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Cardiology 2 > Pharm - Heart Failure > Flashcards

Pharm - Heart Failure Flashcards

1
Q

ACC/AHA and NYHA classification

A

She said she wouldn’t test over this - review just to get general idea

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2
Q

Goals of therapy for HFrEF

A
  • reduce morbidity

- reduce mortality

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3
Q

reducing morbidity in therapy of HFrEF

A
  • reducing symptoms
  • improving sx can be achieved by putting pts on:
  • diuretics
  • beta blockers
  • ACEIs
  • ARBs
  • ARNIs
  • hydralazine + nitrate
  • dig
  • aldosterone antagonists
  • improve quality of life and functional status
  • decrease rate of hospitalization
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4
Q

reducing mortality in therapy of HFrEF

A
  • pt survival has been prolonged w/ use of:
  • beta blockers
  • ACEis
  • ARNIs
  • hydralazine + nitrate
  • aldosterone antagonists
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5
Q

What is the goal of drug treatment for HFrEF?

A
  • improve sx
  • slow or reverse deterioration in myocardial function
  • reduce mortality
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6
Q

specific drug treatment for HFrEF

A

-all treated w/ ACEi or ARB and beta blocker!!

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7
Q

ACEIs

A
  • lisinopril
  • ramipril
  • quinapril
  • fosinopril
  • enalapril
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8
Q

ARBs

A
  • losartan
  • valsartan
  • candesartan
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9
Q

beta blockers

A
  • carvedilol
  • metoprolol ER
  • bisoprolol
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10
Q

neprilysin/ARB

A

sacubritril/valsartan (entresto)

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11
Q

for all volume overloaded pts, what drug do you add?

A

loop diuretic

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12
Q

for persistently symptomatic african americans add what drug?

A

hydralazine-nitrates

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13
Q

if creatinine clearance is >30 mL/min and serum potassium <5.0 mEq/dl add what drug?

A

aldosterone antagonist: (spironlactone, eplerenone)

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14
Q

be able to…

A

ID meds missing from a med list for a pt with HFrEF

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15
Q

loop diuretics mechanism of action

A

-inhibit reabsorption of Na and Cl in the ascending loop of Henle and distal renal tubule leading to an increased excretion of water, Na, Cl, Mg, and Ca

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16
Q

the diuretic response of the kidney to a loop diuretic is dependent upon what?

A
  • how much diuretic reaches the site of action

- it is a threshold type dose-response curve

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17
Q

why do people w/ HF have a reduced response to a diuretic?

A
  • decreased delivery of diuretic to kidney b/c renal blood flow is reduced
  • increased Na reabsorption at other sites d/t RAAS and SNS
  • delayed intestinal reabsorption d/t gut edema
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18
Q

indication for loop diuretics HFrEF

A
  • only drugs used for tx of HF that can adequately control fluid retention of HF
  • prescribe to all pts who have evidence of fluid retention
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19
Q

contraindications to loop diuretics

A
  • hypersensitivity

- anuria

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20
Q

loop diuretics monitoring parameters

A
  • weight
  • resolution of sx: pulm. congestion, peripheral edema, elevated jugular venous pressure
  • serum potassium (very important)
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21
Q

patient factors that may lead to diuretic resistance

A
  • significant impairment of renal fxn/perfusion
  • increase in Na-retaining hormones (AII and aldosterone)
  • hypoalbuminemia
  • consuming lg amounts of dietary Na
  • taking agents that can block effects of diuretics: NSAIDs
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22
Q

why does hypoalbuminemia cause diuretic resistance?

A
  • all diuretics are highly protein bound which limits them to the vascular space and ensures better delivery of drug to kidneys
  • reduced albumin = less protein binding of diuretic
  • more “free” diuretic to move into extravascular space
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23
Q

how can diuretic resistance be overcome?

