Download severe COPD - Millennium Organization

•Chronic Obstructive Pulmonary
Disease
• It is a progressive disease,
• Characterized by air flow
limitations (irreversible),
• It adds to the heart work.
1. Chronic bronchitis with an obstructive ventilatory
pattern that is defined by the existence of chronic
bronchitis with permanent obstruction of airways
(FEV1/FVC<70%)
2. Chronic respiratory failure, which is defined by
the existence of chronic obstructive bronchitis with
hypoxaemia.
3. Emphysema with or without α1-anti-trypsin
deficiency
 Chronic productive cough for 3 months in
each of 2 successive years in a patient in
whom other causes of productive chronic
cough have been excluded.
Permanent enlargement of airspaces distal to
the terminal bronchioles, accompanied by
destruction of their walls and without obvious
fibrosis.
EPIDEMIOLOGY
was the 6th cause of death in USA in 1990
 2000: 120,000 died from COPD
 2002: 12.1 million were reported having COPD
 2020: is expected to be the 3rd cause of death
However, the exact prevalence of COPD is
under-estimated, due to it is an underdiagnosed
(and undertreated) disease, because most
patients do not present for medical care until
the disease is in a late stage.
 It
ETIOLOGY
 Cigarette smoking (the leading cause, 80-90%)
 Occupational exposure to dusts & chemicals (fumes, vapors,
irritants….)
 Environmental air pollution (exact role ?)
 Genetic factors, viz., of α1 antitrypsin (AAT)
 Asthma & hyper-responsiveness are risk factors, but how they
COPD is ?
 Recurrent infections &/or exposure to tobacco smoke during
childhood → ↑ risk to COPD
 Intravenous drug use of methadone or methylphenidate
pulmonary vascular damage that results from the insoluble filler
(e.g, cornstarch, cotton fibers, cellulose, talc) contained in them
Chronic inflammation
dt repeated exposure to
noxious particles &
gases
• Proteinases ≠ Antiproteinases
Pathologic changes in
Central airways
Peripheral airways
Lung Parenchyma
• Oxidative stress (OS,
tobacco + inflammation)
Pulmonary vasculature
1- Chronic inflammation is mediated primarily by the
activation of inflammatory cells, e.g. neutrophils,
macrophages, CD8+T-lymphocytes and eosinophils (during
exacerbation) inflammatory mediators (LTB4, IL-8, TNF-α).
2- Proteinases ≠ Anti-proteinases → unopposed proteinase
activity (elastase, proteinase-3, etc…….)
3-
OS
ROS & RNS →damage of cell macromolecules & cell
dysfunction
promotes inflammation & prot./anti-prot. imbalance
oxidants constrict airway smooth muscle→ narrowing
airways
Central Airways (trachea, bronchi, bronchioles >2mm
diameter) [mainly hypersecretory phase]
 hyperplasia & hypertrophy of mucus
secretory glands & goblet cells ↑ mucus
secretion ciliary dysfunction
chronic
cough & sputum production + susceptibility
to respiratory infections (viral followed by
Peripheral Airways obstruction
(bronchioles<2mm diameter)bacterial, Steptococcus pneumoniae and
Obstruction phase Haemophilus influenzae).
1- Inflammatory exudates & mucus hypersecretion → cell remodeling
+ thickening the airway walls + narrowing of the airways.
2- Advanced chronic bronchitis: squamous metaplasia and fibrosis →
↑fixed limitation of airflow.
3- Loss of alveolar wall & elasticity → closure of small airways during
expiration & fixed obstruction.
Hyperplesia: ↑ in the number of normal cells in a tissue or organ
Hypertrophy: ↑ in the size of cells → overgrowth of an organ or part
of it.
 Worsened airflow obstruction → slow emptying of the
lung

→ lung hyperinflation (1st upon exercise, then even at
rest )
 Airflow obstruction + damaged alveoli & bronchioles +
pulmonary vascular abnormality (inadequate ventilation/
perfusion V/Q) → hypoxemia/hypercapnia.
