MCB 136 Review | Respiration

Review Answers | Mechanics of respiration

a. Recoil tendency of the lungs. b. Intrapleural pressure is less negative during expiration.

1. TV is volume of air inhaled in the lungs during a single breath of quiet breathing and leaves the lungs passively during expiration. Measured by spirometry.
2. IRV is the amount of air that can be inhaled from the end of a normal inspiration to the maximal point of inspiration. Measured by spirometry.
3. FRC includes the ERV + RV. It can be measured by a "dilution" technique from a gas that is inspired in a single inhalation.
4. TLC is the total amount of air within the intrapulmonary space at the point of maximum inspiration and would include VC + RV. VC can be measured by spirometry, and RV by an application of the dilution technique as in (c).
Minute volume (V) = resp. rate x tidal volume. V at rest = 6 L/min; during exercise = 24 L/min; increase = 18 L/min. (Alveolar ventilation, V_A, for these two conditions, assuming a dead space of 0.15 L, would be 4.2 L/min and 21 L/min, respectively.)
Lung compliance is defined as the ratio of the change in lung volume to the change in transpulmonary pressure. The two major elements in lung compliance are the elastic properties of the lung tissue itself and the surface tension at the air-water interface within the lung.
Wall tension is higher at the end of a normal inspiration. Intrapulmonary pressure is the same at end of inspiration or expiration (i.e., equal to atmospheric pressure) but intrapleural pressure is more negative at the end of inspiration, therefore the transpulmonary pressure gradient is larger. Also, elastic tension of the tissue increases as it is stretched. At the end of inspiration, the transpulmonary pressure gradient is larger and the radius of an individual alveolus is greater, so simple physical relationships from the law of Laplace (T = Pr/2) predict greater tension. In addition, dilution of surfactant as alveolar surface area increases will increase surface tension, further increasing total wall tension at larger lung volumes.
Surfactant decreases alveolar surface tension.
1. A low surface tension in alveoli increases lung compliance and reduces the work of lung expansion with each breath.
2. Alveolar stability is promoted. Since surfactant must be at the surface, it is more concentrated — and more profoundly decreases surface tension — when alveoli are small than when they are expanded. Thus, the tendency for small alveoli to collapse into larger ones is prevented (with P ∼ T/r, P would increase as r decreases unless T also decreases).
3. Reduction of alveolar surface tension tends to prevent transudation, or "sucking", of fluid from capillaries into alveolar spaces.
1. Elasticity of elastic fibers, muscle and connective tissue.
2. The tendency of the chest wall to recoil in the opposite direction from the lung — these opposing forces tend to produce a sub-atmospheric pressure between the visceral and parietal pleura (intrapleural pressure), as long as the intrapleural space remains completely sealed.
16 times. Increased caliber of airways as total lung tissue expands — especially bronchi, because of tethering to surrounding parenchyma.
Dead space is 0.25 of tidal volume, or 125 ml.
(c).
(c)
(b). L, D, D
(c). A, P, D
(f). ΔV/ΔP, D
1. No. Airways begin to close only as residual volume is approached in healthy young people.
2. No. When resistance to flow increases, the tidal excursion moves to a higher lung volume, so FRC is increased.
3. Yes. Because tidal volume is small relative to the volume remaining in the lungs continuously, there is very little fluctuation in CO₂ and O₂ concentrations in alveoli, and therefore in blood.
1. Yes. This is the definition.
2. Yes. Compliance is increased by surfactant, decreased by surface tension.
1. No. They use only a tiny fraction; somewhat less than one twenty-fifth of the whole-body oxygen consumption.
2. Yes. During forced expiration the intrathoracic pressure becomes positive, and tends to close small airways, increasing the resistance to airflow.
3. Yes. The position of rest is above the tidal range.
1. Yes. This is a normal tidal breath, so inspiration starts from the functional residual capacity.
2. No. The volume change shown is about 400 ml. 16 x 0.4 = 6.4 liters which is a possible vital capacity, but not a possible tidal volume in exercise. Oxygen consumption can increase by 16 times, and minute volume by a comparable factor; tidal volume does not usually become more than half the vital capacity.
3. Yes. Resistance to airflow is one of the factors which make it necessary to exert a greater pressure change to cause a given volume change, during inflation and deflation, than if the lungs were simply elastic structures. The greater the resistance, the further would the curves be from the straight line of compliance.
1. Yes. Alveolar CO₂ = 3%: alveolar PCO₂ = 3/100 barometric pressure. P_ACO₂ is less than 23 mmHg. By definition, this is hyperventilatlon.
2. Yes. The inspired PO₂ will be about 380 mmHg. Alveolar PO₂ is roughly this minus alveolar PCO₂, which has been calculated as less than 3kPa (23 mmHg). So the range is right for alveolar PO₂, and if pulmonary gas exchange is normal, arterial PO₂ will be not more than l0mmHg lower.
3. No. To answer this you need to know that RQ is expressed as CO₂ output/O₂ uptake. 195/240 is clearly less than 1.

