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2020 CPR II Cardio Exam 1 > Drugs Used for Heart Failure (Wolff) > Flashcards

Drugs Used for Heart Failure (Wolff) Flashcards

1
Q

Left-sided systolic heart failure is due to failure of what?

A

Failure of the pump function of the heart (EF <45%) due to dysf. or destruction of cardiac myocytes or their molecular components

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2
Q

Left-sided diastolic heart failure occurs due to what?

A

Ventricular capacitance is diminished and/or when ventricle becomes “stiff” and cannot fully relax during diastole

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3
Q

What are 2 common causes of left-sided diastolic heart failure?

A
  • Ventricular hypertrophy due to chronic HTN
  • CT disease such as amyloidosis
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4
Q

What occurs to both afterload and preload in systolic heart failure?

A
  • Increased afterload
  • Increased preload
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5
Q

What is the LVEF like in systolic HF and there is usually progressive what?

A
  • LVEF <50% = HFrEF
  • Usually progressive chamber dilation w/ eccentric remodeling
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6
Q

Diastolic heart failure is now especially common in whom?

A

Elderly women

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7
Q

What occurs to the ejection fraction in diastolic heart failure?

A

Usually normal = HFpEF

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8
Q

What occurs to preload in diastolic heart failure?

A

Decreased preload

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9
Q

Diastolic heart failure has a poor tolerance of what 2 things and is worsened by an increase in what?

A
  • DHF –> poor tolerance of atrial fibrillation
  • DHF –> poor tolerance of tachycardia
  • DHF is worsened by ↑ MAP
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10
Q

Worsening of diastolic HF by ischemia raises left atrial pressure which can lead to which life threatening condition?

A

“Flash” pulmonary edema

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11
Q

With a drop in cardiac output, what are the adpative mechanisms (i.e., what gets increased) contributing to HF?

A
  • ↑ renin + ↑ aldosterone + ↑ natriuretic peptides
  • ↑ sympathetic discharge
  • ↑ preload and afterload
  • ↑ remodeling of heart
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12
Q

ACE-I and ARB’s lead to less angiotensin II which has what 3 positive effects in pt’s with HF?

A
  • Less vasoconstriction (↓ afterload)
  • Less aldosterone and less Na+/H2O retention (↓ preload)
  • ↓ cell proliferation and remodeling
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13
Q

Define the terms inotropic agent and chronotropic agent.

A
  • Ionotropic agents alter the force/strength of muscle contractions
  • Chronotropic agents may change the heart rate and rhythm
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14
Q

ACE-I (-prils) are used clinically for what heart conditions?

A
  • Heart failure w/ reduced EF (HFrEF) = systolic HF
  • LV dysfunction following MI
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15
Q

What are 2 major AE’s associated with ACE-I’s?

A
  • Cough
  • Angioedema
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16
Q

Which 2 ACE-I are now widely used due their longer half-life permitting 1x/day dosing?

A
  • Benazepril
  • Lisonopril
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17
Q

Which drugs can be used for HF if patient is intolerant to ACE-I’s?

A

ARBs (-sartans)

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18
Q

Which ARB is noteworthy in that it is not a prodrug requiring activation?

A

Valsartan

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19
Q

Which ARB is noteworthy in that it displays relatively irreversible binding?

A

Candesartan

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20
Q

What is the MOA of sacubitril and what is it co-crystalized with as a combo drug for HF?

A
  • Prodrug that inhibits neprilysin (neutral endopeptidase [NEP])
  • Co-crystalized with the ARB, Valsartan
  • Valsartan/sacubitril
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21
Q

What does the neutral endopeptidase blockade by sacubitril lead to?

A

Increased levels of natriuretic peptides

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22
Q

What are3 common AE’s of valsartan/sacubitril?

A
  • HYPOtension
  • HYPERkalemia
  • ↑ serum creatinine
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23
Q

What is the effect of ↑ ANP on GFR, renin/aldosterone secretion, Na+/H2O reabsorption, and ADH secretion?

A
  • ↑ GFR
  • ↓ renin + ↓ aldosterone secretion
  • ↓ Na+/H2O reabsorption
  • ↓ ADH secretion and ADH effects in collecting duct
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24
Q

ACE-I’s/ARBs should be administered to all pt’s with LV systolic failure or LV dysfunction w/o HF except in what 5 situations?

A
  • Not tolerated (cough, angioedema; try ARB)
  • Pregnant
  • HYPOtensive
  • Serum creatinine >3 mg/dL
  • HYPERkalemia
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25
Q

Which beta-blocker has been shown to work best in HF?

