NR 507 Week 2 FINAL STUDY GUIDE FOR QUIZ., Quizzes of Nursing

Download NR 507 Week 2 FINAL STUDY GUIDE FOR QUIZ. and more Quizzes Nursing in PDF only on Docsity! NR 507 Week 2-Final Study Guide for Quiz Respiratory Disorders and Alterations in Acid/Base Balance, Fluid and Electrolytes Chapter 35: Structure and Function of the Pulmonary System Tara Morgan • The primary function of the pulmonary system is the exchange of gases between the environmental air and the blood. • There are three steps in this process: ○ Ventilation, the movement of air into and out of the lungs ○ Diffusion, the movement of gases between air spaces in the lungs and the bloodstream ○ Perfusion, the movement of blood into and out of the capillary beds of the lungs to body organs and tissues • The first two functions (ventilation and diffusion) are carried out by the pulmonary system and the third (perfusion) by the cardiovascular system. • Normally the pulmonary system functions efficiently under a variety of conditions and with little energy expenditure. Structures of the Pulmonary System • The pulmonary system includes two lungs and the upper and lower airways, and the blood vessels that serve them; the chest wall, or thoracic cage; and the diaphragm. • The lungs are divided into lobes: ○ 3 in the right lung (upper, middle, lower) ○ 2 in the left lung (upper, lower) • Each lobe is further divided into segments and lobules. • The mediastinum is the space between the lungs and contains the heart, great vessels, and esophagus. • A set of conducting airways, or bronchi, delivers air to each section of the lung. • The diaphragm is a dome-shaped muscle that separates the thoracic and abdominal cavities and is involved in ventilation. • • FIGURE 35.1 Structural Plan of the Respiratory System. The inset shows alveolar sacs where the interchange of oxygen and carbon dioxide takes place through the walls of the grapelike alveoli. Capillaries surround the alveoli. • The lungs are protected from a variety of exogenous contaminants by a series of mechanical and cellular defenses. • These defense mechanisms are so effective that in the healthy individual, contamination of the lung tissue itself, particularly by infectious agents, is rare. STRUCT URE OR SUBSTA NCE MECHANISM OF DEFENSE Upper respirator y tract mucosa Maintains constant temperature and humidification of gas entering the lungs; traps and removes foreign particles, some bacteria, and noxious gases from inspired air Nasal hairs and Trap and remove foreign particles, some bacteria, and noxious • Epiglottis • Thyroid • Cricoid ○ And three smaller cartilages-connected by ligaments  Arytenoid  Corniculate  Cuneiform • The supporting cartilages prevent collapse of the larynx during inspiration and swallowing. • The internal laryngeal muscles control vocal cord length and tension, and the external laryngeal muscles move the larynx as a whole. • The internal muscles contract during swallowing to prevent aspiration into the trachea and contribute to voice pitch. • The trachea, which is supported by U-shaped cartilage, connects the larynx to the bronchi, the conducting airways of the lungs. • The trachea divides into the two main airways, or bronchi, at the carina • This area is very sensitive and when stimulated can cause coughing and airway narrowing. • The left mainstem bronchus branches from the trachea at about a 45 -degree angle. The right mainstem bronchus is slightly larger and more vertical than the left (branches at about a 20- to 30- degree angle from the trachea). • Aspirated fluids or foreign particles thus tend to enter the right lung rather than the left. • The right and left main bronchi enter the lungs at the hila, or “roots” of the lungs, along with the pulmonary blood and lymphatic vessels. • From the hila the main bronchi branch into lobar bronchi and then to segmental and subsegmental bronchi, and finally end at the sixteenth division in the smallest of the conducting airways, the terminal bronchioles FIGURE 35.3 Conducting Airways and Respiratory Unit. A, Structures of respiratory airways. B, Changes in bronchial wall with progressive branching. C, Electron micrograph of alveoli: long white arrow identifies type II alveolar cells (pneumocytes - secretes surfactant); short white arrowhead identifies pores of Kohn; red arrow identifies alveolar capillary. D, Plastic cast of pulmonary capillaries at high magnification. • The bronchial walls have 3 layers: • Epithelial lining • Smooth muscle layer • Connective tissue layer • In the large bronchi (up to approximately the tenth division), the connective tissue layer contains cartilage. • The epithelial lining of the bronchi contains single - celled exocrine glands—the mucus- secreting goblet cells—and ciliated cells. • High columnar pseudostratified epithelium lines the larger airways and becomes progressively thinner, changing to columnar cuboidal epithelium in the bronchioles and squamous epithelium in the alveoli • The submucosal glands of the bronchial lining produce a mucous blanket that protects the bronchial epithelium. • The ciliated epithelial cells rhythmically beat this mucous blanket toward the trachea and pharynx, where it can be swallowed or expectorated by coughing. • Toward the terminal bronchioles, ciliated cells and goblet cells become more sparse, and smooth muscle and connective tissue layers thin Gas-Exchange Airways • The conducting airways terminate in the respiratory (terminal) bronchioles, alveolar ducts, and alveoli • These thin-walled structures participate in gas exchange, and the clusters of alveoli are sometimes called the acinus • The bronchioles from the sixteenth through the twenty-third divisions contain increasing numbers of alveoli and are called respiratory bronchioles. • The walls of the respiratory bronchioles are very thin, consisting of an epithelial layer devoid of cilia and goblet cells, very little smooth muscle fiber, and a very thin and elastic connective tissue layer. • These bronchioles end in alveolar ducts, which lead to alveolar sacs made up of numerous alveoli. • The alveoli are the primary gas-exchange units of the lung, where oxygen enters the blood and CO2 is removed • Tiny passages called pores of Kohn permit some air to pass through the septa from alveolus to alveolus, promoting collateral ventilation and even distribution of air among the