HAP 12e Ch 22 The Respiratory System PDF

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This document is a chapter on the respiratory system from a human anatomy and physiology textbook. It covers the different parts of the respiratory system, including the upper and lower respiratory systems, major organs, functions and more. It also includes diagrams and tables.

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Marieb Human Anatomy & Physiology Twelfth Edition Chapter 22 The Respiratory System PowerPoint® Lecture Slides prepared by Justin A. Moore,...

Marieb Human Anatomy & Physiology Twelfth Edition Chapter 22 The Respiratory System PowerPoint® Lecture Slides prepared by Justin A. Moore, American River College Copyright © 2025 Pearson Education, Inc. All Rights Reserved Respiratory System (1 of 2) Our bodies continuously absorb oxygen and nutrients, and excrete carbon dioxide and other wastes into the external environment Major function of respiratory system is gas exchange: supply cells with O2 dispose of CO2 from, cellular respiration To do this, respiratory and cardiovascular systems work together to carry out four processes collectively called respiration – Respiratory system responsible for: 1. Pulmonary ventilation, or breathing (moving air in and out of lungs) 2. Pulmonary gas exchange (of O2 and CO2 between lungs and blood) Copyright © 2025 Pearson Education, Inc. All Rights Reserved Respiratory System (2 of 2) – Cardiovascular system responsible for: 3. Transport of respiratory gases ( O2 and CO2 in blood) 4. Tissue gas exchange (of O2 and CO2 between blood and tissues) Also functions in olfaction and speech (because it moves air) Copyright © 2025 Pearson Education, Inc. All Rights Reserved Respiration Consists of Four Processes Figure 22.1 Respiration consists of four processes. Copyright © 2025 Pearson Education, Inc. All Rights Reserved BioFlix Video: Gas Exchange Click here to view ADA compliant Animation: Gas Exchange https://mediaplayer.pearsoncmg.com/assets/gMkhizjcFfow76d8E7_kC9ZIQ2UM8TeH Copyright © 2025 Pearson Education, Inc. All Rights Reserved Part 1 Functional Anatomy Major organs – Upper respiratory system ▪ Nose and paranasal sinuses ▪ Pharynx – Lower respiratory system ▪ Larynx ▪ Trachea ▪ Bronchi and their smaller branches ▪ Lungs and alveoli Respiratory muscles classified as part of muscular system Copyright © 2025 Pearson Education, Inc. All Rights Reserved The Major Respiratory Organs in Relation to Surrounding Structures Figure 22.2 The major respiratory organs in relation to surrounding structures. Copyright © 2025 Pearson Education, Inc. All Rights Reserved Table 22.1 The Upper Respiratory System Structure Description, General and Distinctive Function Features Nose Jutting external portion is supported by bone Produces mucus; filters, warms, (external and cartilage. Internal nasal cavity is divided by and moistens incoming air; nose and midline nasal septum and lined with mucosa. resonance chamber for speech nasal cavity) Roof of nasal cavity contains olfactory Receptors for sense of smell epithelium. Paranasal Mucosa-lined, air-filled cavities in cranial bones Lighten skull; may also warm, sinuses surrounding nasal cavity ( p. 215). Leftward arrow moisten, and filter incoming air Pharynx Passageway connecting nasal cavity to larynx Passageway for air and food and oral cavity to esophagus. Three Facilitates exposure of immune subdivisions: nasopharynx, oropharynx, and system to inhaled antigens laryngopharynx. Houses tonsils (lymphoid tissue masses involved in protection against pathogens). Copyright © 2025 Pearson Education, Inc. All Rights Reserved Table 22.2 The Lower Respiratory System Structure Description, General and Distinctive Features Function Blank Larynx Connects pharynx to trachea. Has framework of cartilage Air passageway; prevents food from and dense connective tissue. Open glottis can be closed by entering lower respiratory tract epiglottis or vocal folds. Voice production Larynx connected to the hyoid bone superiorly, in an anterior view. Houses vocal folds (true vocal cords). Trachea Flexible tube running from larynx and dividing inferiorly into Air passageway; cleans, warms, and two main bronchi. Walls contain C-shaped cartilages that moistens incoming air are incomplete posteriorly where connected by trachealis. Trachea Bronchial tree Consists of right and left main bronchi, which subdivide Air passageways connecting trachea within the lungs to form lobar and segmental bronchi and with alveoli; cleans, warms, and Left and right bronchial tree. bronchioles. Bronchiolar walls lack cartilage but contain a moistens incoming air complete layer of smooth muscle. Constriction of this muscle impedes expiration. Alveoli Microscopic chambers at termini of bronchial tree. Walls of Main sites of gas exchange simple squamous epithelium overlie thin basement membrane. External surfaces are intimately associated Surfactant reduces surface tension; Alveol with pulmonary capillaries. helps prevent alveolar collapse Special alveolar cells produce surfactant. Lungs Paired composite organs that flank mediastinum in thorax. House respiratory passages smaller Composed primarily of alveoli and respiratory than the main bronchi passageways. Stroma is elastic connective tissue, allowing Left and right lung. lungs to recoil passively during expiration. Pleurae Serous membranes. Parietal pleura lines thoracic cavity; Produce lubricating fluid and Blank visceral pleura covers external lung surfaces. compartmentalize lungs Copyright © 2025 Pearson Education, Inc. All Rights Reserved 22.1 The Upper Respiratory System Warms, Humidifies, and Filters Air Copyright © 2025 Pearson Education, Inc. All Rights Reserved The Nose and Paranasal Sinuses (1 of 3) Nose only externally visible part of respiratory system Functions of nose – Provides an airway for respiration – Moistens and warms entering air – Filters and cleans inspired air – Serves as resonating chamber for speech – Houses olfactory receptors Divided into two regions: external nose and nasal cavity Copyright © 2025 Pearson Education, Inc. All Rights Reserved The External Nose Figure 22.3 The external nose. Copyright © 2025 Pearson Education, Inc. All Rights Reserved The Nose and Paranasal Sinuses (2 of 3) Nasal cavity – Found within and posterior to external nose – Divided by midline nasal septum – Posterior nasal apertures (choanae): openings that allow air to pass posteriorly from nasal cavity into nasopharynx – Floor formed by the palate (separates oral cavity below) ▪ Hard palate (bone) ▪ Soft palate (muscle) Copyright © 2025 Pearson Education, Inc. All Rights Reserved The Nose and Paranasal Sinuses (3 of 3) – Nasal conchae protrude medially from lateral walls of nasal cavity ▪ Shape increases mucosal area exposed to air and enhances turbulent airflow – More air particles get trapped in mucus (better cleaning) ▪ During inhalation, conchae and nasal mucosa filter, heat, and moisten air – During exhalation they reclaim most of the heat and moisture Paranasal sinuses – The paranasal sinuses (in the frontal, sphenoid, ethmoid, and maxillary bones) surround and connect with the nasal cavity – Functions include: ▪ Lighten skull; may help warm and moisten air ▪ Secrete mucus, flows into nasal cavity – Blowing nose creates suction to help drain sinuses Copyright © 2025 Pearson Education, Inc. All Rights Reserved Paranasal Sinuses Copyright © 2025 Pearson