Exam 1 Blueprint - Exam 1 study topics PDF

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PCC2

Exam 1 Blueprint I. Respiratory Conditions: A. Asthma (pg. 563-571) – 6 questions 1. Asthma: chronic disease in which reversible airway obstruction occurs intermittently, reducing airflow a. Airway obstruction occurs by both inflammation and airway tissue sensitivity (hyperresponsiveness) w bronchoconstriction i. Bronchoconstriction is the cause of reduced airflow, so bronchodilators are first treatment  Beta-blockers cause bronchoconstriction  Avoid beta-adrenergic blockers in asthma pts, opposite effect of bronchodilators  End in -lol 2. Etiology: inflammation of the mucous membranes lining the airways is a key event in triggering an asthma attack

a. b. ~1/2 of adults w asthma also had asthma in childhood c. Uncontrolled asthma: asthma symptoms no more than 2x/week d. Common asthma triggers: i. Specific allergens, ex: mold, animal product, pollen, dust ii. General irritants, ex: cold air, dry air, fine airborne particles, chemicals, vapors, smoke, gases, dust, fumes, humidity, temperature iii. Microorganisms, ex: viruses iv. Aspirin and other NSAIDS v. Stress vi. GERD vii. Exercise viii. Upper respiratory illness e. Types of asthma: i. Exercise-induced asthma ii. Child-onset asthma iii. Adult-onset asthma iv. Occupational asthma v. Nocturnal asthma vi. NSAID induced asthma or ASA (aspirin induced asthma)

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When asthma is well controlled airway changes are temporary and reversible. With poor control, chronic inflammation leads to airway damage and altered cellular regulation w enlargement of the bronchial epithelial cells, including mucus-secreting cells, and changes in the bronchial smooth muscle g. Chart 30-1: Nursing Focus on the Older Adult Chronic Respiratory Disorder      

Provide rest period between activities, ex: meals, bathing, ambulation Place pt in an upright position for meals to prevent aspiration Encourage nutritional fluid intake after meal to promote ↑ caloric intake Schedule drugs around routine activities to ↑ adherence to drug therapy Arrange chairs in strategic locations to allow pts w dyspnea to stop and rest Urge pt to receive pneumococcal vaccine and annual influenza vaccination For pts w home O2, keep tubing coiled when walking to ↓ risk of tripping

 3. Assessment: asthma is classified based on how well controlled the symptoms are and on the patient’s responses to asthma drugs a. History: i. Symptoms: pt w asthma usually has a pattern of intermittent episodes of dyspnea (SOB), chest tightness, coughing, wheezing, increased mucus production ii. Timing: continuous, seasonal, associated w specific activities or exposures, exercise, at work, at night, etc  Some pts have symptoms for 4-8 weeks following cold or upper resp infection iii. Genetic: family hx of asthma or other respiratory problems iv. Habits: smoking, atopic (skin allergic rxn then asthma) b. Signs/symptoms: audible wheeze (musical sound), ↑ RR (30-35/min), coughing (may be early indicator of breathing problems in children) i. Breathing cycle is longer, requires more effort, w prolonged expiration ii. Pt may be unable to speak more than a few words iii. Pt may use accessory muscles to help breathe during attack, observe for muscle retraction at the sternum and the suprasternal notch and between ribs  Pt w long-standing, severe asthma may have “barrel chest” caused by air trapping iv. Hypoxia occurs w severe attacks  asthma, COPD, pneumonia, cystic fibrosis  Pulse oximetry shows hypoxemia (poor blood O2 levels)  Examine oral mucosa and nail beds for cyanosis  Changes in level of cognition or consciousness, tachycardia v. Absent breath sounds  medical emergency, prepare to intubate c. Diagnostic tests: i. Vitals: tachycardia (↑HR), tachypnea (↑RR), severe hypotension (↓BP), desaturation (↓O2) indicate hypoxia  Any pt w asthma, COPD, pneumonia, cystic fibrosis will present w same vital sign changes w hypoxia ii. Arterial blood gases (ABG): shows the effectiveness of gas exchange

