Copd and Asthma

AN ESICM MULTIDISCIPLINARY DISTANCE LEARNING PROGRAMME
FOR INTENSIVE CARE TRAINING

COPD and asthma

Organ specific problems

Update 2012

Module Authors (Update 2012)

Raymond Friolet
Dept of Intensive Care Medicine, University of Bern, Switzerland; Dept of Intensive
Care Medicine, Sion Hospital, Centre Hospitalier du Centre du Valais, Wallis,
Switzerland

Marco Conti
Service of Intensive Care, Department of Anesthesiology, Pharmacology, and Intensive
Care, Geneva University Hospital, University of Geneva, Geneva, Switzerland

Module Authors (first edition)

Raymond Friolet/Roland Dietler
Dept of Intensive Care Medicine, University of Bern, Switzerland

For The Bernese PACT Working Group (in alphabetical order)
Roland Dietler, Raymond Friolet, Roger Lussmann, Hans-Ulrich Rothen, Kay Stricker,
Jukka Takala, Eva-Maria Weiss-Guillet, Jeannie Wurz

Module Reviewers Joanna Brown, Fernando Suarez Sipmann,
Janice Zimmerman

Section Editor Anders Larsson

COPD and asthma
Update 2012
Editor-in-Chief Dermot Phelan, Dept of Critical Care
Medicine, Mater Hospital/University College
Dublin, Ireland
Deputy Editor-in-Chief Position vacant
Medical Copy-editor Charles Hinds, Barts and The London School
of Medicine and Dentistry
Self-assessment Author Hans Flaatten, Bergen, Norway
Editorial Manager Kathleen Brown, Triwords Limited, Tayport,
UK
Business Manager Estelle Flament, ESICM, Brussels, Belgium
Chair of Education and Training
Committee
Marco Maggiorini, Zurich, Switzerland

PACT Editorial Board
Editor-in-Chief Dermot Phelan
Deputy Editor-in-Chief Position vacant
Respiratory failure Anders Larsson
Cardiovascular critical care Jan Poelaert/Marco Maggiorini
Neuro-critical care Mauro Oddo
Critical Care informatics,
management and outcome
Carl Waldmann
Trauma and Emergency Medicine Janice Zimmerman
Infection/inflammation and Sepsis Johan Groeneveld
Kidney Injury and Metabolism.
Abdomen and nutrition
Charles Hinds
Peri-operative ICM/surgery and
imaging
Torsten Schrder
Professional development and
Ethics
Gavin Lavery
Education and assessment Lia Fluit
Consultant to the PACT Board Graham Ramsay

Copyright 2012.European Society of Intensive Care Medicine. All rights reserved.

LEARNING OBJECTIVES

After studying this module on Chronic Obstructive Pulmonary Disease (COPD) and
Asthma, you should be able to:
1. Evaluate the severity of respiratory distress and triage patients to the
appropriate level of care
2. Understand the pathophysiologic mechanisms that lead to decompensation
in COPD and asthma patients
3. Manage ventilatory support of COPD and asthma patients in the ICU
4. Provide non-ventilatory support and manage complications
5. Know how to wean the patient from mechanical ventilation and develop a
weaning protocol.

FACULTY DISCLOSURES
The authors of this module have not reported any disclosures.

DURATION
7 hours

Copyright2012. European Society of Intensive Care Medicine. All rights reserved.

Introduction .......................................................................................................................1
1/ Initial evaluation and triage of patients with respiratory distress .............................. 2
Initial assessment and management on ward/in ED ................................................... 2
Differential diagnosis ................................................................................................. 3
Severity assessment and risk assessment for respiratory exhaustion ....................... 3
2/ Why do COPD and asthma patients decompensate? .................................................. 9
The chain of events ........................................................................................................ 9
How does expiratory obstruction occur? .................................................................... 10
COPD ........................................................................................................................ 10
How does airflow obstruction affect respiratory mechanics? .................................... 12
Asthma .......................................................................................................................... 15
3/ Managing ventilatory support of COPD and asthma in the ICU ............................... 17
Defining a strategy and initial setting of the ventilator .............................................. 19
Assessment of dynamic hyperinflation ....................................................................... 21
When to apply PEEPe............................................................................................... 26
How much PEEPe should be applied? ..................................................................... 26
Clinical problems in applying PEEPe ...................................................................... 27
Cardiopulmonary interactions .................................................................................... 27
4/ Providing non-ventilatory support and managing complications ............................ 29
Drug treatment ............................................................................................................ 29
Asthma ...................................................................................................................... 29
COPD ........................................................................................................................ 32
Supportive therapies ................................................................................................... 35
Correction of fluid imbalance ................................................................................... 35
Correction of acidosis ............................................................................................... 35
Alkalosis .................................................................................................................... 36
Nutritional support .................................................................................................. 36
Treatment of common complications ......................................................................... 36
Fever ......................................................................................................................... 36
Atelectasis and sputum retention ............................................................................ 37
Tachycardia, tachyarrhythmia ................................................................................. 38
5/ Weaning the patient ................................................................................................... 40
When to start weaning ................................................................................................ 40
How to wean ............................................................................................................. 42
Weaning failure ........................................................................................................... 46
Role of non-invasive ventilation in weaning ............................................................... 47
Role of tracheostomy ................................................................................................ 49
Long-term outcome ..................................................................................................... 49
Conclusion ....................................................................................................................... 51
6/ Glossary ...................................................................................................................... 52
Self-assessment .............................................................................................................. 59
Patient challenges ........................................................................................................... 64

1

INTRODUCTION

Chronic obstructive pulmonary disease (COPD) is a worldwide and rapidly
growing health problem: it was the sixth leading cause of death worldwide in
1990 and is expected to become the third leading cause by 2020. COPD places a
huge economic burden on society.

Transient worsening of the chronically altered lung function (so-called
exacerbation of COPD) may lead to life-threatening respiratory insufficiency
requiring ventilatory support.

Mortality from asthma is also not negligible: it is estimated at 1.4 per 100,000
annually in the United States. Although most deaths from acute asthma occur
outside the hospital, patients who are admitted to the emergency department
(ED) or a general ward and fail to improve should be admitted to an ICU or at
least to a high-dependency unit (HDU), where ventilatory support and
appropriate monitoring is possible.

It is of paramount importance to properly triage patients with COPD and asthma
so that those at risk of deterioration or death can benefit from ICU/HDU
management.

Global Strategy for the Diagnosis, Management and Prevention of COPD, Global
Initiative for Chronic Obstructive Lung Disease (GOLD) 2011. Available
from: http://www.goldcopd.org/
Global Strategy for Asthma Management and Prevention, Global Initiative for
Asthma (GINA) 2011. Available from: http://www.ginasthma.org/
National Heart, Lung, and Blood Institute, National Asthma Education and
Prevention Program. Expert Panel Report 3: Guidelines for the Diagnosis
and Management of Asthma. Full Report 2007.
http://www.nhlbi.nih.gov/guidelines/asthma/index.htm
Hinds CJ, Watson JD. Intensive Care: A Concise Textbook. 3rd edition. Saunders
Ltd; 2008. ISBN: 978-0-7020259-6-9.
2

1/ INITIAL EVALUATION AND TRIAGE OF PATIENTS
WITH RESPIRATORY DISTRESS

Initial assessment and management on ward/in ED

The terminal event of respiratory distress in COPD and asthma is respiratory
arrest. Regardless of the origin of the distress, any patient, who is not known to
be for palliative care, who presents with impending respiratory arrest should
immediately receive mechanical ventilatory support, via a tracheal tube or a non-
invasive procedure (for details of ventilatory support see Task 3). Warning signs
of impending respiratory arrest are lethargy, obtundation, silent chest, cyanosis,
bradycardia and hypotension.

There is no universal predictive model for survival or weaning failure in severe
exacerbation of COPD. Thus, unless the patients refusal of intubation has been
declared in advance care planning (which should take place for each severe
COPD patient during the stable phase), ventilatory support is initiated in patients
with severe exacerbation of COPD requiring ventilatory assistance. Indeed, the
presence of severe COPD in itself is not enough to withhold ventilatory support.
Such a decision has to integrate other prognostic factors such as disease severity,
major co-morbidities, age and previous quality of life.

In addition to providing mechanical respiratory support as needed, concurrent
immediate treatments include:

Asthma COPD
Inhaled -
mimetics
++ ++
Inhaled
anticholinergics
+ ++
Systemic
corticosteroids
++ +
Antibiotics +
Oxygen
++
+ (cautious
titration)
Non-invasive
ventilation
(+) ++
Theophylline
Mucokinetics

++ good evidence; + relatively good evidence; no evidence

For further information, see Task 4.

Oxygen therapy: If the patient is hypoxaemic, oxygen is applied in acute
asthma and also in an exacerbation of COPD.
It is, however, important to know that in COPD, pCO
2
may rise in association
with the O
2
therapy. This necessitates iterative blood gas measurement to avoid
CO
2
narcosis, and corresponding titration of FiO
2
so that SaO
2
reaches but does
not exceed 90%.
3

Ventilatory support: If reaching this target induces a significant worsening of the
respiratory acidosis, there is a clear indication for ventilatory support.

THINK If you are told that the respiratory drive is not dampened by the application
of oxygen, what pathophysiological mechanism could explain the increase of pCO
2
?
The following references can provide information on the mechanism.

Robinson TD, Freiberg DB, Regnis JA, Young IH. The role of hypoventilation and
ventilation-perfusion redistribution in oxygen-induced hypercapnia during
acute exacerbations of chronic obstructive pulmonary disease. Am J Respir
Crit Care Med 2000; 161(5): 15241529. PMID 10806149
http://ajrccm.atsjournals.org/content/161/5/1524.long
Aubier M, Murciano D, Milic-Emili J, Touaty E, Daghfous J, Pariente R, et al.
Effects of the administration of O
2
on ventilation and blood gases in
patients with chronic obstructive pulmonary disease during acute
respiratory failure. Am Rev Respir Dis 1980; 122(5): 747754. PMID
6778278

Q. What is the definition of an exacerbation of COPD?

A. There is no universal answer. According to the GOLD update 2011: An exacerbation
of COPD is defined as an acute event characterised by a worsening of the patients
respiratory symptoms (baseline dyspnoea, cough and/or sputum) that is beyond normal
day-to-day variations and leads to a change in medication.

Di ffer enti al di agnosi s

After initiating the required level of respiratory support (which may include
intubation and ventilation), review the possible aetiologies of ventilatory failure
e.g. acute pulmonary oedema, pneumothorax, upper airway obstruction. To rule
out these pathologies, which can clinically mimic COPD or asthma exacerbation,
and to look for the aetiology triggering the exacerbation, the most useful
investigation is a baseline chest radiograph. This in turn always has to be
evaluated in relation to a patients symptoms, clinical findings and preferably a
previous radiograph.

Heart failure is often present in decompensated COPD (more often right
ventricular than bi- or left ventricular) even in the presence of other possible
aetiologies (pulmonary infection, pneumothorax, pulmonary embolism). See the
PACT module on Heart failure.

Severi ty assessment and ri sk assessment for respi rator y
exhausti on

It is more difficult to gauge the severity of respiratory distress when respiratory
arrest is not impending. It is important to recognise and properly treat patients
who are at risk of exhaustion, as exhaustion can rapidly end up in respiratory
arrest.
4

Severity assessment depends on medical history, clinical findings and initial
response to therapy.

Medical history (COPD)
(see below for asthma)

Prognosis of COPD exacerbation depends on baseline severity of COPD, on the
presence of significant co-morbidities, and the number of previous
exacerbations. The severity of the baseline COPD is best evaluated by the GOLD
spirometric classification.

Severity Post-
bronchodilator
FEV1/FVC*
FEV1
% predicted
Stage 1 Mild
COPD
<0.7
80
Stage 2
Moderate COPD
<0.7 5080
Stage 3 Severe
COPD
<0.7 3049
Stage 4 Very
severe COPD
<0.7 <30
* FEV1 = forced expiratory volume in one second; FVC = forced vital capacity

Other clinical features which raise the suspicion of a severe disease:
Cachexia
Cough syncope
Signs of chronic right heart failure


Medical history (asthma)

In asthma, the risk factors for near-fatal asthma are a combination of
features of severe asthma recognised by one or more of:
A history of prior mechanical ventilation and intensive care unit
admission
Prescription of oral corticosteroids and theophylline
Evidence of worsening asthma over a period of 27 days with
increasing use of short-acting 2-adrenergic receptor agonists
Poor compliance with inhaled corticosteroid therapy
Difference in perception of dyspnoea
Age >40 years
Brittle asthma
5

o Type 1: wide peak expiratory flow rate (PEFR) variability
(>40% diurnal variation for >50% of the time over a period
>150 days) despite intense therapy.
o Type 2: sudden severe attacks on a background of apparently
well controlled asthma.

And adverse behavioural or psychosocial issues recognised by one or more
of:
Failure to attend appointments
Self-discharge from hospital
Psychosis, depression, other psychiatric illness or deliberate self-harm
Alcohol or drug abuse
Obesity
Employment and income problems
Social isolation.

Papiris SA, Manali ED, Kolilekas L, Triantafillidou C, Tsangaris I. Acute severe
asthma: new approaches to assessment and treatment. Drugs 2009; 69(17):
23632391. PMID 19911854
Jalaludin BB, Smith MA, Chey T, Orr NJ, Smith WT, Leeder SR. Risk factors for
asthma deaths: a population-based, case-control study. Aust N Z J Public
Health 1999; 23(6): 595600. PMID 10641349
Rea HH, Scragg R, Jackson R, Beaglehole R, Fenwick J, Sutherland DC. A case-
control study of deaths from asthma. Thorax 1986; 41(11): 833839. PMID
3824270
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC460507/?tool=pubmed

Clinical findings (COPD)

Change in mental status, intercostal retraction, paradoxical thoraco-abdominal
movements and use of auxiliary muscles are important clinical findings in
assessment of exacerbation severity. Presence of haemodynamic instability
and/or right heart failure are also signs of severity as is an inadequate response
to initial therapy with persistent or worsening of hypoxaemia and/or of
hypercapnia. A good predictor of impending respiratory exhaustion is the
occurrence of uncompensated respiratory acidosis (pH <7.35), and in particular
its progression over time.

Clinical findings (asthma)

Clinical signs of severe asthma are:

Inability to complete sentences in one breath
Utilisation of accessory muscles and suprasternal retractions
Respiratory rate (RR) >30/min
Tachycardia >120/min
6

PEFR <60% of predicted normal or of best normal if known; or<100
L/min, if not known
An absence of sustained response to treatment (<2 hrs)
Hypoxaemia while breathing air (PaO
2
<8 kPa/60 mmHg) and
hypercapnia (PaCO
2
>6 kPa/45 mmHg)

Asthma (GINA) 2011. Figure p. 72. Available from:
http://www.ginasthma.org/

Patient deterioration despite optimal treatment with progressive
increase of PaCO
2
is a sign of impending respiratory exhaustion and a predictor
of fatal asthma, even before the occurrence of severe hypercapnia.

