Therapeutics: Overview HF and Systolic 1

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Therapeutics: Overview HF and Systolic 1
2014-03-22 15:26:46
Therapeutics Overview HF Systolic
Therapeutics: Overview HF and Systolic
Therapeutics: Overview HF and Systolic 1
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  1. What drugs are usually used to treat Tachycardia caused by receded CO?
  2. What drugs are usually used to treat Increased preload caused by receded CO?
    ACEIs and Diuretics
  3. What drugs have Negative inotropic effects on HF?
    • Antiarrhythmics
    • Beta-blockers (other than the 3)
    • CCB (non-dihydropyridine CI in Systolic HF)
    • Intraconazole
    • Terbinafine
  4. What drugs have Cardiotoxic effects on HF?
    • Doxorubicin
    • Daunomycin
    • Cyclophosphamide
    • Trastuzumab
    • Ethanol
    • Amphetamines
  5. What drugs have Na/Water retention effects in HF?
    • NSAIDs
    • COX-2 Inhibitors
    • TZD’s
    • Glucocorticoids
    • Androgens/estrogens
    • Na-containing drugs
    • Imatinib
  6. What CCB’s are always CI in Systolic HF?
    Non-dihydropyridine CCB (verapamil and diltiazem)
  7. Do Diuretics provide a mortality benefit for HF?
    No, symptom relief only
  8. What aspects of HF are Diuretics used to treat in HF?
    • Symptoms only:
    • Improve exercise tolerance
    • Improve QOL
    • Reduce hospitilizations
    • Reduce preload (main mechanism)
  9. How should you initiate a diuretic in HF?
    • Start low
    • Adjust based on s/s
  10. How should you monitor Diuretic use in HF?
    • By s/s (i.e. body weight)
    • See HCP if:
    • More than 1 lb/day weight gain for several consecutive days
    • More than 3lb/week
  11. What is the main diuretic used in HF?
    • Loops
    • Mainly Furosemide
  12. What is the peak effect time from time of dosing for Loops?
    30-90 minutes after admin
  13. What is the benefit of Loops over other diuretics?
    Maintain efficacy in Renal impairment
  14. What Loops have a long DOA?
  15. What loops have a short DOA?
    Butenamide and Furosemide
  16. What is the MOA of loops?
    Inhibit Na-K transporter in the ascending loop of henle
  17. What is the usually PO dose of Furosemide?
    20-160 mg QD
  18. What is the Ceiling dose for Furosemide in Normal renal function, CrCl 20-50 and CrCl <20?
    • Normal renal function: 80-160 mg
    • CrCL 20-50 mL/min: 160 mg
    • CrCL < 20 mL/min: 400 mg
  19. What is the DOS for Furosemide?
    6-8 hours
  20. What are the beneficial Mechanisms of ACEIs in HF?
    • Decrease BP: reduce AgII and aldosterone
    • Prevent RAAS mediated worsening of myocardial function and remodeling
    • Decrease preload and afterload
  21. What are the benefits of ACEIs in HF?
    • Mortality benefit
    • Reduce reinfarction, hospitalizations, symptoms, QOL, NYHA functional class and Exercise tolerance
  22. Do ACEIs have a mortality benefit for HF?
  23. What should you monitor when giving and ACEI to a HF patient?
    • SCr and K
    • Dosing
  24. Should patients stop their ACEI if they are symptomatic?
    No, should be on for the rest of their lives
  25. Should a patient be on an ACEI if they have renal insufficiency?
    Yes, benefits outweigh the risks
  26. What are the potential adverse reactions of ACEIs in HF?
    • HYPOtension
    • Renal insufficiency
    • Hyperklaemia
    • Cough
    • Angioedma
  27. What are the indications for ACEIs in Stage A HF?
    Atherosclerotic disease (PAD or CAD) or DM and HTN
  28. What stages are ACEIs indicated for in HF?
  29. What are the indications for ACEIs in Stage B HF?
    • History of MI and EF < 40%
    • EF < 40%
  30. What are the indications for ACEIs in Stage C HF?
    EF < 40%
  31. What are the indications for ACEIs in Stage D HF?
    Continue only if tolerating
  32. What are the BBs with a mortality benefit in HF?
    • Carvedilol
    • Metoprolol succinate
    • Bisoprolol
  33. What is the MOA of BBs in HF?
    • Antagonize Sympathetic NS effects
    • Antiarrhythmic effects
    • Decrease HR/ventricular wall stress
  34. What are the benefits of BBs in HF?
    • Mortality benefit
    • Hospitilizations
    • LV systolic function
    • Reverses remodeling
    • Helps with: symptoms, QOL and exercise tolerance
  35. Do BBs have a mortality benefit?
  36. If a patient is having a symptomatic exacerbation to a BB, what would you do?
    • Temorarily reduce dose
    • Only stop dose under dire situations
    • Don’t start a BB under these conditions
  37. What are the key adverse events realetd to BB use in HF?
    • Fluid retention and worseneinf HF
    • Fatigue
    • Bradycardia
    • HYPOtension
  38. What are the CIs for BB in HF?
    • Bronchospastic disease
    • Severe bradycardia
    • Heart Block
    • Very severe acute decompensated HF
  39. What diseases are BBs precautioned in, but should be used unless symptoms make impossible?
    DM, COPD, asthma and PVD
  40. What is the difference in MOA of the various BBs for HF?
    • Metoprolol succinate and Bisoprolol: Only B1 antagonist
    • Carvedilol: B1, B2 and a1 antagonist
  41. Why might Carvedilol cause more BP lower than Metoprolol succinate and Bisoprolol?
    B/C it is an a1, B1 and B2 antagonist and the others are just B1
  42. What is the Initial dose of Carvedilol CR?
    10 mg QD
  43. What is the target dose of Carvedilol?
    80 mg QD
  44. At what interval should you push up the dose of BB?
    Q2weeks, unless symptomatic, then wait, maybe a month
  45. Typically, should you initiate a BB or ACEI first?
    ACEI first
  46. What stage of HF should you use BBs in?
    • Stage B: History of MI and EF <40% or <40%
    • Stage C: all patient with <40%
    • Stage D if tolerated
  47. When should you initiate a BB before and ACEI?
    • Excessive SNS activity (high HR)
    • ACEI CI due to renal dysfunction or K concentration
  48. Why might you stop a BB in Stage D?
    Makes you feel pretty groggy and sluggish sometimes and Stage D, we just want patients to be comfortable
  49. What are the core agents for HF?
    ACEI and BB
  50. What ARBs are usually used in HF clinical trials?
    Valsartan and Candesartan
  51. What are the benefits of ARBs in HF?
    • Mortality benefit
    • Reduction in hospitalizations
  52. What is the MOA of ARBs in HF?
    • BP control by blocking Ag II and aldosterone
    • Prevents RAAS mediated worsening of myocardial function
  53. How should you monitor ARBs?
    • Same as ACEIs
    • SCr and K
    • BP