Nursing care of client with Coronary Artery Disease Part 1 of 2


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Nursing care of client with Coronary Artery Disease: Assessment

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Nursing care of client with Coronary Artery Disease Part 1 of 2

  1. 1. NURSING CARE OF CLIENTWITH ACUTE CORONARYSYNDROMEASSESSMENT, DX EXAMSMaria Carmela L. Domocmat, RN, MSNInstructorSchool of NursingNorthern Luzon Adventist College
  2. 2. CORONARY ARTERY DISEASE CLDomocmat 8/9/2012 2
  3. 3. Coronary Artery DiseaseAKA Ischemic Heart Disease Coronary Heart Disease (CHD) Coronary Occlusive Disease (C.O.D.) Atherosclerotic Heart Disease (A.H.D.) CLDomocmat 8/9/2012 3
  4. 4. Coronary Artery Disease Refers to the diseases of the heart that result from a decrease in blood supply to the heart muscle Disease caused by inadequate supply of blood to the heart. CLDomocmat 8/9/2012 4
  5. 5. CAD Include the disorders 1. Angina pectoris 2. Acute coronary syndrome a. Unstable angina b. MI (STEMI, NSTEMI) CLDomocmat 8/9/2012 5
  6. 6. Incidence Primary cause of morbidity mortality in the PhilippinesEtiology Results from development of obliterative lesions within the coronary arteries CLDomocmat 8/9/2012 6
  7. 7. Ten Leading Causes of Mortality Philippines, 2000 1. Diseases of the Heart 2. Diseases of the Vascular System 3. Malignant Neoplasm 4. Pneumonia 5. Accidents 6. Tuberculosis, all forms 7. Chronic Obstructive Pulmonary Disease & Allied Conditions 8. Certain conditions originating in the Perinatal period 9. Diabetes Mellitus 10. Nephritis, Nephrotic Syndrome and Nephrosis CLDomocmat 8/9/2012 7
  8. 8. Coronary Artery Disease Occlusion of the coronary artery or any of its branches Decrease or absence of blood supply to myocardium1. Transient Hypoxia: Angina Pectoris2. Hypoxia with decreased function: Myocardial Ischemia3. Death and necrosis of myocardium: Myocardial Infarction CLDomocmat 8/9/2012 8
  9. 9. CLDomocmat 8/9/2012 9
  10. 10. Causes of CAD Arteriosclerosis Atherosclerosis CLDomocmat 8/9/2012 10
  11. 11. Atherosclerosis – deposition of fat containing substances along the intima of blood vessels causing its narrowing ; a type of arteriosclerosis CLDomocmat 8/9/2012 11
  12. 12. atherosclerosis CLDomocmat 8/9/2012 12
  13. 13. CLDomocmat 8/9/2012 13
  14. 14. Atheroma Formation CLDomocmat 8/9/2012 14
  15. 15. CLDomocmat 8/9/2012 15
  16. 16. Atherosclerosis develops in the coronaryarteries, causing them to becomenarrowed or blocked. Blood flow to thearea of the heart supplied CLDomocmat 8/9/2012 16
  17. 17. Arteriosclerosis Is hardening of arterie primarily affects the intimal layer of the blood vessels Includes: a. Atherosclerosis – accumulation of fat deposits b. Monckebergs sclerosis – calcium accumulation in medial layers of the arteries c. Arteriolar sclerosis- thickening of the sclerosis- small artery vessels CLDomocmat 8/9/2012 17
  18. 18. CLDomocmat 8/9/2012 18
  19. 19. Theories of Pathogenesis1. Response to injury theory2. Neoplasia Theory CLDomocmat 8/9/2012 19
  20. 20. Theories of Pathogenesis1. Response to injury theory Injurious Stimuli (HPN, Hypercholesterolemia) Endothelial damage Increased permeability/adhesion molecule Lipids and platelets travel to the areas affected CLDomocmat 8/9/2012 20
  21. 21. Migration of macrophages into vessel wallPlaques begin to form from cells which are imbibed into the endothelium Lipids are engulfed by the cells (foam cells) and smooth muscle cells develop Narrowing of blood vessels Plaque disruption CLDomocmat 8/9/2012 21
