Guyton and Hall Physiology Chapter 39 - Pulmonary Circulation, Pulmonary Edema, and Pleural Fluid PDF

CHAPTER 39 UNIT VII Pulmonary Circulation, Pulmonary Edema, and Pleural Fluid The lun...

CHAPTER 39 UNIT VII Pulmonary Circulation, Pulmonary Edema, and Pleural Fluid The lung has two circulations, a high-pressure, low-flow The pulmonary veins, like the pulmonary arteries, are circulation and a low-pressure, high-flow circulation. The also short. They immediately empty their effluent blood high-pressure, low-flow circulation supplies systemic arte- into the left atrium. rial blood to the trachea, bronchial tree (including the Bronchial Vessels. Blood also flows to the lungs through terminal bronchioles), supporting tissues of the lung, and small bronchial arteries that originate from the systemic outer coats (adventitia) of the pulmonary arteries and circulation, amounting to 1% to 2% of the total cardiac veins. The bronchial arteries, which are branches of the output. This bronchial arterial blood is oxygenated blood, thoracic aorta, supply most of this systemic arterial blood in contrast to the partially deoxygenated blood in the pul- at a pressure that is only slightly lower than the aortic monary arteries. It supplies the supporting tissues of the pressure. lungs, including the connective tissue, septa, and large The low-pressure, high-flow circulation supplies venous and small bronchi. After this bronchial and arterial blood blood from all parts of the body to the alveolar capillar- passes through the supporting tissues, it empties into the ies where oxygen (O2) is added and carbon dioxide (CO2) pulmonary veins and enters the left atrium, rather than is removed. The pulmonary artery, which receives blood passing back to the right atrium. Therefore, the flow into from the right ventricle, and its arterial branches carry the left atrium and left ventricular output are about 1% to blood to the alveolar capillaries for gas exchange, and the 2% greater than that of the right ventricular output. pulmonary veins then return the blood to the left atrium to be pumped by the left ventricle though the systemic Lymphatics. Lymph vessels are present in all the support- circulation. ive tissues of the lung, beginning in the connective tissue In this chapter, we discuss the special aspects of the spaces that surround the terminal bronchioles, coursing pulmonary circulation that are important for gas exchange to the hilum of the lung, and then mainly into the right in the lungs. thoracic lymph duct. Particulate matter entering the alve- oli is partly removed by these lymph vessels, and plasma protein leaking from the lung capillaries is also removed PHYSIOLOGICAL ANATOMY OF THE from the lung tissues, thereby helping to prevent pulmo- PULMONARY CIRCULATORY SYSTEM nary edema. Pulmonary Vessels. The pulmonary artery extends only PRESSURES IN THE PULMONARY 5 centimeters beyond the apex of the right ventricle and SYSTEM then divides into right and left main branches that supply blood to the two respective lungs. Pressures in the Right Ventricle. The pressure pulse The pulmonary artery has a wall thickness one-third curves of the right ventricle and pulmonary artery are that of the aorta. The pulmonary arterial branches are shown in the lower portion of Figure 39-1. These curves short, and all the pulmonary arteries, even the smaller are contrasted with the much higher aortic pressure curve arteries and arterioles, have larger diameters than their shown in the upper portion of the figure. The normal sys- counterpart systemic arteries. This feature, combined tolic pressure in the right ventricle averages about 25 mm with the fact that the vessels are thin and distensible, gives Hg, and the diastolic pressure averages about 0 to 1 mm the pulmonary arterial tree a large compliance, averaging Hg, values that are only one-fifth those for the left ventricle. almost 7 ml/mm Hg, which is similar to that of the entire systemic arterial tree. This large compliance allows the Pressures in the Pulmonary Artery. During systole, pulmonary arteries