Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
25 Cards in this Set
- Front
- Back
|
Henry's Law of Dissolved gasses
|
[Gas] dissolved in liquid is proportional to partial pressure of the gas in the liquid
- Ex. = If PO2 = 100 mmHg, [O2] dissolved = 0.3mL/dL - When PO2 = 200 mmHg, [O2] = 0.6mL/dL *** Important because O2 in plasma is taken up by RBC - Need certain PO2 to get certain [O2] |
|
|
Importance of Hb
|
- Hb is O2 carrier = necessary!
- If O2 only randomly diffused into plasma (not carried), CO would have to be ~83 L/min to sustain O2 consumption... |
|
|
Saturation of Hb factor
|
- Hb O2 saturation entirely dependent on PO2!
- PO2 determines how much O2 gets on Hb, and how much O2 is dissolved in plasma! |
|
|
O2 dissociation curve
|
- Sigmoid from cooperativity
- Plateau of curve = large changes in PO2 don't radically affect O2 saturation - Can still maintain high levels of O2 in blood despite lower PO2 - Safety net! |
|
|
How low does PO2 need to be to reach P50?
|
- P50 = PO2 when Hb is 50% saturated
- 27 mmHg = pretty low! |
|
|
Factors that decrease Hb O2 affinity
|
Increased H+, PCO2 (↓pH)
- Increased temperature - Increased 2,3 DPG - Causes overall shift to the right! |
|
|
Importance of decreased Hb O2 affinity
|
Increased PCO2, H+ decreases O2 affinity
- As RBC's move into tissues, they encounter progressively higher PCO2's - This causes lower affinity for O2 - O2 delivery to tissues where needed! |
|
|
Factors increasing Hb O2 affinity
|
- Decreased H+, PCO2
- Decreased temperature - Decreased 2,3 DPG - Presence of Fetal hemaglobin - Overall shift of curve to left! |
|
|
Arterial vs. Venous blood curve shift
|
Venous = shifted to the right, arterial to the left
- Venous has higher PCO2, H+ - Arterial blood has higher affinity for O2 |
|
|
Calculation of O2 content
|
O2 content = amount of O2 in the plasma for use
- Determined by 1) O2 physcially bound to Hb and 2) O2 dissolved in plasma - NOT PO2 directly! - PO2 affects both, but does NOT contribute directly! - O2 content = [O2 on Hb] + [O2 in plasma] = [(Hb g/dL x Hb carrying capacity) x O2 saturation] + (0.003 x PO2) = [(Hb g/dL x 1.34 mL/g) x some%] + (0.003 x PO2) - Normal value = ~20mL/dL |
|
|
Effects on O2 content: PO2 vs. Hb
|
- Change in PO2 has large safety buffer, so even big PO2 variance = small O2 content changes
- Effects of Hb drop are much more severe! |
|
|
O2 saturation curve for patients with normal vs. reduced Hb
|
- They are exactly the same!
- The % saturation will remain the same! - The O2 is what changes! |
|
|
Factors affecting O2 content
|
- Anemic patients = will have normal PO2, lower O2 content
- Venous PO2 will be low - high metabolic demand for O2 that just isn't there... - CO poisoning = will have normal PO2 and Hb, but low O2 content - Curve shifts left - Hb holds O2 tighter - can't deliver well... - PO2 has to get much lower before O2 is released - Also large drop in O2 content *** End of the day = content mostly controlled by Hb! |
|
|
CO2 transport overview
|
~200 mL/min produced
Transport mechs = Dissolved in plasma = 8% - HCO3 in plasma (57%) RBC (24%) - Carbaminohemaglobin (11%) |
|
|
CO2 exchange at tissues
|
- PO2 is lower in tissues than RBC carrying O2
- Hb lets O2 go - At same time, PCO2 is higher in tissues -> RBC will eq. with them - CO2 + H20 -> HCO3 + H+ - HCO3 will leave RBC, Cl- enters |
|
|
CO2 exchange at lungs
|
Complete opposite of CO2 exchange at tissues
- PO2 at alveoli is 100, so RBC's will eq. to 100 mmHg - Very little CO2 at alveoli, so HCO3 -> CO2 + H2O - Cl- leaves RBCs |
|
|
Carbonic anhydrase reaction
|
Facilitates the CO2 + H2O -> HCO3 + H+ reaction in RBC's
|
|
|
Bohr effect
|
- PCO2 inversely affects Hb affinity for O2
- Higher PCO2 -> curve shifted right, O2 released more easily |
|
|
Haldane effect
|
- Amount of O2 carriage affects Hb affinity for CO2
- Opposite of Bohr effect - At a given PCO2, deoxygenated blood = higher CO2 content! *** Affinity for CO2 and O2 depend on relative concentrations! |
|
|
CO2 effects on ventilation
|
1) Affects ventilation
- Measure of alveolar ventilation (VA) is PCO2 - VA = VCO2/PaCO2 - Body produces CO2 at constant rate - If VA is reduced by 0.5, then PCO2 will be double! - Ventilating half as much means PCO2 will be twice as high - Ventilation affects PAO2 PAO2 = PIO2 - PaCO2/R 2) CO2 -> HCO3 produces H+ -> lowers pH - Higher the PCO2 = the lower the pH |
|
|
Respiratory acidosis
|
- Hypoventilation -> High PCO2
- Reduced ratio of HCO3/PCO2 - HCO3 will buffer H+, but the HCO3 produced is not enough to completely buffer all H+ - Overall lower pH |
|
|
Respiratory alkalosis
|
- Patient hyperventilates -> low PCO2!
- Higher HCO3/PCO2 ratio - Overall higher pH! |
|
|
pH shift based on PCO2
|
pH change of 0.08 for every 10 mmHg change in PCO2
- PCO2 from 40 -> 50 mmHg = pH drops by 0.08! |
|
|
Renal compensation for acidosis/alkalosis
|
- Change in pH not tolerated well by kidneys
- Ex. If pH = 7.2 for a while, kidneys will hold on to HCO3 - Respiratory acidosis with renal compensation! - HCO3 levels in plasma rise/fall based on renal compensation one way or another! |
|
|
Steps to determine situation
|
1) Check to see if pH is high or low
- Tells us either kidneys are jacked or lungs are jacked, but not which 2) Look at PaCO2 and HCO3 - whichever is driving the pH in the abnormal direction is the one causing the problem! - One moving away from pH shift is the compensation |
