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Cardiac Disorders and ManagementCoronary Vascular Disorders CADAnginaMyocardial Infarction (MI)Acute Coronary Syndrome (ACS)-describe an array of clinical presentations of CAD that ranges from unstable angina to acute MI Coronary Artery Disease (CAD) Cardiovascular (CV) disease is the leading cause of death in the USCAD is most prevalent type of CV disease in adultsCoronary atherosclerosis is most common cause of CV What’s the Problem With CAD? Narrowing of the arterial lumen Thrombus formationObstruction of blood flow to myocardiumAHA CAD progression Risk factorsHigh lipidsSmoking HTNDMObesityFamily historyInactive lifestyleAgeGender/raceWhich ones are modifiable?What can be done to prevent CAD? What problems can CAD lead to?IschemiaAnginaMIHow is CAD diagnoses?Health historyPhysical examECGStress testingAngiography Angina Pectoris infoChest pain caused by myocardial ischemiaCan occur anywhere in chest, neck, arms, or backMost common is behind sternumLack of Oxygen in Tissue=Pain (in ANY tissue)Types of Angina Pectoris Stable anginaUnstable anginaIntractable or refractoryVariant Angina (AKA Prinzmetal’s)Silent Ischemia What is the problem?oxygen demand > oxygen supplyMyocardium uses a large amount of oxygen from coronary circulation. Obstruction of a major coronary artery (commonly from atherosclerosis) causes ischemia and results in episodes of pain or pressure in the chest.Medical ManagementObjective: to decrease oxygen demand of the myocardium and to increase O2 supplyPharmacological therapyNitrates, ASA, BB, CCB, antiplatelets, O2Reperfusion proceduresPercutaneous transluminal coronary angioplastyIntracoronary stentsCABG Nitroglycerin Vasodilator used to ↓ myocardial O2 consumption→decreased ischemia→pain Sublingual, tablet, or spray, oral capsule, topical agent of IVSL placed under tongue or in buccal pouchMay be taken 3x in 5-minute intervals for unrelieved CPPatient Teaching on Nitroglycerin Moisten mouth before takingCarry with them at all timesKeep in original (dark) bottle-very unstableRenew supply every 6 monthsTake note of how long it takes for nitro to relieve painAnticipated side effects: headache, hypotension, tachycardia and flushingSit down when taking Nursing ManagementPQRST to gather information about CPReduce anxietyPrevent/reduce pain (stop all activity, semi-Fowler’s position)Patient and family education PQRST Assessment of CP P: position/location (where? And provocation (what makes it worse?)Q: quality (describe the pain)R: radiate? Relief?S: severity (pain scale); other symptomsT: timing (when did it start?) Myocardial Infarction (MI) infoSustained ischemia → injury → death of heart muscle cellsImmediate recognition of signals is crucialTime is muscleCPR is essential! Basics! ABCDSigns and SymptomsSudden and continued CP despite rest and medicationShortness of breathDiaphoresisIndigestionNauseaAnxietyCool, pale, clammy skin Assessment and Diagnostic findingsDiagnosis usually made based on S/S, ECG, and lab testsGoal: ECG within 10 minutes of reported CP or arrival to EDReview of cardiac labsTroponin: elevates in 3-4 hrs, peak 4-24, stay up for 1-3 weeksCK-MB: predominately cardiac specific, first enzyme to increase, elevated short timeMyoglobin: not very cardiac specific, increases 1-3 hrs after MI, peaks 4-12 hrs, normal within 24 hrs.Diagnosis? Unstable angina: symptoms of ischemia without evidence of acute MI on ECG or cardiac labsST-segment elevation MI (STEMI): ECG changes in two leads; indicates significant damage to myocardiumNon-ST elevation MI (NSTEMI): elevated cardiac markers without definitive ECG evidenceMedical Management for MIGoal: minimize myocardial damage, preserve myocardial function, and prevent complicationsThrombolytics (stretokinase, tPA) within 3 hours of symptomsInotropic support (dobutamine)- ↓ SVRPreload/afterload reduction to decrease O2 demand, diuretics, vasodilators (nitro)Emergent PCICABGPharmacological Management of MI’s Thrombolytics (stretokinase, tPA) within 3 hours of symptomsInotropic support (dobutamine)- ↓ SVRPreload/afterload reduction to decrease O2 demand, diuretics, vasodilators (nitro)AnticoagulantsEarly Treatment of MI’s AspirinNitroVS12-lead ECGMorphine for painOxygenBeta Blocker (metoprolol) MONA M-morphineO-oxygenN-nitroglycerineA-aspirin (have them chew it so it gets into their system faster)Cardiac Rehabilitation Active program started once symptoms are resolvedReduces risk through education and physical activityGoal: to extend life and improve quality of life Nursing Process Assessment: important to assess baseline symptoms and identify changes in theseNursing Diagnoses: Ineffective cardiac perfusionRisk for imbalanced fluid volumeRisk for ineffective peripheral tissue perfusionCollaborative problems/potential complications Acute pulmonary edemaAcute pulmonary edemaHeart failureCardiogenic shockDysrhythmia’s and cardiac arrestPericardial effusion and cardiac tamponade Cardiogenic Shock Info↓ CO → inadequate tissue perfusion and initiation of shock syndromeMay occur after MI (due to areas of ischemia and necrosis)Also can occur with end-stage HF, cardiac tamponade, PE, cardiomyopathy, and dysrhythmia Life-threatening/high mortality rate Who is at risk?Elderly (>65 yrs)FemalesDiabeticsPre-existing CADAnterior wall MISigns and symptomsCerebral hypoxia (restlessness, confusion, agitation), decreased BP, rapid & weak pulse, cold clammy skin, tachypnea Assessment findings↓CO , ↓SV, ↑ SVR , ↓BP, ↓ tissue perfusionManagement/TreatmentMedications: diuretics, vasodilators, vasopressors Circulatory assist devices (IABP)Hemodynamic monitoringIntra-aortic Balloon Pump (IABP) Primary goal: decrease workload and maintain adequate perfusionA catheter with an inflatable balloon at the tip is inserted through the femoral artery and the balloon is placed in the descending thoracic aorta. Balloon inflates during diastole and aortic valve closure to augment the pumping action of the heart and decrease afterload Inflation and deflation synchronized to ECG Indications: cardiogenic shock, LV failure, post-op open heart, unstable angine, post MIContraindications: aortic valve incompetence, Peripheral vascular occlusive disease, aorto-femoral/ or illiac bypass grafts, aortic aneurysmComplications: ↓circulation to leg, left arm or balloon ruptureWean by decreasing ratio 1:1, 2:1, 4:1 Cardiac Arrest InfoHeart ceases to produce an effective pulse and circulate bloodMost reliable sign of this is by absence of a pulse… check carotidsLoss of consciousness, pulse and BPineffective or absent breathing. Emergency managementABCDMaintain open airwayProvide artificial ventilationPromote artificial circulationDefibrillate (*defibrillate for pulseless Vtach and Vfib)Invasive Coronary Artery ProceduresPercutanous Coronary Interventions (PCI’s)Variety of procedures used to treat diseases of the arteries of the heartPreviously known as angioplasty, PTCA, and balloon angioplastyBalloon-tipped catheter threaded from groin artery to blocked/diseased area of the heart. When inflated it widens the narrowed artery →increased blood flow. RandomsAnti-clotting meds are used before, during, and after PCIPlavix, Lovenox Time is muscleGoal: restore blood flow to heart muscle within 90 minutes of arrival in ED“door to balloon time of 90 minutes” ComplicationsBleeding, swelling at insertion site, CPPost-procedure careAssess for back pain (retroperitoneal bleeding)Check pulses (15 min x 2 hrs, then Q1-2 hrs)HOB <30 degrees while sheath in placeLeg straight for several hoursDirect pressure for 15-30 minutes after removal of sheath Stent Placementmesh wire tubes inserted during PCI to keep vessel open“permanent scaffolding”Cardiac CatheterizationGuidewire, then sheath, threaded into artery or chamber of heartOpaque dye injected; fluoroscopyHelps determine whether an intervention is needed Coronary Artery Bypass Surgery infoSurgical revasculization (of areas that have been blocked off)Can be used when several arteries have significant blockageBlood vessel grafted distal to coronary artery lesion, bypassing the area of obstructionSaphenous vein or LIMA (left internal mammary artery) vessels most commonly usedOff-pump vs on-pumpImmediate Post-Op Period Recovered in critical care unit or PACUVery critical period of timeFocus: achieving hemodynamic stabilityIssues: managing pain, cardiopulmonary status, wound careAssessment for complications↓ CO, fluid volume and electrolyte imbalances, impaired gas exchange, impaired cerebral circulationStructural Disorders Mitral Valve Prolapse InfoLeaflets papillary muscle of mitral valve do not work correctly leading to prolapse of leaflets, allowing them to go back into the atriumRegurgitation?Cause is unknownMost common form of vavular heart disease2x women over men S/SOften patient is asymptomaticPalpitationsDyspnea CPActivity intoleranceMitral Regurgitation PathoCaused by defect in mitral valve allowing blood to flow back from LV to LA during systoleAcute: causes: rupture of papillary muscle following an acute MI and rupture or one or more chordae teninae Forceful jet of blood sent retrograde into lt. atrium →sudden increase atrial pressure→acute pulmonary edema, ↓CO and possibly cardiogenic shockChronicElderly most common as structures sag and stretch over timeMitral Stenosis Obstruction of blood flow from LA to LV due to narrowing of mitral valve orificeLow-pitched murmurOccurs during diastoleBest heard in mitral areaCan lead to a-fib and atrial thrombi↑ left atrial pressure creates pulmonary congestion, breathlessness, moist cough, and rt. sided heart failureAortic Regurgitation Aka aortic insufficiencyIncompetent aortic valve “leaking valve”High-pitched blowing murmurEarly diastolic Heard best at aortic area Aortic Stenosis Narrowing of aortic valve orificeLV has ↑ difficult ejecting blood into aorta → increased intraventricular pressure→LV hypertrophy (↑ muscle mass)→loss of contractile force in LVLeads to ↓ decreased blood flow to aorta means less efficient filling of coronary arteries→Chest PainTwo yrs of symptoms→Survival rate of <50% without valve replacementLow-pitched, systolic murmur, heard in aortic areaTreatment of Valvular Disorders Valvuloplasty-repair of the valveCommissurotomy Annuloplasty Leaflet repairValve replacement-Mechanical valvesBiologic valvesXenografts Homografts Autografts Infectious Diseases of the HeartAny of 3 layers can be affected by infectionsNamed by layer of heart most involvedRheumatic Endocarditis (endocardium)Infective Endocarditis Myocarditis (myocardium)Pericarditis (pericardium) Infective Endocarditis infoAn infectious process which leads to vegetation in heart, usually the leaflets or endocardium Usually caused by strep or staphPortals of entry: dental procedures, tonsillectomy, burns, rheumatic heart disease, IV drug abuse, prosthetic valvesPrevention: oral antibiotics for dental procedures Signs and SymptomsSystemic signs: mild fever, malaise, murmur, chills, abd. pain, dypsnea Petechiae Osler nodes: small, red, raised nodules on fingers or toesJaneway lesions: hemorrhages, flat, red, nontender macules on palms and solesClubbingAnemia, ↑ WBC’s, + blood culturesInfective Endocarditis cont’d Treatment: antibiotics, may need valve replacementComplications: HF, myocardial abscess (from staph), pericarditis, myocarditis, emboli Myocarditis Causes: infectious agent invading myocardiumS/S: may be asymptomatic or have s/s of HF, ST-T changes, fatigue, dypsnea, temp, CPTreatment: tx for dysrhythmia’s and HF, O2, steroids, interferon Pericarditis Causes: MI, viruses, bacteria,trauma, lupus, post-open heartS/S: Positional CP (worse when lying down, improved when sitting up/leaning forward), friction rub (heard best at lower sternal border)Complications: pericardial effusion, pericardial tamponade Treatment: NSAIDS, steroids Pericardial Effusion & Cardiac Tamponade Pericardial sac normally contains <50 mL of fluid needed to decrease friction of beating heartIncrease in the fluid raises pressure within the sac and compress the heartCardinal signs: falling SBP, narrowing pulse pressure, rising venous pressure (inc. JVD) and distant (muffled) heart sounds Cardiomyopathy InfoDisease of the