Education, Inc. All Rights Reserved The Nasal Cavity Figure 22.4 The nasal cavity. Copyright © 2025 Pearson Education, Inc. All Rights Reserved Clinical—Homeostatic Imbalance 22.1 Rhinitis – Inflammation of nasal mucosa ▪ Excessive mucus production, nasal congestion, postnasal drip – Nasal mucosa lines first part of respiratory tract, so infections spread from nose to throat to chest ▪ May spread to tear ducts and paranasal sinuses, causing inflammation (sinusitis) ▪ Air pressure in blocked sinus has difficulty equalizing with atmospheric pressure; can cause sinus headache Copyright © 2025 Pearson Education, Inc. All Rights Reserved The Pharynx Funnel-shaped pharynx is commonly called the throat – Connects nasal cavity to larynx, and mouth to esophagus – Wall contains skeletal muscle along its length, from base of skull to vertebra C6 – Divided into three regions: nasopharynx, oropharynx, and laryngopharynx Copyright © 2025 Pearson Education, Inc. All Rights Reserved The Pharynx, Larynx, and Upper Trachea (1 of 2) Figure 22.5a The pharynx, larynx, and upper trachea. Copyright © 2025 Pearson Education, Inc. All Rights Reserved Clinical—Homeostatic Imbalance 22.2 Infected and swollen adenoids can block air passage in nasopharynx, making it necessary to breathe through the mouth – Air is not properly moistened, warmed, or filtered before reaching lungs When chronically enlarged, adenoids may disrupt both speech and sleep Copyright © 2025 Pearson Education, Inc. All Rights Reserved The Pharynx (3 of 3) Oropharynx is posterior to, and continuous with, the oral cavity – Passageway for food and air from level of soft palate to epiglottis ▪ Lined with protective stratified squamous epithelium – Palatine tonsils located in lateral walls, posterior to oral cavity – Lingual tonsil covers posterior surface of tongue Laryngopharynx is directly posterior to the larynx – Also, a passageway for food and air; also lined with stratified squamous epithelium – Extends to bottom of larynx, where it is continuous with esophagus ▪ If swallowing, food has “right of way” and airflow temporarily stops Copyright © 2025 Pearson Education, Inc. All Rights Reserved The Pharynx, Larynx, and Upper Trachea (2 of 2) Figure 22.5b The pharynx, larynx, and upper trachea. Copyright © 2025 Pearson Education, Inc. All Rights Reserved 22.2 The Lower Respiratory System Consists of Conducting and Respiratory Zone Structures Anatomically, lower respiratory system divided into: – Larynx, trachea, bronchi, and lungs Functionally, respiratory system divided into: – Respiratory zone ▪ Sites of gas exchange (all microscopic structures) ▪ Consists of respiratory bronchioles, alveolar ducts, and alveoli – Conducting zone ▪ Consists of all other airways, from nose to respiratory bronchioles ▪ Functions: – Conduits that transport air to and from sites of gas exchange – Cleanse, warm, and humify incoming air Copyright © 2025 Pearson Education, Inc. All Rights Reserved The Larynx – Larynx (voice box) extends from vertebra C3 to C6 and attaches to the hyoid bone – Three functions: 1. Provides patent (open) airway 2. Routes air and food into proper channels 3. Voice production (houses vocal folds) Epiglottis (elastic cartilage) Covers laryngeal inlet during swallowing as larynx is pulled superiorly Covered in taste bud–containing mucosa Copyright © 2025 Pearson Education, Inc. All Rights Reserved The Larynx (3 of 6) Figure 22.6 The larynx. Copyright © 2025 Pearson Education, Inc. All Rights Reserved Movements of the Vocal Folds Figure 22.7 Movements of the vocal folds. Vocal folds Form core of mucosal folds called vocal folds, or true vocal cords Vibrate to produce sound as air passes through during expiration Opening between vocal folds called glottis Copyright © 2025 Pearson Education, Inc. All Rights Reserved The Larynx Voice production – Speech: intermittent release of expired air during opening and closing of glottis – Pitch determined by length and tension of vocal folds (tenser folds vibrate faster to produce higher pitch) – Loudness depends upon force of airflow vibrating folds – Pharynx and oral, nasal, and sinus cavities act as resonating chambers ▪ Amplify and enhance sound quality – Sound “shaped” into language by muscles of pharynx, tongue, soft palate, and lips Copyright © 2025 Pearson Education, Inc. All Rights Reserved Clinical—Homeostatic Imbalance 22.3 Laryngitis: inflammation of vocal folds – Vocal folds swell, interfering with vibrations ▪ Changes vocal tone, causing hoarseness ▪ In severe cases, speaking limited to a whisper – Most often caused by viral infections ▪ Can also result from overuse of the voice, very dry air, bacterial infections, tumors on the vocal folds, or inhalation of irritating chemicals Copyright © 2025 Pearson Education, Inc. All Rights Reserved The Trachea Trachea (windpipe) descends from larynx into mediastinum, dividing into main bronchi – It is about 4 inches long, and very flexible Trachealis muscle (smooth muscle) connects posterior parts of cartilage rings – Contracts during cough to constrict trachea, raises airflow speed to expel mucus Last tracheal cartilage (carina) marks point where trachea branches into main bronchi – Mucosa highly sensitive, violent coughing triggered if contacted by foreign object Copyright © 2025 Pearson Education, Inc. All Rights Reserved Tissue Composition of the Tracheal Wall (1 of 2) Figure 22.8 Tissue composition of the tracheal wall. Copyright © 2025 Pearson Education, Inc. All Rights Reserved Tissue Composition of the Tracheal Wall (2 of 2) Figure 22.8c Tissue composition of the tracheal wall. Copyright © 2025 Pearson Education, Inc. All Rights Reserved Clinical—Homeostatic Imbalance 22.4 Smoking inhibits and ultimately destroys cilia Without ciliary activity, coughing only way to prevent mucus accumulation in lungs When person stops smoking, ciliary function usually recovers within a few weeks – “Smoker’s cough” subsides once ciliary function restored Copyright © 2025 Pearson Education, Inc. All Rights Reserved Clinical—Homeostatic Imbalance 22.5 Tracheal obstruction is life threatening: many people have suffocated after choking on a piece of food that suddenly closed off their trachea Heimlich maneuver: procedure in which air in victim’s lungs is used to “pop out,” or expel, an obstructing piece of food Maneuver is simple to learn and easy to do but is best learned by demonstration; when done incorrectly, may lead to cracked ribs Copyright © 2025 Pearson Education, Inc. All Rights Reserved The Bronchi and Subdivisions Airways undergo about 23 generations of branching, forming bronchial tree – At tips of tree conducting zone structures give rise to respiratory zone structures Conducting zone structures – Trachea divides into right and left main (primary) bronchi, one for each lung ▪ Enter lung at hilum ▪ Right is wider, shorter, and more vertical than left – Each primary branches into lobar (secondary) bronchi, one for each lobe ▪ Three in right lung, two in left – Secondary branch into segmental (tertiary) bronchi ▪ Divide repeatedly into smaller and smaller branches; less than 1 m m in diameter called bronchioles – Terminal bronchioles are less than 0.5 mm in diameter Respiratory zone structures Begin where terminal bronchioles feed into respiratory bronchioles, which lead into alveolar ducts and finally into alveolar sacs (saccules) Alveolar sacs contain clusters of alveoli (sites of gas exchange) - ~ 300 million