Pulmonary Circulation

Respiratory Physiology > Pulmonary Circulation and Non‐Respiratory Functions > Evolving Therapy of Pulmonary Vascular Pathophysiology

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Alfred P. Fishman

10.1002/cphy.cp030103

Source: Supplement 10: Handbook of Physiology, The Respiratory System, Circulation and Nonrespiratory Functions

Originally published: 1985

Published online: January 2011

Full Article on Wiley Online Library

Abstract
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References

Abstract

The sections in this article are:

1 Pulmonary Hemodynamics

1.1 Pulmonary Blood Flow: General Aspects

1.2 Pulmonary Blood Flow and Pressure Waves

1.3 Mechanical Influences on Pulmonary Blood Flow

1.4 Pulmonary Vascular Pressures

1.5 Pulmonary Blood Volume

1.6 Pressure‐ Volume, Pressure‐Flow Relationships

2 Vasomotor Regulation

2.1 Level of Initial Tone

2.2 Detection of a Vasomotor Response

2.3 Sites of Pulmonary Vasoconstriction

2.4 Vasomotor Mechanisms

3 Bronchial Circulation

3.1 Determination of Bronchial Blood Flow

3.2 Normal Levels of Bronchial Blood Flow

3.3 Bronchial Circulation in the Normal Lung

3.4 Bronchial Circulation in Disease

4 Fetal and Neonatal Pulmonary Circulation

4.1 Morphologic Changes

4.2 Regulation of Fetal Pulmonary Circulation

4.3 Postnatal Pulmonary Vasodilation

5 Pulmonary Hypertension

5.1 Pathogenesis

5.2 Experimental Chronic Pulmonary Hypertension

5.3 Pulmonary Vasodilators

5.4 Endothelium‐Dependent Pulmonary Vasodilation

	Figure 1. gRenin‐angiotensin system. The lungs play a central role in control of systemic blood pressure because of the converting enzyme on the luminal aspect of pulmonary capillary endothelium. Strategic disposition of the enzyme and huge expanse of pulmonary capillary endothelium enable rapid and efficient conversion of angiotensin I to angiotensin II as blood courses through the lungs.
	Figure 2. Muscular pulmonary arteries (resistance vessels) in pulmonary circulation of various animal species. Elastic Van Gieson's stain. A: dog; × 500. B: cat; × 500. C: human; × 200. D: rat; × 800. A‐D: tunica media is relatively thin. E: guinea pig; × 200. Tunica media consists of crescentic masses of circular smooth muscle disposed in discontinuous segments resembling sphincters. In areas between sphincterlike masses of smooth muscle the wall consists only of an elastic lamina. F: cow; × 500. Tunica media is thick. Micrographs courtesy of J. M. Kay
	Figure 3. Four‐quadrant diagram illustrating respiratory and circulatory adaptation by which O₂ requirement is satisfied at rest (inner rectangle) and during exercise (outer rectangle). , concentration of O₂ in arterial blood; Cvo₂, concentration of O₂ in venous blood; CAP area, capillary area; D_L, diffusing capacity of the lungs; Hb, hemoglobin; , O₂ capacity of hemoglobin; , mean alveolar O₂ tension; , mean capillary O₂ tension; , arterial O₂ saturation; , venous O₂ saturation. Adapted from Barcroft 538
	Figure 4. Pulsatility in pulmonary circulation of the dog. A: transformation of pressure‐flow pulses along length of pulmonary circulation. Transmission time for pressure pulse from pulmonary artery to capillaries ∼0.09 s; from capillaries to veins, transmission time ∼0.03 s. B: top, changes in pulmonary blood volume of the dog at rest and exercise during a single cardiac cycle. Rate of change in pulmonary blood volume (striped area) equals difference between flows in main pulmonary artery and in pulmonary veins . Bottom, storage as calculated from discharge curves at consecutive sections of pulmonary vascular tree during a cardiac cycle. Spa, storage in pulmonary arteries; Spv, storage in pulmonary veins; ST, total storage. Most storage occurs within the pulmonary arterial tree. [A from Wiener, Fishman, et al. 527, by permission of the American Heart Association, Inc. B from Skalak, Fishman, et al. 443.]
	Figure 5. Propagation of pressure pulses (left) and flow pulses (right) through pulmonary circulation. Left: top and bottom curves, measured boundary pressures from which all other pressures and flows in the model were calculated. Dashed curves, sum of the mean pressure plus pressure oscillations propagated from right ventricle (arterial pulse). Solid curves include contribution of oscillatory part of left atrial pressure (venous pulse) and represent total (mean + arterial pulse + venous pulse) pressure at each location. Right: corresponding curves for flow. In contrast to left panel, for which top and bottom curves were determined experimentally, all curves in right panel were computed. Tracings, from top to bottom: main pulmonary artery, segmental pulmonary artery (generation 6), precapillaries, postcapillaries, segmental pulmonary vein (generation 38), and left atrium. From Wiener, Fishman, et al. 527, by permission of the American Heart Association, Inc
	Figure 6. Principle of a Starling resistor. Thin‐walled collapsible tube traverses a closed chamber (A) in which pressure can be varied at will. Fluid flows from reservoir (R) into collecting vessel (striped area), traversing collapsible tube en route. When outflow pressure exceeds chamber pressure (left), flow is determined by difference between inflow and outflow pressure. However, when chamber pressure exceeds outflow pressure, so that collapsible tube closes (arrow), flow is determined by difference between inflow and chamber pressure. Adapted from West et al. 524
