Topic 4 Respiratory Pathophysiology and Treatment

Reading: Gould Ch 13, Lehne 76 (See 2200 Topic 9.1)

Key Terms
Term Definition
apnea
bronchodilation Sympathetic stimulation relaxes the smooth muscle, dilating or enlarging the bronchioles
caseation A form of necrosis characteristic of tuberculosis, in which diseased tissue forms a firm, dry mass like cheese in
appearance
clubbing Painless, firm, fibrotic enlargement at the end of the digit
cohesion “sticking together” (high surface tension)
compliance Used to refer to the ability of the lungs to expand. It is affected by the alveolar surface tension and the shape, size,
and flexibility of the thorax
empyema Collection of pus in the pleural cavity
eupnea Normal, rhythm is smooth and even with expiration longer than inspiration
expectorant
hemoptysis Blood-tinged (bright red) frothy sputum that is usually associated with pulmonary edema
Hering-Breuer reflex Stretch receptors in the lungs which prevent excessive lung expansion
hypercapnia High levels of carbon dioxide in the blood
hypoxemia Marked decreased in oxygen in the blood
orthopnea Dyspnea that occurs when a person is lying down
paroxysmal nocturnal Sudden acute type of dyspnea common in patients with left-sided CHF
dyspnea
proteases Destructive enzymes released by neutrophils during an inflammatory response
pulsus paradoxus Pulses differ on inspiration and expiration
rales Light bubbly or crackling sounds associated with serous secretions
residual volume The volume of the air remaining in the lungs after maximum expiration. This air continues to provide gas exchange
and maintains partial inflation of the lungs – 1200 mL
rhonchi Deeper and harsher sounds resulting from thicker mucous
sputum Mucoid discharge from the respiratory tract, normally thin, clear, and colorless or cream color
steatorrhea Bulky, fatty, foul stools
stridor A high-pitched crowing noise, usually indicated an upper airway obstruction
surface tension The tendency for fluid to reduce its surface area by forming droplets
vital capacity Represents the maximal amount of air that can be moved in and out of the lungs. It can be altered by lung disease,
size of the thorax, amount of blood in the lungs or body position – 4600 mL
wheezing Indicates obstruction of the small airways
Notes
Learning Objective Notes
Ventilation
Airflow during inspiration and expiration depends on a pressure gradient. If atmospheric pressure is higher than the air pressure inside the lungs than
inspiration will occur.

Boyle’s Law: as the size of the thoracic cavity decreases, the pressure inside the cavity increases

Inspiration
1. Muscles contact, chest wall moves out
2. Diaphragm descends
3. Intrapulmonic pressure becomes negative (usually less than atmosphere – 758 mm Hg)
4. Intrapleural pressure becomes more negative (754 mm Hg)
5. Atmospheric air (760 mm Hg) flow in
Expiration
1. Muscles relax, chest wall moves in
2. Diaphragm ascends
3. Intrapleural pressure remains negative
4. Intrapulmonic pressure becomes positive (greater than atmosphere – 763 mm Hg)
5. Air out

Dead space refers to the passageways or areas where gas exchange cannot take place. This is the space first filled by newly inspired air. Anatomic dead
space includes bronchi and bronchioles, it can be increased by obstruction or collapse of alveoli.

Pulmonary Volumes
Name Volume Meaning
Tidal volume (TV) 500 mL Amount of air entering lungs with each normal breath
 Residual volume (RV) 1200 mL Amount of air remaining in the lungs after forced expiration
Inspiratory reserve (IRV) 3000 mL Maximal amount of air that can be inhaled in excess of normal
quiet inspiration
Expiratory reserve (ERV) 1100 mL Maximal amount of air expired following a passive expiration
Vital capacity (VC) 4600 mL Maximal amount of air expired following a maximal inspiration
Total lung capacity (TLC) 5800 mL Total volume of air in the lungs after maximal inspiration

Control of Ventilation
Medulla: controls the basic rhythm by stimulating phrenic nerves to the diaphragm and intercoastal nerves to the external intercostal muscles.
Pons: role in coordinating inspiration, expiration and the intervals for each

Chemoreceptors sense changes in the levels of CO2, H+, and O2 in blood or CSF.
 Central chemoreceptors in medulla respond quickly to slight elevations in PCO 2 or to a decrease in pH of the CSF
 Peripheral chemoreceptors in the carotid bodies at the bifurcation of the common carotid arteries in the aortic arch are sensitive to decreased
O2 levels in the arterial blood as well as low pH

A marked decreased in O2 is required for chemoreceptors respond to hypoxemia. This is important in COPD patients, who move to a hypoxic drive
where they adopt to a sustained PCO2. When hypercapnia occurs, gas diffuses into the CSF, lowering the pH and stimulating the respiratory center,
resulting in increased rate and depth of respirations.

Gas Exchange
Dalton’s law: each gas in a mixture moves or diffuses according to its own partial pressure gradient and independent of other gases

Diffusion can be affected by variety of factors, including the:

 Thickness of the respiratory membrane (can increase with edema, which causes impeded blood flow to the capillaries and increased surface
tension in the alveoli)
 Total surface area available for diffusion and the thickness of the alveolar membranes

Inspired air: PO2 = 160 mm Hg, PCO2 = 0.3 mm Hg

Expired air: PO2 = 120 mm Hg, PCO2 = 27 mm Hg

If airflow into the alveoli is obstructed or the capillaries are damaged, the involved surface area becomes nonfunctional. This imbalance is measured by
the ventilation-perfusion ratio.
Transport of Oxygen and Carbon Dioxide
Most oxygen is transported bound to hemoglobin by the iron molecules – oxyhemoglobin. O2 is dissolved out of the blood into interstitial fluid and the
cells, and it is replaced with O2 bound to the hemoglobin. Approximately 25% of oxygen is released to the cells for metabolism during the RBCs trip
through the systemic circulation.