to accommodate the stroke volume the pressure in the pulmonary artery is essentially equal output of the right ventricle. to the pressure in the right ventricle, as also shown in 503 UNIT VII Respiration Aortic pressure curve the right atrium, then through the right side of the heart 120 and through the pulmonary artery into one of the small branches of the pulmonary artery, and finally pushing the catheter until it wedges tightly in the small branch. Pressure (mm Hg) The pressure measured through the catheter, called the 75 “wedge pressure,” is about 5 mm Hg. Because all blood flow has been stopped in the small wedged artery, and because the blood vessels extending beyond this artery make a Right ventricular curve direct connection with the pulmonary capillaries, this Pulmonary artery curve wedge pressure is usually only 2 to 3 mm Hg higher than 25 the left atrial pressure. When the left atrial pressure rises 8 to high values, the pulmonary wedge pressure also rises. 0 Therefore, wedge pressure measurements can be used to 0 1 2 estimate changes in pulmonary capillary pressure and left Seconds atrial pressure in patients with congestive heart failure. Figure 39-1. Pressure pulse contours in the right ventricle, pulmo- nary artery, and aorta. BLOOD VOLUME OF THE LUNGS 25 S The blood volume of the lungs is about 450 ml, about 9% of the total blood volume of the entire circulatory system. Pressure (mm Hg) Approximately 70 ml of this pulmonary blood volume Pulmonary 15 M capillaries Left is in the pulmonary capillaries; the remainder is divided atrium about equally between the pulmonary arteries and veins. 8 D 7 Lungs Serve as a Blood Reservoir. Under various physi- 2 ological and pathological conditions, the quantity of blood 0 Pulmonary Pulmonary Left in the lungs can vary from as little as half-normal up to artery capillaries atrium twice normal. For example, when a person blows out air Figure 39-2. Pressures in the different vessels of the lungs. The red so hard that high pressure is built up in the lungs, such as curve denotes arterial pulsations. D, Diastolic; M, mean; S, systolic. when blowing a trumpet, as much as 250 ml of blood can be expelled from the pulmonary circulatory system into the systemic circulation. Also, loss of blood from the sys- Figure 39-1. However, after the pulmonary valve closes temic circulation by hemorrhage can be partly compen- at the end of systole, the ventricular pressure falls pre- sated for by the automatic shift of blood from the lungs cipitously, whereas the pulmonary arterial pressure falls into the systemic vessels. more slowly as blood flows through the lungs. As shown in Figure 39-2, the systolic pulmonary arte- Cardiac Pathology May Shift Blood From Systemic rial pressure normally averages about 25 mm Hg in the Circulation to Pulmonary Circulation. Failure of the human being, the diastolic pulmonary arterial pressure is left side of the heart, or increased resistance to blood flow about 8 mm Hg, and the mean pulmonary arterial pres- through the mitral valve as a result of mitral stenosis or sure is 15 mm Hg. mitral regurgitation, causes blood to dam up in the pul- monary circulation, sometimes increasing the pulmonary Pulmonary Capillary Pressure. The mean pulmonary blood volume as much as 100% and causing large increas- capillary pressure, as diagrammed in Figure 39-2, is about es in the pulmonary vascular pressures. Because the vol- 7 mm Hg. The importance of this low capillary pressure is ume of the systemic circulation is about nine times that of discussed in detail later in the chapter in relation to fluid the pulmonary system, a shift of blood from one system to exchange functions of the pulmonary capillaries. the other affects the pulmonary system greatly but usually Left Atrial and Pulmonary Venous Pressures. The has only mild systemic circulatory effects. mean pressure in the left atrium and major pulmonary veins averages about 2 mm Hg in the recumbent person, BLOOD FLOW THROUGH THE LUNGS varying from as low as 1 mm Hg to as high as 5 mm Hg. AND ITS DISTRIBUTION It