 Severe hypoxemia → pulmonary artery V.C. →
pulmonary H.T. → right-sided HF (cor pulmonale)
 Cor pulmonale → venous stasis, thrombosis →
pulmonary embolism
Fibroblast
proliferation
↑ Proteases
Chronic lung
inflammation
Airway mucus
cells metaplasia/
hyperplasia
↓Immune
response to
infection
Hypoxemic V.C
& vascular
remodeling
Small airway
fibrosis
Destructed
parenchyma
Airway obstruction,
hyperinflation,
hypercapnia,
hypoxemia, chronic
dyspnea
↑Mucus
secretion &
viscosity
Bacterial
colonization
Pulmonary
hypertension
Mucus
plug
Chronic
cough &
pneumonia
Corpulmonale
Hypoxic pulmonary vasoconstriction a si
hcihw ni nonemonehp lacigoloisyhp ,lacixodarap
fo ecneserp eht ni tcirtsnoc seiretra yranomlup
ainpacrepyh tuohtiw )slevel negyxo wol( aixopyh
ot wolf doolb gnitcerider ,)slevel edixoid nobrac hgih(
.tnetnoc negyxo rehgih a htiw iloevla
The process might at first seem illogical, as low
ot dael yllaciteroeht dluohs slevel negyxoincreased
suoesag desaercni eviecer ot sgnul eht ot wolf doolb
taht tcaf eht yb denialpxe si ti ,revewoH .egnahcxe
ot wolfdoolb fo noitubirtsider ot sdael noitcirtsnoc
sesaercni hcihw ,gnul eht fo saera detalitnev-retteb
.egnahcxe suoesag ni devlovni aera latot eht
Types of respiratory failure
1- Type one respiratory failure:
• caused by a ventilation-perfusion mismatch
• This processes impairs oxygen transfer in the
lung & causes hypoxaemia (acute or
hypoxaemic respiratory failure) →
hypoxaemia.
• Treatment: correction of hypoxaemia with a
high conc. of O2 to establish a PaO2 > 60
mmHg to ensure O2 saturation is maintained
above 92 %, as tissue hypoxia will not occur
at this level.
2- Type two respiratory failure:
• caused by alveolar hypoventilation, e.g. patient
with an exacerbation of COPD may not be able to
ventilate alveoli sufficiently to remove CO2
leading to retention of CO2, with hypercapnia
and hypoxaemia (chronic, ventilatory or
hypercapnic respiratory failure).
- Treatment is a high conc. of O2 despite a high
CO2 level.
- The aim is to achieve acceptable PaO2 without a
fall in pH below 7.35. A pH below 7.26 is
predictive of a poor outcome, so monitoring O2
saturation alone is not advisable & blood gas
analysis is recommended to detect rise in PaCO2.
Normal Arterial Values Range:
• pH 7.35-7.45,
• pCO2 35-45,
• pO2 80-100,
• O2 Sat. 95-100% ,
• HCO3 22-26
Abnormal values:
• pH 7.30 (acidotic),
• pCO2 58 (acidotic),
• pO2 50 (low)
• O2 Sat. 80% (low)
-In case of respiratory failure we can use resp. stimulants
as I.V. infusion of Doxapram (1-4 mg/min).
S.E. narrow therap. index, HT, tachycardia, convulsion
1. A diagnosis of COPD should be considered
in patients over the age of 35 who have a
risk factor (generally smoking)
2. and who present with exertional
breathlessness, chronic cough, regular
sputum production, frequent winter
‘bronchitis’ or wheeze.
3. The presence of airflow obstruction should
be confirmed by performing spirometry.
•A suspected diagnosis of COPD should be based on
the patient’s symptoms and/or history of exposure to
risk factors.
- History:
•Do you smoke?
•Have you had chronic exposure to dust or air pollutants?
•Do other members of your family have lung disease?
•Are you short of breath?
•Do you get short of breath with exercise?
•Do you have chronic cough and/or wheezing?
•Do you cough up excess mucus?
- COPD is asymptomatic at first, then symptoms develop when
FEV1/FVC post-bronchodilator<70%. This’ll confirm airflow
limitation that is not fully reversible.
-SYMPTOMS & SIGNS:
-Symptoms:
•Initial: 1- chronic cough > 3 months in 2 successive years
2- chronic sputum production
3- dyspnea on exertion
• As COPD progresses: 1- dyspnea at rest develops
- decreased ability to perform daily
activities
N.B. Breathlessness is one of the 1ry symptoms of COPD.
Graded by “The Medical Research Council (MRC)
dyspnoea scale.
