What is Pulmonary Fibrosis What is Pulmonary Fibrosis Home » What is Pulmonary Fibrosis What is Pulmonary Fibrosis? The medical term "fibrosis'' is the development of fibrous connective tissue, thickening and scarring of connective tissue, as a reparative response to damage or injury. The term fibrosis can be used to refer to: the connective tissue deposition that occurs as part of the normal healing process or to the excess deposition of tissue as part of a pathological process. There are different types of fibrosis that can occur in the body, depending on the affected organ: pulmonary fibrosis, cardiac fibrosis, liver cirrhosis. Pulmonary fibrosis is not cystic fibrosis , even if this involves scarring as well. Cardiac fibrosis is usually a result of myocardial infarction and can affect the muscles in the heart but also the valves. Liver cirrhosis presents areas of scar tissue and nodules that replace the normal liver tissue and alter liver function being caused by alcoholism, hepatitis viruses and fatty liver disease. Pulmonary fibrosis – refers to multiple lung conditions that cause interstitial lung damage and scarring. It can also occur as a secondary condition in various other diseases.

If the underlying cause is not known the term idiopathic pulmonary fibrosis is used. In pulmonary fibrosis the interstitial damage, scarring and fibrosis will cause loss of lung elasticity and functionality. The main symptoms in pulmonary fibrosis are: persistent cough fatigue due to lack of oxygen There are three types of pulmonary fibrosis: Replacement fibrosis – occurs as a result of disrupt repairing process in lung damage caused by infarction or a pneumonia or tuberculosis infection. Focal fibrosis – occurs as a response to inhaled substances that cause irritation in lymph tissue where the fibrosis begins, substances such as asbestos and silica (silicosis). Diffuse parenchymal lung disease (DPLD) – this occur in allergies and affects the lung alveoli, causing fibrosis in the alveoli due to persistent inflammation caused by allergic triggers (dust, animal dander, pollen, etc.) In most cases the underlying factors that cause pulmonary fibrosis develop over many years and the most affected age range is between 50 to 70 years. Avoiding the risk factors will help to prevent pulmonary fibrosis.

The risk factors are: Pulmonary system - definition of Pulmonary system by The Free Dictionary Pulmonary system - definition of Pulmonary system by The Free Dictionary respiratory system n. The system of organs and structures, such as lungs in mammals and gills in fish, involved in the exchange of oxygen and carbon dioxide between an organism and its environment. respiratory system n (Anatomy) the specialized organs, collectively, concerned with external respiration: in humans and other mammals it includes the trachea, bronchi, bronchioles, lungs, and diaphragm res′piratory sys`tem n. the system of organs and tissues involved in drawing oxygen into the body and removing carbon dioxide: in mammals, includes the nasal cavity, pharynx, trachea, bronchi, lungs, and the diaphragm.

[1935–40] res·pi·ra·to·ry system (rĕs′pər-ə-tôr′ē) The system of organs and structures in which gas exchange takes place, consisting of the lungs and airways in air-breathing vertebrates, gills in fish and many invertebrates, the outer covering of the body in worms, and specialized air ducts in insects. respiratory system In humans, the mouth, nose, pharynx, larynx, trachea, bronchi, bronchioles, alveoli, and lungs. ThesaurusAntonymsRelated WordsSynonymsLegend: Pulmonary | definition of pulmonary by Medical dictionary Pulmonary | definition of pulmonary by Medical dictionary 1. pertaining to the lungs ; called also pulmonic and pneumonic . 2. pertaining to the pulmonary artery. pulmonary acid aspiration syndrome a disorder produced as a complication of inhalation of gastric contents; it may progress to a syndrome resembling acute respiratory distress syndrome .

pulmonary alveolar proteinosis a disease of unknown etiology marked by chronic filling of the alveoli with a proteinaceous, lipid-rich, granular material consisting of surfactant and the debris of necrotic cells. Some patients have a history of exposure to irritating dusts or fumes. The condition is treated by whole lung lavage with balanced salt solution; most patients need repeated lavage. pulmonary artery the large artery originating from the superior surface of the right ventricle of the heart and carrying deoxygenated blood to the lungs for oxygenation; it starts as the pulmonary trunk, which divides between the fifth and sixth thoracic vertebrae to form the right pulmonary artery that enters the right lung and the left pulmonary artery that enters the left lung. See Appendix 3-1. pulmonary circulation the circulation of blood to and from the lungs. Unoxygenated blood from the right ventricle flows through the right and left pulmonary arteries to the right and left lungs. After entering the lungs, the branches subdivide, finally emerging as capillaries which surround the alveoli and release the carbon dioxide in exchange for a fresh supply of oxygen. The capillaries unite gradually and assume the characteristics of veins.

These veins join to form the pulmonary veins, which return the oxygenated blood to the left atrium. See also circulatory system . pulmonary function tests tests used to evaluate lung mechanics, gas exchange, pulmonary blood flow, and blood gases and pH. They are used to evaluate patients in the diagnosis of pulmonary disease, assessment of disease development, or evaluation of the risk of pulmonary complications from surgery. Lung Volumes and Capacities. The total lung capacity (TLC) is divided into four volumes. The tidal volume (VT) is the volume inhaled or exhaled in normal quiet breathing. The inspiratory reserve volume (IRV) is the maximum volume that can be inhaled following a normal quiet inhalation. The expiratory reserve volume (ERV) is the maximum volume that can be exhaled following a normal quiet exhalation. The residual volume (RV) is the volume remaining in the lungs following a maximal exhalation. The vital capacity (VC) is the maximum volume that can be exhaled following a maximal inhalation; VC = IRV + VT + ERV. The inspiratory capacity (IC) is the maximum volume that can be inhaled following a normal quiet exhalation; IC = IRV + VT.

