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  1. What is ventilation?
    It is the air that reaches the lungs.
  2. What is perfusion?
    It is the blood which reaches the lungs.
  3. What is the normal V/Q ratio?
  4. What is FVC?
    It is forced vital capacity, which is defined as the amount of air that you can forcibly blow out after full inspiration.
  5. What is FEV1?
    Forced Expiratory Volume: the amount of air that you can forcibly blow out in one second.
  6. What is the significance of FVC and FEV1?
    When taken together, they are considered one of the primary indicators of lung function.
  7. In which conditions do you expect to see high V/Q?
    High V/Q ratios indicate dead space. For example, in pulmonary embolism you would have ventilation with very little perfusion.
  8. In what conditions do you expect to see low V/Q?
    Low V/Q ratios have poor ventilation in well-perfused areas. If severe, it will lead to R to L shunting. For example, mucus plugging could block the alveolus to diminish ventilation while perfusion remains unchanged. Supplemental O2 may be relatively ineffective.
  9. How accurate is SaO2 in reflecting oxygenation?
    • It measures the % of Hb saturated with oxygen, and it is an indirect measurement. Therefore, it is prone to error. 
    • You need good perfusion and enough Hb to have adequate oxygenation.
  10. What are some characteristics of obstructive pulmonary disease?
    • Decreased FEV1
    • Dyspnea
    • Wheezing
    • V/Q mismatching
  11. How do changes in V/Q mismatches occur in some obstructive diseases?
    Capillary destruction alters perfusion
  12. What are some examples of obstructive diseases?
    • Asthma
    • COPD: chronic bronchitis and emphysema
  13. What are some mechanisms of airway obstruction in chronic obstructive lung disease?
    • Hypertrophy of the bronchial wall
    • Inflammation and hypersecretion of mucus
    • Loss of elastic fibers. (Normally, elastin and elastic fibers provide traction to keep the airways open.)
  14. What are some symptoms of bronchial asthma?
    • SOB
    • Wheezing
    • Coughing
    • Activity intolerance
    • Conscious effort to breathe

    Remember that asthma can be either intermittent or chronic and onset can be sudden or gradual.
  15. What is status asthmaticus?
    It is an asthma exacerbation that does not respond to treatment.
  16. What happens during an episode of asthma?
    • Linings of the the airways become swollen
    • Airways produce a thick mucus
    • Muscles around the airways tighten and made the airways narrower.
  17. Is the etiology of asthma based on genetics or on the environment?
    Both! Probably.

    They have identified about 20 chromosomal regions associated with asthma.
  18. Describe the pathogenesis of asthma and how that leads to the manifestation of symptoms.
    • Acute inflammation >> bronchoconstriction
    • Chronic inflammation >> exacerbations non-specific hyperreactivity
    • Airway remodeling >> persistent airflow obstruction

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  19. How do you treat asthma?
    You must consider the pathophysiology when deciding how to treat it. NEED bronchodilator (rescue) and steroid (treat inflammation)
  20. What IS asthma?
    It is inflammation resulting in hyperresponsiveness of reactive airways (reversible).
  21. Describe the characteristics of early response asthma.
    • IgE binding to antigen
    • Mast cell degranulation
    • Release of mediators that induce bronchospasm
    • Edema
    • Mucus secretions
  22. Describe the characteristics of late response asthma.
    • Epithelial damage
    • Inflammatory changes
    • Increased airway responsiveness
    • Diminished mucociliary action -- accumulation

    Attacks can last for days.
  23. What are the main differences between early and late stage asthma reactions?
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  24. You would expect to see respiratory acidosis in asthma. 

    True or false?
    • True and false.
    • Initially, hypoxemia may occur without CO2 retention. 
    • Hyperventilation eventually causes hypocapnia and respiratory alkalosis. 
    • The obstruction worsens/persists to the point where FEV1 decreases to 15-20% of predicted value. This leads to respiratory acidosis and hypercapia.
  25. How is asthma severity determined?
    It is determined by the frequency of symptoms.
  26. What are the goals of asthma treatment?
    • Reduce impairment: prevent chronic symptoms, reduce use of SABAs, maintain normal lung and activity levels
    • Reduce risk: prevent loss of lung function, prevent exacerbation
  27. What medications are involved in asthma treatment?
    • Relievers: short onset B2 agonists, anticholinergics
    • Controllers: LABA, steroids, cromolyn (mast cell inhibitor), leukotriene inhibitors, Anti-IgE
  28. COPD is comprised of two diseases. What are they?
    Chronic bronchitis and emphysema.

