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239 Cards in this Set
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CAD
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manifestations:
1. coronary atherosclerosis 2. Myocardial infraction |
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Coronary Atherosclerosis
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1.common
2.blockages in arterial BV walls 3.narrow the lumen 4.reduces bl.flow to myocardium 5.produces a repetitous inflammatory response |
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Pathophysiology of Atherosclerosis
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fatty streaks,lipids stick, leads to injury of cvasculr endothelium, then the injury leads to accumulation of macrophages, which cause the cells to become foam like
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Continued breakdown (Atherosclerosis)
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biochemical release attracts platelets that clot, smooth muscle forms fibrous caps called atheromas or plaque, two types, stable or ruptured
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platelets form clots that form atheromas
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ruptured atheromas or Thrombus
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cause of MI
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Clinical Manifestation (Atherosclerosis)
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depends on location & degree of occlusion
can be asymptomatic, can lead to ischemia which cause anginia pectoris which lead to irreversible damage & sudden cardiac death |
ischemia>angina>irreversible damage>sudden cardiac death
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Risk factors (CAD)
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1.high bl. lipids
2.smoking 3.hypertention 4.DM 5. Age: 45+ for men, 55+ for women 6.obesity 7.history |
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Prevention of CAD
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PRIMARY prevention: Preventing the occurrence
1.find out if have DM 2.insulin resistence 3.abd. obesity 4.dyslipidemia 5.HTN 6.Proinflammatory state (increased C-reactive protein) 7.Prothrombotic state (high fibrinogen) SECONDARY prevention: Preventing the progression 1.control lipid intake 2.decrease LDL 3.increase HDL |
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4 Modifiable risks (CAD)
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1. cholesterol
2.smoking 3.hypertension 4. DM |
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4 Non-modifiable risks (CAD)
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RASH
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4 types of fat
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cholesterol,
LDL HDL Triglycerides |
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To control CAD
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1. diet, watch fats
2.exercise 3. meds 4.quit smoking 5.manage hypertension 6.control DM 7 control stress |
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Meds. used with CAD
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1. Cholesterol synthesis blockers-Lipitor, Zocar (Statins)
2. Nicotinic acids-Niacor, Niaspan 3. Fibric acids - Atromid-S, Tricor 4. Bile acid sequestrants or resins - lo-Cholest, Questran, Prevalite |
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Cholesterol synthesis blockers
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block cholestrol
decrease-LDL,TRIG. levels, increases- HDL |
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Nicotinic acids
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decreases Lipoproteins synthesis, LDL & Trig.
must be titrated to achieve therapeutic |
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Fibric Acids
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decreases: cholesterol, trig levels,
increases: HDL |
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Bile Acid sequestrants
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binds chol. in intestine
increases its breakdown lowers LDL levels no effect on HDL or trig |
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Hypertension affects CAD
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vasoconstriction increases vessel wall thickness
accelerates atherosclerosis |
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How DM affects CAD
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1. strong relationship
2. kills most DM patients 3. fosters dyslipidemia, increases platelet clotting, alters red blood cell function which leads to thrombus formation 4. impairs vasodilation & smooth muscle function |
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Another Modifiable Risk factor (CAD)
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stress
releases catecholamines type A's |
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Non-Modifiable Risks (CAD)
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RASH
angina pectoris |
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Angina Pectoris (AP)
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pain and/or pressure
-cause is insufficient blood flow -decreases O2 when it is needed -effects ADLs |
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Pathophysiology of AP
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1.atherosclerotic disease
2. significant obstr. of major coronary artery 3. O2 cannot be met when needed 4. becomes problem in cold, eating heavy meal, stress or emotional situation |
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Clinical Manifestations of AP
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1.pain (can radiate into neck, jaw, back, arm)
2. apprehension 3.N, V, dizziness |
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Assessment & Diagnosis of AP
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1. pt. history
2.12-lead ECG 3. Lab values (C-reactive proteins) |
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Management of AP
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1. decrease O2 demand of myocardium
2.increase O2 supply (cannula) 3.reestablish perfusion |
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Methods (AP)
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Pharm:
1.nitro, Beta blockers, Calcium blockers, antiplatelets & anticoagulants, O2 admin 2. Anxiety & stress reduction 3. pain prevention |
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Nitrates for AP
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Nitrates
1.nitrostat, nitrol, nitro-bid vasodilators, reduce preload, -in higher doses-relaxes systemic arteriolar bed, lowering BP & decreases afterload |
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Calcium Channel Blockers for AP
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1. Norvasc, Cardizem, Tiazac, Plendil(preferred in CHF)(2nd gen)
2.decrease SA automaticity which decreases workload 3.1st gen: decrease myocardial contractility & contraindicated with CHF pts |
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Antiplatelets & Anticoagulants for AP
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1. prevents clotting
2. ASA's, Plavix & Ticlid, Heparin, Glycoprotein IIb/IIIa agents |
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O2 admin for AP
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increase o2 & decrease pain
pulse oximetry to measure |
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MI Pathophysiology
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1. a pc of mycardium is permanetly destroyed
2. caused by thrombus 3.Unstable angina & MI are the same but different;ACS together |
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ACS
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Acute Coronary Syndrome
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Clinical Manifestations of MI
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1. sudden onset and not stopped by rest & meds
2.no previous symptoms 3. or may have: chest pain, SOB, Indigestion, Nausea, Anxiety, Cool,pale & moist skin |
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Assessment & Diagnosis of MI
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1.history
2.ECG 3.Echocardiogram 4. Lab. test (creatine, myoblobin, Troponin) |
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Medical Management of MI
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1. meds
2. PTCA emergent percutaneous coronary intervention 3. cardiac rehabilitation |
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Meds for MI
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1. Thrombolytics-within 6 hrs
2. Analgesics-morphine 3. ACE inhibitors |
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PTCA for MI
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Emergent Percutaneous Coronary Intervention
