Drugs used in heart failure Flashcards Preview

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Flashcards in Drugs used in heart failure Deck (14):
1

Furosemide

  • MOA
    - loop diuretic: decreases NaCl and KCl reabsorption in thick ascending loop of Henle
  • Effects
    - increased excretion of salt and water
    - reduces preload and afterload
    - reduces pulmonary and peripheral edema
  • Clinical
    - acute & chronic heart failure
    - severe hypertension
    - edema
  • Kinetics, tox, int.
    - oral, IV, duration 2-4h
    - tox: hypovolemia, hypokalemia, orthostatic hypotension, ototoxicity, sulfonamide allergy

2

Hydrochlorothiazide

  • MOA
    - decreases NaCl reabsorption in distal convoluted tubule
  • Effects
    - same as furosemide, but much less efficacious
  • Clinical
    - mild chronic failure, mild-moderate hypertension
    - hypercalcuria
  • Kinetics, tox, int.
    - oral, duration 10-12h 
    - tox: hyponatremia, hypokalemia, hyperglycemia, hyperuricemia, hyperlipidemia, sulfonamide allergy

3

Spironolactone

  • MOA
    - blocks cytoplasmic aldosterone receptors in collecting tubules
  • Effects
    - increases salt & water excretion, reduces remodeling
  • Clinical
    - chronic heart failure
    - aldosteronism
    - hypertension
  • Kinetics, tox, int. 
    - oral, duration 24-72h (slow onset & offset)
    - tox: hyperkalemia, antiandrogen actions

4

Captopril

  • MOA
    - inhibits ACE - reduction of AII by inhibiting conversion from AI
  • Effects
    - arteriolar and venous dilation
    - reduces aldosterone secretion
    - reduces cardiac remodeling
  • Clinical
    - chronic heart failure, hypertension, diabetic nephropathy
  • Kinetics, tox, int.
    - oral, t1/2 2-4h but given in large doses so duration 12-24h
    - tox: cough, hyperkalemia, angioneurotic edema
    - int: additive with other angiotensin antagonists

5

Losartan

  • MOA
    - antagonize AII effects at AT1 receptors (angiotensin receptor blocker, ARB) 
  • Effects
    - like ACE inhibitors
  • Clinical 
    - like ACE inhibitors, used in pt intolerant to ACE inhibtors
  • Kinetics, tox, int.
    - oral, duration 6-8h
    - tox: hyperkalemia, angioneurotic edema
    - int: additive with other angiotensin antagonists 

6

Carvedilol

  • MOA
    - competitively blocks β1 receptors
  • Effects
    - slows heart rate, reduces blood pressure
  • Clinical
    - chronic heart failure - slows progression
    - reduce mortality in moderate and severe heart failure
    - other indications - see ch.10 
  • Kinetics, tox, int.
    - oral, duration 10-12h
    - tox: bronchospasm, bradycardia, AV- block, acute decompensation 

7

Digoxin

  • MOA
    - Na+/K+-ATPase inhibition→reduced Ca2+ expulsion & increased Ca2+ stored in SR
  • Effects
    - increases cardiac contractility, cardiac parasympathomimetic effect (slowed HR, slowed AV conduction)
  • Clinical
    - chronic symptomatic heart failure
    - rapid ventricular rate in atrial fibrillation 
  • Kinetics, tox, int. 
    - oral, parenteral, duration 36-40h
    - tox: nausea, vomiting, diarrhea, arrythmias

8

Isosorbide dinitrate

  • MOA
    - venodilator
    - releases NO, activates guanylyl cyclase
  • Effects
    - venodilation, reduces preload and ventricular stretch
  • Clinical
    - acute and chronic heart failure, angina
  • Kinetics, tox, int.
    - oral, duration 4-6h
    - tox: postural hypotension, tachycardia, headache
    - int: additive with other vasodilators and synergistic with phosphodiesterase type 5 inhibitors

9

Hydralazine

  • Arteriolar dilator
  • MOA
    - increases endothelial NO synthesis
  • Effects
    - reduces blood pressure and afterload, results in increased output 
  • Clinical
    - reduced mortality with hydralazine + nitrates
  • Kinetics, tox, int. 
    - oral, duration 8-12h
    - tox: tachycardia, fluid retention, lupus-like syndrome

10

Nitroprusside

  • Combined arteriolar and venodilator
  • MOA
    - releases NO spontaneously
    - activates guanylyl cyclase
  • Effects
    - marked vasodilation
    - reduces preload and afterload
  • Clinical
    - acute decompensation, hypertensive emergencies
  • Kinetics, tox, int.
    - IV only, duration 1-2min
    - tox: excessive hypotension, thiocyanate and cyanide toxicity
    - int: additive with other vasodilators 

11

Dobutamine

  • MOA
    - β1 selective agonist, increases cAMP synthesis
  • Effects
    - increases contractility, output
  • Clinical
    - acute decompensated heart failure
    - intermittent therapy in chronic failure reduces symptoms
  • Kinetics, tox, int.
    - IV only, duration a few minutes
    - tox: arrythmias
    - int: additive with other sympathomimetics 

12

Dopamine

  • MOA
    - D receptor agonist, higher doses activate β and α receptors
  • Effects
    - increases renal blood flow, higher doses increase cardiac force and blood pressure
  • Clinical
    - acute decompensated heart failure
    - shock
  • Kinetics, tox, int. 
    - IV only, duration a few minutes
    - tox: arrythmias
    - int: additive with other sympathomimetics

13

Milrinone

  • MOA
    - phosphodiesterase type 3 inhibitor
    - decreases cAMP breakdown
  • Effects
    - vasodilator, lowers peripheral vascular resistance
    - increases contractility 
  • Clinical
    - acute decompensated heart failure
    - increases mortality in chronic failure
  • Kinetics, tox, int.
    - IV only, duration 3-6h
    - tox: arrythmias
    - int: additive with other arrythmogenic agents

14

Nesiritide

  • Natriuretic peptide
  • MOA
    - activates BNP receptors, increases cGMP
  • Effects
    - vasodilation, diuresis 
  • Clinical
    - acute decompensated heart failure
  • Kinetics, tox, int.
    - IV, duration 18 minutes
    - tox: renal damage, hypotension, may increase mortality