Summary

This document is a chapter from a textbook on respiratory disorders, providing an outline, learning objectives, and a review of normal respiratory system structures. It explores various aspects of respiratory disease, including infectious diseases, obstructive lung diseases, and others.

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Pathophysiology (2) (MBS 214) Respiratory Disorders Textbook; Pathophysiology for the Health Professions, 4th edition, 2011 Chapter 19 (p.323-375) Respiratory Disorders Chapter outline:-  Review of Normal Structures in the Respiratory System  Infectious Di...

Pathophysiology (2) (MBS 214) Respiratory Disorders Textbook; Pathophysiology for the Health Professions, 4th edition, 2011 Chapter 19 (p.323-375) Respiratory Disorders Chapter outline:-  Review of Normal Structures in the Respiratory System  Infectious Diseases  Obstructive Lung Diseases  Vascular Disorders  Expansion Disorders Lecture 3 Respiratory Disorders Learning objectives: After studying this chapter ,the student is expected to: Describe the common upper respiratory tract infections Compare the different types of pneumonia. Differentiate the effects of primary from secondary tuberculosis. Describe the pathophysiology and complications of cystic fibrosis. Describe the etiology and pathophysiology of bronchogenic carcinoma Compare the types of asthma and describe the pathophysiology and manifestations of an acute attack Compare emphysema and chronic bronchitis Describe the causes of pulmonary edema and explain how it affects oxygen levels. Compare the effects of small, moderate, and large-sized pulmonary emboli. Describe the causes of atelectasis and the resulting effects on ventilation and oxygen levels Explain the effects of pleural effusion on ventilation. Compare the types of pneumothorax. Explain how a flail chest injury affects ventilation, oxygen levels, and circulation. Describe the pathophysiology and signs of infant respiratory distress syndrome. Describe the possible causes of adult respiratory distress syndrome and the pathophysiology. Describe the etiology and changes in blood gases with acute respiratory failure. Explain the cause of sleep apnea and describe the effects and complications of this disorder. REVIEW OF NORMAL STRUCTURES IN THE RESPIRATORY SYSTEM The respiratory system consists of two anatomic areas. The upper respiratory tract is made up of the passageways that conduct air between the atmosphere and the lungs, The lower respiratory tract consists of the trachea, bronchial tree, and the lungs, where gas exchange takes place Lungs are covered by pleura In addition, the pulmonary circulation, the muscles required for ventilation, and the nervous system, which plays a role in controlling respiratory function, are integral to the function of the respiratory system. Respiratory disorders may result from airway obstructions, alveolar damage, reduced lung expansion, or interference with pulmonary blood flow. Mechanism of Breathing Inspiration Expiration The external intercostal The internal intercostal muscles contract while the muscles contract while the internal intercostal muscles external intercostal muscles relax. relax. Elevate the ribs  Lower the ribs  Tidal volume (TV): The amount Inspiratory and expiratory reserve volume (IRV exits with each breath. Volumes of Air Exchanged of air that normally enters & & ERV): The difference between normal amounts and the maximum effort amounts of air moved. during Ventilation Vital capacity (VC): The amount of air that Residual volume (RV): The amount of moves in plus the amount that moves out air that stays in the lungs even after a with maximum effort (Deep breathing). very deep exhalation. 