alveoli. The lungs contain approximately 50 million alveoli at birth and about 480 million by adulthood. FIGURE 35.4 Alveoli. Bronchioles subdivide to form tiny tubes called alveolar ducts that end in clusters of alveoli called alveolar sacs. • Lung epithelial cells provide a protective interface with the environment • Essential for adequate gas exchange • Preventing entry of foreign agents • Regulates ion and water transport • Maintains mechanical stability of the alveoli • The alveolar septa consist of an epithelial layer and a thin, elastic basement membrane but no • The shared alveolar and capillary walls compose the alveolocapillary membrane, a very thin membrane made up of the; • alveolar epithelium • the alveolar basement membrane • an interstitial space • the capillary basement membrane • and the capillary endothelium • Gas exchange occurs across the alveolocapillary membrane. • These extremely thin alveolar walls are easily damaged and can leak plasma and blood into the alveolar space. • With normal perfusion, approximately 100 mL of blood in the pulmonary capillary bed is spread very thinly over about 70 to 100 m2 of alveolar surface area. FIGURE 35.6 Cross Section Through an Alveolus Showing Histology of the Alveolar - Capillary Membrane (Respiratory Membrane). The dense network of capillaries forms an almost continuous sheet of blood in the alveolar walls, providing a very efficient arrangement for gas exchange. • Each pulmonary vein drains several pulmonary capillaries. • Unlike the pulmonary arteries, which follow the branching bronchi, pulmonary veins are dispersed randomly throughout the lungs and then leave the lung at the hila and enter the left atrium. • They are similar to veins in the systemic circulation, but they have no valves. • The bronchial circulation is part of the systemic circulation and receives 1% of the cardiac output. • The bronchial arteries supply blood to the: • trachea • bronchi and its branches • esophagus • visceral pleura • the vasa vasorum of the thoracic aorta • and the pulmonary arteries • and to the nerves • pulmonary veins • and lymph nodes in the thorax. • Not all of the capillaries drain into their own venous system. Some empty into the pulmonary vein and contribute to the normal venous admixture of oxygenated and deoxygenated blood or right-to-left shunt • The bronchial circulation does not participate in gas exchange. • Lung vasculature also includes deep and superficial pulmonary lymphatic capillaries. • The deep lymphatic capillaries begin at the level of the terminal bronchioles. • Fluid and alveolar macrophages migrate from the alveoli to the terminal bronchioles, where they enter the lymphatic system. • The superficial lymphatic capillaries drain the membrane that surrounds the lungs. • Both deep and superficial lymphatic vessels leave the lung at the hilum through a series of mediastinal lymph nodes. • The lymphatic system plays an important role in keeping the lung free of fluid and providing immune defense. Control of the Pulmonary Circulation • The caliber of pulmonary artery lumina decreases as smooth muscle in the arterial walls contracts. • Contraction increases pulmonary artery pressure. • Caliber increases as these muscles relax, decreasing blood pressure. • Contraction (vasoconstriction) and relaxation (vasodilation) primarily occur in response to local humoral conditions, even though the pulmonary circulation is innervated by the autonomic nervous system (ANS), as is the systemic circulation. • The most important cause of pulmonary artery constriction is a low alveolar partial pressure of oxygen (PAO2). • Vasoconstriction caused by alveolar and pulmonary venous hypoxia, often termed hypoxic pulmonary vasoconstriction, results from an increase in intracellular calcium levels in vascular smooth muscle cells in response to low oxygen concentration and the presence of charged oxygen molecules called oxygen free radicals. • If only one segment of the lung is involved, the arterioles to that segment constrict, shunting blood to other, well-ventilated portions of the lung. This reflex improves the lung's efficiency by better matching ventilation and perfusion. • If all segments of the lung are affected, vasoconstriction occurs throughout the pulmonary vasculature, and pulmonary hypertension (elevated pulmonary artery pressure) can result. • Chronic alveolar hypoxia can result in inflammation and structural remodeling in pulmonary arterioles, causing permanent pulmonary artery hypertension that eventually leads to right heart failure. • An elevated PaCO2 value without a drop in pH does not cause pulmonary artery constriction. • Other biochemical factors that affect the caliber of vessels in pulmonary circulation are: • histamine • prostaglandins • endothelin -PaO2 values >60 reflects flatter curve on oxyhemoglobin dissociation curve due to maximum saturation of hemoglobin with oxygen in lungs PAO2- partial pressure of alveolar O2, normal PAO2 = 104mmHg at sea level with relaxed breathing Therefore a pressure gradient of about 60mmHg facilitates diffusion of oxygen from the alveolus into the capillary (Fig 35.15) -Different values for PAO2 can be calculated if there are changes in the inspired oxygen content or the PaCO2, which are common occurrences in clinical settings. Figure 35.9 Neurochemical Control of Ventilation (Fig 35.9)- occurs in neurons located in brainstem: 1. Ventral Respiratory Group (VRG)- inspiratory nerve cells (located in medulla) that transmit impulses out to diaphragm & intercostal muscles 2. Dorsal Respiratory Group (DRG)- receives impulses from various receptors & various stimuli which alter breathing patterns to restore normal blood gases a. Receives impulses from: i. PNS receptors in carotid & aortic bodies ii. Receptors in the lung iii. Various stimuli (mechanical, neural, chemical) _ Chemoreceptors- monitor pH, PaCO2, & PaO2 levels A. Central Chemoreceptors- monitor arterial blood indirectly by sensing pH changes in CSF a. Sensitive to very small changes in pH of CSF = 1-2mmHg PaCO2 b. Central chemoreceptors respond to PaCO2 leads to pH ( H+) by: i. Depth & rate of ventilation which leads to ii. PaCO2 of arterial blood gas < PaCO2 CSF from CO2 diffusing out CSF leads to iii. Return to normal pH level c. Central chemoreceptors often able to maintain a normal PaCO2 level under many conditions