each) [18–20]. Thirty three percent [20] to 46 % [21] of all
patients admitted to an ICU need PPMV for more than 12–24 h and the overall
median duration of PPMV is reported to be 3 days [20]. However, a wide range
exists: from 2 days in postoperative cases [22], over 4 days in COPD [20], up to 11
days in pneumonia [23] and 6–15 days in ALI/ARDS [20]. Only a very small number (3 %) needed more than 3 weeks of ventilatory support [20].
Ventilator-associated pneumonia (VAP) occurs in 8–28 % of cases [24], and the
incidence increases with the duration of PPMV [25]. Interestingly, the risk rate


1  Mechanical Ventilation

4

lowers the longer the patient is ventilated, as shown by Cook [26], with the risk rates
of 3% on day 5, of 2% day 10 and of 1% on day 15. However, the cumulative risk
is estimated to be 7 % at 10 days and 19 % at 20 days [27]. However, differences in
the definitions require some caution when generalizing this data.
Published mortality rates vary widely [28, 29], and it is important to note that
ventilator settings have changed fundamentally since the implementation of lung
protective ventilation in 2000, specifically regarding rates of acute lung injury/acute
respiratory distress syndrome (ALI/ARDS) [30]. In unselected populations of
PPMV patients, the reported mortality rates range from 64 % in an older (1993)
study [31] to 39 % in a publication in 2002 [20]. Ideally therefore, when comparing
ventilator-related mortality rates, the disease-specific rates should be considered.

1.3 Ventilator Modes Nomenclature
There is a profusion of terms used to describe ventilator modes which may be inconsistent and confusing, and multiple different names may be used to describe the same
function [32, 33]. However, there are a number of main general principles.
The mode of mechanical ventilation refers to the method of inspiratory support
[34] and comprises three components: (a) the control variable which may be volume
or pressure controlled, or dual switching from one mode to the other during one
breath may be permitted; (b) the breath sequence which may be continuous mandatory, intermittent mandatory or spontaneous; and (c) the targeting scheme, feedback
or type of control mechanism(s) referring to the programmed ventilator target settings, i.e. respiratory rate, tidal volume, minute volume or combined targets [32, 33].
The new generation of ventilators are equipped with adaptive features and use modelled algorithms which calculate how to achieve set goals. However, it is not possible
to control both pressure and volume simultaneously [33, 35].
Based on these principles, eight ventilation modes can be identified [32, 36]:
Control variable
Volume
Pressure

Dual

Breath sequence
Continuous mandatory ventilation
Intermittent mandatory ventilation
Continuous mandatory ventilation
Intermittent mandatory ventilation
Continuous spontaneous ventilation
Continuous mandatory ventilation
Intermittent mandatory ventilation
Continuous spontaneous ventilation

Acronym
VC – CMV (IPPV)
VC – IMV
PC – CMV (IPPV)
PC – IMV
PC – CSV (PSV/ASB)
DC – CMV (CMV, pressure limited)
DC – IMV (IMV, pressure limited)
DC – CSV (CSV, pressure limited)

PC pressure control, VC volume control, DC dual control, IPPV intermittent positive pressure
ventilation, PSV pressure support ventilation, ASB assisted spontaneous breathing

Pressure support ventilation (PSV) or just pressure support (PS) amplifies the
patient’s own respiratory efforts on patient-initiated breaths [37, 38]. With contemporary ventilators, triggering requires the patient to create a small negative inspiratory
flow of −1 to −2 cm H2O [39] which will, if achieved, lead to the initiation of the set
support pressure [40]. Compared to conventional pressure triggering, flow triggering


