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Document Details

Lamar University

Shannon Marsh

Tags

pulmonary system pathophysiology nursing respiratory system

Summary

These notes cover the pathophysiology of the pulmonary system. They include information on the structural organization, gas exchange, and various respiratory disorders. These notes are likely for a nursing program, university level.

Full Transcript

Lamar University JoAnne Gay Dishman School of Nursing NURS 2373 Pathophysiology: Alterations in the Pulmonary System Shannon Marsh, MSN, RN, CCRN Objectives: 1. Describe the structural organization, exchange and transpor...

Lamar University JoAnne Gay Dishman School of Nursing NURS 2373 Pathophysiology: Alterations in the Pulmonary System Shannon Marsh, MSN, RN, CCRN Objectives: 1. Describe the structural organization, exchange and transport of gases, and control of breathing within the pulmonary system. 2. Discuss how the body adapts to chronic hypoxia. 3. Discuss the etiology, pathogenesis, manifestations, and consequences of upper and lower infectious respiratory disorders. 4. Discuss the etiology, pathogenesis, manifestations, and consequences of lung cancer. 5. Discuss the etiology, pathogenesis, manifestations, and consequences of obstructive airway disorders. 6. Discuss the etiology, pathogenesis, manifestations, and consequences of ventilation/perfusion ratio and gas exchange disorders. Norris, (2025). Porth’s pathophysiology: concepts of altered health states. (11th ed). Wolters Kluwer. Chapter 29; Chapter 30 p. 912-922, p. 928-931; Chapter 31 STRUCTURE & FUNCTION OF THE PULMONARY SYSTEM Primary function of the respiratory system: GAS EXCHANGE Other functions: 2) Lungs serve as a host defense by providing a barrier between the inside of the body and the external environment; 3) Lung is a metabolic organ that synthesizes and metabolizes certain compounds ---A&P REVIEW--- Structural Organization Conducting Airways o Section in which air moves as it passes between the atmosphere and the lungs (do not participate in gas exchange) o Warms, filters, moistens, and removes foreign materials via mucociliary blanket from air as it moves through structures o Structures: § Nasal passages Preferred route of entrance for air Filters, warms, humidifies air; coarse hairs filter and trap large particles from the air § Mouth and pharynx Mouth is alternate airway when nasal passages are plugged or large volumes of air are needed (Exercise) 1 Oropharynx is the only opening between nose, mouth, and lungs- obstruction leads to immediate cessation of ventilation § Larynx Connects oropharynx with trachea between upper airways and lungs Two functions: speech & protecting the lungs from foreign substances Epiglottis is located above the larynx- opens during breathing and closes during swallowing to keep foreign substances out Substances other than air (liquid, food, etc.) that enter the airway are not easily removed. When they enter the lungs, aspiration pneumonia can occur § Tracheobronchial Tree Trachea- “windpipe;” connects larynx with major bronchi Bronchi- right and left mainstem bronchus; carina is a highly sensitive area between bronchi; each bronchus enters the lungs through a slit called the hilum; bronchi divide into segments and get smaller at the distal ends Bronchioles- Segmental bronchi continue to branch until they become the smaller, terminal bronchioles. Bronchospasm can narrow these conducting airways and impair airflow. Lungs & Respiratory Airways o Area of gas exchange o Other functions: inactivate vasoactive substances such as bradykinin, convert angiotensin I to angiotensin II, & serve as a reservoir for blood storage o Lobules § Smallest functional units of lungs § A branch of a terminal bronchiole, an arteriole, the pulmonary capillaries, and a venule supply each lobule § Blood enters lobules through a pulmonary artery and exits through a pulmonary vein. o Alveoli § Specific site of gas exchange § Alveolar sacs are thin-walled, cup shaped structures separated from each other by thin alveolar septa. A single network of capillaries occupies most of the septa. § Approximately 300 million alveoli in an adult lung (large surface area) § Type I and Type II alveolar cells (Type II synthesize pulmonary surfactant) § Surfactant: Lipoprotein that reduces surface