Case Myocardial Infarction Type two .pptx

myocardial infarction case report

1. Case Report The Approach to Diagnosis and Management of MI Type 2 Departemen Kardiologi dan Kedokteran Vaskuler , Fakultas Kedokteran , Universitas Padjadjaran , Indonesia, Selasa , 10 Desember 2019 Pembimbing : Dr. dr . Chaerul Achmad ., Sp.JP (K) Presentan : dr. Andra Naufal P

2. Outline Introduction Case Presentation Discussion Conclusion

3. INTRODUCTION

4. Myocardial Infraction Type 2 (type 2 MI) mechanism leading to ischaemic myocardial injury in the context of a mismatch between oxygen supply and demand . Most studies show a higher frequency of type 2 MI in women In this case MI in patients with CKD and elevated cTn levels may be difficult if symptoms or ECG changes indicating myocardial ischaemia are absent. U ndergo timely coronary angiography, description of a ruptured plaque with thrombus in the infarct-related artery may be helpful in making the distinction between type 2 MI vs type 1 MI. Thygesen K, Alpert JS, White HD; Joint ESC/ACC/AHA/WHF Task Force for the Redefinition of Myocardial Infarction. Universal definition of myocardial infarction. Eur Heart J 2007;28:2525–2538; Circulation 2007;116:2634–2653; J Am Coll Cardiol 2007;50:2173–2195. Thygesen K, Alpert JS, Jaffe AS, Simoons ML, Chaitman BR, White HD; Writing Group on the Joint ESC/ACC/AHA/WHF Task Force for the Universal Definition of Myocardial Infarction. Third universal definition of myocardial infraction. Eur Heart J 2012;33:2551–2567; Circulation 2012;126:2020–2035; J Am Coll Cardiol 2012;60:1581–1598.

5. CASE PRESENTATION

6. Mrs. E, 70 years old C ame with complained of heartburn at 4 hours of SMRS during dialysis, felt continuously more than 30 minutes, spread to the back, accompanied by cold sweat and vomiting. N o history of DOE, PND, orthopnea, and edema extremities. N o previous history of chest pain The patient had risk factor hypertension and smooking .

7. Patients were referred from the Habibie hospital with a diagnosis of Inferoanterolateral STEMI and carrying laboratory results of Hb 4.4 , Leukocytes 11,200, Erythrocytes 1.5, Platelets 258,000, GDS 124, Ureum 187 , Creatinine 8.5 .

8. Physical Examination B lood pressure 110/60 mmHg, heart rate 76x/minutes, respiratory rates 20x/minutes, and saturation O2 98% room air. Conjungtiva anemis (+), JVP 5+2, HJR (-), cardiomegaly (+) with normal heart sound, and no sign of congestion.

9. EKG RSKG Habibie onset 30 minutes Diagnosis EKG: Sinus rhythm, STEMI Inferoanterolateral

10. EKG RSHS onset 4 hours Diagnosis EKG: Sinus rhythm, STEMI inferoposteroapicolateral - RV

11. Chest X-ray Expertise: cardiomegaly without lung oedema .

12. The laboratory examination showed Hb 6.7 g/ dL , Ht 21.4%, leukosit 11.650/mm 3 , ureum 63.0 mg/ dL , creatinin 4.66 mg/ dL , eGFR 6 ml/min/1.73m 2 , random blood glucose 98 mg/ dL , natrium 139 mEq /L, kalium 2.4 mEq /L, calcium 2.89 mg/ dL , magnesium 1.8 mg/ dL and troponin I 5.99 ng/ mL . P atient was likely to diagnosed MI Type II dd / CAD STEMI Inferoposteroapicolateral -RV, Killip I, ESRD on hemodiyalisis , and hypertensive heart disease, hypertensive on therapy. Patients planned diagnostic angiography and hemodiyalisis . Patient get therapy Aspilet 1x81mg, Clopidogrel 1x75mg, Diazepam 1x5mg, Laxadine 1x15cc, and transfusion PRC with target Hb more than 8 .

13. On the next day, patient no complaints with hemodynamics stable. Laboratory post hemodialysis and transfusion intra hemodyalisis showed Hb 9.8 g/ dL , leukosit 8.400/mm 3 , ureum 38 mg/ dL , creatinin 3.07 mg/ dL , random blood glucose 95 mg/ dL , kalium 2.9 mEq /L. The ECG post transfusion showed sinus rhythm, ischemic anterior.

14. Echocardiography Normal all chamber Reduced LV systolic function (EF biplane 50%) hypokinetic anterior, anterolateral (mid-apex), inferior, inferoseptal (apex) LV diastolic dysfunction Mild AR due to calcification NCC, low probability of PH Normal RV contractility

15. A ngiography examination and result showed normal coronary

16. From that result patient was diagnosed MI Type II, ESRD on routine hemodialysis and Hypertensive heart disease.

17. DISCUSSION Patients with type 2 MI have less chest pain and more often have dyspnea or other atypical presentations. For patients with cardiac troponin ( cTn ) increases with a rising and/or falling pattern, a diagnosis of acute MI is possible if ischemia is present. Thygesen K, Alpert JS, Jaffe AS, Chaitman BR, White HD; the Executive Group on behalf of the Joint ESC/ACC/AHA/WHF Task Force for the Universal Definition of Myocardial Infarction. Fourth universal definition of myocardial infraction. European Heart Journal (2019) 40, 237–269 Lippi G, Sanchis-Gomar F, Cervellin G. Chest pain, dyspnea and other symptoms in patients with type 1 and 2 myocardial infarction. A litera - ture review. Int J Cardiol 2016;215:20–2.

