Transcript Document 7269345

Asthma and COPD
November 28, 2002
Cass Djurfors
Dr. M. Betzner
Objectives:
Asthma:
Definition
 Epidemiology
 Pathophysiology
 Clinical features
 Diagnostic tests
 Management
 Disposition

Objectives:
COPD
Definition
 Epidemiology
 Pathophysiology
 Clinical Presentation
 Diagnostic Criteria
 Treatment:

Chronic
 Acute

Asthma: definition
Chronic inflammatory disease
characterized by reversible airflow
obstruction, exacerbations and
remissions.
NAEPP Diagnostic Criteria
1. Intermittent airflow obstruction indicated by a
history of nighttime cough, recurrent wheeze
or recurrent chest tightness.
2. Reversible airflow obstruction as
documented by pulmonary function testing,
worsening symptoms in the presence of any
of several triggers, or symptoms that occur
at night.
3. All other possible diagnoses are excluded.
National Asthma Education and Prevention Program. Expert panel report 2: Guidelines for the
diagnosis and management of asthma. DHHS pub # NIH 97-4051. 1997
Epidemiology:
Affects 4-6% of population in the United
States
Most common chronic disease of childhood,
fourth leading cause of disability in children,
increasing in prevalence
30% of children will have persistent
symptoms of asthma into adulthood
Fatalities are real: 4657 in U.S. in 1998
Etiology:
Currently believed that asthma is the
result of a combination of genetic
predisposition and environmental
exposures
Common Triggers:

Tobacco smoke, air pollutants, animal
allergens, dust mites, viral respiratory
infections, cockroach allergens, weather
changes, molds, outdoor allergens, gerd…
Pathophysiology:
Acute and chronic inflammation and airway
hyperresponsiveness
Partially reversible airflow obstruction results
from bronchial smooth muscle constriction,
airway edema and inflammation, and mucus
plugging; bronchoconstriction is
superimposed in the acute setting
Permanent changes can eventually be seen
at the microscopic level…including collagen
deposition and fibrosis below the basement
membrane from mast cell activity and
inflammatory cell migration
History:
Symptoms:

Cough, wheeze, SOB, chest tightness, sputum, fever, poor
feeding
Pattern of disease:

Course, onset, duration, seasonal variation, frequency
Aggravating factors/triggers

Usual triggers, current trigger
History of disease:






previous hospitalization
previous intubation/ICU
previous ED visits
typical episode
Age at onset and method of diagnosis
Present management, meds and history of steroid use
History:
Family History
Social History:


Home environment (smoking, pets, allergens)
Identification of precipitating cause
Exacerbation profile:

Usual exacerbation pattern and outcome
Past best spirometry measures
Medical history, allergies, anaphylaxis
Treatment:


Medications at home and timing of last dose
Treatment before arrival
Physical Exam:
Vital signs:
RR increases
 HR-tachycardia from anxiety, increased
work of breathing, and hypoxia
 BP-hypotension may be present in patients
with impending resp failure due to
decreased venous return and increased
pleural pressures. Pulsus paradoxus may
be present

Physical Exam:
Accessory muscle use
Indrawing: subcostal, intercostal,
supraclavicular
Paradoxical abdominal and chest wall
movements
Nasal flaring in young children
Physical Exam:
Mental status
Prolonged expiratory phase
Lung findings:
Wheeze
 “Silent chest”

Diagnostic Tests:
Pulse Oximetry:


Continuous monitoring
<91% may be a predictor of hospital admission in
kids (Geelhoed et al, BMJ, 1988)
PEF:



An approximation of FEV1
Should be measured in all but the sickest of
patients or those younger than 5 years
Compare with predicted age/size appropriate
value and with personal best
Diagnostic Tests:
CXR:
 Of limited utility
 Useful in those with concern for
complications of asthma (pneumothorax)
or those patients in whom another
diagnosis is suspected
 Recommended for children with first
episode of wheeze to rule out foreign
bodies, congenital anomalies (Scarfone,
Emergency Asthma, 1999)
Diagnostic Tests:
ABG:

Useful as supportive evidence for the
clinical diagnosis of respiratory failure
Asthma Severity: CAEP
Mild
exertional dyspnea/cough
 ± nocturnal symptoms.
 Increased use of ß agonist
for symptom control.
 Good response to ß agonist
 FEV1,PEFR > 60% predicted or best.
(FEV1 > 2.1L; PEFR > 300L/min)

