Acute Myocardial Infarct Dr. Lenka Katila Kemi-Tornio Polytechnic school Health care institute Objectives: 1. Etiology 2. Incidence 3. Path physiology 4. Symptomathology 5. Diagnose 6. Therapy 7. Complications 8. Prevention 9. Control questions 1. Etiology See arteriosclerosis 2. Incidence 375/100 000 inhabitants 30 000 AMI / year Sweden AMI – 2,5% of all health care visits for men and 1,2% for women Mortality: 1960…30-40%, 2000…15% 6500 pat. Dies outside of the hospital because of AIM in Sweden 3. Path physiology Insufficient perfusion of the myocardial muscle is causing a necrosis – death of the cells. This happens principally because of ? Thromboses of the artery: Endotel damage >>>>activation of the coagulation process>>>contractile substances>>>>spasms>>>complete occlusion of the artery>>>> all the muscles distal of the occlusion is damaged -, mostly in whole wall – TRANSMURAL INFARCT ? a. Slow process – collaterals – compensational mechanism b. Quick process – no collaterals – no chance to compensate ? Incomplete occlusion of the artery –SUBENDOCARDIAL INFARCT ? Longer time low perfusion – cardiac failure, tachyarhytmia, hypertrophy of the myocardial – DIFFUSE SUBENDOCARDIAL INFARCT The intensity of the necrosis is varying, depends on the time of the compromised circulation and lack of oxygen. We can approve this with the EKG monitoring. That's why early diagnostic and therapy start are crucial in the prognosis of AMI. 4. Symptomathology: a. Anamnesis: i. Acute burning pain in the central chest not varying with the breathing movements. Pain can irradiate to the neck, chews, left hand, left shoulder, back. ii. Pain last longer than 30 minutes and does not react to the Nitro- glycerin treatment. iii. Patient have seldom feeling of arrhythmias, though they are often seen on the EKG monitor iv. Symptomatic start may be coming (silent infarct) b. Clinical status: i. Vegetative symptoms, patient is scared, nausea, vomiting, cold sweat. ii. Left ventricle infarct – higher symphaticus tonus – tachypnoe, pale face, cold sweat. iii. Left cardiac failure iv. Inflammation process – subfebrilia 5. Diagnostic a. Minimally two of following 3 criteria must be recognized: i. Central chest pain with or without radiation ii. Typical presence of the biochemical markers iii. Typical changes on the EKG, i e changes in the QRS complex b. Central chest pain – one must exclude the other reasons for central chest pain c. Biochemical markers: i. CKMB – Creatinkinase – isoenzym MB – start to increase 2 hours after ischemia and lasts about 2-3 days ii. Myoglobin – increase almost immediately, is highly in specific, lasts few hours. iii. Troponin – T or I – highly specific – increase within 2-4 hours, decrease after 5-6 days. 1. There were recognized even other markers earlier, but their specificity is very low – LD, ALAT; ASAT; CK. d. EKG diagnostic: i. Typical church-tower-like QRS complex ii. Deep Q – transmural infarct iii. ST –elevations which with the time changes to ST- negativity as the sign of previous ischemia e. Completing methods: i. Cardiac ECHO: to recognize immobility of the cardiac wall and quantify the level of the cardiac failure through the measurements of the flows and volumes through the heart ii. Thorax X rays – heart failure, ev. Pericardial exudates iii. Thallium scintigraphy of the heart – marked isotopes accentuate the necrotic areas in the heart 6. Treatment a. Immobilization of the patient immediately – minimizing the heart work-out b. ASA 500mg po immediately when the first suspicion comes c. Pain treatment – morphine – minimizing the symphatic activation d. Thromolysis – streptokinasis, urokinasis, alteplasis, etc – direct to dissolve thrombus e. Or PTCA – percuttan transluminal angioplasty – immediate diagnostic of the infarct, balloon dilatation as well as intraluminal stent of the artery f. Beta-blockers – prevention of the arrhythmia, positive protective effect g. ACE- inhibitors – protective effect, treatment of the heart failure 7. Complications a. Heart failure – see the chapter heart failure b. Rupture of the cardiac wall because of the ischemia – haemopericard – heart tamponade – death c. Rupture of the papillary muscles – acute mitral insufficiency – lung edema d. Pericarditis – sub pericardial infarct e. Thrombosis end emboli - prevention with early mobilization f. Post myocardial syndrome – autoimmune reaction to the muscle damage g. Aneurysm of the cardiac wall h. Hypotension and chock – if not treated immediate death i. Arrhythmias – reperfusion arrhythmia after thrombolyse 8. Prevention: a. Motion b. Low cholesterol and diet c. Normal weight d. Stress-free life e. No smoking f. No alcohol g. Diabetes mellitus – compensated diabetes h. If there has been infarct previously – following the medication and the regularly controls Control questions: 1. What is the acute myocardial infarct 2. What should be recognized to be able to say surely, that the patient does have the acute myocardial infarct 3. How do you recognize the transmural infarct 4. Draw the three typical EKG signs of myocardial infarct 5. What are the methods of treatment of acute myocardial infarct