RESPIRATORY DISORDERS

ATELECTASIS
An area of collapsed or non-expanded lung
Predisposed to infection
Reversible disorder
Dull percussion note due to the edema that comes with it
Decreased breath sounds on affected lung
Collapse of large sections of dependent lung markedly decreases lung compliance
Intrapulmonary shunting and hypoxemia develop
Resistance to blood flow due to the collapse leads to pulmonary hypertension

Major types

1. Obstruction/resorption atelectasis
Collapse of lung due to resorption of air distal to an obstruction
E.g. Foreign body aspiration, COPD, or post-op

2. Compression atelectasis
Due to fluid, air, blood, or tumor in the pleural space

3. Contraction (scar) atelectasis

Due to fibrosis and scarring of the lung

4. Patchy atelectasis
Due to a lack of surfactant
E.g. hyaline membrane disease, or ARDS

RESPIRATORY INFECTIONS

Bacterial pneumonia

Acute inflammation and consolidation (solidification) of the lung due to a

bacterial agent
Fever and chills
Productive cough with purulent, or rusty sputum
Tachypnea
Pleuritic chest pain
Decreased breath sounds, rales, and dullness to percussion
Elevated WBC
Chest X-ray lobar or segmental consolidation (opacification), pleural effusion
Clinical key identification of the organism and early treatment with antibiotics

Lobar pneumonia

Consolidation of entire lobe

Organism Streptococcus pneumonia (95%), or Klebsiella (in alcoholics)
Intra-alveolar suppurative inflammation (neutrophils) and edema

Bronchopneumonia

Scattered patchy consolidation centered around bronchioles

Tends to be bilateral, multilobar, and basilar
Affects the young, old, and terminally ill
Staphylococcus, Streptococcus, H.influenzae, P.aeruginosa
Micro Acute inflammation of bronchioles and surrounding alveoli

Diagnosis of bacterial pneumonia

Sputum gram stain and culture

Blood cultures
Treatment of bacterial pneumonia

Empiric antibiotic treatment modified by the results of cultures and organism

sensitivities

Complications

Fibrous scarring and pleural adhesions

Lung abscess
Empyema
Sepsis

Lung abscess

Localized collection of neutrophils (pus) and necrotic pulmonary parenchyma

Aspiration most common, tends to involve the right lower lobe, mixed oral flora
(anaerobic/aerobic)
Lung abscess follows a pneumonia, especially S.aureus and Klebsiella
Postobstructive
Septic emboli

Complications of lung abscess

Empyema
Pulmonary hemorrhage

Atypical pneumonia

Interstitial pneumonitis without consolidation of the parenchyma

Mycoplasma pneumonia especially in young adults
Influenza virus, Parainfluenza virus
Respiratory syncytial virus especially in young children
Cytomegalovirus especially in immunocompromised individuals
Chest X-ray diffuse interstitial infiltrates
Micro lymphoplasmacytic inflammation within the alveolar septum

Complications of atypical pneumonia

Superimposed bacterial infection, and Reye syndrome

Tuberculosis

Increasing incidence in the US secondary to AIDS

Type IV hypersensitivity reaction (cell-mediated immunity)
Inhalation of aerosolized bacilli
Micro caseating granuloma with acid fast bacilli
Local symptoms cough, hemoptysis, chest pain, dyspnea
Constitutional symptoms fever, weight loss, chills, anorexia

Effects of tuberculosis on the respiratory system

Increased work on the part of the respiratory muscles to cause pulmonary

ventilation and reduced vital capacity and breathing capacity
Reduced total respiratory membrane surface area and increased thickness of the
respiratory membrane, causing progressively diminished pulmonary diffusing
capacity
Abnormal ventilation-perfusion ratio in the lungs, further reducing overall
pulmonary diffusion of oxygen and carbon dioxide
Laboratory diagnostics

Positive skin test (PPD) positive skin test only indicates exposure but not
necessarily active disease
Chest X-ray upper lobe infiltrates and cavitations
Sputum examination shows acid fast positive microorganisms

Classification of the Tuberculin Skin Test Reaction

[Fischbach A Manual of Laboratory & Diagnostic Tests 7th ed.]