Review Answers | Physical principles of gas exchange

PO₂ = 2400 mm Hg; Fractional O₂ = 0.8 or 80%.
Greater solubility.
Surfactant, alveolar epithelium, interstitial layer, capillary endothelium, plasma, red cell membrane, red cell interior. b). Area about 50-100 m²; less than 0.5 痠 in thickness; large area and small thickness are well suited to diffusion as predicted by the Fick equation.
PO₂ will decrease to about 80 mmHg. During the breathing of ambient air, the sum of alveolar PO₂ and PCO₂ is fixed at ~143 mmHg (the sum of their partial pressures in alveolar gas). Increase or decrease in one must be accompanied by an approximately equal and opposite shift in the other.
1. Some of the blood entering the left heart has bypassed the pulmonary circulation through "anatomical shunts." A significant portion of bronchial artery flow enters pulmonary venous circulation, and the Thebesian veins from the heart also add deoxygenated blood to the well oxygenated blood returning to the left heart.
2. 3-5% of the right ventricular output circulates through poorly ventilated portions of lung and therefore is not oxygenated and constitutes a "physiological shunt."
3. Limitation of O₂ diffusion from alveolus to pulmonary capillary. Ordinarily this is no real limitation, but there may be in hypoxia or pulmonary disease. Note: The more rapid the flow through the pulmonary capillaries, the greater the PO₂ gradient between the end-capillary and alveolus will be.
Response to reduced PO₂ in alveolar gas. Blood perfusing an unventilated segment of the lung is "wasted." Shunting occurs to ventilated areas by intense vasoconstriction in the non-ventilated areas.
Dead space would increase. a) and c).
1. Hydrostatic forces: The hydrostatic pressure within most systemic capillary beds averages about 25 mmHg, whereas within the pulmonary capillaries, pressures of about 10 mmHg are observed.
2. Osmotic forces: The relatively high permeability of the pulmonary capillaries results in an interstitial oncotic pressure (plasma protein) that is higher in the lungs than in many systemic vascular beds. Although this is a force that would tend to promote fluid accumulation in the interstitium, and possibly transudation into alveoli, a very effective pulmonary lymphatic circulation rapidly removes interstitial plasma proteins and excess fluid. (High rate of lymph flow is largely due to a continuous pumping action of lungs.)
3. Surfactant in the alveoli helps reduce the surface tension, which if too high would tend to pull fluid into alveolar space. The net result is that the bulk of forces are such that no outward fluid loss occurs in the healthy state (other than that which is accomodated by any evaporative loss). An increased capillary hydrostatic pressure or decreased oncotic pressure could result in fluid moving into the alveoli.
(a). E, N
1. Yes. One of the effects of gravity is to expand the uppermost, and relatively 'squash' the lowermost air spaces. (But note that the larger expanded alveoli are ventilated less than smaller ones, because they are less readily expanded).
2. No. Any excess of fluid lost from capillaries in the lungs is drained, as elsewhere in the body, via lymphatics. Fluid seeps through connective tissue between alveoli, to reach the lymphatics which extend to the end of the bronchial tree. Only when a considerable fluid pressure builds up in the interstitial tissue, does edema extend into the thin alveolar-capillary interface, and ultimately break through the alveolar epithelium into the air spaces.
3. No. There are no cilia between alveoli and respiratory bronchioles. Macrophages must migrate to reach the 'staircase' of cilia which starts at the proximal end of respiratory bronchioles.
1. Yes If PCO₂ is lower than normal, there is by definition a state of hyperventilation. The normal PCO₂ is around 40 mmHg.
2. No. This is the expected increase in alveolar oxygen partial pressure when alveolar CO₂ pressure is this much decreased.
3. Yes. (You should be able to answer this when you have covered acid-base balanc
4. A decrease of PCO₂ depletes plasma bicarbonate and must cause an alkalaemia in accordance with the interrelation between pH, bicarbonate and PCO₂, as defined in the Henderson-Hasselbalch equation. Even if the hyperventilation has continued for a long time and pH has been restored to near normal by other compensatory mechanisms, there is still by definition a respiratory alkalosis when PCO₂ is low.
1. Yes. Surface tension forces tend to create a 'suction' drawing fluid out of capillaries. Surfactant counteracts this.
2. Yes. There is some net loss of fluid and a steady small lymph flow.
3. No. Fluid escapes into the interstitial corners between alveoli; it only bursts through into alveoli when the pressure has risen and increased lymph flow cannot keep up with it.
4. No. It is the intravascular pressure which is the driving force, not flow.
1. Yes. The ventilation increases as metabolic activity increases so that P_ACO₂ is kept normal.
2. Yes. A larger subject would have a greater ventilation at any given PCO₂; his CO₂output at rest would be greater. His resting condition would be represented at b. (The curve could equally refer to the same subject as the solid curve, but at an increased metabolic rate.)

