tvnovellas.info Theory WEST RESPIRATORY PHYSIOLOGY 9TH EDITION PDF

WEST RESPIRATORY PHYSIOLOGY 9TH EDITION PDF

Saturday, October 26, 2019 admin Comments(0)

West's Respiratory Physiology: The Essentials is the gold standard text for learning respiratory Respiratory Physiology: The Essentials, 9th Edition - PDF. Editorial Reviews. Review. FIVE STARS FROM DOODY'S REVIEW SERVICE! Entering its fifth Respiratory Physiology: The Essentials (Respiratory Physiology: The Essentials (West)) 9th Edition, Kindle Edition. by. book review respiratory physiology the essentials eight edition john b west, m.d., ph.d, dsc, west's respiratory physiology the essentials 10th edition pdf.


Author:PAULENE POLEYESTEWA
Language:English, Spanish, French
Country:Ireland
Genre:Lifestyle
Pages:369
Published (Last):16.09.2015
ISBN:785-2-69179-650-7
ePub File Size:16.71 MB
PDF File Size:16.79 MB
Distribution:Free* [*Sign up for free]
Downloads:46977
Uploaded by: DAMIAN

Library of Congress Cataloging-in-Publication Data West, John B. (John Burnard) Respiratory physiology: the essentials / John B. West. — 9th ed. p. ; cm. 4 days ago Physiology The Essentials 9th Edition [PDF] [EPUB] In physiology, dead of respiratory pathophysiology by exploring causes, alterations and. West's Pulmonary Pathophysiology- The Essentials Ninth Edition. John B. West Respiratory Physiology- The Essentials, 9th tvnovellas.info 7 torrent download.

Jump to Navigation These lectures were prepared as ancillary teaching aids for our own medical students and those in other schools. The material is based on my two books Respiratory Physiology: The Essentials, 9th ed. However the lecture format means that more time can be spent discussing the more difficult concepts, and also of course far more illustrations can be included here than in a book. The material may also be useful as a review for residents and fellows in such areas as pulmonary medicine, anesthesiology, and internal medicine, particularly to help with preparation for licensing and other examinations. Some students have requested that the PowerPoint images used in the videos be made available as a separate file so that notes can be added alongside the images by the viewer.

This section was prepared from lung that was rapidly frozen while being perfused. Each red blood cell spends about 0. The lung has an additional blood system, the bronchial circulation that supplies the conducting airways down to about the terminal bronchioles. Some of this blood is carried away from the lung via the pulmonary veins, and some enters the systemic circulation. Such a structure is inherently unstable. Because of the surface tension of the liquid lining the alveoli, relatively large forces develop that tend to collapse alveoli.

Fortunately, some of the cells lining the alveoli secrete a material called surfactantt that dramatically lowers the surface tension of the alveolar lining layer see Chapter 7. As a consequence, the stability of the alveoli is enormously increased, although collapse of small air spaces is always a potential problem and frequently occurs in disease.

Various mechanisms for dealing with inhaled particles have been developed see Chapter 9. Smaller particles that deposit in the conducting airways are removed by a moving staircase of mucus that continually sweeps debris up to the epiglottis, where it is swallowed.

The mucus, secreted by mucous glands and also by goblet cells in the bronchial walls, is propelled by millions of tiny cilia, which move rhythmically under normal conditions but are paralyzed by some inhaled toxins. The alveoli have no cilia, and particles that deposit there are engulfed by large wandering cells called macrophages.

The blood-gas barrier is extremely thin with a very large area, making it ideal for gas exchange by passive diffusion. The conducting airways extend to the terminal bronchioles, with a total volume of about ml. All the gas exchange occurs in the respiratory zone, which has a volume of about 2.

The pulmonary capillaries occupy a huge area of the alveolar wall, and a red cell spends about 0. Concerning the blood-gas barrier of the human lung, The thinnest part of the blood-gas barrier has a thickness of about 3 mm. The total area of the blood-gas barrier is about 1 square meter. If the pressure in the capillaries rises to unphysiologically high levels, the blood-gas barrier can be damaged. Oxygen crosses the blood-gas barrier by active transport.

When oxygen moves through the thin side of the blood-gas barrier from the alveolar gas to the hemoglobin of the red blood cell, it traverses the following layers in order: A.