5,800 maximum inspiratory expiration reserve 4,800 volume maximum inspiration Average Lung Volume (ml) vital 3,600 capacity total 2,900 Lung capacity tidal volume 2,400 expiratory reserve volume 1,200 Dead air space: Volume residual volume residual volume of air that remains in VC = IRV+TV+ERV the airways and is not Total 0 lung capacity (TLC) = VC+RV used for gas exchange. Regulation of Breathing Conscious control in Nervous Control the cortex can modify A respiratory center in the brain automatic regulatory establishes a regular pattern of control but cannot breathing (12 – 20 / min). override it completely. Receptor cells near the respiratory Medulla oblongata center respond to changes in CSF H+ caused by increases in arterial CO2. Nerve signals to and from (CO2 + H2O  H2CO3  H+ + HCO3- the respiratory center ) Chemical Control Carotid Receptor cells in the carotid bodies and aortic bodies respond to Aortic large decreases in arterial O2. bodies Intercostal The rate and depth of normal muscles breathing is determined by the need to get rid of CO2 rather than the need to obtain O2 Diaphragm Gas Exchanges in the Body O2 must be supplied to all the cells, and CO2 must be removed from the body during gas exchange. The principles of diffusion govern whether O2 or CO2 enters or leaves the blood in the lungs and in the tissues. The amount of pressure each gas exerts is called its partial pressure, symbolized as Po2 & Pco2. External Respiration Exchange of gases between air in alveoli and blood in pulmonary capillaries Blood in pulmonary capillaries has a higher Pco2 than atmospheric air. CO2 diffuses out of the plasma into lungs. Most of CO2 is carried in plasma as HCO3-. H+ + HCO3- → H2CO3 → H2O + CO2 carbonic anhydrase Blood in the pulmonary capillaries is low in oxygen, and alveolar air contain a higher Po2. O2 diffuses into plasma and then into red blood cells in the lungs. Hemoglobin (Hb) takes up this oxygen and becomes oxyhemoglobin (HbO₂) Hb + O2 → HbO2 Internal Exchange of gases between the blood in systemic capillaries and the tissue cells. Respiration Oxygen diffuses out of the blood into the tissues because the Po2 of tissue fluid is lower than that of blood. HbO2 → Hb + O2 Carbon dioxide diffuses into blood from tissues because the Pco2 of tissue fluid is higher than that of blood. H2O + CO2 → H2CO3 → H+ + HCO3-  Most CO2 is transported in plasma as HCO3-.  Small amount of CO2 is taken up by hemoglobin, forming carbaminohemoglobin (HbCO2).  The globin of Hb combines with H+ excess becomes HHb (reduced Hb). GENERAL MANIFESTATIONS OF RESPIRATORY DISEASE 1. Sneezing: a reflex response to irritation in the upper respiratory tract 2. Coughing :expel air from the lungs with a sudden sharp sound. 3. Sputum or mucoid discharge; thin, clear, and colorless or cream color. 4. Breathing pattern: The normal rate (eupnea) is 10 to 18 inspirations per minute, regular and effortless. 5. Breath sounds may be abnormal (Rales; light bubbly and Rhonchi; harsh) or absent. 6. Dyspnea is a subjective feeling of discomfort that occurs when a person feels unable to inhale enough air (shortness of breath). GENERAL MANIFESTATIONS OF RESPIRATORY DISEASE 7. Cyanosis is the bluish coloring of the skin and mucous membranes. 8. Pleural pain: a cyclic pain that increases as the inflammed membrane is stretched with inspiration or coughing. 9. Friction rub may be heard; a soft sound produced as the rough membranes move against each other. 10. Clubbed fingers and sometimes toes; enlargement of the tips resembles a drumstick-like shape, result from chronic hypoxia. 11. Changes in arterial blood gases (ABGs): Hypoxemia refers to inadequate oxygen in the blood (PO2). Hypoxia, or inadequate oxygen supply to the cells https://slideplayer.com/slide/6922348/ DIAGNOSTIC TESTS Spirometry-pulmonary function testing (PFT) is used to test pulmonary volumes and airflow (volume vs. times). Arterial blood gas determinations are used to check oxygen, carbon dioxide, and bicarbonate levels as well as serum pH. Oximeters measure O2 saturation. A normal healthy person should be able to achieve normal blood oxygen saturation levels (SpO2) of 94% to 99%. Exercise tolerance testing is useful in patients with chronic pulmonary disease for diagnosis and monitoring of the patient’s progress. DIAGNOSTIC TESTS Radiography may be helpful in evaluating tumors or infections such as pneumonia or tuberculosis. Bronchoscopy may be used in performing a biopsy or in checking for the site of a lesion or bleeding. Culture and sensitivity tests on exudates from the upper respiratory tract or sputum specimens can identify pathogens and assist in determining the appropriate therapy. Spirometry Spirometry is a type of pulmonary function test (PFT), a noninvasive procedure that provides important information about how well the lungs are working. Spirometry measures your airflow, measure how much air you inhale, how much air you exhale and how quickly you exhale. Spirometry is used to diagnose chronic