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GEMC- Cardiovascular Board Review Session 2- Resident Training


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This is a lecture by Joe Lex, MD from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License:

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GEMC- Cardiovascular Board Review Session 2- Resident Training

  1. 1. Project: Ghana Emergency Medicine Collaborative Document Title: Cardiovascular Board Review for Part 2 Author(s): Joe Lex, MD (Temple University School of Medicine) License: Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: We have reviewed this material in accordance with U.S. Copyright Law and have tried to maximize your ability to use, share, and adapt it. These lectures have been modified in the process of making a publicly shareable version. The citation key on the following slide provides information about how you may share and adapt this material. Copyright holders of content included in this material should contact with any questions, corrections, or clarification regarding the use of content. For more information about how to cite these materials visit Any medical information in this material is intended to inform and educate and is not a tool for self-diagnosis or a replacement for medical evaluation, advice, diagnosis or treatment by a healthcare professional. Please speak to your physician if you have questions about your medical condition. Viewer discretion is advised: Some medical content is graphic and may not be suitable for all viewers. 1
  2. 2. Attribution Key for more information see: Use + Share + Adapt Make Your Own Assessment Creative Commons – Attribution License Creative Commons – Attribution Share Alike License Creative Commons – Attribution Noncommercial License Creative Commons – Attribution Noncommercial Share Alike License GNU – Free Documentation License Creative Commons – Zero Waiver Public Domain – Ineligible: Works that are ineligible for copyright protection in the U.S. (17 USC § 102(b)) *laws in your jurisdiction may differ Public Domain – Expired: Works that are no longer protected due to an expired copyright term. Public Domain – Government: Works that are produced by the U.S. Government. (17 USC § 105) Public Domain – Self Dedicated: Works that a copyright holder has dedicated to the public domain. Fair Use: Use of works that is determined to be Fair consistent with the U.S. Copyright Act. (17 USC § 107) *laws in your jurisdiction may differ Our determination DOES NOT mean that all uses of this 3rd-party content are Fair Uses and we DO NOT guarantee that your use of the content is Fair. To use this content you should do your own independent analysis to determine whether or not your use will be Fair. { Content the copyright holder, author, or law permits you to use, share and adapt. } { Content Open.Michigan believes can be used, shared, and adapted because it is ineligible for copyright. } { Content Open.Michigan has used under a Fair Use determination. } 2
  3. 3. Cardiovascular Board Review for Joe Lex, MD, FACEP, MAAEM Professor of Emergency Medicine Department of Emergency Medicine Temple University School of Medicine Philadelphia, PA USA 3
  4. 4. Part Two 5. Diseases of the Myocardium Cardiac Failure Cardiomyopathy CHF Coronary Syndromes Myocardial Infarction Myocarditis Ventricular Aneurysm 4
  5. 5. 3.5 Acquired Diseases of the Myocardium 5 Patrick J. Lynch (Wikimedia Commons)
  6. 6. Cor Pulmonale 6 Mariana Ruiz (Wikipedia)
  7. 7. Cor Pulmonale Cor = heart Pulmonale = of the lungs In other words, pulmonary heart disease Also known as “right heart failure” 7
  8. 8. Cor Pulmonale Chronic: right ventricle hypertrophy Adaptive response to long- term  in pressure Acute: right ventricle dilatation Stretching of ventricle in response to acute  in pressure 8
  9. 9. Acute Cor Pulmonale Massive pulmonary embolization Exacerbation of chronic cor pulmonale 9
  10. 10. Chronic: Many Causes 1 COPD Primary pulmonary hypertension Asthma Recurrent pulmonary embolism Loss of lung tissue following trauma or surgery End stage pneumoconiosis 10
  11. 11. Chronic: Many Causes 2 Sarcoidosis T1-4 vertebral subluxation Obstructive sleep apnea Altitude sickness Sickle cell anemia Bronchopulmonary dysplasia (in infants) 11
  12. 12. Signs & Symptoms 1 Shortness of breath on exertion At rest when severe Wheezing Chronic wet cough Ascites Pedal edema Prominent neck and facial veins 12
  13. 13. Signs & Symptoms 2 Hepatomegaly Abnormal heart sounds Bi-phasic atrial response on EKG due to hypertrophy 13
  14. 14. Chest X-Ray Right ventricular hypertrophy Right atrial dilatation Prominent pulmonary artery Peripheral lung fields:  vascular markings Changes of COPD 14
  15. 15. Chest X-Ray Right ventricular hypertrophy Right atrial dilatation Prominent pulmonary artery Peripheral lung fields:  vascular markings (COPD) 15 Source Undetermined
  16. 16. ECG  RVH Right axis deviation Prominent R wave in lead V1 Inverted T waves in right precordial leads Large S in I, II and III Large Q in lead III Tall peaked P waves (P pulmonale) in II, III and aVF 16
  17. 17. ECG  P pulmonale Peaked P waves in inferior leads >2.5 mm (P pulmonale) Absent R waves in right precordial leads (SV1-SV2-SV3 pattern) 17 Source Undetermined Source Undetermined
  18. 18. What We Need to Know 1 Sildenafil = Revatio® = Viagra® PDE5 inhibitor Relaxes arterial wall   pulmonary arterial resistance and pressure   workload of right ventricle   symptoms Beware of using nitrates  refractory hypotension 18
  19. 19. What We Need to Know 2 Epoprostenol = PGI2 = Flolan® Delivered by pump: very short T½ Sudden cessation  rebound pulmonary hypertension Dyspnea, dizziness, etc. Potent platelet inhibitor  major bleed risk 19
  20. 20. High Output Cardiac Failure 20
  21. 21. High Output Failure Term is misnomer Many conditions: heart is normal, can generate  cardiac output Underlying problem:  in systemic vascular resistance threatens arterial blood pressure  activation of neurohormones   salt and water retention by kidney 21
  22. 22. High Output: Causes 1 Chronic severe anemia Large AV fistula 22 Source Undetermined
  23. 23. High Output: Causes 2 Multiple small arteriovenous shunts e.g. Paget's disease of bone Some severe hepatic or renal disorders Hyperthyroidism Beriberi 23
  24. 24. High Output: Causes 3 Acutely in septic shock, especially Gram-negative bacteria 24 Source Undetermined
