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Cardiovascular System Nursing 1120 By: Diana Blum RN MSN Metropolitan Community College 1 2 3 Coronary Arteries • Two major coronary arteries – arise from the aorta beyond the aortic valve. – Blood flows to the coronary arteries during diastole • Left main, LAD, Circumflex feeds most of Left side of the heart • Right feeds SA node, AV node, RA, RL 4 5 Collateral circulation is a network of tiny blood vessels, and, under normal conditions, not open. When the coronary arteries narrow to the point that blood flow to the heart muscle is limited (coronary artery disease), collateral vessels may enlarge and become active. This allows blood to flow around the blocked artery to another artery nearby or to the same artery past the blockage, protecting the heart tissue from injury. 6 Conduction Continued 7 Cardiac Cycle • Contraction and relaxation of the heart: • Diastole: • Systole: 8 • Video Mysterious Heart Volume 2 chapter 3 9 Cardiac Output • the volume of blood ejected by the heart each minute and is determined by stroke volume and the heart rate. • Normal stroke volume is 60-100 ml • Normal cardiac output is 4 to 8 L / min • (CO = HR X SV) 10 Factors affecting Stroke Volume • Preload: the amount of blood remaining in the ventricles at the end of diastole or the pressure generated at the end of diastole • Contractility: is the ability of the cardiac muscle fibers to shorten and produce a muscle contraction. (Inotropic, + or -) • Afterload: amount of pressure the Ventricle must overcome to eject blood volume out 11 Heart Rate • SA node : pacemaker of heart 60-100 bpm • AV node : 40 -60 bpm • Heart is innervated by sympathetic and parasympathetic nervous system – Sympathetic: speeds HR, and increases force of contraction – Parasympathetic: slows HR and force 12 Heart Tones • Murmur: Produced by turbulent sounds across valves – Rub: inflamed pericardium-best heard along left sternal border – S3 murmur: sounds like “Kentucky” – S4 murmur: sounds like “Mississippi” http://www.blaufuss.org/ http://www.med.ucla.edu/wilkes/ Rubintro.htm 13 Health History 14 Present Illness 15 Past Medical History 16 Family History: 17 Review of systems • • • • • • • • • • weight gain fatigue dyspnea cough orthopnea palpitations chest pain fainting concentrated urine edema 18 Functional assessment • • • • • effects of illness on ADLs and rest patterns smoker diet stress coping 19 Physical Assessment • General: • VS: orthostatic bp in both arms, apical rate and rhythm, respiratory rate and effort • peripheral pulses: • Skin: color hair distribution, cap refill, temp • Thorax: heart sounds, lung sounds, sputum • Extremities: pulses, color, temp, edema 20 Age Related Changes • Heart less able to adapt to changing needs related to activity • Valves thicken and stiffen • # of pacemaker cells decrease • Nerve fibers decrease • Frequent dysrhythmias 21 Diagnostic Tests • EKG: rate, rhythm, ischemia (T-inverted), injury (ST segment elevation), arrhythmias, strain, infarction (q wave) • Echocardiogram: (TEE) sound wave test detects size of chambers, valve integrity, flow, wall motion, Cardiac Output 22 Diagnostic Tests Continued Biomarkers: Troponin will show elevation 3-4 hr after injury <0.10 is negative 0.10-0.60 is intermediate and may indicate injury >0.60 is positive evidence of MI Myoglobin increases 1-4 hours after MI CPK-MB will show increase 4 hrs after MI BNP can be elevated 48 hrs after MI which indicates heart failure 23 Diagnostic Tests Continued • • • • • CBC: anemia CMP: screening K+, etc PT, INR PTT Lipid profile: see next 2 slides 24 Total cholesterol Below 200 mg/dL Desirable 200-239 mg/dL Borderline high 240 mg/dL and above High LDL cholesterol Below 70 mg/dL Optimal for people at very high risk of heart disease Below 100 mg/dL Optimal for people at risk of heart disease 100-129 mg/dL Near optimal 130-159 mg/dL Borderline high 160-189 mg/dL High 190 mg/dL and above Very high 25 HDL cholesterol Below 40 mg/dL Poor 40-59 mg/dL Better 60 