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MP - Lecture 32
Pulmonary Pathophyysiology
| Question | Answer |
|---|---|
| Medical Physiology – Lecture 32 | Pulmonary Pathophysiology |
| A-a PCO2 gradient difference is: | Insignificant (~0) |
| PCO2 of inspired air is: | ~0 mmHg |
| Largest PCO2 difference is between: | Inspired air and alveoli |
| Hypoventilation always increases: | Alveolar, arterial, and venous PCO2 |
| Hypercapnia | Elevated PCO2 |
| Respiratory acidosis is caused by: | CO2 backup all the way to venous/tissues |
| Respiratory alkalosis is caused by: | Rapid CO2 expiration (Hyperventilation) |
| Alveolar ventilation is ___ proportional to alveolar PCO2 at constant CO2 production. | Inversely (VA decrease = alveolar PCO2 increase) |
| Causes of CO2 retention: | Hypoventilation and decreased blood flow relative to VCO2 |
| Causes of hypoventilation: | Increased airway resistance, reduced lung/thorax compliance, depressed respiratory center, or muscle dysfunction |
| If alveolar PCO2 is 60 to 75 mmHg: | Severe dyspnea |
| If alveolar PCO2 is 80 to 100 mmHg: | Lethargy, possible coma |
| If alveolar PCO2 is greater than 100 mmHg: | Depressed ventilation, increased PCO2, decreased PO2, and death |
| Difference between inspired PO2 and alveolar PO2 is increased by: | Hypoventilation |
| Diffusion impairment (low VA/Q) caused by: | Absolute shunt, physiological shunt, and pulmonary embolism |
| Effect of VA/Q mismatch on alveolar PCO2 is: | Minimal |
| Pneumonia creates a: | An absolute right to left shunt |
| Saturation of blood if one long is completely consolidated but still equal flow is: | (98 + 60) /2 = 79% |
| Saturation of shunted blood is: | Equal to mixed venous blood (~60%) |
| If 100% O2 is given to lungs with one side completely consolidated: | Minimal effect, unsaturated shunted blood outweighs small gain by good lung |
| Atelectasis causes: | Absolute right to left shunt |
| Hypoxia and decreased volume in collapsed lung causes: | Increased vascular resistance and blood flow less than half of cardiac output |
| Pulmonary Embolism | Venous thrombus from lower extremity or pelvis travels through right heart and lodges in pulmonary artery |
| Large pulmonary embolism causes: | severe VA/Q mismatch resulting in increased physiological dead space and wasted ventilation |
| Increased arterial to venous PO2 difference caused by: | Low flow, left shifted Hb, anemia, and CO poisoning |
| CO compared to O2: | Same size but more polarized |
| CO binds Hb: | 200x stronger than O2 |
| CO bound Hb increases: | affinity for O2 (left shift) |
| CO poisoning causes: | Decreased arterial O2 content and increased O2 affinity (decreased unloading) |
| In the placenta, O2 transfer is from: | Blood to blood |
| How does fetal blood pick up O2 in placenta: | Lower p50 with more hematocrit than maternal Hb and double Bohr effect |
| Double Bohr Effect | Bohr effect in maternal blood helps O2 unloading and in fetal blood helps O2 loading |
| Effect of CO in fetal O2 delivery | Maternal HbCO lowers arterial O2 content and p50, lowering PO2 in maternal side of placenta which lowers fetal arterial PO2, CO also bound to Hbf increases affinity |
| Effect of cyanide (CN-) | Competes with O2 and inhibits cytochrome oxidase |
| Venous PO2 in cyanide poisoning is: | Increased because O2 consumption reduced (Fick) |
| Forced expiration test measures: | Forced vital capacity (FVC) |
| FEV1 is: | Volume forcefully expired in 1 second, ~80% of FVC |
| Flow-volume curve shows: | max flow at each volume |
| Maximum flow for each volume caused by: | Dynamic airway collapse |
| Dynamic Airway Collapse | During forced expiration pressure surrounding airway becomes larger than inside pressure and causes airway collapse |
| Restrictive flow-volume curve has: | Decreased compliance and lower max volume, but normal slope for max flow because normal airway resistance |
| Obstructive flow-volume curve has: | Higher initial volume, but decreased overall volume with decreasing curve due to increased resistance |
| Hazards of O2 therapy | CO2 retention in COPD, retrolental fibroplasia in infants, damage to alveolar endothelium leading to edema, hyperbaric PO2 causing CNS convulsions, and absorption atelectasis |
| Absorption Atelectasis | Obstructed alveoli eventually collapses after absorbing gases into venous blood, N2 slows atelectasis because of slow diffusion rate |
Created by:
emyang
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