CHRONIC OBSTRUCTIVE PULMONARY DISEASE ETIOLOGY AND RISK FACTORS

GOLD GUIDELINES  Tobacco Smoke

Chronic Obstructive Pulmonary Disease (COPD) o Major risk factor
 A common, preventable and treatable disease o Smoker have higher prevalence of
that is characterized by persistent respiratory respiratory symptoms and lung
symptoms and airflow limitation that is due to function abnormalities and greater
airway and/or alveolar abnormalities usually mortality rate than non-smoker
caused by significant exposure to noxious  Indoor air pollution
particles or gases o Burning of wood and other biomass
 Defined as a disease state characterized by fuels for cooking and heating
airflow limitation that is not fully reversible o Commonly affects women
 COPD is currently the fourth leading cause of  Occupational Exposures
death in the world o Exposure to organic and inorganic
 COPD is projected to be the 3rd leading cause dusts, chemical agents and fumes
of death by 2020  Outdoor air pollution
 More than 3 million people died of COPD in o Relatively small effect on COPD
2012 accounting for 6% of all deaths globally.  Genetic Factors
 Globally, the COPD burden is projected to o Alpha 1 antitrypsin
increase in coming decades because of o MMP-12
continued exposure to COPD risk factors and o Glutathione S-transferase
aging of the population  Age and Gender
ETIOLOGY, PATHOBIOLOGY & PATHOLOGY OF COPD
o Aging and female sex increase COPD
LEADING TO AIRFLOW LIMITATION & CLINICAL
risk
MANIFESTATIONS
 Lung Growth and Development
o Any factor that affects lung growth
Etiology
-Smoking and pollutants
during gestation and childhood (Low
-Host Factors BW. Respiratory infections) has the
potential to increase risk for
developing COPD
 Socioeconomic status
Pathobiology
-Impaired lung growth
 Asthma and Airway Hyperactivity
-Accelerated decline  Infections
-Lung Injury
-Lung & Systemic o History of severe childhood
inflammation
respiratory infection-> reduced lung
function and increase respiratory
symptoms in adulthood
CLINICAL MANIFESTATIONS
 The most common respiratory symptoms
PATHOLOGY include DYSPNEA, COUGH and/or SPUTUM
-Small airway disorders or
abnormalities
-Emphysema
PRODUCTION
-Systemic Effects  Advanced cases: worsening dyspnea, resting
hypoxemia
 Physical Examination:
o Early COPD: NORMAL PE
CLINICAL MANIFESTATIONS o Later of more severe: Prolonged
AIRFLOW LIMITATION
-Symptoms
-Persistent airflow
limitation
-Exacerbation Expiratory phase, expiratory
-Comorbidities
wheezing, signs of hyperinflation
(barrel chest, poor diaphragmatic
excursion with enlarged lung
volumes), significant weight loss,
bitemporal wasting
 COPD may be punctuated by periods of acute
worsening of respiratory symptoms-
EXACERBATIONS  Symptoms of COPD
 In most patients, COPD is associated with o Chronic and progressive dyspnea
significant concominant chronic diseases, o Cough
which increase its morbidity and mortality o Sputum production
DIAGNOSIS AND INITIAL ASSESMENT o Wheezing and chest tightness
o Others: including fatigue, weight loss,
anorexia, syncope, rib fractures,
ankle, swelling, depression, anxiety

 The goals of COPD assessment are:

o Determine the level of airflow
limitation
o Impact of disease on the patient’s
MEDICAL HISTORY
health status
 Patient’s exposure to risk factors
o Risk of future events (exacerbations,
 Past medical history
hospital admissions or death)
 Family history of COPD or other chronic
 Concominant chronic disease occur frequently
respiratory disease
in COPD patients and should be actively
 Pattern of symptom development
sought and teated appropriately when
 History of exacerbations or previous
present as they can influence mortality and
hospitalizations for respiratory disorder
hospitalizations independently
 Presence of comorbidities
o CV disease
 Impact of disease on patient’s life
o Skeletal muscle dysfunction
 Social and family support available to the
o Metabolic syndrome
patient
o Osteoporosis
 Possibilities for reducing risk factors,
o Depression
especially smoking cessation
o Anxiety SPIROMETRY
o Lung Cancer

POST-BRONCHODILATOR FEV1
CHOICE OF THRESHOLDS
 COPD Assessment Test (CATTM)
 Chronic Respiratory Questionnaire (CCQ)
 St. George’s Respiratory Questionnaire (CRQ)
 Modified Medical Research Council (mMRC)
Questionnaire
COPD ASSESSMENT TEST
MODIFIED MRC DYSPNES SCALE
ABCD ASSESSMENT TOOL
ALPHA-1 ANTITRYPSIN DEFICINECY (AATD)
AATD SCREENING
 The world health organization recommends
that all patients with a diagnosis of COPD
should be screened once especially in areas
with high AATD prevalence
 AATD patients are typically <45 years with
panlobular basal emphysema
 Delay in diagnosis in older AATD patients
presents as more typical distribution of
emphysema (Centrilobular apical)
 A low concentration (<20% normal) is highly
suggestive of homozygous deficiency
DIFFERENTIAL DIAGNOSIS OF COPD
MANAGEMENT OF STABLE COPD
 Management strategy for stable COPD should
be predominantly based on the individualized
assessment of symptoms and future risk of
exacerbations
 Smoking cessation should emphasized
 Management is both pharmacologic and non-
pharmacologic
 Once COPD has been diagnosed, effective
management should be based on an
individualized assessment to reduce both
current symptoms and future risks of
exacerbations

