Agents used in heart failure Flashcards

1
Q

Meaning of Pre-load and after-load

A

P - how much blood comes to the heart

A - peripheral resistance

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2
Q

Compensatory responses that occur in heart failure

A
  1. Decrease cardiac output
  2. Decrease carotid firing
  3. Increase sympathetic discharge
  4. Increase cardiac output - force, rate, preload
  5. Decrease cardiac output
  6. Decrease renal blood flow
  7. Increase renin release
  8. Increase Angiotensin II
  9. Increase preaload, afterload, remodeling
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3
Q

Acute heart failure

-drugs

A
  1. Digoxin
  2. Beta adrenoreceptos agonists
  3. Milrinone
  4. Levosimendan
  5. Diuretics - increase H20 and sodium elimination
  6. Vasodilator drugs - increase preload and afterload

All increase inotropic function

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4
Q

Chronic heart failure

-drugs

A
  1. Digoxin
  2. Beta adrenoreceptos blockers
  3. Ivabradin
  4. ACEi and ARB
  5. Diuretics - increase H20 and sodium elimination
  6. Vasodilator drugs - increase preload and afterload

All decrease workload (preload and afterload)

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5
Q

DIGOXIN

-mechanism of action (6)

A
  1. it binds to sodium-potassium pump and competes with potassium for it
  2. it inhibits sodium-potassium pump
  3. increases intracellular sodium levels
  4. calcium-sodium pump recognizes that there is a lot of calcium intracellulary
  5. this pump is less active
  6. accumulation of calcium intracellulary –> beneficial to cause beta contraction
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6
Q

DIGOXIN

  • principal effects
  • why are there negative effects?
A

+ –> inotropic and bathmotropic effect –> parasympathetic system effect directly
- –> chronotropic and dromotropic effect –> parasympathetic system effect indirectly

Positive inotropic effects will cause a higher cardiac output

  1. more drugs goes to periphery
  2. more blood to carotid sinus
  3. N. vagus active
  4. Parasympathetic system activity is increased in the heart
    - that’s how decrease heart rate is caused indirectly
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7
Q

DIGOXIN

  • pharmacokinetics
  • indications
  • unwanted effects
A
  • high volume of distribution, mainly eliminated by the kidneys
  • to slow ventricular rate in rapid persistent atrial fibrillation, heart failure
  • the effects increase if extracellular K+ is low, pro-arrhythmic effects, GI: nausea, vomiting, diarrhea, vision disturbances
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8
Q

Beta adrenoreceptos agonists used in acute heart failure

A

DOBUTAMINE

DOPAMINE

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9
Q

Dobutamine

  • mechanism of action
  • indications
  • unwanted effects
  • contraindications
A
  • more inotropic effects –> less effect in heart rate, it mainly causes better contraction
  • doesnt have effect to peripheral resistance
  • cardiogenic shock, acute heart failure, after heart surgery
  • tachycardia, dysrhythmia, increase of myocardial damage
  • hypertension, narrowing of the aortic valve, atrial fibrillation
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10
Q

Dopamine

-mechanism of action

A

Low doses - D1 receptors (decrease intracellular cAMP) –> vasodilation of kidney, mesenteric, coronary vessels

Medium doses - B1-adrenoreceptors (increase intracellular cAMP) –> positive inotropic effects

High dose - B1-adrenoreceptors + alpha-adrenoreceptors –> peripheral vasoconstriction

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11
Q

Dopamine

  • indications
  • unwanted effects
A
  • cardiogenic shock, other shock

- tachycardia, dysrhythmias, hypertension

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12
Q

Milrinone

  • indications
  • mechanism of action
  • effects
A

-acute heart failure

  • inhibit phophodiesterase-3
  • prevents degradation of cAMP –> increase intracellular cAMP –> increase calcium –> better cardiac contractility

-increase heart contractility, vasodilator effect

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13
Q

Levosimendan

  • effects
  • mechanism of action
A
  • increase cardiac output without increasing myocardial O2 demand, vasodilator (opens ATP sensitive K+ channels in vascular smooth muscle)
  • calcium sensitizer (increases heart’s sensitivity to Ca2+) –> increases cardiac contractility without rise in intracellular calcium
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14
Q

Ivabradin

  • indications
  • effects
  • mechanism of action
  • contraindications
  • unwanted effects
A
  • chronic stable angina pectoris, chronic heart failure
  • lowers heart rate
  • inhibits If (funny channels) in the heart that controls the spontaneous diastolic depolarization in the SN without affecting any other cardiac ionic channels
  • HR<70 bpm prior to treatment, cardiogenic shock, acute MI, hypotension, sick sinus syndrome, sino-atrial and AV block, unstable or acute heart failure
  • luminous phenomena, blurred vision, bradycardia, AV block, arrhythmia, uncontrolled BP
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15
Q

Sacubitril/Valsartan

  • mechanism of action
  • indications
  • contraindications
  • unwanted effects
A
  • angiotensin receptor and neprilysin inhibitor
  • inhibition of neprilysin leads to reduced breakdown and increased concentration of endogenous natriuretic peptides in addition to increased levels of vasoconstricting hormones such as angiotensin II.
  • However, when combined with valsartan, would result in blocking of angiotensin II to its receptor, preventing the vasoconstrictive effects and resulting in a decrease in vascular resistance and blood pressure.
  • chronic heart failure with reduced ejection fraction
  • concomitant use with ACEi
  • hypotension
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