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NUR2502/MDC Exam 3 Focused Review (Chapters 34, 35, 36, 38, 39, 40) Fall 2020,100% CORRECT

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NUR2502/MDC Exam 3 Focused Review (Chapters 34, 35, 36, 38, 39, 40) Fall 2020 ● Heart failure o causes ▪ A common chronic health problem with acute episodes often causing hospitalization. Acute... coronary disease and other structural or functional problems of the heart can lead to acute HF. ▪ Caused by systemic HTN in most cases ▪ Common causes and Risk factors for HF: ● HTN, coronary artery disease, cardiomyopathy, substance abuse, valvular disease, congenital defects, cardiac infections and inflammations, dysrhythmias, DM, smoking/tobacco use, family history, obesity, severe lung disease, sleep apnea, hyperkinetic conditions (hyperthyroidism) o left vs right ▪ Left sided heart (ventricular) failure includes HTN, coronary artery disease, and valvular disease. Decreased tissue perfusion from poor cardiac output and pulmonary congestion from increased pressure in the pulmonary vessels indicate left ventricular failure ● Formerly referred to as congestive HF; not all cases of LVF involve fluid accumulation ● May be acute or chronic and mild to severe. ● Two types: o Systolic: heart cannot contract forcefully enough during systole to eject adequate amounts of blood into the circulation o Diastolic: left ventricle cannot relax adequately during diastole- ventricle can not fill with sufficient blood to ensure an adequate cardiac output ▪ Right sided heart (ventricular) failure may be caused by left ventricular failure, right ventricular MI, or pulmonary HTN (cor pulmonale). The right ventricle cannot empty completely. Increased volume and pressure develop in the venous system and peripheral edema results. o diagnosis ▪ Labs: ● Electrolytes - may occur from complications or diuretics ● Hgb and HCT - identify HF resulting from anemia ● BNP - used when dyspnea to r/o HF ● U/A - proteinuria/high specific gravity ● ABGs- respiratory acidosis ▪ B-type natriuretic peptide (BNP) ● is used for diagnosing HF (in particular, diastolic HF), in patients with acute dyspnea ▪ Microalbuminuria ● An early indicator of decreased compliance of the heart and occurs before the BNP rises ▪ CXR ● “early warning detector” that lets HCP know that the heart is experiencing early signs of decreased compliance long before symptoms occur ● Helpful in diagnosing left ventricular failure because the heart is enlarged, representing hypertrophy or dilation ▪ Echocardiography ● Best tool in diagnosing HF- ejection fraction between 50-70% ● Cardiac valvular changes, pericardial effusion, chamber enlargement, and ventricular hypertrophy can be diagnosed with this noninvasive technique ● Can also be used to determine ejection fraction ▪ Hemodynamic Monitoring ● PA catheter allows for assessment of cardiac function and fluid volume ● PAP (positive airway pressure) /PAWP (pulmonary artery wedge pressure) elevated with L sided HF because volumes and pressures are increased in the left ventricle o s/s ● ▪ Left HF: ● Decreased cardiac output: o Fatigue, weakness, oliguria during the day (nocturia at night), angina, confusion, restlessness, dizziness, tachycardia, palpitations, pallor, weak peripheral pulses, cool extremities o Priority problems: ▪ Impaired gas exchange r/t ventilation/perfusion imbalance ▪ Decreased cardiac output r/t altered contractility, preload, and afterload ▪ Fatigue/weakness r/t hypoxemia ▪ Potential for pulmonary edema r/t L sided HF ● Pulmonary congestion: o Hacking cough, worse at night, dyspnea/breathlessness, crackles or wheezes in lungs, frothy, pink-tinged sputum, tachypnea, s3 s4 summation gallop ▪ Right HF: ● jugular neck vein distention, enlarged liver and spleen, anorexia and nausea, dependent edema (legs and sacrum), distended abdomen, swollen hands and fingers, polyuria at night, weight gain, increased BP from excess volume or decreased BP from failure o treatment ▪ Drugs: ● ACE inhibitors: increase stroke volume (can cause hyperkalemia) ● ARBs: block aldosterone decreased fluid overload (can cause hyperkalemia) ● Human BNP: increases sodium loss in renal tubules ● Diuretics: reducing sodium and water retention to decrease the workload of the heart o Loop and thiazide ● Venous vasodilators - nitrates: nitrate free periods to reduce tolerance ● Digoxin: o Increased contractility, decreased HR, slowing of conduction through AV node, inhibition of sympathetic activity o Possibility of toxicity ● Beta-adrenergic blockers: o Improve morbidity, mortality, and QOL for patients o Helps to increase activity tolerance o Improvement in symptoms ● Morphine sulfate: o Reduce anxiety, decrease preload and afterload, slow respirations, and reduce pain associated with MI ▪ Nutrition therapy: ● Sodium and fluid restrictions ▪ CPAP: improve cardiac output and ejection fraction by decreased afterload and preload, BP, and dysrhythmias ▪ CRT-biventricular pacing: ● Synchronous ventricular contractions to improve EF, CO, and mean arterial pressure (EF less than 35%) ▪ Gene therapy: ● End-stage HF ● Replaces damaged genes with modified genes to improve regrown of cardiac cells ▪ Heart transplant ▪ VADs- ventricular assist devices o nursing interventions ▪ Promoting oxygenation and gas exchange: ● Ventilation assistance ● Monitor RR q 1-4 hr ● Auscultate breath sounds q 4-8hr ● Position in high Fowler’s if patient dyspneic ● Maintain oxygen sat of 90% o education ▪ Activity schedule, indications of worsening or recurrent HF, drug therapy, nutrition therapy, advanced directives, energy management ▪ MAWDS (medications, activity, weight, diet, symptoms) ▪ Indications of worsening or recurrent HF ● Rapid weight gain (3lbs in a week or 1-2 lbs overnight) ● Decrease in exercise tolerance ● Cold symptoms lasting more than 3-5 days ● Excessive awakening at night to urinate ● Development of dyspnea/angina at rest ● Increased edema in feet, ankles, and hands ● MI o s/s ▪ substernal chest pain / pressure radiating to left arm ▪ Pain / discomfort in jaw, back, shoulder, abdomen ▪ Pain lasting 30 min + ▪ N/V ▪ Diaphoresis, dizziness, disorientation ▪ Dyspnea, fatigue ▪ Fear & anxiety ▪ Dysrhythmias, palpitations ▪ Epigastric distress ▪ Feeling “short of breath” o diagnosis: EKG o treatment: MONA, heparin, beta blockers, ca+ channel blockers, nitro, o nursing interventions o education ● MONA o Morphine, Oxygen, Nitroglycerin, Aspirin ● Valvular disorders (mitral regurgitation, aortic stenosis, mitral stenosis, aortic regurgitation, mitral valve prolapse) causes, s/s, treatment, diagnosis, complications, nursing interventions o Mitral Stenosis: ▪ Valve leaflets fuse and become stiff narrowing valve opening and preventing blood flow from the left atrium to left ventricle ▪ Increases pressure in left atrium leading to R ventricular hypertrophy ▪ Pulmonary congestion and R sided HF first ▪ Later, left HF and reduced CO ▪ S/S: ● Mild usually asymptomatic ● As narrows: o DOE, orthopnea, PND, palpitations, dry cough, hemoptysis, and further signs of right HF o Rumbing, diastolic murmur o Mitral Regurgitation (insufficiency) ▪ Prevent mitral valve from closing completely during systole allowing backflow of blood into left atrium when left ventricle contracts ▪ Left ventricular hypertrophy to compensate for increased volume and pressure ▪ S/S: ● Remain symptom free for decades ● Atrial fibrillation ● High-pitched systolic murmur at apex with radiation to left axilla o Mitral Valve Prolapse (MVP) “clicks” ▪ Valvular leaflets enlarge and prolapse into left atrium during systole ▪ Marfan syndrome (tall man- “abe lincoln is the MVP”) and familial tendency ▪ S/S: ● Most asymptomatic ● May have CP, palpitations, exercise intolerance ● Midsystolic click and late systolic murmur at apex of heart o Aortic Stenosis: ▪ Most common cardiac valve dysfunction in US ▪ Aortic valve opening narrows and obstructs left ventricle outflow during systole ▪ Ventricular hypertrophy ▪ S/S: ● Signs of L HF ● Dyspnea, angina, syncope on exertion ● Systolic crescendo-decrescendo murmur o Aortic Regurgitation (insufficiency) ▪ Aortic valve leaflets do not close properly during diastole ▪ Allows flow of blood from aorta back into the left ventricle during diastole ▪ L ventricular hypertrophy ▪ S/S: ● Asymptomatic for many years ● Signs of L HF ● High-pitched, blow, decrescendo diastolic murmur o MR ASS twerks - systolic ▪ Mitral regurgitation (axilla) ▪ Aortic stenosis (neck) ▪ RADIATES o MS ARD - diastolic ▪ Mitral stenosis ▪ Aortic regurgitation o Assessment of Valve Disease: ▪ Hx of rheumatic disease and infective endocarditis ▪ S/S: ● Fatigue, activity tolerance, angina, dyspnea, palpitations ▪ Echocardiogram o Interventions of Valvular Disease ▪ Nonsurgical: ● Drug therapy: Diuretics, beta blockers, ACEI, digoxin, and oxygen to improve symptoms of HF ● CCB for aortic or mitral stenosis to reduce regurgitant flow ● lifelong ABX (prior to dental procedures) ▪ Prophylactic antibiotics therapy ● Prior to invasive dental or oral procedure ▪ Balloon valvuloplasty ▪ Valve replacement: ● Stop anticoagulants at least 72 hrs prior to surgery ● Management post-op pain, incision care, infection prevention ● Mechanical valves require anticoagulation lifelong (goal 3-4 INR) o Care Coordination and Transition Management ▪ Home care - may require home health nurse ▪ Self-care: ● Possibility of HR, drug therapy, prophylactic abx use, activity plan for rest ● Teaching related to Vit K when on Coumadin (Warfarin) ● Can usually return to normal activity after 6 weeks, but no heavy lifting with arms for 3-6 months ▪ Wallet