CARDIAC INFLAMMATORY PROBLEMS/INFECTIOUS DISEASES OF THE HEART ENDOCARDITIS INFECTIVE ENDOCARDITIS - a microbial infection of the endothelial surface of the

he heart - develops in people with prosthetic heart valves or structural cardiac defects Clinical Manifestations: - primary presenting symptoms of infective pericarditis 1. fever 2. heart murmur Other S/S: 1. Clusters of petechiae on the body 2. Osler nodes in the pads of fingers or toes 3. Janeway lesions on palms, fingers, hands or soles and toes 4. Roth spots in the fundi of the eyes 5. Splinter hemorrhages under the fingernails and toenails 6. Petechiae in the conjunctiva and mucous membranes *Cardiomegaly, heart failure, tachycardia or splenomegaly may occur Assessment & Diagnostic Findings: 1. Blood cultures 2. Elevated white blood cells 3. Anemia 4. Elevated erythrocyte sedimentation rate 5. Microscopic hematuria on urinalysis 6. Doppler echocardiography Prevention: for high risk patients 1. Antibiotic prophylaxis 2. Good oral hygiene to prevent bacteremia 3. Avoid nail biting 4. Advise not to use IUD for females 5. Avoid body piercing Medical Management: Goal: eradicate the invading microorganism 1. Antibiotic therapy continuous IV infusion for 2-6 weeks 2. Antifungal agent (AmphotericinB) 3. Monitor temp. at regular intervals Surgical Management: 1. Valve debridement or excision 2. Debridement of vegetations 3. Debridement and closure of abscess 4. Closure of a fistula 5. Surgical valve replacement Nursing Management: 1. Monitor patients temp. 2. Assess heart sounds 3. Monitor signs of sytemic embolization 4. Assess signs of organ damage (stroke, meningitis, heart failure, MI, glomerulonephritis, splenomdegaly) 5. Assess invasive lines and wounds daily 6. Emphasize antibiotic prophylaxis 7. Provide emotional support and facilitate coping strategies

 RHEUMATIC ENDOCARDITIS - acute rheumatic which occurs most commonly in school-aged children - may develop after an episode of GABHS pharyngitis * RHEUMATIC HEART DISEASE is an inflammatory disease primarily affecting connective tissue, especially Cardiac valves * Myocardial involvement ASCHOFFS bodies, *Mitral and aortic valve are most commonly affected, either by valvular stenosis or valvular insufficiency Risk Factors/Etiology 1. Previous infection by beta-hemolytic streptococcus 2. Higher incidence in crowded living conditions and lower socio-economic groups 3. Occurs primarily in school-aged children Assessment 1. Symptoms vary 2. No specific symptom or sign is diagnostic of rheumatic fever Criteria for the diagnosis of RF requires a combination of symptoms to be present: 1. two major and one minor criteria 2. one major and two minor A. Major Criteria 1. Carditis murmur; Pericarditis tachycardia 2. Migratory Polyarthritis 3. Chorea 4. Erythema maarginatum 5. Subcutaneous nodules B. Minor Criteria 1. fever 2. arthralgia 3. hx of previous rheumattic fever 4. increase in sedimentation rate 5. anemia 6. positive C-reactive protein 7. Increased white count 8. EKG changes Complications - severe valvular damage may develop to CHF Treatment: 1. Adequate treatment of streptococcal infection 2. Bedrest until tachycardia subsides 3. Salicylates 4. Prophylactic tx initiated after acute therapy Nursing Management A. GOAL: To assist parents and family to provide home environment conducive to healing and recovery 1. Decrease activity 2. Encourage routine activities within the home 3. Friends may visit for short periods 4. Arrange for school work to be continued at home as appropriate 5. Maintain adequate nutrition - soft or liquid foods as tolerated - assist child with feeding - maintain adequate hydration 6. administer analgesics for arthralgia 7. reassure child that chorea and joint involvement is only temporary and there will be no residual damage B. GOAL: To assist parents to understand need for long-term prophylactic antibiotic therapy 1. importance of preventing recurring infections 2. include child in planning, especially when numerous injections are involved 3. importance of prophylactic therapy prior to invasive medical procedures 4. continued medical follow-up for the development of valvular problems as child grows