A

Carvedilol

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26
Q

Which other beta-blocker is a non-selective alpha/beta blocker, used primarily for severe HTN and tx of hypertensive emergencies?

A

Labetalol

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27
Q

What condition should patient be in for use of carvedilol in HF and what are it’s recommended uses?

A
  • IF clinically stable
  • Recent or remote hx of MI or ACS and ↓ EF (rEF; <40%)
  • rEF to prevent SYMPTOMATIC HF (even if no hx of MI)
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28
Q

Carvedilol is used to prevent what in the heart as a result of excessive sympathetic stimulation during HF?

A

Prevent down-regulation of the β1-receptors

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29
Q

List 5 benefits of carvedilol in HF by preventing the down-regulation of β1-receptors?

A
  • Keeps heart responsive to sympathetic drive
  • Protects against dysrhythmias
  • ↓ renin secretion
  • ↓ myocardial O2 consumption
  • Limits heart muscle remodeling
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30
Q

Carvedilol should only be administered to which patients?

A

Clinically stable

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31
Q

Which type of HF’s is carvedilol useful in and should be given along with ACE-I to which pt’s?

A
  • Pts with diastolic HF will benefit from a lower HR
  • Should be given to all pt’s w/ symptomatic CHF and LVEF <40% unless contraindications exist
  • Given along w/ ACE-I to all pt’s w/ LV systolic dysfunction caused by MI to reduce mortality
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32
Q

What is the MOA of ivabradine and effects on heart?

A
  • Selective and specific inhibition of the HCN channels (f-channels) within SA node
  • Disrupts If (“funny” current) to prolong diastole and slow HR
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33
Q

What is the clinical application of ivabradine; specifically in which pt’s?

A
  • Tx of resting HR ≥70 bpm in pt’s w/ stable, symptomatic chronic HF w/ LVEF ≤35% who are in sinus rhythm with:
  • Maximally tolerated doses of β-blockers

OR

  • Contraindications to β-blocker use
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34
Q

What is the MOA of spironolactone and its effects on ion and volume levels?

A
  • Competitive antagonist of aldosterone receptors
  • K+-sparing diuretic due to ↓ ability of aldosterone to promote Na+-K+ exchange in collecting ducts
  • ↓ plasma Na+ and volume
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35
Q

Which K+-sparing diuretic is a more selective aldosterone antagonist, approved for use in post-MI heart failure or in combo for tx of HTN?

A

Eplerenone

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36
Q

What are the pharmacokinetics of spironolactone like and why is a single dose effective for 2-3 days?

A

Steroid effects are slow on and slow off

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37
Q

What are some possible AE’s associated with Spironolactone?

A
  • HYPERkalemia (duh.)
  • Amenorrhea, hirsutism, gynecomastia, and impotence
  • Tumorigen in chronic animal toxicity studies (boxed warning)
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38
Q

What are 3 beneficial effects of spironolactone on the heart?

A
  • ↓ myocardial fibrosis
  • Reduces early morning rise in HR
  • Reduces mortality and morbidity in pt’s with severe HF
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39
Q

Explain the purpose of aldosterone inhibition when treating post-myocardial infarction heart failure?

A

- Damaged heart vasculature synthesizes aldosterone after MI

- Locally produced aldosterone contributes to cardiac fibrosis

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40
Q

What are some of the effects blocked by spironolactone that occur as a result of aldosterone release following an MI?

A
  • Na+/H2O retention; K+ and Mg2+ loss
  • ↓ baroreceptor reflex
  • Sympathetic activation
  • Cardiac fibrosis + ischemia
41
Q

Spironolactone is approved for what application in HF?

A

Tx of symptomatic HF w/ reduced systolic function

42
Q

Why is spironolactone (and eplerenone) the most underutilized of all classes of meds for HF?

A

Primarily due to fear of HYPEkalemia

43
Q

Which loop diuretic has a longer t1/2, better oral absorption and som evidence that it works better in HF?

A

Torsemide

44
Q

Furosemide and other loop diuretics are useful in the management of acute pulmonary edema by decreasing what?

A

Preload

45
Q

Which class of diuretics is useful in patients with low GFR?

A

Loop diuretics

46
Q

When using diuretics to control the congestive heart failure state, which class is used first and then followed by what 2 classes if needed?

A
  • Use loop diuretic first
  • Add K+-sparing next if needed
  • If still need more diuresis, finally add thiazide
47
Q

What is the purpose of using diuretics to relieve congestion in HF?

A

Return ventricular fiber length to more optimal range

48
Q

Which vasodilator combo is especially useful in tx of chronic HF in African Americans?

A

Isosorbide dinitrate plus hydralazine

49
Q

Where are the vasodilatory effects of isosorbide dinitrate and hydralazine seen and what is the effect on preload/afterload?

