Perfusion Learning Outcomes At the end of the lecture the student will: Identify risk factors for developing selected perfusion disorders. Articulate the recommended screening practices, laboratory and diagnostic studies for selected perfusion disorders. Discuss clinical manifestations of selected disorders of perfusion. Plan and prioritize nursing interventions for a patient with an alteration in perfusion. Develop a teaching plan, utilizing current research, for a patient with an alteration in perfusion. Apply principles of pharmacologic management to the care of patients with an alteration in perfusion. Discuss management of care for patients receiving transfusion therapy. Exemplars Peripheral Vascular Disease Arteriosclerosis & Atherosclerosis Hypertension Cardiovascular Disease Stable Angina Chronic Heart Failure Hematologic diseases Anemia Leukemia Perfusion Central Perfusion: a normal physiologic process that requires the heart to generate sufficient cardiac output to transport blood through patent blood vessels for distribution in the tissues throughout the body. Tissue perfusion refers to the flow of blood through target tissues. The blood flows through arteries and capillaries, delivering nutrients and oxygen to cells, and removing cellular waste products. Normal Physiological Process Central Perfusion Cardiac Output Preload Stroke Volume HR Afterload Contractility Impaired Central Perfusion Impairment of central perfusion occurs when cardiac output is inadequate. Conduction or valve problems Disease of the heart muscle Increased SVR (afterload)-HTN, Aortic stenosis Decreased SVR (afterload)-hemorrhage Reduced cardiac output results in a reduction of oxygenated blood reaching the body tissues (systemic effect). If untreated, leads to ischemia, cell injury and cell death If severe, associated with shock Impaired Tissue Perfusion Impaired tissue perfusion occurs when there is reduced blood flow to the target tissues through the arteries and capillaries. Poor central perfusion Blockage of the vessel leading to target organ or tissue Excessive edema interferes with cellular oxygen exchange Results of impaired tissue perfusion is impaired blood flow to target tissue Ischemia, irreversible cell injury and necrosis (cell death) Risk Factors Associated with Impaired Perfusion Increased age Male Genetics Congenital Heart Defects Cardiovascular Disease Peripheral Vascular Disease Impaired Perfusion Risk Factors Non-Modifiable Modifiable Age Smoking Sex Obesity Genetics Hyperlipidemia Ethnicity HTN DM Sedentary lifestyle Hypertension Copyright © 2020 by Elsevier, Inc. All rights reserved. 11 Hypertension Modifiable risk factor to prevent CVD As BP increases, so does the risk of: MI Heart failure Stroke Renal disease Retinopathy Affects ~46% adults in United States Heart disease associated with HTN leads to 23.7% of deaths in United States Copyright © 2020 by Elsevier, Inc. All rights reserved. 12 Hypertension Promoting health equity All ethnicities: Three factors for decreased prevalence Born outside United States; do not speak English; limited time living in United States Blacks Highest prevalence; more resistant HTN; develop at younger age; female greater than male; more nocturnal nondipping BP; more end-organ damage; highest death rate Less response to renin inhibiting meds; better control with calcium channel blockers and diuretics Increased risk of angioedema with ACE inhibitors Copyright © 2020 by Elsevier, Inc. All rights reserved. 13 Hypertension Promoting health equity Hispanics Less likely to receive treatment Lower rate of: awareness, treatment, and control Gender differences Men—more common before middle age Women increased 2-3x with oral contraceptives Preeclampsia—possible early sign More common after menopause; harder to control with older women Copyright © 2020 by Elsevier, Inc. All rights reserved. 14 Normal Regulation of Blood Pressure Blood pressure (BP)—force exerted by blood against walls of blood vessels Involves both systemic factors and peripheral vascular effects Important to maintain tissue perfusion during activity and rest. Function of cardiac output (CO) and systemic vascular resistance (SVR) CO = SV × HR Copyright © 2020 by Elsevier, Inc. All rights reserved. 15 Gu Copyright © 2020 by Elsevier, Inc. All rights reserved. 16 Audience Response Question The nurse determines that the patient has stage 2 hypertension when the patient’s average blood pressure is: (Select all that apply.) a. 150/96 mm Hg. b. 155/88 mm Hg. c. 172/92 mm Hg. d. 160/110 mm Hg. e. 182/106 mm Hg. Copyright © 2020 by Elsevier, Inc. All rights reserved. 17 Etiology of Hypertension Primary hypertension Also called essential or idiopathic HTN Elevated BP of unknown cause 90% to 95% of all cases Many contributing factors Altered endothelial function, increased SNS activity, increased Na+ intake, overproduction of Na+ retaining hormones, overweight, diabetes, tobacco, excess alcohol Copyright © 2020 by Elsevier, Inc. All rights reserved. 18 Etiology of Hypertension Secondary hypertension Elevated BP with a specific cause; sudden development 5% to 10% of adult cases Clinical findings relate to underlying cause (See Table 32-3 in the textbook) Cirrhosis; aortic problems; drug-related; endocrine, neurologic, or renal problems; pregnancy-induced, or sleep apnea Treatment aimed at removing or treating cause Copyright © 2020 by Elsevier, Inc. All rights reserved. 19 Risk Factors for Primary Hypertension Age Family history Alcohol use Obesity Tobacco use Ethnicity Diabetes Sedentary lifestyle Elevated serum lipids Socioeconomic status Excess dietary sodium Stress Gender Copyright © 2020 by Elsevier, Inc. All rights reserved. 20 Audience Response Question While performing blood pressure screening at a health fair, the nurse counsels which person as having the greatest risk for developing hypertension? a. A 56-year-old man whose father died at age 62 from a stroke b. A 30-year-old female advertising agent who is unmarried and lives alone c. A 68-year-old man who uses herbal remedies to treat his enlarged prostate gland d. A 43-year-old man who travels extensively with his job and exercises only on weekends Copyright © 2020 by Elsevier, Inc. All rights reserved. 21 Hypertension Clinical Manifestations “Silent killer”—asymptomatic until severe and target organ disease occurs Symptoms of severe hypertension Fatigue Dizziness Palpitations Angina Dyspnea Copyright © 2020 by Elsevier, Inc. All rights reserved. 22 Hypertension Complications Target organ diseases occur most frequently in: Heart Coronary Left ventricular hypertrophy (Fig. 32-4) Heart artery disease; atherosclerosis failure Brain—cerebrovascular disease TIA/Stroke; atherosclerosis Hypertensive encephalopathy; changes in autoregulation Copyright © 2020 by Elsevier, Inc. All rights reserved. 23 Left ventricular hypertrophy (A) Normal thickness (B) (Fig. 32-4) Copyright © 2020 by Elsevier, Inc. All rights reserved. 24 Hypertension Complications Peripheral vascular disease Atherosclerosis leads to PVD, aortic aneurysm, aortic dissection Intermittent claudication Kidney Nephrosclerosis disease (CKD) Eyes—retinal damage Blurry leads to chronic kidney or loss of vision; retinal hemorrhage Damaged retinal vessels indicate concurrent damage to vessels in heart, brain, and kidneys. Copyright © 2020 by Elsevier, Inc. All rights reserved. 25 Hypertension Diagnostic Studies Measurement of BP Labs to: 1) identify or rule out secondary HTN 2) evaluate target organ disease 3) determine CV risk 4) establish baselines before starting therapy (Table 32-5) Renal function, U/A, BMP, CBC, serum lipid profile, uric acid, ECG, ophthalmic exam Other; Echo, LFTs, TSH Ambulatory blood pressure monitoring (ABPM); avoids “white coat” HTN Noninvasive, fully automated system that measures BP at preset intervals over 12 to 24-hour period. Teach patient to hold arm still while device reads BP and keep diary of activities Copyright © 2020 by Elsevier, Inc. All rights reserved. 26 Hypertension Interprofessional Care Overall goals (Table 32-5) Achieve and maintain goal BP Reduce CV risk factors and target organ disease Lifestyle modifications AHA Life’s Simple 7: (1) Manage BP, (2) Control cholesterol, (3) Reduce blood sugar, (4) Get active, (5) Eat better, (6) Lose weight, (7) Stop smoking Copyright © 2020 by Elsevier, Inc. All rights reserved. 27 Hypertension Lifestyle Modifications Weight Reduction Dash Diet Low Sodium Dietary Intake Moderation of Alcohol Intake Physical activity Avoid tobacco products Management of risk factors Copyright © 2020 by Elsevier, Inc. All rights reserved. 