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Heart Failure Drugs > Heart Failure Drugs > Flashcards

Heart Failure Drugs Flashcards

1
Q

Furosemide

A
  • loop diuretic
  • blocks NKCC2 in thick ascending loop
  • most common
  • monitor K+ levels
  • induce prostaglandin and NO generation from endothelial cells
  • 4-8 hrs duration
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2
Q

Ethacrynic Acid

A
  • loop diuretic
  • indicated for patients allergic to sulfonamides
  • can cause more ototoxicity than furosemide
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3
Q

Torsemide

A

-loop diuretic

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4
Q

Bumetanide

A

-loop diuretic

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5
Q

Chlorothiazide

A
  • thiazide diuretic
  • blocks Na+/Cl- cotransporter NCC in distal convoluted tubule
  • PO
  • cause hypokalemia, metabolic alkalosis, hypomagnesemia, hyponatremia, hypercalcemia, hyperglycemia, hyperurecemia
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6
Q

HCTZ

A
  • thiazide diuretic
  • blocks Na+/Cl- cotransporter NCC in distal convoluted tubule
  • PO
  • cause hypokalemia, metabolic alkalosis, hypomagnesemia, hyponatremia, hypercalcemia, hyperglycemia, hyperurecemia
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7
Q

Chlorthalidone

A
  • thiazide diuretic
  • blocks Na+/Cl- cotransporter NCC in distal convoluted tubule
  • PO
  • cause hypokalemia, metabolic alkalosis, hypomagnesemia, hyponatremia, hypercalcemia, hyperglycemia, hyperurecemia
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8
Q

Metolazone

A
  • thiazide diuretic
  • blocks Na+/Cl- cotransporter NCC in distal convoluted tubule
  • PO
  • cause hypokalemia, metabolic alkalosis, hypomagnesemia, hyponatremia, hypercalcemia, hyperglycemia, hyperurecemia
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9
Q

Indapamide

A
  • thiazide diuretic
  • blocks Na+/Cl- cotransporter NCC in distal convoluted tubule
  • PO
  • cause hypokalemia, metabolic alkalosis, hypomagnesemia, hyponatremia, hypercalcemia, hyperglycemia, hyperurecemia
  • UNIQUE VASODILATORY EFFECTS
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10
Q

Triamterene

A
  • K+ sparring diuretic
  • blocks ENaC channel
  • side effects: hyperkalemia, hyperchloremic metabolic acidosis
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11
Q

Amiloride

A
  • K+ sparring diuretic
  • blocks ENaC channel
  • side effects: hyperkalemia, hyperchloremic metabolic acidosis
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12
Q

Spironoloactone

A
  • K+ sparring diuretic
  • direct aldosterone antagonist
  • opposes aldosterone action in late distal tubule and collecting duct
  • side effects: hyperkalemia, hyperchloremic metabolic acidosis, gynecomastia
  • aldosterone antagonists may be preventing myocardial and vascular fibrosis
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13
Q

Eplerenone

A
  • K+ sparring diuretic
  • direct aldosterone antagonist
  • opposes aldosterone action in late distal tubule and collecting duct
  • side effects: hyperkalemia, hyperchloremic metabolic acidosis
  • aldosterone antagonists may be preventing myocardial and vascular fibrosis
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14
Q

Vasodilators (ACEi)

A
  • decrease afterload by lowering peripheral resistance
  • reduce preload by reducing aldosterone secretion, thereby lowering salt and water retention
  • can cause hyperkalemia
  • decrease in the degradation of bradykinin, which stimulates NO output
  • decrease sympathetic activity by reducing norepinephrine release
  • decrease long-term remodeling of the heart vessels
  • used in conjunction with diuretics and digitalis
  • prolonged treatment reduces CHF and reduces mortality
  • in acute MI, ACEi decrease LV diastolic volume, prevent further ventricular dilation, and improve exercise tolerance
  • Side Effects: cough, angioedema, hypotension, hyperkalemia, increased fetal mortality
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15
Q

ARBs

A
  • block AT1
  • decrease afterload by lowering PVR
  • reduce preload by reducing aldosterone secretion, thereby lowering salt and water retention
  • long-term therapy reduces the risk of death and other cardiovascular events in patients with HF
  • does NOT effect bradykinin duration, or production of NO
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16
Q

Aliskiren

A
  • renin blocker
  • binds to active site of renin
  • similar side effects to ACEi
17
Q