A
  • Isosorbide dinitrate dilates veins and ↓ preload
  • Hydralazine dilates arteries and ↓ afterload
50
Q

Nitroglycerin has a more prominent effect on what vasculature?

A

Veins

51
Q

What is the clinical application of nitroglycerin in HF?

A

Acute decompensated HF (especially when assoc. w/ MI)

52
Q

Hydralazine’s MOA is dependent on what, requires activation by, and is mediated by what receptor?

A
  • Endothelium dependent
  • Requires activation of COX
  • Mediated by PGI2 receptor
53
Q

What are the clinical applications of hydralazine in HF and use in pregnancy?

A
  • HF w/ reduced EF if intolerance to ACEI or ARB
  • HF w/ reduced EF in self-identified African Americans
  • Hypertensive emergency in pregnancy
54
Q

What are some of the major AE’s associated with Hydralazine?

A
  • Angina pectoris
  • Flushing
  • Peripheral edema
  • Tachycardia
  • Pruritus
  • Drug-induced lupus-like syndrome
55
Q

What is the MOA of digoxin?

A

Inhibition of Na+-K+ ATPase pump in myocardial cells

56
Q

What are the effects of digoxin on myocardial cells via inhibition of the Na+-K+ ATPase?

A
  • Transient ↑ of intracellular Na+ which promotes Ca2+ influx leading to increased contractility (+ inotropic effect)
  • Direct suppression of AV node conduction –> ↑ effective refractory period and ↓ conduction velocity
57
Q

What is the effect of digoxin on inotropy, vagal tone, and ventricular rate?

A
  • Positive inotropic effect
  • Enhanced vagal tone
  • ↓ ventricular rate to fast atrial arrhythmias
58
Q

Increased myocardial contractility produced by digoxin has what effect on cardiac output, sympathetic, and vagal tone?

A

↑ cardiac output –> ↓ sympathetic tone + ↑ vagal tone

59
Q

What are the clinical applications of digoxin?

A
  • Control of ventricular response rate in adults w/ chronic atrial fibrillation
  • Tx for mild-to-moderate HF in adults/kids to increase myocardial contractility
60
Q

What is the route of administration for digoxin and it’s half-life?

What is required to get beneficial effects immediately?

A
  • Oral w/ t1/2 = 36-48 hrs
  • Needs a loading dose
61
Q

What are the major AE’s associated with Digoxin?

A

Severe dysrhythmias

62
Q

Digoxin cardiac toxicity occurs in part because myocytes becomes overloaded with what?

How does this contribute to arrhythmias?

A
  • Overloaded w/ Ca2+ and spontaneous oscillatory uptake and release from SR causes delayed afterdepolarizations and aftercontractions
  • Excess free radicals also contribute
63
Q

What are 3 hemodynamic benefits of Digoxin due to increased cardiac output?

A
  • ↓ sympathetic tone
  • ↑ urine production
  • ↓ renin release
64
Q

Digoxin increases the responsiveness of the SA node to what?

A

ACh

65
Q

What are the 2 most important effects of Digoxin on the AV node in regard to duration of refracory period and conduction velocity?

A
  • ↑ duration of refractory period
  • ↓ conduction velocity
66
Q

The most important effect of digoxin on purkinje fibers is an increase in what?

A

Automaticity

67
Q

What is the major effect of digoxin on the duration of the refractory period in ventricular myocardium?

A

↓ duration of refractory period

68
Q

What are typical changes seen on an EKG with therapeutic levels of digoxin?

A
  • Depression of S-T segment
  • Longer P-R interval
69
Q

Toxic effects of digoxin on A-V conduction will be seen how on an EKG?

A
  • A-V dissociation
  • Lack of relationship between P and QRS complexes
70
Q

Toxic effects of digoxin on purkinje automaticity and ventricular refractory period will appear how on EKG?

A

Ectopic ventricular beats

71
Q

What are some of the non-cardiac AE’s associated with Digoxin?

A
  • Anorexia, N/V, salivation
  • Excessive urination
  • Fatigue
  • Visual disturbances (blurred vision, halos, and yellowish or greenish tinge to objects)
72
Q

What are 4 tx’s for digoxin toxicity?

A
  • KCl
  • Lidocaine
  • Phenytoin
  • Antidigitalis Abs
73
Q

Why are digoxin drug interactions with diuretics a big deal?

A

Diuretics cause hypokalemia, which leads to ↑ digoxin binding —> digoxin toxicity

74
Q

Digoxin competes with what ion for binding to Na+-K+-ATPase?

