1. Myocardial Infarction Angina Pectoris What is an MI?

2. Myocardial Infarction What causes an MI? Blood flow is abruptly and severely deprived of oxygen.

3. MI Circumstances that decrease the supply of blood flow/oxygen to the heart….

4. MI Circumstances that increase the demand for oxygen (MV02) by the myocardium….

5. MI Is angina and MI the same thing? Is it managed the same?

6. MI Angina Pectoris Angina Pectoris is temporary chest pain. No permanent damage is done to the myocardium.

7. MI Why does pain occur when there is a deficit of blood and therefore oxygen to the myocardium?

8. MI Stable Angina Stable Angina: is usually prompted by something (exertion, stress) and is relieved with rest, nitroglycerine, and pharmacologic therapy taken prophylactically.

9. MI What meds did you talk about in pharm could be taken to address this problem?

10. MI Unstable angina Unstable angina : can occur at rest, or while sleeping and is unrelieved with intervention. Requires prompt treatment!

11. MI Prinzmetal’s angina Prinzmetal’s angina : is associated with coronary vasospasm. May be relieved by exercise or spontaneously.

12. MI – Prinzmetals angina What type of pharmacologic therapy do you think is appropriate for a patient with this type of angina?

13. MI Silent Ischemia = Asymptomatic What type of patient(s) that we studied are likely to experience silent ischemia? Why?

14. MI The degree of altered function depends on the area of the heart involved, and the size of the infarct. The occlusion of which vessel do you think is associated with poor left ventricular ejection?

17. MI Why do you think that younger people who suffer MIs with the same degree of occlusion as their older counterparts suffer more serious cardiac debilitation?

19. MI- Definitions Transmural MI- the entire thickness of the myocardium in a region is involved. Subendocardial MI- the damage has not penetrated through the entire thickness of the myocardial wall.

21. MI -Location The location of the infarct correlates with the part of the coronary circulation involved. Inferior wall MI- right coronary artery Anterior wall MI- left anterior descending artery Lateral/Posterior/Inferior MI- left circumflex artery

23. MI- Signs and Symptoms Chest pain P-- precipitating event Q-- quality of pain or discomfort R-- radiation of pain S-- severity of pain –T-- Time

24. MI-Signs and Symptoms Abdominal pain Nausea SOB/dyspnea Anxiety, weakness, fatique Palpitations, diaphoresis, pallor

25. Women and MI symptoms In a multi-center study of 515 women who had an acute myocardial infarction (MI), the most frequently reported symptoms were unusual fatigue, sleep disturbances, shortness of breath, indigestion and anxiety.

28. MI- Management Keep calm Give 02 ECG IV Pain control Labs..CK-MB, Troponin, Mypglobin, WBC

29. Cardiac Markers Troponin T and I- Have a wider diagnostic time frame than CK-MB (myocardial muscle protein released when there is injury to myo muscle.) Creatine Kinase MB-peaks after 24 h (enzyme specific to cardiac muscle) Myoglobin- Not specific but pekas in 2 hours

30. Others- associated risk CRP-Detects inflammation. Found that it was elevated in MI pts Homocysteine- An amino acid found to be elevated in MI pts. Both of these are used as detectors of MI to find who is a high risk pts. Used for primary prevention.

33. MI -Management Antithrombotic therapy o ASA o Heparin o Thrombolytics

34. MI-Management Anti-ischemic therapy- nitrates beta-blockers

35. MI Management Nitrates: Nitroglycerine Primarily affect venous blood flow. Dilate large coronary arteries. Prevents Vasospasm. Increases coronary collateral blood flow.

36. MI Management - nitro Therefore, what happens to myocardial O2 supply?

37. Nitroglycerine By causing venodilation, the nitrates bring about a decrease in venous return, and therefore lower preload. (LVEDV). There is decreased pressure in the ventricle, resulting in decreased workload on the heart

38. MI Management - nitro Therefore, what happens to myocardial O2 demand?

39. MI- Management Anti-ischemic therapy Beta adrenergic blocking agents compete with epinephrine and norepinephrine at the receptor sites located throughout the body.

40. MI- Management- beta blockers When these beta blocker drugs block the B1 receptors on the surface of the heart: Heart rate is decreased Conduction through the AV node is slowed Myocardial contractility is decreased

41. MI- Management- beta blockers Therefore, what do you thing happens to myocardial O2 consumption?

42. Catecholamine- s/p MI What effect would catecholamine release have on myocardial O2 consumption? Why is consumption critical to reduce s/p MI?

43. MI- Complications 1.Dysrhythmias: Why? What to do? 2.Cardiogenic Shock: Why? What to do 3.Heart Failure/Cardiogenic pulmonary edema: Why? What will you see? What to do? 4.Pulmonary embolism: Why after an MI?(afib) What to do? 5.Recurrent MI: Why? What to do?

45. EKG changes