1.4  Volume-Controlled (VC) Versus Pressure-Controlled (PC) Ventilation

5

probably decreases the work of breathing [41, 42] and minimizes the risk of development of auto-PEEP/gas trapping inherent to the ventilator settings [43, 44].
Synchronized intermittent mandatory ventilation (SIMV), or now just shortened to
IMV [32], refers to a volume- or pressure-controlled mode where the patient is able to
trigger set mandatory breaths. This is allowed to occur only during a limited, short
phase at the end of expiration prior to the next mandatory breath being delivered, and
in addition to a set rate of breaths per minute supplied by the ventilator (whether patient
triggered or not), the patient may spontaneously activate further breaths. These will
usually be pressure supported [32, 36, 40], in order to ensure an adequate tidal volume
which otherwise may vary according to the patient’s respiratory muscle capability [40].
The term dual control was coined by Branson [45]to describe the technical ability
to switch from one control mode to the other during a single breath cycle, i.e. starting
with volume control in order to achieve a set tidal volume (VT) target but limiting
the pressure automatically generated to meet that VT [32]. The same intention is
also known as volume target pressure control which, in line with the results from the
ARDSnet group in 2000 [30], limits the pressure to match the lung protective ventilation settings [40]. In recent years the dual or adaptive pressure-control algorithms have become widely available and combine pressure-limiting and
volume-­cycling features. This is achieved either by regulating the pressure in a
volume-­controlled mode (PRVC) or by assuring a specific volume in a pressure-­
controlled manner. It is physically achieved by affecting the flow delivered over a
variable time, and the pressure is held after flow has stopped [46]. However, this
approach has its limits; a minimum VT is guaranteed but will not be constant because
VT depends on a complex relationship between respiratory compliance, airway
resistance and patient effort and the ventilator is unable to distinguish between
changes in lung mechanical properties and improved patient effort [46].

1.4 V
 olume-Controlled (VC) Versus Pressure-Controlled
(PC) Ventilation
Positive pressure mechanical ventilation (PPMV) either in VC or PC mode replaces
the physiological negative pressure respiration by the exact opposite mechanism
[40]. Indeed, negative-pressure ventilatory support was used in at the advent of
mechanical ventilation, but following the results observed during the polio epidemics in the 1950s, where those patients ventilated with negative-pressure generating
mechanical ventilators had worse outcomes compared to those treated with PPMV,
the technology shifted completely towards the positive pressure variant [47, 48].
Mechanical ventilatory support mainly increases lung volume that decreases in
various disease states due to altered lung mechanics, namely, diminished lung and/
or chest wall compliance and elevated airway resistance. This considerably supports
the work of breathing by unloading the exhausted respiratory muscles, allowing
them to recover, and thus improves pulmonary gas exchange, the latter further
improved by a revised ventilation–perfusion mismatch [49–52].
Volume-controlled ventilation is the most frequently used mode worldwide as
physicians are more familiar with this type of ventilatory support rather than with


6

1  Mechanical Ventilation

pressure-controlled [18]. This may also represent a desire to safeguard tidal and minute volumes which have traditionally been considered the most important target of
respiratory support, and high VT may avoid formation of atelectasis by avoiding alveolar hypoventilation [53]. In VC, the tidal volume set is delivered; however, the pressure necessary to reach the desired VT will vary and may exceed our limits of peak
and plateau pressure [35, 54, 55]. In contrast, in PC mode the pressure set will definitely be generated, but the consecutive tidal volumes will vary as it follows a complex function (see below) largely determined by the respiratory mechanics [54, 55].
The pressure level has to be adjusted if compliance or resistance change, in order to
avoid too low or too high VTs which may risk atelectasis or over-distension, respectively [46]. Although a large body of literature concludes that no significant differences exist between PC and basic modes of ventilation, in terms of outcome, duration
of ventilation or ICU and hospital stay exist [56–58], PC may still have some advantages. Even in VC, the maximal pressures applied need to be limited as there is good
evidence that plateau pressures higher than 26–28 cm H2O [59–61] or a peak inspiratory pressure (PIP) higher than 30–35 cm H2O [53, 62] may have detrimental effects
and should be avoided [54]. Moreover, in PC mode a more favourable pressure distribution and dissemination of the airway pressures including a significant reduction
in peak pressure are found compared to VC [63, 64]. Decelerating inspiratory flow
patterns are applicable in PC but not in VC (only constant patterns) and are associated with improved air distribution in the lungs which have heterogeneous mechanical properties [65–67] and will facilitate gentle and tissue preserving airway pressure
and air distribution conditions. Decelerating inspiratory flow is shown to be especially of value in lungs with poor compliance [40, 68]. At the least, PC may be more
comfortable for patients due to a better interaction between patient and ventilator,
particularly in obstructive lung diseases [69].
In PC the main disadvantage is potential hypoventilation due to varying lung and
chest wall mechanics which allows variations in VT, whereas in VC the high pressures applied may be harmful, VC cannot compensate for leaks [54, 69] and the fixed
flow may lead to patient–ventilator dyssynchrony [46]. However, VC will control the
ventilation, may better manage hypoventilation during the first phase of respiratory
failure and exhibits the lowest degree of hyperinflation if high inspiratory flows are
applied and long expiratory times allowed [69].
In order to better synchronize patient and ventilator, two very similar pressure-­
controlled methods of ventilation have been developed, the so-called bilevel, BiPAP
or BiLevel ventilation, and airway pressure release ventilation, APRV. Biphasic
positive airway pressure (BiPAP, BiLevel) and airway pressure release ventilation
are modified pressure-controlled modes [40, 70]. APRV combines repetitive application of a constant high positive airway pressure (PHIGH or high PEEP level), generating a tidal volume with intermittent pressure releases to a lower pressure level
(PLOW or low PEEP level) causing expiration [71]. As the inspiratory time is kept
very prolonged there is only a short exhalation time in this pressure-controlled
(IMV) ventilatory mode, potentially and intentionally creating auto-PEEP [70].
However, spontaneous breathing is possible at any time, making patient–ventilator
interaction much more comfortable [32, 72]. Biphasic positive airway pressure