opens occluded coronary artery, promotes reperfusion |
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Phases of Cardiac Rehabilitation
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Phase I-diagnosis of atherosclerosis
Phase II-occurs after pt is discharged Phase III- on maintaining cardovascular stability & long-term conditioning |
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Phase I (Cardiac Rehab)
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a.light activity & ed
b. mobilization occurs early c. self-care 4.in hospital teaching;call 911, s/s, maintenance of med, rest, keep appointments |
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Phase II (Cardiac Rehab)
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a.from 4-6 wks to 6 mths
b. supervised, exercise training c. lifestyle modification d. short & long term goals |
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Phase III (Cardiac Rehab)
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1. maintains stability & long-term conditioning
2. self-directed without supervision 3. builds on accomplishments |
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Nursing Process-Assessment of MI
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1.establish baseline
2.history related to symptoms 3.physical assessment(critical) 4.IV sites examined alot |
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Nursing Process-Nursing Diagnoses for MI (4 of them)
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1.ineffective cardiac tissue perfusion
2.risk for imbalanced fluid volume 3.acute pulmonary edema 4.heart failure |
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Nursing Process-Planning for MI
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1.pain relief
2. relief of ischemis s/s 3. prevention of further damage 4. decrease workload 5.reduce anxiety |
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Nursing Process- Nursing Interventions (MI)
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1. pain relief
2. O2 3.meds 4.ed 5.work together 6. monitor VS |
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Nursing Process- Evaluation (MI)
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1.relief of angina
2.no resp.problems 3. tissue perfusion 4. no anxiety |
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Invasive Coronary Artery Procedures
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PTCA-balloon-shaped catheter-
done in cardiac cath lab. through femoral artery, |
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Coronary Artery Stent
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stops all ways of artery occlusion
must take antiplatelets from then on |
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Atherectomy
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drill
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Brachytherapy
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inhibits smooth muscle cell proliferation with gamma or beta radiation
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Problems with invasive procedures
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destroying the artery
MI bleeding Hematoma Pseudoaneurysm Embolus Fistula Arterial thrombus Acute renal failure |
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Post care with invasive procedures
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1.No complications
-a.Usually discharged same day or next day -b.If emergent, patient may be admitted for a few days -c.Patients monitored closely for complications, i.e. bleeding, restenosis, MI, etc. 2.Complications -a.Interventions & length of hospital stay will depend on the problem that develops |
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Surgical Coronary Artery Revascularization
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1. angina that cannot be controlled
2.treats left main cor. artery stenosis or multi-vessel CAD 3. treats MI, dysrhythmias, heart failure |
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Coronary Artery Bypass Graft -Traditional
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CABG
graft from saphenous vein or left internal mammary artery 1.pt put on machine for surgery 2. CPB machine circulates & oxygenates blood 3. cannula in vena cava 4.use harvested graft |
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Coronary Artery Bypass Graft - Alternative
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done without CPB machine, heart continues to beat during surgery
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Assessment for these surgeries for MI
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1.health history, physical, psychosocial & learning
2. do not offer false reassurance 3. answer questions honestly |
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Nursing Diagnosis (Pre-Op)
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preop:
a. fear b.deficient know c. ineff.tissue perf. postop: a.decreased CO b.impaired gas exch c. r. for imbalanced fluid vol |
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Nursing Process-Planning (Pre-Op)
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goals for pt
a.reduce fear b.ed about procedure & aftercare c. avoid complications |
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Complications of procedures
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1. decreased CO
2. Fluid vol. & electrolyte imbalance 3. impaired gas exchange 4. impaired cerebral circulation |
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Problem of Decreased CO
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a. preload: 2 little bl. vol
b. afterload: arterial constriction from postop HTN c. alterations in HR d. Contractility alterations |
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Problems of Fluid volume & electrolyte imbalance
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a. hemodynamic instability
b. elevated. bl glucose c. neck vein distention d. altered breath sounds |
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Problems of impaired gas exchange
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a. altered bl. gas values
b. restlessness c. anxiety d. cyanosis e. breathing diff. on ventilator |
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Problems of cerebral circulation
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a. restlessness
b. headache c. confusion d. hypotension |
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Nursing process-Interventions (Pre-Op)
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1. emotional support & ed of pt and family
2. establish rapport 3. clarify info etc |
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Nursing process-Evaluation (Pre-Op)
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must be realistic, fear addressed/reduced, etc
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Nursing process in Postoperative Phase:
Assessment |
a.pt admitted to critical care
b. total assessment c. observation |
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Nursing Diagnoses (Post-Op)
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Postop:
a. decreased CO b. Impaired gas exch c. R.for imbalanced fluid vol |
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Planning (Post-Op)
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goals for pt
a. restoration of CO & gas ex b. maintenance of fluid & elec. balance (at least 30 cc's an hr) c. reduction of sensory-perception alterations d. relief of pain etc |
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Interventions (Post-Op)
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1. restore CO
2. Promote gas exchange 3. adequate tissue perfusion 4. pain relief 5 home & community based care |
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1. Restoring CO
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a. close monitoring of BP, HR, CVP, arterial pressure & pulmonary artery pressures
b. fluid vol. & intake c. VS, wgt, hemodynamamics d.intervene with changes |
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2. Promoting Gas Exchange
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a. suctioning
b.compression devices c. quality & quantity of output |
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Evaluation of Postoperative care
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expected outcomes
a. adequate CO, gas exc. fluid & elec. balance, tissue perfusion & body temp maintenance b. self-care activities c. no complications |
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Valvular Disorders
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a. Mitral valve prolaspe
b. Mitral regurgitation c. mitral stenosis d. Aortic regurgitation e. Aortic stenosis |
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Mitral Valve Prolaspe
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1. deformity/no s/s