including strenuous activity i. Except not under long-term conditions such as COPD as receptors become insensitive to small changes in PaCO2 from hypoventilation 1. Which results in prolonged PaCO2 bicarbonate retention from renal compensation 2. Bicarbonate diffuses in CSF to normalize pH ii. Peripheral Chemoreceptors take over when central chemoreceptors reset by chronic hypoventilation B. Peripheral Chemoreceptors-kick in primarily when central chemoreceptors reset by chronic hypoventilation a. Primarily sensitive to O2 levels in arterial blood (PaO2) i. As PaO2 & pH peripheral chemoreceptors in carotid bodies respond by ventilation ii. Additive effect ventilation if PaCO2 in addition to PaO2 & pH b. Somewhat sensitive to PaCO2 Lung is innervated by ANS and has 3 types of lung sensory receptors: 1. Irritant receptors- cause bronchoconstriction & ventilatory rate a. Cough reflex from noxious aerosols (vapors), gases, and particulate matter (inhaled dust) b. Also stimulated by inflammatory mediators (histamine, serotonin, prostaglandins), by drugs c. Located primarily in epithelium of proximal larger airways (nearly absent in distal airway) 2. Stretch receptors- cause ventilatory rate & volume leads to Hering-Breuer expiratory reflex a. This reflex assists with ventilation and may protect against excess lung inflation b. This reflex active in newborns & only in adults with high tidal volumes (exercise, mechanical ventilation) c. Located in smooth muscles of airways & sensitive to increases in size or volume of the lungs 3. Pulmonary C-fiber receptors- cause rapid, shallow breathing; laryngeal constriction on expiration and mucous secretion; hypotension; and bradycardia; may be associated with dyspnea a. Located near capillaries in the alveolar septa and in other airway locations as nociceptors b. Sensitive to increased pulmonary capillary pressure ANS- control diameter of airway lumen by stimulating bronchial smooth muscle to contract (parasympathetic receptors) and relax (sympathetic receptors). Advanced Patho Page 10 or pleural pressure) ii. compliance indicates lungs or chest wall is abnormally easy to inflate and has lost some elastic recoil 1. Occurs with normal aging and disorders such as emphysema iii. compliance indicates lungs or chest wall is abnormally stiff or difficult to inflate 1. Occurs with ARDS, pneumonia, pulmonary edema, & fibrosis 2. Work of breathing may be increased considerably when lung (pulmonary edema) & chest wall compliance (spinal deformity or obesity) leading to increased O2 consumption & inability to maintain adequate ventilation 9. Resistance to airflow through the conducting airways a. Airway resistance- determined by length, radius, diameter, & cross - sectional area of the airways i. Normally very low airway resistance (especially in conducting airways of lungs due to large cross-sectional area) ii. 1/2 to 2/3 resistance occurring primarily in the nose, followed by oropharynx & larynx b. Bronchodilation- airway resistance c. Bronchoconstriction- airway resistance from irritants, inflammatory mediators d. Other means of airway resistance i. Edema of the bronchial mucosa ii. Airway obstructions such as mucus plugging (asthma or bronchitis), tumors, or foreign bodies Gas transport involves delivery of O2 to the cells of the body (#1) and removal of CO2 (#2) (gas exchange is compromised if respiratory or cardiovascular disorder impairs any step in this Advanced Patho Page 11 process) 10. Ventilation of the lungs, diffusion of oxygen from alveoli into capillary blood, perfusion of systemic capillaries with oxygenated blood, & diffusion of oxygen from systematic capillaries into cells 11. Diffusion of CO2 from the cells into the systematic capillaries, perfusion of the pulmonary capillary bed by venous blood, diffusion of CO2 into alveoli, removal of CO2 from the lung by ventilation Blood remains in pulmonary capillary bed for about 3/4 second, but only 1/4 second required for oxygen concentration to equalize across the alveolocapillary membrane. This allows for ample time for oxygen to diffuse into the blood even during increased cardiac output, which speeds blood flow. Barometric pressure (PB) (atmospheric pressure)- pressure exerted by gas molecules in air at specific altitudes A. Sea level (barometric pressure is 760mm Hg) B. Partial pressure-portion of total pressure exerted by any individual gas a. Calculated by % gas x barometric pressure b. Measurement of gas pressure i. Greater in smaller area due to more collisions of gas molecules ii. with heat as heat speed of gas molecules which collisions c. Partial pressure of water vapor exerts pressure 47mm Hg at 98.6F regardless of barometric pressure. However, before determining partial pressures of other gases in the mixture, water vapor must be subtracted from barometric pressure [ie. (760-47) x % gas]. That is why pulmonary function laboratories specify temp & humidity of a gas at time of all pressure & volume measurements. a. Partial pressure of oxygen molecules (PO2) is much greater in alveolar gas than in capillary blood which promotes rapid diffusion from alveolus into the capillary i. Amount of oxygen in alveoli (PAO2) estimated by using alveolar gas Advanced Patho Page 12 equation: ii. PAO2 = PiO2 (inspired partial pressure of O2) - PaCO2/0.8 (the respiratory quotient) iii. PiO2 = Barometric pressure (760) - vapor pressure (47mmHg) x FiO2 [fraction (%) of inspired air (0.21)] b. Figure 35.15 shows partial pressure of respiratory gases in normal respiration Figure 35.15 Figure 35.13 Figure 35.14 -Ventilation & perfusion are greatest in the lower lobes as most tidal volume occurs in alveoli lung bases and because greater pressure causes greater perfusion. Ventilation-Perfusion Ratio or V/Q: ratio of ventilation to perfusion A. Ventilation exceeds perfusion in apexes B. Perfusion exceeds ventilation in bases Advanced Patho Page 15 *Bohr effect-The shift in oxyhemoglobin dissociation curve caused by changes in CO2 & H+ concentration in the blood Carbon Dioxide Transport: -CO2 is 20x more soluble than O2 and diffuses quickly from tissue cells into blood & enhanced when O2 diffuses out of blood and into cells -Approximately 200mL of CO2 is produced by the tissues per minute at rest as byproduct of cellular metabolism transported in blood by: 1. Dissolved in plasma as CO2 diffuses out