mg/dL and above Best Triglycerides Below 150 mg/dL Desirable 150-199 mg/dL Borderline high 200-499 mg/dL High 500 or above Very high 26 Diagnostic Tests Continued • • • • • ABG: assess acid/base levels Pulse Oximetry: generally >92% Holter monitoring: 24+ hr of EKG + events Stress test: treadmill or pharmacological Cardiac Catheterization: invasive, NPO 6-8h, consent. Visualizes chambers, valves, arteries, pressures, CO • Heart-CT scan: assesses CAD, MRI • Nuclear scans: assess heart muscle viability • EPS: NPO, consent, IV, assess electrical activity 27 • http://preop.medselfed.com/as p/center.asp?centerId=heart&p artnerId=preop&id=&cachedate =&emailId=&affId=&campId=&hi deNav= 28 CAD Video-mysterious heart volume 3 chapter 2 29 Etiology of CAD • CAD occurs when the intimal lining of the coronaries begin to plaque resulting in jagged edges and narrowed passageway for blood flow • Atherosclerosis results in impaired blood flow to the heart muscle 30 Risk Factors for CAD Non-controllable Controllable- 31 s/s of CAD • Angina which results from a lack of 0xygen to the heart muscle – 4Es= • Weakness, diaphoresis, SOB • N/V 32 MI: Myocardial Infarction • Occlusion of a coronary artery resulting in necrosis of the heart muscle. • Risk factors: same as for CAD • Pathophysiology: AMI-over 4-6 hrs ischemia injury and infarction develop. Ischemia=lack of 02 to heart muscle, if not relieved=injury. After 20 min of ischemia=infarction • Main S/S: chest pain and accompanying S/S 33 • Within 24 hours after infarction, healing begins, collateral circulation begins. • 10-14 days after MI=extension of MI may occur due to myocardial tissue vulnerability to stress • Complete scar formation and healing takes about 6 weeks • Video- mysterious heart volume 1 chapter 2 34 Data Collection Same as for CAD but will assess symptom of chest pain with accompanying s/s May have EKG changes with or with-out ST-T wave changes or Q wave changes Cardiac Bio-markers (Troponin, Myoglobin, CPK, CKMB) May proceed with Echocardiogram to assess if wall motion sluggish May go to cath lab 35 Angina or MI • Angina without MI} often relieved with rest and NTG • Angina with MI } may be relieved with rest, NTG, 02, MS, rescue angioplasty, etc. • Think MONA – Morphine – Oxygen – Nitroglycerin – Aspirin http://www.youtube.com/watch?v=4GlQmTlP2jE&feat ure=related http://www.youtube.com/watch?v=rEqw3AKM_g 36 Treatment continued…video mysterious heart volume 3 chapter 37 ASA: MS: Beta-blocker ACE inhibitor: 37 Treatment continued – May need antiarrhythmic meds • like what??? – Stool softeners to reduce valsalva maneuver and prevent constipation r/t narcotic use and bed rest – Treat: HTN, DM other co-morbid illnesses – Cardiac Rehab to follow 38 Treatments • Low fat low cholesterol diet • Prescribed exercise program 5-7 days a week • Knows correct use of NTG for angina • Management of DM, HTN • Stop smoking • Medications to reduce work load or dilate 39 Low salt diet (<2000mg) does not include: • Soups: • Snacks: 40 Low fat <30% Low cholesterol <200mg • • • • Lean meat: skinless Dairy limited: egg beaters, skim milk Olive oil, canola oil Avoid: fried, fatty or heavily marbled meats, sausage, lunch meat, spareribs, frankfurters, salt pork, canned fish in oil, yolks, duck. Cream sauces, gravy, buttered vegetables, sweet rolls, other processed foods 41 Exercise • 5-7 X week is goal to include stretches with warm-up, progressive walking program, light weights, stretches with cool down. • Strengthens heart muscle, reduces BP, BS, weight, stress, tension, appetite, LDLs. • Increases HDLs, energy and self esteem and improves immune system 42 Principles of Exercise • Practice on regular basis • Know how to do own pulse • Strive for target heart rate • Stop if chest pain occurs • Complications: CHF & Dysrhythmias 43 Nursing interventions for MI • Comfort measures • Freq VS, cardiac monitoring, I&O, CMS checks, spacing activities • Heart & lung sounds, assess fluid volume status, IV responsibilities, note BP & Pulse prior to heart