Carbon dioxide is either dissolved in the plasma, reversely bound to hemoglobin (attached to an amino group - carbaminoglobin), or enters the RBC
where is transitions into carbonic acid and then bicarbonate ions (ratio of 20 bicarbonate ions to 1 carbonic acid)

General Manifestations of Respiratory Disease

Symptom Details
Sneezing Reflex response to irritation of upper respiratory tract
Coughing Cough reflex is controlled by a center in the medulla and consists of coordinated actions that inspire
air and then close the glottis and vocal cords
Sputum Discharge from the upper respiratory tract
 Yellow/green - bacterial infection
 Rusty or dark-colored – pneumococcal pneumonia
 Purulent – foul odor may be bronchiectasis
 Thick, sticky – asthmas or cystic fibrosis
 Hemoptysis – usually associated with pulmonary edema
Breathing patterns Eupnea (normal) – 10-18 bpm – smooth and even with longer expiration than inspiration
Cheyne-Stokes – periodic breathing associated with periods of apnea, alternating regularly
Ataxic breathing – periods of apnea alternating irregularly with a series of shallow breaths of equal
depths
Kussmaul respiration - deep regular sighing respirations with an increase in respiratory rate
Apneusis - long, gasping inspiratory phase followed by a short, inadequate expiratory phase
Breath sounds Wheezing - indicate obstruction in the small airways
Stridor - usually indicates an upper airway obstruction
Rales - associated with serous secretions
Rhonchi - deeper sounds from thicker mucous
Absent - indicate non-aeration or collapse of lung
Dyspnea Subjective feeling of discomfort that occurs when a person feels unable to inhale enough air. Severe
dyspnea may be accompanied by nostril flaring, use of accessory muscles, retraction of muscles above
ribs.
 Cyanosis Bluish coloring of the skin and mucous membranes resulting from large amounts of unoxygenated
hemoglobin in the blood
Pleural pain Results from inflammation or infection of the parietal pleura, cyclic pain that increases with
inspiration or coughing
Friction rub A soft sound produced as rough, inflamed pleural membranes move against each other
Clubbed fingers Chronic hypoxia associated with respiratory or cardiovascular diseases
Arterial blood gas Hypoxemia - refers to inadequate oxygen in the blood
(ABGs) Hypoxia - inadequate oxygen supply to the cells, may have many causes
 Deficient RBC or hemoglobin levels
 Circulatory impairment
 Excessive release of oxygen from RBCs if circulation is sluggish
 Impaired respiratory function
 Carbon monoxide poisoning

Other Respiratory Disorders

Histoplasmosis
Fungal infection in the midwestern US as an opportunistic infection and found as a parasite inside of macrophages
Similar to TB with asymptomatic first stage with second stage of granuloma formation and necrosis and consolidation in the lungs
Anthrax
Bacterial infection of the skin, respiratory tract, or GI tract that has gained attention as a biologic weapon
Gram (+) bacillus that forms grey spores
Inhalation causes flu-like symptoms and leads to severe acute respiratory distress with mediastinal widening on x-ray and fever
Symptoms depend on form of anthrax
 Cutaneous - blisters/bumps on skin, open sores with black centers
 Inhalation – fever/chills, shortness of breath, cough, v/n, headache, tiredness, body aches
 Gastrointestinal – swelling of neck or neck glands, sore throat, diarrhea, stomach pain
Treated with ciprofloxacin and anthrax antitoxin
Restrictive Lung Disorders
Applies to a group of disease in which lung expansion is impaired and total capacity is reduced
1. The abnormality of the chest wall limits lung expansion
a. Kyphosis, scoliosis – affecting the thorax
b. Poliomyelitis, botulism – respiratory muscle paralysis
c. Muscular dystrophy – weak muscles
2. Diseases affecting the tissues providing supportive framework of the lungs
 a. Idiopathic pulmonary fibrosis
b. Occupations diseases (such as pneumoconiosis from asbestos)
c. ARDS
Flail Chest
Falls and MVCs cause the most chest injuries, usually fractures of three to six ribs in two places or fracture of the sternum and several consecutive
rubs. Atelectasis does not occur as a direct result of the injury but may occur as a complication if rib punctures the pleura.
Pathophysiology
Chest wall rigidity is lost, resulting in paradoxical movement
Inspiration:
 Broken section moves inwards as intrathoracic pressure is decreased – prevents expansion of the affected lung
 Air from affected lung can cross into the unaffected lung, transferring “stale” air
Expiration:
 Broken section moves outward by the increasing intrathoracic pressure, altering airflow

Caroline’s Notes
Cyanosis: healthy adults have a hemoglobin level of 120-150 g/L, a person exhibits the blue discoloration when about 50 g/L is desaturated
Describe several common
upper respiratory tract
infections
Infectious Disease Pathophysiology/Etiology Signs/Symptoms Treatment
Common Cold Caused by a viral infection of Red, swollen mucous Acetaminophen (fever/headache)
(Infectious Rhinitis) the upper respiratory tract membranes with increased Decongestants (decrease edema
Spread through respiratory secretions and congestion)
droplets Nasal congestion Antihistamines (reduce secretions)
Highly contagious due to large Mouth breathing Humidifiers (keep secretions liquid
number of virus that is shed Sore throat and easily drained)
from the infected nasal Headache
mucosa Fever
Malaise
Cough from secretions
dripping into pharynx
Sinusitis Bacterial infection secondary Pain in facial bones Dx through radiograph or
to a cold or an allergy that Nasal congestion transillumination
has obstructed the drainage Fever Decongestants
of one or more paranasal Sore throat Analgesics
sinus into the nasal cavity Antibiotics
 Common pneumococci,
streptococci, or H.
influenzae
Exudate accumulates,
pressure increases, causes
severe pain in the facial
bone
Laryngotreacheo- Common viral infection in
bronchitis children between 1 and 2
(Croup) years of age
Parainfluenza viruses and
adenoviruses
Begins as upper respiratory
infection and the larynx and
subglottic area become
inflamed with swelling and
exudate
Epiglottis Acute infection usually caused
by H. influenzae
Common 3 to 7 years,
increasing in adults
Swelling of larynx, supraglottic
area, and epiglottitis
Influenza Viral infection affecting upper
(Flu) and lower, type A (most
prevalent), B or C
Highly contagious, 2 days
before symptoms and 5 days
after
Scarlet Fever Caused by group A B-
hemolytic streptococcus (S.
Pyogenes)
Incubation 1 to 2 days
Nasal congestion Cool, moisturized air from
Barking cough (croup) humidifier/shower/croup tent
Hoarse voice
Inspiratory stridor
More severe at night
Rapid onset fever and sore Careful exam due to reflex spasm
throat Oxygen
Refusing to swallow Antibiotics
Drooling of saliva Intubation or tracheotomy if
Inspirator stridor necessary
Anxious, pale, tripoding
Sudden, acute onset fever Symptomatic and supportive unless
Marked fatigue and aches bacterial infection occurs
Antivirals (amantadine, zanamivir,
oseltamivir) may reduce symptoms
and duration and reduce risk of
infecting others
Vaccination
-Fever and sore throat Antibiotics
-Chills
-Vomiting, abdominal pain
-Malaise