Immediately life-threatening clinical features are:

Silent chest, weak respiratory efforts with paradoxical thoraco-
abdominal movement
Confusion or coma
Bradycardia and hypotension
Cyanosis.

Triage

In asthma, the initial response to therapy is an important prognostic finding and
will be decisive in triage. If a patient who demonstrates criteria of a severe
exacerbation does not improve rapidly, i.e. within 12 hours, s/he needs to be
admitted to a ward where ventilatory support is possible. Improvement is
monitored clinically, physiologically as demonstrated by the blood gases
(decreasing pCO
2
) and by lung mechanics (i.e. PEFR).

Since in COPD the therapeutic response is usually not as fast, triaging patients
does not have the same implications as in asthma. Nevertheless, if the patient
responds rapidly to initial treatment, admission to a normal ward may be
considered.

The three tests that are the most useful in evaluating acute respiratory
distress are arterial blood gas analysis, PEFR, and baseline radiography of the
lungs.

7

Summary of severity assessment and risk of respiratory failure

COPD Asthma
Medical history Co-morbidities
Severity of baseline
COPD (spirometry)
Number of previous
exacerbations
Previous ICU
admission
Previous mechanical
ventilation for asthma
Deterioration despite
optimal treatment
including oral steroids
Increasing use of -
mimetics over several
days

Clinical signs Severity of dyspnoea:
Resp. Rate Auxiliary
muscle use
Change in mental
status
Haemodynamic
instability
PEFR not useful

Severity of dyspnoea:
Resp. Rate Auxiliary
muscle use
Silent chest
Haemodynamic
alterations:
tachycardia
Agitation, anxiety or
stupor, coma
Failure to improve
within 12 hours of
initial treatment
PEFR useful

Blood gases Hypoxaemia
Respiratory acidosis
No improvement with
treatment
Normocapnic or
hypercapnic
hypoxaemia
No decrease of pCO
2

with treatment
No correction of
hypoxaemia

The most important question to address in triaging is whether the patient might
need ventilatory support. The above-mentioned severity criteria, as well as the
initial response to treatment, are the cornerstones for triage: patients with severe
COPD exacerbation with respiratory acidosis (pH <7.35), or with severe asthma
not clearly improving under initial treatment, should be admitted to a ward with
the capability for ventilatory support (non-invasive and/or intubation) such as
the ICU or HDU.

Criteria for admission to ICU:

COPD
Inadequate response to initial therapy (severe dyspnoea, altered
mental status)
Persistent or worsening hypoxaemia (PaO
2
<5.3 kPa/40 mmHg)
despite supplemental oxygen and non-invasive ventilation
When in
doubt, admit
the patient: A
night in the
ICU is better
than a life in
the grave
8

Persistent or worsening respiratory acidosis (pH <7.25) despite non-
invasive ventilation
Need for invasive mechanical ventilation
Haemodynamic instability requiring vasopressors.

Asthma
Poor response to initial 1 to 2 hours of treatment
Risk factors for near-fatal asthma
Persistent or worsening of clinical symptoms (respiratory distress,
decreased mental status)
PEFR <30%
PaO
2
<8 kPa/60 mmHg
PaCO
2
>6 kPa/45 mmHg

Asthma (GINA) 2011. Table p. 74. Available from:
http://www.ginasthma.org/
23632391. PMID 19911854
Initiative for Chronic Obstructive Lung Disease (GOLD) 2011. p. 43.
Available from: http://www.goldcopd.org/

For the next patient you see with asthma, evaluate the severity and the risk of
near-fatal asthma and decide where the patient should be treated after initial
management in the emergency department. Is there a protocol in your institution? If
not, consider approaching your colleagues with suggestions for creating one.

Q. The first blood gases of a patient with acute asthma show
hypoxaemic respiratory alkalosis. Thirty minutes after initiation of
treatment with inhaled -mimetics and systemic steroids, the patient
tells you that he still feels dyspnoeic. The clinical evaluation is
unchanged but the arterial blood gases now show hypoxaemic
normocarbia. Can you now transfer the patient to the ward? Give
your reasons.
A. No! The fact that the patient is no longer able to hyperventilate in response to the
hypoxaemia means that he is beginning to have exhaustion. The initial evolution of this
patient (with a rising PaCO
2
) is worrisome, and he should be kept under intensive
surveillance.

It is of paramount importance to clinically reassess asthma patients
frequently during the first few hours, with iterative blood gases and peak flow
measurements (initially at least hourly). If there is no clear and sustained
improvement, the patient should be admitted to a ward with mechanical
ventilation capability usually the ICU.
9

2/ WHY DO COPD AND ASTHMA PATIENTS
DECOMPENSATE?

The chain of events

The hallmark of COPD is a mainly irreversible, expiratory airflow limitation
caused by either an increase in the resistance of the small conduction airways, or
an increase in lung compliance due to emphysematous lung destruction, or both.
The product of resistance and compliance (the time constant, reflecting the time
necessary for lung emptying) is always increased in COPD patients, and is best
reflected by measurements of the FEV1 (the maximal volume that can be expired
in one second) and its ratio to the forced vital capacity (FEV1/FVC).

There are two pathophysiological mechanisms leading to hyperinflation:

Increased airway resistance, which impedes airflow and can lead to so-
called dynamic hyperinflation if expiratory time is too short to exhale
the whole tidal volume (predominant in asthma). We will refer to this
as without expiratory flow limitation or without EFL during normal,
quiet tidal volume expiration.
Airway collapse, leading to the stopping of airflow in the airway and
loss of communication with the airway opening; this leads to air
trapping distal to the point(s) where airflow has stopped and is
predominant in COPD. We will refer to this as with expiratory flow
limitation or with EFL during normal, quiet tidal volume expiration.

These two pathophysiological pathways are important to keep in mind when you
are applying external PEEP (PEEPe) to COPD and asthma patients:

In situations where there is no EFL, serial resistances are additive,
and therefore PEEPe should not be used because it may increase the
dynamic hyperinflation.
Serial resistances in situations with EFL are not additive: the airways
are collapsing (COPD) or are plugged (asthma), and there is no more
airflow downstream from the obstruction during expiration. Thus any
further resistance has no effect on airflow or on resistance upstream.
In this case the Starling resistor (waterfall principle) applies (see
Figure 4-9 and 7-18 in JB West chapters 4 and 7) and there is no
hazard in using PEEPe, as long as PEEPe < PEEPi.
See the references below and also Task 3, How much PEEPe to apply.

Not infrequently of course, a certain degree of both phenomena co-exist in the
same patient.

Techniques for bedside detection of EFL are based on the lack of an increase in
expiratory flow in response to an increase in the driving pressure (Alveolar
Pressure Mouth Pressure). This should help to determine which patient might
benefit from PEEPe (see When to apply PEEPe section).

10

West JB. Respiratory Physiology The Essentials. Philadelphia 7
th
ed. Lippincott
Williams & Wilkins; 2005. ISBN 0-7817-5152-7
Koulouris NG, Hardavella G. Physiological techniques for detecting expiratory flow
limitation during tidal breathing. Eur Respir Rev 2011; 20(121): 147155.
PMID 21881143
Ninane V, Leduc D, Kafi SA, Nasser M, Houa M, Sergysels R. Detection of
expiratory flow limitation by manual compression of the abdominal wall.
Am J Respir Crit Care Med 2001; 163(6): 13261330. PMID 11371396

See the PACT module on Respiratory assessment and monitoring

How does expiratory obstruction occur?

COPD

Exposure to inhaled noxious particles and gases (such as cigarette smoke or
environmental pollution) causes an inflammatory response of the lungs. In at
least 15% to 20% of smokers, this leads to the classical pathological findings of
COPD narrowing of the airways by excessive mucus secretion, inflammatory
mucosal oedema and increased fluid and cell exudation in the airways. These
phenomena are reversible and are the target of our therapy.

Even more important, however, is the structural remodelling of the airway wall
caused by the repeated injury and repair process, which leads to irreversible
airway obstruction (decreased diameter caused by increased fibrous wall
thickness).

Only a minor portion of airway obstruction is reversible in COPD.

The impact of these alterations on total airway resistance is most important in
the peripheral airways (<2 mm diameter), which are the major site(s) of airway
obstruction in COPD.

Q. Given that most of the airway resistance in healthy lungs is located
in the intermediate sized bronchi (about the 4th to 5th bronchus
generation), why is the major airway resistance located in the small
airways in COPD patients?

A. The alterations of the airway wall occur throughout the bronchial tree, but since the
resistance to laminar flow (Poiseuilles law) is inversely proportional to the 4th power of
the radius, the relative narrowing of the airways due to the wall thickening is greatest in
the small airways.

11

Hogg JC, Chu F, Utokaparch S, Woods R, Elliot WM, Buzatu L, et al. The nature of
small-airway obstruction in chronic obstructive pulmonary disease. N Engl
J Med 2004; 350(26): 26452653. PMID 15215480
http://www.nejm.org/doi/full/10.1056/NEJMoa032158
Hogg JC. Pathophysiology of airflow limitation in chronic obstructive pulmonary
disease. Lancet 2004; 364(9435): 709721. Review. PMID 15325838
Initiative for Chronic Obstructive Lung Disease (GOLD) 2010. Chapter 4.
Available from: http://www.goldcopd.org

The other pathological finding contributing (although to a lesser extent) to
expiratory airflow impediment is destruction of the parenchyma (emphysema).
This destruction is believed to originate from an imbalance of proteinases and
antiproteinases (as in 1-antitrypsin deficiency) and/or an imbalance of oxidative
stress and anti-oxidants as in smoking.

The destruction of the lung parenchyma has two deleterious effects on expiratory
airflow:

The ability of the small airways to maintain patency is impaired by the
loss of surrounding lung parenchyma. This leads to airway collapse, to
so-called air trapping, and to an increase in residual volume
(functional residual capacity, FRC), and so to hyperinflation.
The pathological decrease in lung elastic recoil forces. These recoil
forces are responsible for the negative pleural pressure and their
compromise results in a less negative pleural pressure.

The difference between the alveolar pressure and the pleural pressure (i.e.
transpulmonary pressure) is the maximal effective driving force in expiration,
and thus the limiting factor for airflow in forced expiration. If recoil forces are
diminished and this driving force becomes very small, as in severe emphysema,
expiration can become flow-limited even during normal tidal breathing (as
mentioned above: EFL).

The extent of the expiratory flow limitation is of course compounded by
increased airway resistance. This increases the pressure reduction along the
airways so that the point of collapse (the equal pressure point see below) is
reached faster.

West JB. Respiratory Physiology The Essentials. Philadelphia 7
th
ed. Lippincott
Williams & Wilkins; 2005. Chapter 7. ISBN 0-7817-5152-7

Q. Bronchi act as starling resistors i.e. they collapse and no longer
allow any flow as soon as the pressure around the airway exceeds that
inside (collapsible tube in a pressure chamber).What are the two
determinants of airway collapse during expiration?
12

A. The first determinant of airway collapse during expiration is the transalveolar
pressure, which is the gradient between the pressure in the adjacent interstitial space
and the alveolar pressure. The other is the pressure drop along the airway which is
related to airway resistance.

Q. Explain the equal pressure point, the point at which airway
collapse occurs?

A. This is the point where the pressure within the airway has fallen to a level which is
equalled (or overcome) by the transalveolar/intrathoracic pressure.

Note that in terms of therapeutic options we have capacity to influence the airway
resistance but given that transalveolar pressure is dependent on passive factors, we do
not have pharmacologic options to influence it.

How does airflow obstruction affect respiratory
mechanics?

Airflow impediment increases the work of breathing (WOB), and alters the
effectiveness of respiratory muscles in several ways:

It increases the change in pressure necessary to overcome airway
resistance for a given airflow (P = Airway resistance Airflow).

It creates hyperinflation, which partly counteracts increased resistance
by increasing airway diameter, but also decreases compliance of the
respiratory system if tidal volume is shifted to the very right of the
lung pressurevolume curve (see figure below).

Pressurevolume curve showing the increased pressure (P2) required to
achieve the same Vt, when tidal ventilation is shifted to the right on the curve.

Hyperinflation (and destruction of lung parenchyma) increases dead
space ventilation and so the total minute ventilation required to
maintain normal alveolar ventilation
13

Auto-PEEP (intrinsic PEEP or PEEPi)) greatly increases the
inspiratory trigger workload. At the beginning of each inspiration,
auto-PEEP must first be overcome before air can flow in, either
during spontaneous breathing or in order to trigger the ventilator
during assisted mechanical ventilation (trigger work). See diagrams
below.

Alveolar pressure and flow curves during spontaneous breathing in the
absence of auto-PEEP (PEEPi) demonstrating the minimal inspiratory pressure
change required (trigger work) to initiate inspiration.

Alveolar pressure and flow curves during spontaneous breathing in the
presence of auto-PEEP (PEEPi) where the pressure change required to initiate
inspiration (trigger work) is evidently increased.

14

At the same time, the ability of the muscles to deal with this increased WOB is
impaired in several ways:

The altered geometry of chest wall and diaphragm (flattened
diaphragm, shortened diaphragm and intercostal muscles) due to
hyperinflation leads to a large decrease in muscle efficiency.
Hypoxaemia and respiratory acidosis disturb the energy metabolism
of the muscles.
Respiratory cachexia, as seen in severe COPD, also impairs muscle
strength.

In severe COPD, the balance between respiratory workload and respiratory
working capacity is difficult to maintain. Even a small disturbance can precipitate
a vicious circle ending up in respiratory failure:

Increased hyperinflation decreased compliance increased minute
ventilation and tachypnoea increased auto-PEEP increased hyperinflation.

All of this increases the work of breathing and leads to increased muscle fatigue
due to decreased muscle perfusion/oxygenation and to respiratory acidosis see
figure (Pathophysiological mechanisms) below.

Pathophysiological mechanisms leading to acute decompensation of
COPD

Based on what you have learned about the pathophysiology of COPD and COPD
exacerbation, you will of course specifically treat triggering factors such as
infection. How do you consider these further possible therapies:

15

Q. How useful is bronchodilator therapy?

A. The reversible components of bronchial obstruction are smooth muscle contraction
and inflammatory oedema of the bronchial epithelium, for which bronchodilating
therapy (2-agonists) and anti-inflammatory drugs (steroids) are given. We have to be
aware, though, that the reversible part is minor.

Airflow limitation, which is substantially dependent on the destroyed lung parenchyma
and the decreased recoil forces, is further limited by dynamic airway collapse.

Q. Are there pharmacological options in this area?

A. No. These parenchymal parameters are fixed and not responsive to any
pharmacologic treatment.

Q. You may wish to increase maximal expiratory airflow by
increasing the lung volume at end inspiration. Is there a hazard to
this approach?

A. Yes. In EFL patients with an exacerbation of COPD, lungs are already overinflated and
further increase in lung volume could be deleterious (high Pplat, worsening heart lung
interactions).

THINK Try to imagine how external PEEP could help a patient with decompensated
COPD.

The most common acute event resulting in severe COPD exacerbation
and thus leading to respiratory failure is airway infection.