1.5  Indications for Intubation and Mechanical Ventilation

7

ventilation (BiPAP) also allows, in principle, for unrestricted spontaneous ventilation (inspiration as well as expiration) at any time during the respiratory cycle,
resulting in reduced sedation requirements and promoting weaning [54, 70]. This
mode also applies two different pressure levels, PHIGH and PLOW, and is conceptually
equal to AVPR [70] with the exception that the duration of the lower pressure level
is far longer than in AVPR where it is by convention less than 1.5 s [33] and that
BiPAP is supportive in spontaneous breaths [70]. AVPR represents a form of
inversed ratio ventilation (IVR) which means that the inspiratory time is extremely
prolonged in order to strongly support oxygen replenishment [33]. In BiPAP, I:E
ratio can be determined by the physician and generally any ratio is available (e.g.
inversed, 1:1, up to 1:4 [5]) [33]. In both types, the lower pressure level applies
PEEP while with the change to the higher level, air will be inflated [33, 70].
Unfortunately, in AVPR the inversed ratio which may be necessary in severe hypoxaemia requires sedation or even paralysis [54]. However, as both techniques significantly improve oxygenation, attributed to alveolar recruitment and improved
ventilation–perfusion matching [73], and as the more moderate settings in BiPAP
allow spontaneous breathing, they are commonly applied in patients with hypoxaemic respiratory failure and BiPAP may routinely be the initial ventilation mode.
Recommended settings are an initial fairly high-pressure level of 12–15 cm H2O
above set PEEP [74]. The potential for spontaneous breathing at any time is of very
high value as it not only facilitates patient–ventilator interaction and synchrony but
helps to avoid respiratory muscle fatigue and longer-term respirator dependency of
which the main cause is diaphragm dysfunction and fatigue [75–77].
CPAP is a PC mode delivering a constant level of positive pressure throughout
the respiratory cycle [40]. It may be applied in a broad range of causes of respiratory
failure as by increasing mean airway pressure, collapsed and hypoventilated lung
units will be reinflated and kept open during expiration with consecutive increase in
functional residual capacity (FRC). This results in improved gas exchange and oxygenation [78] and so this technique is particularly indicated in hypoxaemic respiratory failure [40]. Moreover, as CPAP will improve the lung compliance as well, it
reduces the work of breathing and thus may avert the development of overt muscle
or ventilatory failure [79–81].

