The flow reduction may be caused by a completely occlusive thrombus (right) or subtotally occlusive thrombus (left). Patients with ischemic discomfort may present with or without ST-segment elevation. Of patients with ST-segment elevation, the majority (wide red arrow) ultimately develop a Q-wave on the ECG (QwMI), while a minority (thin red arrow) do not develop Q-wave and in older literature where said to have sustained a non-Q-wave MI (NQMI). Patients who present without ST-segment elevation are suffering from either unstable angina or a non-ST-segment elevation MI (NSTEMI) (wide green arrows), a distinction that is ultimately made on the presence or absence of a serum cardiac marker such as CK-MB or a cardiac troponin detected in the blood. The majority of patients presenting with NSTEMI do not develop a Q-wave on the ECG; a minority develop a QwMI (thin green arrow).
1. AcuteMyocardialInfarctionSoM-340Khos-Od E.Munkhtulga G.
4. Definition• Acute myocardial infarction (MI) isa clinical syndrome that resultsfrom occlusion of a coronaryartery, with resultant death ofcardiac myocytes in the regionsupplied by that artery.• Удаан хугацааны миокардын ишемийнулмаас үхжлийн голомт үүсэхийг ЗЦШ гэнэDefined by “Current diagnosis and treatment in Cardiology - 2013”
5. Definition• Acute Coronary Syndrome isfollowing disruption of a vulnerableplaque, patients experienceischemic discomfort resulting froma reduction of flow through theaffected epicardial coronary artery.– STEMI– NSTEMI– Unstable angina• Defined by: Harrison’s Cardiovascular medicine
6. Acute Coronary SyndromeResource: Harrison’s Cardiovascular medicine
7. Causes of Acute CoronarySyndromes• Atherosclerotic plaque rupture with superimposedthrombus/95%/• Vasculitic syndromes• Coronary embolism (e.g., from endocarditis, artificial heartvalves)• Congenital anomalies of the coronary arteries• Coronary trauma or aneurysm• Severe coronary artery spasm (primary or cocaine-induced)• Increased blood viscosity (e.g., polycythemiavera, thrombocytosis)• Spontaneous coronary artery dissection• Markedly increased myocardial oxygen demand (e.g., severeaortic stenosis)
8. Risk factors• American Heart Association guide to risk factors forcoronary artery disease.• Resource: “Cardiology explained”
9. Risk factorsEuropean Society of Cardiology table of lifestyles and characteristicsassociated with an increased risk of a future coronary heart disease event.Resource: “Cardiology explained”
16. • Anamnesis• Signs and symptoms• ECG• Serum analyze• Echocardiography
17. Anamnesis:• Complains• Onset of disease• Time– initial of disease - calling 103– Initial of disease – arrive of a Doctor• Risks/HTN, Smoking, Diabetes,stress, hereditary/• Whether having MI, AP, coronaryartery by pass graft before that
18. Symptoms• By CHEST PAIN:Typical or classical type of MIAtypical type of MI Asthmatic Abdominal Low blood pressure Arrhythmatic Brain’s
19. Chest pain of MIPainindicatorsDescriptionLocation Behind side of sternum, left side of chestRadiation Left arm, jaw, neckCharacterizes Pressure, dull, squeezing, aching, crushing,burning /elephant sitting in the chest/Duration >10-20minsRelievingfactorNo abatement of nitroglycerin, relievedwith analgesic/morphine/AssociatedsymptomsWeakness, dyspnea, fainting fit/syncope/Cold sweat, apprehensive.Dyspnea, orthopnea, cough, wheezing,nausea and vomiting, or abdominalbloatingOccurs at rest, more commonly in the early morning
20. Painless infarction• One-third of patients with acute myocardialinfarction present without chest pain, andthese patients tend to be undertreated andhave poor outcomes.• Older patients, women, and patients withdiabetes mellitus are more likely to presentwithout classic chest pain. As many as 25%of infarctions are detected on routine ECGwithout any recallable acute episode.
22. General signs• Patients may appear anxious and sometimesare sweating profusely.• The heart rate may range from markedbradycardia (most commonly in inferiorinfarction) to tachycardia, low cardiacoutput, or arrhythmia.• The BP may be high, especially in formerhypertensive patients, or low in patients withshock.• Respiratory distress usually indicates heartfailure.• Fever, usually low grade, may appear after 12hours and persist for several days.
23. Chest• The Killip classification is the standard way to classifyheart failure in patients with acute myocardial infarctionand has powerful prognostic value.• Killip class I is absence of rales and S3• Class II is rales that do not clear with coughingover one-third or less of the lung fields orpresence of an S3• Class III is rales that do not clear with coughingover more than one-third of the lung fields• Class IV is cardiogenic shock (rales,hypotension, and signs of hypoperfusion).