Inflammatory oedema of the airway mucosa, mucus hypersecretion, and
bronchoconstriction result in increased airway resistance and contribute to
worsening of the VA/Q relationship; these may trigger the vicious circle
mentioned above.

Q. Other than pneumonia, name some other causes/disease
processes that could disturb the fragile balance between respiratory
workload and respiratory working capacity?

A. There are numerous events that can disturb the balance, either by increasing
workload or decreasing the work capacity. These include cardiac failure, inhalation of
noxious gases, pneumothorax (rupture of bullae), pulmonary embolism, strenuous
physical activity, decreased inspired partial oxygen pressure as in high altitude, air
travelling.

Asthma

Although inflammation is important in both COPD and asthma, the
inflammatory response is quite different in the two diseases. In asthma, a chronic
inflammatory disorder of the airways, many cells (mast cells, eosinophils, ) and
cellular elements (cytokines, histamine, ) play a central role (see figure 1-4 to 1-
16

6 pp. 7 and 8, GINA 2011). Hypertrophy and hyperplasia of smooth muscle or
goblet cells and submucosal glands for instance (see figure 1-7 p. 8 GINA 2011)
are the structural changes in airways resulting from this chronic inflammatory
disease.

Acute exacerbation may occur as a result of exposure to risk factors for asthma
symptoms (see figure 1-2 p. 4 GINA 2011), or triggers such as exercise, air
pollutants or allergens, for instance. Occasionally infections can trigger acute
exacerbation (mostly viral).

The chronic inflammation is associated with airway hyperresponsiveness (see
figure 1-9 p. 9 GINA 2011) that leads to recurrent episodes of obstructive
symptoms (wheezing, breathlessness, chest tightness) or coughing, particularly
at night or in the early morning. These episodes are usually associated with
widespread, but variable, airflow obstruction within the lung that is often
reversible (in contrast to COPD).

The final pathophysiological mechanisms leading to airway narrowing (see figure
1-8 p. 8 GINA 2011) in asthma exacerbation are:
Exaggerated and abnormal contraction of airway smooth muscle cells
(predominant and reversible mechanism)
Airway oedema (important component during exacerbation)
Mucus hypersecretion (airway plugging)
Airway thickening (due to structural changes, not fully reversible).

Thus, even if in obstructive patients, EFL or no EFL often co-exist, in asthma
patients, no EFL is predominant. However, as for COPD patients (mostly EFL),
hyperinflation is the main mechanism leading to respiratory muscle fatigue.


17

3/ MANAGING VENTILATORY SUPPORT OF COPD
AND ASTHMA IN THE ICU

Once the ventilatory muscles can no longer match the ventilatory demand,
patients become progressively exhausted. At this point ventilatory support is
needed to interrupt the above vicious circle. The aim of ventilatory support is to
give the respiratory muscles the opportunity to rest until the cause of
exacerbation is treated and the bronchial obstruction and inflammation has been
reversed.

In severe COPD exacerbation with respiratory acidosis, ventilatory support
should first be applied non-invasively (if not contraindicated), since the
intubation rate, the length of stay in the ICU and even mortality, have been
shown to be reduced.

In asthmatic patients, non-invasive ventilation could have potential benefits such
as off-setting the PEEPi, re-expanding collapsed lung and reducing the work of
breathing. An early non-invasive mechanical ventilation trial may be individually
assessed but only in an ICU environment. These benefits have not been
established for severe asthma.

The indications for ventilatory support include:

Signs of respiratory distress (dyspnoea, with use of accessory muscles
and paradoxical abdominal motion, tachypnoea)
Hypercapnic acidosis (pH <7.35).

See the following references:

Brochard L, Mancebo J, Wysocki M, Lofaso F, Conti G, Rauss A, et al. Noninvasive
ventilation for acute exacerbations of chronic obstructive pulmonary
disease. N Engl J Med 1995; 333(13): 817822. PMID 7651472
http://www.nejm.org/doi/full/10.1056/NEJM199509283331301
Evans TW. International Consensus Conferences in Intensive Care Medicine: non-
invasive positive pressure ventilation in acute respiratory failure. Intensive
Care Med 2001; 27(1): 166178. Review. PMID 11280630
Soroksky A, Stav D, Shpirer I. A pilot prospective, randomized, placebo-controlled
trial of bilevel positive airway pressure in acute asthmatic attack. Chest
2003; 123(4): 10181025. PMID 12684289
http://chestjournal.chestpubs.org/content/123/4/1018.long
Keenan SP, Sinuff T, Cook DJ, Hill NS. Which patients with acute exacerbation of
chronic obstructive pulmonary disease benefit from noninvasive positive-
pressure ventilation? A systematic review of the literature. Ann Intern Med
2003; 138(11): 861870. PMID 12779296

18

Non-invasive ventilatory support

The most commonly used ventilatory mode is pressure support with PEEP or
bilevel positive-pressure ventilation with a minimal mandatory frequency in case
of insufficient respiratory drive.

Practical aspects:
Patient must be seated and reassured
Choose a facial mask for the interface
Start with pressure support mode
Initial settings:
o Inspiratory pressure 68 cmH
2
O
o PEEP 35 cmH
2
O, FiO
2
to ensure SaO
2
88%
o Inspiratory trigger set at 0.5 to 1 L/min
o Expiratory trigger set in the upper range (4070% of maximal
inspiratory flow)
o Pressurisation time set at shorter range (o.1 to 0.2 sec)
Titrate PEEP by steps of 12 cmH
2
O according to patients comfort
(observe and assess ineffective triggering attempts)
Titrate pressure support level by steps of 2 cmH
2
O to patients
comfort, respiratory rate (25/min) and tidal volume (68 mL/kg),
avoid total airway pressure above 20 cmH
2
O.

As titration of settings is guided by patient comfort, communication is
paramount.

Failure criteria (see also below):
Absence of improvement (or a deterioration) within first two hours
using clinical and PaCO
2
/PaO
2
criteria
pH <7.25, respiratory rate >35/min, GCS <11 after the first two hours
of NIV.

Dont delay intubation if patient worsens during NIV trial.

Nava S, Hill N. Non-invasive ventilation in acute respiratory failure. Lancet 2009;
374(9685): 250259. PMID 19616722
Confalonieri M, Garuti G, Cattaruzza MS, Osborn JF, Antonelli M, Conti G, et al.;
Italian noninvasive positive pressure ventilation (NPPV) study group. A
chart of failure risk for noninvasive ventilation in patients with COPD
exacerbation. Eur Respir J 2005; 25(2): 348355. PMID 15684302
http://erj.ersjournals.com/content/25/2/348.long

Invasive ventilatory support

There are no clearly defined criteria for the initiation of invasive mechanical
ventilation in COPD or asthma.
19

In COPD, the current approach is to intubate the patient if non-invasive
ventilation fails, i.e. if blood gases and clinical status do not improve within the
first two hours of initiation of non-invasive mechanical ventilation (see Figures
5.49, pp. 4244 GOLD update 2011).


In asthma, the primary goal of intubation and mechanical ventilation is to
maintain oxygenation and prevent respiratory arrest; thus intubation should not
be deferred too long, but should rely on worsening of clinical signs (changes in
alertness, speech and posture as well as respiratory rate decrease, for instance).
Once a decision to intubate has been made, the goal is to gain rapid and complete
control of the patients cardiorespiratory status. The most experienced physician
available should handle the intubation.

Whenever possible, use a large diameter tracheal tube to decrease total airway
resistance and facilitate clearance of secretions.

In obstructive lung disease, it is the avoidance of further overinflation and the
threat of volu-/barotrauma what should guide the ventilator settings. Thus, in
patients ventilated for severe asthma, for instance, the therapeutic targets are
limited to obtain an adequate oxygenation and minimise overinflation and its
consequences, using the minimum minute ventilation required to avoid severe
respiratory acidosis.

In very severe cases of bronchial obstruction, neuromuscular paralysis
might be necessary to ventilate the patient. We should, however, be aware of the
high risk of myopathy in these patients, who are often treated with
corticosteroids, and thus balance the risk against the benefits. Heavy sedation
might obviate the necessity for neuromuscular paralysis.

For information on myopathy see the PACT module on Neuromuscular
conditions. See Task 5, for information on weaning difficulties.

Defining a strategy and initial setting of the ventilator

The main problem in ventilating a patient with bronchial obstruction is
hyperinflation and its associated complications: volutrauma, barotrauma and
haemodynamic compromise.

Hyperinflation arises when the inspired air cannot be totally expired (so-called
dynamic hyperinflation).

20

The main determinants for the occurrence of dynamic hyperinflation are:

The expiratory time
The volume of air that has to be expired (tidal volume: Vt).

In the initial phase, we choose a controlled mode and set the parameters so that
expiration is as long as possible (low RR and low I:E ratio) and tidal volume is
kept low. The general strategy also called controlled hypoventilation or
permissive hypercapnia, combines a relatively low expired minute volume (Ve =
RR Vt) with a high inspiratory flow (to ensure a short Ti and thus a low I:E
ratio).

Regarding respiratory terminology see combined glossary of
respiratory terms:
RR for respiratory rate is synonymous with the term Fr (frequency).
I:E ratio, the ratio of time in inspiration to time in expiration, is sometimes
written as Ti:Te ratio.

There is consensus on how to start mechanical ventilation in severe bronchial
obstruction:

Minute ventilation <115 mL/kg
Tidal volume <8 mL/kg
Respiratory rate 10 to 14 per minute
Inspiratory flow 80 to 100 L/min

There is no consensus as to which ventilator mode should be initially set.

Be careful to avoid overventilating patients with chronic compensated
respiratory acidosis as this may lead to dangerous metabolic/respiratory alkalosis. Aim
at normal pH rather than normal PaCO
2
.

21

Williams TJ, Tuxen DV, Scheinkestel CD, Czarny D, Bowes G. Risk factors for
morbidity in mechanically ventilated patients with acute severe asthma.
Am Rev Respir Dis 1992; 146(3): 607615. PMID 1519836

Assessment of dynamic hyperinflation

See Glossary.

You can suspect hyperinflation, when inspiration starts before expiratory flow
returns to zero in the monitored flow time curve.

The only measure that has been shown to predict complications of hyperinflation
(hypotension and barotrauma) is the end-inspiratory volume (Vei) above
functional respiratory capacity (FRC). It is measured by collecting total exhaled
volume in a paralysed patient over 60 seconds of apnoea.

Tuxen DV, Williams TJ, Scheinkestel CD, Czarny D, Bowes G. Use of a
measurement of pulmonary hyperinflation to control the level of
mechanical ventilation in patients with acute severe asthma. Am Rev
Respir Dis 1992; 146(5 Pt 1): 11361142. PMID 1443862

Vei: the end-inspiratory volume above functional residual capacity
(FRC)

Vei >20 mL/kg is predictive of complications such as hypotension and
barotrauma.

Since Vei is difficult to determine in clinical practice, surrogate measures are
used to reflect hyperinflation:

Intrinsic PEEP
Pplateau (also called Pplat or Ppause)
22

Ppeak (peak or maximal inspiratory airway pressure) also increases
proportionally to Pplat and PEEPi with hyperinflation, but it has no pathological
implication in the clinical setting, since Ppeak is not transmitted to alveoli.

See PACT module on Acute respiratory failure.

COPD and asthma patients always have high Ppeak because of increased
airway resistance and of the high inspiratory flow rate often required to shorten
the inspiratory time (Ti), thus ensuring a longer expiratory time(Te).

PEEPi is measured at end-expiration and is the lowest average alveolar pressure
achieved during the respiratory cycle, and is best measured during an end-
expiratory hold manoeuvre on the ventilator in a relaxed, but not necessarily
(pharmacologically) paralysed, patient. See the following figure and the PACT
module on Mechanical ventilation.

How to measure PEEPi by expiratory breath-hold

During this manoeuvre there is no airflow, and pressures equilibrate within the
respiratory system and so reflect the mean end-expiratory alveolar pressure.

Measuring PEEPi (also called auto-PEEP) in a spontaneously breathing patient is
more difficult. If you measure oesophageal pressure (Poe, also called P
es
) in your
unit, you might approximate PEEPi in spontaneous, assisted ventilation, by the
negative inflexion of Poe at the beginning of a triggered inspiration, until
inspiratory flow starts (see figure below).

Poe Ptrigger + PEEPi and thus
PEEPi Poe Ptrigger where Ptrigger is the set trigger on the ventilator.

23

Oesophageal pressure trace during triggered assisted positive
pressure ventilation.

The value determined this way (so-called PEEPi
dyn
as opposed to PEEPi static) is
usually lower than with the expiratory hold method, since inspiratory flow starts
to the region with the lowest PEEPi (non-homogeneity of time constant) as soon
as auto-PEEP is balanced. Thus this method gives the value of the lowest auto-
PEEP in the lungs, whereas the expiratory hold method gives the mean value.

Appendini L. About the relevance of dynamic intrinsic PEEP (PEEPi, dyn)
measurement. Intensive Care Med 1999; 25(3): 252254. PMID 10229157

There is no value for auto-PEEP (PEEPi) that is predictive of barotrauma, but
successive measurements give an indication of the evolution of hyperinflation:
increasing auto-PEEP (PEEPi) reflects increasing hyperinflation. There is general
agreement that to minimise the risk of volutrauma and barotrauma of the lungs,
Pplateau (Ppause) should be kept below 30 cmH
2
O.

Slutsky AS. Consensus conference on mechanical ventilation--January 2830,
1993 at Northbrook, Illinois, USA. Part I. European Society of Intensive
Care Medicine, the ACCP and the SCCM. Intensive Care Med 1994; 20(1):
6479. PMID 8163765
Slutsky AS. Consensus conference on mechanical ventilation--January 2830,
1993 at Northbrook, Illinois, USA. Part 2. Intensive Care Med 1994; 20(2):
150162. PMID 8201097

Dont keep Ppeak below an arbitrary limit; you may increase hyperinflation by
decreasing inspiratory air flow. Pplateau (Ppause) is the parameter to watch for.

24

Evaluate one of your intubated patients with regard to whether hyperinflation
could be present. Measure auto-PEEP (PEEPi).

Q. In a severe asthma patient, you set the initial settings in Volume-
controlled ventilation: Minute ventilation (Vm) <115 mL/kg, Tidal
volume(Vt) <8 mL/kg, Respiratory rate(Fr) 10 to 14 per minute,
Inspiratory flow 80 to 100 L/min to ensure a short Ti and thus a low
Ti:Te (I:E) ratio and you measure the following values: Ppeak of 80
cmH
2
O, Pplateau of 40 cmH
2
O, as measured by an end-inspiratory
occlusion manoeuvre, auto-PEEP of 12, and respiratory acidosis of
pH 7.30 with good oxygenation. What is your assessment, particularly
of the Ppause?