Epithelial cell, surfactant, interstitium, endothelial cell, plasma, red cell membrane. This means that CO2 diffuses about 20 times more rapidly than does O2 through tissue sheets because it has a much higher solubility but not a very different molecular weight. Diffusion through a tissue sheet. The constant is proportional to the gas solubility Sol but inversely proportional to the square root of its molecular weight MW. How rapidly will the partial pressure in the blood rise?

Figure shows the time courses as the red blood cell moves through the capillary, a process that takes about 0. Uptake of carbon monoxide, nitrous oxide, and O2 along the pulmonary capillary. Note that the blood partial pressure of nitrous oxide virtually reaches that of alveolar gas very early in the capillary, so the transfer of this gas is perfusion limited.

By contrast, the partial pressure of carbon monoxide in the blood is almost unchanged, so its transfer is diffusion limited. O2 transfer can be perfusion limited or partly diffusion limited, depending on the conditions. As a result, the content of carbon monoxide in the cell rises. However, because of the tight bond that forms between carbon monoxide and hemoglobin within the cell, a large amount of carbon monoxide can be taken up by the cell with almost no increase in partial pressure.

Thus, as the cell moves through the capillary, the carbon monoxide partial pressure in the blood hardly changes, so that no appreciable back pressure develops, and the gas continues to move rapidly across the alveolar wall.

It is clear, therefore, that the amount of carbon monoxide that gets into the blood is limited by the diffusion properties of the blood-gas barrier and not by the amount of blood available. Contrast the time course of nitrous oxide.

When this gas moves across the alveolar wall into the blood, no combination with hemoglobin takes place. As a result, the blood has nothing like the avidity for nitrous oxide that it has for carbon monoxide, and the partial pressure rises rapidly. Indeed, Figure shows that the partial pressure of nitrous oxide in the blood has virtually reached that of the alveolar gas by the time the red cell is only one-tenth of the way along the capillary.

After this point, almost no nitrous oxide is transferred. The transfer of nitrous oxide is therefore perfusion limited. What of O2? Its time course lies between those of carbon monoxide and nitrous oxide.

O2 combines with hemoglobin unlike nitrous oxide but with nothing like the avidity of carbon monoxide. In other words, the rise in partial pressure when O2 enters a red blood cell is much greater than is the case for the same number of molecules of carbon monoxide.

Figure shows that the Po2 of the red blood cell as it enters the capillary is already about four-tenths of the alveolar value because of the O2 in mixed venous blood. Under typical resting conditions, the capillary Po2 virtually reaches that of alveolar gas when the red cell is about one-third of the way along the capillary.

Under these conditions, O2 transfer is perfusion limited like nitrous oxide. However, in some abnormal circumstances when the diffusion properties of the lung are impaired, for example, because of thickening of the blood-gas barrier, the blood Po2 does not reach the alveolar value by the end of the capillary, and now there is some diffusion limitation as well. For a gas like carbon monoxide, these are very different, whereas for a gas like nitrous oxide, they are the same.

Figure A shows that the Po2 in a red blood cell entering the capillary is normally about 40 mm Hg. Across the blood-gas barrier, only 0. Oxygen time courses in the pulmonary capillary when diffusion is normal and abnormal e. A shows time courses when the alveolar PO2 is normal. B shows slower oxygenation when the alveolar PO2 is abnormally low. Note that in both cases, severe exercise reduces the time available for oxygenation. Thus, under normal circumstances, the difference in Po2 between alveolar gas and end-capillary blood is immeasurably small—a mere fraction of an mm Hg.

In other words, the diffusion reserves of the normal lung are enormous. Therefore, the time available for oxygenation is less, but in normal subjects breathing air, there is generally still no measurable fall in end-capillary Po2. However, if the blood-gas barrier is markedly thickened by disease so that oxygen diffusion is impeded, the rate of rise of Po2 in the red blood cells is correspondingly slow, and the Po2 may not reach that of alveolar gas before the time available for oxygenation in the capillary has run out.

Respiratory Physiology: The Essentials, 9th Edition

In this case, a measurable difference between alveolar gas and end-capillary blood for Po2 may occur. Another way of stressing the diffusion properties of the lung is to lower the alveolar Po2 Figure B.