meds!! • Client education r/t diet, meds, pulse taking activity, elimination, reporting chest pain and correct use of nitro products for angina 44 Medications for Heart Disease • • • • Anti-Anginal: Anti-Hypertensive: Anti-Arrhythmic: l Cardiac glycoside: 45 Medication continued • • • • • • Thrombolytic: Anti-coagulant: Anti-platelet aggregate: Lipid-Lowering agents: Diuretics: Electrolyte replacement: 46 Medication continued • 02 to maintain 02 sat > 92% to reduce chance of angina/ischemia • If Angina the nurse needs to have the client lie down, take VS then report to charge nurse ,met team, call md. • Instruct client: If develops chest pain, sit down take 1 nitro every 3- 5 min x 3. If chest pain not relieved call 911 47 •POST MI Complications 48 • 90% will develop complication and 80% will demonstrate arrhythmia which is the most common cause of death in clients in the pre-hospital period. (VT>>>VF) • CHF and severe Left ventricular failure • Papillary muscle dysfunction • Pericarditis • Thromboembolism • Ventricle rupture 49 Nursing Diagnosis • Decreased cardiac output r/t Dysrhythmias • Acute Pain r/t lack of 02 to myocardium • Anxiety r/t to feeling of doom, lack of understanding of medical diagnosis 50 •Surgical Procedures 51 Pacemaker • New in 1958 having purpose to restore the regular rhythm and to improve tissue perfusion and cardiac output. • Temporary / permanent • Single chamber or double chamber • Teach client how to take 1 min pulse, s/s to report to MD-dizzy, angina, dyspnea • Carry card and know precautions 52 Video- mysterious heart volume 2 chapter 4 53 AICD • Implantable defibrillator to correct a life threatening rhythm disturbance. – Has pacemaker back-up. • check battery q2months • Instruct on how to take pulse for 1 min • s/s to report to MD: firing, s/s of dizziness, dyspnea, weakness, carry card and wear bracelet, CPR for family. Know precautions 54 • Nursing care for client with newly implanted pacemaker or AICD. – Assess cardiac monitor for capture/pacing (pacer) – VS post-op then q 4 hours, IV, bed rest till am – Dressing dry and intact until AM then often may remove. Increase activity progressively – Instruct client not to raise arm above shoulder for 5days. May shower in 5 days 55 Angioplasty with Stent • Procedure done at the time of cardiac cath. • Balloon angioplasty is accomplished to widen or open specific coronary vessel-stent is inserted to maintain patency of the vessel. • pre-procedure Plavix given with follow up Plavix http://preop.medselfed.com/asp/center.asp ?centerId=heart&partnerId=preop&id=&ca chedate=&emailId=&affId=&campId=&hid eNav= 56 EP with Ablation • Mapping of myocardial tissue to determine irritable focus. • Low voltage current delivered to ablate tissue causing SVT or VT • 90% effective • http://video.google.com/videop lay?docid=5590000557631435292 57 Nursing Care • NPO prior • Coumadin stopped 4 days prior, Heparin 4 hours prior • Post – procedure same as heart cath – Cardiac monitoring – Muscloskeletal and groin checks – VS – Ambulate prior to discharge 58 Cardiac Surgery • Coronary artery bypass • • Valve replacement or repair • Septal repair and other congenital repairs – CCU post op, chest tubes – Pre-op teaching with post op expectations – See client teaching for CABG, Valve repair/replacement, care of PTCA, MI 59 • http://preop.medselfed.com/as p/center.asp?centerId=heart&p artnerId=preop&id=&cachedate =&emailId=&affId=&campId=&hi deNav= 60 Congestive Heart Failure • Video..the mysterious heart volume1 chapter 3 61 62 • DEFINITION:EF < ____% or when the myocardium is no longer able to pump efficiently 63 • Systolic failure= most common 64 Causes of CHF • CAD, advancing age • HTN is a major factor > CHF x 3 • DM, Smoking, Obesity • Valvular incompetency, alcohol or other chemicals, idiopathic,(unknown) 65 S/S of Left Sided CHF • • • • • • • • Fatigue Angina Tachycardia Cool extremities Hacking cough Crackles Frothy sputum Gallop 66 S/S of Right Sided CHF • Jugular distention • Anorexia/nausea • Dependent edema • Distended abdomen • Weight gain • BP problems 67 Assessment Findings • C/O SOB, weakness, dry cough, fatigue, can not lie down must sit up to breath, has gained weight • Auscultation of the heart} rapid HR, extra heart sounds • Auscultation of the lungs} rales, wheezing • Examination of the extremities for peripheral edema 68 69 System Compensation • Mediated thru Sympathetic Nervous System: as CO drops, baroreceptors alert brain • – This causes stimulation Beta 1=>> – Stimulation Beta 2= – Activate Alpha receptors peripherally=constriction=>> 70 Compensation • Causing S/S of CHF because: • Contractility decreases • Stroke volume and CO continue to decrease • Afterload (pressure on the other side of the aorta) increases • Preload ( pressure caused by increase volume to heart creating an exaggerated stretch in the muscle) increases 71 Renal Compensation • CO drops initiating renin-angiotensin mechanism – Results in powerful vasoconstrictor 72 Ventricular Hypertrophy • The heart enlarges which results in strain • The increase in volume causes the ventricles to dilate • Eventually remodeling will occur 73 Diagnostic Tests • • • • • • • • • H&P Chest x-ray EKG: Echocardiogram: CBC: CMP: Thyroid function ABGs BNP=B type natriuretic peptide= hormone released in response to Ventricular stretch ( CHF peptide) • Nuclear studies to determine heart function, EF, tissue viability • Cardiac Cath to determine exact nature of heart74 function 75 CHF Management • Directed at: Improving LV function (Contractility) by decreasing intravascular volume and decreasing vascular resistance • Decreasing venous return (Preload) • Decreasing BP (Afterload) • Improving gas exchange and 02 • Increasing the CO and reducing anxiety 76 continued • ACE inhibitors to < afterload by dilating vessels and < BP (ARBs) • Beta blockers to < 02 demand by reducing the contractility of the heart and HR (not given in acute period) • Diuretics <preload by reducing volume returning to the heart-Lasix & (Aldosterone Antagonists) K+ supplement 77 continued • ASA in low doses or Plavix to help prevent blood clot formation • Anticoagulants for those with poor EFs to prevent CVA • Antiarrhythmics to control ectopy • Biventricular pacing (CRT=cardiac resynchronization therapy) to improve CO • Digoxin to increase contractility of myocardial fibers and improving cardiac output. +inotropic agent 78 Treatment of CHF • Treat underlying cause • Rest and hi Fowlers to reduce work load and improve ventilation • 02 at 2-6 L/min with 02 sats >92% to increase available 02 and prevent hypoxemia • Freq VS and cardiac monitoring 79 Treatment continued • I & O q shift • Daily am weights before breakfast and after voiding. 2-3# weight gain in 1-4 days call MD • Sodium restricted diet • Medications: to decrease intravascular volume thus reducing venous return, dilate and reduce BP and improve contractility • http://chfsolutions.com/zip_how_aquapher esis_works.html# 80 Educating the CHF Client • Education re: heart failure – Explanation of heart failure – Expected S/S and when to call MD – Self monitoring of daily weights – Know medications and need to take them – 2000mg sodium restricted diet – Importance of low level daily exercise program (energy conservation) – Prognosis / advanced directives 81 • Telemetry Interpretation/ Dysrhythmias 82 Lead Placement 83 • A dysrhythmia is a disturbance of the rhythm of the heart caused by a problem in the conduction system. • Categorized by site of origin: atrial , AV nodal, ventricular • Blocks are interruptions in impulse conduction: 1st, 2nd type 1&2, 3rd or complete heart block 84 Each small box measures 0.04 1 big box (5 small boxes) is equal to a HR of 300 2 big boxes is hr of 150 3 big boxes is hr of 100 4 big boxes is hr of 75 5 big boxes is hr of 60 6 big boxes is hr of 50 7 big boxes is hr of 43 8 big boxes is hr of 38 85 • P-wave = atrial electrical activity • QRS= ventricular electrical activity • T wave= resting phase of ventricle 86 87 P wave Measures: 0.12-0.20 88 QRS WAVE Measures: 