A. The Pplateau (Ppause) is definitely above the safe range and is indicative of
hyperinflation.

Q. What is your priority in terms of minimising the risk of
barotrauma? What do you do?

A. Even if there is already respiratory acidosis, the priority is to decrease Ppause
(Pplateau) and the likely related hyperinflation. This may be achieved by reducing Vm by
decreasing Vt. Vm may also be decreased by reducing RR, thereby prolonging expiration
and also allowing a reduction in hyperinflation.

Q. Is the elevated Ppeak a concern?

A. The high Ppeak is not bothersome, since it arises from the increased airway resistance
and the high inspiratory flow rate and is mainly dissipated in the airways and so does not
reach the alveoli.

25

If it is not possible to reach normoventilation within the safe parameters as
mentioned above, it is recommended to use so-called permissive hypercapnia
to avoid mechanical lung damage. Hypercapnic acidosis is usually well tolerated.

Permissive hypercapnia is contraindicated in the presence of intracerebral
hypertension because of the cerebral vasodilation that it induces.

Q. You decide to reduce the respiratory rate alone from 12 to 8
breaths/min and you achieve the following findings:
Ppeak 70 cmH
2
O,
Pplateau 30 cmH
2
O,
PEEPi of 4 cmH
2
O,
pH and pCO
2
unaltered (slight hypercapnic acidosis) and good
oxygenation.

Are you satisfied that safety criteria have been achieved?

A. Yes, the safety criteria are now satisfied.

The presumed mechanism is that there has been a significant reduction in
hyperinflation.

Q. Since the Vm has been reduced, how can we explain the unchanged
pCO
2
?

A. We can assume that the hyperinflation was associated with an increase in dead space.
So despite a decrease in Vm, alveolar ventilation (VA) may have remained unchanged
due to the decrease in dead space ventilation.

Q. And how do you interpret the fact that the change in Pplateau
(Ppause) is greater than the change in intrinsic PEEP (PEEPi)?

A. Hyperinflation shifted the ventilation toward the right and upper part of lung
pressurevolume curve, where the compliance was lower. So by changing the setting we
reached the steeper (more compliant) part of the lung pressure-volume curve.

For the next intubated patient who is ventilated in volume-controlled mode,
calculate expiratory time (Te) with the actual setting. Then, increase Te by decreasing
RR, and calculate the new Te. Afterwards, increase Te by shortening Ti e.g. by increasing
inspiratory flow.

Decreasing RR is the most effective manoeuvre to increase Te and thus decrease
hyperinflation. As in ARDS, the solution to prevent volutrauma and barotrauma
in obstructive lung disease may be permissive hypercapnia (see above).

26

When to apply PEEPe

Anytime that auto-PEEP (PEEPi) is present, external PEEP (PEEPe) can and
should be applied to decrease inspiratory trigger efforts.

Attempts to overcome PEEPi are thought to be one of the major causes of
respiratory failure in acute exacerbations of COPD, as well as a major cause of weaning
failure in mechanically ventilated patients with airway obstruction. External PEEP may
be of use in counterbalancing PEEPi thus diminishing work of breathing but does not
minimise hyperinflation (see the references below and the PACT module on Mechanical
ventilation).

In obstructive patients, be careful in applying PEEPe during fully
controlled mode since you might worsen hyperinflation without any proven
benefit on lung mechanics. The main indication for applying PEEPe in this
context is to improve oxygenation; start applying PEEPe as soon as the patient is
on assisted mode since it reduces inspiratory trigger work.

Brochard L. Intrinsic (or auto-) PEEP during controlled mechanical ventilation.
Intensive Care Med 2002; 28(10): 13761378. PMID 12373460
Ward NS, Dushay KM. Clinical concise review: Mechanical ventilation of patients
with chronic obstructive pulmonary disease. Crit Care Med 2008; 36(5):
16141619. PMID 18434881

How much PEEPe should be appli ed?

Defining an adequate amount of external PEEP is difficult. Thinking of the
waterfall principle (situation with airflow limitation), setting PEEPe = PEEPi
would bring the greatest relief to inspiratory efforts, without carrying the risk of
increasing hyperinflation.

There are two reasons, however, why PEEPe should be set lower than measured
PEEPi.

There might be a mixed picture of airflow limitation and no-airflow
limitation.
The PEEPi distribution within a COPD or an asthma lung is uneven
(because of an inhomogeneous time constant distribution) and thus,
in some areas, the effective PEEPi might be lower than the measured
static PEEPi (see above figures on PEEPi measurement).

Both of these reasons might lead to an increased total PEEP (PEEPtot), if PEEPe
were equal to PEEPi.

27

The current consensus is that external PEEP (PEEPe) should be set at
about 80% of PEEPi, in order to give a substantial relief on inspiratory workload
without risk of increasing hyperinflation.

Brochard L. Intrinsic (or auto-) positive end-expiratory pressure during
spontaneous or assisted ventilation. Intensive Care Med 2002; 28(11):
15521554. PMID 12583374

In a controlled mechanically ventilated COPD patient, determine auto-PEEP
(PEEPi) and then apply different levels of PEEPe ( to PEEPi). Observe the absence of
change in total PEEP as long as PEEPe is below 80% of PEEPi.

Cli ni cal pr oblems i n applyi ng PEEPe

In clinical practice, there is another everyday difficulty: PEEPi changes in
relation to the respiratory parameters (RR, Vm), body position, and variability of
changes in respiratory mechanics related to disease course and response to
treatment. Thus the measured values of PEEPi under controlled ventilation in a
relaxed patient might be quite different from the actual PEEPi in spontaneous
ventilation, the situation in which we want to apply external PEEP.

Measuring PEEPi in a spontaneously ventilating patient is rather difficult (see
figures on how to measure PEEPi). In clinical practice it is therefore helpful to
ask the patient about his comfort and his dyspnoea, while increasing external
PEEP (PEEPe) very gradually. He will notice the relief of workload due to
counterbalancing of PEEPi until hyperinflation is increasing. Dyspnoea is
proportional to Vei and thus the patient can notice increasing hyperinflation.

Cardiopulmonary interactions

Since the lung, heart, and pulmonary circulation are within the same box, i.e.
the thoracic cage, intra-pleural pressure variations might greatly influence
cardiac function.

Positive intrathoracic pressure:

Decreases venous return and thus the preload of both ventricles
Increases pulmonary vascular resistance, and thus the afterload of the
right ventricle.

Hyperinflation further increases intrathoracic pressure and thus accentuates
these haemodynamic effects.

Hypotension is the more common effect of the decreased preload, and is
accentuated by hypovolaemia.

28

Always consider hyperinflation in the mechanically ventilated patient with
hypotension, especially if bronchial obstructive lung disease is present.

If you suspect hyperinflation in a mechanically ventilated patient, briefly
disconnect the ventilator and hypotension will rapidly improve.

Due to the increasing afterload of the right ventricle, hyperinflation could induce
acute right ventricular failure with ensuing RV dilation, septal shift and LV
filling deficiency due to ventricular interdependency.

Intrathoracic pressure is partially transmitted to the circulation and thus
influences the measured values of central venous pressure (CVP) and pulmonary
capillary wedge pressure (PCWP). This has to be taken into account when
haemodynamic measurements are assessed. The extent of alveolar pressure
transmission is proportional to the compliance of the lungs and is thus
minimised in the presence of severe ARDS. However, it is inversely proportional
to the compliance of the chest wall.

Feihl F, Broccard AF. Interactions between respiration and systemic
hemodynamics. Part I: basic concepts. Intensive Care Med 2009; 35(1):
4554. PMID 18825367
Feihl F, Broccard AF. Interactions between respiration and systemic
hemodynamics. Part II: practical implications in critical care. Intensive
Care Med 2009; 35(2): 198205. PMID 18825366
Jardin F. Ventricular interdependence: how does it impact on hemodynamic
evaluation in clinical practice? Intensive Care Med 2003; 29(3): 361363.
PMID 12577152
Jardin F, Genevray B, Brun-Ney D, Bourdarias JP. Influence of lung and chest wall
compliances on transmission of airway pressure to the pleural space in
critically ill patients. Chest 1985; 88(5): 653658. PMID 3902386
29

4/ PROVIDING NON-VENTILATORY SUPPORT AND
MANAGING COMPLICATIONS

The basic ICU management of an acute exacerbation of COPD or asthma is
supportive, (euvolaemia, correction of acid-base balance and electrolytes,
adequate nutrition, and the treatment of common complications) and specific,
particularly the drug treatment.

Drug treatment

The drugs and their importance partly differ in the treatment of patients with
acute exacerbations of asthma or COPD.

Asthma

THINK about a patient with status asthmaticus. If an airway obstruction is
responsible for the exacerbation, does it make sense to perform intubation as early as
possible?

Beta-sympathomimetic agents

2-adrenergic agonists are the most effective bronchodilating
agents, and are the first-line treatment for smooth-muscle-
mediated bronchoconstriction. Nebulised therapy has a rapid
onset of action and is as effective as intravenous therapy, but is
less likely to cause cardiac arrhythmias, hypokalaemia, tremor,
and lactic acidosis.

Oxygen-driven nebulised therapy should be given until an adequate clinical
response is achieved or until adverse side effects limit further administration.
Intubated patients need higher drug doses to accomplish adequate delivery of
drugs to the lung. If the response is poor or the patient is moribund, use the
intravenous form (e.g. albuterol 200 g over 10 min, then 320 g/min). (Note:
in the USA, albuterol has not been approved for intravenous use).

Corticosteroids

Airway-wall inflammation is central to the pathogenesis of asthma, and thus
systemic corticosteroid therapy is an essential part of the first-line treatments for
status asthmaticus. Hydrocortisone and methylprednisolone have both been
demonstrated to be very effective.

No definitive consensus exists in the dose and molecule to use. There is no
efficacy difference between oral and parenteral administration. The British
Thoracic Society guidelines recommend parenteral hydrocortisone 400 mg daily
(100 mg six-hourly) or oral prednisolone 4050 mg daily. There is no evidence
that higher doses of steroids are more effective. Lower doses are probably as
effective but there are no sufficient data to support this. Duration of systemic
corticosteroid therapy should be 5 to 10 days.

Epinephrine isnt a
more potent
bronchodilator than 2-
mimetics. It should be
avoided (either
nebulised or
systemically) because of
its numerous side effects
30

Inhaled corticosteroids can be continued or added to the systemic therapy when
possible in order to prepare for the chronic asthma management plan.

The peak response for steroid action does not occur until four to six
hours after administration, therefore start early with the steroid treatment.

Manser R, Reid D, Abramson M. Corticosteroids for acute severe asthma in
hospitalised patients. Cochrane Database Syst Rev 2001; (1): CD001740.
PMID 11279726
http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD001740/full
23632391. PMID 19911854
British Guideline on the Management of Asthma (2011 revision). http://www.brit-
thoracic.org.uk/guidelines.aspx
and Management of Asthma. Full Report 2007. http://www.nhlbi.nih.gov/

Additional bronchodilators

Anticholinergics such as ipatroprium bromide inhibit the vagal tone with
medium-potency bronchodilation. In combination with inhaled 2-adrenergic
agonists, the effect of bronchodilation will be increased and it has been shown
that it can lead to a faster recovery and reduce hospitalisation rates.
Anticholinergic treatment is not necessary and may not be beneficial in milder
exacerbations of asthma or after stabilisation.

Add nebulised ipratropium bromide (0.5 mg 46 hourly) to 2 agonist treatment
for patients with acute severe or life-threatening asthma or those with a poor
initial response to 2 agonist therapy.

Leukotriene receptor antagonists

Leukotrienes are derived from arachidonic acid metabolism through the 5-
lipoxygenase pathway. They are potent mediators of inflammation implicated in
asthma. Leukotriene receptor antagonists have bronchodilator and anti-
inflammatory effects and are clinically active following a single dose. There is
only sparse literature, however, suggesting that montelukast is effective in the
treatment of acute asthma as an adjunct therapy to avoid intubation.

31

23632391. PMID 19911854

Magnesium sulfate

There are randomised controlled trials suggesting that a single intravenous dose
of 2 gm of magnesium sulfate can have an additional bronchodilatory benefit in
patients with severe acute asthma, even with normal serum magnesium levels. It
may be that magnesium inhibits calcium channels.

Rowe BH, Camargo CA Jr. The role of magnesium sulfate in the acute and chronic
management of asthma. Curr Opin Pulm Med 2008; 14(1): 7076. PMID
18043278

Methylxanthines (aminophylline, theophylline)

Aminophylline is an inhibitor of phosphodiesterase. It causes weak
bronchodilation, dilation of the pulmonary vessels, and has a positive inotropic
effect, especially for the right heart. The use of methylxanthines in acute asthma
is not routinely recommended (no additional benefit, increased frequency of side
effects).

However, some patients with near-fatal asthma or life-threatening asthma with a
poor response to initial therapy may gain additional benefit from IV
aminophylline, (5 mg/kg loading dose over 20 minutes (unless on maintenance
oral therapy) and then by infusion (0.50.7 mg/kg/hr). Such patients are likely
to be rare and could not be identified in a meta-analysis of trials.

Toxicity should be monitored and levels checked regularly in patients on
aminophylline infusions.

Parameswaran K, Belda J, Rowe BH. Addition of intravenous aminophylline to
beta2-agonists in adults with acute asthma. Cochrane Database Syst Rev
2000; (4): CD002742. PMID 11034753
http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD002742/full
32

23632391. PMID 19911854
British Guideline on the Management of Asthma (2011 revision). http://www.brit-
thoracic.org.uk/home.aspx

Heliox

Heliox is a mixture of 6080% helium and 2040% oxygen, and has a lower gas
density. It decreases respiratory work by reducing airflow resistance, but requires
substantial technical adaptation of the respirator and thus is limited to
experienced centres. It has no effect on bronchospasm although it could improve
the spirometric effect of albuterol, if used to nebulise it instead of oxygen. It
might, however, be a bridge to resolution of bronchospasm thus avoiding
intubation in patients not responding to standard therapy. There is no proven
benefit on relevant outcomes. Heliox cannot be used in patients who require a
high FiO
2
(the benefit of low density is lost with FiO
2
above 0.4).

Rodrigo G, Pollack C, Rodrigo C, Rowe BH. Heliox for nonintubated acute asthma
patients. Cochrane Database Syst Rev 2006 Oct 18; (4): CD002884. PMID
17054154
http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD002884.pub2/full
Kress JP, Noth I, Gehlbach BK, Barman N, Pohlman AS, Miller A, et al. The utility
of albuterol nebulized with heliox during acute asthma exacerbations. Am J
Respir Crit Care Med 2002; 165(9): 13171321. PMID 11991886

Anti-infective therapy

Most exacerbations of asthma are due to non-infective factors or to viral
infections. Anti-infection therapy should only be given for asthma if there is very
good evidence of bacterial infection.

Acute asthma often shows discoloured or purulent sputum (due to
eosinophils) even in the absence of infection.

COPD

Beta-sympathomimetic agents and other bronchodilators

Patients with COPD have a limited degree of reversible airflow obstruction
compared to patients with asthma. Nevertheless, the role of bronchodilators
remains prominent in the management of exacerbated COPD.

