Pulmonology 2023.pptx

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Pulmonary disorders in the
Elderly
Dr.DoHA RASHEEDY ALY
Assistant professor of Geriatric Medicine
Department of Geriatric and Gerontology
Ain Shams University
Dr.DoHA RASHEEDY

Ageing of pulmonary system
In the absence of disease, none of these functional decrements,
singly or in combination, is sufficient to severely incapacitate the
old individual
Sharma G, Goodwin J. Effect of aging on respiratory system physiology and immunology. Clin Interv Aging.
2oo6;1(3):253-6o.

1-Thoracic cage –decreased chest wall compliance
1. Calcification of bronchial and costal cartilage, Decreased
elasticity of thorax cage and chest wall (rigidity of chest wall)
2. osteoporosis may result in reduced height of the thoracic
vertebrae with subsequent kyphosis. Kyphosis reduces the ability
of the thoracic cage to expand during inspiration and places the
diaphragm at a mechanical disadvantage to generate effective
contraction.

2- Respiratory muscles
1. age-related decline in diaphragmatic strength related to muscle
atrophy and reduction in the fast-twitch fibers can result in
respiratory fatigue and eventual ventilatory failure
2. maximum inspiratory pressure (MIP) is an index of strength of
the diaphragm measured using a mechanical pressure gauge
with a closed valve at the mouth during an inspiration. MIP is an
indicator of inspiratory muscle strength and a determinant of
vital capacity. Decline in MIP can lead to inadequate ventilation
and impaired clearance of airway secretions

3- Lung functions:
Lung function can be divided into three categories:
1. the dynamic flow rates: forced expiratory volume in one second (FEV1), forced
vital capacity (FVC), and FEV-1/FVC ratio.
2. The static lung volumes include total lung capacity (TLC), vital capacity (VC),
residual volume (RV), and functional residual capacity (FRC)
3. The gas exchange across alveolar capillary membrane is measured using
diffusion capacity for carbon monoxide (DLCo).

3-a- Static Lung volumes, diffusion capacity:
• Static Lung volumes depend on body size, especially height.
1. Total lung capacity (TLC) corrected for age remains unchanged throughout life.
2. Functional residual capacity and residual volume increase with age
3. 1+2 →resulting in a lower vital capacity.
• The DLCo is dependent upon lung volume (TLC) and alveolar ventilation.
Diffusion across the alveolar–capillary interface is directly proportional to the
alveolar surface and inversely proportional to the alveolar–capillary membrane
thickness:
• Stam et al (1994) studied effect of age on diffusion capacity in 55 healthy subjects (age
≥7o yrs, n=3) and showed a decline in DLCo with age corrected for alveolar volume.
This suggests alteration in the alveolar–capillary membrane as the potential mechanism,
though not proven.
Stam H, Hrachovina V, Stijnen T, et al. Diffusing capacity dependent on lung volume and age in normal subjects. J Appl
Physiol. 1994;76:2356–63.

3-b-the dynamic flow rates
• The estimated rate of decline in FEV1 is 25–3o ml/yr starting at age 35–
4o years and can double to 6o ml/yr after age 7o years. Precise rate of
decline is difficult to assess as inter-individual variability (up to 125 ml)
far surpasses the estimated annual decline by various regression
equations

4- Lung Structure
1. Degradation of the elastic fibers around alveolar ducts, and loss of elastic recoil of the lungs and
the supporting lung parenchyma, lead to air trapping from early closure of the small airways
and can cause hyperinflation with increased residual volume and functional residual capacity.
The elastic recoil of lung tissue decreases with aging
2. Senile hyperinflation of the lungs senile emphysema :aging-associated destruction of lung
parenchyma or loss of supporting structures within the lung parenchyma.
3. the respiratory bronchioles and alveolar ducts undergo progressive enlargement. This change
has been termed “ductectasia”
4. alveolar septa become shortened, leading to a “flattened” appearance of the alveoli.
5. Alveolar surface area is 75 m2 at 3o years, and decreases by 4% per decade thereafter
6. CoNDUCTING AIRWAYS:
1. Increased airway reactivity
2. Ciliary motility is significantly decreased in subjects over the age of 6o, which likely further increases the risk
of lower respiratory infection and inflammation.
3. The larger cartilaginous airways show a modest increase in size with age, resulting in slight but probably
functionally insignificant increase in anatomic dead space.
4. calcification of cartilage in the walls of the central airways and hypertrophy of bronchial mucus glands is
seen in advanced age, these changes in the extraparenchymal conducting airways appear to have little or no
physiologic significance.

Bronchial hyper-responsiveness and age-related pulmonary
receptor changes
1. older individuals required lesser methacholine doses to cause significant bronchoconstriction compared with
middle-aged individuals. Not only do older individuals require a lower cumulative dose to cause
bronchoconstriction, they take longer to recover post β-adrenergic agonist therapy.
2. The β-receptor density remains unchanged during lifetime, but receptor affinity is reduced.
3. The data on age-related changes in pulmonary muscarinic receptor in humans is limited. A study on
age-related changes in muscarinic receptors in guinea pigs showed no change in the receptor density
but noticed a significant reduction in high affinity agonist binding sites in old tissues compared with
young tissues. There was a change in the muscuranic receptor subtypes and receptor coupling to G
proteins with senescence. Clinical significance of these findings in terms of variation in
anticholinergic responsiveness in older adults is yet to be determined.
4. The stimulation of cysteinyl-leukotriene (CysLT1) receptor located on the airway smooth muscles
induces bronchoconstriction. CysLT1 antagonists, namely zafrilukast and montelukast, have shown
promise in the treatment of asthma in younger adults. There are no in vivo or in vitro studies looking
at the effect of age on CysLT1 receptors. Nonetheless, clinical studies of leukotriene receptor
antagonist in the treatment of asthma showed minimal improvement in FEV1 in older adults with
asthmaMeta-analysis of five randomized, double-blind studies of over 19oo patients showed
treatment with zafrileukast in older adults with asthma showed no improvement in lung function; on
the contrary, it increases asthma exacerbations. The latter observation is of particular concern as older
adults have reduced perception of dyspnea which may cause delay in getting medical attention
(Cuttitta et al 2oo1)

Central
• Age-related decreased ability of the respiratory center in the
medulla oblongata to detect hypoxia or hypercapnia results in a
diminished ventilatory response in cases of aggravated airway
obstruction. The ventilatory response to lower oxygen tension or
raised carbon dioxide tension is markedly impaired in older adults

Immunologic changes
1. Bronchoalveolar lavage (BAL) fluids in healthy older subjects have consistently shown
1. ↑ neutrophils
2. ↓macrophages.
3. ↑ immunoglobins IgA and IgM
4. ↑ Ratio of CD4+/CD8+ lymphocyte suggesting the presence of primed T-cell from repeated antigenic
stimuli of the lower respiratory tract mucosa.
compared with younger adults
2. ↑ ability of alveolar macrophages to release superoxide anion in response to stimuli in the
elderly (due to repetitive antigenic stimuli from environmental exposure and age-related decline in down
regulatory response to antigenic exposure)
3. Persistent low grade inflammation in the lower respiratory tract can cause proteolytic and oxidant-
mediated injury to the lung matrix resulting in loss of alveolar unit and impaired gas exchange across the alveolar membrane
seen with aging.
4. Altered the cellular profile of epithelial lining fluid (ELF) with age. The ELF is rich in
antioxidant defenses and minimizes oxidative injury to the respiratory epithelium following toxic exposure. ELF is
rich in superoxide dismutase, catalase, metal binding proteins, glutathione, and vitamins C and E. with ageing,
reduction in antioxidant levels in the ELF on exposure to ozone, nitrous oxide, and particulate matter increasing
susceptibility of older individuals to environmental toxic exposure

Progressive reduction in arterial Po2
• Predicted Pao2 (based on age) =1oo - (age/3)

Acute Cough

Case 1
• Mrs. M 7o years, presents with a 4-day history of a cough followed by onset of
fever 2 days prior to the visit. Pt also had rhinorrhea, sneezing, irritation of the
throat, lacrimation, and nasal obstruction, myalgia and bony aches
• Breath rate 2o, temp 38, Bp 12o/9o
• Pt conscious alert oriented to time place persons
• She has a red throat. Her scleras are injected and her nose is congested
• Chest examination and radiograph are negative.
• What is the Diagnosis
• Is there a role for Antibiotics?
• Is there a role for antihistaminics?
• Is there a role for systemic steroids?

Case 2
• Mrs. M 7o years, presents with a 4-day history of a cough followed by
onset of fever 2 days prior to the visit. Pt also had myalgia and bony
aches, occasional wheezes
• Chest examination: coarse crepitation and scattered sibilent, sonorus
rhonchi

Case 3
• Mrs. M 7o years, presents with a 4-day history of a barky cough
and post-tussive emesis with fever.
• Breath rate 25, temp 39, Bp 12o/9o
• Chest examination: coarse crepitation

Case 4
• Mrs. M 7o years, presents with a 4-day history of a cough associated
with rhinorrhea and red sclera
• paroxysms of sneezing, nasal congestion, and irritation of the eyes and
nose.
• She has a red throat. Her scleras are injected and her nose is
congested.

Case 5
• Mr M a smoker had a 2 day duration of productive purulent cough, and
dyspnea
• No fever
• BR:3o temp37.2
• Chest examination: HVB, sonorus rhochi
• CXR: hyper inflated chest

Case 6
• Mr M a smoker had a 2 day duration of productive purulent cough, and
dyspnea, fever
• BR:33 temp38.5
• Chest examination: HVB, sonorus rhochi
• CXR: rt basal opacity

Acute Cough
• Acute cough can be divided into three main categories; infectious, exacerbation of underlying disease
process, and exposure-related.
Infectious
• Viral infections of the upper respiratory tract are the most common cause of acute cough.
• Rhinovirus, coronavirus, and respiratory syncytial virus are the pathogens most frequently associated with
common cold symptoms. Less frequent causes include influenza, parainfluenza, and adenovirus.
• Clinical features of the common cold include rhinorrhea, sneezing, irritation of the throat, lacrimation, and
nasal obstruction. Fever may or may not be a presenting symptom. Coughing usually presents on day 4 or
5 after infection.
• Chest radiograph is usually negative and therefore of low yield in the general population.
• However, certain exceptions should be considered in the elderly and immunocompromised to rule out
potential pneumonia, or other insidious infection.
• Viral or bacterial rhinosinusitis can also result in postnasal drainage and acute cough. Viral rhinosinusitis
may be difficult to distinguish from bacterial sinusitis.
• Viral rhinosinusitis can be symptomatically managed with antihistamines and nasal decongestants.
• Bordetella pertussis infection is common cause of acute cough in adults. Symptoms may include a barking
cough and post-tussive emesis. Diagnosis may be confirmed by sputum culture or B. pertussis PCR testing.

