Drug Induced cardiac toxicity

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Drug Induced cardiac toxicity
2011-05-04 16:55:05
Drug Induced cardiac toxicity

Drug Induced cardiac toxicity
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  1. which electrolyte disorder?
    tall peaked T
    decrease P wave
    increase PR interval
    P is lost
    depressed ST
    QRS blends into T
    sine wave
    cardiac arrest
  2. how do you get hyperkalemia? (drugs, conditions)
    from potassium salt, K sparing diuretics (spironolactone, triamterene), increased K+ (ACEi), acute OD of digoxin esp in decreased renal fxn, NSAID
  3. which electrolyte disorder?
    decreased ST
    u wave (comes after T but before next P) PVCs
  4. what are the causes of hypokalemia?
    • diuretics (esp. loop)
    • vomiting
    • ingestion of magic shave (b/c contains soluble barium salt that drives potassium into cells --> profound hypokalemia)
  5. which electrolyte disorder?
    wide QRS
    ventricular arrhythmias
  6. what causes hypermagnesemia?
    • from Mg (i.e. antacids, cathartic)
    • repeat dose, renal function issue
  7. antidote for hypermagenesemia?
    IV calcium
  8. which electrolyte disorder?
    dysrhythmia especially if treated with digoxin
  9. which electrolyte disorder?
    short QT
    occasional depressed ST
    sinus arrest
    AV block
  10. which electrolyte disorder?
    long QT
    some broadening of T
  11. why does myocardial ischemia happen?
    • mismatch btwn myocardial O2 demand and supply
    • demand exceeds supply
  12. similarity btwn angina and myocardial ischemia
    sympts are similar
  13. difference btwn myocardial ischemia and angina
    • MI: oxygen supply is decreased due to clots (use fibrinolytics and thrombolytics), "supply" issue
    • angina: chronic exertinal angina, "demand" issue, use NTG to relieve
  14. two mechanisms behind myocardial ischemia
    • increased demand (increased heart rate, BP, underlying CAD)
    • oxygen supply (coronary blood flow, oxygen carrying capacity of the blood)
  15. during MI, there is increased HR and BP due to increased demand. which drugs cause this?
    • sympathomimetics (einephrine, cocaine)
    • abrupt d/c of BB and central a-agonist
  16. during MI, vasoconstriction affects oxygen supply and coronary blood flow. which drugs affect this?
    • cocain
    • ergots
  17. during MI, oxygen supply is affected by hypotension. which agents affect this mechanism?
    • PDE5 inhibitor + nitrates
    • dipyridamole
  18. during MI, oxygen supply is affected by oxygen carrying capacity of blood. which agents affect this mechanism?
    • methemoglobin inducers (benzocaine, dapsone)
    • Fe3+, not Fe2+, thus cannot carry O2 and decreased O2 supply.
  19. antidote for methemoglobin inducers (benzocaine, dapsone)?
    methylene blue
  20. ruptured plaque and thrombosis of MI is caused by..
    • estrogens
    • cocaine
  21. vasospasm of MI is caused by...
    • cocaine
    • ergots
    • triptans.
  22. how to correct vasospasm (MI) caused by cocaine?
    • IV phentolamine
    • alpha blocker
  23. how to correct ergot-induced vasospasm (MI)?
    • IV NTG, IV vasodilator
    • (ergot and cocaine cause vasoconstriction)
  24. accelerated atherosclerosis of MI is caused by ...
    protease inhibitor and cocaine
  25. how would you manage MI?
    • with CAD: according to guidelines
    • without CAD: d/c drug and treat ischemia
  26. how does cocaine cause myocardial infarction?
    • 1) ruptured plaque = thrombosis
    • 2) vasospasm
    • 3) accelerated atherosclerosis
  27. what should you AVOID acutely in cocaine associated chest pain?
    beta blockers b/c causes unopposed alpha and worsens
  28. how to manage cocaine associated chest pain?
    • 1) ASA and benzo (central cooling)
    • 2) IV NTG, nitroprusside for persistent htn (IV pentolamine)
    • 3) high risk vs. low risk
    • 4) if high risk: avoid BB acutely; antiplatelet/antithromb tx
    • 5) discharge - ASA, clopidogrel, statin, ACEi (chronic BB if high risk like systolic dysfx, dysrhythmia)
  29. how does HF affect the body?
    heart fails to pump enough blood to meet the metabolic demand of the body
  30. drug induced HF without pre-existing disease is... common or rare?
  31. what are two types of HF?
    • systolic HF: <40% EF (amount that is squeezed out)
    • diastolic HF: EF is fine but stiff left ventricle so cannot be filled with blood
    • both have problem pumping blood
  32. risk factors for HF
    • pre-existng LV dysfxn
    • history of MI
    • CAD
    • HTN
    • LVH
    • aortic or mitral valve disease
    • >70 yo
    • pre-existing edema
    • chronic kidney disease
  33. agents that exacerbate HF by reducing myocardial contractility?
    • acute use of beta blocker
    • CCB (diltiazem and verapamil are contraindicated in HF)
    • anthracycline
    • trastuzumab
  34. agents that exacerbate HF by increasing preload?
    • glucocorticoids
    • glitazones (Actos is dose-dep)
    • NSAID
    • COX 2 inhibitor
  35. agents that exacerbate HF by increasing after load
    sympathomimetic due to vasoconstriction
  36. 2 medication options to treat HF?
    • diuretics
    • ACEi
  37. risk factors for doxorubicin induced CHF?
    • cumulative dose >550mg/m2
    • cumulative dose >400mg/m2 if prior mediastinal radiation, >70yo or <15yo, or prior anthracycline
    • concurrent use of other chemo
  38. how to prevent doxorubicin related cardiac toxicity?
    • dexrazoxane (esp if doxo >300mg/m2; may decrease dox efficacy)
    • questionable: coQ10, carnitine, pretreat with antihistamines, cromolyn sodium, probucol
  39. normal PR second?
  40. normal QRS sec?
    <0.12 sec
  41. normal QT sec?
    <0.4 sec
  42. P wave signifies what in EKG?
    atrial depolarization
  43. Q waves signifies what in EKG?
    ventricular depolarization
  44. T wave signifies what in EKG?
    ventricular repolarization
  45. in sinus pause/arrest, what happened?
    • sinus node is impaired transiently
    • thus there are pauses without P wave on EKG
  46. what is an important clinical feature in sinus bradycardia, sinus pause and sinus arrest?
    HR is low to cannot pump enough blood with oxygen thus leading to dizziness
  47. how does AV block occur?
    conductino of impulse from atria to ventricle thru the AV node is delayed or inhibited.
  48. which degrees of AV block result in bradycardia?
    2nd and 3rd degrees