Pulmonary Respiration System PDF

**The Respiration System and Homeostasis:** Overview - The respiratory system contributes to homeostasis by providing for the exchange of gases (oxygen and carbon dioxide) b/w the atmospheric air, blood, and tissue cells - It also helps adjust the pH of body fluids - Reminders:...

**The Respiration System and Homeostasis:** Overview - The respiratory system contributes to homeostasis by providing for the exchange of gases (oxygen and carbon dioxide) b/w the atmospheric air, blood, and tissue cells - It also helps adjust the pH of body fluids - Reminders: - Hydrogen bonds that link neighboring water molecules give water considerable cohesion and create a very high surface tension - Cilia are short hair-like projections that extend from the surface of a cell - Each cilium contains a core of microtubules surrounded by plasma membrane - Cellular respiration is the process by which a nutrient molecule (glucose, fatty acid, or amino acid) is broken down in the presence of oxygen to form CO2, water, and energy (ATP + heat) Respiration -- the process of supplying the body with O2 and removing CO2 - 5 steps: - 1\. Ventilation - Air flows in and out of the lungs - 2\. Pulmonary gas exchange - Gas exchange b/w alveoli and capillaries in lungs - 3\. Transport of O2 and CO2 by the blood - 4\. Systemic gas exchange - Gases exchanged b/w blood and tissues - 5\. Cellular Respiration - Cells consume O2 and give off CO2 as metabolic reactions break down nutrient molecules in order to produce ATP Components of the respiratory system: - Structures - Nose - Major fxn filters, warms, and humidifies incoming air - Air enters the nostrils passes coarse hairs that trap and filter out large dust particles flows over shelflike extensions of bone called conchae that extend from the wall of the nasal cavity - Turbulence also allows the incoming air to be warmed by blood circulating in abundant capillaries and to be humidified by droplets of water evaporating from the mucosal surface - Pharynx - Larynx -- epiglottis - Trachea - Lungs - Contain smaller bronchi, bronchioles, and numerous alveoli - Primary bronchi -- right and left - Alveoli -- microscopic air sacs which are the site of gas exchange b/w air and blood - Each lung is enclosed in a double-layered membrane of epithelium and connective tissue called the pleura - Outer layer -- parietal pleura - Lines the wall of the thoracic cavity - Inner layer -- visceral pleura - Covers the lungs themselves - b/w the visceral and parietal pleura is a small space -- pleural cavity - contains a few milliliters of lubricating fluid secreted by the membranes - the fluid helps reduce friction b/w the membranes allowing them to slide easily over one another during breathing - intrapleural fluid also causes the two membranes to adhere to one another - inflammation of the pleural membranes (pleurisy) -- may cause pain d/t friction b/w parietal and visceral layers - if inflammation persists, excess fluid accumulates in the pleural space pleural effusion - All of the structures that carry air to and from the alveoli of the lungs are collectively referred to as the airways Functional Zones: - 23 generations of branching - Est. 300 million alveoli with a surface area of 75m^2^ - 2 functional zones: - Conducting zone - From nose to terminal bronchioles - Filters, warms, humidifies air - Conducts air to the lungs - No gas exchange - Respiratory zone - Portion of respiratory system that contain alveoli - Carries out gas exchange - Respiratory bronchioles, alveolar ducts, alveolar sacs *Each lung contains all the branches of a primary bronchus (Figure 18.2a, c). On entering the lungs, the primary bronchi divide to form smaller bronchi---the secondary bronchi, one for each lobe of the lung. (The right lung has three lobes; the left lung has two.) The secondary bronchi continue to branch, forming still smaller bronchi, called tertiary bronchi, that divide several times, eventually giving rise to smaller bronchioles. Bronchioles in turn branch into even smaller tubes called terminal bronchioles. Terminal bronchioles subdivide into microscopic branches called respiratory bronchioles, which have a few alveoli that extend from their walls. As the respiratory bronchioles penetrate more deeply into the lungs, they subdivide into several alveolar ducts, which contain more alveoli. The alveolar ducts give rise to alveolar sacs, which contain large numbers of alveoli arranged in clusters. An alveolar sac is comparable to a bunch of grapes, with each grape being an alveolus. It has been estimated that the lungs contain 300 million alveoli, providing an immense total surface area of 75 m2---about the size of a racquetball court---for gas exchange. The respiratory passages from the trachea to the alveoli contain about 23 generations of branching (Figure 18.2f). This extensive branching from the trachea resembles an inverted tree and is commonly referred to as the bronchial tree.* Respiratory Epithelium: - Mucociliary escalator -- the movement of mucus along resp. tract toward the pharynx - Larger bronchi - Outer layer = cartilage plates - Middle layer = smooth muscle - Inner layer = mucous membrane - Airway lines with mucosa - Layer of epithelial cells - Epithelium of many portions have ciliated cells, scattered goblet cells - Goblet cells -- cells that secrete mucus - Mucus -- traps inhaled particles and act as a lubricant for the lining of the resp. tract - Underlying layer of connective tissue - Branching -- changes - Plates of cartilage less abundant - finally disappear in the bronchioles - Amount of smooth muscle increases - the smooth muscle encircles the lumen in spiral bands - Mucosa change from ciliated epithelium to nonciliated in the terminal bronchioles - In regions where cilia are absent, inhaled particles are removed by macrophages - movement of cilia is paralyzed by nicotine in cigarette smoke smokers cough often to remove foreign particles - Some goblet cells in larger bronchi to no goblet cells in terminal bronchioles *Only the tips of the cilia of the respiratory mucosa actually make contact with mucus. Beneath the mucus and surrounding the remaining parts of the cilia is a thin, watery saline layer known as periciliary fluid. Periciliary fluid facilitates movement of mucus along the respiratory tract. If the volume of periciliary fluid is reduced, the mucus thickens and entangles the cilia, the cilia are unable to move the mucus, and the mucus clogs the airways.* Bronchodilator -- impacts smooth muscle The Nose Brings Air into the Respiratory System *The lack of cartilage and the presence of smooth muscle in bronchioles allows these tubes to change their diameters, altering the flow of air to the alveoli. Bronchioles are the main sites of resistance to airflow, just as arterioles are the main sites of resistance to blood flow. Bronchiolar smooth muscle is innervated by both the sympathetic and parasympathetic divisions of the autonomic nervous system (ANS). During exercise, norepinephrine released from sympathetic neurons, and epinephrine and norepinephrine secreted from the adrenal medulla bind to β2-adrenergic receptors, causing relaxation of bronchiolar smooth muscle, which dilates the bronchioles (bronchodilation). Because more air reaches the alveoli, lung ventilation increases. During periods of rest, acetylcholine (ACh) released from parasympathetic neurons binds to muscarinic ACh receptors, causing contraction of bronchiolar smooth muscle, which results in constriction of the bronchioles (bronchoconstriction). Because less air reaches the alveoli, lung ventilation decreases. Mediators of allergic reaction such as histamine also promote bronchoconstriction by causing contraction of bronchiolar smooth muscle. The bronchoconstriction may be so severe that very little air reaches the alveoli.