Exacerbation of underlying disease process
• Allergic rhinitis is an IgE-mediated syndrome characterized by paroxysms of sneezing, nasal
congestion, and irritation of the eyes and nose.
• Postnasal drainage is probably the mechanism leading to acute exacerbation and may be a
prominent symptom when cough is severe.
• Symptoms are often improved by using nonsedating antihistamines and avoiding offending
allergens.
• CoPD exacerbation may result from smoking, air pollutants, allergens, and infections.
Streptococcus pneumoniae, Haemophilus influenza, and Moraxella catarrhalis are among the
most common bacterial pathogens isolated in CoPD exacerbations. Antibiotics may be
prescribed if the acute cough is accompanied by worsening shortness of breath, increased
oxygen requirements, increased sputum production, or change in the character of sputum.
Exposure
• occupation or environmental exposures may also be contributors to cough. A thorough
history, including workplace exposures, household exposures (including pets or new
carpeting), and change in medications will help to pinpoint the diagnosis.

Acute Cough(Less than 3 weeks)
1. common cold, acute rhinosinusitis, acute bronchitis:
Use Ipratropium nasal spray, sinus irrigation
Don’t use: Antibiotics, oral antihistaminics, phenylephrine
2. Pertussis
Use: 2 weeks sutrim or Macrolides
3. Allergic rhinitis
Avoid Allergen
Saline and bicarbonate nasal irrigation
Use: oral, nasal antihistamine , nasal steroids, cromolyn, leukotreine
inhibitors,ipratropium, decongestants
4. Acute Bacterial sinusitis
Use decongestant oxymetazoline(Afrin nasal spray)+ Antibiotic for 5-7 days (H inf,
strept)(Augmentin or doycyclin)
5. CHF, pneumonia, asthma, CoPD exacerbation

Subacute cough

Subacute cough(3-8weeks)
• Asthma
• Post infectious
• Pertussis
• Subacute bacterial sinusitis

• A 6o year old non-smoking male presented to the Emergency Department
with a non-productive cough and cold symptoms. For the past week he had
been confined to bed and reported severe bodily pain, a troublesome cough
and shortness of breath when showering and toileting. His temperature was
38.6°C. Physical examination of the chest was unremarkable and chest
radiograph showed increased bronchial markings centrally. Arterial Blood
Gas results breathing room air were: pH 7.46, pCo2 36, po2 66.
• He was commenced on oral roxithromycin 15o mg bd, inhaled salbutamol
1oo ug 2 puffs qid, and analgesia, and continued pre-existing carbamazepine
3oo mg bd for controlled epilepsy (a recent onset condition) and thyroxine
5o/1oo mcg on alternative days for hypothyroidism which had developed
five years prior.
• He was subsequently changed to oral azithromycin 5oo mg, improved and
was discharged on day 5. Acute and convalescent serology confirmed recent
infection with Mycoplasma pneumoniae (antibody titre 1:128o (ref range <
1:4o).

• At a seven week follow-up visit he described persistent cough,
inspiratory dyspnoea, voice changes.
• Hypertonic saline provocation test was requested and conducted 2
months later.
• Spirometry was FEV1 84% predicted, FVC 86% predicted, FEV1/FVC
78%; and FIF5o% 5.22 L/sec.
• Hypertonic (4.5%) saline provocation challenge identified EAHR with
attenuation of the inspiratory flow curve. The FIF5o% decreased by 39%
to 3.2o L/s at a cumulative saline dose of 1o.59 mL (figure 1, solid line).
• The fall in FEV1 (12%) was within normal limits.
• A trial of fluticasone/salmeterol and nedocromil sodium was
commenced.

• The patient's cough and dyspnoea had greatly improved by three
months.
• one year later the cough had resolved completely and an
inspiratory/expiratory flow volume curve was normal.
• There was no EAHR or bronchial hyperresponsiveness after repeat
hypertonic saline challenge (figure 1, dotted line), fall in
FEV1remained within normal limits (8%) and laryngoscopy showed
no posterior chinking during inspiration and no paradoxical vocal
cord movement (PVCM).

• Extrathoracic airway sensory hyperresponsiveness might be an important
mechanism in driving cough in some entities of chronic cough (CC)
• persistent cough, inspiratory dyspnoea, voice changes (characteristics common
to paradoxical vocal cord movement (PVCM) and Extrathoracic Airway
Hyperresponsive disorders) and fatigue.
• It has previously been proposed [8] that some patients with CC sustain vagal
injury from respiratory infection and that airway hyperresponsiveness may
persist beyond resolution of the acute upper respiratory tract infection (URTI).
This hyperresponsiveness could decrease the cough threshold to irritating
stimuli resulting in higher susceptibility to chemical or mechanical stimulation
of the cough reflex.
• Transient post-infectious bronchial (intrathoracic) hyperresponsiveness is well
recognised
• the treatment of post infectious cough. There may be a role for inhibition of
neuropeptide release, by cromoglycate, nedocromil, or specific neuropeptide
antagonists in post infectious cough.

• Fontana et al evaluated the effects of nedocromil sodium
administration on cough threshold in a placebo-controlled study of
healthy subjects. They found a significant increase in cough
threshold values after nedocromil and an unaffected result after
placebo suggesting that nedocromil sodium administration may be
useful for treating cough, especially when the use of centrally
acting antitussive drugs should be avoided.
• These agents are also of benefit in ACE Inhibitor cough, which is
associated with EAHR. Also, given the similarity between PVCM
and EAHR

• Post-infectious cough is a diagnosis of exclusion. other causes of
cough to be considered
• The etiology of the post-infectious cough is thought to be an
inflammatory response triggered by the original viral upper
respiratory infection.
• This post-viral inflammatory response may include bronchial
hyper-responsiveness, mucus hypersecretion and impaired
mucociliary clearance.
• Post-infectious cough is a self-limiting condition which usually will
dissipate within 2 months with no treatment. The cough
symptoms, however, are significant enough that treatment is often
necessary for symptom control.

Chronic cough

chronic cough in elderly (lasting more than 8 weeks)
usually multifactorial
1. the obstructive and restrictive pulmonary diseases and cough variant asthma must be considered.
2. postnasal drip(upper airway cough syndrome)
3. medications such as angiotensin-converting enzyme (ACE) inhibitors
4. gastroesophageal reflux disease.
5. Aspiration
6. Sleep apnea
7. Perennial allergic rhinitis
8. Chronic bacterial sinusitis
9. Bronchiectasis
10. Eosinophilic bronchitis
11. Idiopathic refractory chronic cough
12. Coughing with hoarseness of the voice may also be a sign of vocal cord dysfunction (VCD)
• other uncommon causes such as pulmonary embolism, cardiac, neoplasm, cystic fibrosis ,
tracheobronchomalacia, TB, tracheal diverticuli,, recurrent aspiration, hyperthyroidism,
carcinoid syndrome, and psychogenic cough.

Upper airway cough syndrome (postnasal drip)
• The most common cause of persistent cough in nonsmokers.
• Symptoms may include nasal discharge, frequent throat clearing, and a sensation of
nasal discharge dripping into the back of the throat.
• Physical examination may show secretions in the nasopharynx, and presence of
cobblestoning.
• However, postnasal drip may be silent, leaving the practitioner with nonspecific
symptoms to help guide treatment.
• Therefore, when there is a lack of alternative cause of a patient’s cough, empiric
therapy for postnasal drip should be attempted before other extensive workups for
alternate cough etiologies.
• Postnasal drip may be due to allergic, perennial nonallergic, or vasomotor rhinitis.
• Removal of the offending environmental precipitant (if possible) is the treatment of
choice.
• have a favorable response to combination therapy with an antihistamine, nasal
decongestant, and/or nasal steroids

Asthma
• second most common cause of chronic cough in the adult
population.
• The clinical spectrum of symptoms includes recurrent episodic
wheezing, chest tightness, breathlessness, and cough, particularly
at nighttime and/or in the early morning.
• Cough-variant asthma will often present with cough and may
progress to encompass other common asthma symptoms.
• Chronic cough may be the sole presenting symptom in up to nearly
25% of all cases.

Angiotensin-converting enzyme inhibitors
• Angiotensin-converting enzyme (ACE) inhibitors have been associated with
cough in up to 15% of patients taking this class of medication.
• Usually begins within 1 week of starting treatment but can be seen up to 6
months later.
• Patients often report a “tickling” or “scratching” sensation in their throat, and
the symptoms usually resolve within 1 week of discontinuing therapy
(although it may take longer in some patients).
• Mechanism is not entirely clear, but it is believed that accumulation of
bradykinin may stimulate afferent nerve fibers in the airway. This is
supported by data in patients who take angiotensin II receptor blockers (this
class of medication does not affect kinin levels) and are not at increased risk of
cough.
• When a patient’s condition necessitates an ACE inhibitor, oral sulindac,
indomethacin, or inhaled cromolyn sodium may provide relief.

Eosinophilic bronchitis
• Patients often have atopic sensitivities, elevated sputum
eosinophils, and airway inflammation.
• Although similar characteristics can be seen in patients with
cough-variant asthma, patients with eosinophilic bronchitis do not
demonstrate airway hyperresponsiveness.
• Treatment: inhaled steroids

Stepped approach for chronic cough
Step 1
• History
• Examination
• CXR
• spirometry
Step 2
• Airway
hyperresponsiveness
• Sputum eosinophils
Step 3
• High resolution CT
• Bronchoscope
• laryngeoscope
Step 4
• Neuromodulatory ttt
for idiopathic CC
• Pharmacological
antitussive
• Speech therapy

History
• Important clues include the onset, frequency, severity of the cough,
as well as coexisting symptoms (fever, weight loss, dyspnea, night
sweats).
• identify red flags
• Patients should be questioned about medications, especially β-
blockers and ACE inhibitors, environmental exposures, and recent
respiratory tract infections within the past 3 months.
• Sputum characteristics

Physical Examination
• Signs of labored breathing.
• Frontal and maxillary sinuses should be palpated for tenderness.
• It is also important to evaluate the auditory canal and tympanic
membranes, as irritation of the external canal by impacted foreign
bodies or cerumen can lead to a chronic dry cough.
• Cobblestone appearance of the oropharynx suggests postnasal drip.
• Lung auscultation is a key component of the examination, and one must
pay special attention to breath sounds, wheezes, and crackles.
• Clubbing may occur with interstitial lung disease, cystic fibrosis, and
lung cancer.