Suppose that this has been reduced to 50 mm Hg, by the subject either going to high altitude or inhaling a low O2 mixture. Now, although the Po2 in the red cell at the start of the capillary may only be about 20 mm Hg, the partial pressure difference responsible for driving the O2 across the blood-gas barrier has been reduced from 60 mm Hg Figure A to only 30 mm Hg.

O2 therefore moves across more slowly. In addition, the rate of rise of Po2 for a given increase in O2 concentration in the blood is less than it was because of the steep slope of the O2 dissociation curve when the Po2 is low see Chapter 6. For both of these reasons, therefore, the rise in Po2 along the capillary is relatively slow, and failure to reach the alveolar Po2 is more likely. Thus, severe exercise at very high altitude is one of the few situations in which diffusion impairment of O2 transfer in normal subjects can be convincingly demonstrated.

By the same token, patients with a thickened blood-gas barrier will be most likely to show evidence of diffusion impairment if they breathe a low oxygen mixture, especially if they exercise as well.

By contrast, the transfer of carbon monoxide is limited solely by diffusion, and it is therefore the gas of choice for measuring the diffusion properties of the lung. At one time O2 was employed under hypoxic conditions Figure B , but this technique is no longer used. The laws of diffusion Figure state that the amount of gas transferred across a sheet of tissue is proportional to the area, a diffusion constant, and the difference in partial pressure, and inversely proportional to the thickness, or A D P1 — P2 T.

V gas g Now, for a complex structure like the blood-gas barrier of the lung, it is not possible to measure the area and thickness during life.

Current Lectures Categories

Instead, the equation is rewritten. V gas g DL P1 — P2 where DL is called the diffusing capacity of the lungg and includes the area, thickness, and diffusion properties of the sheet and the gas concerned. Thus, the diffusing capacity for carbon monoxide is given by. But as we have seen Figure , the partial pressure of carbon monoxide in capillary blood is extremely small and can generally be neglected.

This is usually done by measuring the inspired and expired concentrations of carbon monoxide with an infrared analyzer. The alveolar concentration of carbon monoxide is not constant during the breath-holding period, but allowance can be made for that.

Helium is also added to the inspired gas to give a measurement of lung volume by dilution. However, Figure shows that the path length from the alveolar wall to the center of a red blood cell exceeds that in the wall itself, so that some of the diffusion resistance is located within the capillary.

When O2 or CO is added to blood, its combination with hemoglobin is quite fast, being well on the way to completion in 0. Thus, the uptake of O2 or CO can be regarded as occurring in two stages: The diffusing capacity of the lung DL is made up of two components: We can add the resistances offered by the membrane and the blood to obtain the total diffusion resistance. As a result, the measured diffusing capacity is reduced by O2 breathing. In fact, it is possible to separately determine DM and Vc by measuring the diffusing capacity for CO at different alveolar Po2 values.

In this way, the separate contributions of the diffusion properties of the blood-gas barrier and the volume of capillary blood can be derived. Furthermore, in the diseased lung, the measurement is affected by the distribution of diffusion properties, alveolar volume, and capillary blood.

However, the reaction of CO2 with blood is complex see Chapter 6 , and although there is some uncertainty about the rates of the various reactions, it is possible that a difference between end-capillary blood and alveolar gas can develop if the blood-gas barrier is diseased. Examples of diffusion- and perfusion-limited gases are carbon monoxide and nitrous oxide, respectively.

Oxygen transfer is normally perfusion limited, but 3. The diffusing capacity of the lung is measured using inhaled carbon monoxide. The value increases markedly on exercise. Carbon dioxide transfer across the blood-gas barrier is probably not diffusion limited.

An exercising subject breathes a low concentration of CO in a steady state. If the alveolar PCO is 0. In a normal person, doubling the diffusing capacity of the lung would be expected to A. Decrease arterial PCO2 during resting breathing. Increase the uptake of nitrous oxide during anesthesia. Increase the arterial PO2 during resting breathing. Increase maximal oxygen uptake at extreme altitude. If a subject inhales several breaths of a gas mixture containing low concentrations of carbon monoxide and nitrous oxide, A.

The partial pressures of carbon monoxide in alveolar gas and end-capillary blood will be virtually the same. The partial pressures of nitrous oxide in alveolar gas and end-capillary blood will be very different. Carbon monoxide is transferred into the blood along the whole length of the capillary. Little of the nitrous oxide will be taken up in the early part of the capillary. The uptake of nitrous oxide can be used to measure the diffusing capacity of the lung.