-Signs:
• Observation of the patient:
1- pat. starts to respire in a see-saw
movement + use of accessory muscles
2- pursed-lips breathing
3- hyperinflation of the chest with increased
anterior-posterior diameter (barrel chest).
- On auscultation of the lungs: 1- wheezing,
2- a prolonged expiratory
phase
3- rhonchi (breathing sound as
snoring, due to obstructed airways with mucus & swollen mucus
membrane).
• In advanced COPD: 1- cyanosis & tachycardia (signs of
hypoxemia)
• Cor-pulmonale signs: 1- jugular venous distention (JVD),
2- lower extremity edema
3- hepatomegaly
• Infection signs: yellowish or greenish sputum, which
involves bacteria, macrophages & epithelial cells with no
fever.
GOLD Spirometric Criteria for COPD Severity
I. Mild COPD
FEV1/FVC < 0.7
* FEV1 > or = 80%
predicted
At this stage, the patient is
probably unaware that lung
function is starting to decline
II. Moderate
COPD
FEV1/FVC < 0.7
* FEV1 50% to 79%
predicted
Symptoms during this stage
progress, with shortness of
breath (SOB) developing upon
exertion.
III. Severe
COPD
FEV1/FVC < 0.7
* FEV1 30% to 49%
predicted
SOB becomes worse at this
stage & COPD exacerbations
are common.
IV. Very Severe FEV1/FVC < 0.7
* FEV1 < 30% predicted OR
COPD
FEV1 < 50% predicted with
chronic respiratory failure
Quality of life at this stage is
gravely impaired. COPD
exacerbations can be life
threatening.
GOLD: Global Initiative for Obstructive Lung Disease
GOLD I: Mild COPD
• There may be mild airflow limitation, but one may be
unaware that lung function has started to decline.
• FEV1≥ 80% of the predicted normal values with an FEV1/FVC
<70%. One may not yet have any COPD symptoms, or may
have symptoms of chronic cough and excessive mucus.
• People at this stage are not likely to associate symptoms with
the disease process and therefore, rarely seek treatment.
GOLD II, Moderate COPD
• Airflow limitation worsens and one may start to
notice symptoms, particularly shortness of breath (SOB) upon
exertion along with cough and sputum production.
• FEV1 will be anywhere between 50% - 79% of the predicted
normal values and FEV1/FVC <70%.
• During this stage most people seek medical treatment.
GOLD III, Severe COPD
• Limitation of airflow significantly worsens, shortness of
breath becomes more evident and COPD exacerbation is
common.
• FEV1 will be between 30% - 49% predicted and
• FEV1/FVC <70 %.
• This stage, is accompanied by ↓ in activity tolerance & ↑in
fatigue-ability.
GOLD IV, Very Severe COPD
• Quality of life is greatly impaired & COPD exacerbations are
life threatening.
• Airflow limitation is severe (FEV1 <30% predicted,
FEV1/FVC <70 %).
• Chronic respiratory failure is often present at this stage, and
may lead to complications with heart, such as cor
pulmonale and/or eventually, death.
GROUP SYMPTOMS
L
O
W
R
I
S
K
H
I
G
H
R
I
S
K
A
Mild or
infrequent
B
Moderate
to severe
C
Mild or
infrequent
D
Moderate
to severe
RISK
FEV1 ≥ 80% predicted &
0-1 exacerbations within the past
year, mMRC dyspnea score: 0-1
FEV1 ≥ 50% predicted &
0-1 exacerbations within the past
year, MRC ≥ 2
FEV1 < 50% predicted & ≥ 2
exacerbations within the past year or
≥ 1 + hospitalization, MRC: ≥ 2
FEV1 < 30% predicted & ≥ 2
exacerbations within the past year or
≥ 1 + hospitalization, mMRC ≥ 2
From: The MRC breathlessness scaleFrom: The MRC breathlessness scale
CAT: COPD assessment test
mMRC: modified Medical Research Council dyspnea
scores
ody mass index, bstruction, yspnea, xercise
POINTS
BMI
FEV1
Medical
research
council
dyspnea
score
Distance
walked in 6
min. (m)
0
1
2
3
> 21
≥ 65
0-1
≥ 21
50 - 64
2
36-49
3
≥ 35
4
≥ 350
250-349
150-249
≥ 149
•Laboratory tests:
1- Hematocrit (polycythemia: no. of RBCs may be
>55%).