* Alveoli - Air-filled sacs that extend from the respiratory bronchioles, alveolar ducts, and alveolar sacs - Thin, single layer of epithelium supported by a basement membrane - Types of cells: - Type I alveolar cells - Main site of gas exchange - More numerous - Dorm a nearly continuous alveolar wall - Type II alveolar cells - Secretes alveolar fluid -- includes surfactant - Surfactant: - Complete mixture of lipids and proteins - Lowers the surface tension of alveolar fluid - Reduces the tendency of alveoli to collapse - Keeps surface b/w cells and the air moist - Alveolar macrophages - Roam alveolar spaces and phagocytize fine dust particles, debris, any microbes - Elastic fibers - Thin layer beneath alveolar cells -- allows for elastic recoil when lung are stretched - Capillaries - Extensive yet thin network covering outer surface of alveoli - Rapid diffusion/gas exchange - Each capillary consists of a single layer of endothelial cells and a basement membrane - The capillary supply is so dense that the alveoli are considered to be surrounded by a nearly continuous "sheet" of blood - Respiratory membrane: - Gas exchange - Diffusion across alveolar and capillary walls (respiratory membrane) - Composed of: - A layer of type I and type II alveolar cells make up the alveolar epithelium - Epithelial basement membrane -- underlying the alveolar epithelium - Capillary basement membrane -- often fused to epithelial basement membrane - Capillary endothelium - 0.5 micrometers thick (1/16 the diameter of an erythrocyte) *The exchange of O2 and CO2 between the air spaces in the lungs and the blood takes place by diffusion across the alveolar and capillary walls, which together form the respiratory membrane. Extending from the alveolar air space to the blood, the respiratory membrane consists of four layers: (1) A layer of type I and type II alveolar cells that constitutes the alveolar epithelium, (2) an epithelial basement membrane underlying the alveolar epithelium, (3) a capillary basement membrane that is often fused to the epithelial basement membrane, and (4) the capillary endothelium. Despite having several layers, the respiratory membrane is very thin---only 0.5 μm thick, about one-sixteenth the diameter of an erythrocyte---to allow rapid diffusion of gases.* Blood flow to the lungs: - Pulmonary circulation - Consists of blood vessels that carry blood from heart to alveoli of lungs and back to the heart - Lungs pulmonary arteries smaller pulmonary arterioles even smaller pulmonary capillaries surrounding alveoli - Blood is oxygenated and then enters pulmonary venules veins heart for circulation of oxygenated blood - Blood flow is high (rate of blood flow is high) - Lungs received the entire Cardiac Output from right ventricle (5.25 L/min) - Right ventricle does not have to pump as hard to get blood to the lungs - Higher rate than any other tissue of the body - Blood pressure is low (resistance of blood flow is low) - Pulmonary blood vessels have larger diameters, thinner wall, and are more compliant than systemic blood vessels - Normal pulmonary pressure 25/8 mmHg **Ventilation** (Breathing): - Mechanical flow of air into and out of the lungs - Dependent on: - Atmospheric pressure: - Atmospheric pressure is the pressure of the air in the atmosphere, which at sea level is about 760 millimeters of mercury (mmHg), or 1 atmosphere (atm) - Alveolar pressure - Alveolar pressure is the pressure of air within the alveoli of the lungs - Depending on the stage of the breathing cycle, it may be equal to, lower than, or higher than atmospheric pressure. Air flows into or out of the lungs because a pressure gradient exists between the atmosphere and the alveoli - Resting phase = alveolar pressure and atmospheric pressure is the same - Inspiration = air moves into the lungs when alveolar pressure is lower than atmospheric pressure. - muscles contract and alveolar pressure decreases, causing air to flow into the lungs - Expiration = air moves out of the lungs when alveolar pressure is higher than atmospheric pressure - Intrapleural pressure -- always negative pressure (lower than atmospheric pressure) -- functions as a vacuum - the pressure within the pleural cavity - Recall that the pleural cavity is the space between the parietal and visceral layers of the pleura. A small amount of intrapleural fluid is present in this space. Intrapleural pressure is always a negative pressure (lower than atmospheric pressure), ranging from 754--756 mmHg during normal quiet breathing. - Because the pleural cavity has a negative pressure, it essentially functions as a vacuum. The suction of this vacuum couples the lungs to the chest wall via the pleura to form the lung--chest wall system. - Lung-chest wall system - If thoracic cavity increases in size, lungs also expand - If thoracic cavity decreases in size, the lungs recoil (become smaller) - The changes in lung volume caused by alterations in thoracic cavity size in turn cause a change in alveolar pressure - Air flow is dependent on pressure gradients - Boyles law and the lungs: - Volume increase = pressure decreases - Volume decreases = pressure increases Breathing Cycle: - Normal respiratory rate = 12 breaths / minute - Three phases: - Rest - No air movement into or out of the lungs - Inspiration - Brining air into the lungs from the atmosphere - Achieved by increasing the volume of the lungs and thereby, decreasing alveolar pressure - Respiratory muscles contact to cause an increase in thoracic volume - Results in a drop in alveolar pressure - Air moves into the lungs - Boyle's law -- the volume of a gas varies inversely with its pressure - Gas always moves from an area of higher pressure to an area of lower pressure - Muscles of inspiration - Diaphragm (most important) - Innervates by fibers of the phrenic nerve - Contraction causes it to flatten - Responsible for about 75% of air that enters lungs during quiet breathing - External intercostals - Intercostal nerves - Pull ribs upward and outward - Accessory muscles of inspiration - SCM -- elevates the sternum - Scalenes -- elevates the upper two ribs - Expiration - Expelling air into the environment from the lungs - Normal expiration is a passive process -- no muscles contraction involved - Respiratory muscles relax - Rib cage decreases volume - Alveolar pressure increases - Air flows out - Forced expiration (active process) -- accessory muscles contract - Abdominal muscles (rectus abdominis, ext/int obliques, transverse abdominis - Forces diaphragm upward - Internal intercostals - Pulls ribs downward - Although intrapleural pressure is always less than alveolar pressure, it may exceed atmospheric pressure briefly during forceful expiration, such as during a cough Factors Affecting Ventilation: - Surface tension of alveolar fluid - Reduced by surfactant - Intersperses between water molecules at the air-water interface - Disrupts cohesive forces b/w water molecules = decrease in surface tension - Reduces work of breathing and increase lung compliance - Infant respiratory distress syndrome -- deficiency of surfactant - Can be calculated using the law of Laplace - Compliance of Lungs - How much effort is being required to stretch the lungs and chest wall -- based on elasticity and surface tension - High compliance = lung and chest walls expand easily - The lungs normally have high compliance and expand easily because elastic fibers that are present in lung tissue are easily stretched and surfactant in alveolar fluid reduces surface tension - increased lung compliance occurs in emphysema because there is less elastic recoil of the lungs due to destruction of elastic fibers in alveolar walls. - Low compliance = lungs and chest wall resist expansion - Decreased compliance is a common feature in pulmonary conditions that - \(1) scar lung tissue, - \(2) cause lung tissue to become filled with fluid (pulmonary edema) - \(3) produce a deficiency in surfactant, - \(4) impede lung expansion in any way (for example, paralysis of the intercostal