ACS/MI

Card Set Information

Author:
Corissa.Stovall
ID:
256321
Filename:
ACS/MI
Updated:
2014-01-20 10:59:09
Tags:
Patho Exam One Spring 2014
Folders:

Description:
Section set of powerpoints from Lecture 1 from pg 1 - 10
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user Corissa.Stovall on FreezingBlue Flashcards. What would you like to do?


  1. What does the pericardium envelop??
    the heart and the roots of the great vessels
  2. There are two parts of the pericardium... what are they??
    the visceral and partial part
  3. The visceral and parietal part of the pericardium are separated by the ______.
    potential space
  4. ____ are the priming chambers for the ventricles.
    Atria
  5. ___ acts as a reservoir for the RV.
    RA
  6. The heart receives blood flow from what 3 areas??
    • superior vena cava
    • inferior vena cava
    • coronary sinus
  7. What is unique about the left atrium??
    It serves as a pump.  Gives a atrial kick to help maintain CO.
  8. Which side of the heart is thicker?? L or R?
    LEFT... bc of increased pressures
  9. What separates the right and left ventricular cavities??
    ventricular septum
  10. What are the 3 layers of the heart??
    • outer --epicardium
    • middle -- myocardium
    • inner --endocardium
  11. The heart requires a constant supply of what??
    oxygen... if oxygen supply is cut of the heart becomes ischemic and a MI can occur.
  12. The left main artery divides into ___ and ___.
    LAD and left circumflex
  13. What is acute coronary syndrome??
    a hypercoagulable state where there is focal disruption of atheromatous plaque that triggers the coagulation cascade with subsequent generation of thrombin and partial or complete occlusion of a coronary artery
  14. If you have ST elevation...an MI is classified as a ??
    STEMI
  15. What would be your diagnosis with ST depression noted on an EKG and elevations in CK-MB or troponins???
    Non-STEMI
  16. how would you diagnosis a patient is they have ST depression on an EKG but normal cardiac lab values??
    Unstable Angina
  17. The prognosis after a STEMI is determined by??
    the severity of the L ventricular dysfunction, presence and degree of residual ischemia and potential for malignant dysrhythmias


    most people with poor function die within 3 mos. Ventricular function can improve during the first few weeks after an acute Mi if reperfusion is achieved.
  18. When should an echo be obtained post MI?
    • in 2 to 3 months
    • this is the most accurate predictor of long term prognosis

    • **
    • if you get an echo immediately after an MI you have tissue that is not functioning correctly yet so your results will be inaccurate.
  19. Atherosclerosis
    is considered a ____ disease.
    inflammatory

    inflammation is import in the cascade of events leading to plaque rupture
  20. What serum markers are increased with CAD & what do these markers represent??
    • c-reactive
    • protein and fibrinogen

    they are markers of inflammation
  21. What are the 5 steps in the inflammatory process that occurs with atherosclerosis??
    • starts
    • with injury to the cell:
    • 1. injured endothelial cells become inflamed
    • 2. numerous inflammatory cytokines are released
    • 3. macrophages adhere to injured endothelium by way of adhesion molecules
    • 4. macrophages release enzymes and toxic oxygen radicals
    • 5. growth factors are released
  22. Why is oxidation of LDL such an issue with atherosclerosis??
    • LDL is bombarded with oxygen to yield free radicals when it enters the wall of an
    • artery.  Oxidized LDL then promotes atherosclerosis by attracting other
    • cells and chemicals to the site causing inflammation at the site of the artery
    • and laying the foundation for cholesterol and other factors to build up in the
    • artery. 

    **got this definition online bc the book didn't explain it well
  23. Oxidized LDL is engulfed by _____.
    macrophages
  24. What are foam cells?
    • Macrophages
    • filled with oxidized LDL
  25. what do foam cells form??
    the fatty streak within the artery.



    • then
    • produce oxygen radicals and cause immunological and inflammatory changes
  26. How do
    smooth muscle cells contribute to plaque formation??
    • smooth muscle cells proliferate with the vessel well and produce
    • collagen.  They migrate over the fatty streak formed by foam cells and
    • form a fibrous plaque.  This action is mediated by inflammatory
    • cytokines.  The plaque may calcify at this time
  27. Why does the plaque within a vessel rupture??
    because of the inflammatory activation of proteinases
  28. What happens after the plaque ruptures??
    the underlying tissues are exposed and platelet adhesion occurs.  this initiates the clotting cascade and rapid thrombus formation occurs at the site.
  29. When a STEMI occurs.. blood flow is decreased abruptly.. why is this???
    due to the thrombus formation at the site where the atherosclerotic plaque fissures, ruptures and ulcerates
  30. 2 of 3 things are required to diagnosis Acute MI... what are these??
    • 1. chest pain (new onset or
    • changes in pain)
    • 2. serial electrocardiographic changes indicative of MI
    • 3. increased cardiac enzymes
  31. When a patients has changes in the chest pain what is the risk??
    risk that the patient will have an MI within 30 days
  32. Which lab
    is most specific when diagnosing an MI?
    troponin
  33. Troponin increases in ___ hours of an MI.
    4-6
  34. how long will the Troponin remain elevated after an MI?
    7-10days
  35. CK-MB isoenzymes increase within ___ hours of an MI.
    6 hours
  36. If the troponin does not increase within ___ hours of pain... the diagnosis is not an
    MI.
    12 hours
  37. Why would you use an echo when assessing for an MI???
    • if the patient has a LBBB or abnormal EKG where a definite diagnosis of
    • an MI is uncertain.

