Prof. S.M.Andreychyn

1. Myocardial infarction. Clinical forms, laboratory and ECG diagnosis. Early signs and complications. Principles of treatment of noncomplicatedmyocardial infarction Prof. S.M.Andreychyn

2. 1. Sudden coronary death or heart arrest (HA) • 1.1. HA with following resuscitation. • 1.2. HA with following mortal outcome. • 2. Angina pectoris (AP) • 2.1 Stable angina at exertion. • 2.1.1 Stable angina at exertion( functional class should be determined). • 2.1.2 Stable angina at exertionin angiographically intact vessels (coronary syndrome X). Clinical forms of IHD

3. 2.2. Angiospastic angina (angina in rest, spontaneous, variant, Prinzmetals’ angina) • 2.3. Unstable angina. • 2.3.1. Primary angina. • 2.3.2. Progressive angina. • 3. MYOCARDIAL INFARCTION (МI) • 4. CARDIOSCLEROSIS (postinfarctional, focal and diffuse) • 5. MYOCARDIAL ASCHEMIA WITHOUT PAIN • 6. CARDIAC RRHYTHM DISORDERS (form) • 7. HEART FAILURE (stage, functional class)

4. Acute myocardial infarction with the presence of wave Q (transmural). • Acute myocardial infarction without Q wave. • Acute subendocardial myocardial infarction. • Acute myocardial infarction (undefined). • Recurrent myocardial infarction. • Repeated myocardial infarction. • Acute coronary insufficiency. Classification of IM

5. It is necrosis of area cardiac to the  muscle, that is predefined by an ischemia that arises up sharply as a result of disparity of coronal blood stream  to the requirements of myocardium in oxygen. Myocardial infarction (MI)

6. 85 % - stenotic atherosclerosis of coronary arteries • 10 % - spasm of coronary arteries • 5 % - transitory thrombocytes aggregates • 100 % - combination of these factors • Morbidity in males is 4 times higher than in females Causes of IHD

7. Smoking • Dyslipidemia • Arterial hypertension • Diabetes mellitus • Obesity • Dietary factors • Thrombogenic factors • Lack of physical activity • Alcohol abuse Provocation factors

9. The accumulation of cholesterol in the vascular wall - atherosclerotic plaque

11. Schematic of MI: 1 - subendocardial 2 - transmural 3 - subepicardial 4 - intramural 2

12. Time of occurrence: • -primary; • -second (after 1 month. following the first); • - recurrent (in the range of 72 hours. Before 28 days after the first). Myocardial infarction can be:

13. Anginousvariant • Abdominal variant • Asthmatic variant • Arrythmiccariant • Cerebral variant • Asymptomatic variant Clinical variants of MI

14. Pain pattern simillar to angina pectoris but pain intensity is much more severe that is why nitrates can’t release pain. Pain duration is longer. Clinics – main symptom

15. If patient feels pain, you must ask him about: • 1. The nature of pain. • 2. Localization. • 3. Duration. • 4. Irradiation. • 5. Contact with the physical, emotional stress, movements, breathing, eating, and other factors. • 6. Effect of different drugs on pain.

16. Pain syndrom

17. Pain syndrom

18. The second severity of symptoms is dyspnea. It may be accompanied by pain or be the only sign of MI.

20. Next complains can be tachycardia, different arrhythmias, high temperature, swelling.

21. Typical history and clinical presentation. • Characteristic of ECG changes. • There are three zones on ECG: •    - Zone of ischemia - negative or high T wave; •    - Zone of damage - shift segment S-T; •    - Zone of necrosis – Q wave larger then ¼ R wave Diagnosis of MI:

22. Shows the process of rapid ventricular repolarisation. • Always positive in I - II, aVF, V2 - V6. • In the third, aVL, V1 can be positive or negative. • Duration 0.12 - 0.16 s, amplitude 2.5 - 6mm. Wave T

23. It is excitation interventricular septum. • Duration to 0.03 sec., height does not exceed ¼ wave R. • Sometimes can not register. • Registration Q wave even small amplitude in leads V1 - V3 pathology. Wave Q

24. І. Superacute (before the development of necrosis) – clinical pattern of prolonged attack of anginous pain (duration 30 min – 2 hours). Stages of MI

25. ІІ. Acute stage(development of myocardial necrosis) – 2 – 7 days • - pain disappears; • - manifestation of heart failure Acute stage

26. ІII. Subacute period (initial organization of a scar, displacement of nectoric tissues with connective one) – 3 weeks. Subacute period

27. IV. Postinfarctional stage (final organization of a scar),lasts for 3-6 month). Postinfarctional stage

28. ST segment elevation

29. QS wave

30. I- the front wall of the left ventricle • II - intermediate (repeats I or III toward pathology) • III - postlateraldiaphragmatic or right ventricle • aVR - basal parts of the left ventricle • aVL - upper lateral departments of left ventricle • aVF - diaphragmatic departments or right ventricle Display units infarction on ECG

31. V1 - front wall • V2 - front wall • V3 – partition (septum) • V4 - top • V5 – lower lateral departments of the left ventricle • V6 – lower lateral departments of the left ventricle

32. Anterior MI - presence of Q or QS waves in V1 - V4. • Lower (posterior diaphragmatic) - the presence of Q or QS waves in II, III and aVF leads. • Side - the presence of Q or QS waves in and aVL, V5 - V6. • Posterior - reciprocal ECG changes in V1 - V2 leads. ECG signs of acute myocardial infarction with Q wave

33. Serum troponin I or T levels (or CK-MB if troponin is not available). • Full blood count. • Serum creatinine and electrolyte levels, particularly potassium concentration, as hypokalaemia is associated with an increased risk of arrhythmias, especially ventricular fibrillation (grade B recommendation). • Serum creatinekinase(CK) level. • ALT, AST, LDG levels • Leucocitosis • Serum lipid levels (fasting levels of total cholesterol, low-density-lipoprotein cholesterol, high-density-lipoprotein cholesterol and triglycerides) within 24 hours. • Blood glucose level. Blood tests

34. Scheme of coronarography

35. A - Aspirin and Antianginal therapy • B - Beta-blocker and Blood pressure • C - Cigarette smoking and Cholesterol • D - Diet and Diabetes • E - Education and Exercise Treatment of MI

38. Thank you!