Therapeutics: Overview HF and Systolic 2

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  1. If and ARB causes symptoms, should you continue it?
  2. What adverse events can and RB cause?
    • HYPOtension
    • Renal insufficiency (10-20% increase is normal)
    • HYPERkalemia
    • Angioedema (less risk than ACEIs)
  3. If a patient has HYPOtension, Renal insufficiency or HYPERkalemia in an ACEI, would it be useful to switch them to an ARB?
    • No, ARBs cause those things too
    • Only with Angioedema or Cough would you switch
  4. What is the initial dose of Candesartan?
    4-8 mg QD
  5. What is the Maximum dose of Candesrtan?
    32 mg QD
  6. What is the mean dose of Candesartan achieved in clinical trials?
    24 mg QD
  7. In what stages of HF would you use ARBs?
    Stage A-D instead of an ACEI
  8. When would you use an ACEI and ARB?
    ACEI escape – very controversial
  9. What might be a better option for a patient on an ACEI and BB than adding an ARB?
    Add Aldosertone antagonist
  10. Do Aldosterone antagonists have a mortality benefit in HF?
    Yes, when added to an ACEI/BB combo
  11. What are the benefits of Aldosterone antagonists?
    • Mortality benefit when added to ACEI/BB combo
    • Reduction in hospitilizations
  12. What are the Mechanism for Aldosterone antagonists in HF?
    • BP control by blocking aldosterone receptors
    • Prevent RAAS-mediated worsening of myocardial function
    • Attenuate cardiac fibrosis and remodeling
    • Diminish systemic pro-inflammatory state and oxidative stress by aldosterone
  13. When is adding an aldosterone antagonist to an HF therapy CI?
    • Women: SCr >2 mg/dL
    • Men: SCr >2.5 mg/dL
    • CrCl < 30 mL/min
    • Worsening of renal function
    • K >5 mEq/L
    • History of sever HYPERkalemia
  14. What is the initial dose for Spirolactone?
    12.5-25 mg QD
  15. What is the Max dose of Spirolactone?
    25 mg QD or BID
  16. What is the mean dose achieved in clinical trials for Spirolactone?
    26 mg QD
  17. How can you reduce the risk of HYPERkalemia with aldosterone antagonists?
    • Decrese or D/C K supplements
    • Avoid concomitant NSAID/COX inhibitors, high dose ACEIs or ARBs
    • Avoid ACEI, ARB AA triple therapy
    • Monitor renal function and serum K
  18. How often Should Serum K and renal function be monitored in a patient on an Aldosterone antagonist?
    • Between 3 days and 1 week after initiation or titration
    • Monthly for first 3 months
    • Then every 3 months
  19. If a patient’s K goes over 5.5 mg/dL, what should you do?
    • D/C any K supplementation
    • Reduce of stop aldosterone antagonists
  20. Under what conditions should you temporarily D/C AA therapy?
    • Diarrhea
    • Diuretic therapy is interrupted
  21. What Stage of HF would you initiate an AA?
    Stage C
  22. Under what conditions would you initiate an AA?
    • Stage C HF (or D)
    • Optimal ACEI/BB therapy
    • Class II if elevated BNP or cardiac hospitalization
    • Class III-IV ( even if they don’t meet all the rest of this criteria)
    • EF <35%
    • SCR < 2.5 in men or <2 in women
    • GFR > 30 mL/min
    • K <5
    • OR Acute MI w/ EF < 40% and symptoms of HF or history of DM
  23. What group of HF patients benefits the most from Isosorbide Dinitrate and Hydralazine therapy?
    Stage III-IV African Americans already on optimal ACEI and BB with systolic HF that are still symptomatic
