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S2B6: Pharm > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

discuss the body’s short term response to heart failure & what its consequences are.

A
  • chronic HR
    • due to systolic dysfunction
      • inability of heart to pump sufficiently.
      • intitially - BP drops & the body is inadequately perfused.
        • body’s response is to: activate:
          • baroreceptor reflex is activated: HR, contractility, vasoconstriction
          • RAAS: promotes fluid retention, increasing afterload/preload

temporarily - cardiac output & blood pressure are restored

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2
Q

discuss the long term effects of the body’s response to heart failure & its consequences.

A

continuous SNS activation puts extreme workload on an already weak heart.

  • ultimately, there will be back up in pulmonary & systemic cirulcation
    • –> pulmonary & systemic congestion
  • decreased cardiac ouput
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3
Q

describe the activity of natruiretic peptides in chronic heart failure

A
  • although ANP/BNP release is high during CHF due to persistent SNS activity creating a hypertensive streat, their metabolizer, neprilysin, is also expressed high levels, and they don’t have an effect
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4
Q

what is the MOA & clinical uses of ACE inhibitors/ARBs in the treatment of heart failure?

A

“-sartans” and “-prils”

  • overall MOA:
    • reduce preload & afterload
    • inhibit cardiac remodeling
  • clinical uses:
    • both: top choice drug for HR
      • ​can reduce mortality in patients with reduced ejection fraction (HFrEF)
    • ARBS: indicated especially in patients with persistent dry cough/angioedema (those are AEs of ACE inhibitors)
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5
Q

what are the MOA & clinical uses of aldosterone receptor blockers in the treatment of heart failure?

A

= spironoloactone, epleronone

  • clinical uses: can be administered at a lower dose to reduce morbidity/mortality in patients with
    • symptomatic HFrEF not corrected by standard therapy (ACE inhibitor + B-blocker)
    • symptomatic of HFrEF that:
      • just had an MI
      • have an hx of diabetes
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6
Q

adverse effects and contraindications of of aldosterone receptor antagonists?

A

spironolactone, eplerenone

adverse effects:

  • hyperkalemia
  • spironolactone specifically:
    • gynecomastia
    • menstrual irregularities
    • decreased libido

contraindications:

  • renal insufficiency
  • serum [K+] > 5 mmol/L
  • combination w/other K+ sparing diuretics (amiloride, triamterine)
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7
Q

what is ARNI?

  • what is its MOA /clinical use in the treatment of heart failure?
  • what are its AEs/contraindications?
A

= sacutratibril + valsartan

  • MOA:
    • sacutribril: enhance action (vasodilation) of natruiretic peptides (NPs) by inhibiting their metabolizer, valsartan
    • valsartan: is an ACE inhibitor
  • clinical uses:
    • patients with chronic symptomatic HF with preserved ejection fraction (HFreF) who can tolerate but don’t prefer ACE inhibitors/ARBS
  • AEs:
    • similar to ACEs/ARBS:
      • hypotension
      • hypokalemia
      • angioedema
  • contraindications:
    • co-administration with ARB: leads to angioedema
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8
Q

what are the beta blockers used to treat HF and what are their indications?

A
  • indications:
    • are a part of a standard therapy (in combo w/ ACE inhibitors) - along with diuretics as needed - in the treatment of HFreF as long as pts are hemodynamically stable
  • drugs:
    • selective B1 antagonists:
      • bisoprolol
      • metoprolol
    • nonselective antagonists:
      • carvedilol: blocks a1, B1 and B2
        • also has anti-oxidant and anti-proliferative properties
        • due to B2 blockage, is C/I in pts with:
          • COPD
          • asthma
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9
Q
  • what are the vasodilators used to treat chronic heart failure?
    • what are their specific indications?
    • AEs?
    • contraindications?
A
  • types of vasodilators:
    • arteriolar dilators: relax arteriole smooth muscle
      • hydralazine
    • venodilators: relax venous smooth muscle
      • isorbiside dinitrates
  • clinical uses:
    • for pts with HFrEF intoleant to standard therapy (ARBs/ACE inhibitors)
      • eg: African Americans
  • AEs:
    • headache, flushing, postural hypotension, reflex tachycardia
  • contraindications:
    • hypotension due to PDE Inhibitors
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10
Q
  • what are the SGLT inhibitors?
  • what is their MOA and indications in the treatment of heart failure?
A
  • “-glifozin”
  • MOA: inhibit Na+/glucose reabsorption
    • increased Na+ reabsorption induces natriuresis diruesis –> reducing circulating blood volume –> reducing preload/afterload
  • indications: added to standard therapy (B-blocker + ACE/ARB) in patients with HFrEF w/out diabetes.
    • reduces hospitalization
    • decreases mortality
    • protect renal function
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11
Q

AEs, drug drug interaction, and contraindications of SGLT2 inhibitors

A
  • AEs
    • urogenital: UTIs, yeast infections, increased urine output
    • DKA
    • hypotension
  • major drug-drug interactions: hypoglycemic drugs
  • contraindications:
    • end stage renal disease
    • dialysis
    • hypersensitivity
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12
Q

vericiguat

  • MOA and indications in the treatment of heart failure?
A
  • MOA: is a soluble gaunylate cyclase stimulator –> induces vasodilation while serving as an anti-fibrotic
  • clinical uses: combined with standard therapy for HFreF to r_educe mortality/hospitalizatio_n time in patients who
    • have recently been hospitalized
    • received IV diuretic therapy
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13
Q
  • veriguat - AEs, contraindications and drug drug interactions
A
  • AEs
    • hypotension
    • anemia
  • contraindications: pregnant women - potential fetal toxicity
  • drug drug interactions: NO donors, PDE inhibitors
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14
Q

loop diuretics

  • MOA and clinical uses in treatment of heart failure
A

= furosemide

  • MOA: promote renal loss of sodium and water
  • clinical uses: first choice for the rapid relief of pulmonary/peripheral congestive symptoms
    • ​often combined with other agents to increase effectiveness
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15
Q

adverse effects of loop diuretics

what cautions should be taken when giving loop diuretics?

