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Respiratory Physiology Gideon Daniel DVM. What are the LFT test you should know? Compliance Resistance.

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Presentation on theme: "Respiratory Physiology Gideon Daniel DVM. What are the LFT test you should know? Compliance Resistance."— Presentation transcript:

1 Respiratory Physiology Gideon Daniel DVM

2 What are the LFT test you should know? Compliance Resistance

3 Dynamic hyperinflation and what it means to you \

4 Overview DEFINITONS SMALL AIRWAYS EFFECT ON LUNG MECHANICS DIAGNOSIS THERAPY

5 Definitions Air-trapping Intrinsic (auto) PEEP Dynamic hyperinflation

6 Air-trapping/dynamic hyperinflation

7 Intrinsic (auto) PEEP Typically refers to ventilated patients Inadequate time for exhalation (may or may not be pathologic) Small airway disease/mucus

8 What are negative effects of autoPEEP? Potential for worsening cardiac pressure Barotrauma or hypoventilation if pressure limited ventilation

9 AutoPEEP Volume limited ventilator (increasing barotrauma and mean AWP) 35 cmH20

10 Pressure limited ventilator (increasing risk of hypoventilation) 18 cmH20

11 Inadequate time for expiration Inverted I: E ratio Short Te and fast rate Altered time constant

12 Time constant Lung volume changes are due to compliance of the lung and the pressure applied Lung volume = Compliance X ΔP When pressure is applied to the lung, there is a time lag until the volume change occurs The time point at which to inflate or deflate to 63% of volume is termed time constant Given also by compliance X resistance

13 Using time constant calculation to predict air-trapping Need to permit 4-5 time constants for complete inhalation or exhalation Normal lungs, ARDS, emphysema/small airway disease Healthy dog – compliance 10 ml/cmH20; resistance 10 cmH20/L/sec ARDS dog- compliance 3 ml/cmH20; resistance 12 cmH20/L/sec COPD dog with air-trapping- compliance 25 ml/cmH20; 14 cmH20/L sec

14 Healthy Healthy dog – compliance 10 ml/cmH20; resistance 10 cmH20/L/sec Time constant Convert ml to liter (10 ml = 0.01 L) 0.01 l/cmH20 X 10 cmH20/L/sec= 0.1 seconds X 3-5 = normal inspiration/expiration should be fine in

15 ARDS ARDS dog- compliance 3 ml/cmH20; resistance 12 cmH20/L/sec X 12= X 5= 0.18 seconds

16 COPD COPD dog with air-trapping- compliance 25 ml/cmH20; 14 cmH20/L sec X 14 = 0.35 X5 = 1.75 seconds

17 What are small airways? < 2 mm in diameter Conducting airways Very small contribution to resistance

18 Small airway disease Asthma Bronchiolitis

19 When might we suspect air- trapping Clinically, we would worry with COPD Ventilated animals * not so much ARDS

20 Effects of lung function Increased lung volume Increased work of breathing since operating off the ideal P-V curve Increase WOB leads to exhaustion and respiratory fatigue

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22 Diagnosis Ventilated patients Spontaneous breathing patients

23 Ventilated Increasing PEEP higher than set PEEP Lower compliance (since at higher part of PVC curve) Breath-stacking at time

24 Spontaneous breathing Chest shape (barrel shaped) Longer expiratory time/effort Imaging Radiographs Computed tomography

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26 Treatment Ventilated patients BD Adjust rates Spontaneous breathing patients BD Lung volume reduction Surgical Bronchoscopic

27 Jack Cleary NOVA (arterial sample): pH PCO2 58 PO Na K 4.94 Cl 105 Ca 1.23 BG 74 Lac 3 Crea 13.6 (BUN did not register) TCO BE 4 Characterize the Acid-base disturbance Is the dog on supplemental oxygen, why or why not? Is this acute or chronic?