28 Causes of Secondary HTN Neurological Increased Sleep Disorders ICP apnea Vascular: Coarctation of aorta Pregnancy Medications Renal Disease Hypertension: Drug Therapy High Blood Pressure Clinical Practice Guidelines—antihypertensive recommendations Age > 65, SBP > 130 mmHg, ambulatory in community setting: Goal SBP < 130 mmHg Age > 65, SBP >130 mmHg, care facility or multiple comorbidities or limited life expectancy: Goal—patient/team decision Age> 18 with HTN, known CVD or other risk factors: Goal—130/80 All others without CVD or other risk factors: Goal BP <130/80 Copyright © 2020 by Elsevier, Inc. All rights reserved. 30 Hypertension: Drug Therapy Two primary actions: Decrease circulating blood volume Reduce SVR See: Tables 32-6, 32-7, and 32-8 and Fig. 32-5 Copyright © 2020 by Elsevier, Inc. All rights reserved. 31 Sympathetic Nervous System Receptors Affecting BP Receptor Location Response When Activated α1 Vascular smooth muscle Vasoconstriction Heart Increased contractility (positive inotropic effect) Presynaptic nerve terminals Inhibition of norepinephrine release Vascular smooth muscle Vasoconstriction Heart Increased contractility (positive inotropic effect) Increased heart rate (positive chronotropic effect) Increased conduction (positive dromotropic effect) Juxtaglomerular cells of the kidney Increased renin secretion β2 Smooth muscle of blood vessels in heart (e.g., coronary arteries), lungs (e.g., bronchi), and skeletal muscle Vasodilation Dopamine receptors Primarily renal blood vessels Vasodilation α2 β1 Copyright © 2020 by Elsevier, Inc. All rights reserved. 32 Drug Therapy (Fig. 32-5) Copyright © 2020 by Elsevier, Inc. All rights reserved. 33 Hypertension: Drug therapy Beta Blockers Cardioselective: Blocks β1-adrenergic receptors, reduces BP by blocking β-adrenergic effects, decreases CO and reduce sympathetic vasoconstrictor tone, decreases renin secretion by kidneys (Metoprolol) Non-Cardioselective: Blocks β1- and β2-adrenergic receptors, reduces BP by blocking β1- and β2-adrenergic effects (Propranolol) Copyright © 2020 by Elsevier, Inc. All rights reserved. 34 Hypertension: Drug therapy Adrenergic inhibiting agents—Decrease SNS stimulation; work centrally on vasomotor center and peripherally to inhibit NE release or block adrenergic receptors on blood vessels (Prazosin) ACE Inhibitors—prevent conversion of angiotensin I to angiotensin II; reduce vasoconstriction and sodium and water retention (Lisinopril) A-II receptor blockers—prevent angiotensin II from binding to receptors in blood vessel walls (Losartan) Copyright © 2020 by Elsevier, Inc. All rights reserved. 35 Hypertension: Drug Therapy Calcium channel blockers (CCB)—increase Na+ excretion and cause arteriolar vasodilation by preventing the movement of extracellular Ca+ into cells (Amlodipine) Direct vasodilators—relax vascular smooth muscle and reduce SVR (Nitroglycerine) Diuretics—reduce plasma volume by increased sodium and water excretion and reduce vascular response to catecholamines (Loop: Furosemide; Potassium Sparing: Spironolactone; Thiazide: Hydrochlorothiazide) Copyright © 2020 by Elsevier, Inc. All rights reserved. 36 Hypertension: Drug Therapy Patient with HTN—nonpharmacologic treatment + 1 first line pharmacologic drug Patient with stage 2 HTN— nonpharmacologic therapy + 2 antihypertensives from two different classifications If a drug is not tolerated, then another classification will be used Monthly follow-up visits until at goal BP; then 3 to 6 months Stage 2 HTN or comorbidities—more frequent Copyright © 2020 by Elsevier, Inc. All rights reserved. 37 Hypertension: Drug Therapy Patient and caregiver education—*report all side effects; different medication may be tried if severe or undesirable; need to continue adherence to therapy Common side effects Orthostatic hypotension—feel dizzy or faint when change position Sexual problems—reduced libido or erectile dysfunction Dry mouth—sugarless gum or candy Frequent voiding—take diuretic early in the day to avoid getting up at night Copyright © 2020 by Elsevier, Inc. All rights reserved. 38 Chronic Stable Angina Chronic Stable Angina (CSA) Temporary imbalance between coronary artery’s ability to supply oxygen and cardiac muscle’s demand for oxygen Ischemia limited in duration Frequent, familiar Subsides with rest Assessment of Chest pain (P) Provocative What makes the symptom(s) better or worse? (Q) Quality Describe the symptom(s). (R) Region or Radiation Where in the body does the symptom occur? Is there radiation or extension of the symptom(s) to another area of the body? (S) Severity On a scale of 1-10 how bad is the symptom(s)? (T) Timing Does it occur in association with something else (e.g. eating, exertion, movement?) Chronic Stable Angina Treatment Home Rest SL Nitroglyercin Repeat every 5 minutes X3 If pain persists call 911 Acute setting EKG within 10min. of onset Monitor Frequent VS O2 2-4L via nc if Spo2 <94% NTG SL every 5 min X3 Nitroglycerin Sublingual Tablet or spray for angina Given every 5 minutes X 3 If pain not relieved notify MD/911 IV gtt for acute MI patient must have continuous cardiac monitoring, ICU level of care Potent vasodilator VS every 3-5 minutes Heart Failure Inability of heart to work effectively as a pump Major types: Left-sided Right-sided Etiology of Heart Failure Any interference with mechanisms regulating cardiac output (CO) Primary causes Conditions that directly damage the heart Precipitating causes Conditions that increase workload of the heart Copyright © 2020 by Elsevier, Inc. All rights reserved. 47 Risk Factors Primary risk factors Hypertension Modifiable risk factor If aggressively treated and managed, incidence of HF can be reduced by 50% CAD Co-morbidities contribute to development of HF Copyright © 2020 by Elsevier, Inc. All rights reserved. 48 Left-Sided Heart Failure Inability of the left ventricle to pump enough blood Pooling of blood in the left ventricle and atrium Eventually backing up into the pulmonary vasculature causing congestion Cardiac output Typical Causes Left-sided Heart Failure Hypertension Coronary Artery Disease Left Ventricular Myocardial Infarction Valvular Disease Aortic and Mitral valve stenosis/insufficiency Other Common Causes of HF Cause Mechanism Anemia ↓ O2-carrying capacity of the blood stimulating ↑ in CO to meet tissue demands, leading to increase in cardiac workload and increase in size of LV Bacterial endocarditis Infection: ↑ metabolic demands and O2 requirements Valvular dysfunction: causes stenosis or regurgitation Dysrhythmias May ↓ CO and ↑ workload and O2 requirements of myocardial tissue Hypervolemia ↑ Preload causing volume overload on the RV Hypothyroidism Indirectly predisposes to ↑ atherosclerosis. Severe hypothyroidism decreases myocardial contractility. Infection ↑ O2 demand of tissues, stimulating ↑ CO Nutritional deficiencies May ↓ cardiac function by ↑ myocardial muscle mass and myocardial contractility Obstructive sleep apnea Frequent nighttime apnea results in ↑ afterload, intermittent hypoxia, and ↑ sympathetic nervous system activity. Paget’s disease ↑ Workload of the heart by ↑ vascular bed in the skeletal muscle Pulmonary embolism ↑ Pulmonary pressure resulting from obstruction leads to pulmonary HTN, ↓ CO. Thyrotoxicosis Changes the tissue metabolic rate, ↑ HR and workload of the heart Left-Sided Heart Failure Clinical Manifestations Decreased Cardiac output Weakness Fatigue Dizziness/ lightheaded Restless/anxious Acute confusion Dysuria/Oliguria Pulmonary congestion Dyspnea Cough Pulmonary crackles Low SpO2 Pink frothy sputum Third heart sound (S3) Right ventricle cannot empty completely Increased volume and pressure in venous system and peripheral edema Causes: Left ventricular failure Right ventricular MI Pulmonary hypertension Pulmonary COPD ARDS emboli Right-sided Heart Failure Clinical manifestations Jugular vein distention (JVD) Increased abdominal girth Dependent edema Hepatomegaly Hepatojugular reflux Ascites Weight gain Fatigue Compensatory Mechanisms Sympathetic nervous system stimulation Increase in HR, BP = increase in CO increased preload Vasoconstriction increased afterload RAAS activation Reduced blood flow to the kidneys Sodium and H2O retention Chemical responses BNP-Brain-type natriuretic peptide Normal <100pg/ml Pituitary-ADH in response to low CO Myocardial hypertrophy Myocardial muscle wall thickening Classification Patient Assessment History Heart disease MI Rheumatic fever HTN Smoke Weight gain Current medications Activity tolerance Diet Sleep Assessment Subjective data Past health history Drugs Functional Health Patterns Sleep/Rest Elimination Cognitive/Perceptual Copyright © 2020 by Elsevier, Inc. All rights reserved. 