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    Pathophysiology

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    Josh Lazo
    Coronary artery disease is caused by both modifiable and non-modifiable risk factors that lead to endothelial injury, lipid and platelet assimilation in the arterial wall, and plaque formation. Disruption of plaques can cause thrombus formation and rapid expansion, reducing blood flow to the myocardium and causing myocardial ischemia, infarction, and further complications like heart failure, hypotension, and death if left untreated.

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    Pathophysiology

    Uploaded by

    Josh Lazo
    54 views3 pages
    Coronary artery disease is caused by both modifiable and non-modifiable risk factors that lead to endothelial injury, lipid and platelet assimilation in the arterial wall, and plaque formation. Disruption of plaques can cause thrombus formation and rapid expansion, reducing blood flow to the myocardium and causing myocardial ischemia, infarction, and further complications like heart failure, hypotension, and death if left untreated.

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    Coronary artery disease is caused by both modifiable and non-modifiable risk factors that lead to endothelial injury, lipid and platelet assimilation in the arterial wall, and plaque formation. Disruption of plaques can cause thrombus formation and rapid expansion, reducing blood flow to the myocardium and causing myocardial ischemia, infarction, and further complications like heart failure, hypotension, and death if left untreated.

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    © All Rights Reserved
    Download as DOCX, PDF, TXT or read online from Scribd
    Flag for inappropriate content
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    54 views3 pages

    Pathophysiology

    Uploaded by

    Josh Lazo
    Coronary artery disease is caused by both modifiable and non-modifiable risk factors that lead to endothelial injury, lipid and platelet assimilation in the arterial wall, and plaque formation. Disruption of plaques can cause thrombus formation and rapid expansion, reducing blood flow to the myocardium and causing myocardial ischemia, infarction, and further complications like heart failure, hypotension, and death if left untreated.

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    CORONARY ARTERY DISEASE

    PATHOPHYSIOLOGY
    Non Modifiable Factors
    Age
    Gender
    Family History

    Modifiable factors
    Smoking
    Lack of exercise
    Stress
    Diet high in fat
    Hypertension
    Elevated Serum cholesterol
    levels
    Alcohol consumption
    Diabetes Mellitus

    Non-specific injury to arterial wall (Endothelial Injury)

    Desquamation of endothelial lining


    Increased Permeability or Adhesion of Molecules
    Lipids (LDL) and Platelets Assimilate in the Area
    Oxydized LDL attracts

    monocytes and macrophages to the site

    Plaques begin to form from

    cells which imbibed into the endothelium

    Lipids are engulfted by the cells (foam cells) and Smooth Muscle Cells Develop

    Disruption of Plaque
    Continuous aggregation of platelets
    Thrombus Formation

    www.NursesLabs.com

    Rapid increase in size of the thrombus in Coronary Artery Wall


    Coronary Atherosclerotic Heart Disease/CAD

    Reduction of blood flow


    Decreased Blood Supply to the Myocardium
    Decreased Myocardial Oxygen Supply

    Myocardial
    Ischemia
    Anaerobic metabolism

    Myocardial Cell Necrosis

    More Lactic Acid Production

    Inflammatory response
    Increase WBC

    Chest Pain

    Acidosis
    Myocardial cells
    are sensitive to
    changes in pH and
    become less
    functional

    Released of endogenous pyrogens


    Pyrogens will stimulate the release of
    prostaglandins

    Conduction System Disorder


    will reset the
    Hypothalamic thermostat to high temperature

    Prostaglandins

    Decreased myocardial contractility


    Fever/Hyperthermia
    Decreased Cardiac Output

    Decreased systemic

    circulation
    www.NursesLabs.com

    Hypotension
    skin to

    away from the

    Redirection of blood
    the major organs

    Sympathetic
    are stimulated

    receptors
    Inadequate

    perfusion of

    Pallor
    cerebral

    Increase in heart
    organs
    rate/ pumping action
    as a compensatory
    mechanism
    Dyspnea,
    /Dizzine
    ss

    Decreased

    oxygenated blood to
    perfusion

    other

    Loss of Consciousness
    Fatigue
    and Body Weakness

    Tachycardia
    Deterioration of hearts ability to pump
    Moderate left ventricular failure
    Decreased arterial pressure

    Stimulation of Baroreceptors

    Right side of the heart continuously


    propel blood to the lungs
    Left

    eject
    Peripheral Vasoconstriction

    ventricle is unable to fully

    the returning blood to systemic circulation


    Pulmonary

    Congestion
    Hypertension
    Dyspnea

    Adventitious breath

    sounds

    www.NursesLabs.com

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