NU 545 Unit 5 Study Guide FINAL ASSURED SUCCESS, Exams of Nursing

Download NU 545 Unit 5 Study Guide FINAL ASSURED SUCCESS and more Exams Nursing in PDF only on Docsity!

Unit 5 Study Guide NU 545 FINAL

Unit 5 Study Guide NU 545 FINAL

UNIT 5: RESPIRATORY AND RENAL SYSTEMS

Physio-Pathological Basis of Advanced Nursing (NU 545)

Study Guide and Resources: Chapters 34 – 39

SECTION 1: STUDY GUIDE

1. KNOW TYPE I AND TYPE II ALVEOLAR CELLS. (p. 1229; key search term: “lipoprotein that coats”) - Bronchioles subdivide to form tiny tubes called alveolar ducts that end in clusters of alveoli called alveolar sacs. - Alveoli are the primary gas-exchange units of the lung, where O 2 enters the blood and CO 2 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. - At birth, there are 50 million alveoli, by adulthood you have 480 million. - The alveolar septa (what separates each alveoli sac) has 2 layers (there is NO muscle layer ) — Epithelial layer — Thin elastic basement membrane - Two major types of epithelial cells appear in the alveolus: — Type I alveolar cells: provide structure — Type II alveolar cells: (or “pneumonocytes”) secrete surfactant (lipid protein that coats the inner surface of the alveolus and facilitates its expansion during inspiration, lowers alveolar surface tension at end expiration, thus preventing lung collapse) - Alveoli contain cellular components of inflammation and immunity, particularly the mononuclear phagocytes. — Called alveolar macrophages — Ingest foreign material that reaches the alveolus and prepares it for removal through lymphatics.

during expiration. Surfactant impairment can occur because of premature birth, acute respiratory distress syndrome, anesthesia, or mechanical ventilation. Surfactant and Infants (p. 1292)

• Without surfactant, the alveoli tend to stay closed, demanding greater inspiratory force and work of breathing to re-expand on the next breath.
• Deficiency of surfactant is often seen in premature infants and causes respiratory distress syndrome (RDS), also known as hyaline membrane disease.
• Surfactant is produced by 20 to 24 weeks of gestation and is secreted into the fetal airways by 30 weeks.
• The more premature the infant, the higher the risk of RDS.

Which statement indicates the nurse has a correct understanding of surfactant? Surfactant: Reduces surface tension. Type I alveolar cells provide structure, and type II alveolar cells secrete surfactant, a lipoprotein that coats the inner surface of the alveolus and facilitates its expansion during inspiration, lowers alveolar surface tension at end- expiration, and, thereby, prevents lung collapse.

is a lipid-protein mix produced by type II alveolar cells, which reduces surface tension and prevents alveolar collapse. Surfactant is a lipid-protein mix produced by type II cells. Surfactant is critical for maintaining alveolar expansion and allows for normal gas exchange, as well as lines the alveoli and reduces surface tension, preventing alveolar collapse at the end of each exhalation.

3. KNOW CHRONIC BRONCHITIS. (see figure 35 - 14 on p. 1268; pp. 1267 - 1268; key search term: “usually the winter”) Chronic Bronchitis - Hypersecretion of mucus and chronic productive cough that continues for at least 3 months out of the year for at least 2 years (usually winter months). ➢ PATHO - Inspired irritants = airway inflammation caused by neutrophils, macrophages, and lymphocyte infiltration of the bronchial wall. Tobacco smoke directly injures airway epithelial cells. - Bronchial inflammation = bronchial edema, ↑ size and # of mucous glands and goblet cells (cells that secrete mucus found in the epithelial layer of the bronchi) in the airway epithelium. - Due to impaired ciliary function, thick/tenacious mucus cannot be cleared. - Defense mechanisms are compromised = ↑ risk to infection and airway injury. - Frequent infectious exacerbations are complicated by bronchospasm with dyspnea and productive cough. - Larger bronchi affected first, but then all airways are involved later on. - Thick mucus + hypertrophied bronchial smooth muscle = narrowing of the airways = obstruction, usually during expiration when the airways are constricted. - Obstruction → ventilation/perfusion mismatch with hypoxemia. - The airways collapse early in expiration, trapping gas in the distal portion of the lung - Air trapping expands the thorax = mechanical disadvantage for airway muscles = decreased tidal volume, hypoventilation and hypercapnia

