Gas Exchange and Transport

Gas Exchange and Transport

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 (O2 or CO2) 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

CO2 highly soluble

Gas Exchange and Transport

PO2 – 100 mm Hg: regulates breathing and 02 loading of HbPCO2 – 40 mm Hg: chemical basis for ventilatory control via respiratory center

Saturation with water vapor - lower PO2

Constant loading and unloading of CO2 and O2FRC necessary to prevent swings in CO2 and O2 concentration in alveoli

Fig 13.2

Gas Exchange and Transport

Fig 13.2

Time Required for Gas ExchangeCapillary transit time is ~0.75 sDuring maximal exercise, capillary transit time is ~0.4 sGas 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

O2 Transport:

•Dissolved oxygen in blood only sustains life for about 4 seconds (0.3 mL O2 / dL)

•Small amount establishes PO2 which regulates breathing and oxygen loading of hemoglobin

Gas Exchange and Transport

O2 Transport:

•Hemoglobin (Hb) – Protein in red blood cells that transports 02 bound to iron

•Each Hb has 4 iron atoms (can bind 4 O2)

•Hb transports 19.7 ml/dL (vs 0.3 ml/dL - plasma)

(65 x that in plasma) Fig 13.3Anemia: Low iron in red blood cells results in low oxygen carrying capacity

Gas Exchange and TransportOxyhemoglobin dissociation curve:

Describes Hb saturation with O2 at various PO2 levels100 mm Hg:

98% saturation

60 mm HG: decline in % saturation

40 mm HG: 75% of O2 remains with Hb - 5 ml delivered to tissues

Athletes?

Fig 13.4

Gas Exchange and Transport

Bohr effect –

•Increased blood acidity (lactic acid), temperature, CO2 causes downward shift to the right

•Facilitates dissociation of O2 from Hb

•No effect on capillary blood Hb-O2 binding

Fig 13.4

Gas Exchange and TransportOxyhemoglobin dissociation curve:

Myoglobin:

•Intramuscular O2 storage protein

•Transfers O2 to mitochondria when PO2 falls

•At 40 mm Hg, Mb 95% saturated with O2

•No Bohr effect occurs with myoglobin

Fig 13.4

Dynamics of Pulmonary Ventilation

Pulmonary VentilationVentilatory 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

PO2, PCO2, acidity (lactate), temperaturePO2 – no effect on medulla (peripheral chemoreceptors detect arterial hypoxia, altitude)

PCO2 – 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 CO2, H+, K+, and temperature during strenuous exercise

Pulmonary VentilationPhases of Ventilatory Response During Exercise:I. Neurogenic – central command, peripheral input stimulates medullaII. Neurogenic – continued central command, peripheral chemoreceptors (carotid)

Rapid rise

Slower exponential rise

Steady state ventilation

Abrupt decline

III. Peripheral - CO2, H+, lactate (medulla), peripheral chemoreceptors Recovery – removal of central, peripheral, chemical input

Fig 14.4