Concerning the diffusing capacity of the lung, A. It is best measured with carbon monoxide because this gas diffuses very slowly across the blood-gas barrier. Diffusion limitation of oxygen transfer during exercise is more likely to occur at sea level than at high altitude.

Respiratory edition west pdf 9th physiology

Breathing oxygen reduces the measured diffusing capacity for carbon monoxide compared with air breathing. It is decreased by exercise. The diffusing capacity of the lung for carbon monoxide is increased by A. Asbestosis, which causes thickening of the blood-gas barrier. Pulmonary embolism, which cuts off the blood supply to part of the lung.

Exercise in a normal subject. Severe anemia. First the pressures inside and outside the pulmonary blood vessels are considered, and then pulmonary vascular resistance is introduced. Finally, other functions of the pulmonary circulation are dealt with, particularly the metabolic functions of the lung.

This artery then branches successively like the system of airways Figure , and, indeed, the pulmonary arteries accompany the airways as far as the terminal bronchioles. Beyond that, they break up to supply the capillary bed that lies in the walls of the alveoli Figures and The oxygenated blood is then collected from the capillary bed by the small pulmonary veins that run between the lobules and eventually unite to form the four large veins in humans , which drain into the left atrium.

However, there are important differences between the two circulations, and confusion frequently results from attempts to emphasize similarities between them. The mean pressure in the main pulmonary artery is only about 15 mm Hg; the systolic and diastolic pressures are about 25 and 8 mm Hg, respectively Figure The pressure is therefore very pulsatile.

Comparison of pressures mm Hg in the pulmonary and systemic circulations. Hydrostatic differences modify these. The pressures in the right and left atriums are not very dissimilar— about 2 and 5 mm Hg, respectively.

In keeping with these low pressures, the walls of the pulmonary artery and its branches are remarkably thin and contain relatively little smooth muscle they are easily mistaken for veins. This is in striking contrast to the systemic circulation, where the arteries generally have thick walls and the arterioles in particular have abundant smooth muscle.

The reasons for these differences become clear when the functions of the two circulations are compared. The systemic circulation regulates the supply of blood to various organs, including those which may be far above the level of the heart the upstretched arm, for example. By contrast, the lung is required to accept the whole of the cardiac output at all times. It is rarely concerned with directing blood from one region to another an exception is localized alveolar hypoxia; see below , and its arterial pressure is therefore as low as is consistent with lifting blood to the top of the lung.

The pressure within the pulmonary capillaries is uncertain. The best evidence suggests that it lies about halfway between pulmonary arterial and venous pressure, and that probably much of the pressure drop occurs within the capillary bed itself.

Certainly the distribution of pressures along the pulmonary circulation is far more symmetrical than in its systemic counterpart, where most of the pressure drop is just upstream of the capillaries Figure In addition, the pressure within the pulmonary capillaries varies considerably throughout the lung because of hydrostatic effects see below.

It is true that there is a very thin layer of epithelial cells lining the alveoli, but the capillaries receive little support from this and, consequently, are liable to collapse or distend, depending on the pressures within and around them.

The latter is very close to alveolar pressure. The pressure in the alveoli is usually close to atmospheric pressure; indeed, during breath-holding with the glottis open, the two pressures are identical. But usually, the effective pressure is alveolar pressure, and when this rises above the pressure inside the capillaries, they collapse.

The pressure difference between the inside and outside of the capillaries is often called the transmural pressure. What is the pressure around the pulmonary arteries and veins? This can be considerably less than alveolar pressure. As the lung expands, these larger 4.

The second are pulled open by the radial traction of the surrounding lung parenchyma, and the effective pressure around them is therefore lower than alveolar pressure. Consequently, the effective pressure around them is low; in fact, there is some evidence that this pressure is even less than the pressure around the whole lung intrapleural pressure.

This paradox can be explained by the mechanical advantage that develops when a relatively rigid structure such as a blood vessel or bronchus is surrounded by a rapidly expanding elastic material such as lung parenchyma.

