1. Outline the anatomy of the respiratory system and the process of gas exchange.
● The Upper Respiratory System protects the lungs from foreign matter. It warms, filters,
and humidifies air.
○ Includes the larynx and trachea
● The Lower Respiratory System participates in gas exchange at the alveoli, oxygenates
the blood, and excretes carbon dioxide.
○ Includes the right and left bronchus.
■ The right bronchus allows aspirated contents to enter the right middle and
lower lobe because it points straight down, and aspirated materials will
fall with gravity instead of having to go almost perpendicular to go into the
left more curved bronchus.
● Gas exchange occurs within the respiratory bronchioles, alveolar ducts, alveoli (alveoli
are surrounded by pulmonary capillaries) and they transfer oxygen and carbon dioxide.
2. Describe the processes of ventilation, perfusion, and diffusion and explain the
ventilation-perfusion ratio.
● Ventilation - The movement of air through the pulmonary airways
● Perfusion - The movement of blood through the pulmonary circulation
● Diffusion - Exchange of oxygen to carbon dioxide
● Oxygenation - Providing cells with oxygen
● Ventilation Perfusion Ratio - Ratio of the amount of air (ventilation) reaching the alveoli
○ Ideally, ventilation and perfusion are equal
○ When ventilation and perfusion are unequal, there is a ventilation/perfusion
mismatch
3. Define common signs of lung pathophysiology: dyspnea, cough, hemoptysis, and
atelectasis.
● Dyspnea - Difficulty breathing, laboured breathing
● Cough - Expelling air quickly, is in response to a mechanical or chemical stimulus.
● Hemoptysis - Coughing up blood or blood stained mucus from the bronchi
● Atelectasis - Partial or complete collapse of the lung
4. Define hypercapnia and hypoxemia. Relate these terms to respiratory failure.
● Hypercapnia - Increased levels of CO2
○ Usually caused by inadequate respiration, respirations are not expelling CO2
from the lungs, making the body more acidic.
● Hypoxemia - Decreased levels of O2
○ Oxygen deprivation can cause damage to many different organs, including the
brain. Oxygen is not making its way into the lungs and bloodstream.
5. Apply the concept of oxygenation to Pulmonary Embolism (PE).
An embolus lodged in the pulmonary artery suddenly raises pressure from within. This acute
rise in pressure within the pulmonary artery pressure places an overwhelming amount of
Tessier Patho Study Guide EXAM 1
resistance against the right ventricle. This can rapidly and severely weaken the right ventricular
muscle, causing acute right ventricular failure.
a. Explain the risk factors for the development of a Pulmonary Embolism.
Age, Ethnicity, Family history and genetics, diabetes, obesity, lifestyle factors, medications,
sleep apnea, congenital heart defects, viruses, alcohol abuse, kidney conditions.
b. Outline the pathophysiology of a Pulmonary Embolism and explain the ventilationperfusion mismatch that is occurring.
● Patho - A thrombus develops, and travels from the leg vein into the inferior vena cava,
continue upward into the into the right side of the heart and into the pulmonary arterial
circulation. When the thrombus enters the pulmonary circulation, it becomes a Pe which
is frequently fatal.
● Pulmonary Embolism creates a ventilation-perfusion mismatch because it is ventilation
without perfusion. Air is still reaching the alveoli, but perfusion in the pulmonary
circulation is blocked by the pulmonary embolism.
c. Explain the typical clinical presentation, common diagnostics, and expected treatments.
● S/S - Dyspnea, chest pain, increased respiratory rate, sudden respiratory distress,
tachycardia
● Diagnosis - V-Q scan shows decreased perfusion in the area of embolism blocking
circulation.
● Treatment - Anticoagulants, thrombolytic agents, pain medication, inferior vena cava
filter can inhibit clot travel into the right heart and pulmonary artery.
6. Apply the concept of oxygenation to Pneumonia.
Pneumonia is the inflammation of the lung tissue in which alveolar air spaces fill with purulent,
inflammatory cells, and fibrin.
a. Discuss the epidemiology and etiology of pneumonia. List and define the different types.