Asthma Severity: CAEP
Moderate
dyspnea at rest, cough,
congested, chest tightness,
 nocturnal symptoms.
 Partial relief from ß agonist
and or ß agonist needed
more often than Q4h
 FEV1 PEFR 40%-60% predicted or best.
(FEV1 1.6-2.1L, PEFR 200-300L/min)

Asthma Severity: CAEP
Severe






laboured respirations
agitated, diaphoretic
difficulty speaking
tachycardic,
no prehospital relief
with ß agonist
FEV1,PEFR - unable or <40% predicted or best
(FEV1 <1.6L PEFR <200L/min O2 saturation
<90%)
Asthma Severity: CAEP
Near Death
exhausted, confused,
 diaphoretic, cyanotic,
 silent chest, decreased resp. effort
 falling heart rate
 FEV1,PEFR not appropriate
 O2 saturation <90% (despite supplemental
O2)

Treatment Goals:
Correct hypoxia
Reverse airflow obstruction
Treat underlying inflammatory response
Management: CAEP
Mild:
O2
 ß agonist (MDI* ± chamber**)
*MDI (Metered Dose Inhaler) - MDI
adapters available for ET tube
**Chamber (valved spacer device) - use of
chamber is recommended

Management: CAEP
Moderate:
O2
 ß agonist (MDI* ± chamber**)
 systemic corticosteroids
 anticholinergics may be helpful in some
cases
 Frequent FEV1 /PEFR to evaluate
response to treatment

Management: CAEP



Severe:
100% O2
anticipate the need for intubation
frequent/continuous ß agonist
and anticholinergic (nebulized or
MDI* with chamber**)
Management: CAEP
Severe:
Systemic corticosteroids
 Cardiac monitoring
 Oximetry, ABG's, CXR
 Frequent reassessment
 Spirometry when possible
 Physician and nursing
supervision until clear signs
of improvement
UNRESPONSIVE: Consider near death
management


Management: CAEP
Near Death:


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
100% O2
paralysis, intubation: modified RSI technique
Intubation is a clinical decision
continuous ß agonist and
anticholinergic (nebulized or
MDI* + ETT adaptor)
UNRESPONSIVE
Rule out pneumothorax or upper airway obstruction
consider alternative drugs: I.V. ß agonists,
inhalational anesthetic agents
Management: CAEP
Near Death:
Systemic corticosteroids
 Cardiac monitoring
 Oximetry, ABG's, CXR
 Frequent reassessment
 Spirometry when possible
 Physician and nursing
supervision until clear signs
of improvement

Ventilatory Strategies:
Cautious CO2 reduction with permissive
hypercapnea until lung function improves
“Controlled mechanical hypoventilation”
Bicarb as needed to keep pH>7.2
Slow RR (6-8 breaths/min) to reduce
barotrauma and volutrauma
Low I:E ratios
Low tidal volumes (6-8 mL/kg)
Frequent suctioning of mucous secretions as
required
OXYGEN
Will not suppress respiratory drive in
acute asthma
Start high: FiO2 40-100%
Achieve O2Sat 92-95%
ß agonists: first line therapy
titrate to response (adults and children)
e.g. inhaled salbutamol: 100 µg/puff
Relaxes bronchial smooth muscle and
promotes mucociliary clearance
MDI 4-8 puffs q15-20 min X 3 is usual,
increase to 1 puff q 30-60 sec (4-20 puffs) prn
wet nebulizer 5.0 mg ( 1 ml/3ml ns)
q 15-20 min. X3; continuous if necessary
administer with oxygen
Increase dose for intubated patients
ß agonists: first line therapy
Several RCT’s have shown equivalent
efficacy between MDI + spacer and
nebulizers in the emergency treatment of
acute asthma
Rodrigo et al, American Journal of Emergency Medicine, 1998
Schuh et al, J Pediatr, 1999
For outpatient ß agonist use, MDI’s are
equivalent to all other hand held inhaler
devices, and remain the most cost effective
delivery system.
Ram et al, BMJ, 2001
Anticholinergics
e.g. inhaled ipratropium bromide (20 µg/puff)
Inhibits acetylcholine-mediated
bronchoconstriction and decreases mucous
production.
Not systemically absorbed
Peak effect in 60 minutes
Indicated for moderate and severe asthma in
both adults and children
Anticholinergics
Zorc et al, Pediatrics, 1999:
427 children>12 months were randomized
in a blinded fashion to either ipratropium
(250 mcg/dose) or normal saline with each
of the first three nebulized albuterol doses.
 The addition of the ipratropium to a
standard ED treatment protocol for acute
asthma was associated with reductions in
duration and amount of treatment before
discharge