1.5 Indications for Intubation and Mechanical Ventilation
The decision to intubate a patient is a complex assessment process requiring the
consideration and integration of numerous aspects and facts, but remains largely a
clinical judgement, and in daily practice is essentially concurrent with the determination to apply PPMV [5, 17, 35, 82–84].
A review by Esteban revealed that the indications for PPMV include [18]:
• Acute respiratory failure 66 %
• Coma 15 %
• Acute exacerbation of COPD 13 %


1  Mechanical Ventilation

8

• Neuromuscular disorders 5 %
Frequently designated/specified indications for PPMV [85]:











Acute respiratory arrest
Apnoea and impending respiratory arrest
Acute hypoxaemic respiratory failure
Coma and acute neuromuscular diseases
Acute exacerbation of COPD
Heart failure and cardiogenic shock
Cardiac arrest
Acute severe asthma
Acute brain injury
Flail chest

The physiological consequences of a sustained pH >7.65 or <7.10 are considered dangerous in itself if not quickly reversible and thus may require mechanical
­ventilation [35]. Within this range from pH 7.1 to 7.65, the clinical condition is
seminal in how to approach the patient [86]. Some indicators in the setting of respiratory dysfunction and distress which support the initiation of PPMV are [50]:
Respiratory rate
Tidal volume, spontaneously
Vital capacity
Rise in PaCO2 from baseline
Negative inspiratory force
PaO2 with supplemented
Alveolar–arterial gradient (on FiO2 = 1.0)
PaO2/PAO2 ratio
GCS

>35/min
<5 ml/kg
<10 ml/kg
>10 mmHg
<−25 cm H2O
O2 <55 mmHg
>450 mmHg
<0.15
<8

A GCS less than eight comes with the risk of not protecting the airway.
Intubation should generally be considered and may be mandatory in head injuries [87]; however, a GCS <8 is otherwise not an absolute indication for intubation [88].
Aside from the clinical assessment, other features may help in making the decision whether to intubate or not [17]:
• Initiation of PPMV necessary and needs facilitation
• Protection from aspiration, particularly in patients not able to protect their airway, which is generally the case in altered mental status as indicated by a
GCS <8
• Facilitation of tracheobronchial suction
• Relief of upper airway obstruction
Further, specific indications for ventilatory support and/or intubation are depicted
in the paragraphs on ventilation in patients suffering from non-ARDS ventilator
failure, COPD, asthma and the separate chapter on ALI/ARDS.


1.6  Patient–Ventilator Interaction

9

1.6 Patient–Ventilator Interaction
PPMV is applied to patients struggling with substantial respiratory difficulties in
order to largely unload the respiratory muscles by taking over or sharing the work of
breathing, facilitating lung inflation and gas exchange, thus reducing dyspnoea [89–
91]. Spontaneous breaths and breathing efforts may be initially replaced by the ventilator, but as passive mechanical ventilation will lead to considerable respiratory
muscle dysfunction and atrophy [92, 93], its timely withdrawal is of pivotal importance [89]. In order to facilitate this, the ventilator actions/responses must synchronize
with patients’ spontaneous breathing efforts and demands [89–91, 94, 95].
When considering why a patient is combating the ventilators, multiple factors may
be contributing; these include underlying lung functional abnormalities, the ventilator
settings set by the clinician, the specific ventilator functions, the patient–ventilator
interface, and not at least the patients’ own airway responses [89, 91, 96, 97].
NIV intolerance is most clearly related to asynchrony [94]. Of particular importance and interest are trigger asynchronies [89, 90, 94, 95], reported to be found in
up to 58 % of all patients [94]. Asynchronies (patient–ventilator interactions) in
general are associated with adverse outcomes, prolonged duration of PPMV and
higher rate of tracheostomy [98–100] due to ineffective ventilation with increased
work of breathing, lung over-distension, impaired gas exchange and patient discomfort [89]. Anxiety and dyspnoea often result from dyssynchronous interactions [90].
Particularly predisposed to mismatch between patients’ request (ventilatory drive
and muscular effort) and the machine’s reply (airflow and pressure delivered) are
patients with COPD and ALI/ARDS [89].
Trigger asynchronies comprise ineffective trigger efforts, auto-triggering,
delayed triggering and premature and delayed release of flow and pressure–volume
[89, 91] with the most common problem being ineffective or wasted efforts [101].
A trigger effort, in the vast majority occurring during the expiratory period, indicated by an abrupt decrease in airway pressure of >0.5 cm H2O is ineffective if not
resulting in an assisted breath from the ventilator (if the trigger occurs during expiration, accompanied by a decrease expiratory flow) [99]. Ineffective efforts, also
known as ineffective triggering, untriggered breaths or trigger asynchrony, may
occur as well during inspiration, indicated by an abrupt increase in inspiratory flow
(in PC mode) or transient abrupt decrease in airway pressure (VC mode) [89, 95].
Dynamic hyperinflation, limited respiratory drive, weakness of respiratory muscles
and insensitive trigger settings are causally underlying ineffective efforts [102].
Since resolving a dys-synchrony in one area often facilitates other adverse interactions as well [90], the most common problem is discussed in detail below.
Although the specific analysis of disadvantageous patient–ventilator interactions
and how to tackle them have been more and more recognized in recent years, the
first systematic approach of how to analyse and manage trigger asynchronies has
been recently done by Sassoon [95]. In brief, low PEEP (5 cm H2O are very common) should be applied, but adjusted in case of measured or suggested intrinsic
PEEP (PEEPi) to 75–80 % of PEEPi as with Nava [103]. If there is still an asynchrony