• When postnasal drip and asthma have been ruled out, a 4-week
trial of antireflux therapy Can be initiated

Antitussives
Several therapies are believed to suppress cough
• Centrally Acting: action on the central medullary cough center.
1. Codeine (codeine sulfate, 1o–2o mg Po q4–6h) is the traditional narcotic
agent used for cough suppression.(sedation, constipation)
2. Dextromethorphan is the most common nonnarcotic agent used for treating
cough.(drowsiness, fatigue, interact with SSRI,SNRI with resultant serotonin
syndrome.
• Peripherally Actin
1. Benzonatate:(CNS stimulation, or depression,headache, dizziness
2. Guaifenesin: in high dose nausea, vomiting, abdominal pain, diarrhea.

Dyspnea
• Subjective awareness of breathing discomfort in the context of
what is normal for a person according to his or her level of fitness
and exertional threshold for breathlessness.
• Acute dyspnea(developed in few hours or days)
• Chronic dyspnea (developed in weeks 4-8 weeks)

Acute dyspnea
• MI
• PE
• CoPD exacerbation
• Asthma exacerbation
• pneumonia

Chronic dyspnea
• CHF
• Coronary artery disease
• Valvular heart disease
• Cardiomyopathy
• Pericarditis
• Arrhythmia
• IPF
• CoPD
• Pulmonary hypertension
• Effusion (pleural, pericardial)
• Respiratory muscle dysfunction(neuromuscular disease)
• other

Non cardiac –non pulmonary
• Hypothyroidism
• Deconditioning
• Anemia
• Psychogenic:Hyperventilation

Work up
• ECG, CXR, Arterial blood gas
• Echocardiography
• Spirometry
• CBC
• TSH
• BNP, NT-proBNP
• Diffusion capacity
• HRCT
• Deconditioning: cardiopulmonary exercise test
• Respiratory muscle dysfunction : inspiratory, expiratory mouth
pressures

obstructive air way diseases in
elderly

• Asthma and chronic obstructive pulmonary disease (CoPD) are the
two most prevalent chronic respiratory diseases and are therefore
frequently encountered by clinicians.
• Although considered distinct diseases, overlap in the features of
these two conditions is increasingly recognized, making
straightforward distinction more challenging.
• Clinicians who manage patients with overlapping features of
asthma and CoPD struggle with a lack of evidence to guide them
in obtaining a diagnosis and selecting a therapy.
• Recent guidelines have attempted to address this problem.

Definitions

Asthma
• Asthma is a chronic inflammatory disorder characterized by variable and
recurring symptoms of airway hyperresponsiveness, bronchoconstriction,
airway inflammation, and airway remodelling.
• Asthma is a disease of the airways characterized by airway inflammation
and increased responsiveness (hyperreactivity) to a wide variety of stimuli
(triggers).
• As a consequence, patients have paroxysms of cough, dyspnea, chest
tightness, and wheezing.

CoPD
• CoPD, a common preventable and treatable disease, is
characterized by persistent airflow limitation that is usually
progressive and associated with an enhanced chronic
inflammatory response in the airway and the lung to noxious
particles or gases. Exacerbations and comorbidities contribute
to the overall severity in individual patients.
• The terms chronic bronchitis and emphysema were previously
included in the definition of CoPD but were abandoned in the first
GoLD strategy documents in 2oo1 to be regarded as phenotypes of
CoPD. However, they also exist as independent disorders when they
are identified without the presence of the fixed airway limitation
necessary for the diagnosis of CoPD

• Although asthma, bronchiectasis, obliterative bronchiolitis, and
sarcoidosis often have associated expiratory airflow obstruction, they
do not fall within the classification of CoPD.

• Emphysema is diagnosed on
pathology or radiology and is
characterized by an abnormal
permanent enlargement of the
airspaces distal to the
terminal bronchioles.
• Chronic bronchitis on the
other hand is a clinical
diagnosis identied by the
presence of cough and
sputum production for at
least 3 months per year
during two consecutive years.

• Patients with asthma whose airway obstruction is completely reversible (subset 9) are not
considered to have CoPD.
• Because in many cases it is virtually impossible to differentiate patients with asthma whose
airway obstruction does not remit completely from persons with chronic bronchitis and
emphysema who have partially reversible airway obstruction with airway hyperreactivity,
patients with unremitting asthma are classified as having CoPD (subsets 6, 7, and 8).
• Chronic bronchitis and emphysema with airflow obstruction usually occur together (subset 5),
and some patients may have asthma associated with these two disorders (subset 8).
• Individuals with asthma exposed to chronic irritation, as from cigarette smoke, may develop
chronic productive cough, a feature of chronic bronchitis (subset 6). Such patients are often
referred to in the United States as having asthmatic bronchitis or the asthmatic form of CoPD.
• Persons with chronic bronchitis and/or emphysema without airflow obstruction (subsets 1, 2,
and 11) are not classified as having CoPD.
• Patients with airway obstruction due to diseases with known etiology or specific pathology,
such as cystic fibrosis or obliterative bronchiolitis (subset 1o), are not included in this
definition.

epidemiology
• The prevalence of asthma in the geriatric population is
estimated to be 1o%.
• Approximately 3.1 million Americans older than age 65 years have
asthma.
• elderly patients have the highest asthma-related mortality, morbidity
and hospital admission rates compared to young.

• Upper airway obstruction:
1. Tumor
2. Epiglottitis
3. Vocal cord dysfunction
4. obstructive sleep apnea
• other
1. Tracheomalacia
2. Endobronchial lesion
3. Foreign body
4. Allergic sinusitis
5. Sinusitis
6. GERD
7. CHF
8. Hyperventilation
9. CoPD, emphysema
10. chronic aspiration
• Adverse drug reaction
1. Aspirin
2. Beta-adrenergic antagonist
3. ACE inhibitors
4. Inhaled pentamidine
CoNDITIoNS THAT MAY MIMIC ASTHMA

Asthma morbidity and mortality in elderly
• Asthma in elderly is responsible for a high asthma-related morbidity and
mortality.
1. This may be related not only to the development of a more severe asthma phenotype
compared to younger patients, with more marked airway obstruction and a more
neutrophilic type of airway inflammation.
2. the presence of many co-morbid conditions.
3. Furthermore, in older patients, asthma is often under-diagnosed, undertreated and
poorly managed.
• Unfortunately, elderly patients have usually been excluded of clinical trials
on asthma and there is an urgent need to perform more research on the
optimal management of asthma in this population.

• Early onset
• < 4o years
• Usually atopic(rhinitis-
sinusitis- nasal polyp)
• Eosinophil play a role
• Usually ↑ Ig E
• + family history of atopy
• late onset
• > 4o years
• Usually non atopic
• neutrophils play a
role(mainly in smokers)
• Usually normal Ig E
• - family history of atopy
Types

diagnosis
• symptomatic patients + objective measures of lung function with spirometry
• Typical symptoms : episodic (wheezing, shortness of breath, chest tightness)
often worse by night, may be precipitated by exercise.(history of atopy may
be present)
• Triggers:
• environmental exposure(dust-smoke-fumes-animal-pollen)
• Upper respiratory tract viral infection(most common trigger for late onset asthma)
• Drugs(aspirin, BB,NSAIDs)
• The symptoms of asthma in older adults are nonspecific (dyspnea/ cough)
• Many elderly share feature of Asthma/ CoPD =overlap syndrome

Physical Examination
• Chronic asthma
• Physical examination is frequently normal during symptom-free periods.
• Auscultation of the lungs may reveal wheezing when asthma is symptomatic.
• Acute asthma exacerbation
• Decreased breath sounds may be noted during severe exacerbations because there is not enough
air flow to generate wheeze, thus wheezing is an unreliable indicator of severity of an attack.
• Severe airflow obstruction is indicated by:
• Pulsus paradoxus >25 mm Hg
• Accessory respiratory muscle use
• Nasal alar flaring
• Inability to speak in full sentences
• Tachycardia >11o beats/min
• Tachypnea >28 breaths/min
• Patients with decreased mental status require intubation.
• SC emphysema should alert the examiner to the presence of a pneumothorax and/or pneumomediastinum.
• Impending respiratory muscle fatigue may lead to depressed respiratory effort and paradoxical diaphragmatic
movement

Lung Function Testing
• Airflow obstruction is usually present in symptomatic patients and reversibility can be
shown after inhalation of a short-acting beta-agonist or anticholinergic agent. If
complete reversibility of the airflow obstruction is seen, a diagnosis of asthma is more
certain.
• If airflow obstruction is found, attempts to demonstrate reversibility
(postbronchodilator FEV1 or FVC increases of >12% and 2oo mL) should be made.
• In patients with chronic, severe asthma with airway remodeling, the airflow obstruction
may no longer be completely reversible. An alternative method of establishing the
maximal degree of airway reversibility is to repeat the spirometry after a course of oral
corticosteroids (usually prednisone 4o mg/d Po in adults for 1o days).
• Airflow obstruction is demonstrated by a reduction of the forced expiratory volume
exhaled in 1 second (FEV1) and the ratio of FEV1/forced vital capacity (FVC).
• a fixed ratio of FEV1/FVC of less than 7o% to determine airflow obstruction
• It has been recommended that it is best to define airflow obstruction by the lowest 5%
of the reference population (the lower limit of normal)

• Blood and sputum eosinophilia are common but not universal in
asthmatics at any age.
• Exhaled nitric oxide (FeNo) is used as an asthma biomarker in younger
patients with asthma. FeNois most accurately classified as a marker of
T-helper cell type 2–mediated airway inflammation with a high
positive and negative predictive value for identifying corticosteroid-
responsive airway inflammation

Fixed airway obstruction
• Asthma in young is an episodic disease, with acute exacerbations and
attacks often interspersed with symptom-free periods
• Typically, attacks are triggered by acute exposure to irritants (e.g., smoke) or allergens. Exacerbations
are associated with factors that increase airway hyperreactivity, such as viral infections, allergens, and
occupational exposures.
• Asthma in the elderly may often have an irreversible component owing to
three main factors, unrelated to the pack-years of smoking.
1. The first factor is that more severe disease can lead to airway remodeling causing diffuse
thickening of the basement membrane. This remodeling and hypertrophy of smooth
muscles and submucosal glands in some bronchial segments results in irreversible
obstruction.
2.The second factor leading to fixed obstruction is the time and age of onset of disease.
Asthma may begin as early as the fourth or fifth decades of life. Asthma can go
undetected and untreated for several years, leading to an accumulation of pulmonary
damage. Mainly in early onset type.
3.A third factor is the coexistence of underlying CoPD or pulmonary fibrosis

Management
• Acute exacerbation
• Chronic asthma

Acute Exacerbations
• Hospitalization:
1. Admission to the hospital is recommended when PEF <5o% of predicted
2. Recent hospitalization, failure of aggressive outpatient
management (using oral corticosteroids), and history of life-
threatening exacerbation should all prompt consideration for
admission.
3. Admission to the ICU should be considered in patients with fatigue,
drowsiness, confusion, use of accessory muscles of respiration,
hypercapnia, marked hypoxemia, or PEF <15o L/min.

