Respiratory System PDF

SAMUEL K. APPIAH (Ph.D Candidate) Office: SAHS – Rm#. SF19 Contact: 0245900367 Email: [email protected]/ [email protected] The Anatomy and Physiology of the Respiratory System  Respiratory system  T...

SAMUEL K. APPIAH (Ph.D Candidate) Office: SAHS – Rm#. SF19 Contact: 0245900367 Email: [email protected]/ [email protected] The Anatomy and Physiology of the Respiratory System  Respiratory system  The respiratory system consists of tubes that filter incoming air and transport it into the microscopic alveoli where gases are exchanged.  Consists of:  Nose  Pharynx = throat  Larynx = voicebox  Trachea = windpipe  Bronchi = airways  Lungs  Organs of the Respiratory System  The organs of the respiratory tract can be divided into two groups:  the upper respiratory tract (nose, nasal cavity, sinuses, and pharynx),  the lower respiratory tract (larynx, trachea, bronchial tree, and lungs).  Locations of infections  upper respiratory tract is above vocal cords  lower respiratory tract is below vocal cords  The branch of medicine that deals with the diagnosis and treatment of diseases of the ear, nose, and throat (ENT) is called otorhinolaryngology.  Major Functions of Respiratory System  Oversees gas exchanges (oxygen and carbon dioxide) between the blood and external environment  Exchange of gasses takes place within the lungs in the alveoli(only site of gas exchange)  Passage ways to the lungs purify, warm, and humidify the incoming air  Shares responsibility with cardiovascular system  Upper Respiratory tract  Nose  Functions  The only externally visible part of the respiratory system that functions by:  Providing an airway for respiration  Moistening and warming the entering air  Filtering inspired air and cleaning it of foreign matter  Serving as a resonating chamber for speech  Housing the olfactory receptors  Structure of the Nose  The nose is divided into two regions  The external nose, including the root, bridge, dorsum nasi, and apex  The internal nasal cavity  Philtrum – a shallow vertical groove inferior to the apex  The external nares (nostrils) are bounded laterally by the alae Nasal Cavity  Nasal Cavity  Lies in and posterior to the external nose  Is divided by a midline nasal septum  Opens posteriorly into the nasal pharynx via internal nares  The ethmoid and sphenoid bones form the roof  The floor is formed by the hard and soft palates  Vestibule – nasal cavity superior to the nares  Vibrissae – hairs that filter coarse particles from inspired air  Olfactory mucosa  Lines the superior nasal cavity  Contains smell receptors  Respiratory mucosa  Lines the balance of the nasal cavity  Glands secrete mucus containing lysozyme and defensins to help destroy bacteria  Nasal Cavity  Inspired air is:  Humidified by the high water content in the nasal cavity  Warmed by rich plexuses of capillaries  Ciliated mucosal cells remove contaminated mucus  Superior, medial, and inferior conchae:  Protrude medially from the lateral walls  Increase mucosal area  Enhance air turbulence and help filter air  Sensitive mucosa triggers sneezing when stimulated by irritating particles  Paranasal Sinuses:  Sinuses in bones that surround the nasal cavity  Sinuses lighten the skull and help to warm and moisten the air Pharynx  The pharynx (throat) is a muscular tube lined by a mucous membrane  It is divided into three regions:  Nasopharynx: functions in respiration  Oropharynx  Laryngopharynx o Both the oropharynx and laryngopharynx function in digestion and in respiration (serving as a passageway for both air and food).  Lower Respiratory Tract  Larynx (Voice Box)  The larynx (voice box) is a passage way that connects the pharynx with the trachea.  It contains the thyroid cartilage (Adam’s apple); the epiglottis, the cricoid cartilage, the paired arytenoid, corniculate, and cuneiform cartilages  The three functions of the larynx are:  To provide a patent airway  To act as a switching mechanism to route air and food into the proper channels  To function in voice production Framework of the Larynx  Trachea  Connects larynx with bronchi  Lined with ciliated mucosa  Beat continuously in the opposite direction of incoming air  Expel mucus loaded with dust and other debris away from lungs  Walls are reinforced with C- shaped hyaline cartilage  Bronchi  The trachea divides into the right and left pulmonary bronchi.  