(BQ) Part 1 book “Pocket companion to guyton and hall textbook of medical physiology” has contents: Introduction to physiology - the cell and general physiology; membrane physiology, nerve, and muscle; the heart; the circulation; the body fluids and kidneys; blood cells, immunity, and blood coagulation;… and other contents.
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FPO: Peel Off Sticker For technical assistance: email studentconsult.help@elsevier.com call 1-800-401-9962 (inside the US) call +1-314-447-8200 (outside the US) Use of the current edition of the electronic version of this book (eBook) is subject to the terms of the nontransferable, limited license granted on studentconsult.inkling.com Access to the eBook is limited to the first individual who redeems the PIN, located on the inside cover of this book, at studentconsult.inkling.com and may not be transferred to another party by resale, lending, or other means GUYTON AND HALL The world’s foremost medical physiology resources Guyton and Hall Textbook of Medical Physiology, 13th Edition John E Hall, PhD 978-1-4557-7005-2 Unlike other physiology textbooks, this clear and comprehensive guide has a consistent, single-author voice and focuses on the content most relevant to clinical and pre-clinical students The detailed but lucid text is complemented by didactic illustrations that summarize key concepts in physiology and pathophysiology Pocket Companion to Guyton and Hall Textbook of Medical Physiology, 13th Edition John E Hall, PhD 978-1-4557-7006-9 Guyton and Hall Physiology Review, 3rd Edition John E Hall, PhD 978-1-4557-7007-6 ORDER TODAY! elsevierhealth.com NOTE TO INSTRUCTORS: Contact your Elsevier Sales Representative for teaching resources, including slides and image banks, for Guyton and Hall Textbook of Medical Physiology, 13e, or request these supporting materials at: http://evolve.elsevier.com/Hall13 Pocket Companion to Guyton and Hall Textbook of Medical Physiology Thirteenth Edition John E Hall, PhD Arthur C Guyton Professor and Chair Department of Physiology and Biophysics Director of the Mississippi Center for Obesity Research University of Mississippi Medical Center Jackson, Mississippi 1600 John F Kennedy Blvd Ste 1800 Philadelphia, PA 19103-2899 POCKET COMPANION TO GUYTON AND HALL TEXTBOOK OF MEDICAL PHYSIOLOGY, THIRTEENTH EDITION ISBN: 978-1-4557-7006-9 Copyright © 2016 by Elsevier, Inc All rights reserved No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein) Notices Knowledge and best practice in this field are constantly changing As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein Previous editions copyrighted 2012, 2006, 2001, 1998 by Saunders, an imprint of Elsevier, Inc Library of Congress Cataloging-in-Publication Data Hall, John E (John Edward), 1946- , author Pocket companion to Guyton and Hall textbook of medical physiology / John E Hall Thirteenth edition p ; cm Complemented by: Guyton and Hall textbook of medical physiology / John E Hall Thirteenth edition [2016] Includes index ISBN 978-1-4557-7006-9 (paperback : alk paper) I Hall, John E (John Edward), 1946- Guyton and Hall textbook of medical physiology Complemented by (expression): II Title [DNLM: Physiological Phenomena QT 104] QP35 612 dc23 2015002946 Senior Content Strategist: Elyse O’Grady Senior Content Development Manager: Rebecca Gruliow Publishing Services Manager: Patricia Tannian Senior Project Manager: Carrie Stetz Design Direction: Julia Dummitt Printed in The United States of America Last digit is the print number: 9 8 7 6 5 4 3 2 1 Contributors Thomas H Adair, PhD Professor of Physiology and Biophysics University of Mississippi Medical Center Jackson, Mississippi Membrane Physiology, Nerve, and Muscle (Chapters 4–8) Respiration (Chapters 38–43) Aviation, Space, and Deep-Sea Diving Physiology (Chapters 44–45) The Nervous System: A General Principles and Sensory Physiology (Chapters 46–49) The Nervous System: B The Special Senses (Chapters 50–54) The Nervous System: C Motor and Integrative Neurophysiology (Chapters 55–60) Gastrointestinal Physiology (Chapters 63–67) John E Hall, PhD Arthur C Guyton Professor and Chair Department of Physiology and Biophysics Director, Mississippi Center for Obesity Research University of Mississippi Medical Center Jackson, Mississippi Introduction to Physiology: The Cell and General Physiology (Chapters 1–3) The Circulation (Chapters 14–19) The Body Fluids and Kidneys (Chapters 25–32) Blood Cells, Immunity, and Blood Coagulation (Chapters 33–37) The Nervous System: C Motor and Integrative Neurophysiology (Chapters 61–62) Metabolism and Temperature Regulation (Chapters 68–74) Endocrinology and Reproduction (Chapters 80–84) Sports Physiology (Chapter 85) Thomas E Lohmeier, PhD Professor Emeritus of Physiology and Biophysics University of Mississippi Medical Center Jackson, Mississippi Endocrinology and Reproduction (Chapters 75–79) R Davis Manning, PhD Professor Emeritus of Physiology and Biophysics University of Mississippi Medical Center Jackson, Mississippi The Heart (Chapters 9–13) The Circulation (Chapters 20–24) v This page intentionally left blank Preface Human physiology is the discipline that links the basic sciences with clinical medicine It is integrative and encompasses the study of molecules and subcellular components, cells, tissues, and organ systems, as well as the feedback systems that coordinate these components of the body and permit us to function as living beings Because human physiology is a rapidly expanding discipline and covers a broad scope, the vast amount of information that is applicable to the practice of medicine can be overwhelming Therefore, one of our major goals for writing this Pocket Companion was to distill this enormous amount of information into a book that would be small enough to be carried in a coat pocket and used often but still contain most of the basic physiological principles necessary for the study of medicine The Pocket Companion was designed to accompany Guyton and Hall Textbook of Medical Physiology, 13th Edition, not substitute for it It is intended to serve as a concise overview of the most important facts and concepts from the parent text, presented in a manner that facilitates rapid comprehension of basic physiological principles Some of the most important features of the Pocket Companion are as follows: • It was designed to serve as a guide for students who wish to review a large volume of material from the parent text rapidly and efficiently The headings of the sections state succinctly the primary concepts in the accompanying paragraphs Thus, the student can quickly review many of the main concepts in the textbook by first studying the paragraph headings • The table of contents matches that of the parent text, and each topic has been cross-referenced with specific page numbers from the parent text The pocket companion has been updated in parallel with the Textbook of Medical Physiology, 13th edition • The size of the book has been restricted so it can fit conveniently in a coat pocket as an immediate source of information Although the Pocket Companion contains the most important facts necessary for studying physiology, it does not contain the details that enrich the physiological concepts or the clinical examples of abnormal physiology that are contained in the parent book We therefore recommend that the Pocket Companion be used in conjunction with the Textbook of Medical P hysiology, 13th Edition vii viii Preface I am grateful to each of the contributors for their careful work on this book Contributing authors were selected for their knowledge of physiology and their ability to present information effectively to students We also greatly appreciate the excellent work of Rebecca Gruliow, Elyse O’Grady, Carrie Stetz, and the entire Elsevier team for continued editorial and production excellence We have strived to make this book as accurate as possible and hope that it will be valuable for your study of physiology Your comments and suggestions for ways to improve the Pocket Companion are always greatly appreciated John E Hall, PhD Jackson, Mississippi 304 UNIT VII Respiration curve shown in Figure 41–1 demonstrates a progressive rise in the percentage of hemoglobin that is bound with oxygen as the blood Po2 increases, which is called percent saturation of the hemoglobin Note the following features in the curve: • When the Po2 is 95 mm Hg (arterial blood), the hemoglobin is about 97 percent saturated with oxygen and the oxygen content is about 19.4 ml/ dl of blood; an average of nearly four molecules of oxygen are bound to each molecule of hemoglobin • When the Po2 is 40 mm Hg (mixed venous blood), the hemoglobin is 75 percent saturated with oxygen and the oxygen content is about 14.4 ml/dl of blood; an average of three molecules of oxygen are bound to each molecule of hemoglobin • When the Po2 is 25 mm Hg (mixed venous blood during moderate exercise), the hemoglobin is 50 percent saturated with oxygen, and the oxygen content is about 10 ml/dl of blood; an average of two molecules of oxygen are bound to each molecule of hemoglobin The Sigmoid Shape of the Oxygen-Hemoglobin Disso ciation Curve Results From Stronger Binding of Oxygen to Hemoglobin as More Molecules of Oxygen Become Bound Each molecule of hemoglobin can bind four molecules of oxygen After one molecule of oxygen has bound, the affinity of hemoglobin for the second