MYOCARDITIS - an inflammatory process involving the myocardium - can cause heart dilation, thrombi on the heart wall (mural thrombi), infiltration of circulating blood cells around the coronary vessels and between the muscle fibers and degeneration of the muscle fibers - may result from viral, bacterial, rickettsial, fungal, parasitic, protozoal or spirochetal infections

Clinical Manifestations: Depend on the type of infection, degree of myocardial damage and the capacity of the myocardium to recover *Patient may be asymptomatic with an infection that resolves on its own 1. Fatigue 2. Dyspnea 3. Palpitations 4. Occasional discomfort in the chest and abdomen Most common symptoms are flu-like

Assessment & Diagnostic Methods: Patient may reveal no detectable abnormalities Patients may be tachycardic or may report chest pain Cardiac MRI ST-T wave changes on ECG Elevated WBC and ESR Prevention: Appropriate immunization and early treatment Medical Management: 1. Specific treatment for the underlying cause 2. Bedrest to decrease cardiac workload Nursing Management: 1. Assess for resolution of tachycardia, fever and other S/S 2. Continuous cardiac monitoring for patients with dysrhythmias 3. Anti-embolism stockings and passive and active exercises should be used PERICARDITIS refers to the inflammation of the pericardium may occur 10 days to 2 months after acute MI (Dressler Syndrome) occur following cardiac surgery Causes: 1. idiopathic or non-specific cause 2. infection (viral) 3. disorders of connective tissue 4. hypersensitivity states (immune reactions, medication reactions) 5. disorders of adjacent structures (MI, pleural and pulmonary disease) 6. neoplastic diseases 7. radiation therapy of chest and upper torso 8. trauma 9. renal failure and uremia 10. tuberculosis Clinical Manifestastions: 1. May be asymptomatic 2. Chest pain most characteristic symptom 3. Creaky or scratchy friction rub heard at left lower sternal border most characteristic sign 4. Mild fever 5. Increased WBC count 6. Anemia 7. Elevated ESR or C reactive protein level 8. Non-productive cough 9. dyspnea

Assessment And Diagnostic Methods: 1. Made on the basis of hx, s/s 2. Echocardiogram help confirm diagnosis 3. TEE 4. CT 5. MRI 6. ECG concave elevations, decreased PR segments, atrial dysrhythmias Medical Management: OBJECTIVE : Determine the cause, administer therapy for tx and symptom relief and detect s/s of cardiac tamponade 1. Bedrest until fever, chest pain and friction rub has subsided 2. Analgesics and NSAIDs 3. Corticosteroids if severe Nursing Management: 1. Administer analgesic as ordered 2. Position properly 3. Provide psychological support 4. Help client with activity restrictions 5. Educate client and family about healthy lifestyle to enhance the patients immune system 6. Monitor patient for heart failure HEART FAILURE Is failure of the heart to pump an adequate amount of blood It is the inability of the heart to pump adequate amounts of blood into the systemic circulation in order to meet tissue metabolic demands Causes 1. Infection 2. Anemia 3. Thyrotoxicosis and pregnancy 4. Arryhthmias 5. Rheumatic, viral, and other forms of myocarditis 6. Infective endocarditis 7. Physical, dietary, fluid, environmental and emotional excesses 8. Systemic HPN 9. MI 10. Pulmonary embolism Clinical Manifestation 1. Left Sided Heart Failure (respiratory manifestations) Dyspnea Orthopnea PND cheyne-stokes respirations cough extra heart sound, S3/ventricular gallop crackles hemoptysis 2. Right Sided Heart Failure neck vein distention hepatomegaly edema ascites hypoglycemia palpitations 3. Impaired Cardiac Function Tachycardia displaced PMI S3 or S4 In infants, a failure to thrive and gain adequate weight 4. fatigue and weakness

