Pulmonary Circulation Linda Costanzo Ph.D.

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1 Pulmonary Circulation Linda Costanzo Ph.D. OBJECTIVES: After studying this lecture, the student should understand: 1. The differences between pressures in the pulmonary and systemic circulations. 2. How to calculate pulmonary vascular resistance. 3. How (and why) blood flow is unevenly distributed in the upright lung. 4. Regulation of pulmonary blood flow, especially the concept of hypoxic vasoconstriction. 5. The relationship between alveolar ventilation and alveolar P CO2 and how it is described by the alveolar ventilation equation. 6. The relationship between alveolar ventilation and alveolar P O2 and the alveolar ventilation equation. I. BIG PICTURE OF PULMONARY CIRCULATION AND PRESSURES Figure 1. Blood is supplied to the lungs by the pulmonary artery, which receives mixed venous blood from the right heart. The pulmonary arteries branch (like the

2 airways) as far as the terminal bronchioles, then break up to form dense capillary networks in the alveolar walls. The density of the capillary network makes for extremely efficient gas exchange. Pulmonary vascular pressures are much lower than their counterparts in the systemic circulation. For example, mean pulmonary artery pressure is 15 mm Hg (25/8) compared with mean aortic pressure of 100 mm Hg (120/80). Consistent with these low pressures, the walls of the pulmonary arteries are thin and contain relatively little smooth muscle. One important issue for the pulmonary capillaries is the fact that they are surrounded by alveoli, which are gas-filled. Capillary pressures are actually close to alveolar pressures. Thus, it is possible under some circumstances for capillaries to be compressed and even collapse under the alveolar pressure (more later). Figure 2. II. PULMONARY VASCULAR RESISTANCE In cardiovascular physiology, we talk about total peripheral resistance, or systemic vascular resistance (SVR). We apply the pressure, flow, resistance relationship that is analogous to Ohm s law for electrical circuits. In similar fashion, we describe pulmonary vascular resistance (PVR): PVR = Pulmonary artery pressure - pulmonary venous pressure Blood flow Mean pulmonary artery pressure is 15 mm Hg, pulmonary venous pressure is approximately 8 mm Hg, and blood flow is cardiac output of the right heart. Pulmonary pressures are much lower than systemic pressures, yet blood flow

3 (cardiac output) is the same on both sides of the circulation. Logically, pulmonary vascular resistance must also be much lower than systemic vascular resistance. III. DISTRIBUTION OF PULMONARY BLOOD FLOW (ZONES OF LUNG) Because of gravitational forces, pulmonary blood flow is not evenly distributed in the lungs of an upright person. Blood flow is highest at the base of the lung (Zone 3), lowest at the apex of the lung (Zone 1), and intermediate in the middle (Zone 2). This is because gravitational forces increase pulmonary arterial pressure more at the base than at the apex. Figure 3. A. Zone 1 (apex), lowest blood flow. Because of gravitational effects, arterial pressure is lowest in this zone. Because alveolar pressure (PA) is approximately equal to atmospheric pressure, it turns out that arterial pressure (P a ) is very close to PA. If P a is lower than PA, the pulmonary capillaries will be compressed by the higher alveolar pressure, reducing or even eliminating blood flow in that region. Normally arterial pressure is just high enough to prevent this capillary closure. In hemorrhage, where arterial pressure is reduced, P a in Zone 1 is well below PA, and the capillaries are smushed. In this condition, Zone 1 will be

4 ventilated, but not perfused ( dead space ) and no gas exchange can occur. B. Zone 2, medium blood flow. P a is higher in Zone 2 than in Zone 1, and is higher than PA. However, PA is still higher than venous pressure in this zone and so blood flow is driven by the difference between arterial and alveolar pressures, rather than the more familiar difference between arterial and venous pressures. Compression of capillaries is not normally a problem in Zone 2 because of the higher P a. C. Zone 3 (base), highest blood flow. In this zone, both arterial and venous pressures are higher than alveolar pressure and blood flow is driven in the traditional way by the difference between arterial and venous pressure. Zone 3 has the greatest number of open capillaries, and the highest blood flow. IV. REGULATION OF PULMONARY BLOOD FLOW A. Passive factors. Several passive forces can change pulmonary blood flow. We have already discussed gravitational effects on Pa in the upright lung, which increases blood flow to the base and reduces blood flow to the apex. Lung volume also affects pulmonary vascular resistance (PVR), whereby high lung volumes pull the blood vessels open, decreasing their resistance and increasing blood flow; low lung volumes are associated with higher vascular resistance and lower blood flow. B. Active factors 1. Hypoxic vasoconstriction is one concept in pulmonary physiology that you will (hopefully) remember forever! It is memorable, in part, because it is so different from what occurs in other tissues (e.g., coronary circulation) where hypoxia causes vasodilation to provide more blood flow and more O 2. Hypoxic vasoconstriction describes the effect of alveolar hypoxia (decreased PA O2 ) to increase the resistance of nearby arterioles, thus reducing blood flow in that region. Hypoxic vasoconstriction is a protective mechanism in the lungs. It diverts blood flow away from unventilated (hypoxic) regions where blood flow would be wasted because gas exchange cannot occur, and directs it toward regions that are ventilated and where gas exchange can occur. When we discuss V/Q ratios, you will further appreciate that hypoxic vasoconstriction attempts to maintain V/Q matching. The mechanism of hypoxic vasoconstriction is a direct effect of low alveolar P O2 on pulmonary arterioles. (The anatomical relationships permit this.) The likely mediator is inhibition of