● Epidemiology - Causes more disease and death in the US than any other infection, and
more than 3 million cases occur each year. Various kinds include community acquired,
hospital acquired, and ventilator associated.
○ Community acquired (CAP) - is most often caused by Streptococcus
pneumoniae, influenzae, mycoplasma, Klebsiella, staphylococcus, and legionella
species, as well as gram negative organisms.
○ Aspiration pneumonia is commonly caused when anaerobic bacteria is
swallowed from the oropharynx.
○ Hospital acquired (HAP) - Major cause of mortality, Methicillin resistant
Staphylococcus (MRSA) as well as vancomycin resistant enterococcus.
○ Walking pneumonia is where the patient may not be appearing very ill but has
persistent cough and more commonly, headache and earache.
b. Explain risk factors for the development of pneumonia.
Tessier Patho Study Guide EXAM 1
●
●
●
●
●
Influenza infection. Viruses alter the makeup of the pulmonary immune defense system
and make the lungs vulnerable to bacterial infection referred to as secondary
pneumonia.
Other respiratory problems may also predispose individuals to a secondary bacterial
infection like pneumonia.
Immunosuppression can predispose people to pneumonia, such as HIV/AIDS.
Aspiration can predispose patients to pneumonia by accidental inhalation of substances
refluxed by the stomach. (those in a coma or with impaired gag reflexes are most at risk
for this occurring, as well as those with chronic gingivitis and periodontitis.
Other risk factors include lung cancer or tumours, COPD, bronchiectasis, smoking,
(alcohol and drug intoxication are relevant for aspiration pneumonia).
c. Outline the pathophysiology of pneumonia and explain the ventilation-perfusion
mismatch that is occurring.
● Patho - Caused by the inhalation of droplets containing bacteria or other pathogens. The
droplets enter the upper airways and gain entry into the lung tissue. Pathogens adhere
to respiratory epithelium and stimulate an inflammatory reaction. The acute inflammation
spreads to the lower respiratory tract and alveoli. At the sites of inflammation,
vasodilation occurs with the attraction of neutrophils out of capillaries and into the air
spaces. Neutrophils phagocytize microbes and kill them with reactive oxygen species,
antimicrobial proteins, adn degradative enzymes. There is an excessive stimulation of
respiratory goblet cells that secrete mucus. Mucous and exudative edema accumulate
between the alveoli and capillaries. The alveoli attempt to open and close against the
purulent exudate, however, some cannot open. The sounds heard with the stethoscope
over the alveoli opening against the exudative fluid are crackles. There is a layer of
edema dn infectious exudate at the capillary alveoli interface that hinders optimal gas
exchange. The patient can become hypoxic and hypercapnic, with obstructed exchange
of O2 and CO2 at the pulmonary capillaries.
● Ventilation-Perfusion Mismatch occurs because the fluid involved in pneumonia does not
assist in ventilation-perfusion balance. There is perfusion without ventilation. Blood is still
flowing through the pulmonary circulation, but the alveoli are blocked with mucus, etc,
and are not able to participate in gas exchange.
d. Explain the typical clinical presentation, common diagnostics, and expected treatments.
● Rule of Thumb - Assess exposure to other persons who are ill, evaluate if the patient
has any aspiration risks, or immunosuppression factors.
● Clinical presentation - Fever, crackles, and cough are the typical characteristics of
pneumonia. In elderly patients who are elderly, hypothermia may present instead of
fever. a
● Diagnosis - Chest x ray is most important. CBC with differential will suggest if it's
bacterial or viral in origin, and ABGs and pulse oximetry can demonstrate oxygenation.
Sputum culture and sensitivity can exhibit the organism and antibiotic susceptibility.
Tessier Patho Study Guide EXAM 1
●
Treatment - Antibiotic therapy and oxygenation of the patient are key priorities. Patients
may require intravenous fluids if dehydrated. Analgesia, antipyretics, and
bronchodilators may be needed.
