C

32 l Nursing2009Critical Care l Volume 4, Number 2

Caring for a patient with an acute asthma exacerbation or
status asthmaticus is quite common in critical care. In this
article, Ill review the pathophysiology and management of a
severe asthma exacerbation so youll be prepared to monitor
your patients response to therapy and intervene appropri-
ately should the patients clinical status deteriorate rapidly.
A chronic inflammation
Asthma is a chronic inflammatory disorder of the airway
characterized by airway hyperresponsiveness, mucus hyper-
secretion, and reversible airflow limitation. Chronic inflam-
mation associated with asthma thickens the airway walls or
changes their structure, a process known as airway remodel-
ing. In an acute episode, the patient also has airway edema
and bronchoconstriction. Asthma is variable in terms of
genotypes, clinical phenotypes, susceptibility to environmen-
tal factors, pathogenesis, expression, severity, and response
to treatments.
1-3
Asthma triggers include viral respiratory infection, expo-
sure to an allergen or irritant, exercise, stress, smoking, cold
air, gastroesophageal reflux, nonadherance to pharmacolog-
ic therapies or sudden withdrawal from corticosteroids, and
consumption of certain foods or intake of certain drugs such
as aspirin, beta-blockers, nonsteroidal anti-inflammatory
drugs, cocaine, or heroin.
1,2,4-6
Asthma exacerbations can be classified as mild, moder-
ate, severe, or respiratory arrest imminent.
1
(For more
details, see Severity of asthma exacerbations.) A severe exacer-
bation, the focus of this article, is characterized by severe
airflow limitation and dynamic hyperinflation (also called
air trapping), in which end-expiratory lung volume increases
because patients cant exhale fully, but are trying to main-
tain near-normal gas exchange.
2,4-8
Bronchospasm, edema,
Act fast to
prevent
respiratory
collapse
By Jin Xiong Lian, RN
Managing a severe acute
asthma exacerbation
34 l Nursing2009Critical Care l Volume 4, Number 2 www.nursingcenter.com
Managing a severe acute asthma exacerbation
excessive secretions, and mucus
plugs lead to progressive airway
narrowing, increased airway
resistance, insufficient expiratory
time, and respiratory muscle
fatigue. As a result, dynamic
hyperinflation and elevated
intrinsic positive end-expiratory
pressure (PEEPi) occur. (In a
healthy patient, a small amount
of air remains in the lungs at
end-expiration, creating normal
PEEP of 3 to 5 cm H
2
O. However,
in a patient with dynamic hyper-
inflation secondary to an asthma
exacerbation, more air is left in
the lungs at end-expiration than
the physiologic normal volume,
resulting in increased PEEPi.)
Airflow obstruction diminish-
es ventilation, reduces oxygen
intake, and increases ventila-
tion/perfusion (V

/Q

) mismatch-
ing. In addition, frequent cough-
ing to clear sputum or airway
secretions, using accessory mus-
cles of respiration, and being
agitated increase oxygen con-
sumption and carbon dioxide
(CO
2
) production. Without time-
ly and appropriate treatment,
a patient with an acute severe
asthma exacerbation will devel-
op hypoxemia and hypercapnia,
leading to anaerobic metabolism,
lactic acidosis, and acid-base
imbalance.
