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46 Cards in this Set
- Front
- Back
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Where is the highest resistance in the airway? |
Mid bronchi |
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What is tidal volume? |
Inspired volume |
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What is the alveolar volume? |
The tidal volume (fresh air) that actually enters the lungs. Approximately 350mL |
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What is the dead space volume? |
Fraction of tidal volume taken into the dead space. Approximately 150mL |
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What is minute ventilation? |
Tidal volume x breaths per min |
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What is alveolar ventilation? |
Alveolar volume x breaths per minute |
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IRV |
Inspiratory reserve volume. Top of normal inspiration to top of VC |
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ERV |
Expiratory reserve volume. From end expiration to RV |
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IC |
Inspiratory capacity. From bottom normal expiration to top vital capacity |
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VC |
From forced expiration to force inspiration |
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FEC1 |
Forced expiratory capacity 1 second. How much can ya get it in 1 second? |
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FRC |
At rest. Begins at bottom of normal expiration. |
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TLC |
Total lung capacity. From top of vital capacity to minimal volume |
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What values can we only estimate from spirometry? |
TLC, RV, FRC. We have to use that crazy box to find these |
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The forced vital capacity test. Normal v obstructive v restrictive |
Used to determine FEV1 and FEV1/FVC ratio . WE CANNOT USE FVC ALONE TO DECIDE ETIOLOGY!! Normal: FEV1 approximately 4L. Ratio approximately 80%. Above 70% is normal. FVC is 5L.
Obstructive: FEV1 approximately 1.3L. FVC is 3.1L. Ratio of 40%.
Restrictive: FEV1 approximately 2.7L. FVC is 3.1L. Ratio of 90%. Normal seeming! |
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What is the effect of hypoxia on vessels in the lungs? |
Vasoconstriction. Increase vascular resistance, decrease flow. Allows for more efficient exchange of O2. Can lead to PAH |
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How do we calculate oxygen content in normal air? |
PO2 is always 21% of mmHg |
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PO2/PCO2 air? PO2 /PCO2 +water vapor? PO2 /PCO2 alveoli? PO2/PCO2 of arteries? PO2/PCO2 of veins? . In what direction does gas move? |
PO2/PCO2 air? 160, 0 PO2 /PCO2 +water vapor? 150, 0 PO2 /PCO2 alveoli? 105, 40 PO2/PCO2 of arteries? 100, 40 PO2/PCO2 of veins? 40, 46 . In what direction does gas move? High to low |
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How do we determine the alveolar PO2 concentration? |
PO2 water vapor/air - (PCO2 alveolar/R) R when we eat lots of carbs is 1 R with mixed diet is .8 |
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What are the different ways we can decrease diffusion? |
1. Thicken the membrane of the alveoli (ex pulmonary fibrosis). 2. Decrease pressure 3. Increase CO so much so that no time for diffusion (1 sec, but mostly first .25 seconds) 4. High affinity for Hb OR inability to dissolve - If high affinity for Hb, once saturated, will not diffuse |
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Which diseases effect diffusion? |
1. Emphysema: wasted ventilation! Multiple alveoli are ineffective at carrying O2. Thus, the area available to perform diffusion is small. 2. Fibrosis: thicc 3. Pulmonary edema: thicc |
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What does it mean that O2 is diffusion limited? |
. If we increase pulmonary perfusion, we can increase the diffusion of O2 |
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What does it mean that CO is diffusion limited? |
After hb is saturated, no more CO can enter the body. |
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What happens when we CO enters the blood? |
. Attaches to Hb. However, the body does not recognize that O2 binding is not occurring, since chemoreceptors only register DISSOLVED O2 |
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The partial pressures of O2 and CO2 at the APEX of the lung are... |
Increased and decreased, respectively. Think (apex is high up, so contents are more like Patm) |
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Stupid rate of O2 transfer equation (including diffusion) |
D (A/T) (delta P) |
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Hyperventilation causes... |
. High PO2 and low PCO2 |
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Hypoventilation causes? |
. Low PO2 and high PCO2 |
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V/Q ratios in 3 conditions: 1. Normal 2. Obstructed 3. Embolus
Also note compensatory steps! |
1. V/Q = 1 2. V/Q = 0/1. Approaching 0. In this condition, PO2 falls and PCO2 rise. Similar ABG to that of mixed venous blood. Compensatory effect: vasoconstrict in the obstructed area and shunt blood to other lung. Alveolar hypoxia response. 3. V/Q approaches infinity. PO2 of the alveoli is near 150 and PCO2 is very low (both conditions near PO2 atm). As a compensatory mechanisms (1) bronchoconstriction in affected lung. Shunting to good lung. (2) Decrease Type II cell production of surfactant in affected lung. Note PO2 of the arterial will be normal or a little low. PCO2 of arterials will be lower than usual.