2- Arterial blood gases (ABGs) [sp. in patients with
an FEV1 less than 40% predicted [severe] or
respiratory failure (hypoxemia with or without
hypercapnia) or S&S of cor pulmonale.
3- α1-antitrypsin level [sp. pat.<45 years, with COPD
S&S, & family history of emphysema].
4- sputum bacterial analysis in case of pat. with
infection signs.
Besides the spirometry test [FEV1, FEV1/FVC]
Typically begins
in childhood
No direct
relationship
Episode attacks with
exposure to allergen,
irritant or exercise
Typically a dry
cough at night
Proximal airways
IL-4+ IL-5+IL-13
CD4+ T cells + EOSINOPHILS +
mast cells + plasma cells
Age?
Typically > 40
years age
Smoking?
Mainly smokers &
ex-smokers
Dyspnea?
Progressive shortness
of breath, usually
with exertion
Cough?
Productive cough,
typically in the
morning
Site of inflammation
Key mediators
Primary involved
cells
Distal Airways + parenchyma
IL-18+TNF-α
CD8+T cells, NEUTROPHILS+
macrophages
I- Smoking Cessation
1-slow the rate of decline in pulmonary function
2- Reduce cough & sputum,
3- decrease airway reactivity
Patients should be treated with a combination of counseling on
behavioral and cognitive strategies and pharmacotherapy ( mainly
nicotine replacement therapy).
II- Pulmonary Rehabilitation
•It should cover a range of non-pulmonary problems including:
1- exercise de-conditioning,
2- relative social isolation,
3- altered mood states (especially depression),
4- muscle wasting, and
5- weight loss.
III- Long-term O2 therapy
1- In patients with chronic respiratory failure: give O2 therapy > 15
hrs/day to reduce mortality & improve life quality.
2- Very severe COPD with:
a. resting PaO2 at or below 55 mm Hg
b. PaO2 between 55 and 60 mm Hg & evidence of pulmonary
hypertension, peripheral edema (suggesting CHF), or polycythemia.
• Use the dual-prong nasal cannula to deliver continuous O2flow to O2
baseline saturation to at least 90% to oxygenate vital organs.
The flow rate(L/minute), must be during exercise, sleep & air
travel (2L/min).
Oxygen therapy should be continued indefinitely.
IV- Surgery Bullectomy, & lung transplantation (v. severe COPD)
improved spirometry, lung volumes, exercise capacity, dyspnea, healthrelated quality of life, and possibly survival.
A- β2-Agonists:
• cause airway smooth muscle relaxation( adenyl cyclase
cAMP)
•Short acting [SABA]:
- albuterol, salbutamol; levalbuterol, pirbuterol, & terbutaline.
- “rescue” therapy for acute symptom relief (Releivers)
• Long-acting [LABA]: (Controllers)
-salmeterol & formoterol, last at least 12 hours, allowing for
twice-daily dosing, better in maintenance schedule
N.B. - salmeterol (partial agonist, slower onset of action
than short-acting β2-agonists).
- formoterol (pure full agonist, onset of action = albuterol)
Adverse effects: palpitations, tachycardia, tremor & sleep
disturbance
B- Anticholinergics: (Controllers)
• act by competitively blocking M3 receptors in bronchial
SM.M [bronchodilation] & mucus secretory cells [dec.
mucus]
Ipratropium (half-life =2 hours, so dosing every 6 - 8 hrs).
Tiotropium LAMA (long acting muscarinic antagonist)
- once daily bec. it dissociates slowly from
receptors, with half-life > 36 hrs)
- improves lung function > ipratropium &
salmeterol, but expensive).
- tiotropium as maintenance + albuterol as
rescue therapy.
C- Theophyllines: (Controllers)
• they ↓ phosphodiesterase (PDE) → ↑ cAMP
• have a modest bronchodilator effect in patients with
COPD.
• limited use (narrow therapeutic index, multiple drug
interactions [cimetidine, phenytoin alter metabolism], &
adverse effects).
• Caution in: CV complicated patients & hepatic
impairment.
•Theophylline should be reserved for patients who
remained symptomatic despite appropriate use of inhaled
bronchodilators.
•Common adverse effects: heartburn, restlessness,
insomnia, irritability, tachycardia, tremor & dose-related
nausea, vomiting, seizures, & arrhythmias.