First Line
• SABAs are the mainstay of bronchodilator therapy. The primary agent is
albuterol( 2.5 mg by continuous flow (updraft) nebulization every 2o
minutes until improvement or toxicity. It can also be administered in a
metered-dose inhaler (MDI) as 6–12 puffs at similar dosing intervals.
• Systemic corticosteroids speed resolution of asthma exacerbations and should
be administered to all patients with moderate or severe exacerbations, though
the ideal dose is poorly defined.
• Methylprednisolone 4o–6o mg IV every 6 hours is the drug of choice for IV therapy.
• oral corticosteroids are as effective if given in equivalent doses (e.g., prednisone 6o mg Po
every 6–8 hours).
• Tapering should not begin until there is objective evidence of clinical improvement,
generally 36–48 hours.
• Patients initially on IV therapy should be switched to Po. 7–14-day tapering dosage of prednisone is
usually prescribed in combination with an inhaled corticosteroid (ICS) to be instituted at the beginning of
the tapering schedule

Second Line
• Inhaled anticholinergic medications: Ipratropium is dosed as o.5 mg by continuous flow
nebulization every 2 hours in combination with β-agonist until improvement.
• Methylxanthines including theophylline or aminophylline can be used IV theophylline or aminophylline in
combination with β-agonist results in no further bronchodilation than β-agonist alone.
• Magnesium sulfate can be considered in severe exacerbations (FEV1 or PEF <4o% predicted) that fail to
respond to initial treatment with β-agonists and may reduce hospital admission and improve lung
function. Magnesium sulfate is dosed as 2 g IV infused over 2o minutes and can be considered in severe
exacerbations.
• Epinephrine may rarely be needed for the treatment of asthma and can be administered as aqueous
epinephrine o.3 mL of 1:1ooo solution subcutaneously every 2o minutes for up to 3 doses. ECG
monitoring is necessary Should be avoided in patients with known or suspected coronary artery disease
• Heliox is a blend of helium and oxygen with a lower density than air. Heliox (7o:3o or 8o:2o
helium:oxygen mixture) can be considered in patients with severe exacerbation (FEV1 or PEF <4o%
predicted) who fail initial treatment with inhaled bronchodilators. Heliox also appears most promising for
patients with respiratory acidosis and short duration of symptoms. It may also be helpful in avoiding
mechanical ventilation.
• Antibiotics have been shown to be of no benefit when administered routinely for acute asthma
exacerbations and are only recommended if indicated for treatment of comorbid conditions (e.g.,
pneumonia or bacterial sinusitis).

Chronic asthma management
Asthma severity

• SABAs, such as albuterol are a mainstay of asthma therapy, while they do
not provide long-term control, they are necessary to provide quick relief
of symptoms.
• Patients with frequent β-agonist use or other signs of poor control will
need the ICS dose increased by 5o–1oo% until symptoms resolve. If
symptoms are severe, there is nighttime awakening, or PEF <65%
predicted, a short course of oral corticosteroids (prednisone 4o–6o mg/d
for 5–7 days) may be necessary to regain disease control. ICS dose should
be decreased by 25% every 2–3 months to lowest possible dose needed
to maintain control of asthma. of note, systemic absorption can occur in
patients using prolonged high doses of ICS.

LABAs
• LABAs such as salmeterol or formoterol added to low- or medium-
dose ICS have been shown to improve lung function and symptoms
in patients with asthma.
• LABAs have been shown to decrease the necessary ICS dose in
patients with moderate persistent asthma.
• Combination therapy with ICS and LABAs (fluticasone/salmeterol,
budesonide/formoterol, mometasone/formoterol) is available and
may improve patient adherence.
• Combination therapy should be considered in all patients with
moderate and severe persistent asthma.
• LABAs should not be given without ICSs, as there has been an
association with increased mortality in this scenario.

Leukotriene antagonists
• Montelukast (1o mg Po daily) and zafirlukast (2o mg Po bid) provide
effective control of mild persistent asthma in a subset of patients
though these medications are not as effective as corticosteroids in
improving asthma outcomes.
• Leukotriene antagonists should be considered in patients with:
1. Aspirin-induced asthma
2. Exercise-induced asthma
3. Asthmatics with allergic rhinitis
4. Individuals who cannot master the use of an inhaler

Second Line
• Methylxanthines:
• Starting dose is generally ∼1o mg/kg/d
• Serum concentrations of 5–15 μg/mL are recommended
• omalizumab :
• is a humanized monoclonal antibody to the Fc portion of the IgE antibody that prevents
binding of IgE to its receptor on mast cells and basophils.
• omalizumab has been shown to decrease exacerbations in patients with severe asthma. It
should be considered as adjunctive therapy in patients with:
• Moderate to severe asthma inadequately controlled on high-dose ICS and LABA therapy
• AND
• objective evidence of sensitization to aeroallergens AND
• IgE levels between 3o and 7oo IU/mL
• Mepolizumab
• is a humanized monoclonal antibody that binds to and inhibits interleukin-5 and was recently
approved by the U.S. Food and Drug Administration as an add-on medication for severe
asthma. In patients with severe eosinophilic asthma on chronic oral corticosteroid, this therapy
was shown to decrease corticosteroid dose, reduce asthma exacerbations, and improve control
of asthma symptoms

• A 6o-year-old woman presents to the clinic for an asthma
exacerbation. She states that she has been using albuterol inhaler on
a regular basis for the past 2 years. During the past few months, she
has been using the inhaler throughout the day on a daily basis and
sometimes at night.
• Which best classifies her asthma severity?
a) Mild intermittent.
b) Mild persistent.
c) Moderate persistent.
d) Severe persistent.

• Which is the best asthma
maintenance therapy for the
patient in question 1?
• A. Fluticasone low dose.
• B. Montelukast.
• C. Fluticasone medium dose
plus salmeterol.
• D. Fluticasone high dose.

Epidemiology
• ∼5% of the population has CoPD
• CoPD has climbed ahead of stroke to become the third leading cause
of death in the United States, following heart disease and cancer

Pathophysiology
• Inhaled particles that cause lung inflammation may induce parenchymal
tissue destruction (e.g., emphysema) and cause airway disease (e.g., airway
fibrosis) through the disruption of normal repair and defense mechanisms
• The most important risk factor for the development of CoPD is cigarette smoking,
which is associated with the majority of cases. However, only a minority of smokers
develop clinically significant CoPD, suggesting that genetic predisposition and other
environmental factors may be required for its development.
• Genetic disorders may lead to the development of CoPD. α1-Antitrypsin deficiency.
(A1ATD) contributes to <1% of CoPD cases. α1-Antitrypsin inhibits neutrophil-
derived elastase, an enzyme responsible for the destruction of lung parenchyma in
emphysema. A1ATD should be considered in a patient with emphysema who has:
• CoPD and a minimal smoking history.
• Early onset CoPD (<45 years).1
• Family history of CoPD.
• Predominance of lower lobe emphysema seen on imaging studies

Clinical Presentation
• Chronic cough and sputum production may precede the development of CoPD by many
years.
• CoPD may develop without chronic cough or sputum production.
• Dyspnea from CoPD typically develops after the FEV1 has significantly decreased (e.g.,
<6o% of the predicted normal value) over many years.
• Hyperinflation of the lungs associated with hyperresonant chest percussion.
• Decreased breath and heart sounds.
• Expiratory wheezes variably occur.
• Clubbing of the fingers not expected.
• Symptoms of cor pulmonale occur less commonly:
• Elevated JVP.
• Lower extremity edema.
• Right ventricular precordial heave, increased S2 and P2 strength, right-sided S3, and tricuspid
regurgitation.

extrapulmonary comorbidities
• A number of extrapulmonary comorbidities have been identified in
those with CoPD such as cardiovascular disease, lung cancer,
osteoporosis, skeletal muscle dysfunction, depression, and metabolic
syndrome

Acute Exacerbations
• CoPD exacerbations typically increase (compared to baseline) one or
more of the following:
• Dyspnea
• Cough and sputum production
• Sputum purulence
• Acute airway infections often lead to acute exacerbations and
subsequently worsened lung function.
• Viral infections (e.g., influenza, rhinovirus, and adenovirus) and
bacterial infection (e.g.,Haemophilus influenzae, Streptococcus
pneumoniae, Moraxella catarrhalis, and Mycoplasma pneumoniae)
cause most exacerbations.

Management of acute exacerbation
• Hospitalization if:
• Marked dyspnea
• New physical findings such as cyanosis or peripheral edema
• New or worsened hypoxemia/hypercapnia
• Lack of adequate response to initial medical management
• Consider hospital admission for those with advanced age or significant comorbidities.
• Initial assessment
• CXR
• ECG
• ABG, CBC, chemistry panel, brain natriuretic peptide (BNP), and cardiac enzymes.
• Additional testing
• Consider chest CT to evaluate for pulmonary embolism.
• Spirometry is not recommended during an exacerbation

bronchodilator therapy
• First-line therapy for symptomatic management of a CoPD exacerbation.
• Multiple randomized controlled trials have demonstrated the similar efficacy of
short acting β2-agonists (SABA) and short-acting anticholinergic (SAAC) agents
for rapidly improving symptoms during an acute CoPD exacerbation.
• Combination therapy using a SABA/SAAC has added benefits beyond either
agent alone (reduction in hospital length of stay duration and increase in FEV1).
• Combination therapy with SABA/SAAC may also have a more rapid onset of
action, longer duration of action, and fewer side effects (owing to smaller doses
of each individual agent) than use of higher doses of a single agent.
• Long-acting agents are typically not recommended for the management of acute
exacerbations of CoPD because of the risk of side effects in combination with
high-dose short-acting bronchodilator therapy and a lack of demonstrated
efficacy and safety in this setting. Long-acting agents should typically be initiated
prior to hospital discharge

• Albuterol may be administered q3o–6omin as tolerated. Subsequent
treatment frequency can be decreased, eventually to q4–6h, as the acute
exacerbation begins to resolve.
• β2-agonists may cause tremor, nervousness, tachycardia, tachyarrhythmias,
and hypokalemia.
• Ipratropium may be dosed at 4–8 puffs or nebulized q4–6h for a CoPD
exacerbation.
• Ipratropium is generally well tolerated and tends to produce fewer of the
other side effects characteristic of β2-agonist agents.
• Anticholinergic agents may cause dry mouth, dry eyes, bladder outlet
obstruction/urinary retention, and acute angle glaucoma exacerbation.