Explain how secondary
bacterial infections occur in
the respiratory tract
Compare the different types
of pneumonia
-”strawberry” tongue by
exotoxin of bacteria
-Rash on chest, neck, groin,
and thighs
Bronchiolitis Children 2 to 12 months of Wheezing and dyspnea with Supportive and symptomatic
Respiratory age rapid, shallow respirations Monitoring of blood gases
Syncytial Virus RSV virus, a mycovirus Cough RSV immunoglobulin serum or
(RSV) Transmitted by oral droplet Rales palivizumab may be administered
and more frequent in winter Chest retractions to reduce severity of infection
months Fever and malaise
Predisposing factors: history
of asthma, and presence of
cigarette smoke
Necrosis and inflammation in
small bronchi and
bronchioles, with edema,
increased secretions, and
reflex bronchospasm leading
to obstruction of the small
airways
Hyperinflation with air
trapping or areas of
atelectasis or non-aeration
resulting from total
obstruction
Usually caused by streptococcus invading inflamed and necrotic mucous membranes. A purulent exudate forms and
systemic signs such as fever develop. Bacteria should be identified by culture and treated quickly with antimicrobial
drugs to reduce risk of rheumatic fever or ace glomerulonephritis from group A S. pneumonia
Pneumonia may develop as a primary acute infection or secondary to another respiratory or systemic condition.
Pneumonia is a risk following any aspiration or inflammation of the lung, when fluid pools or defense mechanisms
such as cilia are reduced. May be caused by a virus, bacterium or fungus. Most cases the organism enters the lungs
directly, by inhalation, resident bacteria spreading along the mucosa, or aspiration. Can occasionally be blood borne.
A vaccine that provides protection against the seven most common causative agents of pneumonia is available for
those with chronic respiratory or cardiovascular disease as well as clients over the age of 65. Nosocomial pneumonia
(hospital acquired) usually affects those with less resistance: the elderly, the debilitated, the malnourished or the
immune suppressed

Legionnaires Disease
Caused by gram (-) bacterium Legionella pneumophila. Thrives in warm, moist environments, such as air conditioning
systems and spas. Difficult to identify because it is found inside pulmonary macrophages and requires a special culture
medium. Without treatment causes severe congestion and consolidation, with necrosis in the lungs.
Lobar Pneumonia Bronchopneumonia Interstitial Pneumonia (Primary
Atypical Pneumonia [PAP])
Distribution All of one or two lobes Scattered small patches, more Scattered small patches
often in lower lobes
Cause Streptococcus pneumoniae Multiple bacteria Influenza virus Mycoplasma or
Influenza A, B; adenoviruses; or RSV
Pathophysiology Inflammation of alveolar wall and Inflammation and purulent Interstitial inflammation around
leakage of cells, fibrin, and fluid exudate in alveoli often alveoli
into alveoli causing consolidation arising from prior pooled Necrosis of bronchial epithelium
of exudate secretions or irritation
Pleura may be inflamed Hypostatic pneumonia
Onset Sudden and acute Insidious Variable
Signs High fever and chills, marked Mild fever Variable fever, headache
fatigue, and leukocytosis Productive cough with yellow- Aching muscles
Dyspnea, tachypnea, tachycardia green sputum Nonproductive hacking cough
Pleuritic pain with splinting or Dyspnea
restriction of respiration on
affected side
Productive cough with rusty
sputum
Rales progressing to absence of
breath sounds in affected lobes
Treatment Antibiotics Antibiotics Mycoplasma responds to
Supportive fluids and medications erythromycin or tetracycline therapy
for fever
Oxygen
 Pneumocystis carinii Pneumonia
Atypical pneumonia that occurs as an opportunistic and often fatal infection in patients with AIDS and in premature
infants. Considered a fungus and inhaled and attaches to alveolar cells, causing necrosis and diffuse interstitial
swelling. Alveoli then fill with exudate and fungi.