muscles) - Airway resistance - Rate depends on both the pressure gradient and resistance - Airflow = the pressure gradient b/w the alveoli and the atmosphere divided by the resistance Ventilation-Perfusion Matching (V:Q matching) - Ventilation of alveoli must be matched with perfusion (blood flow) to maximize gas exchange - Regulatory mechanisms for this: - Local chemical mediators - CO2-CO2 level in an alveolus controls ventilation by altering bronchiolar diameter - O2-O2 level in blood of pulmonary arteries control perfusion by altering arteriolar diameter - Ventilation \> perfusion - CO2 levels decrease (increased CO2 exhaled) and O2 levels increase and diffuses into blood (both the result of increased ventilation) - Low levels of CO2 causes constriction of bronchiolar smooth muscles (bronchoconstriction) - High levels of O2 causes relaxation of pulmonary arteriolar smooth muscles (vasodilation) -- opposite of how systemic circulation responds to low O2! - Bronchoconstriction decreases airflow to match smaller blood flow - Vasodilation increases blood flow to the overventilated alveolus - Perfusion \> Ventilation - Level of CO2 increases b/c excess blood flow drops off more CO2 than is exhaled in the air - O2 level decrease b/c the excess blood flow carries more O2 than the alveoli can bring in - High level of CO2 in the alveolus causes relaxation of bronchiolar smooth muscles (bronchodilation) - Low levels of O2 in the blood cause constriction of pulmonary arteriolar smooth muscle (vasoconstriction) - The bronchodilation increases airflow to match the larger blood flow and the vasoconstriction reduces blood flow to the underventilated alveolus If ventilation exceeds perfusion (Figure 18.7a), the CO2 level in the alveolus and surrounding tissue decreases because too much CO2 is exhaled due to the excess ventilation. In addition, the O2 level increases because the excess ventilation brings in more O2, which diffuses into the blood. To compensate for the ventilation--perfusion mismatch, the low level of CO2 in the alveolus causes contraction of bronchiolar smooth muscle (bronchoconstriction), and the high level of O2 in the blood causes relaxation of pulmonary arteriolar smooth muscle (vasodilation). The bronchoconstriction decreases airflow to match the smaller blood flow, and the vasodilation increases blood flow to the overventilated alveolus. If perfusion exceeds ventilation (Figure 18.7b), the level of CO2 in the alveolus and surrounding tissue increases because the excess blood flow drops off more CO2 than is exhaled into the air. In addition, the level of O2 decreases because the excess blood flow carries away more O2 than the alveoli can bring in. To compensate for the ventilation--perfusion mismatch, the high level of CO2 in the alveolus causes relaxation of bronchiolar smooth muscle (bronchodilation), and the low level of O2 in the blood causes constriction of pulmonary arteriolar smooth muscle (vasoconstriction). The bronchodilation increases airflow to match the larger blood flow and the vasoconstriction reduces blood flow to the underventilated alveolus. Note that an important difference between the pulmonary and systemic circulations is their autoregulatory response to changes in O2 level. The walls of blood vessels in the systemic circulation dilate in response to low O2. With vasodilation, O2 delivery increases, which restores the normal O2 level. By contrast, the walls of blood vessels in the pulmonary circulation constrict in response to low levels of O2. This response ensures that blood mostly bypasses those alveoli (air sacs) in the lungs that are poorly ventilated by fresh air. Thus, most blood flows to better-ventilated areas of the lung. (Shunting) Modified Respiratory Movements: A screenshot of a computer Description automatically generated Dead space -- air that is ventilated that is nor perfused. Too much air and not enough blood flow can increase dead space. Lung Volumes and Capacities: - Lung Volumes: - Tidal Volume (Vt) - Volume of air inspired or expired during a single breathing cycle, resting conditions - Inspiratory reserve volume (IRV) - Max volume of air that can be inspired after a normal inspiration - Expiratory reserve volume (ERV) - Max volume of air that can be expired after a normal respiration - Residual Volume (RV) - Volume that remains after maximum expiration - Lung Capacities: calculated by adding two or more lung volume - Functional residual capacity = RV + ERV - Volume of air in lungs at the end of normal respiration - Inspiratory capacity = Vt + IRV - Max volume of air that cab be inspired after a normal expiration - Vital capacity = IRV + Vt + ERV - Max volume of air that can be expired after a max inspiration - FEV1 -- forced expiratory volume in 1 second - Volume of that can be exhaled in 1 second w/ maximal effort following maximum inspiration - Total lung capacity = VC + RV Two Types of gas exchange: - 1\. Pulmonary Gas Exchange - Diffusion of oxygen from alveolar air to capillary blood - Diffusion of carbon dioxide in the opposite direction - Pulmonary capillaries pick up O2 from the alveolar air and unloads CO2 - Each gas diffuses independently from an area of its higher partial pressure to where its partial pressure is lower - 2\. Systemic Gas Exchange - Exchange of O2 and CO2 b/w systemic capillaries and tissue cells - Both types depend on several factors - Partial pressure differences of gases - Surface area available for gas exchange - Diffusion distance - Molecular weight and solubility of the gases Summary of Gas Laws - Dalton's Law - Each gas in a mixture of gases exerts its own pressure as if no other gases was present - The pressure of a specific gas in a mixture is called its partial pressure - The total pressure of the mixture can be calculated by adding together all of the partial pressures - atmospheric pressure is 760 mm/Hg -- this is determined by adding together all the partial pressures of nitrogen, oxygen, argon, carbon dioxide, and water vapor - Each gas diffuses across a permeable membrane from an area where its partial pressure is greater to the area where its partial pressure is less - The greater the difference in partial pressure, the faster the rate of diffusion - Henry's Law - The quantity of a gas that will dissolve is liquid is proportional to the partial pressure of the gas and its solubility - The ability of a gas to stay in solution is greater when its partial pressure is higher and when It has a high solubility in water - Solubility of CO2 is 24x greater than that of O2 O2 diffuses from alveolar air, where its partial pressure is 105 mmHg, into the blood in pulmonary capillaries, where PO2 is only 40 mmHg in a resting person. If you have been exercising, the PO2 is even lower because contracting muscle fibers are using more O2. Diffusion continues until the PO2 of pulmonary capillary blood increases to match the PO2 of alveolar air, 105 mmHg. Because there is a small amount of ventilation--perfusion mismatching from the apex to the base of the lungs due to gravitational effects, the PO2 of blood in the pulmonary veins is slightly less than the PO2 in pulmonary capillaries, about 100 mmHg. While O2 is diffusing from alveolar air into deoxygenated blood, CO2 is diffusing in the opposite direction. The PCO2 of deoxygenated blood is 45 mmHg in a resting person, and the PCO2 of alveolar air is 40 mmHg. Because of this difference in PCO2, carbon dioxide diffuses from deoxygenated blood into the alveoli until the PCO2 of the blood decreases to 40 mmHg. Expiration keeps alveolar PCO2 at 40 mmHg. Oxygenated blood returning to the left side of the heart in the pulmonary veins thus has a PCO2 of 40 mmHg. The number of capillaries near alveoli in the lungs is very large, and blood flows slowly enough through these capillaries that it picks up a maximal amount of O2. During vigorous exercise, when cardiac output is increased, blood flows more