	Figure 7. Zones of the lungs in different body positions as determined by interplay between pulmonary vascular (Ppv) and alveolar pressures (PA). For simplicity, only zones 1, 2, and 3 are shown. Ppa, pulmonary arterial pressure.a Adapted from Hughes 231
	Figure 8. Blood flow in upright lung as function of vertical height. Adapted from Glazier et al. 172
	Figure 9. Topographical distribution of pulmonary blood flow according to relationship among pulmonary arterial pressure (Ppa), pulmonary venous pressure (Ppv), and alveolar pressure (PA). Because of effect of surface tension, PA is more accurately pericapillary pressure. Zone 1 (apex): PA > Ppa > Ppv. No flow (except through corner vessels) because collapsible vessels close when pericapillary pressure exceeds the pressure inside the vessels. Vessels that close are capillaries and other alveolar vessels up to ∼30 μm diam. Zone 2: Ppa > PA > Ppv. Driving pressure is Ppa — PA. This difference increases down lung and so does flow. Zone 3: Ppa > Ppv > PA. Driving pressure is Ppa — Ppv. Although Ppa — Ppv does not change down lung, Ppa and Ppv continue to increase from top to bottom. Flow down zone 3 is less than zone 2. Zone 4 (appears at residual volume): this region of decreased flow appears during forced exhalation and has been attributed to either an increase in interstitial pressure at lung bases or to closure of small airways at low lung volumes as the increase in PA creates either zone 1 or zone 2 conditions. Adapted from West et al. 524 and Anthonisen and Milic‐Emili 13
	Figure 10. Alveolar, corner, and extra‐alveolar vessels. A: large extra‐alveolar artery (A) showing its muscle layer surrounded by a loose connective tissue sheath. Alveolar septa, inserted radially, presumably exert a radial outward pull that is responsible for dilation of these vessels as the lung is inflated. Lung parenchyma is characteristic of zone 2. a, Bundles of capillaries (corner vessels); b, flat septa containing open but smoothened, slitlike capillaries; c, septa containing completely closed (derecruited) capillaries. Normal rabbit lung fixed under zone 2 conditions by vascular perfusion of OsO₄ into the pulmonary artery. After 2 full inflations, peak arterial pressure = 11–12 mmHg, alveolar pressure = 10 mmHg. Thin epoxy section. B: bundle of wide‐open capillaries (a) within reversible folds of alveolar walls in a corner area. Bundles communicate with vessels (V) larger than capillaries, here probably a small nonmuscular artery that is part of the corner arrangement. Although this vessel cannot expand with inflation, it is also protected against collapse. In other locations, small veins are also visible in this arrangement. Normal rabbit lung fixed under zone 2 conditions by vascular perfusion of OsO₄ into the pulmonary artery. Thin epoxy section. C: capillaries inside a bundle of capillaries (a) in corner presumably connect small arteries with small veins (cf. B) and are protected against excess alveolar pressure. Arrangement is due to reversible pleating of alveolar walls. Some septal capillaries (b) are open but flattened, whereas others (c) are derecruited. Normal rabbit lung fixed under zone 2 conditions by vascular perfusion of OsO₄ into the pulmonary artery. Thin epoxy section. D: large extra‐alveolar vein (V) is surrounded by a loose connective tissue sheath. Bottom right, pleural surface. Normal rat lung fixed by instillation of fixatives into trachea after lung collapse. Relatively thick paraffin section, hematoxylin and eosin stain. Micrographs courtesy of J. Gil
	Figure 11. Cross section of alveolar capillary from human lung lined by endothelium (EN). Endothelial nucleus is striking. Alveolar‐capillary barrier is organized into thick (right) and thin (left) portions. Thick side includes considerable interstitial space (IN), containing connective tissue elements, e.g., fibers (cf). In contrast, interstitial space on thin side is obliterated by fusion of basement membranes, which forms a minimal air‐blood barrier. C, capillary containing 3 red corpuscles in its lumen; EP, alveolar epithelium; F, fibroblast. From Weibel 515
	Figure 12. Schematic representation of fascial sheath extending down wall of pulmonary arteriole. Adapted from Hayek 207
	Figure 13. Pulmonary vascular pressures in consecutive segments of the pulmonary vascular tree and in comparable segments of a systemic artery. Measurements were made by direct puncture of arterial and venous segments of the subpleural microcirculation. Adapted from Bhattacharya et al. 49,50
	Figure 14. Simultaneous tracings in the dog of pulmonary arterial and venous flow and pulmonary arterial and venous pressure. Variations in pulmonary arterial and venous flow are nearly simultaneous; maxima and minima in venous flow lag from corresponding points in arterial flow record only by the 0.09 s necessary for flow pulse to be propagated across pulmonary circulation. From Morkin, Fishman, et al. 342
	Figure 15. Principle of determination of pulmonary wedge pressure. Pressure sensed by wedged catheter (left, balloon inflated) is same as that at conjunction of flowing (2 arrows) and static streams (distal to wedged catheter). Nonocclusive constriction distal to occlusive catheter does not affect determination of pulmonary wedge pressure. However, constriction distal to confluence, as in pulmonary venule (PV), may cause pulmonary wedge pressure to exceed left atrial (LA) pressure. Adapted from Marini 304