➢ CLINICAL MANIFESTATIONS

• Decreased exercise tolerance = hypoxia with exercise
• Wheezing
• SOB
• Productive "smokers cough"
• Evidence of airway obstruction: decreased FEV (forced expiratory volume 1 = 1 second) on spirometry Disease progression: — Copious sputum and frequent pulmonary infections — FVC and FEV values ↓ and FRC and residual (RV) ↑ as obstruction and air trapping become more pronounced
• Airway obstruction= ↓ alveolar ventilation and ↑ PaCO 2
• Hypoxemia = polycythemia (overproduction of erythrocytes) and cyanosis; if not reversed: hypoxemia
  • pulmonary hypertension and results in cor pulmonale
  • severe disabilities or death ➢ EVALUATION
• Diagnoses is based on symptom hx, physical exam, cxr, pulmonary function tests, ABG
• These tests reflect progressive nature of the disease ➢ TREATMENT — Prevention is the BEST treatment (pathologic changes are NOT reversible) — By the time medical care is sought, most have considerable airway damage — Stop smoking = halted disease progression — Bronchodilators + expectorants = reduced dyspnea cough control — Chest physical therapy = deep breathing and postural drainage — Acute exacerbations (infections and bronchospasm) requires antibiotics + corticosteroids and may need mechanical ventilation — LAST RESORT: chronic oral corticosteroids — Severe hypoxemia requires continuous O 2 therapy (beware of CO 2 retainers) — Teaching includes: nutrition, respiratory hygiene, early infection signs, techniques to relive dyspnea (such as pursed lip breathing)

volume

— Pores of Kohn ▪ Tiny passages that allow air to pass from alveolus to alveolus, promoting collateral ventilation and even distribution of air among alveoli. ▪ Like the bronchi, alveoli contain cellular components of inflammation and immunity. ▪ Contain alveolar macrophages ▪ Alveolar septa consist of an epithelial layer and thin, elastic basement membrane but no muscle layer — Epithelial cells ▪ Type I alveolar cells: alveolar structure ▪ Type II alveolar cells: surfactant production (prevents lung collapse)

Pulmonary and bronchial circulation: the pulmonary circulation facilitates gas exchange, delivers nutrients to lung tissues, acts as a blood reservoir for the left ventricle, and serves as a filtering system that removes clots, air, and other debris.

• Pulmonary artery divides and enters the lung at the hilus, travels with each main bronchus, and branches with the bronchus at every division so that every bronchus and bronchiole has an accompanying artery or arteriole. The arterioles, less than 1 mm in diameter, regulate blood flow through their respective capillary beds. - Pulmonary capillaries are a network around the acinus. — They are an integral part of the alveolar septa — Capillary walls consist of an endothelial layer with a basement membrane of the alveolar septa; there is little separation between blood in the capillary and gas in the alveolus Alveolocapillary membrane is the name for where the capillary fuses with the septa membrane and is the SITE OF GAS EXCHANGE: — Made up of the alveolar epithelium, alveolar basement membrane, and the capillary endothelium — Normal perfusion of 100mg of blood in the capillary bed is spread very thinly over about 140m^2 of alveolar surface area (efficiently exposes large quantities of blood to gas in the alveoli) — Any disorder that thickens the membrane impairs gas exchange.

