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Pharm Exam 2 > Topic 10 > Flashcards

Topic 10 Flashcards

1
Q

Heart Failure definitions

A
  1. Inability to effectively return all the blood volume
    it (the heart) receives to the patients circulation
  2. (The heart’s)…inability to deliver adequate oxygen
    to the patients body to maintain normal function and homeostasis
  3. “The heart is unable to effectively provide the patietns tissues with necessary metabolites and remove metabolic wastes
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2
Q

Symptomatic definition for heart failure

A

A mismatch between right and left heart volume

outputs: Right sided vs. Left sided HF
- implies 2 different set of syndromes

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3
Q

Cardio-centric definition for heart failure

A

The heart’s impaired ability to adequately
fill with &/or eject blood
-implies dual causation

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4
Q

Definition of what causes heart failure

A
  • systolic failure= thin walls
  • diastolic failure= thick walls
  • -implies 2 types of myocardial remodeling
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5
Q

Systolic HF=

A

decreased Contractility
decreased Ejection Fraction
~ ½ of the HF patients which tend to be “younger”

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6
Q

Diastolic HF=

A

decreased Ventricular Filling
decreased Cardiac Output
~ ½ of patients which tend to be older

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7
Q

Main HF causes

A

1) Ischemia
2) Idiopathic
3) Viral
4) Immune-mediated
5) HTN

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8
Q

Ischemia can contribute to

A

both systolic and diastolic dysfunction

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9
Q

Most common type of HF in America? %?

A

Ischemia

70%

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10
Q

Idiopathic=

A 
Familial? (~ 1/3?)
Toxins?
Parasitic?
Undiagnosed viral?
Pregnancy-related?
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11
Q

Viral=

A

Viruses “errantly” take up residence in
myocardial cells…Moderate/severe cardiomyopathy develops…and may or may not fully or completely
resolve (eventually)
•Might require valvular Sx due to new cardiac “geometry”

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12
Q

Immune mediated

A

Specific cardiac antibodies attack cardiomyocytes
•Possible link to other immune-mediated diseases
•Acute myocardial infarctions (AMIs) may expose novel cardiac antigens affecting long-term prognosis

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13
Q

Phase 0

A

Fast upstroke

  • Na+ channels open
  • Na+ current is blocked by anti-arrhythmic drugs
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14
Q

Phase 1

A

Partial re-polarization

-Inactive Na+ channels, Fast Active K+

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15
Q

Phase 2

A

Plateau

-Ca++ opens

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16
Q

Phase 3

A

Re-polarization

-Ca++ close, K+ open

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17
Q

Phase 4

A

Forward current

-increasing depolarization from gradual increase in Na+

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18
Q

What forces contribute to the chronic downhill HF slide?

A 
#1= ANS
#2= Renin-Angiotensin-Aldosterone system
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19
Q

Why Does the Heart “Remodel”?

A

Heart cells die…they’re replaced with fibrotic tissues…and remaining cells hypertrophy.

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20
Q

What are the Goals of Therapy for HF?

A

1) Improve/alleviate critter’s symptoms
2) Slow that “downhill slide” towards
transplant/VAD/death
3) Improve survival
4)Increase critter’s QALYs

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21
Q

Six Classes of QALY-Improving Drugs

A

1) Positive Inotropes
2) Diuretics
3) Renin/Angiotensin Blockers
4) Primary Vasodilators
5) β-Blockers
6) Aldosterone Antagonists
7) Neprilysin Inhibitor (the future?)

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22
Q

1: Positive Inotropes=

A
  • Cardiac Glycosides
  • Catecholamines
  • Bipyridines
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23
Q

Cardiac Glycosides: drug name

A

Digitalis (Digoxin)

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24
Q

Digitalis

A

Digoxin

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25
Q

Digitoxin (historical use)

A

Positive Inotrope
Negative Chronotrope
Increased Baroreceptor sensitivity

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26
Q

Cardiac Glycosides Narrow therapeutic window for

A

Arrhythmias, GI symptoms

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27
Q

Digitalis blocks

A

Na⁺/K⁺ -ATPase “The Sodium Pump”

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28
Q

Administration of Digoxin shifts the ventricular function curve toward

A

normal

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29
Q

Digoxin treatment effects on the heart

A

Increased contractility and CO

Decreased sympathetic reflexes and vascular tone= decrease in ventricular end diastolic pressure

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30
Q

decompensated HF=

A
  1. initial contractility due to HF

2. symptoms of low CO (Dyspnea, edema)

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31
Q

compensated HF=

A
  1. ventricular end diastolic pressure increase in an effort to maintain adequate CO
  2. Symptoms of congestion (Dyspnea)
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32
Q

Catecholamines are classic

A

β-1 adrenergic receptor stimulants

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33
Q

Catecholamines- drugs

A

Epinephrine
Norepinephrine
Dopamine
Dobutamine

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34
Q

Catecholamines are powerful

A

positive inotropes and chronotropes

35
Q

PREFERRED DRUG FOR CARDIAC ARREST

A

Epinephrine (Adrenaline)

36
Q

Epinephrine (Adrenaline) is handy for _____ reactions and has predictable ______ ______

A

anaphylactic

side effects

37
Q

Dopamine is a relatively non-specific ______ and acts on ______ receptors

A

catecholamine

dopaminergic

38
Q

Dopamine improves cardiac function in _____ and is also used for ____ and ____

A

heart failure
renal failure
shock

39
Q

Dopamine is given by

A

IV drip infusion

40
Q

Dobutamine also acts on dopaminergic receptors is but

more

A

cardioselective

41
Q

Bipyridines are referred to as

A

phosphodiesterase inhibitors

42
Q

Bipyridines: drugs

A

Inamrinone (Inocor)

Milrinone (Primacor)

43
Q

Inamrinone

A

(Inocor)

44
Q

Milrinone

A

(Primacor)

45
Q

Bipyridines have what effects

A

increase intracelular levels of cAMP=
increased intracellular levels of Ca⁺⁺ =
increased myocardial contractility

46
Q

Bipyridines: ***Surprisingly, longer-term use of these drugs results in

A

significantly higher mortality than that seen in untreated patients!