	Figure 16. Effect of location of tip of wedged catheter on validity as measure of left atrial pressure (Pla); one catheter was wedged high (Pwh) and the other low (Pwl) in the lung. Initially the upper catheter was located in zone 2 of the lung and did not reflect left atrial pressure. Saline infusion increased left atrial pressure and converted lung containing upper wedged catheter to zone 3 conditions; both catheters then reflected left atrial pressures. Subsequent hemorrhage restored zone 2 conditions and original discrepancy between pulmonary wedge and left atrial pressures. Catheter that was wedged low operated throughout under zone 3 conditions. From Todd et al. 481
	Figure 17. Effect of exercise on upright lung. Increase in mean pulmonary arterial pressure, coupled with increase in pulsatility, favors apical perfusion. Adapted from West 522
	Figure 18. Pulmonary hemodynamics at rest and during steady‐state supine exercise in humans. A: normal males, avg age 23.6 ± 2.1 SD. B: normal females, avg age 23.8 ± 3.9 SD. BA, brachial arterial pressure; C.O., cardiac output; d, diastolic pressure; HR, heart rate; m, mean pressure; PAP, pulmonary arterial pressure; PCW, pulmonary capillary wedge pressure; PVR, pulmonary vascular resistance; s, systolic pressure. Adapted from Gurtner et al. 187
	Figure 19. Passive changes in pulmonary vascular resistance (R) at different levels of driving pressure and pulmonary blood flow (). Pulmonary venous pressure is assumed to remain constant. Pulmonary vascular resistance decreases as either blood flow or pressure drop increases.
	Figure 20. Pulmonary vascular pressure‐flow curves for detection of pulmonary vasomotor activity. A: theoretical basis for detecting pulmonary vasomotor activity with respect to passive pressure‐flow curves in the same individual. Solid line, passive pressure‐flow curve for the individual. Points A and B, linear incremental changes in pressure and flow along passive pressure‐flow curve. Point C, active change in pulmonary vascular resistance. B: practical application of passive pressure‐flow curves to detect vasomotor activity. Left: passive pressure‐flow curve has been established for the individual by measurements at 2 levels of blood flow, i.e., at rest and during exercise (EX). During a single trial of acute hypoxia, point falls above passive pressure‐flow curve, i.e., on a new curve that lies above the passive curve, suggesting that pulmonary vasoconstriction has occurred. Right: similar plot with calculated pulmonary vascular resistance instead of pressure drop as ordinate. A courtesy of D. Silage
	Figure 21. Use of linear portions of a family of pulmonary vascular resistance curves as isopleths to display effect of test procedure on pulmonary vascular resistance. Right, resistance values (R units). At rest (•), pulmonary vascular resistance is higher at sea level than at altitude. During exercise (→), resistance values decrease in both instances, moving in each case to a lower resistance isopleth.
	Figure 22. Top: input impedance spectrum in main pulmonary artery of normal anesthetized dog. Pattern is similar to that of the ascending aorta but lower in amplitude. Minimal value of impedance modulus and crossover of impedance phase occurs at ∼6–8 Hz. Pulmonary hypertension secondary to valvular heart disease is associated with an increase in pulmonary arterial input impedance and a shift of minimal impedance modulus to right. Bottom: impedance phase. Flow in normal lung leads pressure at lower frequencies (negative phase); situation is reversed at higher frequencies. Adapted from Milnor 332
	Figure 23. Arachidonic acid cascade, illustrating 2 pathways and some metabolic products able to change pulmonary vasomotor tone. Metabolic pathways of arachidonic acid initiated by cyclooxygenase and lipoxygenase catalyzed reactions. By stimulating a phospholipase the leukotrienes may in turn cause release of products of cyclooxygenase pathway.
	Figure 24. Putative sites of action of acute hypoxia. Pulmonary microvessel (artery, capillary, and vein) is shown traversing alveolar portion of the lung. Precapillary vessel is subdivided into proximal conducting segment (A), in which mixed venous blood (MVB ) affects some critical element of the vascular smooth muscle, and terminal segment (B), in which alveolar ordinarily is the major influence (striped area). Top: air breathing. Low mixed venous is responsible for normal tone of proximal pulmonary vascular segments; high alveolar is responsible for tone of distal segments. Bottom: hypoxia (breathing 10% O₂ mixture). During hypoxia the mixed venous in proximal segment (A) undergoes little change, whereas alveolar decreases to a level that is not appreciably different from blood in distal segment (B); to the high tone of proximal segment is added the increase in tone of distal segment. Main component of pressor response to hypoxia is due to smooth muscle contraction in distal segment. FI_o2, fraction of O₂ in inspired gas. From Fishman 141, by permission of the American Heart Association, Inc