usually is not feasible to measure someone’s left atrial pressure using a direct measuring device because it is Blood flow through the lungs is essentially equal to the difficult to pass a catheter through the heart chambers cardiac output. Therefore, the factors that control car- into the left atrium. However, the left atrial pressure can diac output—mainly peripheral factors, as discussed in be estimated with moderate accuracy by measuring the Chapter 20—also control pulmonary blood flow. Under so-called pulmonary wedge pressure. This is measured most conditions, the pulmonary vessels act as distensible by inserting a catheter first through a peripheral vein to tubes that enlarge with increasing pressure and narrow 504  Chapter 39 Pulmonary Circulation, Pulmonary Edema, and Pleural Fluid Exercise (per unit of tissue) UNIT VII Blood flow NORMAL Alveolus Alveolus Standing at rest Increased Top Middle Bottom flow Lung level Vasoconstriction Figure 39-4. Blood flow at different levels in the lung of an upright person at rest (red curve) and during exercise (blue curve). Note that when the person is at rest, the blood flow is very low at the top of the HYPOXIA PO2 lungs; most of the flow is through the bottom of the lung. and causing the influx of calcium ions. The rise of calcium concentration then causes constriction of small arteries and arterioles. Figure 39-3. Regulation of blood flow in the lungs during local tis- The increase in pulmonary vascular resistance as a sue hypoxia. Local tissue blood flow and alveolar ventilation are nor- result of low O2 concentration has the important function mally matched for optimal gas exchange (top panel). Decreased PO2 of distributing blood flow where it is most effective. That in tissue surrounding poorly ventilated alveoli causes vasoconstriction is, if some alveoli are poorly ventilated and have a low O2 of adjacent arterioles and diverts blood flow to alveoli that are well ventilated (bottom panel). concentration, the local vessels constrict. This constric- tion causes the blood to flow through other areas of the lungs that are better aerated, thus providing an automatic with decreasing pressure. For adequate aeration of the control system for distributing blood flow to the pulmo- blood to occur, the blood must be distributed to the seg- nary areas in proportion to their alveolar O2 pressures. ments of the lungs where the alveoli are best oxygenated. This distribution is achieved by the following mechanism. EFFECT OF HYDROSTATIC PRESSURE Decreased Alveolar Oxygen Reduces Local Alveolar GRADIENTS IN THE LUNGS ON Blood Flow and Regulates Pulmonary Blood Flow REGIONAL PULMONARY BLOOD FLOW Distribution. When the concentration of O2 in the air of the alveoli decreases below normal, especially when it In Chapter 15, we pointed out that the blood pressure in falls below 70% of normal (i.e., 0 mm Hg), which allows dumping 1. Left-sided heart failure or mitral valve disease, with of fluid from the interstitial spaces into the alveoli. consequent great increases in pulmonary venous pres- Now let us see how these quantitative differences sure and pulmonary capillary pressure and flooding of affect pulmonary fluid dynamics. the interstitial spaces and alveoli 2. Damage to the pulmonary blood capillary membranes Interrelationships Between Interstitial Fluid Pressure caused by infections such as pneumonia or by breathing and Other Pressures in the Lung. Figure 39-7 shows a noxious substances such as chlorine gas or sulfur diox- pulmonary capillary, pulmonary alveolus, and lymphatic ide gas capillary draining the interstitial space between the blood Each of these mechanisms causes rapid leakage of plas- capillary and alveolus. Note the balance of forces at the ma proteins and fluid out of the capillaries and into the lung blood capillary membrane, as follows: interstitial spaces and alveoli. Pulmonary Edema Safety Factor. Experiments in ani- mm Hg mals have shown that the pulmonary capillary pressure Forces tending to cause movement of fluid outward normally must rise to a value at least