  22. 22. Thrombus formation Obstruction of coronary arteriesDecreased Myocardial Oxygenation Angina pectoris Myocardial Infarction CLDomocmat 8/9/2012 22
  23. 23. 2. Neoplasia Theory - vessel injury cause cell proliferation stemming from a single cell (monoclonal origin) CLDomocmat 8/9/2012 23
  24. 24. Aortic atherosclerotic plaques CLDomocmat 8/9/2012 24
  25. 25. Cross section of a coronary artery. A thrombus occludes thelumen and rests upon a mature atherosclerotic plaque. Note the relative thickness of the intima and media. CLDomocmat 8/9/2012 25
  26. 26. Etiology and risk factors Nonmodifiable risk factors Modifiable risk factors CLDomocmat 8/9/2012 26
  27. 27. Nonmodifiable risk factors Heredity Increasing age Gender CLDomocmat 8/9/2012 27
  28. 28. Heredity family history of first degree relative with CVD at 55 yrs old or younger (M), 65 yrs old or younger (F) CLDomocmat 8/9/2012 28
  29. 29. Increasing age ›45 yrs old (M); ›55 yrs old (F) CLDomocmat 8/9/2012 29
  30. 30. Gender affects men more than women before they have menopause with OCP use after menopause increase risk of developing CAD especially with smoking history with early menopause- 3x’s increase risk menopause- of developing CAD lifestyle changes that increase risk of CAD in women a. more women have entered the work force b. increase number of smokers CLDomocmat 8/9/2012 30
  31. 31. Modifiable risk factors Cigarette smoking Homocysteine levels Hypertension Metabolic syndrome Increase serum Physical inactivity cholesterol Lack of exercise Obesity Diabetes Stress Inflammatory Response CLDomocmat 8/9/2012 31
  32. 32. Cigarette smoking Nicotine – initiate release of catecholamine Endothelial dysfunction and increased vessel wall thickness Increase blood CO level Beware! Passive smoking Oral contraceptives (OC) + smoking CLDomocmat 8/9/2012 32
  33. 33. Hypertension men >45 y/o with BP exceeding 140/90 all adult women with pressures above 160/95 have a 50% increase in mortality the higher the BP = the higher the risk of CAD CLDomocmat 8/9/2012 33
  34. 34. Increase serum cholesterol > 259mg/dl = 3x’s more likely to develop CAD Patients with LDL to HDL ratios greater than 4:1 are prone to CAD CLDomocmat 8/9/2012 34
  35. 35. Modifiable Risk Factors cont. Lack of exercise Obesity Distribution of body fat Waist measurement: N: less than 40 inches (M); less than 35 (F) BMI – N: 18.5 to 24.9 Diabetes Stress: increases BP CLDomocmat 8/9/2012 35
  36. 36. Metabolic syndrome Diagnosis of this includes 3 of the ff: Insulin resistance (FBS › 100 mg/dl or abnormal GTT) Central obesity (waist circum › 35 inches for F; › 40 for M Dyslipedemia (Tg ›150 mg/dL; HDL ‹ 50 mg/dL for F; ‹ 40 mg/dL for M) BP persistent ›130/85 Proinflammatory state (high CRP level) Prothtombin state (high fibrinogen level) CLDomocmat 8/9/2012 36
  37. 37. Inflammatory responses chronic inflammation cause increase C- reactive protein (CRP) levels which tend to disrupt plaque inside arterial walls Lab test : high sensitivity C-reactive protein (hs-CRP) CLDomocmat 8/9/2012 37
  38. 38. Homocystein levels Essential amino High homocysteine acid levels increase the risks of a heart High serum levels attack or stroke. block production of nitric oxide Normal value: ‹ 12 mmol/dL CLDomocmat 8/9/2012 38
  39. 39. Physical inactivity Goal: 30 minutes, regular moderate aerobic exercise (ex: brisk walking) CLDomocmat 8/9/2012 39
  40. 40. Let’s Review CLDomocmat 8/9/2012 40
  41. 41. Modifiable risk factors Cigarette smoking Homocysteine levels Hypertension Metabolic syndrome Increase serum Physical inactivity cholesterol Lack of exercise Obesity Diabetes Stress Inflammatory Response CLDomocmat 8/9/2012 41
