Pulmonary Disorders Lecture Notes PDF

1 Nursing 3366 Pathologic Processes: Implications for Nursing Lecture Notes: Disorders of the Pulmonary System Objectives /outcomes for this subject: DESCRIBE/DISCUSS/IDENTIFY: 1. The relationship between key aspects of normal pulmonar...

1 Nursing 3366 Pathologic Processes: Implications for Nursing Lecture Notes: Disorders of the Pulmonary System Objectives /outcomes for this subject: DESCRIBE/DISCUSS/IDENTIFY: 1. The relationship between key aspects of normal pulmonary function and the pathophysiology involved in: select restrictive pulmonary conditions, including: o pleural alterations such as effusion and pneumothorax o airway & pulmonary tissue disorders such as croup, pneumonia, pulmonary edema, tuberculosis, and bronchogenic cancer. o vascular disorders such as pulmonary embolus. select obstructive pulmonary conditions, including o asthma, chronic bronchitis, emphysema, 2. Signs and symptoms related to above pathological conditions, including significance of diagnostic test results used to evaluate and monitor pulmonary function, including peak flow test, ABGs, and V/Q computations. *************************** Outline: I. Basics of breathing B. Overview of pulmonary concepts A. Overview 1. phases in the breathing cycle see B. Properties of ventilation, perfusion, gas 2. healthy lungs prep exchange 3. increased work of breathing C. Work of breathing 4. categorizing pulmonary diseases D. Gas transport and delivery C. Restrictive lung diseases II. Pulmonary alterations 1. overview A. Review of blood gas concepts 2. low V/Q disorders 1. ABGs purpose a. chest wall restriction a. pH b. airway restriction b. gas levels in the blood c. pleural restriction d. lung tissue restriction: 2. disturbances in acid / base balance 3. high V/Q disorders and what they mean a. structural problems a. 5 steps to analyzing & b. pulmonary embolus interpreting ABGs D. Obstructive pulmonary diseases b. key points of acid/base 1. overview imbalances & compensation 2. asthma 3. a note on compensation 3. COPD—emphysema & bronchitis 4. summary of evaluating ABGs ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ II. Pulmonary alterations ABGs are a lab test obtained by drawing blood from artery A. Review of blood gas concepts (See “ABGs interpretation summary for pulmonary lecture”) 1. purpose of ABGs (arterial blood gases)-- to check for efficacy/disruption of gas exchanges and acid/base balance; they measure:  2 a. pH 1) indicates level of acidity of blood (decreased = lots of acid gang; increased = less acid gang) 2) normal range = 7.35-7.45; < 7.35 = acidosis; > 7.45 = alkalosis b. gas levels in the blood: 1) PO2 a) partial pressure of oxygen in arterial blood (O2 gas dissolved in plasma) b) norm = ~ 80 to 100mmHg; cigarette smoking—one in 10 smokers will develop lung cancer b) patho: carcinogens in tobacco smoke (has > 40)→ causes multiple genetic abnormalities in bronchial cells including deletions of chromosomes, activation of oncogenes, inactivation of tumor suppressor genes→ carcinoma in situ→ invasive carcinoma c) types of bronchogenic cancer: to establish diagnosis, a bronchoscopy is done→ a sample of the suspicious area is taken and sent for biopsy→ usually classified as small cell lung cancer (SCLC) or non- small cell (NSCLC) d) S&Ss—pleural effusion, cough, sputum, chest wall pain, SOB; anorexia, weight loss 3. problems that result in HIGH V/Q (can’t get blood to the air—less perfusion than normal), ie, obstruction of vessel in lung a. structural problems of vessels can cause this: strictures in pulmonary vessels, malformations, birth defects  12 b. most common perfusion problem is pulmonary embolus--occlusion of portion of pulmonary vessels by an embolus, which can be a blood clot, some type of tissue fragment, or an air bubble. 1) increased risk in patients with Virchow’s triad ( endothelial injury, hypercoagulability, venous stasis)→ venous thrombosis (DVT)→ dislodges & travels to lung 2) once embolus lodges in portion of pulmonary artery or its branches, it prohibits deoxygenated blood from getting to the air in the alveoli to be oxygenated, so the blood in the pulmonary veins that returns to the heart & beyond is less saturated with O2 & person will start to feel SOB & often chest pain; hemoptysis also occurs… see box below. 