Inhalation of short-acting 2-adrenergic agonists is recommended and combine
them with anticholinergics if a prompt response does not occur. Both nebulisers
33

and hand-held inhalers can be used to administer inhaled therapy during
exacerbations of COPD, depending on the severity of the exacerbation. If a
patient is hypercapnic or acidotic, it is advised that the nebuliser should be
driven by compressed air rather than oxygen (to avoid worsening hypercapnia).
If oxygen therapy is needed, administer it simultaneously by nasal cannulae.

Intravenous 2-adrenergic agonists are not indicated.

The addition of theophylline adds minimal, if any, efficacy and should only be
considered if there is an inadequate response to nebulised bronchodilators.
Theophylline levels are monitored daily in the acute setting.

Corticosteroids

The efficacy of systemic corticosteroids has been demonstrated for patients with
severe exacerbations of COPD.

Systemic corticosteroids are indicated only for patients with severe exacerbation
or lack of response to other therapy. There is no consensus about the exact dose
or the route of administration (oral or intravenous). Guidelines suggest 3040
mg of prednisolone (or equivalent) per day for no longer than 710 days.

Duration of mechanical ventilation (invasive or not) is shortened with systemic
corticosteroids therapy as is the rate of NIV failure.

Walters JAE, Gibson PG, Wood-Baker R, Hannay M, Walters EH. Systemic
corticosteroids for acute exacerbations of chronic obstructive pulmonary
disease. Cochrane Database Syst Rev 2009 Jan 21; (1):CD001288. PMID
19160195
Walters JAE, Wang W, Morley C, Soltani A, Wood-Baker R. Different durations of
corticosteroid therapy for exacerbations of chronic obstructive pulmonary
disease. Cochrane Database Syst Rev 2011 Oct 5; (10): CD006897. PMID
21975757
Ala I, de la Cal MA, Esteban A, Abella A, Ferrer R, Molina FJ, et al. Efficacy of
corticosteroid therapy in patients with an acute exacerbation of chronic
obstructive pulmonary disease receiving ventilatory support. Arch Intern
Med 2011; 171(21): 19391946. PMID 22123804
http://archinte.jamanetwork.com/article.aspx?doi=10.1001/archinternmed.2011.
530

34

Anti-infective therapy

Bronchial infections are the most common precipitating factor for an acute
exacerbation of COPD. Viral infections are an important trigger, and a majority
of these are due to rhinovirus.

Between 25% and 50% of patients with COPD have lower airway colonisation by
bacteria. This colonisation is variable over time, and is associated with greater
airway inflammation.

If the patients initial symptoms are increased dyspnoea, sputum volume and
purulence, treat with an antibiotic that is effective against Haemophilus
influenzae, Streptococcus pneumoniae, and Moraxella catharalis. If available,
previous bacterial airway samples are used to target initial antibiotic therapy
especially if the patient is known to be colonised with Gram negative bacteria
such as Pseudomonas aeruginosa.

Check the immunisation status of your COPD patients. If they have not
received a seasonal influenza vaccination and a pneumococcal vaccination, it
should be administered after recovery from the acute illness.

Rothberg MB, Pekow PS, Lahti M, Brody O, Skiest DJ, Lindenauer PK. Antibiotic
therapy and treatment failure in patients hospitalized for acute
exacerbations of chronic obstructive pulmonary disease. JAMA 2010;
303(20): 20352042. PMID 20501925
http://jama.jamanetwork.com/article.aspx?doi=10.1001/jama.2010.672

Mucolytic agents such as N-acetylcysteine have no place in the treatment
of acute exacerbation of asthma and COPD.

Be aware of using sedatives in COPD patients because it decreases the ventilatory
drive.

A patient with exacerbated COPD and severe shortness of breath
became increasingly agitated and frightened while using his auxiliary breathing
muscles. He was therefore put on non-invasive ventilatory support. Afterwards
the patient was absolutely calm without any sedation. The relief of his exhausted
breathing muscles with good ventilatory support was the best anxiolytic for this
patient.

35

Supportive therapies

Cor r ecti on of flui d i mbalance

The chronic inflammation seen in patients with COPD and asthma leads to lung
remodelling and in the end stages to emphysema. The capacity of pulmonary
lymphatic drainage is decreased and there is a greater chance of developing lung
oedema thus causing more respiratory problems, even at moderate levels of fluid
replacement.

COPD patients are frequently elderly with chronic heart disease. In the context of
an acute exacerbation, congestive heart failure can be superimposed.
Measurement of plasma B-type natriuretic peptide level can be useful to guide
diagnosis and treatment, especially the fluid balance.

Chest radiographs are often unremarkable in spite of too much water in the
lungs.

Mueller C, Laule-Kilian K, Frana B, Rodriguez D, Scholer A, Schindler C, et al. Use
of B-type natriuretic peptide in the management of acute dyspnea in
patients with pulmonary disease. Am Heart J 2006; 151(2): 471477. PMID
16442916

Cor r ecti on of aci dosi s

There are several reasons why acidosis develops in critically ill patients with
exacerbated COPD and asthma. Although metabolic acidosis (e.g. lactic acidosis)
may (co-)exist, most of the patients with severe exacerbations of COPD and
asthma have respiratory acidosis (hypercapnia).

Increased PCO
2
may lead to:
Increased cerebral blood flow and intracranial pressure
Increased pulmonary artery pressure and overloading of the right
heart
Decreased peripheral vascular tone/resistance
Increased levels of epinephrine and norepinephrine
Increased cardiac output
Inadequate oxygenation due to hypercapnia by reducing FAO
2

FAO
2
= FiO
2
FACO
2
where
FAO
2
= alveolar fraction of O
2,
FiO
2
= inspired fraction of O
2
and
FACO
2
= alveolar fraction of CO
2

Identify the causes of acidosis and correct the factors which may be reversible.
Increase FiO
2
in case of hypoxaemia and respiratory acidosis
Optimise the mechanical ventilation
Optimise the circulatory situation.
36

THINK Metabolic acidosis increases the work of breathing; where possible, correct it
appropriately e.g. extra-renal replacement, correction of haemodynamics.

Alkalosi s

Alkalosis may become symptomatic when pH exceeds 7.55. Above pH 7.6,
seizures, coma, arrhythmias and cardiac arrest are possible.

Iatrogenic respiratory alkalosis due to excessive minute ventilation in patients
requiring ventilatory support can aggravate pre-existing compensatory metabolic
alkalosis in chronically hypercapnic COPD patients. See section: Defining a
strategy and initial setting of the ventilator.

Nutri ti onal support

Patients with asthma normally have no nutritional deficit, whereas patients with
severe COPD have an imbalance between energy intake and energy consumption.
The chronic inflammation and increased effort needed to breathe lead to higher
energy consumption. COPD patients are characterised by loss of weight, loss of
muscle mass and intrinsic changes in the muscles, so-called pulmonary cachexia.

Early nutritional support, preferably delivered enterally, should aim to meet the
increased metabolic needs of the COPD patient. Care should be given to avoid
overfeeding because it can lead to increased CO
2
production and O
2

consumption. Measuring the energy requirements with a calorimeter may be
considered.

For the next two intubated COPD patients, make a nutritional plan after
calculating the caloric requirements.

THINK Does additional administration of vitamins have a place in the feeding plan
of a patient with exacerbated COPD?

For more information see the PACT module on Nutrition.

Treatment of common complications

Fever

Fever is a common symptom during the ICU stay. Both asthma and COPD
exacerbations are inflammatory syndromes with increased numbers of
infiltrating cells, alterations of epithelial cells and the non-cellular components of
the airway wall accompanied by increased levels of pro-inflammatory cytokines.
Infections and superinfections play a major role during exacerbations. A large
number of COPD patients have bacterial colonisation of lower airways, and
deterioration of asthma is often triggered by chronic sinusitis or gastro-
oesophageal reflux disease with micro-aspiration.

37

If fever appears or persists, look for a pulmonary superinfection and exclude
sinusitis. Of course, all other possible causes of fever during an ICU stay should
be excluded as well.
See the PACT modules on Pyrexia and Severe infection.

Atelectasi s and sputum retenti on

Often the clinical course of patients with COPD and asthma is negatively affected
by atelectasis and sputum retention. Atelectasis is a collapse of alveoli with
reduction of intrapulmonary air and an abnormal ventilation-to-perfusion ratio.
This causes an intrapulmonary shunt, with passage of venous blood into the
arterial system without oxygenation, leading to hypoxaemia. Atelectasis is one
major risk factor for developing a pulmonary infection.

Mechanisms of atelectasis

Chronic hyperinflation leads to an increase in lung volume.
The diaphragm stays deeper and is flatter, so the potential for sufficient
diaphragmatic contractility is reduced
If high concentrations of oxygen have to be inspired, with high
differences of the partial gas pressures between alveoli and venous
(pulmonary arterial) blood, the oxygen diffuses rapidly from the
poorly-ventilated alveoli into the venous blood, leading to volume loss
and subsequent collapse of these alveoli known as absorption
atelectasis
Extrapulmonary compression (pneumothorax, pulmonary contusion)
results in passive atelectasis
Accumulation of bronchial secretions can lead to airway obstruction

Development of atelectasis in COPD patients is most commonly caused
by the stagnation of bronchial secretions in conjunction with increased sputum
volume, sometimes called sputum retention.

Mechanisms underlying the stagnation of bronchial secretions

Mucociliary clearance
o Chronic inflammation destroys the normal airway wall, and
particularly interferes with the normal function of the cilia
o Drugs such as opioids and anticholinergics depress the
mucociliary clearance
o Mechanisms associated with mechanical ventilation (high
oxygen concentration, high inspiration pressure) reduce
mucociliary clearance
Cough
o Reduced ability to cough due to absent occlusion of the glottis
during tracheal intubation. Drug-induced suppression (opioids,
anaesthetics)
o Diaphragmatic weakness (anatomical configuration, critical
illness polyneuromyopathy)
o Depression of consciousness.
38

The successful treatment of atelectasis and sputum retention is important in the
prevention of infective and other complications and in shortening the ICU stay.

Wean as early as possible from mechanical ventilation
Perform endotracheal aspiration if abundant tracheal secretions are
present
Suction in accordance with a standard safe procedure
o Hand hygiene and sterile catheters
o Be careful not to injure the tracheobronchial mucosa
o Use pre- and post-oxygenation with 100% oxygen to avoid severe
hypoxia
o Do not suction too often (loss of surfactant) or for too long (risk of
aspiration atelectasis)
Fibre-optic bronchoscopy only performed when indicated e.g. for
lobar/lung collapse. Aspiration can be harmful; suctioning can induce
bronchial collapse or injure the mucosa

For the next five long-term intubated patients, work with the physiotherapist
to make a plan for preventing or treating atelectasis and sputum retention.

Q. An intubated patient with an exacerbation of COPD also has a
hypertensive crisis. You treat the hypertension with an infusion of the
vasodilator, sodium nitroprusside. Afterwards, a higher FiO
2
is
required. Why?

A. Sodium nitroprusside causes vasodilation of the pulmonary vessels also. In a patient
with atelectasis, the hypoxic vasoconstriction in these badly ventilated areas may be
compromised resulting in these areas being supplied with more blood. The consequence
may therefore be an increase in rightleft shunting, thereby delivering more poorly
oxygenated blood to the left heart.

Initiative for Chronic Obstructive Lung Disease (GOLD) update 2010.
http://www.goldcopd.org/.
PACT module on Hypertension

Tachycar di a, tachyar r hythmi a

Patients with an exacerbation of COPD or asthma have several reasons for
developing a sinus tachycardia or tachyarrhythmia.

Pathogenic mechanisms

Tachycardia can result from hypoxia, stress, and high work of
breathing.
39

If severe hyperinflation exists, decreased systemic venous return and
heart-lung interaction affect steady-state cardiac output, with
resulting decreased cardiac output, hypotension and shock.
Cardiomyopathy can occur with pulmonary hypertension, right heart
insufficiency (and sometimes coronary vascular disease) in association
with COPD.
Tachycardia and tachyarrhythmia can result from aggressive therapy
with -sympathomimetics and/or aminophylline.

Management

If clinically relevant tachycardia or tachyarrhythmia persists,
reduction or discontinuation of -sympathomimetics and
aminophylline should be considered.
Reduce stress and work of breathing with sedation and controlled
ventilation.
Exclude the possibility of myocardial ischaemia.
Optimise the mechanical ventilation to reduce hyperinflation and
intrathoracic pressure.

40

5/ WEANING THE PATIENT

Mechanical ventilation, especially in COPD patients, is associated with many life-
threatening complications and it should be discontinued as early as possible.
Weaning patients from a ventilator is one of the everyday and sometimes most
challenging problems for an ICU physician. Using an empirical approach alone to
manage the weaning process can prolong the duration of mechanical ventilation.
Indeed, using only intuitive clinical assessments of the status of the patients
respiratory failure is not enough to make decisions on the discontinuation of
ventilator support. The sensitivity of clinical judgment is only 35%; the specificity
is 79%. Prospective studies have shown that the application of weaning protocols
leads to a more rapid weaning process without increasing weaning failure. No
specific weaning strategy for obstructive patients has been proven superior to
others.

Aggressive weaning and extubation criteria maximise the withdrawal from
ventilatory support, with fewer complications (such as nosocomial infections)
and shorter ICU stays.

For more information, see the PACT modules on Mechanical ventilation and
Respiratory assessment and monitoring.

When to start weaning

To identify the right moment to start the process of weaning from the ventilator,
a persistent search for and assessment of possible underlying causes of
continuing ventilator dependency is important.

Optimally, weaning begins with the onset of mechanical ventilation. A
protocol implemented by intensivists, nurses (and respiratory therapists where
applicable) begins testing for the opportunity to reduce support very soon after
intubation and at every further opportunity.

Causes of ventilator dependency/weaning problems

Gas-exchange factors Ventilationperfusion imbalance
Shunts (e.g. atelectasis, pulmonary
embolism)
Ventilatory muscle factors Muscle fatigue
Atrophy and remodelling
Disadvantageous muscle position
Hyperinflation
High resistance with elevated
ventilatory muscle work
Ventilator factors High resistance to gas flow by
tracheal tube, ventilator hoses,
humidifiers, demand valves
Metabolic factors Overfeeding with excess CO
2

production
Malnutrition with protein
41

catabolism
Electrolyte abnormalities
(phosphate/magnesium deficiency)
Cardiovascular factors Left heart failure with pulmonary
oedema
Pulmonary arterial hypertension
with right heart failure
Changes of preload and afterload
Neurological factors Cortical feedback failure from
chemo- and mechanoreceptors by
sedation, narcotics and metabolic
disturbances
Critical illness polyneuromyopathy
Severe agitation and delirium

Critical illness neuromyopathy is a common cause of weaning failure in
COPD/asthma, since the combined treatment with corticosteroids and
neuromuscular blockade is not rare

See the PACT module on Neuromuscular conditions.