The functional residual capacity (FRC) is the volume remaining in the lungs following a normal quiet exhalation; FRC = ERV + RV. The vital capacity and its components are measured using a spirometer , which measures the volumes of air inhaled and exhaled. The functional residual capacity is usually measured by the helium dilution method using a closed spirometry system. A known amount of helium is introduced into the system at the end of a normal quiet exhalation. When the helium equilibrates throughout the volume of the system, which is equal to the FRC plus the volume of the spirometer and tubing, the FRC is determined from the helium concentration. This test may underestimate the FRC of patients with emphysema. The FRC can be determined quickly and more accurately by body plethysmography . The residual volume and total lung capacity are determined from the functional reserve capacity. Forced Vital Capacity (FVC). In the forced vital capacity maneuver, the patient exhales as forcefully and rapidly as possible, beginning at maximal exhalation. Several parameters are determined from the spirogram. The forced vital capacity is the total volume of air exhaled during the maneuver; it is normally equal to the vital capacity.

The forced expiratory volume (FEV) is the volume expired during a specified time period from the beginning of the test. The times used are 0.5, 1, 2, and 3 seconds; corresponding parameters are FEV0.5, FEV1.0, FEV2.0, and FEV3.0. The maximal expiratory flow is the slope of the line connecting the points where 200 ml and 1200 ml have been exhaled; it is also called FEF200–1200 (forced expiratory flow). The maximal midexpiratory flow is the slope of the line connecting the points where 25 per cent and 75 per cent of the forced vital capacity have been exhaled; it is also called FEF25–75%. Maximal Voluntary Ventilation (MVV). This is the maximal volume of air that can be breathed by the patient, expressed in liters per minute; it was formerly called maximal breathing capacity. The patient breathes as rapidly and deeply as possible for 12 to 15 seconds and the volume exhaled is determined by spirometry. Predicted Values.

Because the results of pulmonary function tests vary with size and age, the normal values are calculated using prediction equations or nomograms, which give the normal value for a specific age, height, and sex. The prediction equations are derived using linear regression on the data from a population of normal subjects. The observed values are usually reported as a percentage of the predicted value. Interpretation. These tests provide evidence of impairment of ventilatory function; they do not point to specific disease processes. Abnormal test results may show either an obstructive or a restrictive pattern; sometimes both are present. The Obstructive Pattern. This pattern occurs when there is airway obstruction from any cause, as in asthma, bronchitis, emphysema, or advanced bronchiectasis; these conditions are grouped together in the nonspecific term chronic obstructive pulmonary disease . In this pattern, the residual volume is increased and the PV/TLC ratio is markedly increased. Owing to increased airway resistance, the flow rates are decreased. The FEV/FVC ratios, maximal midexpiratory flow, and maximal expiratory flow are all decreased; FEV1.0/FVC is less than 75 per cent. The Restrictive Pattern.

This pattern occurs when there is a loss of lung tissue or when lung expansion is limited as a result of decreased compliance of the lung or thorax or of muscular weakness. This pattern occurs in conditions such as pectus excavatum, myasthenia gravis, diffuse idiopathic interstitial fibrosis, and space-occupying lesions (tumors, effusions). The vital capacity and forced vital capacity are less than 80 per cent of the predicted value, but the FEV/FVC ratios are normal. The total lung capacity is decreased and the RV/TLC ratio is normal. pulmonary vein any of the four large veins (two right and two left branches) that carry oxygenated blood from the lungs to the left atrium of the heart. See anatomic Table of Veins in the Appendices. pul·mo·nar·y (pul'mō-nār'ē), Relating to the lungs, to the pulmonary artery, or to the aperture leading from the right ventricle into the pulmonary artery. adjective Referring to lungs.

anthrax Greek, anthrax, a burning coal, charbon, milzbrand Infectious disease An often fatal bacterial infection which occurs when Bacillus anthracis endospores, primarily of grazing herbivore–cattle, sheep, horses, mules–origin enter via skin abrasions, inhalation, or orally Pathogenesis Anthrax endospores germinate within macrophages, become vegetative bacteria, multiply within the lymphatics, enter the bloodstream and cause massive septicemia Clinical URI-like symptoms, followed by high fever, vomiting, joint pain, SOB, internal and external hemorrhage, hypotension, meningitis, pulmonary edema, shock sudden death; intestinal anthrax is caused by ingestion of contaminated meat; cutaneous anthrax is rare Diagnosis ELISA for capsule antigens–95+% senstivity, for protective antigen–72% sensitivity; detection of exotoxins in blood is unreliable Prevention Prophylaxis–6 wks with doxycycline or ciprofloxacin; vaccination, with anthrax vaccine absorbed; decontamination with aerosolized formalin Management Penicillin, doxycycline; if allergic to penicillin, chloramaphenicol, erythrom

ycin, tetracycline, ciprofloxacin See Bacillus anthracis , Cutaneous anthrax, Industrial anthrax , Inhalation anthrax .