molecule is increased, and so forth Note that the affinity for oxygen is high in the lungs where the Po2 value is about 95 mm Hg (at the flat portion of the curve) and low in the peripheral tissues where the Po2 value is about 40 mm Hg (at the steep portion of the curve; see Figure 41–1) The Maximum Amount of Oxygen Transported by Hemoglobin Is About 20 Milliliters of Oxygen per 100 Milliliters of Blood In a normal person, each 100 milliliters of blood contains about 15 grams of hemoglobin, and each gram of hemoglobin can bind with about 1.34 milliliters of oxygen when it is 100 percent saturated (15 × 1.34 = 20 milliliters of oxygen per 100 milliliters of blood) However, the total quantity of oxygen bound with hemoglobin in normal arterial blood is about 97 percent, so about 19.4 milliliters of oxygen are carried in each 100 milliliters of blood The hemoglobin in venous blood leaving the peripheral tissues is about 75 percent saturated with oxygen, so the amount of oxygen transported by hemoglobin in venous blood is about 14.4 milliliters of oxygen per 100 milliliters of blood About milliliters of oxygen are therefore normally 305 Transport of Oxygen and Carbon Dioxide in Blood and Tissue Fluids 20 Hemoglobin saturation (%) 90 Oxygenated blood leaving the lungs 80 18 16 70 14 60 12 10 50 Reduced blood returning from tissues 40 30 20 10 Volumes (%) 100 0 10 20 30 40 50 60 70 80 90 100 110 120 130 140 Pressure of oxygen in blood (PO2) (mm Hg) Figure 41–1 Oxygen-hemoglobin dissociation curve transported to and used by the tissues in each 100 milliliters of blood Hemoglobin Functions to Maintain a Constant Po2 in the Tissues Although hemoglobin is necessary for the transport of oxygen to the tissues, it performs another major function essential to life as a tissue oxygen buffer system • Under basal conditions, the tissues require about milliliters of oxygen from each 100 milliliters of blood For the milliliters of oxygen to be released, the blood Po2 must fall to about 40 mm Hg The tissue Po2 normally does not rise above 40 mm Hg because the oxygen needed by the tissues at that level is not released from the hemoglobin; therefore, the hemoglobin sets the tissue Po2 level at an upper limit of about 40 mm Hg • During heavy exercise, oxygen utilization increases to as much as 20 times normal This increased utilization can be achieved with little further decrease in tissue Po2—down to a level of 15 to 25 mm Hg— because of the steep slope of the dissociation curve and the increase in tissue blood flow caused by the decreased Po2 (i.e., a small fall in Po2 causes large amounts of oxygen to be released) The Oxygen-Hemoglobin Dissociation Curve Is Shifted to the Right in Metabolically Active Tissues in Which Temperature, Pco2, and Hydrogen Ion Concentration Are Increased The oxygen-hemoglobin dissociation curve shown (see Figure 41–1) is for normal, average blood A shift in the curve to the right occurs when the affinity for oxygen is low, facilitating the unloading of oxygen from hemoglobin Note that for any given value of Po2, 306 UNIT VII Respiration the percent saturation with oxygen is low when the curve is shifted to the right The oxygen-hemoglobin dissociation curve is also shifted to the right as an adaptation to chronic hypoxemia associated with life at high altitude Chronic hypoxemia increases the synthesis of 2,3-diphosphoglycerate, a factor that binds to hemoglobin, decreasing its affinity for oxygen Carbon Monoxide Interferes With Oxygen Transport Because It Has About 250 Times More Affinity for Hemo globin Carbon monoxide combines with hemoglobin at the same point on the hemoglobin molecule as does oxygen and therefore can displace oxygen from hemoglobin Because carbon monoxide binds with about 250 times as much tenacity as oxygen, relatively small amounts of carbon monoxide can occupy a large portion of the hemoglobin binding sites, making them unavailable for oxygen transport A patient with severe carbon monoxide poisoning can be helped by the administration of pure oxygen because oxygen at high alveolar pressures displaces carbon monoxide from its combination with hemoglobin more effectively than does oxygen at low alveolar pressures TRANSPORT OF CARBON DIOXIDE IN THE BLOOD (p 534) Under Resting Conditions, About Milliliters of Carbon Dioxide Are Transported From the Tissues to the Lungs in Each 100 Milliliters of Blood Approximately 70 percent of the carbon dioxide is transported in the form of bicarbonate ions, 23 percent in combination with hemoglobin and plasma proteins, and percent in the dissolved state in the fluid of the blood • Transport in the form of bicarbonate ions (70 percent) Dissolved carbon dioxide reacts with water