 Following implementation of therapy, patients
should be reassessed for attainment of
treatment goals and identification of any
barriers for successful treatment
 Following review of the patient response to
treatment initiation, adjustments
pharmacological treatment may be needed
 Based on GOLD groups, personalized design
could include:
o Groups A,B,C & D- addressing
behavioural risk factors, including
smoking cessation, maintaining or
increasing physical activity, and
ensuring adequate sleep and a
healthy diet
o Groups B & D- learning to self-manage
breathlessness, energy conservation
techniques, and stress management
strategies
o Groups C & D- avoiding aggravating
factors, monitoring and managing
worsening symptoms, having a
in written action plan and maintaining
regular contact/communication with
a healthcare professional.
o Group D- discussing with their
healthcare providers palliative
strategies and advance care directives

NON-PHARMACOLOGICAL TREATMENT
Education & Self-management
 Self-management education and coaching by
healthcare professionals should be a major
component of the “Chronic Care Model”
within the context of the healthcare delivery
system
 The aim of self-management interventions is
to motivate, engage and coach the patients to
positively adapt their health behaviour(s) and
develop skills to better manage their disease
on a day-to-day basis
 Venturi mask 25-35% FiO2,
hypercarbia i.e., PaCO2
increased compared with
baseline or elevated 50-60
mmHg
o Acute Respiratory Failure-Life-
threatening:
 Respiratory rate:> 30 breaths
per minute, using accessory
respiratory muscles; acute
changes in mental status,
hypoxemia not improved with
supplemental oxygen via
Venturi mask or requiring
FiO2 > 40%; hypercarbia i.e.,
PaCO2 increased compared
with baseline or elevated > 60
mmHg or the presence of
acidosis (ph < 7.25)
MANAGEMENT OF EXACERBATIONS
 COPD exacerbations are defined as an acute
worsening of respiratory symptoms that result
in additional therapy
 They are classified as:
o MILD (treated with short acting
bronchodilators only, SABDs)
o MODERATE (treated with SABDs plus
antibiotics and/or oral corticosteroids)
or
o SEVERE (patient requires
hospitalization or visits the emergency
room). Severe exacerbations may also
be associated with acute respiratory
failure
 Classification of hospitalized patients:
o No Respiratory Failure:
 Respiratory rate: 20-30
breaths per minute, no use of
accessory respiratory
muscles, no changes in
mental status, hypoxemia
improved with supplemental
oxygen given via Venturi mask
28- 35% inspired oxygen
(FiO2); no increase in PaCO2
o Acute Respiratory Failure-non-life-
threatening:
 Respiratory rate: > 30 breaths
per minute; using accessory
respiratory muscles; no
change in mental status;
hypoxemia improved with
supplemental oxygen via

