LEVEL II

Global Initiative for Chronic Obstructive Lung Disease (GOLD)

MODULE 4Dr. Nichelle Jan M. Valmoria FPCP, FPCCP, FPSCCM
INTERNAL MEDICINE 03 NOVEMBER 2022

OUTLINE LUNG GROWTH AND DEVELOPMENT

CHRONIC OBSTRUCTIVE PULMONARY DISEASE ............ 1 • Positive association between birthweight and FEV1 in
FACTORS THAT INFLUENCE DISEASE DEVELOPMENT adulthood
AND PROGRESSION .......................................................... 1 • the lower the birthweight, the more likely that the patient will
PATHOLOGY, PATHOGENESIS, AND have a lower FEV1 by adulthood
PATHOPHYSIOLOGY .......................................................... 2 • Factors in early life termed “childhood disadvantage factors”
DIAGNOSIS AND INITIAL ASSESSMENT .......................... 2 are as important as heavy smoking in predicting lung
MEDICAL HISTORY............................................................. 3 function in adult life
PHYSICAL EXAMINATION .................................................. 3
SPIROMETRY.......................................................................... 3
ROLE OF SPIROMETRY ..................................................... 3
CONSIDERATIONS IN PERFORMING SPIROMETRY ....... 4
CHOICES OF THRESHOLDS .............................................. 4
TREATMENT ........................................................................... 6
MANAGEMENT OF COPD .................................................. 6
GOALS FOR TREATMENT OF STABLE COPD .................. 6
PHARMACOLOGICAL TREATMENT .................................. 6
BRONCHODILATORS IN STABLE COPD ........................... 6
ANTI-INFLAMMATORY STABLE COPD.............................. 6
NON-PHARMACOLOGIC TREATMENT.............................. 8
MANAGEMENT OF EXACERBATIONS ................................. 9
OVERALL KEYPOINTS ....................................................... 9
INDICATIONS FOR HOSPITALIZATIONS........................... 9
CLASSIFICATION OF HOSPITALIZED PATIENTS ............. 9
MANAGEMENT OF SEVERE BUT NOT LIFE-
THREATENING EXACERBATION ....................................... 9 Figure 1. Progression of FEV1 over time
INDICATIONS FOR NON-INVASIVE MECHANICAL
VENTILATION .................................................................... 10
INDICATIONS FOR INVASIVE MECHANICAL EXPOSURE TO PARTICLES
VENTILATION .................................................................... 10
• Cigarette smoking
DISCHARGED CRITERIA AND RECOMMENDATIONS
o Most common cause of COPD
FOR FOLLOW-UP.............................................................. 11 o Associated with:
PALLIATIVE, END-OF-LIFE, AND HOSPICE IN COPD .... 11 ▪ More respiratory symptoms & lung function
abnormalities
▪ Higher COPD mortality rate
CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) ▪ Greater annual rate of decline in FEV1
• A heterogeneous disease/ syndrome that is characterized • Cigarette smoking would affect the lungs depending
by persistent respiratory symptoms and airflow limitations on:
that is due to airway and/or alveolar abnormalities usually o Length of smoking
caused by significant exposure to noxious particles or o Amount of cigarette smoking
gases and influenced by host factors including abnormal o Onset of smoking – when smoking started before full
lung development. lung development, there is a higher risk of having a
severe form of COPD compared to those who started
smoking late
FACTORS THAT INFLUENCE DISEASE DEVELOPMENT • Environmental tobacco smoke (ETS)
AND PROGRESSION o i.e., Passive/secondhand smoking
GENETIC FACTORS • Indoor air pollution
• Best documented by alpha-1 antitrypsin deficiency, o Biomass fuels, burning of wood, animal dung, coal
secondary to serine protease inhibitor o Burning of wood – 2nd most common cause of COPD
• Significant familial risk of airflow limitation in people who in PH
smoke and are siblings of patients with severe COPD • Outdoor (urban) air pollution
• MMP 12: related to a decline in lung function o Occupational exposures
o Organic and inorganic dust (e.g., miners)
o Chemical agents and fumes (e.g., painters, carpenters)
AGE AND GENDER
• Aging of the airways and parenchyma mimics some of the
structural changes associated with COPD SOCIOECONOMIC STATUS
• Recent studies: men = women • Lower socioeconomic status
• Greater burden of small airway disease in females (vs • Exposure to indoor and outdoor air pollution
males) with COPD despite a similar history of tobacco • Crowding
smoke exposure • Poor nutrition
• Susceptible to respiratory infection