heart muscle associated with cardiac dysfunctionDifferent classifications according to the structural and functional abnormalities of the heart musclePatho: decreased stroke volume→ sympathetic nervous system stimulation and the renin-angiotensin-aldosterone resonse→ ↑SVR and ↑ Na and fluid retention →workload on the heart Known CausesCardiotoxic agents: alcohol, cocaine, Adriamycin Aortic stenosis HTNIschemiaCan occur acutely or over time. TypesDilated cardiomyopathy (DCM)InfoMost common type (~90%)Significant dilation of ventricles without simultaneous hypertrophy (increased muscle wall thickness) and systolic dysfunctionDiminished ability of the heart to contract↑ stystolic and diastolic volumes and ↓ ejection fractionS/STachycardiaFatigueS3, S4 heart soundsMurmursS/S HFEcho-easy observation of structure and function of ventriclesECG may show dysrhythmia’s Cardiac catheterization may be used to r/o CAD for the cause of the symptomsManagementTreating underlying causesTreatment similar to that for HFEnhance contractility of heartDecrease afterload Hypertrophic Cardiomyopathy (HCM)Restrictive Cardiomyopathy Arrhythmogenic RV Cardiomyopathy Unclassified CardiomyopathiesHeart Failure (HF) InfoPreviously referred to as Congestive Heart Failure (CHF)HF is a clinical syndrome with s/s of fluid overload or inadequate tissue perfusionProblem is with either contraction (systolic dysfunction) or filling (diastolic dysfunction)Number of patients with HF is increasing in the U.S. Over 5 million in US have HF, 550,000 new cases each year; 300,000 die each year from HFHeart failure is a response to cardiac dysfunctionAny condition which impedes the ability of the heart to pump blood at a volume required to meet the body’s needs can lead to HFCAD→necrotic damage to LV, Valvular dysfunction, Cardiomyopathy, Infection (myocarditis or endocarditis)TypesSystolic (more common) is characterized by a weakened heart muscleDiastolic is characterized by a stiff and non-compliant heart muscle, making ventricular filling difficultEjection fraction is used to help determine the type of dysfunction nl=55%-65%EF is severely ↓ in systolic HF and nl in diastolicSigns of Left vs. Right Heart Failure LEFT RIGHTtachypneaPeripheral edemaTachycardiaHepatomegalycoughSplenomegalyBibasilar cracklesHepatojugular reflexS3 and S4AscitesIncrease PA pressuresJVDHemoptysisIncreased CVPCyanosisPulmonary HTNPulmonary EdemaSymptoms of Left vs. Right HF LEFTRIGHTfatigueWeaknessdyspneaAnorexiaorthopneaIndigestionParoxysmal nocturnal dyspneaWeight gainNocturiaMental ChangesAcute vs. Chronic HF ACUTECHRONICRapid onsetongoingPulmonary EdemahypervolemicLow CONa and H2O retentionCardiogenic shockStructural changes in chambers of the heart Chronic Heart Failure InfoDiagnosis usually made with echocardiogram (ultrasound)Ejection fraction (EJ) is determined through echoCXR is also helpfulBNP is key diagnostic indicator of HFExercise testing or cardiac catheterization can be used to determine whether CAD or cardiac ischemia is the cause Medical ManagementPharmacological therapyACE inhibitorsBBDiureticsDigitalisNutritional therapyAdditional therapyO2ICD Nursing ManagementCareful assessment and monitoringFluid balance, I/O’sDaily weightMonitoring JVD, VSMonitor for complications r/t diuretic therapyHypokalemia, hyponatremia, hyperuricemmia Nursing Diagnosis Activity intoleranceExcess fluid volumePowerlessnessAcute Heart Failure (Pulmonary Edema) InfoAcute event related to HFMay occur with MIExacerbation of chronic HF Clinical manifestationsPulmonary edema: abnormal accumulation of fluid in the lungsRapid onsetPatient becomes restless and listlessSense of suffocationCold hands, cyanotic nail beds, ashen skinWeak, rapid pulseJVDProductive coughMedical ManagementO2 therapyMorphineDiureticsIV medicationsDobutamine Nesiritide milrinone Nursing managementPosition patient to promote circulation and reduce venous return to the heart (upright and feet dangling)Provide emotional supportMonitor effects of medications ................
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