of cells into the blood (5% arterial, 10% venous) 2. Transported as bicarbonate (HCO3-) out of RBC into the plasma (60% arterial, 90% venous) -CO2 combines with H20 with the help of the enzyme carbonic anhydrase, which forms carbonic acid that quickly dissociates into H+ and bicarbonate (HCO3-) 3. Combined with blood proteins (hemoglobin in particular) to form carbamino compounds (Fig 3.13) -Drop in SaO2 at tissue level increases ability of Hb to carry CO2 back to lung by attaching to reduced hemoglobin (desaturated hemoglobin) Haldane effect (effect of O2 on CO2 transport)- In tissue capillaries, O2 dissociation from hemoglobin facilitates the pickup of CO2 & binding of O2 to hemoglobin in the lungs facilitates the release of CO2 from the blood. -Diffusion of CO2 in the lung is so efficient that diffusion defects that cause hypoxemia (low O2 content in blood) do not cause hypercapnia (excessive CO2 in blood). Chapter 36 -Clinical manifestations of pulmonary alterations-Carlo Enrico Yap Advanced Patho Page 16 I. Signs and Symptoms of Pulmonary Disease A. Dyspnea - Subjective breathing discomfort - Most common symptom of cardiac and respiratory dse - Evolves across 3 constructs: sensory (intensity), affective (distress), and impact on daily activities - Severity of the experiences DOES NOT DIRECTLY correlate severity of disease - Mechanism: stimulation of mechanoreceptors and chemoreceptors that interact with the respiratory centers and motor cortex - Signs: flaring of nostrils, use of accessory muscles, retractions (common in children OR adults who are thin) - Dyspnea on exertion: dyspnea that presents during exercise - Paroxysmal Nocturnal Dyspnea (PND): pulmonary or cardiac dse = waking at night gasping for air and must sit up or stand to relieve the dyspnea B. Cough - A protective reflex to clear airway with explosive expiration, occurs when irritants stimulate the receptors in the airway → vagus nerve stimulation - Fewer irritant receptors in the distal bronchi = secretions can accumulate w/o stimulating cough reflex - Opiates and serotonergic agents can modulate cough reflex - Acute cough: resolves in 2-3 weeks OR resolves w/ treatment of underlying dse o Ex: Upper resp tract infections, acute bronchitis, PNA, CHF, PE, or aspiration - Chronic cough: >3 weeks, up to 7-8 weeks, seen in some cases of viral infection o Non-smokers chronic cough = post nasal drainage, nonasthmatic eosinophilic bronchitis, asthma, GERD, heightened cough reflex sensitivity o Smokers chronic cough = chronic bronchitis o A inhibitors → chronic cou resolved when d C. Abnormal Sputum - Provides info about disease progression and effectiveness of therapy - Hemoptysis: bloody sputum → bright red, alkaline pH, + frothy sputum o Not to be confused with hemoptysis: vomiting blood → dark, acidic pH + food o Indicates: damage to bronchi d/t infection/inflammation, cancer, pulmonary Infarction D. Abnormal Breathing Patterns - Eupnea = normal breathing, 8-15/min; tidal volume = 400 to 800 mL - Pathophysiologic changes →change in rate, depth, regularity, and effort of breathing - Kussmaul breathing (hyperpnea) = slight increase in rate, very large tidal volume, and no expiratory pause o Caused by metabolic acidosis i.e. strenuous exercise - Labored breathing: increased work of breathing ←obstruction of airway o Obstruction of LARGE airways→ slowed rate but increased effort, long inspiration and expiration, stridor (high-pitched during inspiration), and wheezing (whistling sounds on expiration). o Obstruction of SMALL airways→ rapid ventilation, small tidal volume, increased Advanced Patho Page 17 effort, prolonged expiration - Restricted breathing: stiffened lungs or chest wall, decreased compliance i.e. Pulmonary fibrosis→ small tidal volume, rapid rate - Gasping: irregular and quick inspiration with expiratory pause o i.e. shock and severe cerebral hypoxia - Cheyne-Stokes respirations: alternating periods of deep and shallow. o Apnea Æ high-volume ventilations Æ Apnea o Results from conditions that lead to slow blood flow to the brain stem Æ slowed impulses that send info to brain stem E. Hypo/Hyperventilation - Hypoventilation: inadequate alveolar ventilation →increased PaCO2 (hypercapnia) →increased pH in the blood→ respiratory acidosis o Can cause somnolence or disorientation; secondary hypoxemia (high CO2 displaces O2 in the alveolus). - Hyperventilation: lungs expel CO2 at a higher rate → decreased PaCO2 (hypocapnia)→respiratory alkalosis o Common is severe anxiety and acute head injury F. Cyanosis: bluish discoloration of the skin and mucus membranes - Increased desaturated Hgb (appears bluish in the blood). - Peripheral cyanosis = poor circulation → peripheral vasoconstriction e.g. Raynaud's dse, cold environments, severe stress - Central cyanosis = decreased oxygen in arteries (low PaO2, seen in oral mucus membranes and lips o Caused by pulmonary dses and cardiac right-to-left shunts - NO CYANOSIS DOES NOT MEAN NORMAL OXYGENATION e.g. severe anemia and carbon monoxide poisoning G. Clubbing: bulbous enlargement of the end of a digit - Painless - Develops gradually - Seen in dses that cause chronic hypoxemia e.g. bronchiectasis, cystic fibrosis, lung abcess,CHF H. Pain: usually originates in the pleurae, airways, or chest wall. - Pleural pain is most common: sharp or stabbing during inspiration d/t infection/inflammation of parietal pleura i.e. pleuritis, pleurisy, PE Advanced Patho Page 20 Pleural Abnormalities  Pneumothorax: the presence of air or gas in the pleural space cause by a rupture in the visceral pleura (which surround the lungs) or the parietal pleura and chest wall. Clinical manifestations: sudden pleural pain, tachypnea, and dyspnea. Absent or decreased breath sounds. Tension pneumo: hypoxemia, tracheal deviation away from affected lung, and hypotension. Diagnosis: Chest XR, ultrasound, CT scan Treatment: Aspiration, usually with insertion of chest tube that is attached to a water seal drainage system with suction 4. Primary (spontaneous) pneumothorax: Advanced Patho Page 21 -Spontaneous rupture of blebs (blister-like formations) on the visceral pleura. Ruptured blebs damage visceral pleura creating a conduit for air to travel from the lower airways into the pleural space (bronchopleural fistulae) -Risk factors: smoking, family history of folliculin gene, Birt-Hogg-Dube syndrome 5. Secondary (Traumatic) pneumothorax: -Caused by chest trauma such as rib fractures, stab or bullet wounds, surgical procedure that tears pleura Primary and secondary can present as either open or tension:  Open pneumothorax: air pressure in the pleural space equals barometric pressure because Advanced Patho Page 22 air that is drawn into the pleural space during inspiration is forced back out during expiration.  