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Pharmacology- Test 3 Material > 27- Heart Failure > Flashcards

27- Heart Failure Flashcards

1
Q

bisoprolol

A

sustained release beta blocker

  • anti-arrhythmic benefit, impair SNS, improved LV structure and function by preventing remodeling
  • improvement of abnormal Ca2+ handling in HF- preventing hyperphosphorylation of RyR which causes diastolic leak of Ca2+ from SR
  • should be prescribed to all patients with reduced LVEF (stage C) unless contraindicated (bradycardia/reactive airway)
  • side effects- fluid retention, fatigue, weakness, bradycardia, heart block, hypotension
  • reduce death from HF
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2
Q

carvedilol

A

beta 1/2 and alpha 1 blocker

  • anti-arrhythmic benefit, impair SNS, improved LV structure and function by preventing remodeling
  • improvement of abnormal Ca2+ handling in HF- preventing hyperphosphorylation of RyR which causes diastolic leak of Ca2+ from SR
  • should be prescribed to all patients with reduced LVEF (stage C) unless contraindicated (bradycardia/reactive airway)
  • alpha 1 block reduces afterload and workload of heart
  • side effects- fluid retention, fatigue, weakness, bradycardia, heart block, hypotension
  • reduce death from HF
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3
Q

metoprolol

A

beta 1 blocker

  • anti-arrhythmic benefit, impair SNS, improved LV structure and function by preventing remodeling
  • improvement of abnormal Ca2+ handling in HF- preventing hyperphosphorylation of RyR which causes diastolic leak of Ca2+ from SR
  • should be prescribed to all patients with reduced LVEF (stage C) unless contraindicated (bradycardia/reactive airway)
  • side effects- fluid retention, fatigue, weakness, bradycardia, heart block, hypotension
  • reduce death from HF
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4
Q

digoxin

A

inhibit Na/K pump- reduced the gradient for Na/Ca exhange pump

  • increases force of cardiac contraction by increasing intracellular free Ca2+
  • the increased CO decreases reflex SNS activity and increases renal perfusion
  • sensitizes cardiac baroreceptors, may increase vagal tone by increasing SA nodal cell sensitivity to ACh which decreases SNS, increase paraSNS activity on heart
  • also inhibits Na/K pump in kidney reducing renal tubular reabsorption of Na and reducing renin release
  • used for HF with Afib, or severe symptoms of HF despite other therapy
  • Toxicity causes arrhythmias and heart block, it is recommended to keep levels below 1 ng/ml
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5
Q

digitoxin

A

inhibit Na/K pump- reduced the gradient for Na/Ca exhange pump

  • increases force of cardiac contraction by increasing intracellular free Ca2+
  • the increased CO decreases reflex SNS activity and increases renal perfusion
  • sensitizes cardiac baroreceptors, may increase vagal tone by increasing SA nodal cell sensitivity to ACh which decreases SNS, increase paraSNS activity on heart
  • also inhibits Na/K pump in kidney reducing renal tubular reabsorption of Na and reducing renin release
  • used for HF with Afib, or severe symptoms of HF despite other therapy
  • Toxicity causes arrhythmias and heart block, it is recommended to keep levels below 1 ng/ml
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6
Q

eplerenone

A

aldosterone antagonist

  • used for moderately severe HF with LV dysfunction after MI
  • it is not recommended to give without concomitant diuretic therapy
  • side effects- hyperkalemia, NSAIDS decrease efficiency, diarrhea, gastritis, GI bleed, CNS symptoms, rash, cross reaction with other steroid receptors
  • clearance rate significantly decreased by CYP3A4 inhibitors
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7
Q

spironolactone

A

aldosterone antagonist

  • used for moderately severe HF with LV dysfunction after MI
  • it is not recommended to give without concomitant diuretic therapy
  • side effects- hyperkalemia, NSAIDS decrease efficiency, diarrhea, gastritis, GI bleed, CNS symptoms, rash, cross reaction with other steroid receptors
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8
Q

hydralazine (Apresoline)

A

Arterial Vasodilator

  • little effect on venous tone and filling pressure
  • reduces renal vascular resistance and inc. renal BF so can be used in those intolerant to ACEIs
  • used in combo with isosobide dinitrate (BiDil)
  • used alone or in combo with nitrates may provide hemodynamic improvement for those in advanced HF and being treated with other agents
  • together with isosorbide, inc. survival but not as effectively as ACEIs
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9
Q

isosorbide (Isordil)

A

Vasodilator

  • inc. venous capacitance thus lowering preload
  • inc. coronary artery flow via vasodilation enhances ventricular function
  • not effective as arterial dilator thus limiting use as single agent
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10
Q

nitroglycerin (Nitrostat)

