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K 305 27 June 03

K 305 27 June 03. Contractile Dysfunction. Reversible stunning hibernation Irreversible necrosis apoptosis. Contractile Dysfunction. This cell damage produces: hypocontractility enhance the likelihood of arrhythmias both of which can be lethal.

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K 305 27 June 03

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  1. K 305 27 June 03

  2. Contractile Dysfunction • Reversible • stunning • hibernation • Irreversible • necrosis • apoptosis

  3. Contractile Dysfunction • This cell damage produces: • hypocontractility • enhance the likelihood of arrhythmias • both of which can be lethal

  4. Etiology of Ischemia - Reperfusion Injury • osmotic overload • number of particles in cytosol as lactate accumulates and ATP is broken down • immune response • neutrophils and complement system • pH paradox

  5. Etiology of Ischemia - Reperfusion Injury • pH paradox • ¯ pHi which increases: • Na+-H+ activity • [Na+]I • Na+-Ca2+ exchange reverse activity • [Ca2+]i overload • contractile dysfunction

  6. Regulation of Intracellular H+ • H+ extrusion (acidosis) • NHE-1 • pH paradox

  7. EKG changes with ischemia/ MI Subendocardium • results in ST segment depression • injury current at rest causes baseline elevation • during plateau causes ST segment depression • observe a J point at the point between the QRS complex and the ST segment and this point represents zero current in the heart as all parts of the ventricles are depolarized • ST segment depression is usually due to imbalance between supply and demand and will reverse when exercise is stopped during a stress test

  8. EKG changes with ischemia/ MI

  9. EKG changes with ischemia/ MI Subepicardium or transmural • immediately results in heightened T waves • may be followed by T wave inversion • T wave inversion problems with directionality of repolarization • ST segment elevation occurs due to injury current during plateau phase of the action potential which is moving towards epicardium • deep (dirty, pathological) Q waves reflect scarring

  10. EKG changes with ischemia/ MI

  11. Plasma markers of MI • 24-72 hours after MI - increases in: • CK • LDH • TnI

  12. Radionuclide Imaging of Heart • Technetium-99m-MIBI • MIBI - 2-methoxy isobutyl isonitrile • MIBI travels via CBF becomes trapped within healthy, active muscle cells in the heart • radioactivity monitored with a gamma camera • during an MI, some muscle cells will not trap the MIBI • also occurs with CAD except the lack of MIBI in some of the muscle cells is due to inadequate CBF

  13. Cardiac Ischemia

  14. Ischemic Preconditioning

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