An induration of 5 or more millimeters is considered positive for:

HIV-infected persons
Close contacts of a person with infectious TB
Persons who have abnormal chest radiographs

An induration of 10 or more millimeters is considered positive for:

Foreign-born persons
Medically underserved, low-income populations
Residents and staffs of long-term care facilities
Persons with certain medical conditions

An induration of 15 or more millimeters is considered positive for:

Persons who do not have any risk factors for TB

Primary pulmonary tuberculosis

Initial exposure
Often seen in children and is frequently localized to the middle and lower lung
zones
Ghon focus subpleural caseous granuloma above or below the interlobar fissure
Most lesions (95%) will undergo fibrosis and calcification

Secondary pulmonary tuberculosis

Endogenous reactivation of latent infection or reinfection

Erosion of granulomas into airways later in life under conditions of reduced T-cell
immunity leads to mycobacterial replication and disease symptoms
Simon focus granuloma at lung apex

Miliary systemic spread

Meninges, liver, spleen, kidneys, adrenals, ileum, cervical lymph nodes (scrofula)
Potts disease, fallopian tubes and epididymis

Indications of active PTB

(+) AFB sputum smear

Presence of constitutional symptoms more reliable than local symptoms
Apical infiltrates on chest x-ray
American Thoracic Society Classification Of PTB
Class Exposure PPD skin test CXR infiltrates Indications of
active disease
0 (-) (-) (-) (-)
1 (+) (-) (-) (-)
2 (+) (+) (-) (-)
3 (+) (+) (+) (+)
4 (+) (+) (+) (-)
5 (+) (+) (+) (-/+)

Treatment of PTB

First line antibiotics Isoniazid, Rifampicin, Pyrazinamide, Ethambutol,

Streptomycin

OBSTRUCTIVE and RESTRICTIVE PULMONARY DISORDERS

[The Washington Manual of Medical Therapeautics, 30th ED]
[Frizzell Handbook of Pathophysiology Jan, 2001]
[Cecils Textbook of Medicine]

Normal Lung Volumes

Inspiratory reserve volume 3500 ml
Tidal volume 500 ml
Expiratory reserve volume 1500 ml
Residual volume 1200 ml

Obstructive Airway Disease Restrictive Lung Disease

Increased resistance to airflow secondary Decreased lung volume and capacity
to obstruction of airways
FEV1/FVC ratio is decreased Decreased TLC and VC
Chronic obstructive airway disease Chest wall disorders
Asthma Obesity
Chronic bronchitis Kyphoscoliosis
Emphysema Interstitial/infiltrative dis.
Bronchiectasis ARDS, pneumoconiosis
Pulmonary fibrosis
Summary of Obstructive versus Restrictive Pattern
Variable Obstructive Pattern Restrictive Pattern
Total lung capacity
FEV1
Forced vital capacity
FEV1/FVC or normal
Peak flow
Functional residual capacity
Residual volume

COPD

Chronic bronchitis

Persistent cough and copious sputum production for at least 3 months in 2

consecutive years
Highly associated with smoking (90%)

Clinical findings of chronic bronchitis

Cough, sputum production, dyspnea, frequent infections

Hypoxia, cyanosis
Prolonged expiration
Barrel-shaped chest
blue bloater

Micro of chronic bronchitis

Hypertrophy of bronchial mucous glands (Reid index)

Increased number of goblet cells
Hypersecretion of mucus
Bronchial squamous metaplasia and dysplasia (smokers)

Complications of chronic bronchitis

Increased risk for recurrent infections

Pulmonary HPN and even lung CA

Treatment of chronic bronchitis

Smoking cessation
Bronchodilators, corticosteroids
Oxygen inhalation at 2-5LPM via nasal cannula
Antibiotics
Flu vaccination, pneumococcal vaccination

Emphysema

An abnormal, permanent enlargement of the terminal air spaces due to destruction

of alveolar walls
Obstruction results from tissue changes rather than mucus production
Airflow limitation caused by a lack of elastic recoil in the lungs