inside red blood cells to form carbonic acid This reaction is catalyzed in the red blood cells by the enzyme carbonic anhydrase Most of the carbonic acid immediately dissociates into bicarbonate ions and hydrogen ions; the hydrogen ions in turn combine with hemoglobin Many of the bicarbonate ions diffuse from the red blood cells into the plasma, and chloride ions diffuse into the red blood cells to maintain electrical neutrality This phenomenon is called the chloride shift • Transport in combination with hemoglobin and plasma proteins (23 percent) Carbon dioxide reacts directly with amine radicals of the hemoglobin molecules and plasma proteins to form the compound Transport of Oxygen and Carbon Dioxide in Blood and Tissue Fluids 307 carbamino-hemoglobin (HbCO2) This combination of carbon dioxide with hemoglobin is easily reversible, so the carbon dioxide is easily released into the alveoli, where the partial pressure of carbon dioxide (Pco2) is lower than that in the tissue capillaries • Transport in the dissolved state (7 percent) Only about 0.3 milliliters of carbon dioxide is transported in the form of dissolved carbon dioxide by each 100 milliliters of blood, representing about percent of all of the carbon dioxide transported in the blood CHAPTER 42 Regulation of Respiration The rate of alveolar ventilation is regulated by the nervous system to maintain the arterial blood oxygen tension (partial pressure of oxygen [Po2]) and carbon dioxide tension (partial pressure of carbon dioxide [Pco2]) at relatively constant levels under a variety of conditions This chapter describes the operation of this regulatory system RESPIRATORY CENTER (p 539) The Respiratory Centers Are Composed of Three Main Groups of Neurons • The dorsal respiratory group generates inspiratory action potentials in a steadily increasing ramplike fashion and is responsible for the basic rhythm of respiration This group is located in the distal portion of the medullae and receives input from peripheral chemoreceptors and other types of receptors by way of the vagus and glossopharyngeal nerves • The pneumotaxic center, located dorsally in the superior portion of the pons, helps control the rate and pattern of breathing It transmits inhibitory signals to the dorsal respiratory group and thus controls the filling phase of the respiratory cycle Because it limits inspiration, it has a secondary effect of increasing the respiratory rate • The ventral respiratory group, which is located in the ventrolateral part of the medulla, can cause either expiration or inspiration, depending on which neurons in the group are stimulated The ventral respiratory group is inactive during normal quiet breathing but stimulates the abdominal expiratory muscles when higher levels of respiration are required The Hering-Breuer Reflex Prevents Overinflation of the Lungs The Hering-Breuer reflex is initiated by nerve receptors located in the walls of bronchi and bronchioles When the lungs become overly inflated, the receptors send signals through the vagi into the dorsal respiratory group, which “switches off ” the inspiratory ramp and thus stops further inspiration This mechanism is called the Hering-Breuer inflation reflex 308 Regulation of Respiration 309 CHEMICAL CONTROL OF RESPIRATION (p 541) The Ultimate Goal of Respiration Is to Maintain Physiological Concentrations of Oxygen, Carbon Dioxide, and Hydrogen Ions in the Tissues Excess carbon dioxide or hydrogen ions mainly stimulate the respiratory center, causing increased strength of inspiratory and expiratory signals to the respiratory muscles Oxygen, in contrast, acts on peripheral chemoreceptors located in the carotid and aortic bodies These chemoreceptors in turn transmit appropriate nervous signals to the respiratory center for control of respiration Increased Pco2 or Hydrogen Ion Concentration Stimulates a Chemosensitive Area of the Central Respiratory Center The sensor neurons in the chemosensitive area are especially excited by hydrogen ions; however, hydrogen ions not easily cross the blood-brain barrier For this reason, changes in blood hydrogen ion concentration have little acute effect on stimulation of the chemosensitive neurons compared with carbon dioxide However, carbon dioxide is believed to stimulate these neurons secondarily by increasing the hydrogen ion concentration Carbon dioxide diffuses into the brain and reacts with water to form carbonic acid, which in turn dissociates into hydrogen ions and bicarbonate ions The hydrogen ions then have a potent direct stimulatory effect Increased Blood Carbon Dioxide Concentration Has a Potent Acute Effect but Only a Weak Chronic Effect in Stimulating the Respiratory Drive Excitation of the