  42. 42. Prevention CLDomocmat 8/9/2012 42
  43. 43. An ounce of prevention is better than a pound of cure CLDomocmat 8/9/2012 43
  44. 44. Preventive measures Lifestyle modifications Reduce stress BP control, DM control Lower Serum chole Reduce CRP levels (hs-CRP) hs- Lower Homocystein levels Boost “good cholesterol” levels (HDL) CLDomocmat 8/9/2012 44
  45. 45. Lifestyle modifications Diet: low fat , low cholesterol, low salt quit smoking , avoid passive smoking exercise and weight reduction adequate time for rest and relaxation CLDomocmat 8/9/2012 45
  46. 46. Medications statins Glycoprotein IIb/IIIa receptor IIb/ antagonists aspirin, plavix Aspirin in low doses is the best known agent for the prevention of coronary heart disease. CLDomocmat 8/9/2012 46
  47. 47. Cigarette smoking cessation Educational program, Counseling, Consistent motivation, reinforcement messages, support group, meds nicotine patch [NicoDerm CQ, Habitrol] antidepressant bupropim [Zyban]) CLDomocmat 8/9/2012 47
  48. 48. Exercise and weight reduction Goal: 30 minutes, regular moderate aerobic exercise (ex: brisk walking) EBP: Men who had weights 30 min or more per week had a 23% risk reduction in coronary heart disease CLDomocmat 8/9/2012 48
  49. 49. Reduce Serum chole Serum fasting lipid profile at least q 5 yrs Lipid-lowering meds Statins Nicotinic acid Fibric Acids Bile acid sequestrants Cholesterol absorption inhibitor Omega-3-acid-ethyl esters CLDomocmat 8/9/2012 49
  50. 50. Statins block a substance liver needs to make cholesterol. This reduces cholesterol in liver cells, which causes liver to remove cholesterol from your blood. may also help body reabsorb cholesterol from built up deposits on your artery walls. CLDomocmat 8/9/2012 50
  51. 51. Statins atorvastatin (Lipitor) fluvastatin (Lescol) lovastatin (Altoprev, Mevacor) pravastatin (Pravachol) rosuvastatin (Crestor) simvastatin (Zocor) CLDomocmat 8/9/2012 51
  52. 52. EBP: Statins Statin Drugs and Dietary Supplements – Vit. E and C, selenium plus statin resulted into reduced LDL levels compared to statins alone. CLDomocmat 8/9/2012 52
  53. 53. Reduce CRP levels (hs-CRP) hs- Low fat, low chole diet Smoking cessation Exercise Statin Aspirin CLDomocmat 8/9/2012 53
  54. 54. Lower Homocystein levels B-complex vitamin (esp folic acid) CLDomocmat 8/9/2012 54
  55. 55. Boost your “good cholesterol” levels (HDL): Set your target HDL cholesterol level At risk Desirable Less than 40 60 mg/dL (1.6 Men mg/dL (1.0 mmol/L) or above mmol/L) Less than 50 60 mg/dL (1.6 Women mg/dL (1.3 mmol/L) or above mmol/L) CLDomocmat 8/9/2012 55
  56. 56. Boost your “good cholesterol” levels (HDL) Dont smoke. Lose weight Get more physical activity. Drink alcohol only in moderation Choose healthier fats. Monounsaturated and polyunsaturated fats — found in olive, peanut and canola oils Nuts, fish and other foods containing omega-3 fatty acids CLDomocmat 8/9/2012 56
  57. 57. EBP: Alcohol Compared with men who consume alcohol less than once a week, men who consume alcohol 3-7 days a week had a 32%-37% reduction of MI. CLDomocmat 8/9/2012 57
  58. 58. Boost your “good cholesterol” Choose healthier fats. Monounsaturated and polyunsaturated fats — found in olive, peanut and canola oils Nuts, fish and other foods containing omega-3 fatty acids CLDomocmat 8/9/2012 58
  59. 59. Boost your “good cholesterol” Niacin (Niaspan) Fibrates The medications fenofibrate (Lofibra, Tricor) and gemfibrozil (Lopid) can also help increase HDL cholesterol level. CLDomocmat 8/9/2012 59
