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Pharm II > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

Goals of therapy

A 
Improve QOL
-Prevention of symptom onset
-Reduction of sx and/or severity of sx
Prolong survival
Slow dz progression
Prevent exacerbations
-Reduce hospitalization
Treat modifiable risk factors
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2
Q

Guidelines for HFpEF

A

Control BP
Use diuretics to control sx due to volume overload
Reasonable to have coronary revascularization in pts with angina/MI that is making HF worse
Manage a fib according to published guidelines

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3
Q

Stage A

A

Pts at high risk for HF

Not symptomatic and NO current evidence of structural heart dz

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4
Q

Stage A tx

A

Aggressive risk factor control

  • Control HTN per current guideline recommendations
  • Smoking cessation
  • Control dyslipidemia per current guideline recommendations
  • Increased physical activity
  • Encourage weight loss if obese
  • Control diabetes per current guideline recommendations
  • Discourage EtOH and illicit drug use
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5
Q

Stage B

A

Pts with structural heart dz but are asymptomatic

-Previous MI, LV remodeling, low EF, valvular dz

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6
Q

Stage B tx

A 
All txs for Stage A
ACE inhibitor or ARB
-Pts s/p ACS/MI or reduced EF
BB (select medications)
-Pts s/p ACS/MI or reduced EF
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7
Q

MOA of BBs

A

Inhibitor/block beta receptors
Net effect:
-Decreased sensivity to circulating catecholamines (SNS)
-Decreased HR/BP

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8
Q

Caution for BBs

A

Only initiate beta blocker when HF is stable and pt is euvolemic

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9
Q

HF indication for BBs

A

1st line for all pts with HFrEF
-Reduction in all-cause mortality, hospitalizations, improve EF
Not a class effect!! Only 3 meds indicated:
-Carvedilol
-Bisoprolol
-Metoprolol succinate

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10
Q

Goal dose carvedilol

A

25 mg PO BID (wt <85 kg)

50 mg PO BID (wt >85 kg)

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11
Q

Goal dose bisoprolol

A

10 mg PO daily

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12
Q

Goal dose metoprolol succinate

A

200 mg PO daily

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13
Q

Side effects of BBs

A 
Depression
Worsening HF sx
Sexual dysfunction
Alterations in glucose metabolism
Bradycardia/hypotension
Bronchospasm
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14
Q

HF indications for ACE inhibitors

A

1st line for all pts with HFrEF
-Reduction in all-cause mortality and hospitalizations, improved QOL, improved LV side and function, reduces likelihood of developing HF in at risk pts

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15
Q

MOA of ACE-Is

A

Block conversion of angiotensin I to angiotensin II
-Decreased vasoconstriction and cardiac remodeling
-Reduction in bradykinin breakdown (increased vasodilation)
Net effect:
-Arterial and venous vasodilation
-Reduction of preload and afterload (reduced workload on heart)

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16
Q

Absolute CIs for ACE-Is

A

Hx of angioedema secondary to ACE-I
Pregnancy (category X)
Bilateral renal artery stenosis

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17
Q

Relative CIs/SEs of ACE-Is

A 
Cough
Unilateral renal artery stenosis
Renal insufficiency
Hypotension
Hyperkalemia
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18
Q

Additional facts of ACE-Is

A

0.5 increase in SrCr is fine, anything above, d/c and try again
K over 5.0, stop drug for a few weeks, and try again
ACE and ARBs are indicated in preventing nephropathy in DM

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19
Q

HF indication for ARBs

A

2nd line for all pts with HFrEF who cannot tolerate an ACE inhibitor
Reduction in all-cause mortality and hospitalizations, improved QOL

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20
Q

MOA of ARBs

A

Block the AT1 receptor to stop the actions of angiotensin II
Decreased vasoconstriction, aldosterone release, cellular growth promotion
Net effect:
-Arterial and venous vasodilation
-Reduction of preload and afterload (reduced workload on heart)

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21
Q

Situations when ACE and ARBs can be combined

A 
Pt already on BB and ACE inhibitor AND
Symptomatic AND
Cannot take an aldosterone antagonist
Carefully monitor K, SCr, BUN
Should not combine ACE inhibitor, ARB and aldosterone antagonist
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22
Q