Beta-Blockers

A
  • suggested in patients with a decreased LVEF

- bisoprolol, carvedilol, metoprolol succinate

18
Q

Beta Adrenergic Antagonists

A
  • attentuation of the adverse effects of high concentrations of catecholamines (including apoptosis)
  • up-regulation of beta-1 receptors for increased catecholamine responsiveness
  • decreased heart rate and decreased arrhythmogenesis
  • reduced remodeling through inhibition of the mitogenic activity of catecholamines
  • short term: no acute lowering of CO; myocardial depression is balanced with vasodilation
  • long term: prevents deterioration of myocardial function and reverses adrenergically mediated myocardial dysfunction and remodeling in dilated caridomyopathy
19
Q

Digitalis, Digoxin, Digitoxin, Ouabain

A
  • inotropic agents
  • cardiac glycosides
  • block the Na/K pump
  • increased Na oppose action of Na-Ca exchanger NCX, thus raising intracellular cytosolic Ca++ concentration
  • increased cytosolic Ca++ increases Ca++ levels in sacroplasmic reticulum
  • action potential then release greater-than-normal Ca++ to increase contraction
  • K+ antagonizes action of digitalis
  • decrease sympathetic output (direct and reflex) and increased vagal activity
  • decrease in HR and increased vasodilation
  • increased renal perfusion
  • some inhibition of renal Na/K ATPase promoting Na+ excretion and diuresis
  • improved renal perfusion dynamics and reduced renin output
20
Q

Digoxin

A
  • reduces morbidity and hosptializations in CHF
  • fewer deaths from failure are balanced with more from sudden death
  • does seem to support the ability of ACEi to retard progressive cardiac deterioration in CHF
21
Q

Effects of Ouabain

A
  • increases calcium releasse
  • at toxic levels, action potential shortens further and a oscillatory depolarization is evoked, causing a calcium increment and an additional contraction
  • Ouabain has low lipid solubility and is almost never used
22
Q

Istaroxime

A

-investigational steroid derivative that inhibits Na/K pump, but in addition facilitates Ca++ sequestration by the SR, which may render the drug less arrhythmogenic than digoxin

23
Q

Digitalis on Cardiac Electrical Fxns

A
  • enhances vagal tone and reduces sympathetic activity
  • slows conduction velocity and increases refractoriness in AV node
  • reduces rate of ventricular stimulation in patients with atrial fibrillation or flutter
  • can convert some SVT reentrant arrhythmias to normal rhythm
24
Q

Digitalis at Toxic Levels

A
  • AV block
  • promotes many forms of arrhythmia due to enhancement of vagal tone and extreme inhibition of Na/K pump
  • increases sympathetic outflow, sensitizing the myocardium
  • nausea, vomiting, visual disturbances
  • digitalis induced tachyarrythmias treated with K+ if hypokalemia present, lidocaine, or Digitalis antibody
25
Q

Milrinone

A
  • bipyridines
  • selective for phosphodiesterase isozyme 3 (PDE3)
  • increased cAMP and phosphorylation/activation of L-type calcium channels, raising Ca++ and increasing myocardial contractility
  • increased cAMP –> vasodilation
  • safe and effective for short term (<24 hrs) support of decompensated HF or for an exacerbation of CHF
  • useful when other txts are failing
  • less prone to produce arrhytmmias than adrenergics or digitalis
  • more likely to promote fatal arrhythmias than Inamrinone
  • produces less bone marrow and liver toxicity
26
Q

Inamrinone

A
  • bipyridines
  • selective for phosphodiesterase isozyme 3 (PDE3)
  • increased cAMP and phosphorylation/activation of L-type calcium channels, raising Ca++ and increasing myocardial contractility
  • increased cAMP –> vasodilation
  • safe and effective for short term (<24 hrs) support of decompensated HF or for an exacerbation of CHF
  • useful when other txts are failing
  • less prone to produce arrhytmmias than adrenergics or digitalis
  • increases mortality relative to placebo
  • tachyphylaxis (receptor desensitization)
  • toxicity includes nausea, vomiting, arrhythmias, thrombocytopenia, liver enzyme changes
27
Q

Dobutamine

A
  • beta-adrenergic agonist
  • activates adenylate cyclase to make cAMP
  • increased Ca++ levels in the SR to increase contraction
  • useful in txt of HF not accompanied by hypotension
  • synthetic analog of dopamine that stimulates beta-1 and beta-2 and alpha receptors
  • incrases contractility thorugh beta-1
  • does not increase peripheral resistance because beta-2 and alpha-1 balance each other out
28
Q

Norepinephrine

A
  • acts at beta-1 and peripheral alpha-receptors

- used for “warm” septic shock (good PVR)

29
Q

Epinephrine

A
  • acts at beta-1, beta2, and peripheral alpha-receptors
  • useful for increasing contraction and HR
  • used for cardiac arrest
  • contraindicated in pts receiving beta-blocker therapy because of risk of alpha-mediated severe hypertension

Heart Failure Drugs (1 decks)

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