7. Apply the concept of Acid-Base balance to Arterial Blood Gas (ABG) interpretation.
a. Define the components of an ABG and list expected values.
b. Interpret ABG results to determine acidotic vs alkalotic and the likely cause.
c. Identify common causes and clinical manifestations for each category of Acid-Base
Imbalance:
Imbalance
Metabolic Acidosis
Metabolic Alkalosis
Respiratory Acidosis
Respiratory Alkalosis
Lab Results
pH < 7.35
HCO3 decreased
(primary)
PCO2 decreased
(compensatory)
pH > 7.45
HCO3 increased
(primary)
PCO2 increased
(secondary)
pH < 7.35
PCO2 increased
(primary)
HCO3 is increased
(compensatory)
pH > 7.45
PCO2 decreased
(primary)
HCO3 is decreased
(compensatory)
Clinical
Presentation
Widespread changes
in neurological,
respiratory, GI, and
cardiovascular
function
Widespread changes
in neurological,
respiratory, GI, and
musculoskeletal
system.
Anxiety, restlessness,
headache, lethargy,
fatigue, SOB, tachypnea,
confusion, possible
coma
Tingling, muscle
cramps, dizziness,
confusion, anxiety,
palpitations
Potential
Causes
Excess acids in the
bloodstream (DKA,
lactic acidosis) or
excessive loss of
bicarbonate (diarrhea)
Ingestion or
administration of
excess bicarbonate or
other alkaline
substances. Excess
loss of H+, Cl-, and K+
(Gastric suctioning,
vomiting, and
potassium wasting
diuretics)
The body accumulates
too much CO2 or cannot
exhale enough. COPD,
pulmonary edema,
pneumonia, airway
obstruction,
hypoventilation, CF
(cystic fibrosis), OD
(Overdose), CNS
depression, cardiac
arrest
Lungs blow off too
much CO2 most
common acid base
abnormality in critically
ill patients.
Hyperventilation, PE,
asthma, anxiety, pain,
fever/sepsis
Compensatio Increased respiratory
n
rate and depth (reduce
PCO2) and increase
renal excretion of H+
and increased
reabsorption of HCO3
Decreased respiratory
rate and depth
(Increase PCO2)
Decreased renal
excretion of H+ and
decreased
reabsorption of HCO3
Kidneys attempt to
compensate by
reabsorbing HCO3 and
excreting H+
Kidneys attempt to
compensate by
reabsorbing H+ and
excreting HCO3
Treatments
Electrolyte and fluid
replacement.
Potassium-sparing
diuretics. Treat the
Improve ventilation,
administer oxygen,
bronchodilators, treat
respiratory infections,
Identify the trigger that
has caused
hyperventilation. Pain
management or
Identifying and
correcting the
underlying disorder. IV
sodium bicarbonate in
Tessier Patho Study Guide EXAM 1
severe cases. Treat
the cause is better.
cause is better
potential intubation
sedation to slow
breathing. Breathe into
a paper bag.
Define Ventilation - The process of inspiration and expiration of air through the pulmonary
airways. It is a continuous renewal of the air in the gas exchange areas of the lungs where the
air is in close proximity to the blood. Affected by body position and lung volume as well as by
disease conditions that affect the heart and respiratory system.
Define Perfusion - The flow of the blood through the gas exchange portion of the lung.
Deoxygenated blood travels from the large pulmonary artery (right side of the heart) and travels
to the capillary network that surrounds the alveoli. The oxygenated blood is then collected in the
pulmonary veins and moves to the pulmonary veins and moves to the large pulmonary veins
that empty into the left atrium. Adequate oxygenation of the blood and removal of CO2 depend
on the perfusion or movement of the blood through the pulmonary blood vessels and
appropriate contact between ventilated alveoli and perfused capillaries of the pulmonary
circulation.
Define Diffusion - The movement of gasses across the alveolar-capillary membrane. It is
affected by different pressures of gas on either side of the membrane, the surface area
available for diffusion, the thickness of the alveolar-capillary membrane and the diffusion
characteristics of the gas.
Define Oxygenation - The process of providing cells with oxygen through the respiratory
system and is accomplished by pulmonary ventilation, respiration, and perfusion. Nurses
encounter potential and actual alterations in oxygenation in all types of clients and must detect
problems and intervene early to prevent life-threatening complications.
