Management of Common Respiratory Disorders

in the ICU: Asthma, COPD, and ARDS

Mark A Bowling1*and Hunter A Coore2
1Assistant Professor of Medicine, Brody School of Medicine, East Carolina University, Greenville,
USA
2Chief Resident/Clinical Instructor, Brody School of Medicine, East Carolina University, Greenville,
USA
*Corresponding author: Mark R Bowling, Assistant Professor of Medicine, Brody School of
Medicine East Carolina University, Department of Internal Medicine, Division of Pulmonary,
Critical Care and Sleep Medicine, 3 E-149 Brody Medical Sciences Building, 600 Moye Blvd., Mail
Stop 328, Greenville, NC, USA; Tel: 278834-4354; Off: 252-744-4650; Fax: 252-744-1115; E-mail:
bowlingm@ecu.edu

Abstract
Pulmonary disorders are frequently encountered in the intensive care unit (ICU).
Complications of asthma, chronic obstructive pulmonary disease (COPD) and
acute respiratory distress syndrome (ARDS) are three of the most common
respiratory disorders faced by the ICU physician. This chapter will focus on the
basic ICU management for these pulmonary disorders.
Keywords: ARDS; Asthmaticus; COPD exacerbation; Hypercapnia; Status
respiratory failure
1. Introduction
Respiratory disorders are a common problem faced in the intensive care unit. In
this section we will discuss three of the most common pulmonary disorders seen
in critical care medicine; this includes chronic obstructive pulmonary disease
(COPD) exacerbation, acute asthma, and acute respiratory distress syndrome
(ARDS).
2.

Chronic Obstructive Pulmonary Disease Exacerbation

2.1

Background

Chronic obstructive pulmonary disease (COPD) is characterized by persistent

non-reversible airflow obstruction due to destruction of the distal airways from
local inflammation as a result of exposure to noxious particles and gases (mostly
from tobacco abuse). This permanent change in lung structure coupled with
chronic inflammation leads to a progressive decline in lung function, abnormal
gas exchange, pulmonary hypertension, air trapping (inability to deflate the
lung), increased sputum production, skeletal muscle wasting and cachexia [1].
The Global Initiative for Chronic Obstructive Lung Disease (GOLD
guidelines)defines COPD as a ratio of forced expiratory volume in 1second
(FEV1) over forced vital capacity<0.70 (FEV1/FVC<0.70) [1]. The severity of

airflow obstruction measured by spirometry is based on the measurement of the

FEV1:
Stage 1 = mild (FEV1>70 ml)
Stage 2 = moderate (FEV1 50-70 ml)
Stage 3 = severe (FEV1 30-50 ml)
Stage 4 = very severe (FEV1 <30)
The Center for Disease Control and Prevention (CDC) in 2011 reported that
COPD was the third leading cause of death in the United Statesand
approximately fifteen million people have been diagnosed with the disease [2].
It is has been predicted that in 2020 it will be the 3rd leading cause of mortality
worldwide and the 5th leading cause of burden of disease [3,4]. Many of the
patients that are diagnosed with COPD will have acute symptoms of the disease
termed exacerbations. In the United States, acute exacerbations of COPD
(AECOPD) are responsible for about 500,000 admissions to the hospital yearly,
with half of these admissions requiring ICU level care [4]. The mainstays of
therapy for AECOPD include the maintenance of adequate oxygenation and
ventilation, bronchodilator therapy, corticosteroids and antibiotics [5]. Below we
will describe the definition, risk factors and therapy in the care of patients with
these exacerbations.
2.2

Definition and risk factors

COPD exacerbations are defined by the GOLD criteria as an increase in the

frequency or severity of a cough, worsening dyspnea and a change in
character or volume of sputum production [1]. There are several identifiable
predictors for patients at risk for COPD, which include: the duration of COPD
diagnosis, number of hospitalizations, sputum production, steroid use, antibiotic
use, and co-morbidities (cardiovascular disease) [6]. Additionally, those with
GOLD Stage 3-4 are at an increased risk for exacerbations [1].
2.3