In any event, both the arteries and veins increase their caliber as the lung expands. The behavior of the capillaries and the larger blood vessels is so different they are often referred to as alveolar and extra-alveolar vessels, respectively Figure Alveolar vessels are exposed to alveolar pressure and include Figure Section of lung showing many alveoli and an extra-alveolar vessel in this case, a small vein with its perivascular sheath.

Their caliber is determined by the relationship between alveolar pressure and the pressure within them. Extra-alveolar vessels include all the arteries and veins that run through the lung parenchyma. Their caliber is greatly affected by lung volume because this determines the expanding pull of the parenchyma on their walls.

The very large vessels near the hilum are outside the lung substance and are exposed to intrapleural pressure. We have seen that the total pressure drop from pulmonary artery to left atrium in the pulmonary circulation is only some 10 mm Hg, against about mm Hg for the systemic circulation.

The normal value is then in the region of Fall in pulmonary vascular resistance as the pulmonary arterial or venous pressure is raised. When the arterial pressure was changed, the venous pressure was held constant at 12 cm water, and when the venous pressure was changed, the arterial pressure was held at 37 cm water.

Data from an excised animal lung preparation. Figure shows that an increase in either pulmonary arterial or venous pressure causes pulmonary vascular resistance to fall. Two mechanisms are responsible for this. As the pressure rises, these vessels begin to conduct blood, thus lowering the overall resistance. This is termed recruitmentt Figure and is apparently the chief mechanism for the fall in pulmonary vascular resistance that occurs as the pulmonary artery pressure is raised from low levels.

The reason some vessels are unper- Recruitment Distension Figure Recruitment opening of previously closed vessels and distension increase in caliber of vessels. These are the two mechanisms for the decrease in pulmonary vascular resistance that occurs as vascular pressures are raised. This increase in caliber, or distension, is hardly surprising in view of the very thin membrane that separates the capillary from the alveolar space Figure There is evidence that the capillary wall strongly resists stretching.

Distension is apparently the predominant mechanism for the fall in pulmonary vascular resistance at relatively high vascular pressures. However, recruitment and distension often occur together. Another important determinant of pulmonary vascular resistance is lung volume. The caliber of the extra-alveolar vessels Figure is determined by a balance between various forces. As we have seen, they are pulled open as the lung expands. As a result, their vascular resistance is low at large lung volumes.

On the other hand, their walls contain smooth muscle and elastic tissue, which resist distension and tend to reduce the caliber of the vessels. Consequently, they have a high resistance when lung volume is low Figure This is called a critical opening pressure.

Effect of lung volume on pulmonary vascular resistance when the transmural pressure of the capillaries is held constant. At low lung volumes, resistance is high because the extra-alveolar vessels become narrow.

At high volumes, the capillaries are stretched, and their caliber is reduced. Data from an animal lobe preparation. If alveolar pressure rises with respect to capillary pressure, the vessels tend to be squashed, and their resistance rises. This usually occurs when a normal subject takes a deep inspiration, because the vascular pressures fall. The heart is surrounded by intrapleural pressure, which falls on inspiration. However, the pressures in the pulmonary circulation do not remain steady after such a maneuver.

An additional factor is that the caliber of the capillaries is reduced at large lung volumes because of stretching and consequent thinning of the alveolar walls. Because of the role of smooth muscle in determining the caliber of the extra-alveolar vessels, drugs that cause contraction of the muscle increase pulmonary vascular resistance. These include serotonin, histamine, and norepinephrine. These drugs are particularly effective vasoconstrictors when the lung volume is low and the expanding forces on the vessels are weak.

Drugs that can relax smooth muscle in the pulmonary circulation include acetylcholine and isoproterenol. The volume of blood passing through the lungs each minute Q can be calculated. This states that the O2 consumption per minute Vo2 measured at the mouth is equal to the amount of O2 taken up by the blood in the lungs per minute.

Because the O2 concentration in the blood entering the lungs is C VO and that in the blood leaving is CaO , 2 2 we have. Mixed venous blood is taken via a catheter in the pulmonary artery, and arterial blood by puncture of the brachial or radial artery. Both these methods are of great importance, but they will not be considered in more detail here because they fall within the province of cardiovascular physiology. When it reaches the pulmonary capillaries, it is evolved into alveolar gas because of its low solubility, and the distribution of radioactivity can be measured by counters over the chest during breath-holding.