5. Anorexia and nausea 6. Cerebral symptoms alterations in mental state Pathogenesis 1. Activation of neurohormonal compensatory mechanisms 2. Systolic HF blood volume from ventricles 3. Decrease ventricular stretch sense by baroreceptors in aortic and carotid bodies 4. Sympathetic NS stimulation release epinephrine and norepuinephrine 5. Increased HR and contractility 6. Causes vasoconstriction in the skin, GIT and kidneys 7. Decreased renal perfusion release of renin 8. Promotes formation of Angiotensin I 9. Angiotensin I converted to Angiotensin II by ACE in the lumen of pulmonary blood vessels Increased BP and afterload 10. Angiotensin II stimulates release of Aldosterone 11. Fluid retention and stimulation of antidiuretic hormone 12. Fluid volume overload 13. Increased heart workload, decreased contractility of myocardial muscle fibers 14. Increased end diastolic blood volume in the ventricles 15. Stretching myocardial muscle fibers and increase ventricular size 16. Compensatory mechanism (ventricular hypertrophy) Assessment and Diagnostic Methods Undetected until the patient presents with signs and symptoms of pulmonary and peripheral edema Assessment of ventricular function Echocardiogram Chest x-ray ECG Serum electrolytes BUN creatinine Thyroid stimulating hormone CBC BNP Routine urinalysis Cardiac stress testing or cardiac catheterization Treatment Goal relieve patients symptoms, improve functional status and quality of life, and to extend survival Divided into four components: 1. removal of the precipitating cause 2. correction of the underlying cause 3. prevention of deterioration of cardiac function 4. control of congestive HF state 3 Ds in Treatment: 1. Diet 2. Digitalis 3. Diuretics Several medications routinely prescribed: 1. ACE inhibitors 2. Angiotensin II receptor blockers 3. Hydralazine and Isosorbide dinitrate 4. Beta blockers 5. Diuretics a. loop diuretic b. thiazide c. aldosterone blocking 6. Digitalis 7. Calcium channel blockers 8. Intravenous infusions a. Nesiritide

b. Milrinone c. Dobutamine Additional Therapy 1. Supplementtal O2 2. Coronary artery bypass surgery if the patient has underlying CAD 3. Cardiac resynchronization therapy (CRT) Complications: 1. Intractable heart failure 2. Pulmonary infarction 3. MI 4. Digitalis toxicity 5. Cardiac arrythmias 6. Pneumonia 7. Pulmonary edema 8. Cardiogenic shock Nursing Interventions: 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. Place client in high fowlers position with legs in dependent position Administer O2 in high concentrations by mask or cannula as prescribed Prepare for intubation and ventilator support if required; monitor lung sounds for crackles and decreased breath sounds Suction fluids as needed Assess level of consciousness Provide reassurance to the client Monitor V/S closely, noting tachycardia or pulsus alterans Monitor for hypotension resulting from decreased tissue perfusion or hypertension resulting from anxiety or hx of hypertension Monitor heart rate and for dysrhythmias by using a cardiac monitor Assess for edema in dependent areas and in the sacral, lumbar and posterior thigh region in the client on bed rest. Insert a foley catheter as prescribed and monitor urine output closely following administration of diuretics Monitor intake and output Avoid the unnecessary IV administration of fluids Administer diuretic, digitalis as prescribed Administer bronchodilators and vasodilators as prescribed Monitor weight to determine response to treatment Assess for hepatomegaly and ascites and measure and record abdominal girth Monitor peripheral pulses Analyze ABG results and electrolyte values for imbalances Monitor potassium level closely

CORONARY ARTERY DISEASE Risk Factors A. Non-modifiable 1. family hx of CAD 2. Increasing age more than 45 for men and more than 55 in women 3. Gender 4. Race - higher incidence in African Americans than in Caucasians B. Modifiable factors 1. hyperlipedemia 2. cigarette smoking, tobacco use 3. HPN 4. DM 5. Metabolic syndrome 6. Obesity 7. Physical inactivity Clinical Manifestations

1. 2. 3. 4. 5. 6. 7.

Cardiac ischemia inadequate oxygenated bloodsupply to the cardiac muscle cells Chest pain Palpitations Dyspnea Syncope Cough or hemoptysis Excessive fatigue