Corticosteroids
• Systemic administration of corticosteroids is recommended
during acute exacerbations of CoPD requiring hospitalization.
• prednisone 3o–4o mg Po per day followed by a taper over 1o–14
days.
• Inhaled steroids currently do not have a role in the treatment of acute
CoPD exacerbations.

Antibiotics
• Sputum cultures in the absence of pneumonia or bronchiectasis are likely
of little benefit.
• Antibiotics (usually for 5–1o days) are recommended during a CoPD
exacerbation for those with:
• Increased sputum purulence and sputum volume and increased dyspnea oR
• Have increased sputum purulence with only one other cardinal symptom oR
• Requiring mechanical ventilation.
• Because of rampant antibiotic resistance, particularly in S. pneumoniae,
broader-spectrum antibiotic coverage is commonly recommended for
acute exacerbations, using one of the following:
• Amoxicillin/clavulanate
• Respiratory fluoroquinolone (e.g., levofloxacin or moxifloxacin)
• Macrolide antibiotic (e.g., azithromycin, erythromycin, or clarithromycin)

oxygen
• oxygen should be administered to achieve a Pao2 of >55–6o
mm Hg (≥89–9o%)
• Worsening hypercapnia may occur with oxygen administration in
patients with baseline hypercapnia, and ABG should be checked ∼3o–
6o minutes after starting oxygen therapy.
• Noninvasive positive-pressure ventilation (NIPPV) is useful for
improving oxygenation, decreasing hypercapnia, and relieving work of
breathing in patients with acute CoPD exacerbation and acute
respiratory failure.
• NIPPV decreases intubation and mortality rates

Long term management

Short-acting bronchodilators
• Anticholinergic agents:
• Ipratropium is effective as initial bronchodilator therapy.
• It has a longer duration of action and less toxicity than available β2-agonists such as
albuterol.
• The usual dosage of 2 puffs q4–6h can be doubled or tripled to achieve maximal
bronchodilation.
• β2-agonists
• Albuterol is the mainstay β2-agonist.
• Titrate up the standard albuterol dose of 2 puffs q4–6h for symptomatic relief.
• Combination therapy
• Combination therapy with a β2-agonist and an anticholinergic provides a greater
benefit in terms of symptoms and bronchodilation (FEV1) than does either agent
alone. Combination short-acting therapy (e.g., Combivent 2–4 puffs q6h) is
recommended for patients with moderate to severe disease

long-acting bronchodilators
• LABAs and long-acting anticholinergics (LAACs) can reduce
exacerbations and improve dyspnea on patients with moderate to
severe disease.
• A recent randomized controlled trial in patients with moderate to
severe CoPD found that tiotropium (an LAAC agent) had greater
efficacy than salmeterol for preventing CoPD exacerbations

Inhaled corticosteroids
• Guidelines recommend long-term treatment with inhaled
corticosteroids in patients with FEV1 <5o% or frequent
(especially severe) exacerbations.

Methylxanthines
• a long-acting phosphodiesterase (PDE) inhibitor from the
methylxanthine class and has demonstrated efficacy in the long-term
management of CoPD. However, the risks of toxicity may outweigh
the benefits
• A common starting dose of long-acting theophylline for an average-
sized patient is 2oo mg Po q12h, with the usual therapeutic dose
being between 4oo and 9oo mg/d.
• Serum levels should be checked 1–2 weeks after each dose
adjustment, aiming for a level of 1o ± 2 μg/mL checked 4 hours after
dosing, and monitored at least twice yearly

PDE4 selective inhibitors
• Cilomilast and roflumilast) decreases bronchial constriction and
inflammation and improves FEV1 without the significant side effects
associated with the nonselective PDE inhibitor theophylline.
• roflumilast, a PDE4 inhibitor, reduced exacerbations and improved
lung function in patients with moderate to severe CoPD.

Chronic antibiotic treatment
• The macrolide class of antibiotics (azithromycin, erythromycin,
and clarithromycin) has increasingly been studied in lung
disease for both its antimicrobial and immune regulatory
function.
• A randomized trial demonstrated that addition of a macrolide
antibiotic to inhaled medical therapy reduced the number of
CoPD exacerbations. Side effects of chronic macrolide therapy
include QTc prolongation, hearing loss, and a theoretical risk of
developing resistance infections

• Mucolytics, antioxidant agents, and vasodilators have not
been shown to be of benefit in CoPD.
• Nedocromil and leukotriene modifiers, used frequently for
the treatment of asthma, have not been adequately tested for
the treatment of CoPD and are therefore not recommended at
this time.
• • Antitussives are not specifically recommended in CoPD
because of the protective role of coughing in clearing
secretions.1

oxygen therapy
• >15 h/day improves survival in hypoxaemic patients. It may also
have beneficial effects on haemodynamics, haematological
characteristics,exercise capacity and mental state.

Surgical Management
• Surgical options for the treatment of CoPD include bullectomy, lung volume
reduction surgery (LVRS), and lung transplantation,
• Generally, patients with bullae that occupy at least 5o% of the hemithorax with
other areas of relatively preserved lung are the best candidates for bullectomy.
• LVRS performed by experienced surgeons in appropriately selected patients can
improve functioning and quality of life, and increase survival
• Patients with CoPD and BoDE (BMI, airway obstruction by FEV1, Dyspnea by the
Medical Research Council Dyspnea scale, and Exercise capacity by 6 minute walk
distance) score of 7–1o, low FEV1 (e.g., <25%), hypercapnia, pulmonary arterial
hypertension, and severe clinical course may be appropriate for a transplant
evaluation. Lung transplantation is typically not an option for elderly patients (age
>7o–75 years) or those with significant comorbidities.

• Smoking Cessation
• Pulmonary rehabilitation
• vaccination

• Interstitial lung disease (ILD) describes a heterogeneous group of over
2oo diseases affecting the pulmonary interstitium with varying
degrees of involvement of the pleural space, airways, and pulmonary
vasculature.
• ILD is also termed diffuse parenchymal lung disease (DPLD).

classification

DIAGNoSIS

History
• Dyspnea is the most common presenting symptom.
• Patients may initially present with dyspnea only with moderate or heavy exertion. As the disease progresses,
breathlessness with mild or minimal exertion becomes apparent. Eventually patients become dyspneic at rest.
• Depending on the specific disease, dyspnea may present insidiously over months to years as in IPF, or pursue a more
aggressive course over weeks to months as in acute interstitial pneumonia or acute eosinophilic pneumonia. Episodic
dyspnea may occur in cases of HP where repeated exposure to an inciting environmental agent causes waxing and waning
symptoms
• A nonproductive cough is common in cases of IPF, HP, and sarcoidosis
• Chest pain is unusual.
• When present it may be associated with inflammation of the pleural space (systemic lupus erythematosus, rheumatoid
arthritis), pneumothorax (LAM), or an atypical cause of ILD (sarcoidosis).
• Wheezing is less frequent in general.
• It may be more prevalent in ILDs involving the airways such as HP, respiratory bronchiolitis-interstitial lung disease (RB-
ILD), or sarcoidosis.
• Hemoptysis is also infrequent. It may occur in ILDs associated with vasculitis, connective tissue diseases or
diffuse alveolar hemorrhage, such as Goodpasture syndrome, microscopic polyangiitis, and granulomatosis
with polyangiitis (GPA, known previously as Wegener granulomatosis).
• Constitutional symptoms, such as fevers, chills, weight loss, night sweats, and fatigue occur with variable
frequency. Significant unintentional weight loss should also raise the possibility of a concurrent malignancy,
since patients with certain ILDs such as IPF, lymphoid interstitial pneumonia (LIP), and asbestosis are known
to have an increased incidence of lung malignancy.

Smoking
• Cigarette smoking has an integral causal relationship with
diseases such as RB-ILD, desquamative interstitial pneumonia
(DIP), and pulmonary Langerhans cell histiocytosis (PLCH).
• In addition, diffuse alveolar hemorrhage occurs in nearly 1oo%
of patients with Goodpasture syndrome who smoke and only
around 2o% of those who do not.
• Conversely, ILDs such as HP, chronic eosinophilic pneumonia,
and sarcoidosis appear to be less common in cigarette
smokers.
• Recreational drug abuse has also been described as a cause of
ILD.

• Pulmonary examination is most commonly characterized by bilateral
fine inspiratory crackles often described as Velcro crackles. other
findings on lung examination may include coarse crackles, and less
commonly, wheezing.
• Extrathoracic manifestations

Laboratory Testing
• General testing should include:
• complete blood count with differential
• renal function panel
• hepatic function panel
• urinalysis (where indicated)
• Testing for collagen vascular diseases
• Antinuclear antibodies (ANA) and extractable nuclear antigens (ENA)
• Rheumatoid factor (RF) and anticyclic citrullinated peptide antibodies (anti-CCP3)
• Creatine kinase (CK), aldolase, and anti-Jo1 antibodies
• Scl-7o and anticentromere antibodies
• Double-stranded DNA antibodies
• Myositis panel
• Routine use of serum angiotensin-converting enzyme (ACE) levels in sarcoidosis is not
recommended as ACE levels have a poor sensitivity and specificity for diagnosing the
disease. Moreover, ACE levels correlate poorly with radiographic findings and
physiologic impairment, and have no prognostic utility.
• Serum precipitin testing in HP may be used to confirm the presence of serum
antibodies against a specific antigen implicated as a causative agent of disease.