1  Mechanical Ventilation

10

index of >10 %, increase PEEP by steps of 1 cm H2O up to max 8 cm H2O. If still
wasted efforts are present, adjust VT to 6–8 ml/kg PBW [104]. Thereafter, increases
in inspiratory flow rate (VC) or pressure (PC) are recommended. Further steps and
details, see Fig. 1.1 below:
[Def asynchrony index (AI) = number of wasted efforts/number of wasted efforts
plus triggered breaths during a period of 2 min [105] in percent [99]]
Keep in mind that some degree of asynchrony may always be present [95].

1.7 B
 asics of Respiratory Physiology
and Pathophysiological Issues
To breathe and thus inflate the lungs, a pressure gradient between the nose/mouth
(atmosphere) and the lungs (alveoli) is needed as air, like fluid, moves from the
higher pressure level towards the lower one [106, 107]. During inspiration the contraction of the respiratory muscles, diaphragm and external intercostal muscles
enlarges the thoracic cage. Due to the (elastic) recoil properties of the lungs, adhered
to the chest wall by a thin layer of fluid, the enlarging thoracic cavity generates a
negative intrapleural pressure which is accompanied by a subatmospheric, negative
alveolar pressure, establishing a pressure gradient within the airways, called the
distending or transpulmonary pressure [106, 108, 109]. Mathematically this distending or transpulmonary pressure (gradient) being the driving force of airflow can
be described and is defined by


PTRANS = PAL - PPL ( formula A )



with PAL being the pressure within the alveoli, and PPL represents the pressure in the
intrapleural space [106, 108, 110]. In mechanically ventilated patients, the airway pressure (PAW) can be measured and equals alveolar pressure (PAL) if there is no airflow
[111, 112]. This is usually determined at end inspiration, as the end-­inspiratory pressure is considered as being the most critical one since it distends the alveoli/alveolar
units [113], but is otherwise influenced by lung and chest specific factors and properties

Fig. 1.1  Algorithm to improve patient–ventilator synchrony (With permission from Sassoon [95]).
Start up to fine-tune PEEP as depicted. If PEEPi (intrinsic PEEP) cannot be measured or is ≤5 cm
H2O, go ahead with PEEP of 5 cm H2O! With persisting asynchrony index (number of wasted
efforts/number of wasted efforts + triggered breaths during a period of 2 min [%]) >10 %, increase
applied PEEP by 1 cm H2O steps up to a max of 8 cm H2O, if measurable PEEPi apply 75–85 % of
that. If after PEEP adjustment still a relevant asynchrony (asynchrony index >10 %) remains, adopt
VT: 6–8 ml/kg IBW. With ongoing asynchrony, increase respiratory flow rate in case of VCV or
pressurization rate if the patient is on PCV. In the end, in case of time-cycled pressure target settings decrease inspiratory time, while in pressure support-ventilation, adjustment of the flowcycling threshold is recommended: upward in case of prolonged expiration, otherwise downward


1.7  Basics of Respiratory Physiology and Pathophysiological Issues

11

Identify
candidate
patient

Assess patient
Measurable static
PEEPi?

