Acute Coronary Syndrome - BMH/Tele


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Acute Coronary Syndrome - BMH/Tele

  1. 1. Acute Coronary Syndromes Natalie Bermudez, RN, BSN, MS Clinical Educator for Cardiac Telemetry
  2. 2. Learning Objectives Define the differences of ischemia, injury, and infarct. Define angina pectoris, etiology, s/s, diagnosis, and treatment Differentiate between UA, NSTEMI, & STEMI: s/s, diagnosis, and treatment Localize area of infarct on a 12-lead EKG Discuss women & heart disease
  3. 3. National Statistics Coronary Artery DiseaseCardiovascular disease is the leading cause of death among men and women in all racial and ethnic groups.Affects approximately 58 million Americans and costs the nation $274 billion each year, including health expenditures and loss of productivity (Woods et al, 2005, p.115)
  4. 4. National StatisticsAccording to the AHA, 785,000 Americans will have an MI this year, and nearly 500,000 of them will experience another (Overbaugh, 2009, p. 42)
  5. 5. National Statistics In 2006, nearly 1.4 millionpatients were discharged with aprimary or secondary diagnosisof ACS, including 537,000 with unstable angina and 810,000 with either NSTEMI or STEMI (Overbaugh, 2009, p. 42)
  6. 6. Atherosclerotic PlaqueThe usual cause of an acute coronary syndrome is the rupture of an atherosclerotic plaque (Phalen and Aehlert, 2006, p. 61)
  8. 8. Angina PectorisLatin phrase literally means “pain in the chest” Many different conditions are responsible for causing angina pectoris
  9. 9. Stable (Classic) Angina Remains relatively constant and predictable in terms of frequency of episodes, severity, duration, time of appearance, precipitating factors, and response to therapyUsually related to emotional upset, exercise orexertion, exposure to cold weather, consumption of heavy mealsDuration of symptoms is typically 2 – 5 minutes; occasionally 10 – 15 minutes
  10. 10. Stable (Classic) Angina Treatment Includes:Lifestyle Modifications (Diet & Exercise) Antiplatelet Agents (aspirin) Beta-Adrenergic Blockers Antianginal Meds (SL nitroglycerin)
  11. 11. Prinzmetal’s Angina AKA Variant AnginaIt is the result of intense spasm of a segment of an epicardial coronary artery Occurs exclusively at rest; early morningLasts only a few minutes; however long enough to produce dysrhythmias including v-tach or v-fib, as well as sudden death
  12. 12. Prinzmetal’s Angina Difficult to identify this type of anginaHas been reported to occur with migraine, Raynaud’s phenomenon, and aspirin- induced asthma It is relieved by administration of nitroglycerin
  13. 13. Silent AnginaObjective evidence of ischemia(i.e. EKG changes with stress test) No reports of symptoms
  15. 15. Acute Coronary SyndromesACS’s are a physiologic continuum of conditions caused by a similar sequence of pathologic events: atransient or permanent obstruction of a coronary artery (Phalen and Aehlert, 2006, p. 60)
  16. 16. Acute Coronary Syndromes These conditions are characterized by an excessive demand or inadequate supply of O2 and nutrients to the heart muscle associated with:  Plaque Disruption  Thrombus Formation  Vasoconstriction(Phalen and Aehlert, 2006, p. 60)
  17. 17. ACS’s: 3 Categories Unstable Angina Non-ST-Segment Elevation MI (NSTEMI)ST-Segment Elevation MI (STEMI)
  18. 18. Blood Vessel Wall Layers
  19. 19. Coronary Artery Obstruction How does it happen? Fatty Streak Fibrous Plaque Ruptured Plaque Advanced Atheromatous Plaque
  20. 20. Endothelial DamageProgression from a fatty streak to an advanced lesion is associated withinjured endothelium that activates the inflammatory response (Phalen and Aehlert, 2006, p. 61)
  21. 21. Rupture of Plaque Rupture of the plaque surface occurs frequently during plaque growth and is probably the most significant mechanism underlying the progression of coronary lesions(Phalen and Aehlert, 2006, p. 61)
  22. 22. Stable & Unstable Plaque As plaque builds up, it can become either stable or unstable.Unstable plaque is more prone to sudden rupture, a potentially life-threatening even.