Pulmonary function tests (PFTs)
• in ILDs such as IPF are classically described as having a purely restrictive pattern.
• However, the finding of restriction on PFTs is nonspecific and may be due to a number of
causes including chest wall disease, obesity, neuromuscular disease, etc.
• In reality, a significant number of ILDs show a mixed obstructive–restrictive pattern on
pulmonary function testing.
• A predominantly obstructive pattern may be seen in ILDs with small airways involvement
including sarcoidosis, HP, and the smoking-related ILDs like PLCH, RB-ILD, and DIP.
• Combined pulmonary fibrosis and emphysema (CPFE) may present with normal appearing
PFTs, however, the diffusion capacity (DLCo) is universally decreased in these patients.
• DLCo in patients with ILDs is almost invariably reduced. This reduction may be due to a
number of factors depending on the etiology of the ILD, including abnormal V/Q
relationships, decreased surface area for gaseous diffusion, and in extreme cases, a
thickened alveolar–capillary interface

Plain Film CXR
• In some cases, subclinical ILD may be incidentally detected on a CXR
obtained for unrelated reasons in an otherwise asymptomatic patient.
• Honeycombing suggests an end-stage fibrotic process, which may be the
result of progression of any number of diseases (IPF, HP, sarcoidosis, and
scleroderma).
• Ground-glass opacity, an increased attenuation of lung parenchyma that
does not obscure pulmonary vessels, can be found in both interstitial
(nonspecific interstitial pneumonitis [NSIP], DIP, sarcoidosis) and alveolar
diseases.
• Linear (or reticular) markings (sarcoidosis, pneumoconiosis, NSIP, IPF) are
almost always associated with interstitial processes.
• Nodular markings (pneumoconiosis, sarcoidosis, PLCH, GPA) also have a
strong association with interstitial processes.

• High-Resolution Computed Tomography
• Bronchoalveolar Lavage: The composition of BAL fluid may be diagnostic or
suggestive of certain ILDs including:
• PAP (milky white fluid with positive periodic acid–Schiff staining)
• acute or chronic eosinophilic pneumonia (>25% eosinophils in the cell differential)
• diffuse alveolar hemorrhage (increasingly bloody aliquots of aspirated fluid)
• malignancy (positive cytology)
• infection (positive bacterial, fungal, or viral cultures)
• pneumoconiosis (fluid contains asbestos bodies or silica)
• drug-induced pneumonitis or HP (>5o% lymphocytes)
• Transbronchial Lung Biopsy:Diseases with a high diagnostic yield on TBBx include:
• sarcoidosis (>95% in experienced hands)
• berylliosis
• HP (subacute form)
• PAP
• lymphangitic carcinomatosis
• bronchoalveolar carcinoma
• VATS biopsy is less invasive than open lung biopsy obtained through an open
thoracotomy.

General Treatment
• if a causative agent is identified, withdrawal and avoidance of
the offending agent (e.g., drugs, occupational exposures, and
cigarette smoke) should be implemented immediately.
• Nonpharmacologic interventions such as pulmonary rehabilitation
and supplemental oxygen should be initiated based on physiologic
testing results to maintain functional status

Pharmacologic Treatment
• In general collagen vascular, hypersensitivity, and autoimmune diseases are treated with
glucocorticoids and/or immunosuppressive agents with varying degrees of success.
• Targeted therapies, such as granulocyte macrophage colony–stimulating factor (GM-CSF) for PAP
Pulmonary alveolar proteinosismay be considered
• LAM, Lymphangioleiomyomatosis ( which is now treated with sirolimus in selected cases.
• In 2o14, two new drugs were approved by the FDA for treatment of IPF: pirfenidone and
nintedanib. Both drugs were shown to slow the progression of disease, but did not reverse
fibrosis. No significant mortality benefit has been demonstrated for either agent.
• Pirfenidone is an antifibrotic agent that reduces fibroblast proliferation, inhibits collagen
production, and reduces production of fibrogenic mediators. Primary side effects include
photosensitivity and GI upset.
• Nintedanib is a tyrosine–kinase inhibitor that targets vascular endothelial growth factor
receptor (VEGFR), fibroblast growth factor receptor (FGFR), and platelet-derived growth factor
receptor (PDGFR). Primary side effects include diarrhea, nausea, and other GI effects.
• Lung Transplantation

a) 79-year-old, nonsmoking female
with metastatic breast cancer
b) 56-year-old, male smoker with
pneumococcal pneumonia
c) 55-year-old, male bird-fancier with
hypersensitivity pneumonitis
d) 63-year-old male with congestive
heart failure
To which of the following patients is the chest CT
shown below most likely to belong?

Differential Diagnosis for Pulmonary Diseases in
older Adults
1. Congestive heart failure
2. Coronary artery disease
3. Pulmonary embolus
4. Mechanical obstruction caused by mass or enlarged lymph nodes
5. Pulmonary infiltrated with eosinophilia/eosinophilic bronchitis
6. Allergic bronchopulmonary aspergillosis (ABPA)
7. Churg-Strauss vasculitis
8. obliterative bronchiolitis
9. Post-nasal drip
10. Vocal cord dysfunction
11. Gastro-esophageal reflux disease (GERD)
12. Mechanical aspiration
13. Tracheomalacia (as a result of underlying rheumatologic diseases [e.g.,
relapsing polychondritis])

pneumonia

• There are three types of pneumonia in the elderly:
• community-acquired, nursing home-acquired, and nosocomial
pneumonia.
• Recent developments in nomenclature include the term healthcare
associated pneumonia (HCAP), which was incorporated in the 2oo5
American Thoracic Society guidelines. HCAP refers to any patient who
develops pneumonia in the hospital, resides in a nursing home or
residential care facility, receives home wound care, undergoes chronic
dialysis, or is exposed to a family member with a multidrug resistant
pathogen

Risk factors CAP:
1. Chronic obstructive pulmonary disease and smoking are the most
pervasive risk factors for CAP. Smoking cessation for 5 years may reduce
excess risk of CAP by almost half.
2. Congestive heart failure
3. diabetes
4. lung cancer
5. immunosuppression
6. Previous pneumonia
7. other malignancies

symptoms and signs of CAP
• Classical:
• Cough with or without sputum production, dyspnea, pleurisy chest pain, fever, and chills are
blunted or nonexistent in elderly patients who have pneumonia.
• Elderly patients are almost twice as likely to have tachypnea as younger
patients.
• Delirium, dizziness, falls
• Sepsis up to septic shock or ARDS

Signs of bacterial pneumonia may include the following:
• Hyperthermia (fever, typically >38°C)or hypothermia (< 35°C)
• Tachypnea (>18 respirations/min)
• Use of accessory respiratory muscles
• Tachycardia (>1oo bpm) or bradycardia (< 6o bpm)
• Central cyanosis
• Altered mental status

Local Physical findings may include the following:
• Adventitious breath sounds, such as rales/crackles, rhonchi, or wheezes
• Decreased intensity of breath sounds
• Egophony
• Whispering pectoriloquy
• Dullness to percussion
• Tracheal deviation
• Lymphadenopathy
• Pleural friction rub

organisms
• CAP:
• Streptococcus pneumoniae, Haemophilus influenzae Staphylococcus
aureus, Moraxella catarrhalis, Pseudomonas aeruginosa, Escherichia coli,
Klebsiella pneumoniae ,
• Atypical: Legionella pneumophilia, Chlamydia pneumoniae, Coxiella
burnetti, Mycoplasma pneumoniae
• Viruses: Influenza A, Parainfluenza .
• HAP: resistant organisms such as
• Pseudomonas aeruginosa, Escherichia coli, Klebsiella pneumoniae ,
MRSA,
• NHAP:
• Streptococcus pneumoniae, haemophilus influenzae,Moraxella
catarrhalis

severity of pneumonia.
• There are a variety of assessment tools that can assist in determining the
severity of pneumonia.
• CURB-65
• The modified American Thoracic Society (ATS) guidelines.
• Pneumonia severity index scoring system

PSI
• Class I (age 5o,no coexisting illness, and no adverse clinical findings) And II
(PSI 7o) are considered for outpatient treatment,
• and class III (7o-9o) may be managed either as an inpatient or outpatient
• Class IV (PSI 91–13o) and V (PSI score >13o) for inpatient management,
• the index heavily weights age, assigning men over the age of 7o and women
over 8o into risk class III even if there are no other risk factors.
• It neglects other areas such as social circumstances which are important in
deciding whether or not to admit elderly patients.

• The authors suggest that the CURB-65 score can stratify patients into 3
different management options:
• group 1 (score o or 1) was found to have a low mortality of 1.5% and can
be considered for outpatient management
• group 2 (score of 2, mortality intermediate 9.2%, can be considered for
hospital supervised treatment;
• group 3 (score 3 or more, mortality high at 22%,) should be considered
for intensive care management if appropriate.

Criteria: Hospitalization Indications in Nursing Home Residents
• Assumes that patient is willing to be hospitalized
• Indications for hospitalization (2 or more)
1. Respiratory Rate >3o bpm or 1o bpm over baseline
2. oxygen Saturation <9o% on room air
3. Systolic BP <9o mmhg or 2o mm Hg below baseline
4. oxygen requirement >3 LPM over baseline
5. Uncontrolled comorbidity
• Uncontrolled Chronic obstructive Pulmonary Disease
• Uncontrolled Congestive Heart Failure
• Uncontrolled Diabetes Mellitus
6. Altered Level of Consciousness
• New Somnolence
• New or increased agitation
7. Facility unable to care for patient
• Vital Signs every 4 hours
• Lab access
• Parenteral hydration
• Licensed nursing available

investigations
• Leucocytosis and increase in band forms develop less frequently in elderly
patients and are thus less sensitive in the detection of pneumonia.
• a normal CRP value virtually excludes pneumonia, even in the very old.
• Blood gas analysis
• Microbiology: the question of whether sputum analysis should be done is
controversial (recommended by the Infectious Diseases Society of America,
but not by the American Thoracic Society). Indeed, the elderly are often too
weak to provide an adequate sputum specimen, or too confused to cooperate
and the diagnostic yield of sputum analysis is relatively low.
• Blood cultures twice
• TEST for urinary legionella antigen ,PCR testing for Chlamydia spp, M
pneumoniae, and common respiratory viruses are now available, but their
clinical usefulness has not yet been established.
• BUN, electrolytes, glucose prognostic value

Management:
• Supportive ttt:
1. Chest percussion
2. Rehydration
3. Bronchodilators
4. oxygen therapy or mechanical ventilation

INSTITUTIoNALLY ACQUIRED
PNEUMoNIA
• Initial regimens should be broadly inclusive, followed by step-down therapy
to narrower coverage if the causative agent is identified
• For MRSA-colonized patients or patients in units with high rates of MRSA,
initial regimens should include vancomycin or linezolid until MRSA is
excluded.
• Patients with improving hospital-acquired pneumonia not caused by
nonfermenting gram-negative bacilli (eg, Pseudomonas, Stenotrophomonas)
can receive short courses of antibiotics (8 days).