    an echo will indicate abnormalities in most patients experiencing an MI
  38. Why are echo's typically not used to evaluate a patient of an acute MI???
    • The time required to perform an echo and identify if there are changes limits its use in
    • early diagnosis of MIs.
  39. What do changes on an EKG look like in general with an MI??
    • ST elevation
    • abnormal Q waves
  40. What makes the Q wave abnormal??
    if it is more than 0.04 secs (0.03 seconds for an inferior MI)
  41. Define a STEMI based on an EKG reading...
    ST elevation greater than 1 in 2 or more contiguous leads or 2 or more adjacent limb leads
  42. How long is a normal PR interval??
    0.12 to 0.20 seconds
  43. What is the normal QT interval??
    0.38 to 0.42 secs

    if this length increases---- arrhythmias
  44. What is the normal QRS length??
    0.12 secs
  45. Where is the J point??
    It is at the location where the QRS segments and the ST segments overlap.
  46. how do you measure ST elevation on an EKG??
    find the J point, then go 1mm or 0.04 (or one little block) to the right from to this point and measure ST elevation from there on the EKG
  47. How do you determine what is the Q wave on an EKG??
    it is the first downward deflection in the QRS complex.
  48. 1mm = __ secs?
    0.04
  49. what determines if a Q wave is pathological??
    • if it is >0.04 wide
    • if it is taller than 25% of the R wave in the same lead
    • and if there are also abnormalities of the T waves and/or ST segments
  50. how would a posterior wall infarction represent on a EKG??
    There would be reciprocal changes in the anterior leads V1 to V3


    Changes--- abnormal tall R waves, ST segment depression, Tall T waves
  51. How would a inferior wall MI present on an EKG??
    There would be pathologic Q waves and ST changes in 2, 3, and AVF

    Q waves are typically largest in lead 3
  52. if you have an inferior wall MI, which vessel is affected??
    RCA
  53. What leads are affected with a Right Ventricular Infarction??  What vessel would you expect to have occlusion??
    • 2, 3, aVF
    • V4R


    RCA
  54. With a R ventricular infarction would should you observe for??
    Signs of HF
  55. What drug should you not give to patients with R ventricular infarction??
    Nitrates
  56. You should suspect a _____ infarction in the setting of inferior wall infarction.
    R ventricular infarction
  57. What leads are affected with an anterior wall MI? & what vessel would you expect to be occluded??
    • Q waves in V3 and V4
    • may see elevation in V1-V6 (from book)

    LAD
  58. What leads are affected with a Septal wall MI??? What vessel is affected??
    Q waves in V1 and V2

    LAD
  59. What leads are affected with a Lateral wall MI??? What vessel is affected??
    • I, AVL, V5, V6
    • Q waves in V5 and V6

    Left circumflex
  60. When must thrombolytic therapy be started if the patient is experiencing a STEMI??
    within 30 to 60 mins of arriving to the hospital
  61. what is the biggest complication with reperfusion therapy??
    intracranial hemorrhage
  62. Direct coronary artery angioplasty must be performed within ___ of arrival to the hospital and within ___  of symptom onset.
    90 mins

    12 hours
  63. Why should patients with an MI receive IV beta blockers as early as possible??
    they decrease the size of the infarction (decrease HR, BP, and contractility)

    they should be continued post MI as well to decrease early and long term mortality and reinfarction)
  64. ACE/ARBs should be given to all patients post MI if (name 4 things)
    • DM
    • EF<40%
    • Large Anterior wall MI
    • evidence of L ventricular failure
  65. when are calcium channel blockers ordered post MI?
    typically not administered routinely

    ordered if persistent myocardial ischemia despite optimal use of ASA,BB,Nitrates and Heparin
  66. What are some conditions that increase oxygen demand??
    thyrotoxicosis, sepsis, fever, tachycardia, anemia, cocaine, and amphetamine use

What would you like to do?

Home > Flashcards > Print Preview