  23. 23. Stable PlaqueHard, consist primarily of collagen- rich sclerotic tissue, and have a thick fibrous cap over the lipid core that separates it from contact with blood70%-diameter stenosis is required to produce anginal symptoms (Phalen and Aehlert, 2006, p. 62)
  24. 24. Unstable Plaque Soft and have a thin fibrous tissue over the lipid core that separates it from the vessel lumen Rupture tends to occur near the normal part of the vessel wall It is unknown whether plaque rupture is triggered on spontaneously (Phalen and Aehlert, 2006, p. 63, 64)
  25. 25. Ischemia, Injury, and Infarction
  26. 26. Ischemia Myocardial ischemia is the result of an imbalance between the metabolic needs of the myocardium and the flow of oxygenated blood to it EKG Changes: ST-segment depression & T-wave inversion(Related to delays in depolarization and repolarization)
  27. 27. IschemiaMay occur as a result of either or both of the following: Demand Ischemia: Increased myocardial O2 demand (Anemia, hypoxemia, coronary artery narrowing due to a thrombus, vasospasm, or rapid progression of atherosclerosis) Supply Ischemia: Reduced myocardial O2 supply(Exercise, smoking, heavy meals, fever, HF, tachydysrhythmias, OCM, cocaine, amphetamines, emotional stress, hypertension, cold weather, aortic stenosis, pheochromocytoma, thyrotoxicosis)
  28. 28. Injury Ischemia prolonged more than just a few minutes results in myocardial injury.Injured myocardial cells are still alive but will infarct if the ischemia is not quickly corrected EKG Changes: ST-segment elevation (Injured myocardial cells do not depolarize completely, remaining electrically more positive than the uninjured areas surrounding them)
  29. 29. InfarctionA myocardial infarction occurs when blood flow to the heart muscle stops or is suddenly decreased long enough to cause cell death Infarcted cells are without function and cannot respond to electrical stimulus or provide any mechanical function (Thalen and Aehlert, 2006, p, 67) EKG Changes: ST-segment elevation, T-wave inversion, abnormal Q waves
  30. 30. Abnormal Q Waves An abnormal Q wave indicates the presence of dead myocardial tissue and subsequently a loss of electrical activity (Thalen and Aelhert, 2006, p. 77)Pathological Q waves represent transmural MI and are most commonly seen with STEMI (Davis, 2004)Sometimes occurs within hours of onset of chest pain More commonly appears 1-3 days after the event Most Post MI Q waves are permanent
  31. 31. Pathologic Q Waves1/3 or greater than the amplitude of an R wave R Wave 5 mm Q Wave 2.5 mmAnd/or greater than 40 ms (0.04 secs)
  32. 32. Risk Factors for DevelopingCORONARY ARTERY DISEASE
  33. 33. Risk FactorsNon-Modifiable Modifiable Contributing Heredity  ETOH Intake Inactive  Age  Hypertension Lifestyle  Race  Lipids &  Diabetes  Gender Cholesterol  Obesity  Smoking  Drug Use  Stress
  34. 34. Causes and Diagnostic Findings for Unstable Angina NSTEMI STEMI
  35. 35. Unstable Angina Cause:Thrombus partially or intermittently occludes the coronary artery Diagnostic Findings:ST-segment depression or T-wave inversion Normal Cardiac Markers (Overbaugh, 2009, p. 46)
  36. 36. NSTEMI Cause: Thrombus partially or intermittently the occludes coronary artery Diagnostic Findings:ST-segment depression or T-wave inversion Elevated Cardiac biomarkers (Overbaugh, 2009, p. 46)