The bronchial tree consists of the trachea, primary bronchi, secondary bronchi, tertiary bronchi, bronchioles, and terminal bronchioles.  Walls of bronchi contain rings of cartilage.  Walls of bronchioles contain smooth muscle. Full extent of airways is visible starting at the larynx and trachea  Tracheostomy and Intubation  Re-establishing airflow pass an airway obstruction  crushing injury to larynx or chest  swelling that closes airway  vomit or foreign object  Tracheostomy is incision in trachea below cricoid cartilage if larynx is obstructed  Intubation is passing a tube from mouth or nose through larynx and trachea  Bronchi and Bronchioles  Primary bronchi supply each lung  Secondary bronchi supply each lobe of the lungs (3 right + 2 left)  Tertiary bronchi supply each bronchopulmonary segment  Repeated branchings called bronchioles form a bronchial tree  Histology of Bronchial Tree  Epithelium changes from pseudostratified ciliated columnar to non-ciliated simple cuboidal as pass deeper into lungs  Incomplete rings of cartilage replaced by rings of smooth muscle & then connective tissue  sympathetic NS & adrenal gland release epinephrine that relaxes smooth muscle & dilates airways  asthma attack or allergic reactions constrict distal bronchiole smooth muscle  nebulization therapy = inhale mist with chemicals that relax muscle & reduce thickness of mucus  Lungs :Gross Anatomy  Lungs occupy all of the thoracic cavity except the mediastinum  Root – site of vascular and bronchial attachments  Costal surface – anterior, lateral, and posterior surfaces in contact with the ribs  Apex – narrow superior tip  Base – inferior surface that rests on the diaphragm  Hilus – indentation that contains pulmonary and systemic blood vessels  Gross Anatomy of Lungs  Cardiac notch (impression) – cavity that accommodates the heart  Left lung – separated into upper and lower lobes by the oblique fissure  Right lung – separated into three lobes by the oblique and horizontal fissures R lung has three lobes separated by two fissures;  There are 10 L lung has two lobes separated by one fissure and bronchopulmonary a depression, the cardiac notch segments in each lung  Pleurae  Thin, double-layered serosa  Parietal pleura  Covers the thoracic wall and superior face of the diaphragm  Continues around heart and between lungs  Visceral, or pulmonary, pleura  Covers the external lung surface  Divides the thoracic cavity into three chambers  The central mediastinum  Two lateral compartments, each containing a lung Pleural Membranes & Pleural Cavity  Visceral pleura covers lungs --- parietal pleura lines ribcage & covers upper surface of diaphragm  Pleural cavity is potential space between ribs & lungs contains a lubricating fluid Structures within a Lobule of Lung The 2o bronchi give rise to branches called tertiary (segmental) bronchi, which supply segments of lung tissue called bronchopulmonary segments. Each bronchopulmonary segment consists of many small compartments called lobules, which contain lymphatics, arterioles, venules, terminal bronchioles, respiratory bronchioles, alveolar ducts, alveolar sacs, and alveoli  Respiratory Zone  Defined by the presence of alveoli; begins as terminal bronchioles feed into respiratory bronchioles  Respiratory bronchioles lead to alveolar ducts, then to terminal clusters of alveolar sacs composed of alveoli  Approximately 300 million alveoli:  Account for most of the lungs’ volume  Provide tremendous surface  area for gas exchange  Alveoli: Cells Types  Type I alveolar cells  simple squamous cells where gas exchange occurs  Type II alveolar cells (septal cells)  free surface has microvilli  secrete alveolar fluid containing surfactant  Alveolar dust cells  wandering macrophages remove debris  Alveolar-Capillary Membrane & Gas exchange: Details of Respiratory Membrane  Respiratory membrane = 1/2 micron thick  Exchange of gas from alveoli to blood  4 Layers of membrane to cross  alveolar epithelial wall of type I cells  alveolar epithelial basement membrane  capillary basement membrane  endothelial cells of capillary  Vast surface area  Blood Supply to the Lungs  The lungs have a double blood supply.  