Respiratory System
I. MECHANICS OF BREATHING
A. Pulmonary Ventilation
1. Inspiration = Inhalation
a. Diaphragm contracts and flattens, increasing volume of thoracic cavity.
b. Contraction of intercostal muscles lifts rib cage, increasing thoracic volume.
c. Volume increase lowers intrapulmonary pressure.
d. Air rushes in until pressures equalize.
2. Expiration = Exhalation
a. Mostly passive. Muscles relax, lungs recoil, volume decreases, pressure (intrapulmonary) increases.
b. Forced expiration uses abdominals.
B. Physical Factors Influencing Pulmonary Ventilation
1. Resisting in Respiratory Passageway (Friction).
a. Greatest resistance in medium sized bronchi.
b. Bronchiole diameter controlled by smooth muscle.
2. Lung Compliance = Expandability
a. Depends on elasticity.
b. Depends on flexibility of thoracic cage.
3. Lung Elasticity- Necessary for Expiration
4. Alveolar Surface Tension Forces
a. "Surface Tension" resists expansion.
b. Surfactant reduces surface tension of the water coating alveolar walls, making it easier to expand the lungs.
C. Respiratory Volumes and Pulmonary Function Tests. All of this is in fig 23.16
1. Respiratory volumes and capacities
a. Respiratory volumes
1) Tidal volume (TV) = amount that goes in and out with each breath.
2) Inspiratory reserve volume (IRV) = amount forcibly inhaled beyond TV.
3) Expiratory reserve volume (ERV) = amount forcibly exhaled beyond TV.
4) Residual volume (RV) = What's left after strenuous expiration.
b. Respiratory capacities (sums of 2 or more volumes)
1) Inspiratory capacity = IRV+TV
2) Functional residual capacity (FRC) = ERV+RV
3) Vital capacity = total exchangeable air = TV+IRV+ERV
4) Total lung capacity (TLC) = TV+IRV+ERV+RV
2. Dead Space- Some air is in passageways, doesn't get involved in gas exchange. TV- Dead Space = amount involved in alveolar ventilation.
3. Pulmonary Function Tests- Spirometer measures volumes of air.
a. Minute Ventilation = total volume in and out in one minute (rate)
b. FVC = forced vital capacity
c. FEV = forced expiratory volume is considered over time in terms of % of FVC.
4. Alveolar Ventilation- better index of effective ventilation than minute volume. AVR = Frequency x (TV- Dead Space)
a. Increasing volume inspired has a greater effect than increasing frequency because dead space is fixed.
b. Rapid shallow breathing is less effective.
D. Non-Respiratory air movements. Sneezing, coughing, hiccups, yawn, laughing/crying
II. GAS EXCHANGES IN THE BODY
A. Basic Stuff
1. Dalton's law of partial pressures
a. total pressure = sum of partial pressures
b. Partial pressures are in proportion to the percentage of that gas in the mixture.
Example: Air pressure at sea level = 760 mmHg
Air:  78.6% nitrogen     PN2  =   760 x 0.786 = 597 mmHg
        20.9% oxygen      PO2  =   760 x 0.209 = 159 mmHg
c. If the total atmospheric pressure changes, the partial pressures change proportionately.
Example: At 2 miles above sea level, one atmosphere= 563 mmHg. PO2 would then = .209x 563= 110

2. Henry's Law

a. Gasses dissolve into liquids in proportion to their partial pressures.
b. The direction of gas movement (between dissolved and undissolved) is determined by the partial pressures in the two phases.
Examples: Suppose we have this mixture:
Pgas x = 100
Pgas y= 50
When this mixture comes in contact with a liquid, gas x will dissolve faster than gas y.
Suppose our mixture and liquid have been in contact for a while. Pgas x in the air will equal Pgas x in the liquid, that is, they reach equilibrium. If Pgas x is lowered in the air, then some gas x will go out of solution until a new equilibrium is reached.
 
B. Composition of Alveolar Gas. Gas in the alveoli is not the same as air. )See the alveolus in fig 23.17)
1. Less O2 and more CO2 from diffusion.
2. More water vapor from conducting passages.
3. Gas in alveoli is a mix of old and fresh air.
C. Exhaled air isn't exactly like alveolar air either. O2 is a little higher and CO2 is a little lower because of the air in the "dead space".
D. Gas exchange between lungs and blood, blood and tissues. External respiration is lungs-to-blood. Internal is blood-to-tissues.
1.Pulmonary gas exchange (external respiration) influenced by the following:
a. Partial pressure gradients and gas solubilities.
1) PO2 in alveoli is 104 mmHg vs. 40 mmHg for the deoxygenated blood of the pulmonary arteries. So after .25 seconds, equilibrium is reached. That means that PO2 in the pulmonary capillary blood = 104 mmHg.
2) PCO2 in alveoli is at 40 mmHg vs. 45 mmHg in blood returning from tissues. So gas goes from blood to alveolar air in this case.