61 Assessment Objective ata Skin color and temperature Edema Respiratory rate and sounds Frothy, blood-tinged sputum Heart rate and sounds Abdominal distention Changes in LOC Copyright © 2020 by Elsevier, Inc. All rights reserved. 62 Assessment of Heart Failure Laboratory Electrolytes Hemoglobin and hematocrit B-type natriuretic peptide (BNP) Urinalysis (proteinuria/high specific gravity) ABGs Assessment of Heart Failure Imaging CXR Echocardiography ECG Pulmonary artery catheter Pulmonary Edema http://www.heartf ailure.org/heartfailure/lungs/ Goals of Therapy Symptom relief Optimizing volume status Supporting oxygenation and ventilation Identifying and addressing causes Avoiding complications Teaching related to exacerbations Copyright © 2020 by Elsevier, Inc. All rights reserved. 66 Improving Gas Exchange Promoting oxygenation and gas exchange Ventilation assistance Monitor respiratory rate every 1-4 hr Auscultate breath sounds every 4-8 hr Position in high Fowler’s if patient dyspneic Maintain oxygen saturation of 90% Interventions that Reduce Preload Nutrition therapy Sodium restriction <2400mg/daily Fluid restriction 2L/daily Drug therapy Diuretics Loop, Thiazide, and K sparing Furosemide, HCTZ, Spironolactone Venous vasodilators Nitrates, IV, PO Morphine Drug Therapy Diuretics Decrease volume overload (preload) Loop diuretics—Furosemide Vasodilators Reduce circulating blood volume and improve coronary artery circulation IV nitroglycerin IV sodium nitroprusside IV nesiritide Copyright © 2020 by Elsevier, Inc. All rights reserved. 69 Drug Therapy Morphine Reduces preload and afterload Relieves dyspnea and anxiety Positive inotropes β-agonists (dopamine, dobutamine, norepinephrine [Levophed]) Phosphodiesterase inhibitors (milrinone) Digitalis Copyright © 2020 by Elsevier, Inc. All rights reserved. 70 Medications to Reduce Afterload ACE inhibitors Captopril, Lisinopril, Enalapril Angiotensin Receptor Blockers-ARB Losartan, Valsartan, Olmesartan Drugs that Affect Contractility Inotropic drugs Positive Negative Other + Inotropes Dobutamine Milrinone Digoxin Cardiac glycoside Positive Inotrope Negative Chronotrope Side effects: h/a, weakness, drowsiness Yellow halo ★ Beta- blockers Metoprolol, Carvedilol Not for use in acute heart failure Negative Inotrope Negative Chronotrope Indications for Worsening or Recurrent Heart Failure Rapid weight gain Decrease in exercise tolerance Excessive awakening at night to urinate Development of dyspnea/angina at rest Increased edema in feet, ankles, hands Patient Teaching Signs and symptoms of worsening HF Telehealth and device remote monitoring technology Therapeutic interventions can be implemented to avoid re-hospitalization Copyright © 2020 by Elsevier, Inc. All rights reserved. 74 Patient Teaching/Expected Outcomes Drug therapy Exercise Training/Cardiac Rehab Health Promotion Influenza & Pneumococcal Vaccines Pallative Care Expected outcomes for patient with HF Maintain adequate O2/CO2 exchange to meet O2 needs of the body Maintain adequate blood pumped by heart to maintain metabolic demands Reduction or absence of edema and stable baseline weight Achieve a realistic program of activity that balances with energy conserving activities Copyright © 2020 by Elsevier, Inc. All rights reserved. 75 Coronary Artery Disease Copyright © 2020 by Elsevier, Inc. All rights reserved. 76 Coronary Artery Disease (CAD) Occurs when there is decrease in perfusion to the myocardium Arteriosclerosis Atherosclerosis Leads to: Ischemia Infarction Risk Factors for CAD Non Modifiable Risk Factors Age Gender Ethnicity Genetics Copyright © 2020 by Elsevier, Inc. All rights reserved. 78 Risk Factors Major modifiable risk factors High serum lipids (Table 31-6) Cholesterol >200 mg/dL High-density lipoproteins (HDL) < 40 mg/dL Low-density lipoproteins (LDL) > 130 mg/dL High LDLs increase atherosclerosis and CAD Fasting triglycerides >150 mg/dL High HDLs prevent lipid accumulation in arteries High levels increase risk for CAD http://www.cvriskcalculator.com Copyright © 2020 by Elsevier, Inc. All rights reserved. 79 Risk Factors Major modifiable risk factors Hypertension (HTN) Normal BP <120/<80 mm Hg Elevated BP 120 to 129/<80 mm Hg Stage 1 HTN 130 to 139/80 to 89 mm Hg Stage 2 HTN >140/>90 mm Hg Lifestyle changes for elevated BP and HTN; treat stage 1 or 2 HTN with drugs (Table 32-5) Elevated BP—endothelial injury leads to left ventricular hypertrophy and reduced stroke volume Copyright © 2020 by Elsevier, Inc. All rights reserved. 80 Risk Factors Major modifiable risk factors Tobacco use Nicotine: Increased catecholamine results in increased HR and BP, peripheral vasoconstriction Increased LDL, decreased HDL, increased oxygen radicals—vessel inflammation and thrombosis Increased carbon monoxide—reduces O2 carrying capacity of Hgb Second-hand smoke - Increased CAD 25% to 30% Tobacco cessation Copyright © 2020 by Elsevier, Inc. All rights reserved. 81 Risk Factors Major modifiable risk factors Physical inactivity Lack of regular exercise 30 to 60 minutes brisk walking 5 days/week Obesity BMI > 30 kg/m2 Waist circumference > 40” men; 35” women Increased LDLs, triglycerides; HTN; insulin resistance Apple figure > CAD than pear figure Copyright © 2020 by Elsevier, Inc. All rights reserved. 82 Risk Factors Contributing modifiable risk factors Diabetes—2-4 × CAD Increased endothelial dysfunction Altered lipid metabolism, increased cholesterol and triglycerides Metabolic syndrome Multiple risk factors related to insulin resistance including central obesity, HTN, abnormal serum lipids, and high fasting blood glucose (Table 40-2) Copyright © 2020 by Elsevier, Inc. All rights reserved. 83 Risk Factors Contributing modifiable risk factors Psychologic states Type A personality Acute and chronic stress, depression, anxiety, hostility and anger, lack of social support results in increased SNS stimulation results in increased catecholamines results in endothelial injury, increased HR, increased force of myocardial contraction results in increased O2 demand Altered coagulation Copyright © 2020 by Elsevier, Inc. All rights reserved. 84 Risk Factors Contributing modifiable risk factors Increased homocysteine level Breakdown of essential amino acid methionine (protein) Damage endothelium, promote plaque buildup, enhance clotting Substance use Cocaine and methamphetamine results in coronary artery spasm resulting in chest pain and MI Copyright © 2020 by Elsevier, Inc. All rights reserved. 85 Audience Response Question (1 of 2) Two risk factors for coronary artery disease that increase the workload of the heart and increase myocardial oxygen demand are: a. obesity and smokeless tobacco use. b. hypertension and cigarette smoking. c. elevated serum lipids and diabetes. d. physical inactivity and elevated homocysteine levels. Copyright © 2020 by Elsevier, Inc. All rights reserved. 86 Audience Response Question (1 of 2) Which patient is most at risk for developing coronary artery disease? a. A patient with hypertension who smokes b. An overweight patient who uses smokeless tobacco c. A patient with diabetes who uses methamphetamines d. A sedentary patient with elevated homocysteine levels Copyright © 2020 by Elsevier, Inc. All rights reserved. 87 Interprofessional and Nursing Care Health promotion Identifying high-risk persons Health history, including family history Presence of cardiovascular symptoms Lifestyle patterns Psychosocial history Employment history Values and beliefs about health and illness; education and literacy Copyright © 2020 by Elsevier, Inc. All rights reserved. 88 Interprofessional and Nursing Care Managing high-risk persons Prevention: control modifiable risk factors Encourage lifestyle changes Education Clarify personal values Set realistic goals Copyright © 2020 by Elsevier, Inc. All rights reserved. 89 Interprofessional and Nursing Care Physical activity FITT formula: Frequency, Intensity, Type and Time 30 minutes most days plus weight training 2 days/wk Regular physical activity helps with: Weight reduction Reduction Increase of systolic BP in HDL cholesterol Copyright © 2020 by Elsevier, Inc. All rights reserved. 90 Interprofessional and Nursing Care Nutritional Therapy See: Tables 33-4, and 33-5 Reduced Saturated fats and cholesterol Increased Complex carbohydrates and fiber Reduced Red meat, egg yolks, and whole milk Increased Omega-3 fatty acids Copyright © 2020 by Elsevier, Inc. All rights reserved. 