Severe Acute Respiratory Syndrome

First diagnosed in China in 2002 and by July 2003 an excess of 8000 cases and 800 deaths were reported in 29
countries. Previously unknown microorganism, a coronavirus names SARS-CoV, an RNA virus that is transmitted by
respiratory droplets in close contact. Incubation of 2 to 7 days. Initial flu like symptoms and later effects on the lungs,
with dry cough and dyspnea. Patchy areas of interstitial congestion. Liver damage can be caused by the virus.
Treatment is antiviral ribavirin and glucocorticoid methylprednisolone. High fatality rate.
Describe primary and Tuberculosis
secondary TB Pathophysiology Mycobacterium tuberculosis, primarily affects the lungs. Acid-fast, aerobic, slow-growing bacillus that
can survive for weeks and is protected by cell wall against body defenses.
Primary infection – occurs when the microorganism first ender the lungs
Bacteria become engulfed by macrophages, and cause a local inflammatory reaction
Some bacilli will migrate to lymph nodes, activating a type IV or CMI hypersensitivity response
Lymphocytes and macrophages cluster to form a granuloma at the site of inflammation
The granuloma contains the bacilli, forming a tubercle
At the center of the tubercle, caseation necrosis develops, forming a core of cheese-like material of
dead macrophages and necrotic tissue
In a healthy person these remain very small and are walled off by fibrous tissue and calcify (Gohn
complexes)
Bacilli in complex may still be alive, and a therefor a potential danger
Miliary or extrapulmonary TB more often occurs in children and immunosuppressed and has
granulomas that affect large areas of the lung and rapidly disseminate into the circulation
Secondary infection – stage of active infection
Usually arises years after infection when bacilli in tubercles is reactivated, generally due to decreased
host resistance
Cavitation occurs, the formation of large open area in the lung and erosion of bronchi and blood
vessels
Hemoptysis is common are blood vessels are damaged
Etiology Transmitted by oral droplets from person with active infection that are inhaled into the lungs. Potential
for unpasteurized milk to Mycobacterium bovis, which infects cows and may cause tuberculosis.
 Factors
Immunodeficiency, malnutrition, alcoholism, conditions of war, or chronic disease, genetic
susceptibility, age
Signs and Primary TB is asymptomatic
Symptoms Onset of secondary or active TB is insidious:
Anorexia
Malaise
Fatigue
Weight loss
Afternoon low-grade fever and night sweats
Prolonged cough that becomes increasingly severe and, as cavitation develops, more productive
Purulent sputum often contains blood
Diagnostic Tests Mantoux tuberculin test
CMI hypersensitivity is basis for test
After exposure to bacilli, the person will produce a positive skin reaction with a large area of
induration (hard, raised, red area)
Chest x-ray
Acid-fast staining of bacterium
CT scan to detect TB lesions
Nucleic acid amplification (NAA) from microbial genetic material
Treatment Latent TB (goal is to prevent active TB)
Isoniazid (INH), rifapentine, rifampin
Active TB (6 months to 1 year)
Isoniazid, rifampin, ethambutol, pyrazinamide, streptomycin
Outline the pathology of Common inherited disorder in children with a mean survival age of 37 years
cystic fibrosis Pathophysiology
Mutations to the CFTR (cystic fibrosis transmembrane conductance regulator) gene have been identified and relate to
protein involve in chloride ion transport in the cell membrane
Exocrine glands cause thick secretions, primarily in the lungs and pancreas where it obstructs passageways
 Lungs: mucus obstructs airflow, causing air trapping and atelectasis as well as frequent infections
 Digestive tract: first abnormality may be meconium ileus in newborns were small intestine is blocked by
mucous
 Pancreas: ducts become blocked, deficiency in pancreatic digestive enzymes to the intestine causing
 malabsorption and malnutrition. Can also cause damage to islets of Langerhans, causing DM
 Bile ducts: become blocked, preventing proper digestion and absorption of fats and fat-soluble vitamins
 Salivary glands: secretions are high in NaCl and cause patchy fibrosis of the submaxillary and sublingual glands
 Sweat glands: secretions high in NaCl, becomes a problem if excessive electrolytes are lost
 Reproductive system: blocked by mucous causing infertility
Etiology
CFTR mutation on 7th chromosome and disease is transmitted as an autosomal recessive disorder. More common in
Caucasians from northern Europe
Signs and Symptoms
Meconium ileus at birth
Salty skin may lead to a sweat test and the diagnosis
Steatorrhea
Distended abdomen
Inability to gain weight
Chronic cough and frequent respiratory infections
Failure to meet normal growth milestones
Diagnostics
Genetic testing
Sweat analysis for electrolyte content
Treatment
Replacement therapy for pancreatic enzymes
Well-balanced diet
Intensive chest physiotherapy
Bronchodilators and humidifiers
Regular moderate aerobic exercise
Immediate, aggressive treatment for any infections

Describe the pathology of Lungs are common site of primary and secondary cancer, ranks as third most common cancer in the US
bronchogenic cancer Pathophysiology
Metaplasia occurs- a change in the epithelial tissue. Lung tissue is now more vulnerable to irritants and inflammation. Dysplasia
or carcinoma in situ then develops. Bronchogenic cancer arises from the bronchial epithelium

