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Cardiology > Lecture 5: Drugs used in Congestive HF > Flashcards

Lecture 5: Drugs used in Congestive HF Flashcards

1
Q

Decreased CO in CHF causes what two things (largely)

A

Decreased sinus firing and decreased renal blood flow

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2
Q

Decreased sinus firing leads to…

A

Increased sympathetic discharge (increased force, rate, preload, afterload)

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3
Q

Decreased renal blood flow leads to…then what?

A

Increased renin release –> increased angiotensin II –> increased preload, afterload, remodeling

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4
Q

T/F: Angiotensin II is good for CHF

A

False!

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5
Q

Conceptually, what do we want HF drugs to do? (2)

A

Act as positive inotropes and vasodilate

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6
Q

How does Furosemide work?

A

Inhibits Na-K-2 CL symporter, Na+ not reabsorbed, water follows

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7
Q

Clinical indications of Furosemide for HF? (2)

A

Acute pulmonary edema and peripheral edema

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8
Q

What is another relevant effect of Furosemide?

A

Acutely increases systemic venous capacitance –> decreased cardiac preload and edema BEFORE diuresis occurs

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9
Q

Furosemide causes…what side effects is this related to? (2)

A

Volume depletion; hypotension, decreased GFR (due to decreased hydrostatic pressure in Glomerulus)

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10
Q

What is another SE of Furosemide that’s important, describe mechanism. What hormone is involved in this?

A

Hypokalemia due to negative charge left in lumen after Na+ is reabsorbed in collecting duct, so K+ will go into lumen; aldosterone

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11
Q

Hypokalmeia predisposes patients to…

A

Arrhythmias

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12
Q

Why does Furosemide cause hypomagnesemia?

A

Inhibition of Na-K-2 CL symporter, means less K+ backleak (required to maintain Na-K-2 CL symporter) into lumen, so lumen is less (+) charged, so less paraceulluar transport (reabsorption) of Mg2+

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13
Q

Why is lasix called lasix?

A

“Lasts 6 hours”

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14
Q

What kind of drug is spironolactone

A

Also a diuretic (but NOT strong)! And an aldosterone receptor antagonist

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15
Q

What does aldosterone DO?

A

Reabsorb a lot of sodium via increase activation of and synthesis of ENaC and basolateral Na/K-ATPase

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16
Q

What else does aldosterone do that is bad for CHF?

A

Vasculature: fibrosis, endothelial dysfunction, inhibition of NO synthesis; Heart: fibrosis, LV hypertrophy, arrhythmias

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17
Q

What is the site of action of aldosterone?

A

Late distal tubule and collecting duct

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18
Q

Clinical indications of spirnolactone

A

Decreases morbidity and mortality in CHF

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19
Q

How does spirnolactone affect K+ levels?

A

HYPERkalemia; Less Na+ reabsorption –> less K+ excretion

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20
Q

Vasoactive peptides classes (3)

A

Natiuretic peptides, ACE inhibitrs, angiotensis receptor blockers

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21
Q

What are the two natiuretic peptides?

A

ANP and BNP

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22
Q

Describe ANP (where it’s secreted and when)

A

Secreted by atrial myocytes due to atrial stretch

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23
Q

Describe BNP (where it’s secreted and when)

A

Secreted by left ventricle due to myocardial stretch

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24
Q

What do ANP and BNP do? (3)

A

Natural diuresis (due to decreased proximal tubular Na+ reabsorption); decrease renin, aldosterone, and ADH; vasodilation (decreases BP)

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25
Q

You can see ANP/BNP effects being opposite to…

A

Angiotensinogen II actions

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26
Q

What is nesiritide?

A

Synthetic recombinant human BNP

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27
Q

Clinical indication of nesiritide? What does it do to cause this indication? Specifically…

A

ST treatment of CHF; improves CO: decrease afterload (vasodilation) and lower pulmonary capillary wedge pressure (natriuresis) –> decrease preload

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28
Q

SE of nesiritide

A

Hypotension

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29
Q

What is aliskiren?