alveoli Copyright © 2025 Pearson Education, Inc. All Rights Reserved Conducting Zone Passages Figure 22.9 Conducting zone passages. Copyright © 2025 Pearson Education, Inc. All Rights Reserved Respiratory Zone Structures Figure 22.10a Respiratory zone structures. Copyright © 2025 Pearson Education, Inc. All Rights Reserved Respiratory Zone Structures Figure 22.10b Respiratory zone structures. Copyright © 2025 Pearson Education, Inc. All Rights Reserved The Bronchi and Subdivisions – The respiratory membrane is extremely thin ( 0.5 m) ▪ Blood air barrier allowing gas exchange by simple diffusion ▪ Consists of alveolar and capillary walls with a shared basement membrane – Alveolar wall made of a simple squamous epithelium ( type I alveolar cells) ▪ Scattered cuboidal type II alveolar cells secrete surfactant and antimicrobial proteins along inner surface ▪ Mobile alveolar macrophages keep inner surfaces clean and sterile, consuming bacteria and other debris – 2 million macrophages/hour carried by cilia to throat and swallowed – Alveoli surrounded by fine elastic fibers and dense network of pulmonary capillaries – Alveolar pores connect adjacent alveoli ▪ Equalize air pressure throughout lungs ▪ Provide alternate routes in case of airway blockages Copyright © 2025 Pearson Education, Inc. All Rights Reserved Alveoli and the Respiratory Membrane (1 of 2) Figure 22.11 Alveoli and the respiratory membrane. Copyright © 2025 Pearson Education, Inc. All Rights Reserved Alveoli and the Respiratory Membrane (2 of 2) Figure 22.11c Alveoli and the respiratory membrane. Copyright © 2025 Pearson Education, Inc. All Rights Reserved IP Anatomy Review Animation: Respiratory Click here to view ADA compliant Animation: IP Anatomy Review Animation: Respiratory https://mediaplayer.pearsoncmg.com/assets/secs-ipweb-respiratory-anat-rev Copyright © 2025 Pearson Education, Inc. All Rights Reserved Gross Anatomy of the Lungs (1 of 2) Lungs occupy all of the thoracic cavity except for mediastinum Each surrounded by pleurae and connected to mediastinum by lung root (vascular and bronchial attachments); features include: – Costal surface: anterior, lateral, and posterior surfaces deep to ribs – Apex: superior tip, deep to clavicle – Base: inferior surface that rests on diaphragm – Hilum: at mediastinal surface; entry/exit point for blood vessels, nerves, bronchi, and lymphatic vessels Copyright © 2025 Pearson Education, Inc. All Rights Reserved Anatomical Relationships of Organs in the Thoracic Cavity Figure 22.12 Anatomical relationships of organs in the thoracic cavity. Copyright © 2025 Pearson Education, Inc. All Rights Reserved Anatomical Relationships of Organs in the Thoracic Cavity (2 of 3) Figure 22.12c Anatomical relationships of organs in the thoracic cavity. Copyright © 2025 Pearson Education, Inc. All Rights Reserved A Cast of the Bronchial Tree Figure 22.13 A cast of the bronchial tree. Copyright © 2025 Pearson Education, Inc. All Rights Reserved Blood Supply and Innervation of the Lungs (1 of 2) Lungs perfused by two circulations that differ in size, origin, and function – Pulmonary circulation of the lungs ▪ Pulmonary arteries carry systemic venous blood from heart to lungs for oxygenation – Branch extensively, leading into pulmonary capillary networks that surround alveoli ▪ Pulmonary veins carry oxygenated blood from alveoli back to heart ▪ Low-pressure, high-volume system – Entire blood volume passes through each minute – Capillary endothelium perfect place to house enzymes that act on blood E.g., angiotensin-converting enzyme (ACE) activates important blood pressure hormone (Angiotensin II) Copyright © 2025 Pearson Education, Inc. All Rights Reserved Blood Supply and Innervation of the Lungs (2 of 2) – Bronchial circulation ▪ Bronchial arteries provide oxygenated blood to lung tissue – Arise from aorta and enter lungs at hilum – Part of systemic circulation – Supply all lung tissue except alveoli ▪ Tiny bronchial veins anastomose with pulmonary veins – Pulmonary veins carry most venous blood back to heart Innervation of the lungs – By parasympathetic and sympathetic fibers, as well as visceral sensory fibers ▪ Parasympathetic fibers cause bronchoconstriction ▪ Sympathetic fibers cause bronchodilation Copyright © 2025 Pearson Education, Inc. All Rights Reserved The Pleurae Pleurae: thin, double-layered serosal (serous) membrane that divides thoracic cavity into two pleural compartments and a central mediastinum – Parietal pleura: layer that lines inner surface of thoracic wall and superior face of diaphragm; continues inward to form lateral mediastinal walls – Visceral pleura: layer that lines external lung surface, dipping into fissures Pleural fluid fills slitlike pleural cavity – Provides lubrication as visceral and parietal pleurae slide past each other – Provides surface tension that resists separation of pleurae ▪ Helps keep lungs (visceral pleura) connected to thoracic wall and diaphragm (parietal pleura) Copyright © 2025 Pearson Education, Inc. All Rights Reserved Anatomical Relationships of Organs in the Thoracic Cavity (3 of 3) Figure 22.12c Anatomical relationships of organs in the thoracic cavity. Copyright © 2025 Pearson Education, Inc. All Rights Reserved Clinical—Homeostatic Imbalance 22.6 Pleurisy: inflammation of pleurae (often from pneumonia) – Inflamed pleurae become rough, causes friction and stabbing pain with each breath – As it progresses, pleurae may produce excessive amounts of (protective) fluid, which may exert pressure on the lungs (hindering breathing) Other fluids that may accumulate in pleural cavity – Blood leaked from damaged blood vessels – Capillary filtrate when left-sided heart failure occurs Fluid accumulation in pleural cavity called pleural effusion Copyright © 2025 Pearson Education, Inc. All Rights Reserved Part 2—Respiratory Physiology Copyright © 2025 Pearson Education, Inc. All Rights Reserved 22.4 Volume Changes Cause Pressure Changes, Which Cause Air to Move Pulmonary ventilation (breathing) consists of two phases: – Inspiration: period of air (gas) flow into lungs – Expiration: period of air (gas) flow out of lungs Copyright © 2025 Pearson Education, Inc. All Rights Reserved Pressure Relationships in the Thoracic Cavity Atmospheric pressure (Patm ) – Pressure exerted by air (gases) surrounding the body – At sea level, Patm 760 mm Hg (or 1 atmosphere) Respiratory pressures always described relative to Patm – Negative respiratory pressures are less than Patm – Positive respiratory pressures are greater than Patm – Zero respiratory pressure Patm Copyright © 2025 Pearson Education, Inc. All Rights Reserved Pressure Relationships in the Thoracic Cavity Intrapulmonary pressure (Ppul ), also called intra-alveolar, is the pressure in the alveoli – Fluctuates during breathing, but equalizes with Patm to end each phase of breathing—inspiration and expiration Copyright © 2025 Pearson Education, Inc. All Rights Reserved Pressure Relationships in the Thoracic Cavity Intrapleural pressure (Pip ) is the pressure in pleural cavity – Fluctuates with breathing, but always negative ( Patm ); 4 mm Hg less than Ppul ▪ Kept negative as opposing forces try to pull visceral and parietal pleurae apart – Surface tension of pleural fluid helps secure layers of pleura together ▪ Fluid level must be kept at a minimum, excess removed by lymphatic system – If fluid accumulates, positive Pip pressure develops Copyright © 2025 Pearson