Heart failure medications

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Heart failure medications
2014-11-10 21:13:25
heart failure medications
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  1. Loop diuretics exert their action at the ____.
    Ascending loop Henle
  2. The diuretics are not filtered through the ___, but instead undergo active transport into the tubular lumen via the organic acid pathway.
  3. In the diuretics oral diuretic efficacy may vary based on the different bioavailability, which is almost complete for ___ and ____, but averages only 50% for ___.
    torsemide and bumetanide

    only 50% with furosemide
  4. Diuretics should be initiated at a latus, and titrated to achieve a weight loss up to _____ pounds per day.
    2 lbs per day or 0.91 kgs per day
  5. Metolazone is a thiazide that can be dose _____ or _____ in use with a loop diuretic
    once a day or once a week
  6. Metolazone must be with caution because
    Metabolic abnormalities
  7. Absolute contraindications to using an ace inhibitor include history of ____, bilateral ____, and _____.
    angioedema, bliateral renal artery stenosis, pregnancy
  8. Relative contraindications for using its inhibitor includes_________,_________,_________, _________, and _________.
    Unilateral renal arterial stenosis, renal insufficiency, hypertension, hyperkalemia, and cough
  9. Ace inhibitors should be used in patients with serum creatinine less than _________ to_________.
    2.5 to 3 mg/dL
  10. A small increase of _________ is possible with the addition of any ace inhibitor, it usually becomes transient or becomes patients new serum creatinine baseline level
    0.5 mg/dL
  11. Ace inhibitor should be held if the serum potassium increases above _________.
    5 mEq per liter
  12. Cough is coming soon with its inhibitors and may be related to chelation of tissue_________
  13. In patients truly intolerant or contraindicated to ace inhibitors or ARB's the combination of _________and _________should be considered.
    Hydralazine and isosorbide dinitrate
  14. Nitrates reduce presented by causing primarily venous vasodilation to reactivation of _________and _________in vascular smooth muscle
    guanylate cyclase and cGMP vascular smooth muscle.
  15. The beneficial effect of external nitric oxide source may be more appropriate and_________ population.
  16. Combination therapy with hydralazine and isosorbide dinitrate is an appropriate substitute for a key to antagonists and those who are unable to tolerate an ace inhibitor or ARB or as add-on therapy and African-Americans. True or false.
  17. Isosorbide dinitrate is given_________ times per day.
    3 to 4 times daily at 40 mg.
  18. Hydralazine was given _________ times per day
    3 to 4 times at 75 mg
  19. Hydralazine is also associated with a dose-dependent risk for_________.
  20. Instead of giving isosorbide dinitrate 2 to 4 times daily to increase patient adherence _________ could be given once daily.
    Isosorbide Mononitrate
  21. A nitrate free interval is still required when using nitrates for heart failure. true or false
  22. Beta adrenergic antagonists are also called_________.
    Beta blockers
  23. Beta blockers competitively blocks the influence of the SNS at the _________site.
    Beta-adrenergic receptors
  24. As recently as 15 years ago, beta blockers were thought to be detrimental in heart failure due to their negative inotropic actions. True or false
  25. Chronic beta blockade reduces _________mass, improves _________shape, and reduces _________volumes.
    VentricularventricularLeth ventricle in systolic and diastolic pressures
  26. Beta blockers improve ejection fraction, reduce all causes and heart failure related hospitalizations, and decrease all cause mortality in patients with diastolic heart failure. True or false
    False systolic heart failure , not diastolic
  27. Beta blockers also exhibit antiarrhythmic effects, slow or reverse catecholamine induced ventricular remodeling, decrease myocyte death from catecholamine induced necrosis or apoptosis, and prevent myocardial fetal gene expression. True or false
  28. The three beta blockers that have been shown to reduce mortality and systolic heart failure include bisoprolol (selective or nonselective), metoprolol succininate (selective or nonselective), and carvedilol (selective or nonselective).
    • Selective for metoprolol succinate and bisoprolol
    • Nonselective beta-1 beta-2 and alpha-1 antagonists carvedilol
  29. The key to utilizing beta blockers and systolic heart failure is initiation with high doses and fast hydration to target over days. True or false
    False, start low and go slow over weeks to months
  30. Beta blockade should begin with the lowest possible dose, after which the dose may be double every 2 to 4 weeks, depending on the left ventricular ejection fraction and short-term worsening of heart failure symptoms upon each dose titration. True or false
  31. If the left ventricle ejection fraction is less than 20% metoprolol succinate or carvedilol would be a better choice?