91 Audience Response Question The nurse determines that teaching about implementing dietary changes to decrease the risk of CAD has been effective when the patient says, a. “I should not eat any red meat such as beef, pork, or lamb.” b. “I should have some type of fish at least 3 times a week.” c. “Most of my fat intake should be from olive oil or the oils in nuts.” d. “If I reduce the fat in my diet to about 5% of my calories, I will be much healthier.” Copyright © 2020 by Elsevier, Inc. All rights reserved. 92 Interprofessional and Nursing Care Lipid-lowering drug therapy Lipid profile screening Statin therapy recommended: Patients LDL with known CVD cholesterol > 190 mg/dL Age 40 to 75 with diabetes and LDL 70 to 189 mg/dL Age 40 to 75 with LDL 70 to 189 mg/dL and 10-year risk for CVD at least 7.5% Copyright © 2020 by Elsevier, Inc. All rights reserved. 93 Interprofessional and Nursing Care HMG-CoA Reductase Inhibitors (Statins) atorvastatin (Lipitor) fluvastatin (Lescol XL) lovastatinpitavastatin (Livalo) pravastatin (Pravachol) rosuvastatin (Crestor) simvastatin (Zocor) Copyright © 2020 by Elsevier, Inc. All rights reserved. 94 Gerontologic Considerations: CAD Increased incidence and mortality associated with CAD in older adults Strategies to reduce risk and treat CAD are effective Treat: hypertension and increased lipids Smoking cessation, increased physical activity Most likely to change when hospitalized or have chest pain Copyright © 2020 by Elsevier, Inc. All rights reserved. 95 Peripheral Artery Disease Copyright © 2020 by Elsevier, Inc. All rights reserved. 96 Peripheral Artery Disease (PAD) Involves thickening of the artery walls and progressive narrowing of arteries of upper and lower extremities Symptomatic age 60 to 80; earlier with diabetes In United States, 8.5 million have PAD prevalence with blacks Strongly related to other cardiovascular disease (CVD) and risk factors Higher risk of mortality, CVD mortality, major coronary events and stroke Copyright © 2020 by Elsevier, Inc. All rights reserved. 97 Etiology and Pathophysiology Atherosclerosis is leading cause in majority of cases Gradual thickening of the intima and media due to cholesterol and lipid deposits Exact cause unknown; inflammation and endothelial injury play a major role; See Fig. 33-1 (next slide) Copyright © 2020 by Elsevier, Inc. All rights reserved. 98 Fig. 33-1 Pathogenesis of Atherosclerosis Copyright © 2020 by Elsevier, Inc. All rights reserved. 99 Etiology and Pathophysiology Risk factors: Tobacco use Atherosclerosis Diabetes HTN High cholesterol Age greater than 60 See Gender Differences Box Multiple risk factors increase the risk of PAD Atherosclerosis often affects coronary, carotid, and lower extremity arteries Symptoms occur when arteries are 60% to 75% blocked Copyright © 2020 by Elsevier, Inc. All rights reserved. 100 PAD of Lower Extremities Fig. 37-1 Common Sites of Atherosclerotic Lesions Copyright © 2020 by Elsevier, Inc. All rights reserved. 101 Clinical Manifestations Classic symptom of PAD—intermittent claudication Ischemic muscle pain that is caused by a constant level of exercise Build up of lactic acid from anaerobic metabolism Resolves within 10 minutes or less with rest Reproducible Copyright © 2020 by Elsevier, Inc. All rights reserved. 102 Clinical Manifestations Paresthesia Numbness or tingling in the toes or feet from nerve tissue ischemia Neuropathy causes severe shooting or burning pain Produces loss of pressure and deep pain sensations from reduced blood flow Injuries often go unnoticed by patient Copyright © 2020 by Elsevier, Inc. All rights reserved. 103 Clinical Manifestations Reduced blood flow to limb: Thin, shiny, and taut skin Loss of hair on the lower legs Diminished or absent pedal, popliteal, or femoral pulses Pallor of foot with leg elevation Reactive hyperemia of foot with dependent position Copyright © 2020 by Elsevier, Inc. All rights reserved. 104 Clinical Manifestations Pain at rest Progressive disease Occurs in feet or toes Aggravated by limb elevation Occurs from insufficient blood flow to distal tissues Occurs more often at night Pain relief by gravity Copyright © 2020 by Elsevier, Inc. All rights reserved. 105 Complications Prolonged ischemia leads to: Atrophy of skin and underlying muscles Delayed healing Wound infection Tissue necrosis Arterial ulcers over bony prominences See: Table 37-1 Copyright © 2020 by Elsevier, Inc. All rights reserved. 106 Complications Most serious: Nonhealing arterial ulcers and gangrene Collateral circulation may prevent gangrene May result in amputation If adequate blood flow is not restored and if severe infection occurs Indicated with uncontrolled pain and spreading infection Copyright © 2020 by Elsevier, Inc. All rights reserved. 107 Diagnostic Studies (Table 372) Doppler ultrasound Duplex imaging Bidirectional, color Doppler Ankle-brachial index (ABI) (Table 37-3) Segmental blood pressure Done using a hand-held Doppler Angiography and magnetic resonance angiography (Table 31-7) Copyright © 2020 by Elsevier, Inc. All rights reserved. 108 Interprofessional Care Risk Factor Modification Goal: reduce CVD risk factors BP control (reduce sodium; DASH diet) Tobacco cessation (Tables 10-3 to 10-6) Hemoglobin A1C <7.0% for diabetics Aggressive treatment of hyperlipidemia—diet and statins Copyright © 2020 by Elsevier, Inc. All rights reserved. 109 Interprofessional Care Drug Therapy ACE inhibitors—reduce PAD symptoms Ramipril (Altace) Decreases cardiovascular morbidity Decreases mortality Increases peripheral blood flow Increases ABI Increases Walking distance Copyright © 2020 by Elsevier, Inc. All rights reserved. 110 Interprofessional Care Drug Therapy Antiplatelet agents Aspirin Clopidogrel (Plavix) See Drug Alert Copyright © 2020 by Elsevier, Inc. All rights reserved. 111 Interprofessional Care Drug Therapy Drugs prescribed for treatment of intermittent claudication Cilostazol (Pletal)—See Drug Alert Inhibits platelet aggregation Increased vasodilation Pentoxifylline (Trental) Improves flexibility of RBCs and WBCs Decreases fibrinogen concentration, platelet adhesiveness, and blood viscosity Copyright © 2020 by Elsevier, Inc. All rights reserved. 112 Interprofessional Care Exercise Therapy Walking is most effective exercise for individuals with claudication 30 to 45 minutes daily, 3 times/wk Women have faster decline and mobility loss than men Daily exercise increases survival rates Copyright © 2020 by Elsevier, Inc. All rights reserved. 113 Interprofessional Care Nutritional Therapy BMI <25 kg/m2 Waist circumference is less than 40 in for men and less than 35 in for women 3% to 5% weight loss yields reduced triglycerides, glucose, A1C, and decreased risk of type 2 diabetes Recommend reduced calories and salt for obese or overweight persons Copyright © 2020 by Elsevier, Inc. All rights reserved. 114 Nursing Management Planning Overall goals for patient with PAD Adequate tissue perfusion Relief of pain Increased exercise tolerance Intact, healthy skin on extremities Increased knowledge of disease and treatment plan Copyright © 2020 by Elsevier, Inc. All rights reserved. 115 Nursing Management Nursing Implementation Health promotion Acute care Ambulatory care Copyright © 2020 by Elsevier, Inc. All rights reserved. 116 Nursing Management Evaluation Adequate peripheral tissue perfusion Increased activity tolerance Effective pain management Knowledge of disease and treatment plan Copyright © 2020 by Elsevier, Inc. All rights reserved. 117 Acute Arterial Ischemic Disorders Copyright © 2020 by Elsevier, Inc. All rights reserved. 118 Acute Arterial Ischemic Disorders Etiology and pathophysiology Sudden interruption in arterial blood supply to a tissue, organ, or extremity. If untreated, can result in tissue death Causes: embolism, thrombosis, or trauma Copyright © 2020 by Elsevier, Inc. All rights reserved. 119 Clinical Manifestations 6 P’s Pain Pallor Pulselessness Paresthesia Paralysis (late sign) Poikilothermia Immediate intervention needed to avoid ischemia, necrosis, and gangrene Copyright © 2020 by Elsevier, Inc. All rights reserved. 120 Venous Thrombosis Formation of a thrombus (clot) with vein inflammation Most common venous disorder Superficial vein thrombosis Deep vein thrombosis (DVT) See Table 37-7 for comparison Venous thromboembolism (VTE) DVT to pulmonary embolism (PE) Copyright © 2020 by Elsevier, Inc. All rights reserved. 121 Venous Thrombosis: Etiology Virchow’s triad (Fig. 37-9) Venous stasis Damage to endothelium Hypercoagulability of blood Risk factors for VTE: Table 37-8 Copyright © 2020 by Elsevier, Inc. All rights reserved. 122 Fig. 37-9 Pathophysiology of VTE Copyright © 2020 by Elsevier, Inc. All rights reserved. 