Pulmonary circulation, V/Q Balance week 5 Flashcards
The pulmonary circulation is in series with the systemic circulation so therefore, they have the same blood flow. The total cardiac output travels through the lungs every passage through the body except for a small physiological left to right shunt. How much of the cardiac output is this shunt in normal individuals? Why does this occur?
The total cardiac output travels through the lungs every passage through the body, except for a small physiological right-to-left shunt (1-2% of total cardiac output in a normal individual), comprising the Thebesian veins and the bronchial circulation. The bronchial circulation supplies bronchi, pulmonary nerves, etc. and empties into pulmonary veins. The Thebesian veins empty severely hypoxic blood (that has supplied cardiac muscle) into the left ventricle. These right-to-left shunts occur in normal individuals, but that does not mean they are desirable!
What are the differences in pressure btwn the pulmonary and systemic circulation? Why do they occur?
What are some anatomical consequences of the differences in pressure (in the heart and pulmonary circulation)?
Local blood pressure in the pulmonary and systemic circulations. The pressures are much lower in the pulmonary circulation, because the pulmonary circulation has a much lower resistance. Teleologically, it takes less work to pump the blood against gravity to all parts of the lung, so lower pressures are needed. Blood flow to pulmonary circulation is pulsatile. note more than 2 fold difference in systolic and diastolic pressures (24/9 vs 120/80 in systemic circulation). Some consequences of the low pressures:
Differences between pulmonary and systemic circulations:
• pulmonary arteries have thin, ‘97-pound weakling’ walls (are more like veins) in contrast with the muscular systemic arteries
• the right side of the heart has less work to do, and hence has thinner walls than the left heart
• low hydrostatic pressure minimizes the tendency for fluid to filter out of the pulmonary capillaries into the airspaces.
What is pulmonary edema? Why does it occur?
What type of edema occurs before pulmonary edema?
What is the worst consequence of pulmonary edema?
Normally the lungs are ‘dry.’ There is a very thin layer of liquid (0.2 µm thick) lining the interior of the airspaces (subphase). Any increase in the amount of liquid in the lungs increases the diffusion distance for O2 and CO2. Excess fluid in the lungs is called ‘pulmonary edema,’ and results when hydrostatic pressure exceeds colloid osmotic pressure. Pulmonary edema is bad for several reasons; one of the worst being that it can greatly impair DL, the diffusing capacity of the lung. The two opposing forces are:
- Hydrostatic pressure – tends to push fluid out of vessels.
- Colloid oncotic pressure – tends to pull fluid into vessels.
Bottom line: Pulmonary edema results when the balance btwn the hydrostatic pressure in the pulmonary blood vessels and colloid oncotic pressure in the blood is disrupted.
What are some causes of pulmonary edema?
Explain the reason for the differences in blood flow at the apex, middle, and base of the lung.
Gravity causes the regional differences in blood flow through the lung. PA is uniform throughout the lung, because the air spaces are all interconnected. In contrast, Pa and Pv change substantially from the top (apex) to the bottom (base) of the lung, due to hydrostatic pressure. The distension of the flimsy alveolar capillaries depends on the pressure difference (PA vs. Pa). If PA > Pa (zone 1) the capillary is squeezed shut. If PA < Pa the capillary will be open (zones 2-3), but if Pv < PA the capillary will close at its distal end until the pressure inside builds up enough to allow flow (zone 2). If Pv > PA the capillary will be open and possibly distended (zone 3).
What effect does increasing blood pressure have on pulmonary vascular resistance?
Why is the response of the pulmonary vessels to increasing blood pressure beneficial?
What are the 2 mechanisms by which pulmonary vessels respond to increasing blood pressure?
As shown in the attached figure, increasing pulmonary blood pressure decreases vascular resistance.
What good is it? Blood flow through the lung increases as vascular resistance decreases. In other words, the right ventricle is happy whenever the pulmonary vascular resistance decreases, because this means less work. When pressure is increased, ventilation and CO are also increased. If resistance decreases, this makes it easier to sustain high levels of flow.
- *How does it work?** Two main mechanisms are responsible for the decrease in pulmonary vascular resistance at higher pressures, and both are passive.
1. Dilatation = distension of the blood vessel by pressure, increasing its diameter, and hence decreasing its resistance, due to Poiseuille’s equation.
2. Recruitment = opening of previously closed blood vessels. With low blood pressure, some small blood vessels at the top of the lung may be closed, but they will open when the blood pressure increases. This results in more blood vessels in parallel, so the resistance decreases.
Using the attached graph, explain why pulmonary vascular resistance is dependent on lung volume.
