ACUTE CORONARY SYNDROME BY DR.NITHA , 2022

ACS- STEMI, NSTEMI
LATEST ADVANCES - OMI

1. ACUTE CORONARY SYNDROME By Dr. Nitha Thomas 1st year MEM

2. Topics covered Anatomy and physiology of the heart ACS and its types Clinical features Investigations - ECG, Cardiac markers Treatment Complications of ACS

3. A NATOMY AND PATHOPHYSIOLOGY

4. PATH OF BLOOD FLOW THROUGH THE HEART

5. ACUTE CORONARY SYNDROME

6. DEFINITION (AHA) Acute coronary syndromes (ACS) is an umbrella term for situations in which blood supplied to the heart muscle is suddenly/abruptly blocked. The occlusion is usually due to a thrombus/atheroma and can be sudden and complete. If a clot forms due to a plaque rupture , a part of the clot may break away and clog one of the coronary arteries causing ACS. Though less common, spasms in the coronary artery may also limit blood flow (prinzmetal’s angina). Regardless of the cause of the blockage, it’s damaging to the heart and a medical emergency .

7. ETIOLOGY

8. Why ischemia Ischemia occurs due to imbalance b/w O2 demand and O2 supply. O2 supply → O2 carrying capacity and Coronary artery blood flow O2 CC→ by Hb levels CABF—> duration of diastolic relaxation + peripheral vas resistance OTHER CAUSES OF ACS : Coronary arterial spasm, microvascular dysfunction, Increased myocardial O2 demand situations eg, fever, tachycardia, arrhythmias , thyrotoxicosis, Reduced blood flow eg hypotension Reduced O2 delivery eg anemia or hypoxemia

9. TYPES

10. TYPES ST-segment elevation myocardial infarction ( STEMI ) — there is usually complete blockage of a coronary artery, which leads to extensive damage to a large area of the heart. This is suspected when there is ST-segment elevation in two or more anatomically contiguous ECG leads, TROP /CKMB>> , extends throughout the thickness of the myocardium result of complete occlusion , irreversible Non-ST-segment elevation myocardial infarction ( NSTEMI ) — supply of blood to the heart is only partially blocked, so a smaller section of the heart is damaged. Without treatment it can progress to STEMI, TROP /CKMB>> , involves a small area in the subendocardial wall of lv , ventricular septum or papillary muscles due to decreased blood flow Unstable angina — blood supply to the heart is restricted, but there is no permanent damage to the heart muscle.- crescendo pattern. The ECG may be normal and troponin levels will not be raised. TROP /CKMB- N

11. TYPES - 2 1. TRANSMURAL extends throughout the thickness of the myocardium result of complete occlusion STEMI 2. SUBENDOCARDIAL involves a small area in the subendocardial wall of lv , ventricular septum or papillary muscles NSTEMI

12. CLINICAL FEATURES H/O - chest discomfort/ pain ,with radiating to the arm, jaw or neck (20min) ,Nausea, diaphoresis , shortness of breath SILENT MI - atypical features like fatigue, weakness vague discomfort, epigastric pain , palpitations —----> women + DM , worse prognosis since its often missed PHYSICAL EXAMINATION CVS - tachy/brady arrhythmias(IWMI) , hypo/<<<hypertension ( sympathetic activation) , S3 gallop+ - papillary muscle dysfunction/ MR/VSD S3 gallop +/- rales = LV dysfunction,LHF Raised JVP + peripheral edema + hepatojugualr reflex = RHF RS - rales , hypoxia, GI - nausea and vomiting, Skin - cool clammy, diaphoretic, pale appearance Decreased Urine o/p

13. DD of acute chest pain

14. Dr.Willem Einthoven

15. INVESTIGATIONS - ELECTROCARDIOGRAPHY ST Elevation MI STEMI - New STEMI at J point at 2 contiguous leads with cut points more that 0.1 mV in all leads except V2- V3 For leads V2 - V3 : >/= 0.2mV in men above 40 y , >/= 0.25mV in men <40y , >/= 0.15 in women

16. Evolution of STEMI

17. IWMI - ?RCA/LCX Dominant right coronary artery (RCA) in 80% of cases → medial part of IW Dominant left circumflex artery (LCx) in 18% →lateral part of IW ?RV infarction .. to do a right sided ecg … RCA occlusion is suggested by: ST elevation in lead III > lead II Presence of reciprocal ST depression in lead I Signs of right ventricular infarction : STE in V1 and V4R Circumflex occlusion is suggested by: ST elevation in lead II = lead III Absence of reciprocal ST depression in lead I Signs of lateral infarction: ST elevation in the lateral leads I and aVL or V5-6 Changes in Rx plan if RV infarction is present In RCA occlusion if hypotension ++ , fluids can be given , to increase venous return In LCX infarction fluids will lead to pulmonary edema

18. STEMI EQUIVALENTS De Winter’s sign New onset LBBB Hyperacute t waves Wellen’s syndrome Posterior wall MI South african flag sign