PHARMACOLOGIC TREATMENT
 The three classes of medications most
commonly used for COPD exacerbations are:
o BRONCHODILATORS: although there is
no high-quality evidence from RCTs, it
is recommended that short-acting
inhaled beta2 –agonists, with or
without short-acting anticholinergics,
are the initial bronchodilators for
acute treatment of a COPD
exacerbation
o CORTICOSTEROIDS: Data from studies
indicate that systemic glucocorticoids
in COPD exacerbations shirten
recovery time and improve lung
function (FEV1). They also improve
oxygenation, the risk of early relapse,
treatment failure, and the length of
hospitalization
o ANTIBIOTICS
DISORDERS OF VENTILATION
INTRODUCTION:
 VENTILATION:
o Process of air exchange between the
lungs and the ambient air
o Delivery of air into the alveoli
o Transfer of CO2 from the blood to the
alveoli out of the body
 GAS EXCHANGE:
o Ability to move cross the alveolar-
capillary membrane
o “Oxygenation”
 Ventilatory Failure-> Hypercapnic Respiratory
Failure
 Gas exchange failure-> Hypoxemic Respiratory
Failure
o BOTH LEADS TO HYPOXEMIA
 NORMAL BREATHING:
o Respiratory Rate (RR): Number of
breaths per minute (12-15bpm)
o Tidal Volume(TV): volume of gas
inspired in a single breath (500ml)
o Minute Ventilation: volume of gas
inspired per minute= RR x VT (6 li per
min)
 PaCO2 is used to determine alveolar
ventilation
o Normal PaCo2= 37 to 43mmhg
o PaCO2 > 43 mmHg= alveolar
hypoventilation
o PaCO2 < 37 mmHg= alveolar
hyperventilation
HYPOVENTILATION
 Decreased in minute ventilation
 Categories:
o Parenchymal lung and chest wall
disease
o Sleep Disorder breathing
o Neuromuscular disease
o Respiratory drive disorders
 Clinical presentation:
o Dyspnea during activities of daily
living
o Orthopnea in diseases affecting
diaphragm function
o Daytime Hypersomnolence
o Early morning headaches
o Anxiety
o Impaired cough in neuromuscular
diseases
 Increase PaCO2= hallmark of alveolar
hypoventilation syndromes
o Increase in plasma bicarbonate
o Decrease in alveolar oxygen->
hypoxemia
*SEVERE HYPOXEMIA-> Clubbing and
Secondary erythrocytosis
 Diagnosis:
o Arterial blood gas
 Elevated plasma HCO3
 Increased PaCO2
 Normal pH
o Evaluate for lung disease or chest wall
abnormalities, screen for OSA
 o If ventilator apparatus is normal ->  Treatment:
evaluate for neuromuscular and o Weight loss
respiratory drive disorders o PAP Therapy ( CPAP or various NIV
modes)
 Delivery of continuous
pressure during the
OBESITY HYPOVENTILATION SYNDROME respiratory cycle to prevent
obstructive apneas and
hypopneas
 Permits unloading of carbon
dioxide accumulated during
OBESITY
long-lasting complete or
partial obstructive events
CHRONIC DAYTIME
during sleep
ALVEOLAR
HYPOVENTILATION
SLEEP DISORDER
BREATHING (90% OSA)
SLEEP APNEA
(PaCO2>45 and PaO2
<70) OBSTRUCTIVE SLEEP APNEA/HYPOPNEA SYNDROME
(OSAHS)
 Coexistence of unexplained excessive daytime
sleepiness with at least 5 obstructed
 Prevalence: breathing events (apnea or hypopnea) per
o 8-20% of obese patients hour of sleep
o Equal in men and women  Most common type of sleep-disordered
 Pathophysiology breathing characterized by recurrent episodes
o Major Mechanisms: of upper airway collapse during sleep
 Obesity-related changes in  APNEA: cessation of airflow for more than or
respiratory system equal to 10 seconds
 Alterations in respiratory  HYPOPNEA: recognizable transient reduction
drive of breathing for at least 10 seconds; decrease
 Increased respiratory of atleast 50% from baseline during sleep or
drive to remain reduction of less than 50% from baseline but
eucapnic but unable with oxygen desaturation of atleast 4%
to sustain during PATHOPHYSIOLOGY:
sleep
 Breathing abnormalities
during sleep
 Obese patient have
higher frequency of
OSA

 Clinical Manifestation:
o Excessive daytime somnolence**
o Non-refreshed sleep
o Nocturia
o Loud snoring
o Apneas
o Choking during sleep
o Morning headaches
o Sexual dysfunction
 Risk Factors:
o Obesity
o Shortening of mandible or maxilla
o Hypothyroidism
o Acromegaly
o Male gender
o Enlarged tonsils or adenoids
o Ehlers-Danlos
o Smoking/alcohol use
 Consequences of OSAHS
o Neurobehavioral and social
o Cardiovascular
o Diabetes Mellitus
o Hepatic dysfunction
o Perioperative and postoperative
 Clinical Assessment
o History:
 Breathing disturbances during
sleep  Diagnostic Examinations:
 Quality of sleep o Polysomnography
 Excessive daytime sleepiness-  Overnight polysomnography
> ESS is the gold standard for
o Physical Examination: diagnosis of OSA
 Craniofacial and soft tissue  Full somnographic study with
enlargement associated with complete monitoring of
upper airway resistance such respiratory and
as retrognathia, deviated neurophysiologic signals
nasal septum, and low lying during sleep
soft palate. Enlarged uvula  Determine the apnea
and base of tongue hypopnea index (AHI)
 BMI (>28)  Diagnostic criteria: AHI >5 +
 Neck Circumference (>42cm) symptoms of daytime
sleepiness or AHI > 15
 SEVERITY based on AHI:
 5-14: mild
 15-30: moderate
 >30: severe
  Not cost effective
 Contraindicated in
pregnancy and
lactation

 Treatment:
o Conservative treatment:
 Lifestyle modification: weight
loss. Reduction of alcohol,
drugs and smoking, avoidance
of sedatives, adjustment of
sleep poisoning
 Across all severity
o CPAP:
 Use positive pressure to keep
airway open and help
unloading of carbon dioxide
o Surgical:
 Bariatric surgery can be
curative in patients with
morbid obesity
 Tonsillectomy is highly
effective in children
 Tracheostomy is curative lbut
rarely used because of
increased morbidity
 Jaw advancement surgery,
especially maxilla-mandibular
osteotomy, is effective in
patients with retrognathia
o Medical
 Modafinil:
 Offers marginal
improvement in
sleepiness in patients
with OSAHS who
remains sleepy
despite CPAP