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MJ- Pharm exam 2 > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

Heart failure results from…

A

the inability of the heart to pump sufficient blood to meet the metabolic needs of the body.

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2
Q

Systolic Dysfunction

A

reduced contractility and reduced ejection fraction

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3
Q

Diastolic dysfunction

A

stiffening and loss of adequate relaxation, which reduces filling and CO

ejection fraction may be normal

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4
Q

Systolic etiologies

A
  • ischemic heart disease
  • chronic HTN
  • dilated cardiomyopathy
  • myocarditis
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5
Q

Diastolic etiologies

A
  • HTN with LV Hypertrophy
  • restrictive and hypertrophic cardiomyopathies
  • fibrosis
  • amyloidosis
  • sarcoidosis
  • constrictive pericarditis
  • hemochromatosis
  • valvular disease
  • aging
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6
Q

You will hear an S3 gallop in ______ heart failure

A

systolic

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7
Q

You will hear an S4 gallop in ______ heart failure

A

diastolic

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8
Q

_______ limits diastolic filling time and coronary flow, further stressing the heart.

A

Tachycardia

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9
Q

Primary and signs and symptoms of all types of heart failure

A
  • tachycardia
  • decreased exercise tolerance
  • shortness of breath
  • cardiomegaly
  • peripheral and pulmonary edema are often but not always present
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10
Q

ACC/AHA Stage A HF

A

Patients at high risk for developing heart failure

Ex: HTN, ASCVD, DM, obesity, metabolic syndrome

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11
Q

ACC/AHA Stage B HF

A

pts w/structural heart dz but no HF signs or symptoms

Ex: Previous MI, LVH, LV systolic dysfunction

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12
Q

ACC/AHA Stage C HF

A

pts w/structural heart disease and current or previous symptoms

Ex: LV systolic dysfunction & symptoms like dyspnea, fatigue, and reduced exercise tolerance

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13
Q

ACC/AHA Stage D HF

A

refractory HF requiring specialized interventions

Ex: pts with treatment refractory symptoms at rest despite maximal medical therapy: pts requiring recurrent hospitalization or who cannot be discharged without mechanical assist devices or inotropic therapy.

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14
Q

NYHA Class I

A

no limitation of physical activity

ordinary physical activity does not cause symptoms

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15
Q

NYHA Class II

A

slight limitation of physical activity

comfortable at rest

ordinary physical activity causes symptoms

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16
Q

NYHA Class III

A

marked limitation of physical activity

comfortable at rest

less than ordinary activity causes symptoms

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17
Q

NYHA Class IV

A

severe limitation and discomfort with any physical activity

symptoms present even at rest

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18
Q

Goals of pharmacologic therapy of HFrEF

A

improve symptoms (risk of hospitalization)

slow or reverse deterioration in myocardial function, and reduce mortality

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19
Q

Improvement in symptoms is achieved by which drugs?

A
  • diuretics
  • BB
  • ACE-I
  • ARBs
  • ARNI (angiotensin receptor-neprilysin inhibitor)
  • hydralazine plus nitrate
  • digoxin
  • aldosterone antagonists
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20
Q

Prolonged survival rate has been documented with which drugs?

A
  • Beta Blockers
  • ACE-I
  • ARNI
  • hydralazine plus nitrate
  • aldosterone antagonists
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21
Q

T/F: drug therapy should be titrated as tolerated to target ranges for optimum clinical benefit

A

TRUE

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22
Q

T/F: benefits observed from aggressive monitoring strategies suggest treatment beyond clincial congestion may improve outcomes

A

TRUE

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23
Q

What medications would you use for Stage A HF pts?

A

ACE-I or ARB or BB

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24
Q

What meds would you use for Stage B pts with HF

A

ACE-I or ARB as appropriate

BB as appropriate

In select patients:

  • ICD
  • Revascularization or valvular surgery as appropriate
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25
Q

What meds would you use in patients with Stage C HF

A

HFrEF:

  • diuretics
  • ACE-I or ARB
  • BB
  • Aldosterone antagonists
  • Ivabradine
  • Sacubitril/Valsartan

In select pts:

  • hydralazine/isosorbide dinitrate
  • Digitalis
  • CRT
  • ICD
  • Revascularization or valvular surgery as appr.

HFpEF:

  • Diuresis
  • Guidelines driven indications for comorbidites
  • Aldosterone antagonism to reduce HF hospitalizations
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26
Q

What meds would you give pts with Stage D HF?

A
  • advanced care measures
  • heart transplant
  • temporary or permanent MCS (mechanical circulatory support)
  • Experimental surgery or drugs
  • Palliative care and hospice
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27
Q

MOA: Decreases NaCl, KCl, Calcium, Magnesium reabsorption in thick ascending limb of the loop of Henle in the nephron

What drug is this?