Ventilation-Perfusion Ratio - Ratio of the amount of air (ventilation) reaching the alveoli to the
amount of blood (perfusion) reaching the alveoli. Ideally, these are equal to allow for optimal gas
exchange.
A Ventilation-Perfusion Mismatch occurs when the ventilation and perfusion levels are
unequal
Pneumonia creates a ventilation-perfusion mismatch because it is perfusion without ventilation.
Blood is still flowing through the pulmonary circulation, but the alveoli are blocked with mucus,
etc, and are not able to participate in gas exchange.
Tessier Patho Study Guide EXAM 1
Pulmonary Embolism creates a ventilation-perfusion mismatch because it is ventilation without
perfusion. Air is still reaching the alveoli, but perfusion in the pulmonary circulation is blocked by
the pulmonary embolism.
Tessier Patho Study Guide EXAM 1
WEEK 2
1. Describe and characterize the clinical presentations for chronic hypoxia and chronic
hypercapnia in terms of ventilation and oxygenation.
● Chronic hypercapnia - Occurs when lungs cannot fully expel carbon dioxide. Clinical
features include headache, drowsiness, intellectual impairment and disorientation. Can
develop due to bradypnea. Can occur with asphyxiation, aspiration, pneumonia,
pulmonary edema, thoracic muscle paralysis, and opiate toxicity.
● Chronic hypoxia - Occurs when lungs cannot fully ventilate or acquire maximal
oxygenation. Clinical presentations include increased ventilation, stimulating pulmonary
vasoconstriction, and having erythropoietin secreted from the kidneys (erythropoietin
stimulates bone marrow to synthesize more RBCs) Can also cause pulmonary arterial
vasoconstriction, leading to pulmonary hypertension.
2. Define and characterize the pathophysiology for obstructive and restrictive alterations
in oxygenation.
Obstructive Lung Diseases - The hallmark patho is an increased resistance to airflow.
Decreased volume and speed of airflow (low FEV1 and FVC ratio) with excessive mucus,
inflammation, loss of lung elastic recoil, oxygenation, and perfusion impairment
Restrictive Lung Diseases - Characterized by either reduction expansion of lung tissue with a
decreased total lung capacity, or that the lungs are stiff and inflexible.
3. Describe the following diagnostic studies: PFT (spirometry), arterial blood gas
analysis, chest radiographs, thoracentesis, and explain the changes that occur with
obstructive and restrictive alterations in oxygenation.
● PFT (spirometry) measures air on inhalation and exhalation
● ABG analysis determines acid/base imbalance, identifies the cause of the imbalance is
respiratory or metabolic, and shows whether or not compensatory mechanisms are
working.
● Thoracentesis - a needle is inserted into the pleural space between the lungs and the
chest wall to remove excess fluid from the pleural space to help you breathe easier.
● Chest radiographs - A chest xray is a fast and painless imaging test using
electromagnetic waves to create pictures of the struftures in and around your chest. This
test can help diagnose and monitor conditions such as pneumonia, heart failure, lung
cancer, tuberculosis, sarcoidosis, and lung tissue scarring (fibrosis)
4. Describe the interaction between heredity, alterations in the immune response, and
environmental agents in relation to the pathophysiology of obstructive asthma.
Asthma is a chronic inflammatory disease causing episodesof spastic reactivigtiy in the
bronchioles.
● Allergens is a common stimulus of asthma, where the allergen triggers the immune
system, causing bronchoconstriction, inflammation, and an increase in the size and
number of goblet cells that secretes mucus.
Tessier Patho Study Guide EXAM 1
●
●
People with allergies, occupational and chemical exposure, viral infections, a triad of
conditions like asthma, aspirin sensitivity, and nasal polyps, NSAID use, and exercise
can all trigger asthma.
Asthma is also commonly triggered by viral respiratory infections that stimulate the
production of IgE directed towards the viral antigens. This causes bronchospasm and
copious mucus production.
5.Relate the clinical presentations and complications of asthma to the pathologic
changes that occur in obstructive asthma.