card, ID bracelet ● Pulmonary edema o Life-threatening event that can result from severe HF (with fluid overload), acute MI, mitral valve disease, and possibly dysrhythmias o The L ventricle fails to eject sufficient blood, and pressure increases in the lungs as a result. The increased pressure causes fluid to leak across the pulmonary capillaries and into the lung airways and tissues o S/S: o Tx: ▪ Crackles, dyspnea at rest, disorientation or acute confusion (especially in older adults as early symptom), tachycardia, HTN or hypotension, reduced urinary output, cough with frothy, pink-tinged sputum, premature ventricular contractions and other dysrhythmias, anxiety, restlessness, lethargy ▪ Diuretics: Furosemide or Bumetanide ▪ Morphine: if patients BP is adequate ▪ In severe cases of fluid overload and renal dysfunction or diuretic resistances, ultrafiltration may be used ● Ultrafiltration can remove up to 500mL/hr and uses a blood flow rate of 10-40mL/hr ● Decrease in cardiac filling pressures, decrease in pulmonary arterial pressure, increase in cardiac index, reduction in norepinephrine, rennin, and aldosterone ● Infective endocarditis o Microbial infection involving the endocardium o causes/risk factors: ▪ IV drug abusers ▪ Valve replacement recipients ▪ Systemic infections ▪ Structural cardiac defects: blood may flow from a high pressure area to a low pressure area eroding a section of the endocardium ▪ HIGH MORTALITY RATE o s/s: Fever, murmur, heart failure (most common complication), arterial embolization, splenic infarction, neurological changes, petechiae, splinter hemorrhages o diagnosis ▪ Positive blood cultures ▪ New regurgitant murmur ▪ Evidence of endocardial involvement by echocardiography o treatment ▪ Nonsurgical: ● Antimicrobials ● Activities balanced with adequate rest ▪ Surgical: ● Removal of infected valve ● Repair or removal of congenital shunts ● Repair of injured valves and chordae tendineae ● Draining of abscess in heart or elsewhere o nursing interventions ● Pericarditis o Inflammation or alteration of pericardium (membranous sac that encloses the heart) o causes ▪ Acute pericarditis is most commonly associated with: ● Infective organisms (bacteria, viruses, or fungi, usually respiratory) ● Post-myocardial infarction syndrome (Dressler’s syndrome) ● Postpericardiotomy syndrome ● Acute exacerbations of systemic connective tissue disease o s/s ▪ Substernal precordial pain ● Radiating to left side of neck, shoulder, or back ● Grating, oppressive pain, aggravated by breathing, coughing, swallowing ● Pain worsened by supine position; relieved by sitting up and leaning forward ▪ Pericardial friction rub ▪ May have elevated WBC and fever o treatment ▪ NSAIDs for pain ▪ Corticosteroid therapy - pts who do not have bacterial pericarditis ▪ Colchicine 0.5 mg orally twice a day for 3 months has been shown to prevent pericarditis recurrence ▪ Bacterial pericarditis (acute) usually requires antibiotics and pericardial drainage ▪ Chronic pericarditis may be caused by malignant disease my need radiation or chemo ▪ Uremic pericarditis is treated by hemodialysis ▪ The definitive treatment for chronic constrictive pericarditis is surgical excision of the pericardium - pericardiectomy o nursing interventions ▪ Patient should sit upright and leaning slightly forward for comfort ▪ NSAIDs for pain management ▪ antibiotics for bacterial form o complications ▪ Pericardial effusion: which occurs when the space between the parietal and visceral layers of the pericardium fills with fluid ● This complication puts the patient at risk for cardiac tamponade, or excessive fluid within the pericardial cavity ▪ Cardiac tamponade may occur when small volumes of fluid accumulate rapidly in the pericardium and cause a sudden decrease in cardiac output ● If the fluid accumulates slowly, the pericardium may stretch to accommodate several hundred mL of fluid ● S/S: ● Pericardial effusion o Restlessness o Tachycardia - always first sign of low cardiac output o Jugular vein distention o Paradoxical pulse - systolic BP 10mm Hg or more higher on expiration than on inspiration = narrow pulse pressure o Decreased HR, dyspnea, and fatigue o Muffled heart sounds o Hypotension o Pericardial effusion: which occurs when the space between the parietal and visceral layers of the pericardium fills with fluid ▪ This complication puts the patient at risk for cardiac tamponade, or excessive fluid within the pericardial cavity o Cardiac tamponade may occur when small volumes of fluid accumulate rapidly in the pericardium and cause a sudden decrease in cardiac output ▪ If the fluid accumulates slowly, the pericardium may stretch to accommodate several hundred mL of fluid ▪ S/S: ● Jugular vein distention ● Paradoxical pulse - systolic BP 10mm Hg or more higher on expiration than on inspiration ● Decreased HR, dyspnea, and fatigue ● Muffled heart sounds ● Hypotension o Cardiac tamponade is an emergency ▪ Manage the decreased CO with increased fluid volume administration while awaiting an echocardiogram or x-ray to confirm the diagnosis ▪ Tests are not always helpful because the fluid volume around the heart may be too small to visualize ▪ Hemodynamic monitoring in a specialized critical care unit usually demonstrates compression of the heart, with all pressures (right atrial, pulmonary artery, and wedge) being similar and elevated (plateau pressures) ▪ Pericardiocentesis: removes fluid and relieve the pressure on the heart ● Pressures should return to normal as the fluid compressing the heart is removed and the s/s of tamponade should resolve ● Cardiomyopathy o Disease of the heart muscle that makes it harder for your heart to pump out blood to the rest of your body o Can lead to HF o types: ▪ dilated: most common, both ventricles dilated, systolic function impaired, decreased cardiac output ▪ hypertrophic: ventricular hypertrophy, diastolic filling abnormalities, (athletes who die suddenly) ▪ restrictive: rare, stiff ventricles that restrict filling during diastole ● Tx like HF ▪ arrhythmogenic right ventricular o s/s: ▪ dilated: fatigue, weakness, LSHF, heart block, dysrhythmias, systemic or PE,s3/s4 gallops, cardiomegaly ▪ hypertrophic non-obstructed: dyspnea, angina, fatigue, syncope, palpitations, cardiomegaly, s4 gallop, ventricular dysrhythmias, sudden death, HF ▪ hypertrophic obstructed: (same as non-obstructed) + mitral regurgitation murmur, aFib o diagnosis o treatment ▪ dilated: tx symp. HF, vasodilators, control dysrhythmias, heart transplant ▪ hypertrophic: tx symptoms, beta blockers, aFib conversion, ventriculomyotomy w. mitral valve replacement o nursing interventions ● Heart transplants o nursing interventions ▪ immunosuppressants, s/s rejection, potential for tamponade o education ▪ rejection: SOB, fatigue, weight gain (fluid), abdominal bloating, new bradycardia, hypoTN, aFib or atrial flutter, decreased activity tolerance, decreased ejection fraction (late sign) ● Hypertension o causes ▪ Primary: family hx, Af. Am, hyperlipidemia, smoking, > 60 y/o, postmenopausal, excessive Na+ or caffeine intake, obese, overweight, physical inactivity, excessive alcohol intake, LOW potassium- mg+ - Ca+ intake, stress ▪ Secondary: kidney disease, primary aldosteronism, pheochromocytoma, cushing’s disease, coarctation of the aorta, brain tumors, encephalitis, pregnancy, drugs (estrogen -OCs, glucocorticoids, mineralocorticoids) o s/s: typically no symptoms ▪ h/a, facial flushing, dizziness, fainting o treatment ▪ lifestyle modifications ▪ drug therapy: diuretics (spironolactone, furosemide, hydrochlorothiazide), calcium channel blockers (verapamil), beta blockers (metoprolol), ACE inhibitors (lisinopril, enalapril, captopril), ARBs (losartan) ● vasodilation decreases BP o nursing interventions o complications ▪ target organ damage ▪ HTN crisis (BP > 180/120) ● give O2 ● admin IV antiHTN (nitroprusside, nicardipine, fenoldopam, labetalol) ● high fowler’s ● IV NS slowly ● monitor BP Q5-15m until diastolic <90, then monitor Q30m o education ▪ fruits, veggies, whole grains, low fat diet ▪ limit sweets, sugar beverages, red meats ▪ low sodium < 2400 mg/day ▪ aerobic physical activity 3-4x week for 40 minutes each ▪ decrease modifiable risk factors ● Atherosclerosis: plaque formation w/i arterial wall- leading risk factor for CVD o s/s ▪ extremity cool to touch w. diminished pulse & cap refill ▪ bruits in large arteries ▪ elevated lipids, cholesterol, triglycerides ● ^ LDL, decreased HDL o diagnosis: cholesterol screening + hx o treatment: lifestyle changes - modifiable risk factors (smoking, weight mgmt, exercise) ▪ diet to reduce LDL levels ● ^ intake fruits, veggies, whole grains ● low fat diet ● 5-6% Kcal from saturated fat ● reduce intake of trans fats ● fiber 30g/ day ● physical activity 3-4 times weekly for 40 minutes ▪ cholesterol lowering agents (“statins”, ezetimibe- inhibits cholesterol absorption) o complications: arterial occlusion ● Peripheral artery disease: causes decreased perfusion to tissues o Having trouble getting blood flow to the legs o Main cause is atherosclerosis o Risk factors: ▪ HTN, DM, smoking, obesity, hyperlipidemia o s/s ▪ stage I: asymptomatic, pedal pulses decreased or absent ▪ Stage 2: claudication, muscle pain = cramping or burning w. exercise but relieved with rest ▪ Strage 3: rest pain- awakens pt at night, pain (numbness, burning), distal part of extremity, relieved by placing extremity in dependent position ▪ Stage 4: necrosis/gangrene, ulcers & blackened tissue on toes-forefoot-heel, gangrenous odor present ▪ Pain in leg during exercise, relieved when put in dependent position ▪ Decreased cap refill in toes ▪ Decreased pedal pulses ▪ Lack of hair on calves ▪ Thick toe nails ▪ Pallor with elevation ▪ Wounds that show up on toes that form ulcers or gangrene, thick eschard, dry o diagnosis: o treatment ▪ drug therapy ( antiplatelet agents, hemorheologic) ● Aspirin and clopidogrel to reduce blood viscosity ● Statins ▪ Surgeries: ● Angioplasty- balloon or stent ● Peripheral bypass graft o Graft occlusion: reduced peripheral pulses on feet, increase pain, extremities have pallor or cold temp o Compartment syndrome: numbness, pain with passive movement, edema, decreased pedal pulses, increased cap refill time o nursing interventions ▪ palpate pulses bilaterally ▪ Education: ● Walk until the point of pain, then stop and rest, and then walk a little more ● Avoid crossing legs or restrictive garments ● Maintain a warm environment with insulated socks ● Avoid cold, stress, caffeine, and nicotine which can lead to vasoconstriction ● Deep vein thrombosis o cause ▪ smoking, HTN, certain diseases resulting to scraping along the blood vessels thus a platelet plug is formed ▪ A blood clot that has formed in the lower legs like the calf or below the knee o s/s ▪ calf/groin tenderness or pain ▪ unilateral leg swelling ▪ localized edema ● CPR o treatment ▪ rest + preventative measures ▪ treatment goal: revolves along preventing dislodgement of clot → PE ▪ D- don't walk or move too fast (bed rest), no hot pads, only warm & moist, no leg massage ▪ V- venous return, elevate extremity ▪ T- teaching DVT prevention: ● Calf exercise ● Hydration ● Ambulation ● No long sitting (car, airplane, bedrest) ● Ted (tight knee length socks) & SCDs (sequential compression device) after clot has resolved ▪ During clot: ● Thrombectomy - removal of clot ● Fibrinolytics ▪ After clot: ● ▪ anticoagulants ▪ thrombectomy, ligation or external clips o complications ● Abdominal aortic aneurysm o s/s ▪ usually asymptomatic at first ▪ gnawing pain that is unaffected by movement, can last for hours or days ▪ pain in abdomen, flank, back ▪ pulsating abdominal mass o diagnosis: xray (eggshell), CT for size & location, aortic arteriography, u/s, o treatment ▪ maintain BP to avoid rupture ▪ Abdominal aortic aneurysm resection ▪ Thoracic aortic aneurysm repair ▪ Endovascular repair o nursing interventions o complications ▪ rupture > hypovolemic shock ● hypoTN, diaphoresis, decreased LOC, oliguria, loss of pulses distal to rupture, dysrhythmias ● Aortic dissection: blood enters aortic wall r/t sudden tear in aortic intima o s/s ▪ pain- ripping, stabbing, tearing o treatment ▪ eliminate pain, reduce BP, decrease velocity of left ventricular ejection o nursing interventions ● Sickle cell disease: chronic anemia, pain, disability, organ damage, increased risk for infection, & early death r/t poor perfusion o S/S ▪ decreased perfusion distal from occlusion leading to skin cool to touch & decreased cap refill, reduced or absent pulses ▪ pain ▪ fatigue, weakness, SOB ▪ pallor, cyanosis ▪ jaundice (RBC reduction = bilirubin release) ● darker skin pts assess roof of mouth, sclera ▪ ulcers lower legs, outer sides & inner aspect of ankle or shin ▪ hepatomegaly, splenomegaly - has a lumpy texture upon palpation ▪ proteinuria, CKD > kidney failure ▪ necrotic degeneration of joints ▪ low grade fever (during crises) ▪ seizure, stroke o treatment ▪ pain management ● large dose opioids o for acute pain episodes involving chest, back, abdomen, extremities ● 48 hrs IV analgesics o morphine, hydromorphone (Dilaudid) round the clock via PCA pump ▪ taper after obtaining relief then give PO ● Hydroxyurea- stimulates fetal hemoglobin possibly reducing pain & sickling episodes- INCREASES risk for leukemia ● hydration- oral or IV o reduces duration of pain episodes o 250 mL.hr for 4 hours ▪ prevent sepsis, multiple organ dysfunction syndrome, & death ● prophylaxis- Penicillin BID ● pneumococcal vaccination ● annual influenza vaccination ● O2- nebulized ● RBC transfusion ● Hematopoietic Stem Cell transplant (HSCT) for children - only “cure” o nursing interventions ▪ administer O2 & pain meds ▪ hydrate w/ NS IV & orally (except caffeine sources) ▪ remove constrictive clothing ▪ keep extremities extended to promote venous return ▪ do NOT raise the knee position of bed ▪ HOB < 30 degrees ▪ room temp kept around 72 F ▪ Q4h assess pulse ox fingers & toes, cap refill, peripheral pulses, toe temp o complications ▪ vaso-occlusive event (VOE) ● further tissue hypoxia ● more sickle shaped cells ● further blood vessel obstruction, inadequate perfusion, ischemia of affected tissues ▪ pulmonary HTN > pneumonia risk ▪ acute chest syndrome (common cause for hospitalization & death) ● fat embolism, pulmonary debris > respiratory infection ● SOB, cough, abnormal breath sounds, infiltrate on chest X-ray ▪ organ damage > death ▪ priapism > anuria o education ▪ causes