Cardiovascular and Peripheral Vascular System: Part II PDF

Cardiovascular and Peripheral Vascular System: Part II NRSG311 – Week R. Stent Winter 2025 Adapted from K. Curtis-Harford Content Covered: Inflammatory disorders of the...

Cardiovascular and Peripheral Vascular System: Part II NRSG311 – Week R. Stent Winter 2025 Adapted from K. Curtis-Harford Content Covered: Inflammatory disorders of the heart Vascular disorders R. Stent Winter 2025 NRSG 311 2 Objectives Describe the etiology, pathophysiology, clinical manifestations, interprofessional care, and nursing management of infective endocarditis, pericarditis, and myocarditis Describe the etiology, pathophysiology, clinical manifestations, interprofessional care, and nursing management of rheumatic fever and rheumatic heart disease Relate major risk factors to the etiology and pathophysiology of peripheral artery disease Select appropriate nursing interventions for a patient undergoing an aortic aneurysm repair Differentiate between superficial vein thrombosis and VTE Prioritize key aspects of nursing management of a patient receiving anticoagulant therapy Explain collaborative care and management of patients with varicose veins, chronic venous insufficiency, and venous leg ulcers Provide patient education on primary and secondary prevention for patients with vascular disorders R. Stent Winter 2025 NRSG 311 3 Inflammatory Disorders of the Heart Infective Endocarditis (IE) Acute Pericarditis Chronic Constrictive Pericarditis Myocarditis Rheumatic Fever and Heart Disease R. Stent Winter 2025 NRSG 311 4  Infection of endocardial surface of heart Infective Affects cardiac valves Endocarditi Causative organisms: s (IE) Most common: staphylococcus aureus, oral Streptococcus, and Enterococci; can also be caused by fungi or viruses Risks: prior endocarditis, prosthetic valves, acquired valvular disease, cardiac lesions Blood flow turbulence in heart allows causative organism to infect previously damaged valves or endothelial surfaces Vegetations: primary lesions of IE, adhere to valve surface or endocardium Can embolize to organs (brain, kidneys, spleen from left-sided lesions; lungs from right-sided lesions) and extremities, cause infarction Infection may spread locally and damage valves, or to supporting structures: Results in dysrhythmias, valvular incompetence, and eventual invasion of myocardium, leading to heart failure (HF), sepsis, and heart block R. Stent Winter 2025 NRSG 311 5  Infective Endocarditis (IE) Classification: four categories, describe site of infection, presence of cardiovascular devices, and how infection was acquired: Left-sided native valve IE Left-sided prosthetic valve IE Right-sided IE (includes intravenous [IV] drug use) Intracardiac and intravascular devices (e.g. pacemaker/defibrillator wires, hemodialysis) Identified as: Community-acquired Health care–associated R. Stent Winter 2025 NRSG 311 6  Infective Endocarditis: Clinical Manifestations Nonspecific, can involve multiple organ systems and include: Low-grade fever, chills, weakness, malaise, fatigue, anorexia Arthralgia, myalgia, back pain, abdominal discomfort, weight loss, headache, clubbing of fingers Splinter hemorrhages in nail beds: black longitudinal streaks Petechiae in conjunctivae, lips, buccal mucosa, palate, over ankles, feet, antecubital and popliteal areas: result of fragmentation and microembolization of vegetative lesions Osler’s nodes: painful, tender, red/purple, pea-sized lesions on fingertips or toes, last 1-2 days Janeway’s lesions: flat, painless, small, red spots on palms and soles Roth’s spots: hemorrhagic retinal lesions, found on funduscopic examination Onset of new or changing murmur or heart failure may occur Clinical manifestations R. Stent Winter 2025 secondary to embolization NRSG 311 in body organs may occur 7  Infective Endocarditis (IE): Diagnostic Studies Obtain recent health history: Recent (3–6 months) dental, urological, surgical, or gynecological procedures, including obstetrical delivery History of illicit IV drug use; valvular or congenital heart disease; intracardiac prosthetic device; recent cardiac catheterization; skin, respiratory, or urinary tract infections Laboratory data: Blood cultures: Two cultures drawn 60 min apart, positive in >90% of patients Mild leukocytosis may occur in acute endocarditis Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) may be elevated Imaging and other diagnostics: Echocardiography: negative blood cultures or surgical candidates; detect vegetation, destructive lesions, valve abscess Chest radiography: detect cardiomegaly Electrocardiogram (ECG): may show 1st or 2nd degree atrioventricular block Cardiac catheterization: evaluate coronary artery patency and valvular function (if surgical intervention being considered) R. Stent Winter 2025 NRSG 311 8  Infective Endocarditis (IE): Collaborative Care Antibiotic prophylaxis: clients with specific cardiac conditions before certain dental or surgical procedures Medication therapy: long-term treatment with IV antibiotics; blood cultures to evaluate effectiveness of antibiotic therapy Early valve replacement followed by prolonged (6 weeks +) drug therapy recommended for fungal infection and prosthetic valve endocarditis (most frequently seen with IV drug use) Treat fevers with ASA, acetaminophen, ibuprofen, fluids, rest Complete bed rest usually not indicated unless temperature remains elevated or signs of HF R. Stent Winter 2025 NRSG 311 9  Infective Endocarditis (IE): Nursing Management Patient and caregiver education: Understand and follow treatment regimen Avoid exposure to infection (e.g. upper respiratory), report cold, flu Goals: Avoid excessive fatigue: plan rest before/after activities Elastic compression stockings, ROM exercises, cough and deep- Normal or baseline breathing every 2 hours to prevent complications of immobility cardiac function Good oral hygiene and nutrition Perform ADLs Inform providers of IE history prior to dental, medical, or surgical without fatigue procedures, prophylactic antibiotic therapy before invasive Knowledge of procedures therapeutic Recognize signs and symptoms of life-threatening complications: regimen Cerebral emboli, pulmonary edema, heart failure Prevent Fever (chronic/intermittent) common early sign that drug therapy is recurrence ineffective R. Stent Winter 2025 NRSG 311 10  Condition caused by: Acute Pericarditi Inflammation of pericardial sac (pericardium) s Most often idiopathic, can be caused by: Fungal or bacterial infection, acute MI, tuberculosis, neoplasm, autoimmune conditions (e.g. lupus), drug reactions, metabolic disorders, trauma Pericarditis with acute MI: Two distinct syndromes Acute pericarditis: within 48-72 hours after MI Dressler’s syndrome: late pericarditis, 4-6 weeks after MI R. Stent Winter 2025 NRSG 311 11  Acute Pericarditis: Clinical Manifestations Progressive, frequently severe chest pain Sharp and pleuritic, worse with deep inspiration and when lying supine Pain relieved by sitting upright, can be referred to trapezius muscle (shoulder, upper back) Dyspnea: rapid, shallow breaths to avoid chest pain Aggravated by fever, anxiety Pericardial friction rub: Hallmark finding Scratching, grating, high-pitched sound believed to arise from friction between roughened pericardial and epicardial surfaces Complications: Pericardial effusion: Accumulation of excess fluid in pericardium Cardiac tamponade: Develops as fluid accumulates in pericardial sac (pericardial effusion), causing increase in intrapericardial pressure and producing compression of heart R. Stent Winter 2025 NRSG 311 12  Acute Pericarditis: Diagnostic Studies ECG: Changes in 90% of cases, covered in more detail in NRSG 415 Chest radiography: Generally normal, may see cardiomegaly with large pericardial effusion Echocardiograph: More useful determining pericardial effusion than cardiac tamponade Tissue Doppler imaging, colour M-mode Doppler imaging: Help assess diastolic function and diagnose constrictive pericarditis CT and cardiac MRI: Visualization of pericardium and pericardial space Laboratory findings: Leukocytosis, elevation of CRP and ESR, may see elevated troponin (indicates concurrent myocardial damage) Evaluation of fluid from pericardiocentesis or tissue from pericardial biopsy: may help determine cause R. Stent Winter 2025 NRSG 311 13  Acute Pericarditis: Collaborative Care Antibiotics for bacterial pericarditis NSAIDs, ASA for pain