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Cardio CP1 > 9 Heart Failure Drugs > Flashcards

9 Heart Failure Drugs Flashcards

1
Q

What are the effects of digoxin?

A
  • positive inotrope
    • increases contractile state of myocardium
    • increases SV
  • increases vagal tone
    • decreases HR
  • arterial/venous dilation (decreased venous pressure)

**shifts frank-starling curve to I+V point

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2
Q

What is the MOA of digoxin?

A
  • inhibits Na/K ATPase
    • increases intracellular Na -> decreases drive to extrude Ca via Na/Ca exchanger- -> indirect increase in intracellular Ca
  • K competes for binding of digoxin to Na/K ATPase
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3
Q

What are some side effects of digoxin?

A

Affects all excitable tissues:

  • GI tract (N/V/D)
  • Visual disturbances
  • Neurologic (hallucinations)
  • Muscular
  • Cardiac (arrhythmias)

**toxicity enhanced with hypokalemia

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4
Q

What is the clinical use of digoxin?

A

Limited to heart failure patients with LV systolic dysfunction in atrial fibrillation (or in sinus patients with continued symptoms despite maximal therapy)

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5
Q

What are the effects of diuretics?

A
  • promote elimination of Na and water -> reduce intravascular volume -> decreased venous return
  • decreased preload= no longer in range promoting pulmonary congestion
    • ​reduce EDP without reducing SV (move to point D on frank starling curve)
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6
Q

Describe furosemide

A
  • loop diuretic (potent)
  • widely used (many heart failure patients require chronic loop diuretic therapy to maintain euvolemia)
  • promotes K loss -> hypokalemia
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7
Q

Describe chlorothiazide

A
  • thiazide diuretic
  • rarely used alone
    • use in combo therapy with loop diuretics in patients refractory to loop diuretics alone
  • promotes K loss -> hypokalemia
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8
Q

Describe amiloride

A
  • K-sparing diuretic
  • weak diuretic activity but limits K and Mg wasting
    • commonly used in combo therapy
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9
Q

Describe triamterene

A
  • K-sparing diuretic
  • weak diuretic activity but limits K and Mg wasting
    • commonly used in combo therapy
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10
Q

What are the effects of angiotensin II?

A
  1. potent arterial constrictor (increases BP)
  2. Na and water retention (via aldosterone stimulation)
  3. promote neuronal and adrenl medulla catecholamine release -> enhances sympathetic activity
  4. arrhythmogenic
  5. promotes cardiac remodeling (hypertrophy, fibrosis, apoptosis)
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11
Q

What are the effects of aldosterone?

A
  1. promotes Na and water retention
  2. promotes K secretion
  3. promotes cardiac remodeling (fibrosis)
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12
Q

What are the effects of ACE inhibitors?

A
  • decrease systemic vascular resistance (afterload)
    • block constricting activity of Ang II
  • reduce intravascular volume and systemic/pulmonic congestion
    • block Ang II/aldosterone retention of Na and water
  • limit maladaptive ventricular remodeling
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13
Q

Describe captopril

A
  • ACE inhibitor
    • decrease vascular resistance/afterload
    • block Ang II/aldosterone retention of Na and water
    • limit maladaptive ventricular remodeling
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14
Q

Describe enalapril

A
  • ACE inhibitor
    • decrease vascular resistance/afterload
    • block Ang II/aldosterone retention of Na and water
    • limit maladaptive ventricular remodeling
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15
Q

What are some side effects of ACE inhibitors?

A
  • hyperkalemia (esp when combined with K sparing diuretics)
  • angioedema (from bradykinin)
  • dry cough (from bradykinin)
  • hypotension
  • renal failure
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16
Q

Describe angiotensin receptor blockers

A
  • competitively block AT1 receptor
  • do NOT prevent degradation of bradykinin
  • potential alternative for heart failure patients who can’t tolerate an ACE inhibitor
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17
Q

Describe losartan

A
  • angiotensin receptor blocker
  • potential alternative for heart failure patients who can’t tolerate an ACE inhibitor
18
Q

Describe valsartan

A
  • angiotensin receptor blocker
  • potential alternative for heart failure patients who can’t tolerate an ACE inhibitor
19
Q

What are some side effects of angiotensin receptor blockers?

A
  • hypotension
  • renal failure
  • hyperkalemia (esp with K sparing diuretics)
20
Q

Describe the Valsartan/Sacubitril combination pill

A
  • Valsartan= angiotensin blocker
  • Sacubitril= neprilysin inhibitor
    • decreases breakdown of vasoactive peptides (ANP, bradykinin, etc)
    • counters the neurohormonal activation that leads to vasocontstriciton, Na retention, and maladaptive remodeling
  • Combo= superior to enalapril in reducing risks of death and hospitalizations for heart failure
21
Q

Describe aldosterone antagonists

A
  • decreases fibrosis and adverse ventricular remodeling normally induced by excess aldosterone in heart failure
  • improves mortality rates
  • reduces symptoms such as…
    • edema
    • arrhythmias
    • fibrosis (in myocardium and vessels)
22
Q

Describe spironolactone

A
  • aldosterone antagonist
  • decreases fibrosis and adverse ventricular remodeling normally induced by excess aldosterone in heart failure
23
Q

Describe eplerenone

A
  • aldosterone antagonist
  • decreases fibrosis and adverse ventricular remodeling normally induced by excess aldosterone in heart failure
24
Q

What is an adverse effect of aldosterone antagonists?