Clinical presentation and initial evaluation

Patients experiencing an AECOPD may present with several complaints and

symptoms, including increased dyspnea and cough, worsened hypoxemia,
hypercapnia (resulting in an acute metabolic acidosis), mental status changes,
and symptoms related to a primary issue such as pneumonia, cardiovascular
events, arrthymias, and organ failure [7]. Many of these patients will require ICU
admission [7]. The initial approach in the care of these patients starts with a
history and physical examination focusing on potential causes of the
exacerbation (infections, cardiac events) and evidence of impending
respiratory failure. It is important to remember that many of these patients will
have significant co-morbidities, which may add to the complexity of the
situation. For example, it is rare that a patient with COPD and heart failure will
present with just heart failure or COPD symptoms alone, it is usually a

combination of both. Therefore, both problems need to be addressed. A quick

evaluation of the patients ability to maintain adequate oxygenation and
ventilation is necessary and pertinent. The following may help in this assessment:
Oxygen saturation <88% on room air
Use of accessory muscles
Increase respiratory rate
Inability to talk clearly due to difficulty breathing
Mental status changes and evidence of inability to adequately protect the
airway (i.e. decrease gag reflex).
Arterial blood gas demonstrating hypoxia and hypercapnia with an acute
respiratory acidosis
If there is concern that the patient cannot adequately protect the airway or
experiencing significant hypercapnic respiratory failure, either endotracheal
intubation or non-invasive mechanical ventilation should be considered
immediately. If airway protection is of a concern, non-invasive mechanical
ventilation should not be utilized. Other studies to consider include a chest
roentogram (to evaluate for lung parenchymal abnormalities such as
pneumonia, pneumothorax, or pulmonary edema, etc.), measurement of
arterial blood gas, and appropriate studies focusing on the underlying cause of
the exacerbation.
2.4

Mechanical ventilation and Oxygen therapy

2.4.1 Non-invasive mechanical ventilation:

Most patients with acute respiratory failure from a COPD exacerbation can be
managed with non-invasive positive pressure ventilation (NIPPV). NIPPV is
considered first-line therapy for patients with COPD exacerbations that have
acute hypercapnic respiratory failure and no contraindications to NIPPV [1].
Several studies have reported improvement in clinical outcomes such as a
decrease in mortality, need for intubation, treatment failure, improvement in
respiratory failure, and decreased respiratory rate [8]. It is unclear as to what
initial settings one should consider when treating these patients. An approach
can be to place these patients on a bi-levelventilator mode, triggered by
spontaneous breathing. The inspiratory pressure is initially started at 10-12
cmH2O and expiratory pressures at 5 cmH2O. The inspiratory pressure is adjusted
to ensure comfort and ventilator synchrony. The goal of therapy is to relieve the
work of breathing and increase ventilation. Attempt to correct the hypercapnia
by following the change in pH to near normal levels and not to a normal pCO2,
since a majority of these patients have a baseline chronic hypercapnia.
2.4.2 Invasive mechanical ventilation: Some AECOPD patients, based on
clinical judgment, require endotracheal intubation and mechanical ventilation
to maintain adequate oxygenation and ventilation. There are several different
strategies for managing patients on a mechanical ventilator with COPD and it is

unclear if which particular strategy is best. However, it has been well described
that liberation from the ventilator should begin early to prevent muscle atrophy.
2.4.3 Oxygen therapy: Oxygen therapy and smoking cessation remains a
corner stone of COPD treatment. Best practices with oxygen therapy are to
observer the arterial hemoglobin saturation with pulse oximetry and maintain
the level of approximately 90%, commonly between 88-92%, but not higher [4].
2.5

