Acute Coronary Syndrome diagnosis and treatment.pptx

Acute coronary Syndrome

1. Dr Vignesh DM Critical Care Medicine Myocardial Infarction

2. MI Coronary circulation Pathogenesis ECG (Ant wall ,Inf wall, RV, PW) ECHO Cardiac markers Broad management of STEMI (PCI / Thrombolysis) & NSTEMI Angiogram / Angioplasty/ CABG

3. Coronary Circulation

4. Type 1 MI Plaque erosion/rupture with occlusive thrombus Plaque erosion/rupture with non-occlusive thrombus

5. Type 2 MI Atherosclerosis and Oxygen supply demand/mismatch Vasospasm or coronary microvascular dysfunction Non-Atherosclerotic coronary dissection Oxygen supply/demand imbalance alone

6. Other Types Type 3 – Sudden Cardiac death when biomarkers are not available Type 4 - Associated with PCI (4a – PCI / 4b – Stent Thrombosis) Type 5 - Associated with CABG

7. Universal definition of MI D etection of a rise and/or fall of cardiac Troponin values (Evidence of Myocardial injury) with at least one value above the 99th percentile URL and at least one of the following: Symptoms of myocardial ischemia; New ischemic ECG changes ; Development of pathological Q waves; Imaging evidence of new loss of viable myocardium or new RWMA consistent with an ischemic etiology; Identification of a coronary thrombus by angiography or autopsy j.jacc.2018.08.1038

8. Acute Myocardial Infarction STEMI - ST-segment elevation in at least two contiguous leads NSTEMI/ Unstable angina - Persistent or transient ST-segment depression, T inversion, or the ECG may be normal Cardiomyocyte necrosis [(NSTEMI)] or myocardial ischaemia without cell damage (unstable angina) MINOCA - MI with non-obstructive coronary arteries

9. ECG lead placement

10. ECG – J Point

11. ECG Diagnosis J-point elevation: in atleast two contiguous leads with ST-segment elevation 2.5mm in men < 40 years, 2mm in men > 40 years, 1.5mm in women in leads V2–V3 and/or 1 mm in the other leads [in the absence of left ventricular (LV) hypertrophy or LBBB)] Left main coronary obstruction: The presence of ST depression: 1 mm in eight or more surface leads (inferolateral ST depression), C oupled with ST-segment elevation in aVR and/or V1 , suggests multivessel ischemia or left main coronary artery obstruction

12. ECG changes

13. ECG changes

14. ECG changes

15. ECG changes

16. ECG changes

17. ECG changes

18. Inferior wall MI - Diagnosis on ECG ST-segment elevation (measured at the J-point) ≥1 mm in II, III and AVF R ecord right precordial leads (V3R and V4R) to identify concomitant RV infarction If there is ST-segment depression ≥ 0.5mm in leads V1–V3 especially when the terminal T-wave is positive do a posterior ECG ST-segment elevation ≥ 0.5mm recorded in leads V7–V9 should be considered as a means to identify posterior MI 2017 ESC Guidelines

19. ECG – Inferior wall MI (RCA occlusion) Greater ST ↑ in lead III > lead II and ST-segment ↓ of more than 1 mm in leads I and aVL suggest involvement of RCA

20. ECG – Inferior wall MI (Proximal RCA occlusion)

21. ECG - RVMI The most sensitive ECG sign of RVMI is ST ↑ o f > 1 mm in lead V 4 R with an upright T wave in that lead - Rarely present >12 hrs

22. ECG – Posterior wall MI (1) Horizontal ST depression, (2) Tall broad R waves (>30ms), (3) Upright T waves, (4) Dominant R wave (R/S ratio > 1) in V2