● Clinical presentations like dyspnea, wheeze, or cough, environmental allergens like dust
or pet dander, episodes of respiratory infection or GERD. Are the symptoms worse at
night or after exercise?
● Asthma is characterized by wheezing, cough, dyspnea, and chest tightness. The
severity of the symptoms depend on the degree of bronchial hyperresponsiveness and
reversibility of the bronchial obstruction.
○ Prolonged exhalations are commonly an early sign of airway obstruction.
○ Severe attacks are accompanied by the use of accessory muscles, distant breath
sounds, and diaphoresis. The patient may only be able to speak one or two
words before taking a breath.
○ Patients going into respiratory failure caused by marked airway constriction have
inaudible breath sounds and a repetitive hacking coughing sounds. Rhonchi may
be present if larger bronchial airways are involved.
○ If asthma is related to allergies, signs of chronic rhinitis may be present, including
nasal edema, nasal polyps, rhinorrhea, and oropharyngeal erythema. Eczema,
which indicates allergy, may be present on the patient's skin, particularly the neck
and antecubital or popliteal spaces.
6. Compare and contrast the categories of obstructive asthma (mild intermittent, mild
persistent, moderate persistent, and severe persistent) and the impact on oxygenation.
●
●
●
●
Mild Intermittent - Symptoms occur less than 2 times a week during waking hours, and
less than 2x a month during the night. Attacks are brief, but varying in intensity.
FEV1/FVC ratio is normal.
Mild Persistent - symptoms are occurring more than 2x a week, but not as often as daily.
Night symptoms happen less than 2x a month. Asthma attacks may interfere with activity
temporarily. FEV1 is greater than or equal to 80% of normal. FEV1/FVC ratio is normal.
Moderate Persistent - Symptoms are occurring daily, and patients need to use quick
relief inhaler daily. Attacks are occuring at least 2x a week, interfering activity, and may
last for days at a time. Night symptoms wake patients 1 or more times a week. FEV1 is
between 60-80% of normal. FEV1/FVC ratio is reduced by 5%.
Severe Persistent - Symptoms are basically continuous. Activity is severely limited, and
asthma attacks and night symptoms are frequent. FEV1 is 60% of normal, and
FEV1/FVC ratio is decreased by more than 5%
Tessier Patho Study Guide EXAM 1
7. Characterize rescue and maintenance treatment methods in the pathophysiology of
obstructive asthma and relate them to complications in oxygenation.
●
●
Maintenance - long acting bronchodilators and antiinflammatory corticosteroids often in
the form of an inhaler medication. A common combination is adrenergic beta 2 agonist
and a corticosteroid. Alternatively an anticholinergic inhaler can be administered if an
adrenergic agonist is not effective. If additional maintenance control is needed, an oral
leukotriene antagonist can be added to the daily regimen. All of these work to long term
enhance bronchodilation.
Rescue - Short acting bronchodilators are used for acute asthma attacks. These rescue
medications are rapid acting, adrenergic beta2 agonists are administered through an
inhaler. If this is not sufficient, an oral corticosteroid is added to the regimen. An injection
of epinephrine can also be used if asthma exacerbation is severe.
8. Define and explain the distinction between chronic bronchitis and emphysema in
terms of pathophysiology and clinical presentations of obstructive COPD.
Chronic Bronchitis
Emphysema
Patho
- Chronic inflammation and edema in the airways.
Bronchial lining thickens, narrowing airways,
bronchoconstriction, destruction of cilia, increase
infection risk, and greater tissue damage.
- Chronic bronchitis is thought to be caused by
overproduction and hypersecretion of mucus by goblet
cells. Epithelial cells lining the airway response to toxic,
infectious stimuli by releasing inflammatory mediators
- During an exacerbation of chronic bronchitis, the
bronchial mucous membrane becomes hyperemic and
edematous with diminished bronchial mucociliary
function.This, in turn, leads to airflow impediment
because of luminal obstruction to small airways. The
airways become clogged by debris and this further
increases the irritation.The characteristic cough of
bronchitis is caused by the copious secretion of mucus
in chronic bronchitis.