4,5,7
Clinical manifestations of an
acute asthma exacerbation vary
among patients and by the severity
of asthma. The common signs and
symptoms include cough, wheez-
ing, shortness of breath, chest
tightness, diaphoresis, tachypnea,
and tachycardia. Remember that
the absence of typical signs and
symptoms doesnt mean that the
patients condition isnt getting
Severity of asthma exacerbations
Mild Moderate Severe Respiratory arrest
imminent
Breathlessness Patient can walk, Patient prefers Patient is leaning
lie down, and sitting, talks forward and can
talk in sentences in phrases only say a few words
between breaths
Alertness May be agitated Usually agitated Usually agitated Drowsy or confused
Respiratory rate Increased Increased Often greater than
30 breaths per
minute
Use of accessory Usually not Usually Usually Paradoxical
muscles of thoraco-abdominal
respiration movement
Wheezing Moderate, Loud Usually loud Absent
and often only
at end-expiration
Pulse Less than 100-120 Greater than 120 Bradycardia
100/minute
Pulsus Absent (less May be present Often present Absent, suggesting
paradoxus than 10 mm (10 to 25 mm Hg (greater than 25 respiratory muscle
Hg difference) difference) mm Hg difference) fatigue
PaO
2
Normal Greater than Less than
60 mm Hg 60 mm Hg
PaCO
2
Less than Less than Greater than
45 mm Hg 45 mm Hg 45 mm Hg
SaO
2
Greater than 95% 91%-95% Less than 90%
Adapted from the Global Initiative for Asthma guidelines, 2008.
1
www.nursingcenter.com March l Nursing2009Critical Care l 35
worsein a drowsy or confused
patient, it can signal imminent
respiratory arrest.
1,2,4,6,9
Management strategies
Because of great variability in
clinical manifestations, severity,
and response to treatments, your
patient may need to be admitted
to the ICU for close monitoring
and aggressive treatment.
1,2
Here
are the recommended interven-
tions for an asthma exacerbation:
Administer supplemental oxygen
as soon as possible to achieve oxy-
gen saturation of 90% or greater. A
patient in an acute exacerbation
inevitably suffers from hypoxia.
Supplemental oxygen reduces
V

/Q

mismatching, promotes
bronchodilation, and reduces
pulmonary vasoconstriction.
6,10
If your patient also has chronic
obstructive pulmonary disease
(COPD), administering a large
amount of supplemental oxygen
may blunt his respiratory
drive.
4,8,11
These patients also
are at risk of oxygen toxicity
if they receive a fraction of
inspired oxygen concentration
(F
I
o
2
) greater than 0.5 to 0.6
for a prolonged period.
11-14
However, the benefit of adminis-
tering a large amount of oxygen
(relieving hypoxemia in an acute
asthma exacerbation) may out-
weigh the risks. Monitor your
patient closely and titrate the
oxygen to minimize the risks.
Administer rapid-acting inhaled
bronchodilators as prescribed.
Beta
2
-agonists stimulate beta
2
receptors on airway smooth
muscles, relieving bronchocon-
striction, reducing the work of
breathing, and decreasing resis-
tance to airflow. Short-acting
beta
2
-agonists (SABAs), quick-
relief medications, are used to
relieve bronchoconstriction, and
are indicated for acute episodes
and exacerbations.
1
The com-
monly prescribed SABAs are
albuterol (also known as salbuta-
mol), terbutaline, levalbuterol,
and pirbuterol.
1,4,5,7,15
Nebulized salbutamol can be
given intermittently or continu-
ously. However, salbutamol that
is given via inhaled or aerosolized
routes may be unable to reach
lower airways and lung tissues
due to severe airflow obstruction
and decreased tidal volume. If
the patients initial response to
SABA therapy is poor, consider
I.V. beta
2
-agonists.
1
In the ICU, continuous I.V.
infusion of terbutaline (the I.V.
beta-agonist of choice in the
United States) or salbutamol
may be used to treat refractory
asthma exacerbations.
4,5,10,15
Subcutaneous injections of epi-
nephrine or terbutaline may be
considered if the patient fails
to improve with nebulized beta
2
-
agonists.
3-5,15
Nebulized or I.V.
epinephrine also may be effective
in treating a severe attack.
7
Anticholinergics cause mild
bronchodilation by inhibiting
muscarinic cholinergic receptors
and lowering intrinsic vagal tone
of the airway. Administering
inhaled ipratropium bromide in
conjunction with a nebulized
beta
2
-agonist produces profound
bronchodilation and significant-
ly improves a patients pul-
monary function, with minimal
cardiovascular adverse
reactions.