of sickling: dehydration, hypoxia, infection ▪ autosomal recessive trait ▪ prevent crisis: ● drink 3-4L fluids daily ● avoid alcohol, tobacco ● avoid extremes in temperatures (too hot / too cold) ● avoid traveling to high altitude locations ● genetic counseling ● avoid strenuous physical activities o mild, low impact exercise >= 3 times weekly when not in crisis ● Polycythemia vera: viscous blood w/ ^ RBCs- cancer o causes ▪ massive production of RBCs ▪ excessive leukocyte production ▪ excessive platelet production o s/s ▪ facial skin: plethoric (flushed), cyanotic or purple, distended veins ▪ intense itching ▪ HTN (r/t slowwwww moving blood & ^ heart demands) ▪ Polycythemia vera, a condition in which too many RBCs are produced in the blood serum, can lead to an increase in the hematocrit and hypervolemia, hyperviscosity, and hypertension. Subsequently, the client can experience dizziness, tinnitus, visual disturbances, headaches, or a feeling of fullness in the head. The client may also experience cardiovascular symptoms such as heart failure (shortness of breath and orthopnea) and increased clotting time or symptoms of an increased uric acid level such as painful swollen joints (usually the big toe). Hearing loss and weight loss are not manifestations associated with polycythemia vera. o treatment ▪ apheresis (withdrawal whole blood, remove RBCs, plasma reinfused) ▪ increase hydration ▪ promote venous return - prevents clot formation ▪ anticoagulants o nursing interventions o complications ▪ thrombosis r/t vascular stasis > tissue hypoxia, anoxia, infarction & necrosis ● heart, spleen, kidneys o education ▪ 3L fluids daily ▪ avoid tight, restrictive clothing ▪ contact HCP at 1st sign of infection ▪ take anticoagulants as prescribed ▪ support hose or stockings when awake & up ▪ elevate feet when seated ▪ stop activity if chest pain occurs ▪ bleeding precautions ● NO flossing ▪ smoking cessation ● Hereditary hemochromatosis: autosomal-recessive disorder of HFE = increased intestinal absorption of iron o s/s ▪ abdominal pain ▪ hepatomegaly ▪ hyperglycemia ▪ gradual darkening of the skin ▪ LATE problems: ● diabetes, liver cirrhosis, endocrine gland failure, heart disease, death o treatment ▪ reduce overall iron load ● phlebotomy & removal of 500 mL blood at a time o twice weekly at first o GOAL: reduce blood ferritin levels (9-50 mcg/L) o nursing interventions ▪ education on genetic testing ● Myelodysplastic syndrome: formation of abnormal cells in bone marrow > decrease in all blood cell types (pancytopenia) o s/s ▪ anemia, neutropenia, thrombocytopenia o treatment ▪ allogeneic HSCT ▪ supportive care ● blood transfusions, platelet transfusions ● erythrocyte stimulating agents (ESA): eopoetin alfa, darbepoetin alfa o nursing interventions ▪ “precancerous state” pt education ▪ administer transfusions ● Leukemia: uncontrolled production of immature WBCs in bone marrow > reduced production of normal blood cells o causes ▪ risk factors: ionizing radiation exposures, chemicals & drugs, chemotherapy agents, genetic & immunity risk factors ▪ incidence increases with age o s/s ▪ excessive bleeding episodes ● bruise easily, increased menstrual flow, nosebleeds, gums bleeding, rectal bleeding, hematuria ▪ weakness, fatigue, anorexia, weight loss, fever ▪ h/a, behavior changes, decreased alertness, increased somnolence ▪ decreased attention span, muscle weakness ▪ murmurs, bruits, tachycardia, orthostatic hypTN, palpitations ▪ slow cap refill ▪ HTN + bounding pulse (extremely ^ WBCs & viscous blood) ▪ cough, dyspnea, abnormal breath sounds ▪ pallor, petechiae, open infected lesions ▪ occult blood, reduced bowel sounds, constipation, hematuria ▪ bone & joint tenderness, swelling ▪ seizures ▪ hepatomegaly, splenomegaly ▪ Labs: decreased Hct, low plts, abnormal WBC (mostly blast cells = poorer prognosis) o treatment ▪ stem cell transplant ▪ blood transfusion: for pts with fatigue - replace RBCs ▪ maintenance therapy: remission ▪ drug therapy ● combo chemotherapy o nursing interventions ▪ frequent handwashing ▪ strict asepsis ▪ private room to reduce cross-contamination ● HEPA filter ▪ consistently assessing for s/s infection ▪ monitor daily CBC with WBC diff. & absolute neutrophil count ▪ vitals Q4h ▪ culture specimens ▪ pulmonary hygiene Q2-4h (auscultate for wheezes, crackles) ● turn, cough, deep breath or incentive spirometer Q1h o education ▪ conserve energy ▪ importance of follow up care ▪ coordinate home care for pt ▪ hygiene & daily bathing o complications ▪ infection - major cause of death ● Stem cell transplants o allogeneic : someone else ▪ bone marrow harvest, umbilical cord blood, peripheral stem cell apheresis ▪ identical sibling is best ▪ two closely matched HLA pts ▪ blood match is NOT a concern, TISSUE type is what matters o autologous: self donation o complications ▪ death- need replacement of stem cells by transplantation to prevent infection or hemorrhage ▪ pancytopenia (low levels of ALL circulating blood cells) ▪ failure to engraft: donated cells fail to grow & function ● pt will die if another transplantation does not occur ▪ graft vs host disease (GVHD): donated marrow immunocompromised cells attack the recipient's cells, tissues, & organs ● usually affected: skin, eyes, GI tract, liver, genitalia, lungs, immune system, musculoskeletal system ▪ Veno-occlusive disease (VOD): blockage of liver vessels through phlebitis & clotting ● w/i first 30 days following transplant ● s/s: jaundice, RUQ pain, ascites, weight gain, hepatomegaly o education ▪ preventing infection ▪ poor clotting times = bleeding risk ● Lymphoma o hodgkin’s ▪ peaks in teens/young adults, adults in 50s-60s, more so in men ▪ Epstein-Barr virus, HIV possible causes ▪ starts in single lymph node, Reed-Sternberg Cells ▪ predictable spread from one lymph node/group to the next o non-hodgkin’s ▪ ALL lymphoid cancers that do NOT have reed-sternberg cells ▪ spreads in an unpredictable manner ▪ possible causes: solid organ transplants, immunosuppressive drug tx, HIV o s/s ▪ large, PAINLESS, lymph node(s) ▪ drenching night sweats ▪ unexpected weight loss ▪ some pts have NO symptoms o treatment ▪ very treatable & curable ▪ external radiation for Hodgkin’s ● sperm banking for young men ▪ monoclonal antibodies ▪ HSCT ▪ chemotherapy combo tx o education ▪ pancytopenia ● risk for infection & bleeding ● permanent sterility- sperm banking options ● secondary cancer development- need for continual follow-up ● Multiple myeloma: WBC cancer, plasma cell secretes antibodies, overtakes bone marrow, increases cancer cell growth o progressive bone destruction, bleeding issues, kidney failure, reduced immunity, death o chemotherapy, steroids, autologous stem cell transplant ● Autoimmune thrombocytopenic purpura: platelet PRODUCTION is NORMAL, with a massive DECREASE in CIRCULATING plts (plt destruction > platelet production) o causes: unknown, suspected viral infections o Diagnosis: low plts + ^ megakaryocytes in bone marrow o s/s ▪ 1st in skin + mucous membranes ● large bruises, mucosal bleeding easily ● petechial rash on arms, legs, upper chest, neck o treatment ▪ therapy for underlying conditions + protection from bleeding episodes ▪ IV anti-Rho - prevent destruction of antibody coated plts ▪ plt transfusions (when cts are <10,000) ▪ splenectomy (site of excessive plt destruction) o nursing interventions ▪ maintain safe env’t ● monitor any bleeding closely ● infection prevention ● bleeding precautions o complications ▪ intracranial stroke (bleeding-induced) ● assess LOC & neuro function ▪ poor clotting = bleeding risk o education ▪ vaccinations: meningococcal, pneumococcal, Haemophilus influenzae ▪ increased risk for infection (protocols) ▪ follow up with HCP ● Hemophilia: hereditary bleeding disorder (A- lacks factor VIII (8) & B- lacks factor IX (9)) o s/s ▪ excessive bleeding ▪ joint & muscle hemorrhage - disabling long term issues ▪ bruise easily o diagnosis: PROLONGED aPTT, normal PT o treatment ▪ regularly scheduled infusions of missing factor o nursing interventions o education ● Blood transfusions o nursing care before ▪ verify prescription with another RN, assess lab values ● type of product, dose, transfusion time ▪ assess pt vitals, output, skin color, hx of transfusion reaction ▪ test donor & recipient for compatibility (good for 72 hrs) ▪ central catheter or minimum 18 gauge needle ▪ verify pt identity w/ another RN ● name & number, blood compatibility, expiration time o during ▪ check blood tubing - NEED a filter & ONLY normal saline ▪ remain w/ pt for first 15-30 mins ▪ infuse at prescribed rate ▪ monitor vitals o and after transfusion ▪ dispose of bag & tubing properly after discontinuing infusion ▪ document o reactions: usually occur w. the first 50 mL of blood ▪ report chills, SOB, hives, itching, back pain ▪ hyperkalemia ▪ febrile: anti WBC antibodies ● chills, tachycardia, fever, hypoTN, tachypnea ▪ hemolytic: blood type or Rh incompatibility ● fever, chills ● DIC + circulatory collapse o apprehension, h/a, angina, low back pain, tachycardia, tachypnea, hypoTN, hemoglobinuria ▪ allergic: anaphylactic transfusion reaction ● urticaria, itching, bronchospasm ▪ bacterial: infusion or contaminated blood products ● tachycardia, hypoTN, fever, chills, shock o RAPID ▪ transfusion-related acute lung injury (TRALI) ● rapid onset of dyspnea & hypoxia w/i 6 hrs of transfusion ▪ transfusion-associated circulatory overload (TACO) ● infusion too quickly- whole blood or RBCs ● HTN, bounding pulse, JVD, dyspnea, restlessness, confusion ▪ transfusion-associated graft-versus-host-disease (TA-GVHD) ● life threatening- usually in immunocompromised pt ● symptoms w/i 1-2 