Etiology of emphysema

Protease/antiprotease imbalance
Proteases (including elastase) are produced by neutrophils and macrophages
which are stimulated by smoke and pollution
 Antiprotease include -1-antitrypsin, -1-macroglobulin, and secretory
leukoprotease inhibitor
Cigarette smoke inactivates alpha1-antitrypsin
Cigarette smoke impairs respiratory epithelial ciliary movement

Manifestations Related to Area of Involvement

Centriacinar (Centrilobular) Panacinar (Panlobular)
Proximal respiratory bronchioles Entire acinus involved
involved, distal alveoli spared
Most common type (95%) Seen in young patients
Associated with smoking -1-antitrypsin deficiency
Worst in apical segments of upper lobes Entire lung, worse in bases of lower
lobes

Gross picture of emphysema

Overinflated, enlarged lungs

Enlarged, grossly visible air spaces
Formation of apical blebs and bullae (centriacinar type)

Clinical findings of emphysema

Progressive dyspnea
Pursing of lips and use of accessory muscles to breathe
Barrel chest
Weight loss
Decreased breath sounds due to air trapping
Clubbed fingers and toes due to chronic hypoxia
Decreased chest expansion
Hyperresonance on chest percussion
Crackles and wheezes as bronchioles collapse
pink puffer

Complications of emphysema

RVH
Respiratory failure
Respiratory tract infection
Peripheral muscle dysfunction with loss of muscle bulk
osteoporosis

Treatment of emphysema

Same with chronic bronchitis

Asthma

Hyperreactive airways resulting in episodic bronchospasm when triggered by

certain stimuli

Extrinsic (type I hypersensitivity reaction)

Allergic most common type, childhood and young adults with family history,
induced by dust, pollen, food, and etc.

Occupational exposure fumes, gases, and chemicals

Intrinsic (unknown mechanism)

Respiratory infections (usually viral)

 Stress
Exercise
Cold temperature
Drug induced (Aspirin)

Microscopic picture of asthma

Hypertrophy of mucous glands with goblet cell hyperplasia

Inflammation (especially with eosinophils)
Edema, hypertrophy of bronchial wall smooth muscles

Mild asthma

Asymptomatic between attacks

Moderate asthma

Barrel chest starts to appear due to air trapping and retention

Severe asthma

Marked respiratory distress due to failure of compensatory mechanisms and

decreased oxygenation levels
Marked wheezing due to increased edema and increased mucus secretion
Chest wall contractions due to use of accessory muscles

Complications of asthma

Status asthmaticus potentially fatal unrelenting attack unresponsive to standard

bronchodilators and corticosteroids
Respiratory failure

Laboratory diagnostics of asthma

Curschmann spirals twisted mucous plugs admixed with sloughed epithelium

Pulmonary function tests indicative of an obstructive pattern
Clinical diagnosis of asthma is supported by an obstructive pattern that improves
after bronchodilator therapy
ABG initially PaCO2 is low due to hyperventilation but with prolonged attacks,
PaCO2 will rise signifying impending respiratory failure

Treatment of asthma

Supplemental oxygen
Bronchodilators
Systemic corticosteroids
Mast cell stabilizer drug
Methylxanthines
Leukotriene antagonists

Bronchiectasis

Abnormal permanent airway dilatation due to chronic necrotizing infection

Cough, fever, malodorous purulent sputum, dyspnea

Causes

Bronchial destruction by foreign bodies, tumors, necrotizing pneumonias

Cystic fibrosis
Kartageners syndrome autosomal recessive, immotile cilia due to defect of
dynein arms, triad of bronchiectasis, sinusitis, situs inversus
Gross picture of bronchiectasis

Dilated bronchi and bronchioles extending out to the pleura

Complications of bronchiectasis

Abscess
Septic emboli
Cor pulmonale

Laboratory diagnostics of bronchiectasis

Chest X-ray subsegmental atelectasis with walls of cylindrically dilated bronchi

Treatment of bronchiectasis

Elimination of an identifiable underlying problem

Improve clearance of tracheobronchial secretions (chest physical therapy)
Control of infection (antibiotics)
Reversal of airflow obstruction (bronchodilators)

