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MP - Lecture 27
Tissue Gas Exchange and CO2 Transport
| Question | Answer |
|---|---|
| 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 |
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