0.06-0.10 89 QT Wave 90 Heart rates • NSR: heart rate is ___bpm • ST: heart rate ____ bpm • SB: heart rate ____bpm 91 NSR 92 Sinus rhythm •PR interval- 0.12-0.20sec • QRS-0.06-0.10sec • QT segment 0.36-0.44 sec •Heart rate 60-100 93 •Hr= 60-100 bpm •On strip it looks regular but does not map out •PR interval= 0.12-0.20 94 HR 40-60 bpm <60 bpm is accelerated Rhythm is regular Pwaves not always present 95 SB 96 Sinus Bradycardia • All criteria same except rate < 60bpm • S/S: dizziness, syncope, angina, hypotension, sweating, nausea, dyspnea • Sometimes no S/S • Treat underlying cause • IV atropine, pacemaker 97 ST 98 Sinus Tachycardia • All criteria same as with NSR except rate >100 • Causes: fever, dehydration, hypovolemia, increased sympathetic nervous system stimulation, stress, exercise, AMI • S/S: Palpations #1, angina and < CO from < V filling time • Treatment: correct cause, eliminate caffeine, nicotine, alcohol. Beta blockers may be ordered 99 Rate is usually WNL Rhythm is regular Pwaves are normal in size and shape The PR interval is prolonged (>0.20 sec) but constant 100 www.unm.edu/~lkravitz/EKG/avblocks.htm l 101 Pwaves are normal in size and shape; Some pwaves are not followed by QRS PR interval: lengthens with each cycle until it appears without QRS Complex then the cycle starts over QRS is usually narrow 102 www.unm.edu/~lkravitz/EKG/avblocks.htm l 103 Ventricular rate is usually slow Rhythm is irregular Pwaves are normal in size and shape (more pwaves than QRS) PR interval is within normal limits QRS is usually wide 104 www.unm.edu/~lkravitz/EKG/avblocks.htm l 105 Ventricular rate is regular but there is no correlation between pwaves and QRS Pwaves are normal in size and shape No true PR interval 106 www.unm.edu/~lkravitz/EKG/avblocks.htm l 107 Atrial Fibrillation Erratic wavy base Pr is not measurable QRS 0.10 sec or less usually http://www.youtube.com/watch?v=VKxQgjj2yVU&f 108 A fib continued • Atrial rate > 400 bpm with a varying Ventricular rate • Overall rhythm irregular • No P waves, unable to measure PR interval • QRS=normal: Twave undeterminable • Causes: Rheumatic fever, mitral valve stenosis, cad. HTN, MI, hyperthyroidism, COPD, CHF see pp. 604 109 A fib continued • Concern with A fib is the development of atrial thrombus and loss of atrial kick from ineffective atrial function. • Treatment: Ca channel blockers and anti- arrhythmics to convert, beta blockers to < HR, anticoagulants to prevent embolization. • Synchronized cardioversion 110 Atrial rate of 250-450 bpm ventricular rate varies Atrial rhythm is regular ventricular rate is irregular No identifiable p waves P wave is not measurable Qrs: 0.10 or less usually 111 Pacer spike should fall before the P wave unless a dual Chamber pacemaker; if it does not there could be a problem 112 Extra beat Types uniform=go the same direction multifocal= go in different direction R on T=when the pvc fall on the preceding twave couplet= 2 pvcs together bigeminy= pvc every other beat trigeminy=pvc every third beat 113 114 Ventricular tachycardia Monomorphic: beats are same size and shape Polymorphic: different size and shape 115 This is a polymorphic VT Usually electrical imbalance in nature r/t NA+ or K+ 116 Ventricular Fibrillation Rate can not be determined because of no identifiable waves Rapid chaotic rhythm with no pattern No p waves No PR interval No QRS 117 Vtach/Vfib • • • • • • • Both can be life threatening VT= V HR 100-250 bpm Causes: AMI, CAD, hypokalemia, dig toxic S/S: palpitations, dizzy, angina, <LOC Treatment: assess for pulse, if none, defib VF=Rate undeterminable Cause: same Treatment: CPR 118 http://videos.reinolla.tv/winners/pe/ 119 Hypertension 120 • HTN is described as persistent elevation of arterial blood pressure greater than 140/90 on at least 2 or more readings on different dates. • The Joint National Committee, Detection, Evaluation, and Treatment of High Blood Pressure defines normal: – BP as S < 120 mm Hg and D < 80 mm Hg – PreHTN: SBP 120-139 DBP 80-89 – Stage 1: SBP 140-159 DBP 90-99 – Stage 2: SBP >160 DBP >100 121 Types of Hypertension • Essential HTN: (Primary) which is the most common 90-95% of population • Secondary HTN: is a result of another disease, kidney, pregnancy. 