and inflammation Management: Corticosteroids (e.g. prednisone) for pericarditis secondary to Identify and systemic inflammatory disease (e.g. systemic lupus erythematosus) treat Also for patients whose symptoms do not respond to/are contraindicated for underlying NSAIDs (e.g. renal failure, pregnancy, anticoagulants) issue/cause Pericardiocentesis: needle to remove fluid from pericardial space Manage For large pericardial effusion with acute cardiac tamponade, purulent symptoms pericarditis, and high suspicion of neoplasm Complications from pericardiocentesis: dysrhythmias, further cardiac tamponade, pneumothorax, myocardial laceration, coronary artery laceration R. Stent Winter 2025 NRSG 311 14  Primary consideration: Acute Pericarditis: Nursing Assess and manage Management pain and anxiety ECG monitoring: distinguish ischemic pain from pericardial pain Ischemia: localized ST-segment changes Acute pericarditis: diffuse ST segment changes Pain relief: Maintain bed rest, head of bed elevated 45 degrees, overbed table for support Anti-inflammatory medications Anxiety reduction: Provide simple, complete explanations of procedures and possible cause of pain Monitor for: Sign of upper GI bleed (high doses of anti-inflammatory medications increase risk) Decreased cardiac output, cardiac tamponade Prepare for possible pericardiocentesis R. Stent Winter 2025 NRSG 311 15  Chronic Constrictive Pericarditis Results from scarring and loss of elasticity of pericardial sac; typically begins with initial episode of pericarditis Clinical manifestations: Over extended period, mimic heart failure and cor pulmonale Symptoms related to decreased cardiac output Dyspnea on exertion, peripheral edema, ascites, fatigue, anorexia, weight loss, elevated jugular venous pressure, pericardial knock on auscultation Interprofessional management: Treatment of choice is pericardiectomy unless asymptomatic or inoperable R. Stent Winter 2025 NRSG 311 16  Focal or diffuse inflammation of myocardium caused by: Myocarditi Viruses, bacteria, fungi, parasites s Radiation therapy Pharmacological factors Chemical factors Immune-mediated disease Idiopathic in some cases When myocardium becomes infected: Causative agent invades myocytes  cellular damage and necrosis Immune response activated Infection progresses, autoimmune response is activated  further destruction of myocytes  cardiac dysfunction R. Stent Winter 2025 NRSG 311 17  Myocarditis: Clinical Manifestations Variable, range from benign to severe, up to sudden cardiac death Early systemic manifestations: Fever, fatigue, malaise, myalgias, pharyngitis, dyspnea, lymphadenopathy, nausea, vomiting Early cardiac manifestations appear 7-10 days after viral infection: Pleuritic chest pain with pericardial friction rub and effusion Late cardiac signs relate to development of heart failure: S3 heart sound, crackles, jugular venous distension, syncope, peripheral edema, angina R. Stent Winter 2025 NRSG 311 18  Myocarditis: Diagnostic Studies ECG changes often non-specific, reflect associated pericardial involvement Dysrhythmias and conduction disturbances may be present Laboratory findings often inconclusive: May include mild to moderate leukocytosis; atypical lymphocytes; increased ESR and CRP; elevated myocardial markers (e.g. troponin); elevated viral titres Endomyocardial biopsy (EMB): Removing several small pieces of myocardial tissue percutaneously from right ventricle with special instrument called a bioptome Microscopic examination of heart samples May use echocardiography, nuclear scans, MRI to evaluate cardiac function R. Stent Winter 2025 NRSG 311 19  Myocarditis: Collaborative Care Treatment for patients with myocarditis with fulminant HF: Cardiovascular support with inotropic and/or vasopressor therapy Mechanical circulatory support (e.g., left ventricular assist device [LVAD]) Treatment for patients with both myocarditis and HF with reduced ejection fraction: Usual care for HF: β blockers, ACE-inhibitors/angiotensin receptor blocker or angiotensin- neprolysin inhibitor, mineralocorticoid receptor antagonist, and diuretic therapy Immuno-suppressive therapy: Help reduce myocardial inflammation and prevent irreversible myocardial damage General supportive