Tension pneumothorax: the site of pleural rupture act as a one-way valve, permitting air to enter on inspiration but preventing its escape by closing on expiration. As more air enters the pleural space, air pressure begins to exceed barometric pressure pushing against the recoiled lung causing compression atelectasis, displacing the heart, great vessels, and trachea.  Tension Pneumothorax. Air in the pleural space causes the lung to collapse around the hilum and may shift the trachea and mediastinal contents (heart and great vessels) toward the other lung.  Pleural Effusion: The presence of fluid in the pleural space. TYP E OF EFFU SION SOURCE OF ACCUMALATIO N PRIMARY OR ASSOCIATED DISORDER Trans udate (Hydr othor ax) Watery fluid that diffuses out of capillaries beneath the pleurae (i.e., capillaries in lung or chest wall) Cardiovascular disease-causing hypertension: liver or kidney disease that disrupts plasma protein production, causing hypoproteinemia (decreased oncotic pressure in the blood vessels) Exuda te Fluid rich proteins (leukocytes, plasma proteins of all kinds) that migrate out of capillaries Infection, inflammation, or malignancy of the pleurae that stimulates mast cells to release biochemical mediators that increase capillary permeability Empy ema Detritus of infection (microorganisms, Pulmonary infections, such as pneumonia; Advanced Patho Page 25 Environmental lung disorders: Exposure to toxic gases- Common toxic gases are ammonia, hydrogen chloride, sulfur dioxide, chlorine, phosgene, and nitrogen dioxide. Inhaled particles can cause damage to airway epithelium, cilia, and alveoli. Oxygen toxicity occurs with high concentrations of supplemental oxygen. Pneumoconiosis- inhalation of inorganic dust particles. The dust of silica, asbestos and coal are most common cause. Hypersensitivity pneumonitis- inhalation of organic particles or fumes. Is an allergic inflammatory disease. Systemic disorders Granulomatosis disorders: Sarcoidosis, Wegener granulomatosis, lymphomatoid granulomatosis, eosinophilic granuloma. Connective tissue diseases: RA, lupus, scleroderma, polymyositis, Sjogren syndrome, cystic fibrosis, Goodpasture syndrome. Pulmonary edema- excess water in the lung. Most common cause left-sided heart disease. Pulmonary edema begins to develop at the pulmonary capillary wedge pressure or left atrial pressure of 20mmHg. Factors for pulmonary edema left-sided heart disease, causing increased pulmonary venous pressure; injury to pulmonary capillary endothelium (ARDS) and inhalation of toxic gases; lymphatic obstruction. Postobstructive pulmonary edema is a rare life- threatening complication that can occur after relief of upper airway obstruction. High-altitude pulmonary edema occur at altitudes usually more than 8000-10000 feet. Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS)- acute lung inflammation and diffuse alveolocapillary injury. ARDS most severe. Acute onset of bilateral infiltrates on xray not explained by cardiac failure. A low ratio of partial pressure of arterial oxygen to the fraction of inhaled oxygen. Most common factors genetic, sepsis, trauma. ARDS 3 phases: Exudative (inflammatory)- 72 hours release of inflammatory cytokines. Lungs become less compliant and work of breathing increases, Advanced Patho Page 26 ventilation of alveoli decreases, and hypercapnia develops. Proliferative- within 1-3 weeks after injury resolution of pulmonary edema and proliferation of fibroblasts, myofibroblasts and type II pneumocytes with surfactant recover. Fibrotic- 2-3 weeks after injury remodeling and fibrosis occur. Clinical manifestation of ARDS: Evaluation and treatment: History of lung injury, examination (Fine inspiratory crackles), ABG’s and chest x -ray. Treatment include early detection, supportive care, prevention of complications. Obstructive Pulmonary Disease- airway obstruction that is worse with expiration. Infiltration of the lung by inflammatory cells with the release of large number of cytokines that cause airway damage and mucus production. Most common are asthma and COPD. Asthma- chronic inflammation of the bronchial mucosa that cause bronchial hyperresponsiveness, constriction of the airway, and variable airflow obstruction that is reversible. Can develop at any age. Asthma phenotypes are observable characteristics that include eosinophilic asthma (allergic) vs. neutrophilic asthma, exercise-induced asthma, aspirin-sensitive asthma, age-at-onset asthma, or steroid nonresponsive asthma. Endotypes are subgroups that describe the underlying pathophysiology to the phenotypes. Early asthmatic response- acute bronchoconstriction that reaches a maximum in the first 30 minutes and resolves within 1-3 hours. Antigen exposure to the bronchial mucosa activates dendritic cells to present the antigen to T helper cells, which differentiate into Th2 cells releasing cytokines. These activate inflammatory cells and cytokines causing vasoconstriction, increased capillary permeability, mucosal edema, bronchial smooth muscle constriction and increased mucus secretion. Late asthmatic response- 4-8 hours after early response. Bronchospasm, edema and mucus secretion with obstruction to airflow. Impaired expiration causes Advanced Patho Page 27 air trapping, hyperinflation distal to obstructions and increased work breathing. With progressive obstruction of expiratory airflow, air trapping is severe and lungs and thorax become hyperexpanded, respiratory muscles are mechanically disadvantaged leading to decrease in tidal volume with increasing CO2 retention and respiratory acidosis, Advanced Patho Page 30 Pulmonary artery hypertension- caused by elevated left ventricular pressure, increased blood flow through the pulmonary system, obstruction of vascular bed, active constriction caused by hypoxemia or acidosis. Mean pulmonary pressure greater than 25mmHg at rest. Cor Pulmonale- caused by pulmonary hypertension which causes right ventricular