tension, allowing alveoli to stay “open” § Alveolar macrophages: Responsible for destroying inhaled pathogens and removing inhaled particulate matter (dust or pollen). Expelled after activation by coughing or swallowing. Pleura 2 o Thin, transparent, double-layered serous membrane lining the thoracic cavity and encasing the lungs o Allows for no separation between the lungs and chest wall o Pleural cavity is an area where inflammation can occur and exudate can accumulate. o Pleural effusion: Pulmonary Vasculature o Pulmonary circulation § Review circulation of blood through the heart to and from the lungs Pulmonary arteries vs Pulmonary veins § Participates in gas exchange o Bronchial circulation § Distributes blood to the conducting airways and the supporting structures of the lungs § Does not participate in gas exchange Innervation o Pain fibers found only in the pleura o Parasympathetic nervous system stimulation = airway constriction and increased glandular secretions o Sympathetic nervous system stimulation = airway relaxation, blood vessel constriction, and inhibition of glandular secretions EXCHANGE AND TRANSPORT OF GASES Basic Properties of Gases o Nitrogen is the most abundant gas in the air o Oxygen is about 21% o Arterial Blood Gases o Inhale O2 à Exhale CO2 GAS EXCHANGE Ventilation o Exchange / movement of gases into and out of the lungs o Influenced by: § Body position § Lung volumes § Blockages in the airway o Degree to which the lungs inflate and deflate depends on the respiratory pressures inflating the lungs, compliance of the lungs, and resistance. o Factors affecting ventilation: 3 o Pressure § Atmospheric pressure = 0 mmHg § Intrathoracic pressure is negative (assists to stay inflated) § Air moves between the lungs and atmosphere because of a pressure difference o Lung Compliance § Ease with which the lungs can be inflated § Dependent upon elastin, collagen fibers, water, and surface tension within the lungs/thoracic cavity § Decreased lung compliance: Stiff lungs or chest wall, lungs are difficult to inflate (pneumonia, pulmonary edema, fibrosis, ARDS) § Increased lung compliance: Lungs are very easy to inflate and have lost some elastic recoil (aging, emphysema) o Airway Resistance § Opposition to flow caused by the forces of friction. § Impacted by bronchial smooth muscle, lung volume, and the bronchial tree Lung Volumes o Amount of air exchanged during ventilation Perfusion- Primary functions of pulmonary circulation are to provide blood flow to gas exchange portion of lung and facilitate gas exchange. Remember blood flow thru heart again o Pulmonary circulation: § Pulmonary artery pressure (PAP) = about 25/10 mmHg § Increased pressures may lead to pulmonary edema o Hypoxia-induced vasoconstriction § Pulmonary blood vessels are highly sensitive to hypoxia § Severe pulmonary vasoconstriction when oxygen levels drop to 60 mmHg § Prolonged hypoxia may lead to pulmonary hypertension, cor pulmonale (right- sided heart failure) o Shunt § Blood moves from the right to the left side of circulation without being oxygenated § Anatomic shunt: Blood moves from venous to arterial without moving through the lungs. May happen with some congenital heart defects. § Physiologic shunt: “mismatching” of ventilation and perfusion within the lung; results in insufficient ventilation to be able to oxygenate the blood flowing through alveolar capillaries. Occurs with certain respiratory or heart diseases. 4 Mismatching of Ventilation & Perfusion o Perfusion without ventilation (atelectasis or obstruction) o Ventilation without perfusion (pulmonary embolism) Diffusion- Transfer of gases between the alveoli and the pulmonary capillaries to the red blood cells. o Increased when high concentration of oxygen is supplied o Decreased with diseases that destroy lung tissue or increase the thickness of the alveolar- capillary membrane O2 and CO2 Transport: the movement of oxygen molecules to the cells and carbon dioxide molecules to the lungs by hemoglobin attached to red blood cells (RBCs). (Lungs à hemoglobin à Cells) § Oxyhemoglobin- Hemoglobin bound with oxygen. 