SEs of ARBs

A

Similar to ACE-Is
Not associated with cough
Can be considered if ACE-I associated angioedema
-Cross reactivity has been reported

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23
Q

Monitoring for ARBs

A

BUN, SCr, K, BP

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24
Q

Stage C

A

Pts with structural heart dz AND prior/current sx of HF

-Sx can be classified via NYHA system

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25
Q

Tx for Stage C

A 
All tx for Stage A
ACEI or ARB
BB (select meds)
Diuretics
Devices
-Biventricular pacing
-Implantable defibrilators
Can add spironolactone or bidil
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26
Q

HF indication for loop diuretics

A

Decreases sx associated with fluid retention
-Shown to decrease hospitalizations
Use in pts with hx of or current sx of fluid retention to maintain euvolemia

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27
Q

MOA of loop diuretics

A

Block Na reabsorption at the thick ascending loop of Henle

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28
Q

SEs of loop diuretics

A 
Azotemia (increased BUN)
Hypokalemia
-Arrhythmias
Hypomagnesemia
AKI
Ototoxicity
Hypotension
Hyperuricemia
Hyponatremia
Caution in true sulfonamide allergy
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29
Q

HF indication for aldosterone antagonist

A

Pts with stage II-IV HFrEF to reduce morbidity and mortality

30
Q

MOA for aldosterone antagonists

A

Inhibits aldosterone
-Increased levels of aldosterone in HF to increase NA/H2O retention and “improve” CO
Weak diuretic effect

31
Q

SEs of aldosterone antagonists

A

Hypotension
Hyperkalemia
Gynecomastia (spironolone only)
Breast tenderness/menstrual irregularities (spironolactone only)

32
Q

Spironolactone initial dose

A

12.5-25 mg once daily

33
Q

Target/max dose of spironolactone

A

25 mg once or twice daily

34
Q

Monitoring for spironolactone and eplerenone

A

BP
Electrolytes (K)
Baseline
1 wk after starting or changing dose

35
Q

Initial dose of eplerenone

A

25 mg once daily

36
Q

Max/target dose of eplerenone

A

50 mg once daily

37
Q

Caution in aldosterone antagonists

A

SCr >2.5 (men)
SCr >2.0 (women)
K >5.0

38
Q

HF indication of hydralazine-isosorbide dinitrate

A

Pts with stage II-IV HFrEF to reduce morbidity and mortality

-First med to show mortality benefit

39
Q

MOA of hydralazine-isosorbide dinitrate

A

Hydralazine
-Directly causes smooth muscle relaxation
-Net effect: reduced afterload
Isosorbide dinitrate
-Activation of guanylate cyclase that causes an increase in cGMP in vascular smooth muscle
-Net effect: reduced preload via venous vasodilation

40
Q

Place of hydralazine-isosorbide dinitrate in therapy

A

Substitute in pts who cannot tolerate either an ACE inhibitor or ARB
-ACEI and ARBs are vasodilators that have higher mortality benefit than hydralazine/isosorbide dinitrate
Add-on therapy in pts self-described as AA who are on optimal therapy with ACE-I/ARB and BB but still symptomatic
-Prospective-randomized trial found more mortality benefit in this pt group

41
Q

HF indication of digoxin

A

Add-on therapy in pts already on ACE-I/ARB, BB and other mortality benefiting meds who are still symptomatic

  • Reduction in hospitalizations only
  • No effect on mortality or dz progression
  • -If levels >1.2 ng/mL may have increased relative risk of mortality
42
Q

MOA of digoxin

A

Inhibition of Na/K ATPase pump in myocardial cells leads to increase in intracellular Na leads to increased Ca influx

  • Neurohormonal modulation
  • Net effect: Increased contractility (pos inotrope)
43
Q

When to start with a lower dose in digoxin

A

Age >65-70 yo
CrCl <60 mL/min
Low lean body mass

44
Q

Dosing of digoxin

A

0.125-0.25 mg PO once daily
Titrate to goal level of 0.5-0.9 ng/mL
Can dose every other day in decreased renal function

45
Q

Monitoring of digoxin

A

If signs of toxicity, change in renal function, new drug interaction, dose change, after IV load (atrial fibrillation)

46
Q

When is cardiac manifestation more likely in digoxin?

