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Main symptoms and syndromes in ischemic heart disease • Prof. S.M.Andreychyn DEFINITION IHD - synonims – coronary disease, coronary insufficiency – is severe chest pain due to ischemia (a lack of blood and hence oxygen supply) of the heart muscle, generally due to obstruction or spasm of the coronary arteries (the heart's blood vessels). 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) RISK FACTORS Smoking alcohol abuse high arterial pressure Dislipidemia Diabetes mellitus Obesity Excessive consumption of animal fats thrombogenic factors Lack of physical activity 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 Angina pectoris Angina is attack of retrosternal pressing pain or chest dyscomfort which occures in physical load or emotional strain and is caused by myocardial ischemia. Provoking factors: • • • • • physical load; Emotional strain; cold; overeating; smoking; Factors which decrease pain: • Refuse of physical load; • Nitroglycerin/ • Patient try to stay or lie down in attack. Stable angina at exertion • Occurs in the same provoking factors, is often follows with the same complains and changes on ECG. AP functional classes • І FC – attacks occur in a whery high load 1 – 2 times a year. Coronary arteries lumen is narrowed not more than on 50 %. • ІІ FC – attacks occur in walking on the plane surface on the diastance more than 500м, in going more than on 1 floor upstairs 2 – 3 times a week. Coronary arteries lumen is narrowed not more than on 75 %. • ІІІ FC – attacks occur in walking on the plane surface on the diastance 200 – 300 м, in going 1 floor upstairs. Postinfarctional angina. Coronary arteries lumen is narrowed more than on 75%. • ІV FC – attacks occur in walking on the plane surface on the diastance less than on 100 м, in rest. Combination of coronary and myocardial insufficiency. Complete obturation of coronary arteries. Clinical pattern • The major sign of stenocardia is attack-like pain in the area of heart. It has squeezing, cutting or burning character with localization behind a breastbone, irradiates in a left arm (left shoulder-blade, left half of neck, lower jaw, sometimes – in a right shoulder or shoulder-blade). Duration of pain of 5-10 min (more frequently – 2-5 min). Coronary syndrome X • This is a stable angina at exertion when small coronary arteries are affected. • Clinical pattern is the same as for stable angina but coronarography does not show obturation of coronary arteries. Angiospastic angina • Caused by spasm of coronal arteries. Arises up in young persons, mainly at night, in rest, when tone of vagus nerve prevails. Duration of attack till 30 min, during this time ECG shows changes typical for MI (depression of ST segment) which disappear after stopping of attack or application of spasmolysants. Nitrates are uneffective with the purpose of removal of attacks. Unstable angina Acute coronary syndrome • This is a result of myocardial ischemia caused by thrombosis of coronaty artery and its complete occlusion. • The syndrome includes: • 1. Unstable angina pectoris. • Non-Q myocardial infarction. • 3. Q- myocardial infarction. Unstable angina pectoris • At a stenocardia which arose up first, the attacks of pain are observed during 28 days for persons, which did not have clinical signs of stenocardia before. Usually this is angina at exertion. • Progressing angina is the state, at which duration, intensity and frequency of anginal attacks, grow in a dynamics, and the usual dose of medications which take off an attack becomes insufficient, that requires its permanent increase. • Characteristic for progressing stenocardia is pressing pain behind the sternum, which periodically calms down and grows, is not removed by nitrates, is accompanied with swweating, dyspnea, arrhythmia, fear of death. The episodes of attacks of anginal pain become more frequent, and periods between attacks shorten. • Every next attack is heavier, than previous. Nitrates (nitroglycerine, Nitrosorbidum), which removed the attacks of anginal pain before, are uneffective, although a patient uses considerably increased their amount. Associated manifestations • Pain can arise up not obviously due to emotional or physical loading, but also in rest. Sometimes only narcotic facilities remove him. On a background a stenocardia there can be an attack of sharp leftventricular insufficiency with dyspnea, dry cough, bubbling in the chest. Diagnostics of angina pectoris functional tests: • - exposure to cold; • - test with hyperwentilation; tests with dynamic physical load: • а) veloergometry; • б) tredmile test; emotional stress-test; pharmacological tests; • а) test with dityridamole; • б) test with isadrine; • в) test with ergometrine; transesophageat atrial electrostimulation; daily ECG-mpnitoring coronary angiography. Tests with physical load Echocardiography 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