Gas Exchange and Transport
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Transcript of Gas Exchange and Transport
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Gas Exchange and Transport
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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)
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Gas Exchange and Transport
Pressure Differential
Fig 13.1
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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
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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
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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
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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)
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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
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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
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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
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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
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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
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Dynamics of Pulmonary Ventilation
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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
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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
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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
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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