  25. 25. High Output Failure Many high output states are curable conditions Untreated leads to systolic failure Since associated with  peripheral vascular resistance, use of vasodilator therapy may aggravate the problem 25
  26. 26. Low Output Cardiac Failure 26
  27. 27. Low Output Cardiac Failure  cardiac output but normal demand for blood Manifestations of impaired peripheral circulation and vasoconstriction Most forms of heart disease Covered in Section 3.5.3: Congestive Heart Failure 27
  28. 28. 3.5.2 Cardiomyopathy 28
  29. 29. Cardiomyopathy Literally “heart muscle disease” Measurable deterioration of myocardial function Usually leads to heart failure Most common form: dilated Common symptoms: dyspnea and peripheral edema At risk for dysrhythmias, sudden cardiac death 29
  30. 30. Extrinsic Causes Primary pathology: outside myocardium itself Most cardiomyopathies are extrinsic Most common cause: ischemia 30
  31. 31. Intrinsic Causes Not due to identifiable external cause Causes can be found for most 31
  32. 32. Signs & Symptoms Can mimic virtually any form of heart disease Chest pain: common Severe cases associated with heart failure, arrhythmias, and systemic embolization 32
  33. 33. Dilated Cardiomyopathy Ventricular dilatation and global myocardial dysfunction (<40%) Usually present with biventricular failure, e.g. fatigue, dyspnea, orthopnea, ankle edema 2-year survival = 50% Progressive cardiogenic shock or sudden cardiac death 33
  34. 34. Dilated Cardiomyopathy Ischemic: following massive anterior MI due to extensive myocardial necrosis and loss of contractility Non-ischemic: most are idiopathic ECG usually abnormal, but no features unique to DCM 34
  35. 35. Non-Ischemic Cardiomyopathy HOCM Restrictive Dilated Myocarditis Tako-Tsubo 35 Source Undetermined
  36. 36. Restrictive Cardiomyopathy Least common Occurs in advanced stages of myocardial infiltrative disease Hemochromatosis, amyloidosis, sarcoidosis, etc. Diffuse myocardial infiltration leads to low voltage QRS complexes No specific ECG findings 36
  37. 37. Peripartum Cardiomyopathy Symptoms and signs of heart failure that present initially during last 3 months of pregnancy or first 5 months postpartum Clinically identical to dilated CM Complain of chest pain, palpitations May be in CHF: rales, dyspnea, cardiomegaly, +S3 37
  38. 38. Peripartum Cardiomyopathy ECG  left ventricular hypertrophy NSST-T wave changes Echocardiography: all 4 chambers enlarged,  left ventricular systolic function preload & afterload, contractility If pregnant: hydralazine, labetalol Mortality ~2% 38
  39. 39. Hypertrophic Cardiomyopathy 39
  40. 40. Hypertrophic Cardiomyopathy Leading cause of sudden cardiac death in young athletes Frequently asymptomatic until sudden cardiac death Prevalence 0.2 – 0.5% of general population 40
  41. 41. Mechanism Asymmetric septal hypertrophy (~2/3) Aortic stenosis & HTN have symmetric hypertrophy Dynamic outflow obstruction At rest ~25% Can be provoked in ~70% If obstruction  HOCM 41
  42. 42. Symptoms Dyspnea  most common Chest pain Palpitations Lightheadedness Fatigue Syncope Sudden cardiac death 42
  43. 43. Findings: Murmur 1 Murmur similar to aortic stenosis Classically, murmur is loudest at left parasternal edge, 4th intercostal space, rather than aortic area 43
  44. 44. Findings: Murmur 2 HCM murmur  in intensity with any maneuver that  volume of blood in left ventricle Stand abruptly Valsalva Amyl nitrite  murmur by  venous return to heart 44
  45. 45. ECG Findings LVH  precordial voltages, non- specific ST / T-wave abnormalities 45 Source Undetermined
  46. 46. ECG Findings Asymmetric hypertrophy  “dagger Q-waves” infero-lateral 46 Source Undetermined
  47. 47. Management Beta-blockers & calcium channel blockers: slow heart rate, improve diastolic function Amiodarone: reduces ventricular dysrhythmias 47
  48. 48. 3.5.3 Congestive Heart Failure 48
  49. 49. Types of Failure Systolic dysfunction: failure of ventricular contractility AHA / ACC: left ventricular ejection fraction <40% Diastolic dysfunction: failure of diastolic ventricular relaxation  high filling pressures 1/3 – ½: some renal insufficiency 49
  50. 50. Left-Sided Heart Failure Left ventricle does not pump enough blood  backs up into lungs, causing pulmonary edema LV heart failure eventually causes right-sided heart failure 50
  51. 51. Left-Sided Heart Failure  rate of breathing  tachypnea  work of breathing Rales or crackles: initially in lung bases  fluid in alveoli (pulmonary edema Cyanosis: late, severe 51
  52. 52. Left-Sided Heart Failure Laterally displaced apex beat Gallop rhythm: from  blood flow or  intra-cardiac pressure Murmur can be cause (e.g. aortic stenosis) or result (e.g. mitral regurgitation) of heart failure 52
  53. 53. Extra Heart Sound Occurs soon after the normal two “lub-dub” heart sounds (S1 and S2) Associated with heart failure Occurs at beginning of diastole, ~0.12 to 0.18 seconds after S2 Mnemonic ken-TUC-ky, with “ky” representing S3 53
  54. 54. Right-Sided Heart Failure 54
  55. 55. Right-Sided Heart Failure Right ventricle does not pump enough blood  backs up into body  systemic edema Nocturia common: leg fluid returns to circulation when flat If severe: ascites, hepatomegaly Possible jaundice, coagulopathy 55
  56. 56. Peripheral Edema & Anasarca 56Source Undetermined Source Undetermined
  57. 57. Right-Sided Heart Failure Jugular venous pressure: marker of fluid status Can be accentuated by eliciting hepatojugular reflux If  right ventricular pressure  parasternal heave Signifies compensatory  in contraction strength 57
  58. 58. Jugular Venous Distention 58 Source Undetermined
  59. 59. Biventricular Failure Left + right + pleural effusions Dull to percussion +  breath sounds at bases Pleural veins drain both into both systemic and pulmonary venous system If unilateral: usually right sided 59
  60. 60. Radiographic Findings 60 The radiological signs of heart failure: • Fluid in lung fissures • Kerley B lines • Prominent upper lobe pulmonary arteries • Fluid in the lung interstitium • Large heart • Pleural effusion
  61. 61. Radiographic Findings Cardiomegaly  large heart 61 Source Undetermined
  62. 62. Radiographic Findings Cephalization = upper lobe blood diversion Occurs when PAWP 12-18 mmHg 62Source Undetermined
  63. 63. Radiographic Findings Kerley B lines: short parallel lines at lung periphery Interlobular septa: usually <1 cm PAWP 18–25 MMHg 63Source Undetermined