A

Renin inhibitor

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30
Q

Why is Angiotensin II bad for the heart in HF? (4)

A

Cardiac and vascular hypertrophy, systemic vasoconstriction, increased blood volume (via thirst), sodium retention

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31
Q

Where is renin released? What does renin do?

A

JG cells; angiotensinogen –> angiotensin I

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32
Q

What causes renin release (at the macula densa)? What inhibits?

A

Decreased delivery of NaCl to macula densa; increased delivery of NaCl

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33
Q

How is renin release related to pressure?

A

Intrarenal baroreceptor can detect decreased renal perfusion –> increase renin release

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34
Q

What renal receptor regulates renin?

A

Beta-1 (sympathetic activity) receptors in the JG

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35
Q

What feeds back to inhibit renin?

A

Angiotensin II

36
Q

Three ACE inhibitors

A

Lisinopril, captopril, enalapril

37
Q

What is the mechanism of action of ACE inhibitors?

A

Competitive inhibitor of ACE –> less angiotensin II

38
Q

What is the effect of ACE inhibitors on renin?

A

Less negative feedback to renin, more renin

39
Q

Clinical indications of ACE inhibitors? (2)

A

CHF and HTN (due to decreased vasoconstriction –> decreased BP w/out reflex tachycardia)

40
Q

ACEI is the #1 choice for HTN treatment in which patients? Why?

A

Diabetic patients with chronic kidney disease; decreases risk of diabetic nephropathy via decreased glomerular pressure

41
Q

Why are ACEI good for the kidneys?

A

Decrease intraglomerular pressure because angiotensin II constricts afferent arterioles > efferent arterioles; ACEI causes bigger dilation of efferent arterioles –> decreased hydrostatic pressure

42
Q

What is the effect of ACEI on mortality in CHF?

A

Decreases! Prevents/decreases progression of heart failure.

43
Q

ACEI: Discuss the decrease of vasoconstriction in CHF

A

Decreased vasoconstriction –> decreases afterload –> increased CO

44
Q

ACEI: Discuss the decrease of aldosterone in CHF

A

Decreased aldosterone –> less Na+ reabsorption –> decreased volume, preload, edema

45
Q

What are three other (besides decreased vasoconstricion and decreased aldosterone) cool/good effects of ACEI?

A

Venodilation (decreased preload), reverses ventricular remodeling, no increase in HR

46
Q

Besides HTN and CHF, what are two other heart-related problems ACEI could be prescribed for?

A

Acute MI and CAD

47
Q

SEs of ACEI (6)

A
  1. Hypotension, 2. Cough (5-20%, dry cough w/in 6 months, bradykinin thought to be indicated); 3. Hyperkalemia, 4. Decreased GFR; 5. Angioedema (rare; rapid swelling of lips/tongue); 6. Teratogenic
48
Q

Why does an ACEI cause decreased GFR

A

Because the efferent arteriole is dilated > afferent arteriole with ACEI, you have decreased hydrostatic pressure –> decreased GFR

49
Q

What is special about lisinopril?

A

Most commonly used

50
Q

What is special about captopril?

A

Short half-life which is good for very sick patients if you’re worried about them “bottoming out”

51
Q

What is special about enalapril?

A

Can be given IV

52
Q

Mechanism of ARBs

A

Selective AT-I receptor antagonists

53
Q

What is our key-worded ARB?

A

Losartan

54
Q

Clinical indications for Losartan (4)

A

HT, CHF, MI, diabetic nephropathy

55
Q

Losartan SEs that are similar to ACEIs

A

Hypotension, hyperkalemia, decreased GFR, teratogenic

56
Q

What’s different about ARBs compared to ACEIs SE profiles

A

Lower incidence of cough and rare cases of angioedema

57
Q

What do beta-blockers do to plasma renin?

A

Decrease concentration and activity

58
Q

What three drugs increase renin concentration?