	Figure 25. Calcium and smooth muscle contraction. A: block diagram of compartmentalization of Ca²⁺ in muscle fibers. Also shown are main pathways and transport systems for Na⁺ and Ca²⁺: 1) ATP‐dependent, ouabain‐sensitive Na⁺‐K⁺ exchange pump; 2) sarcolemmal Na⁺‐Ca²⁺ exchange mechanism (shown operating in forward or Ca²⁺ extrusion mode); 3) sarcoplasmic reticulum (SR) ATP‐dependent Ca²⁺ pump. Most of entering Na⁺ and Ca²⁺ is assumed to come through voltage‐sensitive conductance channels associated with action potential, k, Rate coefficient for fluxes of Na⁺ and Ca²⁺ across sarcolemma and sarcoplasmic reticulum membranes in directions indicated. B: contraction of vascular smooth muscle. When intracellular Ca²⁺ levels exceed a critical level (10⁻⁶ M), Ca²⁺ binds to calmodulin, a Ca²⁺‐binding protein; Ca²⁺‐calmodulin complex binds in turn to myosin kinase, thereby activating the enzyme. Active kinase then catalyzes phosphorylation of myosin, which can interact with actin to produce contraction. Cyclic AMP plays an important role in activating a cAMP‐dependent protein kinase that can transfer phosphate from ATP to proteins directly involved in regulation of intracellular Ca²⁺ levels and in interaction of actin with myosin. A adapted from Blaustein 53
	Figure 26. Native resident of Lake Titicaca (Peruvian Andes, ∼4,500 m). Barrel chest is generally held to be one of several adaptations to life in rarified atmosphere. Courtesy of R. B. Eckhardt
	Figure 27. Relation in Peruvian Andes between altitude, arterial O₂ saturation , and mean pulmonary arterial pressure . Appreciable levels of arterial hypoxemia and of pulmonary hypertension occur at ∼3,000 m. During exercise (EX) arterial hypoxemia and pulmonary arterial pressure increase. From Penaloza and Gamboa 371
	Figure 28. Effect of age on mean pulmonary arterial pressure at sea level and at altitude (Peruvian Andes). From Penaloza and Gamboa 371
	Figure 29. Mean pulmonary arterial pressure and arterial O₂ saturation (ART O₂ SAT) in 3 groups of individuals. In healthy highlanders, arterial oxygenation is lower than in healthy sea‐level residents. This discrepancy is greatly widened in chronic alveolar hypoventilators (Monge's disease) at high altitude. Level of pulmonary arterial pressure is inversely related to degree of arterial hypoxemia. Adapted from Heath and Williams 210
	Figure 30. A: schematic representations of bronchial circulation in different disorders. Top: bronchial arteries (BA). In chronic suppurative diseases of the lungs, bronchial arteries undergo considerable proliferation. Bottom: bronchial veins (BV). Proximal bronchial veins drain either into right atrium (RA) or left atrium (LA), depending on pressure levels in these 2 cardiac chambers. Normally most bronchial venous outflow from the lungs enters right atrium (thicker curved arrow). However, in right ventricular failure, bronchial venous drainage to left atrium increases. B, bronchus; C, expanded bronchial arterial circulation; PA, pulmonary artery. B: indicator‐dilution curves from pulmonary artery and brachial artery (BA) in a normal individual (left) and in a patient with bronchiectasis (right). Curves from the patient are identical in appearance, time, and height, indicating that catheter tip in pulmonary artery (in vicinity of bronchiectatic area) had sampled systemic arterial blood.a A from Fishman 136, by permission of the American Heart Association, Inc. B from Cudkowicz 93
	Figure 31. Fetal circulation in the lamb. BCA, brachiocephalic artery; DA, ductus arteriosus; DV, ductus venosus; FO, foramen ovale; IVC, inferior vena cava; LA, left atrium; LV, left ventricle; RV, right ventricle; SVC, superior vena cava.a From Dawes 103
	Figure 32. Schematic representation of changes in mean pulmonary arterial pressure, proportion of combined ventricular output (CVO) distributed to the lungs, actual pulmonary blood flow, and calculated pulmonary vascular resistance in fetal lambs during gestational development from 0.4 to 1.0 gestation. Progressive decrease in resistance is attributable to an increase in cross‐sectional area of pulmonary vascular bed, in large measure due to growth of new vessels. From Rudolph 423. Reproduced, with permission, from the Annual Review of Physiology, vol. 41, © 1979 by Annual Reviews, Inc
	Figure 33. Changes in patterns of pulmonary arterial (PA) pressure and flow after birth. Left: in the fetus. Right: after birth. From Rudolph 423. Reproduced, with permission, from the Annual Review of Physiology, vol. 41, © 1979 by Annual Reviews, Inc
	Figure 34. Schematic representation of effects of progressive restriction of pulmonary vascular bed by successive amputation of lobes of the lungs on mean pulmonary arterial (PA) pressure (assuming that pulmonary blood flow remains unchanged). Pneumonectomy (middle) evokes only a modest increase in pulmonary arterial pressure (to 22 mmHg). Subsequent removal of right lower and middle lobes leads to considerable pulmonary arterial hypertension (to 55 mmHg). Data from Lategola 267
	Figure 35. Gut‐liver‐lung axis. Serotonin, brought to the liver via the portal vein, is partially removed by the liver. Removal is completed in the lungs.
	Figure 36. Influence of endothelium on responses of different vessels to acetylcholine (ACH). Increasing concentrations of acetylcholine were applied to rings of femoral, saphenous, splenic, and pulmonary arteries (circles) that had previously been contracted with norepinephrine. Those vessels in which endothelium was intact (solid curves) responded with increasing vasodilation. In vessels without endothelium (dashed curves), virtually no vasodilation occurred. Adapted from De Mey and Vanhoutte 113