respiratory center by carbon dioxide is greatest during the first few hours of increased carbon dioxide tension in the blood, with the degree of excitation gradually declining during the next to days The following mechanisms cause this decline: • The kidneys facilitate return of the hydrogen ion concentration toward a normal level after the carbon dioxide first increases the hydrogen ion concentration The kidneys increase the blood bicarbonate, which binds with hydrogen ions in blood and cerebrospinal fluid, reducing their concentration • More importantly, the bicarbonate ions diffuse through the blood-brain barrier and combine directly with the hydrogen ions near the respiratory neurons PERIPHERAL CHEMORECEPTORS FUNCTION TO REGULATE ARTERIAL OXYGEN LEVELS DURING HYPOXEMIA (p 542) Oxygen Is Not Important for Direct Control of the Central Respiratory Center Changes in oxygen concentration 310 UNIT VII Respiration have virtually no direct effect on the respiratory center with regard to altering the respiratory drive, but when arterial oxygen levels decrease greatly, the body has a special mechanism for respiratory control that is located in the peripheral chemoreceptors, outside the brain respiratory center This mechanism responds when the arterial oxygen tension falls to 60 to 70 mm Hg Peripheral Chemoreceptors Detect Changes in Arterial Po2 Peripheral chemoreceptors also respond to changes in Pco2 and hydrogen ion concentration The following two types of chemoreceptors transmit nervous signals to the respiratory center to help regulate respiratory activity: • The carotid bodies are located in the bifurcations of the common carotid arteries; their afferent nerve fibers innervate the dorsal respiratory area of the medulla • The aortic bodies are located along the arch of the aorta; their afferent nerve fibers also innervate the dorsal respiratory area The Oxygen Lack Stimulus Is Often Counteracted by Decreases in Blood Pco2 and Hydrogen Ion Concentration When a person breathes air that has too little oxygen, the decrease in arterial Po2 excites the carotid and aortic chemoreceptors, thereby increasing respiration The increase in respiration leads to a decrease in both arterial Pco2 and hydrogen ion concentration These two changes severely depress the respiratory center, so the final effect of increased respiration in response to low Po2 is mostly counteracted The effect of low arterial Po2 on alveolar ventilation is far greater under some other conditions, including the following: • Pulmonary disease With pneumonia, emphysema, or other conditions that prevent adequate gas exchange through the pulmonary membrane, too little oxygen is absorbed into the arterial blood, and at the same time, the arterial Pco2 and hydrogen ion concentration remain near normal or are increased because of poor transport of carbon dioxide through the membrane • Acclimatization to low oxygen When climbers ascend a mountain over a period of days rather than a period of hours, they can withstand far lower atmospheric oxygen concentrations because the respiratory center loses about four fifths of its sensitivity to changes in arterial Pco2 and hydrogen ions, and the low oxygen can then drive the respiratory system to a much higher level of alveolar ventilation Regulation of Respiration 311 REGULATION OF RESPIRATION DURING EXERCISE (p 545) During Strenuous Exercise, the Arterial Po2, Pco2, and pH Values Remain Nearly Normal Strenuous exercise can increase oxygen consumption and carbon dioxide formation by as much as 20-fold, but alveolar ventilation ordinarily increases almost exactly in step with the higher level of metabolism through two mechanisms: • Collateral impulses The brain, upon transmitting impulses to the contracting muscles, is believed to transmit collateral nerve impulses into the brain stem to excite the respiratory center • Body movements During exercise, movements of the arms and legs are believed to increase pulmonary ventilation by exciting joint and muscle proprioceptors, which in turn transmit excitatory impulses to the respiratory center Chemical Factors Can Also Play a Role in the Control of Respiration During Exercise When a person exercises, the nervous factors usually stimulate the respiratory center by the proper amount to supply the extra oxygen needed for the exercise and to blow off the extra carbon dioxide Occasionally, however, the nervous signals are either too strong or too weak in their stimulation of the respiratory center Then, the chemical factors play a significant role in bringing about the final adjustment in respiration required to keep blood gases as normal as possible CHAPTER 43 Respiratory Insufficiency— Pathophysiology, Diagnosis, Oxygen