Anthrax, clinical forms Pulmonary Almost universally fatal–due to inhalation of anthrax spores which germinate and produce toxins resulting in pleural effusions, hemorrhage, cyanosis, SOB, stridor, shock, death Inhalation Anthrax pneumonia, inhalational anthrax, pulmonary anthrax An almost universally fatal form due to inhalation of 1 to 2 µm pathogenic endospores which are deposited in alveoli, engulfed by macrophages and germinate en route to the mediastinal and peribronchial lymph nodes, produce toxins Clinical Mediastinal widening, pleural effusions, fever, nonproductive cough, myalgia, malaise, hemorrhage, cyanosis, SOB, stridor, shock, death, often accompanied by mesenteric lymphadenitis, diffuse abdominal pain, fever Cutaneous Once common among handlers of infected animals, eg farmers, woolsorters, tanners, brushmakers and carpetmakers in an era when brushes were from animals Clinical Carbuncle–a cluster of boils, that later ulcerates, resulting in a hard black center surrounded by bright red inflammation; rare cases which become systemic are almost 100% fatal Gastrointestinal After ingesting contaminated

 meat–2 to 5 days; once ingested spores germinate, causing ulceration, hemorrhagic and necrotizing gastroenteritis Clinical Fever, diffuse abdominal pain with rebound tenderness, melanic stools, vomit, fluid and electrolyte imbalances, shock; death is due to intestinal perforation or anthrax toxemia Oropharyngeal Physiology II -- Pulmonary ventilation Respiratory Physiology Pulmonary Ventilation Readings required or recommended: Guyton and Hall (9th edition).

Chap. 37; Ganong (19th edition), Chap. 34; Key Words ventilation: The inflow and outflow of air btw the atmosphere and the lung alveoli. The process of exchange of air btw the lungs and the ambient air. Pulmonary ventilation refers to the total exchange, whereas alveolar ventilation refers to the effective ventilation of the alveoli, where gas exchange with the blood takes place. perfusion: The act of pouring through or over: especially the passage of a fluid through the vessels of a specific organ. Blood flow through the pulmonary vessels where gas exchange occurs. oxygen consumption: The amt of oxygen needed to meet the metabolic needs of the tissues. diffusion: The movement of O2 and CO2 btw the alveoli and the pulmonary capillaries which is a random molecular motion of molecules intertwining their ways in both direction through the respiratory membrane. convection: The removal of heat from the body by a process called convection so that the heated air moves away from the skin, so that new, unheated air is continually brought in contact with the skin. inspiration: Contraction of the diaphragm pulls the lover surfaces of the lungs downward.

expiration: The diaphragm simply relaxes and the elastic recoil of the lungs, chest wall, and abd structures compress the lungs. anatomical dead space: The nose, pharynx, and trachea where no gas exchange occurs. physiological dead space: This is the anatomical dead space and any alveoli that do not take part in gas exchange. work of breathing: Work of inspiration can be divided into 3 fractions: 1)That required to expand the lungs against the lungs and chest elastic forces, called compliance work or elastic work. 2) that required to overcome the viscosity of the lungs and chest wall structures, called tissue resistance work. And 3) that required to overcome airway resistance during the movement of air into the lungs, called airway resistance work. partial pressure: An absolute number of a concentration of a gas in a mixture of gases or a liquid where the partial pressure is indicated in mm of Hg are represents the concentration of that gas and the pressure that gas exerts on the total volume. Each gas exerts its own partial pressure on the whole and the total of all the partial pressures must add up to the total pressure on that volume.

water vapor pressure: The pressure that the water molecules exert to escape through the surface is called the vapor pressure of the water. At normal body temp this is 47 mm Hg. Once the gas mixture has become fully humidified ï¿½ or at equilibrium with the surrounding water ï¿½ the partial pressure of the water vapor in the gas mixture is 47. minute ventilation: The amt of air moved in and out of the lungs in a minute. frequency: The respiratory rate per minute. tidal volume: The volume of air inspired or expired with each normal breath ï¿½ usually about 500ml. dead space ventilation: Alveoli that are ventilated but not perfused. alveolar ventilation: The volume of air entering and leaving the alveoli per minute. pulmonary volumes and capacities: Total lung capacity (TLC) - the volume of air in the lungs after a maximal inspiratory effort. Determined by the strength of contraction of the inspiratory muscles in opposition to the inward elastic recoil of the lungs and chest wall. About 6 liters in a healthy 70 kg adult Residual Volume (RV) - the volume of gas left in the lungs after a maximal forced expiration.

Determined by the force generated by the muscles of expiration and the inward elastic recoil of the lungs as the oppose the outward elastic recoil of the chest wall. Dynamic compression of the airways during the forced expiratory effort is also an important determinant of the residual volume - as airway collapse occurs gas is trapped in the alveoli. The residual volume of a healthy 70-kg adult is 1.5 liters. Functional Residual Capacity (FRC) - the volume of gas remaining in the lungs at the end of a normal tidal expiration. Balance point between the inward elastic recoil of the lungs and the outward elastic recoil of the chest wall. About 3 liters in a healthy 70-kg adult. Tidal Volume (VT) - the volume of air entering or leaving the nose or mouth per breath. During normal, quiet breathing (eupnea) the tidal volume of a 70-kg adult is about 500 ml per breath. Expiratory Reserve Volume (ERV) - the volume of gas expelled from the lungs during a maximal forced expiration that starts at the end of normal tidal expiration. About 1.5 liters.

Inspiratory Reserve Volume (IRV) - the volume of gas inhaled into the lungs during a maximal forced inspiration starting at the end of a normal tidal inspiration. About 2.5 liters. Inspiratory Capacity (IC) - the volume of air inhaled into the lungs during a maximal inspiratory effort that begins at the end of a normal tidal expiration. About 3 liters. Vital Capacity (VC) - the volume of air expelled from the lungs during a maximal forced expiration starting after a maximal forced inspiration. About 4.5 liters. hyperventilation: Abnormally prolonged and deep breathing, usually associated with acute anxiety or emotional tension. A transient respiratory alkalosis commonly results from hyperventilation. hypoventilation: Reduction in the amt of air entering the pulmonary alveoli. alveolar ventilation equation: Tells you the measure of alveolar ventilation by measuring the CO2 and the end tidal CO2. It also tells you that alveolar ventilation is very important in CO2 elimination. The amt of CO2 would go up if you couldnï¿½t get it out. Anything that impairs alveolar vent will also increase the partial pressure of CO2.