  60. 60. Stable and Unstable Angina PectorisSee separate presentation CLDomocmat 8/9/2012 60
  61. 61. Acute Myocardial Infarction CLDomocmat 8/9/2012 61
  62. 62. Acute Myocardial Infarction Occurs when myocardial tissue is abruptly and severely deprived of O2 When blood flow is reduced by 80-90% 80- ischemia develops CLDomocmat 8/9/2012 62
  63. 63. prolonged ischemia lasting more than 35- 35-45 minutes produces irreversible cellulardamage and necrosis of themyocardiumischemic injury evolves over several hourstoward complete necrosis and infarction CLDomocmat 8/9/2012 63
  64. 64. The autonomic nervous system attemptsto compensate for the depressed cardiacperformance.This results to further imbalance betweenmyocardial oxygen supply and demandThe 3 areas which develop in MI are: CLDomocmat 8/9/2012 64
  65. 65. CLDomocmat 8/9/2012 65
  66. 66. Zone of infarction Zone of hypoxic injury Zone of ischemia CLDomocmat 8/9/2012 66
  67. 67. Most common site for MI is the anterior wall of the left ventricle.MI may be classified as follows: Transmural infarct – extends from endocardium to epicardium Subendocardial – affects the endocardial muscles Intramural – seen in patchy areas of the myocardium and is usually associated with longstanding angina pectorisHealing requires formation of scar tissuesthat replace the necrotic myocardium; scartissue inhibits contractility CLDomocmat 8/9/2012 67
  68. 68. javascript:eml2(dorland,infarction_myocardial.jpg) CLDomocmat 8/9/2012 68
  69. 69. CLDomocmat 8/9/2012 69
  70. 70. Clinical Manifestations CLDomocmat 8/9/2012 70
  71. 71. Clinical Manifestations Pain crushing, severe, prolonged, unrelieved by rest or nitroglycerine, radiating to one or both arms, neck, back Signs of shock - hypotension, cold diaphoresis, peripheral cyanosis, tachy/brady, tachy/brady, thready pulse CLDomocmat 8/9/2012 71
  72. 72. Women often present with a “triad” ofsymptoms, including indigestion orabdominal fullness, chronic fatigue despiteadequate rest, and inability to catch one’sbreath. CLDomocmat 8/9/2012 73
  73. 73. Clinical Manifestations fever apprehension indigestion dob n/v pallor, cyanosis, coolness of extremities increase BP, HR, S4, transient murmur CLDomocmat 8/9/2012 74
  74. 74. PE thorough and focused health hx and PE goal: presence of CAD risk factors, angina, previous infarctions focused assessment chest pain general appearance determination of frequent VS cont monitoring of cardiac and pulse ongoing eval of mental status, heart, lungs, abd UO, extremities Maria Carmela L.Domocmat, RN, MSN 8/9/2012 75
  75. 75. Diagnostic exams CLDomocmat 8/9/2012 76
  76. 76. Diagnostic exams ECG Serum Markers of Myocardial Damage : Cardiac biomarkers Cardiac catheterization with coronary arteriography Echocardiography Radionuclide imaging PET Scan CT scan Magnetic Resonance Imaging Intravascular ultrasound (IVUS) CLDomocmat 8/9/2012 77
  77. 77. CLDomocmat 8/9/2012 78
  78. 78. Stress ECG ST segment depression of 1mm or more during exercise ECG changes during testing may indicate ischemia CLDomocmat 8/9/2012 79
  79. 79. 12 lead ECG changes T wave inversion ST segment elevation (subepicardial (subepicardial injury) ST segment depression (subendocardial injury) abnormal Q wave (infarction) CLDomocmat 8/9/2012 80
  80. 80. Maria Carmela L.Domocmat, RN, MSN 8/9/2012 81
  81. 81. CLDomocmat 8/9/2012 83
  82. 82. CLDomocmat 8/9/2012 84
  83. 83. Abnormal Q wave CLDomocmat 8/9/2012 85
  84. 84. 12- lead ECG Note: 1 single ECG is NOT sufficient to confirm or exclude dx of AMI cardiac conduction system is dynamic process that is subject to change overtime Recommendation serial ECGs q 30 min for pt at high risk for AMI Maria Carmela L.Domocmat, RN, MSN 8/9/2012 86