  64. 64. Radiographic Findings Bat wing = central interstitial edema PAWP >25 mmHg 64 Source Undetermined
  65. 65. B-Natriuretic Peptide From distended ventricles >500 pg/mL: highly associated with heart failure (LR = 8.1) 100-500 pg/mL: indeterminate (LR = 1.8) <100 pg/mL: highly unlikely (LR = 0.13) 65
  66. 66. Acute Management 1 Immediate therapeutic goals Improve respiratory gas exchange Maintain adequate arterial saturation  left ventricular diastolic pressure Maintain adequate cardiac and systemic perfusion 66
  67. 67. Acute Management 2 Noninvasive positive pressure ventilation (NIPPV) Continuous (CPAP) or inspiratory / expiratory (BiPAP) Recruit collapsed alveoli  functional residual capacity  improve oxygenation  work of breathing 67
  68. 68. Acute Management 3 Result:  left ventricular preload and afterload by  intrathoracic pressure More rapid restoration of normal vital signs and oxygenation Fewer intubations 68
  69. 69. Management: Nitroglycerin 1 Lower doses: venodilation  preload Higher doses: arteriolar dilation  blood pressure  afterload 69
  70. 70. Management: Nitroglycerin 2 Sublingual 400 mcg x 3 Total 1200 mcg in 10 minutes Good bioavailability Start IV 50 – 80 mcg/min Can go to 200 – 300 mcg / min for BP control 70
  71. 71. Management: Loop Diuretic Furosemide standard In volume overload:  plasma volume,  preload,  pulmonary congestion Diuresis unnecessary in low plasma volumes 71
  72. 72. Management: Morphine Controversial: central sympatholytic that releases vasoactive histamine  causes peripheral vasodilation 72Vaprotan (Wikimedia Commons)
  73. 73. Management: ACE Inhibitor Controversial: good  afterload Enalaprilat IV (0.625 – 1.25 mg) Captopril sublingual (12.5 – 25 mg) No good, large studies Some sources say “theoretically harmful” 73
  74. 74. 3.5.4 Coronary Syndromes 74
  75. 75. Acute Coronary Syndromes Continuum or progression of coronary artery disease from myocardial ischemia to necrosis Stable angina unstable angina acute myocardial infarction 75
  76. 76. Classic Presentations 76J. Heuser (Wikipedia)J. Heuser (Wikipedia)
  77. 77. 3.5.5 Ischemic Heart Disease 77
  78. 78. Classic Presentations Stable Angina Transient, episodic chest discomfort that is predictable and reproducible Familiar symptoms occur from a characteristic stimulus Improve with rest or sublingual nitroglycerin within few minutes 78
  79. 79. Classic Presentations Unstable Angina New onset Occurs at rest or with  frequency Severely limiting Lasts longer than a few minutes Resistant to meds that previously relieved the symptoms 79
  80. 80. Classic Presentations Acute Myocardial Infarction Retrosternal chest discomfort lasting > 15 minutes Dyspnea, diaphoresis, light- headedness, palpitations, nausea and/or vomiting Radiation to arms, shoulders, neck  probability of ischemia 80
  81. 81. Atypical Presentations More common in elderly History of angina often absent Epigastric discomfort / indigestion or nausea and vomiting Shortness of breath Syncope or confusion Fatigue, dizziness, or generalized weakness 81
  82. 82. Atypical Presentations So-called “Silent MI”  vague ~12.5% of all MIs Worse prognosis than “classic” Suspect in elderly, diabetics, those with spinal cord injuries or disease, alcoholics 82
  83. 83. Risk Factors, Major Cigarette smoking Hypertension Diabetes Mellitus Hypercholesterol Hypercoagulability Family history of CAD at < 55 in first degree relative Prior history of CAD PVD Carotid arteriosclerosis 83
  84. 84. Risk Factors, Other Male sex Advanced age Methamphetamine use Cocaine use Obesity Inactive Lifestyle Post-menopause 84
  85. 85. Factors Predicting AMI History ischemic heart disease Chest pain / discomfort worse than usual angina Pain similar to a prior AMI lasts longer than an hour radiates to jaw / neck / shoulder / arm 85
  86. 86. Diagnosis Normal initial EKG / troponin does NOT rule out MI History: most important tool Suspect history: admit “ROMI” Typically ≤ 25%of ROMI have discharge diagnosis of “Acute MI” Improvement after nitroglycerin / antacid dose NOT rule in / out 86
  87. 87. EKG Most important adjunctive diagnostic test Initial EKG diagnostic in only ~25- 50% Normal / non-diagnostic initial EKG does not rule out ACS 87
  88. 88. NSTEACS Non-ST-elevation acute coronary syndrome (NSTEACS)  Non-ST-elevation myocardial infarction (NSTEMI) Unstable angina (UA) Differentiation may be retrospective based on cardiac biomarkers 88
  89. 89. NSTEACS Non-ST-elevation acute coronary syndrome (NSTEACS)  Main ECG abnormalities ST segment depression T wave flattening or inversion 89
  90. 90. Causes of ST Depression Myocardial ischemia / NSTEMI Reciprocal change in STEMI Posterior MI Digoxin effect Supraventricular tachycardia Hypokalemia RBBB Right ventricular hypertrophy LBBB Left ventricular hypertrophy Ventricular paced rhythm 90
  91. 91. Causes of T Wave Inversion Normal in children Persistent juvenile T wave pattern Myocardial ischemia / infarction Bundle branch block Ventricular hypertrophy (‘strain’ patterns) Pulmonary embolism Hypertrophic cardiomyopathy  intracranial pressure 91
  92. 92. Ischemic T Wave Inversions Ischemia: contiguous leads based on anatomical location of area of ischemia / infarction: Inferior = II, III, aVF Lateral = I, aVL, V5-6 Anterior = V2-6 92
  93. 93. Ischemic T Wave Inversions Dynamic inversions with acute myocardial ischemia 93 Source Undetermined Source Undetermined
  94. 94. Ischemic T Wave Inversions Fixed inversions follow infarction, usually in association with pathological Q waves 94 Source Undetermined Source Undetermined
  95. 95. Biphasic T Waves Two main causes: Hypokalemia Myocardial ischemia Waves go in opposite directions: Hypokalemic: go  then  Ischemic: go  then  95
  96. 96. Biphasic T Waves Due to hypokalemia:  then  96 Source Undetermined
  97. 97. Biphasic T Waves Due to ischemia:  then  97 Source Undetermined
  98. 98. Biphasic T Waves: Wellens’ Inverted / biphasic T waves in V2-3 Patient presents with ischemic chest pain Highly specific for critical stenosis of left anterior descending artery 98
  99. 99. Biphasic T Waves: Wellens’ Type 1 Wellens’ T-waves: deeply and symmetrically inverted 99 Source Undetermined
  100. 100. Biphasic T Waves: Wellens’ Type 2 Wellens’ T-waves: biphasic, with initial deflection positive and the terminal deflection negative 100 Source Undetermined
