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13 Cards in this Set
Anatomic Dead Space vs Physiological Dead Space
Anatomic Dead Space: is the volume of conducting a/w's.
Physiological Dead Space: is the volume of gas that does not eliminate CO2
The 2 dead spaces are almost the same in healthy individuals. but physiological dead space might be higher in lung disease (air trapping, like in pulmonary fibrosis)
Tidal Ventilation = Alveolar Ventilation + Anatomic Dead Space
V(T) = V(A) +V(D)
if n is respiratory frequency
n(V(T)) = n(V(A)) + n(V(D))
Alveolar Ventilation can be increased by increasing n or anatomic dead space
How can we measure anatomic dead space? Alveolar Ventilation?
Uses 100% O2 to displace the N2 from alveolar gas to dead space, while N2 levels are continiously measured at the mouth.
Alveolar Ventilation - CO2 concentration in expired gas is used, b.c no gas exhange occurs in the anatomic dead space so all of the expired CO2 comes from the alveolus.
The application is this:
If Alveolar Ventilation is halved, arterial pCO2 will double, once steady state is established. So pCO2 helps evaluate the progression of alveolar hypoventilation in impending resp failure.
How do we measure physiological dead space?
The normal ratio of dead space to TV is in the range of .2 to .35 during resting breathing
What are the important features of Fick's Law of Diffusion? (**)
1. Rate of diffusion of a gas is proportional to the area, and inversely proportional to thickness.
2. Diffusion rate is proportional to the partial pressure difference.
3. Diffusion rate is proportional to solubility of the gas, and inversely proportional to the square root of the mw. (so a less dense gas = increase diffusion rate)
4. Diffusion of oxygen is effecient. Equilibrium of alveolar and arterial O2 occurs almost immediately! So **O2 transfer into the pulmonary capillaries is perfusion limited.**
(pp of O2 in capillaries is 40 mmHg and the alveolar air pp is 100 mmHg. So O2 flows down this gradient)
5. CO2 has 20 times the solubility of O2. Hence Diffusion of CO2 through tissue is 20 times faster. So in hypoventilation, high CO2 levels at the alveoli cause impaired O2 exchange, causing hypoxemia.
1. At high altitudes, alveolar pO2 is reduced and the gradient btwn air and blood is less, so rise in arterial O2 is slower. (**High Altitude Hypoxia can be fixed with O2**)
2. In diseased states, where the blood-gas barrier is thickened, as in interstitial lung disease, diffusion of O2 and more rarely CO2, may be impaired. (remember thickness is inversely proportional to diffusion rate) These disease cause thickness to increase: coal workers lungs, pnemonconeosis, pulmonary edema, interstitial fibrosis, sacoidosis. b/c of increased thickness the transport of alveoli to the artery is impaired and hypoxemia occurs.
3. Carbon Monoxide is diffusion limited so it's used to evaluate the diffusion properties of the lung. It forms a tight bond with Hgb.
What are the physiologic causes of hypoxemai? Explain the first cause.
1. Hypoventilation, 2. Diffusion limitation, 3. Shunt, 4. Ventilation-perfusion inequality.
1. Hypoventilation: caused by:
b) Damage to chest wall
c) Weakness of respiratory muscles
d) Dense gas decreasing air flow (deep sea diving)
(THP is that hypoventilation always increases PCO2 and can often be fixed with high percent O2 infusion)
Back to the **Alveolar Gas Equation**
PAO2=PIO2-PACO2/R + F
PA is alveolar, R is the Respiratory quotient, and PI is inspired.
Can fix by increasing PIO2.
(F is a small factor or 2 mmHg which can be ignored)
Explain the third and fourth physiologic causes of hypoxemia.
Before we start: **Shunted blood cannot be fixed by giving 100% FiO2, b/c shunted blood is not exposed to the increased O2 concentration!** In addition, a shunt does not raise CO2 b/c sensitive chemoreceptors will respond to an increased CO2 by ^RR.
Shunt: refers to blood that enters the arterial system without going through ventilated areas of the lung. In the normal lung, bronchial arteries and coronary veins drain back to the Left ventricle w/o passing through the lung. This deoxygenated arterial blood causes a shunt. The shunt ratio (QS/QT) refers to shunted volume over total volume. V/Q = 0
4. Ventilation-Perfusion Mismatch:
Hypoxemia may occur when there is a mismatch between ventilation and perfusion.
Shunt: V/Q=0 (no ventilation)
Dead Space: V/Q = 0 (no flow) in this situation O2 rises (150 mmHg), b/c it's not being soaked up and CO2 decreases (0) because it's not being dumped. Both approaching inspired levels.
What is the dynamic of the V/Q relationship of the upright lung?
In the upright lung V/Q is very high at the top of the lung (much more ventilation then perfusion). By going down the lung perfusion (Q) increases rapidly with ventilation (V) increasing much slower. Because Q increases much faster and higher and it's the denominator so it lowers the V/Q ratio.
Now Alveolar concentration also decreases, being max at apex and lowest at base (40 mmHg difference). But since Q is so low at the apex, the apex's overall contribution to O2 uptake is minimal.
pO2 is higher at the apex b/c of a high V/Q ratio.Tuberculosis affects the apex, where the aerobic bacilli are exposed to more O2 in the alveolus.
During exercise, pulmonary BF increases causing the apex to assume a larger share of O2 uptake.
A 50 y/o man with pneumonia is breathing air at sea level, and has an arterial pO2 of 50 mmHg, and arterial pCO2 of 60 mmHg, and R is 0.8. Explain the cause of hypoxemia in this patient.