A nurse recalls that the acinus contains: alveolar ducts. The gas-exchange airways are made up of respiratory bronchioles, alveolar ducts, and alveoli. These structures together are sometimes called the acinus and all of them participate in gas exchange

5. HOW IS THE PATIENT'S ALVEOLAR VENTILATION MEASURED? (p. 1232; key search term: “cannot be accurately”) - Ventilation — Is the mechanical movement of gas or air into and out of the lungs. — Often misnamed "respiration," which is actually the exchange of O 2 and CO 2 during cellular metabolism. — Ventilatory rate (respiratory rate) is the number of times gas is inspired and expired per minute. — Effective ventilation is calculated by: — Ventilatory rate (breaths per minute) x volume of air per breath (liters per breath, tidal volume) = minute volume or minute ventilation and is expressed in li ter s/ m inu te. — CO 2 , the gaseous form of carbonic acid (H 2 CO 3 ), is a product of cellular metabolism. — The lung eliminates about 10,000 milliequivalents (mEq) of carbonic acid per day in the form of CO 2 , which is produced at the rate of approximately 200 ml/minute. — CO 2 elimination is necessary to maintain a normal partial pressure of arterial CO 2 (PaCO 2 ) of 40 mmHg and normal acid-base balance. - Alveolar ventilation - Cannot be accurately determined by the observation of ventilator rate, pattern, or effort. - Alveolar ventilation adequacy must be measured by arterial blood gases. - Measures partial pressure of carbon dioxide (PaCO 2 ). 6. KNOW ASTHMA (ADULT AND CHILDHOOD; ACUTE AND CHRONIC). (pp. 1263 - 1266 [adult] and 1308 - 1310 [children]; key search term: “asthma occurs at all”) Adult Asthma ▪ Chronic inflammatory disorder of the bronchial mucosa. ▪ Causes bronchial hyper-responsiveness, constriction of the airways and variable airflow obstruction that is reversible. ▪ 50% of all cases develop during childhood and 1/3 of those left before age 40. ▪ Death rates highest for adult females, blacks, and adults > 65. ▪ Is a familial disorder; over 100 genes have been identified. ▪ Risk factors: allergen exposure, urban residence, air pollution exposure, tobacco smoke, and environmental tobacco smoke, recurrent respiratory tract viral infections, esophageal reflux, and obesity. ▪ Exposure to high levels of allergens during childhood increases risk for asthma. ▪ Decreased exposure to certain infectious organisms = immunologic imbalance that favors the development of allergy and asthma = hygiene hypothesis. ➢ Pathophysiology - Episodic attacks of bronchospasm, bronchial inflammation, mucosal edema, and increased mucus production: caused by macrophages (dendritic cells), T helper 2 (Th2) lymphocytes, B lymphocytes, mast cells, neutrophils, eosinophils, and basophils. — Early asthmatic response

➢ Clinical manifestations

• Asymptomatic between attacks and pulmonary function tests are normal
• During partial remission: no clinical symptoms, but pulmonary function tests abnormal
• Beginning of an attack = chest constriction, expiratory wheezing, dyspnea, nonproductive coughing, prolonged expiration, tachycardia, tachypnea
• Severe attack = accessory muscle use, and wheezing during inspiration and expiration o Pulsus paradoxus: ↓ of SBP during inspiration of > 10 mmHg noted
• O 2 sats ↓ 90%, check ABG tensions (usual finding respiratory alkalosis + hypoxemia)
• Late asthma response = more severe symptoms than the original attack
• Status asthmaticus: ▪ Bronchospasm not reversed by usual measures ▪ Hypoxemia worsens, expiratory flow ↓ and effective ventilation ↓; ↑ PaCO 2 = acidosis = life-threatening
• Ominous signs of impending death : ▪ Silent chest (no audible air movement) and a PaCO 2 greater than 70 mm Hg ➢ Diagnosis ▪ History of allergies and reoccurring episodes of wheezing, dyspnea, and cough, or exercise intolerance ▪ Spirometry = reversible decreases in FEV1 during induced attack ▪ Acute attack = rapid assessment of ABG and expiratory flow rates and search for underlying cause (infection); hypoxia + respiratory alkalosis expected. Development of hypercapnia + respiratory acidosis = need for ventilator. ● Treatment ➢ Acute attack
• Immediate administration of O 2 and inhaled β -agonist bronchodilators
• Oral corticosteroids administration early in the course of management
• Careful monitoring of gas exchange and airway obstruction in response to therapy
• Antibiotics are not indicated for acute asthma unless a bacterial infection is documented ➢ Asthma in General
• Education over allergens and irritants and peak flow meters
• Due to underestimation of severity, education on action plan adherence is good ➢ Pharmacologic treatments
• Mildest form of asthma (intermittent): short-acting β -agonist inhalers
• Persistent asthma: anti-inflammatory medications and inhaled corticosteroids —the mainstay of therapy
• Not adequately controlled on inhaled corticosteroids: leukotriene antagonists
• Severe asthma: long-acting β agonists persistent bronchospasm (can actually worsen asthma in some individuals)
• Reduction of asthma exacerbations: immunotherapy (can be sublingual)
• Monoclonal antibodies to IgE (omalizumab)

