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MP - Lecture 27

Tissue Gas Exchange and CO2 Transport

Medical Physiology – Lecture 27 Tissue Gas Exchange and CO2 Transport
Rate limiting factor of O2 consumption is: ADP levels, other factors
Myoglobin functions as a ___ in skeletal muscle: Cytoplasmic O2 sink
Cytoplasmic O2 store in the CNS and retina is by: Neuroglobin
In absence of Hb, downstream capillary diffusion rates: Decrease
If PO2 = 100 and Hb is absent: Tissue hypoxia can still occur
Hb serves as a: O2 reservoir
How does Hb maintain downstream diffusion of O2? Replenishes dissolved O2 to maintain PO2
Venous PO2 is an index of: Tissue O2 levels (deficiency indicator)
Factors that determine venous PO2: Fick principle (metabolic demands vs. blood flow), PaO2, O2 dissociation curve
Fick Principle O2 Content = (O2 concentration)/ (Blood Flow)
High consumption but low flow results in: O2 content change
Venous PO2 of each tissue depends on: Fick principle
Normal value for difference in O2 content of the brain is: ~7.4 mL O2 / 100 mL blood
Mixed venous blood has a ___ PO2 and O2 content. Single
Arterial PO2 is the same in carious tissues because: O2 does not diffuse until it reaches venules and capillaries
Tissues extract different % of O2 from blood based on: Metabolic needs
At arterial PO2 = 90, saturation is: 98%
At arterial PO2 = 40, saturation is: 75%
At arterial PO2 = 26, saturation is: 50%
Average O2 extraction over whole body is: 25%, 5 mL/100 mL out of 20 mL/100 mL
Normal value for difference in O2 content is: 5 mL O2/100 mL blood
A safety factor in the dissociation curve, moderate change in VA and PaO2 at high PaO2 produces: little change in arterial content to prevent premature unloading
A safety factor in the dissociation curve, a small pressure drop at moderate to low PaO2 produces: A large amount of O2 delivery/unloading
Patient with anemia (1/2 normal [Hb]) but with same cardiac output and O2 consumption has: Same O2 content change, but reduced total O2 content and lower mixed venous O2
Change in O2 content in an anemic patient (1/2 normal [Hb]) with increased cardiac output (10 L/min) and O2 consumption of 300 mL/min equals: (300 mL O2/min) / (10,000 mL blood/min) = 3 mL O2/100 mL blood
Effect of increasing cardiac output in anemic patients Increased mixed venous PO2, higher O2 content
Effect of left-shift on mixed venous PO2 Increased O2 affinity, decreased unloading potential
Compensate for effect of left-shift by: Polycythemia (increase RBC/Hb)
Effect of polycythemia on dissociation curve Increase venous PO2, leaving higher PO2 after O2 extraction
Cyanide (CN-) causes: Increased PvO2, decreased a-v O2 content
Mixed venous PO2 is elevated if a-v O2 content is: Decreased
CN- works by: Competing with O2 for cytochrome a/a3, inhibiting O2 consumption
Respiratory exchange ratio of high carbohydrate diet: R = 1
Respiratory exchange ratio of high hydrocarbon diet: R = 0.67
Respiratory exchange ratio of balanced diet: R = 0.8
CO2 is transported as: HCO3- in blood (plasma)
At arterial pH 7.4, concentration of HCO3- is: 20 times concentration of CO2
Formation of HCO3- takes primarily takes place in: RBC by carbonic anhydrase
Function of anion exchanger in RBC is to: Bring in Cl- to remove HCO3-
Hb buffering ability is due to: Histidine residues
CO2 is formed in ___ by reverse steps. Pulmonary capillaries
Intracellular H+/HCO3- formation increases: O2 dissociation (Bohr effect)
Normal arterial PO2 ~90 mmHg
Normal mixed venous PO2 40 mmHg
Normal arterial PCO2 40 mmHg
Normal mixed venous PCO2 46 mmHg
Normal arterial pH 7.4 pH
Normal mixed venous pH 7.37
Normal change in O2 content: 5 mL O2 / 100 mL blood
CO2 dissociation curve compared to O2 dissociation curve: Steeper curve, shape dependent on bicarbonate buffers
Bohr Effect Incoming CO2 produces H+ to shift curve right, increasing venous PO2 and O2 delivery
Haldane Effect Incoming O2 causes H+ dissocation from Hb, increasing CO2 formation and expiration
Created by: emyang



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