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Pharmacology part 3 > Drugs for heart failure > Flashcards

Drugs for heart failure Flashcards

1
Q

most common reason for hospitalization

A

heart failure

-in those over 65

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2
Q

types of CHF

A
  • diastolic (can’t relax heart)

- systolic (can’t contract, or weak contraction)

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3
Q

symptoms seen in both types of CHF

A
  • dyspnea
  • fatigue
  • palpitations
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4
Q

diastolic pathology

A
  • increased left ventricular diastolic pressure with increase interstitial collagen
  • low ATP
  • increased Ca (cause of trouble of cant relax)
  • pulmonary HTN: left atrium enlarged and pulmonary edema
  • ventricles may not be enlarged
  • some cardiac remodeling
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5
Q

what isn’t tolerated well with diastolic pathology

A

tachycardia

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6
Q

systolic pathology

A

Cardiac remodeling:

  • decrease number of cells, giants cells,
  • decrease capillary density,
  • decrease mito,
  • decreased rate contraction due fetal actin and myosin
  • increase fibroblast
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7
Q

what causes increased gene expression in systolic HF

A

exposure to excessive NE, angio II, aldosterone and pro-Inflammatory cytokines, possibly endothelin, vasopressin

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8
Q

what does digitalis glycosides do for CHF?

A

improve function of systolic HF

-mild positive inotropes (heart can’ handle strong ones)

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9
Q

what is used to increase CO in HF

A

-digoxin
“dobutamine holiday” (beta-1 agonist): positive inotrope, used a pressor agent. Causes increase in force without increase in HR. Very short half life, a few seconds

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10
Q

what is given to relieve edema

A

-diuretics (furosemide, strong diuretic)
-spironolactone (aldosterone antagonist)
(*wound healing inhibited and circulation is inhibited by Pulmonary edema)

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11
Q

what is given to decrease angio II

A
  • improve quality of life
  • ACE-I
  • ARB’s if cough severe
  • decrease preload and decrease afterload
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12
Q

what is given to decrease in PR

A
  • isosorbide dinitrate (has tolerance)
  • hydralazine (causes strong reflex tachycardia so must use with BB)
  • unload stressed heart
  • decrease mortality
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13
Q

what is given to decrease HR

A
  • beta blockers can decrease mortality and improve life quality
  • low starting dose
  • carvedilol especially good
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14
Q

what does carvedilol do

A
  • blocks beta1/2 and alpha 1
  • has antioxidant effect
  • decreases remodeling
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15
Q

treatments to increase survival in CHF

A
  • spironolactone
  • ACEI-I
  • vasodilators
  • beta-blockers
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16
Q

MOA of digoxin

A
  • inhibits Na/K/ATPase in plasma membrane of myocyte and cell Na accumulates
  • decrease Na gradient across membrane
  • Na gradient drives ca extrusion during repolarization-> reduced Na gradient leads to less Ca- extrusion- by Na/Ca exchanger
17
Q

digoxin causes

A

CA ACCUMULATION IN CELL

18
Q

vagal effect of digitalis glycosides

A
  • action of brain stem
  • strong cardiac slowing
  • also some direct slowing of conduction in heart due to partial depolarization
  • glycosides may still be used in atrial tachycardias when other drugs don’t work.
19
Q

digoxin usage

A
  • oral absorption ~ 70%
  • does get in brainstem to cause vagal response
  • plasma half life= 36 hours
  • 80% secreted unchanged in urine
20
Q

toxicity of cardiac glycosides

A
  • low TI (~2%)

- therapeutic blood level 1.5 ng/ml

21
Q

three common symptoms of toxicity of cardiac glycosides

A
  1. anorexia, nausea
  2. arrhythmias
  3. neurological: headache, drowsiness, confusion
    - green, yellow vision
    - also gynecomastia and increase blood coagulation
22
Q

factors that influence digoxin toxicity

A
  1. diuretics: increase K loss and increase toxicity
  2. antidiarrheals and Al-containing antacids (Rolaids) bind to glycosides and inhibit absorption
  3. digoxin 25% bound to plasma protein, may be displaced by other drugs (thyroid hormones)
23
Q

how does loss in K lead to digoxin toxicity?

A

low potassium increased glycoside binding to ATPase

24
Q

how is cardiac toxicity treated?

A
  • KCL when K low
  • antiarrythmic drugs
  • atropine for excess vagal activity
  • digoxin antibody: onset 30 min, most patients recover completely
25
Q

duration of digoxin therapy

A
  • long term for most patients

- temporary after heart attack

26
Q

drugs for diastolic HF

A
  1. first line: BB, slow HR
  2. some CCB’s can decrease ventricular stiffness
    - verapamil: decrease HR
  3. ACE-I: prevent remodeling and lower BP (maybe)
  4. diuretics: hypotension can result
27
Q

what is taken for dyspnea

A

nesiritde

  • IV (not available in oral form)
  • h-l: 18 mins
  • causes vasodilation, natriuresis relieves edema
28
Q

what does nesiritde work on?

A

GPCR to increase cGMP and NO

-known as BNP (made by recombinant DNA technology)

29
Q

another positive inotrope for HF

A

milrinone

  • caffeine analog
  • short term use in those who don’t respond to digoxin
30
Q

what does milrinone inhibit?

A

inhibits PDE-3: specific for heart and blood vessels

-good TI

31
Q

side effects of milrinone

A

fever

-some hepatotoxicity

Pharmacology part 3 (13 decks)

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