23. ECG – Posterior wall MI ST-elevation ≥ 0.5 mm in one lead indicates posterior ST-elevation MI (STEMI)

24. Cardiac enzymes

25. Cardiac enzymes

26.  Parasternal Long Axis View - PLAX

27. Parasternal Short Axis Views - PSAX

28. Apical  View (A4C, A5C)

29. Subxiphoid view

30. LV function – Eye ball

31. Hyperdynamic LV P apillary apposition (kissing ventricles) – Parasternal short axis view

32. Obstructive Shock

33. LVH

34. Cardiogenic shock

35. Hypovolemic shock

36. Pulmonary Embolism

37. Pericardial Effusion

38. Noninvasive tests are available to establish the diagnosis of CAD Exercise ECG , generally using a treadmill and standardized protocols. Echocardiography using either exercise or pharmacologic (dobutamine) stress. Radionuclide myocardial perfusion imaging using either exercise or pharmacologic stress and imaging with either single photon emission computed tomography (SPECT) or positron emission tomography (PET). Coronary CT Angiogra phy and CT perfusion and perfusion reserve. Cardiac magnetic resonance imaging Hybrid imaging using either SPECT/CT, PET/CT, or PET/MR.

39. Angiogram (Calculate Syntax Score)

40. CABG CABG is preferred to PCI in patients with: T hree-vessel disease and diabetes or elevated SYNTAX score (>22) Patients with LMS and SYNTAX score of more than 22 Cardiac surgery is usually reserved for the complications of MI: Ventricular septal defect or Mitral regurgitation Operative mortality is highest in the first 72 hours after STEMI

41. Indications for Admission to ICCU Acute Coronary Syndrome Cardiogenic shock Arrhythmias (Brady and Tachyarrhythmia) Congestive Heart Failure Right Heart Failure Hypertensive emergency Aortic Dissection Cardiac Tamponade PR < 40 or > 150/min SBP < 90 mmHg MAP < 65 mmHg DBP >120 RR > 30 /min

42. Initial Management Monitor and support A irway, B reathing and C irculation If O2 saturation>90% - No Oxygen therapy Obtain IV access and send blood for Troponin & Coagulation studies Obtain 12 lead ECG and interpret as STEMI/NSTEMI/UA Aspirin 325 mg (Non-enteric coated and should be chewed) (Rectal suppository of 300mg if vomiting) NTG C/I: RVMI, SBP<90 mmHg and Recent Phosphodiesterase inhibitor use

43. Anti-coagulation for Primary PCI UFH (Class I,C) and Bivalirudin Enoxaparin (Class IIa , A) Fondaparinux is not recommended ATOLL trial

44. Primary PCI Indications STEMI and cardiogenic shock - Only the occluded artery responsible for the STEMI should be treated because clinical trial evidence demonstrates no advantages and potential harms from treating multiple coronary arteries

45. Fibrinolytic therapy Ischemic symptoms < 12 h (Class I , Level A) Evidence of ongoing ischemia 12 to 24 h after symptom onset and a large area of myocardium at risk or hemodynamic instability (Class II a, Level C) Largest benefit when given within 2 hrs of symptom onset ( A meta-analysis showed that thrombolysis within 6 hours of STEMI or LBBB MI prevented 30 deaths in every 1000 patients treated. Between 7 and 12 hours, 20 in every 1000 deaths were prevented . After 12 hours the benefits are limited, and there is evidence to suggest less benefit for older patients, possibly because of the increased risk of strokes) Fibrin-specific agent + Aspirin + Clopidogrel - recommended Enoxaparin i.v. followed by s.c. preferred over UFH ( Anticoagulation is recommended in patients treated with lytics until revascularization (if performed) or for the duration of hospital stay up to 8 days) In patients treated with streptokinase: Fondaparinux preferred

46. Contraindication for Fibrinolytic therapy Absolute contraindications Any prior ICH Known structural cerebral vascular lesion (e.g., AV malformation) Known malignant intracranial neoplasm Ischemic stroke within 3 months Suspected aortic dissection Active bleeding or bleeding diathesis Significant Closed-head or facial trauma within 3 months Intracranial or intraspinal surgery within 2 months For streptokinase, prior treatment within the previous 6 months Relative contraindications (SBP > 180 mm Hg or > DBP 110 mm Hg) History of prior ischemic stroke > 3 mo Traumatic or prolonged (> 10 min) CPR Major surgery (< 3 wk ) Recent (within 2 to 4 wk) internal bleeding Noncompressible vascular punctures Pregnancy Active peptic ulcer Oral anticoagulant therapy

47. “Do not forget” interventions in STEMI patients undergoing a primary PCI strategy

48. “Do not forget” interventions in STEMI patients undergoing a successful fibrinolysis strategy

49. Thank you