PACO2 Learning Objectives: describe the general anatomical features of the lung, chest wall, pulmonary circulation, and bronchial circulation: To move air into or out of the lungs we must create pressure differences between the atmosphere and the alveoli. To move air into the alveoli we must make alveolar pressure less than atmospheric pressure (except during positive pressure ventilation). Alveoli expand passively in response to an increased transmural pressure gradient. As they expand, their elastic recoil increases. Alveolar pressure = intrapleural pressure + alveolar elastic recoil pressure. describe in detail the structure of the terminal respiratory units, including the anatomical matching of airway and pulmonary arterial branching as well as the venous admixture of pulmonary venous and bronchial venous blood: The upper sections of the alveoli in the apex of the lung in an upright human are somewhat dilated and have less blood flow than the bases where the alveoli are more compact and can then expand more with air since they arenï¿½t as full as the alveoli at the apex. There is more blood flow in the bases due to the hydrostatic pressure gradient.

The alveoli are surrounded by a thin layer of liquid lining them. The alveoli epithelial cells are flat and thin with a tiny area of interstitial space and a basement membrane separating the alveoli epithelium from the vascular endothelium. The gases easily pass through these membranes. There is a great deal of blood flow around each alveoli to maximize ventilation/perfusion ratios. There is some blood flow that comes from the upper apices that have very little blood flow and therefore have poor perfusion. This blood mixes in with the blood that came from areas that were well perfused and the combination of well perfused and poorly perfused blood has a slight overall decrease in the PaO2. identify the primary and accessory muscles of inspiration and expiration: Muscles of Breathing Inspiration - expansion of thoracic cavity lowers intrathoracic pressure. "Negative pressure." Normally no true intrathoracic space. Only about 7 - 15 ml pleural fluid. The Diaphragm. The diaphragm is the primary muscle of inspiration. During supine eupneic breathing it is responsible for at least 2/3 of the tidal volume.

The muscle fibers of the diaphragm are inserted into the sternum and the lower ribs, and into the vertebral column by the two crura. The other ends of these muscle fibers converge to attach to the fibrous central tendon. During eupnea, contraction of the approximately 250 cm diaphragm causes its dome to descend 1 to 2 cm into the abdominal cavity, with little change in its shape, except that the area of apposition decreases in length. This elongates the thorax and increases its volume. These small downward movements of the diaphragm are possible because the abdominal viscera can push out against the relatively compliant abdominal wall. During a deep inspiration the limit of the compliance of the abdominal wall is reached and the indistensible central tendon becomes fixed against the abdominal contents. After this point contraction of the diaphragm against the fixed central tendon elevates the lower ribs (the "bucket handle motion"). External and Parasternal Intercostal Muscles - contraction pulls ribs up. Increases antero- posterior diameter of the chest. Innervation from T -1 to T-11.

Accessory muscles - not involved in eupnea but may be called into action during exercise, cough, sneeze, chronic obstructive pulmonary diseases, etc. Include sternocleidomastoid and others. Act to raise the upper ribs (" pump handle motion") and the sternum. Expiration during eupneic breathing is passive. Relaxation of the inspiratory muscles allows the increased alveolar elastic recoil to decrease the volume of the alveoli, increasing alveolar pressure above atmospheric pressure. The muscles of expiration are involved in active expiration: exercise, speech, cough, sneeze, forced expiration, etc. Internal intercostals - Perpendicular to external intercostals. Action pulls rib cage down and inward. Muscles of abdominal wall - raise intra-abdominal pressure. Displace diaphragm upward into thorax. Includes rectus abdominis, internal and external oblique muscles, and transversus abdominis. During expiration there is a "braking action" of the inspiratory muscles at high lung volumes. Although all of the respiratory muscles are usually considered to be completely relaxed at the FRC, diaphragmatic tone probably plays an important role.

identify, in words or by drawing a reasonably accurate graph depicting a spirometric tracing, the four pulmonary volumes and four pulmonary capacities, discuss how these are measured or calculated, and state typical values for these volumes and capacities in a healthy human subject: Guyton page 483 Ganong page 622 Total lung capacity (TLC) - the volume of air in the lungs after a maximal inspiratory effort. Determined by the strength of contraction of the inspiratory muscles in opposition to the inward elastic recoil of the lungs and chest wall. About 6 liters in a healthy 70 kg adult. Functional Residual Capacity (FRC) - the volume of gas remaining in the lungs at the end of a normal tidal expiration. Balance point between the inward elastic recoil of the lungs and the outward elastic recoil of the chest wall. About 3 liters in a healthy 70-kg adult. Vital Capacity (VC) - the volume of air expelled from the lungs during a maximal forced expiration starting after a maximal forced inspiration. About 4.5 liters. Inspiratory Capacity (IC) - the volume of air inhaled into the lungs during a maximal inspiratory effort that begins at the end of a normal tidal expiration.

