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Chapter 22 Gas Exchange
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Surviving in Thin Air The high mountains of the Himalayas
Surviving in Thin Air The high mountains of the Himalayas Have claimed the lives of even the world’s top mountain climbers The air at the height of the world’s highest peak, Mt. Everest Is so low in oxygen that most people would pass out instantly if exposed to it
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Twice a year, flocks of geese migrate over the Himalayas They are able to fly at such a high altitude because of the efficiency of their lungs These birds have blood with hemoglobin with a very high affinity for oxygen This adaptation allows them to carry large amounts of oxygen to their tissues to exchange with carbon dioxide
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The process of gas exchange, often called respiration Is the interchange of O2 and CO2 between an organism and its environment
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MECHANISMS OF GAS EXCHANGE
Overview: Gas exchange involves: breathing, transport of gases, and exchange of gases with tissue cells 1 Breathing O2 CO2 Lung Circulatory system 2 Transport of gases by the circulatory 3 Exchange of gases with body cells Capillary Cell Mitochondria The three phases of gas exchange Figure 22.1
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Animals exchange O2 and CO2 across moist body surfaces
Respiratory surfaces Must be thin and moist for diffusion of O2 and CO2 to occur
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Some animals, like the earthworm
Some animals, like the earthworm Use their entire skin as a gas-exchange organ Cut Cross section of respiratory surface (the skin covering the body) CO2 Capillaries O2 Figure 22.2A
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In most animals Specialized body parts provide large respiratory surfaces for gas exchange Body surface Respiratory surface (air tubes) Body cells (no capillaries) O2 CO2 Body surface Respiratory surface (gill) Capillary CO2 O2 Figure 22.2C Body surface Respiratory surface (within lung) Capillary CO2 O2 Figure 22.2B Figure 22.2D
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Gills are adapted for gas exchange in aquatic environments
Gills are extensions of the body That absorb O2 dissolved in water Figure 42.20b (b) Marine worm. Many polychaetes (marine worms of the phylum Annelida) have a pair of flattened appendages called parapodia on each body segment. The parapodia serve as gills and also function in crawling and swimming.
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In a fish, gas exchange is facilitated by feathery gills
Figure 42.1
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In a fish, gas exchange Is enhanced by ventilation and the countercurrent flow of water and blood Gill arch Direction of water flow Blood vessels Gill filaments Oxygen-rich blood Oxygen-poor Lamella 15% 40% 70% 100% 60% 80% 30% 5% % O2 in water flowing over lamellae % O2 in blood flowing through capillaries in lamellae Countercurrent exchange Figure 22.3
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The tracheal system of insects
--provides direct exchange between the air and body cells --Transport O2 directly to body cells through a network of finely branched tubes Air sacs Tracheae Opening for air LM 250 Body cell Tracheole Air sac Trachea Body wall CO2 O2 Figure 22.4A, B
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Terrestrial vertebrates have lungs
(Heart) Diaphragm Bronchiole Bronchus Right lung Trachea Larynx (Esophagus) Pharynx Nasal cavity Left lung In mammals, air inhaled through the nostrils Passes through the pharynx and larynx into the trachea, bronchi, and bronchioles Figure 22.5A
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The human respiratory system
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The Nasal Cavity Olfactory receptors are located in the mucosa on the superior surface The rest of the cavity is lined with respiratory mucosa Moistens air Traps incoming foreign particles Slide 13.4a
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Trachea (Windpipe) 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 cartilage
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Coverings of the Lungs Pulmonary (visceral) pleura covers the lung surface Parietal pleura lines the walls of the thoracic cavity Pleural fluid fills the area between layers of pleura to allow gliding
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Respiratory Membrane (Air-Blood Barrier)
Thin squamous epithelial layer lining alveolar walls Pulmonary capillaries cover external surfaces of alveoli
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The bronchioles end in clusters of tiny sacs called alveoli
The bronchioles end in clusters of tiny sacs called alveoli Where gas exchange occurs Colorized SEM 6,200 Oxygen-rich blood Bronchiole Oxygen-poor Alveoli Blood capillaries Figure 22.5B, C