47
Q

Bipyrides are only used in

A

short-term (acute) HF patients

48
Q

2: Diuretics: First-line D.O.C.’s for

A

heart failure (particularly furosemide/lasix)

49
Q

Diuretics: drugs

A

furosemide (lasix)

50
Q

furosemide

A

lasix

51
Q

Diuretics are ideal for nasty symptoms of excessive

A

venous pressure

52
Q

Diuretics Decrease plasma volume, which does what

A

Decrease afterload and blood pressure
Decrease preload as well as edema
*Net affect is to decrease the heart’s workload and mycardial O2 demand

53
Q

3: Renin-Angiotensin Converting Enzyme Blockers (Angiotensin-Converting Enzyme Inhibitors) have what effects

A

decrease venous tone which in turn decreases SVR.

decreases preload & afterload

54
Q

Renin -Angiotensin Converting Enzyme Blockers: DOC

A
  • all stages of HF, particularly in patients with low EF

- Often used as part of a progressive multi-modal Rx

55
Q

initiation of ACE-Inhibitor Rx after _____ is widely considered a standard of care

A

acute myocardial infarction

56
Q

Angiotensin Receptor Blockers “ARBs”: Historically

not a first-line drug- Used as a

A

replacement for ACE-Inhibitors in intolerant patients BUT may also be used with ACE-Inhibitors in decompensating patients

57
Q

Angiotensin Receptor Blockers: drug name

A

Losartan (Cozaar)

58
Q

Losartan

A

(Cozaar)

59
Q

4: Primary Vasodilators: have what effects

A

Dilation =

  • decreased preload due to increased venous capacitance
  • decreased SVR
  • decreased afterload
60
Q

Primary Vasodilators: _____ are frequently D.O.C. venous dilators for acute CHF episodes

A

Nitrates

61
Q

Those intolerant of ACE-Inhibitors and Angiotensin Blockers &/or β-Blockers frequently respond well to

A

Hydralazine (Apresoline)

Isosorbide (Isordil)

62
Q

Hydralazine

A

(Apresoline)

63
Q

Isosorbide

A

(Isordil)

64
Q

5: β-Blockers: Block chronic (and deadly) SNS stimulation which contributes to

A

cardiomyocyte apoptosis

mitogenic remodeling

65
Q

B-Blockers have what effects

A

Negative chronotrope= decreased myocardial O2 needs

66
Q

β-Blockers: Drugs

A

Metoprolol (Lopressor, Toprol-XL)

Carvedilol (Coreg)

67
Q

Metoprolol

A

(Lopressor, Toprol-XL)

68
Q

Carvedilol

A

(Coreg)

69
Q

β-Blockers: Metoprolol and Carvedilol- have been show to improve

A

long-term HF survivability. NOT for acute HF!!!

70
Q

6: Aldosterone Antagonists: have what effets

A

help prevent salt/fluid retention, myocardial hypertrophy, and K⁺
*Improve long-term mortality post-MI

71
Q

Aldosterone Antagonists: drugs

A

Spironolactone (Aldactone)

Eplerenone (Inspra)

72
Q

Spironolactone

A

(Aldactone)

73
Q

Spironolactone (Aldactone) is a

A

DIRECT aldosterone antagonist

74
Q

Eplerenone

A

(Inspra)

75
Q

Eplerenone (Inspra) is a

A

COMPETITIVE aldosterone antagonist

76
Q

7: LCZ696: A 50/50 mix of

A

Losartan and Sacubitril

•Sacubitril is metabolized into a neprilysin inhibitor

77
Q

LCZ696: Neprilisyn is an enzyme which breaks down

A

atrial (ANP) & brain (BNP) natriuretic peptides

78
Q

ANP is mostly released in response to

A

excessive blood volume (mostly in response to excessive atrial “stretch”) and causes an increased
GFR, increased sodium loss, and decreased renin secretion

79
Q

Stage A (Pre-faliure)

  • Description
  • Management
A
  • Description: No symptoms but risk factors present

- Management: Treat obesity, HTN, Diabetes, Hyperlipidemia

80
Q

Stage B (I)

  • Description
  • Management
A
  • Description: Symptoms with severe exercise

- Management: ACEI/ ARB, B-Blocker, Diuretic

81
Q

Stage C (II/III)

  • Description
  • Management
A
  • Description: Symptoms with markes (Class II) or mild (class III) exercise
  • Management: Add aldosterone antagonist, digoxin, CRT, hydralazine/nitrate
82
Q

Stage D (IV)

  • Description
  • Management
A
  • Description: Severe symptoms at rest

- Management: Transplant, LVAD

83
Q

Morphine used in acute heart failure to

A

reduce preload, heart rate, and (maybe?) afterload

84
Q

Morphine has what effects for chronic HF

A
  1. Lowers respiratory rate which decreases cardiac workload
  2. Decreases preload and afterload
  3. EASES ANXIETY!

Pharm Exam 2 (9 decks)

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