About 3 liters. Residual Volume (RV) - the volume of gas left in the lungs after a maximal forced expiration. Determined by the force generated by the muscles of expiration and the inward elastic recoil of the lungs as the oppose the outward elastic recoil of the chest wall. Dynamic compression of the airways during the forced expiratory effort is also an important determinant of the residual volume - as airway collapse occurs gas is trapped in the alveoli. The residual volume of a healthy 70-kg adult is 1.5 liters. Tidal Volume (VT) - the volume of air entering or leaving the nose or mouth per breath. During normal, quiet breathing (eupnea) the tidal volume of a 70-kg adult is about 500 ml per breath. Expiratory Reserve Volume (ERV) - the volume of gas expelled from the lungs during a maximal forced expiration that starts at the end of normal tidal expiration. About 1.5 liters. Inspiratory Reserve Volume (IRV) - the volume of gas inhaled into the lungs during a maximal forced inspiration starting at the end of a normal tidal inspiration. About 2.5 liters.

write from memory an equation representing the relationship between minute ventilation, respiratory frequency, and tidal volume: E = VT * F E = Minute ventilation, VT = tidal volume, and F = frequency. E can also = (VD x F) + (VA x F) compare and contrast the effects of changes in respiratory frequency and tidal volume on alveolar ventilation, including a quantification of these effects using typical values for the parameters involved: When you change frequency or tidal volume, you can increase or decrease alveolar ventilation. If you doubled frequency both VD and VA would then double. If you increased VT then VA would double but the dead space would not so more air would go to the alveoli and thus more ventilation could occur. Thus to increase tidal volume is a more effective way to increase alv. ventilation. compare and contrast the anatomical and physiological dead spaces and describe how each might be measured: Anatomical dead space is the physical structures that are not involved in the gas exchange process. These include the nasopharynx, the larynx, the trachea, brochi, and bronchioles to the edge of the alveolus.

Physiological dead space is the anatomical plus any alveoli that do not participate in gas exchange for whatever reason. One way to measure this is the nitrogen washout method that would entail breathing in 100% oxygen and then having your expired breath measured. The first air out would be the 100% O2 sitting in the dead space and then as the expiration continued you would begin to pick up nitrogen. The volume of air that was all oxygen would be the amt of dead space. The other method to measure dead space is to measure the amt of CO2 present on expiration. CO2 is essentially not existent in the room air so if you measured inspired air and the amt of CO2 that comes out in expired air, you can get a measurement of dead space. The equation begins like this: CO2 = A * FACO2 since CO2 isnï¿½t the only gas coming out, you have to consider the fraction of [CO2] in the air in the alveoli. In essence you are measuring the end tidal CO2 and the equation becomes the alveolar ventilation equation which tells us the measure of alveolar ventilation by measuring the CO2 and the end tidal CO2.

The significance of this equation is that it tells us that alveolar ventilation is very important in CO2 elimination. A = ----------------- x K PACO2 define the term "alveolar ventilation", discuss its relationship to dead space and minute ventilation, and state its significance in pulmonary gas exchange: Since alveolar ventilation is the volume of air entering and leaving the alveoli per minute, any changes in this volume will greatly affect the overall rate of gas exchange in the lungs. Anything that impairs the alv vent will increase the partial pressure of CO2. An increased PaCO2 will be a reflection of decreased alv vent. Alv vent and PaCO2 are reciprocally related. If you decreased A and increased PaCO2 and since this gas mixture is in communication with the outside world, and if you added more CO2 the AO2 would have to decrease since as you add more gas the mixture becomes diluted. A hallmark of low alv vent is to have an increased PaCO2 and a decreased PaO2. See two questions above for a relationship btw dead space, min vent and alv vent.

write from memory the alveolar ventilation equation and use it to demonstrate the effects of changes in alveolar ventilation on the alveolar partial pressure of carbon dioxide: A = ----------------- x K PACO2 The bodyï¿½s way of controlling alv ventilation to properly supply the tissues with adequate oxygenation and CO2 removal is to control PaCO2. The changes in partial pressure of this gas will reciprocally effect a change on the partial pressure of oxygen and total alveolar ventilation. write from memory the simplified form of the alveolar air equation and use it to calculate alveolar PO2 when given values for inspired PO2, the respiratory exchange ratio, and arterial or alveolar PCO2: Alveolar air equation: PAO2 = PIO2 ï¿½ Where R = the respiratory quotient or the ratio of VCO2 production divided by the O2 consumption. PIO2 = 150 mm Hg, PACO2 = .40, the resp quotient is .8, and so you can calculate the PAO2 to be 100.

demonstrate an understanding of the effect of hypoventilation and hyperventilation on the arterial partial pressures of oxygen and carbon dioxide: Hypoventilation is defined as an increase in arterial PCO2. Hyperventilation is defined as a decrease in arterial PCO2. If someone is hypoventilating, then they are not blowing off enough carbon dioxide or breathing in enough oxygen. The two values are usually reciprocal since the partial pressures of each, along with any other gases present in the arterial system must = the total pressure in the system. Hyperventilating can decrease the CO2 and could thus increase the O2. Last Updated 09/06/01 08:53:26 PM Circulatory System: Pulmonary and Systemic Circuits Circulatory System: Pulmonary and Systemic Circuits Sign Up for Our Free Newsletters Thanks, You're in! Health Tip of the Day Recipe of the Day There was an error. Please try again. Please select a newsletter. Please enter a valid email address. Did you mean ? About PF About PF Subscribe to receive the most current news and updates from the Pulmonary Fibrosis Foundation. About PF Feeling confused or overwhelmed about pulmonary fibrosis?

You are not alone. The Pulmonary Fibrosis Foundation is here to help you understand what it means to have pulmonary fibrosis. You can always reach us through our Patient Communication Center at 844.Talk.PFF or by email at pcc@pulmonaryfibrosis.org . Please remember that this information is a brief overview and is for educational purposes only. It is not intended to be a substitute for professional medical advice. Always consult your health care provider with any questions you may have regarding your specific medical condition. What is Pulmonary Fibrosis? The word "pulmonary" means “lung” and the word "fibrosis" means scar tissue – similar to scars that you may have on your skin from an old injury or surgery. So, in its simplest sense, pulmonary fibrosis (PF) means scarring in the lungs. But, pulmonary fibrosis is more serious than just having a scar in your lung. In PF, the scar tissue builds up in the walls of the air sacs of the lungs, and eventually the scar tissue makes it hard for oxygen to get into your blood. Low oxygen levels (and the stiff scar tissue itself) can cause you to feel short of breath, particularly when walking and exercising.