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How much O2 is carried per 100mL blood? How is it carried? |
21mL O2 per 100mL blood . 20mL are on hemoglobin. 0.3mL dissolved |
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Calculate how much O2 per 100mL blood men v women carry on their hemoglobin. |
16g men 14g women We are able to carry 1.34 mL O2 per 1 g hb Hemoglobin has 4 spots open. We have to include this in our calculation. If CO involved. <1 (16)x (1.34mL O2 per 1g hb)x 1.0 |
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What causes the hemoglobin sigmoidal curve to shift right? |
DAT - DPG - acidosis - high temp
. Recall, shifting to the right means O2 is offloading at a higher PO2 |
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How is CO2 carried in the blood? |
70% as bicarb 23% as carbamjno compound 7% dissolved CO2 |
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Equation for determining acidosis/alkalosis |
[H+] = [24 x (PCO2)]/[HCO3] Normal values: PCO2= 40mmHg H+= 40 nmol/L HCO- = 24 mmol/L |
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Inducing respiratory acidosis |
. Increase CO2 (hypercapnea, hypercarbia) via: - hypoventilating - brain damage/injury - neuromuscular disorders - lung disease COMPENSATORY MECHANISM? Increasing HCO3 |
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Inducing metabolic acidosis |
Decrease HCO3 via: - DM - diarrhea - lactic acidosis - uremia (waste products in the blood) COMPENSATORY MECHANISM? decrease CO2. Hyperventilate. |
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Inducing respiratory alkalosis |
Decrease CO2 (hypocapneia) - hyperventilate - anxiety - fever - brain disorder COMPENSATORY MECHANISM? decrease bicarb (pee pee) |
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Inducing metabolic alkalosis |
Increasing HCO3: - poisoning - alkali ingestion - vomiting - diuretic COMPENSATORY MECHANISM? Increase CO2. Hypoventilate |
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What do the chemoreceptors in the aortic sinus and cartoid bodies sense? What effect do chemoreceptors have? |
. Increase PCO2, H+, K+ . Decrease PO2 . Signal via glossopharyngeal n to DRG to increase ventilation |
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Which three abnormalities lead to an increased A-a gradient? What is that btw? |
DVS: diffusion, V/Q dysfunction, shunting (R to L) - This occurs when the difference between the P of the alveoli and the P of the arterial is LARGER than 5mmHg. Typically, 105mmHg- 100mmHg |
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At what PO2 do we see large increases in minute ventilation? |
. 60mmHg
. Normally, minute ventilation is about .5mL/breath at about 16 RR. So, minute ventilation is about 8L/min |
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When do central chemoreceptors become activated? |
. Upon registering increase [H+] in CSF . Note, CO2 is soluble in the CSF, but it does not directly cause central chemoreceptor response. Only the conversion to H+ does. . Effect is to stimulate DRG and increase ventilation |
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Difference between Herring-Breuer reflex in animals and humans. |
. "Stretch reflex" . Lots of stretch stimulates vagal n and tells medulla to end inspiration . In animals, this effect is much more important: upon performing vagatomy, inspiration lasts WAY longer . In humans, Herring-Breuer has the effect: 1. Decreasing WOB 2. Sensing dyspnea. Dyspnea occurs when minute ventilation and actual lung volume (sensed by reflex) do not match |
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Irritant receptors - Where? (3) - What do they do? |
. Nasal: Sneeze. Trigeminal n. . Pharynx: Aspiration. glossopharyngeal n. . Larynx/trachea: Cough. Vagal n. . Irritant receptors trigger large inhalation and then huge forced exhalation |
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Asthma and the irritant receptors |
Asthma already causes bronchoconstrictors to be secreted. However, when secreted, they also trigger irritant receptors, which cause further bronchoconstriction. |
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J-receptors |
Sense engorgement of the alveolar capillaries from edema, interstitial abnormalities. When engorgement sensed, leads to tachypnea and sometimes apnea |