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Respiratory Membrane (Air-Blood Barrier)
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Gas Exchange Gas crosses the respiratory membrane by diffusion
Oxygen enters the blood Carbon dioxide enters the alveoli Macrophages add protection Surfactant coats gas-exposed alveolar surfaces
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Breathing ventilates the lungs
Is the alternation of inhalation and exhalation
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The contraction of rib muscles and the diaphragm
Rib cage expands as rib muscles contract Air inhaled Rib cage gets smaller as relax exhaled Lung Diaphragm Diaphragm relaxes (moves up) Diaphragm contracts (moves down) Inhalation Exhalation Expands the chest cavity and reduces air pressure in the alveoli (negative pressure breathing) Figure 22.7A
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Inspiration Diaphragm and intercostal muscles contract
The size of the thoracic cavity increases External air is pulled into the lungs due to an increase in intrapulmonary volume Slide 13.22a
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Exhalation Largely a passive process which depends on natural lung elasticity As muscles relax, air is pushed out of the lungs Forced expiration can occur mostly by contracting internal intercostal muscles to depress the rib cage Slide 13.23a
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The pleural cavity is maintained at a negative pressure compared to the atmosphere
The thin liquid film between the chest wall and lungs, keeps the lungs from being pulled away from the chest wall. Because of inward elastic force of the lungs and the outward elastic forces of the chest wall, the pressure between the lungs and the chest wall is negative.
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Pressure differences between pleural fluid and lung
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the pressure between the two glass slides is negative
The lungs are like the lower slide being pulled with a fixed rubber band. The chest wall is like the upper slide with a handle. There is liquid between the chest wall and lungs. This liquid, which is in a thin film-like form, keeps the two together. The inward elastic force in the lungs works towards decreasing the lung volume (Note that the rubber bands in the lungs are lightly stretched). The outward elastic force of the chest wall increases the volumes of the thoracic cavity and of the lungs. The pressure between the lungs and chest wall (pleural pressure) is negative (note that the blue pressure gauge, with its tip between the lung and chest wall, is elevated on the lung side, compared to the outer-side, which is opened and thus indicates the atmospheric pressure).
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Pressure changes during breathing
Inspiratory muscles, such as the diaphragm, contract, increasing the volume of the thoracic cavity. Because of the thin liquid film, the lung volume is also increased. Since this is in the opposite direction of the lung elasticity (note that the 'rubber bands' are further stretched), the pleural pressure becomes more negative (note the blue pressure gauge). This is similar to: A rubber band is attached to a desk and the lower glass slide. With water in between, when the upper glass slide is lifted, pulling the rubber band lightly, the negative pressure inbetween is small, but when the rubber band is pulled strongly, the negative pressure inbetween is large. Inspiration is like the latter situation.
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Pressure Differences in the Thoracic Cavity
Normal pressure within the pleural space is always negative (intrapleural pressure) Differences in lung and pleural space pressures keep lungs from collapsing --due to elastic tissues in the lung and surface tension in the alveoli. Slide 13.24
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What happens if the pleural membrane is punctured?
When the pleural membrane is punctured, atmospheric air rushes into the pleural cavity, and the intrapleural pressure immediately changes from -4 mm Hg to 0 mm Hg (760mmHg). The negative pressure that holds the lung open is now eliminated, and the stretched lung collapses due to its elasticity and surface tension. If the lung collapses, it can no longer be, inflated by inhalation, even when the diaphragm and ribs can still carry out normal breathing movements.
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Micconception: “When one is shot in the lung, he couldn’t breathe because the lungs would collapse.” The fact is: When one is shot in one side of the two lungs, provided that the other side of the thoracic cage and pleural membranes are intact, he could still breathe with ONE side of his lung—which wouldn’t collapse because the two sides of the lungs are separately wrapped with pleural membranes.