Boles JM, Bion J, Connors A, Herridge M, Marsh B, Melot C, et al. Weaning from
mechanical ventilation. Eur Respir J 2007; 29(5): 10331056. PMID
17470624
MacIntyre N. Discontinuing mechanical ventilatory support. Chest 2007; 132(3):
10491056. PMID 17873200

Prognostic factors for successful weaning

Reversal of underlying cause for
respiratory failure

Pulmonary criteria PaO
2
/FiO
2
ratio >19.926.6
kPa/150200 mmHg
Positive end-expiratory pressure
(PEEP) 8 cmH
2
O
pH >7.3
Rapid shallow breathing index <105
(breathing frequency/tidal volume
in litres)
Less important factor:
Maximum inspiratory pressure
>minus 2030 cmH
2
O
42

Haemodynamic stability Absence of:
Low cardiac output
Pulmonary oedema
Myocardial ischaemia
Important arrhythmias
Adequate respiratory forces and
coordination
No thoracic instability
Normal intra-abdominal pressure
Capacity for inspiratory effort (i.e.
enough force to breathe)
No need for respiratory accessory
muscles
No paradoxical breathing
No relevant hyperinflation/intrinsic
PEEP

See also the PACT modules on Respiratory assessment and monitoring and
Mechanical ventilation.

Some patients with unresolved respiratory failure who required high
levels of ventilatory support and who did not meet these criteria have
nonetheless been shown to be capable of successful weaning from the ventilator.

How to wean

The two most widely used methods are pressure support ventilation (PSV) with
stepwise reductions of support and daily T-piece trial.

Pressure support ventilation (PSV)

The level of pressure support is set to avoid Vt over 8 mL/kg of ideal body weight
(IBW) and is reduced accordingly during weaning. The inspiratory fraction of
oxygen (FiO
2
), the positive end-expiratory pressure (PEEP), and the level of
pressure support can be reduced in steps. The criteria for the speed of the
different reductions are, as above, the Vt, respiratory pattern, adequacy of gas
exchange, haemodynamic stability and subjective patient comfort.

In a mechanically ventilated patient with broncho-obstruction who has already
begun the weaning process, talk with the patient to try to determine optimal PEEP
(consider different levels of pressure support at different times of the day).

It is important to consider inefficient triggering attempts because they increase
substantially the work of breathing. Spontaneous ventilation in pressure support
depends on four distinct phases: inspiratory trigger, flow rate, amount of
pressure support, and expiratory trigger. Inefficient triggering and patient
ventilator interactions can originate from any of these phases. To improve
patient comfort and reduce work of breathing, the inspiratory trigger must be set
at the more sensitive value possible while avoiding auto-triggering phenomena.

43

To favour expiration and avoid dynamic hyperinflation, a high flow rate is used
with a pressurisation time between 0.1 and 0.2 sec. If available, the expiratory
trigger has to be set to a highest value (40 to 70% of the maximal inspiratory
flow).

Interestingly, the number of unsuccessful triggering attempts may increase with
the level of ventilator assistance. These triggering failures seem to be due to an
increased level of hyperinflation and might thus be reduced by reducing the level
of pressure support and/or applying higher PEEPe.

In clinical practice, the occurrence of inefficient triggering attempts means that
it:
Should not necessarily impede the weaning process
Warrants a trial of increasing PEEPe, decreasing pressure support,
and checking the trigger level (inspiratory and expiratory).

Jolliet P, Tassaux D. Clinical review: patient-ventilator interaction in chronic
obstructive pulmonary disease. Crit Care 2006; 10(6): 236. PMID
17096868
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1794446/?tool=pubmed
Leung P, Jubran A, Tobin MJ. Comparison of assisted ventilator modes on
triggering, patient effort, and dyspnea. Am J Respir Crit Care Med 1997;
155(6): 19401948. PMID 9196100
Nava S, Bruschi C, Rubini F, Palo A, Iotti G, Braschi A. Respiratory response and
inspiratory effort during pressure support ventilation in COPD patients.
Intensive Care Med 1995; 21(11): 871879. PMID 8636518
Vitacca M, Bianchi L, Zanotti E, Vianello A, Barbano L, Porta R, et al. Assessment
of physiologic variables and subjective comfort under different levels of
pressure support ventilation. Chest 2004; 126(3): 851859. PMID
15364766

Daily T-piece trial

In a spontaneous breathing trial (SBT), warm and moistened air is brought to the
patient via a T-piece, in a flow high enough to avoid CO
2
rebreathing. The T-piece
is placed on top of the intratracheal tube and the patient breathes spontaneously,
without ventilator support. Research has shown successful discontinuation from
the ventilator 77% of the time after a tolerance of 30 minutes of SBT. Because a
tracheal tube increases resistance and breathing work, the duration of SBT
should not be longer than 120 minutes to avoid breathing muscle fatigue. The
criteria mentioned earlier are used to assess weaning success.

44

Neither of these two weaning methods has been proven superior.
Whichever mode is chosen, a weaning protocol is generally recommended see
example below. Synchronised intermittent mandatory ventilation (SIMV) is no
longer recommended since it has been proven less efficient for weaning.

Boles JM, Bion J, Connors A, Herridge M, Marsh B, Melot C, et al. Weaning from
mechanical ventilation. Eur Respir J 2007; 29(5): 10331056. PMID
17470624
Kollef MH, Shapiro SD, Silver P, St John RE, Prentice D, Sauer S, et al. A
randomized, controlled trial of protocol-directed versus physician-directed
weaning from mechanical ventilation. Crit Care Med 1997; 25(4): 567574.
PMID 9142019

45

Example of a protocol for difficult to wean patients

46

Check whether your ICU has a weaning protocol. If it does, do the staff use the
protocol? In the next five patients, strictly adhere to the protocol. Evaluate how weaning
differs with and without the protocol.

In asthma patients, if the mucous membrane hyperactivity/airway obstruction is
resolved, early extubation is generally possible.

COPD patients, on the other hand, not only have airway obstruction with
hyperinflation but also several other organ problems e.g. muscle fatigue,
cardiocirculatory problems, infections, metabolic and nutrition problems. If
these patients are alert, cooperative, and ready to breathe without an artificial
airway, there may nevertheless be a benefit to early extubation, with the
institution of non-invasive positive-pressure ventilation (NPPV) after the
extubation. See below for the Role of non-invasive ventilation in weaning.

Nava S, Ambrosino N, Clini E, Prato M, Orlando G, Vitacca M, et al. Noninvasive
mechanical ventilation in the weaning of patients with respiratory failure
due to chronic obstructive pulmonary disease. A randomized, controlled
trial. Ann Intern Med 1998; 128(9): 721728. PMID 9556465

Q. Weaning is proceeding successfully for a patient with an
exacerbation of COPD, but the patient has persistently high PCO
2

levels. What do you do?

A. Normally, patients with advanced COPD have chronically higher levels of PCO
2
thus
aim at pH rather than PCO
2
. You should look at the values before exacerbation and the
corresponding pH. If these values correspond to the typical pre-exacerbation levels, and
the patient is otherwise ready for extubation, extubate the patient and then consider
following with non-invasive ventilation.

Weaning failure

If patients receiving mechanical ventilation fail the weaning procedure,
immediate evaluation of the cause is necessary (see Causes of ventilator
dependency/weaning problems, above), along with specific therapeutic
measures.

Except in patients recovering from sedatives, muscle relaxants,
pneumothorax and atelectasis, respiratory system abnormalities are rarely
resolved over a short period (a few hours).

47

Patients who fail a weaning trial should have a stable, non-fatiguing, and
comfortable form of ventilatory support for at least 24 hours. Which ventilatory
form to use is patient-dependent. Controlled ventilation is often necessary to
enable the patient to relax, but whenever possible, assisted modes of ventilation
with levels of pressure support high enough to ensure comfortable breathing
(with Vt not exceeding 8 mL/kg of IBW) should be used as this should allow
better patientventilator synchrony and prevent muscle atrophy. After a rest of
at least 24 hours, a new protocol-driven weaning trial should be started.

New ventilatory modes such as proportional assist ventilation, adaptive support
ventilation, knowledge-based expert system, or neurally adjusted ventilatory
assist could be useful for difficult to wean patients. You will find further
information in the PACT module on Mechanical ventilation.

Q. Is it helpful to use the carbo-anhydrase inhibitor acetazolamide in
treating a patient who has COPD, hypercapnia and a pH of 7.34?

A. No.

Q. Give reasons for not using acetazolamide?

A. A patient with severe COPD has a decreased ability to eliminate the CO
2
; hypercapnia
allows the patient to keep the alveolar ventilation and thus respiratory workload low.
Chronic hypercapnia leads to a compensatory increase in serum bicarbonate and thus to
normalisation of pH.

Once the patient is compensated again and the blood gases show metabolic
alkalosis, there is some controversy as to whether acetazolamide should be given.
It can accelerate the return to steady state values of bicarbonate and induce
helpful diuresis (decreasing water load, leading to better respiratory system
compliance). Trying to normalise bicarbonate levels, however, might lead to
weaning failure by mandating increasing ventilatory workload.

There are some data showing that if normalisation of bicarbonate is possible, the
interval to the next exacerbation might be prolonged.

Role of non-invasive ventilation in weaning

There are three different situations when NIV can be considered.

Shortening of invasive ventilation:
It has been demonstrated that application of NIV in case of failed spontaneous
breathing test shortens invasive mechanical ventilation duration, length of ICU
stay and lowers nosocomial pneumonia incidence.

48

Nava S, Ambrosino N, Clini E, Prato M, Orlando G, Vitacca M, et al. Noninvasive
mechanical ventilation in the weaning of patients with respiratory failure
due to chronic obstructive pulmonary disease. A randomized, controlled
trial. Ann Intern Med 1998; 128(9): 721728. PMID 9556465
Burns KE, Adhikari NK, Keenan SP, Meade MO. Noninvasive positive pressure
ventilation as a weaning strategy for intubated adults with respiratory
failure. Cochrane Database Syst Rev 2010 Aug 4; (8): CD004127. PMID
20687075

Prevention of post-extubation respiratory failure:
Early NIV application after extubation prevents post-extubation respiratory
failure, decreases re-intubation rate and ICU mortality.

Nava S, Gregoretti C, Fanfulla F, Squadrone E, Grassi M, Carlucci A, et al.
Noninvasive ventilation to prevent respiratory failure after extubation in
high-risk patients. Crit Care Med 2005; 33(11): 24652470. PMID
16276167
Ferrer M, Valencia M, Nicolas JM, Bernadich O, Badia JR, Torres A. Early
noninvasive ventilation averts extubation failure in patients at risk: a
randomized trial. Am J Respir Crit Care Med 2006; 173(2): 164170. PMID
16224108

Treatment of post-extubation respiratory failure:
No study has proven any benefit of NIV in post-extubation respiratory failure and
there is even an increased ICU mortality. Nevertheless, in very selected, mainly
COPD patients, a trial of NIV could be considered as long as it does not delay re-
intubation in the case of failure.

Esteban A, Frutos-Vivar F, Ferguson ND, Arabi Y, Apeztegua C, Gonzlez M, et al.
Noninvasive positive-pressure ventilation for respiratory failure after
extubation. N Engl J Med 2004; 350(24): 24522460. PMID 15190137
http://www.nejm.org/doi/full/10.1056/NEJMoa032736
Keenan SP, Powers C, McCormack DG, Block G. Noninvasive positive-pressure
ventilation for postextubation respiratory distress: a randomized controlled
trial. JAMA 2002; 287(24): 32383244. PMID 12076220
http://jama.jamanetwork.com/article.aspx?volume=287&page=3238

49

Role of tr acheostomy

When it becomes apparent that a patient will require prolonged ventilator
assistance, a tracheostomy should be considered. The right timing and the impact
on the duration of mechanical ventilation have not been clearly answered by
literature.

Durbin CG Jr. Tracheostomy: why, when, and how? Respir Care 2010; 55(8):
10561068. PMID 20667153
http://www.rcjournal.com/contents/08.10/08.10.1056.pdf
Diehl JL, El Atrous S, Touchard D, Lemaire F, Brochard L. Changes in the work of
breathing induced by tracheotomy in ventilator-dependent patients. Am J
Respir Crit Care Med 1999; 159(2): 383388. PMID 9927347
Link to the PACT module on Airway management

Long-term outcome

A precise prediction of outcome for individual patients with acute respiratory
failure and COPD or asthma is not realistic, and each case must be considered
individually.

The majority of patients with asthma have a good long-term prognosis,
depending on the longitudinal changes in lung function triggered by airway
inflammation. A patient with status asthmaticus and the need for intubation and
ventilation does not make the long-term outcome worse per se.

The outcome of patients with COPD and acute exacerbation depends on their
clinical situation before exacerbation. Factors predicting a poor long-term
outcome are:

Dyspnoea at rest with hypoxaemia and hypercapnia
Pulmonary hypertension and cor pulmonale
Irreversible airway obstruction despite treatment with -
sympathomimetics
Pulmonary cachexia with weight loss
Several acute exacerbations in the history
Other organ diseases, such as cardiomyopathy or nephropathy.

Studies of mortality associated with exacerbated COPD have had varying results,
but mortality is generally extremely high. The hospital mortality is around 10%,
at one year it is approaching 40% and is even higher for elderly patients.

50

For each patient with end-stage COPD and acute respiratory failure, we
have to consider an ICU stay with the possibility of prolonged intubation and
ventilation. If possible, the patient and family should be consulted in advance
regarding their preferences for the use of mechanical ventilation and
prolongation of life under these circumstances.

Seneff MG, Wagner DP, Wagner RP, Zimmerman JE, Knaus WA. Hospital and 1-
year survival of patients admitted to intensive care units with acute
exacerbation of chronic obstructive pulmonary disease. JAMA 1995;
274(23): 18521857. PMID 7500534
Weiss SM, Hudson LD. Outcome from respiratory failure. Crit Care Clin 1994;
10(1): 197215. PMID 8118729
51

CONCLUSION

Proper triage of patients with exacerbated COPD or severe asthma is very
important: the aim of the assessment is to identify patients who might need
ventilatory support and hospitalise them on a ward with ventilatory assistance
capability such as the ICU.

If ventilatory assistance is necessary for COPD patients, a non-invasive route is
tried first.

If a COPD patient in respiratory distress has not refused mechanical ventilation
in advance care planning, do not hesitate to intubate, since there are no criteria
that predict weaning failure.

In a ventilated patient with bronchial obstruction, be aware of hyperinflation to
avoid its haemodynamic and pulmonary complications.

The long-term prognosis of asthma is quite good; thus asthma patients should
always be admitted to the ICU if required. The long-term prognosis for patients
with severe COPD is worse, and patients and their relatives should be encouraged
to consider (and write down) their preferences concerning the intensity of
intervention in advance, in case of a later worsening of the patients status. This
is best done while the patient is in a stable situation.

[52]

6/ GLOSSARY

Combined glossary of terms for the modules Mechanical Ventilation, Respiratory Assessment
and Monitoring and COPD and asthma with acknowledgement to Dr Ed Carton for finalising
its composition.

Airway pressure Pressure at a specified point in the patients airway.