  101. 101. Flattened T Waves Non-specific Dynamic or in contiguous leads: think ischemia Generalized: think electrolyte abnormality, like hypokalemia 101 Source Undetermined
  102. 102. Inverted U Wave Infrequently recognized but specific sign of myocardial ischemia 102 Source Undetermined
  103. 103. TIMI Risk Score 1 Thrombolysis In Myocardial Infarction Assesses risk of death and ischemic events in patients with unstable angina or a non-ST elevation myocardial infarction 103
  104. 104. TIMI Risk Score 1 1. Age >= 65 2. ASA use in last 7 days 3. 2 angina episodes in last 24hrs 4. ST changes 0.5mm on admit EKG 5.  serum cardiac biomarkers 6. Known CAD: stenosis  50% 7. 3 risk factors for CAD: cigarette smoking, hypertension, HDL < 40, diabetes, family history 104
  105. 105. TIMI Risk Score 14 day risk: all-cause mortality, new or recurrent MI, or ischemia requiring urgent revascularization 0 or 1 = 4.7% risk 2 = 8.3% risk 3 = 13.2% risk 4 = 19.9% risk 5 = 26.2% risk 6 or 7 = 40.9% risk 105
  106. 106. NSTEACS 50% of UA patients will show evidence of myocardial necrosis based on  cardiac serum markers such as troponin T or I and creatine kinase isoenzyme (CK)-MB Diagnosis of non-ST elevation myocardial infarction 106
  107. 107. NSTEACS: Treatment Oxygen: evidence unclear Nitroglycerin: vasodilate coronary arteries,  blood flow to heart Antiplatelet agent: aspirin / clopidogrel to reduce progression of clot formation Anticoagulant: heparin, unfractionated or LMWH 107
  108. 108. 3.5.6 Myocardial Infarction 108
  109. 109. EKG for STEMI  amplitude R and T waves (“giant” R / “hyperacute” T) 1st change to occur in evolving MI Transient finding: may resolve by presentation 109 Source Undetermined
  110. 110. EKG for STEMI  amplitude R  “giant” R waves 110 Source Undetermined
  111. 111. EKG for STEMI ST usually earliest recorded sign ± reciprocal changes Initial up-sloping portion of ST segment usually convex or flat (horizontally or obliquely) Q waves: represent myocardial necrosis but not severity of infarct Inverted T waves 111
  112. 112. Other Causes of  ST 1 Early repolarization Acute pericarditis: all except aVR Pulmonary embolism: V1 and aVR Hypothermia: V3-V6, II, III and aVF Hypertrophic cardiomyopathy: V3-5 Hyperkalemia: V1-V2 (V3) 112
  113. 113. Other Causes of  ST 2 Acute neurologic events: all leads, primarily V1-V6 Acute sympathetic stress: all leads, especially V1-V6 Brugada syndrome Ventricular aneurysm Cardiac contusion 113
  114. 114. Other Causes of  ST 3 Left ventricular hypertrophy Idioventricular rhythm including paced rhythm 114 Source Undetermined
  115. 115. Early Repolarization 1  ST segment elevation without underlying disease Probably has nothing to do with actual early repolarization Commonly seen in young men 115
  116. 116. Early Repolarization 2 Characteristics Upward concave elevation of RS-T segment with distinct or “embryonic” J waves Slurred downstroke of R waves or distinct J points or both RS-T segment elevation in precordial leads 116
  117. 117. Early Repolarization 3 Characteristics Rapid QRS transition in precordial leads with counterclockwise rotation Persistence of these characteristics for many years Absent reciprocal ST depression Large symmetrical T waves 117
  118. 118. Early Repolarization 4 Generalized concave ST elevation in precordial (V2-6) and limb leads (I, II, III, aVF) 118 Source Undetermined
  119. 119. Early Repolarization 5 J-point notching evident in inferior leads (II, III and aVF) 119 Source Undetermined
  120. 120. Early Repolarization 6 J-point notching evident in inferior leads (II, III and aVF) 120 Source Undetermined
  121. 121. Early Repolarization 7 Prominent, slightly asymmetrical T waves that are concordant with main vector of QRS complexes 121 Source Undetermined
  122. 122. Early Repolarization 8 Descending limb of T wave is straighter and slightly steeper than ascending limb 122 Source Undetermined
  123. 123. Early Repolarization 9 Descending limb of T wave is straighter and slightly steeper than ascending limb 123 Source Undetermined
  124. 124. Specific Infarcts 124
  125. 125. 125 Effects of Myocardial Ischemia, Injury, and Infarction on the ECG
  126. 126. 126 Patrick J. Lynch (Wikipedia)
  127. 127. Left Main Occlusion Widespread horizontal ST depression, most prominent in leads I, II and V4-6 ST elevation in aVR ≥ 1mm ST elevation in aVR ≥ V1 127
  128. 128. Left Main Occlusion Widespread ST depression, most prominent in lateral leads (V4-6, I, aVL) ST elevation > 1mm in aVR 128 Source Undetermined
  129. 129. Left Main Occlusion Widespread ST depression, most prominent in lateral leads (V4-6, I, aVL) ST elevation > 1mm in aVR 129 Source Undetermined
  130. 130. Left Main Occlusion Widespread ST depression, most prominent in lateral leads (V4-6, I, aVL) ST elevation > 1mm in aVR 130 Source Undetermined
  131. 131. Left Main Occlusion Widespread ST depression, most prominent in lateral leads (V4-6, I, aVL) ST elevation > 1mm in aVR 131 Source Undetermined
  132. 132. 132 Patrick J. Lynch (Wikipedia)
  133. 133. Anterior STEMI Occlusion of left anterior descending artery (LAD) Worst prognosis   infarct size ST segment  with Q wave formation in precordial leads (V1-6) ± high lateral leads (I and aVL) Reciprocal ST  in inferior leads (mainly III and aVF) 133
  134. 134. Anterior STEMI: Hyperacute 134 Source Undetermined Source Undetermined
  135. 135. Anterior STEMI: Acute 135 Source Undetermined Source Undetermined
  136. 136. Anterior STEMI: Acute Q waves in V1-2 Reduced R wave height (Q-wave equivalent) in V3-4 136 Source Undetermined
  137. 137. Anterior STEMI: Tombstone 137 Source Undetermined
  138. 138. Anterior STEMI: Tombstone Proximal LAD large infarction with poor LV ejection fraction High likelihood of cardiogenic shock and death 138 Source Undetermined
  139. 139. STEMI: High Lateral Occluded 1st diagonal branch (D1) of LAD  isolated ST in I, aVL Occlusion of circumflex artery  ST in I, aVL, V5-6 139
  140. 140. 140 Patrick J. Lynch (Wikipedia)
  141. 141. STEMI: High Lateral ST elevation primarily localized to leads I and aVL Associated with reciprocal ST depression and T wave inversion in inferior leads 141
  142. 142. STEMI: High Lateral Occluded 1st diagonal branch (D1) of LAD  isolated ST in I, aVL 142 Source Undetermined
