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
2
Q
Ethacrynic Acid
A
- loop diuretic
- indicated for patients allergic to sulfonamides
- can cause more ototoxicity than furosemide
3
Q
Torsemide
A
-loop diuretic
4
Q
Bumetanide
A
-loop diuretic
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
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
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
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
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
10
Q
Triamterene
A
- K+ sparring diuretic
- blocks ENaC channel
- side effects: hyperkalemia, hyperchloremic metabolic acidosis
11
Q
Amiloride
A
- K+ sparring diuretic
- blocks ENaC channel
- side effects: hyperkalemia, hyperchloremic metabolic acidosis
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
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
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
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
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