Therapy Successful diagnosis and treatment of respiratory disorders require knowledge of the basic physiological principles of respiration and gas exchange Pulmonary disease can result from inadequate ventilation, abnormalities of gas exchange in the lungs, or transport of oxygen from the lungs to peripheral tissues METHODS FOR STUDYING RESPIRATORY ABNORMALITIES (p 549) The Most Fundamental Tests of Pulmonary Performance Are Determinations of Blood Partial Pressure of Oxygen, Partial Pressure of Carbon Dioxide, and pH It is often important to measure partial pressure of oxygen (Po2), partial pressure of carbon dioxide (Pco2), and pH rapidly to help determine appropriate therapy for persons with acute respiratory distress or acute abnormalities of acidbase balance MEASUREMENT OF MAXIMUM EXPIRATORY FLOW (p 550) A Forced Expiration Is the Simplest Test of Lung Function Figure 43–1B shows the instantaneous relationship between lung volume and expiratory air flow when a healthy person expires with as much force as possible after having inspired as much air as possible Thus, expiration begins at total lung capacity and ends at residual volume (see Figure 43–1B) The middle curve shows the maximum expiratory flow at all lung volumes in a normal person Note that the expiratory flow reaches a maximum value of more than 400 L/min at a lung volume of liters and then decreases progressively as the lung volume decreases An important aspect of the curve is that the expiratory flow reaches a maximum value beyond which the flow cannot be increased further, even with additional effort For this reason, the descending portion of the curve representing the maximum expiratory flow is said to be effort independent The Maximum Expiratory Flow Is Limited by Dynamic Compression of Airways Figure 43–1A shows the effect of pressure applied to the outsides of the alveoli and 312 Respiratory Insufficiency—Pathophysiology, Diagnosis, Oxygen Therapy 313 A Expiratory air flow (L/min) 500 400 300 200 100 B Normal Airway obstruction Constricted lungs TLC RV Lung volume (liters) Figure 43–1 A, Collapse of the respiratory passageway during a maximum expiratory effort, an effect that limits the expiratory flow rate B, Effect of two respiratory abnormalities—constricted lungs and airway obstruction—on the maximum expiratory flow-volume curve TLC, total lung capacity; RV, residual volume respiratory passageways as a result of compression of the chest cage The arrows indicate that the same amount of pressure is applied to the outsides of both the alveoli and bronchioles Not only does this pressure force air from the alveoli into the bronchioles, it also tends to collapse the bronchioles at the same time, which in turn opposes the movement of air to the exterior Once the bronchioles have become almost completely collapsed, further expiratory force can still greatly increase the alveolar pressure, but it can also increase the degree of bronchiolar collapse and airway resistance by an equal amount, thus preventing a further rise in flow Beyond a critical degree of expiratory force, a maximum expiratory flow has been reached The Maximum Expiratory Flow-Volume Curve Is Useful for Differentiating Between Obstructive and Restrictive Lung Diseases Figure 43–1B shows a normal maximum flow-volume curve, along with curves generated from patients with obstructive lung disease or restrictive (or constrictive) lung disease • Restrictive lung disease The flow-volume curve in a restrictive lung disease (e.g., interstitial fibrosis) is 314 UNIT VII Respiration characterized by low lung volumes and slightly higher than normal expiratory flow rates at each lung volume, as shown • Obstructive lung diseases The flow-volume curve in obstructive lung diseases (e.g., chronic bronchitis, emphysema, asthma) is characterized by high lung volumes and lower than normal expiratory flow rates The curve may also have a “scooped-out” appearance, as shown PATHOPHYSIOLOGY OF SPECIFIC PULMONARY ABNORMALITIES (p 551) Obstructive Lung Disease Is Characterized by Increased Resistance to Airflow and High Lung Volumes Patients with obstructive lung disease find it easier to breathe at high lung volumes because doing so increases the caliber of the airways (by increasing radial traction) and thus decreases the resistance to airflow Mechanisms of airway obstruction include the following: • The airway lumen may be partially obstructed by excessive secretions (e.g., chronic bronchitis), edema fluid, or aspiration of food or fluids • The airway wall smooth muscle may be contracted (e.g., asthma) or thickened because of inflammation and edema (e.g., asthma, bronchitis), or the mucus glands may be hypertrophied (e.g., chronic