1. Chapter 23 Disorders of Ventilation and Gas Exchange

2. Physiological Effects of Ventilation and Perfusion
Major function of the lung is to oxygenate blood and remove carbon dioxide
Certain disorders disrupt this exchange of gases
Disorders of lung inflation
Obstructive airway disorders
Chronic interstitial lung disorders
Disorders of the pulmonary circulation
Acute respiratory disorders

3. Hypoxemia A reduction in the PO2 of arterial blood
Potential causes include:
Inadequate O2 in the air
Disease of the respiratory system
Dysfunction of the neurologic system
Alterations in circulatory function
Mechanisms
Hypoventilation
Impaired diffusion of gases
Inadequate circulation of blood
V/P mismatch

4. Hypoxemia
Produces it’s effect through tissue hypoxia and the compensatory mechanisms
Brain and heart have the greatest O2 needs
Mild hypoxemia may go unnoticed
Pronounced hypoxemia may cause:
Personality changes
Restlessness
Uncoordinated body movements
Impaired judgement
Stupor and coma

5. Cyanosis
Bluish coloration of the skin and mucus membranes (lips, nailbeds, ears and cheeks)
Central
Tongue and lips
Caused by an increased amount of deoxygenated hemoglobin in the arterial blood
Peripheral (cold exposure, shock, heart failure)
Extremities and tip of the nose
Slowing of blood flow to an area of the body
Chronic hypoxemia- body compensates by
Increased ventilation
Increased production of RBCs
Pulmonary vessel vasoconstriction

6. Hypercapnia Increase in the carbon dioxide content in the blood
Manifestations are those seen with a decrease in pH
Vasodilation of blood vessels

7. Disorders of the Pleura
Pleuritis
Pleural effusion
Pneumothorax

8. Pleurisy
Inflammation of the parietal pleura that typically results in pleuritic pain
Pleuritic pain is usually unilateral, abrupt in onset, and worsened by deep breathing and cough
Commonly caused by viral infections or pneumonia
Treatment involves treating the underlying disease
Anti-inflammatory agents

9. Pleural Effusion Hydrothorax (serous) usually caused by CHF
Empyema (purulent)
infection in pleural cavity
Invasion by adjacent tissue
Chylothorax (lymph)
Trauma, inflammation, malignancy
Hemothorax (blood)
Chest injury, chest surgery, rupture of a great vessel

10. Pleural Effusion Manifestations
Dullness to percussion and diminished breath sounds
Hypoxemia, dyspnea, pleuritic pain
Diagnosis
Chest x-ray
Ultrasound CT
Thoracentesis to test fluid

11. Pneumothorax The presence of air in the pleural cavity
Air takes up space, restricting lung expansion
Partial or complete collapse of the affected lung
Spontaneous air-filled blister (bleb) on the lung ruptures
Occurs in tall, thin persons
Traumatic air enters through chest injuries
Tension air enters pleural cavity through wound on inhalation, cannot leave on exhalation
Medical emergency (causes shift in mediastinum)
Open air enters pleural cavity through the wound on inhalation and leaves on exhalation

12. Pneumothorax

13. Pneumothorax Clinical features
RR, asymmetry of chest, hyperresonance on percussion, ipsilateral pain
Tracheal deviation to opposite side of the chest (tension)
Diagnosis
Chest x-ray, ultrasound or CT
Treatment
Relief of tension pneumo with large bore needle
Chest tube

14. Airway Obstruction in Asthma
Inflammatory mediators
 Airway inflammation
 Increased mucociliary function
 Edema
 Epithelial injury 
 Increased airway responsiveness
 Bronchospasm
 Airflow limitation

15. Atelectasis Incomplete expansion of the lung or part of the lung
Caused by airway obstruction, lung compression, loss of surfactant
Common postop complication
Primary-newborn
Acquired-adult
manifested by tachypnea, tachycardia, dyspnea, cyanosis, absence of breath sounds

16. Obstructive Airway Disease
Bronchial asthma
COPD
Emphysema
Chronic bronchitis
Bronchiectasis
Cystic Fibrosis

17. Bronchial Asthma
Chronic inflammatory disease of the airways involving recurring symptoms of airflow obstruction and bronchial hyper- responsiveness
An exaggerated hypersensitivity response to a variety of stimuli
Two types
Extrinsic (allergic)
Intrinsic
Episodes can be triggered by:
URIs
Exercise
ASA
Irritants (cigarette smoke)

18. Pathogenesis of Bronchial Asthma

19. Extrinsic (Atopic) Asthma
Type I hypersensitivity reaction induced by exposure to an extrinsic antigen or allergan (dust mite, cockroach)
Onset is usually childhood or adolescence
Often have other allergies (eczema, hay fever)
Early-phase response (acute phase) min of exposure
Antigen binds with previously sensitized mast cells
 inflammatory response
Bronchospasm, mucosal edema, increased mucus secretions
Late phase response (4-8 hrs after exposure)
Inflammation and increased airway responsiveness
Prolongs the attack and starts a cycle of exacerbations

