CHF Flashcards

1
Q

DRUGS USED TO TREAT CHF

A
  1. RAAS inhibitors
    a. ACEI
    b. ARBs
    dec afterload, dec preload, dec remodeling
  2. Other vasodilators
    a. hydralazine + isosorbide dinitrate
    b. amlodipine
    dec afterload, dec preload, less
    effect on remodeling
  3. B antagonists
  4. diuretics
  5. inotropic drugs
    a. cardiac glycosides (digoxin) used chronically
    b. B-agonists (dobutamine) used acutely
    c. Phosphodiesterase inhibitors (inamrinone,
    milrinone) used acutely
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

ACE INHIBITORS/ARBs moa

A

a. inhibit the vasoconstrictor effects of angiotensin II
inhibit the retention of sodium and water by
inhibiting aldosterone
prevent aldosterone-mediated cardiac remodeling;
aldosterone may act directly on cardiac muscle to
promote increased collagen deposition and fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Cardiovascular actions

A

induce venous as well as
arterial vasodilation
a. preload: preload is reduced by reducing salt and
water retention and also by increasing venous
capacitance
b. afterload: afterload is reduced by arterial
vasodilation and improves signs of mitral regurgitation
c. ACEI/ARBs reduce the long-term remodeling of
the heart and vessels and is likely responsible for the
reduction in morbidity and mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

B-Antagonists

A

Metoprolol, Bisoprolol, and Carvedilol are the -blockers studied extensively in heart failure

  1. Clinical use: improve symptoms, exercise tolerance, and several measures of ventricular function; effective in patients with mild to moderate cardiomyopathies in combination with ACE inhibitors +/- diuretics +/- digoxin; effective at decreasing mortality
    Dosage: dosing is critical for B-blockers used in CHF; start
    with a low initial dose and titrate upwards for the next 4-6
    weeks; high doses could be lethal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Diuretics

A
1.  Mechanism:  reduce extracellular fluid volume and 
ventricular filling pressures (preload) but usually do not 
affect cardiac output due to the flatness of the ventricular 
function curve in patients with heart failure

Loops = furosemide, torsemide, bumetanide;
Thiazides: hydrochlorothiazide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Spironolactone, Eplerenone

A

a. aldosterone receptor antagonists
b. not very potent as diuretics (K+ sparing)
c. although ACE inhibitors and ARBs block
aldosterone production, there is a benefit of using one
of them with aldosterone receptor blockers; the main
concern with that combination is K+ retention so K+
levels must be monitored closely

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Hydralazine

A

a. is mainly an arterial vasodilator so it reduces
afterload
b. reduces renal vascular resistance and increases
renal blood flow to a greater degree than most other
vasodilators
c. may be a drug of choice in patients with renal
dysfunction who cannot tolerate ACE inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Isosorbide dinitrate

A

a. is a venodilator so it reduces preload
b. the combination of hydralazine with isosorbide
dinitrate is less effective than ACE inhibitors/ARBs at
reducing mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Calcium Channel Blockers

A
  1. Most calcium channel blockers actually worsen the
    symptoms of systolic dysfunction and increase mortality
    due to negative inotropic effects (verapamil and diltiazem
    especially)
    Amlodipine has less negative inotropic effects and
    may be useful in CHF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Digitalis (cardiac glycosides)

A

a. a group of compounds derived from the plant digitalis (foxglove); these drugs increase the contractility of the heart (positive inotropic effect); includes the drug digoxin; this drugs has a low therapeutic index (

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Digitalis (cardiac glycosides) effects on cardiac contractility

A

the cardiac glycosides inc the force of contraction and inc cardiac output which more closely resembles the normal heart; the net result is improved circulation -> dec sympathetic activity -> dec peripheral vascular resistance; Note: in the normal heart, the positive inotropic effect of digitalis is counteracted by compensatory autonomic reflexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Digitalis (cardiac glycosides) use

A

patients in sinus rhythm with mild to moderate heart failure will often respond to treatment with ACE inhibitors, diuretics, and -blockers and do not require digoxin; digoxin is preferred in heart failure with concurrent atrial fibrillation or patients who have not responded to standard therapies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Digitalis (cardiac glycosides) kinetics & adverse

A

e. pharmacokinetics: digoxin has a half-life of 36-48 hrs and an onset of action of 20 minutes
f. adverse effects: digitalis toxicity is one of the most
commonly encountered adverse drug reactions; the major effect is severe arrhythmias which include complete heart block; v-tach and v-fib; anorexia, nausea vomiting, headache, fatigue, confusion, and blurred vision are common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

factors predisposing to digitalis toxicity:

A

1) hypokalemia can precipitate serious arrhythmia and
the toxicity is treated with discontinuation of digoxin
and potassium supplementation; severe digitalis toxicity
is treated with antidigoxin antibodies; 2) drugs:
quinidine and verapamil can both displace digoxin from
plasma proteins; potassium depleting diuretics
(thiazide or loop) can enhance digoxin toxicity
digoxin has no net effect on
survival in CHF patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

B-Adrenergic agonists

A

B-agonists improve cardiac performance by positive
inotropic effects (1); only used short-term due to
tachyphylaxis (rapid tolerance)
b. dobutamine: has actions on 1 receptors to
enhance cardiac contractility (maybe some 1 antagonist)
c. dobutamine is given by i.v. infusion to treat acute
heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

B-Adrenergic agonists: dopamine

A

at low doses (≤2 g/kg per minute) will
act via D1 receptors to vasodilate renal blood vessels;
at intermediate doses (2-5 g/kg per minute) will act
via a1 receptors to enhance contractility; at high doses
(5-15) will act via 1 receptors to vasoconstrict blood
vessels and increase TPR
D1 -> B1 -> a1

17
Q

Phosphodiesterase inhibitors

A

inamrinone and milrinone
a. act by inc cAMP which can phosphorylate a calcium
channel and inc the entry of calcium into the myocardial
cells to enhance contraction
have limited utility in treating heart failure; only
used short-term in acute failure
both drugs have been shown to increase mortality
with long-term use

18
Q

Nesiritide

A

is a recombinant form of human brain
natriuretic peptide (BNP). It is approved for treatment
of dyspnea due to CHF. It activates cGMP in target
tissues including vascular, endothelial, and smooth
muscle cells. Vasodilation occurs in both arterial and
venous beds. It is mainly used short-term in acutely
decompensated patients experiencing peripheral edema.

19
Q

HTN

CHF

A

ABCD

ABD…..D