A
  • IV admin of diuretics by intermittent bolus therapy or continuous IV infusions
  • switch from oral furosemide to torsemide or bumetanide
  • add diuretic w/ different MoA (thaizide)
  • for pts w/ systolic HF, add spironolactone or eplerenone
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24
Q

ADRs for loop diuretics

A
  • electrolyte and fluid depletion
  • hypotension and azotemia
  • depeletion of K and Mg can predispose pts to serious cardiac arrhythmias (higher risk when using 2 diuretics)
  • hyperuricemia
  • photosensitivity
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25
Q

positive patient outcomes when using an ACEI to treat HFrEF

A
  • lead to symptomatic improvement
  • reduce hospitalization
  • enhance survival
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26
Q

ACEI MoA

A
  • not completely understood

- she said she wouldn’t test on this, just have general understanding

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27
Q

contraindications for ACEIs

A
  • if they have experienced life-threatening adverse rxns during previous exposure
  • pregnant or plan to become pregnant
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28
Q

prescribe ACEI with CAUTION if pt has 1 or more of the following:

A
  • symptomatic or very low systemic BP
  • marketdly increased serum levels of creatinine (>3 mg/dL)
  • b/l renal artery stenosis
  • elevated levels of serum K (>5 mEq/L)
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29
Q

describe the prescribing pattern when initiating an ACEI and beta-blocker for a pt w/ HFrEF

A
  • ACEI benefit is a class effect
  • ACEIs are used w/ beta blockers
  • ACEI is initiated 1st and titrated to moderate dose
  • then beta blocker is titrated to max dose, followed by uptitration of the ACEI to max tolerated dose
  • begin at low doses and advance as tolerated
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30
Q

ACEI monitoring parameters

A
  • assess renal fxn and serum K w/i 1 week and 1 month of initiation and periodically thereafter
  • abrupt withdrawal of treatment can lead to clinical deterioration and should be avoided
31
Q

mechanism of ACEI induced cough

A
  • not fully known
  • increased local concentrations of kinins, substance P, prostaglandins, or thromboxane may be involved
  • kinins and substance P are metabolized by ACE so their levels are increased by ACEI
32
Q

what is the most appropriate tx for ACEI induced cough

A
  • improvement begins w/i 4-7 days after ACEI is dc
  • re-admin of an ACEI is associated w/ high occurrence rate
  • pts w/ good antihypertensive response to ACEI can be switched to ARB (lower rate of cough)
33
Q

What is the mechanism of ACEI induced hyperkalemia

A
  • ACEIs block release of aldosterone through blocking AII
  • this impairs efficiency of urinary K excretion
  • generally raise the serum K by less than .5 meq/L in pts w/ normal renal fxn
34
Q

more prominent hyperkalemia may be seen in pts with:

A
  • renal insufficiency
  • DM
  • concurrent use of a drug promoting K retention such as K-sparing diuretic
  • concurrent use of a nonsteroidal anti-inflammatory drug
  • elderly
35
Q

explain the mechanism of ACEI induced renal impairment

A
  • GFR is maintained in part by AII-induced increase in resistance at efferent arteriole
  • blocking it w/ ACEI will sequentially relax the efferent arteriole, lower intraglomerular pressure and reduce GFR
36
Q

what is the clinical effect of a pt w/ renal impairment secondary to an ACEI

A
  • rise in serum creatinine concentration generally begins a few days after starting ACEI
  • renal fxn should be checked at 3-5 days after starting when pt has renal a. stenosis or at high risk
37
Q

In renal impairment secondary to an ACEI, when should termination of the drug be considered?

A
  • hyperkalemia cannot be controlled

- serum creatinine concentration increases more than 30% above baseline value w/i the first 6-8 weeks when BP is reduced

38
Q

what are the pt risk factors for renal impairment when taking an ACEI

A
  • b/l renal a. stenosis
  • hypertensive nephrosclerosis
  • HF
  • polycystic kidney dz
  • chronic kidney dz
39
Q

what are the techniques to minimize first dose hypotension w/ ACEIs?