Figure 1.

gRenin‐angiotensin system. The lungs play a central role in control of systemic blood pressure because of the converting enzyme on the luminal aspect of pulmonary capillary endothelium. Strategic disposition of the enzyme and huge expanse of pulmonary capillary endothelium enable rapid and efficient conversion of angiotensin I to angiotensin II as blood courses through the lungs.

Figure 2.

Muscular pulmonary arteries (resistance vessels) in pulmonary circulation of various animal species. Elastic Van Gieson's stain. A: dog; × 500. B: cat; × 500. C: human; × 200. D: rat; × 800. A‐D: tunica media is relatively thin. E: guinea pig; × 200. Tunica media consists of crescentic masses of circular smooth muscle disposed in discontinuous segments resembling sphincters. In areas between sphincterlike masses of smooth muscle the wall consists only of an elastic lamina. F: cow; × 500. Tunica media is thick.

Micrographs courtesy of J. M. Kay

Figure 3.

Four‐quadrant diagram illustrating respiratory and circulatory adaptation by which O₂ requirement is satisfied at rest (inner rectangle) and during exercise (outer rectangle). , concentration of O₂ in arterial blood; Cvo₂, concentration of O₂ in venous blood; CAP area, capillary area; D_L, diffusing capacity of the lungs; Hb, hemoglobin; , O₂ capacity of hemoglobin; , mean alveolar O₂ tension; , mean capillary O₂ tension; , arterial O₂ saturation; , venous O₂ saturation.

Adapted from Barcroft 538

Figure 4.

Pulsatility in pulmonary circulation of the dog. A: transformation of pressure‐flow pulses along length of pulmonary circulation. Transmission time for pressure pulse from pulmonary artery to capillaries ∼0.09 s; from capillaries to veins, transmission time ∼0.03 s. B: top, changes in pulmonary blood volume of the dog at rest and exercise during a single cardiac cycle. Rate of change in pulmonary blood volume (striped area) equals difference between flows in main pulmonary artery and in pulmonary veins . Bottom, storage as calculated from discharge curves at consecutive sections of pulmonary vascular tree during a cardiac cycle. Spa, storage in pulmonary arteries; Spv, storage in pulmonary veins; ST, total storage. Most storage occurs within the pulmonary arterial tree. [A from Wiener, Fishman, et al. 527, by permission of the American Heart Association, Inc. B from Skalak, Fishman, et al. 443.]

Figure 5.

Propagation of pressure pulses (left) and flow pulses (right) through pulmonary circulation. Left: top and bottom curves, measured boundary pressures from which all other pressures and flows in the model were calculated. Dashed curves, sum of the mean pressure plus pressure oscillations propagated from right ventricle (arterial pulse). Solid curves include contribution of oscillatory part of left atrial pressure (venous pulse) and represent total (mean + arterial pulse + venous pulse) pressure at each location. Right: corresponding curves for flow. In contrast to left panel, for which top and bottom curves were determined experimentally, all curves in right panel were computed. Tracings, from top to bottom: main pulmonary artery, segmental pulmonary artery (generation 6), precapillaries, postcapillaries, segmental pulmonary vein (generation 38), and left atrium.

From Wiener, Fishman, et al. 527, by permission of the American Heart Association, Inc

Figure 6.

Principle of a Starling resistor. Thin‐walled collapsible tube traverses a closed chamber (A) in which pressure can be varied at will. Fluid flows from reservoir (R) into collecting vessel (striped area), traversing collapsible tube en route. When outflow pressure exceeds chamber pressure (left), flow is determined by difference between inflow and outflow pressure. However, when chamber pressure exceeds outflow pressure, so that collapsible tube closes (arrow), flow is determined by difference between inflow and chamber pressure.

Adapted from West et al. 524

Figure 7.

Zones of the lungs in different body positions as determined by interplay between pulmonary vascular (Ppv) and alveolar pressures (PA). For simplicity, only zones 1, 2, and 3 are shown. Ppa, pulmonary arterial pressure.a

Adapted from Hughes 231

Figure 8.

Blood flow in upright lung as function of vertical height.

Adapted from Glazier et al. 172

Figure 9.

