Acute coronary syndrome. myocaridal infraction,heart attack.pptx

Acute coronary syndrome. myocaridal infraction,heart attack. introduction,diagnosis and managements from new guideline and standard text book of emergency medicine

1. DR PANKAJ PARMAR JR2 EMERGENCY MEDICINE DEPARTMENT ACUTE CORONARY SYNDROME

2. Exam Que. 11. A 68 year old male presents to ED with chest pain. His ECG shows ST- segment elevation in V2-V6. a) Enumerate causes of ST segment elevation b) How will you manage this patient in the ED? c) Discuss HEART score and TIMI score in a patient with chest pain. d) How will you decide between percutaneous coronary intervention and fibrinolytic therapy?

3. CASE :- A 51-year-old diabetic male came in the emergency department with chest pain that radiated to his left hand and was associated with diaphoresis and dizziness for 2 hours, He went to a nearby hospital where ECG was done and primary treatment was given. Primary survey- A irway patent, RR- 18/MIN., SPO2- 97 ON RA, PULSE-78/MIN, BP134/78mmhg, temp. afeb . Rbs 202 mg/dl, GCS-15/15 Secondary survey - HEENT- normal, S1S2 heard, B/L air entry equal , conscious , NO P/I/LN/E

4. ECG- RATE- 60/MIN, RHTYM- REGULAR ST ELEVATION – 2/3/ aVF D/D? - INFERIOR WALL MI

5. Importance of Chest Pain in Emergency Medicine Chest pain is one of the most common and high-risk complaints in the emergency department (ED). The primary goal is to rapidly differentiate life-threatening from benign conditions. Misdiagnosis or delayed treatment can lead to severe morbidity or mortality.

6. MYOCARDIAL INFRACTION – blood circulation of heart

7. Type of ACS Unstable Angina (UA) → No troponin rise, no ST elevation NSTEMI → Troponin ↑, no ST elevation STEMI → ST elevation + troponin rise Pathophysiology of ACS Atherosclerotic plaque rupture → platelet aggregation → thrombus → partial or complete occlusion of coronary artery → myocardial ischemia/infarction

8. Differential diagnosis of chest pain 2. Life-Threatening Causes of Chest Pain (Mnemonic: " ThE Big 6") Acute Coronary Syndrome (ACS) → Myocardial infarction (MI), Unstable Angina Aortic Dissection → Sudden onset tearing pain, radiates to back Pulmonary Embolism (PE) → Sudden dyspnea , pleuritic pain Pneumothorax (Tension/Spontaneous) → Sudden sharp pain, decreased breath sounds Pericarditis with Tamponade → Pulsus paradoxus, hypotension, muffled heart sounds Esophageal Rupture (Boerhaave Syndrome) → Severe vomiting, mediastinitis, subcutaneous emphysema

9. Signs and symptoms- Classic cardiac chest pain is retrosternal left anterior chest crushing, squeezing, tightness, or pressure. ACS presentations include radiation of the pain to the arms, neck, or jaw; diaphoresis; dyspnea; and nausea or vomiting. Nonclassic presentations are common and include chest pain lasting for seconds , constant pains lasting for 12 to 24 hours or more without waxing and waning intensity, or pain worsened by specific body movements or positions Risk Factors- >40 years old, male or postmenopausal female, hypertension, tobacco use, hypercholesterolemia, diabetes, truncal obesity, family history, and a sedentary lifestyle

10. Initial ED Approach to Chest Pain (Algorithm-Based) Primary Survey (ABCDE) → Ensure airway, breathing, and circulation History (OPQRST, Risk Factors) Onset: Sudden vs. gradual Provocation: Exertion, rest, deep breathing Quality: Sharp, crushing, tearing Radiation: Back, jaw, left arm Severity: 1-10 scale Time: Duration, intermittent vs. constant Risk Factors: CAD, smoking, HTN, diabetes, previous MI Echocardiogram → Pericardial effusion, tamponade Physical Exam Findings Levine’s sign (clenched fist over chest) → ACS Unequal BP in arms → Aortic dissection JVD + muffled heart sounds + hypotension → Cardiac tamponade Clear lungs + hypotension → Massive PE Initial Workup ECG → Immediate for ST-segment changes (STEMI, NSTEMI) Cardiac Biomarkers (Troponin I/T, CK-MB) CXR → Pneumothorax, aortic dissection D-dimer → If PE suspected (Wells’ criteria)

