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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
You can see ANP/BNP effects being opposite to...
Angiotensinogen II actions
26
What is nesiritide?
Synthetic recombinant human BNP
27
Clinical indication of nesiritide? What does it do to cause this indication? Specifically...
ST treatment of CHF; improves CO: decrease afterload (vasodilation) and lower pulmonary capillary wedge pressure (natriuresis) --> decrease preload
28
SE of nesiritide
Hypotension
29
What is aliskiren?
Renin inhibitor
30
Why is Angiotensin II bad for the heart in HF? (4)
Cardiac and vascular hypertrophy, systemic vasoconstriction, increased blood volume (via thirst), sodium retention
31
Where is renin released? What does renin do?
JG cells; angiotensinogen --> angiotensin I
32
What causes renin release (at the macula densa)? What inhibits?
Decreased delivery of NaCl to macula densa; increased delivery of NaCl
33
How is renin release related to pressure?
Intrarenal baroreceptor can detect decreased renal perfusion --> increase renin release
34
What renal receptor regulates renin?
Beta-1 (sympathetic activity) receptors in the JG
35
What feeds back to inhibit renin?
Angiotensin II
36
Three ACE inhibitors
Lisinopril, captopril, enalapril
37
What is the mechanism of action of ACE inhibitors?
Competitive inhibitor of ACE --> less angiotensin II
38
What is the effect of ACE inhibitors on renin?
Less negative feedback to renin, more renin
39
Clinical indications of ACE inhibitors? (2)
CHF and HTN (due to decreased vasoconstriction --> decreased BP w/out reflex tachycardia)
40
ACEI is the #1 choice for HTN treatment in which patients? Why?
Diabetic patients with chronic kidney disease; decreases risk of diabetic nephropathy via decreased glomerular pressure
41
Why are ACEI good for the kidneys?
Decrease intraglomerular pressure because angiotensin II constricts afferent arterioles > efferent arterioles; ACEI causes bigger dilation of efferent arterioles --> decreased hydrostatic pressure
42
What is the effect of ACEI on mortality in CHF?
Decreases! Prevents/decreases progression of heart failure.
43
ACEI: Discuss the decrease of vasoconstriction in CHF
Decreased vasoconstriction --> decreases afterload --> increased CO
44
ACEI: Discuss the decrease of aldosterone in CHF
Decreased aldosterone --> less Na+ reabsorption --> decreased volume, preload, edema
45
What are three other (besides decreased vasoconstricion and decreased aldosterone) cool/good effects of ACEI?
Venodilation (decreased preload), reverses ventricular remodeling, no increase in HR
46
Besides HTN and CHF, what are two other heart-related problems ACEI could be prescribed for?
Acute MI and CAD
47
SEs of ACEI (6)
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
Why does an ACEI cause decreased GFR
Because the efferent arteriole is dilated > afferent arteriole with ACEI, you have decreased hydrostatic pressure --> decreased GFR
49
What is special about lisinopril?
Most commonly used
50
What is special about captopril?
Short half-life which is good for very sick patients if you're worried about them "bottoming out"
51
What is special about enalapril?
Can be given IV
52
Mechanism of ARBs
Selective AT-I receptor antagonists
53
What is our key-worded ARB?
Losartan
54
Clinical indications for Losartan (4)
HT, CHF, MI, diabetic nephropathy
55
Losartan SEs that are similar to ACEIs
Hypotension, hyperkalemia, decreased GFR, teratogenic
56
What's different about ARBs compared to ACEIs SE profiles
Lower incidence of cough and rare cases of angioedema
57
What do beta-blockers do to plasma renin?
Decrease concentration and activity
58
What three drugs increase renin concentration?
Renin inhibitors, ACE inhibitors, ARBs
59
What are the effects of ARBs on RAAS and why?
Decrease blood pressure --> higher renin --> higher AT I --> higher AT II
60
Inotropic agents (4)
Dopamine, dobutamine, digoxin, milrinone
61
Dobutamine is a...
Beta-1 agonist
62
Dopamine is a...
D1, beta-1, and alpha agonist
63
What is the mechanism of the inotropic agents?
Increase Ca2+ levels --> better contraction
64
What is the mechanism of Digoxin?
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
If a patient is _____-kalemic, what should you watch out for w/ digoxin?
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
What effect does digoxin have on the ANS? What does this do?
Decrease sympathetic outflow and increases parasympathetic outflow; slows the heart
67
What are the electrical effects of digoxin?
Shortens AP (at therapeutic levels); reduce resting potential (at higher potentials)
68
What happens at moderately toxic levels of digoxin? What does this look like on EKG?
Overload of intracalcium stores --> delayed after depolarizations (DADs) --> bigeminy
69
What happens at very toxic digoxin levels?
Ventricular fibrillation (death)
70
Clinical indications of digoxin (2)
CHF via increasing CO, but narrow therapeutic window; Afib and atrial flutter (rate control)
71
Does digoxin cause a decrease in mortality?
Probably nope
72
AEs of digoxin (4 classes)
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
Why does Van Gogh help us remember digoxin?
Yellow-green paintings, halos, GI problems, psychiatric problems
74
What is important about digoxin's pharmacokinetics? (2)
Huge volume distribution --> digoxin is all over the body; narrow therapeutic window
75
What is important about digoxin and renal function?
Mainly renally cleared, must watch levels closely
76
How do you treat digoxin OD?
Digibind (digoxin immune fab)
77
What is the mechanism of milrinone?
Selective inhibitor of phosphodiesterase (PDE) type 3 --> increased cAMP --> better contraction
78
What else does milrinone do?
By increasing cAMP in vessels --> vasodilaton in arterioles and venules --> decreased preload and afterload
79
Clinical indication of milrinone
ST management of CHF
80
SO milrinone causes _______ in the heart and _______ in the vessels via _______
Contraction; relaxation; cAMP
81
AEs of milrinone
Afib, arrhythmias, hypotension
82
Key worded beta-blocker and it's mechanism
Metoprolol; selective beta-1 antagonist
83
What is the effect of beta-blockers?
Slows down the heart --> less cardiac work; decreases BP --> decrease afterload
84
T/F: Beta blockers reduce CHF mortality?
True
85
Why do we have to think carefully about prescribing beta-blockers? Who are they prescribed to? Who do we NOT prescribe to?
They are negative inotropes --> decreased contractility; stable patients; pts in fluid overload/acute CHF decompensation
86
What does acute decompensation CHF look like? (7)
Very sick: dyspnea, orthopnea, crackles, pink frothy sputum, anxiety, fatigue, decreased urine output

Cardiology (22 decks)

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