CHAPTER 23 DISORDERS OF VENTILATION AND GAS EXCHANGE Essentials of Pathophsiology.
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Transcript of CHAPTER 23 DISORDERS OF VENTILATION AND GAS EXCHANGE Essentials of Pathophsiology.
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CHAPTER 23
DISORDERS OF VENTILATION AND GAS EXCHANGE
Essentials of Pathophsiology
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PRE LECTURE QUIZ TRUE/FALSE
Pleural, musculoskeletal, and myocardial pain are similar in description and almost impossible to differentiate.
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.
Persons with emphysema are often labeled as “blue bloaters” because of the chronic hypoxemia and eventual right-sided heart failure with peripheral edema.
Cystic fibrosis is manifested by pancreatic exocrine deficiency and a noted decrease in levels of sodium chloride in the sweat.
Hypercapnia refers to an abnormal increase in oxygen levels.
F
T
F
F
F
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PRE LECTURE QUIZ
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.
Asthma
Effusion
Embolism
Right
Tension
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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
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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
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HYPERCAPNIA
PCO2 >50 mm Hg
Respiratory acidosis Increased respiration Decreased nerve firing
º Carbon dioxide narcosis
º Disorientation, somnolence, coma
Decreased muscle contractionº Vasodilation
Headache; conjunctival hyperemia; warm, flushed skin
CO2 + H2O H2CO3 H+ + HCO3-
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QUESTION
Tell whether the following statement is true or false.
Both hypercapnia and hypoxemia will lead to respiratory failure if untreated.
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ANSWER
TrueRationale: 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.).
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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
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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
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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 Tension: air enters pleural cavity through the wound on inhalation but cannot leave on exhalation
º Open: air enters pleural cavity through the wound on inhalation and leaves on exhalation
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OPEN PNEUMOTHORAX
Air Comes in
Air goes out
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TENSION PNEUMOTHORAX
Air comes in
Air is trapped
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QUESTION
Tell whether the following statement is true or false.
Open pneumothorax is more life-threatening than tension pneumothorax.
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ANSWER
FalseRationale: 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.
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PLEURAL EFFUSION—FLUID IN THE PLEURAL CAVITY
Hydrothorax: serous fluid
Empyema(em-pī-ē-mə) : pus
Chylothorax: lymph Hemothorax: blood
an accumulation of fluid in one or both pleural cavities, often resulting from disease of the heart or kidneys
fluid in the pleural space secondary to leakage from the thoracic duct
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OBSTRUCTIVE AIRWAY DISORDERS
Bronchial asthma Chronic obstructive airway
diseases Chronic bronchitis Emphysema Bronchiectasis Cystic fibrosis
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PATHOGENESIS OF BRONCHIAL ASTHMA
Early Phase
AntigenIgECytokine ReleaseMuscle Spasm
Late Phase
Mast Cell ActivationVascular porosity Edema and WBC infiltrationEpithelial DamageMuscle Spasm with edema
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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
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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
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AIRWAY OBSTRUCTION IN ASTHMA
inflammatory mediators
airway inflammation
bronchospasm
edema
impaired mucociliary
function
epithelial injury
increased airway
responsiveness
airflow limitation
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QUESTION
Which of the following occurs in asthma?a. Airway inflammationb. Bronchospasm c. Decreased ability to clear mucusd. All of the above
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ANSWER
d. All of the aboveRationale: 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.
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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
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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
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Mechanism of COPD
A) Inflammation, Fibrosis
B) Hypersecretion of mucus
C) Destruction of elastic fibers that hold the airways open
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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
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TYPES OF EMPHYSEMA
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Emphysemia Chest Wall Shape
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CHRONIC BRONCHITIS
Chronic irritation of airways Increased number of mucus
cells Mucus hypersecretion
Productive cough
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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
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QUESTION
Which chronic obstructive pulmonary disease primarily affects the alveoli?
a. Asthmab. Emphysemac. Chronic bronchitisd. Bronchiectasis (dilitation)
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ANSWER
b. EmphysemaRationale: In emphysema, alveolar
walls are destroyed. The other chronic pulmonary diseases listed primarily affect the airways.
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COPD AND BLOOD PH
Discussion: In what range will a COPD client’s
blood pH fall? Why?
Normal when stabilized & down to 7.3 unstabilized
CO2 +H2O H2CO3 H+ + HCO3-
Respiratory acidosis(lung induced): Low pH, High CO2, Low HCO3-
Metabolic (tissue induced): Low pH, High CO2, Normal HCO3-
Venous blood gas
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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
high CO2
levels
hypercapnia
hypoxia
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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?
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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 secretionsº Mucus is thicker
Obstructs airways Obstructs pancreatic and biliary
ducts
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PATHOGENESIS OF CYSTIC FIBROSIS
Cystic Fibrosis Transmembrane Regulator Gene Failure
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CYSTIC FIBROSIS MANIFESTATIONS
Discussion: A client with cystic fibrosis is having
respiratory problems and: Digestive problems Flatulence Steatorrhea Weight loss
Question: He does not understand why a respiratory
disease would cause these problems. How would this be explained to the client?
Steatorrhea is the presence of excess fat in feces. Stools may also float due to excess lipid, have an oily appearance and be especially foul smelling.
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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?
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DISORDERS OF PULMONARY BLOOD FLOW
Pulmonary embolism Pulmonary hypertension
Primaryº Blood vessel walls thicken and
constrict Secondary
º Elevation of pulmonary venous pressure
º Increased pulmonary blood flowº Pulmonary vascular obstructionº Hypoxemia
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PULMONARY EMBOLISM
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Results of Pulmonary Hypertension
Occluded pulmonary artery
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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
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ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)
Exudate enters alveoli Blocks gas exchange Makes inhalation more
difficult Neutrophils enter alveoli
Release inflammatory mediators
Release proteolytic enzymes
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MECHANISMS OF LUNG CHANGES IN ARDS
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QUESTION
Tell whether the following statement is true or false.
Patients suffering from ARDS will be not necessarily be hypoxemic.
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ANSWER
FalseRationale: 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).