  143. 143. STEMI: Lateral Supplied by branches of LAD and left circumflex (LCx) arteries Usually as part of larger territory infarction, e.g. anterolateral STEMI Lateral extension of anterior, inferior or posterior MI indicates large territory of myocardium at risk  worse prognosis 143
  144. 144. STEMI: Lateral Isolated lateral STEMIs uncommon Lateral STEMI as a stand-alone MI is indication for emergent reperfusion 144
  145. 145. STEMI: Inferior 1 ~80%  dominant RCA ~18%  dominant LCx Rare: “type III” or wraparound LAD  concomitant inferior and anterior ST elevation 145
  146. 146. STEMI: Inferior 2 40-50% of all MIs In general, more favorable prognosis than AMI ~40% have concomitant right ventricular infarction Severe hypotension in response to nitrates Worse prognosis 146
  147. 147. STEMI: Inferior 3 ~20% develop significant bradycardia due to 2o or 3o AV block  in-hospital mortality (>20%) May be associated with posterior infarction Worse prognosis due to  area of myocardium at risk 147
  148. 148. STEMI: Inferior 4 ST in leads II, III and aVF Progressive development of Q waves in II, III and aVF Reciprocal ST in aVL (± lead I) 148
  149. 149. STEMI: Inferior 5 149 Source Undetermined
  150. 150. 150 Patrick J. Lynch (Wikipedia)
  151. 151. STEMI: Inferior from RCA ST in lead III > lead II Reciprocal ST in lead I Signs of right ventricular infarction  STE in V1 and V4R 151
  152. 152. STEMI: Inferior from RCA ST in lead III > lead II Reciprocal ST and T wave inversion in aVL 152 Source Undetermined
  153. 153. STEMI: Inferior from RCA ST in lead III > lead II Reciprocal ST and T wave inversion in aVL 153Source Undetermined
  154. 154. 154 Patrick J. Lynch (Wikipedia)
  155. 155. STEMI: Inferior from LCx ST in lead II = lead II Reciprocal ST and T wave inversion in I or aVL Q wave in III, aVF 155 Source Undetermined
  156. 156. Right Ventricular Infarct Isolated RV infarct rare Complicates ~40% of inferior STEMIs Poor RV contractility  preload sensitive Nitrates  severe hypotension Treat with fluid loading 156
  157. 157. Right Ventricular Infarct ST in V1 Only standard ECG lead that looks directly at the right ventricle ST in lead III > lead II Lead III more “rightward facing” than lead II Must do right-sided leads 157
  158. 158. Right Ventricular Infarct 158 V1RV2R V3R V4R V5R V6R Arcadian (Wikimedia Commons)
  159. 159. Right Ventricular Infarct ST in V1 ST in lead III > lead II 159 Source Undetermined
  160. 160. Right Ventricular Infarct Right-sided leads ST in lead III > lead II ST throughout right-sided leads V3R-V6R 160Source Undetermined
  161. 161. Posterior Infarct Accompanies 15-20% of STEMIs, usually inferior or lateral Isolated posterior MI (3-11%) Lack of obvious ST means diagnosis often missed Isolated posterior infarct is indication for emergent coronary reperfusion 161
  162. 162. Posterior Infarct Suggested by changes in V1-3 Leads look at internal surface of posterior myocardium Horizontal ST depression Tall, broad R waves (>30ms) Upright T waves Dominant R wave (R/S ratio > 1) in V2 162
  163. 163. Posterior Infarct ST becomes ST Q waves become R waves Terminal T-wave inversion becomes an upright T wave 163 Source Undetermined
  164. 164. Posterior Infarct Same EKG flipped upside down Now looks like typical STEMI Also with posterior leads 164Source Undetermined
  165. 165. Posterior Infarct Same EKG flipped upside down Now looks like typical STEMI Also with posterior leads 165 Source Undetermined
  166. 166. Posterior Infarct: Leads 166 Scapula V7 V8 V9 Source Undetermined
  167. 167. Posterior Infarct Posterior extension of inferior or lateral infarct implies much larger area of myocardial damage  risk of left ventricular dysfunction and death 167
  168. 168. Posterior Infarct Tall, broad R waves (>30ms) Upright T waves Dominant R wave (R/S ratio>1) in V2 168 Source Undetermined Source Undetermined
  169. 169. Posterior Tall, broad R waves (>30ms) Upright T waves Dominant R wave (R/S ratio>1) V2 169Source Undetermined
  170. 170. Posterior Infarct Same patient, posterior leads V7 – V9 170 Source Undetermined
  171. 171. Posterior Infarct 171 Source Undetermined Source Undetermined
  172. 172. Q-Waves: Normal Depolarization of interventricular septum (“septal Qs”) Lateral leads I, aVL, V5 and V6 172
  173. 173. Q-Waves: Pathologic Electrical signal passes through stunned or scarred myocardium Deflection amplitude of 25% or more of subsequent R wave >0.04 s (40 ms) wide, >2 mm amplitude 173
  174. 174. Q-Waves: Pathologic Deflection amplitude of 25% or more of subsequent R wave >0.04 s (40 ms) wide, >2 mm amplitude 174 Source Undetermined
  175. 175. Initial EKG Useful for… … screening … risk stratification … establishing criteria that determine which therapeutic interventions will be employed 175
  176. 176. Serial EKGs Nondiagnostic EKG but concern for possible ongoing ischemia Capture ischemic changes Demonstrate stability Detect silent ischemia ST segment trend-monitoring MAY improve detection 176
  177. 177. Serum Biomarkers 177 Source Undetermined
  178. 178. Serum Biomarkers Proteins that leak from injured myocardial cells through damaged cell membranes into bloodstream Troponin T / I CK-MB Obsolete: serum glutamic oxaloacetic transaminase (SGOT) / lactate dehydrogenase (LDH) 178
  179. 179. Serum Biomarkers: Troponin 179 Ayacop (Wikimedia Commons)
  180. 180. Serum Biomarkers: Troponin Marker for all heart damage, not just AMI Tachycardia, CHF, myocarditis, pericarditis, defibrillation, contusion  in ~40% of patients with critical illnesses such as sepsis Severe GI bleed: mismatch between myocardial oxygen demand and supply 180
  181. 181. Serum Biomarkers: Troponin Type I MI: coronary artery occlusion Type II MI: low flow state leading to troponin leakage DIFFERENT PATHOLOGIES DIFFERENT TREATMENTS NOT ALWAYS OBVIOUS 181
  182. 182. Serum Biomarkers: Troponin Marker Rise (hrs) Peak (hrs) Remains Elevated Troponin T 6 12 – 18 10 – 14 days Troponin I 6 12 – 18 7 – 10 days CK-MB 4 – 10 20 <2 days Myoglobin 2 – 3 4 – 24 <1 day 182
  183. 183. Serum Biomarkers: Others CK-MB: serum levels of two variants of enzyme phospho- creatine kinase Isoenzymes CKM and CKB Myoglobin: primary oxygen- carrying pigment of muscle tissues Very nonspecific for cardiac damage 183
  184. 184. Serum Biomarkers: Others Marker Rise (hrs) Peak (hrs) Remains Elevated Troponin T 6 12 – 18 10 – 14 days Troponin I 6 12 – 18 7 – 10 days CK-MB 4 – 10 20 <2 days Myoglobin 2 – 3 4 – 24 <1 day 184
