pa tho physiology of myocardial infarction

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  • 8/3/2019 Pa Tho Physiology of Myocardial Infarction

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    Pathophysiology of Myocardial Infarction

    ON on modifiable

    Factor/Predisposing factors- Age- Gender (male)-Genetics abnormalities

    Modifiable Factors: Precipitating

    Factors

    -Diet (high fat and high - Stresscarbohydrates)- Hyperlipoproteinemia - Postmenopausal estrogen- Hypertension

    defficiency- Sedentary lifestyle - Type A personality

    Increase accumulation/deposition of

    blood cholesterol and fibrous tissue in

    Endothelial Injury/

    -Monocyte/lymphocyte adhesion andemigration- LDL & HDL imbalance-Smooth muscle cell migration to theintima.

    Plaque remodeling- progressive

    formation and development of

    - macrophages and t-lymphocytes

    activation of proteolytic enzymes

    ( cytokines & metalloproteases) w/in the

    Disruption of the atheromatous plaque by

    proteolytic enzymes>degradation of ECM

    of the plaques fibrous cap> (Rupture,

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    Activation of coagulation/ clotting cascade1.platelet adhesion2.platelet activation3.platelet aggregation

    Promotes thrombus

    Embolus

    Coronary arterial occlusion

    -Anterior descending

    branch of left coronary

    artery

    Right coronary artery

    -posterior/ inferior wall

    infarction

    Circumflex branch of left

    coronary artery-lateral wall infarction(15-

    Decreased blood supply to

    the myocardium

    Decreased oxygen supply to

    the myocardium

    Anaerobic glycolysis

    Increase production of lactic acid

    Decreased blood ph

    concentration>

    Signs and

    symptoms

    -fatigue

    -palpitation

    -sweating-weakness

    -tachycardia

    -nausea

    -vomiting

    Chest pain/ chest

    tightness

    -stabbing

    -crushing-burning

    -squeezingPrimary somatosensory

    cortexMyocardial

    necrosis

    Stimulation of sympathetic

    nervous system

    Impair Myocardial

    enzymatic and

    metabolic activity

    Decreased

    Stroke volume

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    Decreased Decreased

    cardiac

    vascul

    Increased Increase

    d heart

    Increased

    Stroke

    Increased

    Venous

    Decreased

    Diastolic

    Decreased

    Cardiac

    Inadequate

    tissue

    erfusion

    Decreasedvolume to met

    metabolic needs

    of the bod

    Increased

    Cardiac

    Hypoxia

    Irreversible MI

    >20minutes after

    onset of MI

    Complete infarc-

    large area/size of

    myocardial

    Reversible MI