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Nonrespiratory Air Movements
Can be caused by reflexes or voluntary actions Examples Cough and sneeze – clears lungs of debris Laughing Crying Yawn Hiccup Slide 13.25
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Respiratory Volumes and Capacities
Normal breathing moves about 500 ml of air with each breath (tidal volume [TV]) Many factors that affect respiratory capacity A person’s size Sex Age Physical condition Residual volume of air – after exhalation, about 1200 ml of air remains in the lungs Slide 13.26
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Respiratory Volumes and Capacities
Inspiratory reserve volume (IRV) Amount of air that can be taken in forcibly over the tidal volume Usually between 2100 and 3200 ml Expiratory reserve volume (ERV) Amount of air that can be forcibly exhaled Approximately 1200 ml Slide 13.27a
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Respiratory Volumes and Capacities
Residual volume Air remaining in lung after expiration About 1200 ml Slide 13.27b
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Respiratory Volumes and Capacities
Vital capacity The total amount of exchangeable air Vital capacity = TV + IRV + ERV Dead space volume Air that remains in conducting zone and never reaches alveoli – is therefore NOT involved in gas exchange About 150 ml Slide 13.28
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Respiratory Volumes and Capacities
Functional volume Air that actually reaches the respiratory zone Usually about 350 ml Respiratory capacities are measured with a spirometer Functional volume + Dead space volume = Tidal volume Slide 13.29
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Respiratory Capacities
Figure 13.9 Slide 13.30
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Vital capacity is the maximum volume of air we can inhale and exhale But our lungs still hold a residual volume
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Misconception: Dead space = residual volume
The dead space, with a volume of about 150 ml, comprises the air passage in the nose, pharynx, trachea, bronchi and bronchioles, where no gas exchange can occur. The residual volume refers to the volume of air remaining in the lungs after exhalation and is approximately 2500 ml during quiet breathing and 1200 ml after a maximal active exhalation.
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Misconception: “Inhaled air fills alveoli and gas exchange takes place between the inhaled atmosphere air and the blood capillary directly.” The efficiency of ventilation is higher when a person breathes rapidly and shallowly compared to when he breathes slowly and deeply Of the 500 ml of fresh air taken into the breathing system in each breath, due to the presence of the dead space, only about 350 ml reach the alveoli for gas exchange. Moreover, the relatively large proportion of residual air to tidal air further reduces the efficiency of gas exchange inside the alveoli. As the residual air is in direct contact with the alveolar membrane, the oxygen in the tidal air has to diffuse for some distance before reaching the gas exchange surface and entering into the blood (Fig. 16). This process again reduces the efficiency of the body in extracting oxygen from the tidal air.
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Air sacs empty; lungs fill
Air flows in one direction Through the more efficient lungs of birds (reference only) Air Anterior air sacs Posterior Trachea Lungs tubes in lung 1 mm Exhalation: Air sacs empty; lungs fill Inhalation: Air sacs fill Figure 22.7B
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Breathing is automatically controlled
Brain Cerebrospinal fluid Pons Medulla Nerve signals trigger contraction of muscles Breathing control centers stimulated by: CO2 increase / pH decrease in blood indicating CO2 and O2 levels CO2 and O2 sensors in aorta Diaphragm Rib muscles Breathing control centers in the brain Keep breathing in tune with body needs, sensing and responding to the CO2 level in the blood
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Neural Regulation of Respiration
Activity of respiratory muscles is transmitted to the brain by the nerves Neural centers that control rate and depth are located in the medulla Normal respiratory rate (eupnea) is 12–15 respirations per minute Hypernia is increased respiratory rate often due to extra oxygen needs
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Factors Influencing Respiratory Rate and Depth
Physical factors Increased body temperature Exercise Talking Coughing Volition (conscious control) Emotional factors
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Factors Influencing Respiratory Rate and Depth
Chemical factors Carbon dioxide levels Level of carbon dioxide in the blood is the main regulatory chemical for respiration Increased carbon dioxide increases respiration Changes in carbon dioxide act directly on the medulla oblongata
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Factors Influencing Respiratory Rate and Depth
Chemical factors (continued) Oxygen levels Changes in oxygen concentration in the blood are detected by chemoreceptors in the aorta and carotid artery Information is sent to the medulla oblongata
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Total amount of CO2 produced =
Miconception During vigorous exercise, exhaled air contains a higher conc. of carbon dioxide and a lower concentration of oxygen than that produced at rest. During vigorous exercise, ventilation can increase from the resting level of about 8 litres per minute to well over 90 litres per minute through an increase in rate and depth of breathing. The increase in ventilation is so remarkable that, except in the most exhaustive type of exercise, CO2 is exhaled as fast as it is produced by the active tissues. So the concentration of CO2 is relatively constant regardless of activity. Total amount of CO2 produced = Ventilation rate X CO2 concentration in arterial blood / CO2 concentration in exhaled air during exercise As the total amount of CO2 produced increases rapidly during exercise, it is removed immediately by a corresponding increase in the rate and depth of breathing which leads to a much greater ventilation rate. Thus the concentration of CO2 in the arterial blood or exhaled air remains rather constant (Vander et. al., 1994.)