A
  • AEs
    • dizziness
    • headache
    • hyponatremia
    • hypokalemia
    • alkalosis
    • hyperglycemia, hyperlipidemia, hyperuricemia
  • caution: start off patient at a low dose to avoid over diuresis/electrolyte imbalance
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16
Q

digoxin

  • what type of drug
  • what is its MOA and
    • cardiac effects?
    • extra-cardiac effects?
A
  • digoxin is a cardiac glycoside
    • MOA: it is an ionotropic drug
      • inhibits N/K ATPase (pumps K+ in & Na+ out)
        • this makes Na+ influx less favorable, slowing down the an Na/Ca++ exchanger (pumps Na+ in and Ca+ out), which slows down Ca+ removal from cell, increasing intracellular [Ca++]
    • cardiac effects:
      • increases cardiac contractility
      • but slows HR and AV node conduction at therapuetic dose by inducing PNS activity (?)
    • extra-cardiac effects:
      • renal diuresis (since it increases contractility and CO)
      • GI: PNS activity can stimulate CTZ (chemoreceptor trigger zone) on gut smooth muscle cause –> nausea
17
Q

pharmokinetics of digoxin

A
  • distribution depends on the amount of skeletal muscle
18
Q

what is the role of digoxin in the treatment of heart failure?

A
  • to reduce hospitalization in chronic HF patients:
    • with persistent symptoms depsite already being on a standard therapy (ACE inhibitors + B blockeres, diuretics as needed)
    • with atrial fibrillation

does NOT improve survival (reduce mortality).

19
Q

adverse effects of digoxin

A
  • cardiac:
    • arrythmias (tachy, brady, AV block)
  • GI:
    • anorexia
    • nausea/vomitting/diarrhea
  • CNS:
    • confusion
    • blurred vision, alteration of color perception, halos on dark objects
20
Q

what are the drug drug interactions of digoxin & what effects can it have if administered with these drugs?

A
  • antibiotics - reduce GI metabolism
  • loop & thiazide diuretics - hypokalemia
  • K+ sparing diuretics / K+ supplements - hyperkalemia
  • CCBs & B-blockers - slows HR & AV node conduction
  • sulfacrate & anti-acid drugs - reduce absorption
21
Q

how to treat digoxin toxicity

A
  • lower the dose/ discontinue the drug
  • if there is an electrolyte imbalance: K+, Mg++
  • if there is an arrythmias: give a antiarrhythmic drugs
  • if severe toxiity: give digibind (digoxin antibodies)
22
Q

name the beta receptor agonists used in the treatment of heart failure

  • what is their MOA?
  • clinical uses?
  • cautions?
  • AEs?
A
  • dopamine, dobutamine
  • MOA: ionotropic agents (increase contracility)
  • clinical uses: end stage heart failure (given IV)
  • caution: though they have short term benefits, they may increase mortality with chronic use
  • AES:
    • tachycardia
    • arrtymias
23
Q

name the beta PDE3 used in the treatment of heart failure

  • what is their MOA?
  • clinical uses?
  • cautions?
  • AEs?
A
  • “rinone” - milrinone, inanrinone
  • MOA: ionotropic agents (increase contracility)
  • clinical uses: end stage heart failure (given IV)
  • caution: though they have short term benefits, they may increase mortality with chronic use
  • AES:
    • tachycardia
    • arrtymias

just like beta agonists (dopamine, dobutamine)

24
Q

what is ivabradine and its MOA?

A
  • MOA:
    • funny channel blocker - slowa heart rate by blocking the cardiac pacemaker If current
25
Q

clinical uses of ivabradine

A
  • added to standard therapy to reduce risk of hospitalization in HF patients with:
    • stable, symptomatic HFreF
    • sinus rhythm with a resting heart rate of 70 bmp
    • on max doses of beta blockers/contraindicated to beta blockers
26
Q

AEs of ivabradine

A
  • bradycardia
  • conduction disturbances
  • a-fib
  • HTN
  • transiently ehanced visual brightness
27
Q

drug drug interactions of ivabradine

A
  • CYP - 3A4 inducers/inhibitors (verapamil, diltiazem)
  • drugs that slow HR - could cause bradycardia
28
Q

contraindicaions of ivabradine

A
  • Acute decompensated heart failure
  • pacemaker dependence
  • Low BP (< 90/50 mmHg)*
  • Resting HR < 60 bpm*
  • SA block / 3rd degree AV block*
  • Severe hepatic impairment
  • strong CYP3A4 inhibitors (verapamil or diltiazem)

S2B6: Pharm (3 decks)

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