11. Causes of ST-Segment Elevation Non-Cardiac Causes: Pulmonary Embolism (Massive PE) – May cause ST-segment elevation due to right heart strain. Hyperkalemia – Pseudo-ST elevation with peaked T waves. Subarachnoid Hemorrhage (SAH) – Global ST-segment changes due to catecholamine surge. Takotsubo Cardiomyopathy – Stress-induced cardiomyopathy mimicking STEMI. ST-segment elevation is commonly associated with Acute Myocardial Infarction (STEMI) but can also occur in other conditions: Cardiac Causes: Acute STEMI – Most common cause, localized to a vascular territory. Pericarditis – Diffuse ST elevation without reciprocal changes, PR depression. Left Ventricular Aneurysm – Persistent ST elevation weeks after infarction. Prinzmetal’s (Variant) Angina – ST elevation due to coronary vasospasm, transient. Brugada Syndrome – ST elevation in V1-V3 with RBBB pattern, risk of sudden cardiac death. Early Repolarization – Benign ST elevations in young individuals, with J-point notching.

12. ECG shows ST-segment elevation in limb leads II, III (inferior), and aVF , as well as lead V 6 (lateral). ST-segment depression is evident in leads V 1 , V 2 , and V 3 , reflecting reciprocal changes in the anterior leads. The patient was found to have 100% occlusion of the left circumflex coronary artery at cardiac catheterization.

13. elevation in aVR greater than that of V 1 suggesting left anterior descending artery occlusion

14. ECG showing anterior myocardial infarction . ECG shows ST-segment elevation in V1, V2, and V3, with the absence of ST-segment depression in leads II, III, and aVF . The patient was found to have 100% occlusion of the distal left anterior descending coronary artery at cardiac catheterization.

15. Wellen’s sign D e Winter ST-T–wave complex (upsloping of ST segment with overall ST depression)

16. Score HEART (for chest pain stratification) TIMI Score (Risk Assessment in ACS/UA/NSTEMI) guide risk assessment. H istory: Highly suspicious (2), Moderate (1), Low (0). E CG: ST deviation (2), Nonspecific changes (1), Normal (0). A ge: >65 (2), 45-65 (1), <45 (0). R isk Factors: ≥3 risk factors or CAD (2), 1–2 risk factors (1), None (0). T roponin: >3x normal (2), 1–3x normal (1), Normal (0). Age ≥65 years ≥3 risk factors for CAD (HTN, DM, smoking, FHx , hyperlipidemia ) Known CAD (prior stenosis >50%) Aspirin use in the last 7 days Severe angina (≥2 episodes in 24 hours) ST deviation ≥0.5mm Elevated cardiac markers (Troponin, CK-MB) TIMI 0–2: Low risk (≤5% event rate) TIMI 3–4: Intermediate risk (13–20% event rate) TIMI 5–7: High risk (>40% event rate) HEART Score ≥4 – Higher risk, consider admission. HEART Score <3 – Low risk, early discharge possible.

17. Treatment of STEMI

18. Management in the Emergency Department (ED) MONA-BASH protocol. 3. Reperfusion Strategy Primary Percutaneous Coronary Intervention (PCI): If available within 90 minutes . Fibrinolytic Therapy (tPA, Tenecteplase, Streptokinase): If PCI unavailable within 120 minutes . 4. Monitoring & Additional Measures Serial ECGs & Cardiac Markers – Monitor progression. Echocardiography – Evaluate ventricular function and complications. Complication Management – Shock, arrhythmias, heart failure. 1. Immediate Stabilization Airway, Breathing, Circulation (ABCs) – Ensure hemodynamic stability. Continuous Cardiac Monitoring – Detect arrhythmias or deterioration. IV Access & Blood Work – Obtain cardiac biomarkers, CBC, electrolytes, coagulation profile. 2. Pharmacologic Therapy Aspirin (162-325 mg chewed) – First-line antiplatelet therapy. P2Y12 Inhibitor (Clopidogrel, Prasugrel, or Ticagrelor) – Dual antiplatelet therapy. Anticoagulation (UFH or LMWH) – Prevent further thrombus formation. Nitroglycerin – Symptom relief (avoid in hypotension, RV infarct). Morphine – For persistent pain after nitrates. Beta-Blockers – If no contraindications (e.g., shock, severe bradycardia). High-Intensity Statins (Atorvastatin 80 mg) – Reduce future cardiovascular risk.