lung diseases. Also to monitor current treatment plan. Spirometry indicates whether or not there is airway obstruction or airway restriction Respiratory disorders  Infectious Diseases  Obstructive Lung Diseases  Restrictive Lung Disorders  Vascular Disorders  Expansion Disorders 1- INFECTIOUS RESPIRATORY DISORDERS A- UPPER RESPIRATORY DISORDERS B- LOWER RESPIRATORY DISORDERS 1- INFECTIOUS DISEASES UPPER RESPIRATORY TRACT INFECTIONS – Common Cold (Infectious Rhinitis) viral infection – Sinusitis, bacterial infection secondary to a cold or an allergy – Laryngotracheobronchitis (Croup)-common viral infection – Epiglottitis – Influenza (Flu) https://www.youtube.com/watch?v=jKrpj777YnY 1- INFECTIOUS DISEASES LOWER RESPIRATORY TRACT INFECTIONS – Bronchiolitis (RSV Infection) respiratory syncytial virus , a myxovirus – Pneumonia; Lobar pneumonia Bronchopneumonia Primary atypical pneumonia Pneumocystis carinii pneumonia (PCP) – Severe Acute Respiratory Syndrome – Tuberculosis – Histoplasmosis, a fungal infection – Anthrax is a bacterial infection of the skin, respiratory tract or GI tract of humans and cattle 1- INFECTIOUS DISEASES Viruses cause both upper and lower respiratory tract infections, including the common cold, laryngotracheobronchitis (croup), influenza, bronchiolitis, and primary atypical pneumonia. Describe the common complications of viral respiratory infection? Common childhood respiratory infections Para-infleunza Respiratory syncytial virus virus,a myxovirus. leaning forward, hands on knees https://www.youtube.com/watch?v =GZe_RHLbQWY Stridor; noisy breathing,https://www.youtube.com/watch?v=5DN7xCleoyQ Drooling; flow of saliva outside the mouth https://www.youtube.com/watch?v=N91TUXfTT_E Hoarse: vocal cords impaired with affection of the sound Pneumonia Pneumonia is a type of lung infection that inflames the air sacs in one or both lungs, which impairs oxygen diffusion when exudate fills the alveoli or interstitial tissue in the lungs. Pneumonia is frequently but not always due to infection. The infection may be bacterial, viral, fungal, or parasitic. It can also be caused by inhalation of certain chemicals that irritate the lung tissue (aspiration pneumonia). Symptoms may include fever, chills, cough with sputum production, chest pain, and shortness of breath. Treatment includes antibiotics. Prognosis :Pneumonia can range in seriousness from mild to life- threatening. Those most at risk of severe infection from pneumonia include smokers, people with heart or lung disease, infants and young children, adults age 65 and older, and people with chronic medical conditions or weakened immune systems Classification (types)of the pneumonias (lung) Diffuse through out lung ,bacteria without cell wall (Dry cough) Rales: discontinuous crackling SOUND heard on auscultation, primarily during inhalation , associated with serous secretions. Rhonchi are deeper and harsher sounds resulting from thicker mucus. https://www.easyauscultation.com/rales Interstitial Pneumonia (Atypical) Severe Acute Respiratory Syndrome(SARS)- Respiratory distress syndrome SARS-associated coronavirus is the causative agent which affect the alveolar epithelium, causing failure of gas exchange It is transmitted by respiratory droplets during close contacts Pathophysiology ; – Flu like symptoms are present for 3 to 7 days followed several days later by a dry cough and marked dyspnea. – By day 7,chest radiographs indicate spreading patchy areas of interstitial congestion and severe hypoxia – There may be thrombocytopenia,lymphpenia, and elevated liver enzymes(due to viral damage) – The final stage: is severe respiratory distress Severe Acute Respiratory Syndrome(SARS) Signs and symptoms Stage1; fever, headache, myalgia, diarrhea Stage2; nonproductive cough, severe dyspnea, hypoxia Stage3; severe hypoxia, respiratory and metabolic acidosis Medications included the antiviral ribavirin and the glucocorticoid methylprednisolone Pneumocystis carinii pneumonia (PCP) It is an atypical pneumonia, that occurs as an opportunistic infection Occurs most commonly in immunosuppressed individuals (AIDS) It also causes pneumonia in premature infants. The etiological agent is a fungus that is inhaled and attaches to alveolar cells, causing necrosis and diffuse interstitial inflammation Onset is marked by dyspnea and a nonproductive cough