No

Yes

Apply PEEP 75–80 %
of PEEPi

Yes

PEEPi >5
cm H2O

No

Asynchrony
index >10 %

No

Apply PEEP 5 cm H2O or
increase by 1 cm H2O not to
exceed 8 cm H2O

Yes

Set VT 6–8 ml/kg

Pressuretargeted
mode

No

Increase inspiratory
flow

Yes

Increase pressurization rate

Time
cycled

No

Long time
constant
(COPD)

Yes
Yes

Decrease inspiratory
time

Increase flow cycleoff threshold
(% of peak flow)

No

Decrease flow cycleoff threshold
(% of peak flow)


1  Mechanical Ventilation

12

[110, 114]. Accordingly, the airway pressure needed to inflate the lungs either during
spontaneous breathing or by ventilator is affected by the compliance of the respiratory
system (CRS), the airway resistance (R), the volume (V) inhaled (tidal volume, VT) and
the airflow (Q) [110], depicted by the following relationship:


PAW = V / CRES + R / Q

[110]

In contrast, PTRANS measured at end inspiration is free from such influences, allowing estimation of the actual true distending pressure in the passive lungs [113, 114].
The transpulmonary pressure is negative during spontaneous inspiration, zero at the
functional residual capacity (FRC) of the lungs where the opposing forces of lungs
and chest wall are equal and opposite to each other [110], and at which the PPL is −5 cm
H2O as most authors mention [108], and positive during expiration [110].
Of those features mentioned above affecting the airway pressure, the compliance
is of special interest and relevance.
The compliance of the respiratory system is made up by the compliance of the lungs
(CL) and the compliance of the chest wall (CW), related by 1/CRS = 1/CL + 1/CCW
(or ­alternatively CRS = (CCW × CL)/(CCW + CL)) as both components are arranged in series
[108–110]. The elastic properties of the respiratory system, CRs, correlate well with the
amount of aerated lung tissue in patients with acute lung injury and ARDS [115].
Compliance is the inverse of elastance (ETOT = EL  + ECW [112]-formula (B)), with
ETOT indicating the elastance of the whole respiratory system (RS) as counterpart to
its inverse (CRS) and a measure of the distensibility of the tissues, in this case an
estimate of the ease of the lungs and the chest wall to distend [108, 110]. As compliance per definition equals the change in volume (usually VT) per cm H2O change
in pressure, C = ΔV/ΔP [106, 108, 109], the chest wall elastance can be separated by
pleural pressure and rearrangement of formula (A) and (B):
PPL = PAW  ×  ECW/ETOT [112], at which PAW represents PAL since literally the airway
opening (mouth/tube) pressure in end-inspiratory hold is assessed, also called plateau pressure (see below); thus in a static setting after proximal airway pressure and
distal, alveolar pressures have equalized [116]. As Barberis et al. [117] nicely show,
in the clinical setting this happens 0.5 s after the onset of occlusion. In physiological
circumstances ECW/ETOT ≈ 0.4 to 0.5 at FRC level [112]. Consecutively, transpulmonary pressure reflecting the alveolar distending forces can be calculated by
PTRANS = PAW  ×   EL/ETOT  [112].
The compliances of lung tissue and chest wall are depicted in Fig. 1.3, as obviously, their lung volumes are markedly different at recoil pressure zero and any change
in either compliance will affect total elastance; see Fig. 1.2 by Kacmarek [110].
Pulmonary (lung) and chest compliance may be substantially different, depending on the disease and underlying medical conditions [118–120], and as such may
considerably affect the transpulmonary pressure with potentially marked clinical
implications [112, 116, 121]. The transpulmonary pressure most closely represents
the actual alveolar distending pressure [114] responsible for and considered as
being the main cause of ventilator-induced lung injury [65, 112, 122–124].
Impaired chest wall compliance is common and may be present in ALI/ARDS
patients with abdominal diseases (extrapulmonary ALI/ARDS) associated with
increased intra-abdominal pressure such as bowel distension, ascites, sepsis, pancreatitis, (pre-) eclampsia, multi-trauma or peritonitis [112, 118, 119], or even obesity