2. progress to death 3. more in women 4. inherited connective tissue disorder, enlarges 1 or both mitral valve leaflets |
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Pathophysiology of MVP
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a. backs in atrium during systole
b. valve does not remain closed c. bl goes from L.Vent.to L.atrium d. murmurs, heart enlargement, pulmonary HTN, CHF |
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Clinical Manifestations of MVP
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1. usually asymptomatic
2. activity does not bring it on 3. symptoms if there: a. fatigue b.SOB c.lightheadedness d.dizziness e.syncope (blackout) f.chest pain g. palpitations h. anxiety |
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Assessment of MVP
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1.usually found as extra heart sound
2. mitral click 3. systolic click is leaflet balloning into left atrium 4. echocardiogram for diagnosis |
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Medical management of MVP
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1.control symptoms
2.stop caffeine, alcohol, smoking 3.meds:antidysrhythmics 4. stronger meds than nitrates 5. repair or replacement may be needed |
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Nursing Management of MVP
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1. ed
2. s/s & report them 3. explain prophylatic antibotic therapy b4 dental work, etc |
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Mitral Regurgitation
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1.bl flows back from L.V. into L.A. during systole
2. leaflets cannot close-thickening & fibrosis of leaflets & chordae tendinease 3. Causes |
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Causes of MR
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a. degenerative changes in valve & ischemia of LV
b. Rheumatic heart disease c. infective endocarditis d. collagen-vascular disease e. cardiomyopathy |
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Pathophysiology of MR
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a. problems with leaflets, chordae tend., annulus or papillary muscles
b. w/ ea.heart beat, bl forced back into L.A. c. forces L.Atrial stretching d. Eventual hypertrophy & dilation e. lungs can become congested f. eventually involves lungs & R. Vent. |
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Clinical Manifestations of MR
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1. often asymptomatic
2. manifest as severe heart failure 3. weakness 4. palpitations 5. SOB w/ exertion 6. cough w/ pulmonary congestion |
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Assessment & Diagnosis of MR
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1. high-pitched, blowing sound at apex
2. pulse irregular 3. transesophageal echocardiography (TEE) used |
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Medical management of MR
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1.same as for CHF
2.ACE inhibitors used 3. activity level restrictions, antibiotic theraphy 4. surgical intervention |
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Mitral Stenosis
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1.obstruction of bl. from L.A to L.V.
2.maybe caused by rheumatic endocarditis 3. thickening of mitral valve leaflets & c.tendinease 4. leaflets often fuse 5. orifice narrowing & progressive obstruction of bl into ventricle |
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Pathophysiology of MS
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1. valve opening -width of pencil
2. L.A. has diff. moving bl. into ventricle 3.L.A. dilates & hyprotrophies 4.pulmonary veins engorge 5, bl moves to R. Ven. |
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Clinical Manisfestations (MS)
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1. breathing diff. on exertion
2. s/s after valve opening reduced by 1/3 3. progressive fatigue, low cardiac output 4. pt may; cough blood, cough, wheeze, palpitations, orthopnea, paroxysmal nocturnal dyspnea & repeated respiratory inf. |
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Assessment & Diagnosis (MS)
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1. pulse is weak, often irregular
2. low-pitched rumbling, diastolic murmur at apex 3. atrial dysrhythmia 4. angiography |
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Medical Management (MS)
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1. anticoagulants
2. trmt for anemia-maybe 3. avoid strenuous activity 4. surgical intervention |
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Aortic Regurgitation
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1. bl.flows back into L.Ven.from aorta during diastole
2. inflammatory lesions deform the aortic valve leaflets, preventing full closure 3. may result from infective or rheumatic endocarditis, congenital abn. syphilis, a dissecting aneurysm |
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Pathophysiology of AR
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1. flow of bl. back into L.Ven. from aorta during diastole
2. L.Ven.hypertrophy occurs to compensate for increased vol 3. Arteries compensate for increased pressure by vasodilating 4. diastolic pressure lowers |
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Clinical Manifestations of AR
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1. w/out s/s
2. forceful heartbeat 3. atrial pulsations that are visible or palpitations 4. progressive s/s of L. Ven. failure including breathing diff. |
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Assessment & Diagnosis of AR
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1. diastolic murmur -high-pitched blowing sound at 3rd or 4th Int space at L.sternal border
2. pulse pressure is widened 3. Doppler echocardiography (TEE) |
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Medical management of AR
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a. antibiotic prophylaxis to prevent endocarditis
b. avoid physical exertion, competitive sports, isometric exercise c. med: calcium channel blockers & ACE inhibitors d. tmt is valve replacement b4 L. Ven. failure occurs |
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Aortic Stenosis
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1. narrowing of the orifice btw L ven & aorta
2. result of degenerative calcification 3. calcifications begins on flexion line of leaflets at the base of valve 4. caused by inflammatory changes 5. congenital leaflet malformation |
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Pathophysiology of AS
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1. progressive narrowing over years
2. L. Ven. overcomes obstruction to circulation by contracting more slowly but with greater energy 3. obstruction increases pressure on the L. Ven 4. Vent. wall thickens |
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Clinical Manifestations (AS)
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1. many pts asymptomatic
2.s/s exertional dyspnea, caused by pulmonary venous pressure due to L. V. failure, dizziness, syncope, angina, decreased pulse pressure |
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Assessment & Diagnosis of AS
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1. loud, rough systolic murmur over aortic area
2. systolic crescendo-decrescendo murmur, which radiates into the carotid arteries & to the apex of the L.V. 3. Mumur is low-pitched, rough, rasping & vibrating 4. S4 sound may be heard 5. Vibration may be felt at base of heart 6. Doppler echocardiography |
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Medical Management (AS)
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1. antibiotic prophylaxis
2. meds if failure occurs 3. surgical aortic valve replacemt |
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Nursing Management in Valvular Disorders
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1. ed
2. report new s/s 3. prophylactic antibiotics 4. assess for s/s heart failure, dysrhythmias, symptoms of dizziness, syncope, increased weakness, or angina |
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Valve Repair & Replacement
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1. Valvuloplasty
2. Valve Replacement 3. Septal Repair |
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Valvuloplasty
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Parts of Valves:
1. Commissurotomy(open/closed) 2. Annuloplasty 3. Leaflet repair 4. Chordoplasty |
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Valve Replacement
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1. Mechanical Valves: for pts. w/ renal failure, hypercalcemia, endocarditis, or sepsis
2. Tissue valves: Xenografts, Autografts |
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Xenograft
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a. used for tricuspid replace.