19. De Winter’s sign De Winter’s sign is a sign of an occlusion of the left anterior descending artery, and should be viewed as an equivalent to an anterior STEMI. The ECG findings of De Winter’s sign are: Upsloping ST depression greater than 1mm in the precordial leads Prominent, tall, and symmetrical T waves in the precordial leads Absence of ST elevation in the precordial leads Reciprocal ST elevation of 0.5mm-1mm in AVR

20. Hyperacute T waves first ischemic changes in a STEMI Asymmetrical, increase in the height and width of the T wave

21. LEFT BUNDLE BRANCH BLOCK ( new onset)

22. WELLENS’ SYNDROME highly specific sign for a critically stenotic proximal (LAD) artery causing partial reperfusion NO ECG CHANGES AT THE TIME OF PAIN refers to the presence of deeply inverted or biphasic T waves in V2–V3. Little or no rise in biomarkers However, they are at extremely high risk for extensive AWMI within the next few days to weeks. Needs immediate intervention

23. Posterior wall MI Posterior MI is suggested by the following changes in V1-3: Horizontal ST depression Tall, broad R waves (>30ms) Upright T waves Dominant R wave (R/S ratio > 1) in V2

24. South African flag sign - 1st diagonal branch of LAD stenosis

25. OCCLUSION MI Occlusion Myocardial Infarction (OMI): A branch of the ACS algorithm representing near or total occlusion with insufficient collateral circulation causing active infarction. STEMI plus STEMI-equivalent patterns. Type of AC resulting in total occlusion or near-occlusion of the infarct-related vessel, with insufficient collateral circulation, such that full-thickness infarction will occur unless flow is restored immediately. Non-Occlusion Myocardial Infarction (NOMI) : is any MI that does not satisfy the description of occlusion MI above. ECG patterns are usually reflective of subendocardial ischemia. Patients with OMI are those that benefit from emergent reperfusion therapy What’s wrong with the STEMI label? Patients with acute occlusion not meeting STEMI criteria may be an underserved, underidentified subgroup of ACS patients who would benefit from emergent intervention, whereby classification of AMI by occlusion vs. no occlusion may be more appropriate than classification by ST elevation on the ECG. The STEMI/NSTEMI paradigm is not a reliable tool for diagnosing occlusion MI Eg: IWMI, New Bifascicular block , small hyperacute waves, isolated posterior MI , Diffuse ST Depression with coexistent ST elevation in aVR

26. NEW BIFASCICULAR BLOCK RBBB + LAFB, and a segment of STE in lead V2, all concerning for a proximal LAD occlusion RBBB:- LAFB:- QRS duration > 120ms Left axis deviation (usually -45 to -90 degrees) RSR’ pattern in V1-3 (“M-shaped” QRS complex) qR complexes in leads I, aVL Wide, slurred S wave in lateral leads (I, aVL, V5-6) rS complexes in leads II, III, aVF Prolonged R wave peak time in aVL > 45ms

27. Diffuse ST dep with coexistent STE in aVR Multi-lead ST depression with coexistent ST elevation in lead aVR has been described in patients with left main or proximal LAD insufficiency causing severe ischaemia. Urgent, rather than emergent, catheterisation following medical therapy appears to be optimal management for this Non-Occlusion Myocardial Infarction (NOMI). aVR, the neglected lead

28. DDs of STEMI E - electrolyte , <<K L - LBBB E - Early repolarisation pattern ( benign) V - Ventricular Hypertrophy A - Aneurysm of ventricle (LV) T - Takotsubo disease I - infarction of myocardium O - Osborn waves in hypothermia N - Non atherosclerotic vasospasm ( Prinzmetal’s angina)

29. NSTEMI - New horizontal or down-sloping ST depression ≥0.5 mm in two anatomically contiguous leads or T inversion 1 mm in two anatomically contiguous leads with prominent R wave or R/S ratio >1. NO STE BUT CARDIAC MARKERS +++

30. Cardiac markers TROPONIN ( contractile protein ) , sensitive to cardiac necrosis Trop I —> only in cardia , more specific, 4-6 h after damage and peaks at 18 h, serially taken , stays for 7-10 days Trop false positives - sepsis, ckd, aki, VT, VF , pericarditis, heart failure Trop T → cardia+skeletal muscle , <<< kidney/skeletal muscle damage , 3-4 h after damage and peaks at 24h CREATINE PHOSPHOKINASE ( CK-MB) —> Highly specific , 4-6 h after damage peaks at 24 h (CKMB: TOTAL CK >> 2.5 = MI ) , stays for 3 days , more specific for reinfarcts LDH – > LDH 1> LDH 2, indicator of MI MYOGLOBIN —> low sensitivity , 1-4 h rise, 6-12 h peaks

31. 2d ECHO LV Failure Regional wall motion abnormalities Aneurysm /clots Any ruptures ( LV, septal) MR/AR and other valvular lesions