ALI A descriptor of an Acute Lung Injury process; since a recent
consensus conference, no longer recommended as a
categorisation of the severity of ARDS. Recommended
categorisation of ARDS now changed to Mild, Moderate
and Severe.

AP
L
(Transpulmonary pressure). This is the pressure
distending the respiratory system (and the functional
residual capacity of the lung) and is the airway pressure
minus the pleural pressure. (AP
L
=Ppause Poes).
However, Poes (equivalent to pleural pressure) and FRC
measurement at the bedside are not common in clinical
practice.

ARDS Acute Respiratory Distress Syndrome.

Atelectrauma Lung injury caused by the cyclic collapse and reopening of
unstable small airways and alveoli resulting in shear
injury.

Auto-triggering The inadvertent triggering of inspiratory ventilatory
support when a patient is not breathing.

Barotrauma Lung injury due to high airway (distending) pressure.

Biotrauma A diffuse lung injury and possible injury to other organs
due to the release of inflammatory mediators.

CaO
2
Content of oxygen in arterial blood. CaO
2
is calculated as
1.34 Hb SaO
2
; the normal value is 16 to 20 mL O
2
/100
mL blood.
Compliance
C
rs
Compliance of the respiratory system. It is defined as the
lung volume change per unit airway pressure change or the
slope of the pressurevolume curve.
In positive pressure ventilation, it is measured by dividing
the Vt by the inflation pressure. See below for dynamic
(C
dyn
)and static (C
stat
) compliance.

C
cw
Compliance of the chest wall.

C
dyn
Dynamic compliance. It is calculated as
vt
Pcuk Puw - PLLP

C
L
Lung compliance.

C
qs

Compliancequasi-static. Compliance derived from
measurements made during a relaxed double prolonged

[53]

occlusion manoeuvre i.e. during a four second pause at
end-inspiration and at end-expiration. It mimics true static
compliance and is termed quasi-static compliance. True
static compliance is utilised mainly in research and is
performed using pressure measurements after serial
volume increments with a super syringe.

C
stat
Static compliance (see above).It is calculated as
vt
Ppuusc - PLLP

CO Cardiac output.

COHb Carboxyhaemoglobin.

CPAP
Continuous positive airway pressure. Refers, by
convention, to the end-expiratory airway pressure in a
spontaneous breathing respiratory system.

Cv O
2
Mixed venous oxygen content. It is measured as
1.34 Hb SvO2 (mixed venous oxygen saturation).

PCO
2
Difference between arterial to end-tidal PCO
2
.

De-escalation A continuous effort to reduce the mechanical ventilatory
support as soon and as much as possible.

DO
2
Oxygen delivery measured as CO CaO
2
.

EtCO
2
End-tidal CO
2
see also PetCO
2
.

EVLW Extravascular lung water.

EWS Expert weaning system.

FRC Functional residual capacity. The volume of gas in the
patients respiratory system at end-expiration. Its capacity
is a key determinant of oxygenation.

Fr Frequency.The number of ventilatory or patient breaths
per minute; also termed the ventilatory (or respiratory)
rate.

Hb Haemoglobin content of blood. Usually expressed as in g%
or as g/100mLs (normal value varies between males and
females but is approx. 15 g/dL).

Hypercapnia More than the normal level of carbon dioxide in the blood.

Hypocapnia Less than the normal level of carbon dioxide in the blood.

Hypoxaemia An abnormally low PO
2
in arterial blood.

I:E ratio The ratio between the time (duration) of inspiration
relative to duration of expiration. It is normally 1:1.5 to 1:2.

[54]

Impedance The combined effects of airway resistance, respiratory
system (including chest wall) compliance and intrinsic
PEEP (PEEPi see below) in opposing the flow and
volume change produced by the ventilator.

k Constant that represents the alveolar end-expiratory
pressure (in the driving pressure equation).

LSF Least square fitting.

MetHb Methaemoglobin.

MIP Maximal inspiratory pressure, see also PI
max
.

MVV Maximum voluntary ventilation.

NI(M)V Non-invasive (mechanical) ventilation.

NIF Negative inspired force.

Normoxaemia Normal blood levels of oxygen.

PaCO
2
Partial pressure of arterial carbon dioxide normal range
4.76 kPa (3545 mmHg).

P
alv
Alveolar pressure.

P
AO
Pressure at airway opening.

PaO
2
Partial pressure of arterial oxygen normal range 1013.3
kPa (75100 mmHg).

P
atm
Atmospheric pressure.

P
aw
Airway pressure.

PCV Pressure-controlled ventilation.

Peak airway pressure The peak (or highest) pressure measured by the ventilator;
the pressure at the level of the major airways.

PECO
2
Partial pressure of CO
2
in mixed expired gas usually
collected/measured in a Douglas bag but not a standard
clinical measurement.

PEEP Positive end-expiratory pressure. Defined as an elevation of
airway pressure at the end of expiration. End-expiratory
pressure is normally zero (atmospheric) during
spontaneous breathing but is often set at a positive level
(measured in cms H
2
O) during mechanical ventilation.

PEEPe PEEPexternal. The PEEP effected by the ventilator and set
by the operator.

PEEPi PEEPintrinsic. Elevated positive end-expiratory pressure
which is intrinsic to the patient. It is associated with
certain lung pathologies particularly where there is

[55]

destructive lung disease, dynamic collapse of airways and
active expiration and may be present during normal
spontaneous breathing or while on a ventilator. It is
sometimes termed auto-PEEP.

Its main reversible cause is a limitation to expiratory flow
and it is exacerbated by insufficient expiratory time (Te)
and dynamic pulmonary hyperinflation may result. It is
usually measured during a prolonged, relaxed expiratory
ventilatory pause.

PEEPtot Total PEEP. This is the combination of the above two
pressures (PEEPi and PEEPe). However, in certain
circumstances the effect of external PEEP may be to reduce
the level of PEEPi.

P
es
Oesophageal pressure. Is the pressure in the lower one
third of the oesophagus when the patient is upright. It
equates to pleural/extra-alveolar pressure. It is also called
Poe.

PetCO
2
End-tidal CO
2.
The highest value of CO
2
partial pressure
during the alveolar plateau of the capnography curve.

PI
max
Maximal inspiratory pressure.

PIP Peak inspiratory pressure.

Pmax The sum of the pressures produced by the ventilator to
overcome the elastic and resistive forces (airways and
endotracheal tube) of the respiratory system.

Pmus Pressure generated by muscle contraction.

Ppause The airway pressure observed during prolonged (4-
second), relaxed end-inspiratory pause/hold. Also termed
Plateau(Pplat) or End-inspiratory hold pressure, it is
used in the determination of static compliance. In the
absence of airflow (no resistance), it represents the
pressure applied to the small airways and alveoli during
peak inspiration. It depends on a number of factors
including the Vt, PEEP, intrinsic PEEP and compliance.

PPV Positive pressure ventilation. Process of exerting a
pressure, which is positive relative to atmospheric
pressure, to achieve entry of air or respiratory gases into
the lungs. Term IPPV used for Intermittent Positive
Pressure Ventilation.

P
pl
Pleura pressure.

P
rs
Respiratory system pressure.

PSG Polysomnography.

PSV Pressure support ventilation.

[56]

R Resistance. Respiratory system resistance (R
rs)
refers to
airway resistance and comprises the inflating pressure
divided by the (gas) flow.

Recruitment manoeuvre Manually or ventilator-assisted lung inflation to achieve an
increase in FRC (by alveolar recruitment) and thereby an
improved oxygenation.

RCe Respiratory system expiratory time constant. The product
of resistance and compliance and quantifies the speed of
exhalation. It may vary between different lung units in
pathological circumstances.

Rmax Total resistance.

SaO
2
Oxygen saturation percentage of the available haemoglobin
(normal value is 98%).

Shunt Is due to perfusion of non-ventilated lung regions and is
the commonest cause of clinical hypoxaemia.
Extrapulmonary causes are those (right to left shunts) that
may occur in the presence, for example, of an atrial septal
defect (ASD).

Te (Expiratory time). The time from the start of expiratory
flow to the start of inspiratory flow.

Ti Inspiratory time.

Transthoracic pressure The pressure in the pleural space measured relative to the
pressure of the ambient atmosphere outside the chest.

Trigger Usually relates to inspiratory rather than expiratory
triggering (see below) and as such, it refers to the process
of initiating the inspiratory breath of the ventilator.
Inspiratory triggering is usually effected by a pressure
change or flow change in the breathing system generated
by patient effort.

Triggering The mechanism of initiating the inspiratory (and
expiratory) phase(s) of the ventilator function.

T
TOT
is the respiratory duty cycle

V Volume.

Flow (Volume per unit of time).

VALI (or VILI) Ventilator-associated lung injury or Ventilator-induced
lung injury.

VAP Ventilator-associated pneumonia.

VCV Volume-controlled ventilation.

V

[57]

VA Alveolar volume. The proportion of Vt that is useful in gas
exchange.

VA Alveolar ventilation. The proportion of Vm that is useful in
gas exchange. It is comprised of Alveolar volume (VA)
multiplied by respiratory rate (Fr) i.e. VA = VA Fr. VA is
directly proportional to CO
2
elimination.

Vd Dead space. The volume of inspired gas that does not take
part in gas exchange.

Vd
phys
Physiologic dead space. This is comprised of the anatomic
dead space (Vd
anat
) and the alveolar dead space (Vd
alv
). It
has also been termed total dead space (Vdtot)

Vd
alv
Alveolar dead space (where alveoli are ventilated but are
receiving minimal or no blood flow).

Vd
anat
Anatomic dead space (upper and lower airways to the tips
of the terminal bronchioles).

Vd
ins
Instrumental dead space i.e. the dead space resulting from
parts of the breathing system, ventilator equipment,
endotracheal tubes, humidification devices and connectors.
It is considered part of the anatomic dead space.

V,ee End-expiratory lung volume. The volume of gas in the
patients respiratory system at end-expiration. Though, it is
often used interchangeably with FRC (see above), this
acronym should be used only for patients mechanically
ventilated and receiving PEEP.

Vei End-inspiratory volume above FRC

Ventilation mode Represents a specific operating logic (or software program)
for the mechanical ventilator, based on one or more
approaches to respiratory cycle management. The specific
mode is chosen by the operator.

Vm Minute Volume. The volume of gas ventilating the
respiratory system per minute. It is comprised of Tidal
volume multiplied by the Respiratory rate (Vt Fr).

Ve Expired minute volume.

Vi Inspired minute volume.

VO
2
Oxygen consumption by the tissues.

Volutrauma Lung injury due to alveolar overexpansion secondary to
high lung volume (with or without high pressure).

Vt Tidal volume. The volume of gas intermittently inhaled or
exhaled, by the patient or ventilator, with each breath on

[58]

top of the volume of the functional residual capacity
(FRC).

Weaning Is the final step in de-escalation, involving the patients
complete and continuing freedom from mechanical support
and removal of the artificial airway.

W
exp
Work of breathing performed during the expiratory phase.

W
insp
Work of breathing performed during the inspiratory phase
of the cycle.

WOB Work of breathing. The work required to accelerate gas in
the airways, to overcome airway resistance and to expand
the elastic lung tissue so that air can be brought into the
lungs and then exhaled.

W
pat
Work of breathing performed by the patient.

W
vent
Work of breathing performed by the ventilator.

[59]

SELF-ASSESSMENT

EDIC-style Type K

Q1. In a patient with an exacerbation of COPD or asthma, warning signs of
impending respiratory arrest include:
A. SpO
2
<80%
B. Lethargy
C. Silent chest
D. Tachycardia (110/min)

Q2. Clinical signs of severe asthma include:
A. Tachycardia >120/min
B. Peak expiratory flow rate (PEFR) <200 L/min
C. Hypoxaemia (PaO
2
<8kPa) while breathing air
D. Respiratory rate >30/min

Q3. Hyperinflation of the lung is a central phenomenon in both COPD and
asthma. The pathophysiology underlying hyperinflation includes:
A. Increased airway resistance resulting in dynamic hyperinflation during
expiration
B. Hypoxic hyperventilation with increased functional residual capacity (FRC)
C. Destruction of lung parenchyma resulting in a decrease in pulmonary elastic
recoil forces
D. Airway collapse with trapping of air distal to the point of airflow cessation
(equal pressure point) in the airway

Q4. The work of breathing (WOB) is often found to be increased in COPD
patients. Reasons for such increased WOB are:
A. Increased pressure necessary to overcome increased airway resistance
B. Altered geometry of diaphragm (flattened and shortened)
C. Disturbed energy metabolism in the respiratory muscles as a consequence of
hypoxaemia and acidosis
D. Increased muscle mass as a consequence of increased breathing efforts

Q5. The end inspiratory volume above FRC (Vei) has been shown to be
predictive of the complications of hyperinflation (hypotension and
barotrauma). Hyperinflation may be measured directly or by surrogate
measures (indirectly) in the clinical setting by the following methods:
A. Total exhaled volume (over 60 secs of apnoea)
B. Peak inspiratory pressure
C. Plateau pressure
D. Intrinsic PEEP

[60]

Q6. Intrinsic PEEP (PEEPi) is:
A. Measured by subtraction of set PEEP from the plateau (Pplat) or pause pressure
(Ppause)
B. The lowest average alveolar pressure during respiratory cycle
C. Measured during an end-expiratory hold manoeuvre
D. Normally 510 cmH
2
O

Q7. When you know (have measured) the PEEPi, your applied (external)
PEEP (PEEPe) in a patient with acute exacerbation of COPD should be:
A. Equal to PEEPi
B. 20% above PEEPi
C. 20% less than PEEPi
D. Zero

Q8. Regarding different methods for weaning a patient from the
ventilator:
A. Pressure support ventilation is superior to other methods
B. Pressure support and daily spontaneous breathing trials on a T-piece are
equally effective
C. SIMV is particularly effective in COPD weaning
D. Weaning protocols have a definite role in promoting successful weaning.