A

Furosemide

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28
Q

Effects of this drug:

  • increased excretion of salt and water
  • reduces cardiac preload & afterload
  • reduces pulmonary and peripheral edema

What drug is this?

A

Furosemide

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29
Q

Clinical applications of Furosemide

A
  • Acute and chronic heart failure
  • severe hypertension
  • edematous conditions
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30
Q

Toxicity:

hypovolemia, hypokalemia, orthostatic hypotension, ototoxicity, sulfonamide allergy

A

Furosemide

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31
Q

MOA: Decreases NaCl reabsorption in the distal convoluted tubule

What drug?

A

Hydrocholorothiazide (HCTZ)

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32
Q

Clinical applications of Hydrocholorothiazide (HCTZ)

A
  • mild chronic HF
  • mild-moderate hypertension
  • hypercalciuria
  • has not been shown to reduce mortality
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33
Q

Toxicity:

  • hyponatremia
  • hypokalemia
  • hyperglycemia
  • hyperuricemia
  • hyperlipidemia
A

Hydrocholorothiazide

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34
Q

MOA: blocks cytoplasmic aldosterone receptors in collecting tubules of nephron, possible membrane effect

What drug?

A

Spironolactone (Aldosterone Antagonist)

35
Q

Effects:

- increased salt and water excretion

- reduces remodeling

  • reduces mortality
A

Spironolactone (Aldosterone Antagonist)

36
Q

Clinical applications of Spironolactone

A
  • Chronic heart failure

- aldosteronism (cirrhosis, adrenal tumor)

  • hypertension
  • has been shown to reduce mortality
37
Q

Toxicity:

Hyperkalemia: risk increases if Creatinine >1.6 mg/dL

Avoid is Baseline K+> 5 mEq/L

  • Antiandrogen actions
A

Spironolactone

38
Q

What is the #1 recommended strategy to reduce the risk for hyperkalemia with aldosterone antagonists?

A

counsel pts to:

  • limit intake of high potassium-containing foods and salt substitutes
  • Avoid the use of over the counter NSAIDS
39
Q

MOA: Inhibits angiotensin converting enzyme

Effects:

- ateriolar and venous dilation

- reduces aldosterone secretion

  • reduces cardiac remodeling
A

ACE-I (angiotensin antagonists)

Lisinopril

40
Q

Clinical applications:

  • chronic heart failure
  • diabetic renal disease
  • has been shown to reduce mortality
A

ACE-I (Angiotensin Antagonists)

Lisinopril

41
Q

Toxicity:

  • cough
  • hyperkalemia
  • angioedema

Interactions: additive w/other angiotensin antagonists

A

ACE-I (Angiotensin Antagonist)

Lisinopril

42
Q

MOA: Antagonize AII effects at AT1 receptors

43
Q

Clinical applications:

-chronic heart failure

  • hypertension
  • diabetic renal disease
  • has been shown to reduce mortality
  • used in pts intolerant to ACE-I
A

Losartan (ARB)

44
Q

Can you use ACE-I and ARB together?

45
Q

Toxicity:

  • hyperkalemia
  • angioneurotic edema

Interactions:

  • additive with other angiotensin antagonists
A

Losartan (ARB)

46
Q

MOA: neprilysin blocker/ARB

A

ANRi: Sacubitril/valsartan

47
Q

T/F: discontinue ACE inhibitors at least 36 hours before initiating sacubitril/valsartan treatment

48
Q

MOA: competitively blocks B-1 and A-1 receptors

A

Carvedilol (Beta Blockers)

49
Q

Effects:

  • slowsl heart rate
  • reduces blood pressure
  • poorly understood effects
  • reduces heart failure mortality
A

Carvedilol (Beta Blockers)

50
Q

Clinical Applications:

  • slows progression of chronic heart failure
  • reduces mortality in moderate and severe heart failure
A

Carvedilol (Beta Blockers)

51
Q

Toxicity:

  • bronchospasm
  • bradycardia
  • AV block
  • Acute cardiac decompensation
A

Carvedilol (Beta Blockers)

52
Q

Select group of B blockers that have been shown to reduce heart failure mortality

A

Metoprolol

Bisoprolol

53
Q

Which beta blocker is effective in both systolic (HFrEF) and diastolic (HFpEF) failure?