1 of 11
 INTERNAL MEDICINE GOLD

o Includes intimal hyperplasia and later SM hypertrophy

ASTHMA AND AIRWAY HYPERREACTIVITY or hyperplasia
• Asthma: reversible airflow limitation
• 12-fold higher risk of acquiring COPD

CHRONIC BRONCHITIS
• Mucus hypersecretion → ↑ likelihood of developing COPD
• Mucus clogging of airways
• ↑ Risk in total number and severity of exacerbations

INFECTIONS
• History of childhood infections → reduced lung function and
increased respiratory symptoms in adulthood
• Especially when the infection is recurrent or not properly
treated

PATHOLOGY, PATHOGENESIS, AND PATHOPHYSIOLOGY

PATHOLOGY Figure 2. Pathogenesis of COPD
• Pathologic changes are seen in the airways, lung
parenchyma, and pulmonary vasculature
DIAGNOSIS AND INITIAL ASSESSMENT
• Chronic inflammation
• Increase in the number of inflammatory cell types in specific
parts of the lung.
• Structural changes
o Due to repeated injury and repair

In general, inflammatory, and structural changes in the airways

increase with disease severity and persist on smoking cessation,
which is the reason why even if patients have stopped smoking for
more than a decade, the damage brought about by cigarette smoking
is still present.

PATHOGENESIS
• Inflammation is due to a modification of the normal
inflammatory response of the respiratory tract to a chronic
Figure 3. Pathways to the Diagnosis of COPD
irritant
• Mechanisms involved in COPD:
o Oxidative stress
o Protease-antiprotease imbalance KEY INDICATORS FOR CONSIDERING A
o Inflammatory cells and mediators DIAGNOSIS OF COPD
o Peribronchiolar and interstitial fibrosis • Consider COPD, and perform spirometry, if any of these
indicators are present in an individual over age 40. These
PATHOPHYSIOLOGY indicators are not diagnostic themselves, but the presence
• Airflow limitation and gas trapping of multiple key indicators increases the probability of a
o Results in hyperinflation (static) → main mechanism of diagnosis of COPD. Spirometry is required to establish a
exertional dyspnea diagnosis of COPD
o Impaired contractile properties of respiratory muscles • Dyspnea is
• Gas exchange abnormalities o Progressive over time
o Reduced ventilation due to reduced ventilatory drive or o Characteristically worse with exercise
increased dead space ventilation o Persistent
o Hypercarbia and hypoxemia • Chronic Cough
• Mucus hypersecretion o Often the first symptom of COPD, frequently
o Results in chronic productive cough discounted by the patient as an expected consequence
o Feature of chronic bronchitis and not necessarily of smoking
associated with airflow limitation o May be intermittent and may be unproductive
o Therefore, not all patients with COPD have o But subsequently may be present every day often
symptomatic mucus hypersecretion throughout the day
o Due to an increase in goblet cells and enlarged o Recurrent wheeze
submucosal glands • Chronic Sputum Production
o Both are due to chronic airway limitation by cigarette o Any pattern of chronic sputum production may indicate
smoke or other noxious agents COPD
• Pulmonary hypertension o Often difficult to evaluate because patients often
o Mainly due to hypoxic vasoconstriction of the small swallow sputum rather than expectorate it
pulmonary arteries eventually results in structural • Recurrent Lower Respiratory Tract Infections
changes • History of Risk Factors

2 of 11
 INTERNAL MEDICINE GOLD

o Host factors (such as genetic factors,

congenital/developmental abnormalities, etc.)
o Tobacco smoke (including popular local preparations)
o Smoke from home cooking and heating fuels
o Occupational dust, vapors, fumes, gases, and other
chemicals
• Family History of COPD and/or Childhood Factors
o For example, low birth weight, childhood respiratory
infections, etc.