123 VTE Deep veins of arms or legs, pelvis, vena cava, and pulmonary system Manifestations (Table 37-7) Lower extremity Unilateral edema Pain, tenderness with palpation Dilated superficial veins Full sensation in thigh or calf Paresthesias Red, warm Fever greater than 100.4° F (38° C) Copyright © 2020 by Elsevier, Inc. All rights reserved. 124 VTE Manifestations (Table 37-7) Inferior vena cava Legs edematous and cyanotic Superior vena cava Similar symptoms of arms, neck, back and face Some patients are asymptomatic Diagnosis: Assessment, D-dimer and/or ultrasound Copyright © 2020 by Elsevier, Inc. All rights reserved. 125 VTE: Complications Most serious: PE Chronic thromboembolic pulmonary hypertension Postthrombotic Phlegmasia Copyright © 2020 by Elsevier, Inc. All rights reserved. syndrome (PTS) cerulea dolens 126 VTE Diagnostic Studies Diagnostic studies (Table 37-9) Blood: ACT, aPTT, INR, bleeding time, Hgb, Hct, platelet count, D-dimer, fibrin monomer complex Noninvasive venous: venous compression ultrasound, duplex ultrasound Invasive venous: CT venography, MR venography, contrast venography Copyright © 2020 by Elsevier, Inc. All rights reserved. 127 VTE: Interprofessional Care Prevention and prophylaxis VTE prophylaxis is a core measure of high-quality health care in high-risk hospitalized patients developed by The Joint Commission (TJC) and the National Quality Forum. TJC recommends all hospitals have a VTE prevention policy for all adult patients Copyright © 2020 by Elsevier, Inc. All rights reserved. 128 VTE: Interprofessional Care Early and aggressive mobilization Bed rest—reposition every 2 hours Flex and extend feet, knees and hips every 2 to 4 hours while awake OOB to chair Walk 4 to 6 times/day Copyright © 2020 by Elsevier, Inc. All rights reserved. 129 VTE: Interprofessional Care Graduated compression stockings Thromboembolic deterrent (TED) Often used with anticoagulation Fit and wear correctly: Toe hole under toes, heel patch over heel; thigh gusset on inner thigh No wrinkles; don’t roll down, cut, or alter Not recommended if VTE already exists Copyright © 2020 by Elsevier, Inc. All rights reserved. 130 VTE: Interprofessional Care Intermittent pneumatic compression devices (IPCs) - increased venous return External pressure from electric pump inflates sleeves or boots to compress calf or thigh and/or foot and ankle Use with graduated compression stockings Fit and apply correctly; wear continuously except for bathing, skin assessment, and ambulation Do not use with active VTE; risk of PE Copyright © 2020 by Elsevier, Inc. All rights reserved. 131 VTE: Drug Therapy Drug therapy: anticoagulants Three classifications (Table 37-10) Vitamin K antagonists (VKA) Thrombin inhibitors (direct and indirect) Factor Copyright © 2020 by Elsevier, Inc. All rights reserved. Xa inhibitors 132 Covered in Pharm Vitamin K antagonists: Warfarin Inhibits Vitamin K-dependent coagulation factors II, VII, IX, and X and anticoagulant proteins C and S For long-term or extended anticoagulation Takes 48 to 72 to be effective; often overlap with parenteral anticoagulant for 5 days Monitor INR (Table 37-11) Antidote: Copyright © 2020 by Elsevier, Inc. All rights reserved. Vitamin K 133 Covered in Pharm Warfarin (continued) Do not give with antiplatelet drugs or NSAIDS Many interactions: See Complementary and Alternative Therapies Box Avoid vitamin K in diet; alters INR Green leafy vegetables Genetic variants may alter response Copyright © 2020 by Elsevier, Inc. All rights reserved. 134 Covered in Pharm Thrombin inhibitors Indirect: UH (heparin) and LMWH Affects intrinsic plasma antithrombin coagulation pathway; inhibits thrombin mediated conversion of fibrinogen to fibrin (Fig. 29-4) Prophylaxis—subcutaneously Existing VTE—continuous IV; monitor aPTT (Table 37-11) Copyright © 2020 by Elsevier, Inc. All rights reserved. 135 Covered in Pharm Heparin (continued) Serious side effect: heparin-induced thrombocytopenia (HIT) Long-term side effect: osteoporosis LMWH—enoxaparin More predictable, longer half-life, fewer bleeding complications Antidote: protamine Copyright © 2020 by Elsevier, Inc. All rights reserved. 136 Covered in Pharm Direct thrombin inhibitors (Table 37-10) Hirudin derivative—bivalirudin (Angiomax) Binds with thrombin and inhibits function Continuous IV infusion Synthetic (Argatroban)— Hinders thrombin Both: Indications: patients with or at risk for HIT having a percutaneous coronary intervention Monitor aPTT or ACT (Table 37-11) No antidote Copyright © 2020 by Elsevier, Inc. All rights reserved. 137 Covered in Pharm Direct thrombin inhibitors (Table 37-10) Dabigatran (Pradaxa)—oral Indications: VTE prevention after elective joint replacement, for stroke prevention in nonvalvular atrial fibrillation, and as a treatment for VTE Antidote: idarucizumab Advantages over warfarin Rapid onset, no monitoring, few drugfood interactions, decreased risk of bleeding, predictable response Copyright © 2020 by Elsevier, Inc. All rights reserved. 138 Covered in Pharm Factor Xa Inhibitors (Table 37-10) Inhibit factor Xa; rapid anticoagulation VTE prophylaxis and treatment Fondaparinux (Arixtra)—Subcutaneous Contraindicated with severe renal disease Rivaroxaba (Xarelto), apixaban (Eliquis), edoxaban (Savaysa)—oral Monitoring not required but can use anti-Xa assays (Table 37-11) Andexant Alfa—reverses rivaroxaban and apixaban Copyright © 2020 by Elsevier, Inc. All rights reserved. 139 Covered in Pharm Anticoagulant therapy for VTE prophylaxis Hospitalized patient not bleeding UH, LMWH, or fondaparinux Low risk VTE—no prophylaxis Moderate risk—UH or LMWH General, GYN or urologic surgery High risk—UH or LMWH Trauma, abdominal or pelvic surgery for cancer, or orthopedic surgery Copyright © 2020 by Elsevier, Inc. All rights reserved. 140 Covered in Pharm Anticoagulant therapy for VTE treatment Initial: LMWH, UH, or oral Factor XA or VKA INR—maintain 2.0 to 3.0 (VKA therapy) Continue 3 or more months Co-morbidities, complex issues, or vary large VTE— hospitalization IV UH initially Copyright © 2020 by Elsevier, Inc. All rights reserved. 141 Covered in Pharm Thrombolytic therapy for VTE treatment Thrombolytic drug (tPA or urokinase) administered via catheter to dissolve clots, reduce acute symptoms, improve deep venous flow, reduce valvular reflux, and PTS Indication: patients with low risk of bleeding and acute, extensive, symptomatic, proximal VTE Must have systemic anticoagulation before, during, and after thrombolysis Copyright © 2020 by Elsevier, Inc. All rights reserved. 142 VTE: Interprofessional Care Surgical and interventional radiology therapies Surgical options: Open venous thrombectomy—incision into vein to remove clot Inferior vena cava interruption devices—filters placed via right femoral or internal jugular veins (Fig. 37-11) to trap clots without impeding blood flow Copyright © 2020 by Elsevier, Inc. All rights reserved. 143 Fig. 37-11 Inferior Vena Cava Interruption Device Recommended for acute PE or proximal VTE of leg with active bleeding, or if anticoagulation contraindicated or ineffective Complications: air embolism, improper placement, filter migration, perforation of vena cava with retroperitoneal bleeding, clogged filter Copyright © 2020 by Elsevier, Inc. All rights reserved. 144 VTE: Interprofessional Care Percutaneous endovascular interventional radiology procedures Options: Mechanical thrombectomy, pharmacomechanical devices, postthrombus extraction, angioplasty, and/or stenting Can be used with catheter-directed thrombolytic therapy Nursing care: Maintain catheter systems, monitor for bleeding, embolization, and impaired perfusion; and teach VTE prevention Copyright © 2020 by Elsevier, Inc. All rights reserved. 145 Nursing Management: VTE Nursing assessment (Table 37-12) Subjective data Important health information Past history Medications Surgery or other treatments Functional health patterns Health-perception–Health management Activity–exercise Cognitive–perceptual Copyright © 2020 by Elsevier, Inc. All rights reserved. 146 Nursing Management: VTE Nursing assessment (Table 37-12) Objective data General Integumentary Cardiovascular Possible Copyright © 2020 by Elsevier, Inc. All rights reserved. diagnostic findings 147 Nursing Management: VTE Nursing diagnoses Acute pain Impaired Risk Planning/goals: The patient will have: tissue Pain mobility Increased integrity Impaired for bleeding relief Decreased edema knowledge of disease and treatment plan No skin ulceration No bleeding complications No Copyright © 2020 by Elsevier, Inc. All rights reserved. evidence of PE 148 Nursing Management: VTE Nursing implementation: Acute care Focus on prevention of thrombi and reduction of inflammation See Nursing Management: Caring for the Patient with VTE; all healthcare team members have important roles Review any interfering factors with anticoagulation therapy (see Complementary and Alternative Therapies Box) Monitor anticoagulation and significant lab studies; titrate drug doses and administer reversal agents as needed Copyright © 2020 by Elsevier, Inc. All rights reserved. 