    Metoprolol succinate because it is more selective
  32. In patients with higher blood pressure and heart failure would be better to start metoprolol succinate or carvedilol?
    Carvedilol may provide additional antihypertensive efficacy
  33. Beta blockers should be used with patients who display active respiratory system symptoms. True or false
    False, however, they still can be used if the patient is not exhibiting active symptoms
  34. Metoprolol and carvedilol are metabolized by the liver through the cytochrome P450. Beta blockers should not be used in patients with severe hepatic failure. True or false
  35. Aldosterone antagonists available are _________and _________.
    Spironolactone and eplerenone
  36. Aldosterone antagonists inhibit aldosterone, thus producing week diuretic effects while sparing potassium concentrations. True or false
  37. _________aldosterone antagonists is selective for mineralocorticoid receptor and hence does not exhibit the endocrine adverse effect profile, seen with_________.
    • eplerenone 
    • Spironolactone
  38. _________Should be given to patients with a New York heart Association III to IV,_________ given directly to post MI patients with evidence of LV dysfunction.
    • Spironolactone
    • eplerenon
  39. The major risk related to aldosterone antagonists is _________.
  40. Two parameters that must be assessed before and within one week of initiating aldosterone antagonist therapy include _________and _________
    BMP to assess serum creatinine and potassium
  41. Dosing spironolactone starts at 12.5 225 mg daily, or occasionally _________days for patients with baseline renal insufficiency.
  42. Dosing of aldosterone antagonist should be cut in half or alternate day dosing. If cretin clearance falls below _________ milliliters per minute.
    Creatinine clearance less than 50
  43. When taking aldosterone antagonist potassium supplementation is often decreased or stopped and patient should be counseled to avoid high potassium foods. True or false
  44. Spironolactone has adverse effects, including _________for men and _________ for one and
    Gynecomastia for men and breast tenderness and menstrual irregularities for women
  45. eplereonne is a CYP3A4 substrate and should not be used with other strong inhibitors of 3A4. True or false
  46. Digoxin was shown to slow down heart failure progression and increase survival, but not to decrease heart failure related hospitalizations. True or false
    False. Digoxin has shown to decrease hospitalizations. However, it does not halt the progression of heart failure or increase mortality
  47. Digoxin is initiated at a dose of 0.125 to 0.25 mg daily depending on age, renal function, weight, and risk for toxicity. True or false
  48. Digoxin should be given at the lower dose. If the patient satisfies any of the following criteria; over 65 years of age, creating clearance less than 60 mL per minute, ideal body weight less than 70 kg. Dosing can also be every other day in patients with moderate to severe renal failure. True or false
  49. The desired concentration range for digoxin is _________to _________. Preferably with concentrations at or less than _________.
    • 0.5 to 1.2 ng/mL
    • 0.8 ng/mL
  50. Digoxin toxicity may manifest as nonspecific findings such as fatigue, or weakness, and other CNS effects such as confusion, delirium, and psychosis. True or false
  51. In patients with life-threatening toxicity due to cardiac or other findings while on digoxin administration of _________therapy usually reverses adverse effects within an hour. In most cases.
    Administration of digoxin specific Fab anti-body fragments
  52. Amlodipine and felodipine is the most extensively studied dihydropyridine.  Calcium channel blockers for systolic heart failure.  They have been shown to have a positive effect on patient survival. True or false
    False. They have neither positive or negative patient survival effects. However, they can be safely using heart failure patients to treat uncontrolled hypertension or angina. Once all other appropriate drugs are maximized
  53. Fish oils or omega-3 fatty acids have been recently studied for heart failure and found to mildly decreased cardiovascular permissions and mortality without significant adverse effects. True or false
  54. Hawthorn has been studied in heart failure and is shown to increase exercise capacity and reduce heart failure symptoms. True or false
  55. Treatment of heart failure with preserved left ventricular ejection fraction lacks trials and studies to show optimal treatment. True or false
  56. The current treatment approach for diastolic dysfunction or heart failure with preserved with intricate ejection fraction is correction control of underlying ideologies such as hypertension, CAD and maintenance of normal sinus rhythm, reduction of cardiac filling pressures at rest and enduring in section and increased diastolic filling time. True or false
  57. peripartum cardiomyopathy is defined as clinical and echocardiographic evidence for new onset heart failure occurring during pregnancy and up to six months after delivery.  True or false
    False all other ideologies need to be excluded
  58. The leading hypothesis for peripartum cardiomyopathy is that it is caused by myocarditis via viral infection or abnormal immune response to pregnancy. True or false
  59. Treatment of peripartum cardiomyopathy is similar to that of regular heart failure patients except for _________.
    The use of ace inhibitors and ARB's
  60. Patients with peripartum cardiomyopathy at high risk of thromboembolism. Treatment options during pregnancy are limited to _________ and _________.