1.7  Basics of Respiratory Physiology and Pathophysiological Issues
Fig. 1.2  Depicted are the
compliance curves of the
lungs, thorax and the total
respiratory system. As can
be derived from the curve
progression, any change in
either or both lung and
thoracic compliance affects
the total compliance of the
respiratory system. TLC total
lung capacity, RFC
functional residual capacity
(With permission from
Kacmarek [110])

13

Vol% TLC
100

Lung

Chest
wall

Respiratory
system
FRC

20
cm H2O
–20

–10

0
Recoil pressure

10

20

30

Pressure
(mbar)
B

Peak pressure

C
Resistance
Pressure
(R.V )
A

Flowphase

Plateau pressure

D

Pausephase

Inspiration time

“Resistance
pressure” (R.V )

“Compliance
pressure” (VT/C)
“PEEP”

Expiration time

Time (s)

(Vinsp = const.)

Fig. 1.3  Depicts the course of airway pressures in chronological sequence during mechanical
ventilation. Pressure – time diagram of a volume controlled, constant flow positive pressure
mechanical ventilation mode to explain pressure behaviour and ventilatory parameters. R airway
resistance, VT tidal volume, C compliance of the lungs and the chest – total compliance and of the
mechanically ventilator system (like tubes etc.), V flow. A beginning of inspiration (mechanical
application of air), B peak pressure, C plateau pressure, D end-expiratory pressure, if positive
called PEEP (Modified with permission from Rittner and Döring [146])

[112, 125]. Gattinoni et al [118] established a linear relationship between increases
in intra-abdominal pressures and chest wall elastance:


ECW = 0.47 × intra − abdominal pressure ( cm H 2 O ) + 1.43

[118, 126].

Furthermore, pleural effusions which are often due to a positive fluid balance
[127], obesity, sedation and paralysis in anaesthetized patients, and anatomical
chest abnormalities all may, at least to some degree, cause an increase in chest wall


14

1  Mechanical Ventilation

elastance [120, 128–130]. Thus, for any given applied airway pressure, with
increasing chest wall elastance, the pleural pressure will increase, while the transpulmonary distending pressure will drop [112, 131]. However, in patients with pulmonary ARDS, as may develop in the setting of diffuse pneumonia, aspiration,
inhalation-­trauma or multi-localized pulmonary embolism, the lung elastance may
be considerably altered while the chest wall elastance is not affected, causing the
transpulmonary pressure to increase but leaving the pleural pressure unchanged/
normal [118, 119, 121, 132] as alveolar pressure is not transmitted [112]. Hence,
impaired chest wall compliance (ECW) associated with consecutively altered ECW to
ETOT ratio and abnormally increased pleural pressure as found in a remarkable number (up to 30 %) [133, 134] of patients suffering from extrapulmonary ALI/ARDS
commonly due to abdominal hypertension or compartment syndrome [133, 134]
induces for any given airway pressure a reduction in PTRANS. While patients with
pulmonary ALI/ARDS, although holding the same total elastance of the respiratory
system (ETOT), exhibit considerably altered lung mechanics (EL) and a concomitant
rise of the EL to ETOT fraction, displaying a significant increase in the transpulmonary lung parenchyma distending pressure PTRANS, but leaving the pleural pressures
unchanged as alveolar pressures are not transmitted [112], accordingly characterizing
two subtypes of the same clinical picture, ALI/ARDS [112, 119, 127, 131, 132].
Not to induce a misimpression, an increase in the total elastance of the respiratory system is, in the majority of ALI/ARDS cases, provoked by disturbed lung
parenchymal properties rather than chest wall mechanics [135, 136]. In this setting,
ECW contributes to ETOT by about 20 % [132], but this proportion may increase to up
to 50 % in ARDS patients [112].
In order to further illustrate the relationship and interactions [131], in most
­pulmonary ARDS patients, the mechanical properties of the chest wall contribute to
20 % of the total respiratory elastance, and, let us say the airway pressure is set to
30 cm H2O. Thus, using the formula



PTRANS = PAW ´ EL / ETOT , PTRANS = 30 cm H 2 O
´ 0.8 ( as lung elastance contributes to 80%to ETOT ) ; thus, PTRANS = 24 cm H 2 O.