Also, pulmonary fibrosis isn’t just one disease. It is a family of more than 200 different lung diseases that all look very much alike (see “Causes and Symptoms” below). The PF family of lung diseases falls into an even larger group of diseases called the “interstitial lung diseases.” Some interstitial lung diseases don't include scar tissue. When an interstitial lung disease includes scar tissue in the lung, we call it pulmonary fibrosis. Causes and Symptoms It can be challenging to figure out what caused your pulmonary fibrosis. Sometimes doctors are able to identify one or more causes of your disease, but it is also common to end up without an answer, despite completing a large number of medical tests. Diseases where a specific cause is not identified are often called "idiopathic" - meaning the cause is not identified or the disease occurs spontaneously. There are many forms of pulmonary fibrosis that are idiopathic. The one that many people have heard of is “idiopathic pulmonary fibrosis” or IPF , but there are many others.

A few examples are: Idiopathic nonspecific interstitial pneumonia (NSIP) Cryptogenic organizing pneumonia (COP) When the cause of PF is known, if often falls into one of these categories: Autoimmune diseases Autoimmune diseases are also called connective tissue diseases, collagen vascular diseases, or rheumatologic diseases. “Auto” means “self” and “immune” refers to your immune system. With autoimmune diseases, your own immune system is attacking your lung. If you have an autoimmune disease, your immune system can cause inflammation and scarring in the lungs. Examples of autoimmune diseases that can cause PF include: Rheumatoid arthritis Scleroderma (now called “systemic sclerosis”) Certain muscle diseases (polymyositis, dermatomyositis, and the anti-synthetase syndrome) Occupational exposures Pulmonary fibrosis can develop after significant exposure to a wide variety of inorganic dusts, including asbestos, silica, coal dust, beryllium, hard metal dusts. Environmental exposures Organic dusts, including animal proteins, bacteria, and molds, can also contribute to the development of some types of PF. Diseases caused by inhaled organic dusts are often called “hypersensitivity pneumonitis”.

Exposure to radiation can also contribute to the risk of PF. Drug Induced or Medication exposures Some medications have been linked to the development of PF, including drugs used to treat: Infections (nitrofurantoin, sulfasalazine) Cancer (methotrexate, bleomycin, oxaliplatin, radiation therapy) Genetic/Inherited diseases Approximately 10-15% of those with an “idiopathic” form of PF have another family member afflicted by the disease. This is called familial pulmonary fibrosis (FPF) or familial interstitial pneumonia (FIP) . A number of genes and genetic variants have been identified that are associated with the development pulmonary fibrosis, but frequently genetic tests are not performed when PF is diagnosed, as we are only just beginning to understand the significance of these genetic abnormalities. It is important to discuss the potential risks and benefits of genetic testing with a qualified genetic counselor and your medical provider. To speak with a Certified Genetic Counselor free of charge, contact Janet Talbert, MS, CGC at 800.423.8891, extension 1097.

CLASSIFICATION OF COMMON INTERSTITIAL LUNG DISEASES Symptoms The most common symptoms of PF are cough and shortness of breath. Symptoms may be mild or even absent early in the disease process. As the lungs develop more scar tissue, symptoms worsen. Shortness of breath initially occurs with exercise, but as the disease progresses patients may become breathless while taking part in everyday activities, such as showering, getting dressed, speaking on the phone, or even eating. Due to a lack of oxygen in the blood, some people with idiopathic pulmonary fibrosis may also have “clubbing” of the fingertips. Clubbing is a thickening of the flesh under the fingernails, causing the nails to curve downward. It is not specific to IPF and occurs in other diseases of the lungs, heart, and liver, and can also be present at birth. Other common symptoms of pulmonary fibrosis include: Chronic dry, hacking cough Unexplained weight loss Diagnostics and Tests Interstitial lung diseases (ILD) are a group of disorders that affect the lung tissue around the air sacks and airways. Many types of ILD can lead to scaring of the lungs or PF.

Making an accurate diagnosis of ILD is complicated by the fact that there are more than 200 different types. In fact, one study showed that more than half of people with IPF may have been initially misdiagnosed. The Pulmonary Fibrosis Foundation strongly recommends that everyone with suspected or established PF be seen at least once at a center that specializes in the care of people with PF. To find medical care, click here. If possible, it is very important to determine which type of pulmonary fibrosis you have. Distinct types of PF behave differently in terms of how quickly your disease will progress, and how you may respond to different treatments prescribed by your medical professional. In order to determine the type of PF you have, doctors from a variety of specialties, including pulmonologists (respirologists), radiologists, rheumatologists, and pathologists work together to make an accurate diagnosis. Your medical provider(s) will order a variety of tests; some of the most common tests are discussed below. Comprehensive Medical History It is essential for your medical provider to obtain a comprehensive medical history to learn if any medications, environmental/occupational exposures, familial, or other medical conditions could have contributed to your pulmonary fibrosis.

Physical Examination It is important to undergo an in-depth physical examination. Scar tissue can often be heard as "crackles" or Velcro-like sounds when your medical provider listens to your lungs with a stethoscope. Your provider may also detect signs of other medical conditions that could be affecting your lungs. Upon reviewing your medical history and physical examination, your medical provider may recommend a variety of tests to further diagnose your lung disease. Most people with PF will also undergo one or more of the following tests during their evaluation: High-Resolution Computed Tomography (HRCT) scan of the chest A type of x-ray test that allows your provider to get a detailed look at your lungs and is a critical component of the diagnostic evaluation of PF. Blood Tests Your medical provider may also perform a series of blood tests to see if your immune system is contributing to your lung disease. Pulmonary Function Tests Pulmonary Function Tests (PFTs) measure the size of your lungs, how well air moves in and out of your lungs, and how well your lungs bring oxygen into your body. These tests help your medical provider determine the type and severity of lung disease present. They are also used to monitor for response to therapy and disease progression.

