Ch23

Report
Essentials of Pathophsiology
CHAPTER 23
DISORDERS OF VENTILATION AND
GAS EXCHANGE
PRE LECTURE QUIZ
TRUE/FALSE
F

Pleural, musculoskeletal, and myocardial pain are similar
in description and almost impossible to differentiate.
T

Extrinsic or atopic asthma is typically initiated by a type I
hypersensitivity reaction induced by exposure to an
extrinsic antigen or allergen, such as dust mite allergens,
cockroach allergens, and animal dander.
F

Persons with emphysema are often labeled as “blue
bloaters” because of the chronic hypoxemia and eventual
right-sided heart failure with peripheral edema.
F

Cystic fibrosis is manifested by pancreatic exocrine
deficiency and a noted decrease in levels of sodium
chloride in the sweat.
F

Hypercapnia refers to an abnormal increase in oxygen
levels.
PRE LECTURE QUIZ
Asthma
Effusion
Embolism

A pleural __________ refers to an abnormal collection of
fluid in the pleural cavity.

__________ is a leading cause of chronic illness in
children and is responsible for a significant number of
lost school days; it is also the most frequent admitting
diagnosis in children’s hospitals.

A __________ pneumothorax, a life-threatening
condition, occurs when the intrapleural pressure
exceeds atmospheric pressure, permitting air to enter
but not leave the pleural space.

A pulmonary __________ develops when a blood-borne
substance lodges in a branch of the pulmonary artery
and obstructs the flow.

Cor pulmonale refers to __________-sided heart failure
resulting from primary lung disease and involves
hypertrophy and eventual failure of that ventricle.
Right
Tension
CAUSES OF RESPIRATORY FAILURE

Hypoventilation  hypercapnia, hypoxia





Depression of the respiratory center
Diseases of respiratory nerves or muscles
Thoracic cage disorders
Ventilation–perfusion mismatching
Impaired diffusion  hypoxemia but not hypercapnia




Interstitial lung disease
ARDS
Pulmonary edema
Pneumonia
HYPOXEMIA
 PO2 <60 mm Hg



Cyanosis
Impaired function of vital centers

Agitated or combative behavior, euphoria, impaired
judgment, convulsions, delirium, stupor, coma

Retinal hemorrhage

Hypotension and bradycardia
Activation of compensatory mechanisms

Sympathetic system activation
HYPERCAPNIA

PCO2 >50 mm Hg

Respiratory acidosis
CO2 + H2O H2CO3 H+ + HCO3-

Increased respiration

Decreased nerve firing

º
Carbon dioxide narcosis
º
Disorientation, somnolence, coma
Decreased muscle contraction
º
Vasodilation

Headache; conjunctival hyperemia; warm, flushed skin
QUESTION
Tell whether the following statement is true or
false.
Both hypercapnia and hypoxemia will lead to
respiratory failure if untreated.
ANSWER
True
Rationale: In hypercapnia (PCO2 >50 mm Hg),
tissues accumulate carbon dioxide; in
hypoxemia (PO2 <60 mm Hg), less oxygen is
delivered to the tissues. In both cases, gas
exchange is impaired, and respiratory failure
will result unless the conditions are corrected
(with oxygen, mechanical ventilation, etc.).
PLEURAL DISORDERS DECREASE VENTILATION
Parietal pleura lines
the thoracic wall and
superior aspect of the
diaphragm
 Visceral pleura covers
the lung
 Pleural cavity or space
between the two
layers contains a thin
layer of serous fluid

SCENARIO

Mr. K presents himself with a stab wound

Now he is having breathing problems, and his breath
sounds are diminished on the side with the wound

His trachea seems to be slanting toward the other side of
his chest, and his heart sounds are displaced away from
the wound

He has an increased respiration rate and blood pressure,
is pale and sweating with bluish nail beds, and has no
bowel sounds
Question:

Explain the effects of the wound
PNEUMOTHORAX
 Air enters the pleural cavity
 Air takes up space, restricting lung expansion
 Partial or complete collapse of the affected
lung
Spontaneous: an air-filled blister on the lung
ruptures
 Traumatic: air enters through chest injuries