95%-98% saturated with O2 in arterial blood, and 75% saturated in venous blood. § Carbaminohemoglobin- Hemoglobin bound with carbon dioxide § Binding Affinity of Hemoglobin for Oxygen The hemoglobin molecule should bind to the oxygen molecule. The hemoglobin molecule should release it as needed to the tissues/cells. Affinity- Hemoglobin’s ability to bind to oxygen. o High affinity = Hemoglobin binds more readily to oxygen o Decreased affinity = Hemoglobin releases the oxygen to the cells more easily Factors increasing affinity: o _______ oxygen saturation o _______ pH (alkalosis) o Decreased CO2 concentration o Decreased body temperature 5 Factors decreasing affinity: o ________ oxygen saturation o ________ pH (acidosis) o Increased CO2 concentration o ________ Dissociation: Oxygen Dissociation Curve CONTROL & REGULATION OF BREATHING Control of Breathing: Respiratory Center of the Brain o Muscles that control respiration require continuous input from the nervous system. o Movement of muscles responsible for ventilation is controlled by neurons in the pons and medulla. o Brain injuries in this area affect breathing! Regulation of Breathing o Automatic Components § Chemoreceptors: Monitor O2, CO2, & pH; adjust ventilation to meet the body’s needs Central- Most important; sense changes in PCO2 levels. High PCO2 levels stimulate increase in ventilation for a short time. Peripheral- Monitor PO2 levels. Exert little control over ventilation until PO2 < 60 mmHg, then stimulate increased ventilation. Important for people with chronically elevated PCO2 levels. § Lung Receptors: Monitor breathing pattern and function. o Voluntary Components § Integrate breathing with voluntary acts such as speaking, blowing, singing, etc. § Temporarily suspend automatic breathing § Initiated by motor & premotor cortex Cough Reflex o One of the primary defense mechanisms in the respiratory system o Sensitive receptors located in the tracheobronchial wall o Conditions interfering with the cough reflex: § Weak abdominal or respiratory muscles § Disease conditions affecting the closing of the glottis and laryngeal muscles § Prolonged presence of nasogastric tube § Depressed function of medullary centers in the brain § Drugs that depress the cough center 6 Dyspnea o Subjective sensation of difficulty breathing o “Difficulty breathing” “Shortness of breath” “Breathlessness” o Observed in at least three major cardiopulmonary disease states: § Primary lung diseases § Heart disease characterized by pulmonary congestion § Neuromuscular disorders Changes Across the Lifespan § Older Adults: o Decreased surface area and elasticity à Less effective chest wall expansion; less effective gas exchange o Increased respiratory dead space à Ventilation/perfusion inequality o Decreased ability to quickly increase respiratory rate à Decreased compensation to acid/base imbalances --- RESPIRATORY DISEASES & DISORDERS --- Common characteristics/manifestations associated with respiratory diseases: Cyanosis Dyspnea Hypercapnia Hypoxemia Tachycardia Tachypnea Hypoxemia = Low amount of oxygen in the blood. Manifestations of hypoxemia: Changes in level of consciousness (LOC) o Stupor à Coma o Restlessness, agitation, or combative behavior Cyanosis o Central o Peripheral Diaphoresis Hyperventilation Pallor SNS activation Hypoxemia may be so severe that systemic hypoxic cell injury occurs, resulting in an accumulation of lactic acid (metabolic acidosis) and increased serum lactate levels. 7 Chronic hypoxemia: Increased respiratory rate Pulmonary vasoconstriction Increased production of RBCs Hypercapnia = High levels of CO2 in the arterial blood: Confusion Respiratory acidosis Chronic hypercapnia in some patients may show no symptoms because they have adapted. UPPER RESPIRATORY TRACT INFECTIONS – INDEPENDENT STUDY The Common Cold § Viral infection of upper respiratory tract. § Most common respiratory tract infection § Most adults have 3-4 colds/year; school-age children may have 6-8 colds/year § Etiology and Pathogenesis o Associated with a number of viruses: § Rhinoviruses (most common), parainfluenza, respiratory syncytial virus (RSV), human metapneumovirus (hMPV), coronaviruses, adenoviruses, and bocaviruses (in children) o Factors in identifying the type of virus: § Season § Age RSV and parainfluenza: Children < 6 years old Frequency of infections decreases with age until about 65 years § Immunologic state § Prior exposure o Common source of spread: FINGERS o Common portals of entry: eyes and nasal mucosa o Incubation period = 2 days o Duration of illness = 7 days § Clinical Manifestations o Dryness/stuffiness affecting mainly the nasopharynx o Rhinitis o Secretions are usually clear and watery o Red, swollen mucous membranes of upper respiratory tract o Postnasal dripping leading to sore throat and hoarseness 8 o Possible headache and generalized malaise o Severe cases: chills, fever, and exhaustion § Viral shedding: Rhinosinusitis Inflammation involving the nasal sinuses. Sinuses should remain sterile, but their lower oxygen content and warm/moist environment could facilitate the growth of organisms Most common causes are conditions that obstruct drainage from the sinuses o Swelling from viral upper respiratory tract infection or allergic rhinitis o Nasal polyps o Barotrauma from frequent changes in barometric pressure o Swimming, diving, and abuse of nasal decongestants Acute: o Caused by viruses, bacteria or mixed o May last up to 4 weeks o Common infecting organisms: § Haemophilus influenzae § Streptococcus pneumoniae o Manifestations: Facial pain Headache Purulent nasal Decreased sense of discharge smell Fever o Viral acute rhinosinusitis: 5-7 days o Bacterial: worsening symptoms for 5-7 days or beyond 10 days Chronic o Usually bacterial or fungal in origin o Duration = > 12 weeks o Caused by anaerobic organisms alone or in combination with aerobic organisms: § Strep species § Staphylococuss aureus o Possible presence of biofilms from Pseudomonas aeruginosa in ear, nose, throat o Manifestations: § Sinus pressure with nasal congestion § Dull, constant headache § Symptoms may persist for years with varying severity § Episodes of acute sinusitis § Mucosal changes often irreversible 9 Influenza Combined with pneumonia, “the flu” is the 8th leading cause of death in the US Infection rates – Highest among children and older adults Rates of serious illness/death – Highest among adults > 65 Mode of transmission: Inhalation of droplet nuclei Incubation period: 1-4 days (average of 2 days) Persons may be contagious on day 1, even before showing symptoms, and remain infectious for ~ 1 week after illness onset. Viral shedding: May last up to 3 weeks Type A, B, and C cause epidemics in humans o Influenza Type A § Can infect multiple species (including avian and mammal species) § Two subtypes based on two surface glycoproteins: Hemagglutinin (HA) and Neuraminidase (NA). § Can develop new HA and NA subtypes in which the population is not protected. § Antigenic shift: Major genetic rearrangement in either antigen HA or NA May lead to epidemic or pandemic § Antigenic drift: Lesser change in the virus; may allow partial protection for some individuals due to cross-reacting antibodies Pathogenesis o May cause three types of infections: § Uncomplicated upper respiratory infection (rhinotracheitis) § Viral pneumonia § Viral infection followed by a bacterial infection o Initially an upper airway infection § Virus destroys mucous-secreting, ciliated, and epithelial cells § Holes between cells allow extra-cellular fluid to escape (“runny nose”) o If virus moves lower in the respiratory tract… § Severe shedding of bronchial and alveolar cells § Compromised natural defense mechanisms § Bacteria easily adhere to epithelial cells à Secondary bacterial infection Clinical Manifestations o Fever & chills o Malaise o Muscle aching o Headache o Profuse, watery nasal discharge o Nonproductive cough o Sore throat o Possible diarrhea Symptoms of uncomplicated rhinotracheitis usually peak on day 3-5 and are gone by day 7-10. 10 LOWER RESPIRATORY TRACT INFECTIONS PNEUMONIAS ______________ of parenchymal structures in the lower respiratory tract (bronchioles & alveoli) Infectious or non-infectious causes Pathophysiology: o Defense mechanisms and anatomic structures assist in keeping the lower respiratory tract a sterile environment o Organisms that make it past these barriers are eaten by macrophages in the alveoli o Inflammatory process ensues o Endotoxins are released by some microorganisms – damaging the mucus membranes of the bronchi & alveoli – resulting in inflammation and edema o Exudate can then build up in the distal airways affecting Ventilation and Gas Exchange Classifications of Pneumonia: Community vs Hospital-Acquired Community-Acquired Pneumonia Hospital-Acquired Pneumonia o Infection that begins outside the hospital or is o Lower respiratory tract