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Myocardial infarction. Clinical forms, laboratory and ECG diagnosis. Early signs and complications. Principles of treatment of noncomplicated myocardial infarction • Prof. S.M.Andreychyn Clinical forms of IHD • 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 exertion in angiographically intact vessels (coronary syndrome X). • 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) Classification of IM • 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. Myocardial infarction (MI) • 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. Causes of IHD • • • • • 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 Provocation factors • • • • • • • • • Smoking Dyslipidemia Arterial hypertension Diabetes mellitus Obesity Dietary factors Thrombogenic factors Lack of physical activity Alcohol abuse The accumulation of cholesterol in the vascular wall - atherosclerotic plaque • Schematic of MI: 1 - subendocardial 2 - transmural 3 - subepicardial 4 - intramural 2 Myocardial infarction can be: • • • • Time of occurrence: -primary; -second (after 1 month. following the first); - recurrent (in the range of 72 hours. Before 28 days after the first). Clinical variants of MI • • • • • • Anginous variant Abdominal variant Asthmatic variant Arrythmic cariant Cerebral variant Asymptomatic variant Clinics – main symptom • 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. 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. Pain syndrom Pain syndrom The second severity of symptoms is dyspnea. It may be accompanied by pain or be the only sign of MI. Next complains can be tachycardia, different arrhythmias, high temperature, swelling. Diagnosis of MI: • 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 Wave T • • • • 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 Q • • • • 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. Stages of MI І. Superacute (before the development of necrosis) – clinical pattern of prolonged attack of anginous pain (duration 30 min – 2 hours). Acute stage • ІІ. Acute stage (development of myocardial necrosis) – 2 – 7 days • - pain disappears; • - manifestation of heart failure Subacute period • ІII. Subacute period (initial organization of a scar, displacement of nectoric tissues with connective one) – 3 weeks. Postinfarctional stage • IV. Postinfarctional stage (final organization of a scar), lasts for 3-6 month). ST segment elevation QS wave Display units infarction on ECG • • • • • • I - the front wall of the left ventricle II - intermediate (repeats I or III toward pathology) III - postlateral diaphragmatic or right ventricle aVR - basal parts of the left ventricle aVL - upper lateral departments of left ventricle aVF - diaphragmatic departments or right ventricle • • • • • 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 ECG signs of acute myocardial infarction with Q wave • 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. Blood tests • 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, lowdensity-lipoprotein cholesterol, high-density-lipoprotein cholesterol and triglycerides) within 24 hours. • Blood glucose level. Scheme of coronarography Treatment of MI • • • • • A - Aspirin and Antianginal therapy B - Beta-blocker and Blood pressure C - Cigarette smoking and Cholesterol D - Diet and Diabetes E - Education and Exercise