enlargement. If pulmonary hypertension is not treated will cause right ventricular failure. Malignancies of the respiratory tract Laryngeal cancer- Squamous cell carcinoma of the vocal cords. Occurs most often in men. Causes hoarseness. Lung cancer- Most frequent cancer deaths in the US. Most common cause from smoking. Cancer cell types include non–small cell lung cancer (squamous cell carcinoma, adenocarcinoma, large cell undifferentiated carcinoma) and neuroendocrine tumors (small cell carcinoma and bronchial carcinoid tumors). Other tumors include small cell (oat cell) carcinoma, bronchial adenoma, adenocystic tumors (cylindromas), mucoepidermoid carcinomas (bronchial tumors), and mesothelioma. Each type arises in a characteristic site or type of tissue, causes distinctive clinical manifestations, and differs in likelihood of metastasis and prognosis. Advanced Patho Page 20 Chapter 37 -Structure and function-Mittal Patel Advanced Patho Page 21 en are influenced by: age. developnient, gender. race. sens. sad ers ronmental conditions, Causes: Alterations of res immaturity of the sieays Cireokaien wshest wall and the immune systean Structure and Function: tructural characteristic siructural characteristies ef the upper and lower resparatery 114 chest wall and Hung elynamies, nctabolie requirements, inimunplogig imwiaturity and physiologic contra of respiration, Upper Airway: conducting aineaes present and change en size, Braoiching of the bronehial tree: complete by fen 16th w Children ratorally hax e smaaller-diameter airsayss tha adults so they suffer more ebstraction PEEVE EGY ee bereue lancs up t9 2 69 3 months of age are Yobligatory nose breathers” so nasal congestion is a serious threat wer Airways ural Lung Parenchyneu: “During: Fetal des eloynnent: Long transforms frotn a dense organ to rnore delicately structured “Stunting of second trimester oF pregnancy. loss of nnerstitial Onesenchynal} tissue with soncomitamt expansion “inten scala ftin matuing ie spevtalzed sel tps, sasha pe ell Suristontaipiproten str tht produc op asl cells and Inport or mainsng Prince 90924 eek Sere othe el gays hy 0 ek Ds Respvtory Diss: Syndr ase cil bone nls mannan acne eae by Surat Define seen n Premmtre infants ncrased RDS sth nteased prema Fig 4 & R, Prenatal Development of the Alveolar Unit and Stages of Lung Development, 4. Epithelial cells differentiate into type Hand type I vells, Mature ¢ pe II cells are cuboidal. have apical microvilli. and contain lamellar bodies for surfactant storage and secretion. Type [ cells are derived from type Hells and consist of Mattened epithelium overlying capillaries. thus forming part of the desived (hia air-blood barrier, During fetal development the pulmonary capillaries initially are randomly distributed in mesenchyme. They progressively arrange around the epithelial tubes and establish close contacts to the lining epithelium, Overall the volume of mesenchyme decreases potential air space increases. B. Stages of fetal lung development. nabes way areing cairn st compty smo Advanced Patho Page 24 intrathoracic pressure which can cause collapse of the upper airway.  Clinical Manifestations:  Rhinorrhea (runny nose)  Sore throat  Low grade fever  Harsh (seal-like) cough  Hoarse voice  Inspiratory stridor • Most cases are mild and will resolves in several days • Severe cases require urgent treatment  Evaluation & Treatment:  A barking cough and viral symptoms require no treatment  Having stridor, retractions, or agitation is a sign it’s a sicker child.  The Westley Croup Score is a tool that scores: • Stridor • Retractions • Air entry Advanced Patho Page 25 • Cyanosis • Dyspnea • LOC  Croup is mild, moderate, or severe  Glucocorticoids are oral or injected which improves symptoms in 6 hours • Dexamethasone oral • Budesonide nebulized o Nebulized epinephrine stimulates a- and b- adrenergic receptors which decrease airway secretions and mucosal edema • Oxygen • In rare cases intubation is required  Acute Epiglottis:  Caused by Haemophilus influenzas type B (Hib)  There is an immunization for Hib, so cases are rare but 25% of epiglottis is still caused by Hib. Due to no immunizations.  Infants less than 1 year old are at greater risk.  Non infectious causes include trauma from foreign body inhalation and chemical burns.  Pathophysiology: o Epiglottis is from the posterior tongue base and covers the laryngeal inlet during swallowing. It has a rich blood and lymphatic circulation. o Bacteria of the mucous and inflammation can cause edema, obstructing the upper airway  Clinical Manifestations  Usually occurs in children 2-6 years old  High Fever  Irritability  Sore throat  Hot potato voice  Inspiratory stridor  Respiratory distress  Children will usually be leaning toward (tripod position), drooling and difficult swallowing  Examination of the throat can cause laryngospasm and cause respiratory collapse. Death can occur shortly after.  PNA, cervical lymph nodes inflammation, otitis, and rarely meningitis or septic arthritis may occur.  Evaluation & Treatment:  Don’t exam the throat  Intubation sometimes  Culture of the throat, antibiotics  Corticosteroids  If caused by Hib, rifampin should be administered to the household once daily for 4 days.  Tonsillar Infections (tonsillitis)  Occurs sometimes due to group A beta - hemolytic Streptococci (GABHS) and methicillin-resistant Staphylococcus aureus (MRSA)  It’s swelling of the tonsils and pharynx and may cover the mucosa.  Can also occur from infectious mononucleosis (mono)  Treatment includes antibiotics and corticosteroids  Recurrent tonsillitis may require adenotonsillectomy.  Peritonsillar abscess • Is usually unilateral and most often complication of acute tonsillitis. • Causative agent is GABHS • Symptoms are: o Fever o Sore throat o Difficulty swallowing o Trismus o Pooling of saliva o Muffled voice • Peritonsillar bulging and cervical adenopathy are visible. • The abscess must be drained and antibiotics are given • If the abscess ruptures death can occur  Bacterial Tracheitis (pseudomembranous croup)  Most common, life threatening upper airway infection for children Advanced Patho Page 26  Caused by  MRSA, Hib, GABHS, or Moraxella catarrhalis  Fungus can be the cause in immunocompromised children  Recurring infection • Sinusitis, otitis, PNA, or pharyngitis  Airway edema and copious purulent secretions lead to airway obstruction  Obstruction can be worse due to mucosal sloughing and tracheal pseudomembrane.  