b. women of child bearing age c. Homografts or allografts d. cadaver tissue e. for aortic or pulmonic grafts |
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Autografts
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a. pulmonic valve & portion of pulmonary artery used
b. no anticoagulation needed |
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Nursing management for Valvuloplasty
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a. monitor for s/s heart failure & emboli
b. Hosp. for 24-48 hrs c. ed about anticoagulant therapy |
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Septal Repair
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a. usually congenital (found during infancy or childhood0
b. anesthesia & cardiopulmonary bypass c. proph.antibiotic for 6 mths d. then check Dopplar echo.to see if any more infection |
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Cardiomyopathy
Pathophysiology |
1.events that culminate in imp. CO
2. Decreased SV, stimulates sympathetic NS & renin-angiotensin-aldosterone response 3. increase systemic vascular resistance & increased sodium & fluid retention, increasing CO 4. heart muscle disease |
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Classified according to structural &/or functional abnormalities of the heart muscle
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a. dilated cardiomyopathy (DCM)
b. Hypertrophic cardiomyopathy (HCM) c. restrictive cardiomyopathy d. arrhythmogenic R.V.cardiomyopathy e. unclassified cardiomyopathies |
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Dilated Cardiomyopathy (DCM)
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1.most common
2. 5-8 cases per 100,000 3.men & african american 4. dilation of the Ventricles 5. diminished contractile elements of muscle fibers & diffuse necrosis of myocardial cells 6. results in poor systolic function |
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Hypertrophic Cardiomyopathy (HCM)
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1. rare autosomal dominant
2. heart muscle increase in size & mass,esp. along septum 3. causes diastolic dysfunction 4. decreases contractions, increasing risk of dysrhythmias 5. bl.supply restricted |
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Restrictive Cardiomyopathy
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1. diastolic dysfunction caused by rigid ventricular walls that impair diastolic filling & stretch
2. systolic func.is normal |
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Arrythmogenic Right Ventricular Cardiomyopathy
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1.myocardium of R. Vent.-infiltrated & replaced by fibrous scar & adipose tissue
2. Vent. dilates & develops poor contractility, wall abn. & dysrhythmias 3. not diagnosed easily |
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Unclassified Cardiomyopathies
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1. have comb. of s/s
a. Fibroelastosis b. noncompacted myocardium c. systolic dysfunction w/minimal dilation d. mitochondrial involvement (genetic) |
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Clinical Manifestations (Cardiomyopathy)
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1.may remain stable & symptom free
2. progress |
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Assessment & Diagnosis (Cardiomyopathy)
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1. phy exam may detect tachycardia & extra heart sounds
2. diastolic or systolic murmurs 3. history 4. cardiac cath. &/or endomyocardial biopsy |
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Medical management (Cardiomyopathy)
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a. determ. & manage causes, giving meds, low-sodium diet, exercise regimen
b. pacemaker or implantable cardiac defibrillator c. trmts can be dangerous |
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Surgical management of CM
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1. L.Vent.outflow tract surgery
2. Latissimus Dorsi Muscle Wrap 3. heart transplas. 4. Mechanical Assist devices 5. Total Artificial heart |
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Assessment of
CM |
a. history
b. impact of illness c. reduce anxiety d. phy assessment must include incidence of JVD, edema & severity, ausculatation for murmurs |
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nursing Diagnosis (Cardiomyopathy)
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a. decreased CO
b. ineffective cardiopulmonary, cerebral, peripheral & renal tissue perfusion 3. impaired gas exchange etc |
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Planning in CM
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GOALS:
a.increase CO b. incr. actvity tolerance c. reduction of anxiety |
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Interventions in CM
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1. rest w/ symptoms
2. adequate O2 3. ed. on meds 4. diet 5. grieving process |
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Evalution in CM
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see interventions
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Infectious Cardiac Disease
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1. Rheumatic Endocarditis
2. Infective Endocarditis 3. Myocarditis 4. Pericarditis |
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Rheumatic Endocarditis
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a.school-age children
b. may develop after group A beta-hemolytic Streptococcal pharyngitis c. new heart murmur, cardiomegaly, pericarditis, heart failure d. other factors: malnutrition, overcrowding, lower SES |
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Pathophysiology of RE
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1. inflammatory or sensitivity reaction to streptococci
2. leukocytes form nodules, replaced with scar tissue 3. temp. weakens contractile power 4. shows up as vegetations or growths along free margins of valve leaflets |
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Clinical Manifestations of RE
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a. recover in 3-4 wks
b. Jones criteria c. pt with Group A strep & 1. carditis 2. polyarthritis 3. subcutaneous nodules 4. erythema marginatum 5. chorea |
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Assessment & Diagnosis of RE
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1. sore throat now or within 5 wks
2.throat cultures 3. c-protein may be positive |
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Prevention of RE
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1. early diag. & trmt
2.complete med. regimen 3. report unresolved infections |
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Med. Management of RE
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1. id and get rid of organism
2. prevent complications 3. prophylactic trmt for 3-4 wks |
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Nursing Management for RE