32. MANAGEMENT AIM: RPT in all pts with symptoms of <12h duration and persistent STEMI /new LBBB Door to needle <30min Needle to balloon inflation < 90min ABC O2 , if hypoxic ( target 94%) Pain relief —> SL Nitrate : 10 mg ,can be repeated 3 times max IV NTG : if not better with SLN , 6ml /h of 25mg GTN in 250ml dextrose and titrated according to symptoms. Contraindicated in hypotension, RCA- IWMI, drugs like sildenafil, HOCM, severe aortic stenosis Fentanyl: 50-100u IV in 100ml NS Inj.Morphine : 5-10mg IV with an antiemetic ( watch for brady) Inj PCT 1gm IV

33. Antiplatelets, statins and anticoagulants Aspirin : P2Y12 receptor blocker , 325mg PO Prasugrel/Clopidogrel/Ticagrelol : ADR antagonist /P2Y12 receptor blocker Clopidogrel ,given before fibrinolysis , 300mg Stat PO , also given in pts with true Asp allergy Prasugrel- given before PCI , 60mg PO stat f/b 10mg PO Ticagrelol - given before PCI , 180mg PO stat Asp +Clop 150/75 mg/day to be continued indefinitely GLYCOPROTEIN IIB/IIIA Inhibitors - tirofiban, Eptifibatide

34. Atorvastatin 80 mg PO stat Betablockers : tab.metoprolol 25 PO/Labetolol , to reduce myocardiam O2 demand by reducing HR , to be avoided in asthma, hypotension ,brady, drug use, possibility of coronary artery vasoconstriction Unfractioned Heparin 5,000 U IV stat and q6h , best when +Aspirin, when PCI delayed Enoxaparin 1 mg/kg SC (LMWH) stat and q12h. Fondaparinux ++ ,Factor Xa inhibitor 2.5mg SC OD (needs renal adjustment., not given for pts going for pCI due to catheter thrombosis) , can be given in NSTEMI

35. Thrombolysis Ideally, door to needle time <30m When PCI cant be done , thrombolysis is choice MOA: act on acute thrombus as plasminogen activators . They are inactive proteolytic enzyme which binds to fibrin in a thrombus to form a plasminogen- fibrin complex—> lysis Improves LV function Only used STEMI Contraindications : head injury, recent stroke, tumors, GI bleeds, coagulopathy, severe HTN, aortic dissection, pericarditis , pregnancy, low GCS, active P. ULCER , prolonged PT/INR

36. Reperfusion arrhythmias ? Good prognostic sign After thrombolysis, flow is initiated and myocardium distal to the clot starts receiving blood supply which can cause conduction irritation This results in accelerated idioventricular rhythm ( AIVR)/ slow VT HR :100-150bpm Short runs of accelerated rhythm seen Rx in ischemia related VT : usually selflimiting , Lignocaine/Amiodarone

37. Interventions Primary Percutaneous Coronary Intervention (PCI) 50% reduction in death risk and recurrent infarction done in pts with STEMI and ischemic sym <90-120m Stenting with drug eluting stent or bare metal stent Helps in opening up the infarct increases the size of the arterial lumen through endothelial denudation; cracking, splitting, and disruption of atheroscler otic plaque Antiplatelets and anticoagulants to be given before pci Coronary Bypass graft surgery ( CABG) When >/= 2 arteries are occluded / PCI fails

38. Determining mortality TIMI Risk Score :can predict in hospital mortality and identifies a group of high-risk patients who might develop adverse events.

39. GRACE SCORE:

40. COMPLICATIONS Complications of MI include arrhythmic, mechanical, and inflammatory (early pericarditis and post-MI syndrome) sequelae, and left ventricular mural thrombus (LVMT) . In addition to these broad categories, right ventricular (RV) infarction and cardiogenic shock are other possible complications of acute MI. these complications should be expeditiously clinically recognized and treated to prevent mortality and morbidity.

41. Complication Manifestation Timeline Arrhythmic Heart blocks, atrial and ventricular arrhythmias 1 to 3 days Ischemic Reinfarction, peri-infarct ischemia, infarct extension Most common in the initial few days Mechanical Mitral valve and chordae rupture/tear, ventricular septal defect (VSD), ventricular free wall rupture, tamponade, aneurysm Usually first week to first month Inflammatory Pericarditis, post-myocardial infarction (MI) Dressler syndrome First week to months (Dressler syndrome typically manifests days to weeks later) Systemic Cardiogenic shock, heart failure, embolic cerebrovascular accident, MI, and systemic and lower extremity embolism Within 24 hours.

42. References Tintinalli’s emergency medicine manual 9th edition Oxford handbook of emergency medicine ecgwaves.com AECTM emergency medicine channel Manipal manual of emergency medicine handbook American heart association journal Medscape https://drive.google.com/file/d/1OnPIiSryULB6CgoS9lIroWnrfriPiZ3h/view?usp=drive_link

43. THANK YOU