24. Heart• Jugular venous distention reflects RAhypertension, and a Kussmaul sign (failure ofdecrease of jugular venous pressure withinspiration) is suggestive of RV infarction. Softheart sounds may indicate LV dysfunction.• Atrial gallops (S4) are the rule, whereasventricular gallops (S3) are less common andindicate significant LV dysfunction. Mitralregurgitation murmurs are not uncommon andmay indicate papillary muscle dysfunctionor, rarely, rupture. Pericardial friction rubs areuncommon in the first 24 hours but mayappear later.
25. ECG• It should be performed as soon aspossible, preferably within 10minutes, after the patient’s arrivalin the emergency department orclinician’s office, since the presenceor absence of ST elevationdetermines the preferredmanagement strategy.
26. ECG early changes• Presence of MI• QRS complex, ST segment, T wavesare changed• Tall T wave in contiguous 2 or moreleads
27. MI’s specific changes• Pathological Q wave present in ≥2leads• Pathological Q wave indicatecellular necrosis• It is generated after beginning ofinfarction in 8-6 hours• ST segment’s elevation isformed after beginning ofinfarction in 4-2 hours
28. Ischemic changes in ECG• ST segment elevation• ST segment’s elevation (J-point): elevated in– V2-V3: for men ≥2 mm, for women ≥1,5 mm or– contiguous 2 leads for another leads• ST segment depression and T wave changes• ST segment depressed by horizontal ordownward in contiguous 2 leads ≥0,5 cmdepressed from isoelectric line, invertedand negative poled(≥1 mm) T wave, moreelevated R wave or R/S ratio be >1• It is positive without LV hypertrophy and LBBB
29. Goal of ECG during MI• Confirm or deny DS• Identify location of infarction• Identify size of infarction• Identify time of infarction• Control outcome of treatment
30. ECG abnormalities
31. Unstable angina/ NSTEMI
33. Serum analyzeIndicators:• Troponin T and I(cTnT, cTnI)• CK-MB (creatininephosphokinasemyocardial bound)• Myoglobin• LDH (Lactatedehydro)Goal:• Confirm or deny DS• Identify size of MI• Assess result offibrinolytictreatment• Diagnosing relapseof MI
34. Troponin using method forDS of MI• Result must be ready within 1 hour• Make second analysis after 6-12hours if first result is negative• Negative first result is not enoughto reject MI• Shouldn’t make MI diagnose withonly Troponin (+)
35. Reference intervals
36. Criteria of MI• Troponin or CK-MB increased with oneof these:– Chest pain– Positive ischemic change in ECG (STsegment and T wave’s changes)– Pathological Q wave presence in ECG newly– Patient had CABG– Detected pathological changes in autopsy
37. STEMI NSTEMI
38. Formulation of DS• Diagnosis must be includinglocation of infarction, type andcomplication.• DS: Anterior lateral wall of LV’stransmural MI. Pulmonary edema.
39. General principle of DS• We should take DS as early aspossible. It directly related totreatment result and prognosis.• Use Diagnosis criteria!• DS must be including infarction’slocation, type and complication
40. Assessment of risk/patient with MI/ Age ≥65 years old * ≥3 risk factors for coronary disease Known coronary stenosis of ≥50% by pre-sentation At least 2 anginal episodes in prior 24 hours Use of aspirin in prior 7 days (i.e., implyingresistance to aspirin’s effect) Elevated serum Troponin or CK-MB 1 score given each question* - MI’s hereditary anamnesis, HTN, DM, Smoking, Dyslipidemia
41. Assessment of risk• Total score is TIMI /Thrombolysis inmyocardial infarction/ assessment’sscore• Total scores:– 2-1: Low risk– 4-3: Moderate risk– 7-5: High risk• TIMI is important for deciding esp.NSTEMI prognosis
42.  It should be successively staged Pre-hospital management Emergency department therapy Post discharge As quickly as begin treatment Correctly choose treatment method Correctly combine treatment methods
49. Reference• “Зүрх судлал” Д.Зулгэрэл, Ө.Цолмон нар, 2012 он• “Зүрхний цочмог шигдээсийн эмнэл зүйн удирдамж”2013 он• “Cardiology explained” Euan A Ashley and JosefNiebauer• “Current diagnosis and treatment in Cardiology” MichaelH. Crawford, 3rd edition• “Current Medical diagnosis and treatment – 2013”Maxine A. Papadakis, Stephen J. McPhee• “Harrison’s Cardiovascular medicine” Joseph Loscalzo,17th edition• “Pathophysiology of heart” Leonard S. Lilly, 5th edition• “Pathophysiology concepts of Altered Health States”Carol Mattson Porth, 7th edition