- Emphysema affects the air spaces,
characterized by abnormal permanent
enlargement of lung air spaces with the
destruction of their walls without any fibrosis
and destruction of lung parenchyma with loss
of elasticity.
- Inflammatory response with neutrophils and
macrophages are activated, releasing
proteinases, and destroy elastin in the lungs,
decreasing their elasticity.
- There is abnormal permanent dilatation of
the airspaces and destruction of their walls
due to the action of the proteinases. This
results in a decrease in alveolar and the
capillary surface area, which decreases the
gas exchange.
- Chronic smoking or extreme overexposure to
noxious materials is often implicated.
Clinical
Presenta
tions
- Persistent productive cough lasting for 3 months or
longer.
- Colour dusky to cyanosis, recurrent cough and
increased sputum production, hypoxia, hypercapnia,
respiratory acidosis, increased hemoglobin, increased
respiratory rate, exertional dyspnea.
- Greater incidence occurs in cigarette smokers
- Digital clubbing, cardiac enlargement, use of
- Increased CO2 retention, pink skin, minimal
cyanosis, pursed lip breathing, dyspnea,
hyperresonance on chest percussion,
orthopneic, barrel chest, exertion dyspnea,
prolonged expiratory time, speaks in short,
jerky sentences, anxious, use of accessory
muscles to breathe, and thin appearance.
Tessier Patho Study Guide EXAM 1
accessory muscles to breathe, and leading eventually to
right sided ventricular failure.
●
●
●
COPD is characterized by poorly reversible airflow limitation. Therefore COPD includes
the narrowing, excessive mucus, and fibrosis in the bronchioles, loss of alveolar elastic
recoil, and smooth muscle hypertrophy. There is permanent remodelling of the
pulmonary structure.
The bronchioles and alveoli in COPD with the chronic bronchitis sections, there is
inflammation, edema, and excessive mucus, and in emphysema, there is an excess of
air in the alveoli. The alveolar walls are weakened, distended, and cannot recoil. Some
alveoli are also atelectatic from lack of ventilation.
In severe COPD, particularly in the areas demonstrating changes consistent with chronic
bronchitis, there is poor ventilation and hypoxia. The hypoxia stimulates pulmonary
arterial vasoconstriction/pulmonary hypertension, causing an increased resistance in the
main pulmonary artery, and in turn, increased resistance against the right ventricle. Can
eventually lead to hypertrophy and failure of the right ventricle as well.
9. Describe the treatment methods for obstructive COPD and the impact oxygen therapy
has on oxygenation.
●
●
●
●
Treatment of COPD includes a stepwise approach beginning with short-acting
bronchodilators for patients with mild disease.
Non-pharmacological interventions include smoking cessation, pneumococcal and
influenza vaccines to prevent flare ups exacerbated by more respiratory problems,
pulmonary rehabilitation, and oxygen therapy.
○ Continuous oxygen therapy has to be used in the lowest doses that can enhance
the patient's oxygenation. When oxygen is administered to a patient with severe
COPD, oxygen administration higher than 2 liters per minute will decrease or
interrupt the stimulus for breathing and can result in respiratory arrest
○ In addition to this, tranquilizers, sedatives, and opiates can depress respiratory
drive and cause respiratory failure in patients with severe COPD
Mechanical ventilator support is indicated for patients that are in severe respiratory
distress. There is a very high mortality rate, and for those older than 65 the mortality rate
is already high DOUBLES.
Lung volume reduction surgery is indicated in severe emphysema. This removes the
most damaged alveoli and decreases the degree of lung hyperinflation. These dead
spaces do not allow diffusion of oxygen into circulation.
10. Compare and differentiate among the causes and presentations of (restrictive)
primary spontaneous pneumothorax, traumatic pneumothorax, and tension
pneumothorax pneumothorax.
Pneumothorax is also known as a collapsed lung. It is the presence of air in the pleural cavity
that causes collapse of a large section or a whole lobe of lung tissue.