28 Alternatives to blood gas? Preliminary evaluation of the utility of comparing SpO2/FiO2 and PaO2/FiO2 ratios in dogs. Calabro, et al. JVECC Numerous studies evaluated SF in people May also be an acceptable surrogate for PaO2/FiO2 in dogs Partial pressure of end-tidal CO2 sampled via an intranasal catheter as a substitute for partial pressure of arterial CO2 in dogs. Pang, et al. JVECC Dogs for sedated for intranasal catheter placement Maybe a substitute for blood gas analysis?

29 Variables to consider Effect of body position on the arterial partial pressures of oxygen and carbon dioxide in spontaneously breathing, conscious dogs in an intensive care unit. McMillian, et al. JVECC PaO2 was significantly higher when patients were sternal compared to lateral recumbency PaCO2 levels were not significantly different

30 What are the 5 causes of hypoxemia as outlined by WEST?

31 Inadequate FiO2 Hypoventilation Diffusion impairment Shunt V-Q mismatch

32 T or F CO2 can diffuse about 20x as rapidly as oxygen for a given difference in pressure. True Ficks law

33 All of the following determine diffusion of oxygen across the respiratory membrane EXCEPT 1.Membrane thickness 2.Diffusion coefficient (based on solubility and molecular wt) of the gas 3.Membrane surface area 4.Concentration of oxygen in the inspired air 5.Partial pressure difference of gas on either side of the membrane

34 What is Alveolar ventilation? Is the rate at which new air reaches the gas exchange areas of the lungs During inspiration, some of the air never reaches the gas exchange areas but instead fills respiratory passages This air is called dead space air Alveolar ventilation can be increased by either (or both) Raising tidal volume More effective b/c it reduces the proportions of each breath occupied by anatomic dead space Increasing resp frequency

35 ALI/ARDS Is a syndrome of pulmonary inflammation and edema resulting in acute respiratory failure associated with critical injury/illness Major difference b/w ALI and ARDS is the degree of hypoxemia as defined by the ratio of arterial oxygen tension to fractional inspired oxygen concentration (PaO2:FiO2)

36 Consensus in people Clinical criteria Acute onset of respiratory distress Presence of bilateral pulmonary infiltrates on CXR Pulmonary artery wedge pressure 18mmHg No clinical evidence of left atrial hypertension

37 ALI vs ARDS A PaO2/FiO2 ratio of 500 is considered normal What ratio for ALI? What ratio for ARDS? < 200

38 Risk factors Pulmonary – direct injury Pneumonia Contusion Toxin NCPE Extra pulmonary Poly-trauma Sepsis/SIRS Sepsis and pneumonia most common etiology

39 Clinical signs May be delayed for 1-4 days Progressive hypoxemia Tachypnea Respiratory distress Cyanosis Productive cough- actually rare

40 Mechanism of lung injury Increase in endothelial permeability, allowing leakage of protein-rich serum into the alveolar spaces Alveolar infiltrates impaired gas exchange and decreased lung compliance Relatively surfactant deficiency contributes to alveolar collapse Inflammatory response may represent an overzealous response on the part of both cellular and humoral immune system

41 Stages of lung injury Exudative – reflects presence of protein-rich edema fluid, hyaline membranes and wbc infiltrates Proliferative - As ALI/ARDS progress – proliferation of type II pneumocytes (attempts to restore the damaged epithelium) Fibrotic phase- as dz resolves

42 Cellular mechanism Macrophages Neutrophils Soluble mediators TNFa IL-1B TGF-B PAF IL 6 CXCL-8 Eicosanoids IL-10

43 A patient breathing room air has an arterial P02 of 49mmHg, PCO2 48mmHg and respiratory exchange ratio of 0.8. What is the approximate alveolar-arterial difference for PO2 in this patient? 41mmHg Is this normal or abnormal? Abnormal; normal A-a gradient should be < 10. Cause? Likely NOT hypoventilating –that is the the role of the A-a gradient to exclude! Indicates venous admixture