Anticholinergics
MDI 4-8 puffs q15-20 min X 3 is usual,
increase to 1 puff q 30-60 SEC (4-20 puffs)
prn
Wet nebulizer .25. - .5 mg ( 1 -2ml/3ml NS)
q 15-20 min. X3; continuous if necessary
Decrease frequency in recovery phase
May be mixed with ß agonists
Corticosteroids
All patients seen in ER for asthma should be
considered for oral or IV steroids
Associated with rapid resolution of airflow
obstruction and decreased relapse rate
Oral and IV are equally efficacious
No good evidence regarding best dose
Accepted doses are 100-200 mg of
methylprednisolone or equivalent or 5001000mg of hydrocortisone or equivalent, oral
doses should be in the range of 40mg of
prednisone or equivalent
Corticosteroids at d/c:
Patients discharged from the ED who require
steroid therapy should be given 30-60 mg of
prednisone orally for 7-14 days (CMAJ, Guidelines for the
emergency management of asthma in adults, 1999)
Children: 1-2 mg/kg per day for a total of 5
days
Decadron has not been widely used or
studied but may be an alternative in children
Inhaled Corticosteroids
Should be prescribed at discharge but
not a component of emergency
management
CMAJ, Guidelines for the emergency management of asthma in adults, 1999
Dose-related systemic adverse effects,
especially at doses >0.8mg/d of fluticasone or
equivalent
Lipworth, Systemic Adverse Effects of Inhaled Corticosteroid Therapy, Arch Intern Med, 1999.
Intubation agents:
Induction: Ketamine 1.5 mg/Kg I.V.

Add atropine in kids
Paralysis:
Succinylcholine 1.5 mg/Kg I.V.
 Roc/vec/pavulon for maintenance
of paralysis only

Alternative Drugs
(Not usually required) May be Associated
With More Toxicity
Patients unresponsive to treatment may
benefit from I.V. ß agonists or inhalational
anesthetic agents. These forms of therapy
may require consultation with respirology,
ICU, anesthesia or internal medicine.
Alternative Drugs
Adrenaline (1:1000) S.C. 0.3 - 0.5 ml q
15 - 20 min prn (1 ml 1:1000 in 250
D5W = 4 µg/ml) I.V. Infusion: 4-8 µg/min
Kids: 0.01mL/kg of 1:1000 S.C.
Alternative Drugs
Salbutamol (I.V. solution only) Load: 4µg/Kg
(over 2-5 min) I.V. Infusion: 0.1 - 0.2
µg/Kg/min
Methylxanthines (Aminophylline) Load: 3 - 6
mg/Kg I.V. over 30 min (1/2 if already taking)
infusion: 0.2 - 1 mg/Kg/Hour (follow levels).
Not usually recommended as Bronchodilator
in the first 4 hours of treatment.
Alternative Drugs
Magnesium:
Controversial: Some evidence for IV use in severe
asthma
 Smooth muscle relaxant
Adults (AMA guidelines):
 Severe / Near Death Asthma
sats<90%, PEF/FEV1<40%
 consider 2gm MgSO4 IV over 20 mins
Peds:
 Severe / Near Death Asthma
(sats<92%,PEF/FEV1<50% of pb/predicted
 consider 25mg/kg MgSO4 IV over 20 mins

Alternative Drugs
Heliox:
Mixture of helium and oxygen
 Low-density gas mixture which is thought
to reduce turbulent airflow
 Must be at least 60% helium which
presents a problem in hypoxic patients
 Evidence is limited
 Can be considered in a limited group of
nonhypoxic severe asthmatics

Alternative Drugs
Leukotriene Modifiers:
Potent bronchodilator with additive effect to
B2-agonists
 Direction for the future
 May have a role in acute treatment of
asthma, but that remains to be investigated

Disposition: CAEP guidelines
Pretreatment
< 25% predicted or best
(FEV1 < 1.0 L; PEFR < 100 L/min)*
Admission is
usually necessary
Disposition: CAEP guidelines
Post Treatment



