CCI Exam PDF - Heart Failure, Drug Therapy, & Nursing Management

Heart Failure Heart Failure  Risk factors/Etiology Primary risk factors Hypertension damaged Vessels ↑ workload. Modifiable risk factor If aggressively treated and managed, incidence of HF can be reduced by 50% CAD blockage Co-morbi...

Heart Failure Heart Failure  Risk factors/Etiology Primary risk factors Hypertension damaged Vessels ↑ workload. Modifiable risk factor If aggressively treated and managed, incidence of HF can be reduced by 50% CAD blockage Co-morbidities contribute to development of HF Etiology Any interference with mechanisms regulating cardiac output (CO) Primary causes Conditions that directly damage the heart Heart attack Precipitating causes Conditions that increase workload of the heart  Classification Left-sided HF Most common form of HF Results from inability of LV to Empty adequately during systole, or Fill adequately during diastole Blood backs up into left atrium (LA) Increased pulmonary hydrostatic pressure causes fluid leakage from the pulmonary capillary bed into the interstitium and then the alveoli. crackles , frothy spotom , This results in pulmonary congestion and edema dyspnea Right-Sided Heart Failure COPD RV does not pump effectively Fluid backs up in venous system Fluid moves into tissues and organs liver This results in peripheral edema, JVD, ascites Left-sided HF is most common cause fluid in abdomen (distended Other causes include RV infarction, PE, and cor pulmonale (RV dilation and hypertrophy) (670s (40) Further classified as HFrEF (systolic HF) reduced ejection Fraction HFpEF (diastolic HF) preserved ejection Fraction (prob. w/ relaxation / refilling Or combination of the two  Heart Failure HFrEF (systolic failure) Inability to pump blood effectively Caused by Impaired contractile function Increased afterload Mechanical abnormalities Decreased LV ejection fraction (LVEF) HFpEF (diastolic HF) Inability of the ventricles to relax and fill during diastole, resulting in decreased stroke volume and CO Primary cause is HTN lear space for blood bCa Result of left ventricular hypertrophy from MuscIf hypertension,older age, female, diabetes, obesity Diagnosis based on Symptoms of HF Normal LVEF LV diastolic dysfunction  Chronic Heart Failure Clinical Manifestations Fatigue B Dyspnea L Orthopnea L (positions Paroxysmal nocturnal dyspnea L Cough L Tachycardia L Edema R Palpitations Skin changes both? Neurological manifestations Mental status and behavioral changes Sleep problems Chest pain Weight changes R  Labs & Diagnostics Determine and treat underlying cause Echocardiogram ultrasound Provides information on LVEF, heart valves , presence of effusion or thrombus ECG, ambulatory heart monitors, chest x-ray, 6-minute walk test, MRI, cardiopulmonary exercise stress test, cardiac catheterization/angiogram BNP levels if theres damage Fluid Status k 100 is a problem give diuretic if fluid  Interprofessional Care Main treatment goals Treat the underlying cause and contributing factors Maximize CO Improve ventricular function Improve quality of life Preserve target organ function Oxygen therapy Relieves dyspnea and fatigue Physical and emotional rest Conserve energy and decrease oxygen needs Dependent on severity of HF Structured exercise program CR associated with better outcomes cardiac read 30 min 3x/wk  Interprofessional Care Nutritional Therapy Low sodium diet processed foods canned foods no red meats. , , Individualize recommendations and consider cultural background AHA web site has dietary guidelines Sodium is usually restricted to 2 g/day Fluid restriction for stage D/IV HF patients Daily weights important same time everyday any weight first thing in morning or when discharged = **Weight gain of 3 pounds (1.4 kg) over 2 days or a 3-5 pounds (2.3 kg) gain over a week should be reported to HCP* diuretic  Drug Therapy RAAS inhibitors ACE inhibitors 1-pril) ↓BP ↓after load ethnic background · Angiotensin II receptor blockers useARBs if the cough , allergic , Neprilysin-angiotensin receptor inhibitors Aldosterone antagonists sprinolactone Monitor K+ Vasodilators (reduce preload and afterload) ↓ workload Nitrates Positive inotropic agents (increase contractility which improves CO) Digitalis dig toxicity (G1) Diuretics furosemide (thiazide loop ( * k +, Mg) , Reduce edema, pulmonary venous pressure, and preload Promote sodium and water excretion Loop diuretics Thiazide diuretics Monitor