Topographical distribution of pulmonary blood flow according to relationship among pulmonary arterial pressure (Ppa), pulmonary venous pressure (Ppv), and alveolar pressure (PA). Because of effect of surface tension, PA is more accurately pericapillary pressure. Zone 1 (apex): PA > Ppa > Ppv. No flow (except through corner vessels) because collapsible vessels close when pericapillary pressure exceeds the pressure inside the vessels. Vessels that close are capillaries and other alveolar vessels up to ∼30 μm diam. Zone 2: Ppa > PA > Ppv. Driving pressure is Ppa — PA. This difference increases down lung and so does flow. Zone 3: Ppa > Ppv > PA. Driving pressure is Ppa — Ppv. Although Ppa — Ppv does not change down lung, Ppa and Ppv continue to increase from top to bottom. Flow down zone 3 is less than zone 2. Zone 4 (appears at residual volume): this region of decreased flow appears during forced exhalation and has been attributed to either an increase in interstitial pressure at lung bases or to closure of small airways at low lung volumes as the increase in PA creates either zone 1 or zone 2 conditions.

Adapted from West et al. 524 and Anthonisen and Milic‐Emili 13

Figure 10.

Alveolar, corner, and extra‐alveolar vessels. A: large extra‐alveolar artery (A) showing its muscle layer surrounded by a loose connective tissue sheath. Alveolar septa, inserted radially, presumably exert a radial outward pull that is responsible for dilation of these vessels as the lung is inflated. Lung parenchyma is characteristic of zone 2. a, Bundles of capillaries (corner vessels); b, flat septa containing open but smoothened, slitlike capillaries; c, septa containing completely closed (derecruited) capillaries. Normal rabbit lung fixed under zone 2 conditions by vascular perfusion of OsO₄ into the pulmonary artery. After 2 full inflations, peak arterial pressure = 11–12 mmHg, alveolar pressure = 10 mmHg. Thin epoxy section. B: bundle of wide‐open capillaries (a) within reversible folds of alveolar walls in a corner area. Bundles communicate with vessels (V) larger than capillaries, here probably a small nonmuscular artery that is part of the corner arrangement. Although this vessel cannot expand with inflation, it is also protected against collapse. In other locations, small veins are also visible in this arrangement. Normal rabbit lung fixed under zone 2 conditions by vascular perfusion of OsO₄ into the pulmonary artery. Thin epoxy section. C: capillaries inside a bundle of capillaries (a) in corner presumably connect small arteries with small veins (cf. B) and are protected against excess alveolar pressure. Arrangement is due to reversible pleating of alveolar walls. Some septal capillaries (b) are open but flattened, whereas others (c) are derecruited. Normal rabbit lung fixed under zone 2 conditions by vascular perfusion of OsO₄ into the pulmonary artery. Thin epoxy section. D: large extra‐alveolar vein (V) is surrounded by a loose connective tissue sheath. Bottom right, pleural surface. Normal rat lung fixed by instillation of fixatives into trachea after lung collapse. Relatively thick paraffin section, hematoxylin and eosin stain.

Micrographs courtesy of J. Gil

Figure 11.

Cross section of alveolar capillary from human lung lined by endothelium (EN). Endothelial nucleus is striking. Alveolar‐capillary barrier is organized into thick (right) and thin (left) portions. Thick side includes considerable interstitial space (IN), containing connective tissue elements, e.g., fibers (cf). In contrast, interstitial space on thin side is obliterated by fusion of basement membranes, which forms a minimal air‐blood barrier. C, capillary containing 3 red corpuscles in its lumen; EP, alveolar epithelium; F, fibroblast.

From Weibel 515

Figure 12.

Schematic representation of fascial sheath extending down wall of pulmonary arteriole.

Adapted from Hayek 207

Figure 13.

Pulmonary vascular pressures in consecutive segments of the pulmonary vascular tree and in comparable segments of a systemic artery. Measurements were made by direct puncture of arterial and venous segments of the subpleural microcirculation.

Adapted from Bhattacharya et al. 49,50

Figure 14.

Simultaneous tracings in the dog of pulmonary arterial and venous flow and pulmonary arterial and venous pressure. Variations in pulmonary arterial and venous flow are nearly simultaneous; maxima and minima in venous flow lag from corresponding points in arterial flow record only by the 0.09 s necessary for flow pulse to be propagated across pulmonary circulation.

From Morkin, Fishman, et al. 342

Figure 15.

Principle of determination of pulmonary wedge pressure. Pressure sensed by wedged catheter (left, balloon inflated) is same as that at conjunction of flowing (2 arrows) and static streams (distal to wedged catheter). Nonocclusive constriction distal to occlusive catheter does not affect determination of pulmonary wedge pressure. However, constriction distal to confluence, as in pulmonary venule (PV), may cause pulmonary wedge pressure to exceed left atrial (LA) pressure.

Adapted from Marini 304

Figure 16.

Effect of location of tip of wedged catheter on validity as measure of left atrial pressure (Pla); one catheter was wedged high (Pwh) and the other low (Pwl) in the lung. Initially the upper catheter was located in zone 2 of the lung and did not reflect left atrial pressure. Saline infusion increased left atrial pressure and converted lung containing upper wedged catheter to zone 3 conditions; both catheters then reflected left atrial pressures. Subsequent hemorrhage restored zone 2 conditions and original discrepancy between pulmonary wedge and left atrial pressures. Catheter that was wedged low operated throughout under zone 3 conditions.