  37. 37. STEMI Cause:Thrombus fully occludes the coronary artery Diagnostic Findings: ST-segment elevation or new left bundle branch block Elevated Cardiac Biomarkers (Overbaugh, 2009, p. 47)
  38. 38. Cardiac MarkersCardiac Enzymes
  39. 39. Cardiac EnzymesA.K.A. ACP (Acute Cardiac Profile) Normal Ranges: CPK: 39 – 308 CK-MB: 0 – 3.60 **Troponin I: 0 – 0.099**
  40. 40. Cardiac Enzymes Ordered for patients c/o chest pain and suspected AMI CE’s are drawn in sets of three 6 to 8 hours apart Sometimes initial results are negativeCK-MB & Troponins are released within hours of a cardiac event
  41. 41. Cardiac Enzymes CK-MB or CPK-MB Creatine Phosphokinase Rise within 4-6 hours after an AMIPeak @ 18 – 24 hours (6x > normal)Return to normal within 3 – 4 days
  42. 42. Cardiac Enzymes Troponin I Rise within 3 hours of an AMIPreferred cardiac enzyme in diagnosis of an AMI
  43. 43. Cardiac EnzymesLab will call nursing for critical lab values Physician needs to be notifiedimmediately for elevated Troponin levels
  44. 44. Cardiac EnzymesPatients with elevated CE’s usuallyundergo a stress test and/or cardiac catheterization for furtherinvestigation of cause of chest pain.
  45. 45. Signs and Symptoms of Unstable Angina, NSTEMI, &STEMI
  46. 46. Signs & Symptoms UA, NSTEMI, & STEMI  Pain with or without radiation to arm, neck, back, or epigastric region  SOB, tachypnea, decreased SaO2 Tachycardia, hypotension or hypertension  Diaphoresis, nausea, lightheadedness,  Rhythm abnormalities
  47. 47. Signs & Symptoms: Chest Pain UA: NSTEMI STEMI Occurs with rest  Occurs with rest  Occurs with rest or exertion; limits or exertion; limits or exertion; limits activity activity activity  Longer duration  Longer duration and more severe and more severe than in unstable than in unstable angina angina (irreversible tissue damage [infarction] occurs if perfusion is not restored) (Overbaugh, 2009, pp. 46, 47)
  48. 48. Treatment ofUnstable Angina NSTEMI STEMI
  49. 49. Goals for Treatment Minimize Infarct Size Salvage ischemic Myocardium Alleviate VasoconstrictionReduce Myocardial O2 DemandPrevent & Manage Complications Improve Chances of Survival (Phalen and Aehlert, 2006, p. 60)
  50. 50. Treatment UA NSTEMI STEMI  Oxygen to Same as UA plus: Same as UA & maintain O2 sat >  Cardiac cath & NSTEMI except: 90% possible PCI for  No glycoprotein NTG or MSO4 to IIb/IIIa inhibitors patients with control pain ongoing CP,  PCI should be  BB’s, CCB’s, hemodynamic done within 90 ACEI’s, statins, instability, or minutes of medical clopidogrel, evaluation increased risk of unfractionated heparin or LMWH, worsening clinical  Fibrinolytic glycoprotein condition therapy within 30 IIb/IIIa inhibitors minutes of evaluation (Overbaugh, 2009, pp. 46, 47)
  51. 51. Pharmacologic Treatment Beta-Adrenergic BlockersNegative Inotropic and Chronotropic EffectsReduces myocardial contractility and heart rate resulting in decreased demand for oxygen
  52. 52. Pharmacologic Treatment Calcium Channel Blockers Non-dihydropyridinesNegative Inotropic and Chronotropic EffectsReduces myocardial contractility and heart rate resulting in decreased demand for oxygenAlso work to decrease workload of the heart by coronary arterioles
  53. 53. Pharmacologic Treatment Nitroglycerin Promotes decrease O2 demand by dilating veins which decreases venous return to the heart thus decreasing ventricular filling (decreases preload)Decrease in wall tension decreases O2 demand (Frank-Starling Effect)