Blood enters the lungs via  the pulmonary arteries (pulmonary circulation)  and the bronchial arteries (systemic circulation).  Most of the blood leaves by the pulmonary veins, but some drains into the bronchial veins.  Events of Respiration  Four distinct processes: I. Pulmonary ventilation – moving air in and out of the lungs II. External respiration – gas exchange between pulmonary blood and alveoli III. Respiratory gas transport – transport of oxygen and carbon dioxide via the bloodstream IV. Internal respiration – gas exchange between blood and tissue cells in systemic capillaries  Mechanics of Breathing  Pulmonary ventilation (breathing) is the process by which gases are exchanged between the atmosphere and lung alveoli.  consists of two phases  Inspiration – air flows into the lungs  Expiration – gases exit the lungs  Breathing is an active process - requiring the contraction of skeletal muscles.  The primary muscles of respiration  include the external intercostal muscles (located between the ribs)  the diaphragm (a sheet of muscle located between the thoracic & abdominal cavities).  Pressure Relationships in the Thoracic Cavity  Respiratory pressure is always described relative to atmospheric pressure  Atmospheric pressure (Patm)  Pressure exerted by the air surrounding the body  Negative respiratory pressure is less than Patm  Positive respiratory pressure is greater than Patm  Intrapulmonary pressure (Palv) – pressure within the alveoli  Intrapleural pressure (Pip) – pressure within the pleural cavity  Intrapulmonary pressure and intrapleural pressure fluctuate with the phases of breathing  Intrapulmonary pressure always eventually equalizes itself with atmospheric pressure  Intrapleural pressure is always less than intrapulmonary pressure and atmospheric pressure  Pulmonary Ventilation  A mechanical process Dimensions of the Chest that depends on volume Cavity changes in the thoracic cavity  Volume changes lead to pressure changes, which lead to the flow of gases to equalize pressure V  P  F (flow of gases)  Inspiration  The movement of air into and out of the lungs depends on pressure changes governed in part by Boyle’s law,  which states that the volume of a gas varies inversely with pressure, ( temperature is constant ). P1V1 = P2V2  The first step in expanding the lungs involves contraction of the main inspiratory muscle, the diaphragm. Boyle’s Law  As the size of closed container decreases, pressure inside is increased  The molecules have less wall area to strike so the pressure on each inch of area increases. Inspiration  Lung Collapse  Caused by equalization of the intrapleural pressure with the intrapulmonary pressure  Transpulmonary pressure keeps the airways open  Transpulmonary pressure = difference between the intrapulmonary and intrapleural pressures (Palv – Pip)  Expiration  Inspiratory muscles relax and the rib cage descends due to gravity  Thoracic cavity volume decreases  Elastic lungs recoil passively and intrapulmonary volume decreases  Intrapulmonary pressure rises above atmospheric pressure (+1 mm Hg)  Gases flow out of the lungs down the pressure gradient until intrapulmonary pressure is 0 Expiration  Laboured Breathing  Forced expiration  abdominal muscles contract  internal intercostals contract  Forced inspiration  sternocleidomastoid, scalenes & pectoralis minor lift chest upwards as you gasp for air  Alveolar Surface Tension  The walls of alveoli are coated with a thin film of water & this creates a potential problem.  Water molecules, including those on the alveolar walls, are more attracted to each other and this attraction creates a force called surface tension.  Potentially, surface tension could cause alveoli to collapse and, in addition, would make it more difficult to 're-expand' the alveoli (when you inhaled).  Detergent-like substance called surfactant produced by Type II alveolar cells  lowers alveolar surface tension and prevents alveoli from collapsing  insufficient in premature babies so that alveoli collapse at end of each exhalation (IRDS)-Clinical Application  Surfactant has dipalmitoyl lecithin, (dipolmitoyl phosphotidyl choline=DPPC) as a major constituent.  