3) the seriousness depends on how large & how proximal the blockage is. Be sure you understand how patho of PE links with S&S (SOB, chest pain, hemoptysis, sometimes shock): Embolus enters pulmonary artery → smaller arterioles →blocks deoxygenated venous blood from getting to alveoli to get oxygenated → SOB & chest pain gets stuck → irritates arterial intima→ inflammation→ leakage of blood into lung tissue→ hemoptysis →if large enough portion of lung tissue inflamed→ massive release of inflammatory mediators → systemic vasodilation → shock D. Obstructive pulmonary diseases 1. overview a. as a rule, obstructive lung disease is due to difficulty with exhalation 1) in this category of lung disease, there is some sort of obstruction of airways that results in more force needed to expire air (rather than difficulty with getting air in & oxygenated, as is the problem with restrictive diseases) 2) normally, exhalation is a no-energy, automatic, passive process that works because of the natural elastic recoil of the lungs, but in people with obstructive disease, air (ie, CO2 and other “waste” gases) gets TRAPPED & must be forced out. 3) their S&S often are a result of this “forcing out:“ a) often patients must use accessory muscles to do this; use of accessory muscles is often manifested as retractions—supraclavicular, substernal, Click on the youtube link & intercostal muscles “sucking in” upon expiration to help get air OUT for a visual reminder of lungs. about obstructive b) some patients also have a prolonged expiratory phase as a disorders and peak flow measurement. compensatory mechanism (the length of time to exhale begins to get longer) https://www.youtube.co c) one test that is used to measure how well they can force out air is m/watch?v=6oKupWgDu peak flow (PF) test 80 (1) measured by a PF meter—patient blows “out” into the device “like blowing out a candle” (2) measures how much air can be blown out in first second of exhalation (measured in millimeters) (3) the less the PF, the worse the obstructive pulmonary disease. 4) almost all patients in this category have patterns of maintenance (ie, normal state of daily disease) and exacerbation episodes (periods of worsening)  13 b. most common types: 1) asthma, bronchitis, & emphysema (since many patients have BOTH bronchitis & emphysema, these two are lumped together & often called chronic obstructive pulmonary disease –COPD; if asthma is bad enough and chronic enough, it too is sometimes lumped under COPD) 2) cystic fibrosis (FYI) 2. asthma a. overview 1) asthma is a chronic inflammatory disorder of the airways due to bronchial hyperresponsiveness to stimuli such as allergens in environment. 2) can begin at any age—about half of all cases develop in childhood and 1/3 in adulthood, usually under age 40. b. patho: inhaled irritants→ inflammatory mediators (histamine, leukotriene, prostaglandins) vasodilation & increased capillary also, bronchial smooth muscle directly permeability, infiltration by neutrophils, react to all the mediators→spasm & eosinophils→ swelling of bronchial lining constriction of bronchi 1) patient can usually inhale ok—inhalation is an active process that can get air past swollen bronchi—but exhalation through the swollen & constricted airways is much more difficult 2) often can hear a wheezing sound caused by expiration of air through narrow passageways (if bronchial swelling & constriction gets VERY bad, can also hear wheezing during inhalation) c. S&S 1) pattern of remission & exacerbation, as is true of most obstructive dz’s Some hyperventilation 2) during exacerbation: during an asthma attack is a) usually have wheezing upon exhalation, though in bad cases the desirable—this means the patient is employing an wheezing can also be upon inhalation. adequate compensatory b) often have accessory muscle use—intercostal & supraclavicular response. But needs treatment, as he could retractions while exhaling—and prolonged expirations decompensate-- tire out, be c) SO2 can drop & patient will try to compensate for hypoxemia by unable to maintain the higher rate, and become hyperventilating (RR typically 24-28) during exacerbations, so ABGs hypoxemic, retain CO2, and during an asthma exacerbation usually show respiratory alkalosis. go into respiratory