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Pharm Block 2 > Drugs for Heart Failure > Flashcards

Drugs for Heart Failure Flashcards

1
Q

excitation - contraction coupling machinery of heart

A

primary defect

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2
Q

baroreceptor reflex, SANS, kidneys, AG2, aldosterone, apoptosis of cardiac cells

A

secondary defect

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3
Q

compensation in heart failure #1

A

Baroreceptor reflex increases sympathetic system:

1) increase contractility & HR (B1 adrenergic receptor)
2) increase vasomotor tone (A1 adrenergic receptor) to maintain systemic BP (inc. preload & inc. afterload)

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4
Q

compensation in heart failure #2

A

RAAS activated:

1) AG2 constricts artery - inc afterload & constricts vein - inc preload
2) aldosterone causes Na+/H2O retention - inc preload (edema)
3) AG2 increases fibrosis in heart (collagen)

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5
Q

Signs & Symptoms of Heart Failure

A

1) tachycardia
2) decrease exercise tolerance & SOB
3) peripheral & pulmonary edema (from LHF)
4) myocardial hypertrophy (initially helps maintain cardiac performance), [later leads to ischemic changes, impairment of diastolic filing, remodeling by local AG2 & aldosterone]

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6
Q

1) increases connective tissue proliferation
2) Beta myosin fetal cells
3) eventually apoptosis

A

remodeling

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7
Q

decrease ejection fraction

<50% (dilated/congestive)

A

systolic heart failure

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8
Q

loss of adequate relaxation

A

diastolic heart failure

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9
Q

Direct effects of Digoxin

A
  • ** inhibition of cardiac Na+/K+ ATPase ***
    1) Inc intracellular Na+
    2) Dec Na+/Ca2+ exchange
    3) Inc intracellular Ca2+
    4) Inc Ca2+ release from sarcoplasmic reticulum
    5) Inc actin - myosin interaction
    6) Inc contractile force
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10
Q

Indirect effect of Digoxin

A

inhibition of neuronal Na+/K+ ATPase (results in increase vagal activity)

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11
Q

Decrease ESV
Increase SV & CO
Increase renal perfusion

A

First dose effect of Digoxin

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12
Q 
Decrease EDV (preload) in continued use
Continued large SV
A

Continued use of Digoxin

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13
Q

Autonomic Effects of Digoxin

A

Increase of intracellular Ca2+ –> Inc Ach in PANS (M2) –> Dec HR –> Dec SA, A-V conduction (Tx: SVT)

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14
Q

Effects of Digoxin on GIT (early signs)

A

Anorexia
Nausea
Vomiting
Diarrhea

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15
Q

Effects of Digoxin on CNS (late signs)

A

Disorientation
Visual Effects (hallucinations)
Altered color perception (blue/green)

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16
Q

ECG changes with Digoxin

A

1) Initial early shortening of AP
2) long term use - lengthening of AP
3) Increase PR interval d/t decrease AV cond vol
4) less -ve RMP - easy premature depolarization

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17
Q

toxic dose effects of digoxin

A

any cardiac arrhythmias, bigeminy ventricular premature contraction

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18
Q

What 3 factors cause - Increase Digoxin toxicity

A

hypokalemia
blood magnesium decrease
blood calcium increase

19
Q

what 3 factors cause - decrease digoxin toxicity

A

hyperkalemia
blood magnesium increase
blood calcium decrease

20
Q

Important key btwn K & digoxin

A

K & digoxin inhibit each other’s binding to Na/K ATPase b/c they compete with each other

21
Q

management of digoxin toxicity

A

Fab antibodies

22
Q

Quinidine interaction w/ digoxin

A

replaces digoxin from tissue protein binding & increases serum digoxin

23
Q

verapamil interaction w/ digoxin

A

increase digoxin concentration by: 1) decrease its. clearance; 2) replaces it from tissue protein binding

24
Q

Pharmacokinetics of digoxin

A

1) renal clearance- caution in renal impairment
2) long t1/2 - 1.5 days (min. 6 day -Css)
3) large vd - tissue protein binding

25
Q

MOA: Increase cAMP

only given IV for short term therapy

A

Phosphodiesterase inhibitors: Inamrinone and Milrinone

26
Q

Use for PDE inhibitors

A

Acute CHF

27
Q

MOA of PDE inhibitors

A

Increase cAMP on heart - increase inotropy

Increase cAMP on smooth muscle - decrease TPR

28
Q

ADR of PDE inhibitors

A

GI upset
Thrombocytopenia
liver toxicity

29
Q

Sympathomimetics used for Acute CHF (systemic fxn decreases)

A

Dobutamine (B1 adrenergic agonist)

Dopamine

30
Q

Drugs that decrease mortality in HF

A

1) ACE-I, ARB
2) B-Blocker
3) Spironolactone/Eplerenone
4) Carvedilol
5) Vasodilators: Nesiritide and Bosentan

31
Q

recombinant human BNP, for acute decompensated CHF

ADR: decrease BP

A

Nesiritide (vasodilator)

32
Q

Endothelin receptor blocker

A

Bosentan

33
Q

decrease AG2 > + vasodilation
decrease aldosterone > decrease fluid retention
slows cardiac remodeling

A

angiotensin antagonist

34
Q

Diuretics in HF

A

1) Furosemide - decrease volume immediately in pulm congestion and severe edema secondary to acute HF
2) Hydrochlorothiazide - mild chronic failure
3) Spironolactone/Eplerenone - long term benefits and decrease mortality in chronic HF

35
Q

1) secreted by ventricular myocytes secondary to stretch
2) increase HF
3) binds to receptor on plasma membrane in vasculature, kidney and other organs

A

BNP

36
Q

-ve Sa node funny channel > decrease HR but does not suppress heart contraction

A

Ivabradine

37
Q

enzyme to degrade BNP and bradykinin

A

neprilysin

38
Q

neprilysin derivative

decreases morbidity and mortality

A

sacubitril

39
Q

symptoms of acute LHF

A 
orthopnea 
dyspnea
pink sputum 
sweating 
anxiety
40
Q

sign of LHF

A

whole lung rales
Gallop HR
cyanosis

41
Q

CXR of LHF

A

cardiomegaly

butterfly infiltration

42
Q

management of acute LHF

A

1) O2
2) morphine
3) furosemide
4) digoxin
5) nitroprusside
6) life support
7) treat the cause

43
Q

Stages of HF

A

1) SOB with heavy exercise
2) SOB with ordinary activities
3) SOB with less than ordinary activities
4) SOB at rest

Pharm Block 2 (22 decks)

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