PAO2=PIO2-PACO2/R + F
PIO2 = .21 x 760-47
PIO2 = 150 - 60/.8
PAO2 = 150 - 75
PAO2 = 75 mmHg
PAO2 - pO2 = Alveolo (PAO2) Arterial PaO2 difference = 25 mmHg
Normal difference is 5-10 mmHg
This is an abnormally high rating, indicatint the presence of ventilation perfusion inequality, as occurs in a consolidated lung
Zone 1: A>a>v (apex)
Zone 2: a>A>v
Zone 3: a>v>A (base)
What is oxygen dilution (the equation) and how does it compare to oxygen binding to Hgb?
Once O2 gets into the blood it gets transfered to different tissues where it is taken up by mitochondria.
It's transported as dissolved O2 and bound to Hgb.
Henry's Law: states that the amount dissolved is proportional to the partial pressure of the gas. For every mmHg of PO2, there is .003 mL O2/100 ml of blood.
So if the body contains 100 mmHg, the blood contains 100 x .003 = .3 mLs O2/100 mls of blood.
Clearly this is not enough! Remember this is dissolved and not bound to Hgb!
In comes Hgb, four polypeptide chains with two alpha and two beta subunits. Differences in aa sequence give rise to different types of Hgb. Hgb A is adult, Hgb F is fetal, Hgb S is sickle cell. Abnormal Hgb such as SulfHgb and Methemoglobin are not useful for O2 carriage.
**What is the Oxygen Dissociation Curve?**
The Oxygen Dissociation Curve:
The amount of O2 carried by Hgb increases rapidly up to a pO2 of about 50 mmHg, above which the curve becomes flatter, to generate the sigmoidal shape of the O2 dissociation curve.
The max amount of O2 that can be combined with Hgb is called the O2 capacity.
1 gm of pure Hgb can combine with 1.39 mLs O2.
So if the blood has a concentration of 15 gm / 100 mL, O2 capacity is 20.8 mL / 100 mLs. (15 x 1.39)
The O2 saturation of Hgb is the percentage of the available binding sites that have O2 attached. The equation to find this out is:
(O2 combined with Hgb/O2 capacity) x 100
O2sat of arterial blood w/ a pO2 of 100 mmHg is about 97.5%
O2sat of mixed venous blood with a pO2 of 40 mmHg is about 75%
(Remember the Oxygen Dissociation Curve.)
Arterial Oxygen Content or the amount of O2 carried in blood includes dissolved O2 and O2 bound to Hgb. The formula for this is:
(1.39 x Hgb x Sat/100) + .003 x PaO2
Applied Aspects: it's easier to raise O2 content by increasing Hgb, then by increasing O2 administration.
Physiological Implications of the Sigmoidal Oxygen Dissociation Curve:
1. The flat upper portion means that loading of O2 continues even if PO2 in alveolar gas falls.
2. As RBCs take up O2 along the pulmonary capillary bed, a large pressure gradient between alveolar gas and blood continues to exist even after most of the O2 has been transferred and diffusion is hastened. This accounts for the steep lower portion of the curve, and large amounts of O2 can be withdrawn for only a small drop in capillary O2.
3. Reduced Hgb are purple (i think reduced means they don't have O2 bound to them)
4. Shifts of the O2 dissociation curve, or the affinity of Hgb for O2 may occur in certain conditions. The effects of these shifts to the left would cause more avid binding of O2.
Shifts to the right indicate a slower uptake of O2, b/c the O2 is unloading itself. Less of an affinity. As seen in exercise.
**What are causes for shifts of the Oxygen Dissociation Curve?**
To The Left:
Decreases 2-3 DPG (end product of red cell metabolism)
Carbon Monoxide binds avidly to Hgb so its unavailable to bind O2. Further more it shifts the curve to the Left, thus interfering with unloading.
To The Right
Increased pCO2 (the Bohr effect)
*Increased 2-3 DPG* (i.e. in chronic hypoxic state)
2-3 DPG is increased in the face of chronic hypoxia, as in high altitude or in chronic lung disease. Unloading of O2 is helpful by a shift to the right.
Also, exercising muscle is acidic, hypercarbic, and hot. Increasing unloading of O2 by a shift to the Right helps the body cope.
(2-3 DPG is a substance made in RBCs. It's level can help us detect anemia (by a low 2-3 DPG level) The substance helps RBC's in their delivery of O2 at the tissue.
Increased Production of 2-3 DPG are found in certain conditions including:
Anemia, OLD, Cystic Fibrosis, and Congential Heart Disease.
Explain CO2 transport.
CO2 is carried in 3 forms:
1. Dissolved (like O2) obeys Henry's Law. 10% of CO2 is carried in this way.
2. Bicarbonate is formed by the reaction below. 60% of CO2 is transported as bicarbonate.
CO2 + H20 <> H2CO3 <>H+ + HCO3-
This equation happens in the RBC.
H+ is mopped up by Hgb, a buffer to maintain H+ concentration constant.
3. Carbamino compounds are formed by the combination of CO2 with amine groups in blood proteins, and account for 30% of CO2.
CO2 dissociation curve is much more linear than the O2 dissociation curve. The lower the saturation of Hgb with O2, the larger the concentration of CO2 for a given pCO2. This is the Haldane Effect! Reduced Hgb facilitates removal of H+ when carbonic acid dissociates.
Thus lower CO2 saturation shifts the curve to the Left.
The CO2 dissociation curve is also much steeper, so for a smaller pressure change, there is a larger change in CO2 concentration, compared to Oxygen.
So reduced Hgb help load CO2 into the tissue.
(???Research this information! Confusing!???)