MEDICAL HISTORY
• Past medical history
o Asthma, allergy, sinusitis Figure 5. (L) Emphysematous type of COPD, (R) Chronic
o Previous hospitalizations for a respiratory disorder bronchitis type of COPD
o Presence of comorbidities (e.g, heart disease,
malignancies)
• Family history of COPD & other chronic respiratory
diseases
• Pattern of symptom development
o Age of onset
o Type of symptom
o More frequent or prolonged “winter colds”

PHYSICAL EXAMINATION
• Early stages: Normal PE
• Severe COPD
o Barrel chest, poor diaphragmatic excursion Figure 6. (L) Emphysematous type of COPD, (R) Chronic
o Hyperresonance on percussion bronchitis type of COPD
o “Distant” breath sounds
o Prolonged expiratory phase/expiratory wheeze
o Pursed lip breathing
o Tripod positioning
o Hoover’s sign

Figure 7. Chronic bronchitis (Blue bloaters) vs Emphysema

(Pink puffers)

SPIROMETRY
Figure 4. Hoover’s sign ROLE OF SPIROMETRY
• Diagnosis
Usually, the diaphragm during inspiration moves down & during • Assessment of severity of airflow obstruction (for prognosis)
expiration, the diaphragm goes up again. In Hoover’s sign, there is • Follow-up assessment
no such movement of your diaphragm. o Therapeutic decisions
▪ Pharmacological in selected circumstances (e.g.,
• Advanced COPD the discrepancy between spirometry & level of
o Cachexia, weight loss symptoms)
o Bitemporal wasting ▪ Consider alternative diagnoses when symptoms
o Diffuse loss of subcutaneous tissue are disproportionate to the degree of airflow
o Signs of overt right heart failure obstruction
▪ Non-pharmacological (e.g., interventional
procedures)
o Identification of rapid decline

3 of 11
 INTERNAL MEDICINE GOLD

• Both FVC & FEV1 should be the largest value obtained from
any of three technically satisfactory curves & the FVC &
FEV1 values in these three curves should vary by no more
than 5% or 150 mL, whichever is greater.
• The FEV1/FVC ratio should be taken from the technically
acceptable curve with the largest sum of FVC & FEV1.

EVALUATION
• Spirometry measurements are evaluated by comparison of
the results with appropriate reference values based on age,
height, sex, and race.
• The presence of a postbronchodilator FEV1/FVC <0.70
confirms the presence of airflow limitation
Figure 8. (L) Emphysematous type of COPD, (R) Chronic
bronchitis type of COPD To confirm the diagnosis of COPD it is very important that you have
or use you would have a post-bronchodilator FEV1/FVC ratio of >0.7
[L] Body Plethysmograph which is the gold standard of spirometry. same also with your asthma.
This type of machine can perform basic spirometry as well as lung
volume study
[R] Plain bedside spirometry machine, more or less the same as
your body plethysmograph. However, this kind of machine is not
able to do the lung volume studies
CONSIDERATIONS IN PERFORMING SPIROMETRY
PREPARATION
• Spirometers need calibration regularly
• Spirometers should produce hard copies or have a digital
display of the expiratory curve to permit the detection of
technical errors or have an automatic prompt to identify an
unsatisfactory test & the reason for it.
• The supervisor of the test needs training in optimal
technique & quality performance.
Figure 9. Spirometry (Flow volume loop)
• Maximal patient effort in performing the test is required to
avoid underestimation of values & hence errors in diagnosis
& management (R) Normal lung
• The bigger the flow volume loop is, the higher the lung vital
capacity
BRONCHODILATION
• For asthma for patients with obstructive lung diseases it is (L) Patients w/ obstructive lung disorders (asthma & COPD)
important to perform spirometry with a pre-and post- • Most characteristic feature: scalloping or excessive concavity
on the expiratory part of the flow volume loop
bronchodilator study where your post-bronchodilator values
• Concavity signifies the severity of the airway obstruction
are much more important than your pre-bronchodilator • The more concave it is, the more obstructed the airway is
values Severe COPD: much smaller flow volume loop
• After the pre-bronchodilator study is performed wherein the
patient is asked to blow into the earpiece three times, the
patient is given the following doses (approximately): SPIROMETRY
o 400 mcg short-acting beta2-agonist
o 160 mcg short-acting anticholinergic, or the two TEST VALUE
combined FEV1/FVC <0.70
FVC <0.80
• The patient is given two inhalation of salbutamol ventolin FEV1 <0.80
MDI or salbutamol ipratropium combination
• After 15 minutes the patient is again subjected to a
spirometry wherein the patient is asked to perform the FEV CLASSIFICATION OF AIRFLOW LIMITATION SEVERITY
then the machine will be able to get the best result of three. IN COPD (BASED ON POST-BRONCHODILATOR FEV1)
• FEV1 should be measured:
o 10-15 mins. after a short-acting beta2-agonist is given In patients with FEV1/FVC <0.70
o 30-45 mins. after a short-acting anticholinergic; or GOLD
SEVERITY FEV1% PREDICTED %
CLASS
Combination of both classes of drugs
FEV1 ≥ 80%
GOLD 1 Mild 80-100%
predicted
PERFORMANCE 50% ≤ FEV1 <80%
• Spirometry should be performed using techniques that meet GOLD 2 Moderate 50-79%
predicted
published standards 30% ≤ FEV1 <50%
GOLD 3 Severe 30-49%
• The expiratory volume/time traces should be smooth & free predicted
from irregularities. The pause between inspiration and FEV1 <30%
GOLD 4 Very Severe 0-29%
expiration should be <1 second. predicted
• The recording should go on long enough for a volume
plateau to be reached, w/c may take more than 15 seconds CHOICES OF THRESHOLDS
in severe disease. • COPD Assessment Test (CAT) – the most common
• Chronic Respiratory Questionnaire