equal to the colloid from the capillaries and into the pulmonary osmotic pressure of the plasma inside the capillaries before interstitium: significant pulmonary edema will occur. To give an example, s #APILLARY PRESSURE 7 Figure 39-8 shows how different levels of left atrial pressure s )NTERSTITIAL mUID COLLOID OSMOTIC PRESSURE 14 increase the rate of pulmonary edema formation in dogs. s.EGATIVE INTERSTITIAL mUID PRESSURE 8 Remember that every time the left atrial pressure rises to 4/4!, /547!2$ &/2#% 29 high values, the pulmonary capillary pressure rises to a level Forces tending to cause absorption of fluid into the 1 to 2 mm Hg greater than the left atrial pressure. In these capillaries: experiments, as soon as the left atrial pressure rose above s 0LASMA COLLOID OSMOTIC PRESSURE 28 23 mm Hg (causing the pulmonary capillary pressure to rise 4/4!, ).7!2$ &/2#% 28 above 25 mm Hg), fluid began to accumulate in the lungs. This fluid accumulation increased even more rapidly with 508  Chapter 39 Pulmonary Circulation, Pulmonary Edema, and Pleural Fluid Edema fluid per hour Venous system Dry weight of lung 10 9 x Lymphatics x 8 UNIT VII 7 x 6 x Rate of edema formation = 5 4 x x x Pulmonary arteries 3 x x x x 2 x x x 1 x x x xx x 0 x x x x x Pulmonary 0 5 10 15 20 25 30 35 40 45 50 veins Left atrial pressure (mm Hg) Figure 39-8. Rate of fluid loss into the lung tissues when the left atrial pressure (and pulmonary capillary pressure) is increased. (From Guyton AC, Lindsey AW: Effect of elevated left atrial pressure and decreased plasma protein concentration on the development of pul- Figure 39-9. Dynamics of fluid exchange in the intrapleural space. monary edema. Circ Res 7:649, 1959.) further increases in capillary pressure. The plasma colloid osmotic pressure during these experiments was equal to amounts of interstitial fluid transude continually into the this 25 mm Hg critical pressure level. Therefore, in a person, pleural space. These fluids carry tissue proteins with them, whose normal plasma colloid osmotic pressure is 28 mm giving the pleural fluid a mucoid characteristic, which is Hg, one can predict that the pulmonary capillary pressure what allows extremely easy slippage of the moving lungs. must rise from the normal level of 7 mm Hg to more than The total amount of fluid in each pleural cavity is nor- 28 mm Hg to cause substantial pulmonary edema, giving an acute safety factor against pulmonary edema of 21 mm Hg. mally slight—only a few milliliters. Whenever the quan- Safety Factor in Chronic Conditions. When the pulmo- tity becomes more than barely enough to begin flowing nary capillary pressure remains elevated chronically (for in the pleural cavity, the excess fluid is pumped away by at least 2 weeks), the lungs become even more resistant to lymphatic vessels opening directly from the pleural cav- pulmonary edema because the lymph vessels expand great- ity into the following: (1) the mediastinum; (2) the supe- ly, increasing their capability of carrying fluid away from rior surface of the diaphragm; and (3) the lateral surfaces the interstitial spaces perhaps as much as 10-fold. There- of the parietal pleura. Therefore, the pleural space—the fore, in patients with chronic mitral stenosis, pulmonary space between the parietal and visceral pleurae—is called capillary pressures of 40 to 45 mm Hg have been measured a potential space because it normally is so narrow that it without the development of lethal pulmonary edema. is not obviously a physical space. Rapidity of Death in Persons With Acute Pulmonary Edema. When the pulmonary capillary pressure rises even Negative Pressure in Pleural Fluid. A negative force is slightly above the safety factor level, lethal pulmonary ede- always required on the outside of the lungs to keep the ma can occur within hours, or even within 20 to 30 minutes lungs expanded. This force is provided by negative pres- if the capillary pressure rises 25 to 30 mm Hg above the sure in the normal pleural space. The basic cause of this safety factor level. Thus, in acute left-sided heart