    In both diseases there is obstruction of the flow of air through the airways and out of the lungs, and the obstruction generally is permanent and progressive over time.
  29. How do you distinguish between chronic bronchitis and just bronchitis?
    Continual productive cough for at least 3 months of the year for at least 2 consecutive years.
  30. What causes chronic bronchitis?
    Most often by air pollutants and cigarette smoke.
  31. What are the characteristics of chronic bronchitis?
    • Decreased FEV1
    • Dyspnea
    • Wheezing
    • V/Q mismatching
  32. What is the pathogenesis of chronic bronchitis?
    • Pathogens thrive
    • Large bronchi at first, eventually all the airways become involved.
    • Ciliary damage and chronic inflammation
    • Shunting >> hypoxemia (leads to polycythemia, clubbing, hypercapnia, and cyanosis)
    • Eventual pulmonary HTN and cor pulmonale
  33. What is the pathogenesis of emphysema?
    • Abnormal and permanent enlargement of the gas-exchange airways accompanied by the destruction of alveolar walls. 
    • Balance between elastases (trypsin) and antielastases (alpha 1 antitrypsin) is disrupted.
    • Elastases dominate and this leads to alveolar septa breakdown. Parts of pulmonary capillary bed are destroyed
  34. What are the causes of emphysema?
    • Primary (inherited) alpha-1-antitrypsin deficiency, which leads to the early development of emphysema.
    • Smoking leads to inflammation and releases elastase. Smoking also causes a decrease in alpha-1-antitrypsin deficiency
  35. What is barrel chest?
    AP diameter/transverse diameter ratio increases significantly secondary to air trapping
  36. What are the clinical manifestations of emphysema?
    • Less cough and sputum than in chronic bronchitis
    • Dyspnea on exertion or at rest, use of accesory muscles, prolonged expiration
    • Chest XR will show hyperinflation
    • Diminished breath sounds
    • Cachexia
    • Polycythemia, clubbing, increased TLC
    • Decreased FEV1 and FVC
  37. How do you treat COPD?
    • Oxygen (Type A or B?)
    • Glucocorticoids
    • Antibiotics: more for chronic bronchitis
    • SABA/LABAs, anticholinergics inhaled
    • Lung volume reduction surgery
    • Lung transplant
  38. What is the difference between OSA and CSA?
    • OSA: there is an effort to breathe
    • CSA: no signals from the brain
  39. What is included in the pathogenesis of OSA?
    • Upper airway anatomy
    • Upper airway dilator muscle activity
    • Arousal from sleep
    • Ventilatory control stability
    • Lung volume
  40. What is CF?
    Cystic fibrosis is an autosomal recessive disorder in which the CFTS (cystic fibrosis transmembrane regulator) is defective, which leads to defective Cl- secretion.
  41. How does CF affect the respiratory system?
    The defective Cl- secretion with excessive Na+ and H2O absorption leads to very thick and sticky mucus. This leads to chronic obstructions and airway infections >> chronic bronchitis.
  42. What are the characteristics of a restrictive lung disease?
    There is an inhibition of the normal expansion of the lung. There are difficulties with inspiration.
  43. Please give some examples of restrictive lung diseases.
    • Pleural effusion
    • Pneumothorax
    • Pulmonary edema
    • Atelectasis
    • Respiratory depression
    • Pulmonary fibrosis
    • ARDs
    • PNA
  44. What is a pleural effusion?
    • A pleural effusion is excess fluid between the 2 lung membranes (visceral and parietal pleurae). 
    • Normally ~3-4 teaspoons of fluid that acts as a lubricant between the two membranes.
  45. What are symptoms of a pleural effusion?
    Chest pain and difficulty breathing
  46. What are some etiologies of pleural effusion?
    • CHF (increased hydrostatic pressure)
    • PNA
    • Malignancies (increased capillary permeability)
    • Tuberculosis (infection)
    • Rheumatoid arthritis (inflammation)
    • Chylothorax (direct extravasation)
  47. What is a pneumothorax?
    • The presence of air in the pleural space. 
    • It causes partial or complete collapse of the affected lung.
  48. Is a pneumothorax obstructive or restrictive?
  49. What is a closed versus and open pneumothorax?
    Closed is within the lung, not OTA. It can be caused by a ruptured bleb or just be a spontaneous pnemo (tall young men who have less muscle?)

