Inferior myocardial infarction

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a seminar on inferior wall MI by my junior Dr.K.Prashanthi...
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Inferior myocardial infarction

  1. 1. Inferior Wall <br />Myocardial Infarction<br />Dr.K.Prashanthi<br />
  2. 2. Sir William Osler said, “Variability is the law of life, and as no two faces are the same, so no two bodies are alike, and no two individuals react alike and behave alike under the abnormal conditions which we know as disease<br />
  3. 3. <ul><li>INTRODUCTION
  4. 4. DEFINITION
  5. 5. EPIDEMIOLOGY
  6. 6. ETIOLOGY
  7. 7. CLINICAL FEATURES
  8. 8. DIAGNOSIS
  9. 9. TREATMENT
  10. 10. COMPLICATIONS
  11. 11. CONCLUSION
  12. 12. TAKE HOME MESSAGE</li></li></ul><li>THE PIONEERS<br />HAROLD ENSIGN BENNET PARDEE<br />EINTHOVEN<br />PAUL DUDLEY WHITE<br />
  13. 13. 2D ECHO <br />
  14. 14. CHARLES THEODORE DOTTER<br />PERCUTANEOUS TRANSLUMINAL ANGIOPLASTY<br />
  15. 15. DR.andreasgruentzig<br />Balloon angioplasty<br />
  16. 16. Dr.bernardlown<br />EXTERNAL DEFIBRILLATOR<br />
  17. 17. THE LIFE SAVING DRUGS <br />
  18. 18. STREPTOKINASE<br />
  19. 19. The saviour – ATROPINE <br />
  20. 20. Coronary circulation<br />
  21. 21. DEFINITION<br />Criteria for Acute ,Evolving ,Recent MI :<br />Either of the following criteria satisifies the diagnosis:<br />1.Typical rise and /or fall of biochemical markers of myocardial necrosis with atleast one of the following :<br />A.Ischemic symptoms<br />B.Development of the pathological q waves in the ECG.<br />C.Ecg changes indicative of ischemia.(ST segment elevation or depression).<br />D.Imaging evidence of new loss of viable myocardium or new RWMA.<br />2.Pathological findings of an acute myocardial infarction.<br />
  22. 22. EPIDEMIOLOGY<br /><ul><li>Myocardial infarction is a common presentation of Ischemic heart disease.
  23. 23. Worldwide more than 3 million people have STEMIs and 4 million have NSTEMIs a year.
  24. 24. Coronary heart disease is responsible for 1 in 5 deaths in the United States.</li></li></ul><li>EPIDEMIOLOGY-India<br />In India, cardiovascular disease (CVD) is the leading cause of death. 32% of all deaths in 2007 .<br />Relatively new epidemic in India.<br />Mortality estimates due to CVD vary widely by state, ranging from 10% in Meghalaya to 49% in Punjab (percentage of all deaths). Punjab (49%), Goa (42%), <br />Tamil Nadu (36%) and Andhra Pradesh (31%) have the highest CVD related mortality estimates.<br />State-wise differences are correlated with prevalence of specific dietary risk factors in the states. <br />Moderate physical exercise is associated with reduced incidence of CVD in India (those who exercise have less than half the risk of those who don't).<br />
  25. 25. EPIDEMIOLOGY<br /><ul><li>Usually anterior wall MI is more than other segment MI because of conjunction of HTN and diabetes along with the presence of hypercholeosterolemias in C.A.D -----Br heart journal 2000..ncbi.nch.gov/pmc
  26. 26. RVMI is present in one third of patients with IWMI ,but clinically significant in less than 50 % of the one third…. CMDT 2009.
  27. 27. AV block is more common than infranodal block and occurs in approximately 20% of IWMI. (infranodal – AWMI) ………CMDT 2009 .
  28. 28. Sinus bradycardia is more common in IWMI (tahcycardia in AWMI)
  29. 29. Posterior wall MI is assosciated with 5% of IWMI or lateral MI but rarely occurs alone.</li></li></ul><li>ETIOLOGY<br /><ul><li>Atherosclerosis. 90% of MIs result from an acute thrombus that obstructs an atherosclerotic coronary artery. Plaque rupture and erosion - the major triggers for coronary thrombosis.</li></li></ul><li>CAD without atherosclerosis<br /><ul><li>Secondary to vasculitis
  30. 30. Ventricular hypertrophy
  31. 31. Coronary artery emboli
  32. 32. Congenital coronary anomalies
  33. 33. Coronary trauma
  34. 34. Primary coronary vasospasm (variant angina)
  35. 35. Drug use (eg, cocaine, amphetamines, ephedrine)
  36. 36. Arteritis
  37. 37. Heavy exertion, fever, or hyperthyroidism
  38. 38. Hypoxemia of severe anemia
  39. 39. Aortic dissection with retrograde involvement of the coronary arteries
  40. 40. Infected cardiac valve through a patent foramen ovale (PFO)
  41. 41. Significant GI bleed
  42. 42. CO Poisoning </li></li></ul><li>Clinical features<br /><ul><li>Prodromal symptoms:
  43. 43. Fatigue,
  44. 44. Chest discomfort,
  45. 45. Malaise in the days preceding the event;
  46. 46. May occur suddenly without warning
  47. 47. Nausea and/or abdominal pain often are present in infarcts involving the inferior or posterior wall. </li></li></ul><li>CLINICAL FEATURES<br /><ul><li>Symptoms:
  48. 48. Chest pain > 30 min.
  49. 49. Character of the pain –retrosternal,constrciting,crushing,compressing sensation of heavy weight.
  50. 50. Predilection for left side.
  51. 51. Radiates to the ulnar aspect of the left arm
  52. 52. Tingling sensation of the wrist and fingers.
  53. 53. In some patients, the symptom is epigastric, with a feeling of indigestion or of fullness and gas.
  54. 54. Nausea,Vomitings
  55. 55. Profound weakness
  56. 56. Dizziness
  57. 57. Palpitations,
  58. 58. Cold perspiration
  59. 59. Sense of impending doom.</li></li></ul><li><ul><li>occurs most often in the early morning hours, -- increase in catecholamine-induced platelet aggregation and ↑ serum concentrations of plasminogen activator inhibitor-1 (PAI-1) that occur after awakening.
  60. 60. In general, the onset is not directly associated with severe exertion. Instead, it is concomitant with exertion.
  61. 61. The immediate risk of myocardial infarction increases 6-fold on average post MI,CAD and by as much as 30-fold in sedentary people. ncbi.nbl.com
  62. 62. Anginal equivalent --abdominal pain,jaw pain,sharp pain in women,elderly.</li></li></ul><li>High index of suspicion<br /><ul><li>women,
  63. 63. diabetics,
  64. 64. older patients,
  65. 65. dementia,
  66. 66. history of heart failure,
  67. 67. cocaine users,
  68. 68. hypercholesterolemia,
  69. 69. positive family history for early coronary disease ---- any first-degree Male aged≤ 45 years, female relative aged ≤ 55 years who MI </li></li></ul><li>Silent MI<br /><ul><li>Half of myocardial infarctions are clinically silent in that they do not cause the classic symptoms described above and consequently go unrecognized by the patient.
  70. 70. In as many as 25% of elderly patients, a population in whom 50% of myocardial infarctions occur; in such patients, the diagnosis is often established only retrospectively, by applying electrocardiographic criteria or by scanning the patients using 2-dimensional (2D) echocardiography or magnetic resonance imaging (MRI).
  71. 71. On clinical evaluation, ventricular aneurysms may be recognized late, with symptoms and signs of heart failure, recurrent ventricular arrhythmia, or recurrent embolization. </li></li></ul><li>Physical examination<br /><ul><li>Physical examination findings can vary; comfortable in bed, with normal examination results, may be in severe pain, with significant respiratory distress and a need for ventilatory support.
  72. 72. Ongoing pain --- pale and diaphoretic.
  73. 73. Hypotension may indicate ventricular dysfunction due to ischemia.
  74. 74. Hypotension in the setting of myocardial infarction usually indicates a large infarct secondary to either decreased global cardiac contractility or a right ventricular infarct.</li></li></ul><li>Signs<br /><ul><li>Bradycardia
  75. 75. Hypotension----due to parasympathetic hyperactivity.
  76. 76. Increased respiration – cheynes stokes –anxiety and pain.
  77. 77. Raised JVP.--- RVMI.—kussmaul’s sign
  78. 78. Clear lung fields.
  79. 79. On cardiac auscultation--S4 is almost universally present in patients in SR with STEMI.but non specific.
  80. 80. S3 ,S4 heard along the left sternal border and increases on inspiration.—RVMI –RVF</li></li></ul><li>IWMI with RVMI <br /><ul><li>The evidence of right ventricular ischemia should be sought in all patients with acute inferior MI at the time of admission. RT precordial leads, in particular lead V4R must be recorded in all patients with inferior MI. –ACC guidelines
  81. 81. 1-mm ST segment elevation in the right precordial lead V4R is the single most predictive ECG finding in patients with right ventricular ischemia This finding, however, may be transient; half of the patients show resolution of ST elevation within 10 hours of the onset of symptoms .</li></li></ul><li>IWMI with RVMI<br /><ul><li>Distention of neck veins is commonly described as a sign of failure of the RV.
  82. 82. Impaired right ventricular diastolic function also leads to systemic venous hypotension, edema, and hepatomegaly with abdominojugular reflux, which may result in saline-response underfilling of the LV and a concomitant reduction in cardiac output.
  83. 83. Peripheral cyanosis, edema, pallor, diminished pulse volume, delayed rise, and delayed capillary refill may indicate vasoconstriction, diminished cardiac output, and right ventricular dysfunction or failure.</li></li></ul><li>Diagnosis<br /><ul><li>ECG
  84. 84. Cardiac imaging
  85. 85. Cardiac biomarkers
  86. 86. Troponin T levels
  87. 87. CKMB,CK
  88. 88. Myoglobin levels
  89. 89. CBP
  90. 90. ESR
  91. 91. LDH
  92. 92. Lipid profile
  93. 93. CRP
  94. 94. MRI ,technetium 99m pyrophosphate scintigraphy
  95. 95. Scintigraphy with thallium 201
  96. 96. Hemodynamic assessement with PA catheter---cardiogenic shock</li></li></ul><li>ECG<br /><ul><li>Most important tool in the initial evaluation
  97. 97. Triage of patients in whom an ACS is suspected.
  98. 98. Confirmatory of the diagnosis - 80% of cases.
  99. 99. In Inferior myocardial infarction, record a right-sided ECG to rule out right ventricular infarct.
  100. 100. Daily serial ECGs for the first 2-3 days and additionally as needed. </li></li></ul><li><ul><li>High probability of myocardial infarction is indicated either by ST-segment elevation greater than 1 mm in 2 anatomically contiguous leads ,2mm in chest leads or by the presence of new Q waves.
  101. 101. intermediate probability of myocardial infarction are ST-segment depression, T-wave inversion, and other nonspecific ST-T wave abnormalities.
  102. 102. low probability of myocardial infarction are normal findings on ECGs
  103. 103. however, normal or nonspecific findings on ECGs do not exclude the possibility of myocardial infarction. </li></li></ul><li><ul><li>Inferior wall MI –ST segment elevation of > 1mm in inferior leads with reciprocal ST segement depression in anterior leads.
  104. 104. Right ventricular - RV4, RV5
  105. 105. Posterior wall - R/S ratio greater than 1 in V1 and V2; T-wave changes (ie, upright) in V1,ST segment elevation in V8, and V9
  106. 106. Right ventricular myocardial infarction commonly is manifested by ST-segment elevation or Q waves detectable in right-sided precordial leads.</li></li></ul><li>2D ECHO<br /><ul><li>RWMA
  107. 107. RV dysfunction.
  108. 108. Assess the LV function secondary to RVMI --- in case of refractory to IV Fluids --- to rule out cardiogenic shock.
  109. 109. MRI with gadolinium contrast enhacement –most sensitive –2 gm of MI can be detected.
  110. 110. Techntium scan – hot spot with calcium – insensitive to small infarctions.
  111. 111. Thallium scan –cold spots in regions of diminished perfusion –does not differentiate old from new.</li></li></ul><li>Cardiac markers<br /><ul><li>Troponin T and troponin I
  112. 112. Highly specific monoclonal antibodies - not normally detectable in the blood of the healthy individuals but may increase after STEMI to levels greater than 20 times.
  113. 113. Normal troponin T 0-0.1 µg/l,I --- 0 – 0.08 µg/l
  114. 114. Cut off for MI t>0.1µg/l, I . 0.4 µg/l
  115. 115. CK, CK MB --- CK rises within 4-8 hrs and returns to normal by 48-72 hrs.
  116. 116. A ratio (relative index) CKMB mass :CK actvity > 2.5 suggests but not diagnostic of acute MI rather than the skeletal source of CKMB elevation.</li></li></ul><li>Treatment<br /> golden period is 1 hr ….<br />Door to needle time -30 min,door to balloon time is <90 min<br />< 6 hrs <br /><ul><li>PCI = thrombolysis</li></ul> <6 hrs with hypotension,cardiogenic shock<br /><ul><li>PCI</li></ul> < 6 hrs with hypotension ,no PCI center <br /><ul><li>Give IV fluids --
  117. 117. Then thrombolysis with cardiac monitoring.</li></ul> In presenceofbradycardia<br /><ul><li>Give atropine</li></ul> In presence of CHB<br /><ul><li>Temporary pacemaker </li></li></ul><li>Management<br /><ul><li>1.Aspirin
  118. 118. Block the formation of thromboxane A2 in the platelets by COX inhibition.
  119. 119. Dose is 160-325 mg.
  120. 120. 2.Clopidogrel
  121. 121. Thienopyridine class antiplatelet agent
  122. 122. Inhibits P2Y12 subtype of ADP receptor
  123. 123. 300 mg
  124. 124. CLARITY trial –loading dose of 300 mg,75 mg /day therafter along with thormbolysis---coronary patency –no increase in bleed.
  125. 125. COMMIT/CCS2 trial in china
  126. 126. Clopidogrel to be added to apsirin to all patients with STEMI regardless of whether or not perfusion is given and continued for atleast 14 days,and generally for 1 year.</li></li></ul><li>Reperfusion therapy<br /><ul><li>Limitation of the infarct size
  127. 127. PCI --
  128. 128. Fibrinolysis
  129. 129. Option depends upon the duration and the availability of the PCI nearby.
  130. 130. < 6 hrs ---PCI – fibrinolysis
  131. 131. >6 hrs --- PCI > fibrinolysis
  132. 132. The patient at discharge should be sent for angiography in case of absence of PCI not done < 6 hrs….but thrombolysis given, for the evaluation of the vessel blockage …and extent of vessel disease,. </li></li></ul><li>Thrombolysis/fibrinolysis<br />To maintain the patency of the coronary artery.<br />Fibrinolytics agents used :<br />Tissue plasminogen activator<br />Tenectplase<br />Reteplase<br />Alteplase ---GUSTO trial<br />tpA---- 15 mg bolus followed by 50 mg intravenously IV over the first 30 min followed by 30 mg over the next 60 min.<br />Tenectplase – IV bolus of 0.53 mg/kg over 10 sec<br />Reteplase – 10 MU bolus given over 2 -3 min followed by 2nd 10 MU units 30 min later.<br />Streptokinase--- 15 MU given over 1 hr –hypotension. <br />
  133. 133. Contraindications and complications<br /><ul><li>Absolute – cerebrovascular hemorrhage ,ischemia,marked hypertensionSBP > 180mm Hg,DBP > 110 mmHg,aortic dissection,active internal bleeding.
  134. 134. Relative --- pregnancy,hemorrhagic diabetic retinopathy,active peptic ulcer disease,severe HTN ,allergic reactions .<5 days- 2yrs.,trauma within 2-4 weeks,major surgery within 3 weeks,traumatic CPR ,current use of anticoagulants INR >2-3.</li></li></ul><li>Antithrombotic agents<br />Goal is to maintain the patency of the infarct related artery in conjunction with reperfusion related strategies.<br />UFH --- 60 U/kg followed by infusion of 12 U/kg/hr<br />The APTT should be 1.5 – 2 times the control value.<br />LMWH – enoxaparin 30 mg IV bolus –1mg/kg every 12 hrs---ASSENT 3 trial. <br />Decreased the death at day 30 compared to UFH –EXTRACT trial <br />OASIS 6 trial – fondaparinux given at dose of 2.5 mg /day reduced death and reinfarction .no benefit in patients udergoing PCI –catheter thrombosis..<br />Use antacids and an H2 blocker as prophylactically<br />
  135. 135. Asessment of reperfusion<br /><ul><li>Early cessation of pain
  136. 136. The resolution of the ST segment elevation at 90 min.
  137. 137. 50% resolution of ST elevation can occur even without reperfusion –still a strong predictor of better outcome.
  138. 138. Reinfarction – recurrence of pain and ST segment elevation –angio and PCI. </li></li></ul><li>General measures<br /><ul><li>Activity :
  139. 139. Bed rest for the first 12 hrs.
  140. 140. Diet :
  141. 141. Clear liquids for the first 12 hrs .
  142. 142. Fibre but low in sodium diet
  143. 143. Bowels:
  144. 144. Stool softeners are recommended
  145. 145. Sedation:
  146. 146. Lorazepam ,oxazepam,diazepam </li></li></ul><li>3.Analgesics – <br />morphine<br />Very effective analgesic for pain assosciated STEMI<br />Reduces sympathetically mediated arteriolar and venous constriction<br />Reduces arterial pressure and cardiac output.<br />Dose – 2- 8 mg repeated in 5-15 min.<br />Hypotension and bradycardia – atropine 0.6mg<br />4.b blockers:<br />If HR > 60 /min,BP > 100 mm Hg SBP<br />Metoprolol 5 mg every 2-5 min ,3 doses.<br />5.nitrates:<br />Should not be given in inferior wall MI –causes hypotension and bradycardia.<br />If waxing and waning of pain ,systole > 100 mm Hg --- IV NTG. 5µg --- 200 µg /min<br />
  147. 147. <ul><li>6.oxygen:
  148. 148. By face mask/nasal prongs
  149. 149. 2-4 lit /min
  150. 150. 7.ACEI /ARBs:
  151. 151. The benefits in EF < 40% ,presence of left heart failure .