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Normal values:  pH: 7.35-7.45  CO2: 35-45  pO2: 80-100  HCO3: 22-26  O2 Sat: 95-100%  PaO2 (arterial O2 levels) may ↓ during asthma attack  Early in attack, PaCO2 (arterial CO2 levels) may be ↓ as pt ↑ their breathing rate and depth  Later in attack, PaCO2 ↑, indicating CO2 retention iii. Allen’s Test: used to determine if pt’s ulnar circulation is sufficient  Performed before drawing arterial blood from the radial artery  Negative test when blood returns within ~7 sec a. Must have negative Allen’s test prior to ABG  Positive test when normal color does not return within ~7 sec a. If positive, you’ll have to use brachial or femoral artery to draw arterial blood (more painful) iv. Serum eosinophils: allergic asthma often occurs w ↑ serum eosinophil count and ↑ immunoglobin E (IgE) levels  Useful to know disease severity  Rule out activity or medication-induced asthma v. Sputum: rule out upper resp infection as a cause vi. Pulmonary Function Tests: the most accurate tests for measuring airflow using spirometry, baseline PFTs are obtained for all asthma pts  Forced Vital Capacity: records the max amount of air that can be exhaled as quickly as possible after max inspiration  Indicates resp muscle strength and ventilatory reserve  ↓ in obstructive and restrictive diseases  Forced expiratory volume in first second (FEV1): records the max amount of air that can be expelled in first second of expiration  Effort dependent, declines normally w age  Peak expiratory flow rate (PEFR): records force of flow in middle half of FVC  Provides sensitive index of obstruction in smaller airways  15-20% decrease in FEV1 or PEFR is expected in pt w asthma  12% increase after treatment w bronchodilators indicates asthma vii. Methacholine challenge: induces bronchospasm in adults suspected of having asthma, tests airway responsiveness, used to diagnose asthma  Do NOT test if pregnant, nursing, can’t perform spirometry test, airway severely compromised 4. Interventions a. Drug Therapy: pharmacologic measures based on the step category for severity and treatment

PCC2 i. Chart 30-3: Key Features The Step System for Medication Use in Asthma Control Step 1 Step 2

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Step 3

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Step 4

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Step 5

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As-needed rapid-acting beta2 agonist (relief inhaler) No daily drugs needed As-needed rapid-acting beta2 agonist (relief inhaler) Daily treatment involved the use of one of these two options: Low-dose inhaled corticosteroid (ICS) -OR- Leukotriene modifier As-needed rapid-acting beta2 agonist (relief inhaler) Daily treatment involved the use of one of these four options: Low-dose ICS and long-acting beta2 agonist -OR- Medium-dose or high-dose ICS -OR- Lowdose ICS and leukotriene modifier -OR- Low-dose ICS and sustained-release theophylline As-needed rapid-acting beta2 agonist (relief inhaler) Daily treatment involves the use of the Step 3 option that provided best degree of control and was well tolerated along w one or more of these two options: Medium-dose or high-dose ICS and long-acting beta2 agonist -ORLeukotriene modifier and sustained-release theophylline As-needed rapid-acting beta2 agonist (relief inhaler) Daily treatment involves the use of the Step 4 option(s) that provided best degree of control and was well tolerated along w either of these two options: Oral glucocorticosteroid (lowest dose) -OR- Anti-IgE treatment