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1. ed pts
2. long-term cardiac reevaluations 3. monitor for hear failure, pulmonary HTN, valvular disease, dysrhythmias |
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Infective Endocarditis
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1. microbial infection of endothelial surface of the heart
2. develps when there is prosthetic heart valves, struct. cardiac defects 3. older people 4. hosp.-acquired- in pts with debilitating diseases, indwelling caths & pts with IV's long-term or antibiotic therapy |
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Pathophysiology of IE
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a. deformity or injury of endocardium causes accumulation of fibrin & platelets, & clots
b. vegetations may go to other organs, concealing growths from body's defenses c. toxic effects of infection are the s/s |
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Clinical manifestations of IE
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1. 1st: fever & heart murmur
2. fever intermittent or absent 3. clusters of petechiae 4. CNS symptoms: headache, temp or transient cerebral ischemia, stroke |
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Assessment & Diagnosis of IE
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1. diagnosis made when microorganism is found in 2 bl. cultures, in vegetation or in abscess
2. may still have with - bl.cultures 3. Doppler endocardiography is used |
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Prevention of IE
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1. primary prophylactic antibiotic trmt in high risk pts
2. oral care 3. antiseptic mouthwash |
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Complications of IE
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1.can be destructive to heart & other organs
2. heart failure & stroke 3. valvular stenosis, atrioventricular blocks |
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Medical management of IE
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1. Meds
a. antibiotics 2-6 wks b. penicillin 2. Surgical management a. valve debridement or excision b. debridement of vegetations c. debridement & closure of abscess d. valve replacement |
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Nursing Mgmt of IE
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1. temp & heart sounds assessed frequently
2. mgmt of infection 3. s/s/ of systemic embolization, pulmonary infarction & infiltrates |
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Myocarditis (MC)
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1. inflammatory process
2. cause heart dilation, thrombi on the heart wall, infiltration of circulating bl. cells around coronary vessels & btw muscle fibers & degeneration of muscle fibers 3.Mortality w/ greater symptoms |
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Pathophysiology of MC
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1. ususally from viral, rickettsial, fungal, parasitic, metazoal, protozoal, or spirochetal infection
2.can result from immune reaction to meds 3. starts small grows big 4. involvement measured by degree of hemodynamic effect & resulting s/s |
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Clinical Manifestations of MC
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1. symptoms per type of infection, degree of MC damage, & capacity of MC to recover
2. flu-like symptoms |
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Assessment & Diagnosis of MC
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1. no detectable abn.
2. WBC &/or ESR may be elevated |
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Prevention of MC
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1. immunizations
2. early trmt |
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Med. Mgmt of MC
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1. trmt for syptoms
2. rest |
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Nursing Mgmt. for MC
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a. assess for resolution of tachycardia, fever & other clin. manif.
b. cardivascular assessment on s/s of heart failure & dysrhythmias 3. Elastic compression stockings, other preventions of thrombus development |
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Pericarditis (PC)
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1. inflammation of pericardium,
2. may occur 10days to 2 mths after MI 3. may be subacute, acute or chronic 4. classified as adhesive or by accumulation in sac |
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Pathophysiology of PC
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1. causes infection, disorders of connective tissue, hypersensitivity states, TB
2. accum. of fluid with increased pressure on heart leading to Cardiac tamponade |
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Clinical Manifestations of PC
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1. asymptomatic
2. chest pain 3. fairly constant, but can worsen 4. relieved w/ forward-leaning or sitting position 5. most common sign is creaky, friction rub heart at L. lower sternal border |
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Assessment & Diagnosis of PC
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1. history, s/s
2. echocardiogram 3. CT best tool |
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Medical Mgmt of PC
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1. analgesics & NSIDS, hasten reabsorption of fluid
2.Pericardiocentesis |
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Nursing Mgmt of PC
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1. pain mgmt w/ meds
2. activity restrictions 3. monitor s/s for tamponade |
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Assessment of PC
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1. pain
2. look for pain in various positions 3. auscultation of friction rub indicates loss of lube fluid b/c of inflammation |
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Diagnosis of PC
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1. acute pain
2. potential complications a. pericardial effusion b. cardiac tamponade |
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Planning of PC
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relief of pain
absence of complications |
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Interventions of PC
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1. relief of pain
a. by rest b. chair rest c. meds 2. complications a. pericardial effusion i fluid btw linings or in sac b. cardiac tamponade i SOB, Chest tightness or dizziness ii. progressive restlessness, possible decrease in systolic BP with stable diastolic BP during inspiration (pulsus paradoxus) |
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Evaluaton of PC
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1. freedom from pain
2. absence of complications |
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What is Hypertension (HTN)?