A

Parenteral Vasodilator

  • NO source relatively selective for venous capacitence vessels
  • indicated for treatment of L. sided HF due to ischemia or when prompt reduction of filling pressure required
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11
Q

dobutamine

A

Beta-Agonist

  • first choice for patients with systolic dysfunction and congestion associated with HF (no dopa activation)
  • stimulates B1 (inotropy) and B2 (dilation)
  • inotropic effect dominates at typical infusion rates (inc. in renal BF proportional to inc. in CO)
  • can use continually for several days but tolerance develops
  • may cause tachycardia and arrhythmias
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12
Q

dopamine

A

Beta/Alpha Agonist (Dopamine as well but not discussed)

  • stimulates B1 receptors on heart to stimulate contractility (chronotropy and inotropy) and typical infusion rates
  • stimulates a-adrenergic receptors at high infusion rates (may be desirable with circulatory failure but not HF)
  • can cause tachycardia that promotes ischemia in those with CAD
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13
Q

inamrinone

A

cAMP Phosphodiesterase Inhibitor

  • short term support of circulation in advanced HF
  • stimulate contraction and accelerate relaxation by preventing degredation of cAMP
  • cAMP activates PKA resulting in inc. Ca++ entry, inc. SR Ca++ uptake, and inc. Ca++ release– net effect is inc. cytosolic Ca++ to stimulate contraction
  • also stimulate arterial and venodilation
  • CO inc. due to inc. contractility and dec. afterload
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14
Q

milrinone (Primacor)

A

cAMP Phosphodiesterase Inhibitor

  • short term support of circulation in advanced HF
  • stimulate contraction and accelerate relaxation by preventing degredation of cAMP
  • cAMP activates PKA resulting in inc. Ca++ entry, inc. SR Ca++ uptake, and inc. Ca++ release– net effect is inc. cytosolic Ca++ to stimulate contraction
  • also stimulate arterial and venodilation
  • CO inc. due to inc. contractility and dec. afterload
  • has more favorable s/fx profile, shorter half-life, and more selective for PDE-3 and is best among PDE inhibitors for short term inotropic support
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15
Q

Nitroprusside

A

Parenteral Vasodilator

  • NO source that reduces both ventricular filling pressure and SVR
  • used in ICU settings for management of decompensated HF
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16
Q

captopril

A

ACEI

  • block conversion of Ang1 to Ang2
  • decrease effects of ang 2, aldosterone, and increased ang-(1-7)
  • prevent breakdown of bradykinin leading to vasodilation
  • arteries>veins
  • first line therapy: should be started in ALL pts with HF with reduced LVEF
17
Q

lisinopril

A

ACEI

  • block conversion of Ang1 to Ang2
  • decrease effects of ang 2, aldosterone, and increased ang-(1-7)
  • prevent breakdown of bradykinin leading to vasodilation
  • arteries>veins
  • first line therapy: should be started in ALL pts with HF with reduced LVEF
18
Q

enalapril

A

ACEI

  • block conversion of Ang1 to Ang2
  • decrease effects of ang 2, aldosterone, and increased ang-(1-7)
  • prevent breakdown of bradykinin leading to vasodilation
  • arteries>veins
  • first line therapy: should be started in ALL pts with HF with reduced LVEF
19
Q

quniapril

A

ACEI

  • block conversion of Ang1 to Ang2
  • decrease effects of ang 2, aldosterone, and increased ang-(1-7)
  • prevent breakdown of bradykinin leading to vasodilation
  • arteries>veins
  • first line therapy: should be started in ALL pts with HF with reduced LVEF
20
Q

candesartan

A

AT1 antagonist/ ARB

  • Block AT1 receptors leading to an increase in renin and increase activation of AT2 (vasodilation and naturesis).
  • Increases Ang-(1-7): prevent remodeling.
  • Safe alternate to ACEI
21
Q

losartan

A

AT1 antagonist/ ARB

  • Block AT1 receptors leading to an increase in renin and increase activation of AT2 (vasodilation and naturesis).
  • Increases Ang-(1-7): prevent remodeling.
  • Safe alternate to ACEI
22
Q

valsartan

A

AT1 antagonist/ ARB

  • Block AT1 receptors leading to an increase in renin and increase activation of AT2 (vasodilation and naturesis).
  • Increases Ang-(1-7): prevent remodeling.
  • Safe alternate to ACEI
23
Q

loop diuretics

A

decreases preload leading to a decrease in ventricular filling pressures.
-HF operate on plateau of starlling curve,so a reduction in preload will not decrease CO.

24
Q

thiazides

A

decreases preload leading to a decrease in ventricular filling pressures.
-HF operate on plateau of starling curve,so a reduction in preload will not decrease CO.

Pharmacology- Test 3 Material (10 decks)

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