infection not present diagnosed within 48 hours after admission to or incubating on admission to the hospital; the hospital in a person who has not resided usually > 48 hours or more after admission in a long-term care facility for 14 days or o Mostly bacterial more before admission. § P. aeruginosa, S. aureus, o Bacterial or viral Enterobacter species, Klebsiella o Most common organism: S. Pneumoniae species, E. coli, Serratia o Other organisms: § H. influenzae, S. aureus, gram-negative bacilli § Mycoplasma pneumoniae, Legionella, Chlamydia species, viruses (atypical agents) 11 Other Classification of Pneumonia: Acute Bacterial Pneumonia (Typical) o S. Pneumonia is the most common cause of bacterial pneumonia o Organisms in the upper airways may travel to the lower airways by aspiration o Defense mechanisms prevent infection under normal conditions o Manifestations: § Chills § Fever (Elderly???) § Fine crackles § Malaise § Pleuritic chest pain § Productive cough with blood tinged / rusty colored / purulent sputum o **Pneumonia vaccine** Primary Atypical Pneumonia o Often referred to as “walking pneumonia” o Most common organism: Mycoplamsa pneumoniae o Usually mild o Manifestations: § Dry hacking nonproductive cough § Fever § Headache § Muscle aches TUBERCULOSIS (TB) Mycobacterium tuberculosis One of the leading causes of death for people with HIV. People with increased risk for TB: people from foreign countries, living in congested populations, people with HIV, the elderly, and other immunocompromised individuals Waxy outer capsule is difficult to destroy. May be referred to as acid-fast bacilli (retains red dye on waxy capsule) May affect other organs besides the lungs Transmitted via very tiny droplet nuclei (1 – 5 microns [1 inch = 42,540 microns]) that remain in the air for several hours Latent vs Active TB o Latent may develop to active TB if the immune system fails Pathogenesis of latent TB o Droplet nuclei eludes defense mechanisms in upper respiratory tract and lodges in bronchiole or alveoli. 12 o Inflammatory process begins. However, macrophages are unable to kill the bacilli by phagocytosis because of the waxy outer capsule protecting the bacteria. Because it cannot be killed, a cell mediated response is initiated that “contains” the organism. o A “tubercle” is formed. Tissue within the tubercle dies, and a cheese-like center forms. o Scar tissue develops around the tubercle. Lesions calcify and are able to be visualized on a chest x-ray. o Adequate immune system: Bacilli remain contained and the patient will not develop active TB. o If immune system fails: Bacilli will not be contained. Active TB may develop – extensive lung damage can occur. TB skin test BCG vaccine Latent vs Active TB Latent TB Active TB Manifestations Anorexia Blood tinged sputum Cough – dry or productive Fatigue Fever Night sweats Weight loss Skin test result Ability to spread to others Chest x-ray May or may not show small Cavitary lesions, opacities, nodules on a chest xray infiltrates, or consolidations. LUNG CANCER Risk factors: Smoking, occupational/environmental hazards, genetics Most are carcinomas that originate in lung tissue Primary cancers from other tissues can metastasize to the lung 13 Cancer Type Characteristics Small-Cell Carcinoma (“Oat Cell”) Cells grow in clusters Strong association with smoking 20% - 25% Highly malignant Metastases usually evident at time of diagnosis Brain metastases are common Poor prognosis Commonly associated with paraneoplastic syndromes Squamous Cell Carcinoma Found most commonly in men Associated with smoking 25% - 40% Usually originates in central bronchi Hypercalcemia Adenocarcinoma Most common type in North America Weaker association with smoking 20% - 40% Most common type for women and non- smokers Originate in bronchiolar or alveolar tissue Associated with areas of scarring in lungs Large-Cell Carcinoma Poor prognosis Spreads very early 10% - 15% Invade subsegmental bronchi and larger airways Manifestations depend on location, metastasis, stage… o Anorexia o Chronic cough o Hemoptysis o Pain o Shortness of breath o Wheezing o Metastasis is most common to brain, bone, and liver 14 DISORDERS OF VENTILATION / PERFUSION RATIO AND GAS EXCHANGE DISORDERS OF THE PLEURA PLEURAL EFFUSION Abnormal collection of fluid in the pleural cavity. Fluid may be: exudates, purulent drainage (empyema), chyle, blood, or serous transudate (hydrothorax). May be unilateral or bilateral. Causes: o Heart failure o Renal failure o Liver failure o Malignancy o Infections Pathogenesis: o Increased capillary permeability o Decreased colloidal osmotic pressure o Increased negative intrapleural pressure o Impaired lymph drainage Manifestations: o Dyspnea o Decreased lung expansion o Diminished breath/lung sounds o Hypoxemia o Pleuritic pain (Large effusion- constant pain) o Fever, increased WBC, and other signs of inflammation (with empyema) HEMOTHORAX Specific type of pleural effusion: Blood in the pleural cavity Causes: o Chest injury o Complication of surgery o Malignancies o Vessel rupture Variations in severity based on size: o Minimal: < 250 mL o Moderate: 500 mL – 1000 mL (~ 1/3 of pleural space) o Large: > 1000 mL (1/2 or more of one side of the chest) Manifestations: Dyspnea, Hypoxemia, & Hypovolemia à SHOCK 15 PNEUMOTHORAX Condition in which air enters the pleural space, causing a partial or complete collapse of the affected lung. Pneumothorax is usually expressed in percentages (5%-95%). Types: o Spontaneous Pneumothorax (no injury): Rupture of air-filled bleb or blister on the surface of the lung. § Primary pneumothorax: Healthy individuals. Seen most often in tall boys and young mean (10-30 years old). Smoking and family history may play a role. § Secondary pneumothorax: Underlying lung disease. Common cause- emphysema (Other conditions- asthma, TB, cystic fibrosis, lung cancer). o Traumatic Pneumothorax (injury): Penetrating or non-penetrating chest injury § Gun shots, stabbing, medical procedures, rib fractures § Hemothorax commonly occurs with traumatic pneumothorax Manifestations (Depend on severity) o Asymmetrical chest expansion o Chest pain o Decreased or absent breath sounds over site o Dyspnea o Hypoxemia o Tachycardia o Tachypnea TENSION PNEUMOTHORAX Air enters pleural space but cannot escape Pressure increases with each breath. As pressure increases, the affected lung collapses. The heart and great vessels are compressed. Mediastinal structures shift to the opposite side of the chest. The trachea is pushed from the normal, midline position. The unaffected lung becomes compressed. Ventilation is severely impaired: Life-threatening, medical emergency!!! More common with traumatic pneumothorax Manifestations: o Hypotension o Distended neck veins o Subcutaneous emphysema o Tracheal deviation toward unaffected side o May lead to shock 16 ATELECTASIS Incomplete expansion of a lung/portion of a lung Results in partial or complete lung collapse Decreased surface area for gas exchange Causes: o Airway obstruction o Lung compression o Absence or loss of pulmonary surfactant (newborns) o Increased risk after surgery secondary to pain, pain medications, and immobility Manifestations: o Cyanosis o Decreased/absent breath sounds over the affected area o Dyspnea o Fever, s/s infection o Hypoxemia o Tachycardia o Tachypnea OBSTRUCTIVE AIRWAY DISORDERS ASTHMA Chronic disorder of the airways that causes episodes of airway obstruction, bronchial hyperresponsiveness, airway inflammation, and airway remodeling (in some cases). Affects individuals of every age; many cases develop in childhood Risk factors for development: o Genetic predisposition* for the development of an IgE response to common allergens o Allergies o Antenatal exposure to tobacco smoke and pollution Pathophysiology o Exposure to stimulus (allergen) triggers the onset of an “asthma attack” o Inflammatory response ensues o Inflammatory mediators are released- stimulating the PNS, resulting in bronchoconstriction o Mucosal edema and mucous production o Airway narrows o Air becomes trapped distal to the edematous airway- resulting in distended alveoli o Blood flow to distended alveoli is reduced (decreased gas exchange) Manifestations o Anxiety o Chest tightness o Cough 17 o SOB o Tachycardia o Tachypnea o Accessory muscle use o Wheezing CHRONIC OBSTRUCTIVE PULMONARY DISEASE Group of chronic airway diseases characterized by chronic and recurrent obstruction of airflow in the pulmonary airways Leading cause of morbidity and mortality worldwide Most common cause: ________________ Less common cause: Hereditary deficiency in a1 antitrypsin Periodic exacerbations of dyspnea and increased