A

Hyperkalemia

25
Q

What are the types of vasodilators? Give examples

A
  • venous
    • nitrates
  • mixed
    • ACE inhibitors
    • Ang II inhibitors
    • nitroprusside
  • arterial
    • hydralazine
26
Q

What are the hemodynamic effects of different vasodilators?

A
  • venous
    • decreases preload (LV EDV)
    • results in decreased wall stress (little effect on SV)
  • arterial
    • reduces afterload (decreases systemic resistance)
    • results in increased SV and decreased wall stress
  • mixed
    • reduces both preload and afterload
    • results in increased SV and decreased wall stress
27
Q

Describe the isosorbide dinitrate/hydralazine combo

A
  • improves survival in heart failure patients (though less effective than ACE inhibitors)
    • substitute when not able to tolerate ACE inhor ang blocker (e.g. in renal dysfunction)
  • more effective in african americans
28
Q

What are the effects of beta blockers on heart failure?

A

Ultimately stop the chronic sympathetic stimulation that worsens heart failure…

  • decrease arrhythmias, oxygen demans, and BP
  • prevent disease progression/remodeling
  • inhibit cardiotoxic actions of catecholamines
  • reduce Beta 1 receptor down-regulation

**can initially worsen cardiac function, must start at a low dose and gradually increase to maximum dose

29
Q

Describe ivabradine

A
  • slows HR by blocking If channels in pacemaker cells
  • considered for use in heart failure patients with a resting heart rate over 70 bpm (including those already taking a beta blocker)
  • prolongs survival time
30
Q

Describe the best drugs to use in NYHA classes I-IV

A
31
Q

What are some non-medication therapies for heart failure?

A
  • salt restriction
  • rehab/exercise
  • biventricular pacing/cardiac resynch therapy (CRT)
  • implantable cardio-defibrillator devices (ICDs)
  • mechanical circulatory support
    • ventricular assist devices (VADs)
    • implantable artificial hearts
  • heart transplant
32
Q

What therapies are used in heart failure with preserved ejection fraction?

A
  • diuretics (reduce pulmonary congestion/peripheral edema)
    • caution: avoid underfilling left ventricle
    • could reduce SV
  • address correctable causes (e.g. BP) of impaired diastolic function
  • contractile function preserved (inotropes=useless)
  • maybe some benefit from RAAS blockade/beta blockers
33
Q

What are some ways to classify acute heart failure?

A
  • “wet”= volume overload consequent of elevated filling pressures (pulmonary congestion/edema)
  • “cold”= decreased cardiac output consequent of reduced tissue perfusion
34
Q

How would you treat a “warm and wet” patient?

A

Diuretic and/or vasodilator for pulmonary edema

35
Q

How would you treat a “cold and wet” patient?

A

diuretic and/or vasodilator for pulmonary edema

AND

intravenous inotropic therapy to increase cardiac output

36
Q

Describe nitroprusside

A
  • vasodilator for acute heart failure (IV administration)
    • helpful in patients with severe HF with elevated systemic vascular resistance
  • direct NO donor that dilates both arteries and veins
  • reduces preload AND afterload (increases SV)
37
Q

Describe nitroglycerin

A
  • vasodilator for acute heart failure (IV administration)
    • most commonly used for acute dysfunction due to acute ischemia
  • primarily induces venodilation and reduces ventricular filling (preload)
38
Q

Describe dobutamine

A
  • inotropic agent for acute heart failure
  • predominantly affects beta 1 adrenergic receptor stimulation
    • increases contractility and SV
  • little effect on peripheral vascular resistance and arterial pressure
39
Q

Describe dopamine

A
  • inotropic agent for acute heart failure (dose dependent pharmacological effect)
  • low dose (D1 receptors)= renal/mesenteric artery dilation
  • intermediate dose (D1 and B1 receptors)= renal effect PLUS increases HR and contractility
  • high dose (D1, B1, a1 receptors)= vasoconstriction
40
Q

Describe milrinone

A
  • phosphodiesterase inhibitor (selective for cardiac/smooth muscle PDE3)
    • decreases degradation of cAMP
  • positive inotropic effect (increased CO)
  • balanced arterial and venodilator (decreased preload/afterload)
  • inotrope + dilation= increased stroke volume

Cardio CP1 (16 decks)

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