https://www.youtube.com/watch?v=cuZb539SaaY Tuberculosis The causative organism is Mycobacterium tuberculosis which is acid fast, aerobic, slow- growing bacillus that is resistant to dryness and many disinfectants Why it is difficult for host defensive cells to eradicate TB bacilli? – The fatty cell wall of the organisms protect against digestion and destruction by defensive individual cells and antibiotics Who are at high risk of contracting TB? – Those whose resistance are lowered because of immunodeficiency (AIDS), malnutrition, alcoholism , or chronic disease. Pathophysiology of Tuberculosis (Development of tuberculosis) An airborne disease Inhalation or ingestion of the microorganism result in inflammatory reaction at the site of infection (lung, tonsils or small intestine) Depend on the immunity of the individual , there are two stages in the pathogenesis of tuberculosis— Primary infection (TB infection) and Secondary infection or reinfection (TB disease) http://www.fw-ac-deptofhealth.com/images/tbanim2.gif Tuberculosis Primary infection: Pathogens are engulfed by macrophages and causes local inflammatory reaction. A granuloma (Ghon tubercle) is formed at the site of inflammation (macrophages containing bacilli surrounded by T lymphocytes). Minimal caseation necrosis may develops in the center of the tubercle, walled off by fibrous tissue and usually become calcified. Ghon tubercle is the pathognomonic feature for primary TB infection. Some macrophages containing bacilli migrate to the regional lymph nodes, activating a type IV hypersensitivity response (delayed cell mediated response) with enlargement of the lymph nodes. Ghon complex : is formed of Ghon tubercle with tuberculous lymphadenitis. Mycobacterium tuberculosis (Mtb) induces an immune response in the lungs of a host that can lead to formation of a cellular aggregate called a granuloma in which the Mtb can remain dormant in the condition of latent tuberculosis (TB). Direct and indirect upregulation of matrix metalloproteinase (MMP), which is stimulated by the Mtb in infected macrophages in the granuloma and denoted by a dashed arrow, degrades the collagen exterior of the granuloma, triggering leakage of extracellular bacteria (B E ) and formation of a necrotic leaking granuloma called a TB cavity. Tuberculosis It is asymptomatic In case of good immunity—healing by fibrosis and calcification occur In case of moderate immunity---patient pass to secondary TB In case of very low immunity---Miliary tuberculosis Tuberculosis Secondary infection It often arises years after primary infection due to decreased host resistance Increase of the number and size of the tubercle with development of extensive caseation (necrosis, cavitation and tissue destruction)occur. Spread ; – Direct to surrounding tissue or – To lymphatic , – To blood (Miliary TB), Rapidly progressive form in which multiple granulomas affect large areas of the lungs with rapid dissemination via the bloodstream to other organs result in systemic infection with subnormal temperature It is symptomatic, has insidious onset with vague symptoms of : – Anorexia, malaise, fatigue and weight loss (toxemia). – Afternoon low-grade fever and night sweats. – Prolonged and increasingly severe cough and productive, purulent sputum, containing blood. Tuberculosis How diagnosis of active TB (infectious) is confirmed? – Chest x-ray – Acid staining of sputum specimen – Sputum culture What is a Mantoux test? What is a positive Mantoux test indicate? – Mantoux test is the tuberculin test. – A positive skin test does not mean the person active TB. It means that there has been adequate exposure to cause a hypersensitivity reaction.(so BCG is contraindicated?) Treatment of Tuberculosis Medications: antituberculous drugs Multiple drugs required to prevent development of resistant strains. Duration of treatment; months to 1 year or possibly longer, depending upon the health of the individual. An individual will become noncontagious when sputum is negative for microbes, usually 1 to 2 months. Drugs are prescribed for a longer period to ensure eradication of the infection. Prophylactic treatment is essential for: Skin test has converted from negative to positive within the last 2 years Who have radiographic changes consistent with TB Who in close contact with individual with active TB Immunosuppressed individuals