Extraalveolar (larger) blood vessels are depicted as a central circle (in cross section), with four “alveolar walls” extending away from them. The capillaries in the alveolar walls are stretched lengthwise at larger lung volumes and they become narrower. Narrowing the capillary diameter increases their resistance to blood flow (Poiseuille’s equation), which accounts for the increased total pulmonary vascular resistance at large lung volumes. At the same time, the larger extra-alveolar vessels are pulled to a larger diameter when the lung inflates, because (exactly like the airways) they are located within lung parenchyma. Again due to Poiseuille’s equation, the resistance of these larger extra-alveolar vessels increases at lower lung volumes because their diameter decreases. The extra alveolar vessels and the alveolar capillaries are in series (the blood has to go through them both as it passes through the pulmonary circulation), so the total vascular resistance reflects contributions from both.
Minimum of curve is around FRC. We normally breathe around FRC where vascular resistance is minimized
How does positive pressure mechanical ventilation impact pulmonary vascular resistance? What effect does this have on the heart?
Why is positive pressure ventilation used? (specifically positive end expiratory pressure/PEEP ventilation)
Mechanical ventilation (positive-pressure type) increases resistance of both alveolar and extraalveolar blood vessels, making more work for the right ventricle, possibly leading to reduced cardiac output. The high pressures in the air spaces compress the blood vessels which are surrounded by air. This is especially true for PEEP (Positive End Expiratory Pressure) which is used to avoid atelectasis.
What is the pulmonary vasculature response to hypoxia?
How is this response harmful at high altitudes?
The pulmonary vascular bed LACKS important autonomic reflexes. Instead, it has hypoxic pulmonary vasoconstriction, an important control mechanism. This mechanism is intrinsic to pulmonary arterial smooth muscle cells, and does not involve reflexes or any humoral mediator. Pulmonary arterial smooth muscle cells grown in culture without other cells contract at low PO2, whereas systemic arterial muscle does not. Local hypoxia (PO2 < 70 torr) in the vicinity of pulmonary arterioles causes vasoconstriction, which shifts blood flow away from poorly ventilated areas. Normally, this feedback mechanism works well and benefits us. However, at high altitude, where PA,O2 is low everywhere in the lung, there is generalized vasoconstriction, which leads to pulmonary edema (hydrostatic pressure is increased).
List 4 metabolic (non-respiratory) functions of the pulmonary circulation.
- Angiotensin is activated in the pulmonary circulation. Angiotensin Converting Enzyme (ACE), present in pulmonary endothelial cells, converts Angiotensin I to Angiotensin II, a potent vasoconstrictor.
- Several vasoactive agents (bradykinin, serotonin, PG, norepinephrine) are inactivated in the pulmonary circulation.
- The pulmonary circulation filters out particulates and microthrombi.
- The pulmonary circulation provides substrates (i.e., food) for lung parenchymal cells
The main goal of respiratory physiology is to match ____ with ____.
The main goal of respiratory physiology is to match ventilation (V), the movement of gas into and out of alveoli, with perfusion (Q), blood flow through the lungs. Many pulmonary diseases exhibit V/ Q mismatch.
What is the result of V/Q mismatch as it pertains to gas exchange? What is the V/Q ratio if f, VT, and CO are all normal?
The V/Q ratio results in what arterial partial pressures of O2 and CO2?
Ventilation and perfusion are normally matched in the lungs, so that gas exchange (ventilation = V) nearly matches pulmonary arterial blood flow (perfusion = Q). If mismatched, impairment of O2 and CO2 transfer results. If frequency, tidal volume, and cardiac output are normal, the V/Q ratio is approximately 0.8. This V/Q ratio results in an arterial PO2 of 100 mm Hg and an arterial PCO2 of 40 mm Hg.
Where in the lung is ventilation greatest (apex, middle, or base)? How does the difference in ventilation btwn the parts of the lung compare to the difference in perfusion in different parts of the lung?
Just like perfusion, ventilation is higher in the bottom of the lung than at the top. However, the difference in ventilation in areas of the lung is not as dramatic.
Why is ventilation greater at the bottom of the lung than the top of the lung?
We can consider each alveolus to have its own pressure-volume curve. Because gravity tends to compress the nether regions of the lungs (just like those grapes at the bottom of a shopping bag) while pulling the lungs down and away from the parietal pleura at the top of the thoracic cavity, the Ppl is greater at the top than at the bottom of the lungs. In contrast, the pressure inside each alveolus is the same (0 at FRC) because the alveoli are all interconnected. As a result, PTM across each alveolus’ wall will be greater, say at FRC, in alveoli at the top of the lung, and therefore the volume will be larger. During inspiration, the Ppl will decrease by a constant amount throughout the lungs, and each alveolus will expand. However, the alveoli at the bottom of the lung start from a small volume, and operate in the steep part of their P-V curve, so a small increase in pressure produces a large increase in volume. The poor alveoli at the top of the lung were already distended at FRC, so the same increment of pressure only increases their volume a little. It seems paradoxical, because they are already at a large volume to begin with, but the key to ventilation is the difference between the volume before and after inspiration.
Bottom line: ventilation is ‘better’ – meaning greater – at the bottom of the lungs. Ventilation is the change in volume with each breath.