A

Decreased Mg, K, and Ca levels

47
Q

Digoxin toxicity

A 
Associated with levels >2.0 ng/mL
Fatigue/weakness
Confusion
Delirium
Psychosis
N/V/anorexia
Visual disturbances
-Halos, photophobia, red-green/yellow-green vision
Arrhythmias
-Vtach, vfib, AV block, sinus brady
48
Q

Reversal agent for digoxin

A

Digibind

Antibody that binds digoxin to be excreted via kidneys

49
Q

Stage D

A

Pts with significant sx at rest even though on optimal and maximum medical therapy

50
Q

Stage D tx

A 
All txs for Stage A-C
Heart transplant
Chronic inotropic meds
Mechanical support
Palliative care/hospice
51
Q

Causes of HF exacerbation

A 
ACS
Med nonadherence
Na/fluid restriction nonadherence
Uncontrolled BP
A fib
Addition of drugs that worsen HF
Pulmonary embolus
Infection
Excessive EtOH use
52
Q

Warm and dry characteristics

A

Nl pt

53
Q

Warm and wet characteristics

A

Congestion

54
Q

Cold and dry characteristics

A

Hypoperfusion

55
Q

Cold and wet characteristics

A

Congestion and hypoperfusion

Cardiac index is low

56
Q

S/sx of ADHF (acute decompensated HF)

A 
Hypoperfusion
-Cool extremities
-Sleepy
-Declining Na levels
Congestion
-Orthopnea
-DOE
-High JVP
-Pulmonary edema
-Peripheral edema
-Elevated BNP
-Weight gain
57
Q

Goals of tx of ADHF

A 
Correct underlying precipitating factor
Relieve the pt's sx
Improve hemodynamics
-Optimize chronic oral med regimen
-Educate pt on adherence to lifestyle modifications and drug regimen
58
Q

Tx of warm and wet

A

Loop diuretics

+/- vasodilators

59
Q

Tx of cold and dry

A

Pos inotropes

+/- fluid replacement

60
Q

Tx of cold and wet

A

Mixture of diuretics, vasodilators, inotropes

61
Q

Diuretics with warm and wet

A

IV furosemide, bumetanide, torsemide

62
Q

Cautions for diuresing in ADHF

A

Excessive preload reduction can cause decreased CO
-Reflex increase in sympathetic tone
Over-diuresis can cause AKI
-Monitor SCr/BUN daily to assess intravascular volume depletion
Electrolyte depletion
-Monitor and replete K and Mg

63
Q

Diuretic resistance

A

Failure to decrease weight by 0.5 kg (neg fluid balance of 500 mL) after several IV diuretic doses

64
Q

Strategies to overcome diuretic resistance

A

Increase dose of the diuretic
Increase frequency of diuretic administration
Change to continuous infusion of loop diuretic
Change loop diuretic (furosemide to bumetanide)
Combine to loop diuretic with thiazide diuretic

65
Q

Effects of vasodilators for warm and wet

A

Decreased arterial tone causing decreased SVR and increased CO
Decreased wedge pressure and ventricular workload

66
Q

Nitroprusside dose

A

0.25-3 mcg/kg/min

67
Q

Nitroprusside pearls

A

Potent venous and arterial vasodilator
Cyanide and thiocyanate toxicity
-Esp in hepatic/renal insufficient and/or >3 days administration and/or receiving high doses
Monitor: BP, HR, liver and kidney

68
Q

Nitro dose

A

5-200+ mcg/min

69
Q

Nitro pearls

A

Primary venous vasodilator
Tolerance after 12 hrs requiring escalating doses
Adverse effects: HA, hypotension, tachycardia
Monitor: BP, HR, ECG, change in ischemic sx

70
Q

Nesiritide dose

A

Bolus: 2 mcg/kg
Infusion: 0.01 mcg/kg/min

71
Q

Nesiritide pearls

A

Recombinant BNP
Improves dyspnea and fatigue
Adverse effect: hypotension

Pharm II (8 decks)

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