rapidly through both the systemic and pulmonary circulations. As a result, blood\'s transit time in the pulmonary capillaries is shorter. Still, the PO2 of blood in the pulmonary veins normally reaches 100 mmHg. In diseases that decrease the rate of gas diffusion, however, the blood may not come into full equilibrium with alveolar air, especially during exercise. When this happens, the PO2 declines and PCO2 rises in systemic arterial blood. The left ventricle pumps oxygenated blood into the aorta and through the systemic arteries to systemic capillaries. The exchange of O2 and CO2 between systemic capillaries and tissue cells is called systemic gas exchange. As O2 leaves the bloodstream, oxygenated blood is converted into deoxygenated blood. Unlike pulmonary gas exchange, which occurs only in the lungs, systemic gas exchange occurs in tissues throughout the body. The PO2 of blood pumped into systemic capillaries is higher (100 mmHg) than the PO2 in tissue cells (40 mmHg at rest) because the cells constantly use O2 to produce ATP. Due to this pressure difference, oxygen diffuses out of the capillaries into tissue cells and blood PO2 drops to 40 mmHg by the time the blood exits systemic capillaries. While O2 diffuses from the systemic capillaries into tissue cells, CO2 diffuses in the opposite direction. Because tissue cells are constantly producing CO2, the PCO2 of cells (45 mmHg at rest) is higher than that of systemic capillary blood (40 mmHg). As a result, CO2 diffuses from tissue cells through interstitial fluid into systemic capillaries until the PCO2 in the blood increases to 45 mmHg. The deoxygenated blood then returns to the heart and is pumped to the lungs for another cycle of pulmonary gas exchange. In a person at rest, tissue cells, on average, need only 25% of the available O2 in oxygenated blood; despite its name, deoxygenated blood retains 75% of its O2 content. During exercise, more O2 diffuses from the blood into metabolically active cells, such as contracting skeletal muscle fibers. Active cells use more O2 for ATP production, causing the O2 content of deoxygenated blood to drop below 75%. Know numbers of pp What happens when ventilation exceeds perfusion in the lungs? **A. ** The bronchiolar smooth muscles contract (bronchoconstriction) **B. ** The CO2 levels in the alveolus and surrounding tissue increases **C. ** The pulmonary arteriole constricts (vasoconstriction) **D. ** The O2 level in the blood vessel decreases Which type of cell in the lung secretes surfactant?  **A. ** Mucus cells **B. **Type I alveolar cells **C. **Ciliated cells **D. **Type II alveolar cells **E. **Goblet cell The pressure of a specific gas in a mixture is called its:  **A. **Partial pressure **B. **Absolute pressure **C. **Hydrostatic pressure **D. **Differential pressure **E. **Osmostic pressure What is the tidal volume of the lungs? **A. **It is the volume of air that remains in the lungs after a maximum expiration **B. **It is the volume of air inspired or expired during a single breathing cycle under resting conditions **C. **It is the maximum volume of air that can be expired after a normal expiration **D. **It is the maximum volume of air that can be expired after a maximum inspiration **E. **It is the maximum volume of air that can be inspired after a normal inspiration Which action involves a spasmodic contraction of the diaphragm followed by  a spasmodic closure of the larynx? **A. **Yawning **B. **Laughing **C. **Hiccupping **D. **Sneezing **E. **Coughing What factors affect lung compliance? **A. **Rigidity and osmostic pressure **B. **Elasticity and surface tension **C. **Osmolality and surface absorption **D. **Capillarity and airway resistance **E. **Poiseuille flow and gas pressure Identify the true statement about the *resting phase *in a respiratory cycle. **A. **During this phase, alveolar pressure is greater than atmospheric pressure **B. **Alveolar pressure is equal to atmospheric pressure during this phase **C. **Alveolar pressure is lower than atmospheric pressure in this phase **D. **The external intercostal muscles remain contracted during this phase **E. **The resting phase is characterized by a flattened diaphragm Flow of air into and out of the lungs can be attributed to: **A. **The rigidity of the diaphragm that maintains the pressure in the thorax **B. **A pulsating contraction and relaxation movement of the trachea **C. **A change in the volume of the intrapleural fluid **D. **A pressure gradient between the atmosphere and the alveoli **E. **The air turbulence created in the nasal conchae In the process of respiration, the step in which air flows into and out of the lungs is called: **A. **Ventilation **B. **Bronchoconstriction **C. **Inflation reflex **D. **Systemic circulation **E. **Perfusion Where does the process of gas exchange take place in the body during respiration?  **A. **In the tracheal passage **B. **In the right pulmonary bronchus **C. **In the nasal conchae **D. **In the pulmonary capillaries **E. **Between the parietal and visceral pleura Transport of Oxygen and Carbon Dioxide: - O2 transported in the blood by hemoglobin - Oxygen does not dissolve easily in water - Only about 1.5% of inhaled O2 dissolved in blood plasma - 98.5% is bound to hemoglobin in RBCs - Each of 4 heme groups has an iron ion that can bind to one oxygen molecule - A single heme-polypeptide unit can exist in two forms: - Deoxyhemoglobin -- no O2 bound - Oxyhemoglobin -- O2 bound - Oxygen-Hemoglobin Dissociation Curve - Partial pressure of oxygen determines how much binds to hemoglobin - O2 that is bound to hemoglobin is trapped inside erythrocytes. So only dissolved O2 can diffuse out of capillaries into tissue cells - As PO2 increases, more O2 combines with hemoglobin, until all available hemoglobin is saturated - Binding of O2 to subunit of hemoglobin causes the hemoglobin molecule undergoes a conformational change -- increases the affinity of hemoglobin for the next O2 molecule - In pulmonary capillaries, PO2 is low, hemoglobin does not hold as much O2, and dissolved O2 is unloaded via diffusion into tissue cells *Although PO2 is the most important factor that determines the percent saturation of hemoglobin, several other factors influence the affinity with which hemoglobin binds O2. In effect, these factors shift the entire curve either to the left (higher affinity) or to the right (lower affinity). The changing affinity of hemoglobin for O2 is another example of how homeostatic mechanisms adjust body activities to cellular needs. Each one makes sense if you keep in mind that metabolically active tissue cells need O2 and produce acids, CO2, and heat as wastes. The following four factors affect the affinity of hemoglobin for O2:* - Oxygen Transport: - Factors affecting oxygen affinity to hemoglobin - Acidity (pH) - As acidity increases (pH decreases), affinity of hemoglobin for O2 decreases, O2 dissociates more readily from hemoglobin - Increasing acidity enhances the unloading of oxygen from hemoglobin - Partial pressure of carbon dioxide - As PCO2 rises, hemoglobin releases O2 more readily - Increases PCO2 produces a more acidic environment, which helps release O2 from Hgb - Temperature - As temperature increases, so does the amount of O2 released from Hgb - Biphosphoglycerate (BPG) - Substance found in erythrocytes - Decreases the affinity of Hgb for O2 and helps unload O2 from Hgb - Greater levels of BPG, the more O2 unloaded from hemoglobin - Levels higher in people living at higher altitudes - Levels increased by thyroxine, growth hormone, epinephrine, norepinephrine, and testosterone - Carbon Dioxide Transport: - Is transported though the blood in three forms: - Dissolved in plasma -- 7% - Carbamino compounds -- 23% - Carbon dioxide combines the amino acids and proteins in blood - Since most prevalent protein in blood is hgh, most CO2 transported in this manner is bound to hemoglobin - Bicarbonate ions -- 70% - As CO2 diffuses into systemic capillaries and enters erythrocytes, it reacts with water to form carbonic acid, which dissociates into H+ and HCO3- - Net effect of these reactions is that CO2 is removed from tissue cells and transported in blood plasma as HCO2- - As blood passes through pulmonary capillaries in the lungs, all these reactions reverse and CO2 is exhaled Gas Exchange and Transport Can Be Summarized  *Summary of chemical reactions that occur during gas exchange. (a) As carbon dioxide (CO2) is exhaled, hemoglobin (Hb) inside erythrocytes in pulmonary capillaries unloads CO2 and picks up O2 from alveolar air. Binding of O2 to Hb--H releases hydrogen ions (H+). Bicarbonate ions (HCO3−) pass into the erythrocyte and bind to released H+ , forming carbonic acid (H2CO3). The H2CO3 dissociates into water (H2O) and CO2, and the CO2 diffuses from blood into alveolar air. To maintain electrical balance, a chloride ion (Cl−) exits the erythrocyte for each HCO3− that enters (reverse chloride shift). (b) CO2 diffuses out of tissue cells that produce it and enters erythrocytes, where some of it binds to hemoglobin, forming carbaminohemoglobin (Hb--CO2). This reaction causes O2 to dissociate from oxyhemoglobin (Hb--O2). Other molecules of CO2 combine with water to produce bicarbonate ions (HCO3−) and hydrogen ions (H+). As Hb buffers H+ , the Hb releases O2 (Bohr effect). To maintain electrical balance, a chloride ion (Cl−) enters the erythrocyte for each HCO3− that exits (chloride shift).* *Deoxygenated blood returning to the pulmonary capillaries in the lungs (Figure 18.14a) contains CO2 dissolved in blood plasma, CO2 combined with globin as carbaminohemoglobin (Hb--CO2), and CO2 incorporated into HCO3− within erythrocytes. The erythrocytes have also picked up H+, some of which binds to and therefore is buffered by hemoglobin (Hb--H). As blood passes through the pulmonary capillaries, molecules of CO2 dissolved in blood plasma and CO2 that dissociates from the globin portion of hemoglobin diffuse into alveolar air and are exhaled. At the same time, inhaled O2 diffuses from alveolar air into erythrocytes and is binding to hemoglobin to form oxyhemoglobin (Hb--O2). Carbon dioxide is also released from HCO3− when H+ combines with HCO3− inside erythrocytes. The H2CO3 formed from this reaction then splits into CO2, which is exhaled, and H2O. As the concentration of HCO3− declines inside erythrocytes in pulmonary capillaries, HCO3− diffuses in from the blood plasma, in exchange for Cl−. In sum, oxygenated blood leaving the lungs has increased O2 content and decreased amounts of CO2 and H+. In systemic capillaries, as cells use O2 and produce CO2, the chemical reactions reverse* Neurologic Control of Respiratory Drive: - The respiratory center is composed of neurons from: - The medullary respiratory center of the medulla oblongata - The pontine respiratory center of the pons - Medullary Respiratory Center -two collections of neurons - Dorsal respiratory group - Mostly inspiratory neurons - Active during normal quiet breathing -- send action potential to diaphragm and ext. intercostals - Ventral respiratory group - Pre-Botzinger complex -- cluster of neurons that function as a "pacemaker" that set the basic rhythm breathing (exact mechanism unknown) - Also contains inspiratory and expiratory neurons - Do not participate in normal quite breathing but become activated when forceful breathing is required - Send action potentials to accessory muscles - During forceful expiration -- DRG and VRG inspiratory neurons are inactive, VRG expiratory neurons are activated and send signals to accessory muscle of expiration - Pontine respiratory center - Two groups of neurons -- help coordinate the transition b/w inspiration and expiration - Pneumotaxic area (in upper pons) - Also known as the pontine respiratory group - Sends inhibitory signals to the DRG - Function to turn off DRG before lungs become too full of air (shortens the duration of inspiration) - Apneustic area (in lower pons) - Sends excitatory signs to DRG that activate it and prolong inspiration - Result in ling, deep inspiration - When the pneumotaxic area is active, it overrides signals from the apneustic area - These centers can be overridden by higher brain function - We do have ability voluntary control over breathing as well - The ability not to breath is limited by the buildup of CO2 and H+ in the body - If breath is held long enough to cause fainting, breathing resumes when consciousness is lost Regulation of Breathing - Chemoreceptor regulation of breathing - Chemical stimuli modulate rate and depth of breathing - Chemoreceptors -- sensory receptors that are responsive to chemicals - Central chemoreceptors - Located in medulla oblongata - Respond to changes in H+, CO2 (or both) in CSF - Stimulated and respond vigorously to the resulting increase in H+ level - Severe deficiency of O2 depresses activity of the central chemoreceptors and DRG, which then do not respond well to any inputs and send fewer action potentials to the muscles of inspiration - Peripheral chemoreceptors - Located in aortic bodies and carotid bodies (located close to baroreceptors) - Respond to changes in PO2, H+, PCO2 in the blood - Respond to high PCO2 and rise in H+, and low O2 - As a result of increased PCO2, decreases pH (increased H+), or decreased PO2, input from the central and peripheral chemoreceptors causes the DRG to become highly active and the rate and depth of breathing increase - Proprioceptor regulation of breathing - During exercise, input from proprioceptors, which monitor movement of joints and muscles stimulate the DRG of the medulla oblongata - Other influences on breathing - Limbic system stimulation - Anticipation of activity or emotional anxiety - Temperature - Increase in body temperature causes increase RR - Pain - Initially brief apnea, prolonged somatic pain increases RR, Visceral pain may slow RR - Stretching the anal sphincter muscles - Increases RR, used to stimulate ventilation in newborn or person who has stopped breathing - Irritation of airways - Physical or chemical irritation causes immediate cessation of breathing followed by coughing or sneezing - Blood pressure - Sudden rise in BP decreases RR Signs and symptoms of pulmonary disease: - Dyspnea - subjective experience of breathing discomfort - Most common symptom of cardiac and respiratory diseases - May also occur with pain, trauma, anxiety, and psychogenic disorders - Variations -- distinct sensation which may vary in intensity. May complain of: - Breathlessness - Air hunger - SOB - Increased work of breathing - Chest tightness - Causes: - Diffuse or focal disturbances of ventilation, gas exchange, or ventilation-perfusion relationships - Diseases that damage lung tissue (lung parenchyma) - Neurophysiologic mechanisms involved in an impaired sense of effort where the perceived work of breathing is greater than the actual motor response generated - Stimulation of a variety of receptors can contribute to the sensation of dyspnea - Severe sigs of dyspnea -- increased work of breathing - Flaring of the nostrils - Use of accessory muscles of respiration -- suprcostal (SCM, scalenes), intercostal retraction - Timing - Paroxysmal nocturnal dyspnea (PND) - Awaking at night gasping for air; must sit up for relief - Indicative of cardiac or pulmonary disease - Dyspnea on exertion (DOE) - Shortness of breath with activity - Positional - Orthopnea (dyspnea worse in supine position) - Abdominal contents exert pressure on the diaphragm and decreased efficiency of respiratory muscles - classically with congestive heart failure and pulmonary edema but can also be present in emphysema, pneumonia and other disorders - most patients with significant dyspnea have more trouble when lying flat - Quantifying - Is there an impact of the patients daily life - assessing improvement or progression over time or after treatment - Ask how far pt can walk or number of stairs they can climb before getting significant symptoms - Grades: - Grade 1 -- no dyspnea except severe exercise/activity - Grade 2 -- dyspnea when climb the step in hurry or climb a small hill - Grade 3 -- walk slower compared to common people - Grade 4 -- must stop for breathing after 100 yards of walk - Grade 5 -- dyspnea while put on/off clothes - Etiologies of dyspnea **Cardiac** **Pulmonary** **Non-cardiac/pulmonary** -------------------------------- ----------------------------------------- --------------------------------------------------------------------- congestive heart failure (CHF) chronic obstructive lung disease (COPD) renal failure (with volume overload) coronary artery disease asthma anemia pulmonary embolism obesity pericardial disease pneumonia neuromuscular disorders causing weakness of the respiratory muscles pleural effusion arrhythmia malignancy (lung or metastatic cancer) thyroid disease valvular heart disease interstitial lung disease/fibrosis chest wall deformities (kyphosis, scoliosis) bronchiectasis pulmonary hypertension psychogenic causes (panic disorders, anxiety) foreign body airway obstruction - Cough -- protective reflex that helps clear the airways by explosive expiration - Cough reflex - Triggered by inhaled particles, accumulated mucus, inflammation, or the presence of a foreign body - Irritant receptors in the airway are stimulated - Few such receptors in the most distal bronchi are the alveoli; thus it is possible for significant amounts of secretions to accumulate in the distal respiratory tree without cough being initiated - Stimulation of cough receptors is transmitted centrally though the vagus nerve - Cough occurs frequently in healthy individuals, and those with an inability to cough effectively are at greater risk for pneumonia - Acute cough - Resolves within 2-3 weeks of the onset of illness or resolves with tx of underlying condition - Most often with upper respiratory tract infections, allergic rhinitis, acute bronchitis, PNA, CHF, PE, or aspiration - Chronic cough - Persisted more than 3 weeks - Nonsmoker: postnasal drainage, eosinophilic bronchitis, asthma, GERD - Smokers: chronic bronchitis, lung CA - Individuals taking angiotensin-converting enzyme inhibitors (dry cough) - Altered breathing pattern - Hyperventilation - Alveolar ventilation exceeds the metabolic demands - Is caused by anxiety, head injury, or server hypoxemia - Lungs remove CO2 at higher rate than it is produced, resulting in decreased PaCO2, causing hypocapnia (PaCO2 \ 44 mmHg) (also called hypercarbia) - Hypercapnia: - Increased carbon dioxide (CO2) in the arterial blood - Occurs from decreased drive to breathe or an inadequate ability to respond to ventilatory stimulation - Causes include: - Depression of the respiratory center by [drugs] - Diseases of the medulla, including infections of the central nervous system or trauma - Abnormalities of the spinal conducting pathways, as in spinal cord disruption or [poliomyelitis] - Diseases of the neuromuscular junction or of the respiratory muscles themselves, as in [myasthenia gravis] or [muscular dystrophy] - Abnormalities of the thoracic cage, as in chest injury or congenital deformity - Obstruction of the large airways, as in [tumors] or [sleep apnea] - Increased work of breathing or increased physiologic dead space, as in [emphysema] - Leads to respiratory acidosis (increase in H+) - Hemoptysis - Expectoration of blood or bloody secretions from the lower respiratory tract - Blood that is expectorated is usually bright red, has an alkaline pH and is mixed with frothy sputum - Causes - Infection or inflammation that damages the bronchi (bronchitis, bronchiectasis) - Infection or inflammation that damages the lung parenchyma (PNA, TB , lung abscess) - Cancer - Pulmonary infarction - DO NOT CONFUSE with hematemesis which is vomiting of blood - Blood that is vomited is dark red, has an acidic pH and is mixed with food particles - Abnormal sputum - Changes in amount, consistency, color, and odor provide information - The gross and microscopic appearances of sputum enable identification of cellular debris or microorganisms that aid in dx and choice of therapy - Cyanosis - Bluish discoloration of the skin and mucous membranes - Caused by increasing amounts of desaturated hemoglobin in the blood - Peripheral: - Most often caused by poor circulation resulting from peripheral vasoconstriction (Raynaud's, cold, stress) - Best observed in the nail beds - Central cyanosis - Caused by decreased arterial oxygenation -- low partial pressure of oxygen (PaO2) - Most often caused by pulmonary disease or pulm/cardiac right to left shunts - Best observed in buccal mucous membranes and lips - Pain - Pain caused by pulmonary disorder originated in the pleurae, airways, or chest wall - Pleural pain - Most common pain caused by pulmonary diseases - Is usually sharp or stabbing in character - Infection and inflammation of the parietal pleura (pleuritis or pleurisy) can cause pain when the pleura stretch during inspiration and may be accompanied by a pleural friction rub - Central chest pain - Infection and inflammation either of the trachea or of the trachea and bronchi (tracheitis or tracheobronchitis) can cause central chest pain that is pronounced after coughing - Can be difficult to differentiate from cardiac chest pain - Chest wall pain - Likely from muscles or ribs - Common cause: rib fractures and excessive coughing - Clubbing - Selective bulbous enlargement of the end (distal segment) of a digit (finger or toe) - Its severity can be graded from 1-5 based on the extent of nail bed hypertrophy and the number of changes in the nails themselves - It is usually painless and develops gradually over weeks - Associated with diseases that cause hypoxemia - Bronchiectasis - Cystic fibrosis - Pulmonary fibrosis - Lung abscess - Congenital heart disease - It is rarely reversible with treatment of the underlying pulmonary condition - Pathogenesis of clubbing is unknown - Abnormal breathing patterns - Normal breathing -- Eupnea - Rhythmic and effortless - 8-16 bpm - Abnormal - Adjustments made with the body to minimize the work of the respiratory muscles - Labored breathing - Occurs whenever there is increased work of breathing, as in COPD (obstructive) - Prolonged inspiration or expiration, and stridor or expiratory wheezing are typical - Restricted breathing - Commonly caused by disorders that stiffen the lungs or chest wall and decrease compliance - Results in small tidal volumes and rapid ventilatory rate (tachypnea) Patterns of Respirations: - Kussmal respirations (hyperpnea) - Induces by strenuous exercise or metabolic acidosis - Slightly increased ventilatory rate - Very large tidal volume - Cheyne-Stokes Breathing - Characterized by alternating periods of deep and shallow breathing - Apnea lasting 15-60 seconds is followed by ventilations that increase in volume until a peak is reached, after which ventilation (tidal volume) decreases again to apnea - Result from any condition that slows the blood flow to the brainstem, which in turn slows impulses sending information to the respiratory centers of the brainstem  Conditions Caused By pulmonary disease or injury: - Hypoxemia - Reduced oxygenation of arterial blood (reduced PaO2) - Caused by respiratory alterations - Clinical manifestations of acute hypoxemia: - Cyanosis - Confusion - Tachycardia - Edema - Decreased renal output - Results from problems with one or more of the major mechanisms of oxygenation: - Oxygen delivery to the alveoli dependent on: - Oxygen content of the inspired air (FiO2) -- fraction of air composed of oxygen - Ventilating of the alveoli (as in hypoventilation) - Diffusion of oxygen from the alveoli into the blood depended on: - Balance b/w alveolar ventilation and perfusion (V/Q mismatch) - Diffusion of oxygen across the alveolocapillary membrane - Perfusion of