A

K+

75
Q

What is the effect of ACE-I and ARBs on levels of digoxin?

A

ACE-I and ARBs can ↑ plasma K+ levels —> ↓ digoxin effects

76
Q

Digoxin is used in combo w/ diuretics, β-blockers, and ACE inhibitors in what type of HF?

A

LV systolic HF

77
Q

Why is digoxin especially useful in pt’s with atrial fibrillation?

A

Due to prolongation of effective refractory period at AV node

78
Q

Which drugs should be used judiciously in pt’s with diastolic HF, but can also lead to what?

Which drug shows mixed evidence of benefit?

A
  • Loop diuretics to tx edema
  • BUT can ↓ preload too much –> ↓CO, hypotension, and death
  • Mixed evidence with spironolactone
79
Q

Which 3 drug classes show no evidence of benefit in diastolic HF?

A
  • Nitrates
  • PDE5 inhibitors
  • Digoxin
80
Q

What therapy needs to be initiated in pt’s with acute decompensated HF and why?

A
  • Diuretic therapy
  • All pt’s with ADHF are volume overloaded, must get rid of excess volume to relieve congestion and return ventricular fiber length to more optimal range
81
Q

How do the dilatory effects of nitroprusside differ from nitroglycerin?

A
  • Nitroprusside = mixed effects, dilates both arterial and venous sides
  • Nitroglycerin = preferentially venous side, decreases preload
82
Q

Pt’s with ADHF can be hypertensive, normotensive, or hypotensive; how is each treated with vasodilators/diuretics?

A
  • Hypertensive = tx with diuretic + vasodilator (i.e., nitropursside or nitroglycerin)
  • Normotensive = tx with diuretic + vasodilator (i.e., nitroglycerin)
  • Hypotensive = tx with diuretic
83
Q

What is the MOA of nitroprusside?

A

Forms free radical nitric oxide, which in smooth m. activates soluble guanylate cyclase to ↑ cGMP

84
Q

What are the systemic and cardiac effects of nitroprusside?

A
  • Peripheral vasodilation w/ action on venous and arteriolar smooth m.
  • Reduces peripheral resistance
  • Will ↑ cardiac output by decreasing afterload
85
Q

What are 3 clinical applications of Nitroprusside?

A
  1. Management of hypertensive crisis
  2. Acute decompensated HF
  3. Used for controlled hypotension to reduce bleeding during surgery
86
Q

One AE of nitroprusside is metabolic acidosis secondary to what?

A

Cyanide toxicity

87
Q

When are inotropic agents (i.e., sympathomimetics, PDE inhibitors) indicated for HF pt’s?

A

If symptomatic HYPOtension w/ end-organ dysfunction despite adequte filling pressure

88
Q

Before administering inotropic agents to pt with HF what should be discontinued?

A

Carvedilol

89
Q

Dobutamine primarily affects what receptors and what is the effect on the heart?

A
  • Stimulates myocardial β1 and β2 AR’s, also so α1 receptors
  • ↑ contractility and HR
  • Some vasodilation due to β2 receptor stimuation
90
Q

Which adrenergic receptors are activated by Dopamine in a dose dependent manner and effects on heart?

A
  • Activates β1-AR’s at LOW doses = ↑ HR and contractility
  • Stimulates α-AR’s at HIGH doses
91
Q

Dopamine is used as an adjunct in the tx of what?

A

Shock that persists after adequate fluid replacement in cases of: MI, open heart surgery, renal failure, and cardiac decompensation

92
Q

What is the prototypical PDE type III inhibitor used as an inotropic agent in short-term/rescue therapy?

A

Milrinone

93
Q

The PDE inhibitor, Milrinone results in increasd levels of what?

What is the effect on the heart and systemic circulation?

Must be given via which route?

A
  • ↑ cAMP —> ↑ contractility in heart + vasodilation
  • Decrease preload and afterload
  • Must be given via IV
94
Q

What are the clinical applications for Milrinone?

A

Inotropic therapy for pt’s unresponsive to other acute HF therapies (i.e., dobutamine)

95
Q

What are 3 drugs classes to avoid in HF?

A
  • Class I antiarrhythmics
  • CCB’s
  • NSAIDs
96
Q

Which drug may improve cardiac responsiveness during ADHF in a patient who was taking carvedilol/is overdosed on carvedilol?

A

Milrinone

97
Q

What are some of the concerns with using the PDE inhibitor, Milrinone?

A

Some studies show it decreases survival time

98
Q

Which drug classes can be used in diastolic HF if justified by sx’s?

A
  • β-blockers
  • ACEI/ARBs
  • CCB’s

2020 CPR II Cardio Exam 1 (31 decks)

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