  185. 185. Use of Serum Markers Admit / discharge decisions based primarily on history and clinical presentation Marker detection requires sufficient myocardial cell damage AND enough time for markers to be released into serum 185
  186. 186. Use of Serum Markers Initial markers have low sensitivity for detecting ischemia, cannot be used to reliably diagnose or exclude ACS No single determination of one serum biomarker reliably identifies or excludes AMI within <6 hrs of symptom onset 186
  187. 187. Use of Serum Markers This is a moving target High sensitivity troponins MAY change everything (or may not) Should we call them “Low Specificity Troponins” instead? Hot topic over next few years, but will not be tested 187
  188. 188. Diagnosing MI: WHO – 2000 Myocardial cell death Markers of myocardial cell death recovered from blood samples Evidence of myocardial ischemia (ST- T segment changes) Loss of electrically functioning cardiac tissue (Q waves) Reduction / loss of tissue perfusion Cardiac wall motion abnormalities Pathology Biochemistry EKG Imaging 188
  189. 189. Two-Dimensional Echo Detects regional wall motion abnormalities that occur with AMI Abnormality starts on 1st beat Cannot distinguish ischemia, acute infarction and old infarction Operator-dependent Not readily available 189
  190. 190. Coronary Artery CT Very controversial A work in progress Zealots on both sides Something MAY emerge in next few years 190
  191. 191. Radionuclide Scanning 191
  192. 192. Technetium (99mTc) sestamibi Tracer taken up by myocardium in proportion to blood flow Bound to six methoxy-isobutyl- isonitrile (MIBI) ligands Detects perfusion defects and hypokinesia 192
  193. 193. Technetium (99mTc) sestamibi Active chest pain + nondiagnostic EKG  100% sensitive / 83-92% specific Pain-free patient: 65% sensitive 193
  194. 194. Thallium 201 scintigraphy 194 Source Undetermined
  195. 195. Thallium 201 scintigraphy Reversibly taken up by normally perfused cells Areas of  uptake indicate regions of severe ischemia or infarction ≤6hrs of infarct  100% sensitive, 80% specific for AMI Cannot distinguish new from old 195
  196. 196. Stress Testing Recommended by American College of Cardiology and American Heart Association Treadmill test: sensitivity 73-90%, specificity 50-74% (Modified Bruce Protocol) Nuclear test: sensitivity 81%, specificity 85-95% 196
  197. 197. Chest Pain Evaluation Unit Safe, effective alternative to routine admission for low-intermediate risk patients with chest pain Protocols vary but usually involve serial studies (EKGs, markers) and selective stress testing for evaluation of risk stratification 197
  198. 198. Treatment 198
  199. 199. Treatment IV (NS)  cardiac monitor  pulse oximeter Oxygen Antiplatelet agents Anticoagulant therapy Nitroglycerin Morphine Beta-blocker Reperfusion therapy ACE-I 199
  200. 200. Treatment IV (NS)  cardiac monitor  pulse oximeter Oxygen Antiplatelet agents Anticoagulant therapy Nitroglycerin Morphine Beta-blocker Reperfusion therapy ACE-I 200
  201. 201. IV / Monitor / Pulse oximetry 201
  202. 202. Treatment IV (NS)  cardiac monitor  pulse oximeter Oxygen Antiplatelet agents Anticoagulant therapy Nitroglycerin Morphine Beta-blocker Reperfusion therapy ACE-I 202
  203. 203. Oxygen Low flow (2-4L) by nasal cannula High flow associated with  mortality and infarct size 203
  204. 204. Treatment IV (NS)  cardiac monitor  pulse oximeter Oxygen Antiplatelet agents Anticoagulant therapy Nitroglycerin Morphine Beta-blocker Reperfusion therapy ACE-I 204
  205. 205. Antiplatelet Agents: Aspirin Irreversibly acetylates platelet cyclo-oxygenase, Rapid onset: within 60 minutes 205
  206. 206. Antiplatelet Agents: Aspirin 325mg on arrival unless contraindicated Chew to maximize bioavailability  mortality, infarct size, and rate of reinfarction Maximal benefit if given within 4 hours of chest pain onset NNT to save one life = 40 206
  207. 207. Antiplatelet Agents: ADP Clopidogrel / prasugrel / ticagrelor  platelet aggregation by inhibiting ADP platelet activation Second-line therapy for patients who cannot take ASA Less effective than ASA due to delayed onset 207
  208. 208. Antiplatelet Agents: ADP Clopidogrel Onset 2 – 3 hours Can speed up by forced doses Safety profile: similar to ASA  risk of CV events in patients with UA or NSTEMI AND early noninvasive approach is planned 208
  209. 209. Clopidogrel & CABG Clopidogrel treatment 7 days before CABG:  major bleeding Prasugrel: even more bleeding Ticagrelor: less bleeding Urgent CABG likely within 7 days: argument for omitting thienopyridines during initial management of ACS 209
  210. 210. Clopidogrel & CABG Clopidogrel / prasugrel / ticagrelor are all ADP receptor antagonists A stands for “adenosine” What happens when we give our patients adenosine for SVT? 210
  211. 211. Clopidogrel & CABG ST 1 mm in aVR: strong predictor severe LMCA / 3VD requiring CABG Discuss with interventionalist / thoracic surgeon use of clopidogrel ST <1mm in aVR: negligible risk severe LMCA / 3VD requiring CABG Thienopyridine can be safely given 211
  212. 212. Antiplatelet Agents: G2B3A Abciximab / eptifibatide / tirofiban Glycoprotein (GP) IIb/IIIa receptor antagonists Block final common pathway for platelet aggregation Indications:  prior to PCI Discuss with interventional cardiologist 212
  213. 213. Treatment IV (NS)  cardiac monitor  pulse oximeter Oxygen Antiplatelet agents Anticoagulant therapy Nitroglycerin Morphine Beta-blocker Reperfusion therapy ACE-I 213
  214. 214. Anticoagulant Therapy Unfractionated heparin Low molecular weight heparin Direct thrombin inhibitors 214
  215. 215. Anticoagulant Therapy Unfractionated heparin and enoxaparin result in similar outcomes at one year post MI 215 Melissa Wiese (Wikimedia Commons)
  216. 216. Heparin Heparin + ASA more effective than either alone Indicated in high risk patients with ACS (AMI/UA)  incidence of DVT, reinfarction, nonhemorrhagic CVA, and formation / embolization of LV thrombus in AMI 216
  217. 217. Unfractionated Heparin May be useful in unstable angina by  rate of subsequent transmural infarction Preferred by cardiologists taking patients to cath lab because can be turned off 217
  218. 218. Unfractionated Heparin No reperfusion: bolus 50 – 70 U/kg to maximum of 5000 U, then IV drip 12 U/kg per hour Fibrinolysis: bolus 60 – 100 U/kg to maximum of 4000 U, then IV drip 12 U/kg per hour PCI: bolus 50 – 70 U/kg to maximum of 5000 U 218