1,3,5,6,10,16
Administer systemic corticosteroids
as prescribed. Corticosteroids play
a vital role in the suppression of
airway inflammation. By inhibiting
inflammatory cell migration and
activation, and blocking late-phase
reaction to allergens, cortico-
steroids reduce airway hypersensi-
tivity, secretions, and edema.
Systemic corticosteroids are an
integral part of the first-line med-
ication for moderate-to-severe
asthma attacks.
1,3
Prednisone,
methylprednisolone, prednisolone,
hydrocortisone, and dexametha-
sone are commonly prescribed
and should be administered for 3
to 10 days. The dose reduction and
duration of corticosteroid therapy
are determined by the severity and
chronicity of asthma.
1,3-5,10,15,17
To prevent a relapse, the patient
should be discharged with a 5- to
10-day course of oral systemic
corticosteroids.
1
Although corticosteroids are
safe for short-term use, they can
cause hyperglycemia, hyperten-
sion, fluid retention, hypokalemia,
Cushings syndrome, acute
psychosis, gastric ulcer, allergic
reactions, and immune function
suppression.
1,4,10,15
Closely moni-
tor patients on long-term cortico-
steroid therapy for adverse drug
reactions.
Administer noninvasive positive-
pressure ventilation (NPPV) as
indicated. NPPV enhances alveo-
lar ventilation, improves gas
exchange, and reduces the need
for endotracheal intubation and
mechanical ventilation. Applying
extrinsic positive end-expiratory
pressure (PEEPe) with NPPV
overcomes the effect of PEEPi,
reduces the work of breathing,
and rests fatigued respiratory
muscles.
5-8,18,19
No universal guidelines exist
for when to implement noninva-
sive or invasive ventilation for
asthma attacks, or for which ven-
tilation strategy to use. However,
NPPV may be used when aggres-
sive treatments with bronchodila-
tors and corticosteroids dont
reverse a patients condition, and
if the patient can tolerate the
therapy, manage his own airway
secretions, and doesnt need
immediate intubation.
6,7,17-19
NPPV can be administered via
facial or nasal masks, using either
continuous positive airway pres-
sure or bilevel positive airway
pressure. Be aware that inappro-
priately set PEEPe may worsen a
patients hyperinflation. Other
complications associated with
NPPV include gastric distension,
vomiting, aspiration, eye irrita-
tion, and stress ulcer.
7,18,20
Some
patients with severe asthma
attacks cant tolerate NPPV.
5,7
More and larger studies may be
needed to determine the role of
NPPV in managing severe asthma
exacerbations.
9,21
Assist with endotracheal intuba-
tion and mechanical ventilation if
indicated. Your patient may need
to be endotracheally intubated
if he develops respiratory or
cardiac arrest, severe hypoxia,
progressive hypercapnia with
profound acidosis, life-threatening
dysrhythmias, hemodynamic
instability, copious amount of
sputum, exhaustion, or decreased
level of consciousness.
1,4,5,8,10,22
Ventilating a patient with a
severe asthma exacerbation often
is challenging. Although mechan-
ical ventilation improves gas
exchange and rests fatigued respi-
ratory muscles, it may lead to
ventilator-induced lung injuries
(VILI) such as barotrauma and
volutrauma, and other complica-
tions. The ventilation strategy
should aim to improve oxygena-
tion, reduce dynamic hyperinfla-
tion, and PEEPi. The primary
settings are for a low respiratory
rate (8 to 10 breaths/minute),
prolonged expiratory time (inspi-
ratory-expiratory ratio of 1:2 to
1:6), and low tidal volume (4 to 8
mL/kg).
6,9,21
Either volume con-
trol or pressure control ventila-
tion can be used, depending on
the healthcare providers prefer-
36 l Nursing2009Critical Care l Volume 4, Number 2 www.nursingcenter.com
Managing a severe acute asthma exacerbation
Heres your single, most authoritative source for
gaining greater professional autonomy
ensuring maximum reimbursement with fewer delays
avoiding emerging legal risks unique to NPs
developing strategies to grow and manage a practice.