From Todd et al. 481

Figure 17.

Effect of exercise on upright lung. Increase in mean pulmonary arterial pressure, coupled with increase in pulsatility, favors apical perfusion.

Adapted from West 522

Figure 18.

Pulmonary hemodynamics at rest and during steady‐state supine exercise in humans. A: normal males, avg age 23.6 ± 2.1 SD. B: normal females, avg age 23.8 ± 3.9 SD. BA, brachial arterial pressure; C.O., cardiac output; d, diastolic pressure; HR, heart rate; m, mean pressure; PAP, pulmonary arterial pressure; PCW, pulmonary capillary wedge pressure; PVR, pulmonary vascular resistance; s, systolic pressure.

Adapted from Gurtner et al. 187

Figure 19.

Passive changes in pulmonary vascular resistance (R) at different levels of driving pressure and pulmonary blood flow (). Pulmonary venous pressure is assumed to remain constant. Pulmonary vascular resistance decreases as either blood flow or pressure drop increases.

Figure 20.

Pulmonary vascular pressure‐flow curves for detection of pulmonary vasomotor activity. A: theoretical basis for detecting pulmonary vasomotor activity with respect to passive pressure‐flow curves in the same individual. Solid line, passive pressure‐flow curve for the individual. Points A and B, linear incremental changes in pressure and flow along passive pressure‐flow curve. Point C, active change in pulmonary vascular resistance. B: practical application of passive pressure‐flow curves to detect vasomotor activity. Left: passive pressure‐flow curve has been established for the individual by measurements at 2 levels of blood flow, i.e., at rest and during exercise (EX). During a single trial of acute hypoxia, point falls above passive pressure‐flow curve, i.e., on a new curve that lies above the passive curve, suggesting that pulmonary vasoconstriction has occurred. Right: similar plot with calculated pulmonary vascular resistance instead of pressure drop as ordinate.

A courtesy of D. Silage

Figure 21.

Use of linear portions of a family of pulmonary vascular resistance curves as isopleths to display effect of test procedure on pulmonary vascular resistance. Right, resistance values (R units). At rest (•), pulmonary vascular resistance is higher at sea level than at altitude. During exercise (→), resistance values decrease in both instances, moving in each case to a lower resistance isopleth.

Figure 22.

Top: input impedance spectrum in main pulmonary artery of normal anesthetized dog. Pattern is similar to that of the ascending aorta but lower in amplitude. Minimal value of impedance modulus and crossover of impedance phase occurs at ∼6–8 Hz. Pulmonary hypertension secondary to valvular heart disease is associated with an increase in pulmonary arterial input impedance and a shift of minimal impedance modulus to right. Bottom: impedance phase. Flow in normal lung leads pressure at lower frequencies (negative phase); situation is reversed at higher frequencies.

Adapted from Milnor 332

Figure 23.

Arachidonic acid cascade, illustrating 2 pathways and some metabolic products able to change pulmonary vasomotor tone. Metabolic pathways of arachidonic acid initiated by cyclooxygenase and lipoxygenase catalyzed reactions. By stimulating a phospholipase the leukotrienes may in turn cause release of products of cyclooxygenase pathway.

Figure 24.

Putative sites of action of acute hypoxia. Pulmonary microvessel (artery, capillary, and vein) is shown traversing alveolar portion of the lung. Precapillary vessel is subdivided into proximal conducting segment (A), in which mixed venous blood (MVB ) affects some critical element of the vascular smooth muscle, and terminal segment (B), in which alveolar ordinarily is the major influence (striped area). Top: air breathing. Low mixed venous is responsible for normal tone of proximal pulmonary vascular segments; high alveolar is responsible for tone of distal segments. Bottom: hypoxia (breathing 10% O₂ mixture). During hypoxia the mixed venous in proximal segment (A) undergoes little change, whereas alveolar decreases to a level that is not appreciably different from blood in distal segment (B); to the high tone of proximal segment is added the increase in tone of distal segment. Main component of pressor response to hypoxia is due to smooth muscle contraction in distal segment. FI_o2, fraction of O₂ in inspired gas.

From Fishman 141, by permission of the American Heart Association, Inc

Figure 25.

Calcium and smooth muscle contraction. A: block diagram of compartmentalization of Ca²⁺ in muscle fibers. Also shown are main pathways and transport systems for Na⁺ and Ca²⁺: 1) ATP‐dependent, ouabain‐sensitive Na⁺‐K⁺ exchange pump; 2) sarcolemmal Na⁺‐Ca²⁺ exchange mechanism (shown operating in forward or Ca²⁺ extrusion mode); 3) sarcoplasmic reticulum (SR) ATP‐dependent Ca²⁺ pump. Most of entering Na⁺ and Ca²⁺ is assumed to come through voltage‐sensitive conductance channels associated with action potential, k, Rate coefficient for fluxes of Na⁺ and Ca²⁺ across sarcolemma and sarcoplasmic reticulum membranes in directions indicated. B: contraction of vascular smooth muscle. When intracellular Ca²⁺ levels exceed a critical level (10⁻⁶ M), Ca²⁺ binds to calmodulin, a Ca²⁺‐binding protein; Ca²⁺‐calmodulin complex binds in turn to myosin kinase, thereby activating the enzyme. Active kinase then catalyzes phosphorylation of myosin, which can interact with actin to produce contraction. Cyclic AMP plays an important role in activating a cAMP‐dependent protein kinase that can transfer phosphate from ATP to proteins directly involved in regulation of intracellular Ca²⁺ levels and in interaction of actin with myosin.