122 Factors that determine arterial pressure • Cardiac output which is the volume of blood pumped by the heart in 1 minute • Peripheral vascular resistance which is the force in the peripheral blood vessels that the left ventricular must overcome to eject blood out of the heart 123 Possible Causes of PVR • Narrowing of blood vessels, PVD, CAD, kidney disease: > renin/angiotensin =vasoconstriction • Release of catecholamine (epinephrine and adrenalin) = vasoconstriction • > blood volume= more work to pump • > Blood viscosity=harder to pump • Ability of blood vessel to stretch 124 Causative Factors of HTN • • • • • • • Hyperlipidemia Obesity Atherosclerosis Sedentary DM Family Hx Cigarette smoking Age > 60 Men Post menapausal women 125 S/S • Often none • Occipital headache more severe on rising • Lightheadedness • Epistaxis • Known as the ‘Silent Killer’ 126 Complications • Damage to blood vessels of the eyes, heart, kidney, brain resulting in: • Stroke • CHF • AMI • Renal failure • Blindness 127 Lifestyle Change Education • Exercise, dash diet, stop smoking, weight management and control, stress reduction, medications and recording BP frequently • Avoid OTC meds • Instruct on how to do postural BPs 128 Valvular Disorders 129 • STENOSIS: • INSUFFICIENCY: 130 Stenosis • Narrowing of the opening of the valves. Limits the amount of blood which is ejected from one chamber to the next. 131 132 Mitral Stenosis • Mitral valve leaflets become thickened and fibrotic. Affect women age 20-40 • CHF may develop • TX if failure develops: Digoxin, Lasix, beta blockers, and anti arrhythmics, lo Na diet, etc • Will monitor with yearly echocardiogram • Surgery if worsens • Prophylactic antibiotics prior to invasive procedure or dental work 133 Insufficiency • The inability of the valves to close completely. • Allows the blood to backflow. • Mitral valve is the most commonly affected 134 Cardiac insufficiency can be caused by many factors – by a swelling of the heart muscle (1), an enlargement of the hollow chambers in the heart (2), a heart attack (3) or a blood clot (4). 135 Mitral Insufficiency • Often accompanies mitral stenosis as a result of rheumatic fever. • Valve leaflet become rigid and shorten, prevents closure of valve. • Hypertrophy of Left Atrium and Ventricle = L sided heart failure occurs • Murmur heard. F/U with echocardiogram • TX: vasodilators, same as for stenosis 136 Mitral Valve Prolapse • When the Left ventricle leaflets become enlarged, and protrude into the left atrium during systole. • Benign but may progress to Mitral insufficiency • More common in women age 20-55 137 S/S of mitral prolapse • Often none • Others experience chest pain, palpitations, dizziness, syncope, dysrhythmias • Monitor with echocardiogram • May do heart catherization • Manage stress, beta blockers if tachycardia 138 Aortic Stenosis • Occurs when valve cusps become fibrotic and calcify. • Most commonly caused by aging and atherosclerosis. • Occurs most predominantly in men • Untreated will lead to Left sided CHF 139 Aortic Insufficiency • • • • Caused primarily by rheumatic fever May also be caused by chronic HTN Predominantly in men Hypertrophy of the Left ventricle and eventually to left sided CHF • Blood may eventually back up into the pulmonary system and lead to Right Ventricle failure 140 S/S and Treatment • Aortic murmur, tachycardia, palpitations, CHF with fatigue, SOB, ascites • Monitored with echocardiogram assessing L ventricular dilatation • Chest X-ray-enlargement of heart • May do cardiac cath • May need valve repair or replacement 141 •Inflammatory Diseases of the Heart 142 • Inflammation of the heart most often results from systemic infections and may include any layer of the heart: What are they??? 143 Endocarditis • Inner layer: tends to affect the valves (Mitral=L). Organisms (Bacterial or fungal) present in blood stream and collect (colonize) on the valves: Rheumatic heart disease, congenital defects or mitral valve prolapse • IV drug users or invasive procedures 144 • Clients with known valvular disease need to be treated with prophylactic antibiotics prior to any invasive procedure including dental. Immunosuppression and any source of contamination places clients at risk 145 Pathophysiology • Bacteria may enter blood stream: • Bacteria collect on valves and vegetate • Complications: Ventricular septal defect, CHF(#1 cause of death) and embolization 146 S/S • Fever- (99-105) • Chills and night sweats may accompany • Malaise, fatigue and weight loss • Appearance of petechiae in the mouth, conjunctiva and legs • Chest and abdominal pain indicating embolization 147 Treatment and Diagnostics • H&P and Lab tests CBC with diff with leukocytosis, > sed rate, blood cultures • May have heart murmur Echocardiogram to visualize valves and vegetation • Chest x-ray: CHF • Long term antibiotics, rest, limited activity, prophylactic anticoagulants, valve replacement after inflammation treated 148 Nursing Assessment • Frequent VS and assess for fever • Assess for heart murmur • Note cough • Assess peripheral edema • Rest with limited activity, administer meds in a timely manner 149 Nursing Diagnosis 150 • myocarditis 151 • Muscle layer: Local or diffuse inflammation of the myocardium. May be viral or bacterial, an autoimmune process or drug toxicity. • May result in cardiomyopathy= 152 Pathophysiology • Characterized by degeneration and necrosis of myocardial tissue that is different of that caused by MI • Tissue next to necrosed area hypertrophies, loses elasticity, results in CHF and arrhythmias 153 S/S • Asymptomatic • May have fever, fatigue, sore throat, dyspnea, muscle aches • Lymph nodes may be enlarged • Chest pain 7-10 days after virus • CHF S/S 154 Diagnosis • Based on Hx, S/S, and testingenzymes> • May hear friction rub, rales • Jugular vein distention • Chest x-ray, echocardiogram=hypertrophy • EKG=arrhythmias • Biopsy (RV) shows lymphatic infiltration and cell necrosis 155 Treatment • Bed rest • 02 • Meds: cardiac glycosideLanoxin, anticoagulants, antiarrhythmic, antibiotics, steroids • Cardiac monitoring • NI same as for endocarditis • ND same as for endocarditis 156 • Pericarditis 157 • Outer-surrounds heart • Inflammation of the pericardium. • Primary or secondary • Acute or chronic • Acute: virus, bacteria, fungi, chemotherapy, MI • Chronic: TB, radiation or metastases 158 Pathophysiology • Inflammation causes an increase in the amount of pericardial fluid and inflammation of surrounding tissues. • Fluid accumulates in the pericardial space • Adhesions may occur which causes loss of elasticity which causes constriction and prevents adequate filling of ventricles. • May lead to tamponade==pericardiocentesis 159 Tamponade 160 S/S • Chest pain is hallmark • Most severe on inspiration, sharp, stabbing, or dull and burning. • Pain is relieved by sitting up or leaning forward • Dyspnea, chills and fever 161 Diagnosis • WBC elevated • Serial EKG show that ST segment increases and resolves in several weeks. A fib may occur • Echocardiogram to see pericardial thickening and effusion • Enzymes can be increased • Blood cultures to ID organism 162 Treatment • • • • • Analgesics Antipyretics Anti-inflammatory agents Antibiotics May need OR to create a pericardial window to allow for drainage of fluid • NI and ND same as for endocarditis 163 • Nursing the Heart Client 164 Assessment • Heart rate and rhythm, color, temperature, cognition • Circulation: peripheral CMS checks • Vital signs to include 02 saturations and telemetry interpretation • Subjective: c/o chest pain, SOB, fatigue, lightheadedness, dizziness 165 Nursing Diagnosis 166 Ekg practice 167 168 169 170 171 172 173 174 •www.mirule.com retrieved on 4/8/07. •Images found at www.aol.com. Retrieved on 4/8/07. • Aehlert, B. RN BSPA (2006). EKGs Made Easy. Mosby (3rd ed). St Louis. 175 •The End 176