FREE online access to full-text issues since 2001 with
individual paid subscription.
Youll be current on topics such as understanding
glaucoma, detecting osteoporosis, implementing insulin
therapy, managing insomnia, and much more!
Continuing education offerings in every issue,
including exclusive pharmacology CEs
Editor-in-Chief: Jamesetta A. Newland, PhD, APRN, BC, FNP, FAANP, FNAP
BONUS
exclusively for
subscribers!
Annual
Legislative Update*
on state-by-state scope
of authority for NPs
Begin your RISK-FREE subscription today.
Go to NursingCenter.com or LWW.com/nursing
or call 1-800-638-3030.
with updates on the full scope of your responsibilities.
*Available in January issues.
tnpj.com
Wolters Kluwer Health/Lippincott Williams & Wilkins F7NKK434 A7K434ZZ
ence and experience. The mode
and settings should be adjusted in
response to significant changes in
a patients condition.
5-7,10,22
Low tidal volume or controlled
hypoventilation elevates partial
pressure of arterial carbon diox-
ide (PaCO
2
). In patients with a
severe asthma exacerbation,
hypercapnia and respiratory aci-
dosis are allowed to occur grad-
ually in an effort to keep plateau
pressure below 30 cm H
2
O and
reduce VILI.
6,10,23,24
However, excessive hypercap-
nia causes intracellular acidosis
and related cytotoxicity and
induces pulmonary vasocon-
striction that exacerbates preex-
isting pulmonary hypertension.
Hypercapnia also causes cere-
bral vasodilation that increases
intracranial pressure and leads
to cerebral edema.
24-26
No con-
sensus exists on the upper limit
of hypercapnia or the safe level
of acidosis. The prevailing views
are to keep PaCO
2
below 90 mm
Hg and to maintain pH greater
than 7.1.
10,15,22,24,26
The use of PEEPe is controver-
sial, because it reduces venous
return and cardiac output,
induces hypotension, and inten-
sifies hyperinflation. Some
healthcare providers advocate
no PEEPe; others recommend
applying a low PEEPe to reduce
the work of breathing, improve
patient-ventilator synchrony, and
promote recovery of fatigued
respiratory muscles.
6,8-10,24,27
The current prevailing recom-
mendation is to apply PEEPe at a
level of about 80% of a patients
PEEPi for spontaneously breath-
ing patients.
8,22,28
(The various
methods used to detect and
measure a patients PEEPi are
beyond the scope of this article.)
Assist with sedation and neuro-
muscular blockade if indicated.
Patient-ventilator dyssychrony is
common in patients with a severe
asthma exacerbation, because of
extreme anxiety, agitation, and
PEEPi. Sedation and paralysis
rest fatigued respiratory muscles,
reduce oxygen consumption and
CO
2
production, ameliorate
patient-ventilator dyssynchrony,
improve patient comfort, and
enhance the effectiveness of
mechanical ventilation.
8,29
Ketamine, midazolam, and
propofol are commonly used
for intubation and mechanical
ventilation. Rocuronium or sux-
amethonium (neuromuscular
blocking agents) often are pre-
scribed to induce paralysis.
7,10
Sedatives may lead to respiratory
depression and delay weaning
from mechanical ventilation.
Neuromuscular blocking agents
may cause myopathy or muscle
weakness, so they should be used
sparingly and only for a short
time.
5-9,24
Because corticosteroids
may potentiate myopathy, they
shouldnt be administered con-
comitantly with neuromuscular
blockers.
30
Administer adjunctive medica-
tions as prescribed. Magnesium
sulfate causes smooth muscle
relaxation. The Global Initiative
for Asthma (GINA) guidelines
recommend administering I.V.
magnesium sulfate in certain
cases, including adults who fail to
respond to initial treatment.
1
In
combination with beta-agonists
and systemic corticosteroids,
this drug may be beneficial to
patients in a severe asthma exac-
erbation.
4,6,31
However, clinical
evidence is inadequate to prove
that magnesium improves a
patients condition, and its
therapeutic effect remains
controversial.