  54. 54. Pharmacologic Treatment Morphine SulfateDecreases pain and anxiety – decreasing heart rate and oxygen consumption Reduces cardiac preload and afterload – decreasing workload of the heartRelaxes bronchioles – increasing oxygenation
  55. 55. Pharmacologic Treatment Antiplatelet AgentsAspirin (acetalsalicylic acid): Low dose, long- term aspirin use irreversibly blocks formation of thromboxane A2 in platelets, producing an inhibitory effect on platelet aggregation
  56. 56. Pharmacologic Treatment Antiplatelet AgentsPlavix (clopidogrel): Inhibits 1st and 2nd Phases ADP-induced affects of platelet aggregation
  57. 57. Pharmacologic Treatment HMG-CoA Reductase Inhibitors “Statins”Decreases the rate of cholesterol productionLiver needs HMG-CoA reductase to make cholesterol When less cholesterol is produced liver needs to “recycle” LDL from the blood circulation
  58. 58. Women & Heart Disease
  59. 59. National Statistics American Heart Association:About 7.3 million females alive today have a history of heartattack, angina pectoris, or both
  60. 60. National StatisticsWomen with diabetes and CVD, especially African American and Hispanic, die at a higher rate than men or non-diabetic womenSince 1984, the number of CVD deaths for females has exceeded those for males. In 2004, CVD was the cause of death in 459,096 females. Females represent 52.8 percent of deaths from CVD.
  61. 61. National Statistics According to the American Heart Association:More women than men have anginapectoris in total numbers (4.6 million versus. 4.4 million)About 25,000 females diagnosed with angina pectoris were discharged from short-stay hospitals in 2005
  62. 62. Atypical Chest Pain Women experience cardiac chest pain differently!!Discomfort varies greatly and be more generalized or subtle  Chest heaviness, squeezing Pain in left chest, midabdomen, back, or shoulder  Arm pain  Sharp, fleeting pain  Palpitations (Cheek and Sherrod, 2008)
  63. 63. Atypical Chest Pain During an MI:Discomfort is more likely to occur in neck, back, arm, shoulder, jaw, or throat Sometimes occurring with n/v, indigestion, upper abdominal pain, dyspnea, fatigue, diaphoresis, dizziness, or fainting (Cheek and Sherrod, 2008)
  64. 64. Atypical Findings An older women or one with diabetes may not experience any pain during an MI EKG findings are different for men and womenWomen are less likely to have ST-segment elevation (Cheek and Sherrod, 2008, pp. 38, 39)
  65. 65. TJC Core Measures for AMI  Aspirin within 24 hours  PCI within 90 minutes for STEMI  LVF Assessment (echocardiogram)  ACEI or ARB for EF < 40%  If +MI, aspirin & BB ordered at D/C  “STATIN” prescribed at discharge Discharge medications to include aspirin & beta-blocker if positive for MI Adult smoking cessation advice/counseling
  66. 66. Cardiac Catheterization Procedures
  67. 67. Cardiac Catheterization Procedures
  68. 68. Cardiac Catheterization Procedures Before & After
  69. 69. Post Myocardial Infarction Complications
  70. 70. Post MI Complications Arrhythmias Heart Failure Cardiac Arrest Mitral Insufficiencies Cardiac Muscle Pericarditis Dysfunction ThromboembolismCardiogenic Shock GI Complaints (Haworth and Pratowski, 2000 p. 90)
  71. 71. Post MI: Common Arrhythmias Atrial Fibrillation Premature Ventricular Contractions Ventricular Tachycardia Accelerated Idioventricular Rhythm Ventricular Fibrillation Atrioventricular Block (Haworth and Pratowski, 2000 p. 91)