Tessier Patho Study Guide EXAM 1
●
●
●
Primary Spontaneous Pneumothorax - Occurs without underlying lung disease and in
the absence of an inciting event. Air is present in the intrapleural space without
preceding trauma or underlying clinical evidence of lung disease. Mostly seen in tall
young men between 10-30 years old.
Traumatic Pneumothorax - Commonly caused by a penetrating wound of the thoracic
cage and underlying pleural membrane. The punctured thoracic cage and pleural
membrane create an opening between the pleural cavity and outside atmosphere. The
open wound allows the pleural cavity, which is normally a vacuum. To pull air into the
opening of the wound from the atmosphere and build up in pleural space. The
accumulated intrapleural air eventually compresses the lung tissue and causes lung
collapse.
○ Open - Chest wall is penetrated (trauma knife) air is pulled into the opening from
the atmosphere and builds up in the pleural space
○ Closed - Chest wall is intact (fractured rib) lung insult, air to escape into pleural
space and cannot return. Shifts mediastinum.
Tension Pneumothorax - There is an escalating buildup of air within the pleural cavity
that compresses the lung, bronchioles, cardiac structures and the vena cava. There is a
closed, penetrating wound that allows air into the pleural cavity, but will not allow air out.
Increasing air accumulation causes a rapid rise in intrathoracic pressure, which inhibits
venous return and optimal function of the heart and lungs.
11. Characterize the pathophysiology and diagnostics for transudative and exudative
restrictive pleural effusion.
Pleural Effusion is the abnormal collection of fluid in pleural cavities.
● Patho - The pleural space should be free of any additional fluid or air. Pleural effusions
result from disruptions of the balance between hydrostatic and oncotic forces in the lung
tissue. When hydrostatic pressure in the lung tissue greatly exceeds oncotic pressure,
fluid leaks out of the pulmonary capillaries and cells into the pleural space.
● Presentations - Restrictive ventilator, decreased total lung capacity, ventilation issues,
perfusion mismatches that can compromise cardiac output.
○ S/S include dyspnea, tachypnea, shart pleuritic chest pain, dullness to
percussion, diminished breath sounds on affected side.
● Diagnostics - Labs want to determine whether fluid is transudate, exudate, lymph, or
sanguineous.
○ Transudate - Straw coloured and clear, caused by a noninflammatory process
such as ascites, heart failure
○ Exudate is cloudy with a high protein, flank pus. Caused by infectious processes
in the pleural spaces such as cancer or a pulmonary infarction.
12. Differentiate the clinical presentations of pleural effusion from a pneumothorax and
explain the effects of restrictive pleural effusion on oxygenation.
Tessier Patho Study Guide EXAM 1
●
●
Clinical presentations of a Pleural Effusion are dyspnea, tachypnea, sharp pain, dullness
on percussion, and diminished breath sounds on the affected side. The area not filled by
lung is full of fluid.
Clinical presentation of Pneumothorax is chest pain, dyspnea, and increased respiratory
rate. There may be an obvious asymmetry, and percussion may show hyperresonance
because there is an openness in the lung space on the affected side. On auscultation
there may be a lack of breath sounds on the affected side.
How long does the body normally respond to low
oxygen or increased carbon dioxide in the blood
or tissues?
Chemoreceptors will begin firing to maintain
homeostasis. The transmitters will increase
breathing when low O2 in an attempt to get more
O2 or to increase breathing for high CO2 to rid the
excess CO2. The rate of breathing (faster or
slower) will depend on the needs of the body at
the time.
High pitched wheezing sounds are due to what?
Airway Constriction
What is the role of immunoglobulins in asthma?
When exposed to certain allergens, the body
releases IgE which then binds to mast cells, then
stimulates immune response causing the airway to
become narrow and inflamed
Why would someone use pursed-lip breathing?
Ease shortness of breath, it promotes deep
breathing
What causes digital clubbing?
Chronic hypoxia. Either perfusion (cardiac) or
oxygenation (respiratory) or both are related.
Tessier Patho Study Guide EXAM 1
What causes a barrel chest?
Due to lungs being chronically overinflated with
air, so the rib cage stays partially expanded all the
time
How to kidneys compensate for hypoxia?