Pharmacologic therapy

2.5.1 Bronchodilators: Short acting inhaled anticholinergic agents (i.e.

ipratropium) and beta-agonist (i.e. albuterol) are the main stay of therapy for
AECOPD. Although they can be given separately or in combination solutions,
several studies have demonstrated the significant broncho dilatation when
these agents are given concomitantly versus either agent being given alone [911]. These agents have a rapid onset and can be administered in a nebulizer
fashion or a metered dose inhaler (MDI) (Table 1). Evidence suggests that there
is no difference in the efficacy between nebulizer versus MDI with a spacer in
the delivery of inhaled medication [1]. In the acute setting, the nebulizer
method may be easier for the patient to administer [1].
Table 1: Common dosing regimens in AECOPD
Ipratropium bromide
MDI: 18 mcg 2 puffs with spacer every 4 hours
Nebulizer: 500 mcg every 4 hours
Albuterol
1) MDI: 90mcg four puffs every 4 hours with a spacer
2) Nebulizer: 2.5 mg (dilute to 3 ml) every 4 hours
Ipratropium bromide & albuterol combination
1) MDI: (90 mcg albuterol/18 mcg Ipratropium) 2 puffs with a spacer every 4
hours
2) Nebulizer: (2.5 mg albuterol/0.5 mg ipratropium) in 3 ml vial every 4 hours
2.5.2 Glucocorticoids: Systemic corticosteroids have been shown to improve
symptoms, lung function, and decrease hospital length of stay [1,12]. The
optimal dose and duration of glucocorticoids is unknown and may depend on
the patients response to therapy. While the consensus in the literature favors a
moderate dose of steroids (30 to 40 mg daily), this may not pertain to critically ill
patients [1]. Evidence suggests oral administration is just as efficacious as an
intravenous route [13]. A commonly prescribed agent is 125 mg of
methylprednisolone every 6 hours for 72 hours followed by a 2-week oral taper
starting at 60 mg [8]. Prolonged treatment leads to increased adverse reactions
from corticosteroids without improving efficacy, morbidity or mortality [12-15].
Hence, shorter tapering regimens have been suggested starting witha standard

3-day intravenous regimen noted above followed by a 30 mg dose for 5-10

days.
2.5.3 Antibiotics: There is a large and consistent beneficial effect of antibiotics
in AECOPD patients admitted to an ICU [16]. Typical bacteria isolates recovered
in AECOPD patients include Haemophilus influenzae, Streptococcus
pneumoniae and Moraxella catarrhalis [17]. While mild-moderate AECOPD is
usually treated with a conventional broad-spectrum agent (i.e. doxycycline,
trimethoprim-sulfamethoxazole and amoxicillin-clavulonate potassium), severe
AECOPD usually includes a 3rd generation cephalosporin (i.e. ceftriaxone) in
combination with a macrolide (i.e. azithromycin) or a fluoroquinolone (i.e.
moxifloxacin). Agents may be changed based on community or institutional
antibiogram and resistance patterns. While it may not provide efficacy in the
ICU setting, influenza and pneumococcal vaccines should be considered prior
to hospital discharge.
3.

Asthma

3.1

Background

Asthma is a chronic inflammatory disease of the airways similar to COPD in that

patients typically have recurrent respiratory symptoms such as cough, chest
tightness, dyspnea and wheezing. The pathophysiology of asthma includes
airway inflammation, hyper-responsiveness, and remodeling resultingin
completely reversible airflow obstruction either spontaneously or with
therapy.The severe airflow obstruction can result from bronchial constriction,
edema, and/or secretions from inflammation. In turn, this can lead to air
trapping (increasing intrathoracic pressure), hypercapnia, hypoxemia, and an
increase in the work of breathing. If not treated appropriately, the airflow
obstruction can be permanent as a result of this alteration of the bronchial
mucosa.
The CDC reports that 1 in every 12 adults have asthma in the US [18]. In the 2009,
there were 1.9 million adult and child emergency department (ED) visits as a
result of asthma, of which 479,000 required hospital admission and 3,388 died
(an age-adjusted death rate of 1.1 per 100,000 population) [19]. Like COPD,
asthma can have acute worsening of symptoms (exacerbations) and require
ICU admission. The major risk factors for a patient suffering from severe asthma
include a slow onset of symptoms [20] and prior history of poorly controlled or
near fatal asthma [21-23].
3.2

Clinical presentation and initial evaluation

On physical exam you may find the patient in significant respiratory distress with
inability to talk in full sentences or lie flat. An increase in the respiratory rate is
often observed with use of accessory muscles. Pulsus paradoxicus (a significant
decrease in systolic blood pressure upon inspiration) is often present in severe

cases as a result of an increase in the intrathoracic pressure from air trapping. A

chest roentogram may demonstrate hyperinflation and peak flow
measurements may be significantly decreased from the patients baseline
values.
3.3