Infant respiratory disease syndrome (IRDS)  Surfactant (DPPC) production starts late in foetal life so premature infants are often unable to make surfactant properly.  Infants with abnormal surfactant have stiff, fluid-filled lungs with collapsed alveolar. Non-ventilated, collapsed alveoli effectively cause right to left shunting of blood.  [lecithin]/[sphingomyelin] ratio can be analyzed in amniotic fluid to provide an index of gestational maturity of surfactant production.  Sphingomyelin production starts early and remains constant during gestation and is a marker of total phospholipid concentration.  Sphingomyelin has no surface active properties.  Physiological importance of surfactant  Increases lung compliance because surface forces are reduced.  Promotes alveolar stability and prevents alveolar collapse.  Decreased surface area lowers surface tension.  Increased surface area increases surface tension.  Small alveoli are prevented from getting smaller.  Large alveoli are prevented from getting bigger.  Promotes dry alveoli. Alveolar collapse tends to “suck” fluid from pulmonary capillaries. Stabilizing alveoli prevents transudation of fluid by preventing collapse.  Pneumothorax  Pleural cavities are sealed cavities not open to the outside  Injuries to the chest wall that let air enter the intrapleural space  causes a pneumothorax  collapsed lung on same side as injury  surface tension and recoil of elastic fibers causes the lung to collapse  Compliance of the Lungs  Ease with which lungs & chest wall expand  Specifically, the measure of the change in lung volume that occurs with a given change in transpulmonary pressure  Determined by two main factors  Distensibility (elasticity) of the lung tissue and surrounding thoracic cage  Surface tension of the alveoli Factors That Diminish Lung Compliance  Scar tissue or fibrosis that reduces the natural resilience of the lungs  Blockage of the smaller respiratory passages with mucus or fluid  Reduced production of surfactant  Decreased flexibility of the thoracic cage or its decreased ability to expand  Examples include:  Deformities of thorax  Ossification of the costal cartilage  Paralysis of intercostal muscles  Compliance changes in disease  Lungs become somewhat more compliant with natural aging and become markedly more compliant with emphysema.  Lungs become less compliant (stiffer) with pulmonary fibrosis or during oedema caused by rheumatic heart disease.  Chest wall becomes less compliant (stiffer) in condition where the chest wall is deformed (eg. kyphoscoliosis).  Chest wall becomes functionally less compliant when abdominal cavity changes cause upward displacement of the diaphragm (eg. pregnancy).  Breathing Patterns  Eupnea = normal quiet breathing  Apnea = temporary cessation of breathing  Dyspnea =difficult or labored breathing  Tachypnea = rapid breathing  Diaphragmatic breathing = descent of diaphragm causes stomach to bulge during inspiration  Costal breathing = just rib activity involved Modified Respiratory Movements (MRM)  Coughing  deep inspiration, closure of rima glottidis & strong expiration blasts air out to clear respiratory passages  Hiccupping  spasmodic contraction of diaphragm & quick closure of rima glottidis produce sharp inspiratory sound  Check on others  Lung volume and capacities  Air volumes exchanged during breathing and rate of ventilation are measured with a spirometer, or respirometer, and the record is called a spirogram  One inspiration followed by expiration is called a respiratory cycle.  Tidal Volume (TV)  The amount of air that enters or leaves the lungs during one respiratory cycle (Normal - about 500 ml)  Inspiratory Reserve Volume (IRV) (deep breath)  amount of air that can be forcibly inhaled over and above normal. (approx.2100–3200 ml)  Expiratory Reserve Volume (ERV)  additional amount of air forcibly expired after tidal expiration (1000 - 1200 ml)  Lung volume and capacities  Residual Volume (RV)  amount of air that stays trapped in the alveoli (about 1.2 liters)  This is the only lung volume which cannot be measured with a spirometer  Total Lung Capacity (TLC)  The volume of air contained in the lungs at the end of a maximal inspiration (approximately 6000 ml in males)  Called a capacity because it is the sum of the 4 basic lung volumes. TLC=RV+IRV+TV+ERV  Vital Capacity (VC)  The maximum volume of air that can be forcefully expelled from the lungs following a maximal inspiration.  