1. < 40% predicted or best
(FEV1 < 1.6 L; PEFR < 200 L/min)*
Admission recommended
2. 40-60% predicted or best
(FEV1 < 1.6-2.1 L; PEFR < 200-300 L/min)*
Discharge Possible
3. > 60% predicted or best
(FEV1 > 2.1 L; PEFR > 300 L/min)*
Discharge likely
Patients at Risk for Relapse
1. Previous near death episode.
2. Recent E.D. visits.
3. Frequent hospitalizations.
4. Steroid dependent or recent use.
5. Sudden attacks.
6. Allergic/anaphylactic triggers.
7. Prolonged duration of recent attack.
8. Poor compliance or understanding.
9. Returning to same environmental triggers.
Discharge instructions:
MEDICATIONS
A. ß agonists:
1. Regular use often required for 48 hours (24 puffs Q4h).
2. PRN use after 48 hours if symptoms
controlled
3. If unable to control symptoms with ß
agonists return to E.D. or see your
physician.
Discharge instructions:
B. Corticosteroids - indicated for most
patients
1.
2.
3.
Prednisone: 30-60 mg/day for 7-14 days taper
or discontinue based on asthma
control/physician advice
Individual plans based on past
treatment/recent symptoms
Inhaled: Continue at previous dose even if
taking prednisone. Initiate at 500-1000 ug/day
(Beclomethasone/Budesonide or equivalent).
Higher doses may be necessary. Consider as
integral part of long term management.
Discharge instructions:
Anti inflammatory medications (nonsteroid)
1. To be continued on discharge.
2. Role in long term management to be
assessed by family physician or
consultant.
PATIENT INSTRUCTIONS
Review:


1) Drug Delivery Technique (puffer, spacer
device, powder delivery)
2) Role of relievers (ß agonists) and preventers
(anti inflammatory)
Explain:

Treatment failure: indications for emergency
assessment or physician advice. This should
be based on signs, symptoms and medication
requirements, e.g. dose (number and
frequency of puffs) of ß agonist required for
relief or control of symptoms.
PATIENT INSTRUCTIONS
Educate:

The Lung Association, Asthma and Allergy
Information Association and the Asthma Society of
Canada has educational materials and some
communities have formal education programs.
Refer:

Consider respirology, internal medicine, allergy/
immunology consultation for high risk patients.
Worsening/ persisting symptoms, modify dose and
schedule of steroid therapy. Follow up with family
MD or consultant in 1-7 days to assess response.
Chronic Management
Considerations:
Environmental control
Short-acting B2-agonists on demand
Regular inhaled glucocorticoid for all but the mildest
of asthmatics (if B2-agonist is needed>3 times per
week, other than for exercise, inhaled glucocorticoid
should be added)
If asthma is not adequately controlled by moderate
doses (500-1000mcg/d of beclomethasone or
equivalent) additional therapy should be
added…consider long-acting B2-agonists, leukotriene
antagonists or other medications
Severe asthma may require additional treatment with
prednisone

CMAJ, Canadian Asthma Consensus Report, 1999
COPD
ATS Definition:
A disease state characterized by the
presence of airflow obstruction due to
chronic bronchitis or emphysema
 Progressive
 Airway hyperactivity, if present, may be
partially reversible

COPD: Definitions
Chronic Bronchitis:

Presence of chronic productive cough for 3
months in each of 2 successive years in a patient
in whom other causes of chronic cough have been
excluded
Emphysema:

Abnormal permanent enlargement of the
airspaces distal to the terminal bronchioles,
accompanied by destruction of their walls and
without obvious fibrosis
Tintinalli, Emergency Medicine, 2000
Epidemiology
Sixth leading cause of death in the world in
1990 (WHO)
Leading cause of morbidity and mortality
among smokers > 55 yrs
Rare in those under age 40
Men>women, but this is changing as more
women smoke
Mortality for patients hospitalized with a
COPD exacerbation is estimated at 5-14%
Pathophysiology
Smoking accounts for 80-90% of risk
Environmental factors have been suggested:
occupational exposure, air pollution, second
hand smoke
Genetic factors:α1-antitrypsin deficiency
Earliest detectable changes in COPD
evolution are evident as small increases in
peripheral airway resistance or lung
compliance
Pathophysiology
Disease progression is slow and insidious,
spanning decades; may be masked by
sedentary lifestyle of most smokers
Abstinence from smoking is most
advantageous during early course of disease
Variability in disease pattern and progression
between similar patients…much is still
unknown
Pathophysiology
Airflow impedance (expiratory mostly) results
primarily from increased resistance or
decreased caliber of the small bronchi and
bronchioles
Airway secretions, mucosal edema,
bronchospasm, and bronchoconstriction from
decreased airway elasticity are all
responsible for airflow obstruction
Increased airway resistance = reduced
minute ventilation +/- increased work of
breathing
Pathophysiology
Alveolar hypoventilation = hypoxemia +
hypercarbia
V/Q mismatching
Pulmonary hypertension
RV hypertrophy then dilatation
Cor pulmonale
Clinical Presentation
Chronic Stable COPD:

Symptoms:
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Exertional dyspnea
Cough
Exam:
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Tachypnea
Accessory muscle use
“Pursed-lip” breathing
Expiratory wheeze
Coarse crackles
Reduced air entry
Clinical Presentation
Acute exacerbation of COPD:

Patients present complaining of:

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Worsening dyspnea
Increased sputum volume
Increased sputum purulence
Hypoxemia, tachypnea, cyanosis, agitation,
tachycardia, hypertension, acc mm use, pursed-lip
exhalation, “sitting up leaning forward” posture
Hypercapnea may result in confusion, tremor,
decreased LOC
Respiratory failure
Causes of AECOPD
Superimposed respiratory infection
Cardiovascular deterioration
Smoking
Noncompliance with meds
Environmental exposures
Meds: e.g. β-blockers, benzos, narcotics
Misuse of oxygen therapy
Metabolic derangements
DDX AECOPD:
Pneumonia
IHD
CHF
Asthma
PE
Pneumothorax
Etc.
Diagnostic Tests
Pulse Oximetry:
 Easy, immediate, noninvasive test that provides
information about the severity of respiratory
compromise in an acute exacerbation
ABG:
 Provides accurate information about pH, PaO2 and
PaCO2
 Consider in most if not all patients presenting with
an acute exacerbation
Diagnostic Tests
PFTs:
 FEV1 as compared to percent predicted is
an excellent measure of disease severity
 As FEV1 falls below 25-30% of predicted,
both hypoxemia and hypercarbia usually
occur
 PEF can be used in ED to estimate FEV1,
with the understanding that PEF is effort
dependent and tends to overestimate lung
function in the mid ranges
Diagnostic Tests
CXR:
Almost always abnormal, comparisons with
prior exams should be made
 Helpful in the diagnosis of complications
such as pneumothorax, pneumonia, pleural
effusions, pulmonary neoplasia

Infectious Precipitants
Viral infections often implicated in COPD
exacerbations: influenza, PAI, RSV
Atypical organisms may also be involved:
Mycoplasma, Chlamydia pneumoniae,
Legionella
Chronic colonization also occurs, most often
with H. flu, Strep pneumo, and
Moraxella…role of these organisms in
exacerbations is controversial.
CAP in AECOPD
COPD patients are at high risk for CAP
Symptoms of CAP are similar to those of
AECOPD: sputum, fever, cough
Strep pneumo is most common, followed by
H flu, and Moraxella Catarrhalis
Legionella and Pseudomonas should always
be considered
Pneumovax and yearly influenza vaccines
are important prevention
Antibiotics in AECOPD
Controversial and difficult to study
Currently accepted practice based on the
best evidence is that patients presenting with
infectious symptoms:



Fever
Increased sputum production
Change in character of sputum
will have a better outcome with the use of
empiric antibiotic therapy
Antibiotics in AECOPD
Increasing evidence for newer
antibiotics as first line therapy:
azithromycin, respiratory
fluoroquinolones, β-lactamase
inhibitors.
Antibiotics in AECOPD
CHA recommendations:

<4 exacerbations/year:
Amoxicillin 500mg po tid x 7-10d
 Doxycycline 200mg po x 1d then 100mg po od
x 7-10d
 TMP/SMX 1 DS tablet po bid x 7-10d

Antibiotics in AECOPD
CHA recommendations:
 > or = 4 exacerbations per year or failure of
first line agent or Abx last 6 weeks:
Cefuroxime axetil 250-500mg bid x 7-10d
 Amoxicillin-clavulanate 875mg po bid x 7-10 d


For pen allergic patients:
Azithromycin 500mg x 1d then 250mg po od x 4d
 Clarithromycin 250-500mg po bid x 7-10d
 Levofloxacin 500mg po od x 5-10d
 Moxifloxacin 400mg po od x 5-10d

Management of stable COPD
Lifestyle modifications:
Smoking cessation
 Regular exercise
 Weight control
 Pulmonary rehabilitation

Prevention:
Pneumovax
 Influenza

Management of stable COPD
Oxygen

Started after room air ABG’s document PaO2<55
or 56-59 in the face of cor pulmonale
Bronchodilators:



β-agonists
Ipratropium bromide
Long acting β-agonists
+/- Theophylline
Management of stable COPD
Steroids:
20-30% are steroid responders
 Inhaled or oral