PFTs are usually performed in a hospital or clinical laboratory and consist of breathing through a "spirometer." Sometimes they are also performed while you sit inside a large plastic enclosure that looks like a glass telephone booth. Pulse Oximetry A “pulse oximeter” is a device placed on the fingertip or earlobe that indicates the amount of oxygen in the blood. Normally, nearly all of your red blood cells are full of oxygen. When all the red blood cells are carrying oxygen, the blood is called “100% saturated.” A normal saturation level is between 95% - 100% when the test is performed at sea level. Low oxygen saturation values can help your medical professional identify the presence of lung disease. Early on in PF, oxygen levels may be normal while you are resting, but can decrease while exerting yourself. This drop in oxygen saturation (called “de-saturation”) can make you feel breathless. When oxygen levels drop below 89% during exertion, your medical professional may recommend using supplemental oxygen while active.

Arterial Blood Gas Arterial Blood Gas (ABG) is a direct arterial puncture to measure arterial pH, oxygen saturation (PaO2), and carbon dioxide content (PCO2). Arterial blood has been oxygenated by the lungs and thus indicates how much oxygen is available to the body. Bronchoscopy Bronchoscopy is a procedure used to collect samples of cells and small biopsies from your lungs using a bronchoscope. Examination of these samples can be useful in making a diagnosis of certain types of lung diseases. Bronchoalveolar Lavage Bronchoalveolar Lavage (BAL) is a way to remove a tiny sampling of cells from the lower respiratory tract using a bronchoscope. During this test, a small amount of saline is injected through the bronchoscope and, when withdrawn, removes a sample of cells from the respiratory tract. Frequently, this test is not helpful in making the diagnosis of PF, but may be beneficial in other clinical situations. Exercise Testing Exercise testing is a measure of how well the lungs function during exertion. Test methods vary from hospital to hospital, but frequently include the use of a stationary bike or treadmill.

The most common method of exercise testing is the six-minute walk test, where the distance you can walk in six minutes is measured. Blood pressure, electrocardiogram, and oxygen saturation levels may also be monitored during exercise testing. Esophagram Esophagram is an X-ray examination of the esophagus (the tube that carries food to your stomach). This exam will help to determine if you suffer from gastroesophageal reflux disease (GERD) or other disorders of the esophagus, which can accompany certain forms of PF. Echocardiogram Echocardiogram (ECHO) is a test that uses sound waves (ultrasound) to create a picture of your heart. It provides information about your heart function and screens for the presence of pulmonary hypertension, a condition that can accompany PF. Surgical Lung Biospy In some cases a biopsy of the lung is required to make a diagnosis of PF. A biopsy should only be considered after an extensive evaluation. Usually a lung biopsy can be performed by a minimally invasive procedure called a video assisted thoracoscopic surgery, or VATS. A VATS procedure is usually well tolerated, but it may not be recommended for all patients.

If your medical provider recommends a lung biopsy, he/she will discuss the recommended procedure with you and refer you to a thoracic surgeon. GLOSSARY Alveoli: Tiny air sacs in the lungs where carbon dioxide leaves the bloodstream and oxygen enters the bloodstream. Bronchoscope: An instrument used for inspecting the airways of the lungs. Comorbidity: A disease or other medical issue that occurs simultaneously with PF. Diffuse parenchymal lung diseases (DPLD): Another name for interstitial lung diseases. Diffusion capacity (DLCO): A measure of the ability of oxygen to diffuse into the bloodstream. Dyspnea: Difficulty breathing or shortness of breath. Exacerbation: An episode of rapid decline or the emergence of more severe symptoms. Fibroproliferation: Relating to the growth of fibroblasts (and fibrous tissue), one of the basic connective tissue cells. Fibrosis: An increase in fibrous scar tissue. Forced expiratory volume (FEV1): The amount of air you can blow out in one second, which is measured by spirometry.

Forced vital capacity (FVC): How much air you can blow out of your lungs, which is measured by spirometry. Gastroesophageal reflux disease (GERD): A regurgitation of stomach acids into the esophagus and throat, causing heartburn, acid indigestion, and possibly injury to the lining of the esophagus. This is also called acid reflux disease. Hospice care: Palliative care for patients at end-of-life. Idiopathic: Of unknown cause. Idiopathic interstitial pneumonias (IIP): A type of interstitial lung disease. Idiopathic pulmonary fibrosis is a type of IIP. Interstitial lung diseases (ILD): A broad category of over 200 lung diseases that affect the lung interstitium. Interstitium: The space between the alveoli (air sacs). Palliative care: Non-curative therapy that treats symptoms and focuses on improving quality of life. It can be received at the same time as curative therapy. Pathologist: A physician specializing in disease-associated changes in tissue and organs. Pathologists aid in making a medical diagnosis. Pulmonary: Relating to the lungs.