People with HIV or with hematological cancer Measures must be taken by health care professional to protect himself; Have regular skin tests Regular chest radiographs Maintain host resistance (adequate rest and nutrition) 2- OBSTRUCTIVE LUNG DISEASES CYSTIC FIBROSIS LUNG CANCER ASPIRATION OBSTRUCTIVE SLEEP APNEA ASTHMA CHRONIC OBSTRUCTIVE PULMONARY DISEASE – EMPHYSEMA – CHRONIC BRONCHITIS – BRONCHIECTASIS Cystic fibrosis Cystic fibrosis is a recessive inherited disorder, common in children – It is a genetic disorder involving a defect in chloride ion transport in cell membranes This defect in the exocrine glands causes abnormally thick mucus secretions. The primary effects of cystic fibrosis are seen in the lungs and the pancreas, where the sticky mucus obstructs the passages Cystic fibrosis Right sided heart failure from high blood pressure in the arteries of the lungs Fatty stools lung cancer The lungs are a common site of both primary and secondary (metastatic ) lung cancer, where venous return and lymphatics bring tumor cells from many distant sites to the heart and then into the pulmonary circulation. Exposure to cigarette smoke ( 90% ) and industrial carcinogens are predisposing (risk)factors to lung cancer. Bronchogenic carcinoma arising from the bronchial epithelium, is the most common type of malignant lung tumor. The symptoms of hemoptysis, pleural effusion, chest pain, and anemia are diagnostic. Prognosis is poor because : – early diagnosis is rare, and – many types of tumors resist chemotherapy or radiation. ASPIRATION (choking) Definition: The passage of food or fluid, vomitus, drugs, or other foreign material into the trachea and lungs Effects: Aspiration of solids or liquids may cause inflammation, injury, or direct block of airways. Individuals who are at high risks ; – Young children; – children with congenital anomalies, cleft palate , – individuals who eat or drink while lying down or talking while eating EMERGENCY TREATMENT FOR ASPIRATION The Heimlich maneuver The Heimlich maneuver 1. To dislodge the solid object is recommended (stand behind the victim with encircling arms, position a fist, thumb side against the abdomen, below the sternum, place the other hand over the fist and thrust forcefully inward and upward). 2. A foreign object may be ejected from an infant by back blows administered between the infant’s shoulder blades, while the infant’s body is supported over a arm or leg, head lower than the trunk. Obstructive Sleep Apnea - Occurs when the pharyngeal tissues collapse on expiration during sleep, leading to intermittent periods of apnea (cessation of breathing). - Men are more often affected than women. Incidence increases with age & obesity (BMI >30). - Sleep apnea is usually diagnosed when the sleeping partner notes loud snoring with intermittent gasps for air. - Complications are directly related to chronic hypoxia and fatigue and include Type 2 diabetes, pulmonary hypertension, right-sided congestive heart failure, cerebrovascular accident, erectile dysfunction, depression, and daytime sleepiness. - Devices are available to prevent the patient sleeping in a supine position, which predisposes to apnea. ASTHMA Definition: Periodic episodes of severe but reversible bronchial obstruction (bronchospasm) Asthma may be classified in different ways. It may be acute or chronic, acute referring to a single episode, chronic referring to the long-term condition. In the traditional method based on etiology and the presence of a hypersensitivity reaction, there are two basic types of asthma. – The first is often called extrinsic asthma with onset commonly occurs in children and involves acute episodes triggered by a Type I hypersensitivity reaction to an inhaled antigen a familial history of other allergic conditions such as allergic rhinitis (hay fever) or eczema. – The second type of asthma is intrinsic asthma, with onset during adulthood. In this disease other types of stimuli target hyper-responsive tissues in the airway, initiating the acute attack. These stimuli include respiratory infections, exposure to cold, exercise, drugs such as aspirin, stress, and inhalation of irritants such as cigarette smoke. Asthma—acute episode All types of asthma exhibit the same pathophysiologic changes which is based on narrowing of the bronchi and bronchioles related to three changes, – Allergic