List some of the outcomes of
aspiration
 Squamous cell carcinoma – develops from epithelial lining of bronchus near the hilum
 Adenocarcinomas – from the glands
 Bronchoalveolar cell carcinomas – found in periphery of the lungs
 Small cell carcinoma – near major bronchus in central part of lung, invasive and metastasize early
 Mesothelioma – aggressive and potentially caused by asbestos
Effects:
 Obstruction of airflow by tumor growth
 Inflammation surrounding tumor
 Pleural effusion, hemothorax, pneumothorax
 Usual systemic effects of cancer
Etiology
Cigarette smoke is major factor in the development, including second-hand smoke
Potential genetic factor
Occupational or industrial exposure to carcinogens
Signs and Symptoms
Cough, dyspnea, wheezing
Hemoptysis
Pleural involvement
Chest pain, occurs with pleural or mediastinal involvement
Hoarseness, facial or arm headache, dysphagia, or atelectasis
Weight loss, anemia, fatigue
Paraneoplastic syndrome – tumor secretes hormones such as ADH or ACTH
Diagnostics and Treatment
CT scans, MRI, chest x-ray, bronchoscopy
Radiofrequency ablation (RFA), surgical resection or lobectomy, chemotherapy and radiation or photodynamic therapy – a
chemical is injected and migrates to tumor cells, where it is activated by a laser and destroys the cells
Aspiration involved the passage of food or fluid, vomitus, drugs, or other foreign material into the trachea and lungs. The
right lower long is often the location of aspirated material. More common in young children or individuals with impaired
swallowing or gag reflex.
Pathophysiology
Commonly causes obstruction or inflammation and swelling due to a liquid. May interfere with gas exchange and predispose
to pneumonia. Could be life threatening if a large obstruction occurs. Solid objects can cause non-aeration and collapse of the
area distal to the obstacle. Air trapping can occur. Granulomas may occur around the object.
 Signs and Symptoms
Coughing and choking with marked dyspnea
Stridor and hoarseness
Wheezing
Tachycardia, tachypnea
Nasal flaring, chest retractions, marked hypoxia
Describe asthma including Asthma is caused by periodic episodes of severe but reversible bronchial obstruction in persons with hypersensitive airways.
the pathophysiology of an  Extrinsic asthma: acute asthma attacks triggered by type I hypersensitivity reactions to an inhaled antigen
acute attack o In those with extrinsic asthma, the antigen reacts with IgE on the previously sensitizes mast cells in the
mucosa and release histamines, kinins, prostaglandins, and other chemical mediators which cause the above
response. In the second stage of the allergic response, increased leukocytes (eosinophils) release additional
mediators, such as leukotrienes, which result in prolongs inflammation, bronchoconstriction, and epithelial
damage.
 Intrinsic asthma: onset in adulthood with other types of stimuli (cold, exercise, drugs, stress etc.) that target hyper-
responsive tissues in the airway
o Precis mechanism is not determined, but suggest chronic T cell activation do to an internal antigen
Pathophysiologic Changes
1. Inflammation of the mucosa with edema
2. Contraction of smooth muscle (bronchoconstriction)
3. Increased secretion of thick mucus in passages
Partial obstruction: results in air tapping and hyperinflation of the lungs as air passes into distal areas but is only partially
expired
Total obstruction: results when mucous plugs completely block the flow of air, leads to non-aeration or atelectasis
Status asthmaticus: persistent severe attack of asthma that does not respond to therapy
Signs and Symptoms
 Cough, marked dyspnea, tight feeling in chest, agitation
 Wheezing on inspiration or expiration (or both)
 Rapid and labored breathing – use of accessory muscles and possible chest retractions
 Thick and sticky mucous is coughed up
 Tachycardia and perhaps pulsus paradoxus
 Hypoxia
 Initially respiratory alkalosis due to hyperventilation, but moves to respiratory acidosis due to air trapping and weaker
respiratory effort due to fatigue
  Respiratory failure: PaO2 <50 mmHg or PaCO2 > 50 mm Hg
Compare emphysema and
chronic bronchitis Emphysema
Destruction of the alveolar walls and septae, which leads to large, permanently inflated alveolar air spaces. In some
individuals a deficiency in alpha1-antitrypsin inhibits the activity of proteases which are destructive enzymes released by
neutrophils (e.g. one type of protease is elastase, which breaks down elastic fibers). The inhibition of alpha1-antityrpsin
causes increased destruction.

The breakdown of alveolar wall results in the following:

 Loss of surface area for gas exchange
 Loss of pulmonary capillaries, affecting perfusion and the diffusion of gases
 Loss of elastic fibers, affecting the ability of the lung to recoil on expiration
 Altered ventilation-perfusion ration as various changes occur in the alveoli
 Decreased support for other structures such as the small bronchi
Fibrosis and thickening of the bronchial walls have resulted from chronic irritation and frequent infections, which can lead to:
 Narrowed airways
 Weakened walls
 Interference with passive expiratory airflow
Progressive difficulty with expiration leads to:
 Air trapping and increased residual volume
 Overinflation of the lungs
 Fixation of the ribs in an inspiratory position and increased anterior-posterior diameter of the thorax (barrel chest)
 Diaphragm appears flattened on x-rays
In advanced emphysema, and significant loss of tissue:
 Adjacent damaged alveoli coalesce, forming very large air spaces, the lung appears to have many large holes in it.
These air-filled spaces are called blebs or bullae
 Tissue and pleural membrane surrounding large blebs near the surface of the lung may rupture
 Hypercapnia
 Hypoxic drive for inspiration develops as respiratory control adapts to a chronic elevation of carbon dioxide levels
 Infections develop frequently as secretions are more difficult to move and airway defenses are impaired
 Pulmonary hypertension and cor pulmonale may develop as pulmonary blood vessels are destroyed and hypoxia
causes pulmonary vasoconstriction. Increased pressure in pulmonary circulation increases resistance to the right
ventricle and eventually the ventricle fails – signs of heart failure
 Signs and Symptoms
Dyspnea on exertion and then marked at rest
Hyperventilation with prolonged expiratory phase, barrel chest “pink puffer”
Anorexia, fatigue and weight loss
Clubbed fingers
Secondary polycythemia

