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MYOCARDIAL INFARCTION - Coggle Diagram

- - - - PLAQUE DISRUPTION
        
        CORONARY THROMBUS
        
        LYSED SPONTANEOUSLY
        
        MYOCARDIAL NECROSIS EXTENDS ACROSS FULL THICKNESS OF WALL
      - PROLONGED SEVERE REDUCTION IN SYSTEMIC BP
        
        SHOCK SUPERIMPOSED ON CHRONIC, NONCRITICAL CORONARY STENOSES
      - GLOBAL HYPOTENSION
  - - - ACUTE PLAQUE CHANGE
      - SUPERIMPOSED THROMBOSIS
      - CHRONIC CORONARY ATHEROSCLEROSIS
    - - Mechanism to reduced coronary blood flow
        
        vasospasm w/ or w/o coronary atherosclerosis
        
        EMBOLI FR LA
        
        ASSOCIATED W/
        
        VEGETATIONS OF INFECTIVE ENDOCARDITIS
        
        INTRACARDIAL PROSTHETIC MATERIAL
        
        PARADOXICAL EMBOLI FR RIGHT SIDE OF HEART
        
        LEFT SIDE MURAL THROMBUS
        
        ATRIAL FIBRILLATION
        
        Ischaemia w/o significant coronary atherosclerosis & thrombosis
        
        CAUSED BY :-
        
        VASCULITIS
        
        SICKLE CELL DISEASE
        
        AMYLOID DEPOSITION IN VASCULAR WALLS
        
        VASCULAR DISSECTION
        
        AORTIC STENOSIS
        
        SHOCK
        
        INADEQUATE PROTECTION DURING SURGERY
  - - - ENDOGENOUS CATECHOLS
      - DRUGS -- COCAINE // EPHEDRINE
      - VASCULITIS
      - MICROEMBOLIZATION
    - - INCREASE HR & MYOCARDIAL CONTRACTILITY
        
        ISCHAEMIA BY VASOSPASM
        
        CAUSES :-
        
        TAKOTSUBO CARDIOMYOPATHY (broken heart syndrome)
        
        SUDDEN CARDIAC DEATH
- - - - ACUTE CHANGE
        
        ULCERATION
        
        RUPTURE
        
        EROSION
        
        FISSURING
        
        INTRAPLAQUE HAEMORRHAGE
    - - EXPOSED
        
        PLATELETS ADHERE & ACTIVATED
        
        GRANULE CONTENTS RELEASED
        
        AGGREGATION
        
        MICROTHROMBI FORMED
        
        RELEASE MEDIATORS
        
        VASOSPASM !!
        
        TISSUE FACTORS
        
        ACTIVATES COAGULATION PATHWAY
        
        ADD TO BULK OF THROMBUS
        
        EXPAND
        
        OCCLUDE VESSEL WALL
    - - FR EPICARDIUM --> ENDOCARDIUM
      - IRREVERSIBLE INJURY OF ISCHAEMIC MYOCYTES OCCUR AT SUBENDOCARDIAL LAYER
    - - NECROSIS AT MYOCARDIUM
        
        AREA THAT DEPENDS ON OCCLUSAL VESSEL FOR PERFUSION -- AT RISK!!!
        
        VERY NARROW ZONE OF MYOCARDIUM CAN BE SPARED FR NECROSIS
        
        D/T DIFFUSION OF O2 FR VENTRICLE
        
        NECROSIS = HALF OF MYOCARDIUM IN 2-3 HRS OF SEVERE TRANSMURAL W/IN 6 HRS
- - - - TRANSMURAL = ENTIRE THICKENESS OF MYOCARDIUM FR ENDO --> EPI
    - - EMERGENCY ANGIOPLASY
        
        REOPEN OBSTRUCTED ARTERY
  - - - ANTIPLATELET
      - ANTICOAGULANT THERAPY
- - - - CRUSHING
      - STABBING
      - SQUEEZING
    - - PROFUSE SWEATING
      - NAUSEA
      - VOMITTING