44 Which of the following is NOT considered a criteria for dx of ALI/ARDS? 1.Acute onset of respiratory distress 2.Left atrial hypertension 3.Decreased PaO2:FiO2 ratio 4.Known risk factors (sepsis, pneumonia, etc)

45 Regarding ALI/ARDS, which of the following statement is true? 1.Neutrophils are generally the first effector cells of the pulmonary response 2.Coughing is frequently the first CS associated with these syndromes 3.Radiographic signs are generally more unilateral than bilateral 4.Patients with ALI have a PaO2:FiO2 ratio < 300 and those w/ ARDS have a ratio < 200mmHg

46 Which of the following is not a part of the consensus definition of VetALI/VetARDS? 1.Acute onset (< 24hrs) of tachypnea and labored breathing 2.Known risk factors are SIRS, near-drowning, smoke inhalation 3.Evidence of pulmonary capillary leak without increased pulmonary capillary pressure 4.Evidence of inefficient gas exchange 5.Evidence of diffuse pulmonary inflammation

47 Which of the following describes the proliferative phase of ALI/ARDS? 1.Organization of exudates and development of fibrosis with increasing numbers of Type II pneumocytes 2.Collagen deposition in the alveolar, vascular and interstitial beds with development of microcysts in the pulmonary parenchyma 3.Pulmonary vascular leakage and inflammatory cell infiltration with loss of capillary integrity, alveolar epithelial damage, accumulation of protein-rich fluid and development of pulmonary edema

48 Which of the following statements is false? 1.The exudative phase is the first phase of ALI/ARDS, and is characterized by pulmonary vascular leakage and inflammatory cell infiltration 2.During the exudative phase, type II pneumoncytes are replaced with type I pneumoncytes 3.The proliferative phase is the 2 nd phase of ALI/ARDS, and is characterized by proliferation of type II pneumoncytes 4.The fibrotic phase of ALI/ARDS involves collagen deposition in the alveolar, vascular and interstitial beds

49 Which of the following does NOT occur in the proliferative phase of ALI/ARDS? 1.Collapse of alveoli 2.Development of microcysts in pulmonary parenchyma 3.Alerted function of type II pneumocytes 4.Pulmonary hypertension 5.Fibrin filled alveoli

50 All are pathologic changes associated with ALI/ARDS EXCEPT? 1.Ventilation-perfusion mismatch 2.Decreased compliance 3.Increased intra-pulmonary shunt 4.Decreased dead space relative to tidal volume

51 Which of the following does NOT act as a pro- inflammatory mediator in the pathogenesis of ALI/ARDS? 1.IL-6 2.TNF-alpha 3.IL-10 4.PAF 5.TGF-beta

52 All of the following are known risk factors of developing ALI/ARDS except? 1.Pancreatitis 2.GDV 3.Sepsis 4.L CHF 5.DIC

53 What is another role of platelet activating factor (PAF) other than activation of platelets? 1.Signals the release of pro-inflammatory cytokines 2.Causes vasodilation and bronchoconstriction 3.Impairs the vascular endothelial effects of neutrophils 4.Decreases development of lung injury 5.Promotes neutrophil migration

54 Which mediators plays a major role in neutrophils recruitment and activation? 1.PAF 2.TNF alpha 3.TGF beta 4.IL1b

55 What would be the typical BAL result from a dog with ALI/ARDS? 1.Proteinaceous background, neutrophils 2.Pyogranulomatous effusion 3.Suppurative and septic 4.Lymphoplasmacytic

56 Which of the following is a key mediator in tissue fibrosis during the late stages of ALI/ARDS? 1.PAF 2.Alveolar macrophages 3.TGF-beta 4.IL-6

57 Which eicosanoids are suspected to be the major players in the pathogenesis of ALI/ARDS? 1.Prostaglandins 2.Prostacyclins 3.TXA2 4.Leukotrienes 5.1 and 3