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Fig 17 The effects of exercise on ventilation rate, and conc
Fig 17 The effects of exercise on ventilation rate, and conc. of oxygen and carbon dioxide in blood Despite the extremely rapid production of CO2 during exercise and the simultaneous consumption of. O2, ventilation increases so greatly that this prevents the blood concentration of these gases from changing significantly from normal. There is even a drop in blood CO2 level during maximal activity. Therefore, most physiologists believe that the increase in ventilation during exercise is NOT caused by changes in the level of either or both of these two respiratory gases.
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Misconception “During exercise, the production of a large amount of CO2 causes a build-up of CO2 in the blood that stimulates the respiratory centre.” As shown in Fig. 17, there is no increase in CO2 concentration in the arterial blood during vigorous exercise. Therefore, the increase in ventilation rate during exercise cannot be mediated through the stimulation of the respiratory centre by a higher CO2 level in blood. Evidences that a neural mechanism is involved: When the venous levels of C02, 02 and pH of a person are artificially maintained at resting levels, muscular activity results in a marked increase in ventilation. Passive ‘pumping’ of the limbs to excite these stretch receptors also increases the ventilation rate. These findings suggest that the increase in ventilation is caused by impulses reaching the respiratory centre from the stretch receptors (proprioceptors) in contracting skeletal muscles. When the cerebral cortex sends impulses to the contracting muscles, it is also sending parallel signals to the respiratory centre at the same time to increase the rate and depth of breathing. This is similar to the role of the cerebral cortex in increasing the cardiac output during exercise. Consequently, the respiratory and circulatory adjustments to exercise are well integrated through these higher levels of the nervous system.
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TRANSPORT OF GASES IN THE BODY
Blood transports respiratory gases The heart pumps oxygen-poor blood to the lungs Where it picks up O2 and drops off CO2 Then the heart pumps the oxygen-rich blood to body cells Where it drops off O2 and picks up CO2 Exhaled air Inhaled air Air spaces Alveolar epithelial cells CO2 O2 CO2-rich, O2-poor blood O2-rich, CO2-poor Heart Tissue capillaries Interstitial fluid Tissue cells throughout body capillaries of lung
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22.10 Hemoglobin carries O2 and helps transport CO2 and buffer the blood Iron atom Heme group O2 loaded in lungs O2 unloaded in tissues Polypeptide chain Most CO2 in the blood --Is transported as bicarbonate ions in the plasma CO2 + H2O H2CO3 H+ HCO3– Carbon dioxide Water Carbonic acid Hydrogen ions Bicarbonate
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Exchange of gases between blood and body cells
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Hemoglobin also helps transport CO2
Figure 42.30 Tissue cell CO2 Interstitial fluid CO2 produced CO2 transport from tissues Blood plasma within capillary Capillary wall H2O Red blood cell Hb Carbonic acid H2CO3 HCO3– H+ + Bicarbonate Hemoglobin picks up CO2 and H+ Hemoglobin releases CO2 and H+ CO2 transport to lungs Alveolar space in lung 2 1 3 4 5 6 7 8 9 10 11 To lungs Carbon dioxide produced by body tissues diffuses into the interstitial fluid and the plasma. Over 90% of the CO2 diffuses into red blood cells, leaving only 7% in the plasma as dissolved CO2. Some CO2 is picked up and transported by hemoglobin. However, most CO2 reacts with water in red blood cells, forming carbonic acid (H2CO3), a reaction catalyzed by carbonic anhydrase contained. Within red blood cells. Carbonic acid dissociates into a biocarbonate ion (HCO3–) and a hydrogen ion (H+). Hemoglobin binds most of the H+ from H2CO3 preventing the H+ from acidifying the blood and thus preventing the Bohr shift. CO2 diffuses into the alveolar space, from which it is expelled during exhalation. The reduction of CO2 concentration in the plasma drives the breakdown of H2CO3 Into CO2 and water in the red blood cells (see step 9), a reversal of the reaction that occurs in the tissues (see step 4). Most of the HCO3– diffuse into the plasma where it is carried in the bloodstream to the lungs. In the HCO3– diffuse from the plasma red blood cells, combining with H+ released from hemoglobin and forming H2CO3. Carbonic acid is converted back into CO2 and water. CO2 formed from H2CO3 is unloaded from hemoglobin and diffuses into the interstitial fluid.