ii. Control therapy drugs: used to reduce airway sensitivity to prevent asthma attacks from occurring to maintain gas exchange, used every day regardless of symptoms iii. Reliever drugs (aka rescue drugs): used to stop attack once it has started iv. Bronchodilators: cause bronchodilation through relaxing bronchiolar smooth muscle by binding to and activating pulmonary beta 2 receptors, first line of treatment for asthma!  Short-Acting Beta2 Agonist (SABA): fast-acting reliever (rescue) drug to be used either during asthma attack or just before engaging in activity that usually triggers an attack, no effect on inflammation  Albuterol (Ventolin, inhaled drug), Levalbuterol (Xopenex, give to pts w history of heart disease, extremely expensive)  Nursing Implications (Chart 30-6): a. Teach pt to carry drug w them at all times, it can stop or reduce lifethreatening bronchoconstriction b. Teach pt to monitor heart rate, excessive use can cause tachycardia bc drug also stimulates beta1 receptors in heart, assess pulse before administering drug c. When using w other inhaled drugs, teach pt to use at least 5 mins before the other drugs, better penetration of other inhaled drugs d. Teach pt correct technique for using metered dose inhaler (MDI) or dry powder inhaler (DPI) to ensure drug reaches the site of action, if no spacer available hold inhaler 1-2 inches away from mouth

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Long-Acting Beta2 Agonist (LABA): slow onset of action but long duration, used to prevent an asthma attack  Salmeterol (Serevent, inhaled drug)  Nursing Implications: a. Teach pt not to use as reliever drugs, slow onset of action and do not relieve acute symptoms b. Teach pt correct technique for using MDI or DPI c. Teach pt that these drugs need time to build up effect  Cholinergic Antagonist: causes bronchodilation by inhibiting parasympathetic nervous system, used to relieve and prevent asthma and improve gas exchange  Ipratropium (Atrovent, inhaled drug), Tiotropium (Spiriva, DPI, long-acting)  DuoNeb = Albuterol + Ipratropium  Nursing Implications: a. If used at reliever drug, teach pt to carry w them at all times b. Teach pt to shake MDI well before using, drugs separate easily c. Teach pt to ↑ daily fluid intake, drug can cause mouth dryness d. Can’t see, can’t pee, can’t spit, can’t shit – Teach pt to observe for/report blurred vision, eye pain, headache, nausea, palpitations, tremors, inability to sleep, these are systemic signs of overdose and require intervention e. Teach pt correct technique for using MDI or DPI (do NOT shake DPI)  Methylxanthines: last resort medication, only used when other types of management are ineffective  Theophylline, Caffeine  One of first drugs used for asthma and COPD  Therapeutic Range: 10-20 mcg/mL a. Toxicity: > 20 mcg/mL b. Blood levels MUST be monitored closely, every 3-6 months  Nursing Implications: a. Use has declined bc of harsh side effects: dysrhythmia, convulsions, cardiorespiratory collapse i. Do NOT give to those w seizure disorder, heart, renal, liver disease b. Teach pts not to take any other xanthines (ex: Caffeine) when taking Theophylline  causes synergistic effects v. Anti-Inflammatory Agents: improve bronchiolar airflow and ↑ gas exchange by ↓ the inflammatory response of the mucous membranes in the airways  Corticosteroids: used to prevent asthma attacks caused by inflammation or allergies (controller drug), prevent further inflammation so healing can begin  Prednisone (oral drug), Fluticasone (Ellipta, MDI inhaled drug), Methylprednisolone (Solumedrol, given IV in acute situation in hospital) a. Many steroids end in -sone  Steroids given PO can cause hyperglycemia, do NOT give to diabetic pts

