NSG 3280 Patho Exam 2 Study Guide:
Alterations in Respiratory Function Concepts
Chapter 21: Alterations in Oxygenation
,Includes → Asthma, Bronchitis, and Emphysema. These diseases have increased resistance to airflow
***Use spirometry for initial diagnosis of respiratory disease
Vital capacity: total volume of gas that can be exhaled during maximal expiration (~4.8 L)
○ Includes inspiratory reserve volume, tidal volume, and expiratory reserve volume
Forced expiratory flow rate (FEF25, FEF50, FEF75): volume of air forcibly exhaled per unit time (liters per second or liters per
minute) at 25%, 50% and 75% of forced vital capacity (FVC)
Total Lung Capacity: Amount of gas contained in lungs at maximal inspiration (~6.0 L)
Acute Bronchitis (pg 494-495)
● Pathophsyiology
○ Acute inflammation of the trachea and bronchi
● Etiology
○ Viral or non-viral
■ Coronavirus
○ Heat
○ Smoke inhalation
○ Inhalation of irritant chemicals
○ Allergic reactions
● Pathogenesis
○ Airways become inflamed and narrowed from capillary dilation
○ Swelling from fluid exudation (pus)
○ Infiltration with inflammatory cells (Mast cells & Basophils)
○ Increased mucus production
○ Loss of ciliary function (can’t get rid of waste in airways bc no movement of cells)
○ Loss of portions of the cilated epithelium
● Diagnostic Tests
○ Clinical presentation
○ Distinct hallmark of disease: recent onset of cough
■ Not reliable diagnostic indicator
● Purulent sputum
● Increased WBC count
○ Chest x-ray to distinguish acute bronchitis from pneumonia (PNA
displays pulmonary infiltrates= white & hazy on X-ray)
● Clinical Manifestations
○ Usually mild and self-limiting
○ Cough (productive or nonproductive)
■ Recent onset
○ Low-grade fever
○ Substernal chest discomfort
○ Sore throat
○ Postnasal drip
○ Fatigue
Chronic Bronchitis (pg 495-497)
● Pathophysiology
○ Patients with emphysema and chronic bronchitis constitute most
cases of COPD
○ Pts can have both Type A and B
● Etiology (AKA risk factors)
○ Cigarette smoking (90%) (changes cililated cells to squamous cells-aka flat cell- so lungs can’t clear airways and
“junk” builds up)
○ Repeated airway infections
○ Overweight
○ Genetic predisposition
○ Inhalation of physical or chemical irritants
○ Chronic or recurrent productive cough greater 3
months and greater 2+ successive years
○ Type B COPD, “blue bloater”
■ A, A hypoxemic patient with edema from
right-sided heart failure. B, A patient with
chronic obstructive bronchitis. Note the
stocky build and the presence of pursed-lip
breathing. The slight gynecomastia is a side
effect of corticosteroid therapy. The
2
, patient's shoulders are raised because of shortness of breath and increased work of breathing
○ Hypersecretion of bronchial mucus
○ Persistent, irreversible when paired with emphysema
○ 1:2 male to female ration
○ GREATEST risk are those greater than 30-40 years!
● Pathogenesis
○ Chronic inflammation and swelling of the bronchial mucosa resulting in scarring
■ Elevated interleukin 8 (IL8) levels recruit neutrophil activation (1st responders)
■ Elevated CD8 T-lymphocytes
■ Extend into surrounding alveoli prevents proper oxygenation and potentiates airway obstruction
○ Hyperplasia of bronchial mucous gland/goblet cells
■ The mucociliary clearance action is impaired or lost, and some areas of ciliated columnar epithelium are
replaced by squamous cells.
■ Ciliary dysfunction occurs because of a decreased number of cilia and decreased action of available cilia.
■ Increased mucus production with formation of mucus plugs
○ Increased bronchial wall thickness
■ Resistance increases work of breathing and O2 demands High airflow resistance increases the work of
breathing, leading to increased oxygen demands. In areas of greater obstruction to airflow, alveoli empty and
fill more slowly, leading to ventilation–perfusion (V̇A/Q̇) mismatch, thus lowering arterial oxygenation.
■ The chronic bronchitis patient may appear as the “blue bloater” characterizing the pathophysiologic process
of oxygen desaturation (cyanosis) and edema associated with right-sided heart failure in advanced disease or
exacerbations.
■ Ventilation-perfusion mismatch with
hypoxemia and hypercarbia; increases
pulmonary artery resistance - leads to
Pulmonary HTN
○ Pulmonary hypertension
■ Inflammation in bronchial walls with
vasoconstriction of pulmonary vessels
and arteries
■ Right-sided heart failure may occur r/t
high pulmonary resistance
NCLEX questions:
1. A significant increase in the resistance of
the pulmonary vasculature results in
pulmonary_hypertension .
2. Diseases that cause global pulmonary
hypoxemia usually are associated with pulmonary hypertension
because hypoxemia causes vasconstriction of pulmonary
vessels.