  72. 72. Localizing theAffected Area of Ischemia and Infarction
  73. 73. 12-Lead EKG:Precordial & Limb Leads
  74. 74. Limb Leads: I, II, III, aVR, aVL, aVF I, II, IIIaVR, aVL, aVF EKG
  75. 75. Limb Leads: I, II, III Bipolar Each of these leads has a distinct negative pole and a distinct positive poleThese were the 1st leads to be used when EKG’s were developedLimb Leads (Phalen and Aehlert, 2006, p. 24)
  76. 76. Limb Leads: aVR, aVL, aVF “a” = augmented Unipolar “V” = voltage Have a distinct positive pole but “R” = right arm do not have a “L” = left arm distinct negative pole“F” = left foot (leg)Limb Leads (Phalen and Aehlert, 2006, p. 24, 26)
  77. 77. Chest Leads: V1-V6V1-V6
  78. 78. Chest Leads: V1-V6 Aka Precordial Leads Unipolar The positive electrode for each lead is placed on a specific location on the chest and the heart is the theoretical negative electrodeChest Leads (Phalen and Aehlert, 2006, p. 25)
  79. 79. R-wave Progression
  80. 80. Localizing EKG Changes I: lateral V1: septum II: inferior V2: septum III: inferior V3: anterior aVR: none V4: anterior aVL: lateral V5: lateral aVF: inferiorLimb Leads V : lateral 6 (Phalen and Aehlert, 2006, p. 86)
  81. 81. I V1 V4 aVR Lateral Septal Anterior NoneLAD or RCA branch LAD LAD II aVL V2 V5 Inferior Lateral Septal Lateral RCA LAD or RCA branch LAD LAD or RCA branch III aVF V3 V6 Inferior Inferior Anterior Lateral RCA RCA LAD LAD or RCA branch
  82. 82. Anterolateral Wall MI Leads: I, V3-V6, AVL Reciprocal ST-segment Depression in Inferior Leads
  83. 83. Inferior/Posterior Wall MI Leads: II, III, AVF Reciprocal ST depression in Posterior LeadsIf ST elevation is seen in II, III, and/or AVF, then look for reciprocal changes (ST-depression) in V1 – V4, indicates a posterior MI
  84. 84. Posterior Wall MI Hyperacute: Mirror image of acute injury in leads V1-V3Fully Involved: Tall R-wave, Tall upright T-wave in leads V1-V3
  85. 85. STEMI & New BBB Infarct-induced BBB – increased mortality rate between 40% and 60% Increased rate of cardiogenic shock – up to 70% New-Onset BBB is an indication of a bigger problem – extensive infarction – Tissue lost due to infarct is what increases the mortality rate and cardiogenic shock
  86. 86. STEMI & New BBB Patients that have septal or anteroseptal infarcts are more likely to develop new- onset BBB New-Onset BBB also indicates a higher likelihood of developing AV blocks On the other hand, an old LBBB can produce ST-segment elevation and wide Q waves that are similar to infarction
  87. 87. ReferencesCheek, D., & Sherrod, M. (2008). Women and heart disease: What’s new. Nursing 2008, 38(1), 36-42.Davis, L. (2004). Cardiovascular nursing secrets. St. Louis, MO: Mosby ElsevierHaworth, K., & Pratowski, E. R., (Eds.). (2000). Myocardial infarction: An incredibly easy mini-guide. Springhouse, PA: Springhouse Corporation.Lackey, S. A. (2006). Suppressing the scourge of AMI. Nursing 2006, 36(5), 37-41.Lilley, L. L., Harrington, S., & Snyder, J. S. (2007). Pharmacology and the nursing process, (5th ed.). St. Louis, MO: Mosby Elsevier.Overbaugh, K. J. (2009). Acute coronary syndrome. American Journal of Nursing, 109(5), 42-52.Phalen, T., & Aehlert, B. (2006). The 12-lead ECG in acute coronary syndromes, (2nd ed.). St. Louis, MO: Elsevier Mosby.Woods, S. L., Sivarajan Froelicher, E. S., Underhill Motzer, S., & Bridges, E. J. (2005). Cardiac nursing (5th ed.). Philadelphia, PA: Lippincott, Williams, and Wilkins.