Acute Coronary Syndrome

1. Acute Coronary Syndrome APS Fleming College

2. What is an ACS? A sudden event during which the myocardium suffers from a relative or a complete lack of perfusion Covers the continuum between angina and MI This is reflected in: • Signs and symptoms • Electrocardiographic changes • Biochemical changes

3. Symptoms of ACS • Pressure • Burning (hot) • Chest/arms/jaw/back Pain Sympathetic response Parasympathetic response Inflammatory response Other • Sweats • Tachycardia • Cool, clammy skin • Nausea • Vomiting • Weak • Mild fever • Dyspnea • Asymptomatic

4. Physical Findings • Inspection BP - often increase anterior MI - often decrease inferior MI HR - often increase anterior MI - often decrease inferior MI RA po - increase in RV MI

5. Stable CAD Acute Coronary Syndromes Unstable angina Non-ST Elevation MI (Non-Q-wave MI) ST-Elevation MI (Q-wave MI) The continuum of acute coronary syndromes ranges from unstable angina, through non-ST-elevation myocardial infarction (also referred to as “non-Q-wave” myocardial infarction [MI]), to ST-elevation MI (also referred to as “Q-wave” MI).

7. Platelets & ACS • Platelets become activated by various stimuli • Binds to fibrinogen and serves to cross-link and aggregate platelets • Platelet plug becomes the centre of a larger thrombus

8. Triggers to Plaque Rupture Inflammatory cytokines Plaque Rupture Vulnerable Plaque Emotional Stress Physical Stress

9. Extent of Myocardial Injury Determined by: • muscle mass perfused by vessel • Magnitude/Duration of flow • Oxygen demand of affected tissue • Adequacy of collaterals • Tissue response to ischemia

10. Preventing ACS / Reducing Infarct Size • Primary prevention -lifestyle • Stabilizing plaque • Preventing platelet aggregation • Decreasing preload and afterload • Decreasing cardiac workload • Reperfusion • Treating arrhythmia Which ones do you as medics do??

11. Pathophysiology of ACS Myocardial ischemia >>> infarction • Plaque formation with narrowing of coronary artery lumen • Plaque rupture • Thrombus formation with platelet activation and aggregation • Ischemia in downstream territory with reversible cell injury • Myocardial cell death

12. Cardiovascular Pathology • Angina • Unstable angina • Myocardial Infarction • Congestive heart failure • Valvular dysfunction • Cardiogenic shock • Aneurysms • Deep vein thrombosis/arterial occlusion

13. Ischemic Chest Pain • Good history and physical exam • 3 & 12/15lead ECG • OPQRST to guide history investigation • Differential diagnosis Chapter 27 27.24-27.36

14. OPQRST • Onset - when did it start? • Provoked - at rest, exertion, better or worse? • Quality - sharp, dull, ache, heaviness? • Radiating - to shoulder, back, jaw? • Severity - on a scale of 1-10? • Time - does it come and go?

15. Myocardial Ischemia • Blood supply and demand • Causes of ischemia • HR – too slow or too fast • vasospasm (Prinzmetals) • coronary artery occlusion • narrowing of coronary arteries • low blood pressure • hypoxemia

16. Coronary Artery Disease • Poor dietary habits • Imbalance between good cholesterol (HDL) and bad cholesterol (LDL) • Atherosclerosis

17. That’s why there are angiograms!

18. myocardial ischemia angina unstable angina myocardial infarction Decreased perfusion Supply and demand CP pattern changes or complicated Total occlusion and necrosis Angina or MI??

19. Consequences ofCoronary Thrombosis Lilly. Pathophysiology of Heart Disease, 4th Ed. Lippincott Williams, 2007. Page 173

20. The Importance of History • Someone with angina knows their typical pattern • In addition to OPQRST, take an AMPLE history • “are you SOB?” • Similar pain? • MI in past? Is this pain similar? • Other cardiac Hx? e.g. CABG, angioplasty ,stress testing, hospitalizations etc.

21. Angina • Lasts less than 30 minutes • Heaviness, dull, tight or even sharp pain • Can radiate but less common • Usually on exertion and dissipates with rest • Temporary drop in coronary artery blood flow • Rule out rate related problems

22. Angina Management • Rest/relaxation (Be calm!) • O2 therapy • IV access ? • ASA 160mg chewed & swallowed • Vitals • Nitroglycerin 0.4mg SL q 5 min. if SBP >100 and HR > 60 but less than 160 bpm • HR and blood pressure parameters…why?

23. Hemodynamic Parameters • SBP < 100 • preload reduction - vasodilation • decreased coronary perfusion • HR < 60 bpm or > 160 bpm • rate related ischemia?