4 of 11
 INTERNAL MEDICINE GOLD

• St. George’s Respiratory Questionnaire

• Modified Medical Research Council (mMRC) Questionnaire
– most common

It is important to determine the thresholds, so we go to the

symptomatology of the patient because we need to determine the
different symptoms of the patient and other parameters for us to be
able to further classify our patients

We need to classify our patients properly to be able to give the right

medications or inhalers to our patients.

COPD ASSESSMENT TEST (CAT) Figure 12. MMRC Questionnaire Example

The higher the number of your grading, the more breathless

or dyspneic the patient feels.

THE REFINED ABCD ASSESSMENT TOOL

• First, do spirometry to confirm the diagnosis and with the
use of the FEV1/FVC ratio
• Second, use the post-bronchodilator FEV1 to categorize the
patient into GOLD standard
• Then the MMRC and CAT assessments
• Correlate it with the history of the exacerbation
• Use the ABCD method to come up with the classification

Figure 10. CAT Assessment Form

Figure 13. ABCD Assessment Tool

EXAMPLE:
• 70-year-old, male, 50-pack-year smoker, stopped 10 years ago
• With progressive dyspnea and non-productive cough for 2 years
• Spirometry: FEV1/FVC ratio = 58; DEV1 = 42
• Admitted 2x in NMMC in the past year due to worsening of
symptoms -> Pneumonia
• Presently prefers to stay at home

Using ABCD Assessment Tool and MMRC:

Answer: COPD GOLD 3, Class D

Figure 11. CAT Assessment Form (Actual)

The highest score is 50.

The higher the number, the more symptomatic the patient is.

MODIFIED MEDICAL RESEARCH COUNCIL

(MMRC) QUESTIONNAIRE

5 of 11
 INTERNAL MEDICINE GOLD

TREATMENT • Combinations of SABA and SAMA are superior compared

MANAGEMENT OF COPD to either medication alone in improving FEV1 and
symptoms (Evidence A).
• LABAs and LAMAs significantly improve lung function,
dyspnea, and health status, and reduce exacerbation rates
(Evidence A).
• LAMAs have a greater effect on exacerbation reduction
compared with LABAs (Evidence A) and decrease
hospitalization (Evidence B).
• Combination treatment with LABA and LAMA increases
FEV1 and reduced symptoms compared to monotherapy
(Evidence A).
• Combination treatment with a LABA/LAMA reduces
exacerbations compared to monotherapy (Evidence B).
• Tiotropium improves the effectiveness of pulmonary
rehabilitation in increasing exercise performance
(Evidence B).
• Theophylline exerts a small bronchodilator effect in stable
COPD (Evidence A) and is associated with modest
Figure 14. Management of COPD symptomatic benefits (Evidence B)

GOALS FOR TREATMENT OF STABLE COPD ANTI-INFLAMMATORY STABLE COPD

• Reduce Symptoms INHALED CORTICOSTEROIDS
o Relieve symptom • An ICS combined with a LABA is more effective than the
o Improve exercise tolerance individual components in improving lung function and health
o Improve health status status and reducing exacerbations in patients with
• Reduce Risk exacerbations and moderate to very severe COPD.
o Prevent disease progression • Regular treatment with ICS increases the risk of
o Prevent and treat exacerbations pneumonia, especially in those with severe disease.
o Reduce mortality • Tripled inhaled therapy of ICS/LAMA/LABA improves lung
function, symptoms, and health status and reduces
PHARMACOLOGICAL TREATMENT exacerbations compared to ICS/LABA, LABA/LAMA, or
KEYPOINTS FOR INHALATION LAMA monotherapy.
• The choice of inhaler divide must be individually tailored
and will depend on access, cost, prescriber, and most
importantly, patient’s ability and preference.
• It is essential to provide instructions and to demonstrate the
proper inhalation technique when prescribing a device, to
ensure that the inhaler technique is adequate, and re-check
at each visit patients continue to use the inhaler correctly.
• Inhaler technique (and adherence to therapy) should be
assessed before concluding that the current therapy
requires modification.