sputum production; lung tissue progressively worsens after each exacerbation Two types: Emphysema & Chronic Bronchitis (may have both) COPD: Emphysema vs Chronic Bronchitis Emphysema Chronic Bronchitis Known as the “pink puffers” because: “Blue bloaters” 1) no cyanosis 2) accessory muscle use Chronic inflammatory process with Associated with smoking or inherited alpha1- excessive bronchial mucous secretion antitrypsin Airflow is obstructed Pathophysiology: Recurrent inflammation results in the release of proteolytic enzymes causing irreversible enlargement of the distal air spaces Loss of lung elasticity Abnormal enlargement of airspaces distal to terminal bronchioles (results in hyperinflation of lungs) Destruction of alveolar walls and capillary beds Elastic recoil is lost Air trapping results à Volume of air passively expired is reduced Hyperventilation and cardiac output Lung is oxygenated, but limited blood flow prevents oxygenation of body tissues Proportionate decrease in ventilation & perfusion 18 Manifestations of Emphysema: Manifestations of Chronic Bronchitis: Barrel chest there is an increased anterior- Increased sputum production posterior diameter of the chest (related to Coarse lung sounds so you may here hyperinflation) fluid/secretions when you listen to their Diminished lung sounds air trapping lungs Dyspnea begin as exertional, but worsen as Cyanosis the disease progresses Respiratory acidosis (Compensated?) Relatively normal ABG’s (until late stages) Hypercapnia and Hypoxemia Muscle wasting Frequent respiratory infections Sitting upright/leaning forward Polycythemia Prolonged expiration May develop pulmonary HTN and/or right- Pursed lip breathing sided HF Accessory muscle use Accessory muscle use CYSTIC FIBROSIS Genetic disorder: Autosomal Recessive Affects respiratory, gastrointestinal, and reproductive systems More common in Caucasians Excessive, thick mucous that obstructs the lungs and pancreas Pathophysiology: o Genetic mutation increases absorption of sodium and water from the airways into the blood, causing the mucociliary blanket of the respiratory epithelium to become more viscid o Result is the accumulation of thick respiratory secretions that predispose the individual to recurrent pulmonary infections SALTY: Manifestations: o Thick secretions à mucous plugs Skinny o Frequent lung infections Autosomal recessive o Structural changes in bronchial wall o Malnutrition Lung infections o High levels of NaCl in sweat Thick mucous o Abnormal pancreatic function Young age 19 CHRONIC INTERSTITIAL LUNG DISEASES Group of diseases resulting from inflammatory conditions that cause the lung tissue to become stiff and difficult to expand (decreased compliance) Affects collagen and elastic connective tissues in the interstitium of alveolar walls Multiple causes: o Injury à Inflammation à Scarring o Occupational § “Coal miner’s lung” § Asbestosis § Gases/fumes o Drugs / Medications § Cancer drugs and others o Immunologic § Sarcoidosis (inflammation, increased collagen & connective tissue) § Collagen vascular disease (example: Lupus) Manifestations: o Increased work of breathing o Exercise intolerance o Small, frequent breaths o Hypoxemia DISORDERS OF PULMONARY CIRCULATION PULMONARY EMBOLISM Occlusion of pulmonary vessel with an embolus Embolism may be a blood clot, air, fat, amniotic fluid, fat from bone marrow Common cause: Deep vein thrombosis** Risk factors: o Virchow’s Triad o Immobility o Post-surgical o Pregnancy o Oral contraceptives/hormone replacement Massive PE: Occlusion of major artery à Infarction of large portion of lung tissue Smaller PE: Embolism lodged in a more distal site à May not cause infarction of lung tissue May result in loss of alveolar surfactant (alveolar collapse) May result in pulmonary hypertension à right-sided heart failure 20 Ventilation-Perfusion mismatching Manifestations: o Chest pain* o Dyspnea* o Tachypnea* o Anxiety o Cough (may be blood tinged) o Hypoxemia o Tachycardia RESPIRATORY FAILURE Result of another problem o Gas exchange failure / Ventilation failure Failure to oxygenate the blood and/or eliminate CO2 Manifestations: o Change in level of consciousness o Cyanosis o Hypoxemia o Hypercapnia o Tachycardia o Tachypnea Acute Lung Injury Acute Respiratory Distress Syndrome 21

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