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Nursing Implications: a. Teach pt about expected side effects, knowing what to expect may reduce anxiety i. Side effects: osteoporosis (long-term use), ↑ appetite, moodiness, water retention  “moon face” ii. Inhaled steroids have fewer systemic side effects, preferred for long-term use, rinse mouth after every use (can cause yeast infection, oral thrush) b. Teach pt to take drug w food to help reduce side effect of GI ulceration i. Monitor for black, tarry stool  upper GI bleed c. Teach pt to use drug daily even when no symptoms present, max effectiveness requires continuous use for 48-72 hours, depends on regular use d. Teach pt to use good mouth care and check daily for lesions/drainage e. Teach pt not to use as reliever drugs, slow onset of action f. Teach pt correct use for using MDI g. Teach pt not to suddenly stop taking drug FOR ANY REASON, drug suppresses adrenal production of corticosteroids which are essential for life  Leukotriene Modifier: used to prevent asthma attack triggered by inflammation or allergens, for moderate to severe asthma, helps control edema  Montelukast (Singulair, oral drug)  Nursing Implications: a. Teach pt to use drug daily even when no symptoms present, max effectiveness requires continuous use for 48-72 hours, depends on regular use b. Teach pt not to decrease dose or stop taking any other asthma meds unless directed by HCP, this drug is for long-term asthma control and does not replace other drugs, especially corticosteroids and rescue drugs b. Oxygen Therapy: supplemental oxygen by mask or nasal cannula is often used during acute asthma attack, high flow delivery may be needed w severe bronchospasm i. Nasal cannula: delivers 24-44% O2 at rate of 1-6 L/min ii. Non-rebreather: delivers 80-95% O2 at 10-15 L/min  If pt is receiving > 4L O2, use a humidifier  Reduce energy expenditure, ex: talking, eat slow, rest periods between activities iii. Positioning: high Fowlers position, tripod/orthopneic position (leaning over, arms on bedside table), fan in room 5. Self-Management Education a. Personal asthma action plan is developed by HCP and pt, tailored to meet pt’s personal triggers, asthma symptoms, and drug responses, includes: i. Prescribed daily controlled drug(s) schedule ii. Prescribed reliever drug directions

PCC2 iii. Pt-specific daily asthma control assessment questions iv. Directions for adjusting daily controller drug schedule v. When to contact HCP vi. Emergency actions to take when asthma not responding to controller/reliever drugs b. Pt will establish baseline or “personal best” PEFR by measuring PEFR 2x/daily for 2-3 weeks when asthma is well controlled, all further readings will be compared to baseline i. Green zone: at least 80% of/above personal best ii. Yellow zone: between 50-80% of personal best  Pt should use prescribed reliever drug if within this range, and retake PEFR reading within a few minutes  Frequent readings in yellow zone or increasing use of reliever drugs indicates need to reassess asthma plan to change controlled drugs iii. Red zone: below 50% of personal best, indicates serious resp obstruction c. Chart 30-5: Pt and Fam Education: Preparing for Self-Management Asthma Management         

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Avoid potential environmental triggers, ex: smoke, fire-places, dust, mold, weather changes to warm/cold Avoid drugs triggers, ex: aspirin, NSAIDs, beta blockers Avoid food prepared w monosodium glutamate (MSG) or metabisulfite Use bronchodilator inhaler 30 mins before exercise if needed Be sure you know proper techniques and correct sequence when using metered dose inhalers Get adequate rest and sleep Reduce stress and anxiety, learn relaxation techniques Wash all bedding w hot water to destroy dust mites Monitor PEFR w flow meter at least 2x/day Seek immediate emergency care if you experience: gray/blue fingertips or lips (cyanosis), difficulty breathing/walking/talking, retractions of the neck/chest/ribs, nasal flaring, failure of drugs to control worsening symptoms, PEFR declining after treatment, or flow rate 50% below baseline

6. Status Asthmaticus: severe, life threatening acute episode of airway obstruction that intensifies once it begins, often does not respond to usual therapy a. Symptoms: use of accessory muscles, distention of neck veins, extremely labored breathing and wheezing i. If condition is not reversed, pt may develop pneumothorax (collapsed lung) and cardiac or respiratory arrest b. Treatment: IV fluids, potent systemic bronchodilators, steroids, epinephrine, O2 c. Sudden absence of wheezing indicated complete airway obstruction and requires trach B. COPD (pg. 572-581) – 6 questions 1. Chronic Obstructive Pulmonary Disease (COPD): disorders including emphysema and bronchitis that interfere w airflow and gas exchange a. Emphysema: loss of lung elasticity, loss of alveoli surface area, and hyperinflation of the lung, resulting in dyspnea, ↓ gas exchange, and need for ↑ RR