4,6,9,10,15,31,32
Methylxanthines such as
aminophylline and theophylline
were part of the standard treat-
ment for severe asthma exacerba-
tions in the past. But they can
cause severe adverse reactions
such as cardiac dysrhythmias,
headache, nausea, tremor,
seizures, and encephalopathy.
Also, these drugs have a very
narrow therapeutic range. As
a result, aminophylline and
theophylline are seldom pre-
scribed, but may be used as sec-
ond-line therapy for refractory
asthma.
2,4,10,17
Short-acting
theophylline may benefit respi-
ratory drive, although it doesnt
appear to provide additional
bronchodilation over other
SABAs.
1
The GINA guidelines also rec-
ommend administering nebulized
heliox as an adjunct treatment for
severe exacerbations unrespon-
sive to intensive treatments with
SABAs, anticholinergics, and
systemic corticosteroids.
1
Using
adjunct treatments may avoid the
need for intubation. However,
administering aminophylline or
theophylline in the ED isnt rec-
ommended.
3
Other second-line options
include inhaled anesthetic agents,
mucolytics, and nitric oxide. Large
studies are needed to evaluate
the efficacy and safety of these
agents and to determine their
roles in treating severe acute
asthma exacerbations.
4,5,7,17
Your role
Closely monitor and regularly
assess your patient to determine
when therapy needs to be adjusted
to improve patient response and
minimize adverse reactions.
1,2
www.nursingcenter.com March l Nursing2009Critical Care l 37
Assess and support the patients
airway, breathing, and circulation
and monitor his clinical status
and vital signs. Help him assume
a comfortable position (high
Fowlers or sitting, unless con-
traindicated by his hemodynamic
status) and encourage him to
relax. Maintain a calm environ-
ment and reassure the patient that
youre there to ensure his safety.
Explain to him that agitation will
worsen his breathlessness, and
that relaxing will help reduce
oxygen consumption and improve
his condition.
Monitor your patients fluid
balance. He may be dehydrated
because of decreased oral intake
and increased insensible fluid loss
caused by agitation, increased
work of breathing, and tachypnea.
Administer fluid replacement as
needed. Mechanically ventilated
patients are at high risk of devel-
oping hypotension, so main-
taining adequate intravascular
volume is essential. However,
be careful not to overhydrate
your patient because of the risk
of fluid volume overload and
pulmonary edema.
4,7
If your patient needs NPPV,
apply the facial or nasal mask
properly and explain the therapy
to your patient. Provide reassur-
ance and emotional support to
help him tolerate the therapy.
Assess him regularly for the need
for endotracheal intubation and
mechanical ventilation. If he
needs mechanical ventilation,
monitor him for complications
and take steps to identify and
minimize VILI.
Teach the patient and his fam-
ily about asthma control and
prevention. (See Keeping asthma
under control, every day.) Review
potential triggers and how the
patient can control risk factors
for acute attacks. Help him
understand the importance of
taking his medications and tak-
ing an active part in managing
his disease.
Assess his ability to use his
inhalers and to manage his asth-
ma at home. Teach him to use a
peak flowmeter and how to rec-
ognize trends that indicate an
increasing risk of an acute
attack. He should know the
signs and symptoms of asthma
exacerbations and when to seek
medical attention. Arrange a
follow-up appointment and refer
him to an asthma self-manage-
ment education program or
asthma specialist as appropriate.
By understanding the man-
agement of an asthma exacer-
bation and how to empower
patients to prevent future attacks,
you can help your patient breathe
easier.
REFERENCES
1. Global Initiative for Asthma. Global
strategy for asthma management and pre-
vention. December 2008. http://www.
ginasthma.com.
2. Balkissoon R. Asthma overview. Primary
CareClin Office Pract. 2008;35(1):41-60.
3. National Heart, Lung, and Blood Insti-
tute. National Asthma Education and Pre-
vention Program. Expert Panel Report 3:
Guidelines for the diagnosis and manage-
ment of asthma. Full report, 2007. http://
www.nhlbi.nih.gov/guidelines/asthma.
