1. Gas Exchange and Transport

2. The driving force for pulmonary blood and alveolar gas exchange is the Pressure Differential – The difference between the partial pressure of a gas (O 2 or CO 2 ) above a fluid and dissolved in fluid (alveoli or blood)

3. Gas Exchange and Transport Pressure Differential Fig 13.1

4. Gas Exchange and Transport Henry’s Law: The rate of gas diffusion into a liquid depends on: 1)Pressure differential between the gas above the fluid and gas dissolved in fluid 2)Solubility (dissolving power) of the gas in the fluid CO 2 highly soluble

5. Gas Exchange and Transport PO 2 – 100 mm Hg: regulates breathing and 0 2 loading of Hb PCO 2 – 40 mm Hg: chemical basis for ventilatory control via respiratory center Saturation with water vapor - lower PO 2 Constant loading and unloading of CO 2 and O 2 FRC necessary to prevent swings in CO 2 and O 2 concentration in alveoli Fig 13.2

6. Gas Exchange and Transport Fig 13.2 Time Required for Gas Exchange Capillary transit time is ~0.75 s During maximal exercise, capillary transit time is ~0.4 s Gas exchange during maximal exercise not a limiting factor

7. Gas Exchange and Transport Fig 13.2 Time Required for Gas Exchange Pulmonary disease impacts this process: 1. Thicker alveolar membrane 2. Reduced surface area Fick's Law-Gas diffuses at rate proportional to: Tissue thickness (inversely) Tissue area (directly)

8. Gas Exchange and Transport O 2 Transport: Dissolved oxygen in blood only sustains life for about 4 seconds (0.3 mL O 2 / dL) Small amount establishes PO 2 which regulates breathing and oxygen loading of hemoglobin

9. Gas Exchange and Transport O 2 Transport: Hemoglobin (Hb) – Protein in red blood cells that transports 0 2 bound to iron Each Hb has 4 iron atoms (can bind 4 O 2 ) Hb transports 19.7 ml/dL (vs 0.3 ml/dL - plasma) (65 x that in plasma) Fig 13.3 Anemia: Low iron in red blood cells results in low oxygen carrying capacity

10. Gas Exchange and Transport Oxyhemoglobin dissociation curve: Describes Hb saturation with O 2 at various PO 2 levels 100 mm Hg: 98% saturation 60 mm HG: decline in % saturation 40 mm HG: 75% of O 2 remains with Hb - 5 ml delivered to tissues Athletes? Fig 13.4

11. Gas Exchange and Transport Bohr effect – Increased blood acidity (lactic acid), temperature, CO 2 causes downward shift to the right Facilitates dissociation of O 2 from Hb No effect on capillary blood Hb-O 2 binding Fig 13.4

12. Gas Exchange and Transport Oxyhemoglobin dissociation curve: Myoglobin: Intramuscular O 2 storage protein Transfers O 2 to mitochondria when PO 2 falls At 40 mm Hg, Mb 95% saturated with O 2 No Bohr effect occurs with myoglobin Fig 13.4

13. Dynamics of Pulmonary Ventilation

14. Pulmonary Ventilation Ventilatory Control – How does our body control rate and depth of breathing in response to metabolic need Medulla – Inspiratory neurons activate diaphragm and intercostals Expiratory neurons activated by passive recoil of lungs *Mechanisms maintain constant alveolar and arterial gas pressures Fig 14.1

15. Pulmonary Ventilation 1. At rest, chemical state of the blood controls ventilation PO 2, PCO 2, acidity (lactate), temperature PO 2 – no effect on medulla (peripheral chemoreceptors detect arterial hypoxia, altitude) PCO 2 – most important respiratory stimulus to medulla at rest Fig 14.2

16. Pulmonary Ventilation 2. During exercise, no single mechanism explains increase in ventilation (hyperpnea) Neurogenic Factors: Cortical: Motor cortex stimulates respiratory neurons to increase ventilation Peripheral: Mechanoreceptors in muscles, joints, tendons influence ventilatory response Peripheral chemoreceptors become sensitive to CO 2, H +, K +, and temperature during strenuous exercise

17. Pulmonary Ventilation Phases of Ventilatory Response During Exercise: I. Neurogenic – central command, peripheral input stimulates medulla II. Neurogenic – continued central command, peripheral chemoreceptors (carotid) Rapid rise Slower exponential rise Steady state ventilation Abrupt decline III. Peripheral - CO 2, H +, lactate (medulla), peripheral chemoreceptors Recovery – removal of central, peripheral, chemical input Fig 14.4