Chapter 23 Disorders of Ventilation and Gas Exchange

1. Essentials of Pathophsiology Chapter 23Disorders of Ventilation and Gas Exchange

2. 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. Pre lecture quiz True/false F T F F F

3. 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. • Corpulmonale refers to __________-sided heart failure resulting from primary lung disease and involves hypertrophy and eventual failure of that ventricle. Pre lecture quiz • Asthma • Effusion • Embolism • Right • Tension

4. 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 Causes of Respiratory Failure

5. 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 Hypoxemia

6. PCO2 >50 mm Hg • Respiratory acidosis • Increased respiration • Decreased nerve firing • Carbon dioxide narcosis • Disorientation, somnolence, coma • Decreased muscle contraction • Vasodilation • Headache; conjunctival hyperemia; warm, flushed skin Hypercapnia CO2 + H2O H2CO3 H+ + HCO3-

7. Tell whether the following statement is true or false. Both hypercapnia and hypoxemia will lead to respiratory failure if untreated. Question

8. 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.). Answer

9. 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 Pleural Disorders Decrease Ventilation

10. 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 Scenario

11. 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 • 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 Pneumothorax

12. Open Pneumothorax Air goes out Air Comes in

13. Tension Pneumothorax Air comes in Air is trapped

14. Tell whether the following statement is true or false. Open pneumothorax is more life-threatening than tension pneumothorax. Question

15. 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. Answer

16. Hydrothorax: serous fluid Empyema(em-pī-ē-mə) : pus Chylothorax: lymph Hemothorax: blood PleuralEffusion—Fluidin the Pleural Cavity 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

17. Bronchial asthma • Chronic obstructive airway diseases • Chronic bronchitis • Emphysema • Bronchiectasis • Cystic fibrosis Obstructive Airway Disorders

18. 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

19. 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 Extrinsic (Atopic) Asthma Allergen Mast cells release inflammatory mediators WBCs enter region and release more inflammatory mediators

20. 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 Intrinsic (Nonatopic) Asthma

21. Airway Obstruction in Asthma inflammatory airway mediators inflammation increased epithelial impaired airway injury mucociliary responsiveness function bronchospasm edema airflow limitation

22. Which of the following occurs in asthma? • Airway inflammation • Bronchospasm • Decreased ability to clear mucus • All of the above Question

23. 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. Answer

24. 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 Chronic Obstructive Pulmonary Disorders the bronchi are distended, characterized by sudden violent coughing and copious expectoration of sputum, and which often become infected

25. 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 Mechanisms of COPD

26. Mechanism of COPD A) Inflammation, Fibrosis B) Hypersecretion of mucus C) Destruction of elastic fibers that hold the airways open

27. 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 Emphysema

28. Types of Emphysema

29. Emphysemia Chest Wall Shape

30. Chronic irritation of airways • Increased number of mucus cells • Mucus hypersecretion • Productive cough ChronicBronchitis

31. 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 • Corpulmonale Pink Puffers vs. Blue Bloaters

32. Which chronic obstructive pulmonary disease primarily affects the alveoli? • Asthma • Emphysema • Chronic bronchitis • Bronchiectasis (dilitation) Question

33. Emphysema Rationale:In emphysema, alveolar walls are destroyed. The other chronic pulmonary diseases listed primarily affect the airways. Answer

34. Discussion: • In what range will a COPD client’s blood pH fall? • Why? COPD and Blood pH Normal when stabilized & down to 7.3 unstabilized CO2 +H2O H2CO3 H+ + HCO3- Venous blood gas Respiratory acidosis(lung induced): Low pH, High CO2, Low HCO3- Metabolic (tissue induced): Low pH, High CO2, Normal HCO3-

35. Which step in this flow chart will cause the central chemoreceptors to increase respiration? Which will cause the peripheral chemoreceptors to increase respiration? Consequences of COPD COPD decreased ability to exhale stale air in lungs low O2 high levels CO2 levels hypoxia hypercapnia

36. 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? Scenario

37. Recessive disorder in chloride transport proteins • High concentrations of NaCl in the sweat • Less Na+ and water in respiratory mucus and in pancreatic secretions • Mucus is thicker • Obstructs airways • Obstructs pancreatic and biliary ducts Cystic Fibrosis

38. Pathogenesis of Cystic Fibrosis Cystic Fibrosis Transmembrane Regulator Gene Failure

39. 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? Cystic Fibrosis Manifestations 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.

40. 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? Pulmonary Blood Flow

41. Pulmonary embolism • Pulmonary hypertension • Primary • Blood vessel walls thicken and constrict • Secondary • Elevation of pulmonary venous pressure • Increased pulmonary blood flow • Pulmonary vascular obstruction • Hypoxemia Disorders of Pulmonary Blood Flow

42. Pulmonary Embolism

43. Results of Pulmonary Hypertension Occluded pulmonary artery

44. 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 Cor Pulmonale

45. Exudate enters alveoli • Blocks gas exchange • Makes inhalation more difficult • Neutrophils enter alveoli • Release inflammatory mediators • Release proteolytic enzymes Acute Respiratory Distress Syndrome (ARDS)

46. Mechanisms of Lung Changes in ARDS

47. Tell whether the following statement is true or false. Patients suffering from ARDS will be not necessarily be hypoxemic. Question

48. 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). Answer