24. Ischemic Chest Pain • Nitroglycerin 0.4mg SL, q 5 min. PRN • Assess VS after each dose • d/c if SBP <100 or SBP drops by 1/3 • d/c if HR <60 or >160 bpm • ASA 160mg chewable tablets • Morphine Sulphate 2mg IV, q 5 min. x 3 PRN

25. Unstable Angina • Indicates a progression towards serious myocardial disease • 5 Indicators of Unstable Angina • new angina pain • change in the duration • change in Rx (e.g increased NTG use) • onset at rest • change in quality (e.g now radiates)

26. Acute Myocardial Infarction Definition: Necrosis of heart muscle due to absolute or relative lack of blood supply to the myocardium. The site of infarction is determined by the location of the arterial occlusion.

27. Myocardial Infarction • Killing of myocardial tissue • Conventional treatment will only save ischemic zone • Thrombolytics Necrotic zone Ischemic zone

28. Presentation of Myocardial Infarction • Varies widely from patient to patient • Typical vs. Atypical (e.g.. weakness or SOB) • The elderly, alcoholics, and women • CP unresolved with rest or NTG • 12 Lead shows acute ST elevation, Flipped T waves or Q waves (old)

29. Electrocardiographic Changes • Change in rate and rhythm • Most often sinus with: • No discernible change • Hyper-acute T-waves • T wave flattening or inversion • ST segments up or down • Q waves

30. ECG Changes

31. Biochemical Markers of ACS • Enzymes which are unique to cardiac myocytes • Released into the circulation by dead cells • Thus a rise in these indicates that myocardium has suffered damage

32. Biochemical Markers • Troponin (remember its role in actin/myosin binding??) • CPK (Creatine Phosphokinase) • Specifically one isoenzyme -MB band • LDH (Lactose dehydrogenase) • AST Hospital staff will draw blood for these tests early but do NOT generally help in the decision making

33. Cardiac Markers • Myoglobin is found in cardiac and skeletal muscle • Very sensitive if measured early • Not specific • Not often used

34. Use of Nitrates in ACS • Nitrates, typically nitroglycerin • Nitrous Oxide acts as a smooth muscle relaxant leading to vasodilatation • Transdermally, sublingually and/or parenterally

35. Benefits of Nitrates • Reduce preload and afterload • Dilate coronary arteries • Assists coronary perfusion

36. Disadvantages of Nitrates • Not useful in patients who are reperfused • May cause hypotension • Severe hypotension in patients with RV dysfunction • May cause hypotension in inferior MI • 30% have RV involvement-check!!!

37. b-blockers Multi-purpose in the setting of ACS • Anti-arrhythmic • Anti-ischemic • Anti-hypertensive

38. b-blockers Decrease myocardial oxygen demand • Decreased heart rate – increases diastole • Decreased myocardial contractility • Decreased MAP

39. Advantages of b-blockers • Reduction in pain • Decreased morbidity and mortality • Decreased risk of arrhythmia • Decreased infarct size • Decreased risk of re-infarction Treatment with a b-blocker is a standard of care

40. ASA • Anti-inflammatory • prevents the formation of arachidonic acid • A pathway that can be blocked to prevent platelet aggregation • Does not block all platelet activators

41. Other Treatment Modalities in ACS • Heparins (LMWH) • Reperfusion • PCI • Mechanical (the digger!) • Thrombolytic agents • Antiarrhythmic agents

42. Focus of ACS • Common reason for transport • Much can be done during transfer • Reduce risk of morbidity and mortality The first step = recognizing the ACS • Signs and symptoms • ECG changes • Biochemical changes

43. Summary Strategies for reducing morbidity and mortality • Reduce cardiac workload • Improve perfusion to cardiac tissue • Reduce risk of fatal arrhythmias • Reduce extension of clot formation • Reperfuse the ischemic myocardium

44. Myocardial Infarction • ASA (2 x 80 mg) P.O. • O2 therapy • IV access • NTG via SL, transdermal, and/or IV • Morphine (ACP) • Heparin and/or Beta blockers (Hosp) • 12/15 Lead ECG as soon as possible • Angioplasty (hosp) • Thrombolytics if PCI not available or contraindicated

45. PCI Time sensitive

46. Pre-hospital Thrombolysis • Oshawa Land ALS • Northern Ornge Bases • Frequent use • Southern Ornge Bases • Carry it • Positive empirical trends

47. Pre-hospital Thrombolysis • prolonged transport time • no thrombolysis at the sending facility • Long delays

48. Indications - Thrombolysis • Ischemic C.P. • Less than 6 hours duration

49. Ischemic Chest Pain? O - at rest or with exertion P – better or worse Q - heaviness, tightening, sharp, weakness etc R - neck, jaw and/or left arm S - varies T - consistent, does NOT come & go

50. 12 Lead ECG Criteria • ST segment elevation • New onset Left Bundle Branch Block with S&S? • Some acute coronary syndromes (A.C.S.) do not benefit from thrombolysis