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CONNECTION 22.11 The human fetus exchanges gases with the mother’s bloodstream Placenta, containing maternal blood vessels and fetal capillaries Umbilical cord, containing fetal blood vessels Amniotic fluid Uterus A human fetus Exchanges gases with maternal blood in the placenta Figure 22.11
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Fetal hemoglobin Enhances oxygen transfer from maternal blood At birth, increasing CO2 in the fetal blood Stimulates the breathing control centers to initiate breathing
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Smoking is a deadly assaults on our respiratory system
CONNECTION Smoking is a deadly assaults on our respiratory system Mucus and cilia in the respiratory passages Protect the lungs Can be destroyed by smoking
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Causes lung cancer, heart disease, and emphysema
Smoking Causes lung cancer, heart disease, and emphysema Lung Heart Figure 22.6
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Respiratory Disorders: Chronic Obstructive Pulmonary Disease (COPD)
Exemplified by chronic bronchitis and emphysema Major causes of death and disability in the United States
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Respiratory Disorders: Chronic Obstructive Pulmonary Disease (COPD) --reference
Features of these diseases Patients almost always have a history of smoking Labored breathing (dyspnea) becomes progressively more severe Coughing and frequent pulmonary infections are common
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Respiratory Disorders: Chronic Obstructive Pulmonary Disease (COPD)
Features of these diseases (continued) Most victimes retain carbon dioxide, are hypoxic and have respiratory acidosis Those infected will ultimately develop respiratory failure
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Emphysema Alveoli enlarge as adjacent chambers break through
Chronic inflammation promotes lung fibrosis Airways collapse during expiration Patients use a large amount of energy to exhale Overinflation of the lungs leads to a permanently expanded barrel chest Cyanosis appears late in the disease
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Chronic Bronchitis Mucosa of the lower respiratory passages becomes severely inflamed Mucus production increases Pooled mucus impairs ventilation and gas exchange Risk of lung infection increases Pneumonia is common Hypoxia and cyanosis occur early
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Chronic Obstructive Pulmonary Disease (COPD) --reference
Figure 13.13
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Lung Cancer Accounts for 1/3 of all cancer deaths in the United States
Increased incidence associated with smoking
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Sudden Infant Death syndrome (SIDS)
Apparently healthy infant stops breathing and dies during sleep Some cases are thought to be a problem of the neural respiratory control center One third of cases appear to be due to heart rhythm abnormalities
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Asthma Chronic inflamed hypersensitive bronchiole passages
Response to irritants with dyspnea*, coughing, and wheezing Dyspnea--Difficult or laboured respiration
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Developmental Aspects of the Respiratory System (reference)
Lungs are filled with fluid in the fetus Lungs are not fully inflated with air until two weeks after birth Surfactant that lowers alveolar surface tension is not present until late in fetal development and may not be present in premature babies
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Developmental Aspects of the Respiratory System
Important birth defect Cystic fibrosis – oversecretion of thick mucus clogs the respiratory system
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Respiratory Rate Changes Throughout Life
Newborns – 40 to 80 respirations per minute Infants – 30 respirations per minute Age 5 – 25 respirations per minute Adults – 12 to 18 respirations per minute Rate often increases somewhat with old age
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Aging Effects (reference)
Elasticity of lungs decreases Vital capacity decreases Blood oxygen levels decrease Stimulating effects of carbon dioxide decreases More risks of respiratory tract infection
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