Review Problems | Carriage of O₂ and CO₂

1. Formation of oxyhemoglobin by the reaction Hb + O₂ <—> HbO₂
2. Shift in color spectrum of Hb (visual color change from purple to red).
3. Decreased pH of solution due to a decrease in pK of histidine residues near the heme nucleus.
4. An increase in the net negative charge on the HbO₂ molecule (same reason as for 'b').
5. Desorption (release) of some 2,3-DPG molecules (if these were bound to Hb in the first place). The shape of the reaction curve is due to allosteric effects, as individual O₂ molecules bind with Hb, alter the kinetics of the subsequent reactions at different loci. S-shape provides more optimal circumstances for high affinity (complete saturation) at elevated PO₂ and ability to deliver the maximal load of O₂ in capillary beds where PO₂ is lower (but not excessively low).
1. RBCs contain the enzyme carbonic anhydrase, which is required for conversion CO₂ + H₂O <—> H₂CO₃ within the brief capillary residence time. The Cl/HCO₃ anion exchanger in the RBC membrane is also essential for maximum CO₂ carrying capacity.
2. CO₂ combines with amino groups of hemoglobin. Also, deoxygenated hemoglobin acts as a base, buffering H⁺ ions such that the dissociation of carbonic acid is more complete.
1. The gradient between venous PCO₂ and that of the alveolus would account for about half of CO₂ that is exchanged.
2. The high PO₂ of the alveoli has two effects: 1) oxygenation of hemoglobin decreases its tendency to form carbamino-hemoglobin; 2) H⁺ ions, normally buffered by hemoglobin, are released once hemoglobin is oxygenated, increasing the conversion of bicarbonate to carbonic acid which in turn dissociates to form CO₂ and water.
3. As in the systemic capillaries, carbonic anhydrase of RBCs greatly accelerates the CO₂ hydration/dehydration reaction — here, in the dehydration direction.
The increased CO₂ from the tissues diffuses into plasma and red cells. CO₂ is hydrated into HCO₃^- and H⁺, catalyzed by carbonic anhydrase in the red cells, resulting in a net increase in the number of osmotically active particles within the cells. Because of the concentration gradient, HCO₃^- moves from cells to plasma. Without a pathway for rapid exit of soluble cations, electrical balance is maintained by use of the Cl^-/HCO₃^- exchanger, moving Cl^- in as HCO₃^- exits. Inside the red cells, although most of the H⁺ bind to Hb, the soluble anions have increased and the cells swell somewhat as they go from arterial to venous blood.
See answer to #4. Most of the CO₂ (85-90%) in both arterial and venous blood is carried as HCO₃^-.
(d). A, T
(e). metabolic alkalosis
(e). result in movement of HCO₃^- from erythrocyte to plasma
1. Yes. Inspired oxygen is twice normal; because alveolar PCO₂ does not change, the alveolar oxygen percentage is higher than at one atmosphere. So the alveolar and arterial partial pressures are more than twice normal.
2. No. Arterial PCO₂ is determined by the control of ventilation: it is kept at the normal value; therefore the percentage CO₂ will be smaller because the total pressure is higher, and the alveolar partial pressure unchanged.
3. Yes. See 'b'.
4. Yes. The arterial PN₂ is related to alveolar PN₂ and so will be more than twice normal.
5. No. The pressure of the inspired gas and of the surroundings is the same, so lung volume will be normal.
1. Yes. From the Fick principle, cardiac output = oxygen consumption divided by the a-v difference for oxygen content.
2. No. Arteriovenous difference is 50 ml/liter, or 5 ml/100 ml. Arterial oxygen content is (1.34 x 13.5) ml/100 ml in Hb and 0.3 ml/100 ml in solution giving 18.39 ml/100 ml. So mixed venous is lower than 15, i.e., 13.39 ml/100 blood.
3. Yes. This follows from the equation relating the three variables (see (a)).
4. Yes. Oxygen in solution is simply proportional to the PO₂. So it has increased sixfold, from 0.3 to 1.8 ml/100 ml.
5. No. In normal lungs, the blood will virtually equilibrate with the alveolar gas so arterial PO₂ will rise similarly to alveolar.