5 nitric oxide (NO) synthesis in the endothelial cells. NO dilates arterioles (via production of cyclic GMP); inhibition of NO synthesis leads to vasoconstriction. Inhaled NO reverses hypoxic vasoconstriction. a. High altitude. Hypoxic vasoconstriction occurs at high altitude where the barometric pressure is decreased, and the P O2 of inspired air and alveolar air are, accordingly, decreased. The low PA O2 causes pulmonary vasoconstriction, increased pulmonary vascular resistance, increased pulmonary artery pressure, and can even lead to a compensatory enlargement of the right ventricle (which has to pump blood against an increased pulmonary arterial pressure). b. Fetal lungs. Of course, the ultimate alveolar hypoxia is the fetal lung, which is not ventilated at all. No ventilation, no O 2 in the alveoli. Hypoxic vasoconstriction increases fetal pulmonary vascular resistance decreases pulmonary blood flow. With the first breath, the neonate brings O 2 into the alveoli and interrupts hypoxic vasoconstriction, decreasing pulmonary vascular resistance and increasing pulmonary blood flow. 2. Other. In addition to O 2 (NO), many other substances can alter pulmonary vascular resistance and, accordingly, pulmonary blood flow. Thromboxane A 2 is produced in response to lung injuries and is a potent pulmonary vasoconstrictor. Prostaglandin I 2 is a vasodilator. Endothelins, released by pulmonary endothelial cells, are potent vasoconstrictors. V. ALVEOLAR VENTILATION EQUATION Switching gears! This topic and the next topic do not really belong in a lecture on pulmonary circulation. Mea culpa! The alveolar ventilation equation describes the inverse relationship between alveolar ventilation and alveolar P CO2 (or arterial P CO2 ). or, rearranging to solve for PA CO2 :

6 where The constant, K, needs explanation. The value for K is 863 mm Hg under conditions of BTPS and when VA and VCO 2 are expressed in the same units (e.g., ml/min). BTPS means body temperature (310 K), ambient pressure (760 mm Hg), and gas saturated with water vapor. The bold version of the equation is used to predict the alveolar P CO2 (or arterial P CO2 ) if the rate of CO 2 production and alveolar ventilation are known. The most important point is that if CO 2 production is constant, alveolar and arterial P CO2 are determined by alveolar ventilation. The figure below shows the equation graphically. The higher the alveolar ventilation, the lower the P CO2 ; the lower the alveolar ventilation, the higher the P CO2. The figure also shows what happens if CO 2 production increases from 200 ml/min to 400 ml/min. Alveolar ventilation would have to double from 5 to 10 L/min in order to keep arterial P CO2 at its normal value of 40 mm Hg. (Alternatively, if alveolar ventilation did not double, then arterial P CO2 would increase significantly.)

7 Figure 4. VI. ALVEOLAR GAS EQUATION We use the alveolar ventilation equation to predict alveolar P CO2. We use the alveolar gas equation to predict the alveolar P O2. But why would we want to know the alveolar P O2? Why not just measure arterial P O2 and say that alveolar P O2 is the same? Because, they are not always the same! Sure, in normal lungs, O 2 equilibrates between alveolar gas and pulmonary capillary blood, and arterial P O2 is almost exactly equal to alveolar P O2. But, in many lung diseases, the process of O 2 diffusion is abnormal, O 2 does not equilibrate, and arterial P O2 is less than alveolar P O2. So...that s why we want to know the value of alveolar P O2...any difference between alveolar and arterial P O2 indicates a gas exchange problem in the lungs. (See discussion of A-a gradient in next lectures.) where

8 If alveolar ventilation is halved, PA O2 decreases (less O 2 is brought into the alveoli). The alveolar gas equation predicts the change in PA O2 that occurs for a given change in PA CO2. Since the respiratory quotient is normally 0.8 (equal to respiratory exchange ratio in the steady state), when alveolar ventilation is halved, the PA O2 will fall slightly more than the PA CO2 will rise. The figure below shows the relationship between P O2 and P CO2 calculated by the alveolar gas equation (the so-called O 2 - CO 2 diagram). One anchor point on the diagram is inspired air which has a high P O2 of 150 mm Hg but no CO 2. Normal alveolar gas (or equilibrated arterial blood) has a P O2 of 100 mm Hg and a P CO2 of 40 mm Hg. These changes reflect the respiratory exchange ratio of 0.8. (50 mm Hg of O 2 were replaced by 40 mm Hg of CO 2.) Mixed venous blood has a P O2 of 40 mm Hg (O 2 was lost to the tissues) and a P CO2 of 46 mm Hg. Notice that the variations in P O2 are much greater than the variations in P CO2. Figure 5.

9 VII. PRACTICE QUESTION 1. If alveolar ventilation increases two-fold and CO 2 production remains constant, arterial P CO2 changes to how many times its original value? A. 1/4 B. ½ C. No change D. 2 E. 4 EXPLANATIONS 1. Answer = B. Use the alveolar ventilation equation, which describes the inverse relationship between alveolar P CO2 and alveolar ventilation. You will be given this equation on the exam. Use the equation to calculate the change in PA CO2 ; assume the same change in Pa CO2 because CO 2 always equilibrates in the lungs. PA CO2 = V CO2 x K/ VA. Alveolar ventilation is in the denominator; if it doubles, then PA CO2 (and Pa CO2 ) will be reduced to one-half.

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