A adapted from Blaustein 53

Figure 26.

Native resident of Lake Titicaca (Peruvian Andes, ∼4,500 m). Barrel chest is generally held to be one of several adaptations to life in rarified atmosphere.

Courtesy of R. B. Eckhardt

Figure 27.

Relation in Peruvian Andes between altitude, arterial O₂ saturation , and mean pulmonary arterial pressure . Appreciable levels of arterial hypoxemia and of pulmonary hypertension occur at ∼3,000 m. During exercise (EX) arterial hypoxemia and pulmonary arterial pressure increase.

From Penaloza and Gamboa 371

Figure 28.

Effect of age on mean pulmonary arterial pressure at sea level and at altitude (Peruvian Andes).

From Penaloza and Gamboa 371

Figure 29.

Mean pulmonary arterial pressure and arterial O₂ saturation (ART O₂ SAT) in 3 groups of individuals. In healthy highlanders, arterial oxygenation is lower than in healthy sea‐level residents. This discrepancy is greatly widened in chronic alveolar hypoventilators (Monge's disease) at high altitude. Level of pulmonary arterial pressure is inversely related to degree of arterial hypoxemia.

Adapted from Heath and Williams 210

Figure 30.

A: schematic representations of bronchial circulation in different disorders. Top: bronchial arteries (BA). In chronic suppurative diseases of the lungs, bronchial arteries undergo considerable proliferation. Bottom: bronchial veins (BV). Proximal bronchial veins drain either into right atrium (RA) or left atrium (LA), depending on pressure levels in these 2 cardiac chambers. Normally most bronchial venous outflow from the lungs enters right atrium (thicker curved arrow). However, in right ventricular failure, bronchial venous drainage to left atrium increases. B, bronchus; C, expanded bronchial arterial circulation; PA, pulmonary artery. B: indicator‐dilution curves from pulmonary artery and brachial artery (BA) in a normal individual (left) and in a patient with bronchiectasis (right). Curves from the patient are identical in appearance, time, and height, indicating that catheter tip in pulmonary artery (in vicinity of bronchiectatic area) had sampled systemic arterial blood.a

A from Fishman 136, by permission of the American Heart Association, Inc. B from Cudkowicz 93

Figure 31.

Fetal circulation in the lamb. BCA, brachiocephalic artery; DA, ductus arteriosus; DV, ductus venosus; FO, foramen ovale; IVC, inferior vena cava; LA, left atrium; LV, left ventricle; RV, right ventricle; SVC, superior vena cava.a

From Dawes 103

Figure 32.

Schematic representation of changes in mean pulmonary arterial pressure, proportion of combined ventricular output (CVO) distributed to the lungs, actual pulmonary blood flow, and calculated pulmonary vascular resistance in fetal lambs during gestational development from 0.4 to 1.0 gestation. Progressive decrease in resistance is attributable to an increase in cross‐sectional area of pulmonary vascular bed, in large measure due to growth of new vessels.

Figure 33.

Changes in patterns of pulmonary arterial (PA) pressure and flow after birth. Left: in the fetus. Right: after birth.

Figure 34.

Schematic representation of effects of progressive restriction of pulmonary vascular bed by successive amputation of lobes of the lungs on mean pulmonary arterial (PA) pressure (assuming that pulmonary blood flow remains unchanged). Pneumonectomy (middle) evokes only a modest increase in pulmonary arterial pressure (to 22 mmHg). Subsequent removal of right lower and middle lobes leads to considerable pulmonary arterial hypertension (to 55 mmHg).

Data from Lategola 267

Figure 35.

Gut‐liver‐lung axis. Serotonin, brought to the liver via the portal vein, is partially removed by the liver. Removal is completed in the lungs.

Figure 36.

Influence of endothelium on responses of different vessels to acetylcholine (ACH). Increasing concentrations of acetylcholine were applied to rings of femoral, saphenous, splenic, and pulmonary arteries (circles) that had previously been contracted with norepinephrine. Those vessels in which endothelium was intact (solid curves) responded with increasing vasodilation. In vessels without endothelium (dashed curves), virtually no vasodilation occurred.

Adapted from De Mey and Vanhoutte 113

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Alfred P. Fishman. Pulmonary Circulation. Compr Physiol 2011, Supplement 10: Handbook of Physiology, The Respiratory System, Circulation and Nonrespiratory Functions: 93-165. First published in print 1985. doi: 10.1002/cphy.cp030103

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