  85. 85. Acute Cardiac Ischemia Time-Insensitive PredictiveInstrument (ACI-TIPI) Adobe Acrobat Adobe Acrobat Document Document Maria Carmela L.Domocmat, RN, MSN 8/9/2012 87
  86. 86. Serum Markers of MyocardialDamage : Cardiac biomarkers CLDomocmat 8/9/2012 88
  87. 87. Cardiac Serum markers during infarction process – cell membranes rupture, allowing intracell enzymes to spill out into blood stream are substances that are released into the blood when the heart is damaged or stressed. Measurement of these biomarkers is used to help diagnose, risk stratify, monitor and manage people with suspected acute coronary syndrome (ACS) and cardiac ischemia. Maria Carmela L.Domocmat, RN, MSN 8/9/2012 89
  88. 88. Cardiac biomarkers Current cardiac biomarker tests used to help diagnose, evaluate, and monitor individuals suspected of having acute coronary syndrome (ACS) include: Troponin I or T CK-MB CLDomocmat 8/9/2012 90
  89. 89. Cardiac biomarkers Other biomarker tests that may be used: Myoglobin BNP (or NT-proBNP) — although usually used to recognize heart failure, an increased level in people with ACS indicates an increased risk of recurrent events hs-CRP Homocysteine Phased out biomarkers—the tests below are not specific for damage to the heart and are no longer recommended for evaluating people with suspected ACS: AST LDH CLDomocmat 8/9/2012 91
  90. 90. Cardiac Troponin T and I most sensitive to cardiac muscle damage Not found in normal heart quick, rapid test if elevated – indicate AMI become elevated in the blood within 3 or 4 hours after injury and may remain elevated for 10 to 14 days. Maria Carmela L.Domocmat, RN, MSN 8/9/2012 92
  91. 91. Troponin Troponin T similar to CK-MB – with regard sensitivity useful and more accurate than LDH in confirmation of distant AMI Troponin I very specific and sensitive indicator of AMI not affected by any other dse or injury to any other muscle except cardiac muscle Maria Carmela L.Domocmat, RN, MSN 8/9/2012 93
  92. 92. CK MB Enzyme specific to cells of heart (+) in blood indicates tissue necoris or injury CLDomocmat 8/9/2012 94
  93. 93. Myoglobin found in both skeletal and cardiac muscle Detected 2-3 hours post MI 2- CLDomocmat 8/9/2012 95
  94. 94. Myoglobin start to rise within 2-3 hours of a heart attack or other muscle injury, reach their highest levels within 8-12 hours, and generally fall back to normal within one day. Increase is detectable sooner than troponin, but it is not as specific for heart damage and it will not stay elevated as long as troponin. Although a negative myoglobin result effectively rules out a heart attack, a positive result must be confirmed by testing for troponin. CLDomocmat 8/9/2012 96
  95. 95. Test Time to Peak Duration Sampling detectionCK-MBCK- 6-12 hours 1 day 3 days Every 12 hrs x 3 days start 6 hrs after chest painTroponin T 3-12 hours 24 hours 10-14 days 10- One at least 12 hrs after onset of painTroponin I 3-12 hours 24 hours 5-10 days One at least 12 hrs after onset of painMyoglobin 1-3 hrs 12 hrs CLDomocmat 8/9/2012 97
  96. 96. Lactate dehydrogenase (LDH or LD) is an enzyme that is found in almost all of the bodys cells, but only a small amount of it is usually detectable in the blood. is released from the cells into the bloodstream when cells are damaged or destroyed. Because of this, the LDH test can be used as a general marker of injury to cells. CLDomocmat 8/9/2012 98