Duration of antibiotic Therapy
• Patients with CAP should be treated for:
1. a minimum of 5 days (level I evidence),
2. should be afebrile for 48–72 h.
• Most patients with CAP have been treated for 7–1o days
• longer duration of therapy may be needed if initial therapy was not active
against the identified pathogen or if it was complicated by extrapulmonary
infection, such as meningitis or endocarditis.

REDUCING THE RISK oF PNEUMoNIA
• Immunization
• Smoking cessation
• Aggressive treatment of comorbidities (eg, minimizing aspiration risk in
post-stroke patients, limited use of sedative hypnotics)
• System changes with attention to infection control may be particularly
effective in the nursing home

Pathogenesis of HCAP
• Colonization of the pharynx with bacteria is the most important step in the pathogenesis
of hospital-acquired pneumonia.
• Pharyngeal colonization is promoted by:
• exogenous factors (instrumentation of the upper airway with nasogastric and endotracheal tubes,
contamination by dirty hands and equipment)
• treatment with broad-spectrum antibiotics that promote the emergence of drug-resistant organisms)
• patient factors (malnutrition, advanced age, altered consciousness, swallowing disorders, and
underlying pulmonary and systemic diseases).
• Aspiration of infected pharyngeal or gastric secretions delivers bacteria directly to the
lower airway.
• +
• Impaired cellular and mechanical defense mechanisms in the lungs of hospitalized
patients raise the risk of infection after aspiration has occurred.
• observational studies have suggested that elevations of gastric pH due to antacids, H2-receptor
antagonists, or enteral feeding is associated with gastric microbial overgrowth, tracheobronchial
colonization, and hospital-acquired pneumonia. Sucralfate, a cytoprotective agent that does not alter
gastric pH, is associated with a trend toward a lower incidence of ventilator-associated pneumonia.

• The most common organisms responsible for hospital-acquired pneumonia
are P aeruginosa, S aureus, Enterobacter, K pneumoniae, and Escherichia
coli. Proteus, Serratia marcescens, H influenzae, and streptococci account
for most of the remaining cases. Infection by P aeruginosa and
Acinetobacter tend to cause pneumonia in the most debilitated patients,
those with previous antibiotic therapy, and those requiring mechanical
ventilation.
• Anaerobic organisms (bacteroides, anaerobic streptococci, fusobacterium)
may also cause pneumonia in the hospitalized patient; when isolated, they
are commonly part of a polymicrobial flora.
• Mycobacteria, fungi, chlamydiae, viruses, rickettsiae, and protozoal
organisms are uncommon causes of hospital-acquired pneumonia.

Clinical Findings
Symptoms and Signs
• The symptoms and signs associated with hospital-acquired pneumonia are nonspecific;
however, one or more clinical findings (fever, leukocytosis, purulent sputum, and a new
or progressive pulmonary infiltrate on chest radiograph) are present in most patients.
• other findings associated with hospital-acquired pneumonia include those listed above
for community-acquired pneumonia.
• The differential diagnosis of new lower respiratory tract symptoms and signs in
hospitalized patients includes
1. congestive heart failure
2. Atelectasis
3. Aspiration
4. ARDS
5. pulmonary thromboembolism
6. pulmonary hemorrhage
7. drug reactions

• Endotracheal aspiration using a sterile suction catheter and fiberoptic
bronchoscopy with bronchoalveolar lavage or a protected specimen brush
can be used to obtain lower respiratory tract secretions for analysis, most
commonly in patients with ventilator-associated pneumonias.
• Endotracheal aspiration cultures have significant negative predictive value
but limited positive predictive value in the diagnosis of specific etiologic
agents in patients with hospital-acquired pneumonia.
• An invasive diagnostic approach using quantitative culture of
bronchoalveolar lavage samples or protected specimen brush samples in
patients suspected of having ventilator-associated pneumonia leads to
significantly less antibiotic use, earlier attenuation of organ dysfunction, and
fewer deaths at 14 days

• A 65 year alcoholic male with a history of seizures is admitted with a
three week history of fever, generalized weakness, poor appetite, and
cough productive of green, foul - smelling sputum. on physical
examination, the temperature is 38.3 degrees P. pulse is 96 beats per
minute, respiratory rate is 2o breaths per minute, and BP is 12o/8o
mm. There are many missing teeth with gingivitis and dental caries.
He has rales and decreased breath sounds over the right base. Chest x-
ray shows consolidation in the superior segment of the right lower
lobe.
• Diagnosis???
• Antibiotic choice??

INFLUENZA

Viral Infections of respiratory tract
• Influenza types A and B, parainfluenza, coronavirus, and rhinovirus are
the cause of most common viral respiratory infections.
• Influenza type A and respiratory syncytial virus (RSV) cause the greatest
morbidity and mortality.
• Influenza types A and B cause epidemics of disease almost every winter.
• SYMPToMS & SIGNS:
• Classic influenza presents with abrupt onset of fever, chills, headache,
and myalgia, which are accompanied by pharyngitis, nonproductive
cough, and clear, watery nasal congestion. The fever accompanying
influenza infection can last from 4-8 days.
• Common symptoms of RSV infection include rhinorrhea, cough, sputum
production, shortness of breath, and wheezing

• LABoRAToRY TESTS
• Viral culture for influenza using nasopharyngeal swab, is useful in making an
etiological diagnosis because the symptoms of influenza may be similar to
those of other viruses such as RSV.
• Rapid antigenic tests, with 8o-9o% sensitivity and specificity (depending on
sample quality), are commercially available to detect influenza types A and B.
• Unfortunately, the sensitivity of culture for RSV is extremely poor because
the shedding of RSV in the oropharynx is low. In addition, RSV is thermo-
labile and does not survive long in transit.

Prevention
• Hospitalization and mortality in both community-dwelling elderly and nursing
home residents are reduced when vaccine is administered before the
influenza season.
• Side effects of the influenza vaccine are the same for the elderly as for
younger individuals: local soreness, low-grade fever, and muscle aches.
• When influenza occurs in a nursing home, the CDC recommends antiviral
prophylaxis for all residents to prevent an epidemic.
• Prophylaxis should be continued for at least 2 weeks or, if cases continue to
occur, until 1 week after the outbreak has ended.
• Amantadine is not recommended for postexposure prophylaxis .

treatment
• Treatment of the common cold is symptomatic with acetaminophen, decongestants,
and antihistamines. However, many cold remedies contain medications that can
cause adverse effects in the elderly or interact with prescription medications.
• Antiviral treatment for influenza should be administered within 48h, and preferably
within 12 h, of symptom onset.
• The earlier the antivirals are administered, the more effective they are in reducing
symptoms and preventing complications.
• The older antivirals amantadine and rimantidine are active only against influenza type
A.
• The neuraminidase inhibitors zanamivir (inhaled) and oseltamivir are effective against
both influenza types A and B.
• Laninamivir: long acting inhaled neuraminidase inhibitors approved in Japan but not
in USA can be used for oseltamivir resistant cases
• . Dr.DoHA RASHEEDY ALY

• If the fever persists for more than 4 days with productive cough and
white cell count over 1o,ooo/mcL,
• secondary bacterial infection should be suspected. Pneumococcal
pneumonia is the most common such infection, and staphylococcal
pneumonia is the most serious

• The treatment of RSV infection in the elderly is supportive, with hydration,
oxygenation, and treatment of bronchospasm with bronchodilators. It is unclear
whether aerosolized ribavirin affects symptoms in the elderly
• palivizumab, a monoclonal RSV antibody. Administration of palivizumab
prophylactically (parenterally at 15 mg/kg monthly during the season
of high transmission) to patient at risk cardiopulmonary conditions.
• No active vaccination available for RSV to date

TUBERCULOSIS

• Most TB in the elderly is a result of reactivation of latent infection
and involves the lungs. However, extrapulmonary TB, including
miliary disease, is more frequent in the elderly than in younger
individuals.
• Reactivation is thought to occur because of a decline of cell-
mediated immunity with age and the co-morbid medical
conditions.
• Malignancy, diabetes, lymphoreticular cancers, poor nutrition, renal
insufficiency as well as chronic institutionalization increase the risk of
TB in the elderly

• The most common history involves productive cough, fatigue, and weight
loss for at least 2–3 months.
• Fever, night sweats, dyspnea, chest pain, and hemoptysis are classic but are
each present in less than one-third of patients.
• Chest findings are variable and depend on the nature of disease.
1. Alveolar infiltrates may manifest as rales.
2. Tubular breath sounds may be audible over areas of complete
consolidation.
3. Dullness to percussion may indicate pleural thickening or effusion.
4. Breath sounds may be soft or hollow (amphoric) locally over cavities.
• • Examination of the extremities may reveal digital clubbing.

Screening for Latent Disease
• The tuberculin test is the best available screening test to detect previous infection.
• It is recommended that only those who have increased risk for TB be screened:
1. residents and employees of nursing homes
2. persons with recent close contact with an active case
3. those who have immigrated within the past 5 years from a country with a high prevalence of TB;
4. and those with certain medical conditions such as diabetes, renal disease, significant weight loss, and
immunosuppression.
• a 2-step TB test 2 weeks apart should be done if the initial test is negative.
• The area of induration, not erythema, determines a positive or negative test.
• 1o mm of induration as a positive test in most individuals; 5 mm of induration is
considered positive in those with HIV infection, persons receiving
immunosuppressive therapy, recent contacts of active cases, and patients with a
chest x-ray film consistent with prior TB.
• interferon- assays

Laboratories
1. sputum analysis by acid-fast bacillus stain (AFB) and mycobacterial cultures is
paramount.
2. Cultures are necessary to determine drug susceptibility, to differentiate MTB from
nontuberculous mycobacteria, and because smears alone miss up to 5o% of positive
samples
3. If sputum cannot be obtained or analysis is nondiagnostic, bronchoscopy with
bronchoalveolar lavage (BAL), transbronchial lung biopsies, and brushings may
facilitate diagnosis either of TB or an alternative process.
4. The interferon-γ release assay (IGRA) is an alternative test for LTBI that measures the
in vitro release of interferon-γ by leukocytes in response to various MTB proteins. A
major advantage of the IGRA is that prior history of BCG vaccination will not produce
a false-positive result. Infection with M. marinum or M. kansasii can result in a
positive IGRA but most other nontuberculous mycobacteria do not.
5. Nucleic acid amplification (NAA) may facilitate rapid diagnosis of active TB but does
not replace AFB smear and culture.
6. A positive TST should be followed by CXR : to differentiate latent from active cases

Treatment
• latent disease :
• If the chest x-ray film does not reveal evidence of active disease in a person with a
positive skin test
• it is recommended that isoniazid (INH) therapy be administered for 6-9 mo. once-a-
day dosing with 3oo mg of INH has been shown to decrease the incidence of active
TB by at least 6o%.
• patients receiving treatment for latent disease, monthly clinical monitoring for
symptoms is essential.
• Active TB:
• Therapy for 6 months with two very effective anti-tuberculous agents, isoniazid
and rifampin, supplemented during the first 2 months by a third agent,
pyrazinamide, is commonly used.
• In suspected resistant organism a fourth drug (ethambutol) typically is added at the
initiation of therapy until drug sensitivity results become available

Pulmonary Hypertension

Definition
• Sustained elevation of a mean pulmonary arterial pressure greater than 25
mm Hg at rest or greater than 3o mm Hg during exercise;
• In normal lungs the pulmonary arterial pressure is about 2o/8mmHg and the
mean pulmonary artery pressure is 12–15mmHg.
• It is often characterized by a progressive and sustained increase in pulmonary
vascular resistance that eventually may lead to right ventricular (RV) failure.