Which statement is true regarding the pathophysiologic process of asthma? Increased bronchial smooth muscle spasm and increased vascular permeability cause asthma. Asthma is an immunoglobulin E (IgE).

A child has asthma. Which pathophysiologic process occurs in this disease? Chronic inflammatory disorder, causing mucosal edema and reversible airflow obstruction. Asthma is a chronic inflammatory disorder of the bronchial mucosa that causes bronchial hyper- responsiveness, constriction of the airways, and variable airflow obstruction that is reversible. Episodic attacks of bronchospasm, bronchial inflammation, mucosal edema, and increased mucus production occur in asthma.

Childhood Asthma, Acute and Chronic (pp. 1308-1310) Childhood Asthma ● Chronic inflammatory disease with sensitivity to allergens, bronchial hyperreactivity, and reversible airway obstruction. ● Most prevalent chronic disease in childhood: 10% US population 5-17 years old, boys > girls. ● Severity and persistence influenced by: age at time of onset, genetics, behavior, atopy, air pollution, level of allergen exposure, environmental tobacco smoke, gastroesophageal reflux, and respiratory infections. ● Variables that affect disparity: social stress in home, lack of insurance, and access to care. ● Environmental and genetic factors, and ↓ vitamin D (= wheezing due to suppressed Th2- mediated allergic disease. Associated with many genes, including genes that code for increased levels of immune and inflammatory mediators (IL-4, IL-5, IL-3, IgE), adrenergic receptors, nitric oxide, and transmembrane proteins in the endoplasmic retriculum. ● Hygiene hypothesis: allergen exposure shifts the immune system toward Th2-predominant phenotype, with an increase in the production of antibodies, including IgE (this effect is usually balanced by exposure to numerous siblings, daycare, farming, endotoxins, and certain micororganisms, such as Toxoplasma gondii , hepatitis A virus, and Helicobacter pylori ). Those exposed to a highly clean environment and those who receive vaccines to prevent infections lack adequate exposure to common pathogens and do not achieve balance in their immune systems. ● PATHO: (similar to that of adults)

7. AGING AND THE PULMONARY SYSTEM. (pp. 1244 - 1245; key search term: “most knowledge”) - A few normal physiologic (developmental and degenerative) changes are known to occur from birth to old age. - Understand the need to provide care, and to differentiate between normal and disease. - Normal alterations include: ▪ These changes are normal and occur gradually, influenced by environmental, social, and cultural factors, nutrition, respiratory disease, body size, gender, and race. - Loss of elastic recoil - Stiffening of the chest wall - Alterations in gas exchange - Increases in flow resistance ▪ During adulthood and as age advances: - Alveoli tend to lose alveoli wall tissue and capillaries (↓ surface area for gas diffusion) - Chest wall compliance decreases because ribs ossified (less flexible) and joints stiffen

• Vital capacity ↓ and residual volume ↑; however, total lung capacity is unchanged (leads to ↓ in ventilator reserves, causing ↓ ventilation-perfusion ratios)
• ↓ in PaO 2 and diminished ventilatory reserve, causing a decrease in exercise tolerance (does not affect PaCO 2 )
• ↓ in respiratory muscle strength and endurance by up to 20% by age 70
• ↑ Immune dysregulation, asymptomatic low-grade inflammation, and ↑ risk of infection.
• ↑ Risk for respiratory depression due to medications
• A very active, physically fit person, will have fewer changes in function at any age than one who has been sedentary.

8) KNOW HOW O 2 AND CO 2 IS CARRIED IN THE BLOOD. (pp. 1240 - 1243; key search term: “the ideal medium”) O 2 Transport

• 1000ml of O 2 is transported to cells each minute
• Transported in the blood in two forms: dissolves in plasma (small amount) and rest bound to Hgb.
• WITHOUT Hgb, O 2 would not reach cells in adequate #s to complete metabolic function. ● Diffusion across alveolocapillary membrane ➢ Ideal medium for O 2 diffusion
• Large total surface area (70-100m^2 )
• Very thin (0.5 μm)
• Partial pressure of O 2 molecules (PaO 2 ) is much greater in alveolar gas than it is in capillary blood: promotes rapid diffusion from the alveolus into the capillary
• The # of O 2 molecules in the alveoli (PAO 2 ) depends on # O 2 molecules in inspired air and the # that remains in the alveoli and tracheobronchial tree between breaths (physiologic dead space)

• Blood remains in the pulmonary capillary for 0.75 seconds, but only 0. seconds is needed for O 2 concentration to equalize across the membrane
• O 2 always has time to diffuse, even during ↑ cardiac output ● Determinants of arterial oxygenation
• Diffusion ceases when the PaO 2 (partial pressure of O 2 in arterial blood) is equal to PaO 2 (amount of O 2 in the alveoli) = no pressure gradient
• Normal transport of 100 ml of blood = 20 ml of O 2 , only 0.3 ml is in plasma
• The small amount in plasma (0.3 ml) is what is responsible for partial pressure (PaO 2 ) in the blood = provides info about the driving pressure that loads Hgb with oxygen, it gives little about the amount of O 2 in the blood
• O 2 content = amount of O 2 carried in the blood, measured in ml/dl
• Total O 2 content of the blood depends on the amount of O 2 chemically combined with Hgb and the # dissolved in the blood
• To calculate total arterial O 2 content:

1. Hgb concentration
2. O 2 saturation or % of available Hg that is bound to O 2 (SaO 2 )
3. The partial pressure of O 2 (PaO 2 )

• Maximum amount that can be transported by Hgb is 1.34ml/g
• Normal venous O 2 content is 15-16 ml/d ➢ ↓ Hg value < 15 (norm) reduces O 2 content ➢ ↑ Hg value may minimize effect of impaired gas exchange, and is a major compensatory mechanism in pulmonary diseases that impair gas exchange ➢ If cardiovascular function is normal – bodies response to ↓ O 2 = ↑ cardiac output ➢ Cardiovascular disease = ↑ Hg as a compensatory mechanism ● Oxyhemoglobin association and dissociation ➢ Hgb molecules bind with O 2 : oxyhemoglobin (HbO 2 ) ➢ Binding occurs in the lungs and is called oxyhemoglobin association/saturation ➢ When O 2 is released form Hgb in body tissues = Hgb desaturation ➢ When Hgb saturation and desaturation are plotted on a graph, the result is a distinctive s-shaped curve known as the oxyhemoglobin dissociation curve. ➢ Shift to the right depicts the Hgb’s decreased affinity for O 2 or an increase in the ease with which oxyhemoglobin dissociates and O 2 moves into the cells.
• Acidosis (low pH) and hypercapnia (↑PaCO) and hyperthermia ➢ Shift to the left depicts the Hgb’s increased affinity for O 2 , which promotes association in the lungs and inhibits dissociation in the tissues.
• Alkalosis (high pH) and hypocapnia (↓PaCO 2 ) and hypothermia ➢ Bohr effect: shift in the oxyhemoglobin dissociation curve caused by changes in CO 2 and H+^ concentration in the blood.