Pulmonary hypertension: Abnormally high blood pressure in the pulmonary (lung) arteries. Pulmonologist: A physician specializing in the lungs. Radiologist: A physician specializing in using radiology tests(e.g., X-rays) to diagnose illness. Rheumatologist: A physician specializing in rheumatic diseases, which may include arthritis, autoimmune diseases, and joint diseases. Spirometry: A test that measures the amount of air inhaled and exhaled over time. Usual interstitial pneumonia (UIP): A specific abnormal radiologic or pathologic pattern of interstitial lung disease. Book a PFF Ambassador for your event. Call 844.TalkPFF > Fluid in the Lungs in Cats | petMD Fluid in the Lungs in Cats Pulmonary Edema in Cats Pulmonary edema refers to fluid buildup in the lungs and is often associated with pneumonia, although there are many other possible causes. Normal lungs have fluid that is moved from the lungs into the internal space of the body, an on-going process for normal healthy function. If there is added pressure in the lungs or other underlying conditions, this mechanism can become damaged and fluid can begin to build in the lungs. If this excess fluid is not removed, edema forms.

Damage can occur if this condition is left untreated, but when treated appropriately, the outcome is positive. Animals of all ages, genders, and breeds can be diagnosed with pulmonary edema. If you would like to learn more about how this disease affects dogs, please visit this page in the PetMD health library. What is Fibrosis? What is Fibrosis? By Sally Robertson , BSc The term fibrosis describes the development of fibrous connective tissue as a reparative response to injury or damage. Fibrosis may refer to the connective tissue deposition that occurs as part of normal healing or to the excess tissue deposition that occurs as a pathological process. When fibrosis occurs in response to injury, the term “scarring” is used. Some of the main types of fibrosis that occur in the body are described below. Pulmonary fibrosis Pulmonary fibrosis refers to a number of conditions that cause interstitial lung damage, followed by fibrosis and eventually loss of lung elasticity. These conditions lead to symptoms such as persistent cough, chest pain, difficulty breathing and fatigue. Pulmonary fibrosis may occur as a secondary condition in various other diseases, but in many cases the underlying cause is not clear and the term idiopathic pulmonary fibrosis is used.

Pulmonary fibrosis can be divided into the following three types: Replacement fibrosis – This occurs in response to lung damage caused by infarction or an infection such as pneumonia or tuberculosis. Focal fibrosis – This occurs as a response to irritation by substances that are inhaled and then carried to nearby lymph tissue by macrophages. In the lymph tissue, the process of fibrosis begins. Occupational exposure to silica or asbestos are common examples of the substances that can cause this form of pulmonary fibrosis. Diffuse parenchymal lung disease (DPLD) – This occurs in cases of fibrosing alveolitis, which manifests in idiopathic pulmonary fibrosis. DPLD also occurs in extrinsic allergic alveolitis, where there is diffuse inflammation of the lung tissue in response to inhalation of dust antigens such as animal dander. In many cases, the underlying condition that causes pulmonary fibrosis develops over many years, meaning people often develop the condition later on in life, with the incidence peaking between 50 and 70 years of age. The condition appears to affect males and females equally.

Some of the risk factors for pulmonary fibrosis include: Exposure to occupational substances that damage the lung Tobacco smoking Infections such as tuberculosis and pneumonia Many cases of pulmonary fibrosis can be managed with a combination of preventive measures and medications, although some patients may require a lung transplant. Examples of preventive measures include stopping smoking, avoiding exposure to known irritants, attending any flu jabs and oxygen therapy. Some of the drugs that may be used include immunosuppressive agents such as corticosteroids or antifibrotic agents such as ciclosporin or colchicine. Where patients who do not respond to any of these measures, a physician may discuss the option of a lung transplant Liver cirrhosis Systemic sclerosis: an interview with Dr Kristin Highland Cirrhosis refers to the scar tissue and nodules that replace liver tissue and disrupt liver function. The condition is usually caused by alcoholism, fatty liver disease , hepatitis B or hepatitis C. The liver is responsible for several essential functions such detoxifying certain substances in the body, producing essential nutrients and cleaning the blood. Every time the liver undergoes stress or injury, it tries to regenerate and produces scar tissue in the process.

As the scar tissue builds up, liver function worsens and when cirrhosis is advanced, the liver no longer works properly. Cirrhosis does not give rise to symptoms until the damage has become extensive, at which point it may cause a wide range of symptoms. Examples include: Tendency to bleed or bruise early Fatigue Slurred speech The development of spider-like vessels underneath the skin surface If liver cirrhosis is detected and diagnosed during the early stages of disease, any further damage to the liver may be prevented. Treatment depends on the stage of disease and the underlying cause of the cirrhosis, but the overall goal is to slow disease progression and relieve symptoms. This might include the following approaches: Treating alcohol dependency, often through rehabilitation programmes for alcohol addicts Weight loss plans for people with cirrhosis caused by non-alcoholic fatty liver disease Medication that can help prevent liver damage caused by hepatitis B or C Drugs to alleviate symptoms such as pain, tiredness and itching When liver cirrhosis is advanced, a liver transplant using a donor organ may be the only option for some patients. A patient due to receive a transplant needs to undergo extensive testing to ensure they are healthy enough to undergo the procedure.

Patients who have alcohol-related disease will also need to abstain form drinking alcohol for at least six months. Cardiac fibrosis Areas of the heart that have become damaged due to myocardial infarction may undergo fibrosis. Cardiac fibrosis can affect the valves in the heart as well as the muscle, which becomes stiff and less compliant. This can increase the risk of heart failure. Fibrocytes usually secrete collagen and are therefore essential for structural support of the heart. However, when these cells are over activated, fibrosis and thickening of the tricuspid valve and pulmonary valve can occur. This loss of flexibility in the valves can eventually cause valvular dysfunction and heart failure. A compound present in red wine called resveratrol has been shown to slow the progression of cardiac fibrosis and other techniques such as microRNA inhibition are currently being studied in animal models of the disease.

Question: """Pulmonary"" refers to which organ?"
Answer: Lungs