  97. 97. LDH LDH1 subunit – plentiful in heart muscle and released into serum when myocardial damage occurs LDH-1: heart, red cells, kidney, germ cells LDH-2: heart, red blood cells, kidney (lesser amounts than LDH-1) LDH-3: lungs and other tissues LDH-4: white blood cells, lymph nodes, muscle, liver (lesser amounts than LDH-5) LDH-5: liver, skeletal muscle Maria Carmela L.Domocmat, RN, MSN 8/9/2012 99
  98. 98. Nrg considerations: LDH Inform that no need to restrict food or fluids Muscle trauma caused by MI injections can raise LD levels Prosthetic valves or recent surgery or pregnancy can cause elevated result CLDomocmat 8/9/2012 100
  99. 99. Test Time to Peak Duration Sampling detectionSGOT 24 hours 2 days 4 days 1-2 days after chest painLDH 36 hours 3 days 10 days 1-2 days after chest pain CLDomocmat 8/9/2012 101
  100. 100. Other lab tests Serum lipids Hs CRP Homocystein WBC Serum elec CLDomocmat 8/9/2012 102
  101. 101. Fasting lipid profile total cholesterol: ‹ 200 mg/dL triglycerides : ‹ 150 mg/dL LDL : ‹ 100 mg/dL HDL chole: ‹ 60 mg/dL HDL: LDL ratio shld be 3:1 CLDomocmat 8/9/2012 103
  102. 102. Homocystein levels Normal value: ‹ 12 mmol/dL Labs: NPO 1-12 hrs CLDomocmat 8/9/2012 104
  103. 103. High sensitive C- reactive protein C-(hs-CRP) hs- correlates with CK-MB levels but it CK- peaks several days later Most standard marker of inflammation Normal value: 1 mg/dl > 3 – increase risk CAD CLDomocmat 8/9/2012 105
  104. 104. Leukocytosis 10, 000 to 20, 000 mm3 appears on 2nd day disappears in 1 wk Myeloperoxidase – a leukocyte enzyme – recently shown to ne a predictive ofAMI even in clients without elevation in Troponin T Maria Carmela L.Domocmat, RN, MSN 8/9/2012 106
  105. 105. Cardiac catheterization withcoronary arteriography CLDomocmat 8/9/2012 107
  106. 106. Cardiac catheterization withcoronary arteriography direct visualization of the coronary arteries by selective injection of radiographic contrast material most sensitive and specific test CLDomocmat 8/9/2012 108
  107. 107. Cardiac catheterization withcoronary arteriographypre post Determine allergy to iodine Bed rest and seafoods (prep Supine HOB elevate antihistamine) Leg insertion site keep straight Informed consent VS q 15v min for 1 hr; then 2-6 hrs bedrest q 30 for 2 hrs til stable NPO post MN Analgesics VS, auscultate heart and Assess insertion site lungs, eval peripheral VS, auscultate heart and pulses, withheld digitalis or lungs, eval peripheral diuretics pulses, Observe complication CLDomocmat 8/9/2012 109
  108. 108. Health educ post cath For the next 24 hrs Don’t bend at waist Strain Lift heavy objects Avid tub bath Call doctor if Bleeding, swelling, new bruising from peripheral site, temp >38.6C CLDomocmat 8/9/2012 110
  109. 109. Cardiac catheterization CLDomocmat 8/9/2012 111
  110. 110. CLDomocmat 8/9/2012 112
  111. 111. Coronary angiography Let’s watch YouTube - Heart Animation_ Coronary Angiography _Cardiac Catheterization_.flv CLDomocmat 8/9/2012 113
  112. 112. Echocardiography CLDomocmat 8/9/2012 114
  113. 113. Echocardiography - produces images of wallmotion abnormalities CLDomocmat 8/9/2012 115
  114. 114. Transesophageal Echocardiography CLDomocmat 8/9/2012 116
  115. 115. Radionuclide imaging CLDomocmat 8/9/2012 117
  116. 116. Radionuclide imaging Stress scintigraphy - use of thallium 201 or sestamibi -decrease uptake of dye in ischemic tissue Stress radionuclide ventriculography - pyrophosphate injected peripherally binds the radionuclide technetium to RBC used to produce a scintigraphic image of the left ventricle 90% sensitive CLDomocmat 8/9/2012 118
  117. 117. PET Scan CLDomocmat 8/9/2012 119
  118. 118. PET Scan CLDomocmat 8/9/2012 120