Education, Inc. All Rights Reserved Pressure Relationships in the Thoracic Cavity Transpulmonary pressure is the difference between the intrapulmonary and intrapleural pressures (Ppul  Pip ) – Pressure that keeps lung spaces open (prevents collapsing) ▪ Size of transpulmonary pressure determines size of lungs (more pressure causes greater lung expansion) – Any condition allowing P to equalize with Ppul (or Patm ) will cause ip lung collapse ▪ Negative Pip must be maintained to keep lungs inflated Copyright © 2025 Pearson Education, Inc. All Rights Reserved Intrapulmonary and Intrapleural Pressure Relationships Figure 22.14 Intrapulmonary and intrapleural pressure relationships. Copyright © 2025 Pearson Education, Inc. All Rights Reserved Pneumothorax (Air in pleural cavity ) Figure 22.15 Pneumothorax. Copyright © 2025 Pearson Education, Inc. All Rights Reserved Clinical—Homeostatic Imbalance 22.7 Atelectasis (lung collapse) can result from: – Plugged bronchioles, which cause collapse of alveoli (as trapped air is absorbed) – Pneumothorax, air in pleural cavity ▪ Can occur from either wound in parietal pleura or rupture of visceral pleura ▪ Treated by removing air with chest tubes ▪ Allows pleurae to heal and regain normal function (keeping lungs inflated) Copyright © 2025 Pearson Education, Inc. All Rights Reserved Pulmonary Ventilation Consists of inspiration and expiration; mechanical process that requires volume changes – Volume changes lead to pressure changes, and pressure changes lead to the flow of gases to equalize the pressure Boyle’s law: relationship between pressure and volume of a gas – Gases always fill their container ▪ If container volume is reduced, gas molecules will be forced closer together and the pressure rises (if volume is increased, pressure falls) – pressure (P) varies inversely with volume (V) ▪ Mathematically: PV 1 1 P2V2 Copyright © 2025 Pearson Education, Inc. All Rights Reserved IP2: Boyle’s Law and Respiratory Pressures Click here to view ADA compliant Animation: Boyle's Law and Respiratory Pressures https://mediaplayer.pearsoncmg.com/assets/sci-ip2-pv-boyles-law-and-re spiratory-pressures Copyright © 2025 Pearson Education, Inc. All Rights Reserved Pulmonary Ventilation (2 of 4) Inspiration – Active process involving inspiratory muscles (diaphragm, external intercostals) ▪ Action of the diaphragm increases height of thoracic cavity (thus volume) – Dome-shaped diaphragm moves inferiorly and flattens out as it contracts ▪ Action of intercostal muscles increase diameter of thorax (thus volume) – Pull ribs up and out, like raising a bucket handle Copyright © 2025 Pearson Education, Inc. All Rights Reserved The Mechanics of Breathing at Rest (1 of 2) Focus Figure 22.1 The Mechanics of Breathing at Rest Copyright © 2025 Pearson Education, Inc. All Rights Reserved IP2: Breathing Cycles and Muscles Click here to view ADA compliant Animation: Breathing Cycles and Muscles https://mediaplayer.pearsoncmg.com/assets/sci-ip2-pv-breathing-cycle-and-muscles Copyright © 2025 Pearson Education, Inc. All Rights Reserved The Mechanics of Breathing at Rest (2 of 2) Focus Figure 22.1 The Mechanics of Breathing at Rest Copyright © 2025 Pearson Education, Inc. All Rights Reserved Changes in Intrapulmonary and Intrapleural Pressures During Inspiration and Expiration Figure 22.16 Changes in intrapulmonary and intrapleural pressures during inspiration and expiration. Copyright © 2025 Pearson Education, Inc. All Rights Reserved Physical Factors Influencing Pulmonary Ventilation Airway resistance, alveolar surface tension, and lung compliance influence the ease (or work) of ventilation, and therefore the amount of energy required Airway resistance – Friction is the major nonelastic source of resistance to gas flow in airways – Flow (F) is directly proportional to the difference in pressures (Ppul  Patm ), or pressure gradient ( P), and inversely proportional to airway resistance (R): P F R ▪ P ~ 1– 2 mm Hg during normal quiet breathing, enough to move 500 ml of air Copyright © 2025 Pearson Education, Inc. All Rights Reserved Physical Factors Influencing Pulmonary Ventilation – Resistance in respiratory tree usually insignificant for two reasons: 1. Conducting zone airways have huge diameters (relative to low air viscosity) 2. All the bronchioles running in parallel (creates huge cross-sectional area) – Greatest resistance in medium-sized bronchi – At terminal bronchioles flow stops and diffusion of gases takes over Copyright © 2025 Pearson Education, Inc. All Rights Reserved Resistance in Respiratory Passageways Figure 22.17 Resistance in respiratory passageways. Copyright © 2025 Pearson Education, Inc. All Rights Reserved Clinical—Homeostatic Imbalance 22.8 Whenever airway resistance rises, breathing movements become more strenuous Severe constriction or obstruction of bronchioles can prevent life-sustaining ventilation – During acute asthma attack, bronchoconstriction may be severe enough to stop ventilation Epinephrine dilates bronchioles, reducing resistance to airflow Copyright © 2025 Pearson Education, Inc. All Rights Reserved Physical Factors Influencing Pulmonary Ventilation Alveolar surface tension – At gas-liquid interface, liquid molecules are more strongly attracted to each other than to gas molecules, producing surface tension ▪ Tends to draw liquid molecules closer together ▪ Resists any force that tends to increase surface area of liquid – Water, which has very high surface tension, lines alveolar walls in a thin film ▪ Tends to shrink (collapse) alveoli to smallest size – Type II alveolar cells secrete surfactant (detergent-like complex of lipids and proteins) ▪ Lessens surface tension of alveolar fluid to prevents alveolar collapse and reduce work of lung inflation Copyright © 2025 Pearson Education, Inc. All Rights Reserved Clinical—Homeostatic Imbalance 22.9 Lack of surfactant causes infant respiratory distress syndrome (IRDS) – Alveoli collapse after each breath due to excessive surface tension ▪ Lots of energy used to reinflated lungs each inspiration – Common in premature babies ▪ Fetal lungs don’t produce enough surfactant until last two months of development Treatment: – Spray natural or synthetic surfactant into newborn’s airways – Positive pressure devices can help to keep alveoli open between breaths – Severe cases may require mechanical ventilation ▪ Can cause bronchopulmonary dysplasia in IRDS survivors (a chronic lung disease that begins in childhood) Copyright © 2025 Pearson Education, Inc. All Rights Reserved Pulmonary Volumes Four pulmonary (lung) volumes of interest – Tidal volume (TV): amount of air moved into and out of lung with each breath ▪ Averages 500 ml at rest – Inspiratory reserve volume (IRV): amount of air that can be forcibly inspired beyond a tidal volume inspiration ▪ 2100–3200 ml – Expiratory reserve volume (ERV): amount of air that can be forcibly expired beyond a tidal volume expiration ▪ 1000–1200 ml – Residual volume (RV): amount of air that always remains in lungs; keeps alveoli open (prevents collapse) ▪ ~ 1200 ml Copyright © 2025 Pearson Education, Inc. All Rights Reserved Pulmonary Volumes and Capacities Figure 22.18a Pulmonary volumes and capacities. Copyright © 2025 Pearson Education, Inc. All Rights Reserved Dead Space Anatomical dead space – Volume of inspired air filling the conducting zone airways (does not contribute to gas exchange) – ~ 150ml (out of 500 ml TV) Alveolar dead space – Volume of inspired air occupying nonfunctional alveoli – Can be due to collapse or obstruction by mucus Sum of these unusable volumes = total dead space Copyright © 2025 Pearson Education, Inc. All Rights Reserved Pulmonary Function Tests Spirometry can distinguish between (not diagnose): – Obstructive pulmonary diseases: increased airway resistance (e.g., bronchitis) – Restrictive diseases: e.g., tuberculosis or exposure to environmental agents (e.g., fibrosis) Pulmonary functions tests also assess the rate at which air is moved – Forced vital capacity (FVC): amount of gas forcibly expelled, as quickly as possible, after a maximal inspiration (with fully inflated lungs) – Forced expiratory volume (FEV): amount of gas expelled during specific time interval of FVC; e.g., FEV1 is amount of air expelled in the first second ▪ Normal is 80% of FVC for healthy lungs; patients with: – Obstructive disease exhale less than 80% Copyright © 2025 Pearson Education, Inc. All Rights Reserved Alveolar Ventilation Minute ventilation: amount of air (gas) flowing in/out of respiratory tract each minute – 12 breaths per min (frequency) 0.5 L per breath (TV) = 6 L/min at rest ▪ Up to 200 L/min during exercise – Poor estimate of respiratory efficiency since it includes air filling conducting zone Alveolar ventilation (AV): amount of air flowing in/out of respiratory zone each minute – This is site of gas exchange, so AV is a good measure of effective ventilation ▪ AV takes dead space into account; it can be calculated as follows: AV  frequency  (TV  dead space) (ml/min) (breaths / min) (ml / breath) Because dead space in an individual is constant, AV is affected by TV and frequency Large increases in AV are brought about by increasing TV more than frequency – In contrast, rapid, shallow breathing (panting) dramatically reduces AV; and as TV approaches the dead space value, effective ventilation approaches zero Copyright © 2025 Pearson Education, Inc. All Rights Reserved Effects of Breathing Rate and Depth on Alveolar Ventilation of Three Hypothetical Patients Table 22.3 Effects of Breathing Rate and Depth on Alveolar Ventilation of Three Hypothetical Patients. Breathing Dead Tidal Respirator Minute Alveolar % Effective Pattern of Space Volume y Rate* Ventilation (MV) Ventilation Ventilation Hypothetical Volume (TV) (AV) (A V/M V) Patient (AV /MV) —Normal 150 ml 500 ml 20/min 10,000 ml/min 7000 ml/min 70% I and depth Roman numeral 1 rate —Slow, Roman numeral 2 150 ml 1000 ml 10/min 10,000 ml/min 8500 ml/min 85% deep II breathing —Rapid, 150 ml 250 ml 40/min 10,000 ml/min 4000 ml/min 40% III Roman numeral 3 shallow breathing *Respiratory rate values are artificially adjusted to provide equivalent minute ventilation as a baseline for comparing alveolar ventilation. Copyright © 2025 Pearson Education, Inc. All Rights Reserved Clinical—Homeostatic Imbalance 22.12 Breathing O2 gas at 2 atm is not a problem for short periods; however, oxygen toxicity develops rapidly when PO is greater than 2.5–3 atm 2 Excessively high O2 concentrations generate huge amounts of harmful free radicals Results in CNS disturbances, coma, and even death Copyright © 2025 Pearson Education, Inc. All Rights Reserved Clinical—Homeostatic Imbalance 22.13 Effective thickness of respiratory membrane increases dramatically if the lungs become waterlogged and edematous – Seen in pneumonia or left heart failure (pulmonary congestion) – The 0.75 seconds that red blood cells spend in transit through pulmonary capillaries may not be enough for adequate gas exchange ▪ Tissues may suffer from oxygen deprivation Copyright © 2025 Pearson Education, Inc. All Rights Reserved Clinical—Homeostatic Imbalance 22.14 Certain pulmonary diseases drastically reduce alveolar surface area – In emphysema, walls of adjacent alveoli break down, and alveolar chambers enlarge Tumors, mucus, or inflammatory material can reduce surface area by blocking gas flow into alveoli Copyright © 2025 Pearson Education, Inc. All Rights Reserved Tissue Changes in Emphysema Figure 22.21 Tissue changes in emphysema. Copyright © 2025 Pearson Education, Inc. All Rights Reserved Pulmonary Gas Exchange Ventilation-perfusion coupling – Ventilation (amount of gas reaching alveoli) and perfusion (amount of blood flowing through pulmonary capillaries) must be coupled for optimal, efficient gas exchange – Both controlled by local autoregulatory mechanisms ▪ Alveolar PO (Partial pressure of oxygen in blood) controls 2 perfusion by changing arteriolar diameter ▪ Alveolar PCO (Partial pressure of carbon dioxide in blood) 2 diameter controls ventilation by changing bronchiolar diameter Copyright © 2025 Pearson Education, Inc. All Rights Reserved Pulmonary Gas Exchange – Influence of local PO on perfusion 2 ▪ Changes in local alveolar PO cause changes in diameters 2 of local arterioles ▪ Directs blood to go to well ventilated alveoli, where O2 is high (and CO2 is low), so blood can pick up more oxygen (and remove more CO2 ) ▪ Opposite mechanism seen in systemic arterioles that dilate when oxygen is low and constrict when high Copyright © 2025 Pearson Education, Inc. All Rights Reserved Pulmonary Gas Exchange – Influence of local PCO on perfusion 2 ▪ Changes in local alveolar PCO cause changes in diameters 2 of local bronchioles – Where alveolar PCO is high, bronchioles dilate to 2 increase alveolar ventilation (allows elimination of CO2 more rapidly) – Where alveolar PCO is low, bronchioles constrict 2 – Balancing ventilation and perfusion ▪ Poor alveolar ventilation results in low alveolar PO (high PCO ), 2 2 causing pulmonary arterioles serving these alveoli to constrict (bronchioles dilate) Copyright © 2025 Pearson Education, Inc. All Rights Reserved Ventilation-Perfusion Coupling Figure 22.22 Ventilation-perfusion coupling. Copyright © 2025 Pearson Education, Inc. All Rights Reserved Tissue Gas Exchange Involves capillary gas exchange in body tissues, where partial pressures and diffusion gradients are reversed compared to pulmonary gas exchange – Tissue PO is always lower than in arterial blood PO 2 2 (40 v s 100 mm Hg) er us ▪ O2 diffuses from blood to tissues until equilibrium is reached – Tissue PCO is always higher than arterial blood PCO 2 2 (45 v s 40 mm Hg) er us ▪ CO2 diffuses from tissues into blood until equilibrium is reached – Venous blood returning to heart has: ▪ PO of 40 mm Hg (after equilibrating with tissue PO ) 2 2 ▪ PCO2 of 45 mm Hg (after equilibrating with tissue PCO ) 2 Copyright © 2025 Pearson Education, Inc. All Rights Reserved Partial Pressure Gradients Promoting Gas Movements in the Body Figure 22.19 Partial pressure gradients promoting gas movements in the body. Copyright © 2025 Pearson Education, Inc. All Rights Reserved 22.7 Oxygen Is Transported by Hemoglobin, and Carbon Dioxide Is Transported in Three Different Ways Copyright © 2025 Pearson Education, Inc. All Rights Reserved Oxygen Transport Molecular O is carried in blood in two ways: 2 – 1.5% is dissolved in plasma – 98.5% is loosely bound to hemoglobin (Hb) in RBCs Association of oxygen and hemoglobin – Each Hb composed of four polypeptide chains, each with an iron-containing heme group, so each Hb can transport four O2 molecules ▪ Binding (loading) of O2 to Hb forms oxyhemoglobin (HbO2 ) ▪ Release (unloading) of O2 from Hb forms reduced hemoglobin (HHb), or deoxyhemoglobin Copyright © 2025 Pearson Education, Inc. All Rights Reserved Oxygen Transport Association