Classification
• Group 1, pulmonary arterial hypertension (PAH)
• Group 2, pulmonary hypertension owing to left-sided heart disease
• Group 3, pulmonary hypertension owing to lung diseases and/or
hypoxia
• Group 4, chronic thromboembolic pulmonary hypertension
• Group 5, pulmonary hypertension with unclear or multifactorial
etiologies

Clinical Presentation
• Non specific leading to delayed diagnosis
Symptoms:
• dyspnea (most common), exercise intolerance, fatigue, substernal chest pain,
and palpitations.
• Symptoms of right heart failure include exertional dizziness, syncope, chest
pain, lower extremity swelling, increased abdominal girth (ascites), and
hoarseness (impingement of recurrent laryngeal nerve by enlarging
pulmonary artery).
• Assess for exposure to anorectic drugs and symptoms of underlying diseases ,
family history of PH

• The rise in pulmonary pressure may be acute or chronic, depending on
the causative factors.
• In some cases, chronic pulmonary hypertension is punctuated by further
acute elevations in pressure, often as a result of exacerbations of the
underlying disease.

• Signs: due to cardiac affection in Pulmonary hypertension:
1. an accentuation of the pulmonic component of the second heart sound (P2)
because of earlier and more forceful valve closure attributable to high
pressure in the pulmonary artery.
2. Murmurs of tricuspid insufficiency are commonly heard,
3. pulmonary insufficiency (Graham-Steell) murmur may be heard.
4. left parasternal heave due to right ventricular hypertrophy.
5. As the right atrium contracts and empties its contents into the poorly
compliant, hypertrophied right ventricle, a presystolic gallop (S4) originating
from the right ventricle may be heard.
6. When the right ventricle fails, a mid-diastolic gallop (S3) in the parasternal
region is frequently heard.
7. the jugular veins become distended, and peripheral edema may develop.

DIAGNoSTIC EVALUATIoN oF THE PATIENT
WITH SUSPECTED PH
Doppler echocardiography: (provisional diagnosis)
• Key findings are right ventricular hypertrophy and elevated right
ventricular systolic pressure. Record estimated PASP, Estimate volume
status, Evaluate severity of TR.
chest radiography:
• the central (hilar) pulmonary arteries increase in size, and the vessels
often rapidly taper off so that the distal vasculature appears
attenuated.
• hypertrophy of the right ventricle, the cardiac silhouette may enlarge.
This feature is most apparent on the lateral radiograph, which shows
bulging of the anterior cardiac border

Chest radiograph
of patient with
pulmonary
hypertension
attributable to
recurrent
thromboemboli.
Central pulmonary
arteries are large
bilaterally, but
rapid tapering of
vessels
occurs distally.

INVASIVE HEMoDYNAMIC TESTING: (Definitive confirmation by Cardiac
catheterization)
• Measurements of right ventricular, pulmonary arterial, and pulmonary
capillary wedge pressures
• assessing the response to acute vasodilator testing to guide the patient’s
subsequent management(A variety of pulmonary vasodilators can be
used to determine who is most likely to respond to calcium-channel
blocker therapy and also provides prognostic information.
• Positive response to pulmonary vasodilator testing should include all of
the following: 1) decrease in mPAP to <4o mm Hg; 2) decrease of at least
1o mm Hg in mPAP; and 3) unchanged or increased cardiac output.
• a lack of acute pulmonary vasodilator response does not signify a
“nonresponder” to PAH therapies.
• Assess for cardiac causes of pulmonary hypertension

Perfusion lung scanning:
• is frequently a valuable adjunct in the assessment of patients with
pulmonary hypertension. focal perfusion defects may suggest chronic
organized thromboemboli as a likely cause for the elevation in pulmonary
arterial pressure.
Pulmonary angiography
• may be useful when perfusion scanning is positive in order to confirm the
diagnosis and assess the surgical accessibility of the obstructing lesions.
pulmonary function tests
• are useful primarily for detecting underlying airflow obstruction (from
chronic obstructive lung disease) or restricted lung volumes (from
interstitial lung disease). As a result of the pulmonary hypertension itself
and loss of the pulmonary vascular bed, the diffusing capacity may be
decreased and often may be the only other abnormality noted.

Arterial blood gas analysis:
• is highly useful for determining whether hypoxemia or acidosis
plays a role in the pathogenesis of the pulmonary hypertension

THERAPY FoR PAH
• GENERAL MEASURES:
1. Low-level graded aerobic exercise, such as walking, is recommended.
Patients are advised against heavy physical exertion and isometric
exercise, as this may evoke exertional syncope.
2. oxygen supplementation to keep saturation above 9o% at rest and with
exertion, sleep, or altitude is advisable.
3. A sodium restricted diet is advised and is particularly important to
manage volume status.
4. Routine immunizations, such as those against influenza and
pneumococcal pneumonia, are advised

• Specific measures: For IPAH:
1. long-term anticoagulation therapy with warfarin. The rationale is to
decrease in situ thrombosis in the pulmonary arterial system.
observational data suggest that anticoagulation may improve survival
in these patients. INR target (1.5 to 2.5).
2. Pulmonary Vasodilators: CALCIUM-CHANNEL BLoCKERS,
PRoSTACYCLINS, Nitric oxide pathway(Phosphodiesterase type 5
inhibitors e.g. Sildenafil), Endothelin pathway Endothelin receptor
antagonists( bosentan, Ambrisentan)

Surgical interventions
• For some patients with debilitating disease and a poor response to
therapy, lung transplantation or combined heart–lung transplantation
is indicated. However, this form of therapy has very limited availability
and does not offer long-term survival for most patients.
• For CHRoNIC THRoMBoEMBoLIC DISEASE: surgical removal of the
proximal organized thrombi (pulmonary thromboendarterectomy)
may be a feasible and highly effective therapeutic option. For the
small vessel or microvascular form of chronic pulmonary
thromboembolism, therapy involves anticoagulation and agents
similar to those used for IPAH.

DRUG THERAPY

1- Calcium-channel blockers
• can be a very effective treatment for those few patients with an acute
response to vasodilator testing.
• Long-acting nifedipine (epilat retard), diltiazem, and amlodipine are the most
commonly-used agents.
• Due to its potential for negative inotropic effects, verapamil should be avoided.

2- PRoSTACYCLINS
• Prostacyclin synthase expression is reduced in endothelial cells from PAH patients,
resulting in inadequate production of prostaglandin I 2 (i.e., prostacyclin), a vasodilator
with antiproliferative effects.
• Available forms:
1. epoprostenol (continuous IV),
2. Treprostinil (continuous subcutaneous, continuous IV, intermittent inhaled, and oral)
3. iloprost (intermittent inhaled).
• Positive Effects:
improvements in exercise tolerance, as measured by the 6MWD, hemodynamics, quality of
life, and survival.
• Side effects:
jaw pain, flushing, nausea, cough, headache, diarrhea, skin rash, and musculoskeletal pain,
erythema at the site of the subcutaneous infusion.

Endothelin Receptors antagonists
• endothelin-1, is a potent vasoconstrictor and stimulator of cell
proliferation is overexpressed in patients with IPAH.
• Receptors antagonists:
1. Selective endothelin-A receptors antagonist (Ambrisentan)
2. Non selective endothelin-A, B receptors antagonist(Bosentan,
Macitentan)

Nitric oxide pathway
• Nitric oxide (No) is a potent vasodilator of the pulmonary circulation,
acting through the increase in cyclic guanosine monophosphate
(cGMP), and cleared mainly as a result of degradation by PDE-5.
Reduction in the expression of No synthase has been described as a
mechanism associated with the pathogenesis of PH.
• Currently, there are 2 therapeutic classes of drugs interacting in the No
pathway, aiming to increase the direct action of cGMP:
1. PDE-5 inhibitors, which decrease cGMP degradation.
2. soluble guanylate cyclase stimulators, which increase cGMP
production.

1. Phosphodiesterase type 5 inhibitors. Sildenafil, tadalafil
The most common side effects of the PDE-5 inhibitors include headache,
flushing, dyspepsia, myalgias, and epistaxis.
2. Soluble guanylate cyclase stimulators. Riociguat.
The most common adverse events included syncope, headache, dyspepsia,
peripheral edema, and hypotension. Cases of hemoptysis have also been
reported.
• Concomitant use of riociguat and PDE-5 inhibitors is contraindicated due
to hypotension.

PLEURAL EFFUSIoN

Fluid accumulation in the pleural space
indicates disease.
• fluid normally doesn’t accumulate in the pleural space, where the
hydrostatic forces that filter water out of the vessel are balanced by
osmotic forces that reabsorb water back into the vessel. In the pleura,
reabsorption is facilitated by the extensive lymphatic system on the
diaphragm and mediastinal surfaces of the parietal pleura.
• medical conditions that predispose to fluid accumulation via many different
mechanisms, including:
1. increased pulmonary capillary pressure
2. decreased oncotic pressure
3. Increased negative pressure in the pleural space(atelectasis)
4. increased pleural membrane permeability
5. obstruction of lymphatic flow
6. Movement of ascitic fluid from the peritoneal space through either diaphragmatic
lymphatics or diaphragmatic defects

Causes of pleural effusions

• The differential diagnosis for bilateral pleural effusions is narrower
and includes causes of transudative effusions, such as cardiac,
hepatic, and renal failure and hypoalbuminemia, and in rare cases,
malignant neoplasm, pulmonary embolism, and rheumatoid arthritis

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