bronchitis) • Outside the airway, the destruction of lung parenchyma may decrease radial traction, causing the airways to be narrowed (e.g., emphysema) Restrictive Lung Disease Is Characterized by Low Lung Volumes Patients with restrictive lung disease find it easier to breathe at low lung volumes because it is difficult to expand the lungs Expansion of the lungs may be restricted for the following reasons: • Abnormal lung parenchyma in which excessive fibrosis increases lung elasticity (e.g., pulmonary fibrosis, silicosis, asbestosis, tuberculosis) • Pleural disorders (e.g., pneumothorax, pleural effusion) • Neuromuscular problems (e.g., polio, myasthenia gravis) Chronic Pulmonary Emphysema (p 551) The Term Pulmonary Emphysema Means Excess Air in the Lungs Chronic pulmonary emphysema signifies a complex obstructive and destructive process of the lungs and is usually a consequence of long-term smoking Respiratory Insufficiency—Pathophysiology, Diagnosis, Oxygen Therapy 315 The following pathophysiological events contribute to its development: • Airway obstruction Chronic infection, excess mucus, and inflammatory edema of the bronchiolar epithelium combine to cause chronic obstruction of many smaller airways • Destruction of alveolar walls The obstruction of the airways makes it especially difficult to expire, causing entrapment of air in the alveoli with subsequent overstretching of the alveolar walls This overstretching, combined with local inflammatory processes, can cause marked destruction of the epithelial cells lining the alveoli The Physiological Effects of Chronic Emphysema Are Extremely Varied These effects depend on the severity of the disease and the relative degree of bronchiolar obstruction versus lung parenchymal destruction Chronic emphysema usually progresses slowly over many years Emphysema has the following consequences: • Increased airway resistance This is caused by bronchiolar obstruction Expiration is especially difficult because the force on the outside of the lung compresses the bronchioles, which further increases their resistance • Decreased diffusing capacity This is caused by the marked loss of alveolar walls, which reduces the ability of the lungs to oxygenate the blood and remove carbon dioxide ˙ ) Areas • Abnormal ventilation-perfusion ratio (V˙ A /Q of the lung with bronchiolar obstruction have a very ˙ (physiological shunt), resulting in poor low V˙ A /Q aeration of blood, whereas other areas with loss of ˙ (physiological alveolar walls have a very high V˙ A /Q dead space), resulting in wasted ventilation • Increased pulmonary vascular resistance Loss of alveolar walls decreases the number of pulmonary capillaries The loss of capillaries causes the pulmonary vascular resistance to increase, which can cause pulmonary hypertension Pneumonia (p 552) The Term Pneumonia Includes Any Inflammatory Condition of the Lung in Which Alveoli Are Filled With Fluid and Blood Cells A common type of pneumonia is bacterial pneumonia, which is caused most often by pneumo cocci The infected alveoli become progressively filled 316 UNIT VII Respiration with proteinaceous transudate and cells Eventually, large areas of the lungs, sometimes whole lobes or even a whole lung, become “consolidated,” which means they are filled with fluid and cellular debris Atelectasis (p 553) Atelectasis Is a Collapse of Lung Tissue Affecting All or Part of One Lung Two common causes of atelectasis are as follows: • Airway obstruction Air trapped beyond a bronchial obstruction is absorbed, causing alveolar collapse If the lung cannot collapse, negative pressure develops in the alveoli, causing edema fluid to collect • Lack of surfactant With hyaline membrane disease (also called respiratory distress syndrome), the quantity of surfactant secreted by the alveoli is greatly diminished As a result, the surface tension of the alveolar fluid is increased, causing the lungs to collapse or become filled with fluid Asthma (p 554) Asthma Is an Obstructive Lung Disease The usual cause of asthma is hypersensitivity of bronchioles to foreign substances in the air The allergic reaction produces (1) localized edema in the walls of small bronchioles, as well as secretion of thick mucus into the bronchiolar lumens, and (2) spasm of bronchiolar smooth muscle In both instances the airway resistance increases greatly A Person With Asthma Can Usually Inspire Adequately but Has Great Difficulty Expiring Clinical measurements show a greatly reduced maximum expiratory rate in asthma, resulting in dyspnea, or “air hunger.” The functional residual capacity and residual volume of the lung are increased during the asthmatic attack because the air is difficult to expire Tuberculosis (p 554) In tuberculosis, the tubercle bacilli cause (1) macrophage invasion of the infected region and (2) walling off of the lesion by fibrous tissue to form the so-called tubercle Tuberculosis in its late stages causes many areas of fibrosis and reduces the total amount of functional lung tissue Respiratory Insufficiency—Pathophysiology, Diagnosis, Oxygen Therapy 317 HYPOXIA AND OXYGEN THERAPY (p 554) Hypoxia Can Result From Multiple Causes The following outline is a descriptive classification of the causes of hypoxia: Inadequate oxygenation of blood in normal lungs a Deficiency of oxygen in the atmosphere b Hypoventilation (e.g., in neuromuscular disorders, narcotic abuse) Pulmonary disease a Hypoventilation due to increased airway resistance or decreased pulmonary compliance ˙ b An uneven alveolar V˙ A /Q c Decreased diffusion through respiratory membranes Venous-to-arterial cardiac shunts (“right-to-left” shunts) Inadequate oxygen transport by blood to tissues a Anemia or abnormal hemoglobin b General circulatory deficiency c Localized circulatory deficiency (peripheral, cerebral, coronary vessels) d Tissue edema Inadequate capability of tissues to use oxygen a Poisoning of cellular enzymes (cyanide) b Diminished cellular metabolic capacity because of toxicity, vitamin deficiency, or other factors Oxygen Therapy in Different Types of Hypoxia (p 555) Oxygen Therapy Is of Great Value in Certain Types of Hypoxia but of Almost no Value in Others Recalling the basic physiological principles of the various types of hypoxia, one can readily decide when oxygen therapy may be of value and, if so, how valuable • Atmospheric hypoxia Oxygen therapy can correct the depressed oxygen level in inspired gases and therefore provide 100 percent effective therapy • Hypoventilation hypoxia A person breathing 100 percent oxygen can move five times more oxygen into the alveoli with each breath compared with breathing normal air Again, in the case of hypoventilation hypoxia, oxygen therapy can be extremely beneficial • Hypoxia caused by impaired alveolar membrane diffusion Essentially the same result occurs in this situation as with hypoventilation hypoxia because oxygen therapy can increase the Po2 in the lungs from a normal 318 UNIT VII Respiration value of about 100 mm Hg to as high as 600 mm Hg, thus raising the oxygen diffusion gradient • Hypoxia caused by oxygen transport deficiencies For hypoxia caused by anemia, abnormal hemoglobin transport of oxygen, circulatory deficiency, or physiological shunt, oxygen therapy is of less value because oxygen is already available in the alveoli Instead, the problem is deficient transport of oxygen to tissues Extra oxygen can be transported in the dissolved state in blood when alveolar oxygen is increased to the maximum level; this extra oxygen may be the difference between life and death • Hypoxia caused by inadequate tissue use of oxygen With this type of hypoxia, the tissue metabolic enzyme system is simply incapable of utilizing the oxygen that is delivered It is therefore doubtful that oxygen therapy can be of any measurable benefit HYPERCAPNIA (p 556) Hypercapnia Means Excess Carbon Dioxide in Body Fluids When the alveolar Pco2 rises higher than about 60 to 75 mm Hg, the person responds by breathing as rapidly and deeply as possible, and air hunger, or dyspnea, becomes severe As the Pco2 rises to 80 to 100 mm Hg, the person becomes lethargic and sometimes even semicomatose Cyanosis Means Bluish Skin Cyanosis is caused by deoxygenated hemoglobin in the skin blood vessels, especially capillaries This deoxygenated hemoglobin is dark blue–purple In general, definite cyanosis appears whenever the arterial blood contains more than grams of deoxygenated hemoglobin in each 100 milliliters of blood A person with anemia almost never becomes cyanotic because there is not enough hemoglobin for grams of it to be deoxygenated in the arterial blood By comparison, in a person with excess red blood cells (polycythemia), the great excess of available hemoglobin often leads to cyanosis, even under otherwise normal conditions ... key concepts in physiology and pathophysiology Pocket Companion to Guyton and Hall Textbook of Medical Physiology, 13 th Edition John E Hall, PhD 978 -1- 4557-7006-9 Guyton and Hall Physiology Review,... Guyton and Hall Textbook of Medical Physiology, 13 e, or request these supporting materials at: http://evolve.elsevier.com /Hall1 3 Pocket Companion to Guyton and Hall Textbook of Medical Physiology. .. means GUYTON AND HALL The world’s foremost medical physiology resources Guyton and Hall Textbook of Medical Physiology, 13 th Edition John E Hall, PhD 978 -1- 4557-7005-2 Unlike other physiology textbooks,