inflammation of the mucosa with edema – Contraction of smooth muscle (bronchoconstriction), – Increased secretion of thick mucus in the passages. Release of interleukins, histamine, leukotrienes are involved in the pathway of asthma. CHRONIC OBSTRUCTIVE PULMONARY DISEASE – EMPHYSEMA; state of hyperinflation of the lung – CHRONIC BRONCHITIS – BRONCHIECTASIS; abnormal dilation of the bronchi surrounded by collapsed alveoli, both are full of pus Emphysema (COPD) (Hyperinflation of the Lung) Pathogenesis of Emphysema : 1- Bronchial asthma with narrowing bronchi and bronchioles leading to air trap (progressive accumulation of air inside the lung result in hyperinflation. 2- alpha1-antitrypsin deficiency lead to loss of elastic fiber in the wall of the alveoli which are responsible for recoil of alveoli during expiration. So, air is trapped in alveoli with hyperinflation of the lung. Chronic bronchitis Chronic bronchitis is associated with constant irritation in the airways and frequent infections, leading to fibrosis. It is characterized by constant productive cough. Cor pulmonale is a common complication. (Alteration in the structure and function of the right ventricle (RV) of the heart caused by a primary disorder of the respiratory system.) Chronic Obstructive Lung Disease Chronic Obstructive Lung Disease Individuals with emphysema are sometimes referred to as Pink buffers; Hyperventilation is a compensatory mechanism that alone helps maintain adequate oxygen, patient’s color is normal –pink Individuals with chronic bronchitis are sometimes referred to as blue bloaters; hypoxia is characteristic feature, particularly during coughing episodes. This result in poor color or cyanosis. Pulmonary congestion and cor pulmonale also commonly occur with chronic bronchitis, resulting in peripheral edema BRONCHIECTASIS Abnormal dilation of the bronchi surrounded by collapsed alveoli, both are full of pus. Develops in patients with cystic fibrosis or COPD. Characterized by chronic cough and production of copious amounts of purulent sputum (1-2cups/day). Treatment: antibiotics, bronchodilators, chest physiotherapy, and treatment of the primary cause. 3- RESTRICTIVE LUNG DISORDERS Applies to a group of diseases in which lung expansion is impaired and total lung capacity is reduced. (expansion disorder) A-Restrictive disorders include those with chest wall dysfunction, such as kyphosis or respiratory muscle paralysis, and those disorders causing pulmonary fibrosis B-Diseases affecting lung tissue as occupational diseases; Pneumoconioses (silicosis); industrial Chronic disorders resulting from continued or long term exposure to irritating particles – Occupational diseases in which inhaled irritants cause irreversible damaging inflammation and fibrosis over a long period of time. PNEUMOCONIOSES (Occupational diseases) Pleural fibrosis and lung cancer, particularly in cigarette smokers (Grass) 4- VASCULAR DISORDERS Respiratory disease occurs in the respiratory tract, – which includes the alveoli, bronchi, bronchioles, pleura, pleural cavity, trachea and the nerves and muscles of breathing. There are three main types of respiratory disease: – airway diseases, – lung tissue diseases and – lung circulation diseases include : A-Pulmonary edema B-Pulmonary embolus 4- VASCULAR DISORDERS Pulmonary edema: – Characterized by too much fluid in the interstitial space. – increased fluid in the alveoli reducing oxygen diffusion, lung expansion, and oxygenation of blood leading to severe hypoxemia. – Manifestations; orthopnea, sputum often frothy and pink or blood- tinged – The cause is left sided heart failure. Pulmonary embolus: – blood clot or a mass of other material that obstructs the pulmonary artery or a branch of it, blocking the flow of blood through the lung tissue. – Most pulmonary emboli (90%) arise from thrombi in leg deep veins. (It is a potential complication of thrombophlebitis in leg veins) – Moderate-sized emboli cause respiratory impairment; – large emboli interfere with cardiovascular function (right sided heart failure). – Other types of emboli, e.g. Fat emboli cause ARDS. Pulmonary edema refers to fluid collecting in the alveoli and interstitial area a b B, Photomicrograph showing acute pulmonary edema due to congestive heart failure: a, alveolar air space; b, fluid-filled A:Pulmonary edema associated with