  119. 119. PET Scan 3 dimensional images Inject isotopes Avoid tobacco and caffeine 4 hrs before CLDomocmat 8/9/2012 121
  120. 120. CT scan CLDomocmat 8/9/2012 122
  121. 121. CT scan Xray Cross sectionial images of the chest (heart, great vessels) Evaluate cardiac masses and dse of aorta , pericardium CLDomocmat 8/9/2012 123
  122. 122. Magnetic Resonance ImagingMagnetic resonance angiography CLDomocmat 8/9/2012 124
  123. 123. Magnetic Resonance Imaging CLDomocmat 8/9/2012 125
  124. 124. Magnetic Resonance Imaging No metal can enter the exam room clothing with metal snaps or pins should not be worn. Jewelry, watches, rings etc should be left in a locker. Hairpins and dentures, should also be removed and left in a locker or outside the exam room Heavy facial makeup should not be worn as it may create artifacts on the image. Labs are not required unless have a history of impaired kidney function. However, allergy history records are necessary for contrast studies. CLDomocmat 8/9/2012 126
  125. 125. Magnetic Resonance Imaging Contraindication Patients cannot have halter monitors, telemetry units, nerve stimulation units or a IV pump in the magnet room If have a heart pacemaker or pacing wires, cerebal aneurysm or Swan Ganz catheter cannot have an MRI under any circumstances! Pregnancy is a contraindication and will require patient consent for an MRI. All other history of metal fragments in the eye require orbit screening x-rays prior to your MRI. All other history of implants or surgery must be indicated to the technologist. The make and model of implants may be necessary (i.e. ear implants, heart valve replacements). CLDomocmat 8/9/2012 127
  126. 126. Intravascular ultrasound (IVUS) CLDomocmat 8/9/2012 128
  127. 127. B-mode ultrasonography CLDomocmat 8/9/2012 129
  128. 128. Intravascular ultrasound (IVUS) Ultrasound - coronary artery; Endovascular ultrasound; Intravascular echocardiography CLDomocmat 8/9/2012 130
  129. 129. IVUS Alternative to injecting medium More reliable than angiography in indicating distribution and composition, arterial dissection, degree of stenosis of the occluded artery CLDomocmat 8/9/2012 131
  130. 130. Intravascular ultrasound(IVUS) A tiny ultrasound wand is attached to a catheter. This ultrasound catheter is inserted into an artery in your groin area and moved up to the heart. A computer measures how the sound waves reflect off blood vessels, and changes the sound waves into pictures. IVUS gives the health care provider a look at coronary arteries from the inside-out. CLDomocmat 8/9/2012 132
  131. 131. IVUSIVUS is almost always done at the end of angioplasty with stent placement, or coronarycatheterization. Angioplasty gives a general look at the coronary arteries, but it cannotshow the walls of the arteries. IVUS images show the artery walls and can revealcholesterol and fat deposits (plaques). Buildup of these deposits can increase your risk of aheart attack.IVUS has provided a lot of insight into how stents become clogged (stent restenosis). CLDomocmat 8/9/2012 133
  132. 132. Let’s review CLDomocmat 8/9/2012 134
  133. 133. Diagnostic exams ECG Serum Markers of Myocardial Damage : Cardiac biomarkers Cardiac catheterization with coronary arteriography Echocardiography Radionuclide imaging PET Scan CT scan Magnetic Resonance Imaging Intravascular ultrasound (IVUS) CLDomocmat 8/9/2012 135
  134. 134. Prognosis of CAD CLDomocmat 8/9/2012 136
  135. 135. Prognosis of CAD >80 y/o = 60 %mortality other diseases Dm, COPD= 30% mortality anterior wall MI= 30% mortality CLDomocmat 8/9/2012 137