4. Mannix R, Bachur R. Status asthmaticus
in children. Curr Opin Pediatr. 2007;19(3):
281-287.
5. Restrepo RD, Peters J. Near-fatal asthma:
recognition and management. Curr Opin
Pulm Med. 2008;14(1):13-23.
6. Corbridge SJ, Corbridge TC. Severe exac-
erbations of asthma. Crit Care Nurs Q.
2004;27(3):207-230.
7. Phipps P, Garrard CS. The pulmonary
physician in critical care: acute severe
asthma in the intensive care unit. Thorax.
2003;58(1):81-88.
8. Peigang Y, Marini JJ. Ventilation of pa-
tients with asthma and chronic obstructive
pulmonary disease. Curr Opin Crit Care.
2002;8(1):70-76.
9. Kaza V, Bandi V, Guntupalli KK. Acute
severe asthma: recent advances. Curr Opin
Pulm Med. 2007;13(1):1-7.
10. Marcoux KK. Current management of
status asthmaticus in the pediatric ICU.
Crit Care Nurs Clin North Am. 2005;17(4):
463-479.
11. Pruitt WC, Jacobs M. Breathing lessons:
basics of oxygen therapy. Nursing. 2003;33
(10):43-45.
12. Fenstermacher D, Hong D. Mechanical
ventilation: what have we learned? Crit
Care Nurs Q. 2004;27(3):258-294.
13. Spritzer CJ. Unraveling the mysteries of
mechanical ventilation: a helpful step-by-
step guide. J Emerg Nurs. 2003;29(1):29-36.
14. Woodruff DW. A quick guide to vent
essentials. RN. 2005;68(9);acute care fo-
cus:32ac2-7,2p.
38 l Nursing2009Critical Care l Volume 4, Number 2 www.nursingcenter.com
Managing a severe acute asthma exacerbation
Keeping asthma under control, every day
The goal of asthma therapy is to keep asthma under control. Therapy is
based on asthma severity and adjusted according to periodic monitoring
of asthma control.
1
Here are steps you can help your patient take.
Identifying potential asthma triggers and avoiding exposure to them.
Establishing an individual asthma management plan and adhering to it.
Maintaining a healthful lifestyle.
Long-acting beta
2
agonists such as salmeterol and formoterol, in com-
bination with inhaled corticosteroids, are recommended for long-term
control, and to prevent exacerbations or relapses. Inhaled corticosteroids
such as beclomethasone, budesonide, flunisolide, and fluticasone are the
most effective long-term control medications for persistent asthma.
1
Leukotriene modifiers such as montelukast, zafirlukast, and zileuton,
can be used as additional therapy in patients with persistent asthma or
aspirin-sensitive asthma. These adjuncts may help reduce the dosage of
corticosteroids needed, and the adverse effects of corticosteroids.
1
Understanding ventilator
waveforms: Erratum
In the article that started on page 43 in the
January issue, waveform B was incorrectly
positioned in Figure 5 on page 45. The corrected
waveform is shown below. This error has been
corrected in the online version of the article,
which is available at www.nursingcenter.com.
Reference: Lian JX. Understanding ventilator waveforms and
how to use them in patient care. Nurs2009 Crit Care. 2009;4(1):
43-55.
15. Werner HA. Status asthmaticus in
children: a review. Chest. 2001;119(6):
1913-1929.
16. Kanazawa H. Anticholinergic agents in
asthma: chronic bronchodilator therapy, re-
lief of acute severe asthma, reduction of
chronic viral inflammation and prevention
of airway remodeling. Curr Opin Pulm Med.
2006;12(1):60-67.
17. Higgins JC. The crashing asthmatic.
Am Fam Physician. 2003;67(5):997-1004.
18. Beers SL, Abramo TJ, Bracken A,
Wiebe RA. Bilevel positive airway pres-
sure in the treatment of status asthmati-
cus in pediatrics. Am J Emerg Med. 2007;
25(1):6-9.