of oxygen and hemoglobin (cont.) inued – Loading and unloading of O2 is facilitated by a change in shape of H b ▪ As O2 binds, Hb changes shape, increasing its affinity for O 2 ▪ As O is released, Hb shape change decreases its affinity for O2 2 – Hb fully saturated when all four heme groups carry O2 , partially saturated when one to three heme groups carry O2 – To ensure adequate oxygenation of blood and delivery of O2 to cells, rate of loading and unloading of O2 is influenced by the following factors:  PO 2  Temperature  Blood pH ▪ PCO2 ▪ Concentration of BPG Copyright © 2025 Pearson Education, Inc. All Rights Reserved Oxygen Transport Influence of PO on hemoglobin saturation 2 – Local PO controls O2 loading and unloading from Hb 2 – Percent Hb saturation can be plotted against PO ,2 producing an S-shaped curve called the oxygen-hemoglobin dissociation curve Copyright © 2025 Pearson Education, Inc. All Rights Reserved The Oxygen- Hemoglobin Dissociation Curve Focus Figure 22.2 The Oxygen-Hemoglobin Dissociation Curve. Copyright © 2025 Pearson Education, Inc. All Rights Reserved IP2: Tissue Oxygen Exchange Click here to view ADA compliant Animation: Tissue Oxygen Exchange https://mediaplayer.pearsoncmg.com/assets/sci-ip2-ote-systemic-oxygen-exchange Copyright © 2025 Pearson Education, Inc. All Rights Reserved The Oxygen-Hemoglobin Dissociation Curve Focus Figure 22.2 The Oxygen-Hemoglobin Dissociation Curve. Copyright © 2025 Pearson Education, Inc. All Rights Reserved The Oxygen-Hemoglobin Dissociation Curve Focus Figure 22.2 The Oxygen-Hemoglobin Dissociation Curve. Copyright © 2025 Pearson Education, Inc. All Rights Reserved Oxygen Transport Influence of other factors on hemoglobin saturation – Temperature, H concentration, PCO , and 2,3- bisphosphoglyceric acid (BPG) 2 therefore affinity of Hb for, O levels affect the shape and 2 – Increases in these factors reduce affinity of Hb for O2 ▪ Occurs in systemic capillaries (tissues) ▪ Enhances O2 unloading, shifting the O2 -Hb dissociation curve to the right – Decreases in these factors increase the affinity of Hb for O2 ▪ Occurs in pulmonary capillaries (lungs) ▪ Enhances O2 loading, shifting the O -Hb dissociation curve to the left 2 – Note the higher saturation at any PO 2 Copyright © 2025 Pearson Education, Inc. All Rights Reserved Effect of Temperature, PCO2 , and Blood pH on P sub C O 2, the Oxygen-Hemoglobin Dissociation Curve Figure 22.23 Effect of temperature, PCO2 , and blood pH on the oxygen-hemoglobin dissociation curve. Copyright © 2025 Pearson Education, Inc. All Rights Reserved Oxygen Transport – Influence of other factors on hemoglobin saturation (cont.) inued ▪ RBCs produce BPG during glycolysis – Levels rise as temperature rises (and O2 levels fall) ▪ The more glucose and O2 cells consume to make ATP, the more heat and CO2 they release, increasing PCO and H in local capillary blood 2 – Increasing temperature directly and indirectly decreases H b affinity for O2 – Reduced affinity of Hb for O2 resulting from falling blood pH and rising PCO2 called the Bohr effect – These factors enhanced O2 unloading occurs where it is needed most Copyright © 2025 Pearson Education, Inc. All Rights Reserved IP2: Oxygen Transport and Exchange: Summary Click here to view ADA compliant Animation: Oxygen Transport and Exchange: Summary https://mediaplayer.pearsoncmg.com/assets/sci-ip2-ote-summary Copyright © 2025 Pearson Education, Inc. All Rights Reserved Carbon Dioxide Transport CO2 transported in blood in three forms: 1. Dissolved in plasma (7 to 10%), thus responsible for PCO2 2. Chemically bound to hemoglobin (just over 20%) ▪ CO2 binds to globin (not heme) of Hb, forming carbaminohemoglobin 3. As bicarbonate ions in plasma (about 70%) ▪ Formation of HCO3  in plasma involves CO2 combining with water to form carbonic acid (H2CO3 ), which quickly dissociates into HCO3 and H   ▪ Occurs primarily in RBCs, where enzyme carbonic anhydrase reversibly and rapidly catalyzes this reaction Copyright © 2025 Pearson Education, Inc. All Rights Reserved Carbon Dioxide Transport In systemic capillaries, after HCO3  is created, it quickly diffuses from R BCs into plasma – Outrush of HCO3  from RBCs is balanced as Cl moves into RBCs from plasma ▪ Referred to as chloride shift In pulmonary capillaries, the processes occur in reverse – HCO3  moves into RBCs while Cl moves out of RBCs back into plasma – HCO3  binds with H to form H2CO3 – H2CO3 is split by carbonic anhydrase into CO2 and water – CO2 diffuses into alveoli Copyright © 2025 Pearson Education, Inc. All Rights Reserved Carbon Dioxide Transport Haldane effect – Amount of CO2 transported in blood is affected by PO 2 – The lower the PO and Hb saturation, the more CO2 can be carried in 2 blood, called the Haldane effect – Process encourages CO2 exchange at tissues and at lungs ▪ At tissues: – As CO2 enters blood, causes more O2 to dissociate from Hb (Bohr effect) ▪ At lungs, situation is reversed. O2 enters blood and CO2 dissociates. Copyright © 2025 Pearson Education, Inc. All Rights Reserved Transport and Exchange of CCO O2 andOO22 2 and Figure 22.24a Transport and exchange of CO2 and O2. Copyright © 2025 Pearson Education, Inc. All Rights Reserved Transport and Exchange of CCO O2 andOO22 2 and Figure 22.24b Transport and exchange of CO2 and O2. Copyright © 2025 Pearson Education, Inc. All Rights Reserved IP2: Carbon Dioxide Transport and Exchange: Summary Click here to view ADA compliant Animation: Carbon Dioxide Transport and Exchange: Summary https://mediaplayer.pearsoncmg.com/assets/sci-ip2-cdte-summary Copyright © 2025 Pearson Education, Inc. All Rights Reserved Hypoxia Hypoxia is inadequate O2 delivery to tissues – Can result in cyanosis when Hb saturation 75% or less Classified by cause: – Anemic hypoxia: too few RBCs or abnormal or too little Hb – Ischemic (stagnant) hypoxia: impaired or blocked blood circulation – Histotoxic hypoxia: cells unable to use O2 , as in metabolic poisons like cyanide – Hypoxemic hypoxia (hypoxemia): abnormal ventilation-perfusion coupling, pulmonary diseases impairing ventilation, low levels of oxygen in air – Carbon monoxide poisoning: leading cause of death from fire; H b has 200  greater affinity for carbon monoxide than oxygen ▪ Causes confusion and headache, but not characteristic signs of hypoxia ▪ Treated with hyperbaric therapy (if available) or 100% O2 supplemental air Copyright © 2025 Pearson Education, Inc. All Rights Reserved Neural Mechanisms Control of respiration involves neurons in the reticular formation of the medulla and pons Medullary respiratory centers (ventral and dorsal) – Ventral respiratory group (VRG) is rhythm-generating and integrative center ▪ Network of neurons, including both inspiratory and expiratory neurons, in ventral brain stem that extends from spinal cord to pons-medulla junction ▪ Inspiratory neurons send action potentials along phrenic and intercostal nerves to contract the diaphragm and external intercostals, respectively ▪ Expiratory neurons inhibit inspiratory neurons to relax the inspiratory muscles so the lungs can recoil ▪ Cyclic activity of inspiratory and expiratory neurons sets normal respiratory rate and rhythm at rest (12–16 breaths/minute), called eupnea Copyright © 2025 Pearson Education, Inc. All Rights Reserved Neural Mechanisms – Dorsal respiratory group (DRG) ▪ Network of neurons located near root of cranial nerve IX ▪ Integrates input from peripheral stretch