Pharmacologic therapy

The goal of therapy is to quickly reverse the significant airflow obstruction and
inflammation with bronchodilators and glucocorticoids, respectively.
3.3.1 Inhaled beta-agonist: Short-acting -receptor agonists (i.e. albuterol) are
the drugs of choice in acute asthma exacerbations and quickly cause bronchial
smooth muscle relaxation [24]. Long-acting beta-agonist is not typically used in
these acute cases. Inhaled MDI or aerosol delivery is preferred over oral or
intravenousroute due to improved efficacy [25-27]. There does not appear to be
any difference in efficacy between the nebulized versus MDI with a spacer
administration [28]. When giving these therapies one needs to be mindful of the
side effects of the -receptor agonists in high doses, these include tachycardia,
tremor, and hyperglycemia and decreased serum potassium. Dosing can either
be recurring/cyclic or continuous: repetitive nebulizer treatments (2.5-5 mg
dose) or in the case of ventilated patients repetitive use of MDI (4-8 puffs of 90
g of albuterol per puff); continuously given as 1-hour nebulizer treatments using
10-15 mg of albuterol.
3.3.2 Anticholinergic therapy: Inhaled anticholinergic agents (i.e., ipratropium)
are recommended for acute asthma inED, but not hospitalized, patients [29].
However, many studies have suggested that the combination of inhaled
anticholinergics and beta-agonists be utilized in ED patients with severe airflow
obstruction since this combination results in a greater bronchodilation than
either drug alone [10,30,31]. When using ipratropium in combination with
albuterol, the dosing is 0.5 mg every 20 minutes x 3 doses then every 2 to 4 hours
as needed (nebulized). If using an MDI, the dose is 4-8 puffs (18 g per puff) in
the same regimen.then every 2 to 4 hours as needed (nebulized). If using an
MDI, the dose is 4-8 puffs (18 g per puff) in the same regimen.
3.3.3 Systemic steroids: The goal of using corticosteroids is to help reduce
inflammation. It may take a few hours before it is effective and therefore, the
quick relief of bronchoconstriction by a short-acting beta-agonist and
anticholinergic is important. Systemic steroids may help improve long-term
recovery by decreasing airways inflammation. Steroids are recommended in
patients with severe acute asthma and should be administered intravenously
[29]. Based on expert opinion [32], the dosing should include intravenous
methylprednisolone (60-80 mg every 12 hours) followed by a transition to10-14
day course of oral steroids when the patient can tolerate oral medications.

3.3.4 Magnesium sulfate: Magnesium sulfate (2 grams administered IV over 20

minutes) may be helpful in acute asthma due to its ability to relax bronchial
smooth muscle [33]. Its use is recommended to patients with severe symptoms
that have not resolved after one hour of aggressive conventional therapy [29].
3.4
Respiratory failure Approximately 4% of hospitalized asthmatics develop
significant respiratory failure that requires endotracheal intubation and
mechanical ventilation [34]. This can be a very challenging problem to manage
as they can develop various complications from securing the airway to
barotrauma from the mechanical ventilation. In this section, we will highlight
some of the basic ICU principals in the airway management and ventilation
strategies for the patient with respiratory failure due to acute asthma.
3.4.1 Airway management: The decision to intubate is based on clinical
judgment based on the patients ability to protect their airway and maintain
adequate oxygenation with supplemental oxygen and NIPPV. It is important to
remember that the patients respiratory issues can continue post-intubated and
adding a mechanical ventilator may further complicate the problem. It is highly
recommended that experienced physicians and respiratory therapists treat
patients with acute asthma. Additionally, it is also recommended that the
healthcare provider performing the intubation be experienced and trained in
the management of patients with potentially difficult airways.
3.4.2 Non-invasive mechanical ventilation: NIPPV is an excellent option for
patients that do not require immediate endotracheal intubation or have a
contraindication to NIPPV therapy [35-39]. Typically, a bi-level mode with
inspiratory pressure starting at 10-12 cmH2O and expiratory pressures of 5-8
cmH2O is used and adjustments are made to increase ventilation and work of
breathing. Of importance is that if NIPPV is utilized, frequent monitoring is
necessary for response to therapy and a declining respiratory status. NIPPV
should not be a substitute for the patient that requires endotracheal intubation
and mechanical ventilation.
3.4.3 Invasive mechanical ventilation: Due to the physiologic consequences of
significant airway constriction (airflow obstruction, hypoxia, hypercapnia, air
trapping) in asthmatic patients, the ventilator management can be very
challenging and may result in complications. General principles to consider in
the ventilator management of these patients include dynamic hyperinflation as
a result of a prolonged expiration from constricted airways. This can be made
worse by mechanical ventilation if the respiratory rate is not spaced far enough
apart allowing the inhaled gas time to escape before a second breathe is
administered. This can cause a tremendous amount of pressure in the chest,
resulting in hypotension from a decrease in blood return to the right heart,
worsening hypercapnia, and barotrauma (pneumothorax,
pneumomediastinium, etc.).