18. Clinical Framework for type 2 MI Januzzi JL, Sandoval Y. The many faces of type 2 myocardial infarction. J Am . Cardiol Coll 2017;70:1569–1572.

19. Oxygen is carried in the blood in two forms: (1) dissolved in plasma and RBC water (about 2% of the total) and (2) reversibly bound to hemoglobin (about 98% of the total). The oxygen transport system normally operates to maintain Vo 2 in conditions where Do 2 varies widely. If global Do 2 decreases then oxygen extraction ratio ( o2 ER ) increases to maintain adequate supply. If Do 2 continues to decrease, appoint is reached where the o2ER is maximal and cannot increase further. This point is called the ‘critical Do 2 . S. A. McLellan MB ChB BSc MRCP FRCA, T. S. Walsh MB ChB BSc MRCP FRCA MD. Continuing Education in Anaesthesia , Critical Care & Pain | Volume 4 Number 4 2004 Do 2 = Co x Ca o2 o2ER = Vo 2 / Do 2 Oxygen extraction ratio (o2ER). Global oxygen delivery (Do2) . Global oxygen consumption (VO2) .

20. Sandoval Y, Smith SW, Sexter A, Schulz K, Apple FS. Use of objective evidence of myocardial ischemia to facilitate the diagnostic and prognostic distinction between type 2 myocardial infarction and myocardial injury. Eur Heart J Acute Cardiovasc Care 2018 Jul 1 [E-pub ahead of print].

21. Either the positive-negative biphasic T waves or the deeply inverted (≥ 5 mm) T waves, when occurring in the precordial leads V2 and V3, with or without similar changes in V1, V4, and V5, are nearly pathognomonic of very recent severe ischemia or injury in the distribution of the left anterior descending artery and characterize what is known as Wellens syndrome. De Zwaan C, bär FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J 1982; 103:730–736 Glancy Dl, Khuri b, Cospolich b. Heed the warning: Wellens ’ type T- wave inversion is caused by proximal left anterior descending lesion. Proc ( Bayl Univ Med Cent) 2000; 13:416–418. .

22. Wellens -type biphasic T wave in leads V2 and V3 (arrows) and T-wave inversion in leads V4 and V5 . Wellens -type deep T-wave inversion in leads V2 to V4.

23. Biomarkers complement clinical assessment and 12-lead ECG in the diagnosis, risk stratification and treatment of patients with suspected ACS . Measurement of a biomarker of cardiomyocyte injury, preferably high-sensitivity cardiac troponin, is mandatory in all patients with suspected ACS . Thygesen K, Alpert JS, Jaffe AS, Simoons ML, Chaitman BR, White HD; Writing Group on the Joint ESC/ACC/AHA/WHF Task Force for the Universal Definition of Myocardial Infarction. Third universal definition of myocardial infraction. Eur Heart J 2012;33:2551–2567; Circulation 2012;126:2020–2035; J Am Coll Cardiol 2012;60:1581–1598. Thygesen K, Mair J, Giannitsis E, Mueller C, Lindahl B, Blankenberg S, Huber K, Plebani M, Biasucci LM, Tubaro M, Collinson P, Venge P, Hasin Y, Galvani M, Koenig W, Hamm C, Alpert JS, Katus H, Jaffe AS. How to use high-sensitivity cardiac troponins in acute cardiac care. Eur Heart J 2012;33:2252 – 2257.

24. Conditions other than acute myocardial infarction type 1 associated with cardiac troponin elevation Roffi M, Patrono C, et. al. Task Force for the Management of Acute Coronary Syndromes in Patients Presenting without Persistent ST-Segment Elevation of the European Society of Cardiology (ESC). 2015 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. European Heart Journal (2016) 37, 267–315.

25. Diagnostic test flow chart in MINOCA Ibanez B, James S, Agewall S, et. al. The Task Force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC) . 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. European Heart Journal (2017) 00, 1–66.

26. In the acute setting to treat the underlying ischaemic imbalance of oxygen supply and demand. This treatment may include volume adjustment, blood pressure management, administration of blood products, heart-rate control, and respiratory support. Thygesen K, Alpert JS, Jaffe AS, Chaitman BR, White HD; the Executive Group on behalf of the Joint ESC/ACC/AHA/WHF Task Force for the Universal Definition of Myocardial Infarction. Fourth universal definition of myocardial infraction. European Heart Journal (2019) 40, 237–269

27. CONCLUSIONS Myocardial Infraction Type 2 (type 2 MI) mechanism leading to ischaemic myocardial injury in the context of a mismatch between oxygen supply and demand. In case MI in patients with CKD and severe anemia , s erial changes in cTn levels are effective in diagnosing MI. Coronary angiography is recommended for diagnostic test for ruling out obstructive CAD in a patient presenting with STEMI.

28. Thank you