congestive heart alveolus failure PULMONARY EDEMA Etiology : Excess fluid in the alveolar tissue may develop when: Inflammation is present in the lungs, increasing capillary permeability (develops due to inhalation of toxic gases, or in association with tumors) Plasma protein levels are low, decreasing plasma osmotic pressure (e.g. hypoproteinemia due to kidney or liver disease) Pulmonary hypertension develops. (With left-sided congestive heart failure/ obstructive sleep apnea) Blocked lymphatic drainage Signs and symptoms Mild pulmonary edema include cough, orthopnea, and rales. As congestion increases, hemoptysis often occurs. Sputum is frothy owing to air mixed with the secretions, and blood-tinged owing to ruptured capillaries in the lungs. Hypoxemia increases, and cyanosis develops in the advanced stage.  Acute congestive heart failure may cause such an episode, called paroxysmal nocturnal dyspnea, during a sleep period. Pulmonary embolus. Pulmonary embolus due to deep vein thrombosis(DVT) is a leading cause of death in hospitals Pulmonary embolus Other types of pulmonary emboli include: Fat emboli cause ARDS (from the bone marrow resulting from fracture of a large bone.) Vegetation resulting from endocarditis in the right side of the heart, Amniotic fluid emboli from placental tears occurring during labor and delivery, Tumor cell emboli that break away from a malignant mass, or Air embolus injected into a vein Pulmonary embolus Signs and symptoms With small emboli, a transient chest pain, cough, or dyspnea may occur. For larger emboli, chest pain that increases with coughing or deep breathing, tachypnea, and dyspnea develop suddenly. Later, hemoptysis and fever are present. Hypoxia stimulates a sympathetic response, with anxiety and restlessness, pallor, and tachycardia. Massive emboli cause severe crushing chest pain, low blood pressure, rapid weak pulse, and loss of consciousness. Fat emboli are distinguished by the development of acute respiratory distress, a petechial rash on the trunk, and neurologic signs such as confusion and disorientation. Pulmonary embolus Diagnosis can be confirmed with:  x-ray, lung scan , MRI, or pulmonary angiography.  The source of the embolus can be determined using Doppler ultrasound or venography.  Sudden death often results in these cases, which involve greatly increased resistance in the pulmonary arteries because of the embolus plus reflex vasoconstriction due to released chemical mediators such as serotonin and histamine  Risk factors for these emboli include immobility, trauma or surgery to the legs, childbirth, congestive heart failure, dehydration, increased coagulability of the blood, and cancer. 5- EXPANSION DISORDERS Atelectasis: collapse of a part or all of a lung (alveoli are airless) Pleural effusion; excessive fluid in the pleural cavity Pneumothorax; air in pleural cavity results from rib fractures Flail Chest Infant Respiratory Distress Syndrome Adult or Acute Respiratory Distress Syndrome Acute Respiratory Failure Atelectasis When the alveoli become airless, they collapse, interferes with blood flow through the lung. Both ventilation and perfusion are altered, and affects oxygen diffusion. If the lungs are not reinflated quickly, the lung tissue can become necrotic and infected, and permanent lung damage results. PLEURAL EFFUSION A pleural effusion is the presence of excessive fluid in the pleural cavity. Pleurisy or pleuritis is a condition in which the pleural membranes are inflamed, swollen, and rough, often in association with lobar pneumonia. PLEURAL EFFUSION Etiology Different types of fluid may collect in the pleural cavity. Exudative effusions are a response to inflammation, containing protein and white blood cells to leak into the pleural cavity Transudates are watery effusions, sometimes called hydrothorax (kidney & liver diseases). Hemothorax is the term used when the fluid is blood resulting from trauma, cancer, or surgery. Empyema occurs when the fluid is purulent as a result of infection, often related to pneumonia. PNEUMOTHORAX Pneumothorax refers to air in the pleural cavity. The presence of air at atmospheric pressure in the pleural cavity and the separation of the pleural membranes by air prevent expansion of the lung, leading to atelectasis. There are several different types of pneumothorax or Closed Pneumothorax Mediastinum is pushed towards affected lung Mediastinum is pushed towards unaffected lung A large open pneumothorax impairs ventilation and circulation (venous return) due to mediastinal flutter. Interference with venous return leads to hypotension. Mediastinum is pushed towards unaffected lung With each inspiration, air increases in pleural cavity leading to increase pressure on affected side, push mediastinum to other lung, compressing it & inferior vena cava. Severe hypoxia & respiratory distress develop quickly. Life threatening condition Types of Pneumothorax Flail chest injury  Falls and car accidents cause most chest injuries.  