Kidneys secrete erythropoietin - the process of
erythropoiesis
What is cor pulmonale
Condition of right ventricular failure - increased
workload for the right ventricle due to chronic
hypoxia
What is chronic hypercapnia? In addition what
factors contribute to chronic hypercapnia?
Excessive accumulation of CO2. Inadequate
ventilation, obstructed gas exchange all contribute
to chronic hypercapnia.
What is lung compliance
The elasticity of the lungs
Who is at risk for respiratory acidosis
COPD patients - high levels of CO2 accumulation
Why is a tension pneumothorax an emergent
event?
It is a closed event that allows air in, but not out.
An increase in air and pressure then displaces the
heart and other vessels. Significant respiratory
and circulation impairment.
How does a pleural effusion affect oxygenation
The main effect of pleural effusion in oxygenation
is a ventilation-perfusion mismatch. Pleural
effusions cause a restrictive ventilator defect with
decreased total lung capacity which results in poor
delivery of oxygen to the blood vessels
Tessier Patho Study Guide EXAM 1
Tessier Patho Study Guide EXAM 1
Characteristics
Obstructive
Restrictive
Resistance to airflow
increased pressure
Either reduced expansion of
lung tissue with decreased
total lung capacity or that
lungs are stiff and
noncompliant.
- DEcreased expansion space is occupied by air or
fluid or low compliance lungs are stiff and have
decreased flexibility.
Hard to get air OUT
O - obstruct
U - under (decreased) FEV1
T - trapped air
Hard to get air IN
I - impede expansion
N - noncompliant stiff lungs
Causes
COPD, Asthma, emphysema,
chronic bronchitis, secretions,
bronchospasms, trach tubes
Reduced expansion - pleural
effusion, pneumothorax,
hemothorax, lung abscess
Stiff lungs - atelectasis,
pneumonia, pulmonary
edema, pulmonary fibrosis,
ARDS
Diagnosis
PFTs - decreased or low
FEV1 and a low FEV1/FVC
ratio
Chest x-ray or CT scan, pulse
ox, ABGs, percussion, labs
(fluid and secretions analysis)
PFTs normal or decreased
FEV! And the FEV1/FVC ratio
Treatment
Bronchodilators - acute
(short-acting med) or longacting (corticosteroids, O2)
Needle aspiration, chest tube,
O2, thoracentesis,
pleurodesis
Pneumothorax (collapsed lung) - the collection of air in the spaces around the lungs. The air
buildup puts pressure on the lung so it cannot expand normally; this pressure causes the lung to
collapse.
Open vs. Closed Pneumothorax
Tessier Patho Study Guide EXAM 1
Open - there has to be an opening through the chest wall which allows the entrance of air
(positive atmospheric pressure) into the pleural space. Open pneumothorax includes open
traumatic.
Open traumatic pneumothorax occurs when air escapes from a laceration (stab wound) in
the lung itself and enters the pleural space.
Closed - air enters the pleural space through a breach of either the parietal or visceral
pleura. Open pneumothorax includes spontaneous, closed traumatic, and tension. The
most common closed pneumothorax is spontaneous or simple.
Spontaneous Pneumothorax is the rupture of blebs. Blebs are small air blisters that can
develop on the surface of the lungs. These blebs can burst spontaneously (without trauma)
which allows air to leak into the pleural space that surrounds the lungs. Spontaneous
pneumothorax is most common in males between 20 and 40 years old, especially if the person
is very tall and underweight. Other risks include the same risks for all types: smoking, genetics,
lung disease, mechanical ventilation, or previous pneumothorax.
Closed traumatic pneumothorax from a wound in the chest wall (blunt trauma - crush
injury, broken rib).
Tension pneumothorax occurs when air is drawn into the pleural space from a lacerated lung
or through a small opening or closed wound in the chest wall. The most common cause of
tension pneumothorax is penetrating trauma (stabbing injury or a gunshot). The
penetrating wound creates a sucking chest wound. A sucking chest wound produces an
abnormal passageway for gas exchange into the pleural spaces which results in air trapping.
Tessier Patho Study Guide EXAM 1