A

Renin inhibitors, ACE inhibitors, ARBs

59
Q

What are the effects of ARBs on RAAS and why?

A

Decrease blood pressure –> higher renin –> higher AT I –> higher AT II

60
Q

Inotropic agents (4)

A

Dopamine, dobutamine, digoxin, milrinone

61
Q

Dobutamine is a…

A

Beta-1 agonist

62
Q

Dopamine is a…

A

D1, beta-1, and alpha agonist

63
Q

What is the mechanism of the inotropic agents?

A

Increase Ca2+ levels –> better contraction

64
Q

What is the mechanism of Digoxin?

A

Increases Ca2+ levels in cardiac myoctyes via inhibition of the Na/K ATPase –> more Na+ in the cell –> less driving force on Na+ to enter cell via NCX –> less Ca2+ out of the cell

65
Q

If a patient is _____-kalemic, what should you watch out for w/ digoxin?

A

Hypo; because digoxin and K+ compete for the same active site on the Na/K ATPase, low K+ can increase risk of digoxin toxicity

66
Q

What effect does digoxin have on the ANS? What does this do?

A

Decrease sympathetic outflow and increases parasympathetic outflow; slows the heart

67
Q

What are the electrical effects of digoxin?

A

Shortens AP (at therapeutic levels); reduce resting potential (at higher potentials)

68
Q

What happens at moderately toxic levels of digoxin? What does this look like on EKG?

A

Overload of intracalcium stores –> delayed after depolarizations (DADs) –> bigeminy

69
Q

What happens at very toxic digoxin levels?

A

Ventricular fibrillation (death)

70
Q

Clinical indications of digoxin (2)

A

CHF via increasing CO, but narrow therapeutic window; Afib and atrial flutter (rate control)

71
Q

Does digoxin cause a decrease in mortality?

A

Probably nope

72
Q

AEs of digoxin (4 classes)

A

Visual: blurred or yellow-green vision halos; GI: N/V, ab pain; Cardiac: sagging ST segment (Salvidor Dali moustache), AV block, bradycardia, ectopic beats, arrhythmias; psychiatric: fatigue, delerium, confusion

73
Q

Why does Van Gogh help us remember digoxin?

A

Yellow-green paintings, halos, GI problems, psychiatric problems

74
Q

What is important about digoxin’s pharmacokinetics? (2)

A

Huge volume distribution –> digoxin is all over the body; narrow therapeutic window

75
Q

What is important about digoxin and renal function?

A

Mainly renally cleared, must watch levels closely

76
Q

How do you treat digoxin OD?

A

Digibind (digoxin immune fab)

77
Q

What is the mechanism of milrinone?

A

Selective inhibitor of phosphodiesterase (PDE) type 3 –> increased cAMP –> better contraction

78
Q

What else does milrinone do?

A

By increasing cAMP in vessels –> vasodilaton in arterioles and venules –> decreased preload and afterload

79
Q

Clinical indication of milrinone

A

ST management of CHF

80
Q

SO milrinone causes _______ in the heart and _______ in the vessels via _______

A

Contraction; relaxation; cAMP

81
Q

AEs of milrinone

A

Afib, arrhythmias, hypotension

82
Q

Key worded beta-blocker and it’s mechanism

A

Metoprolol; selective beta-1 antagonist

83
Q

What is the effect of beta-blockers?

A

Slows down the heart –> less cardiac work; decreases BP –> decrease afterload

84
Q

T/F: Beta blockers reduce CHF mortality?

A

True

85
Q

Why do we have to think carefully about prescribing beta-blockers? Who are they prescribed to? Who do we NOT prescribe to?

A

They are negative inotropes –> decreased contractility; stable patients; pts in fluid overload/acute CHF decompensation

86
Q

What does acute decompensation CHF look like? (7)

A

Very sick: dyspnea, orthopnea, crackles, pink frothy sputum, anxiety, fatigue, decreased urine output

Cardiology (22 decks)

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