This distribution is affected by change of posture and exercise. The dissolved xenon is evolved into alveolar gas from the pulmonary capillaries. If we consider the pulmonary arterial system as a continuous column of blood, the difference in pressure between the top and bottom of a lung 30 cm high will be about 30 cm water, or 23 mm Hg. There may be a region at the top of the lung zone 1 where pulmonary arterial pressure falls below alveolar pressure normally close to atmospheric pressure.

See text for details. This ventilated but unperfused lung is useless for gas exchange and is called alveolar dead space. Farther down the lung zone 2 , pulmonary arterial pressure increases because of the hydrostatic effect and now exceeds alveolar pressure.

The pulmonary capillary bed is clearly very different from a rubber tube. Nevertheless, the overall behavior is similar and is often called the Starling resistor, sluice, or waterfall effect. In addition, increasing recruitment of capillaries occurs down this zone. The pressure within them lying between arterial and venous increases down the zone while the pressure outside alveolar remains constant. Thus, their transmural pressure rises and, indeed, measurements show that their mean width increases.

At low lung volumes, the A B Figure Two Starling resistors, each consisting of a thin rubber tube inside a container. In some animals, some regions of the lung appear to have an intrinsically higher vascular resistance. However, a remarkable active response occurs when the Po2 of alveolar gas is reduced. This is known as hypoxic pulmonary vasoconstriction and consists of contraction of smooth muscle in the walls of the small arterioles in the hypoxic region.

The precise mechanism of this response is not known, but it occurs in excised isolated lung and so does not depend on central nervous connections. Excised segments of pulmonary artery constrict if their environment is made hypoxic, so there is a local action of the hypoxia on the artery itself.

This can be proved by perfusing a lung with blood of a high Po2 while keeping the alveolar Po2 low. Under these conditions, the response occurs. The vessel wall becomes hypoxic as a result of diffusion of oxygen over the very short distance from the wall to the surrounding alveoli. Recall that a small pulmonary artery is very closely surrounded by alveoli compare the proximity of alveoli to the small pulmonary vein in Figure The stimulus-response curve of this constriction is very nonlinear Figure When the alveolar Po2 is altered in the region above mm Hg, little change in vascular resistance is seen.

The mechanism of hypoxic pulmonary vasoconstriction is the subject of a great deal of research. Recent studies show that inhibition of voltage-gated potassium channels and membrane depolarization are involved, leading to increased calcium ion concentrations in the cytoplasm.

An increase in cytoplasmic calcium ion concentration is the major trigger for smooth muscle contraction. Nitric oxide NO has been shown to be an endothelium-derived relaxing factor for blood vessels. NO activates soluble guanylate cyclase and increases the synthesis of guanosine 3',5'-cyclic monophosphate cyclic GMP , which leads to smooth muscle relaxation. Inhibitors of NO synthase augment hypoxic pulmonary vasoconstriction in animal preparations, and inhaled NO reduces hypoxic pulmonary vasoconstriction in humans.

The required inhaled concentration of NO is extremely low about 20 ppm , and the gas is very toxic at high concentrations. Disruption of the eNOS gene has been shown to cause pulmonary hypertension in animal models.

Data from anesthetized cat. Their roles in normal physiology and disease are the subject of intense study. Blockers of endothelin receptors have been used clinically to treat patients with pulmonary hypertension. At high altitude, generalized pulmonary vasoconstriction occurs, leading to a rise in pulmonary arterial pressure. But probably the most important situation in which this mechanism operates is at birth. Other active responses of the pulmonary circulation have been described.

A low blood pH causes vasoconstriction, especially when alveolar hypoxia is present. Unfortunately, the practical use of this equation is limited because of our ignorance of many of the values. The colloid osmotic pressure within the capillary is about 25—28 mm Hg.

The capillary hydrostatic pressure is probably about halfway between arterial and venous pressure and is much higher at the bottom of the lung than at the top. The colloid osmotic pressure of the 4. The interstitial hydrostatic pressure is unknown, but some measurements show it is substantially below atmospheric pressure.