pulmonary capillaries - Ventilation -- perfusion abnormalities: most common cause of hypoxemia - Inadequate ventilation of well-perfused areas of the lung (low V/Q) - Shunting -- occurs in atelectasis, asthma, pulmonary edema, pneumonia - Right left shunt -- blood passes through a portion of the capillary bed with no ventilation (decreased systemic PaO2 and hypoxemia) - Alveolar dead space: area where alveoli are ventilated but not perfused - Causes: +-----------------------------------+-----------------------------------+ | **Mechanism** | **Common Clinical Causes** | +===================================+===================================+ | Decrease in inspired oxygen | High altitude | | (decreased FiO2) | | | | Low oxygen content of gas mixture | | | | | | Enclosed breathing spaces | | | (suffocation) | +-----------------------------------+-----------------------------------+ | Hypoventilation of the alveoli | Lack of neurologic stim of | | | respiratory center (oversedation, | | | drug overdose, neurologic damage) | | | | | | Defects in chest wall mechanics | | | (trauma, chest deformity) | | | | | | Large airway obstruction (foreign | | | body, neoplasm) | | | | | | Increased work of breathing | | | (emphysema, severe asthma) | +-----------------------------------+-----------------------------------+ | Ventilation-perfusion mismatch | Asthma | | | | | | Chronic bronchitis | | | | | | Pneumonia | | | | | | ARDS (acute respiratory distress | | | syndrome) | | | | | | Atelectasis | | | | | | Pulmonary embolism | +-----------------------------------+-----------------------------------+ | Alveolocapillary diffusion | Edema | | abnormality | | | | Fibrosis | | | | | | Emphysema | +-----------------------------------+-----------------------------------+ | Decreased pulmonary capillary | Intracardiac defects | | perfusion | | | | Intrapulmonary arteriovenous | | | malformations | +-----------------------------------+-----------------------------------+ - Hypoxia (ischemia) - Reduced oxygenation of cells in tissues - May be caused by alterations of other systems as well Acute Respiratory Failure - Gas exchange is inadequate - Hypoxemia in which PaO2 is [\]50 mmHg with a pH [\ the atmospheric pressure - Causes: - Rib fracture, stab or bullet wounds - A surgical procedure that tears the pleura - Rupture of a bleb or bulla (larger vesicle) as occurs in COPD - Mechanical ventilation - Site of pleural rupture acts as a one-way valve - Air can enter on inspiration but can't escape during expiration. - As more and more air enters the pleural space, air pressure in the pneumothorax begins to exceed atmospheric pressure. - Air pressure in the pleural space pushes against the already recoiled lung, causing: - Compression atelectasis - Compression and displacement of the heart, great vessels, and trachea *The cause of bleb formation is not known, although more than 80% of these individuals have been found to have emphysema-like changes in their lungs even if they have no history of smoking or no known genetic disorder. Approximately 10% of affected individuals have a significant family history of primary pneumothorax that has been linked to autosomal dominant mutations in the folliculin gene, which influences cell-to-cell adhesion and cell growth and causes cystic lung disease* *Clinical manifestations of primary or secondary pneumothorax begin with sudden pleural pain, tachypnea, and dyspnea. Depending on the size of the pneumothorax, physical examination may reveal absent or decreased breath sounds and hyperresonance to percussion on the affected side. Tension pneumothorax may be complicated by severe hypoxemia, tracheal deviation away from the affected lung, and hypotension (low blood pressure). Deterioration occurs rapidly and immediate treatment is required. Diagnosis of pneumothorax is made with chest radiographs, ultrasound, and computed tomography (CT). Pneumothorax is treated by aspiration, usually with insertion of a chest tube that is attached to a water-seal drainage system with suction. After the pneumothorax is evacuated and the pleural rupture is healed, the chest tube is removed. For individuals with persistent air leaks, other interventions may be needed including thoracoscopic surgical techniques or pleurodesis (instillation of a caustic substance into the pleural space). Heimlich valves (one-way valves connected to the end of the chest drain) provide an option for home care in persistent spontaneous pneumothorax. Smoking cessation is strongly advised.* - Pleural Effusion -- Presence of fluid in the pleural space - **Transudative effusion** - Is watery and diffuses out of the capillaries. - Cardiovascular disease that causes high BP, or decreased oncotic pressure from hypoproteinemia (liver or renal disease) - **Exudative effusion** - Is less watery and contains high concentrations of white blood cells and plasma proteins. - Infection, inflammation, malignancy of the pleura - Stimulates mast cells to release biochemical mediators that increase capillary permeability - **Chylothorax**: Chyle (lymph and fat) exudate - Traumatic injury or infection disrupting lymph transport - **Hemothorax**: Blood -- hemorrhage into pleural space (injury, surgery, malignancy that damages blood vessels) - **Empyema**: Pus - Byproducts of infection dumped into pleural space by blocked lymphatic vessels - Pulmonary infections: Pneumonia, lung abscess - **Clinical** **manifestations**: Dyspnea and pleural pain - **Treatment**: Thoracentesis, chest tube, and surgery *Pleural effusion is the presence of fluid in the pleural space. The source of the fluid is usually from blood vessels or lymphatic vessels lying beneath either pleura, but occasionally an abscess or other lesion may drain into the pleural space. Pleural effusions that enter the pleural space from intact blood vessels can be transudative (watery) or exudative (proteinaceous) with fluid accumulating at a rate faster than it can be removed by the lymphatics. Other types of pleural effusion are characterized by the presence of pus (empyema), blood (hemothorax), or chyle (lymphatic fluid \[chylothorax\]).* Which of the following accurately describes the reason that obstructive lung diseases cause the loop on a Flow Volume graph to shift to the left.   **A. **The FVC (forced vital capacity) is dramatically reduced and FEV1/FVC ratio increased **B. **The TLC (total lung capacity) is increased, mostlyy due to longer inspiration and increased residual volume **C. **The expiratory phase is shortened but greater volume **D. **The TV (tidal volume) of the lungs is increased **E. **The IV (inspiratory volume) is drastically increased, RV (residual volume) decreased Which of the following is an example of a restrictive lung disease?  **A. **Bronchiectasis **B. **Atelectasis **C. **Blastomycosis **D. **Asbestosis **E. **Asthma Which of the following obstructive lung diseases is characterized by abnormal permanent enlargement of gas-exchange airways accompanied by destruction of alveolar walls without obvious fibrosis leading to loss of elastic recoil and decreased lung compliance?  **A. **Bronchiectasis **B. **Chronic bronchitis **C. **Cystic fibrosis **D. **Mesothelioma **E. **Emphysema COPD manifests in two different phenotypes. Which of the following best describes the issues that accompany \"Blue Bloaters\"?  **A. **Hyperinflation on xray; Quiet lung sounds; Pursed lip breathing **B. **Elevated hemoglobin; Rhonchi and wheezing; Peripheral edema **C. **Chronic inflammation; Stiffening in the interstitium; Limited lung volumes **D. **Thickened visceral pleura; Vasculitis; Overweight **E. **Concentric alveolar scarring; Compression atelectasis; Cachexia Which type of occupational exposure pneumoconiosis is associated with individuals who work in mining, stone cutting, ceramics, and sandblasting?  **A. **Berylliosis **B. **Asbestosis **C. **Silicosis **D. **Sarcoidosis **E. **Allergic Alveolitis 48 year old female presents after having diagnostic thoracentesis. The fluid was sent for testing and was described as having high concentrations of white blood cells and protein. What is the most likely cause of her pleural effusion?  **A. **Hemorrhage into the pleural space **B. **A liver or renal disorder that caused a decrease in oncotic pressure **C. **An injury that disrupted the transport of lymphatic fluid **D. **An infectious process that stimulated the release of biochemical mediators **E. **A malignancy that damaged local blood vessels A 21 year old male presents to the ED after a motorcycle accident on the interstate. He has multiple obvious injuries and arrives in a C-collar and on a backboard. You notice paradoxical movement to the left side of his chest, apparent with each breath. He appears to be in a large amount of pain. What would be an expected injury to be identified on imaging?  **A. **Iatrogenic pneumothorax **B. **Multiple consecutive rib fractures **C. **Tracheal injury **D. **Rupture of a pleural bullae **E. **Aortic dissection During an initial assessment of a trauma patient, you note a 63-year-old male who appears to be in significant distress with dyspnea, tachycardia, and hypotension. He was just brought in by a buddy after being involved in a bar fight. He smells strongly of alcohol. He has decreased breath sounds on the right lung and trachea is obviously deviated to the left. What is the most important first step for this patient?  **A. **Obtain chest xray to confirm suspicion of tension pneumothorax **B. **Apply supplemental oxygen **C. **Administer pain medication **D. **Get more information about injuries from the buddy **E. **Immediately perform needle decompression to the right lung Which of the following diseases is characterized by sheets of macrophages aggregated around a central group of cells to form noncaseating granulomas, concentric scar formation, and bilateral hilar lymphadenopathy?  **A. **Asbestosis **B. **Goodpasture\'s syndrome **C. **Coal worker\'s pneumoconiosis **D. **Sarcoidosis **E. **Idiopathic pulmonary fibrosis Which of the following is TRUE regarding spirometry results expected with a restrictive lung disease? **A. **Increased residual volume **B. **Increased FVC (forced vital capacity) **C. **Decreased FVC (forced vital capacity) **D. **Decreased FEV1/FVC ratio **E. ** Increased TLC (total lung capacity) Aging and the pulmonary system: - There are a few physiological changes (developmental and degenerative) that occur with aging -- typically gradual: - Loss of elastic recoil - Stiffening of the chest wall -- ribs become ossified and joints become stiffer - Changes in gas exchange -- increase in alveolar size - Increases in flow resistance - Change influenced by: - Genetics - Sociocultural factors - Nutrition status - Exercise - Immune fxn - Respiratory distress encountered - Body size - Sex - Race - Also influenced by exposure to environmental toxins: - Seen with some respiratory tract infections - Tobacco smoker - Air pollution - Occupational dusts - Leads to decrease in exercise tolerance, respiratory muscle strength and endurance- reduce ventilatory capacity - Also at greater risk for respiratory depression caused by mediations *During adulthood and as age advances, the alveoli tend to lose alveoli wall tissue and capillaries. This process increases alveolar size, diminishes the alveolar surface area available for gas diffusion, and decreases airway support provided by normal lung tissues. These changes are similar to those seen in emphysema and change the elastic properties of the lungs. Chest wall compliance decreases with age, because the ribs become ossified (less flexible) and the joints become stiffer. As a result the chest wall loses some of its ability to expand. In addition, respiratory muscle strength and endurance decrease by up to 20% by age 70. These mechanical changes in the lung and chest wall, along with structural changes in the alveoli, reduce the ventilatory capacity in older adults. Vital capacity decreases and residual volume increases; however, total lung capacity remains unchanged. These changes decrease ventilatory reserves and lead to decreased ventilation-perfusion ratios. With advancing age there is also increased immune dysregulation, asymptomatic low-grade inflammation ("inflamm-aging"), and increased risk of infection.* **Pulmonary Edema:** - Abnormal accumulation of fluid in the alveoli - Slowly resolves and interferes with gas exchange - Two varieties: - Hemodynamic: - Fluid accumulation when there is increased hemodynamic pressure (BP) in the lung vascular bed - Most common cause of PE: left-sided heart failure (increased afterload) - Hydrostatic pressure exceeds oncotic pressure fluid moves into alveolar interstitium - Microvascular injury - Occurs when capillaries in the alveolar walls are injured and leak protin0rich inflammatory fluid into the alveolar space - Causes: inhalation of toxic fumes, hot gases from a fire, septicemia (bacterial endotoxin), IV drug abuse - "NOT CARDAIC" causes of pulmonary edema - Near drowning - O2 therapy/post intubation - Trauma/transfusion (TRALI) - CNS: neurogenic - Allergic alveolitis - Renal failure - Drugs (ASA) - Inhaled (toxins, chlorine) - Altitude: high altitude (HAPE), ARDS - Contusion *Pulmonary edema is excess water in the lung. The normal lung contains very little fluid and is kept dry by lymphatic drainage and a balance among capillary hydrostatic pressure, capillary oncotic pressure, and capillary permeability. In addition, surfactant lining the alveoli repels water, keeping fluid from entering the alveoli. Common predisposing factors for pulmonary edema include left-sided heart disease, causing increased pulmonary venous pressure; injury to pulmonary capillary endothelium, like that seen with adult respiratory distress syndrome (ARDS) and inhalation of toxic gases; and lymphatic obstruction. The pathogenesis of pulmonary edema is illustrated in Fig. 36.7. Other causes include rapid pulmonary reexpansion after upper airway obstruction and exposure to high altitude.*  - Clinical manifestations include: - Dyspnea, hypoxemia, and increased work of breathing - Physical examination may reveal inspiratory crackles (rales), dullness to percussion over lung bases - In severe edema, pink and frothy sputum is expectorated - Treatment of pulm edema depends of the cause - If from HF - Therapy is guided toward improving cardiac output and volume status w/ diuretics, vasodilators, and drugs that improve the contraction of the heart muscles - If from increased capillary permeability resulting from injury: - The treatment is focused on removing the offending agent and providing supportive therapy to maintain adequate oxygenation, ventilation, and circulation - Think "LMNOP" in treatment - Lasix - Morphine - Nitroglycerine - Oxygen - Position/positive pressure ventilation *ARDS or inhalation of toxic gases causes injury to the alveolocapillary membrane. Capillary injury causes water and plasma proteins to leak out of the capillary and move into the interstitium. When plasma proteins move into the lung interstitium, they increase the interstitial oncotic pressure, which is usually very low. As the interstitial oncotic pressure begins to equal capillary oncotic pressure, water moves out of the capillary and into the lung. (Mechanisms of edema are discussed in Chapter 3.) Lymphatic drainage can be blocked by compression of lymphatic vessels caused by edema, tumors, and fibrotic tissue or by increased systemic venous pressure that elevates the hydrostatic pressure of the large pulmonary veins into which the pulmonary lymphatic system drains.* Key Components of Acute Lung injury or acute respiratory distress syndrome - Acute, meaning onset over 1 week or less - Bilateral opacities consistent with pulmonary edema must be present and may be detected on CT or chest radiograph - PaO2/FiO2 ratio \