KEYPOINTS FOR BRONCHODILATORS

• LABAs and LAMAs are preferred over short-acting agents
except for patients with only occasional dyspnea (Evidence
A), and immediate relief of symptoms in patients already on
long-acting bronchodilators for maintenance therapy.
• Patients may be started on long-acting bronchodilator
therapy or dual long-acting bronchodilator therapy. In
patients with persistent dyspnea, one bronchodilator Figure 15. Factors to Consider When Initiating ICS Treatment
treatment should be escalated to two (Evidence A).
• Inhaled bronchodilators are recommended over oral ORAL CORTISCOSTERIODS
bronchodilators (Evidence A). • Long-term use of oral glucocorticoids has numerous side
• Theophylline is not recommended unless other long-term effects with no evidence of benefits.
treatment bronchodilators are unavailable or unaffordable
(Evidence B). PDE4 INHIBITORS
• In patients with chronic bronchitis, severe to very severe
BRONCHODILATORS IN STABLE COPD COPD, and a history of exacerbations:
• Inhaled bronchodilators in COPD are central to symptom o A PDE4 inhibitor improves lung function and reduces
management and commonly given regularly to prevent or moderate and severe exacerbations.
reduce symptoms (Evidence A). • A PDE4 inhibitor improves lung function and decreases
• Regular and as-needed use of SABA or SAMA improved exacerbations in patients who are on fixed-dose LABA/ICS
FEV1 and symptoms (Evidence A). combinations.

6 of 11
 INTERNAL MEDICINE GOLD

ANTIBIOTICS
• Long-term azithromycin and erythromycin therapy reduce
exacerbations over one year.
• Treatment with azithromycin is associated with an
increased incidence of bacterial resistance and hearing test
impairments.

MUCOREGULATORS AND ANTIOXIDANT AGENTS

• Simvastatin does not prevent exacerbations in COPD
patients at increased risk of exacerbations and without
indications for statin therapy. However, observational
studies suggest that statins may have positive effects on
some outcomes in patients with COPD who receive them
for cardiovascular and metabolic indications.
• Leukotriene modifiers have not been tested adequately in
COPD patients.

BRONCHODILATORS AND COMBINATIONS

BRONCHODILATORS EXAMPLES
SABA Salbutamol
SAMA Ipratropium bromide
Formoterol
Indacaterol
LABA Olodaterol
Salmeterol
Vilanterol
Glycopyrronium bromide
LAMA Tiotropium
Umeclidinium
Indacaterol + Glycopyrronium
bromide (Glycoair & Ultibro)
LABA + LAMA
Olodaterol + Tiotropium (Spiolto)
Vilanterol + Umeclidinium (Anoro)
Figure 16. Initial and follow-up pharmacological treatment.
METHYLXANTHINES
• Theophylline
MANAGEMENT CYCLE
• Aminophylline

Methylxanthines are not recommended for the management of

COPD. You can only make use of Theophylline if there are no
LABA/LAMA or any other inhalations available for the patient. You
may consider using theophylline then, but it is not to be used as a
routine in the management of COPD.

INITIAL PHARMACOLOGIC TREATMENT

• COPD groupings are based on the (see table, in white):
o The number of exacerbations in a year that would lead
to hospitalizations
o mMRC and CAT grading

Figure 17. Management Cycle

Assess: You may assess if the patient is willing or has been on

pulmonary rehabilitation and other non-pharmacologic management
of COPD.
Adjust Accordingly: If there are any problems that you have seen
as you assess the patient with each consultation or follow-up.
→ Escalate: If you think that the patient needs to have an
escalation of inhalers.
→ Switch to another inhaler device if the patient thinks that the
inhaler prescribed was a bit more expensive.
→ De-escalate if the given inhaler if the patient has had no
symptoms or exacerbations within the past 3 to 6 months