potassium levels (hypokalemia)  Nursing Management Nursing Implementation Health promotion Communication and joint decision making with patient, caregiver, and interprofessional team Aggressively identify and treat risk factors for HF to prevent or slow progression Basic principles of care HF is a progressive disease Treatment plans established with quality-of-life goals Symptom management depends on adherence to self-management protocols Precipitating factors, etiologies, and comorbid conditions must be addressed Complex care needs often require multiple settings, increasing fragmented care Support systems are essential to success Nursing Monitor respiratory status Administer oxygen therapy Semi-Fowler’s position Monitor hemodynamic status Daily weights I&O Administer prescribed drugs Monitor edema  Nursing Management Alternate rest with activity Provide diversionary activities Monitor response to activity Collaborate with OT/PT Reduce anxiety Evaluate support system Patient teaching Patient teaching Signs and symptoms of worsening HF Telehealth and device remote monitoring technology Therapeutic interventions can be implemented to avoid re-hospitalization  Nursing Management Drug therapy Basic mechanism of action Signs of drug toxicity check apical pulse for imin (dia) How to take pulse for a full minute Home BP monitoring Signs and symptoms of hypokalemia and hyperkalemia Exercise training (cardiac rehab) Individualize Importance of rest periods Energy conserving behaviors Environmental changes may be needed Consultation with PT, OT  Nursing Management Evaluation/Expected: 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 Cardiomyopathy  Dilated Cardiomyopathy Most common type, causes HF in 25-40% cases Caused by: infectious myocarditis, alcohol, cocaine, ect. Clinical manifestations: Decreased exercise capacity Fatigue Dyspnea at rest Paroxysmal nocturnal dyspnea Orthopnea As the disease progresses: Dry cough Palpitations N/V, anorexia Abnormal S3 and/or S4 Pulmonary crackles, edema Weak PP, pallor, hepatomegaly, JVD peripheral pulse  Dilated Cardiomyopathy Dx Studies Doppler echocardiography CXR ECG BNP Heart cath Endomyocardial biopsy Interprofessional/Nursing Care Nitrates β-Blockers Antidysrhythmics stops et from going into abl. rhythms ACE inhibitors Diuretics Digitalis Nutritional therapy Cardiac rehab Teach CPR HH/Hospice referral Hypertrophic Cardiomyopathy More common men, diagnosed in young adults, active, athletic Causes: Genetic link, HTN, Aortic stenosis Main characteristics: Massive ventricular hypertrophy Rapid, forceful contraction of the LV Impaired relaxation Obstruction to aortic outflow (not all pts) Clinical Manifestations: May be asymptomatic Exertional dyspnea Fatigue Angina Syncope O Interprofessional and Nursing Care: Drug therapy Beta blockers CCBs Digitalis Anti-dysrhythmic drugs Surgery Teach to avoid strenuous activity and dehydration Elevate feet Vasodilators may worsen CP  Restrictive Cardiomyopathy rigid Least common type Causes: *Amyloidosis, cancer, post- radiation, ect. Clinical Manifestations Fatigue Exercise intolerance Dyspnea Angina Orthopnea Syncope Palpitations Signs of HF: Dyspnea, peripheral edema, weight gain, JVD Interprofessional/Nursing Care: Conventional HF therapy Heart Transplant hardastiff Avoid strenuous activities and dehydration Prophylactic antibiotics Cardiomyopathy Valvular Heart Disease  Valvular Heart Disese Heart has Two atrioventricular valves Mitral Tricuspid Two semilunar valves Aortic t issues Pulmonic lungs Types of valvular heart disease defined according to Valve(s) affected Type of dysfunction Stenosis (constriction/narrowing) Valve opening is smaller Forward blood flow is impeded Pressure differences on the two sides of the valve reflect degree of stenosis Regurgitation (incompetence or insufficiency) Incomplete closure of valve leaflets Results in backward flow of blood Blood flow through the heart  Mitral valve stenosis Stiff Most common cause is rheumatic heart disease Scarring of valve leaflets and chordae tendineae Contractures develop with adhesions between commissures of the leaflets Results in decreased blood flow from left atrium to left ventricle Increased left atrial pressure and volume Risk for atrial fibrillation Clinical manifestations Exertional dyspnea Loud S"lub" 1 round Diastolic murmur after rest blowing Palpitations A pressure in LA Hemoptysis backing up into lung Atrial fibrillation