149 Nursing Management: VTE Nursing implementation: Acute care Monitor and reduce the risk of bleeding See: Table 37-13 (Assessment, Injections, Patient Care) See: Drug Alert: Anticoagulant Therapy Acute VTE—initial bed rest Early ambulation Teach importance of physical activity Copyright © 2020 by Elsevier, Inc. All rights reserved. 150 Nursing Management: VTE Ambulatory care Discharge teaching (Table 37-14) VTE risk factors Smoking, hormone therapy, travel, prolonged sitting, signs/symptoms of PE Drug doses, actions, side effects and routine blood tests; wear medic-alert ID Avoid falls and trauma Apply pressure to bleeding sites for 10-15 minutes No ASA or NSAIDs; limit alcohol Copyright © 2020 by Elsevier, Inc. All rights reserved. 151 Nursing Management: VTE Discharge teaching (continued) Dietary and Exercise Instructions Vitamin K and warfarin Obtain and maintain desired weight Guidelines for follow-up Report/call EMS: Copyright © 2020 by Elsevier, Inc. All rights reserved. Bleeding (urine, stool, vomit, nose, gums, skin) Severe headache, stomach pain, chest pain, palpitations, dyspnea, mental status changes Inform all HCP and dentist of anticoagulation 152 Nursing Management: VTE Evaluation Expected outcomes: Minimal Intact to no pain skin Increased knowledge of disorder and treatment plan No signs of hemorrhage or occult bleeding Copyright © 2020 by Elsevier, Inc. All rights reserved. 153 Chronic Venous Insufficiency (CVI) and Venous Leg Ulcers CVI—abnormalities of venous system include edema, skin changes, and venous leg ulcers Etiology and Pathophysiology Ambulatory venous hypertension Serous fluid and RBC leak results in edema and chronic inflammatory changes Hemosiderin—brown Skin Copyright © 2020 by Elsevier, Inc. All rights reserved. skin discoloration is hard, thick, and contracted 154 Chronic Venous Insufficiency (CVI) and Venous Leg Ulcers Clinical Manifestations and Complications Lower leg—brown, leathery and edematous Eczema with itching and scratching (Table 37-1) Venous ulcers (Fig. 37-13) Pain especially with dependent position Risk of infection Copyright © 2020 by Elsevier, Inc. All rights reserved. 155 Fig. 37-13 Venous Leg Ulcer Copyright © 2020 by Elsevier, Inc. All rights reserved. 156 Chronic Venous Insufficiency (CVI) and Venous Leg Ulcers Interprofessional and nursing care Compression for healing and prevention of recurrence Stockings, bandages, IPCs, wraps Teach proper fit and application Assess for PAD prior to compression Activity guidelines and limb positioning Avoid prolonged sitting or standing Elevate legs above heart Daily walking Avoid trauma Daily foot and leg care Copyright © 2020 by Elsevier, Inc. All rights reserved. 157 Chronic Venous Insufficiency (CVI) and Venous Leg Ulcers Interprofessional and nursing care Wound care and dressings—moist environment Nutrition—adequate protein, vitamins A and C, zinc Diabetics—normal blood glucose levels Monitor for infection Debridement, Copyright © 2020 by Elsevier, Inc. All rights reserved. excision, antibiotics 158 Chronic Venous Insufficiency (CVI) and Venous Leg Ulcers Interprofessional and nursing care Drug therapy—pentoxifylline or micronized flavonoid fraction Other: skin replacement (e.g., grafts) Daily moisturizing Copyright © 2020 by Elsevier, Inc. All rights reserved. 159 Tissue Perfusion Hematologic N 1020 Fall 2020 Memorize this slide! RBCs = oxygen WBCs = infection & inflammation (leuko-) Platelets = clotting -cytosis = too many leukocytosis, (erythro-) (thrombo-) thrombocytosis -penia = too few leukopenia, thrombocytopenia Assessment of Hematologic System Objective Data Head to Toe Physical examination Abnormalities that require f/u: Pallor Red tongue or mouth ulcers DOE, tachypnea Weak pulses Hematuria Bone tenderness Palpable spleen or liver Numbness/tingling Lymph node enlargement Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. Anemia A deficiency in the number of erythrocytes (RBCs), quantity or quality of hemoglobin (Hgb) & volume of packed RBCs (hematocrit) The amount of oxygen delivered to body tissues is also diminished Not a specific disease Manifestation of a pathologic process Copyright © 2020 by Elsevier, Inc. All rights reserved. 163 Causes of Anemia 164 Anemia Classified according to Morphology Cellular RBC characteristic size and color Etiology Cause Clinical Copyright © 2020 by Elsevier, Inc. All rights reserved. condition causing anemia 165 Anemia Clinical Manifestations Caused by body’s response to tissue hypoxia (i.e. decreased perfusion) Manifestations vary based on how fast anemia has evolved, its severity, and any coexisting disease Hgb levels are often used to determine severity of anemia Fatigue is the #1 most common symptom Copyright © 2020 by Elsevier, Inc. All rights reserved. 166 166 Anemia Integumentary Manifestations Pallor Decreased Hemoglobin Decreased blood flow to the skin Jaundice Increased concentration of serum bilirubin Pruritus Increased serum and skin bile salt concentrations Copyright © 2020 by Elsevier, Inc. All rights reserved. 167 Anemia Cardiopulmonary Manifestations Result from heart and lungs trying to provide adequate O2 to tissues Results in increased heart rate & respiratory rate Cardiac output maintained by increasing heart rate and stroke volume Low Hgb can result in a “demand MI” Copyright © 2020 by Elsevier, Inc. All rights reserved. 168 Anemia Clinical Manifestations Respiratory Dyspnea on exertion Neurologic Fatigue Headache Paresthesias Gait of hands and feet and balance disorders Anemia Nursing Assessment Subjective data Important Past health information health history Medications Surgery or other treatments Dietary history Functional Copyright © 2020 by Elsevier, Inc. All rights reserved. health patterns 170 Anemia Nursing Assessment Objective data General Integumentary Respiratory Cardiovascular GI Neurologic Diagnostic Copyright © 2020 by Elsevier, Inc. All rights reserved. findings 171 Anemia Nursing Interventions Patients with fatigue Alternate rest and activity Prioritize activities Accommodate Maximize Aid energy levels O2 supply for vital functions to minimize risk of injury from falls Monitor cardiorespiratory response Evaluate Copyright © 2020 by Elsevier, Inc. All rights reserved. nutritional needs 172 Anemia Gerontologic Considerations Anemia is not normal More common in the 70s and beyond Often related to an underlying cause Signs and symptoms may be overlooked Other May health issues be mistaken for normal aging Copyright © 2020 by Elsevier, Inc. All rights reserved. 173 Anemia Decreased Erythrocyte Production RBC production (erythropoiesis) is in equilibrium with RBC destruction/ loss Balance ensures that adequate number of RBCs is always available Three changes in erythropoiesis may decrease RBC production: Decreased Hgb synthesis Defective DNA synthesis in RBCs Diminished availability of erythrocyte precursors Copyright © 2020 by Elsevier, Inc. All rights reserved. 174 Iron-Deficiency Anemia Etiology Most common nutritional disorder Etiology Inadequate dietary intake Pregnant/nursing women, adolescents Malabsorption Blood loss Menstruating women, GI bleending 175 Iron-Deficiency Anemia Etiology Blood loss Major cause of iron deficiency in adults Chronic blood loss most commonly through GI and GU systems Bleeding often not apparent May take time to identify Postmenopausal bleeding, chronic kidney disease, and dialysis may contribute Copyright © 2020 by Elsevier, Inc. All rights reserved. 176 Iron-Deficiency Anemia Clinical Manifestations General manifestations of anemia Pallor is most common Glossitis is second Inflammation Cheilitis is also found Inflammation Copyright © 2020 by Elsevier, Inc. All rights reserved. of tongue of lips 177 Iron-Deficiency Anemia Diagnostic Studies Laboratory findings ↓ RBC, Hgb, Ferritin, Serum Iron RBC ↑ are microcytic (small) TIBC (Transferrin) Stool occult blood test Endoscopy and colonoscopy Bone marrow biopsy Copyright © 2020 by Elsevier, Inc. All rights reserved. 178 Iron-Deficiency Anemia Collaborative Management Goal Treat underlying problem causing loss, reduced intake or poor absorption of iron Replace iron Nutritional therapy Lean beef, turkey, pork & chicken, fish, legumes, dark green leafy vegetables, beans, enriched breads & cereals Iron supplements Transfusion of packed RBCs Copyright © 2020 by Elsevier, Inc. All rights reserved. 