7 of 11
 INTERNAL MEDICINE GOLD

TREATMENT
1. If the response to initial treatment is appropriate, maintain it
and offer
a. Flu vaccination every year and other recommended
vaccinations according to guidelines
b. Self-management education o assessment of
behavioral risk factors such as smoking cessation (if
applicable) and environmental exposures
c. Ensure:
• Maintenance of exercise program and physical
activity
• Adequate sleep and a healthy diet
2. If not, consider the predominant treatable trait to target
a. Dyspnea
• Self-management education (written action plan) with
integrated self-management regarding.
o Breathlessness and energy conservation
techniques, and stress management strategies
Figure 18. Follow-up Treatment in COPD
• Pulmonary rehabilitation (PR) program and/or
maintenance program post PR
NON-PHARMACOLOGIC TREATMENT b. Exacerbations
• Education and self-management • Self-management education (written action plan) that
• Pulmonary rehabilitation is personalized concerning:
o One of the best non-pharmacological management of o Avoidance of aggravating factors
stable COPD. You cannot request a pulmonary o How to monitor/manage worsening symptoms
rehabilitation program if the patient has exacerbation. o Contact information in the event of an
• Exercise training exacerbation
• Nutritional support 3. All patients with advanced COPD should be considered for
• End-of-life and palliative care end-of-life palliative care support to optimize symptom
• Vaccination control and allow patients and their families to make
• Oxygen Therapy informed choices about future management.

PULMONARY REHABILITATION
KEY POINTS FOR THE USE OF NON-
• Pulmonary rehabilitation improves dyspnea, health status,
and exercise tolerance in stable patients PHARMACOLOGICAL TREATMENTS
• Pulmonary rehabilitation reduces hospitalization among • Education, self-management, and pulmonary
patients who have had a recent exacerbation (</= r weeks rehabilitation
from prior hospitalization) o Education is needed to change patient’s knowledge but
no evidence used alone will change patient behavior
o Education self-management with the support of a case
EDUCATION & SELF-MANAGEMENT
manager with or without the use of a written action plan
• Education alone is not effective
is recommended for the prevention of exacerbation
• Self-management intervention with communication with a complications such as hospital admissions
health care professional improves health status and o Rehabilitation is indicated in all patients with relevant
decreases hospitalizations and emergency department symptoms and/or high risk for exacerbations
visits. o Physical activity is a strong predictor of mortality.
INTEGRATED CARE PROGRAMS o Patients should be encouraged to increase their level
• Integrated care and telehealth have no demonstrated of physical activity although we still don’t know how to
benefit at this time (Evidence B) best insure the likelihood of success
• Vaccination
NON-PHARMACOLOGICAL MANAGEMENT OF COPD o Influenza vaccination is recommended for all patients
Depending with COPD
Patient o Pneumococcal vaccination: PCV 13 and PPSV23 are
Essential Recommended On Local
Group
Guidelines recommended for all patients >65 years of age, and in
Smoking younger patients with significant comorbid conditions
Flu
Cessation (can including chronic heart or lung disease
Vaccination,
A include Physical Activity
Pneumococc • Nutrition
pharmacologic
treatment)
al Vaccination o Nutritional supplementation should be considered in
Smoking malnourished patients with COPD
Cessation (can • End of palliative care
include Flu o All clinicians managing patients with COPD should be
B, C, pharmacologic
Physical Activity
Vaccination, aware of the effectiveness of palliative approaches to
and D treatment Pneumococc symptom control and use these in their practice
al Vaccination o End-of-life care should include discussions with
Pulmonary
patients and their families about their views on
Rehabilitation
resuscitation, advance directives, and place of death
preferences
• Treatment of Hypoxemia