measures: Oxygen therapy, bed rest, restricted activity, maintenance of standby emergency equipment R. Stent Winter 2025 NRSG 311 20  Myocarditis: Nursing Management Assess for signs and symptoms of HF Measures to decrease cardiac workload: semi-Fowler’s, space out activity and rest, provide quiet environment Ongoing Monitor effects of cardiac medications Nursing Diagnosis Assess and reduce anxiety : If receiving immunosuppressive therapy: Decrease Awareness of immune response changes, potential for infection, d cardiac complications output Most patients with myocarditis recover spontaneously Some may develop dilated cardiomyopathy If severe HF occurs, patient R. Stent Winter 2025 NRSG 311 may require heart transplantation 21  Case Study A 55-year-old male with a history of IV drug use presents with fever, night sweats, and new-onset murmur. Blood cultures grow staphylococcus aureus. 1. What diagnosis do you suspect? 2. What complications should the nurse monitor for? 3. What patient education is necessary to prevent recurrence? R. Stent Winter 2025 NRSG 311 22  Case Study A 40-year-old female presents with sharp, pleuritic chest pain that improves when sitting forward. She has a pericardial friction rub and diffuse ST elevations on ECG. 1. What are the priority nursing interventions? 2. What diagnosis do you suspect? 3. How does the suspected diagnosis differ from myocardial infarction in presentation? 4. What discharge education should be provided? R. Stent Winter 2025 NRSG 311 23  Rheumatic fever: inflammatory disease Rheumati Affects connective tissues of body (heart, brain, joints, skin) c Fever Potential to involve all layers of heart and Heart Rheumatic heart disease: Disease Chronic condition, results from rheumatic fever Characterized by scarring and deformity of heart valves Acute rheumatic fever (ARF) Complication, delayed result Rare in higher-income countries Myocardial involvement characterized by: Aschoff bodies: tiny, rounded, or spindle-shaped nodules Pericardial effusion may develop R. Stent Winter 2025 NRSG 311 24 Rheumatic Fever and Heart Disease: Clinical Manifestations Symptoms of ARF can include: Chest pain; excessive fatigue; heart palpitations; thumping sensation in chest; dyspnea; swollen ankles, wrists, or stomach When not severe: May be difficult to differentiate from illnesses with similar clinical manifestations R. Stent Winter 2025 NRSG 311 25  Rheumatic Fever and Heart Disease: Diagnostic Studies Diagnosis of ARF suggested by clustering signs and symptoms and laboratory findings No single diagnostic test Echocardiogram: may show valvular insufficiency and pericardial fluid or thickening Chest radiographic study: may show enlarged heart if HF present ECG: most consistent change is delayed AV conduction, evidenced by prolonged PR interval R. Stent Winter 2025 NRSG 311 26 Rheumatic Fever and Heart Disease: Collaborative Care Antibiotic therapy: Does not modify course of acute disease or development of carditis Eliminates organisms remaining in tonsils and pharynx, prevents spread Salicylates, NSAIDs, and corticosteroids Control fever and joint manifestations Salicylates and NSAIDs when arthritis is main manifestation Corticosteroids if severe carditis is present Supportive measures: Bed rest R. Stent Winter 2025 NRSG 311 27  Rheumatic Fever and Heart Disease: Nursing Management History and assessment Prevention, early detection, and immediate treatment of group A β-hemolytic Overall streptococcal pharyngitis to prevent rheumatic fever goals: Normal or Patient, family, and community education: baseline heart Seek medical attention for symptoms of streptococcal pharyngitis function Educate patient about importance of completing full antibiotic course Resume daily Acute intervention: activities Control/eradicate infecting organism without joint Prevent complications pain Relieve joint pain, fever, and other symptoms Verbalize Support patient psychologically and emotionally ability to Monitor fluid intake manage Promote optimal rest to reduce cardiac workload and diminish metabolic needs disease R. Stent Winter 2025 NRSG 311 28  Knowledge Check A patient with acute pericarditis reports increasing chest pain when lying down. Which intervention