Death can occur due to:  PNA, cardiac arrest, acute respiratory distress syndrome (ARDS), multiple organ dysfunction.  Clinical presentation  Tachypnea  Fever  Stridor  Hoarse voice  Cough  Increased secretions from mouth and nose  Treatment  Antibiotics  Inbutation  Retropharyngeal Abscesses: o Caused by  Aerobic, anaerobic, or polymicrobial infection  GABHS, MRSA o Occurs around 4 years old from other nasopharyngeal infection or penetrating Advanced Patho Page 29 o Inflammation from asthma, allergies, or respiratory syncytial virus (RSV) can cause OSAS o In obese children inflammation and elevated C- reactive proteins are linked to OSAS which causes increased risk for cardiovascular and metabolic diseases  Clinical Manifestations:  Snoring  Gasping for air  Labored breathing  Failure to thrive  Sweating in sleep  Restlessness  Children with OSAS usually are mouth breathers and have large tonsils and adenoids  Untreated OSAS can lead to left ventricular hypertrophy, pulmonary HTN, upper and lower RTI and insulin resistance.  Children may have trouble focusing, hyperactive, and poor school performance.  Evaluation & Treatment:  Ask parents about labored breathing, sweating, snoring and restlessness during sleep  Screening tools about sleep patterns are helpful.  A polysomnographic sleep study  Imaging of the upper airway to look for adenoidal hypertrophy or airway narrowing.  Tonsillectomy and adenoidectomy (T&A) may needed for enlarged tonsils.  For severe cases:  CPAP  High flow oxygen  Weight loss  Anti inflammatory meds  Dental treatments Chapter 37 -Sudden infant death syndrome- Amanda Deering Sudden Infant Death Syndrome (SIDS) • Etiology: unknown cause, most common cause of infant death in Western countries • death of infants under 1 year of age when there is no other explanation of death • death rates peak between 2-4 months, uncommon in first month, uncommon after 6 months • more common amongst non-Hispanic black, American Indian and Alaskan Natives • higher frequency in winter months r/t higher incidence of upper respiratory illness • almost always occurs at night • back is best of “back to sleep” campaigns attributed to decreased incidence • hypothesis of cause includes: o predisposing factors; altered/immature cardiorespiratory, circulatory and arousal characteristics, impaired autonomic regulation o environmental factors: soft bed, room to warm, dressed to warm, prone or side sleeping positions, tobacco exposure • growing evidence that there may be a genetic component (those genes associated with immune system regulation, inflammation, cardiac and brainstem function) Fluid Balance From Lesson-Lauren Andrews Fluid Balance:  All living organisms are composed of Water and the solutes Advanced Patho Page 30 dissolved in it o Solutes:  Sodium  Chloride  Potassium  Calcium  Protein  Glucose Why are we water based? o Temperature regulation o Lubrication  Synovium  Pleura  Pericardium o Transportation of nutrients o Waste in and out of cell o Medium for cellular metabolism to occur  TBW = Total body water: the sum of water in all compartments o Equal to approx. 60% of body weight in adults  Compartments: o Intracellular: ICF = fluid within every one of our cells  = to approx. 40% of TBW o Extracellular: ECF = the fluid outside of our cells  = to approx. 20% of TBW ECF LOCATIONS:  Intravascular (IV) = blood plasma approx. 5%  Interstitial (IF) = the fluid between cells but outside of blood vessels approx. 15%  3rd Space locations = other misc. fluids o Lymph vessels o Synovium o Cerebral spinal fluid within ventricles of the brain and around the spinal cord Advanced Patho Page 31 o Intestinal fluid, sweat, urine, intraocular fluid = a few percent of ECF  Electroneutrality o Each compartment has the same amount of positive versus negative charges  The solute levels differ  ICF: o Primary Potassium and Phosphate o Slightly more magnesium  ECF: o Primary Cation Sodium, Chloride o Slightly less magnesium that ICF  There are two Distinct fluid movements: o Between the ICF and ECF  Fluid moves from LOWER concentration to HIGHER concentration.  Driven by osmosis(electrolytes moving across membrane as determined by solute concentration.  CONCENTRATIONAKA Osmolarity or Osmotic Pressure  Normal fluid movements favor isotonic conditions that is ICF and ECF are EQUAL o Between Plasma and Interstitial area  Fluid movement across capillary walls, Occur at the atrial ends of capillaries • Hydrostatic pressure (driven by the heart) mechanical force of water o Blood pressure; pushing against capillary membrane to move fluid out AKA filtration/perfusion creates movement of fluid from vascular space to interstitium  Onotic or colloid pressure (Chemical force excreted by large molecules • Interstitium to blood vessel, occurs at venous end of capillaries to blood stream o Unequal pressures/ shifts can cause flooding (edema) o Fluid shifts  Hypotonic = Low electrolyte or higher than normal water levels = • ECF has lower osmolality than ICF • Draws water into the cell o Water is going to move into an area that in more concentrated with solute • Result: o Cellular swelling o Pulling fluid from the plasma into the cell  Plasma volume will decrease, and hypovolemia occurs  Hypertonic=increased electrolyte level or abnormally low water levels in plasma (Dehydration) • ECF has higher osmolality than ICF • High concentration of solute outside of the cell will draw water out of the cell o Results:  Cellular shrinkage  Hypervolemia  Changes is Osmolality can result in electrolyte concentration and electrical activity of excitable cells o Nerves and muscles  Changes can be characterized by Changes in muscle tone, Cardiac function, Level of consciousness, Edema (unequal fluid shifts) o Causes of Edema o Most common cause is increased sodium level in our body  Decreased kidney function o Blood vessel obstruction  Clot or build up of plaque in vessel calls o Lymph vessel obstruction  Infection o Changes in capillary permeability Advanced Patho Page 34 ic Alkalosi s o pH = alkalosis o PaCO2 = high or normal o HCO3 = retaining too much bicarb  Renal type problem  Metabol ic Acidosis o pH = acidosis o PaCO2 = low o HCO3 = can’t make bicarb  Renal Failure  Lactic Acidosis https://www.youtube.com/watch?v=al9oOyCbCYI&t=292s Pathophysiology of Pulmonary Functions in Adults Tara Morgan  In a normal functioning lung unit we find a match between the ventilation (air that flows into and out of the alveoli) and perfusion (blood circulating past the alveoli).  