    Unfractionated heparin and low molecular weight heparin. Warfarin is contraindicated
  61. After pregnancy with patients with peripartum cardiomyopathy anticoagulation is recommended in patients with LVEF of less than _________ percent.
  62. Types of drugs that may precipitate or exacerbate heart failure
    • Agents causing negative inotropic effects
    • cardiotoxic agents.
    • Agents causing sodium retention
  63. Agents causing negative inotropic effects that may exacerbate HF
    Antiarrhythmic's such as recognized, beta blockers, calcium channel blockers(verapamil and diltiazem) itraconazole, terminafine
  64. What are some cardiotoxic agents that can exacerbate HF
    Doxorubicin daunomycin cyclophosphamide
  65. Agents causing sodium retention of water that exacerbate HF
    NSAIDs, Cox two inhibitors, glucocorticoids, engines, questions, salicylates (high doses), TZDs (rosi and pioglitazone)
  66. Name the 18 symptoms of heart failure
    Dyspnea, orthopnea, shortness of breath, paroxysmal nocturnal dyspnea, kidnapped, cough, fatigue, bacteria and or polyuria, and offices, abdominal pain, anorexia, nausea, bloating, ascites, mental status changes, weakness, lethargy
  67. What are the 13 signs of heart failure
    Pulmonary rails, pulmonary edema, S3 gallop, plural effusions, Cheyne–Stokes respiration, tachycardia, cardiomegaly, peripheral edema, jugular venous distention, hepatojugular reflux, hepatomegaly, cyanosis of the digits, pallor or cold extremes
  68. Acute HF Subset 1 (warm and dry)
    -CI ____ and pulmonary capillary wedge pressure less than ______
    -Pt considered well compensated and perfused without evidence of congestion
    no immediate interventions necessary except to maximize oral meds
    • CI greater than 2.2 L/min/m2
    • PCWP less than 18 mmHg
  69. Acute HF Subset 2 (warm and wet)
    -CI greater than _____ and PCWP less than _____
    -patients adequately perfused and display signs and symptoms of _____
    -mail goal is to reduce _____ with ______
    • - >2.2 CI and >18 mmHg PCWP
    • -congestion
    • -preload (PCWP) with loop diuretics and vasodilators
  70. Acute HF Subset 3 (cool and dry)
    -CI ____ 2.2 L/min/mPCPW ____ 18 mmHg
    -Pt are inadequately perfused and not congested
    -Tx focuses on increasing ____ with ____ agents and replacing fluids
    -fluid replacement must be done conservatively
    • CI LESS than 2.2 and PCPW GREATER
    • tx focuses on increasing CO with positive inotropic agents
  71. Subset IV (cool and wet)
    -CI ____ 2.2 L/min/mPCWP _____ 18 mmHg
    -Pts are inadequately ____ and ____
    -worst prognosis
    -____ are used to maintain blood pressure
    • -CI less than 2.2 and PCWP less than 18
    • -perfused and congested
    • -pressors
  72. Treatment of AHF targets relief of congestion and optimization of cardiac output, utilizing oral and IV_________, IV_________, and when appropriate allotropes based on presenting hemodynamics.
    IV diuretics and IV vasodilators
  73. AHF
    Diuretics reduce_________, but do not increase cardiac index, as do positive inotropes and arterial vasodilators
    PCWP pulmonary capillary wedge pressure (Congestion)
  74. AHF
    onset of action (min)
    duration of action (hours)
    intermittent bolus dosing (mg)
    cont infusion dosing (bolus/infusion)
    • onset of action (min) 2- 5 
    • duration of action (hours) 6
    • intermittent bolus dosing (mg) 20-200+
    • cont infusion dosing (bolus/infusion) 20-40/2.5-10
  75. AHF
    onset of action (min)
    duration of action (hours)
    intermittent bolus dosing (mg)
    cont infusion dosing (bolus/infusion)
    • onset of action (min) less than 10 min
    • duration of action (hours) 6-12 hours
    • intermittent bolus dosing (mg) 10-100
    • cont infusion dosing (bolus/infusion) 20/2-5
  76. AHF
    onset of action (min)
    duration of action (hours)
    intermittent bolus dosing (mg)
    cont infusion dosing (bolus/infusion)
    • onset of action (min) 2-3
    • duration of action (hours) 4-6
    • intermittent bolus dosing (mg) 1-10
    • cont infusion dosing (bolus/infusion) 1-4/0.5-1