  219. 219. Low Molecular Weight Heparin Acceptable in patients <75 years without significant renal dysfunction  recurrent angina, AMI, need for urgent revascularization, mortality rate Preferred agent in absence of renal failure or planned CABG within 24 hours 219
  220. 220. Low Molecular Weight Heparin  bleeding than unfractionated heparin with equivalent or better antithrombotic effects Simple administration and dosing Limited blood monitoring More predictable anticoagulation effect 220
  221. 221. Low Molecular Weight Heparin No reperfusion: no load, 1 mg/kg every 12 hours Fibrinolysis: loading dose 30 mg IV bolus, then 1 mg/kg subcutaneously every 12 hours PCI: unfractionated preferred 221
  222. 222. Nitroglycerin (NTG) 1 Dilates collateral coronary vessels  collateral blood flow to ischemic myocardium Has antiplatelet effects 222
  223. 223. Nitroglycerin (NTG) 2  infarct size and mortality  myocardial oxygen demand  preload  LV end-diastolic volume  afterload May  myocardial susceptibility to ventricular dysrhythmias during ischemia and reperfusion 223
  224. 224. Nitroglycerin (NTG) 3  pain and consequently catecholamine release 224
  225. 225. Nitroglycerin (NTG) 4 For chest pain if systolic BP >90mm Hg Start with sublingual 0.4mg (400 mcg) q3 – 5 minutes prn pain 1200 mcg in 6 – 10 minutes Excellent bioavailability (>80%) Ointment / paste: pretty useless 225
  226. 226. Nitroglycerin (NTG) 5 Intravenous: books say start @ 10 – 20 mcg/min and increase by 5 – 10 mcg/min until pain controlled or SBP  by 10% In real life, start higher Sublingual: 1200 mcg / 10 min = 120 mcg / min 226
  227. 227. Nitroglycerin: Adverse Hypotension: usually responds to fluid bolus and leg elevation Reflex tachycardia: can be moderated by concomitant use of beta-blocking agent Contraindicated in patients taking PDE5 inhibitors (e.g. sildenafil) Avoid for 12–24 hours after using 227
  228. 228. Beta Blockers (BB) Potential benefits 1  oxygen demand:  heart rate,  blood pressure,  contractility  risk of ventricular fibrillation  automaticity,  electro- physiologic threshold for activation, slowing conduction 228
  229. 229. Beta Blockers (BB) Potential benefits 2 Bradycardia prolongs diastole   coronary diastolic perfusion  remodeling, improves left ventricular hemodynamic function  left ventricular diastolic function with a less restrictive filling pattern 229
  230. 230. Beta Blockers (BB) Prefibrinolysis era: mortality benefit 10 – 15% in patients treated with propranolol, metoprolol, atenolol Early IV therapy associated with reduction in infarct size Reperfusion era: ~40% reduction in mortality in both STEMI (Q wave) or non-ST elevation (non-Q wave) MI 230
  231. 231. Beta Blockers (BB) Contraindications HR <60/min SBP <100mmHg Moderate to severe LV dysfunction Hypoperfusion Precipitated by cocaine PR interval >0.24 sec 2o or 3o AV block Active bronchospasm 231
  232. 232. Morphine Chest pain despite adequate treatment with antiplatelet, anticoagulant, anti-ischemics  pain and anxiety   circulating catecholamines   tendency toward dysrhythmias  both pre and afterload   myocardial oxygen demand 232
  233. 233. Morphine Adverse Effects Hypotension / bradycardia  responds to fluid bolus and atropine Respiratory depression 233
  234. 234. Reperfusion Therapy Thrombolytic (fibrinolytic) therapy Percutaneous Coronary Intervention (PCI) 234
  235. 235. Fibrinolytic Streptokinase (SK) Anisoylated Plasminogen Streptokinase Activator Complex (APSAC, Eminase, Anisterplase) Tissue Plasminogen Activator (TPA, Activase, Alteplase) Reteplase (RPA, Retavase) Tenecteplase (TNK) 235
  236. 236. Fibrinolytic Converts plasminogen to plasmin  lyses fibrin content of acute intracoronary thrombosis  reperfusion of coronary arteries   infarction size,  residual LV function,  survival 236
  237. 237. Fibrinolytic Shorter time between symptom onset and administration  greater reduction in mortality Initiate ideally within 30 minutes of ED arrival 237
  238. 238. Criteria for Thrombolysis Class I: treatment benefit established ST > 0.1mV in two or more contiguous leads Time to therapy ≤ 12 hours Age <75 years Bundle branch block (old) obscuring ST segment analysis but history suggesting AMI 238
  239. 239. Criteria for Thrombolysis Class IIa: treatment likely to benefit ST elevation Age >75 years 239
  240. 240. Criteria for Thrombolysis Class IIb: treatment may benefit ST elevation Time to therapy >12-24 hours SBP >180 or DBP >110 240
  241. 241. Criteria for Thrombolysis Class III: not indicated, may be harmful ST elevation, time to therapy >24 hours, Ischemic pain resolved ST depression only No ST elevation True posterior MI Presumed new BBB 241
  242. 242. Absolute Contraindications Any prior cerebral hemorrhage Known structural CNS lesion Ischemic stroke within 3 months (unless TIA < 3 hrs) Significant closed head / facial injury within 3 months Suspicion of aortic dissection Active bleeding / bleeding disorder 242
  243. 243. Relative Contraindications 1 Chronic, severe, poorly controlled HTN or severe HTN on admission (SBP > 180 or DBP > 119) Traumatic / prolonged (>10min) CPR Non-compressible vascular punctures Major surgery or internal bleeding within 3-4 weeks 243
  244. 244. Relative Contraindications 2 Any other CNS disease – structural or functional – not noted above Pregnancy Active peptic ulcer Current use of anticoagulants Prior exposure / allergic reaction to SK or anistreplase if using these agents 244
  245. 245. Complications Systemic bleeding 2 – 10% Cerebral hemorrhage < 1% Hypotension 3 – 10% Allergic phenomena 1.5 – 2% Usually minor; most common with SK Reperfusion dysrhythmias ~50% PVCs, idioventricular rhythms Failure to open occlusion ~20% 245
  246. 246. Percutaneous Coronary Intervention Angioplasty or stent placement 2000 AHA guidelines Class I for patients <75 years with ACS and signs of cardiogenic shock Class IIa for patients >75 years 246
  247. 247. Percutaneous Coronary Intervention Benefits More effective than thrombolysis in opening occluded arteries Treats underlying fixed obstructed coronary artery lesions as well as relieve the acute thrombosis Associated with lower incidence of recurrent ischemia, reinfarction, intracranial hemorrhage, and death 247
  248. 248. Percutaneous Coronary Intervention Cons Needs to be implemented 60 – 90 minutes Not all facilities have PCI available on 24 hour basis Performance varies based on center’s volume and operator’s experience 248