8 of 11
 INTERNAL MEDICINE GOLD

o In patients with severe resting hypoxemia long-term • Methylxanthines are not recommended due to increased
oxygen therapy is indicated side effect profiles.
o In patients with stable COPD and resting or exercise-
induced moderate desaturation, long-term oxygen Anthonisen Criteria
• When the patient has two out of three of the Anthonisen
treatment should be routinely prescribed. However,
criteria, such as:
individual patient factors may be considered when o Increase dyspnea
evaluating the patient’s need for supplemental oxygen o Increase sputum production
o Resting oxygenation at sea level does not exclude the o Increase sputum purulence Then, you may prescribe
development of severe hypoxemia when traveling by antibiotics
air
SEVERITY OF COPD EXACERBATIONS
Recheck in 60 to 90 days to assess: If supplemental oxygen is still CLASS TREATMENT
indicated MILD SABA
MODERATE SABA + Antibiotics ± oral corticosteroids
SEVERE Hospitalizations
• Treatment of Hypercapnia
o In patients with severe chronic hypercapnia and a
history of hospitalizations for acute respiratory failure, INDICATIONS FOR HOSPITALIZATIONS
long-term noninvasive ventilation may be considered • Severe symptoms such as sudden worsening of resting
• Interventional bronchoscopy and surgery dyspnea, high respiratory rate, decreased oxygen
o Lung volume reduction surgery should be considered saturation, confusion, drowsiness
in selected patients with upper-lobe emphysema • Acute respiratory failure
o In selected patients with a large bulla surgical • Onset of new physical signs
bullectomy may be considered o Example: Cyanosis, peripheral edema
o In select patients with advanced emphysema, • Failure of an exacerbation to respond to initial medical
bronchoscopic interventions reduce end-expiratory management
lung volume and improve exercise tolerance, quality of • Presence of serious co-morbidities
life, and lung function at 6-12 months following o Heart failure, newly occurring arrhythmias
treatment. Endobronchial valves; lung coils; vapor • Insufficient home support
ablation
o In patients with severe COPD (progressive disease, CLASSIFICATION OF HOSPITALIZED PATIENTS
BODE score of 7 to 10, and not a candidate for lung
• No respiratory failure
volume reduction) lung transplantation may be
o Respiratory rate: 20-30 breaths per minute
considered for referral with at least one of the following:
o No use of accessory respiratory muscles; no changes
o History of hospitalization for exacerbation associated
in mental status
with acute hypercapnia (Pco2 >50 mmHg)
o Hypoxemia improved with supplemental oxygen given
▪ Pulmonary hypertension and/or cor pulmonale,
via Venturi mask 28-35% inspired oxygen (FiO2)
despite oxygen therapy or
o No increase in PaCO2
▪ FEV1 and either DLCO <20% or homogenous
• Acute respiratory failure- non-life-threatening
distribution of emphysema
o Respiratory rate: > 30 breaths per minute
o Using accessory respiratory muscles
OXYGEN THERAPY AND VENTILATORY SUPPORT IN o No changes in mental status
STABLE COPD o Hypoxemia improved with supplemental oxygen given
• Oxygen Therapy via Venturi mask 25-30% inspired oxygen (FiO2)
o The long-term administration of oxygen increases in o Hypercarbia - Ex. PaCO2 increased compared with
patients with severe chronic resting arterial hypoxemia baseline or elevated 50- 60 mmHg
o In patients with stable COPD and moderate resting or • Acute respiratory failure- life-threatening
exercise-induced arterial desaturation, prescription of o Respiratory rate: > 30 breaths per minute
long-term oxygen does not lengthen the time of death o Using accessory respiratory muscles
or first hospitalization or provide sustained benefit in o Acute changes in mental status - patient with
health status, lung function, and 6-minute walk drowsiness or stupor
distance o Hypoxemia not improved with supplemental oxygen via
o Resting oxygenation at sea level does not exclude the Venturi mask or requiring FiO2>40%
development of severe hypoxemia when traveling by o Hypercarbia - Ex. PaCO2 increased compared with
air baseline or elevated >60 mmHg or the presence of
• Ventilatory Support acidosis (Ph <7.25) Acute respiratory acidosis based
o NPPV may improve hospitalization-free survival in on the ABG)
selected patients after a recent hospitalization,
particularly in those with pronounced daytime MANAGEMENT OF SEVERE BUT NOT LIFE-THREATENING
persistent hypercapnia (PaCO2 > 52 mmHg) EXACERBATION
• Assess the severity of symptoms, blood gases, chest
MANAGEMENT OF EXACERBATIONS
radiograph
OVERALL KEY POINTS • Administer supplemental oxygen therapy, obtain serial
• Antibiotics, when indicated, can shorten recovery time, arterial blood gas, venous blood gas, and pulse oximetry
reduce the risk of early relapse, treatment failure, and measurements
hospitalization duration. (Duration: 5-7 days) (Anthonisen
Criteria). Administer supplemental oxygen therapy either through a nasal cannula
or a face mask; in more severe exacerbations- the patient may need non-

9 of 11
 INTERNAL MEDICINE GOLD

invasive ventilation; you may also consider starting the patient on a short-
acting SABA with or without a SAMA. And consider the LABA once the
patient is more stable.