20. Intrinsic (Nonatopic) Asthma
Triggered by respiratory infections
Epithelial damage and stimulation of IgE production
Increase airway responsiveness to other triggers
Exercise hyperventilation
Loss of heat and water may cause bronchospasm
Cold air
Inhaled irritants
Irritant receptors and vagal reflex
Aspirin and other NSAIDs
Abnormal arachidonic acid metabolism

21. Manifestations of Asthma Attack
Wheezing, chest tightness, dyspnea and fatigue
Usually symptom-free between attacks
Often worse at night
Expiration prolonged because of progressive airway obstruction
FEV1 and PEF
Air becomes trapped behind the occluded and narrowed airways hyperinflation of the lungs

22. Diagnosis of Asthma Based on careful H & P, lab findings and PFTs
Self-monitoring of PEF (peak expiratory flow rate) to establish personal best
PEF < 40% of personal best indicates a severe attack
PEF < 25% of personal best is a life-threatening condition

23. Treatment of Asthma Educate patients to avoid triggers
Desensitization injections (allergy shots)
Quick-relief medications
Short acting β-2 agonists, anticholinergic agents, systemic corticosteroids
Long-term medications
Inhaled corticosteroids, long-acting bronchodilators, cromolyn and nedocromil, leukotriene receptor anatagonists, theophylline

24. Severe (Persistent) Asthma
<10% of asthmatics
Persistent asthma that requires continuous high-dose oral or inhaled steroids for >50% of previous year
Need for additional daily treatment with controller meds
Exhibited evidence of disease exacerbations or instability
Required hospitalizations or ED visits
Increased risk for fatal or near-fatal attacks

25. Childhood Asthma Common chronic illness in children
80% are symptomatic before age 5
More prevalent among black children
Previous infection with RSV is risk factor
Acute night-time attacks are common
Characterized by irritability, nonproductive cough, wheezing, tachypnea, dyspnea, use of accessory muscles of expiration

26. Chronic Obstructive Pulmonary Disease
Respiratory disorders characterized by chronic and recurrent obstruction of airflow in the pulmonary airways
Airflow obstruction is usually progressive and may be accompanied by airway hyperreactivity
Leading cause of morbidity and mortality
Most common cause is smoking
Disease usually far advanced when diagnosed
Mechanisms:
Inflammation and fibrosis of the bronchial wall
Hypertrophy of the submucosal glands
Hypersecretion of mucous
Loss of elastic lung fibers and alveolar tissue

27. Mechanisms of Airflow Obstruction
inflammation and fibrosis hypersecretion destruction of elastic fibers

28. Emphysema
Characterized by loss of lung elasticity and abnormal enlargement of the air spaces distal to the terminal bronchioles with destruction of the alveolar walls and and capillary beds
Hyperinflation of the lungs with in TLC (total lung capacity
Caused by smoking or inherited deficiency of α1- antitrypsin

29. Chest Wall in Emphysema

30. Chronic Bronchitis Airway obstruction of the major and small airways
Seen most often in middle-aged male smokers
Clinical diagnosis: persistent chronic productive cough for at least 3 months in 2 consecutive years
Characterized by excessive productive cough and SOB

31. Manifestations of COPD
Insidious onset
Typically diagnosed in 5th or 6th decade of life
Excessive cough, sputum production and SOB
Cough usually occurs in the morning
Dyspnea becomes more severe as disease progresses
Frequent exacerbations of infection and respiratory insufficiency
Recurrent respiratory failure death

32. Pink Puffers Versus Blue Bloaters
Pink puffers (emphysema)
Lack of cyanosis
Use accessory muscles
Pursed-lip breathing
Barrel chest
Blue bloaters (chronic bronchitis)
Cannot increase respiration enough to maintain oxygen levels
Cyanosis, fluid retention and polycythemia
Right sided heart failure

33. Question
Which chronic obstructive pulmonary disease primarily affects the alveoli?
Asthma
Emphysema
Chronic bronchitis
Bronchiectasis

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

35. Consequences of COPD COPD  decreased ability to exhale
 Stale air in the lungs
 Low O2 levels  hypoxia
 High CO2 levels  hypercapnia
Which step will cause the central chemoreceptors to increase respiration?
Which will cause the peripheral chemoreceptors to increase respiration?