  24. What is the MOA of Isosorbide Dinitrate and Hydralazine in HF?
    • Nitrates cause venodilation = decrease preload
    • Hydralazine causes arterial dilation = decreases afterload
  25. What effect does Hydralazine have on Isosorbide dinitrate?
    May reduce tolerance of the nitrate
  26. What is the benefit of Isosorbide Dinitrate and Hydralazine in HF?
    • Mortality benefits
    • Reduced hospitilizations
    • QOL
  27. Why does Isosorbide Dinitrate and Hydralazine work better in African American patients?
    African American patients have less nitric oxide
  28. When might you use an Isosorbide Dinitrate and Hydralazine combo in a non-AA patient?
    • Add on therapy for symptomatic non-AA pts with EF≤ 40%
    • Alternate therapy for tolerance issues with other drugs
  29. Does Digoxin have a mortality benefit?
  30. What are the benefits of Digoxin in HF?
    • Aids in symptoms
    • QOL
    • Exercise tolerance
    • Reduce hospitilizations
  31. What is the MOA of Digoxin in HF?
    • + inotropic effects
    • Inhibits Na/K transporter in Myocardium
    • Increases Na, causes Ca influx and leads to increased contractility
    • Neurohormonal modulation
    • Increases PNS activity
  32. What are the CIs for Digoxin use in HF?
    Ventricular fibrillation
  33. What are the Precautions for Digoxin use in HF?
    • High arrhythmia risk
    • Acute MI (avoid w/in 6 mo after)
    • Heart block
    • Electrolyte imbalance (important caution = avoid)
    • Hypermetabolic state
    • Renal Impairment
    • Thyroid Disease (important caution = avoid)
  34. What effect does HYPOthyroid have on digoxin therapy?
    Increased risk of digoxin toxicity = higher digoxin levels
  35. What effect does HYPERthyroid have on Digoxin therapy?
    Lower the digoxin levels
  36. What are the DDIs with Digoxin?
    CYP3A4 and Pgp interactions
  37. What is considered Digoxin toxicity>
    >2 ng/mL
  38. What should you monitor when a patient is on Digoxin?
    • HR and rhythm
    • Metabolic panel
    • Serum digoxin levels
  39. What are the Adverse effects of Digoxin in HF?
    • Arrhythmias
    • CNS (dizziness, mental disturbances, HA)
    • Dermatologic (rash)
    • GI (N/V/D)
    • Neuromuscular and skeletal: weakness
    • Ocular: blurred, yellow vision, halos
  40. At what interval should you be monitoring Digoxin serum concentrations?
    • Measure Trough q3-6mo if have been on awhile
    • After initiation: 5-7 days after starting, 6-8 hours after dose (ideally 12-24 hours after)
  41. How long does it take to reach a SS digoxin concentration?
    Several weeks
  42. What is a normal dose of digoxin?
    • .125-0.25 mg QD
    • Reduce to Every other day dosing if they have decreased renal function are elderly or have interacting meds
  43. What is the target serum for Digoxin in HF?
    0.5-0.9 ng/mL ( higher w/ afib)
  44. When would you put a HF patient on Digoxin?
    Stage C or D and All other drugs are optimal, but still symptomatic
  45. Does Hyperthyroidism cause digoxin toxicity?
  46. Does HYPOkalemia cause digoxin toxicity?
  47. Does Renal dysfunction cause digoxin toxicity?
  48. Does HYPcalcemia cause digoxin toxicity?
  49. What agents can be used for blood pressure control in HTN in HF?
    • ACEI/ARB, BB, diuretics
    • Aldosterone antagonists, hydralazine/(ISDN)
    • Amlodipine or felodipine
  50. What drugs should be avoided for BP control in HF?
    • Non-DHP CCB, clonidine, minoxidil
    • Never use these
  51. What drugs are OK to use in a patient with HF and Afib for rate control?
    Digoxin or BB (BB preferred)
  52. What drugs are OK to use in a patient with HF and Afib for Rhythm control?
    Amiodarone or Defetilide
  53. What drusg should be avoided when treating Afin in patients with HF?
    • Non-DHP CCB
    • Class I antiarrhythmics
  54. Are anti-thrombotic therapies acceptable in patients with Afib and HF?
Card Set:
Therapeutics: Overview HF and Systolic 2
2014-03-22 19:27:53
Therapeutics Overview HF Systolic
Therapeutics: Overview HF and Systolic 2
Therapeutics: Overview HF and Systolic 2
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