This ventilation-perfusion (V/Q) matching creates an efficient lung unit that allows desaturated blood from the pulmonary artery to release carbon dioxide in exchange for oxygen.  This exchange occurs through the alveolocapillary membrane and blood then returns to the central circulation through the pulmonary vein.  The alveolar unit will eliminate the carbon dioxide from the body through exhalation and obtain more oxygen through inhalation.  Problems occur when a mismatch between ventilation and perfusion occur, as illustrated in the graphic below. From pulmonary ‘artery Ai way Impaired J ventilation ‘Alveolocapillary* senna To .. Hypoxemia [Normal V/Q pulmonary vein|Low V/@ Blocked | Impaired ventilation | perfusion eo Alveolar Collapsed alveolus dead space > |. Hypoxemia | Fypoenia Shunt (very low) V/Q High V/ Te view the entire animation, click the play button. If you wish to access a segment of the animation ver the progr: each segment and click to access one directly. At the lend of the animation, there is an interactive mode for use in studying the algorithm. You will be able to roll over each box to view its contents. If you wish to access this directly, click on the last segment in the progress bar. To view the entire animation, click the play button. If you wish to access a segment of the animation directly, roll over the progress bar to see each segment and click to access one directly. At the end of the animation, there is an interactive mode for use in studying the algorithm. You will be able to roll over each box to view its contents. If you wish to access this directly, click on the last segment in the progress bar. Hypoxei i Advanced Patho Page 35 Advanced Patho Page 30 *Tends to occur after surgery with general anesthesia *SX’s dyspnea, cough, fever, leukocytosis *TX Deep breathing, incentive spirometer, position changes, ambulation, pain management Bronchiectasis *Persistent abnormal dilation of bronchi *Usually occurs with other respiratory conditions *Associated with systemic disorders such as rheumatologic disease, inflammatory bowel disease, immunodeficiency disorders *Dilation will be cylindrical or saccular *SX’s chronic productive cough – months or years, large amounts of foul smelling purulent sputum, clubbing fingers, hemoptysis, dyspnea, pleuritic chest pain, fatigue *Tx Antibiotics, bronchodilators, anti- inflammatory drugs, chest physiotherapy, supplemental oxygen, surgery to remove portions of lung, lung transplant Bronchiolitis *Diffuse inflammation of bronchioles *Most Common in Children *Sx’s rapid respirations, increased accessory muscles used, low -grade fever, dry nonproductive cough, hyperinflated chest *Tx antibiotics, corticosteroids, immunosuppressive agents, chest physical Obstructive Versus Restrictive- Sheila Tate From Lesson PULMONARY DISORDERS RESTRICTIVE VS OBSTRUCTIVE RESTRICTIVE 1. Decreased compliance of lung tissue 2. Increased effort to inhale 3. Reduces the diffusion of Oxygen from alveoli to the blood = hypoxemia Restrictive Pulmonary Disorders Aspiration * Solids or fluids in the lung * SX’S hoking, intractable cough, fever, dyspnea. Wheezing *TX Supplemental Oxygen, mechanical ventilation, fluid restriction, Corticosteroids, Antibiotics Atelectasis *Collapse of lung tissue *3 Types- Compression, Absorption, Surfactant Advanced Patho Page 33 cardiopulmonary bypass surgery, pancreatitis, drug overdose, smoke or noxious gas inhalation, oxygen toxicity, radiation therapy, DIC *3 Phases *Exudative (Inflammatory) Phase Within 72 hours of lung injury lungs become less compliant, increased work of breathing, ventilation of alveoli decreases, hypercapnia develops *Proliferative Phase is 1-3 weeks from lung injury resolution of pulmonary edema and surfactant recovery overlaps with fibrotic phase *Fibrotic phase 2-3 weeks after lung injury There is abnormal repair and fibrosis leading to respiratory failure and pulmonary hypertension *Leads to a systemic inflammatory response SIRS *SIRS leads to multiple organ dysfunction syndrome MODS *Death is usually from MODS associated with ARDS *Clinical Manifestations Advanced Patho Page 34 *TX is early detection, managing contributing etiologies, supportive therapy to prevent progression of lung injury, prevent complications like pneumonia and stress ulcer *No FDA approved treatments *Use protective ventilation to reduce lung injury, prone position, neuromuscular paralytics, extracorporeal lung assistance OBSTRUCTIVE *More force or time is needed to expire air and empty lungs *Common Disorders Asthma and Chronic Obstructive Pulmonary Disease COPD *COPD is the combination of chronic bronchitis and emphysema ASTHMA *chronic inflammatory of the bronchial mucosa *Develops at any age *6.3 million cases are children *1.7 million cases are adults *death rate highest for female adults, black adults, and those over the age of 65 *familial disorder *asymptomatic and normal pulmonary function tests between attacks *SX’s chest constriction, expiratory wheezing, tachycardia, dyspnea, nonproductive cough, prolonged expiration, tachycardia, tachypnea *severe attacks also have accessory muscle use and wheezing with inspiration and expiration *life threatening if not reversed by treatment *TX inhaled corticosteroids CHRONIC OBSTRUCTIVE PULMONARY DISEASE *preventable disease *progressive disease Advanced Patho Page 35 *Combination of chronic bronchitis and emphysema *3rd leading cause of death in US *Risk factors are tobacco smoke, occupational dusts & chemicals, indoor & outdoor air pollution *SX dyspnea with exertion that progresses to dyspnea at rest *Prevention best treatment, not reversable Lung Cancer From Lesson Lori Eyre  Typically arises from the epithelium of the respiratory tract  Most common cause is smoking  10-15% of active smokers will develop cancer  10-25% of lung cancers occur in non-smokers  25% of non-smoker lung cancers are d/t passive tobacco smoke  Tobacco smoke is also related to cancer in several sites: larynx, oral cavity, esophagus, and urinary bladder  There is not a tool for predicting risk or rate of progression of lung cancer