Flail chest results from fractures of the thorax, usually fractures of three to six ribs in two places or fracture of the sternum and a number of consecutive ribs.  Flail chest injury causes paradoxical (opposite) motion of the chest wall and decreases oxygen concentration in the alveolar air as well as impeding venous return. Respiratory Distress Syndrome Respiratory distress syndrome occurs in newborn infants { Infant Respiratory Distress Syndrome (IRDS) and is associated with prematurity }, and also in adults whose lungs are damaged by ischemia or inhalation of toxic materials. Lung expansion is reduced and oxygen diffusion impaired by fluid in the lungs. INFANT RESPIRATORY DISTRESS SYNDROME IRDS, or neonatal respiratory distress syndrome [NRDS], or hyaline membrane disease) A common cause of neonatal deaths, particularly in premature infants Pathophysiology – During the third trimester of fetal development, the alveolar surface area and lung vascularity greatly increase in preparation for independent lung function immediately after birth. – Surfactant, which reduces surface tension in the alveoli and promotes expansion, is first produced between 28 and 36 weeks of gestation , depending on the maturity of the individual lung – Infant lung maturity can be assessed by measuring the surfactant level of the fetus with a test such as the lecithin-sphingomyelin (L/S) ratio in amniotic fluid, which is obtained by amniocentesis Initially sphingomyelin is high, then it decreases and lecithin increases until the ratio represents adequate surfactant function at around 35 weeks of gestation. INFANT RESPIRATORY DISTRESS SYNDROME – Without adequate surfactant, each inspiration is very difficult because the lungs totally collapse during each expiration, thereby requiring use of the accessory muscles and much energy to totally reinflate the lungs. – The poorly developed alveoli are difficult to inflate, and an inadequate blood and oxygen supply further deters the production of surfactant by alveolar cells – Diffuse atelectasis results, which decreases pulmonary blood flow and leads to reflex pulmonary vasoconstriction and severe hypoxia. – Poor lung perfusion and lack of surfactant lead to increased alveolar capillary permeability, with fluid and protein (fibrin) leaking into the interstitial area and alveoli, forming the “hyaline membrane” INFANT RESPIRATORY DISTRESS SYNDROME Etiology: premature birth, Infants born to diabetic mothers Signs and symptoms Respiratory difficulty may be evident at birth or shortly after birth. Signs include a persistent respiratory rate of more than 60 breaths per minute, nasal flaring, subcostal and intercostal retractions, rales, and low body temperature. Chest retractions are quite marked in a neonate because of the soft chest wall Diagnostic tests Arterial blood gas analysis is helpful in monitoring both oxygen and acid-base balance. Chest x-rays indicate areas of congestion and atelectasis. Retractions of the Infant Chest in IRDS. Compare Infant respiratory distress syndrome Adult respiratory distress IRDS, or neonatal respiratory distress syndrome syndrome [NRDS], or hyaline membrane disease) Etiology Premature birth resulting in decreased Systemic sepsis surfactant Prolonged shock Burns and smoke inhalation aspiration Pathophysiology Lung collapse with each expiration Damage to surfactant-producing resulting in diffuse atelectasis, cells and increased capillary poor lung perfusion, permeability leading to diffuse leakage of fluid and fibrin into alveoli atelectasis that decreases lung expansion and gas Fluid accumulation in lungs, all exchange of which predispose to pneumonia Signs and Respirations

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