acidosis—very dangerous. d) baseline PF lower than normal population, but will worsen even more during exacerbations. d. tx: 1) monitor daily status with baseline PF readings; good indicator of impending exacerbations 2) meds: bronchodilators like ventolin via aerosol nebulization and/or inhalers; anti-inflammation drugs like oral and/or IV steroids (decrease swelling, stabilize capillary membranes) 3. COPD a. collective term for emphysema and/or chronic bronchitis 1) patho is different, but some characteristics are the same in both. a) in MOST cases, the cause of both types of COPD is smoking  14 b) S&S in both include prolonged expirations, certain degree of accessory muscle use, and a chronically low PF; all these S&S are even worse than usual during exacerbation c) treatment of both is similar (and much like treatment of asthma)— smoking cessation (stop smoking); giving O2 appropriately, bronchodilators, sometimes steroids 2) keep in mind that though they will be described separately, elements of emphysema and bronchitis are often BOTH seen in obstructive pulmonary disease and can complicate the “picture” 3) also, some sources include severe, chronic asthma under the COPD category b. emphysema 1) cause: smoking is the main one 2) patho: a) inspired irritants (usually from smoking)→ inability to expel them due to altered cilia →airway inflammation & abnormally increased activity of proteolytic enzymes like elastase (an enzyme that breaks down the proteins that make lungs so flexible & “elastic”) → eventual destruction of patches of the alveolocapillary membrane and some of the walls between alveoli clusters → results in large, stiff, hyperinflated alveoli that have no elastic recoil →due to this loss of elastic recoil, these areas act as air “traps” (large, over-inflated areas sometimes called “blebs”) →once air is inhaled & trapped, it becomes harder to exhale it b) due to destruction of areas of alveolocapillary membrane, O2 diffusion is compromised & hypoxemia develops (“air hunger”) Like someone having an (1) to “tap into” areas where the alveolocapillary membrane has not asthma attack, some been destroyed & get more O2 diffusion, it helps to increase hyperventilation in an emphysemic is desirable— respiratory rate this means the patient is employing an adequate (2) so the emphysemic typically lives in a state of compensatory compensatory response. chronic hyperventilation to try to get more air. Most emphysemics live their3) S&S lives in this compensatory state of tachypnea. a) a degree of tachypnea is almost always present—RR of 26 to 30/min But during exacerbation periods, he needs b) because of hyperventilation, patients with emphysema known as “pink treatment, as he could puffers” --they can stay pink (ie, fairly well-oxygenated) as long as decompensate-- tire out, be they keep “puffing.” unable to maintain the higher rate, and become b) this is hard work, so these patients usually are thin and have no hypoxemic, retain CO2, and appetite (no energy to eat) go into respiratory acidosis—very dangerous. c) they also have a typical feature of increased anteroposterior (AP) To reiterate, if an diameter of chest emphysemic goes into (1) goes from normal AP-to-lateral diameter ratio of 1 to 2, to an respiratory acidosis, he is decompensating→, he is equal diameter both ways (2:2), as a compensatory change to wearing out and cannot accommodate years of air trapping & lungs getting bigger exhale enough CO2 →CO2 (2) the thorax is much “rounder” and is called a barrel chest. retention (hypercapnia→ resp. acidosis); respiratory d) often emphysemics will unconsciously use certain techniques to help acidosis is a danger sign to exhale and to get more air: that patient might go into respiratory failure.  15 (1) “tripod” position forces the diaphragm down and forward, which helps to maximize chest expansion and decrease work of breathing. (2) “pursed lip” breathing to increase pressure in chest to get air out & to prolong expiratory time e) may have wheezing, but usually lung sounds are markedly diminished due to no air flow in many areas f) ABGs: because an emphysemic patient is usually in a chronic state of compensatory hyperventilation, he or she therefore lives in a daily state of some degree of respiratory alkalosis: pH:>7.45;PCO2: