The document provides information on inferior wall myocardial infarction (MI), including: 1. Definitions, epidemiology, etiology, clinical features, diagnosis, treatment and complications of inferior wall MI are discussed. Worldwide over 7 million people experience STEMIs or NSTEMIs annually. 2. Diagnosis involves ECG, cardiac imaging, cardiac biomarkers like troponin and CK-MB. Reperfusion therapy within 6 hours includes PCI or thrombolysis. General treatment measures include aspirin, clopidogrel, anticoagulants, analgesics, beta-blockers, nitrates and oxygen. 3. The history of pioneers in cardiology and development of techniques like echocardi

1. Inferior Wall Myocardial Infarction Dr.K.Prashanthi

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

4. DEFINITION

5. EPIDEMIOLOGY

6. ETIOLOGY

7. CLINICAL FEATURES

8. DIAGNOSIS

9. TREATMENT

10. COMPLICATIONS

11. CONCLUSION

13. 2D ECHO

14. CHARLES THEODORE DOTTER PERCUTANEOUS TRANSLUMINAL ANGIOPLASTY

15. DR.andreasgruentzig Balloon angioplasty

16. Dr.bernardlown EXTERNAL DEFIBRILLATOR

17. THE LIFE SAVING DRUGS

18. STREPTOKINASE

19. The saviour – ATROPINE

20. Coronary circulation

21. DEFINITION Criteria for Acute ,Evolving ,Recent MI : Either of the following criteria satisifies the diagnosis: 1.Typical rise and /or fall of biochemical markers of myocardial necrosis with atleast one of the following : A.Ischemic symptoms B.Development of the pathological q waves in the ECG. C.Ecg changes indicative of ischemia.(ST segment elevation or depression). D.Imaging evidence of new loss of viable myocardium or new RWMA. 2.Pathological findings of an acute myocardial infarction.

23. Worldwide more than 3 million people have STEMIs and 4 million have NSTEMIs a year.

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. AV block is more common than infranodal block and occurs in approximately 20% of IWMI. (infranodal – AWMI) ………CMDT 2009 .

28. Sinus bradycardia is more common in IWMI (tahcycardia in AWMI)

30. Ventricular hypertrophy

31. Coronary artery emboli

32. Congenital coronary anomalies

33. Coronary trauma

34. Primary coronary vasospasm (variant angina)

35. Drug use (eg, cocaine, amphetamines, ephedrine)

36. Arteritis

37. Heavy exertion, fever, or hyperthyroidism

38. Hypoxemia of severe anemia

39. Aortic dissection with retrograde involvement of the coronary arteries

40. Infected cardiac valve through a patent foramen ovale (PFO)

41. Significant GI bleed

43. Fatigue,

44. Chest discomfort,

45. Malaise in the days preceding the event;

46. May occur suddenly without warning

48. Chest pain > 30 min.

49. Character of the pain –retrosternal,constrciting,crushing,compressing sensation of heavy weight.

50. Predilection for left side.

51. Radiates to the ulnar aspect of the left arm

52. Tingling sensation of the wrist and fingers.

53. In some patients, the symptom is epigastric, with a feeling of indigestion or of fullness and gas.

54. Nausea,Vomitings

55. Profound weakness

56. Dizziness

57. Palpitations,

58. Cold perspiration

60. In general, the onset is not directly associated with severe exertion. Instead, it is concomitant with exertion.

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

63. diabetics,

64. older patients,

65. dementia,

66. history of heart failure,

67. cocaine users,

68. hypercholesterolemia,

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).

72. Ongoing pain --- pale and diaphoretic.

73. Hypotension may indicate ventricular dysfunction due to ischemia.

75. Hypotension----due to parasympathetic hyperactivity.

76. Increased respiration – cheynes stokes –anxiety and pain.

77. Raised JVP.--- RVMI.—kussmaul’s sign

78. Clear lung fields.

79. On cardiac auscultation--S4 is almost universally present in patients in SR with STEMI.but non specific.

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.

84. Cardiac imaging

85. Cardiac biomarkers

86. Troponin T levels

87. CKMB,CK

88. Myoglobin levels

89. CBP

90. ESR

91. LDH

92. Lipid profile

93. CRP

94. MRI ,technetium 99m pyrophosphate scintigraphy

95. Scintigraphy with thallium 201

97. Triage of patients in whom an ACS is suspected.

98. Confirmatory of the diagnosis - 80% of cases.

99. In Inferior myocardial infarction, record a right-sided ECG to rule out right ventricular infarct.

101. intermediate probability of myocardial infarction are ST-segment depression, T-wave inversion, and other nonspecific ST-T wave abnormalities.

102. low probability of myocardial infarction are normal findings on ECGs

104. Right ventricular - RV4, RV5

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

107. RV dysfunction.

108. Assess the LV function secondary to RVMI --- in case of refractory to IV Fluids --- to rule out cardiogenic shock.

109. MRI with gadolinium contrast enhacement –most sensitive –2 gm of MI can be detected.

110. Techntium scan – hot spot with calcium – insensitive to small infarctions.

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. Normal troponin T 0-0.1 µg/l,I --- 0 – 0.08 µg/l

114. Cut off for MI t>0.1µg/l, I . 0.4 µg/l

115. CK, CK MB --- CK rises within 4-8 hrs and returns to normal by 48-72 hrs.

118. Block the formation of thromboxane A2 in the platelets by COX inhibition.

119. Dose is 160-325 mg.

120. 2.Clopidogrel

121. Thienopyridine class antiplatelet agent

122. Inhibits P2Y12 subtype of ADP receptor

123. 300 mg

124. CLARITY trial –loading dose of 300 mg,75 mg /day therafter along with thormbolysis---coronary patency –no increase in bleed.

125. COMMIT/CCS2 trial in china

127. PCI --

128. Fibrinolysis

129. Option depends upon the duration and the availability of the PCI nearby.

130. < 6 hrs ---PCI – fibrinolysis

131. >6 hrs --- PCI > fibrinolysis

136. The resolution of the ST segment elevation at 90 min.

137. 50% resolution of ST elevation can occur even without reperfusion –still a strong predictor of better outcome.

139. Bed rest for the first 12 hrs.

140. Diet :

141. Clear liquids for the first 12 hrs .

142. Fibre but low in sodium diet

143. Bowels:

144. Stool softeners are recommended

145. Sedation:

148. By face mask/nasal prongs

149. 2-4 lit /min

150. 7.ACEI /ARBs:

151. The benefits in EF < 40% ,presence of left heart failure .

152. SAVE ,AIRE,SMILE ,TRACE,GISI –III,ISIS 4 ---short and long term benefits

154. Clopdiogrel

155. H2 blockers

156. ACEI /ARBS

158. Grade 0 –complete occlusion of the infarct related artery.

159. Grade 1 – some penetration of the contrast material beyond the point of obstruction,but without the perfusion of the distal coronary bed.

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.

163. RVMI

164. VPCs

165. AF

166. AFL

167. AIVR

168. Sinus bradycardia

169. Pericarditis

170. Septum rupture

172. Electrolyte disturbances

173. Ischemia

174. Slowed conduction in zones of ischemic myocardium

175. 1. Sinus bradycardia—50% CASES

176. 2.PVCs

177. 3.VT

178. 4.VF

179. 5.AIVR

181. Pain radiating to either trapezius muscle is typical.

182. Rub -heard within 24 hrs or as late as 2 weeks…most commonly on second or third day.

183. Audible along the left sternal border or at the point of maximal impulse.

186. Acute Inferior wall MI

187. Acute Inferolateral MI

188. Acute InferoPosterior Myocardial Infarction

189. RIGHT SIDED LEADS

191. Acute Inferior MI with RVMI

192. Acute Inferolateral MI with 2:1 AVblock

193. Acute inferior wall MI and complete AV block

194. Take home message Inferior wall MI presents with nausea and abdominal pain also. Inferior wall in 30-50% cases is assosciated with RV MI. Take right sided V4R in all the patients with IWMI. Presence of RVMI increases the mortality of the patients. IV fluids and inotropes,pacing play a equally contributing role in the management of patients on presentation. Recurrence of IWMI at the same site is more than in the anterior wall MI. Triad of raised JVP ,hypotension and clear lungs think of RVMI. PWMI in case of R wave in V1 with upright T wave and R/S ratio >1 V1 and V2..take leads V7-9.

195. References Braunwald – 7 th edition An Introduction to electrocardiography ---Schamroth ,7 thed Marriott’s practical electrocardiography –Galen Basic and bedside electrocardiography –Romulo.F.Baltazar CMDT 2009 HARRISON’S 17 thed http://www.ncbi.nlm.nih.gov/pmc/articles www.ecglibrary.com www.netterimages.com www.medscape.com www.americanjournalofcaridology.com

196. Thank you