• Adjust dose in COPD pat. bec. chemicals in tobacco
smoke may induce cyt. P-450 that metabolizes
theophylline.
D- Combinations:
• COPD pat. may need combination of 2 or 3
bronchodilators.
• albuterol + ipratropium,
• OR LABA + theophylline,
•OR LABA + tiotropium
•OR LABA + ipratropium OR the 3 bronchodilators
II- Corticosteroids: (Preventers)
• Used in symptomatic patients with severe COPD (FEV1
≤ 50%) + frequent exacerbations [2 or more], requiring
treatment with antibiotics or oral corticosteroids in a
12-months period.
• Corticosteroid is used to ↓ no. of exacerbations/year.
• However, corticosteroids do not slow the long-term
decline in pulmonary function.
• Combination inhaler device is recommended when
using LABD + inhaled corticosteroid [e.g., Advair/
seretide (fluticasone/salmeterol), ].
• Assess after 6-8 weeks, if FEV1 is not improved (>15 %), stop
corticosteroids, BUT reinstitute in pat. who develop
deterioration in lung function, increase in dyspnea & mild
exacerbations.
• Long-term use of oral corticosteroids should be
avoided dt unfavorable risk/benefit ratio.
• Common adverse effects:
1- oropharyngeal candidiasis & hoarse voice
2- bruising & decreased bone density
3- myopathy in long-term use.
• + theophylline: improved response to corticosteroids
in COPD!!!!
III- Immunization:
• annual influenza vaccination (early October through mid-November)
reduces serious illness and death by 50%.
• All patients with COPD should also receive a one-time
vaccination with the pneumococcal polysaccharide vaccine,
even though sufficient data supporting its use in COPD
patients are lacking.
IV- Alpha1-Antitrypsin Augmentation Therapy:
• I.V. augmentation therapy for AAT deficient patients & moderate
airflow obstruction (FEV1 35% - 60% predicted).
• carried out by weekly transfusions of pooled human AAT
to maintain adequate plasma levels of the enzyme.
• not recommended for individuals with AAT deficiency who
do not demonstrate lung disease.
V- Other Pharmacologic Therapies:
A- Selective phosphodiesterase (PDE)4 inhibitor:
• Roflumilast (Daxas, Daliresp)
• is a drug that acts as a selective, long-acting PDE-4
inhibitor.
• It has anti-inflammatory effects and is used as an
orally administered drug for the treatment of
inflammatory conditions of the lungs such as COPD.
• In June 2010, Daxas was approved in the EU for
severe COPD associated with chronic bronchitis.
• In March 2011, Daliresp gained FDA approval in
the US for reducing COPD exacerbations.
B- Leukotriene modifiers (e.g., zafirlukast and
montelukast):
• not adequately evaluated in COPD patients & not
routinely recommended,
• however, small, short-term studies showed better
pulmonary function, dyspnea, & life quality when LT
modifiers were added.
C- Mast cell stabilizer (e.g. Nedocromil),
• not adequately tested in COPD patients &
• is not included in the GOLD (Global Initiative for
Chronic Obstructive Lung Disease) recommendations.
D- N-acetylcysteine:
• has antioxidant & mucolytic activity, can be
suitable for COPD pat. ,
• However, clinical trials have produced conflicting
results, so not routinely recommended.
• One of the largest trials found N-acetylcysteine to
be ineffective at reducing the decline in lung
function & preventing exacerbations.
E- Prophylactic antibiotics:
• no effect, so used only to treat infectious
exacerbations.
• Anti-tussives: contraindicated bec. cough has
protective role.
COPD Treatment: GOLD 2017 Guidelines
Long-acting bronchodilators:
 Almost all patients with COPD who experience more
than occasional dyspnea should be prescribed long
acting bronchodilator therapy.
 This could be a long-acting beta agonist (LABA), a
long acting muscarinic antagonist (LAMA), or both.
 Patients with persistent COPD symptoms while
taking one long-acting bronchodilator should be
prescribed two (or a combination agent containing
two long acting bronchodilators).
Inhaled corticosteroids:
 are not recommended as monotherapy
in COPD.
 Combination agents containing inhaled
corticosteroids along with LABA are
considered appropriate step-up therapy
for
patients
experiencing
COPD
exacerbations while taking long-acting
bronchodilators.