    An open pneumothorax is open to air.
  50. What is a tension pneumothorax?
    A lung collapses and there is air in the pleural space drawn in from the outside, but it is unable to escape. The volume of the pneumothorax gradually increases until the heard is compressed.
  51. What is pulmonary edema? Is it restrictive or obstructive?
    • Pulmonary edema is a restrictive process that involves fluid in the alveoli and tight spaces. 
    • There is swelling and/or fluid accumulation in the lungs >> impaired has exchange and may lead to respiratory failure.
  52. How does one develop pulmonary edema?
    • It begins with an increased filtration through the loose functions of the pulmonary capillaries. 
    • As the intracapillary pressure increases, normally impermeable (tight) junctions between the alveolar ells open, permitting alveolar flooding to occur.
  53. What are the defining characteristics of ARDS?
    ARDS is a severe lung disease caused by a variety of direct and indirect insults.

    Characterized by inflammation of the parenchyma. This leads to many changes.
  54. Describe the mechanism of ARDS.
    • Impaired gas exchange
    • Systemic release of inflammatory mediators
    • Hypoxemia
    • Frequently results in MODS
  55. What causes ARDS?
    • Direct or indirect lung injuries that induce endothelial damage and stimulate inflammatory processes (platelet aggregation, complement activation, release of neutrophil mediators)
    • It is a results of increased capillary permeability, which leads to pulmonary edema and lung hemorrhage >> respiratory failure.
  56. Will oxygen administration correct hypoxemia associated with ARDS?
    Not really.
  57. How does the pathophysiology of ARDS work on a cellular level?
    • Injury and increased permeability of the alveolar capillary membrane allow fluid, protein, cellular debris, platelets, and blood cells to move out of the vascular compartment and enter the interstitium and alveoli. 
    • Activated neutrophils release a variety of products that damage the alveolar cells and lead to edema, surfactant inactivation, and formation of a hyaline membrane. This blocks gas exchange. 
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  58. What is MODS?
    Progressive dysfunction of two or more organ systems resulting from an uncontrolled inflammatory response to severe illness or injury.
  59. What is the pathophysiology/mechanism of MODS?
    • Involves inflammatory mediators, which damage endothelium throughout the body.
    • Neutrophils are attracted to damaged endothelium.
    • Nitric oxide is released from activated endothelial cells.
    • Vascular leaking b/c permeability
    • Activation of coagulation systems (DIC maybe)
    • Damage to gut mucosa (gut barrier) >> organ failure.
  60. How do you treat MODS?
    Supportive measures: ventilation, fluid and electrolyte corrections, control infections
  61. What is RDS? What causes it?
    • Respiratory distress syndrome in premature infants.
    • It is caused by a developmental insufficiency of surfactant and structural immaturity of lungs.
    • May also be caused by genetics.
  62. Pathophysiology of RDS?
    • It is a hyaline membrane disease. 
    • This leads to a deficiency in effective surface area for gas exchange >> atelectasis, shunt, persistence of fetal circulation, leaking plasma proteins, HPV
  63. What is the the composition of a hyaline membrane?
    Consists of cellular debris, RBCs, neutrophils and macrophages.
  64. What are the treatments for RDS?
    • Maternal glucocorticoid administration
    • Surfactant via ETT
    • Ventilatory support methods that minimize lung injury
    • Inhaled NO
  65. Why is maternal glucocorticoid administration an effective treatment for RDS?
    Natural birth causes stress in infants, who produce glucocorticoids. This stimulates lung maturation.
  66. How might an infant with RDS present?
    • Tachypnea
    • Retractions (chest wall)
    • Expiratory grunting
    • Nasal flaring
    • Cyanosis
  67. What are the most common symptoms of lung cancer?
    • SOB
    • Coughing
    • Weight loss
Card Set:
2013-04-30 00:58:45

BC Boston College CRNA NU 672 Pathophysiology
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