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CHAPTER 23 DISORDERS OF VENTILATION AND GAS EXCHANGE Essentials of Pathophsiology.

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Presentation on theme: "CHAPTER 23 DISORDERS OF VENTILATION AND GAS EXCHANGE Essentials of Pathophsiology."— Presentation transcript:

1 CHAPTER 23 DISORDERS OF VENTILATION AND GAS EXCHANGE Essentials of Pathophsiology

2 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

3 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 childrens 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

4 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

5 HYPOXEMIA PO 2 <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

6 HYPERCAPNIA PCO 2 >50 mm Hg Respiratory acidosis Increased respiration Decreased nerve firing º Carbon dioxide narcosis º Disorientation, somnolence, coma Decreased muscle contraction º Vasodilation Headache; conjunctival hyperemia; warm, flushed skin CO 2 + H 2 O H 2 CO 3 H + + HCO 3 -

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

8 ANSWER True Rationale: In hypercapnia (PCO 2 >50 mm Hg), tissues accumulate carbon dioxide; in hypoxemia (PO 2 <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.).

9 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

10 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

11 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

12 OPEN PNEUMOTHORAX Air Comes in Air goes out

13 TENSION PNEUMOTHORAX Air comes in Air is trapped

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

15 ANSWER False Rationale: In open pneumothorax, inhaled air compresses the affected sides 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.

16 PLEURAL EFFUSIONFLUID IN THE PLEURAL CAVITY Hydrothorax: serous fluid Empyema(em-pī-ē-m ə ) : 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

17 OBSTRUCTIVE AIRWAY DISORDERS Bronchial asthma Chronic obstructive airway diseases Chronic bronchitis Emphysema Bronchiectasis Cystic fibrosis

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 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

20 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

21 AIRWAY OBSTRUCTION IN ASTHMA inflammatory mediators airway inflammation bronchospasm edema impaired mucociliary function epithelial injury increased airway responsiveness airflow limitation

22 QUESTION Which of the following occurs in asthma? a. Airway inflammation b. Bronchospasm c. Decreased ability to clear mucus d. All of the above

23 ANSWER d. 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.

24 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

25 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

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

27 EMPHYSEMA Neutrophils in alveoli secrete trypsin Increased neutrophil numbers due to inhaled irritants can damage alveoli Alpha 1 -antitrypsin inactivates the trypsin before it can damage the alveoli A genetic defect in alpha 1 -antitrypsin synthesis leads to alveolar damage

28 TYPES OF EMPHYSEMA

29 Emphysemia Chest Wall Shape

30 CHRONIC BRONCHITIS Chronic irritation of airways Increased number of mucus cells Mucus hypersecretion Productive cough

31 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

32 QUESTION Which chronic obstructive pulmonary disease primarily affects the alveoli? a. Asthma b. Emphysema c. Chronic bronchitis d. Bronchiectasis (dilitation)

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

34 COPD AND BLOOD PH Discussion: In what range will a COPD clients blood pH fall? Why? Normal when stabilized & down to 7.3 unstabilized CO 2 +H 2 O H 2 CO 3 H + + HCO 3 - Respiratory acidosis(lung induced): Low pH, High CO 2, Low HCO 3 - Metabolic (tissue induced): Low pH, High CO 2, Normal HCO 3 - Venous blood gas

35 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 O 2 levels high CO 2 levels hypercapnia hypoxia

36 SCENARIO A client with chronic bronchitis has a barrel chest and cyanosis. His pulse oximeter reads 86% oxygenation. His PO 2 is 54 mm Hg. His PCO 2 is 56 mm Hg. He is put on low-flow oxygen but complains of shortness of breath. Somebody turns the O 2 flow up. He is found in a coma with a PCO 2 of 59 mm Hg and a blood pH of 7.2. Question: What was the cause of the coma? Why?

37 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

38 PATHOGENESIS OF CYSTIC FIBROSIS Cystic Fibrosis Transmembrane Regulator Gene Failure

39 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.

40 PULMONARY BLOOD FLOW In a COPD client, exhalation is inefficient and O 2 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 CO 2 Discussion: What will the pulmonary arterioles do? Which side of the heart will be affected? Why?

41 DISORDERS OF PULMONARY BLOOD FLOW Pulmonary embolism Pulmonary hypertension Primary º Blood vessel walls thicken and constrict Secondary º Elevation of pulmonary venous pressure º Increased pulmonary blood flow º Pulmonary vascular obstruction º Hypoxemia

42 PULMONARY EMBOLISM

43 Results of Pulmonary Hypertension Occluded pulmonary artery

44 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

45 ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS) Exudate enters alveoli Blocks gas exchange Makes inhalation more difficult Neutrophils enter alveoli Release inflammatory mediators Release proteolytic enzymes

46 MECHANISMS OF LUNG CHANGES IN ARDS

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

48 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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