with risk for stroke  Mitral valve regurgitation Normal valve function depends on intact: Mitral leaflets Mitral annulus Chordae tendineae Papillary muscles Damage caused by: MI Chronic rheumatic heart disease Mitral valve prolapse Ischemic papillary muscle dysfunction IE Incomplete valve closure Backward flow of blood Acute MR Pulmonary edema Chronic MR Left atrial enlargement, ventricular dilation, eventual ventricular hypertrophy  Mitral valve regurgitation Acute clinical manifestations Thready peripheral pulses Cool, clammy extremities Chronic clinical manifestations Asymptomatic for years Weakness, fatigue, palpitations, dyspnea Progress to orthopnea, paroxysmal nocturnal dyspnea Peripheral edema Audible S3, murmur  Mitral valve prolapse Abnormality of mitral valve leaflets and the papillary muscle or chordae Leaflets prolapse back into left atrium during systole Usually benign with valve closing effectively Potential complications Unknown cause but genetic link in some Confirmed with echocardiography M-mode or 2-D Clinical manifestations Most patients asymptomatic for life Only 10% with symptoms Murmur d/t regurgitation Severe MR uncommon  Mitral valve prolapse Clinical manifestations Dysrhythmias can cause palpitations, light-headedness, and syncope Infective endocarditis Chest pain unresponsive to nitrates Treat symptoms with β-blockers ↓ workload Valve surgery for MR Patient teaching important Antibiotic prophylaxis if MR present Take drugs as prescribed Healthy diet; avoid caffeine Avoid OTC stimulants Exercise When to call HCP or EMS  Aortic valve stenosis Congenital aortic stenosis (AS) usually found in childhood, adolescence, or young adulthood In adults, can be degenerative or caused by rheumatic fever Obstruction of blood flow from left ventricle to aorta Left ventricular hypertrophy and increased myocardial oxygen consumption Decreased CO leads to decreased tissue perfusion, pulmonary hypertension, and HF Poor prognosis if left untreated Clinical manifestations (SAD) Syncope Angina Exertional dyspnea Auscultatory findings Normal to soft S1 Decreased or absent S2 Use nitroglycerin cautiously Reduces preload and BP Can worsen chest pain  Aortic valve regurgitation Acute AR IE, trauma, or aortic dissection I Life-threatening emergency Chronic AR Rheumatic heart disease, congenital bicuspid aortic valve, syphilis, connective tissue problem, or post-surgical cause Backward blood flow from ascending aorta into left ventricle With chronic AR, left ventricular dilation and hypertrophy Decrease in myocardial contractility Pulmonary hypertension and right ventricular failure Clinical manifestations of acute AR Severe dyspnea Chest pain Hypotension Life-threatening emergency  Aortic valve regurgitation Clinical manifestations of chronic AR May be asymptomatic for years Exertional dyspnea, orthopnea, paroxysmal dyspnea Angina “Water-hammer” pulse if severe Soft or absent S1 S3 or S4 Murmur  Labs & Diagnostics Patient’s history/physical exam Echocardiogram Chest x-ray ECG Heart catheterization  Interprofessional care Conservative therapy Dependent on valve involved and disease severity Prevent exacerbations of HF, pulmonary edema, thromboembolism, and recurrent RF and IE Prophylactic antibiotic therapy to prevent recurrent RF and IE Drugs to treat/control HF Vasodilators (e.g., nitrates, ACE inhibitors) Positive inotropes (e.g., digoxin) Diuretics β-blockers Sodium restriction Anticoagulation therapy afin mech value. Anti-dysrhythmic drugs  Interprofessional care Surgical therapy Valve repair Preferred surgical procedure Lower operative mortality rate May not restore total valve function Valve replacement Valve replacement Mechanical (artificial) More durable, last longer Risk of thromboembolism Require long-term anticoagulation Biologic (tissue) warfarin Bovine, porcine, and human No anticoagulation required Less durable bleeding risk NSALDS  Nursing management Nursing Dx Impaired cardiac output Activity intolerance Fluid imbalance Planning/Goals Normal heart function Improved activity tolerance Understanding of the disease process and health maintenance measures Implementation Health promotion Early treatment of streptococcal infections Prophylactic antibiotics for patients with history Teach patient symptoms to report  Nursing Management Individualize rest and exercise Avoid strenuous activity Discourage tobacco use Ongoing cardiac assessments to monitor drug effectiveness