179 Iron-Deficiency Anemia Drug Therapy Indications Treatment of iron deficiency anemias and may be used as adjunctive therapy in pts receiving Epoetin Alfa Pharmacokinetics Absorbed in small intestines Transported in the blood bound to transferrin Small amounts are lost daily in the sweat, urine, sloughing of skin and mucosal cell and sloughing of intestinal cells. 180 Iron-Deficiency Anemia Drug Therapy Oral iron (ferrous sulfate, ferrous glucontate) Best absorbed in an acidic environment Take @ 1 hr before meals Take with Vit. C to be properly absorbed Do not take at same time as Calcium Undiluted liquid iron may stain teeth Side effects Heartburn, nausea, constipation, diarrhea Discoloration Copyright © 2020 by Elsevier, Inc. All rights reserved. of stools (dark green to black) 181 Iron-Deficiency Anemia Collaborative Management Parenteral iron Indicated for malabsorption, oral iron intolerance, need for iron beyond normal limits, poor patient compliance Can be given IM or IV, IM may stain skin, use Z-track Reassess Hgb and RBC count to evaluate response to therapy Emphasize adherence to dietary and drug therapy Need to take supplement for 2 to 3 months after Hgb returns to normal Monitor for liver problems with lifelong therapy Copyright © 2020 by Elsevier, Inc. All rights reserved. 182 Megaloblastic Anemias Group of disorders Caused by impaired DNA synthesis Presence of large RBCs (megaloblasts) Majority result from deficiency in Cobalamin Folic (vitamin B12) acid Copyright © 2020 by Elsevier, Inc. All rights reserved. 183 Vitamin B12 anemia Deficiency in vitamin B12 (cobalamin) Strict vegetarians Malabsorption Lack of intrinsic factor-this type of anemia is called Pernicious Anemia. Weakness Fatigue Bone marrow and blood changes look like folic acid anemia Folic acid anemia Deficiency in folic acid intake Chronic alcoholism/ Repeated pregnancies Weakness Fatigue Bone marrow and blood changes look like vitamin B12 anemia Neuro dysfunctions Megaloblastic Anemias RBCs will be larger than normal. Cobalamin Vit B12 Deficiency Etiology Most commonly caused by pernicious anemia Caused by absence of intrinsic factor (IF) IF: Protein secreted by parietal cells of gastric mucosa, needed for cobalamin absorption Can also occur: Surgery or chronic diseases of the GI tract Excess alcohol or hot tea ingestion Smoking Long-term users of H2 histamine receptor blockers and proton pump inhibitors Strict vegetarians Familial predisposition Copyright © 2020 by Elsevier, Inc. All rights reserved. 185 Cobalamin Vit B12 Deficiency Clinical Manifestations General manifestations of anemia develop slowly due to tissue hypoxia GI problems: Sore, red, beefy, and shiny tongue (glossitis) anorexia, nausea, vomiting, and abdominal pain Neuromuscular problems: Weakness, paresthesias of feet and hands, decreased vibratory and position senses, ataxia, muscle weakness, and impaired thought processes Copyright © 2020 by Elsevier, Inc. All rights reserved. 186 Glossitis-smooth beefy red tongue and paresthesias are common symptoms of B12 deficiency anemia. 187 Megoblastic Anemias Diagnostic Studies CBC Vitamin B12 level MMA (methylmalonic acid) Homecysteine level RBC Folate level Intrinsic factor assay Bone Marrow staining Copyright © 2020 by Elsevier, Inc. All rights reserved. 188 Cobalamin Vit B12 Deficiency Collaborative Management Medical Management: Nutritional therapy Vit B12 injection (hydroxocobalamin) or intranasal (cyanocobalamin) Milk, eggs, fish, enriched grains, dairy products Early detection and treatment Ensure safety Diminished sensations to heat and pain from neurologic impairment Protect from falling, burns, and trauma Physical therapy may be needed Copyright © 2020 by Elsevier, Inc. All rights reserved. 189 Folic Acid Deficiency Etiology Folic acid is needed for DNA synthesis RBC formation and maturation Manifestations are similar to those of cobalamin deficiency without neurological Common causes: Dietary deficiency, Malabsorption syndromes, Drugs, Increased requirement , Alcohol use and anorexia, Loss during hemodialysis Copyright © 2020 by Elsevier, Inc. All rights reserved. 190 Folic Acid Deficiency Collaborative Management Serum folate level is low Normal is 5 to 25 ng/mL (11 to 57 nmol/L) Serum cobalamin level is normal Treated with replacement therapy Usual dose is 1 mg/day by mouth Nutrition therapy Green leafy vegetables, enriched grain products & breakfast cereals, orange juice, peanuts, avacado Copyright © 2020 by Elsevier, Inc. All rights reserved. 191 Before a transfusion… IV Access- Blood cannot be “piggybacked” or infused with any other solutions except for normal saline (0.9% NS). Separate IV access may be needed if other iv infusions cannot be stopped (TPN, Vasopressors, insulin etc.). A large bore IV (bigger than a 22g for adults in most facilities) is required for blood so the cells aren’t destroyed by being squeezed through a small tube. Each facility has its own policy. A type and crossmatch (patient blood sample)- must be sent to the lab so the blood to be transfused can be tested for compatibility with the patient. Other baseline labs- CBC, electrolytes and coagulation studies may be sent for baseline data. Usually a cbc result is the reason a transfusion is ordered. Before a transfusion… Assess your patient- We’re adding fluid. A baseline assessment should include fluid status i.e. a good cardiovascular assessment should be performed first. BASELINE VITAL SIGNS. MD should be made aware if patient is febrile. Premedication In many facilities patients are premedicated with acetaminophen and diphenhydramine first. Patient teaching Assess knowledge of procedure. Instruct the patient to immediately report any changes-chills, itching, feeling of warmth, difficulty breathing, pain in the back, the abdomen, the chest, or at the IV site once the transfusion has begun. IF possible-ask your patient to void or empty their catheter drainage before starting the transfusion •All blood or blood components not used within 30 minutes must be stored in a monitored refrigerator that has been approved by the blood bank. Do not allow Blood Products to stand at room temperature longer than 30 minutes before administration. •Transfusions should be completed within 4 hours and before the expiration date/time of the blood component. Blood Transfusion Procedure The following elements MUST be double-checked with a second RN or MD prior to administration of the blood or blood products Patient name Patient medical record number Donor unit identification Blood type (ABO group) Rh type Donor unit expiration dates and when applicable time Presence of antibodies and/or agglutinins Product type Copyright © 2020 by Elsevier, Inc. All rights reserved. You cannot delegate Blood Transfusions to UAP 195 Blood Transfusion Procedure Verify that there is a written order from a physician for blood or blood components Verify that there is a signed consent with the patient’s name and medical record number documented Complete a baseline physical assessment of the patient as a basis to assess changes during and after the transfusion Insure the IV line has an appropriate catheter size and is patent Adjust infusion rate of transfusion according to the patient’s need, providers orders and agency policy Assess patient for signs of transfusion reaction Delegate UAP to take vital signs as directed Evaluate for therapeutic effect of blood product (improvement in CBC, increased BP, decreased bleeding) Monitor for signs of circulatory overload (i.e. SOB) if the transfusion is given rapidly Copyright © 2020 by Elsevier, Inc. All rights reserved. 196 Type & Crossmatch Blood 198 Blood Compatibilities for Transfusions Copyright © 2020 by Elsevier, Inc. All rights reserved. 199 Rhesus (“Rh”) Factor Copyright © 2020 by Elsevier, Inc. All rights reserved. Read your book! This will become important when you take Maternity 200 Transfusion Procedure Spike bag of 0.9% sodium chloride (NS) with one of the Y-tubing spikes, hang bag on IV pole and prime IV tubing Gently invert the blood component bag several times to suspend cells (to mix thoroughly before infusion) Spike blood component bag with the other Y-tubing connection. Ensure the drip chamber is half-full and the filter is covered to prevent damage to blood cells Clean the IV port per institution policy, then attach the Y-tubing to the patient’s IV site. Open the roller clamp on the blood. A gentle squeeze on the filter helps start the flow of blood Copyright © 2020 by Elsevier, Inc. All rights reserved. 