Assessmentt & Diagnostic Methods 1. ECG ST segment depression or T wave inversion in ischemia and ST segment elevation and T wave inversion in infarction or cell injury 2. Cardiac catheterization most definitive source of diagnosis, shows atherosclerotic lesion 3. Blood lipid levels are elevated Medical Management A. Pharmacologic therapy 1. cholesterol lowering medications B. Cessation of tobacco use C. Managing HPN and DM D. Dietary measures Mediterrenean diet - ingestion of vegetables and fish and limits red meats low calorie, low sodium, low cholesterol and low fat diet with soluble dietary fibers E. Weight reduction and increased physical activity Surgical Procedures 1. PTCA to compress the plaque against the walls of the artery and dilate the vessels 2. Laser angioplasty to vaporize the plaque 3. Atherectomy to remove the plaque from the artery 4. Vascular stent to prevent the artery from closing and to prevent restenosis 5. Coronary artery bypass graft to improve blood flow to the myocardial tissue Nursing Interventions 1. Assist the client to identify risk factors that can be modified 2. Assist the client to set goals to promote lifestyle changes 3. Instruct the client regarding a low calorie, low sodium, low cholesterol and low fat with increase in dietary fiber 4. Stress that dietary changes must be maintained for life 5. Instruct regarding prescribed medications 6. Provide community resources to the client regarding exercise, smoking cessation and stress reduction as appropriate 7. instruct the client regarding the purpose of diagnostic and surgical procedures ANGINA PECTORIS Is chest pain resulting from myocardial ischemia caused by inadequate myocardial blood and oxygen supply A clinical syndrome usually characterized by episodes or paroxysms of pain or pressure in the anterior chest The causes are atherosclerotic disease, coronary artery spasm & conditions increasing myocardial oxygen consumption TYPES/PATTERNS: 1. Stable angina (classic) occurring intermittentlyover a long period of time with the same pattern of onset, duration and intensity of symptoms occurs on exertion and is relieved by rest or nitroglycerin also called as exertional angina 2. Unstable angina symptoms increase in frequency and severity, may not be relieved with rest or nitroglycerin also called as preinfarction angina occurs with unpredictable degree of exertion or emotion and increases in occurrence, duration and severity over time 3. Variant Angina pain at rest with reversible ST segment elevation thought to be caused by coronary artery vasospasm also called as Prinzmetals angina or vasospastic angina 4. Intractable angina

5.

a chronic, severe incapacitating angina that is unresponsive to intervention

Preinfarction angina associated with acute coronary insufficiency last longer than 15 minutes symptom of worsening cardiac ischemia Postinfarction angina occurs after an MI when residual ischemia may cause episodes of angina Silent ischemia objective evidence of ischemia (ECG) but patient reports no pain Nocturnal angina occurs only at night but not necessarily when the person is in the recumbent position or during sleep

6.

7.

8.

Contributory Factors 1. Physical exertion 2. Exposure to cold 3. Eating a heavy meal 4. Stress or any emotion provoking situations Clinical Manifestations 1. Pain - deep in the chest behind the sternum; radiate to the shoulders, arms, jaw, neck and back - usually lasts less than 5 minutes, however pain can lasts for 15-20 minutes 2. Weakness or numbness in the arms, wrists and hands 3. Shortness of breath 4. Pallor 5. Diaphoresis 6. Dizziness or lightheadedness 7. N/V Assessment and Diagnostic Methods 1. Hx related to the clinical manifestations of ischemia 2. ECG T wave inversion 3. Exercise or Pharmacologic stress test 4. Cardiac catheterization provides a definitive diagnosis ; provides information about the patency of coronary arteries Medical Management 1. Pharmacologic therapy a. Nitroglycerin b. Beta adrenergic blocking agents c. Calcium Channel blocking agents d. Antiplatelet and anticoagulant 2. O2 administration Nursing Management 1. Assess pain 2. Provide bed rest 3. Administer O2 at 3L/min by nasal cannula as prescribed 4. Administer nitroglycerin as prescribed 5. Obtain a 12 lead ECG 6. Provide continuous cardiac monitoring 7. Instruct client regarding prescribed medications 8. Provide dietary instructions 9. Assist client to set goals 10. Provide community resources regarding exercise, smoking cessation and stress reduction

MYOCARDIAL INFARCTION (MI/Coronary Occlusion/Heart Attack) Occurs when myocardial tissue is abruptly and severely deprived of oxygen Does not occur instantly but evolves over several hours Obvious physical changes does not occur in the heart until 6 hours after the infarction when the infarcted area appears blue and swollen after 48 hours it turns to gray with yellow streaks as neutrophils invades the tissues by 8-10 days , granulation tissue forms over 2-3 months, the necrotic area develops into scar which changes the shape of the ventricle

*Danger of death is greatest during the first 2 hours Causes 1.

2.