Oral PDE4 inhibitors are considered an
add-on therapy only for patients with
COPD with chronic bronchitis and
severe airflow restriction who experience
COPD exacerbations despite use of a
combination bronchodilator with inhaled
corticosteroid.
Treatment Algorithm for Stable COPD
GOLD Stage
Recommended Therapy
Avoidance of risk factor(s), especially smoking
cessation; influenza vaccination
ADD
I: Mild
Inhaled short-acting bronchodilator when needed (e.g.,
ipratropium, albuterol, or combination inhaler)
ADD
II: Moderate Pulmonary rehabilitation , Inhaled LABD on a scheduled
basis (e.g. tiotropium, salmeterol, or formuterol)
Inadequate response to Use alternative class or combine classes of
LABD? YES
inhaled LABD
0: At Risk
Inadequate response to LABD?
YES
ADD Inhaled corticosteroids if repeated exacerbations
Add/substitute oral theophylline
III: Severe
IV: v. Severe
ADD Long-term O2 if chronic respiratory failure; Consider
surgical treatment
The 2017 GOLD guidelines
COPD GOLD Grade A: Any bronchodilator (short or
long acting), titrating or switching to another as
appropriate.
COPD GOLD Grade B: A long acting bronchodilator
(LAMA or LABA), and both if symptoms persist on
one drug.
COPD GOLD Grade C: A long acting muscarinic
antagonist (LAMA), switching to LAMA+LABA or to
LABA+ICS if further exacerbations occur.
COPD GOLD Grade D: More complicated, requires
individual management, often multiple drugs,
consideration of roflumilast and azithromycin in
selected patients.
COPD exacerbations are defined as an acute worsening of
respiratory symptoms that result in additional therapy.
• The most common causes of an exacerbation are respiratory
infection & air pollution, but the cause cannot be identified in
about 1/3 of severe exacerbations.
 Mild exacerbations:
• increase bronchodilator therapy with or without oral
corticosteroids
• antibiotics indicated only if clinical signs of airway infection (e.g.,
inc. volume & change in color of sputum and/or fever).
 Moderate – Severe exacerbations: 1- controlled oxygen therapy,
2- bronchodilators, 3- oral or I.V. corticosteroids, 4- antibiotics if
indicated, and 5- consideration of mechanical ventilation (noninvasive or invasive).
A- Bronchodilators:
1- Albuterol (acute exacerbations because of its rapid onset of action).
2- Ipratropium can be added to allow for lower doses of albuterol.
Deliver through nebulizer (in patients with severe dyspnea and/or
cough that would limit delivery of medication through an MDI with
spacer.
3- Theophylline can be considered.
B- Oral Corticosteroids :
•Oral prednisone 30 to 40 mg/day for 10 to 14 days.
•If inhaled corticosteroids are part of the patient’s usual treatment
regimen, they should be continued during systemic therapy.
•Systemic corticosteroids shorten the recovery time, quickly restore
lung function, and may reduce the risk of early relapse.
• Oral cort. should be tappered, then move to inhalers
(beclomethasone 200-500 µg/ twice daily).
C- Antibiotics:
Antibiotics should be used in patients with COPD exacerbations
who have either of the following characteristics:
(1) at least 2 of 3 cardinal symptoms:
- increased dyspnea,
- Sputum volume, or
- sputum purulence (sputum containing a lot of pus); or
(2) a severe exacerbation requiring mechanical ventilation.
Common m.o.:
-Streptococcus pneumoniae,
- Haemophilus influenzae, &
- Moraxella catarrhalis.
•In patients with more severe COPD:
other bacteria, such as
1- enteric gram -ve bacilli (Escherichia coli, Klebsiella
pneumoniae, & Enterobacter cloacae) and
2- Pseudomonas aeruginosa can be detected.
Antibiotic treatment for most patients require 3 to 10 days,
until the patient has been afebrile for 3 consecutive days.
•Exacerbations due to uncommon bacteria require 21 to 42
days.
• If no response in 48 to 72 hrs, adjust antimicrobial therapy
considering sputum Gram’s stain & culture if not already
obtained.
D- Oxygen:
• The goal is to maintain PaO2 > 60 mm Hg or SaO2 > 90% (to
prevent tissue hypoxia & preserve cellular oxygenation). T21 RF
•Increasing the PaO2 much further adds little benefit & may
increase the risk of CO2 retention, which may lead to
respiratory acidosis.