The Essentials, 7th ed. Baltimore, MD: Fluid that reaches the alveolar spaces is actively pumped out by a sodium-potassium ATPase pump in epithelial cells. Alveolar edema is much more serious than interstitial edema because of the interference with pulmonary gas exchange. However, it has other important functions. One is to act as a reservoir for blood. We saw that the lung has a remarkable ability to reduce its pulmonary vascular resistance as its vascular pressures are raised through the mechanisms of recruitment and distension Figure The same mechanisms allow the lung to increase its blood volume with relatively small rises in pulmonary arterial or venous pressures.

This occurs, for example, when a subject lies down after standing. Blood then drains from the legs into the lung. Small blood thrombi are removed from the circulation before they can reach the brain or other vital organs. Many white blood cells are trapped by the lung and later released, although the value of this is not clear.

A number of vasoactive substances are metabolized by the lung Table Because the lung is the only organ except the heart that receives the whole circulation, it is uniquely suited to modifying bloodborne substances.

A substantial fraction of all the vascular endothelial cells in the body are located in the lung. The only known example of biological activation by passage through the pulmonary circulation is the conversion of the relatively inactive polypeptide angiotensin I to the potent vasoconstrictor angiotensin II. The latter, which is up to 50 times more active than its precursor, is unaffected by passage through the lung. The conversion of angiotensin I is catalyzed by angiotensinconverting enzyme, or ACE, which is located in small pits in the surface of the capillary endothelial cells.

The lung is the major site of inactivation of serotonin 5-hydroxytryptamine , but this is not by enzymatic degradation but by an uptake and storage process Table Some of the serotonin may be transferred to platelets in the lung or stored in some other way and released during anaphylaxis. Histamine appears not to be affected by the intact lung but is readily inactivated by slices. Several vasoactive and bronchoactive substances are metabolized in the lung and may be released into the circulation under certain conditions.

Important among these are the arachidonic acid metabolites Figure Arachidonic acid is formed through the action of the enzyme phospholipase A2 on phospholipid bound to cell membranes.

There are two major synthetic pathways, the initial reactions being catalyzed by the enzymes lipoxygenase and cyclooxygenase, respectively. These compounds cause airway constriction and may have an important role in asthma. The prostaglandins are potent vasoconstrictors or vasodilators. Two pathways of arachidonic acid metabolism. The leukotrienes are generated by the lipoxygenase pathway, whereas the prostaglandins and thromboxane A2 come from the cyclooxygenase pathway. Prostaglandins also affect platelet aggregation and are active in other systems, such as the kallikrein-kinin clotting cascade.

They also may have a role in the bronchoconstriction of asthma. There is also evidence that the lung plays a role in the clotting mechanism of blood under normal and abnormal conditions.

For example, there are a large number of mast cells containing heparin in the interstitium. In addition, the lung is able to secrete special immunoglobulins, particularly IgA, in the bronchial mucus that contribute to its defenses against infection. Synthetic functions of the lung include the synthesis of phospholipids such as dipalmitoyl phosphatidylcholine, which is a component of pulmonary surfactant see Chapter 7. Protein synthesis is also clearly important because collagen and elastin form the structural framework of the lung.

Under some conditions, proteases are apparently liberated from leukocytes in the lung, causing breakdown of collagen and elastin, and this may result in emphysema. The pressures within the pulmonary circulation are much lower than in the systemic circulation. Also the capillaries are exposed to alveolar pressure, whereas the pressures around the extra-alveolar vessels are lower. Pulmonary vascular resistance is low and falls even more when cardiac output increases because of recruitment and distension of the capillaries.

Pulmonary vascular resistance increases at very low or high lung volumes. Fluid movement across the capillary endothelium is governed by the Starling equilibrium. The pulmonary circulation has many metabolic functions, notably the conversion of angiotensin I to angiotensin II by angiotensin-converting enzyme. The ratio of total systemic vascular resistance to pulmonary vascular resistance is about A. Concerning the extra-alveolar vessels of the lung, A.

Respiratory Physiology: The Essentials, 9th Edition - PDF Free Download

Tension in the surrounding alveolar walls tends to narrow them. Their walls contain smooth muscle and elastic tissue. They are exposed to alveolar pressure. Their constriction in response to alveolar hypoxia mainly takes place in the veins. The fall in pulmonary vascular resistance on exercise is caused by A. Decrease in pulmonary venous pressure.

Increase in alveolar pressure. Distension of pulmonary capillaries. Alveolar hypoxia. In zone 2 of the lung, A. Alveolar pressure exceeds arterial pressure.