58 Matching- Which receptors? Responsible for bronchodilator? B2 Responsible for bronchoconstriction? Muscarinic

59 Matching Definitions

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61 T or F In health, the greatest resistance to airflow occurs in small terminal bronchioles False

62 The most important factor limiting flow rate during most of a forced expiration from total lung capacity is: 1.Rate of contraction of expiratory muscles 2.Action of diaphragm 3.Constriction of bronchial smooth muscle 4.Elasticity of chest wall 5.Compression of airways

63 What is the difference b/w anatomic and physiologic dead space? 1.Anatomic dead space: represents the volume of conducting airways 2.Physiologic dead space: the part of the tidal volume which does not participate in gas exchange

64 Which of the following are components of the conducting airways? 1.Trachea, bronchioles, alveolar ducts, and bronchi 2.Bronchi, resp bronchioles and alveolar sacs 3.Bronchi, bronchioles, terminal bronchioles and respiratory bronchioles 4.Trachea, bronchi, bronchioles, and terminal bronchioles

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66 Which of the following is NOT true about surfactant? 1.Surfactant decreases alveolar surface tension 2.Surfactant is secreted primarily by type I pneumocytes as well as goblet cells 3.Surfactant is spread over the alveolar surface and reduces the surface tension to 1/12 to ½ of the surface tension of a pure water surface 4.As an alveolus becomes smaller, the surfactant molecules on the alveolar surface are squeezed together, increasing their concentration

67 Which of the following statements is FALSE? Pulmonary surfactant: 1.Reduces the surface tension of the alveolar lining liquid 2.Is secreted by type II alveolar epithelial cells 3.Contains dipalmitoyl phosphatidylcholine 4.Increases the work required to expand the lung 5.Helps to prevent transudation of fluid from the capillaries into the alveolar spaces

68 References/Additional reading Preliminary evaluation of the utility of comparing SpO2/FiO2 and PaO2/FiO2 ratios in dogs. Calabro, et al. JVECC Partial pressure of end-tidal CO2 sampled via an intranasal catheter as a substitute for partial pressure of arterial CO2 in dogs. Pang, et al. JVECC Effect of body position on the arterial partial pressures of oxygen and carbon dioxide in spontaneously breathing, conscious dogs in an intensive care unit. McMillian, et al. JVECC Evaluation of respiratory parameters at presentation as clinical indicators of the respiratory localization in dogs and cats with respiratory distress. Sigrist, et al. JVECC Acute lung injury and acute respiratory distress syndromes in veterinary medicine: consensus definitions: the Dorothy Russell Havemeyer Working Group on ALI and ARDS in Veterinary Medicine. Wilkins, et al JVECC Acute respiratory distress syndrome in dogs and cats: a review of clinical findings and pathophysiology. DeClue, et al. JVECC Acute lung injury and Acute respiratory distress syndrome. Carpenter, et al Compendium Respiratory physiology 8 th edition. West Ch 3-6. Textbook of respiratory disease in dogs and cats. King Ch 68, 23, 24.

69 Airway physiology and clinical function testing. Hoffman. Vet Clinics 2007 Small animal critical care medicine. Silverstein, Hopper, 1 st edition. Chapters 34, 15. Ettinger and Feldman. Textbook of veterinary internal medicine, 7 th edition, Chapter 143, 124, 73. A case-based review of a simplified quantitative approach to acid- base analysis. Hopper, Haskins. JVECC Pulmonary abnormalities in dogs with renal azotemia. Boedec et al. JVIM Indications for and outcome of positive-pressure ventilation in cats: 53 cases ( ). Lee, et al. JAVMA Comparison of two fluid-management strategies in acute lung injury. Weidemann, et al. NEJM Comparison of the SPO2/FIO2 ratio and the PAO2/FIO2 ratio in patients with acute lung injury or ARDS. Rice, et al Chest 2007.


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