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A systolic blood pressure greater than 140 mm Hg & a diastolic blood pressure greater than 90 mm Hg based on an average of 2 or more accurate blood pressure measurements taken during 2 or more contacts with health care providers
(Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure, JNC 7) |
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Facts about HTN
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1. 28% to 31% of adults in US diagnosed with HTN
2. 90% to 95% have primary HTN, high blood pressure from an unidentified cause 3. 5% to 10% have secondary HTN, high blood pressure related to identified causes, including narrowing of renal arteries, renal parehchymal disease, hyperaldosteronism, certain medications, pregnancy, coarction of the aorta |
primary -unidentified
secondary - identified |
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The Silent Killer
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1. Hypertensive adults are often asymptomatic
2. Often accompanies other risk factors for atherosclerotic heart disease, i.e. dyslipidemia, obesity, diabetes mellitus, metabolic syndrome, sedentary lifestyle 3. Can also be caused by medications, physiological responses 4. Contributes to death from cardiac, renal & peripheral vascular disease 5. Eventually damages systemic vessels leading to MI, heart and/or renal failure, stroke, impaired vision |
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Pathophysiology (HTN)
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1. Multifactorial condition
2. May have many causes 3. There must be a change in one or more factors affecting peripheral resistance or cardiac output 4. There must also be a problem with body’s control system that monitors or regulates blood pressure |
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Gerontologic Considerations (HTN)
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1. May be attributed in part to structural & functional changes in heart & blood vessels that come in age
2. Accumulation of plaque, collagen deposits, impaired vasodilation may contribute to decreased elasticity |
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Clinical Manifestations (HTN)
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1. Physical exams may not reveal abnormalities
2. When symptoms do appear, usually indicate vascular damage 3. Long-term disease process can lead to MI, stroke, TIAs, organ insufficiency or failure |
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Assessment & Diagnosis (HTN)
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1. Thorough health history & physical exam
2. Laboratory studies for indications of hyperlipidemia 3. Echocardiography, ECG 4. Urine studies for renal function |
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Medical Management (HTN)
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1. Goal of treatment is to prevent complications & death by achieving & maintaining arterial blood pressure < 140/90 mm/Hg
2. Management options: a. Lifestyle modifications (dietary, activity, decreased alcohol consumption) b. Medications (antihypertensives, diuretics, antihyperlipidemics) c. Weight reduction d. Smoking cessation |
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Pharmacologic Therapy (HTN)
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1. Initially, diuretics &/or beta-blockers, usually in low doses
2. If indicated, doses may increase gradually 3. If unsuccessful, other medications may be added 4. If controlled after 1 year, some medications may be decreased or discontinued |
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Gerontologic Considerations regarding treatment (HTN)
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1. HTN Increases the risk of death & complications in people 50 years & older
2. Treatment reduces the risk 3. Treatment should begin with lifestyle modifications/changes 4. Medications should be started slowly |
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Nursing Process - Assessment (HTN)
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1. After initial diagnosis, frequent monitoring & strict adherence to follow-up care
2. Consistent monitoring at home 3. Thorough health & family history 4. Special attention to heart rate, rhythm, & regularity during physical exam |
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Nursing Process - Diagnoses (HTN)
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1. Deficient knowledge of physiologic processes & treatment
2. Noncompliance with therapeutic regimen |
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Nursing Process - Planning (HTN)
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1. Understanding of disease process & treatment
2. Participation in self-care program 3. Absence of complications |
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Nursing Process – Interventions (HTN)
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1. Focus on lowering & controlling blood pressure
2. Education about use of & side effects of medications 3. Support in making lifestyle modifications, follow-up care, & adherence to treatment regimen a. Patient understanding of correlation of disease process & effects of modifications 4. Review complications that require immediate medical interventions &/or call to 911 |
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Nursing Process – Evaluation (Expected outcomes)
(HTN) |
a. Tissue perfusion maintenance
i. Maintain BP < 140/90 mm/Hg ii. No symptoms of angina or vision changes iii. Stable BUN & serum creatinine levels iv. Palpable peripheral pulses b. Compliance with self-care program i. Adheres to lifestyle modifications ii. Follows medication regimen & follow-up appointments c. No complications from disease or treatment i. No changes in overall health or development of new health problems |
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Hypertensive Crisis
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Usually occur in patients with poorly controlled HTN after abrupt discontinuation of medications
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2 Types of Crises
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-Hypertensive emergency
-Hypertensive urgency |
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Hypertensive emergency
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Blood pressure is extremely elevated (> 180/120 mm/Hg) & must be lowered immediately
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Hypertensive urgency
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Blood pressure is very elevated with no evidence of impending or progressive target organ failure
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Hypertensive Emergency (more info)
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1. Blood pressure must be lowered immediately to halt or prevent damage to target organs
2. Assessment will reveal actual or developing clinical dysfunction of target organs 3. Can include HTN in pregnancy 4. Life-threatening, requiring prompt treatment 5. Goal is to lower BP by 25% within 1st hour of treatment 6. BP to < 160/100 mm/Hg within 6 hours with more gradual reduction during course of treatment |
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Hypertensive Urgency (more info)
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1. Patient may experience severe headaches, nosebleeds, or anxiety
2. Extremely close monitoring & cardiovascular status required during treatment 3. Frequency of VS measurements will depend on treatment response by patient 4. Precipitous drops in BP require immediate act to restore pressure to acceptable levels |
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Cardiac Hemodynamics:
Cardiac output (CO) |
amount of blood pumped per minute; determined by measuring HR X SV = CO
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Cardiac Hemodynamics:
Stroke volume (SV) |
amount of blood pumped out of ventricle with each contraction
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Cardiac Hemodynamics:
Preload |
amount of blood presented to the ventricle just before systole; increases pressure in ventricle stretching the wall
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Cardiac Hemodynamics:
Afterload |
amount of resistance of ejection of blood from ventricle; inversely related to SV
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Cardiac Hemodynamics:
Contractility |
force of contraction; related to status of myocardium
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Mechanisms of Heart Failure (HF)
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1. Inability of the heart to pump sufficient blood to meet needs of tissue for O2 & nutrients
2. Previously referred to as CHF because many patients experienced pulmonary or peripheral congestion 3. Currently recognized as a clinical syndrome 4. Characterized by S/S of fluid overload or inadequate tissue perfusion resulting from heart’s inability to cardiac output sufficient to meet body’s demands |
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Chronic Heart Failure
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1. Incidence increases with age
2. At 5 million people in US 3. 350,000 new cases diagnosed/year 4. Prevalent in older people 5. Epidemic that challenges health care resources 6. Most common reason for hospitalization of people > 65 y/o 7. Reflects advances health & cardiac care & treatments |
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How is HF assessed?
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Identified by assessment of left ventricular function
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Ejection fraction (EF)
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an indication of the volume of blood ejected with each contraction; calculated by subtracting amount of blood at end of systole from amount of blood at end of diastole & calculating % of blood ejected (55% to 65% - normal)
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What does the measurement of Ejection Fraction determine in Heart Failure?