In advanced COPD, (patients with chronic hypercapnia, T2 RF)
caution should be used since overly aggressive administration
of oxygen may result in respiratory depression & respiratory
failure.
In these patients, mild hypoxemia, rather than carbon dioxide
accumulation, triggers their drive to breathe.
• An arterial blood gas should be obtained after 1 to 2 hours to
assess for hypercapnia.
Oxygen Not Recommended
Patients in GOLD 2017
for
Most
COPD
• The
2017
GOLD
guidelines
generally
advise against ecitcarp enituor eht of prescribing
supplemental oxygen to stable COPD patients
without severe resting hypoxemia .
• In randomized trial in 700 >stable COPD patients
with moderate hypoxemia, supplemental oxygen did
not improve clinical outcomes or quality of life during
the followup period .
• COPD patients with severe resting hypoxemia
88% ≤ noitarutas negyxo(and certain other patients
with COPD) should all receive supplemental oxygen
to be worn continuously.
E- Assisted Ventilation
• Mechanical ventilation can be administered as follows:
(1) Invasive (through endotracheal tube);
(2) (NPPV) non-invasive positive pressure ventilation, using +ve
pressure devices, which is preferred whenever possible as it
-improves S&S,
-decreases hospital stay, and
-reduces mortality.
• Appropriate patients to consider for NPPV include those with:
(1) moderate to severe dyspnea with use of accessory muscles and
paradoxical abdominal motion;
(2) moderate to severe acidosis (pH between 7.25 and 7.35) &
hypercapnia (PaCO2 between 45 and 60 mmHg).
(3) respiratory rate between 25 and 35 breaths/min.
• Invasive mechanical ventilation should be used in patients with
more severe symptoms & in those failing NPPV.
Non-Invasive positive pressure
O2
Invasive mechanical ventilation
• Recommended Antibiotic
Patient:
Characteristics
Uncomplicated
exacerbation
1- Not requiring
hospitalization
Therapy in Acute Exacerbations of COPD
Likely Pathogens
Recommended Antibiotics
•Strepto
pneumoniae,
ORAL:
• Macrolide (azithromycin,
clarithromycin)
• Ketolide (telithromycin)
•Haemophilus
influenzae,
2- < 3 exacerbations/
year
•Moraxella
catarrhalis
3- No comorbid
illness
• 2nd or 3rd generation
cephalosporin
(cefuroxime, cefpodoxime,
cefdinir,cefprozil)
4- FEV1 > 50% predicted
5- No recent antibiotic
therapy
• Doxycycline
• β-Lactam/β-lactamase
inhibitor (amoxicillinclavulanate
Above organisms plus:
Complicated
• drug-resistant pneumococci,
exacerbation
• β-lactamase producing H.
1- FEV 1 < 50% predicted
influenzae & M. catarrhalis,
2- Comorbid cardiac
Escherichia coli, Proteus spp.,
disease
Enterobacter spp., Klebsiella
3- >3 exacerbations/
pneumoniae
year
4- Antibiotic in previous
3 months
ORAL:
• amoxicillin-clavulanate
• Fluoroquinolone with enhanced pneumococcal
activity (levofloxacin, gemifloxacin, moxifloxacin)
INTRAVENOUS:
• ampicillin-sulbactam
• 2nd or 3rd generation cephalosporin
(cefuroxime, ceftriaxone)
•Fluoroquinolone(levofloxacin, moxifloxacin)
Complicated exacerbation
with risk factors for P.
aeruginosa
1- Recent hospitalization
2- > 4 courses of antibiotics
in the last year
3- Very severe COPD
4- Previous isolation of P.
aeruginosa
Antipseudomonal
fluoroquinolone
(ciprofloxacin, highdose levofloxacin)
C-
Above organisms
plus P. aeruginosa
ORAL:
Antipseudomonal fluoroquinolone
(ciprofloxacin, high-dose levofloxacin)
INTRAVENOUS:
a- Antipseudomonal β-lactamase
resistant penicillin (piperacillintazobactam)
b- 3rd or 4th generation cephalosporin
with antipseudomonal activity
(ceftazidime, cefepime)
-Videos links:
https://www.youtube.com/watch?v=fmLZrZv10NM
https://www.youtube.com/watch?v=tusMPvA4wU&list=PLYojB5NEEakWxqnCBgl5_5rGXEP7VYGVT&index=2