Strategies to decrease hyperdynamic inflation include [40]:

Increase the ventilator flow rate in order to decrease the inspiratory time and
increase the expiratory time.
Decrease the respiratory rate, allowing the inhaled gas time to be exhaled.
Decrease the tidal volume, allowing less inhaled gas to be exhaled.
3.4.4 Adjunctive therapies: In some severe cases when oxygenation and
ventilation cannot be achieved by conventional methods, other therapies have
been utilized in the management of acute asthma. Listed below is a brief
description of these therapies. We recommend that only those physicians that
are familiar with the utility of these agents should administer these treatments. i.
Heliox Therapy
Heliox is the blend of helium and oxygen that can be helpful by enhancing the
delivery of oxygen and inhaled medication to the distal airway in acute
asthmatics [41]. It has a density less than air and can overcome the significant
airway resistance in these patients [41-44]. ii.
General Anesthesia
Several different agents such as ketamine and isoflurane have been used in the
management of these patients mostly due to their bronchodilatation properties
[45-47].
4
Acute Respiratory Distress Syndrome
4.1
Background
Acute respiratory distress syndrome (ARDS) is a common condition encountered
in the ICU with an estimated 190,000 cases per year in the United States [48].
Respiratory failure results from an acute inflammation resulting in diffuse alveolar
damage, non-cardiac pulmonary edema, poor lung compliance and
significant hypoxemia. In general, there is an indirect (transfusion reactions,
sepsis, pancreatitis,) or direct (trauma, aspiration, pneumonia) insult to the lungs
that results in diffuse alveolar damage from disruption of the alveolar lining and
capillary endothelium. In turn, this leads to alveolar edema and protein
exudation coupled with a marked inflammatory response consequentially
resulting in fibrosis. The physiological effect of this damage manifests as
abnormal gas exchange due to ventilation perfusion disparities [49] and poor
lung compliance [50] and pulmonary hypertension [51].
4.2

Clinical presentation and initial evaluation

The initial signs of ARDS are tachypnea and progressive hypoxemia. Physical
exam may reveal manifestations of the initial insult such as pneumonia, sepsis or
trauma. Typically, the patient will have an increased respiratory rate, use of
accessory muscles and diffuse crackles upon auscultation of the lungs. There
may be signs of peripheral cyanosis and poor perfusion if shock is present. The
chest roentogram is often unrevealing in the first few hours, but will eventually

show dense bilateral infiltrates. As the disease progresses, the patients

hypoxemia often progresses to require mechanical ventilation.
Appropriate laboratory and radiologic studies should be directed to the
underlying disease. For example, if pneumonia is suspected, blood and sputum
cultures may be appropriate. If the patient had significant trauma, radiologic
studies should be directed to evaluate the extent of the injury. It is imperative to
evaluate the arterial oxygen and carbon dioxide tension with arterial blood gas
monitoring in all these patients.
4.3

Diagnosis

In 2011, an expert panel from an initiative of the European Society of Intensive

Care Medicine endorsed by the American Thoracic Society and the Society of
Critical Care Medicine developed the Berlin definition of ARDS [52]. According
to the Berlin ARDS definition, all of the following criteria must be met:
Respiratory symptoms must occur or become worse within one week of the initial
insult
Bilateral pulmonary opacities consistent with pulmonary edema on radiographic
imaging (not be due to pleural effusions, lobar or lung collapse, or pulmonary
nodules)
The respiratory failure must not be due to cardiac failure or volume overload.
This must be verified by an objective measure such as (echocardiogram,
pulmonary occlusion pressure, etc.) to exclude hydrostatic pulmonary edema if
there is no risk factors explain the ARDS.
Impaired oxygen exchange must be present as defined by the ratio of arterial
oxygen tension to fraction of inspired oxygen (PaO2/FiO2).
The severity of hypoxemia defines the severity of ARDS and associated mortality
risk:
Mild (27% mortality risk): PaO2/FiO2>200mmHgbut = 300 mmHg, [positive endexpiratory pressure (PEEP) = 5cmH2O]
Moderate (32% mortality risk): PaO2/FiO2 >100 mmHg but < 200 mmHg. [PEEP =
5cmH2O]
Severe (45% mortality risk): PaO2/FiO2 <100 mmHg [PEEP =5 cm H2O]
4.4