weeks following infusion o thrombocytopenia, anorexia, N/V, chronic hepatitis, weight loss, recurrent infection ▪ acute pain transfusion reaction (APTR) ● during or shortly after ● severe chest pain, back pain, joint pain, HTN, anxiety, redness of head & neck o Nursing interventions for transfusion reactions ▪ STOP transfusion ▪ notify rapid response team ▪ Keep IV access- flush with NS ▪ apply O2 - give diphenhydramine via IV push ● Dysrhythmias- review the dysthymias that we covered in class- please be sure you are able to identify our serious dysrhythmias, causes, s/s, treatment, complications (i.e. SVT, afib, vtach, vfib, etc.) cause s/s treatment complications SVT stimulators, Atrial rate of 100 adenosine, beta angina. HF, caffeine, hypoxia, to 280 blockers, cardiogenic shock heart disease beats/minute, if cardioversion, the impulse calcium channel originates above blockers the ventricles, the P wave may not be visible especially if the rate is high because the P wave is often embedded in the preceding T wave. SVT is seen more often in women. Chest pain, low BP, lethargy, anxiety, palpitations, SOB, elevated HR, dizziness aFib underlying CVD atrial fibrosis, loss of muscle mass heart disease: HTN, HF, CAD no clear P waves, no atrial contractions, loss of atrial kick, irregular ventricular response long term anticoagulants antidysrhythmic drugs (amiodarone) cardioconversion embolic stroke, DVT, PE atrial rate of 350 to 600 beats/min with a ventricular response of 120 to 200 beats/min and irregular maze procedure bi-ventricular pacing cath. ablation irregular apical pulse, poor perfusion, decreased cardiac output = dyspnea, SOB, fatigue, weakness, dizziness, anxiety, syncope, palpitations, chest discomfort/pain cardioconversion, beta blockers, calcium channel blockers vTach hypoxia results from an cardioversion death MI irritable foci in the amiodarone hypokalemia ventricle at a rate lidocaine (no hypomagnesemia of 140 to 180 puse) caffeine beats/min. The immediate CPR + stimulants stress rhythm can be intermittent or defibrillation sustained vFib CAD results from CPR + LIFE valvular heart electrical chaos in defibrillation THREATENING disease the ventricles. epinephrine acid-base & This is a life- amiodarone electrolyte threatening lidocaine abnormalities dysrhythmia. The mag sulfate electrical shock ventricles are quivering, and there is no cardiac output or pulse, which results in loss of organ and tissue perfusion. ● Dosage and Calculation ● Prioritization ● Therapeutic communication ● Heparin induced thrombocytopenia: unexplained drop in platelet count after Heparin o cause: immune-mediated drug reaction caused by heparin-dependent platelet- activating immunoglobulin G (IgG) antibodies o UNFRACTIONATED heparin ▪ risks: duration longer than 1 week ▪ exposure to unfractionated heparin ▪ postsurgical thromboprophylaxis ▪ females o s/s: VTE (DVT, PE) o treatment: anticoagulation therapy ▪ management > direct thrombin inhibitor (argatroban, lepirudin) ● Lab values- INR, PT, PTT, platelets, WBC, etc related to hematological system o INR: 0.8-1.1 times the control ▪ WARFARIN 2.0-3.0 ▪ INCREASED: longer clotting time, w/ WARFARIN = expected ▪ DECREASED: hypercoagulation, risk for DVT o PT: 11-12.5 sec ▪ WARFARIN 18-24 seconds ▪ INCREASED = possible def. of clotting factors V & VII ▪ DECREASED = Vit K excess o aPTT: 1.5-2.0 times normal value ▪ Heparin tx: 60-80 seconds o platelets: 150,000 - 400,000 ▪ INCREASED: polycythemia vera, malignancy ▪ DECREASED: bone marrow suppression, autoimmune disease, hypersplenism o WBC: 5,000 - 10,000 o RBC: Females 4.2-5.4 million - Males 4.7-6.1 million ▪ INCREASED levels = chronic hypoxia, polycythemia vera ▪ DECREASED levels possible anemia, hemorrhage o Hgb: F 12-16 + M 14-18 o Hct: F 37-47% + M 42-52% ● Iron deficiency anemia o causes ▪ inadequate iron intake r/t iron-deficient diet, chronic alcoholism, malabsorption syndromes, partial gastrectomy ▪ rapid metabolic (anabolic) activity caused by: pregnancy, adolescence, infection o s/s ▪ microcytic ▪ weakness, pallor ▪ fatigue, exercise tolerance reduced ▪ fissures corners of mouth o treatment ▪ increase oral iron intake (kidney beans, red meat, organ meat, egg yolk, leafy green veggies, raisins) ▪ PO iron supplements (Vitamin C helps absorption) ▪ (aplastic anemia) HSCT with donor cells ▪ hydration, transfusions o education ● Anemia s/s o pallor (ears, nail beds, palmar creases, conjunctivae, around mouth) o skin cool to touch o cold intolerance o brittle nails / concaving o tachycardia, increases w/ activity & after meals o murmurs, gallops w/ SEVERE anemia o orthostatic hypoTN, h/a, increased fatigue o dyspnea on exertion, decreased O2 sat o Vitamin B12 s/s: glossitis, paresthesia hands & feet, jaundice [Show More]

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