▪ When left ventricle fails → lift sided filling pressures ↑ → ↑ pulmonary capillary

hydrostatic pressure → hydrostatic pressure exceeds oncotic pressure → fluid moving into the interstitium/interstitial space (space within the alveolar septum between alveolus and capillary) → fluid moves to lymphatic vessels → fluid removed from the lung; when fluid moving out of the capillaries exceeds the lymphatics ability to remove it = pulmonary edema ▪ Pulmonary edema occurs at wedge pressure or left atrial pressure of 20 mmHg ▪ If capillary oncotic pressure is ↓ for any reason (anemia/decreased plasma proteins), pulmonary edema develops at a lower hydrostatic pressure ➢ Another cause: capillary injury that ↑ capillary permeability ▪ ARDS and inhalation of toxic gases (ammonia) = capillary injury ▪ Water and plasma proteins leak out of the capillary → move to lung interstitium → ↑ interstitial oncotic pressure (usually very low) → as interstitial oncotic pressure begins to = capillary oncotic pressure → water moves out of the capillary and into the lung = pulmonary edema ➢ Pulmonary edema can also result from obstruction of the lymphatic system ▪ Drainage can be blocked by compression of lymphatic vessels caused by edema, tumors, and fibrotic tissue. ▪ In left-sided heart failure, the systemic venous pressure increases → ↑ hydrostatic pressure of the large pulmonary veins in which the lymphatic system usually drains. ➢ Postobstructive pulmonary edema (POPE)/Negative pressure pulmonary edema

• Is a rare life-threatening complication that can occur after relief of upper airway obstruction (post extubation, laryngospasm after anesthesia, epiglottitis, laryngeal tumor, or obstructive tonsils)
• Attempted inspiration against an occluded airway → excessive intrathoracic negative pressure → ↑ venous return and blood flow to right side of the heart and ↓ outflow from the left side of the heart from ↑ afterload = ↑ pulmonary blood volume and ↑ venous pressure = pulmonary edema ➢ Clinical manifestations
• Dyspnea, orthopnea, hypoxemia, and increased work of breathing
• Physical exam = inspiratory crackles (rales), dullness to percussion over the lung bases, and evidence of ventricular dilation (S3 gallop and cardiomegaly)
• Severe edema (pink, frothy sputum), hypoxemia worsens, and hypoventilation with hypercapnia may develop.

➢ Treatment

• Increased hydrostatic pressure caused by heart failure Improve cardiac output and volume status with diuretics, vasodilators, and drugs that improve the contraction of the heart muscle.
• Increased capillary permeability resulting from injury Remove offending agent and supportive therapy to maintain adequate oxygenation, ventilation, and circulation.
• POPE Provide PEEP (positive end expiratory pressure) ventilation.
• Any type of pulmonary edema Provide supplemental O 2 Mechanical ventilation required if edema significantly impairs ventilation and oxygenation