Using the attached graph, explain the differences in the V/Q ratio btwn the apex and base of the lungs. How does this effect the PA, O2 and PA,CO2?
Remember that perfusion (Q) – blood flow in the lungs - is lowest at the apex and highest at the base. This is in the same direction as we just saw for V, but the differences in ventilation are much smaller than the differences in perfusion. Consequently, the V/Q ratio is higher at the apex of the lung and lower at the base of the lung. Changing the V/Q ratio has the physiological consequence of altering PA,O2 and PA,CO2 together, in accordance with the alveolar gas equation.
Explain the effect of altering the V/Q ratio on the alveolar PO2 and PCO2 using the attached figure.
The middle picture, A, is the normal situation. Air enters the airway, V/Q = 0.8, PA,O2 = 100 mm Hg, and PA,CO2 = 40 mm Hg. If the airway is obstructed, as in B, then ventilation is zero. Blood flow here is normal, so V/Q = 0. No ventilation means no gas exchange! PA,O2 and PA,CO2 approach their values in mixed venous blood: 40 mm Hg and 45 mm Hg, respectively. If blood flow to a region of lung is completely blocked, as in C, then perfusion is zero. Airflow here is normal, so V/Q infinitely increases.This alveolus is now physiologic dead space. Again, there is no gas exchange, so PA,O2 = 150 mm Hg, and PA,CO2 = 0 mm Hg (their values in inspired air). There is no blood flow, but any blood that equilibrates with this alveolus would have these values.
Using the attached graph, explain how alveolar PO2 and PCO2 change with changing the V/Q ratio.
If we change ventilation such that we change V/Q ratio, the changes in PO2 and PCO2 follow this curve. Increased VQ ratio: increased PO2, decreased Pco2.
Decreased VQ ratio: PO2 decreases and PCO2 increases. This occurs because of the interrelatedness btwn PO2 and PCO2 as shown in alveolar gas equation. You cannot change PO2 without changing PCO2.
What is a result (as it pertains to alveolar PO2) of the normal VQ imbalance due to gravity in different parts of the lung?
Explain the A-a difference (difference in PO2 of alveolar and arterial blood).
One result of the normal V/Q imbalance due to gravity is that blood perfusing different parts of the lung will have very different gas pressures. You may notice that in Fig. 63 (attached) the mixed alveolar PO2 is 101 torr, but the mixed arterial PO2 is only 97 torr, yielding an A-a difference of 4 torr. Did I lie to you when I said that the capillary blood fully equilibrates with the alveolar gases? Perish the thought! The origin of the A-a difference is that although the blood gases do equilibrate with the alveolar gases, regional variation in alveolar gases means that the blood coming from different regions of the lung will have different PO2. When you mix blood with different PO2 values, the mixture always has a lower PO2 than the average. {{{You compulsive types can legitimately point out that an exception occurs at the sigmoid ‘foot’ of the curve at very low PO2 (<20 torr).}}}
The A-a difference can increase in some pulmonary diseases.
Using the attached graph, explain what the effects are on PO2 when blood with high and low PO2s are mixed.
Let’s mix equal volumes of blood with PO2 values of 100 torr and 20 torr. From the graph above, we can take values for the O2 content.
When we mix the PO2 20 and 100 units of blood, we first add the O2 content and divide by 2 to get the O2 content/dl of blood: (7.06 + 19.8)/2 = 13.43 ml O2/dl. We then use the oxyhemoglobin dissociation curve to estimate the PO2 of our mixture. We can see that 13.43 ml/dl falls about halfway between 30 and 40 torr, so the mixture has a PO2 ~35 torr. If we had taken the average PO2 we would have expected the mixture to be 60 torr! We would have been wrong!
If a pt has low PO2, what effect would giving 100% oxygen have?
Now let’s imagine that a patient has a low PO2 and you decide that the obvious treatment is to increase FI,O2. You give the patient 100% O2, which by the time it gets to the alveoli may be about 660 torr O2 (adjusting for the omnipresent water vapor pressure of 47 torr and some CO2 which will also be present). What will happen when we mix equal volumes of blood at PO2 660 torr and PO2 20 torr? From the above table we can add the O2 content (we use content because this corresponds with the total number of O2 molecules that are really there, unlike the peculiar and nonlinear PO2 parameter!): (7.06 + 22)/2 = 14.53 ml O2/dl. OOPS! The PO2 that corresponds with this O2 content of our mixture is still <40 torr! What went wrong? The problem here is that blood with PO2 = 660 torr really doesn’t have much more O2 than blood with PO2 = 100 torr. By the time you get to 100 torr, practically all the binding sites on Hb molecules are filled, so the only place you can add O2 beyond this is to physically dissolve it.
Bottom line: When you mix blood with different PO2 values, the mixture always has a lower PO2 than the arithmetic average. This is because the oxyhemoglobin dissociation curve is non-linear!