Chronic Bronchitis
Differentiated from emphysema by changes to the bronchi resulting from constant irritation from smoking or exposure to
pollution. The effects are irreversible and progressive.
Inflammation and obstruction, repeated infections, and chronic coughing characterize bronchitis as the following occurs:
 Mucosa is inflamed and swollen
 Hypertrophy and hyperplasia of the mucous glands – increased secretions, increased goblet cells, decreased ciliated
epithelium
 Fibrosis and thickening of bronchial wall – further obstruction causing secretions to pool distal to obstructions
 Cyanosis, edema - “blue bloater”
Signs and Symptoms
Constant productive cough, tachypnea and shortness of breath
Thick and purulent secretions
Cough and ronchi are more severe in the morning
Describe bronchiectasis Secondary problem, typically in COPD or cystic fibrosis patients. May be localized in one lung, but sometimes diffuse in both.
 Irreversible abnormal dilation or widening, generally in medium-sized bronchi
 Arise from recurrent inflammation and infection in the airways
 Leads to obstruction in the airways or weakening of the muscle and elastic fibers in bronchial wall
 Fibrous adhesions may pull the wall outward, dilating it
 Large amount of fluid collects and becomes infected
 Cause loss of cilia and metaplasia in the epithelium, additional fibrosis, and progressive obstruction
Describe the cause and Pathophysiology
pathology of pulmonary Fluid collecting in the alveoli and interstitial area. Fluid accumulation reduces the amount of oxygen diffusing into the blood
edema and interferes with lung expansion, further reducing oxygenation. Excess fluid develops when:
 Inflammation in the lungs, increasing capillary permeability
 Plasma protein levels are low, decreasing plasma osmotic pressure
 Pulmonary hypertension develops
 Normally pressure in pulmonary capillaries is very low, with minimal fluid in air passages and alveoli.
 Increase in hydrostatic pressure in pulmonary capillaries becomes high (e.g. CHF), there is shift of fluid out of
capillaries into the alveoli
Ultimately there is difficulty in expanding the lungs, causing collapse. Capillaries may rupture, causing blood-streaked sputum.
Etiology
Can result from many primary conditions:
 Left-sided CHF – backup of blood from left ventricle causes high pressure in pulmonary circulation
 Hypoproteinemia due to kidney or liver disease – low serum albumin levels
 Inflammation with increased capillary permeability due to inhalation of toxic gases or tumors
 Blocked lymphatic drainage due to tumors or fibrosis
 Pulmonary hypertension idiopathically or secondary to obstructive sleep apnea
Signs and Symptoms
Mild pulmonary edema:
 Cough, orthopnea, rales
Increased congestion:
 Hemoptysis, frothy sputum
 Labored breathing, “drowning”
 Hypoxemia
 Cyanosis
Outline the pathology of A PE is a blood clot or mass of material that obstructs the pulmonary artery or a branch of it, blocking the blood flow through
pulmonary embolus the lung tissue. An embolus travels from its source through larger and larger veins until it reaches the heart and pulmonary
artery where it becomes lodged in the smaller passages. PE due to DVT is a leading cause of death in hospitals
Pathophysiology
Infarction usually does not follow due to separate bronchial circulation. Small PE can be silent, but a “shower” of small emboli
may have an equal effect of a larger embolus.
 Respiratory impairment occurs due to fluid and blood filling the alveoli of the involved area
 Reflex vasoconstriction – increasing the pressure of the blood vessels
Large emboli (affecting 60% of lung tissue) affect the cardiovascular system:
 Causes right-sided failure and decreased CO
o Increased resistance in the pulmonary arteries with reflex vasoconstriction due to release of serotonin and
histamine
o Resistance to output from right ventricle causes acute cor pulmonale
o Less blood returning from the lungs to left ventricle and then to systemic circulation

Describe the causes of
atelectasis and how it affects
ventilation and oxygen levels
 “saddle embolus” is a large embolus lying across the bifurcation of the pulmonary artery, totally blocking flor of blood
from the right ventricle into the lungs
Etiology
Risk factors include:
 Immobility
 Trauma – fracture of a long bone could cause a fat embolus from bone marrow. A fat embolus will cause acute
respiratory distress, a petechial rash on the trunk, as well as confusion and disorientation
 Surgery to the legs
 Childbirth – amniotic fluid emboli from placental tears
 Congestive heart failure
 Dehydration
 Increased coagulability of the blood
 Cancer – tumor cell emboli that break from malignant mass
Signs and Symptoms
Small emboli
 Transient chest pain
 Cough, dyspnea
Larger emboli
 Chest pain, increases with coughing or deep breathing
 Tachypnea, sudden dyspnea
 Hemoptysis and fever
Massive emboli
 Severe crushing chest pain
 Low blood pressure
 Rapid, weak pulse
 Loss of consciousness
Atelectasis is the non-aeration or collapse of a lung or part of the lung, leading to decreased gas exchange and hypoxia.
Occurs as a complication of many primary conditions.
Pathophysiology
Without air inside them, alveoli shrivel as the natural elasticity of the tissues dominate. Ventilation and perfusion are altered,
affecting oxygen diffusion. If tissue is not inflated quickly, it can become necrotic and infected, causing permanent damage
Etiology

Describe how a pleural
effusion affects ventilation
 Obstructive or resorption atelectasis – total obstruction of airway due to mucous or tumor leads to air diffusion into
the tissue distal to the obstruction; this air is not replaced
 Compression atelectasis – mass such as a tumor exerts pressure on part of the lung and prevents air from entering; or
pressure in pleural cavity increased and the adhesion between the pleural membranes is destroyed and the lung
cannot expand
 Contraction atelectasis - fibrotic tissue in the lungs or pleura restrict expansion and lead to collapse
 Postoperative atelectasis - 24-72 hours after surgery, particularly abdominal surgery – restricted ventilation due to
pain or distension, slow and shallow respirations from anesthetics and increased secretions due to supine position
Signs and Symptoms
Large areas cause dyspnea, increased HR and RR and chest pain
Chest expansion may appear asymmetric
The affected side may “lag” behind the unaffected side in ventilation
Presence of excessive fluid in the pleural cavity, vary in type and mechanism according to the primary problem. One or both
lungs may be involved. Pleurisy may precede or follow. Thoracentesis or chest tubes may be neeeded
Pathophysiology
Lrge fluid volume increases the pressure in the pleural cavity and causes separation of the pleural membranes
 Prevents their cohesion during inspiration
 Prevent expansion of the lung – leading to atelectasis
 Can cause shift into mediastinum (causing tracheal deviation)
 Venous return in the inferior vena cava and cardiac filling may be impaired
Etiology
 Exudative - response to inflammation
 Transudates - watery effusions (hydrothorax) - result from increased hydrostatic pressure or decreases osmotic
pressure in blood vessels leading to a shift of fluid into the potential space
 Hemothorax - blood in pleural cavity resulting from trauma, cancer, or surgery
Signs and Symptoms
Dyspnea, chest pain and increased HR and RR
Dullness to percussion and absence of breath sounds over affected area as air no longer flows through the passages
Tracheal deviation and hypotension indicate massive effusion
Compare the types of Pneumothorax refers to air in the pleural cavity. Air at atmospheric pressure in the pleural cavity and the separation of the
pneumothorax pleural membranes prevent the expansion of the lung, leading to atelectasis.
Types of Closed Open Tension
Pneumothora
x
Cause Spontaneous, idiopathic Puncture wound through chest Open – puncture through thorax
wall
Ruptures emphysematous bleb Closed – tear in lung surface

