Myocardial Infarction (MI)

MORPHULOL-CHAYUCIES IN MYOCARDIAL INFARCTION DURATION CROSS CHANGIE LIGHT MICROSCOPIC CHANGE Reversible injury) o-hour None Nila (Elechon-mitrakopa- relaxation of myofibrils, loss of gheogon and swelling. of mitochondria Irreversible injury Non Nochange but show wavines of flwes at 6-12 hans DARK MELTINGL Early coagulative necrosis 12-24 hours DARK MOLTING (Cogulative neumnis, prakrotic nucleis increased eusi-philic of 41-3 days NA-kal PMNL L (d) 6-7 days Mottling with yellow ton center Conjulative necrosis, loss of cla (Nenbophal mfiltration) Hyprema boder; Central-gellow ton Disintegration of dead myocardinh alls, with disintegratis neutro phils, phasroytosis of dand coll by marerophages at andre of intoret 7-10 days primay yellow- toom and sott •Pringoghsis of dead cells, formatim of granulahin tissues Camerons) well established grondata die & collages deposition 7) 10-14 days REA GREY Red yig inforal by GREY-WHITE Gra-whila scor; antie Wireew collagen depositor decreased call-lent -12-8 weeks SCARINE-COMPLETE. complete Dence ellagerms Scor) Fisive// > a months Melted with central pale yellowich neirotic region with well-do marcatel border of peremin Alo 2 week, →soft rimmed by a hypremic zone of gruriulation tissue Afler 2 weak, Healed in foruts appper Firm, pale gray, & contracted Fibrous scar DIAGNOSIS OF MYOCARDIAL INFARCTION CLINICAL SYMPTOMS I severe, Retrosternal chest Pain-neck-Jaw epigastrium ar Loft Arm 2. Rapid, Weak Pulse 3. Profuse Sweating (diophoresis) 4. Dyspner due to impaired contre tion of ischemic myocardiuon and the resulting pulmonary vedeme. ELECTRO CARDIOGRAPHIC CHANGES Inverted T-waves Elevatel St segments a waves LAB FINDINGS CREATINE KINASE (MR Fractio) CREATINE KINASE (CK, CPK) ASPARTATE TRANSAMINASE (AST) TROPONIN LACTATE DEHYDROGENASE +CK-MIB-Eazyne of choke for diagnoing Reinteritin increase after MI. xnlyoglobin - Farliest enzyme to Reinforchion-CK-MB reapper aite 3-days. X CARDIAC TROPONSIN Gold standard (Aunt mi) Most sensitive Most specific for MI LABORATORY MARKERS Morker onset Peak Normalization Significance TROPONINT& 2-4 has 48 hrs 7-10 days Most sensitive specifi- Morker CK-MB 2-4 hrs 24hs 72 hrs Sensitive but not specific LDH 24-48 hrs Many days 7-14 days Not specific ryoglobin 1-3 hrs. 8-12 has 24-36 hrs Earliest morker. 1 CARDIAC TROPONINS Threased plasma levels establish dingnosis of MI. 2-4 hs 48hrs/ Felbuatch 710dy 2. CARDIAC CREATIVE PHOSPHOKINASE (CK) - Nim-specific morkor. La prentin Brain, myocardium, skeletal muscle. B- MB (Cordiac muscle) LDH Myoglobin = skeletal & cardiac muscle. OIL offs 240mms ath Triphogitetrazolium chloride (Stain) Non-tramworal inforuts PATTERS ATTERS OF INFARCTION Permanent peclosion of Loft dicending 2. branch of Left corry Ar5 (LAD) D 2. Laft cirumfler branch of LCA RCA Po RV LV LCX LAD 5. Transiel Obstmat Revival sabentar infor sbendourdit nere 3. Posterior descending bronch of R.C.A. 1-4- Patterns of tranmural infarction 4 Right main corong Artery microinfurch 7. Smal погони Vessel. ocs SEQUENTIAL CHANGES SEEN IN MT most of the trastomural inforuts (501) Left ventricle or inservetriner septim. a purtin of involves atleast a (15-301) 5ml involves posterior on postero septal also ar tend to involung right ventricle holated imterct & inferrets of atria - Rare XPuttive od Left ventricle infarcto AN-CAO CAO Right coroning ofte of cluvion Loft circumvoflox (30-4-1) (40-50%) CAO (15201) Left and de CGROSS swithin first 12 his: - No Wenlifiablel oppret gross chaps x. Gripireral retrazolium chloride (a Histochemicalstain) can growl infarct within 2-3 in afls onset." -Noinfarcter myourdian > Appears Brick Pad (LD) Inforcled area remains unstained Pula old=white, glistening (CD-lose) 12-24 hrs Pale Reddish-Bine over shorif defined lows tom PATHOGENESI ATHOGENESIS MI 1. ACUTE PLAQUE CHANGE Sudden charge in atheromatris plaque. Those aents plaque changes. convert partially acclusive arthuronlastic plaques to produce Sudden scher -Rupture, fissuring of plage exposure of trrumboganic plaqu constituents sedler THROMBUS FORMATION sudden occlusion of woman EROSION OF PLAQUE RUPTURE EXPOSURE THROMBUS FORM OCCLUSION LIMEN →ERUSJON Facton Intrinsic Exirin sic Plaque composition Blood pressure Sticke Phtelet Reaction 2. FORMATION OF MICRO THROMB/ Acate pliqu hay expose throinhogenic plaqu amais trents→ (platelet adhere platelets aggregation and activation MICRODHRON →portial or complete occlusion of aff. corening artey. 3. VASO SPASM Act platelets, endothelial rells, inf cells release mediators- Vasospus? 4) Act. COACULATION PATHWAY Ine size of Thrombus 5) Completo occlusion of vessel Thiranthus eclude Lumen 6 MYOCARIAL NECROSIS Gmplele scalesion Results in isclismic coagulative necrosis of the over supplied AREA AT RISK CONSEQUENCE OF MYOCARDIAL ISCHEMIA REVERSIBLE INJURY Mahumil-Cescation cerotke glycolysis occurs within seconds. production of acc. of toxi. metabolites Maxtional disturbances - (Loss of contrachtig within 60 sec pptAcute Heart Failove ✓Morphological changes citachundile cwellng, glycogen dopliter, & mafibriller relaxation. IRREVERSIBLE INJURY ocan alte prologed ther 2040 mills, Myoglobin, LDH, CK, Tropom- Used for the dignosis Funchinal disturbana Apomies Coagulative necrosis of fusaf omplek cordian murde within this of onetof MI. COLLATERALS IN HEARY MCH MCA HMCA Collalichidation Morrocand (HighLow) precviet collatit koonds. CLASSIMATONS OF MYOCARDIAL INFARCT Thickness of Tros miral in tacet Entietnickness of ventricule wall -Most intorcks. -ass with Acute plaque change CCA fukaducordial in foret 3% of ventricuhr wall shock superimponal Multi Focel OCL of small vessels Age of Inforet Fresh Heated Anatome region involved -Anteis -Postener Septal Electrocondo graphi Changes STEMI (Tranhmuart) NSTEMI (Subendocordial infort