36. Consequences of COPD COPD  decreased ability to exhale
 Stale air in the lungs
 Low O2 levels  hypoxia
 High CO2 levels  hypercapnia
Which step will cause the central chemoreceptors to increase respiration? PCO2
Which will cause the peripheral chemoreceptors to increase respiration? PO2

37. Diagnosis and Treatment of COPD
Based on H & P
PFTs (FEV1, FVC RV, TLC)
Chest x-ray
Lab tests
Treatment
Smoking cessation
Pulmonary rehabilitation
Avoid exposure to URIs
Bronchodilators including inhaled adrenergic and anticholinergic agents

38. Cystic Fibrosis
Major cause of severe chronic respiratory disease in children and young adults
inherited disorder involving fluid secretion by the exocrine glands in the respiratory, GI and reproductive tracts
Manifested by pancreatic exocrine deficiency and high concentrations of NaCl in the sweat
Caused by mutations of the CFTR (cystic fibrosis transmembrane regulator)
Renders epithelial membrane impermeable to the chloride ion

39. Pathogenesis of Cystic Fibrosis

40. Manifestations of Cystic Fibrosis
Respiratory
Accumulation of viscid mucus in the bronchi, impaired mucociliary clearance, lung infections
Chronic bronchiolitis and bronchitis bronchiectasis (permanent dilation of the bronchi)
Predisposition to URIs (pseudomonas)
Exocrine pancreatic function
Steatorrhea, diarrhea and abdominal pain
Reproductive
Males have congenital bilateral absence of vas deferens

41. Diagnosis and Rx of Cystic Fibrosis
Based on presence of respiratory and GI symptoms typical of CF, history of CF in sibling, or positive newborn screening test
Confirmed by sweat test or DNA test for CTFR gene
Treatment is directed toward early and aggressive measures to slow progression of secondary organ dysfunction
antibiotics, chest physiotherapy
Supplemental pancreatic enzymes, vitamins and minerals

42. Interstitial Lung Disease
“restrictive lung disorders” which result in stiff and noncompliant lungs
Effects on the collagen and elastic connective tissue found in the delicate interstitium of the alveolar walls
Many of these diseases also involve airways, arteries and veins
Diminished lung compliance characterized by dyspnea, tachypnea, and eventual cyanosis

43. Pulmonary Embolism
Occurs when a blood-borne substance lodges in a branch of the pulmonary artery causing obstruction (thrombus, air, fat, amniotic fluid)
Causative factors:
deep vein thrombosis
oral contraceptives
malignancy

44. Pulmonary Embolism
Manifestation depend on size and location of occlusion
Breathlessness, pleuritic pain, apprehension, low grade temp, productive cough of blood streaked sputum
Tachycardia, sudden collapse, shock
Diagnosis:
Clinical signs and symptoms
ABGs
D-dimer tests
Lung perfusion scans
CT chest
Pulmonary angiography
Lower limb US
Treatment:
Thrombolytic therapy and anticoagulation

45. Pulmonary Embolism

46. Pulmonary Hypertension
Caused by an abnormal elevation of pressure within the pulmonary arterial system
Most cases are secondary to cardiac or pulmonary disease (CPOD, heart failure, sleep apnea)
Manifested by
Elevation of pulmonary venous pressure
Increased pulmonary blood flow
Pulmonary vascular obstruction
Hypoxemia
Primary
Persistent elevation of PAP in the absence of a secondary cause

47. Cor Pulmonale
Right-sided heart failure secondary to lung disease or pulmonary hypertension
Decreased lung ventilation
Pulmonary vasoconstriction
Increased workload on the right heart
Decreased oxygenation
Kidney releases erythropoietin  more RBCs made  polycythemia makes blood more viscous
Increased workload on the heart

48. Acute Respiratory Syndrome (ARDS)
Characterized by severe dyspnea of rapid onset, hypoxemia and pulmonary infiltrates
Diffuse epithelial cell injury with increased permeability of alveolar capillary membrane
Can be caused by:
Aspiration of gastric contents
Major trauma
Sepsis
Acute pancreatitis
Hematologic disorders
Metabolic events
Reactions to drugs and toxins

49. Acute Respiratory Distress Syndrome
Exudate enters the alveoli
Blocks gas exchange
Makes inhalation more difficult
Neutrophils enter the alveoli
Release inflammatory mediators, proteolytic enzymes, reactive oxygen species

50. Clinical Features of ARDS
Rapid onset of respiratory distress
RR
Signs of respiratory failure
Diffuse bilateral infiltrates
Marked hypoxemia refractory to supplemental O2
Multi-system organ failure

51. Acute Respiratory Failure
Impaired gas exchange due to either heart or lung failure
Hypoxemic (advanced COPD)
VP mismatch
Impaired diffusion
Hypercapnic/hypoxemic (drug OD, disorders affecting respiratory muscles
Unable to maintain a level of alveolar ventilation

52. Clinical Features of Acute Respiratory Failure
Varying degrees of hypoxemia and hypercapnea
 respiratory drive and sympathetic tone
Cyanosis, restlessness, confusion, anxiety, fatigue, dyspnea, hypertension, cardiac arrhythmias
Pulmonary vasoconstriction in response to hypoxemia right sided heart failure