11. KNOW PULMONARY FIBROSIS. (pp. 1258-1259; key search term: “when no specific”) Pulmonary Fibrosis - Excessive amount of fibrous or connective tissue in the lungs - Idiopathic pulmonary fibrosis: no specific cause for the fibrosis is known - Causes: inhalation of harmful substances (toxic gas, inorganic dusts, organic dusts) and underlying autoimmune disorders (rheumatologic disease) - Fibrotic process results from chronic inflammation, alveolar epithelialization, and myofibroblast proliferation. - Fibrosis causes: loss of lung compliance → lung becomes stiff and difficult to ventilate → diffusing capacity of the alveolocapillary membrane decreases = hypoxemia - Diffuse fibrosis = poor prognosis Idiopathic Pulmonary Fibrosis (IPF) - Most common idiopathic lung disorder, men > women, most cases > 60 years old - Median survival 2-4 years post diagnosis - Results from: chronic inflammation and fibroproliferation of the interstitial lung tissue around the alveoli with disruption of the alveolocapillary basement membrane - Causes: ↓ O 2 diffusion across the membrane and hypoxemia - Disease progresses: ↓ lung compliance → ↑ work of breathing, ↓ tidal volume = hypoventilation and hypercapnia. - Acute exacerbations: rapid decompensation and death rate as high as 50% - Primary symptoms: ↑ dyspnea on exertion; examination reveals diffuse inspiratory crackles - Diagnosis is confirmed by: pulmonary function tests (PFT) ↓ FVC, high resolution CT, and biopsy - Treatment: corticosteroids alone = remission rates of 50%, + cytotoxic drugs = ↑ success rate, but also ↑ toxicity. - Newer therapy = antifibrotic drugs, interferon, and anticoagulation (lung transplant for some) Exposure to Toxic Gases Pulmonary Fibrosis - Inhalation of gaseous irritants such as: ammonia, hydrogen chloride, sulfur dioxide, chlorine, phosgene, and nitrogen dioxide - Inhalation burns to the airway epithelium, cilia, and alveoli are caused by: h o u seh o ld /i n d u str i a l com bu st an t s, hea t, and sm oke part i cle s - Causes: ↑ mucus secretion, inflammation, mucosal/pulmonary edema, surfactant is inactivated - Acute inhalation: leads to ARDS and pneumonia - Initial symptoms: burning of eyes, nose and throat, chest tightness and dyspnea, hypoxemia - Treatment: supplemental O 2 , mechanical ventilation with PEEP, and cardiovascular support, and corticosteroids in some (effect not well documented) - Most respond well, some relapse due to bronchiectasis or bronchiolitis O 2 Toxicity ( not a cause of PF, but a topic covered under this section ) - Prolonged exposure to high concentrations of O 2 can result in rare iatrogenic condition - Severe inflammatory response mediated by O 2 free radicals - Causes: damage to alveolocapillary membranes, disruptions of surfactant production, interstitial and alveolar edema, and decrease in compliance - Treatment: ventilator support and reduction of inspired O 2 concentrations to <60% Pneumoconiosis - Change in the lung caused by inhalation of inorganic dust particles in the workplace - Diagnosis is dependent upon history of exposure - Occurs after years of exposure with progressive fibrosis of lung tissue - Causes: silica, asbestos, and coal (most common) talc, fibercobalt, aluminum, and iron

• Acute = fever, cough, dyspnea, and chills appear few hours after exposure, resolves 1- days
• Chronic = continued exposure → pulmonary fibrosis → weight loss, fever, fatigue, respiratory failure
• Diagnosis: history of allergen exposure, and serum antibody testing, cxr, bronchoscopy, CT, and lung biopsy
• Treatment: avoidance of offending agent, and corticosteroid administration

A person has pneumoconiosis. Which information would the nurse find in the history of this person? Inhaled inorganic dust particles resulting in a change in the lungs. Pneumoconiosis represents any change in the lung caused by inhalation of inorganic dust particles, which usually occurs in the workplace. Pneumoconiosis is caused by long-term inhalation of dust particles. Dust particles that produce this disorder include coal, asbestos, silica, talc, fiberglass, and mica.