and chemoreceptors, then modifies information to VRG neurons Pontine respiratory centers – Pontine respiratory centers influence and modify activity of VRG ▪ Appear to smooth out transitions between inspiration and expiration (damage can cause very prolonged inspirations called apneustic breathing) ▪ Communicate with the VRG during vocalization, sleep, exercise to fine-tune breathing rhythms ▪ Like DRG, receive inputs from higher brain centers and peripheral receptors Copyright © 2025 Pearson Education, Inc. All Rights Reserved Respiratory Centers in the Brain Stem Figure 22.25 Respiratory centers in the brain stem. Copyright © 2025 Pearson Education, Inc. All Rights Reserved Neural Mechanisms Generation of the respiratory rhythm – Origin of breathing rhythm is not yet fully understood ▪ One hypothesis is that pacemaker neurons in VRG control intrinsic rhythmicity (but suppressing pacemaker-like activity in the VRG doesn’t stop breathing) Copyright © 2025 Pearson Education, Inc. All Rights Reserved Factors Influencing Breathing Rate and Depth Depth determined by how actively VRG stimulates respiratory muscles – Greater stimulation activates more motor units, increasing depth (tidal volume) of inspiration Rate determined by how long inspiratory neurons are active (or how quickly switched off) – Both depth and rate of breathing determined by changing demands of body ▪ Respiratory centers are affected by: – Chemical factors – Influence of higher brain centers – Pulmonary irritant reflexes – The inflation reflex Copyright © 2025 Pearson Education, Inc. All Rights Reserved Factors Influencing Breathing Rate and Depth Chemical factors – Rising CO2 levels are the most powerful respiratory stimulant – Fluctuations detected by chemoreceptors ▪ Central chemoreceptors located throughout brain stem, including medulla ▪ Peripheral chemoreceptors found in aortic arch and carotid arteries – Influence of PCO 2 ▪ Strongest influence on ventilation, most closely controlled ▪ If arterial PCO rises (hypercapnia), CO2 accumulates in CSF of brain and 2 joins with water to become carbonic acid, which releases H – Increased H (drop in pH) stimulates central chemoreceptors, which synapse with respiratory centers – VRG increases depth and rate of breathing, causing decrease in blood PCO 2 , causing reduction in H (rise in pH) back to normal levels Copyright © 2025 Pearson Education, Inc. All Rights Reserved Changes in PCO 2 P sub C O 2 Regulate Ventilation by a Negative Feedback Mechanism Figure 22.27 Changes in PCO regulate ventilation by a negative feedback mechanism. 2 Copyright © 2025 Pearson Education, Inc. All Rights Reserved Clinical—Homeostatic Imbalance 22.15 Hyperventilation: increased depth and rate of breathing that exceeds body’s need to remove CO2 – May be caused by anxiety attacks – Leads to low arterial PCO (hypocapnia), causing: 2 ▪ Cerebral vasoconstriction and ischemia, resulting in dizziness or fainting – Earlier symptoms include tingling and muscle spasms in hands and face – Symptoms may be avoided by re-breathing (breathing into paper bag), which increases CO2 in inspired air, so more CO2 is retained in blood Copyright © 2025 Pearson Education, Inc. All Rights Reserved Factors Influencing Breathing Rate and Depth – Influence of PCO (cont.) 2 inued ▪ If arterial PCO falls abnormally low, respiration becomes slow and shallow 2 – Periods of apnea (breathing cessation) can occur until arterial PCO 2 rises again (stimulating respiratory centers) – Swimmers sometimes voluntarily hyperventilate so they can hold their breath longer Causes rapid/large drop in PCO , delaying stimulation of respiratory 2 centers until PCO levels build back up 2 Can cause dangerous drops in PO levels, leading to “black out” 2 Copyright © 2025 Pearson Education, Inc. All Rights Reserved Factors Influencing Breathing Rate and Depth Chemical factors (cont.)inued – Influence of PO 2 ▪ Peripheral chemoreceptors detect fluctuations in arterial blood O2 levels ▪ Declining arterial PO normally has only slight effect on ventilation because of 2 huge O2 reservoir bound to Hb – Arterial PO must drop substantially (60 mm Hg or less) before it 2 becomes a major stimulus for ventilation – Influence of arterial pH ▪ pH can influence ventilation even with normal arterial PCO and PO 2 2 – Mediated by peripheral chemoreceptors ▪ Decreased pH may reflect CO2 retention, accumulation of lactic acid, or excess ketone bodies ▪ Respiratory centers attempt to raise pH by increasing ventilation, which increases CO2 removal from blood, lowering H levels Copyright © 2025 Pearson Education, Inc. All Rights Reserved Factors Influencing Breathing Rate and Depth Pulmonary irritant reflexes – Receptors in bronchioles respond to irritants such as dust, accumulated mucus, or noxious fumes by triggering reflexive bronchoconstriction ▪ Receptors communicate with respiratory centers via vagal nerve afferents – Same irritants in trachea or bronchi trigger a cough, or in nasal cavity a sneeze The inflation reflex – Inflation reflex (Hering-Breuer reflex) ▪ Stretch receptors in pleurae and airways are stimulated by lung inflation – Send inhibitory signals to respiratory centers to end inhalation and allow expiration – May act as protective response more than as a normal regulatory mechanism Copyright © 2025 Pearson Education, Inc. All Rights Reserved Neural and Chemical Influences on Brain Stem Respiratory Centers Figure 22.26 Neural and chemical influences on brain stem respiratory centers. Copyright © 2025 Pearson Education, Inc. All Rights Reserved 22.9 Exercise and High Altitude Bring About Respiratory Adjustments Copyright © 2025 Pearson Education, Inc. All Rights Reserved Exercise Respiratory adjustments reflect both the intensity and duration of the exercise – Increased ventilation in response to metabolic needs is called hyperpnea ▪ Can increase 10  to 20  during exercise – Adjustments during exercise do not appear to be controlled by the usual chemical factors (rising PCO , and falling PO 2 and pH) for two reasons: 2 ▪ Ventilation increases abruptly at the onset, followed by more gradual increase, then reaches steady state; when exercise stops, there is a small, abrupt decline in ventilation, followed by a more gradual decrease ▪ Arterial PCO , PO , and pH remain surprisingly constant during exercise 2 2 – PCO2 may even fall below normal (and PO2 rise slightly) because the respiratory adjustments are so efficient Copyright © 2025 Pearson Education, Inc. All Rights Reserved Exercise Abrupt rise in ventilation that occurs at onset of exercise involves three neural factors: – Psychological stimuli (anticipation of exercise) – Simultaneous cortical motor activation of skeletal muscles and respiratory centers – Excitatory impulses to respiratory centers from proprioceptors in moving muscles, tendons, joints Gradual increase and then leveling of ventilation reflect rate of CO2 delivery to the lungs Exercise leads to anaerobic respiration and the formation of lactic acid – Lack of oxygen in muscles not from poor respiratory function, but from limits in cardiac output as well as the muscle’s ability to increase oxygen uptake Copyright © 2025 Pearson Education, Inc. All Rights Reserved High Altitude Quick travel to altitudes above 2400 meters (8000 feet) may trigger symptoms of acute mountain sickness (AMS) – Atmospheric pressure and PO levels are lower at high elevations 2 – Symptoms: headaches, shortness of