Called a capacity because it is the sum of inspiratory reserve volume, tidal volume, and expiratory reserve volume. VC=IRV+TV+ERV or VC=TLC-RV  Lung volume and capacities  Functional Residual Capacity (FRC) The volume of air remaining in the lung at the end of a normal expiration.  Called a capacity because it equals residual volume plus expiratory reserve volume. FRC=RV+ERV  Inspiratory Capacity (IC)  Maximum volume of air that can be inspired from end expiratory position.  Called a capacity because it is the sum of tidal volume and inspiratory reserve volume.  This capacity is of less clinical significance than the other three. IC=TV+IRV Lung Capacities and Respiratory Diseases A. Restrictive Disease Respiratory disease which make it more difficult to get air in to the lungs. They “restrict” inspiration. (Decreased VC; decreased TLC, RV, FRC.) Includes: o fibrosis o sarcoidosis o muscular diseases o Chest wall deformities Lung Capacities and Respiratory Diseases B. Obstructive Disease Respiratory disease which make it more difficult to get air out of the lungs (Decreased VC; Increased TLC, RV, FRC). Includes o emphysema o chronic bronchitis o asthma EXCHANGE OF OXYGEN AND CARBON DIOXIDE  Composition of Alveolar Gas  The atmosphere is mostly oxygen and nitrogen, while alveoli contain more carbon dioxide and water vapor  These difference result from:  Gas exchanges in the lungs – oxygen diffuses from the alveoli and carbon dioxide diffuses into the alveoli  Air is humidified by the conducting pathways  The mixing of alveolar gas occurs with each breath What is Composition of Air?  Air = 21% O2, 79% N2 and.04% CO2  Alveolar air = 14% O2, 79% N2 and 5.2% CO2  Expired air = 16% O2, 79% N2 and 4.5% CO2  External & Internal Respiration  Gases diffuse from areas of high partial pressure to areas of low partial pressure  External respiration :Exchange of gas between external environment & lungs  Internal (tissue) respiration is the exchange of gases between tissue blood capillaries and cells resulting in the conversion of oxygenated blood into deoxygenated blood.  At rest only about 25% of the available oxygen in oxygenated blood actually enters tissue cells. During exercise, more oxygen is released.  Partial Pressure Gradients and Gas Solubilities  The partial pressure of oxygen (PO2) in venous blood is 40 mm Hg; the partial pressure in the alveoli is 104 mm Hg  This steep gradient allows oxygen partial pressures to rapidly reach equilibrium (in 0.25 seconds), and thus blood can move three times as quickly (0.75 seconds) through the pulmonary capillary and still be adequately oxygenated  Although carbon dioxide has a lower partial pressure gradient:  It is 20 times more soluble in plasma than oxygen  It diffuses in equal amounts with oxygen TRANSPORT OF O2 AND CO2 IN THE BLOOD  Oxygen Transport  Molecular oxygen is carried in the blood bound to haemoglobin (Hb) within RBCs and dissolved in plasma  Each haemoglobin molecule binds 4 O2 in a rapid and reversible process  The haemoglobin-oxygen combination is called oxyhaemoglobin (HbO2)  Haemoglobin that has released oxygen is called reduced haemoglobin (HHb)  Haemoglobin (Hb)  Saturated haemoglobin – when all four haems of the molecule are bound to oxygen  Partially saturated haemoglobin – when one to three haemes are bound to oxygen  The rate in which haemoglobin binds and releases oxygen is regulated by:  PO2, temperature, blood pH, PCO2, and the concentration of 2,3-BPG (an organic chemical)  These factors ensure adequate delivery of oxygen to tissue cells Haemoglobin Saturation Curve Haemoglobin is almost completely saturated at a PO2 of 70 mm Hg Further increases in PO2 produce only small increases in oxygen binding Oxygen loading and delivery to tissue is adequate when PO2 is below normal levels Only 20–25% of bound oxygen is unloaded during one systemic circulation If oxygen levels in tissues drop: – More oxygen dissociates from haemoglobin and is used by cells – Respiratory rate or cardiac output need not increase  Other Factors Influencing Haemoglobin Saturation  Temperature, H+, PCO2, and