º
º
Tension: air enters pleural cavity through the wound on
inhalation but cannot leave on exhalation
Open: air enters pleural cavity through the wound on
inhalation and leaves on exhalation
OPEN PNEUMOTHORAX
Air Comes
in
Air goes
out
TENSION PNEUMOTHORAX
Air comes
in
Air is
trapped
QUESTION
Tell whether the following statement is true or
false.
Open pneumothorax is more life-threatening than
tension pneumothorax.
ANSWER
False
Rationale: In open pneumothorax, inhaled air
compresses the affected side’s lung, but during
exhalation, the lung reinflates somewhat. In
tension pneumothorax, a sort of one-way valve
exists: the air enters the affected side during
inhalation, but is unable to leave when the patient
exhales. Therefore, all of this air exerts increased
pressure on the organs of the thoracic cage.
Unless the pressure is relieved, tension
pneumothorax is fatal.
PLEURAL EFFUSION—FLUID IN THE PLEURAL
CAVITY

Hydrothorax: serous fluid
an accumulation of fluid in one or both pleural cavities,
often resulting from disease of the heart or kidneys

Empyema(em-pī-ē-mə) : pus
fluid in the pleural space secondary
to leakage from the thoracic duct


Chylothorax: lymph
Hemothorax: blood
OBSTRUCTIVE AIRWAY DISORDERS


Bronchial asthma
Chronic obstructive airway diseases
 Chronic bronchitis
 Emphysema
 Bronchiectasis
 Cystic fibrosis
PATHOGENESIS OF BRONCHIAL ASTHMA
Early Phase
Antigen
IgE
Cytokine Release
Muscle Spasm
Late Phase
Mast Cell Activation
Vascular porosity
Edema and WBC infiltration
Epithelial Damage
Muscle Spasm with edema
EXTRINSIC (ATOPIC) ASTHMA
Type I hypersensitivity
 Mast cells’
inflammatory mediators
cause acute response
within 10–20 minutes
 Treat with inhalers
 Airway inflammation
causes late-phase
response in 4–8 hours
 Treat with antiflamatory

Allergen
Mast cells release
inflammatory
mediators
WBCs enter region
and release more
inflammatory
mediators
INTRINSIC (NONATOPIC) ASTHMA




Respiratory infections
 Epithelial damage, IgE production
Exercise, hyperventilation, cold air
 Loss of heat and water may cause
bronchospasm
Inhaled irritants
 Inflammation, vagal reflex
Aspirin and other NSAIDs
 Abnormal arachidonic acid metabolism
AIRWAY OBSTRUCTION IN ASTHMA
airway
inflammation
impaired
mucociliary
function
inflammatory
mediators
epithelial
injury
increased
airway
responsiveness
bronchospasm
edema
airflow limitation
QUESTION
Which of the following occurs in asthma?
a. Airway inflammation
b. Bronchospasm
c. Decreased ability to clear mucus
d. All of the above
ANSWER
All of the above
Rationale: Inflammatory mediators lead to airway
inflammation, edema of the mucous lining of
the airways, bronchospasm, and impaired
ability to clear secretions. All of these things
cause the airways to narrow during an asthma
attack.
d.
CHRONIC OBSTRUCTIVE PULMONARY
DISORDERS



Emphysema
 Enlargement of air spaces and destruction of
lung tissue
Chronic obstructive bronchitis
 Obstruction of small airways
Bronchiectasis
 Infection and inflammation destroy smooth
muscle in airways, causing permanent
dilation
the bronchi are distended, characterized by sudden
violent coughing and copious expectoration of
sputum, and which often become infected
MECHANISMS OF COPD




Inflammation and fibrosis of bronchial wall
Hypertrophied mucus glands  excess mucus
 Obstructed airflow
Loss of alveolar tissue
 Decreased surface area for gas exchange
Loss of elastic lung fibers
 Airway collapse, obstructed exhalation, air trapping
Mechanism of COPD
A) Inflammation, Fibrosis
B) Hypersecretion of
mucus
C) Destruction of elastic
fibers that hold the
airways open
EMPHYSEMA


Neutrophils in alveoli secrete trypsin
 Increased neutrophil numbers due to inhaled
irritants can damage alveoli
Alpha1-antitrypsin inactivates the trypsin before it
can damage the alveoli
 A genetic defect in alpha1-antitrypsin synthesis
leads to alveolar damage
TYPES OF EMPHYSEMA
Emphysemia Chest Wall Shape
CHRONIC BRONCHITIS


Chronic irritation of airways
 Increased number of mucus cells
 Mucus hypersecretion
Productive cough
PINK PUFFERS VS. BLUE BLOATERS

Pink puffers (usually emphysema)
 Increase
respiration to maintain oxygen levels
 Dyspnea; increased ventilatory effort
 Use accessory muscles; pursed-lip breathing

