# RESPIRATORY PHYSIOLOGY. Anaesthesiology Block 18 (GNK 586) Prof Pierre Fourie

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1 RESPIRATORY PHYSIOLOGY Anaesthesiology Block 18 (GNK 586) Prof Pierre Fourie

2 Outline Ventilation Diffusion Perfusion Ventilation-Perfusion relationship Work of breathing Control of Ventilation 2

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4 4

5 Ventilation Function: Supply O 2 to the alveoli and remove CO 2 Airways divided in conducting passages (dead space) and respiratory zone (gas exchange) Respiratory zone blood-gas interface Respiratory bronchiole Alveoli 5

6 Figure 37-8 Respiratory passages. Downloaded from: StudentConsult (on 22 May :53 PM) 2005 Elsevier 6

7 Blood-Gas interface 500 million alveoli Surface area of m 2 Extremely thin um Damaged by high capillary pressures 7

8 Figure 39-7 Respiratory unit. Downloaded from: StudentConsult (on 22 May :53 PM) 2005 Elsevier 8

9 Ventilation Tidal Volume Volume of air entering the lung with a normal breath = Tidal Volume (Vt) Vt = 6-8 ml/kg = 500 ml Vmin = Vt x RR = 500 x 12 = 6000 ml Vt = Alveolar volume (VA) + Physiological dead space (VdPhys) 9

10 Ventilation Dead Space VdPhys = Anatomical dead space (VdAnat) + Alveolar dead space (VdAlv) Vd/Vt = 1/3 2/3 of Tidal volume available for gas exchange Alveolar volume (330 ml) Anaesthesia - Apparatus dead space (VdApp) Total Vd = VdApp + VdAnat + Vd Alv 10

11 Ventilation Dead Space VdPhys = Vt(PaCO 2 - PECO 2 ) PaCO 2 Bohr equation PaCO 2 - PECO 2 = 5 mm Hg Dead space ventilation 11

12 Figure 37-6 Diagram showing respiratory excursions during normal breathing and during maximal inspiration and maximal expiration. Downloaded from: StudentConsult (on 22 May :53 PM) 2005 Elsevier

13 Ventilation Alveolar Gas exchange depends on Alveolar Ventilation (VA) VA = RR x Alveolar volume = 12 x 330 = 4000 ml Alveolar Ventilation Equation: VA = VCO 2 / P a CO 2 + K 13

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16 Ventilation Function: Supply O 2 to the alveoli and remove CO 2 Alveolar gas equation P A O 2 = PiO 2 (P A CO 2 /R) + K = FiO 2 (PB - PH 2 O) (P A CO 2 /R) + K 16

17 Hypoventilation VA Vt Vd HYPERCAPNIA Headache, excitement, restlessness, confusion Respiratory acidosis, sympathetic stimulation tachycardia, pulse pressure, sweating, cyanosis 17

18 Functional Residual Capacity (FRC) FRC = ERV + RV Amount of air that remains in the lungs, end of normal expiration (+/ ml). Volume of air available for gas exchange diffusion of O 2 to blood and of CO 2 from blood to alveoli FRC supine, age, respiratory disease, anaesthesia 18

19 Figure 39-9 Ultrastructure of the alveolar respiratory membrane, shown in cross section. Downloaded from: StudentConsult (on 22 May :53 PM) 2005 Elsevier

20 Diffusion Fick s Law Rate of diffusion of a gas through a tissue slice is proportional to area of tissue Partial pressure difference Solubility of the gas in the tissue Inversely proportional Thickness of the tissue Square root of the molecular weight of the gas 20

21 Oxygen uptake Diffusion limited Perfusion limited RBC time spent in alveolar capillary = 0.75 sec PaO 2 is reached within 0.25 sec Limited High cardiac output Very low mixed venous PO 2 21

22 Perfusion Cardiac output (Qt) = SV x HR Vmin = Vt x RR Pulmonary blood flow (Qp) = Qt Vmin = Qt then ventilation / perfusion ratio = 1 Alveoli perfused but not ventilated = shunt (Qs) Alveoli ventilated but not perfused = dead space (Vd) 22

23 Shunt equation CcO 2 CaO Qs / Qt = 2 CcO 2 - CmvO 2 CcO 2 = O 2 concentration in capillaries of ventilated perfused alveoli (Alveolar gas equation) CmvO 2 = 40 mmhg or 70% saturated Qs / Qt = 2% 23

24 Ventilation Perfusion relationships Ideal V/Q ratio = 1 If V = 0 V/Q = 0 = pure shunt If Q = 0 V/Q = infinity = pure dead space ventilation V/Q ratio > 0 but < infinity = V/Q mismatch High V/Q Hypercapnia Low V/Q Hypoxia 24

25 V/Q mismatch and Anaesthesia Loss of motor tone compression atelectasis low V/Q ratio Vasodilatation and cardiac suppression - Qt high V/Q ratio V/Q mismatch open abdominal and thoracic procedures Atelectasis with high O 2 concentrations (Absorption atelectasis) 25

26 Management of V/Q mismatch Ventilatory support Rx atelectasis Avoid high O 2 concentrations Apply PEEP Circulatory support Rx low cardiac output Fluid management, correct hypovolemia Inotropes Vasopressors 26

27 Work of breathing (WOB) Energy and Work is required to expand the chest and move gas into the lungs and increase the lung volume = WOB Pressure is required to overcome airway resistance and tissue elasticity Volume change per unit of pressure change = Compliance Normal Compliance = 200 ml / cm H 2 0 transpulmonary pressure 27

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29 Work of breathing WOB Diseases that compliance = restrictive lung disease (inspiration) Diseases that airflow resistance = obstructive lung disease (expiration) WOB hypoventilation, hypercapnia and hypoxia Respiratory failure 29

30 Control of Breathing Central Respiratory centres in the brainstem control spontaneous breathing by rhythmic neural activity Dorsal inspiratory and ventral expiratory neurons in the medulla oblongata RR and rhythm fine-tuned by pontine centres (apneustic and pneumotacic) which influence the dorsal neurons H + sensitive chemoreceptors in the medulla is stimulated by low CSF ph ( PCO 2 ) stimulate breathing 30

31 Figure 41-1 Organization of the respiratory center. Downloaded from: StudentConsult (on 22 May :53 PM) 2005 Elsevier

32 Figure 41-2 Stimulation of the brain stem inspiratory area by signals from the chemosensitive area located bilaterally in the medulla, lying only a fraction of a millimeter beneath the ventral medullary surface. Note also that hydrogen ions stimulate the chemosensitive area, but carbon dioxide in the fluid gives rise to most of the hydrogen ions. Downloaded from: StudentConsult (on 22 May :53 PM) 2005 Elsevier

33 Control of Breathing Peripheral Chemoreceptors in the Aortic arch and Carotid body Sensitive to PaO 2 - ventilation Chemoreceptors in the Carotid body Sensitive to ph - ventilation Juxta-capillary receptors Irritation receptors Stretch receptors 33

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35 Anaesthetic implications Central respiratory centres Very sensitive to opioids - Vmin Insensitive by chronic hypercapnia (CSF ph normalized by buffering with HCO3) stimulated by low PaO 2 (hypoxic drive) Peripheral centres Suppressed by Anaesthetic vapours benzodiasipines 35

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