should the nurse implement first? a) Administer sublingual nitroglycerin b) Position the patient in a high-Fowler’s position c) Prepare the patient for emergency pericardiocentesis d) Encourage deep breathing exercises R. Stent Winter 2025 NRSG 311 29  Knowledge Check A patient with infective endocarditis (IE) is at risk for embolization. The nurse should monitor for which of the following as a possible sign of embolism? a) Petechiae on the chest and abdomen b) Splinter hemorrhages on the fingernails c) Sudden onset of left-sided weakness and confusion d) Janeway lesions on the palms and soles R. Stent Winter 2025 NRSG 311 30  Knowledge Check Which statement by a patient with a history of rheumatic fever indicates a need for further teaching? a) “I should take all my prescribed antibiotics, even if I feel better.” b) “I need to inform my dentist that I have a history of rheumatic fever.” c) “I only need antibiotics if I have a sore throat.” d) “I should watch for symptoms like joint pain and fever.” R. Stent Winter 2025 NRSG 311 31  Knowledge Check The nurse is caring for a patient with myocarditis. Which of the following assessment findings would be most concerning? a) Fatigue and generalized weakness b) Crackles in the lungs and S3 heart sound c) Mild chest discomfort and palpitations d) Low-grade fever and sore throat R. Stent Winter 2025 NRSG 311 32  In Class Learning Activity: Rapid Response to Cardiovascular Crisis! Objective: Work in groups of 4-5 (4 groups) to assess, prioritize, and intervene in a simulated cardiovascular scenario 1. Each group is a "nursing team" in a hospital setting 2. You will receive a patient case scenario 3. Each group will answer 3-4 structured questions 4. Each group will present a quick summary of their case and key nursing priorities R. Stent Winter 2025 NRSG 311 33 Break R. Stent Winter 2025 NRSG 311 34 Vascular Disorders Peripheral Artery Disease Acute Arterial Ischemic Disorders Peripheral Arterial Disorders Thromboangiitis Obliterans, Raynaud’s Phenomenon Aortic Aneurysm and Dissection Venous Disorders Phlebitis Venous Thromboembolism Varicose Veins Venous Insufficiency and Leg Ulcers R. Stent Winter 2025 NRSG 311 35 https://www.shutterstock.com/search/arterial-venous- system  Leading cause is atherosclerosis: Periphera Cholesterol and lipids deposited within the vessel walls l Arterial Progressive narrowing of arteries of upper and lower extremities Disease Risk factors: (PAD) Age, smoking, sedentary lifestyle, obesity, stress DM, kidney disease, associated with CAD HTN, hyperlipidemia, hypertriglyceridemia, hyperuricemia, hyperhomocysteinemia May affect: Aortoiliac, femoral, popliteal, tibial, and/or peroneal arteries Femoral popliteal most commonly affected in nondiabetic patients Below-knee arteries more commonly affected in patients with DM R. Stent Winter 2025 Advanced PAD: multiple NRSG 311 levels of occlusions 36 Peripheral Arterial Disease: Clinical Manifestations Intermittent claudication: Precipitated by exercise, resolves with rest, reproducible Physical appearance of limb: Thin, shiny, taught skin, hair loss on lower legs Patients with diabetes: altered foot architecture (e.g. hammer toes, Charcot deformity) Pedal, popliteal, or femoral pulses diminished or absent Changes in CWMS: Colour: pallor on elevation and dependent rubor Warmth: cool, temperature gradient down leg Severity Sensation: paresthesia in toes/feet; neuropathy, especially near ulcers depends on As PAD progresses: site, extent Continuous pain at rest aggravated by limb elevation of Dependent edema obstruction, and amount Complications: of collateral Critical limb ischemia circulation Arterial (ischemic) ulcers R. Stent Winter 2025 NRSG 311 37  Peripheral Arterial Disease: Diagnostic Studies Doppler Ultrasound with duplex imaging: maps blood flow through entire region of artery If cannot palpate peripheral pulse because of severe PAD, use Doppler ultrasound Segmental blood pressures: measured with Doppler ultrasonography and sphygmomanometer at thigh, below knee, and ankle Drop in segmental BP > 30mmHg suggests PAD Ankle-brachial index (ABI): Identifies presence and severity of PAD Normal ABI 1.00-1.40, indicates adequate BP in extremities ABI