• Bronchodilators
o Increase doses and/or frequency of short-acting
bronchodilators.
o Combine short-acting beta 2-agonists and
anticholinergics
o Consider the use of long-active bronchodilators when
the patient becomes stable
o Use spacers or air-driven nebulizers when appropriate
• Consider antibiotics (oral) when signs of bacterial infection
are present
o If the patient is noted to have respiratory distress,
consider IV antibiotics over oral antibiotics
• Consider noninvasive mechanical ventilation (NIV) (As the
Figure 20. The patient is primarily started on NIV with the oronasal interface
first line of oxygen therapy for patients who come in with
severe exacerbations of COPD)
• Oxygen therapy for patients at all times:
o Monitor fluid balance
o Consider subcutaneous heparin or low molecular
weight heparin for thromboembolism prophylaxis.
o Identify and treat associated conditions (e.g., heart
failure, arrhythmias, pulmonary embolism, etc.)

INDICATIONS FOR NON-INVASIVE MECHANICAL

VENTILATION
• At least one of the following:
o Respiratory acidosis (PaCO2 > 6.0 kPa or 45 mmHg
and arterial pH < 7.35)
o Severe dyspnea with clinical signs suggestive of
respiratory muscle fatigue, increased work of
breathing, or both, such as the use of respiratory
accessory muscles, paradoxical motion of the
abdomen, or retraction of the intercostal spaces.
Figure 21. Full face mask interface
o Persistent hypoxemia despite supplemental oxygen
therapy.

Figure 22. Nasal interface

Figure 19. Non–invasive Mechanical Ventilators.
INDICATIONS FOR INVASIVE MECHANICAL VENTILATION
• Upper-leftmost & upper-center left = Nasal interfaces • Unable to tolerate NIV or NIV failure
• Upper center right & upper rightmost = Oronasal interfaces • Status post: respiratory or cardiac arrest
• Lower right = Helmet interface • Diminished consciousness, psychomotor agitation
• Lower center = Full face mask interface
inadequately controlled by sedation
• Lower left = Oral interface
• Massive aspiration or persistent vomiting
• Persistent inability to remove/ expectorate respiratory
secretions
• Severe hemodynamic instability without response to fluids
and vasoactive drugs

10 of 11
 INTERNAL MEDICINE GOLD

• Severe ventricular or supraventricular arrhythmias

• Life-threatening hypoxemia in patients unable to tolerate
NIV

These are primarily the core management of patients with COPD

exacerbations. They would either require NIV or invasive mechanical
ventilation.

DISCHARGED CRITERIA AND RECOMMENDATIONS FOR

FOLLOW UP
• Full review of all clinical and laboratory data
• Check maintenance therapy and understanding
• Reassess the inhaler technique
• Ensure understanding of withdrawal of acute medications
(steroids and/or antibiotics)
• Assess the need for continuing any oxygen therapy (you
can make use of your NIV at home using CPAP)
• Provide a management plan for comorbidities and follow-
up
• Ensure follow-up arrangements: early follow-up < 4 weeks,
and late follow up <12 weeks as indicated
• All clinical or investigational abnormalities have been
identified.
• 1-4 weeks follow up:
o Evaluate the ability to cope in his/her usual
environment
o Review and understand the treatment regimen
o Reassessment of inhaler technique
○ Reassess the need for long-term oxygen
○ Document the capacity to do physical activity and
activities of daily living
○ Document symptom: CAT or mMRC
○ Determine the status of comorbidities
• 12-16 weeks follow up:
o Evaluate the ability to cope in his/her usual
environment
o Review understanding of treatment regimen
o Reassessment of inhaler technique
o Reassess the need for long-term oxygen
o Document the capacity to do physical activity and
activities of daily living
o Measure spirometry: FEV1
o Document symptom: CAT or mMRC
o Determine the status of comorbidities

PALLIATIVE. END-OF-LIFE, AND HOSPICE IN COPD

• Opiates, neuromuscular electrical stimulations (NMEs),
oxygen, and fans blowing air onto the face can relieve
breathlessness
• In malnourished patients, nutritional supplementation may
improve respiratory muscle strength and overall health
status
• Fatigue can be improved by self-management education,
pulmonary rehabilitation, nutritional support, and mind-body
interventions (Evidence B)

Please be smart and don’t start smoking because COPD is a chronic and
progressive respiratory disease that does not only affect our lungs but will
also affect other organs like the heart, respiratory tract, stomach, and GI
tract.
If you know anybody who has been smoking, please advocate for them
to stop as early as possible before it is too late.

11 of 11