54
Q

MOA:

  • Releases Nitric Oxide (NO)
  • activates guanylyl cyclase
A

Isosorbide dinitrate

55
Q

Effects:

  • Venodilation: reduces preload and ventricular stretch
A

Isosorbide dinitrate (Vasodilator)

56
Q

Clinical applications:

  • acute and chronic heart failure
  • angina

Toxicity:

  • postural hypotension, tachycardia, headache

Interactions:

  • additive with other vasodilators
  • synergistic with phosphodiesterase type 5 inhibitors
A

Isosorbide Dinitrate (Vasodilators)

57
Q

Clinical applications:

  • chronic failure in African Americans

**Indicated in conjunction with standard heart failure therapy to improve survival and reduce hospitalizations in self identified African American patients

A

Hydralazine- Isosorbide Dinitrate

58
Q

MOA: increases NO synthesis in endothelium

A

Hydralazine (Aterilar Dilators)

59
Q

Effects:

  • reduces blood pressure and afterload
  • increases Cardiac Output
A

Hydralazine (Arteriolar dilators)

60
Q

Clinical applications of Hydralazine

A

Hydralazine plus nitrates have reduced mortality

61
Q

Toxicity:

  • Tachycardia
  • Fluid retention
  • Lupus-like syndrome
A

Hydralazine (Arteriolar dilator)

62
Q

MOA: rapid, powerful vasodilation reduces preload and afterload

A

Nitroprusside

63
Q

Clinical application: acute severe decompensated failure

A

Nitroprusside

64
Q

P-kinetics:

  • IV only
  • Duration: a few minutes
A

Nitroprusside

65
Q

Thiocyanate and cyanide toxicity

A

Nitroprusside

66
Q

MOA: Na+/K+ -ATPase inhibition results in reduced CA2+ expulsion and increased Ca2+ stored in sarcoplasmic reticulum

67
Q

Effects:

  • increases cardiac contractility

**cardiac parasympathomimetic effect (slowed sinus heart rate, slowed AV conduction)

A

Digoxin (cardaic glycoside)

68
Q

Clinical applications:

  • chronic symptomatic heart failure

- rapid ventricular rate in A-fib

- has not been definitively shown to reduce mortality with HFrEF

A

Digoxin (cardiac glycoside)

69
Q

Toxicity:

  • narrow margin of safety

- nausea, vomiting, diarrhea, cardiac arrhythmias

A

Digoxin (Cardiac Glycoside)

70
Q

MOA: Beta 1 selective agonist

  • increases cAMP synthesis
A

Dobutamine (Beta-adrenoceptor agonist)

71
Q

Effects: increases cardiac contractility, output

A

Dobutamine (Beta-adrenoceptor agonist)

72
Q

Clinical Applications:

  • acute decompensated heart failure
  • intermittent therapy in chronic failure reduces symptoms
A

Dobutamine (Beta-adrenoceptor agonists)

73
Q

P-kinetics, Toxicities, Interactions:

  • IV only
  • Duration a few minutes

Toxicity: arrhythmias

Interactions: additive with other sympathomimetics

A

Dobutamine

74
Q

MOA: dopamine receptor agonist, higher doses activate B and Alpha adrenoceptors

Effects: increases renal blood flow, higher doses increase cardiac force and blood pressure

Clinical applications: acute decompensated heart failure, shock

**IV only

Toxicity: arrhythmias

Interactions: additive with sympathomimetics

A

Dopamine (Beta-adrenoceptor agonists)

75
Q

Mechanism of Action:

Phosphodiesterase type 3 inhibitors

decrease cAMP breakdown

Effects:

vasodilators, lower peripheral vascular resistance

increase cardiac contractility

Clinical Applications:

acute decompensated heart failure

increase mortality in chronic failure

Toxicity: arrhythmias

Interactions: additive with other arrhythymogenic agents

A

Inamrinone, Milrinone

76
Q

MOA: activates BNP receptors, increases cGMP

Effects: vasodilation + diuresis

Clinical Applications: acute decompensated failure, has not been shown to reduce mortality

**IV only

Toxicity: renal damage, hypotension, may increase mortality

A

Nesiritide (Natriuretic Peptide)

77
Q

MOA: prolongs diastolic time by selectively and specifically inhibiting the If current within the HCN channel, reducing heart rate.

Indication: symptoms of heart failure that are stable, a normal heartbeat with a resting heart rate of atleast 70 beats per minute, taking a beta blocker at the highest dose tolerated

**hopefully reduces the risk of being hospitalized for worsening heart failure**

A

Ivabradine

78
Q

Interactions: avoid concomitant use with strong CYP3A4 inhibitors

A

Ivabradine

79
Q

T/F: In patients with NYHA class II and III HF and iron deficiency (ferritin <100 or 100-300 if transferrin saturation is <20), IV iron replacement may be reasonable to improve functional status.

80
Q

In patients with HF and anemia, ________________ shoud not be used to improve morbidity and mortality

A

erythropoeitin-stimulating agents

81
Q

In patients with HF, the optimal blood pressure in those with HTN shoud be less than ______

82
Q

In pts with CVD and OSA, ______ may be reasonable to improve sleep quality and daytime sleepiness

MJ- Pharm exam 2 (19 decks)

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