Gas Exchange and Transport

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)

Gas Exchange and Transport Pressure Differential Fig 13.1

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

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

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

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)

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

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

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

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

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

Dynamics of Pulmonary Ventilation

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

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

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

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