Physical Therapy Intervention of COPD

Submaximal exercise that emphasizes on endurance

Arm bicycle ergometry
Diaphragmatic breathing
Pursed-lip breathing
Secretion clearance such as coughing, huffing, postural drainage, chest tapping

RESPIRATORY DISTRESS SYNDROMES

Adult respiratory distress syndrome (ARDS)

Synonyms diffuse alveolar damage (DAD), shock lung

Diffuse damage of alveolar epithelium and capillaries resulting in progressive
respiratory
Causes shock, sepsis, trauma, gastric aspiration, radiation, pulmonary infections,
etc.
Clinical presentation dyspnea, tachypnea, hypoxemia, cyanosis, and use of
accessory respiratory muscles
X-ray bilateral lung opacity (white out)
Heavy, stiff, noncompliant lungs
Interstitial and intra-alveolar edema and inflammation

Treatment

Treat the underlying cause

Oxygen, PEEP, and mechanical ventilation

Prognosis

Overall mortality 50%

Respiratory distress syndrome of the newborn (RDS)

Synonyms hyaline membrane disease of newborns

Deficiency of surfactant
Associated with:

Prematurity (AOG < 28 weeks has a 60% incidence)

Maternal diabetes

Treatment Steroids and oxygen

Prognosis overall mortality 30%

Prevention delay labor and corticosteroids to mature the lung

PULMONARY VASCULAR DISORDERS

Pulmonary edema

Fluid accumulation within the lungs usually due to disruption of starling forces or
endothelial injury
Increased hydrostatic pressure left-sided heart failure
Decreased oncotic pressure nephrotic syndrome, or liver disease
Increased capillary permeability infections, radiation

Pulmonary emboli (PE) and pulmonary infarction

Most (90-95%) pulmonary emboli arise from DVT in the leg

Only 10% of PE cause infarction
Diagnosis V/Q lung scan shows a mismatch
Large emboli (saddle emboli) may cause sudden death
Septic emboli may result in a pulmonary abscess

Pulmonary hypertension

Increased pulmonary artery pressure, usually due to increased vascular resistance

or blood flow
COPD and interstitial disease (hypoxic vasoconstriction)
Multiple ongoing pulmonary emboli
Mitral stenosis and left heart failure
Congenital heart disease with left to right shunts (ASD, VSD, PDA)
Complication right-sided heart failure

PULMONARY NEOPLASIA

Type Location Characteristics Histology

Squamous cell CA Central Hilar mass Keratin pearls and
arising from intercellular
bronchus bridges
Cavitations
Clearly linked
to smoking
PTHrP
Adenocarcinoma: Peripheral Develops in site Multiple densities
of prior on chest x-ray
Bronchial pulmonary
inflammation or
Bronchoalveolar injury
Most common
lung CA in non-
smokers
Not linked to
smoking
Small-cell (oat cell) CA Central Very aggressive Small, dark blue
Often cells
 associated with
ectopic
production of
ACTH or ADH
May lead to
Lambert-Eaton
syndrome
Large-cell CA Peripheral Highly Pleomorphic giant
anaplastic cells with
undifferentiated leukocyte
tumor fragments in
Poor prognosis cytoplasm
Carcinoid tumor Secretes
serotonin
Can cause
carcinoid
syndrome
(flushing,
diarrhea,
wheezing,
salivation)
Metastasis Very common
From the brain
(seizures)
Bone
(pathologic
fracture)
Liver (jaundice,
hepatomegaly)

DISEASES OF THE PLEURAL CAVITY

Pleural effusion

Accumulation of fluid in the pleural cavity

Empyema pus in the pleural space
Chylothorax due to obstruction of thoracic duct usually by tumor

Pneumothorax

Air in the pleural cavity

Spontaneous pneumothorax rupture of emphysematous blebs
Tension pneumothorax due to penetrating chest wall injuries creating a ball-
valve effect

Mesothelioma

Rare, highly malignant neoplasm

Occupation exposure to asbestos in almost 90%
Recurrent pleural effusions, dyspnea, chest pain
Gross encases and compresses the lung
Poor prognosis