3. Pulmonary compliance is a reflection of
airway resistance and lung elasticity .
4. The respiratory centers of the brain are
located in the Medulla and _Pons.
● Diagnostic Tests
○ Chest x-ray → it will show increased bronchial vascular markings, congested lung fields,
enlarged cardiac silhouette, and evidence of previous pulmonary infection
○ Pulmonary function tests
○ Arterial blood gas (ABG) → increased CO2 and decreased 02 (DO NOT pt pt on too much O2 bc
it will be toxic!!)
○ ECG → atrial dysrhythmias d/t right ventricular enlargement
○ Secondary polycythemia → increased RBC’s r/t hypoxemia leading to increased production
of RBC to carry more 02 to tissues
3
, ● Clinical Manifestations
○ Typical patient is overweight
○ Commonly associated with emphysema
○ SOB on exertion
○ Excessive sputum
○ Chronic cough (more severe in mornings)
○ Evidence of excess body fluids (edema, hypervolemia)
○ Cyanosis (late sign)
○ crackles, rhonchi, and wheezes; use of accessory muscles to breathe; jugular vein
distention; clubbing; and pedal and ankle edema.
Emphysema (pg 498-500)
● Etiology
○ Type A COPD “Pink puffer”
○ Destructive changes of alveolar walls without fibrosis (decrease SA of aveoli)
○ Abnormal enlargement of the distal air sacs
○ Damage is irreversible
○ Associated with chronic bronchitis
○ Smoking >70 packs/year
○ Air pollution
○ Certain occupations (mining, welding, working with or near asbestos)
○ α1-Antitrypsin deficiency
● Pathogenesis
○ Groups of genes
○ Release of proteolytic enzymes from neutrophils and macrophages leading
to alveolar damage
○ α1-Antitrypsin deficiency
○ Smoking causes alveolar damage
○ Inflammation leads to release of proteolytic enzymes
■ See above image Neutrophil elastase
○ Inactivates α1-antitrypsin (normally protects lung
parenchyma)
○ Reduction in pulmonary capillary bed
○ Loss of elastic tissue in lung
○ Air becomes trapped in distal alveoli
○ Loss of alveolar wall and air trapping leads to bullae (large,
thin-walled cysts in the lung) formation
○ *****Acidosis at the beginning → alkalosis after a while bc of
“puffing out” acid
● Classifications (nice to know)
○ Centriacinar (centrilobular)
■ Associated with smoking and chronic bronchitis
■ Destroys respiratory bronchioles
○ Panacinar (panlobular)
■ Destroys the alveoli
○ Paraseptal
4
Alterations in Respiratory Function Concepts
Chapter 21: Alterations in Oxygenation
,Includes → Asthma, Bronchitis, and Emphysema. These diseases have increased resistance to airflow
***Use spirometry for initial diagnosis of respiratory disease
Vital capacity: total volume of gas that can be exhaled during maximal expiration (~4.8 L)
○ Includes inspiratory reserve volume, tidal volume, and expiratory reserve volume
Forced expiratory flow rate (FEF25, FEF50, FEF75): volume of air forcibly exhaled per unit time (liters per second or liters per
minute) at 25%, 50% and 75% of forced vital capacity (FVC)
Total Lung Capacity: Amount of gas contained in lungs at maximal inspiration (~6.0 L)
Acute Bronchitis (pg 494-495)
● Pathophsyiology
○ Acute inflammation of the trachea and bronchi
● Etiology
○ Viral or non-viral
■ Coronavirus
○ Heat
○ Smoke inhalation
○ Inhalation of irritant chemicals
○ Allergic reactions
● Pathogenesis
○ Airways become inflamed and narrowed from capillary dilation
○ Swelling from fluid exudation (pus)
○ Infiltration with inflammatory cells (Mast cells & Basophils)
○ Increased mucus production
○ Loss of ciliary function (can’t get rid of waste in airways bc no movement of cells)
○ Loss of portions of the cilated epithelium
● Diagnostic Tests
○ Clinical presentation
○ Distinct hallmark of disease: recent onset of cough
■ Not reliable diagnostic indicator
● Purulent sputum
● Increased WBC count
○ Chest x-ray to distinguish acute bronchitis from pneumonia (PNA
displays pulmonary infiltrates= white & hazy on X-ray)
● Clinical Manifestations
○ Usually mild and self-limiting
○ Cough (productive or nonproductive)
■ Recent onset
○ Low-grade fever
○ Substernal chest discomfort
○ Sore throat
○ Postnasal drip
○ Fatigue
Chronic Bronchitis (pg 495-497)
● Pathophysiology
○ Patients with emphysema and chronic bronchitis constitute most
cases of COPD
○ Pts can have both Type A and B
● Etiology (AKA risk factors)
○ Cigarette smoking (90%) (changes cililated cells to squamous cells-aka flat cell- so lungs can’t clear airways and
“junk” builds up)
○ Repeated airway infections
○ Overweight
○ Genetic predisposition
○ Inhalation of physical or chemical irritants
○ Chronic or recurrent productive cough greater 3
months and greater 2+ successive years
○ Type B COPD, “blue bloater”
■ A, A hypoxemic patient with edema from
right-sided heart failure. B, A patient with
chronic obstructive bronchitis. Note the
stocky build and the presence of pursed-lip
breathing. The slight gynecomastia is a side
effect of corticosteroid therapy. The
2
, patient's shoulders are raised because of shortness of breath and increased work of breathing
○ Hypersecretion of bronchial mucus
○ Persistent, irreversible when paired with emphysema
○ 1:2 male to female ration
○ GREATEST risk are those greater than 30-40 years!