Management

Initial therapy should focus on treating the underlying cause of ARDS (i.e.
antibiotics for infections, reversing antidote for overdoses, etc) and maintaining
adequate gas exchange while minimizing complications that are common in
patients with ARDS. The following treatment modalities may be used:

4.4.1 Mechanical ventilation lung protective strategy:

Low tidal volume ventilation: In patients with ARDS, positive pressure ventilation
may generate extreme pressure in the distal airways due to the decrease in lung
compliance from pulmonary edema, proteinaceous material, and fibrosis. This
can lead to further lung damage, resulting in worsened hypoxemia,
pneumothorax, and pneumomediastinium (coined ventilator induced lung injury
and barotrauma).Therefore, the lung protective strategy approach to
mechanical ventilation in ARDS patients is to minimize the elevated distal airway
pressure (displayed by the mechanical ventilator as the plateau pressure) by
utilizing low tidal volumes defined as 6-8 mL/kg of ideal body weight [53].
Mortality is also reduced with low distal airway pressures (plateau pressure
<30cm H2O) [54,55]. Our experience has been to utilize lung protective
strategies by targeting tidal volumes to 6-8 mL/kg of ideal body weight.
PEEP: One of the factors that may contribute to ventilator induced lung injury is
inflammation from cyclic atelectasis (termed alectotrauma). PEEP improves
oxygenation and prevents alectotrauma, although it is unclear at what level of
PEEP prevents this complication [55-57]. Several studies have evaluated various
approaches to utilizing PEEP with conflicting results [58-62]. While some studies
report no difference in mortality between higher versus lower levels of PEEP [58],
other studies illustrate an improved mortality with higher levels of peep in
patients with severe hypoxemia (PaO2/FiO2<200mmHg) [61,62]. Furthermore,
studies have shown a decrease in hypoxemia, ventilator free days, and days
free of organ failure when combined with a low tidal volume strategy [59,60].
While nearly all patients should have a minimum PEEP of 5 cmH2O, PEEP is
increased to a plateau pressure of 30-32 cm H2O in patients with severe
hypoxemia (PaO2/FiO2<200mmHg).
Fluid management strategies: Patients with ARDS have non-cardiogenic
pulmonary edema due to vascular permeability from inflammation and
changes in oncotic forces due to damage to the alveolar-capillary interface.
Conservative fluid management approaches have shown to have a significant
clinical benefit by decreasing ventilator free days, ICU days, improved
oxygenation and lung injury scores [63]. A conservative fluid management
strategy should therefore be pursued as long as the patient is not in shock or
experiencing hypo perfusion. Effective fluid strategies can be achieved with
daily diuretics, avoiding unnecessary intravenous fluids, and meticulously
monitoring fluid intake/output and electrolytes if diuretics are utilized.
Novel therapies: Several other therapies and management strategies have
been utilized in the management of ARDS such as systemic steroids [64],
antioxidants [65] and prone positioning [66] to improve oxygenation. The
benefits of these treatment modalities remain controversial and should be
approached with caution under the direction of a physician that is an expert in
the management of patients with ARDS.

Supportive care: Appropriate supportive measures should be given to all

patients in the ICU. Maintaining adequate nutrition, sedation and pain control is
paramount but often overseen. The prevention of secondary infections by
maintaining aggressive hand hygiene, ventilator-associated infection
preventative measures, and diligent central venous and urinary catheter care is
vital. Gastric ulcers and deep venous thrombosis prophylaxis should be
addressed on a case-by-case basis.
5. Conclusion
COPD, asthma and ARDS are common pulmonary disorders encountered in the
ICU. COPD and asthma are initially managed initially with rapid bronchodilators,
anti-inflammatory steroids, and oxygenation via invasive and non-invasive
ventilation. In patients with ARDS, management focuses primarily on treating the
underlying cause, lung protective strategies for those receiving mechanical
ventilation, and adequate supportive care. Management of all these conditions
can be challenging and a consultation by experts in critical care medicine is
often warranted. Providers caring for critically ill patients should be familiar with
the identification and management of patients with COPD, asthma and ARDS.

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NOTE DAME OF TACURONG COLLEGE

COLLEGE OF NURSING
CITY OF TACURONG

Nursing Journal
(Management of Common Respiratory Disorders in the ICU: Asthma, COPD, and
ARDS)

Submitted to:
Mrs. Tina Lumanag, R.N.,M.N
Clinical instructress
Submitted by:
Bai Sandra M. Sinagandal
BSN 4

11.24.14