  152. 152. SAVE ,AIRE,SMILE ,TRACE,GISI –III,ISIS 4 ---short and long term benefits
  153. 153. CURE trial clopidogrel 75 mg/day to be given along with aspirin for 1 year in MI patients. </li></li></ul><li>At discharge <br /><ul><li>Aspirin
  154. 154. Clopdiogrel
  155. 155. H2 blockers
  156. 156. ACEI /ARBS
  157. 157. Stress testing –see for ST segment depression during submximal exercise –positive send him for angiography---revascualrization.</li></li></ul><li>TIMI grading <br /><ul><li>Thrombolysis in myocardial infarction
  158. 158. Grade 0 –complete occlusion of the infarct related artery.
  159. 159. Grade 1 – some penetration of the contrast material beyond the point of obstruction,but without the perfusion of the distal coronary bed.
  160. 160. Grade 2 – perfusion of the entire infarct vessel into the distal bed but with flow that is delayed compared with that of the normal artery.
  161. 161. Grade 3 – full perfusion of the infarct vessel with normal flow. </li></li></ul><li>GRACE score<br />Global Registry of Acute Coronary Events (GRACE) Hospital Discharge Risk Score Accurately Predicts Long-Term Mortality Post Acute Coronary Syndrome<br />
  162. 162. Complications<br /><ul><li>Post infarction ischemia
  163. 163. RVMI
  164. 164. VPCs
  165. 165. AF
  166. 166. AFL
  167. 167. AIVR
  168. 168. Sinus bradycardia
  169. 169. Pericarditis
  170. 170. Septum rupture
  171. 171. Cardiogenic shock</li></li></ul><li>Arryhthmias<br /><ul><li>Autonomic nervous system imbalance.
  172. 172. Electrolyte disturbances
  173. 173. Ischemia
  174. 174. Slowed conduction in zones of ischemic myocardium
  175. 175. 1. Sinus bradycardia—50% CASES
  176. 176. 2.PVCs
  177. 177. 3.VT
  178. 178. 4.VF
  179. 179. 5.AIVR
  180. 180. 6.AF AFL</li></li></ul><li>Pericarditis<br /><ul><li>Pericardial friction RUB and pericardial pain are frequently encountered in patients with MI.
  181. 181. Pain radiating to either trapezius muscle is typical.
  182. 182. Rub -heard within 24 hrs or as late as 2 weeks…most commonly on second or third day.
  183. 183. Audible along the left sternal border or at the point of maximal impulse.
  184. 184. Anticoagulants should be stopped.</li></li></ul><li>Lets have a look at the ECGs <br />
  185. 185.
  186. 186. Acute Inferior wall MI <br />
  187. 187. Acute Inferolateral MI <br />
  188. 188. Acute InferoPosterior Myocardial Infarction<br />
  189. 189. RIGHT SIDED LEADS<br />
  190. 190.
  191. 191. Acute Inferior MI with RVMI<br />
  192. 192. Acute Inferolateral MI with 2:1 AVblock<br />
  193. 193. Acute inferior wall MI and complete AV block<br />
  194. 194. Take home message<br />Inferior wall MI presents with nausea and abdominal pain also.<br />Inferior wall in 30-50% cases is assosciated with RV MI.<br />Take right sided V4R in all the patients with IWMI.<br />Presence of RVMI increases the mortality of the patients.<br />IV fluids and inotropes,pacing play a equally contributing role in the management of patients on presentation.<br />Recurrence of IWMI at the same site is more than in the anterior wall MI.<br />Triad of raised JVP ,hypotension and clear lungs think of RVMI.<br />PWMI in case of R wave in V1 with upright T wave and R/S ratio >1 V1 and V2..take leads V7-9.<br />
  195. 195. References<br />Braunwald – 7 th edition<br />An Introduction to electrocardiography ---Schamroth ,7 thed<br />Marriott’s practical electrocardiography –Galen<br />Basic and bedside electrocardiography –Romulo.F.Baltazar<br />CMDT 2009<br />HARRISON’S 17 thed<br />http://www.ncbi.nlm.nih.gov/pmc/articles<br />www.ecglibrary.com<br />www.netterimages.com<br />www.medscape.com<br />www.americanjournalofcaridology.com<br />
  196. 196. Thank you <br />

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