BPG:  Modify the structure of haemoglobin and alter its affinity for oxygen  Increases:  Decrease haemoglobin’s affinity for oxygen  Enhance oxygen unloading from the blood  Decreases act in the opposite manner  These parameters are all high in systemic capillaries where oxygen unloading is the goal  Factors That Increase Release of Oxygen by Hb  As cells metabolize glucose, carbon dioxide is released into the blood causing:  Increases in PCO2 and H+ concentration in capillary blood  Declining pH is (acidosis) weakens the hemoglobin-oxygen bond (Bohr effect)  Metabolizing cells have heat as a byproduct and the rise in temperature increases BPG synthesis  All these factors insure oxygen unloading in the vicinity of working tissue cells  Carbon Monoxide Poisoning  CO from car exhaust & tobacco smoke  Binds to Hb heme group more successfully than O2  CO poisoning  Treat by administering pure O2  Carbon Dioxide Transport  Carbon dioxide is transported in the blood in three forms:  Dissolved in plasma – 7 to 10%  Chemically bound to haemoglobin – 20% is carried in RBCs as carbaminohaemoglobin  Bicarbonate ion in plasma – 70% is transported as bicarbonate (HCO3–)  Transport and Exchange of Carbon Dioxide  Carbon dioxide diffuses into RBCs and combines with water to form carbonic acid (H2CO3), which quickly dissociates into hydrogen ions and bicarbonate ions CO2 + H2O  H2CO3  H+ + HCO3– Carbon Water Carbonic acid Hydrogen ion Bicarbonate dioxide ion  In RBCs, carbonic anhydrase reversibly catalyzes the conversion of carbon dioxide and water to carbonic acid  At the tissues:  Bicarbonate quickly diffuses from RBCs into the plasma  Chloride shift – to counterbalance the outrush of negative bicarbonate ions from the RBCs, chloride ions (Cl–) move from the plasma into the erythrocytes Summary of Gas Exchange & Transport  Influence of Carbon Dioxide on Blood pH  The carbonic acid–bicarbonate buffer system resists blood pH changes  If hydrogen ion concentrations in blood begin to rise, it is removed by combining with HCO3–  If hydrogen ion concentrations begin to drop, carbonic acid dissociates, releasing H+  Changes in respiratory rate can also:  Alter blood pH  Provide a fast-acting system to adjust pH when it is disturbed by metabolic factors Control of Respiration: Medullary Respiratory Centers Groups of neurons in the brain stem comprise the respiratory center, which controls breathing by causing inspiration and expiration and by adjusting the rate and depth of breathing. The components of the respiratory center include – The medulla rhythmicity center – the pneumotaxic area of the pons. Control of Respiration: Medullary Respiratory Centers The dorsal respiratory group (DRG), or inspiratory center: – Is located near the root of nerve IX – Appears to be the pacesetting respiratory center – Excites the inspiratory muscles and sets eupnea (12-15 breaths/minute) – Becomes dormant during expiration The ventral respiratory group (VRG) is involved in forced inspiration and expiration Control of Respiration: Pons Respiratory Centers Pons centers: – Influence and modify activity of the medullary centers – Smooth out inspiration and expiration transitions and vice versa Pneumotaxic center – continuously inhibits the inspiration center Apneustic center – continuously stimulates the medullary inspiration center Regulation of the Respiratory Center 1. Cortical Influences  Cortical influences allow conscious control of respiration that may be needed to avoid inhaling noxious gasses or water.  Breath holding is limited by the overriding stimuli of increased [H+] and [CO2]. 2.Chemical Regulation  Central chemoreceptors (located in the medulla oblongata) and peripheral chemoreceptors (located in the walls of systemic arteries) monitor levels of CO2 and O2 and provide input to the respiratory center.  Central chemoreceptors respond to change in H+ concentration or PCO2, or both in cerebrospinal fluid. Regulation of the Respiratory Center  Peripheral chemoreceptors respond to changes in H+, PCO2, and PO2 in blood.  A slight increase in PCO2 (and thus H+), a condition called hypercapnia, stimulates central chemoreceptors.  As a response to increased PCO2, increased H+ and decreased PO2, the inspiratory area is activated and hyperventilation, rapid and deep breathing, occurs.  