Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

Acute Myocardial infarction

20,793 views

Published on

Acute Myocardial Infarction
Heart Attack
Acute coronary syndrome
pathogenesis, diagnosis, classification, management

Published in: Education, Health & Medicine

Acute Myocardial infarction

  1. 1. AcuteMyocardialInfarctionSoM-340Khos-Od E.Munkhtulga G.
  2. 2. Outline• Introduction• Etiology and risk factors• Pathogenesis• Classification• Diagnosis• Management
  3. 3. Nomenclature• Зүрхний цочмог шигдээс• Зүрхний хурц шигдээс• Зүрхний шигдээс• Острый инфаркт миокарда/ОИМ/• Acute Myocardial Infarction• Heart attack
  4. 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. 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. 6. Acute Coronary SyndromeResource: Harrison’s Cardiovascular medicine
  7. 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. 8. Risk factors• American Heart Association guide to risk factors forcoronary artery disease.• Resource: “Cardiology explained”
  9. 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”
  10. 10. Formation ofthrombus
  11. 11. Mechanism of coronary thrombus
  12. 12. Main• STEMI• NSTEMI/Unstable angina
  13. 13. 1-р хэлбэрГэнэтийн ЗЦШ: титэм судасны товруу шархлах, задрах, хуулрах зэрэг шалтгааны улмаас титэм судасны цусан хангамж хомсдсоноос үүссэн шигдээс2-р хэлбэрХоѐрдогч ЗЦШ: зүрхний титэм судасны агшилт, судасны б¿лэнт бºглºрºл, цус багадалт, артерийн гипотензи зэрэг шалтгааны улмаас зүрхний булчингийн хүчилтөрөгчийн хэрэгцээ ба шаардлагын тэнцвэрт байдал алдагдсанаас үүссэн шигдээс3-р хэлбэрГэнэтийн з¿рхний ¿хэл: з¿рх зогсох, зүрхний булчингийн ишемийн эмнэл з¿йн шинж нь дараах ¿з¿¿лэлтийн аль нэгтэй хавсран тохиолдох. Үүнд:ÇÖÁ-т ST сегмент шинээр ºргºгдсºн байх, эсвэл Гисийн зүүн хөлийн хориг (ГЗХХ) шинээр ¿¿сэхТитэм судасны шинжилгээнд, эсвэл задлан шинжилгээнд шинэ бүлэн тодорхойлогдохГэхдээ гэнэтийн нас баралт цусны биомаркерийн шинжилгээг авч амжааг¿й байхад эсвэл зүрхний өвөрмөц ферментүүд илрэх хугацаа нь болоогүй байхад тохиолдоно.4à õýëáýð• Титэм судсан дотуурх эмчилгээтэй холбоотой шигдээс4б хэлбэр• Òèòýì ñóäàñíы тэлэгч орчмийн бүлэнгээс гаралтай шигдээс, гэхдээ б¿лэн нь титэм судасны шинжилгээ, эсвэл задлан шинжилгээгээр нотлогдсон байх5-ð õýëáýð• Титэм судасны мэс засалтай холбоотой ЗШ
  14. 14. By necrotic area:• Micro size of MI• Small size of MI (LV muscle damage<10%)• Moderate size of MI (LV muscledamaged 10-30%)• Large size of MI (LV muscle >30%)
  15. 15. By progress: Initial period: (<6 hours) Acute period: (6h – 7 days) Recovering period: (7-28 days) Convalescence period: (≥29 days)
  16. 16. • Anamnesis• Signs and symptoms• ECG• Serum analyze• Echocardiography
  17. 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. 18. Symptoms• By CHEST PAIN:Typical or classical type of MIAtypical type of MI Asthmatic Abdominal Low blood pressure Arrhythmatic Brain’s
  19. 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. 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.
  21. 21. Signs• General• Chest• Heart• Extremities
  22. 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. 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. 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. 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. 26. ECG early changes• Presence of MI• QRS complex, ST segment, T wavesare changed• Tall T wave in contiguous 2 or moreleads
  27. 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. 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. 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. 30. ECG abnormalities
  31. 31. Unstable angina/ NSTEMI
  32. 32. STEMI
  33. 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. 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. 35. Reference intervals
  36. 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. 37. STEMI NSTEMI
  38. 38. Formulation of DS• Diagnosis must be includinglocation of infarction, type andcomplication.• DS: Anterior lateral wall of LV’stransmural MI. Pulmonary edema.
  39. 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. 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. 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. 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
  43. 43. Pre-Hospital management• Chest pain• Dyspnea• Restless
  44. 44. Morphine• Analgesic• Sedative• Reducing fear• Dilate venous reduce heart burden(important inpul.edema)• Reduce sympathetictonus• 4-8 mg by IV• Repeat 2-4 mg by IVin 5-15 mins• Vomiting –Metoclopramide /5-10 mg by IV/• Hypotension, bradycardia – Atropine/0,5-1 mg by IV/• Naloxone /0,1-0,2mg by IV/• The highest dose ofMorphine: 20 mg
  45. 45. Improving heart blood supplyOXYGEN• 2-8 liter per minuteby nasotubule• Saturation: >90%NITROGLYCERIN• Dilating coronaryartery• 0,3-0,6 mg bysublingual or spray• Repeat 2 times in 5minute
  46. 46. Pre-Hospital careAspirin /ASA/• 162-325 mg by chew• If contraindicated:ClopidogrelFibrinolytic therapy• Anistreplase/Streptokinase/ Urokinase• Slowly ejecting by IV/>5 minutes/• If Carrying tohospital requires>30 minutes
  47. 47. STEMImanagement• Key words:• PercutaneousCoronaryIntervention/PCI/• Thrombolytictherapy
  48. 48. • ТСДЭ - PCINSTEMImanagement
  49. 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

×