failure, in negative pressure is pumping of fluid from the space which the pulmonary capillary pressure occasionally does by the lymphatics, which is also the basis of the nega- rise to 50 mm Hg, death may ensue in less than 30 minutes tive pressure found in most tissue spaces of the body. as a result of acute pulmonary edema. Because the normal collapse tendency of the lungs is about −4 mm Hg, the pleural fluid pressure must al- ways be at least as negative as −4 mm Hg to keep the FLUID IN THE PLEURAL CAVITY lungs expanded. Actual measurements have shown When the lungs expand and contract during normal that the pressure is usually about –7 mm Hg, which is breathing, they slide back and forth within the pleural a few millimeters of mercury more negative than the cavity. To facilitate this movement, a thin layer of mucoid collapse pressure of the lungs. Thus, the negativity of fluid lies between the parietal and visceral pleurae. the pleural fluid pressure keeps the normal lungs pulled Figure 39-9 shows the dynamics of fluid exchange against the parietal pleura of the chest cavity, except for in the pleural space. The pleural membrane is a porous, an extremely thin layer of mucoid fluid that acts as a mesenchymal, serous membrane through which small lubricant. 509 UNIT VII Respiration Pleural Effusion—Collection of Large Amounts of Free Guyton AC, Lindsey AW: Effect of elevated left atrial pressure and Fluid in the Pleural Space. Pleural effusion is analogous decreased plasma protein concentration on the development of pulmonary edema. Circ Res 7:649, 1959. to edema fluid in the tissues and can be called edema of the Hughes M, West JB: Gravity is the major factor determining the distri- pleural cavity. The causes of the effusion are the same as bution of blood flow in the human lung. J Appl Physiol 104:1531, the causes of edema in other tissues (discussed in Chap- 2008. ter 25), including the following: (1) blockage of lymphatic Jaitovich A, Jourd’heuil D: A Brief overview of nitric oxide and reactive drainage from the pleural cavity; (2) cardiac failure, which oxygen species signaling in hypoxia-induced pulmonary hyperten- sion. Adv Exp Med Biol 967:71, 2017. causes excessively high peripheral and pulmonary capil- Lumb AB, Slinger P: Hypoxic pulmonary vasoconstriction: physi- lary pressures, leading to excessive transudation of fluid ology and anesthetic implications. Anesthesiology 122:932, into the pleural cavity; (3) greatly reduced plasma colloid 2015. osmotic pressure, thus allowing excessive transudation of Parker JC: Hydraulic conductance of lung endothelial phenotypes and fluid; and (4) infection or any other cause of inflamma- Starling safety factors against edema. Am J Physiol Lung Cell Mol Physiol 292:L378, 2007. tion of the surfaces of the pleural cavity, which increases Stickland MK, Lindinger MI, Olfert IM, Heigenhauser GJ, Hopkins SR: permeability of the capillary membranes and allows rapid Pulmonary gas exchange and acid-base balance during exercise. dumping of plasma proteins and fluid into the cavity. Compr Physiol 3:693, 2013. Suresh K, Shimoda LA: Lung circulation. Compr Physiol 6:897, 2018. Sylvester JT, Shimoda LA, Aaronson PI, Ward JP: Hypoxic pulmonary Bibliography vasoconstriction. Physiol Rev 92:367, 2012. Dunham-Snary KJ, Wu D, Sykes EA, et al: Hypoxic pulmonary va- Tabima DM, Philip JL, Chesler NC: Right ventricular-pulmonary vascu- soconstriction: from molecular mechanisms to medicine. Chest lar interactions. Physiology (Bethesda) 32:346, 2017. 151:181, 2017. Townsley MI: Structure and composition of pulmonary arteries, capil- Effros RM, Parker JC: Pulmonary vascular heterogeneity and the Star- laries, and veins. Compr Physiol 2:675, 2012. ling hypothesis. Microvasc Res 78:71, 2009. Zielinska-Krawczyk M, Krenke R, Grabczak EM, Light RW: Pleural Frise MC, Robbins PA: The pulmonary vasculature--lessons from Tibetans manometry-historical background, rationale for use and methods and from rare diseases of oxygen sensing. Exp Physiol 100:1233, 2015. of measurement. Respir Med 136:21, 2018. 510