Review Answers | Regulation of Respiration and Responses to Respiratory Gases

Long inspiratory gasps; called apneustic breathing.
PCO₂
Arterial blood. CO poisoning does not increase ventilation, since the arterial PO₂ has not been changed (CO decreases the O₂-carrying capacity).
a and b
1. poor alveolar ventilation;
2. decreased diffusion of O₂ across alveolar membrane;
3. increase in venous blood admixing with arterial blood, i.e., anatomic shunts or inequality between perfused and ventilated lung;
4. decreased O₂-carrying capacity of hemoglobin.
1. normal
2. low
3. low (if hemoglobin bound to CO is included)
4. low
5. low.
1. No. They are stimulated only by the types of hypoxia which reduce the arterial oxygen tension (hypoxaemia, 'hypoxic hypoxia').
2. No. Afferents from stretch receptors, irritant receptors and 'J' receptors can certainly take part in the control of breathing.
3. Yes. Voluntary pathways 'bypass' the medullary centers and activate spinal motoneurons.
1. Yes.
2. Yes. After 5 minutes virtually all the nitrogen would be washed out so O₂, CO₂ and water vapour must add up to 1 atmosphere.
3. Yes. The break point in breath-holding depends on the combined stimulus of increasing PCO₂ and decreasing PO₂. After breathing oxygen, the rate of rise of PCO₂ would be unchanged, but the hypoxic enhancement of the stimulus is absent.
1. Yes. Hypoxia causes pulmonary vasoconstriction.
2. No. There is an increase in the red cell mass, and in haematocrit, causing an increase in viscosity.
3. No. Hypocapnia causes alkalaemia: a decreased rate of bicarbonate reabsorption is the compensatory response.
4. Yes

MCB 136 Review | Respiration

Review Answers | Mechanics of respiration

Review Answers | Physical principles of gas exchange

Review Problems | Carriage of O2 and CO2

Review Answers | Regulation of Respiration and Responses to Respiratory Gases

Review Problems | Carriage of O₂ and CO₂