12. HOW DO DIFFERENT DISEASE PROCESSES CAUSE HYPOXEMIA? (pp. 1251 - 1252; key search term: “hypoxemia results from”) Hypoxemia ( disease processes are in chart below ) - Reduced oxygenation of arterial blood (PaO 2 ) is caused by respiratory alterations - Hypoxemia can lead to tissue hypoxia (reduced O 2 of cells in tissues) - Hypoxemia results from: - O 2 delivery to the alveoli (O 2 content of the inspired air FiO2) - Ventilation of the alveoli - Diffusion of O 2 from the alveoli into the blood (balance between alveolar ventilation and perfusion V/Q mismatch, and diffusion of O 2 across the alveolocapillary membrane) - Perfusion of pulmonary capillaries Hypoxia - Reduced oxygenation of cells in tissues, may be caused by alterations of other systems as well

• Tissue hypoxia can result from other abnormalities, such as low cardiac output or cyanide poisoning. An abnormal ventilation/perfusion ratio (V/Q) is the most common cause of hypoxemia, where V = amount of air getting into alveoli, and Q = amount of blood perfusing the capillaries around the alveoli. Hypoventilation: ↑ in PaCO 2 and ↓ PaO 2 , corrected by ↑ rate and depth of breathing Shunting: an abnormal distribution of ventilation and perfusion. Inadequate ventilation of well perfused areas of the lung (low VQ), ventilation perfusion mismatch Right to left shunt = blood passes through portions of pulmonary capillary bed that receives no ventilation → ↓ PaO 2 and hypoxemia High V/Q: poor perfusion of well-ventilated portions of the lung resulting in wasted ventilation, most common cause PE = impaired blood flow to lung segment Alveolar dead space: area where alveoli are ventilated but not perfused

Alveolocapillary barrier: diffusion of O 2 is impaired if membrane is thickened, or surface area is decreased. Thickness ↑ time needed for diffusion, decreased surface area is caused by emphysema. Individuals with impaired diffusion would die from hypoxia before hypercapnia could occur. Hypoxemia associated with: compensatory hyperventilation and respiratory alkalosis (↓ PaCO 2 and ↑ PH) Results in: widespread tissue dysfunction and organ infarction, ↑ pulmonary artery pressure and right sided heart failure and cor pulmonale , cyanosis, confusion, tachycardia, edema, and ↓ renal output

13. KNOW EMPYEMAS. (p. 1255; key search term: “empyema occurs”) Empyema - Infected pleural effusion - Pus in the pleural space - Develops when: pulmonary lymphatics become blocked → outpouring of contaminated lymphatic fluid into the pleural space (source of accumulation is from detritus of infection: microorganisms, leukocytes, cellular debris) dumped into the pleural space by blocked lymphatic vessels) - Most common in older adults and children - Results from: complication of pneumonia, surgery, trauma, or bronchial obstruction from a tumor - Commonly infectious microorganisms: Staphylococcus aureus , Escherichia coli , anaerobic bacteria, and Klebsiella pneumoniae ➢ Clinical manifestations - Cyanosis, fever, tachycardia, cough, and pleural pain, ↓ breath sounds over empyema ➢ Diagnosis: - Chest radiographs, thoracentesis, and sputum culture ➢ Treatment - Administration of antimicrobial medications - Drainage of the pleural space with a chest tube - Severe cases: ultrasound-guided pleural drainage, instillation of fibrinolytic agents, or deoxyribonuclease (DNase) injected into the pleural space to achieve adequate drainage

14. KNOW ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)/ACUTE LUNG INJURY

(ALI). (p. 1261; key search term: “represents a spectrum”) Acute Respiratory Distress Syndrome (ARDS)/Acute Lung Injury (ALI)

• Forms of respiratory failure characterized by acute lung inflammation and diffuse alveolocapillary injury
• 64-78 cases per 100,000 people in US
• Death rate 42-47%, advanced age + immunocompromised + severe infections = ↑ mortality
• Survivors have almost normal lung function 1 year after acute illness, but many have neurocognitive disorders up to 5 years later
• Most common predisposing factors: genetic factors, sepsis, multiple trauma (especially when transfusions are received)
• Other causes: pneumonia, burns, aspiration, cardiopulmonary bypass surgery, pancreatitis, drug overdose, smoke/noxious gas inhalation, O 2 toxicity, radiation therapy, and DIC ➢ Pathophysiology - Acute injury to the alveolocapillary membrane (pulmonary capillary endothelium)