Monitor INR for patient on anticoagulants Patient teaching Drug actions and side effects Importance of prophylactic antibiotic therapy Information related to anticoagulation therapy When to seek medical care Follow-up care Notify HCP for Signs of infection, HF, or bleeding Planned invasive or dental work Medical-alert device or bracelet  Nursing management Evaluation Maintain adequate tissue and organ perfusion Achieve fluid and electrolyte balance Achieve optimal level of activity Describe disease process and measures to prevent complications Week 4 Hypertension & Vascular Disorders 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 Atherosclerosis is leading cause in majority of cases Gradual thickening of the intima and media due to cholesterol and lipids Exact cause unknown; inflammation and endothelial injury play major role Pathogenesis of Atherosclerosis  Tobacco use Atherosclerosis Diabetes HTN High cholesterol Age greater than 60 Risk Factors 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 Clinical Manifestations walking around and develop pain Intermittent Claudication- burning, cramping, and pain in legs during exercise Numbness or burning pain primarily in the feet when in bed Pain that is relieved by placing legs in a dependent position Assessment Findings Bruit over Decreased Decreased or Loss of hair femoral artery capillary refill non palpable on lower calf, and aortic of toes pulses ankle and foot arteries Pallor of the Dependent Ulcers and extremity with rubor possible elevation (redness) gangrene of no blood toes  Arteriography Areas can be treated during procedure with angioplasty and stent Diagnostic Exercise tolerance testing Studies Ankle-brachial index (ABI) Doppler and magnetic resonance angiography  Prolonged ischemia leads to: Atrophy of skin and underlying muscles Delayed healing Wound infection Tissue necrosis Arterial ulcers over bony prominences Complications May result in amputation If adequate blood flow is not restored and if severe infection occurs Indicated with uncontrolled pain and spreading infection Interprofessional Care Drugs prescribed for *Antiplatelets treatment of intermittent Exercise claudication Aspirin Cilostazol (Pletal)—See Drug Alert Walking is most effective exercise for Clopiodogrel (Plavix) Inhibits platelet aggregation individuals with claudication Increased vasodilation 30 to 45 minutes daily, 3 times/wk Pentoxifylline (Trental) Women have faster decline and Improves flexibility of RBCs and WBCs mobility loss than men Decreases fibrinogen concentration, platelet adhesiveness, and blood viscosity Daily exercise increases survival rates  Interprofessional Care Percutaneous transluminal angioplasty (PTA) Catheter has a balloon at the tip Balloon is inflated dilating the vessel by compressing atherosclerotic intimal lining Stent is placed to hold artery open Stent coated with drug (paclitaxel) to limit growth of new tissue in treated area Atherectomy Removal of obstructing plaque Performed using a cutting disc, laser, or rotating diamond tip Peripheral artery bypass surgery Human umbilical vein or composite sequential bypass graft may be used PTA with stenting may also be used in combination with bypass surgery Nursing Management Nursing Dx: Ineffective tissue perfusion Activity intolerance Planning/Goals: 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  Ambulatory care Management of risk factors Smoking cessation Long-term antiplatelet/ASA therapy Supervised exercise training after revascularization ↑ Importance of meticulous foot care Daily inspection of the feet Nursing Comfortable shoes with rounded toes and soft insoles; shoes lightly laced Management Show how to check skin temperature, capillary refill, and palpate pulses Evaluation: Adequate peripheral tissue perfusion Increased activity tolerance Effective pain management Knowledge of disease and treatment plan  Acute care In recovery area, after surgery or radiologic intervention, frequently monitor: Skin color and temperature check for decreased blood Flow Capillary refill Presence of peripheral pulses distal to the operative site Notify HCP immediately with any changes Nursing Sensation and movement of extremity Management Acute care—after leaves recovery Continued circulatory assessment Monitor for potential complications Report: Increased pain, loss of pulses, pallor or cyanosis, numbness or tingling Avoid knee-flexed positions Turn and position