Decrease blood supply - atherosclerosis - spasms of artery - embolic occlusion of artery Decrease O2 in the blood - anemia - carbon monoxide

- alkalemia, shifting O2 supply to tissue - cyanide 3. Increase demand for blood - HPN - hypertrophy - valvular stenosis/insufficiency - hyperthyroidism - hyperthermia - stress producing cathecolamines - dilatation of the heart Risk Factors 1. Atherosclerosis 2. CAD 3. Elevated cholesterol levels 4. Smoking 5. HPN 6. Obesity 7. Physical inactivity 8. Impaired glucose tolerance 9. stress Location of MI Obstruction of the left anterior descending artery results in anterior or septal MI or both Obstruction of the circumflex artery results in posterior wall MI or lateral wall MI Obstruction of the right coronary artery results in inferior wall MI Clinical Manifestations 1. Typical pain severe crushing substernal pain unrelieved by nitroglycerin, rest - occur primarily in the morning and lasts 30 minutes or longer 2. N/V 3. Diaphoresis 4. Dyspnea 5. Dysrhythmias 6. 7. 8. Denial of the seriousness of the problem pale/dusky skin Extreme weakness

9.

Decrease in blood pressure

10. Tachycardia 11. Syncope 12. No signs or symptoms Complications Cardiogenic shock Dysrhythmias CHF Papillary muscle dysfunction Pericarditis Cardiac rupture

Assessment & Diagnostic Methods 1. Total creatine kinase level rises within 3 hrs. after onset of chest pain and peaks in 24 hours after damage and death of cardiac tissue 2. CK-MB Isoenzymes peak elevation at 18-24 hours after onset of chest pain; returns to normal 48-72 hours later 3. Troponin level rises within 3 hours and remains elevated for 7 days 4. Myoglobin rises within 1 hour after cell death, peaks in 4-6 hours and returns to normal within 24-36 hours or less 5. LDH level rises after 24 hours and peaks between 48 and 72 hours and falls to normal in 7 days 6. Elevated WBC 7. ECG ST segment elevation, T wave inversion and abnormal Q wave Medical Management 1. Supplemental O2 2. Rest 3. IV therapy 4. Medications a. analgesics b. antidysrhythmic agents c. Ca Channel blocking agents d. Sedatives e. Stool softeners 5. Thrombolytic therapy 6. Pacemaker if conduction problems occur 7. Dietary restrictions a. initially NPO or on a liquid diet b. progress to DAT-low sodium and low cholesterol c. decrease intake of stimulants 8. Open heart surgery for myocardial revascularization 9. PTCA Nursing Management 1. Assess chest pain and monitor V/S 2. Maintain cardiac monitoring 3. Place in semi-fowlers position 4. Administer O2 at 2-4 L/min by nasal cannula as prescribed 5. Establish an IV access route 6. Administer morphine SO4 as prescribed 7. Administer nitroglycerin and other medicatios as prescribed 8. 8. Obtain ECG 9. 9. Monitor for sing of bleeding if receiving thrombolytic therapy

10. 10. Monitor for complications 11. 11. Assess distal peripheral pulses ands skin temperature 12. 12. Monitor I & O

ANEURYSMS (Aortic, Thoracic, Abdominal, Dissecting, Rupturing) Abnormal dilation of the arterial wall caused by localized weakness and stretching in the medial layer of an artery A dilation or sac formed on the wall of an arterial vessel Can be located anywhere along the abdominal aorta May involve only one layer or all layers of the arterial wall Types of Aortic Aneurysm 1. Fusiform diffuse dilation that involves the entire circumference of the arterial segment 2. Saccular - distnct localized outpouching of the artery wall 3. Dissecting created when blood separates the layers of the artery wall forming a cavity between them 4. False (Pseudoaneyrysm) Occurs when the clot and connective tissue are outside the arterial wall Occurs as a result of vessel injury or trauma to all three layers of the arterial wall Assessment A. Thoracic occurs in men ages 50-70 - caused by atherosclerosis, infection, syphillis and HPN 1. pain extending to the neck, shoulders, lower back or abdomen 2. syncope 3. dyspnea 4. increased pulse 5. weakness B. Abdominal - occur most in men over age 60, caused by atherosclerosis, HPN, trauma, syphillis, other types of infectious process 1. prominent, pulsating mass in the abdomen at or above the umbilicus 2. systolic bruit over the aorta 3. tenderness on deep palpation 4. abdominal or lower back pain C. Rupturing 1. severe abdominal or back pain 2. lumbar pain radiating to the flank and groin 3. hypotension 4. increased pulse rate 5. signs of shock Dignostic Methods Abdominal ultrasound CT Arteriography Treatment Goal: To prevent rupture and improve blood circulation 1. surgical resection or excision 2. antihypertensive drugs