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Measurement of EF determines type of failure
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Two types of HF
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-Systolic heart failure
-Diastolic heart failure |
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Systolic heart failure
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Characterized by weakened heart muscle
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Diastolic heart failure
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Characterized by a stiff & noncompliant heart muscle making ventricular refill difficult
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Pathophysiology (HF)
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1. Results from variety of CV conditions
2. Conditions result in decreased contraction (systole), decreased filling (diastole), or both 3. Significant myocardial dysfunction most often occurs before S/S of HF 4. As HF develops, body activates neurohormonal compensatory mechanisms representing body’s attempt to cope with HF, creating S/S that develop |
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Systolic HF (more info)
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1. Results in decreased blood volume being ejected from ventricle
2. Baroreceptors sense decreased stretch 3. Epinephrine & norepinephrine released, HR & contractility increase to support myocardium; continued response causes vasoconstriction to skin, GI tract, & kidneys 4. Lower CO triggers renin release eventually increasing blood pressure & afterload |
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Cascade of Effects (Systolic HF)
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1. As process continues; angio II triggers Na+ & fluid retention in renal tubules stimulating thirst
2. Fluid volume overload increases pre- & after-load causing increased cardiac workload 3. Natriuretic peptides released causing systemic vasodilation 4. Contractility decreases resulting in end-diastolic blood volume overfill, stretching fibers & increasing size of ventricle |
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Lasting Changes (Systolic HF)
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1. End result – ventricular hypertrophy leading to ventricular remodeling
2. As changed cells die, other myocardial cells assume work of maintaining CO 3. Workload is too much for compensatory cells, which translates to decreased CO 4. “Vicious Cycle of HF” label stems from the continued cycle of cardiac cells trying, failing, & trying again to maintain adequate CO |
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Diastolic HF
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1. Develops because of continued increased workload, responding to increasing numbers & size of myocardial cell
2. Continued resistance to ventricular filling increases ventricular filling pressures despite normal or reduced blood volume 3. Less blood decreases CO & higher pressures triggers similar cascade as Systolic HF |
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Heart Failure Etiology
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1.Dysfunction most often caused by CAD, cardiomyopathy, hypertension, or valvular disorders
2. Systemic conditions associated with HF |
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Systemic conditions associated with HF
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a. Increased metabolic rate
b. Iron overload c. Hypoxia d. Severe anemia e. Acidosis f. Electrolyte abnormalities g. Antiarrhythmic medications |
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Clinical Manifestations (Left-sided HF)
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1. Pulmonary congestion
2. Left ventricular blood volume & pressures increase, decreasing flow from atrium 3. Blood volume & pressure build in pulmonary vessels, forcing fluid into interstitial spaces 4. S/S include dyspnea, cough (non-productive), pulmonary crackles, low O2 saturation levels 5. S3 heart sound may be detected during auscultation based on large volume of fluid entering ventricle at beginning of diastole |
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Paroxysmal Nocturnal Dyspnea (PND)
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Sudden attack of dyspnea at night
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Clinical Manifestations (PND)
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1. Accumulated peripheral fluid is reabsorbed into circulating volume when patient lies down
2. Left ventricle cannot eject added fluid causing further shift of fluid into pulmonary vessels & spaces 3. Body detects decreased gas exchange 4. Ventricle ejection decreases in response to decreased O2 & increased pressures |
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Effects of Left-Sided Heart Failure (LSHF) on Other Organs
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1. Tissue perfusion is decreased
a. Renal perfusion results in reduced urine output (oliguria): -i. Pressure falls, stimulating renin release, causing aldosterone secretion, increasing intravascular volume; during sleep, workload is decreased, perfusion improves leading to nocturia -ii. GI perfusion causes altered digestion -iii. Brain perfusion causes dizziness, lightheadedness, confusion, restlessness, anxiety -iv. EF prompts sympathetic nervous system to increase HR; pulses may weaken |
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Right-sided Heart Failure (RSHF): Clinical Manifestations
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1. Congestion in peripheral tissues & viscera predominates
2. Occurs because right side of heart cannot eject blood & cannot accommodate the systemic blood continuing to enter from normal circulation 3. S/S include: dependent edema, hepatomegaly, ascites, anorexia & nausea, weakness & weight gain |
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Systemic Effects (in RSHF)
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1. Edema
2. Hepatomegaly 3. Anorexia |
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Edema (in RSHF)
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-Lower extremities
-Can accumulate higher when patient reclines -Pitting edema is obvious after retention of at least 4.5 kg of fluid |
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Hepatomegaly (in RSHF)
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Venous engorgement of liver;
increased pressure may interfere with liver function; increased pressure forces fluid from portal vessels into abdominal cavity leading to ascites |
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Anorexia (in RSHF)
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Venous engorgement & venous stasis within abdominal organs;
weakness results from reduced CO, impaired circulation, inadequate removal of catabolic waste products |
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Assessment & Diagnosis of HF
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1. May be undiagnosed until patient presents with S/S of pulmonary & peripheral edema
2. Can be detected with renal failure (RF), liver failure, oncologic conditions, COPD 3. Further assessment & evaluation must be completed to treat HF appropriately 4. Echocardiogram can confirm diagnosis 5. Lab studies necessary (BUN, creatinine, TSH, serum electrolytes, CBC, BNP (important), & UA |
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Medical Management (HF)
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1. Main goals are to relieve symptoms, improve functional status & quality of life, extend survival
2. Education & support to promote adherence to self-care regimen & limitations of condition 3. Treatment options dependent on severity of condition -a. May include lifestyle changes, medications, O2 supplement, implantation of assistive devices, transplant |
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Pharmacologic Therapy (HF)
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1. Angiotensin-converting enzyme inhibitors
2. Angiotensin II receptor blockers 3. Hydralazine & isosorbide dinitrate 4. Beta-blockers 5. Diuretics 6. Digitalis 7. Calcium channel blockers 8. Intravenous infusions 9. Medications for diastolic dysfunction 10. Other medications |
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Nutritional Therapy (HF)
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1. Low-sodium diet
2. Avoidance of excessive amounts of fluid 3. Education regarding patient needs & restriction including patient likes, dislikes, & cultural foods for nutritional value, & sodium limitations in milligrams |