  249. 249. Angiotensin Converting Enzyme Inhibitors When administered within first 24 hours,  incidence of severe ventricular dysfunction and death All with AMI should receive ACE-I Not until 6 hours after initial therapy has started, patient stable Too early  hypotension 249
  250. 250. Angiotensin Converting Enzyme Inhibitors Captopril 12.5mg PO BID Lisinopril 5 mg PO qd Contraindications ACE-I allergy Killip Class III or IV heart failure Hypotension (SBP < 100) Creatinine > 2.5 Renal artery stenosis 250
  251. 251. Complications of AMI 251
  252. 252. Dysrhythmias Prehospital phase associated with highest incidence lethal dysrhythmia Ventricular fibrillation greatest in 1st hour of infarction 252
  253. 253. Dysrhythmias: Treatment 1 Treat if exacerbates myocardial ischemia or could potentially deteriorate into cardiac arrest Consider treatment of PVCs if Frequent (>30 / hour) Multifocal Short runs of ventricular tachycardia Couplets / display R on T phenomenon 253
  254. 254. Dysrhythmias: Treatment 2 Initial treatment: optimally manage underlying ischemia / infarction Lidocaine vs procainamide vs amioadarone: your call 254
  255. 255. Heart Failure Left ventricular failure: congestive heart failure  pulmonary edema  cardiogenic shock Left ventricle impaired ≥25%  CHF / pulmonary edema Left ventricle impaired ≥40%  cardiogenic shock 255
  256. 256. Conduction Disturbances AV Blocks: 1o and Mobitz I 2o Generally due to  vagal tone Rarely progress to complete block Usually associated with inferior MI Generally respond to drug therapy: atropine 256
  257. 257. Conduction Disturbances AV Blocks: Mobitz II 2o Generally due to destruction of infranodal conduction tissue Sudden progression to complete AV block may occur Usually associated with anterior MI Pacemaker indicated 257
  258. 258. Conduction Disturbances Bundle Branch Block Identifies patients more likely to develop CHF, AV block, V-Fib Acute anterior wall MI + new RBBB  high risk of developing complete AV block and / or cardiogenic shock 258
  259. 259. Some Other Complications Cardiac rupture Ventricular septal rupture Papillary muscle dysfunction / rupture Mitral regurgitation LV aneurysm Thromboembolism Pericarditis 259
  260. 260. 3.5.7 Myocarditis 260
  261. 261. Myocarditis Detected in ~10% of routine autopsies Numerous virus (especially enterovirus), bacteria, fungi South America: Chaga’s disease Necrosis and destruction of cardiac tissues 261
  262. 262. Myocarditis Complaints nonspecific: fever, fatigue, myalgias, N/V/D No sign or symptom sensitive or specific Unexplained tachycardia common, but nonspecific Cardiac exam often unremarkable 262
  263. 263. Myocarditis EKG findings nonspecific: sinus tachycardia, low electrical activity May be prolonged corrected Q-T interval, AV block, acute MI pattern Cardiac troponin usually  WBC / ESR / CRP: nonspecific 263
  264. 264. Differential Diagnosis Can masquerade as acute MI: severe chest pain, ECG changes,  cardiac markers, heart failure Patients with myocarditis usually young, few risk factors for CAD ECG abnormalities may extend beyond distribution of single coronary artery 264
  265. 265. Treatment Determined by patient's clinical presentation and severity of disease Extends from limitation of activity to rhythm and CHF treatment, ECMO, VADs, and eventual cardiac transplantation 265
  266. 266. Chaga’s Disease Common in Central America Protozoan Trypanosoma cruzi with transmission by insect vector ~75% have no cardiac symptoms Syncope / presyncope in 2/3 who are seropositive Antitrypanosomal drugs: benznidazole and nifurtimox 266
  267. 267. Trichinosis Ingestion of cysts of Trichinella spiralis in undercooked meat, now mostly game meats Myocardial involvement in ~20% of diagnosed cases, appears 2nd – 3rd week of illness Many cardiac and EKG findings Corticosteroids + anti-helminthic 267
  268. 268. Lyme Disease Spirochete Borrelia burgdorferi Carditis ~21 days after onset of erythema migrans Cardiac complications 4 - 10% Conduction disturbances; BBB, 1st, 2nd, and 3rd degree heart block; cardiac arrest; dysrhythmias; left ventricular dysfunction 268
  269. 269. Lyme Disease Treatment Atropine or isoproterenol to treat stable heart blocks Temporary pacemaker often required in unstable patients IV penicillin or oral tetracycline can reverse AV blocks Erythromycin in kids Ceftriaxone also effective 269
  270. 270. Pharmacologic Causes In addition to ischemia, cocaine can cause myocarditis & dilated cardiomyopathy Doxorubicin can cause pericarditis, dysrhythmias, myocarditis, left ventricular dysfunction 270
  271. 271. Kawasaki Disease Primarily affects children ~25% have coronary artery abnormalities, usually several weeks after symptom onset Usually reversible: may cause aneurysm formation or 2o thrombosis and acute MI Myocarditis / pericarditis also seen 271
  272. 272. Brugada Syndrome Unpredictable ventricular dysrhythmias and syncope or sudden cardiac death More in < 50 years old Inherited disorder of Na+ channels Men > women Most common in Asian patients 272
  273. 273. Brugada Syndrome No structural heart disease Consider in children, teenagers, young adults with unexplained syncope or symptomatic palpitations ECG pattern: ST  with “saddle- back” or coved appearance V1-V3 RBBB often coexists 273
  274. 274. Brugada Syndrome 274 Source Undetermined
  275. 275. Brugada Syndrome Untreated: 10% mortality / year Only proven therapy: implantable cardioverter – defibrillator (ICD) Quinidine is proposed alternative in settings where ICD’s are unavailable or inappropriate (eg: neonates) 275
  276. 276. 3.5.8 Ventricular Aneurysm 276
  277. 277. Ventricular Aneurysm Persistent ST elevation following acute myocardial infarction Some ST elevation remains in 60% of patients with anterior STEMI and 5% with inferior STEMI Associated with paradoxical movement of ventricular wall on echocardiography 277
  278. 278. Ventricular Aneurysm ST elevation >2 weeks after AMI Most common: precordial leads. May be concave or convex Usually associated with well- formed Q- or QS waves. Relatively small T-waves Unlike hyperacute T-waves of AMI 278
  279. 279. Ventricular Aneurysm 279 Source Undetermined
  280. 280. Predispose To Ventricular arrhythmias and sudden cardiac death Myocardial scar tissue is arrhythmogenic Congestive cardiac failure Mural thrombus and embolization Myocardial rupture and death 280
  281. 281. 281