If the chest wall properties are affected by the disease as in peritonitis with
increased intra-abdominal pressure, the chest wall may contribute to 50 % to ETOT.
Hence, PTRANS = PAW  × EL/ETOT = 30  cm  H2O × 0.5 = 15  cm  H2O, quite a highly
significant difference and certainly will affect management.
However, the described differences in mechanical and morphological properties and
the consecutive behaviour of the respiratory system in patients suffering from pulmonary and extrapulmonary ALI/ARDS imply different therapeutic approaches [112,
114, 131, 137]. As the real distending and thus potentially injurious pressure (PTRANS)
for lung tissue is, due to altered chest wall mechanics, markedly lower in patients suffering from extrapulmonary ALI/ARDS [118, 119, 131, 132], the application of
higher airway pressures intending to increase/adjust VT or PEEP may be advisable:
1. Adequate VTs are not only possible but may even be necessary to avoid ­atelectasis
following too low tidal volumes [131, 138] as a relative large amount of the
applied pressure will dissipate against the stiff chest [114, 131].


1.8 Pressures

15

2. Specifically a higher PEEP will contribute to avoid cyclic reopening and collapse
of the diffuse localized and unstable alveolar units [126, 139, 140] typically
found as a result of the diffuse pulmonary oedema and the inflammatory cascade
which originates outside the lung [141] in extrapulmonary ALI/ARDS.
The opposite conclusions could be drawn in cases of pulmonary ALI/ARDS [112].
Furthermore, based on the diverse chest wall and lung mechanics in both subtypes,
recruitment attempts are more successful in extrapulmonary rather than in pulmonary ALI/ARDS [127, 132, 142]. Extrapulmonary ARDS patients demonstrate a
bigger improvement in oxygenation when put into a prone position [143] attributed
to regional changes in transpulmonary pressure resulting in lung density redistributions; however, in pulmonary ARDS, a more even distribution of ventilation will take
a beneficial effect as well [144].
Of note, higher pleural pressures may compromise venous return and thus cardiac
filling, hence resulting in lower cardiac output [145].

1.8 Pressures
Plateau pressure (PPLAT) reflects the applied airway pressure during the end-­inspiratory
hold after inflation has finished and before exhalations starts [147], also called static
elastic recoil pressure, as it largely reflects elastic and resistive properties of the
respiratory system in ARF [117, 148]. The mechanical properties of the respiratory
system are determined by its two main components, lung and chest wall, which are
arranged in series, and their interactions [149]. Thus plateau pressure represents the
sum of pressures required to inflate the lungs and to expand the chest wall [124];
hence the amount of tidal volume applied depends on PPLAT [150]; on the other hand
PPLAT may be decisively influenced by chest wall mechanic properties [124, 151], as
already described in detail above. Nevertheless, it is taken as an estimate of endinspiratory lung distension [117], as such alveolar stretch is reflected by PPLAT [152].
Increases in PPLAT are associated with declines in respiratory system compliance
(CRS) and vice versa [153]. If comparing PPLAT with peak airway pressure (PPEAK) (see
Fig. 1.3) in normal lungs, PPEAK is found to be only slightly above PPLAT [147, 154].
PPEAK indicates the resistive characteristics of the respiratory system, specifically the
airways during inspiratory flow [155]. If respiratory compliance decreases or VT
increases, PPEAK and PPLAT rise proportionately [147, 154]. Situations where PPLAT
remains unchanged while PPEAK increases are indicative for increased total inspiratory resistance which includes tube and airways resistance and should lead to a
check for airway obstruction [153, 154].
Of course, the real distending force of the lungs and hence alveoli is determined
by the pressure difference between the alveolar pressure (PAL) and, more generally
expressed, the surrounding pressure (PSUR), called transpulmonary pressure (PTRANS),
and thus is defined as [106, 108, 112, 156]:


PTRANS = PAL - PSUR




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