Follow the author

Venous pressure exceeds alveolar pressure. Venous pressure exceeds arterial pressure. Pulmonary vascular resistance is reduced by A. Removal of one lung. Exhaling from functional residual capacity to residual volume.

Acutely increasing pulmonary venous pressure. Mechanically ventilating the lung with positive pressure. Hypoxic pulmonary vasoconstriction A. Depends more on the PO2 of mixed venous blood than alveolar gas.

Is released in the transition from placental to air respiration. Involves CO2 uptake in vascular smooth muscle.

The metabolic functions of the lung include A. Producing bradykinin. Secreting serotonin. Removing leukotrienes. Generating erythropoietin. First, a theoretical ideal lung is considered. Then we review three mechanisms of hypoxemia: Then we examine how ventilationperfusion inequality impairs overall gas exchange.

It is emphasized that this is true not only of oxygen but also of carbon dioxide. It would be natural to assume that if all these processes were adequate, normal gas exchange within the lung would be assured.

First, however, we shall examine two relatively simple causes of impairment of gas exchange—hypoventilation and shunt. Because all of these situations result in hypoxemia, that is, in an abnormally low Po2 in arterial blood, it is useful to take a preliminary look at normal O2 transfer. The Po2 of air is Thus, the Po2 of inspired air is Scheme of the O2 partial pressures from air to tissues. The solid line shows a hypothetical perfect situation, and the broken line depicts hypoventilation.

Hypoventilation depresses the PO2 in the alveolar gas and, therefore, in the tissues. This is because the Po2 of alveolar gas is determined by a balance between two processes: Strictly, alveolar ventilation is not continuous but is breath by breath. The rate of removal of O2 from the lung is governed by the O2 consumption of the tissues and varies little under resting conditions.

In practice, therefore, the alveolar Po2 is largely determined by the level of alveolar ventilation. The same applies to the alveolar Pco2, which is normally about 40 mm Hg. However, the lung is an essential link in the chain of O2 transport, and any decrease of Po2 in arterial blood must result in a lower tissue Po2, other things being equal. For the same reasons, impaired pulmonary gas exchange causes a rise in tissue Pco2.

Thus, if the alveolar ventilation is abnormally low, the alveolar Po2 falls. For similar reasons, the Pco2 rises. This is known as hypoventilation Figure Causes of hypoventilation include such drugs as morphine and barbiturates that depress the central drive to the respiratory muscles, damage to the chest wall or paralysis of the respiratory muscles, and a high resistance to breathing for example, very dense gas at great depth underwater.

Hypoventilation always causes an increased alveolar and, therefore, 5. The relationship between alveolar ventilation and Pco2 was derived on p.

This means that if the alveolar ventilation is halved, the Pco2 is doubled, once a steady state has been established. It is sometimes known as the respiratory quotient. This equation shows that if R has its normal value of 0. The full version of the equation is given in Appendix A.

Pdf edition 9th west physiology respiratory

Hypoventilation always reduces the alveolar and arterial Po2 except when the subject breathes an enriched O2 mixture. If alveolar ventilation is suddenly increased for example, by voluntary hyperventilation , it may take several minutes for the alveolar Po2 and Pco2 to assume their new steady-state values.

This is because of the different O2 and CO2 stores in the body. Therefore, the alveolar Pco2 takes longer to come to equilibrium, and during the nonsteady state, the R value of expired gas is high as the CO2 stores are washed out.

Opposite changes occur with the onset of hypoventilation. In real life, this is not so. One reason is that although the Po2 of the blood rises closer and closer to that of alveolar gas as the blood traverses the pulmonary capillary Figure , it can never quite reach it.

Under normal conditions, the Po2 difference between alveolar gas and end-capillary blood resulting from incomplete diffusion is immeasurably small but is shown schematically in Figure As we have seen, the difference can become larger during exercise, or when the blood-gas barrier is thickened, or if a low O2 mixture is inhaled Figure B. Library information skills training programme "Just precisely what is a P value"?

Need to find information to support your clinical practice? Need to make a decision but can't find the supporting evidence?

Starting a course but can't find the study material?

You might also like: API 2000 7TH EDITION PDF

Found the evidence but unsure what it means? Going through nursing re-validation? We can help. All of our training programme dates for are now available on the Library's web site.