3) Something I mentioned in class and its in your book. Yes, equilibrium is reached in #s 1 and 2 above, but if you look in say, the pulmonary veins, which are returning blood to the heart from the lungs, the actual PO2 will be about 100 mmHg, not 104, because some of the pulmonary capillaries didn't go quite as close to well ventilated alveoli. So they didn't get as much O2. This doesn't seem to be a factor with PCO2 in the blood leaving the lungs. Its partial pressure is 40mmHg, just like in the alveoli.

b. Thickness and area of the exchange surface, the respiratory membrane.
1) Thin is good.
2) High surface area is good.
c. Ventilation- Perfusion coupling. ( Perfusion is blood flow- in this case, through pulmonary capillaries.)
1) Pulmonary arteries are constricted in alveoli which are poorly ventilated, dilated when serving well ventilated alveoli.
2) Bronchioles serving alveoli with high CO2 levels dilate to increase ventilation and vice versa.
2. Capillary gas exchange in tissues (internal respiration) is the reverse of pulmonary exchange (sort of ). PO2 in tissues is low (40 mmHg) relative to arterial blood (100 mmHg). O2 moves into tissues, CO2 moves out of tissues, into blood. Figure 23.17 shows all of this quite nicely.


III. Transport OF RESPIRATORY GASSES BY BLOOD

A. Oxygen transport. 98.5% is carried on hemoglobin. (For those of you who took notes in class, please note that 98.5 is the value from your text book. I was using a different reference when I made up the lecture.
1.Association and Dissociation of O2 and hemoglobin.
a. Influence of PO2 on saturation of hemoglobin. Check out figure 23.19 of the oxygen hemoglobin dissociation curve.
1) at rest arterial blood:
has a PO2 = 100 mmHg
has hemoglobin that is 98% saturated

2) after going through the capillaries in the tissues the blood has lost O2:
the PO2 = 40 mmHg
the hemoglobin is at 75% saturation

So...you don't really need a high PO2 (greater than 104 mmHg) in the alveolar air or in arterial blood, the hemoglobin (which is carrying most of the O2) is almost completely saturated when the PO2 is only 70 mmHg (you can see this in figure 23.19). Notice that the region of the curve between PO2 of 100 and PO2 of 40 only accounts for about 25% of the oxygen saturation of the hemoglobin (look at the Y-axis on the graph). So even when we're down to the PO2 of the tissues, where oxygen is being used up, the hemoglobin still has 75% of its oxygen. This 75% is called the venous reserve of the blood. It's oxygen that could be used if the tissues were very demanding - say during exercise.
b. the influence of temp, pH, PCO2 and BPG on Hemoglobin saturation. At a given PO2, increases in Temp, PCO2, H+ ion concentration, and BPG will all cause O2 to be more easily released from hemoglobin. It's as if we draw the oxygen-hemoglobin dissociation curve with the same shape but a little over to the right.
1) temperature increases with activity in a particular area, so we want the O2 to be released easily there, that's where it's needed.
2) PCO2 will increase where cells are working harder, and that's where we'll want the O2 to come off easily.
3) H+ ion concentration increases with dissolved CO2 ( a sign that the cells in that area need more O2) the acidosis (acid in the blood) causes the BOHR effect, a weakening of the hemoglobin-to-oxygen bonds, again allowing hemoglobin to give up its Oxygen where the Oxygen is needed.
4) BPG is produced by Red Blood Cells undergoing anaerobic respiration (that's cellular respiration in the absence of oxygen. That's inefficient. We don't get the most energy from glucose when we do anaerobic respiration) That's a sign that O2 is needed there. So again, hemoglobin has less of a grip on oxygen right when oxygen is need the most.
B. Carbon dioxide transport. CO2 is carried 3 ways:
1. 7% is dissolved in plasma
2. 23% is bound to the globin part of hemoglobin
a. PCO2 affects this, as does
b. The degree of O2 saturation of the hemoglobin. Deoxygenated hemoglobin combines more readily with CO2 than does oxygenated hemoglobin.
3. 60-70% is carried as bicarbonate ion in plasma. (you'll need to look in the book for the arrows that go with this diagram.  Page 736)
CO2 + H2O        H2CO3            H+ + HCO3-


This equation shows carbon dioxide combining with water to form carbonic acid, then carbonic acid dissociating into hydrogen ions and bicarbonate ions. This all could happen in the plasma but it happens a lot more in the Red Blood Cells because they have an enzyme in them called Carbonic Anhydrase which mediated the first part of the equation (CO2 + H2O going to carbonic acid). So... CO2 diffuses into the RBC, which leads to an increase in bicarbonate ions (HCO3-) and an increase in H+ ions. The H+ ions will bind to the hemoglobin, helping to buffer the whole system (remember that if the H+ ions just stayed in solution, the pH would go way down). By binding to the hemoglobin, the H+ ions trigger the Bohr Effect. The Bohr effect causes O2 to come off the hemoglobin, which makes it easier for CO2 to bind to hemoglobin. The HCO3 ions that have built up inside the RBC will diffuse out of the cell to the plasma which has a lower concentration of them. Cl- ions will diffuse into the RBCs to replace the outgoing negatively charged bicarbonate ions, this is called the chloride shift.

At the lungs, some CO2 will leave the RBCs. It will leave the hemoglobin and follow its concentration gradient out to the lungs. This decline in CO2 in the RBCs will cause the equation above to shift toward the left side, that is, the H+ ions and the bicarbonate ions inside the RBCs will combine to form carbonic acid, which will in turn (under the influence of Carbonic Anhydrase) become CO2 and water. the CO2 will diffuse out of the RBC and into the lungs, and now more bicarbonate ions will diffuse from the plasma into the RBCs. This will be converted to CO2 and diffuse out into the lungs to be exhaled.