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Additional Therapies (HF)
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1. Supplemental O2
2. Additional interventions |
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Supplemental O2 (HF)
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Need is based on degree of pulmonary congestions & resulting hypoxia
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Additional interventions (HF)
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a. Surgical interventions may be necessary
b. Implantable cardioverter defibrillator to prevent sudden cardiac death c. Transplantation for end-stage HF d. Cardiac resynchronization therapy (CRT) – biventricular pacemaker |
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Nursing Management (HF)
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1. Mortality is high; promotion of positive outcomes
2. Interventions should include: -a. Administering medications -b. Assessing fluid balance -c. Daily patient weight -d. Auscultation of lung sounds -e. ID & evaluate severity of dependent edema -f. Monitor pulse & BP -g. Assess for dehydration & symptoms of fluid overload |
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Potential Complications (HF)
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1. Repeated use of diuretics can lead to hypokalemia; possibly hypomagnesemia; hyponatremia resulting in disorientation, apprehension, weakness, fatigue, malaise, & muscle cramps
2. Hyperkalemia may develop associated with use of ACE inhibitors, ARBs, or spironolactone |
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Gerontologic Considerations (HF)
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1. Natural changes can increase frequency of HF
2. May present with atypical S/S 3. Diuretic use by elderly men requires close nursing surveillance 4. Frequency & urgency may be very stressful for elderly |
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Nursing Process – Assessment (HF)
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1. Observation for effectiveness of therapy & patient’s ability to understand & implement self-management strategies
2. S/S of pulmonary & systemic fluid overload for therapy adjustments as necessary 3. Exploration of patient’s emotional response to HF 4. Health history must include inclusion of S/S of HF 5. Physical assessment must evaluate areas of fluid dependence & accumulation |
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Nursing Process – Diagnoses (HF)
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1. Activity intolerance
2. Excess fluid volume 3. Anxiety 4. Powerlessness 5. Noncompliance |
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Nursing Process – Planning (HF)
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Major goals:
a. Promotion of activity & reducing fatigue b. Relieving fluid overload symptoms c. Decreasing the incidence of anxiety or increasing the patient’s ability to manage anxiety d. Encouraging the patient to verbalize ability to make decisions & influence outcomes e. Teaching patient about self-care program |
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Nursing Process – Interventions (HF)
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1. Promoting activity tolerance
2. Managing fluid volume 3. Controlling anxiety 4. Minimizing powerlessness 5. Promoting home & community-based care |
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Nursing Process - Evaluation (HF)
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1. Increased activity tolerance
2. Fluid balance maintenance 3. Decreased anxiousness 4. Care & treatment decision-making 5. Adherence to self-care program |
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Acute Heart Failure (Pulmonary Edema)
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1. Abnormal accumulation of fluid in the lungs
2. Accumulation may occur in interstitial spaces & in alveoli |
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Pathophysiology (Pulmonary Edema)
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1.Acute event that results from HF
2. Can accompany an acute event, i.e. with an MI, or as an exacerbation of chronic HF 3. With MI scarring, limited distensibility increases workload, increased resistance backs blood into pulmonary circulation, pulmonary edema develops (flash pulmonary edema) from blood volume overload in lungs 4. Can also be caused by a non-cardiogenic disorder, i.e. renal failure, liver failure, oncologic conditions 5. Impaired lymphatic drainage contributes to accumulation of fluid in lung tissues; classic symptoms – frothy pink sputum |
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classic symptoms (Pulmonary Edema)
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frothy pink sputum
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Clinical Manifestations (Pulmonary Edema)
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1. Increasing restlessness & anxious because of reduced oxygenation
2. Patient may report sudden breathlessness or sense of suffocation 3. Pulse is weak & rapid 4. Neck veins are distended 5. Patient’s hands become cold, clammy, & cyanotic 6. Cough with increasing quantities of mucoid sputum 7. O2 saturation significantly decreased |
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Assessment & Diagnosis (Pulmonary Edema)
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1. Diagnosis confirmed by evaluation of clinical manifestations resulting from pulmonary congestion
2. Chest x-ray for confirmation of pulmonary vein engorgement 3. Abrupt onset of LSHF may occur without signs of RSHF |
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Prevention (Pulmonary Edema)
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1. Easier to prevent than to treat
2. Recognition of early stages: dry, hacking cough, fatigue, weight gain, development or worsening of edema, decreased activity tolerance 3. Alleviation by placing patient in upright position with feet & legs dependent, elimination of overexertion, minimizing emotion stress 4. Long-range prevention includes identifying precipitating factors |
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Medical Management (Pulmonary Edema)
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1. Main goals are to reduce volume overload, improve ventricular function, increase respiratory exchange
2. Medical Management Methods |
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Medical Management Methods include (Pulmonary Edema):
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a. Oxygen therapy
b. Morphine c. Diuretics d. Intravenous infusions |
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Nursing Management (Pulmonary Edema)
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1. Positioning patient to promote circulation
2. Provide psychological support 3. Monitor medications |
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Positioning patient to promote circulation (Pulmonary Edema)
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Can help reduce venous return to heart
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Provide psychological support (Pulmonary Edema)
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a. Impending sense of doom
b. Information in calm, reassuring voice c. Strategies to address/reduce patient anxiety |
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Monitor medications (Pulmonary Edema)
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Morphine & diuretics may compromise patient condition quickly
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Tobacco Use/Cessation
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1.Use contributes to development & severity of CAD
2.Second-hand smoke exposure can be just as dangerous 3.Multiple ways to aid cessation |
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Use of Tobacco contributes to development & severity of CAD
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a.Smoke inhalation increases blood carbon monoxide (CO) levels
b.Nicotinic acid triggers catecholamine release=increased heart rate & blood pressure c.Detrimental vascular response, increases platelet adhesions |
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Multiple ways to aid Tobacco cessation
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a.Education
b.Medication c.Complimentary treatments (acupuncture, guided imagery, hypnosis) |
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