Management: AECOPD
Goals of therapy:
Relieve bronchoconstriction
 Improve oxygenation

Approach to treatment:
Multi-modal
 Be cognizant of previous disease pattern

Management: AECOPD
Oxygen:




All patients in respiratory distress should receive
supplemental oxygen
Target O2sat>90%
Be aware that patients known to be CO2-retainers
may require controlled oxygen therapy
Hypercarbia is likely secondary to the Haldane
effect: a shift of the hemoglobin-CO2 binding
curve, as well as due to increased CO2 production
and changes in physiologic dead space
Management: AECOPD
β2-agonists:
 COPD patients will have some reversibility
to their airflow obstruction that can
effectively be relieved by inhaled short
acting β2-agonist therapy
 Long acting β2-agonist therapy should be
reserved for chronic management only
 No evidence that one specific agent has
any greater efficacy than any other
 Little evidence regarding timing of
administration (q60 min vs. q20 min etc.)
Management: AECOPD
Anticholinergics:





Preferentially dilate larger central airways
compared to β2-agonists which dilate
peripheral airways
Slower onset of action than β2-agonists
Thought to inhibit vagal stimulation of the
bronchi…thereby promoting smooth muscle
relaxation
Atropine and glycopyrrolate have been used
Most common agent is ipratropium bromide
q4-6h by neb or MDI
Management: AECOPD
Theophylline:
Controversial
 Narrow therapeutic window
 Significant side effects: dysrhythmias,
seizures
 Limited evidence for efficacy

Management: AECOPD
Corticosteroids:
Conflicting results in the literature
 In acute exacerbation, there is likely a role
for systemic steroids, but not for inhaled
 Steroid response is likely a continuum
rather than an “all or none” phenomenon

Management: AECOPD
Magnesium:
Studied mostly in asthma
 One study showed benefit in COPD, used
as 1-2g IV over 20 min

Heliox:
No large-scale studies
 Probably should only be considered as a
last alternative

Mechanical Ventilation: the
controversies
Widespread fear among healthcare workers
that patients will become ventilator dependent
Evidence suggests that most patients in fact
will be extubated around day 10 but that 1-5
year mortality rate following an episode of
respiratory failure is very high
Likely a decision that should be addressed by
the patient, family, primary health care
provider PRIOR to the actual event
Mechanical Ventilation
Decision to begin assisted ventilation is a
clinical one
Noninvasive ventilation (BiPAP):



BiPAP works by providing nasal, bilevel
positive airway pressure. This overcomes the
intrinsic PEEP of most COPD patients, and
significantly reduces work of breathing,
thereby improving gas exchange
Response is usually seen within the first hour
Should be considered first line before
endotracheal intubation unless patient has
impaired mental status or cardiovascular
instability
Mechanical Ventilation
Kramer et al

Selection criteria for NPPV (any two):
Moderate to severe dyspnea with use of
accessory muscles and paradoxical abdominal
motion
 Moderate to severe acidosis (pH 7.3-7.35) and
hypercapnia (PaCO2 45-60)
 Respiratory frequency > 25 breaths/min

Mechanical Ventilation
Kramer et al

Exclusion Criteria for NPPV (any one):
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Respiratory arrest
Cardiovascular instability (hypotension, dysrhythmias,
AMI)
Somnolence, impaired mental status, uncooperative
patient
High risk of aspiration
Viscous or copious secretions
Recent facial or gastroesophageal surgery
Craniofacial trauma with fixed nasopharyngeal
abnormalities
Extreme obesity
Mechanical Ventilation
Indications for invasive mechanical ventilation
in AECOPD (Pierson, Respiratory Care, 2002)
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Severe dyspnea with accessory muscle use and
paradoxical abdominal motion
RR>35
Life-threatening hypoxemia (PaO2<40)
Severe acidosis (pH < 7.25) and hypercapnea (PaCO2 >
60)
Respiratory arrest
Somnolence or impaired mental status
Cardiovascular complications
Other complications (sepsis, pneumonia, PE…)
Failure of NPPV
Disposition
Consider
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Overall respiratory status post-treatment
Home environment
Mental status
Comorbid illness
Age
Compliance
Previous pattern of illness
Keep in mind high relapse rate
Disposition
Treatment at home:
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O2 if needed
Inhaled β2-agonists
Inhaled anticholinergic agents
Proper inhaler technique (review prior to
discharge)
Corticosteroids
+/- Theophylline
+/- Antibiotics