19. Carroll CL, Schramm CM. Noninvasive
positive pressure ventilation for the treat-
ment of status asthmaticus in children. Ann
Allergy Asthma Immunol. 2006;96(3):454-459.
20. Manno MS. Managing mechanical ven-
tilation. Nursing. 2005;35(12):36-42.
21. Ram FSF, Wellington SR, Rowe B,
Wedzicha JA. Non-invasive positive pres-
sure ventilation for treatment of respiratory
failure due to severe acute exacerbations of
asthma. Cochrane Database Syst Rev. 2005;3:
CD004360.
22. Pilbeam SP. Final considerations in ven-
tilator setup. In: Pilbeam SP, Cairo JM, eds.
Mechanical Ventilation: Physiological and
Clinical Application. 4th ed. St Louis: Elsevier
Mosby; 2006:127-149.
23. Hager DN, Krishnan JA, Hayden DL,
Brower RG. Tidal volume reduction in pa-
tients with acute lung injury when plateau
pressures are not high. Am J Respir Crit Care
Med. 2005;172(10):1241-1245.
24. Evans N, Skowno J, Hodgson E. The
anaesthesiologist in the intensive care unit.
Curr Opin Anaesthesiol. 2003;16(4):401-407.
25. Chonghaile MN, Higgins B, Laffey JG.
Permissive hypercapnia: role in protective
lung ventilatory strategies. Curr Opin Crit
Care. 2005;11(1):56-62.
26. Mutlu GM, Factor P, Schwartz DE, Sz-
najder JI. Severe status asthmaticus: man-
agement with permissive hypercapnia and
inhalation anesthesia. Crit Care Med. 2002;
30(2):477-480.
27. Pruitt WC. Ventilator graphics made
easy. RT. 2002;15(1):23-24, 50.
28. Blanch L, Bernabe F, Lucangelo U.
Measurement of air trapping, intrinsic posi-
tive end-expiratory pressure, and dynamic
hyperinflation in mechanically ventilated
patients. Respir Care. 2005;50(1):110-124.
29. Hess DR. Thompson BT. Patient-ventila-
tor dyssynchrony during lung protective
ventilation: whats a clinician to do? Crit
Care Med. 2006;34(1):231-233.
30. Larsson L, Li X, Edstrom L, et al. Acute
quadriplegia and loss of muscle myosin in
patients treated with nondepolarizing neu-
romuscular blocking agents and cortico-
steroids: mechanisms at the cellular and
molecular levels. Crit Care Med. 2000;28(1):
34-45.
31. 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):70-76.
32. Beasley R. Aldington S. Magnesium in
the treatment of asthma. Curr Opin Allergy
Clin Immunol. 2007;7(1):107-110.
Jin Xiong Lian is a nurse in the intensive care unit
at Concord Repatriation General Hospital, part of
the University of Sydney in New South Wales,
Australia.
www.nursingcenter.com March l Nursing2009Critical Care l 39
Extend your
nursing skills and
bring stronger purpose
to your care of the sick and dying
with this vital blend of clinical
excellence and Gods sustaining
inspiration. Youll discover a unique,
biblically-based, Christian perspective
on nursing that leads you to higher
professional excellence and a more
fulfilling sense of purpose.
Lippincott Williams & Wilkins 6-K565-4P
Articles available in print and on-line at
www.journalofchristiannursing.com.
Earn Continuing Education credits with Journal of Christian Nursing.
Publication of
the Nurses
Christian Fellowship

To begin your risk-FREE subscription,

call TOLL-FREE 1-800-638-3030 or reply to
LWW.com/nursing or nursingcenter.com.
International requests call 1-301-223-2300.
For more information about Nurses
Christian Fellowship, go to www.ncf-jcn.org.
60
40
20
0
-20
-40
-60
16
Time (second)
.
V
(L/min)
4 2 0 6 8 10 12 14
A
Inspiration
B C D
Expiration