201 Transfusion Procedure Infuse slowly for the first 15 minutes while observing the patient for reactions. This step allows for assessment to make sure the patient is not in need of rapid, life-sustaining interventions. Most serious reactions occur during this time After 15 minutes, reassess vital signs and adjust the flow rate to the desired speed, if no signs of a transfusion reactions are noted. Infusion time for RBCs should not exceed 4 hours. The longer the RBCs are left at room temperature, the greater the danger of bacterial proliferation and RBC hemolysis. Continue the assessment of the patient (always include vital signs) throughout the transfusion as needed, according to the patient’s condition, the number of units being administered and the facility policy. Copyright © 2020 by Elsevier, Inc. All rights reserved. 202 Signs and Symptoms of Transfusion Reactions Fever (Temp increase of > 1Cor 2F) with or without chills Skin changes, including flushing, uticaria localized or generalized edema Shaking chills (rigors) with or without fever Nausea, with or without vomiting Pain at infusion site or in the chest, abdomen or flanks, muscle aches Bradycardia or tachycardia Pruritis, diaphoresis, cyanosis or pallor Blood pressure changes, usually acute, either hypertension or hypotension Respiratory distress, including dyspnea, tachypnea, hypoxemia, shortness of breath, wheezing, cough or rales Copyright © 2020 by Elsevier, Inc. All rights reserved. Basically, if there is ANY CHANGE from baseline assessment…Sometimes it’s as simple as an itchy face or flushing… When in doubt, stop the transfusion and ask for assistance. 203 204 Management of a Transfusion Reaction Immediately STOP the transfusion once a reaction has been suspected or identified. Maintain IV access with normal saline using new primed tubing. Call the patient’s physician STAT! and notify the blood bank. Recheck the identifying tags and numbers Immediately take the patient’s vital signs. Monitor VS and urine output Treat patient’s symptoms per the physician’s orders. Return the blood bag and tubing to the blood bank for examination Collect required blood and urine specimens based on policy Document on transfusion reaction form and patient medical record Copyright © 2020 by Elsevier, Inc. All rights reserved. 205 Blood Transfusion General Principles No medications or solutions (except normal saline) should be added to or transfused concurrently with blood components If the integrity of any component is questioned on visual inspection, the unit should be returned to the blood bank of further evaluation Lactated Ringer’s solution or other electrolyte solutions containing calcium should never be administered concurrently with a blood component mixed with an anticoagulant containing citrate, because calcium binds to citrate Copyright © 2020 by Elsevier, Inc. All rights reserved. 206 Blood Transfusion Documentation Per organizational policy Component infused and amount Unit number and expiration date ABO & Rh type of component and patient Length of infusion time Unexpected outcomes or transfusion reactions Physician notifications of transfusion reactions Signature of both RNs double checking Copyright © 2020 by Elsevier, Inc. All rights reserved. 207 Leukemia A group of cancers affecting the blood and blood-forming tissues of Bone marrow Lymph system Spleen Occurs in all age-groups Overproduction of WBCs Accumulation of dysfunctional cells due to loss of regulation in cell division Copyright © 2020 by Elsevier, Inc. All rights reserved. 208 208 Leukemia Etiology and Pathophysiology No single cause Combination of genetic and environmental influences Oncogenes, or abnormal genes, can cause many types of cancers Chemical agents, chemotherapeutic agents, viruses, radiation, and immunologic deficiencies have been associated with development of leukemia Copyright © 2020 by Elsevier, Inc. All rights reserved. 209 209 Pathophysiology of Leukemia Copyright © 2020 by Elsevier, Inc. All rights reserved. 210 Leukemia Classification Acute vs Chronic Cell maturity and nature of disease onset Acute: Clonal proliferation of immature hematopoietic cells Chronic: More mature forms of WBC and onset is more gradual Based on type of WBC Acute lymphocytic leukemia (ALL) Acute myelogenous leukemia (AML) Chronic myelogenous leukemia (CML) Chronic lymphocytic leukemia (CLL) Copyright © 2020 by Elsevier, Inc. All rights reserved. 211 211 ACUTE MYELOGENOUS LEUKEMIA ACUTE LYMPHOCYTIC LEUKEMIA All age groups impacted; peak > 60 y.o. Children: peak 4 y.o., rare after 15 y.o. Prognosis highly variable -- the younger the patient, the better the prognosis Prognosis: 5 year survival 80% for children but 40% for adults “Undifferentiated” form: worse prognosis Bone/abdominal, CNS pain Neutropenia: fever, weakness, bleeding Chemo: corticosteroids and vinca alkaloids Chemo: aggressive induction therapy Bone marrow transplant Bone marrow transplant CHRONIC MYELOGENOUS LEUKEMIA CHRONIC LYMPHOCYTIC LEUKEMIA Rare: < 20 y.o.; median age 55-60 y.o. Most common form; 2/3 > 60 y.o. Prognosis: 3-5 years while chronic, only months once it becomes acute Prognosis: 2 (late) – 14 (early) years Three stages: chronic, transformation, accelerated (blast) crisis Painful enlarged lymph nodes “B” symptoms: night sweats, weight loss, fever Malaise, anorexia, weight loss possible Chemo: monoclonal antibodies Gleevec, Interferon, hydroxyurea Infections: antibiotics, immunoglobulin Bone marrow transplant Leukemia Manifestations Bruises, petechiae, pallor Open lesions, bleeding gums Anorexia, wt. loss Enlarged liver and spleen Tachycardia, palpitations Orthostatic hypotension D.O.E., fatigue, headache, fever, Bone or joint pain and swelling, hematuria Leukemia from a conceptual view: You will have problems with both PERFUSION and PROTECTION. The patient suffers from symptoms of pancytopenia. The overproduction non-working WBCs will take over, meaning the patient has no ability to PROTECT themselves (either from infection or bleeding) and reduced RBCs which means decreased PERFUSION. Hence, the manifestations on the left. Leukemia Clinical Manifestations Inadequate marrow elements predispose patient to Anemia Thrombocytopenia Decreased number and function of WBCs Copyright © 2020 by Elsevier, Inc. All rights reserved. 214 214 Leukemia Collaborative Care Initial goal is to attain remission Complete, partial, or molecular Prognosis is directly related to ability to maintain a remission Prognosis becomes more unfavorable with each relapse Chemotherapy is the mainstay of treatment Copyright © 2020 by Elsevier, Inc. All rights reserved. 215 215 Leukemia Chemotherapy Regimens Combination chemotherapy Mainstay of treatment Three purposes Decrease drug resistance Decrease drug toxicity by using multiple drugs Interrupt cell growth at multiple points in cell cycle Copyright © 2020 by Elsevier, Inc. All rights reserved. 216 216 Leukemia Other Treatments Corticosteroids Radiation therapy Total body radiation in preparation for bone marrow transplantation Organ- or field-specific such as liver or spleen Immunotherapy and targeted therapy Copyright © 2020 by Elsevier, Inc. All rights reserved. 217 217 Leukemia Hematopoietic Stem Cell Transplant Goal of HSCT Eliminate all leukemic cells using combinations of chemotherapy with or without total body irradiation Eradicates patient’s hematopoietic stem cells Replaced with those of an HLA-matched Sibling HLA-half-matched relative Volunteer donor (allogenic) Identical twin (syngeneic) Copyright © 2020 by Elsevier, Inc. All rights reserved. 218 218 Nursing Management Planning Overall goals Understand and adhere to treatment plan Have minimal side effects and complications of disease and treatment Establish realistic hope and goals, feeling supported during periods of treatment, relapse, and remission Copyright © 2020 by Elsevier, Inc. All rights reserved. 219 219 Nursing Management Acute Care Many physical and psychologic needs Diagnosis evokes great fear Equated with death Family needs help adjusting to stress of sick role May be viewed as hopeless, horrible Copyright © 2020 by Elsevier, Inc. All rights reserved. 220 220 Nursing Management Acute Care Important nursing interventions Maximizing patient’s physical functioning Teaching patients that acute side effects of treatment are usually temporary Encouraging patients to discuss quality of life issues Copyright © 2020 by Elsevier, Inc. All rights reserved. 221 221 Leukemia – Case Study What should be included in this teaching? Your patient has been diagnosed with leukemia after presenting to the office with frequent bruising, bleeding gums, fatigue and fevers. You are to teach the patient about bleeding precautions, managing fatigue and protecting himself from infections Copyright © 2020 by Elsevier, Inc. All rights reserved. 222