19. Cardiac biomarker C. Troponin B-type natriuretic peptite Other – ckmb , ischemia-modified albumin , interleukin-6, vascular cell adhesion molecule, intercellular adhesion molecule , E-selectin, P-selectin, pregnancy-associated plasma protein A, myeloperoxidase, copeptin, and heart-type fatty acid binding protein. Current evidence does not support the use of these novel biomarkers for ED chest pain evaluations.

20. Antiplatelet Agents Aspirin 162–325 milligrams Clopidogrel Loading dose of 600 milligrams PO followed by 75 mg PO daily. No loading dose is administered in patients >75 y old receiving fibrinolytics Prasugrel Loading dose of 60 milligrams promptly and no more than 1 h after PCI once coronary anatomy is defined and a decision is made to proceed with PCI Ticagrelor Loading dose is 180 milligrams PO followed by 90 milligrams twice a day Antithrombins Unfractionated heparin Bolus of 60 units/kg (maximum, 4000 units) followed by infusion of 12 units/kg/h (maximum, 1000 units/h) titrated to a partial thromboplastin time 1.5–2.5 × control Enoxaparin 30 milligrams IV bolus followed by 1 milligram/kg SC every 12 h Fondaparinux 2.5 milligrams SC* Fibrinolytic Agents Streptokinase 1.5 million units over 60 min Anistreplase 30 units IV over 2–5 min Alteplase Body weight >67 kg: 15 milligrams initial IV bolus; 50 milligrams infused over next 30 min; 35 milligrams infused over next 60 min Body weight <67 kg: 15 milligrams initial IV bolus; 0.75 milligram/kg infused over next 30 min; 0.5 milligram/kg infused over next 60 min Reteplase 10 units IV over 2 min followed by 10 units IV bolus 30 min later

21. Tenecteplase Weight Dose (total dose not to exceed 50 milligrams) <60 kg 30 milligrams ≥60 but <70 kg 35 milligrams ≥70 but <80 kg 40 milligrams ≥80 but <90 kg 45 milligrams ≥90 kg 50 milligrams

22. Decision Between PCI and Fibrinolysis Criteria Primary PCI Fibrinolysis (tPA, Tenecteplase) Time Window <90 minutes from first medical contact If PCI not available within 120 min Efficacy Superior (↓ mortality, ↓ stroke risk) Slightly higher bleeding risk Contraindications Limited Many (recent stroke, active bleeding, intracranial hemorrhage, severe hypertension) Preferred In High-risk patients, cardiogenic shock, late presentation Remote areas, delay in PCI PCI is preferred whenever available. Fibrinolysis is used when PCI is unavailable within 120 minutes or in remote settings

23. COMPLICATIONS OF ACUTE CORONARY SYNDROME DYSRHYTHMIAS AND CONDUCTION DISTURBANCES B rady - sinus> 1 st degree block> 2&3 rd T achy – sinus> VPC>APC>AF HEART FAILURE MECHANICAL COMPLICATIONS Rupture of the interventricular septum Ventricular free wall rupture Papillary muscle rupture PERICARDITIS RIGHT VENTRICULAR INFARCTION RECURRENT OR REFRACTORY ISCHEMIA

24. Contraindications to Fibrinolytic Therapy in ST-Segment Elevation Myocardial Infarction Absolute contraindications • Any prior intracranial hemorrhage • Known structural cerebral vascular lesion (e.g., arteriovenous malformation) • Known intracranial neoplasm • Ischemic stroke within 3 mo • Active internal bleeding (excluding menses) • Suspected aortic dissection or pericarditis Relative contraindications • Severe uncontrolled blood pressure (>180/100 mm Hg) • History of chronic, severe, poorly controlled hypertension • History of prior ischemic stroke >3 mo or known intracranial pathology not covered in contraindications • Current use of anticoagulants with known INR >2–3; no evidence with direct oral anticoagulants available as of this writing, but safety data can be extracted from stroke studies with recombinant tissue plasminogen activator and direct oral anticoagulants • Known bleeding diathesis • Recent trauma (past 2 wk ) • Prolonged CPR (>10 min) • Major surgery (<3 wk ) • Noncompressible vascular punctures (including subclavian and internal jugular central lines) • Recent internal bleeding (within 2–4 wk ) • Patients treated previously with streptokinase should not receive streptokinase a second time • Pregnancy • Active peptic ulcer disease • Other medical conditions likely to increase risk of bleeding (e.g., diabetic retinopathy

25. THANK YOU