frequently, OOB, ambulate; avoid out of bed prolonged sitting Graduated compression stockings  Nonatherosclerotic, segmental, recurrent inflammatory disorder of the small and medium arteries and veins of the arms and legs Most common in men younger than 45 years old with history of tobacco and/or marijuana use without other CVD risk factors Thromboangiitis Symptoms Intermittent claudication of feet, hands, or arms; rest Obliteans pain, ischemic ulcerations, changes in color and temperature, paresthesia, superficial vein thrombosis and cold sensitivity (Buerger’s No specific lab or diagnostic tests Disease) Based on history and symptoms and exclusion of other disorders Treatment: no smoking tobacco or marijuana; no nicotine replacements Conservative: Avoid cold exposure; walking program, antibiotics for ulcers, analgesia for pain, avoid trauma  Raynaud’s Phenomenon Episodic, vasospastic disorder of small cutaneous arteries; fingers and toes most commonly involved More common in women, age 15 to 40 years. May occur alone or with other diseases Characteristic change in color of fingers, toes, ears, and nose White, blue, and red Also: coldness, numbness followed by throbbing, aching pain, tingling, and swelling Several minutes to hours Prolonged, frequent attacks causes thick skin, brittle nails, punctate lesions and gangrenous ulcers Triggers: exposure to cold, emotional upset, tobacco use and caffeine genesis Nursing care Patient education: prevent episodes Avoid temperature extremes; wear appropriate clothing No tobacco products; avoid caffeine No vasoconstrictor drugs Chronic Venous Insufficiency (CVI) CVI—abnormalities of venous system include edema, skin changes, and venous leg ulcers Etiology and Pathophysiology Primary varicose veins Ambulatory venous hypertension Serous fluid and RBC leak results in edema and chronic inflammatory changes Hemosiderin—brown skin discoloration Skin is hard, thick, and contracted * bounding pulses CVI Risk Factors Results from periods of prolonged venous hypertension Sitting or standing in one position too long Obesity Pregnancy Thrombophlebitis CVI-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 CVI-Interprofessional and Nursing Care Wound care and dressings—moist environment Nutrition—adequate protein, vitamins A and C, z Diabetics—normal blood glucose levels Medication therapy Flavonoids anti-inflammatory Pentoxifylline (Trental) hemorheologic agent Acetylsalicylic acid (Aspirin) non- steroidal-anti-inflammatory Saponins anti-inflammatory  Peripheral Venous Disease: Nursing Process Recognize Cues (Assessment) Generate Solutions (Planning) Obtain thorough history and physical Decrease pain and edema Identify risk factors Facilitate wound healing History of leg pain Take Action (Intervention) Client occupation Wound care Analyze Cues (Analysis) Pain control Differentiate between venous and Education arterial abnormalities Evaluate Outcomes (Evaluation) Prioritize Hypotheses (Analysis) Improved Decrease pressure in the veins Worsened Decrease pain and edema Stay the Same Facilitate wound healing. 20 Copyright 2022 Assessment Technologies Institute, L.L.C. All rights reserved. Hypertension  Hypertension (HTN) High blood pressure Affects ~46% adults in United States Heart disease associated with HTN leads to 23.7% of deaths in United States National Health and Nutrition Examination Survey (NHANES) 83% of people greater than age 20 with HTN are aware they have high BP 76% are being treated 48% of those aware do not currently have their BP well controlled Modifiable risk factor to prevent CVD As BP increases, so does the risk of: MI Heart failure Stroke Renal disease Retinopathy  HTN Promoting health equity Gender differences Blacks Men—more common before middle age Highest prevalence; more resistant HTN; Women develop at younger age; female greater than increased 2-3x with oral contraceptives male; more nocturnal nondipping BP; more end- Preeclampsia—possible early sign organ damage; highest death rate More common after menopause; harder to Less response to renin inhibiting meds; better control with older women control with calcium channel blockers and diuretics Increased risk of angioedema with ACE inhibitors Hispanics Less likely to receive treatment Lower rate of: awareness, treatment, and control  Normal Regulation of BP 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  Classification of HTN Category SBP (mm Hg) DBP (mm Hg) Normal