Both with flap or one-way valve

Air entry From inside lung through tear in From outside body through Through the thorax or tear in lung
visceral pleura opening in thorax and parietal surface
pleura
Effects Atelectasis Atelectasis Atelectasis

Leak seals as lung collapses
One lung impaired
No additional cardiovascular
effects
Air enters pleural cavity with each
inspiration and leaves with each
expiration
Unaffected lung compressed by
mediastinal shift on inspiration
Air enters pleural cavity with east
inspiration
Flap closes with expiration, and air
pressure increases in pleural cavity
pressure

Mediastinal flutter impairs venous Unaffected lung increasingly

return to heart compressed by mediastinal shift

Mediastinal shift reduces venous

return to heart

Signs Increased, labored respirations
with dyspnea, tachycardia,
pleural pain, and asymmetric
chest movements
Breath sounds absent
Hypoxemia
Increased, labored respirations
with dyspnea, tachycardia,
pleural pain, and asymmetric
chest movements
“Sucking” noise if large
Trachea swing
Increased, labored respirations with
dyspnea, tachycardia, pleural pain,
and asymmetric chest movements
Breath sounds absent on affect side
Tracheal deviation to unaffected side

Describe how ventilation
affects ventilation,
oxygenation and circulation
Describe the signs of infant
respiratory distress
syndrome
Decreased BP Increasing respirato0ry distress
Moderate hypoxemia Shock, distended neck veins, cyanosis
Sever hypoxemia
Treatment
An open pneumothorax or sucking wound is covered with an occlusive dressing to prevent the air moving in or out of the
pleural cavity
Common cause of neonatal deaths, particularly in premature infants
Pathophysiology
Normally, the alveolar surface area and the lung vascularity greatly increased in preparation for independent lung function
after birth. Surfactant is first produced between 28 and 36 weeks. Infant lung maturity can be assessed by measuring the
surfactant levels of the fetus with a lecithin-sphingomyelin ration in the amniotic fluid by amniocentesis. Initially
sphingomyelin is high, then decreases and lecithin increases until there is an adequate surfactant ratio (around 35 weeks).
Without adequate surfactant the initial respirations are very difficult:
 Alveoli completely collapse during expiration
 Accessory muscles and more energy are required to reflate the lungs
 Inadequate blood and oxygen supply further decrease surfactant production by alveolar cells
 Diffuse atelectasis results – leads to pulmonary vasoconstriction and severe hypoxia
 Increased alveolar capillary permeability, with fluid and protein leaking into the interstitial area and alveoli form the
hyaline membrane – further impairing lung expansion and decreasing oxygen diffusion
 Acidosis develops leading to anaerobic metabolism and increased lactic acid
Etiology
Premature birth, male children, cesarean delivery, diabetic mothers
Treatment
Arterial blood gas to monitor oxygen and acid-base balance
 Initially: hypoxemia – low PaO2, and metabolic acidosis – low serum HCO3-
 Later: respiratory acidosis – high PCO2 as ventilation becomes more difficult
Glucocorticoids given to women in premature labor or administration of synthetic surfactant

Describe the causes of adult
respiratory distress
syndrome
Describe the etiology and
changes in blood gases with
acute respiratory failure
Describe the causes of sleep
apnea
CPAP, oxygen therapy, nitrous oxide drugs
ARDS is also known as lung shock, wet lung, stiff lung or postperfusion lung. Considered a restrictive lung disorder and is
caused by a multitude of predisposing conditions such as sepsis, prolonged shock, burns, aspiration, and smoke inhalation. It
is associated with multiple organ dysfunction and failure secondary to a sever insult to the body
Pathophysiology
Injury to the alveolar wall and capillary membrane – leads to release of chemical mediators:
 Causes increased permeability of alveolar capillary membranes
 Increased fluid and protein in the interstitial area and alveoli
 Damage to the surfactant-producing cells
All results in decreased diffusion of oxygen, reduces blood flow to the lungs, difficulty expanding the lungs, and diffuse
atelectasis
 Reductions in tidal volume and vital capacity
Further lung damage from increased neutrophils releasing proteases and other mediators
Hyaline membranes form – protein-rich fluid in alveoli, platelet aggregation and microthrombi develop causing stiffness and
decreased compliance
Etiology
Ischemic damage to the lungs – inflammation from toxic chemicals, excessive oxygen concentration, viral infections, toxins,
fat emboli, explosions, aspiration
Disseminated intravascular coagulation, cancer, acute pancreatitis, and uremia
Acute respiratory failure can be the result of many disorders
ARF PaO2 < 50 mm Hg (severe hypoxia) OR PaCO2 > 50 mm Hg (hypercapnia) and serum pH is decreasing (<7.3)
Normal PaO2 80 – 100 mm Hg
Normal PaCO2 35 – 45 mm Hg
Etiology
May result from acute or chronic disorders
 Emphysema if degenerative tissue changes progress to the point at which ventilation and gas exchange are minimal
 Combination of chronic and acute disorder, such as a COPD patient with a pneumonia or pneumothorax
 Acute chest trauma, pulmonary edema or acute asthma
 Neuromuscular diseases such as myasthenia gravis, ALS or MS
Sleep apnea is a potentially serious sleep disorder in which breathing repeatedly stops and starts. If you snore loudly and feel
tired even after a full night's sleep, you might have sleep apnea.
The main types of sleep apnea are:

Describe the assessment
procedures of a respiratory
examination
Describe the different types
of breath sounds and how
they vary at auscultation
sites
Describe the monitoring
devices used in respiratory
emergencies
Describe the EMS treatment
 Obstructive sleep apnea, the more common form that occurs when throat muscles relax
 Central sleep apnea, which occurs when your brain doesn't send proper signals to the muscles that control breathing
 Complex sleep apnea syndrome, also known as treatment-emergent central sleep apnea, which occurs when
someone has both obstructive sleep apnea and central sleep apnea
1. Initial assessment of airway: opening and clearing the airway, and breathing: assessing breathing and providing any
appropriate interventions
o Patient positioning
o Rise and fall of chest adequate
o Gasping for air?
o Skin color
o Nostril flaring, pursed lips or any retractions (intercostal, suprasternal notch, supraclavicular fossa, subcostal)
o Accessory muscles (sternocleidomastoids)
o Symmetrical chest movement?
2. Listen for air movement at mouth and nose, is ventilation adequate?
3. Auscultate breath sounds with stethoscope, comparing each apex and base to the opposite side
4. Pulsus paradoxus – systolic BP drops 10 mm Hg during inhalation
5. History – onset, trigger, duration, alleviation/exacerbation, other symptoms, pre-EMS interventions?, previous
hospital admissions, medications, risk factors
Breath sounds you hear are made by turbulent flow in the large airways. Sounds move better through fluids than air, thus the
more air that is present in the lungs, the more distant and diminished the breath sounds will be in the periphery. The more
“wet” the lungs, the louder the sounds will be in the periphery.
Wheezes: high pitched, whistle sound from air being forced through narrowed airways (makes them vibrate)
 May be diffuse (asthma, CHF, FBOA)
 Pathological conditions rarely cause bilateral wheezing
Crackles: discontinuous noises (pops, snaps, and clicks) heard and caused by the popping open of air spaces
 Associated with increased fluid in the lungs
Rhonchi: low-pitched continuous sound (low wheeze or death rattle)
 Thick secretions in the large airways, will usually clear with coughing
Pulse oximeter: measures the percentage of hemoglobin in the arterial blood that is saturated (normally with O2 but will be
saturated with CO if available). Device transmits light through the vascular bed, the amount of light transmitted depends on
the amount of saturated hemoglobin
 <95% suggests respiratory compromise
Airway obstruction
(including medication
administration) for airway
obstruction, infected
airways, COPD, asthma,
anaphylaxis, aspiration,
chronic bronchitis,
pneumonia, emphysema,
toxic inhalation, acute
respiratory distress
syndrome, pneumothorax,
pleural effusion, pulmonary
edema, hypoventilation, and
Infected airways / Pneumonia
anxiety
COPD / Asthma / Bronchospasm
 Partial obstruction (conscious – able to speak or cry)
o Place patient in sitting position
o Encourage coughing
 Partial or complete obstruction (poor air exchange – cyanosis, stridor, weak or silent cough)
o Perform abdominal thrusts (chest thrusts if obese or pregnant) until success or unconscious
 Complete obstruction (unconscious)
o Chest compressions x 2 mins
o Clear airway and attempt to ventilate x2
o Set up airway management equipment (including surgical)
o Direct visualization of FB – remove with Magill/suction
o No visualization, attempt ETT x1 (pushing FB into mainstream bronchus)
o Perform cricothyrotomy if there is no success with other measures
 Intravenous hydration
 Oxygenation
 Secretion management (suctioning)
 Trasport to appropriate facility
 Establish vascular access
 Mild/moderate
o MDI salbutamol
o MDI ipratropium bromide
o PO prednisone OR IM/IV dexamethasone
 Severe/near death
o NEB salbutamol
o NEB ipratropium bromide
o PO prednisone OR IM/IV dexamethasone
 Condition not improving?
o Due to CPAP
 Consider CPAP
o Bolus followed by maintenance drip
o Consider IV/IO magnesium sulfate
o Consider IM epinephrine
 o Consider advanced airway management
Anaphylaxis
 Discontinue exposure to allergen (if known)
 IM epinephrine
 Establish vascular access
 IV diphenhydramine
 PO prednisone OR IV/IO dexamethasone
 If there is bronchospasm, treat with appropriate bronchospasm protocols
 Refractory or ongoing symptoms?
o IV epinephrine
o Normal saline bolus
o Refractory hypotension and beta-blocker therapy
 IV/IO glucagon
Aspiration
Aggressively reduce risk of aspiration by avoiding gastric distension when ventilating. Monitor patient's ability to protect their
own airway. Aggressively treat aspiration with suction and airway control
Toxic inhalation
 Remove from contact with substance
 Provide 100% supplemental oxygen or assisted ventilation if breathing is impaired
 Manage a compromised upper airway with aggressive airway management (intubation, cricothyrotomy)
Acute respiratory distress syndrome
 May require mechanical ventilation under high pressure
 You can avoid development of ARDS for your patients by avoiding high pressures and volumes of air
Pneumothorax
 Administer high flow oxygen
 Open pneumothorax
o Close chest wall with occlusive dressing taped on 3 sides to create flutter valve or commercially available
product
 Closed pneumothorax
o Monitor
 Tension pneumothorax
o Perform needle decompression
Pleural effusion
  Proper positioning and aggressive supplemental oxygen administration
Pulmonary edema
 Rapid transport with oxygenation
 Systolic BP >100 mmHg
o SL nitroglycerine
o CPAP
o Transport >30 mins
i. IV/IO nitroglycerine drip
 Systolic BP <100 mmHg
o IV norepinephrine
o CPAP or airway management
 Consider intubation with PEEP if severe hypoxia <85% with altered level of consciousness
Hypoventilation
 Treat underlying cause
 Assist with ventilations
Anxiety
 Coach breathing
 Assist with ventilations