Blue bloaters (usually bronchitis)
 Cannot
increase respiration enough to
maintain oxygen levels
 Cyanosis and polycythemia
 Cor pulmonale
QUESTION
Which chronic obstructive pulmonary disease
primarily affects the alveoli?
a. Asthma
b. Emphysema
c. Chronic bronchitis
d. Bronchiectasis (dilitation)
ANSWER
Emphysema
Rationale: In emphysema, alveolar walls are
destroyed. The other chronic pulmonary
diseases listed primarily affect the airways.
b.
COPD AND BLOOD PH
Discussion:
 In what range will a COPD client’s blood
pH fall? Normal when stabilized & down to 7.3 unstabilized
 Why?
CO2 +H2O
H2CO3
H+ + HCO3-
Venous blood gas
Respiratory acidosis(lung induced): Low pH, High CO2, Low HCO3Metabolic (tissue induced): Low pH, High CO2, Normal HCO3-
CONSEQUENCES OF COPD


Which step in this flow
chart will cause the
central chemoreceptors
to increase respiration?
Which will cause the
peripheral
chemoreceptors to
increase respiration?
COPD
decreased
ability to
exhale
stale air in
lungs
low O2
levels
hypoxia
high
CO2
levels
hypercapnia
SCENARIO
A client with chronic bronchitis has a barrel
chest and cyanosis. His pulse oximeter reads
86% oxygenation. His PO2 is 54 mm Hg. His
PCO2 is 56 mm Hg.
 He is put on low-flow oxygen but complains of
shortness of breath. Somebody turns the O2
flow up. He is found in a coma with a PCO2 of
59 mm Hg and a blood pH of 7.2.
Question:
 What was the cause of the coma? Why?

CYSTIC FIBROSIS

Recessive disorder in chloride transport proteins
 High concentrations of NaCl in the sweat
 Less Na+ and water in respiratory mucus and in
pancreatic secretions
º Mucus is thicker
 Obstructs airways
 Obstructs pancreatic and biliary ducts
PATHOGENESIS OF CYSTIC FIBROSIS
Cystic Fibrosis Transmembrane
Regulator Gene Failure
CYSTIC FIBROSIS MANIFESTATIONS
Discussion:

A client with cystic fibrosis is having respiratory
problems and:
 Digestive problems
 Flatulence
Steatorrhea is the presence of excess fat in
feces. Stools may also float due to excess lipid,
 Steatorrhea
have an oily appearance and be especially foul
 Weight loss
smelling.
Question:

He does not understand why a respiratory disease
would cause these problems. How would this be
explained to the client?
PULMONARY BLOOD FLOW
In a COPD client, exhalation is inefficient and O2 levels in
the lungs decrease
 If blood goes through the lungs filled with stale air, it will not
pick up much oxygen; it might even pick up CO2
Discussion:
 What will the pulmonary arterioles do?
 Which side of the heart will be affected? Why?

DISORDERS OF PULMONARY BLOOD FLOW
Pulmonary embolism
 Pulmonary hypertension

 Primary
º
Blood vessel walls thicken and constrict
 Secondary
º
º
º
º
Elevation of pulmonary venous pressure
Increased pulmonary blood flow
Pulmonary vascular obstruction
Hypoxemia
PULMONARY EMBOLISM
Results of Pulmonary Hypertension
Occluded pulmonary
artery
COR PULMONALE

Right-sided heart failure secondary to
respiratory disease
 Decreased
lung ventilation
 Pulmonary vasoconstriction
 Increased workload on right heart
 Decreased oxygenation
 Kidney releases erythropoietin  more RBCs
made
 Polycythemia makes blood more viscous
 Increased workload on heart
ACUTE RESPIRATORY DISTRESS SYNDROME
(ARDS)


Exudate enters alveoli
 Blocks gas exchange
 Makes inhalation more difficult
Neutrophils enter alveoli
 Release inflammatory mediators
 Release proteolytic enzymes
MECHANISMS OF LUNG CHANGES IN ARDS
QUESTION
Tell whether the following statement is true or
false.
Patients suffering from ARDS will be not
necessarily be hypoxemic.
ANSWER
False
Rationale: In ARDS the alveoli are filled with
exudate, decreasing the available surface area
for gas exchange. If gas exchange decreases,
poorly oxygenated or unoxygenated blood is
sent to the tissues (hypoxemia).

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