EDIC-style Type A

Q9. Which of the following initial treatments of an exacerbation of asthma
is NOT a standard therapy:
A. Inhaled -mimetic
B. Systemic corticosteroids
C. Antibiotics
D. Oxygen
E. Inhaled anticholinergic

Q10. The GOLD classification of COPD baseline severity is based on:
A. Clinical development
B. PaCO
2

C. % of predicted Forced Expiratory Volume 1 (FEV1)
D. PaO
2

E. % of predicted peak inspiratory flow (PIF)

Q11. In making the triage decision as to whether a patient needs to have
ventilatory support initiated quickly, important signs include the
following EXCEPT:
A. Inadequate response to initial therapy
B. Worsening of hypoxaemia (PaO
2
<5.3 kPa
C. PaCO
2
>10 kPa
D. Haemodynamic instability
E. Worsening of respiratory acidosis (pH <7.25)

[61]

Q12. Several benefits have been shown from the use of non-invasive
ventilation in the treatment of severe exacerbations of COPD. The single
most compelling reason for this choice is to:
A. Reduce the need for additive sedation in the patient
B. Reduce ICU length of stay
C. Avoid ventilator-associated pneumonia
D. Decrease hospital mortality
E. Avoid iatrogenic pneumothorax

Q13. The initial settings of non-invasive pressure support in a patient with
COPD include all of the following EXCEPT:
A. Inspiratory pressure 1520 cmH
2
O regardless of tidal volume (Vt) achieved
B. PEEP 35 cmH
2
O
C. Lowest possible FiO
2
to ensure SaO
2
>88%
D. Inspiratory trigger 0.5 to 1 L/min
E. Inspiratory pressure time set at shorter range (0.1 to 0.2 sec)

Q14. A 32-year-old male with a severe asthmatic attack is admitted to the
ED at 20.00 hrs. He is given steroids, inhalation with beta-adrenergic
drugs and inhaled anticholinergic. After two hours of observation and
treatment his vital signs and arterial blood gases (ABGs) have not
improved. On 10-litre oxygen on open mask, they now are:
- BP 140/70
- Pulse rate 130
- Respiratory rate 28
- Still has audible wheezing
- Unable to speak full sentences
- pH 7.23
- PaO
2
10 kPa
- PaCO
2
7.9 kPa
- HCO
3
23 mmol/L
- BE -2 mmol/L

What is your preferred option?
A. Transfer to an intermediate unit for further medical treatment
B. Transfer to an ICU for further observation
C. Transfer to an ICU for immediate intubation and IPPV
D. Keep the patient in the ED for another 23 hours
E. Transfer to the ICU for non-invasive ventilation

[62]

Q15. If you intubate and ventilate an acute asthmatic patient with pressure
support ventilation, what might the main adverse patient consequence be
compared with the choice of volume control ventilation:

A. Unacceptably high Peak inspiratory airway pressure (Pmax) and Pplat
(Ppause)
B. Air trapping
C. High PEEPi
D. A resultant high or low tidal volume (Vt) depending on the evolution of the
disease process
E. Increased airway resistance

Explanation: If the increased airway resistance suddenly improves or decreases
(because of therapy 0r spontaneously), there is a risk to the patient. For example, if
improvement occurs, there is a risk of hyperinflation of the lungs due to a large (Vt) if
the level of pressure support is not reduced immediately. Volume control ventilation
will not have this danger.

Q16. Factors which predict successful weaning include all of the following
EXCEPT:
A. PaO
2
/FiO
2
ratio >26.6 kPa (200 mmHg)
B. PEEP = 10 cmH
2
O
C. Rapid shallow breathing index <105
D. Inspiratory pressure < 2030 cmH
2
O
E. Cardiac index > 3 L/min

[63]

Answers

1. FTTF
2. TFTT
3. TFTT
4. TTTF
5. TFTT
6. FTTF
7. FFTF
8. FTFT
9. Correct: C
10. Correct: C
11. Correct: D
12. Correct: D
13. Correct: A
14. Correct: C
15. Correct: D
16. Correct: B

[64]

PATIENT CHALLENGES

A 63-year-old man is brought by his daughter to the emergency
department of your hospital because of progressive difficulty in breathing. On
arrival, the patient is non-responsive and has a dark purple colour, without perceptible
breathing movements or any perceptible pulse.

Q. What are your immediate actions?

A. Start evaluation and treatment concurrently according to guidelines: address ABC
(Airway Breathing and Circulation) and start CPR if breathing and a pulse is absent.

Given that the current ACLS therapeutic sequence for CPR, after
breathlessness (or gasping) and pulselessness is confirmed, starts with
compressions (>100/min), the ACLS therapeutic acronym is now CAB
(circulation, airway, breathing).

Travers AH, Rea TD, Bobrow BJ, Edelson DP, Berg RA, Sayre MR, et al. Part 4:
CPR overview: 2010 American Heart Association Guidelines for
Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.
Circulation 2010; 122(18 Suppl 3): S676S684. PMID 20956220
http://circ.ahajournals.org/content/122/18_suppl_3/S676.long
Berg RA, Hemphill R, Abella BS, Aufderheide TP, Cave DM, Hazinski MF, et al.
Part 5: adult basic life support: 2010 American Heart Association
Guidelines for Cardiopulmonary Resuscitation and Emergency
Cardiovascular Care. Circulation 2010; 122(18 Suppl 3): S685S705. PMID
20956221
http://circ.ahajournals.org/content/122/18_suppl_3/S685.long
http://www.acls.net

Link to PACT module on Airway management

You intubate the patient, without the need for sedative or neuromuscular blocking
drugs, and ventilate him by resuscitation bag device. After one dose of epinephrine 1
mg intravenously, you have a good carotid pulse, the purple colour is disappearing and
pulmonary auscultation and percussion is symmetrical. You transfer the patient to the
ICU.

Initial evaluation and triage of patients with respiratory distress

The patients daughter tells you that her father is a heavy smoker, that he doesnt like
going to the doctor and that he doesnt take any medicine. She says his condition has
worsened over the past ten days. As well as having increasing difficulty with breathing,

[65]

in the last two days he could no longer walk and he was coughing up a lot of brownish
sputum.

Often at the beginning of an emergency procedure you have only limited
historical information, if it is not possible to speak with the patient. Acute
resuscitative management is more important initially than a refined differential
diagnosis.

Q. What is the most common cardiorespiratory sequence in an adult with
cardiorespiratory arrest?

A. The most frequent pattern is a cardiac arrest either as pulseless ventricular
tachycardia, ventricular fibrillation, asystole or other cause of pulseless electrical
activity (PEA). The respiratory arrest is therefore normally secondary in nature.

The initial electrocardiogram (ECG) showed regular QRS complexes despite an absent
pulse i.e. pulseless electrical activity (PEA). There was a rapid return of spontaneous
circulatory activity after intubation and oxygenation.

Q. Given the clinical picture (history and clinical events), what is the likely sequence of
cardiorespiratory arrest in this patient?

A. This picture is suggestive of hypoxia (+/- respiratory acidosis) as the cause of the
PEA.

Q. Evaluation, using the ABC approach, confirms that airway obstruction has been
excluded by inspection. What B (breathing) causes might be considered?

A. A tension pneumothorax has a low probability because of a symmetrical
auscultation and percussion. Consider, and seek clinical supportive evidence for,
breathing impairment due to central nervous system pathology, CNS intoxication or
neuromuscular disease.

Q. What do you suspect as the cause of the hypoxia/respiratory arrest? Why?

A. The history of a progressive dyspnoea over days in a heavy smoking, COPD patient
makes respiratory exhaustion the most likely diagnosis; the most frequent cause of
exhaustion/decompensation is an infection.

Together with a short clinical examination, a concise and targeted
medical history is the cornerstone of the diagnostic process.

As you re-examine the patient you hear hardly any breath sounds in both lungs and
high airway pressures are required to achieve even a small tidal volume (Vt). The
palpable carotid pulse is disappearing again.

[66]

Q. In this patient with severe hypotension after intubation (which required no
facilitating drug therapy), what complications must be considered?

A. First exclude a misplacement of the tracheal tube then consider a pneumothorax
after auscultation and percussion of the lungs.

Q. How would you confirm or exclude tracheal tube misplacement?

A. Measure the expired CO
2
; consider a check laryngoscopy.

Q. If clinical exam suggests pneumothorax and auscultation findings are asymmetric,
what would you do?

A. Immediately perform a needle decompression on the side on which the
pneumothorax is suspected, followed by a chest tube placement. Then perform a chest
X-ray without delay.

The lung percussion is symmetrical and normal and the breath sounds are also
symmetrical, so pneumothorax is unlikely.

Q. Given the onset of hypotension after initiation of positive pressure ventilation, what
is the diagnosis to consider now, particularly in a COPD patient?

A. Elevated intrathoracic pressure which may be exacerbated by dynamic
hyperinflation an entity which is common in bronchial obstruction.

Q. A high intrathoracic pressure decreases venous return and thus cardiac output.
What common circulatory state might exacerbate this?

A. This phenomenon is exacerbated by hypovolaemia.

Cardiopulmonary interactions

Always consider pneumothorax and auto-PEEP in a ventilated patient
who rapidly becomes hypotensive.

You manage this presumed diagnosis by disconnecting the resuscitation bag from the
tracheal tube for a while and the carotid pulse becomes palpable again. You then re-
connect the patient to the ventilator.

Assessment of dynamic hyperinflation
Disconnection of manual or mechanical ventilation to treat air trapping
Ventilator adjustment

[67]

Link to PACT module on Mechanical ventilation

Q. To minimise the adverse effect of severe air trapping, which two ventilator settings
do you modify?

A. To prolong the expiration time, set a low respiratory rate and keep a low I:E ratio.
To shorten the time needed to exhale inspired gas, give a smaller tidal volume.

Ventilating the patient eight times/min with 500 mL (the patient weighs 70 kg), zero
PEEP, and FiO
2
of 1.0, you measure a PaO
2
of 26.6 kPa/200 mmHg, a PaCO
2
of 8.0
kPa/60 mmHg, and a pH of 7.3. The peak airway pressure is 60 cmH
2
O and the
plateau pressure is 35 cmH
2
O.

Q. What could explain the high peak and plateau pressures and the substantial
difference between them?

A. The peak pressure reflects dynamic compliance. The dynamic measurement (peak
pressure) is related to static compliance and to airway resistance but the plateau
pressure only to static compliance. Hence the majority of the pressure difference
between peak and plateau pressure reflects the elevated airway resistance related to
the obstructive lung disease.

Regarding the high plateau pressure, it could reflect progressive dynamic
hyperinflation.

Q. How can you verify the presence of dynamic hyperinflation?

A. The easiest way to assess dynamic hyperinflation is by assessing and measuring
auto-PEEP, either by measuring pressure at the end of an end-expiratory hold or by
checking (on the ventilator flow-time curve) if there is still an expiratory flow when the
next inspiration cycle starts.

How to measure auto-PEEP
See the PACT module on Respiratory assessment and monitoring (Task 3
monitoring ventilator waveforms)

In the deeply sedated and relaxed patient, you measure a total PEEP of 18 cmH
2
O.

Q. How could you modify the pertinent ventilatory settings?

A. You could further reduce the respiratory rate and the tidal volume.

Sometimes you need very low (RR 45/min and Vt 56 mL/kg of IBW)
ventilatory minute volume (Vm) to avoid air trapping.

[68]

Following tidal volume and respiratory rate reduction, the plateau pressure drops to
30 cmH
2
O and the pH to 7.2 as a result of hypercarbia.

Principles that guide mechanical ventilation, ventilator adjustments
Permissive hypercarbia

Link to PACT module on Mechanical ventilation

Q. Which medical treatments do you start to try to further improve the lung
mechanics?

A. Try to reduce the bronchospasm with inhaled -mimetics and anticholinergics, as
well as intravenous steroids. Treat the probable infective cause of the decompensation
with antibiotics after bacteriologic sampling. Use of sedatives and muscle relaxants
may reduce O
2
demand and CO
2
production.

Non-ventilatory support

Always monitor sedation, analgesia and neuro-blockade on a proper
scale e.g. a sedation scale. Neuromuscular blockade, if required, is monitored
using a nerve stimulator.

After a few days of full mechanical respiratory support and of the above-mentioned
medication, the patient has been stabilised and you decide to start to wean the patient
from the ventilator.

Link to PACT module on Sedation and analgesia

Q. How do you proceed?

A. You stop neuromuscular blockade if still in place, reduce/stop sedation and switch
the ventilator from a controlled (or assist-controlled) mode to an assist mode such as
PSV.

Weaning the patient

Link to the PACT module on Mechanical ventilation

Q. Do you apply PEEP?

[69]

A. In spontaneous ventilation, the patient might profit from a certain level of PEEP,
assuming he still has some auto-PEEP. The set PEEP should never exceed auto-PEEP.

External PEEP: when to apply it
External PEEP: how much

PACT module on Mechanical ventilation

Remember that decompensation in COPD patients e.g. during weaning
reflects respiratory muscle exhaustion resulting from a mismatch between the
required workload of breathing and the workload the patient is able to provide.

Two days later, the patient becomes febrile and hypotensive. You put him on
controlled mechanical support again, after excluding mechanical complications
(pneumothorax and increasing auto-PEEP).

Q. Which complication should you consider?

A. Always consider a nosocomial infection in a febrile intubated patient who remains a
long time in the ICU.

The new infiltrates on the chest X-ray and the copious and purulent bronchial
secretions cause you to suspect a nosocomial pneumonia. After taking blood cultures
and sputum samples, you change antibiotics to a broader spectrum regimen that
covers nosocomial organisms. Two days later, the bacteriological results confirm a
nosocomial pneumonia and you adapt the antibiotics to the antibiogram. Over the
next few days, the patients progress is favourable, so that you again start to wean the
patient from the ventilator. Every time you try to decrease the pressure support below
20 cmH
2
O, however, the patients breathing becomes rapid and shallow.

Diagnosis of nosocomial/ventilator-associated pneumonia
Treatment of ventilator-associated pneumonia (VAP)
See the PACT module on Severe infection

Q. Although the facial expressions are intact, the patient appears to be weak. You have
excluded a mechanical problem with the tube and ventilator. What would you do to
determine the cause of the weaning failure?

A. You examine the patient for other recognised causes of weaning failure particularly
a critical illness polyneuromyopathy.

[70]

You determine that the patient cannot lift his arms and legs from the bed and his deep
tendon reflexes have disappeared. Since the weaning is now likely to be prolonged, it is
decided to carry out a tracheostomy.

Finally, after two months of ICU stay, the patient is weaned from the ventilator and
leaves the ICU for rehabilitation in a specialised clinic. He is expected to return home
approximately two months later.

Causes of failure to wean from mechanical ventilation
Tracheostomy
Long-term outcome

See the PACT modules on Airway management, Mechanical ventilation, Respiratory
assessment and monitoring and Neuromuscular conditions.

On reflection, this module reflects the severity of acute illness which can occur in
COPD and asthma patients, often against a background of quite varying comorbidity.
The critical care treatments and support in severe acute disease are generally life-
saving and, when successful, may allow the rapid return, particularly of a young
asthmatic patient, to a normal life-style in the community. Achieving this will have
required a high level of expertise and critical care input, including a comprehensive
and consistent capacity to provide advanced, individualised ventilatory management.
This will have obvious benefit to the patient and, in terms of healthcare economic
analysis, is also evidently beneficial. However, similar expertise may entail a prolonged
ICU and hospital stay including a higher level of intervention and likely patient
morbidity but with a less evidently favourable outcome for the patient. In times when
healthcare costs and life expectancy are increasing, and the mortality from COPD is
expected, by 2020, to have doubled (relative to 1990), do you think guidelines for
rationing the distribution of medical resources are needed? If so, how and by whom
should these guidelines be created?

See the PACT module on Quality Assurance and cost-effectiveness

Copd and Asthma

Uploaded by

Copyright:

Available Formats

Copd and Asthma

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Copd and Asthma

Uploaded by

Copyright:

Available Formats

AN ESICM MULTIDISCIPLINARY DISTANCE LEARNING PROGRAMME

FOR INTENSIVE CARE TRAINING

You might also like