If arterial PCO2 is lower than 40 mm Hg, a condition called hypocapnia, the chemoreceptors are not stimulated and the inspiratory area sets its own pace until CO2 accumulates and PCO2 rises to 40 mm Hg. Regulation of the Respiratory Center  Severe deficiency of O2 depresses activity of the central chemoreceptors and respiratory center  Hypoxia refers to oxygen deficiency at the tissue level and is classified in several ways.  Hypoxic hypoxia is caused by a low PO2 in arterial blood (high altitude, airway obstruction, fluid in lungs).  In anaemic hypoxia, there is too little functioning hemoglobin in the blood (hemorrhage, anemia, carbon monoxide poisoning).  Stagnant hypoxia results from the inability of blood to carry oxygen to tissues fast enough to sustain their needs (heart failure, circulatory shock).  In histotoxic hypoxia, the blood delivers adequate oxygen to the tissues, but the tissues are unable to use it properly (cyanide poisoning).  Respiratory Adjustments: Exercise  Respiratory adjustments are geared to both the intensity and duration of exercise  During vigorous exercise:  Ventilation can increase 20 fold  Breathing becomes deeper and more vigorous, but respiratory rate may not be significantly changed (hyperpnea)  Exercise-enhanced breathing is not prompted by an increase in PCO2 nor a decrease PO2 or pH  These levels remain surprisingly constant during exercise Respiratory Adjustments: Exercise  As exercise begins:  Ventilation increases abruptly, rises slowly, and reaches a steady-state  When exercise stops:  Ventilation declines suddenly, then gradually decreases to normal  Neural factors bring about the above changes, including:  Psychic stimuli  Cortical motor activation  Excitatory impulses from proprioceptors in muscles  Respiratory Adjustments: High Attitude  The body responds to quick movement to high altitude (above 8000ft) with symptoms of acute mountain sickness – headache, shortness of breath, nausea, and dizziness  Acclimatization – respiratory and haematopoietic adjustments to altitude include:  Increased ventilation – 2-3 L/min higher than at sea level  Chemoreceptors become more responsive to PCO2  Substantial decline in PO2 stimulates peripheral chemoreceptors  Aging & the Respiratory System  Respiratory tissues & chest wall become more rigid  Vital capacity decreases to 35% by age 70.  Decreases in macrophage activity  Diminished ciliary action  Decrease in blood levels of O2  Result is an age-related susceptibility to pneumonia or bronchitis  DISORDERS: HOMEOSTATIC IMBALANCES Asthma  Characterized by dyspnea, wheezing, and chest tightness  Active inflammation of the airways precedes bronchospasms  Airway inflammation is an immune response caused by release of IL-4 and IL-5, which stimulate IgE and recruit inflammatory cells  Airways thickened with inflammatory exudates magnify the effect of bronchospasms  DISORDERS: HOMEOSTATIC IMBALANCES Tuberculosis  Infectious disease caused by the bacterium Mycobacterium tuberculosis  It is communicable and destroys lung tissue, leaving nonfunctional fibrous tissue behind.  Symptoms include fever, night sweats, weight loss, a racking cough, and splitting headache  Treatment entails a 12-month course of antibiotics Chronic Obstructive Pulmonary Disease (COPD)  Exemplified by chronic bronchitis and obstructive emphysema  Patients have a history of:  Smoking  Dyspnea, where labored breathing occurs and gets progressively worse  Coughing and frequent pulmonary infections  COPD victims develop respiratory failure accompanied by hypoxemia, carbon dioxide retention, and respiratory acidosis  Bronchogenic carcinoma: Lung Cancer  Accounts for 1/3 of all cancer deaths in the US  90% of all patients with lung cancer were smokers  The three most common types are:  Squamous cell carcinoma (20-40% of cases) arises in bronchial epithelium  Adenocarcinoma (25-35% of cases) originates in peripheral lung area  Small cell carcinoma (20-25% of cases) contains lymphocyte- like cells that originate in the primary bronchi and subsequently metastasize “When you talk, you are only repeating what you already know. But if you listen, you may learn something new” Dalai Lama