breath, nausea, and dizziness; in severe cases, lethal cerebral and pulmonary edema may occur Acclimatization: long-term respiratory and hematopoietic adjustments to high altitude – Chemoreceptors become more responsive to PCO at lower PO levels 2 2 ▪ Arterial PO  60 mm Hg directly stimulates peripheral chemoreceptors 2 – Ventilation increases to raise arterial PO (also lowering PCO ) 2 2 ▪ PCO of individuals living at high altitudes usually below 40 m m Hg 2 – Hb saturation levels are lower-than-normal because less O2 is available ▪ Decline in arterial blood O2 stimulates kidneys to produce more E PO, which increases RBC numbers for long-term compensation Copyright © 2025 Pearson Education, Inc. All Rights Reserved 22.10 Respiratory Diseases are Major Causes of Disability and Death Copyright © 2025 Pearson Education, Inc. All Rights Reserved Chronic Obstructive Pulmonary Disease (COPD) (1 of 2) The chronic obstructive pulmonary diseases (COPD) are best exemplified by emphysema and chronic bronchitis – Key feature of COPD is irreversible decreased ability to force air out of the lungs 80% of COPD patients have history of smoking; other shared features include: – Dyspnea, or labored breathing, gets progressively worse – Coughing and frequent pulmonary infections – Most develop hypoventilation resulting in respiratory acidosis and hypoxemia Emphysema: permanent enlargement of alveoli (via destruction of their walls) – Reduces lung elasticity, with three consequences: ▪ Exhaustion, as accessory muscles (so more energy) now needed to breath ▪ Trapped air causes hyperinflation, which flattens diaphragm and causes expanded barrel chest, both of which reduce ventilation efficiency ▪ Damaged pulmonary capillaries lead to enlarged right ventricle Copyright © 2025 Pearson Education, Inc. All Rights Reserved Chronic Obstructive Pulmonary Disease (COPD) (2 of 2) Chronic bronchitis – Inhaled irritants cause chronic excessive mucus – Mucosae of lower respiratory passageways become inflamed and fibrosed – Results in obstructed airways that impair lung ventilation and gas exchange – Symptoms include frequent pulmonary infections – Risk factors include smoking and environmental pollutants COPD: symptoms and treatment – Different symptoms seen in different patients due to the strength of their innate respiratory drive ▪ “Pink puffers”: patient usually thin because they burn large amount of energy breathing; near-normal blood gases are maintained, so skin color is normal ▪ “Blue bloaters”: patient usually stocky; cyanosis is due to hypoxia, so skin color takes on bluish hue – Treatments: bronchodilators and corticosteroids; if needed, oxygen can be administered carefully Copyright © 2025 Pearson Education, Inc. All Rights Reserved The Pathogenesis of COPD Figure 22.29 The pathogenesis of COPD. Copyright © 2025 Pearson Education, Inc. All Rights Reserved Asthma Characterized by coughing, dyspnea, wheezing, and chest tightness Sometimes classified as COPD, but episodes are acute, not chronic, with symptom-free periods (so the obstruction is reversible) Active inflammation of airways precedes bronchospasms in allergic asthma – Airway inflammation is an immune response caused by production of IgE antibodies and recruitment of inflammatory cells Airways thickened with inflammatory exudate magnify effect of bronchospasms We now treat the underlying inflammation using inhaled corticosteroids and a variety of other drugs (rather than just treat symptoms with albuterol) Copyright © 2025 Pearson Education, Inc. All Rights Reserved Tuberculosis (TB) Infectious disease caused by bacterium Mycobacterium tuberculosis Symptoms: fever, night sweats, weight loss, racking cough, coughing up blood Deadly strains of drug-resistant (even multidrug-resistant) TB emerge when treatment is incomplete or inadequate – Resistant strains found throughout the world Copyright © 2025 Pearson Education, Inc. All Rights Reserved Lung Cancer Leading cause of cancer deaths in North America; – About 90% of all cases are result of smoking Three most common types: – Adenocarcinoma ( 40% of cases) originates in peripheral lung areas; develops from bronchial glands and alveolar cells – Squamous cell carcinoma ( 20 of cases) arises in bronchial epithelium – Small cell carcinoma ( 15% of cases) contains lymphocyte-sized cells that originate in primary bronchi and subsequently metastasize Treatment for lung cancer – Early detection is key to survival – If metastasis has not occurred: surgery to remove diseased lung tissue – If metastasis has occurred: radiation and chemotherapy (but low success rates) ▪ New targeted drug therapies are having greater success Copyright © 2025 Pearson Education, Inc. All Rights Reserved Sleep Apnea Sleep apnea is characterized by temporary cessation of breathing during sleep – Common disorder, person usually not aware of problem – Leads to excessive daytime sleepiness due to waking up several times each night (can be up to 30 per hour) – Obstructive sleep apnea (most common type) caused by collapse of upper airway ▪ Pharynx muscles relax during sleep and soft tissues sag and obstruct airway Central sleep apnea is caused by reduced drive from respiratory centers of brain stem Consequences of disrupted sleep: – Susceptibility to accidents – Increase in chronic illnesses such as hypertension, heart disease, stroke, diabetes Obstructive sleep apnea can be treated by using C PAP (continuous positive airway pressure) device, which prevents airway collapse Copyright © 2025 Pearson Education, Inc. All Rights Reserved Developmental Aspects of Respiratory System Upper respiratory structures develop first – By week 28, most premature babies can breathe on their own – During fetal life, lungs are filled with fluid, and blood bypasses the lungs ▪ Gas exchange takes place via placenta At birth, respiratory centers are activated, alveoli inflate, and lungs begin to function – Takes 2 weeks after birth before lungs are fully inflated – Respiratory rate is highest in newborns (40–80 breaths/m in) and slows until adulthood (12–16 breaths/min) Lungs continue to mature, and more alveoli are formed until young adulthood – Respiratory efficiency decreases in old age Copyright © 2025 Pearson Education, Inc. All Rights Reserved Embryonic Development of the Respiratory System Figure 22.30 Embryonic development of the respiratory system. Copyright © 2025 Pearson Education, Inc. All Rights Reserved Clinical—Homeostatic Imbalance 22.16 Cystic fibrosis (CF) – Most common lethal genetic disease in North America – Caused by abnormal gene for Cl membrane channel protein, cystic fibrosis transmembrane conductance regulator (CFTR) ▪ Abnormal CFTR protein gets stuck in endoplasmic reticulum (E R), never reaches membrane to carry out Cl transport; as less Cl is secreted less water follows (producing thick mucus) – Faulty gene affects lungs, pancreatic ducts, reproductive ducts, and sweat glands ▪ In lungs, mucus clogs airways and leads to bacterial infections Treatments for cystic fibrosis include: – Mucus-dissolving enzymes and inhalation hypertonic saline to thin mucus – Percussively “clapping” the chest to loosen mucus, followed by coughing and huffing to expel mucus – Antibiotics, bronchodilators, and anti-inflammatory meds to treat symptoms – Drugs that target specific C FTR mutations to modulate CFTR protein function Copyright © 2025 Pearson Education, Inc. 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