A
  • not beginning therapy if the pt is volume depleted
  • dc prior diuretic therapy for 3-5 days
  • can begin w/ very low dose
40
Q

mechanism of ACEI induced angioedema

A
  • one of the functions of bradykinins is to increase vascular permeability
  • ACEIs block the degradation of bradykinin which leads to a build up of it
  • the build up is thought to cause angioedema
41
Q

treatment of ACEI induced angioedema

A
  • airway management
  • dc ACEI - should NEVER be used again
  • icatinat: selective breadykinin receptor antagonist - VERY expensive
42
Q

positive pt. outcomes when using an ARB to treat HFrEF

A
  • they are reasonable to reduce mortality and morbidity as alternatives to ACEIs
  • reduced hospitalization and mortality have been demonstrated even though ACEIs are first choice
43
Q

ARBs MoA

A

directly blocks the actions of AII, a potent vasoconstrictor and stimulator of the release of aldosterone

44
Q

contraindications/precautions for ARB use

A
  • pregnancy/breastfeeding
  • angioedema
  • hyperkalemia
  • hypotension
  • declining renal fxn
45
Q

monitoring parameters for ARB use

A
  • assess renal fxn and serum K w/i 1 week and 1 month of initiation of therapy and periodically thereafter
  • avoid abrupt withdrawal
  • (same as ACEIs)
46
Q

ADRs for ARBs

A
  • dizziness
  • increase in BUN >50%
  • cough (lower incidence than ACEIs)
  • angioedema
  • hypotension
  • hyperkalemia >20%
47
Q

ARNI (angiotensin receptor/neprilysin inhibitor) sacubitril/valsartan (Entresto) MoA

A
  • combines ARB and neprilysin inhibitor
  • neprilysin degrades some vasoactive peptides like bradykinin and natriuretic peptides
  • natriuretic peptides counter regulate the detrimental effect of the upregulation of RAAS (Na/water retention and vasocontriction)
  • inhibition of neprilysin increased peptide levels, decreasing vasoconstriction, Na and water retention
  • valsartan is an ARB
48
Q

contraindications for Entresto

A
  • hx of angioedema

- concomitant use or use w/i 36 hrs of an ACEI

49
Q

MoA of beta blockers

A
  • cardioselective beta blockers block β1 receptors in the heart
  • non selective blocks both β1 receptors in the heart and β2 receptors in the body at all doses
  • related to decreased sympathetic outflow from CNS, reduced CO, and reduced renin release by juxtaglomerular cells in the kidney
50
Q

monitoring parameters for beta blockers

A
  • heart rate
  • BP
  • rhythm
51
Q

what are 3 beta-blockers that are associated w/ decreased mortality?

A
  • bisoprolol (Zebeta)
  • carvedilol (coreg)
  • extended release metoprolol succinate (Toprol XL)
52
Q

positive patient outcomes for beta blockers

A
  • they reduce the risks of dz progession, clinical deterioration and sudden death
  • can reduce the risk of death and combined risk of death or hospitalization
  • long term tx can lessen sx of HF, improve clinical status, enhance overall wellbeing
  • addition of beta blocker to low dose ACEI produced greater improvement in sx and reduction in risk of death more so than increase in ACEI dose
53
Q

beta blocker contraindications

A
  • 2nd or 3rd degree AV blocks
  • severe bradycardia
  • decompensated HF
  • sick sinus syndrome
54
Q

explain the need to prescribe a loop diuretic w/ a beta blocker

A

-diuretics are needed to maintain Na and fluid balance and prevent exacerbation of fluid retention

55
Q

monitoring parameters for beta blockers

A
  • HR
  • BP
  • rhythm
56
Q

what are the 4 types of ADRs that occur w/ beta blockers?