● Pathogenesis
○ Chronic inflammation and swelling of the bronchial mucosa resulting in scarring
■ Elevated interleukin 8 (IL8) levels recruit neutrophil activation (1st responders)
■ Elevated CD8 T-lymphocytes
■ Extend into surrounding alveoli prevents proper oxygenation and potentiates airway obstruction
○ Hyperplasia of bronchial mucous gland/goblet cells
■ The mucociliary clearance action is impaired or lost, and some areas of ciliated columnar epithelium are
replaced by squamous cells.
■ Ciliary dysfunction occurs because of a decreased number of cilia and decreased action of available cilia.
■ Increased mucus production with formation of mucus plugs
○ Increased bronchial wall thickness
■ Resistance increases work of breathing and O2 demands High airflow resistance increases the work of
breathing, leading to increased oxygen demands. In areas of greater obstruction to airflow, alveoli empty and
fill more slowly, leading to ventilation–perfusion (V̇A/Q̇) mismatch, thus lowering arterial oxygenation.
■ The chronic bronchitis patient may appear as the “blue bloater” characterizing the pathophysiologic process
of oxygen desaturation (cyanosis) and edema associated with right-sided heart failure in advanced disease or
exacerbations.
■ Ventilation-perfusion mismatch with
hypoxemia and hypercarbia; increases
pulmonary artery resistance - leads to
Pulmonary HTN
○ Pulmonary hypertension
■ Inflammation in bronchial walls with
vasoconstriction of pulmonary vessels
and arteries
■ Right-sided heart failure may occur r/t
high pulmonary resistance
NCLEX questions:
1. A significant increase in the resistance of
the pulmonary vasculature results in
pulmonary_hypertension .
2. Diseases that cause global pulmonary
hypoxemia usually are associated with pulmonary hypertension
because hypoxemia causes vasconstriction of pulmonary
vessels.
3. Pulmonary compliance is a reflection of
airway resistance and lung elasticity .
4. The respiratory centers of the brain are
located in the Medulla and _Pons.
● Diagnostic Tests
○ Chest x-ray → it will show increased bronchial vascular markings, congested lung fields,
enlarged cardiac silhouette, and evidence of previous pulmonary infection
○ Pulmonary function tests
○ Arterial blood gas (ABG) → increased CO2 and decreased 02 (DO NOT pt pt on too much O2 bc
it will be toxic!!)
○ ECG → atrial dysrhythmias d/t right ventricular enlargement
○ Secondary polycythemia → increased RBC’s r/t hypoxemia leading to increased production
of RBC to carry more 02 to tissues
3
, ● Clinical Manifestations
○ Typical patient is overweight
○ Commonly associated with emphysema
○ SOB on exertion
○ Excessive sputum
○ Chronic cough (more severe in mornings)
○ Evidence of excess body fluids (edema, hypervolemia)
○ Cyanosis (late sign)
○ crackles, rhonchi, and wheezes; use of accessory muscles to breathe; jugular vein
distention; clubbing; and pedal and ankle edema.
Emphysema (pg 498-500)
● Etiology
○ Type A COPD “Pink puffer”
○ Destructive changes of alveolar walls without fibrosis (decrease SA of aveoli)
○ Abnormal enlargement of the distal air sacs
○ Damage is irreversible
○ Associated with chronic bronchitis
○ Smoking >70 packs/year
○ Air pollution
○ Certain occupations (mining, welding, working with or near asbestos)
○ α1-Antitrypsin deficiency
● Pathogenesis
○ Groups of genes
○ Release of proteolytic enzymes from neutrophils and macrophages leading
to alveolar damage
○ α1-Antitrypsin deficiency
○ Smoking causes alveolar damage
○ Inflammation leads to release of proteolytic enzymes
■ See above image Neutrophil elastase
○ Inactivates α1-antitrypsin (normally protects lung
parenchyma)
○ Reduction in pulmonary capillary bed
○ Loss of elastic tissue in lung
○ Air becomes trapped in distal alveoli
○ Loss of alveolar wall and air trapping leads to bullae (large,
thin-walled cysts in the lung) formation
○ *****Acidosis at the beginning → alkalosis after a while bc of
“puffing out” acid
● Classifications (nice to know)
○ Centriacinar (centrilobular)
■ Associated with smoking and chronic bronchitis
■ Destroys respiratory bronchioles
○ Panacinar (panlobular)
■ Destroys the alveoli
○ Paraseptal
4