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↑ levels of protease enzymes (often caused by smoking) damage alveoli and small airways  alveolar sacs lose elasticity over time and small airways collapse/narrow  increased amount of air trapped in lungs  alveoli are destroyed or become large/flabby  less area for gas exchange  Hyperinflated lungs flatten diaphragm, weakening effectiveness  Pts need to use accessory muscles to inhale/exhale  Increased efforts increase need for O2  “Air hunger”: pt starts inhalation before exhalation is completed, resulting in uncoordinated breathing pattern ii. Gas exchange is affected by increased work of breathing and loss of alveolar tissue  Pt may adjust by ↑ RR, so ABG values may not show gas exchange problems until advanced disease  CO2 is produced faster than eliminated  CO2 retention and chronic respiratory acidosis  ↓ PaO2 (arterial O2) level bc it is difficult for O2 to move from diseased alveoli into blood b. Chronic Bronchitis: inflammation of the bronchi and bronchioles caused by exposure to irritants, resulting in inflammation, vasodilation, mucosal edema, congestion, and bronchospasm i. Chronic inflammation ↑ number/size of mucus-secreting glands which produce large amounts of thick mucus  bronchial walls thicken and impair airflow, blocking smaller airways and narrowing larger ones ii. Affects airways, NOT alveoli iii. Impairs airflow and gas exchange bc mucus plugs and infection narrow airways  ↓ PaO2 level (hypoxemia)  ↑ CO2  respiratory acidosis 2. Etiology a. Risk factors for COPD: i. Cigarette smoking: greatest risk factor for COPD  Inhaled smoke triggers release of excessive proteases in lungs  break down elastin (major component of alveoli)  Impair action of cilia  inhibits cilia from clearing bronchi of mucus, cellular debris, and fluid  Pt w 20+ pack-year history often has early-stage COPD w changes in PFT  Calculating pack history: 1 pack/day x 20 years = 20 pack-years ii. Alpha1-antitrypsin (AAT) deficiency: less common risk factor for COPD  AAT inhibits excessive protease activity, so proteases only break down inhaled pollutants/organisms and do not damage lung structures  Can also cause problems in skin and liver iii. Asthma: incidence of COPD is 12x greater among adults w asthma b. Stages of COPD Severity: i. Stage 1 (Mild): FEV1 > 80% of normal lung volume

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Minor airflow limitations, increase in mucus production, chronic cough  20 pack-years ii. Stage 2 (Moderate): FEV1 between 50-80% of normal lung volume  Wheezing, ↑ coughing, SOB, ↑ mucus production limits daily activities  Most pts seek help for COPD symptoms at this stage iii. Stage 3 (Severe): FEV1 between 30-50% of normal lung volume AND severe emphysema  Lung function continues to decline, breathing becomes more difficult, large impact on quality of life iv. Stage 4 (Very Severe): FEV1 < Stage 3 AND low blood O2 levels  Flare-ups and breathing issues may become life threatening  End-stage COPD 3. Complications a. Hypoxemia and acidosis: reduced gas exchange in COPD pts  ↓ oxygenation and ↑ CO2 levels b. Respiratory infection: risk increased bc of ↑ mucus and poor gas exchange, bacterial infections are most common i. Worsens COPD symptoms: increased inflammation, increased mucus production, induces more bronchospasm  airflow becomes more limited, breathing efforts must increase, and dyspnea results c. Cardiac failure: occurs w bronchitis or emphysema i. Air trapping, airway collapse, stiff alveolar walls ↑ lung tissue pressure and narrow blood vessels  increased pressure creates heavy workload on right side of heart  heart chambers enlarge and thicken  right-sided heart failure w backup of blood into general venous system ii. Cor pulmonale: right-sided heart failure caused by pulmonary disease iii. Chart 30-9: Key Features Cor Pulmonale       

Hypoxia and hypoxemia Increasing dyspnea Fatigue Enlarged and tender liver Warm, cyanotic hands/feet, w bounding pulses Cyanotic lips Distended neck veins

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