A
  • fluid retention and worsening HF
  • slowing HR and heart block
  • hypotensive sx
  • fatigue
57
Q

tx of fluid retention in beta blocker use

A
  • usually not a reason for permanent withdrawal of tx
  • pts generally respond well to intensification of conventional therapy and then remain excellent candidates for long term beta blocker tx
58
Q

tx of bradycardia or heart block with beta blocker use

A
  • generally asymptomatic and requires no tx

- if brady is accompanied by dizziness or 2nd/3rd degree block occurs, decrease beta blocker dose

59
Q

tx of hypotensive sx with beta blocker use

A
  • minimize risk of hypotension by admining the beta blocker and ACEI at different times of day
  • may also resolve after decrease in dose of diuretics in pts who are volume depleted
  • if hypotension is accompanied by evidence of hypoperfusion, beta blocker should be decreased or dc
60
Q

tx of fatigue in beta blocker use

A
  • hardest sx to address

- other causes should be considered

61
Q

aldosterone receptor antagonist MoA

A
  • competitively inhibits the mineralocorticoid receptor to block aldosterone effects in collecting ducts of nephron
  • aldosterone stimulates Na reabsorption and K secretion
62
Q

contraindications for aldosterone receptor antagonist use

A
  • acute renal insufficiency

- hyperkalemia

63
Q

positive patient outcomes when using an aldosterone antagonist to treat HFrEF

A
  • recommended to reduce morbidity and mortality following an acute MI in pts who have LVEF of 40% or less who develop sx of HF or have hx of DM
  • recommended in pts w/ NYHA class II-IV and have LVEF of 35% or less
64
Q

monitoring parameters for aldosterone antagonists

A
  • serum K and renal function should be checked:
  • 3 days after initiating
  • 1 week after
  • at least monthly for the first 3 mos
  • every 3 mos thereafter
  • intesify monitoring of K anytime a new med is added that increases serum K
  • beware of salt substitutes (they’re usually KCl)
65
Q

renal function guidelines for aldosterone antagonists

A

-creatinine should be:
*2.5 mg/dL or less in men
*2.0 mg/dL or less in women
(or estimated GFR >30)
-K should be:
*less than 5.0

66
Q

what are the strategies to minimize the risk of hyperkalemia in pts treated w/ aldosterone antagonist?

A
  • risk of hyperkalemia is increased w/ concomitant use of higher doses of ACEIs
  • most cases, K supplements are dc or reduced
  • close monitoring of serum K is required
  • at 3 days, then 1 week, and monthly for first 3 mos
67
Q

hydralazine/nitrate combo MoA

A
  • dilates arteries and veins

- powerful in reducing load on the heart

68
Q

monitoring parameters for hydralazine/nitrate combo

A
  • BP
  • HR
  • ANA titer if drug induced lupus is suspected
69
Q

what is the correct therapeutic digoxin serum concentration?

A

0.5-0.9 ng/mL

70
Q

monitoring parameters for digoxin

A
  • serum creatinine
  • serum K, Mg, Ca
  • serum dig concentration:
  • should be drawn at least 6-8 hrs after last dose
  • or w/i 5-7 days after any dosage change
71
Q

drug interactions of digoxin

A
  • concomitant use of clarithromycin, dronedarone, eryhtromycin, amiodarione, itraconazole, cyclosporine, propafenone, cerapamil or quinidine can increase serum dig concentration and likelihood of toxicity
  • dose should be reduced if tx w/ these drugs
  • low lean body mass and impaired renal function can also elevate serum dig levels (think elderly)
72
Q

adverse effects of digoxin

A
  • primarily occur with lg doses, esp in the elderly
  • major ADRs include:
  • cardiac arrhythmias
  • GI
  • neuro
  • overt dig toxicity
73
Q

What drug should be avoided in people with heart failure?

A
  • NSAIDs and COX-2 inhibitors
  • corticosteroids
  • metformin
  • thiazolidinediones
  • non-DHP CCBs
  • TNF alpha antagonists
  • serotonin agonists

Cardiology 2 (13 decks)

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