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Cardiopulm Exam 1 > Drugs for Heart Failure > Flashcards

Drugs for Heart Failure Flashcards

1
Q

Captopril: MOA

A

competitive inhibitor of
angiotensin- converting
enzyme (ACE)

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2
Q

Captopril: Effects

None emphasized

A 
- prevents
conversion of
angiotensin I to
angiotensin II, a
potent
vasoconstrictor
and mitogen for
cardiovascular
remodeling
- lowers levels of
angiotensin II  -->
↑ plasma renin
activity and ↓ aldosterone
secretion
  • lowers blood pressure
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3
Q

Captopril: Clinical Applications

none emphasized

A
  • hypertension
  • acute hypertension
    (urgency/emergency)
  • heart failure with
    reduced ejection
    fraction (HFrEF)
    (ACCF/AHA)
  • LV dysfunction following
    MI
  • diabetic nephropathy
  • off-label: aldosteronism
    (diagnosis), delay the
    progression of
    nephropathy and
    reduce risks of
    cardiovascular events
    HT + DM
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4
Q

Captopril: Pharmacokinetics

A

t1/2: ~1.7 hrs,
longer in renal
impairment

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5
Q

Captopril: Toxicities

A
  • cough

- angioedema

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6
Q

another early ACEI, a prodrug with active form (enalaprilat) available for IV

A

enalapril (enalaprilat)

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7
Q

now widely used ACE inhibitor, longer half life permitting 1X/day dosing

A

benazepril

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8
Q

now widely used ACE inhibitor, longer half life permitting 1X/day dosing

A

lisonopril

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9
Q

losartan: MOA

A

competitive NONPEPTIDE
ANGIOTENSIN II RECEPTOR
ANTAGONIST

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10
Q

losartan: Effects

A
  • blocks the
    vasoconstrictor and aldosterone-secreting
    effects of angiotensin II
  • does not affect
    the response
    to bradykinin!!
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11
Q

losartan: Clinical Applications

none emphasized

A
  • treatment of diabetic
    nephropathy
  • HT, alone or in
    combination with other
    antihypertensives
  • heart failure if intolerant
    of ACE inhibitors
  • off-label: Marfan
    syndrome
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12
Q

losartan: Pharmacokinetics

none emphasized

A

extensive
first-past
metabolism

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13
Q

losartan: Toxicities

none emphasized

A
  • adverse effects more
    common in those with
    diabetic nephropathy
  • hypotension, first-dose
    hypotension,
    orthostatic hypotension
  • fatigue , dizziness ,
    fever
  • hypoglycemia,
    hyperkalemia
  • diarrhea, gastritis,
    nausea, weight gain
  • anemia
  • weakness , back/knee
    pain
  • cough (< ACEI)
    bronchitis, nasal
    congestion
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14
Q

t1/2 ~ 6 -10 hrs, noteworthy in that NOT A PRODRUG requiring activation, excreted primarily in feces as uncharged drug

A

valsartan

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15
Q

t1/2 5-9 hrs, noteworthy for its relatviely IRREVERSIBLE BINDING

A

candesartan

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16
Q

valsartan/sacubitril: MOA

A 
- sacubitril is a
prodrug that
inhibits neprilysin
(neutral endopeptidase
[NEP])
  • valsartan is an
    ARB
  • drugs are co-
    crystalized
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17
Q

valsartan/sacubitril: Effects

A 
- neutral endopeptidase
blockade leads to
increased levels
of peptides,
including
natriuretic
peptides
  • valsartan
    antagonizes AT1-
    receptors
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18
Q

valsartan/sacubitril: Clinical Applications

A

heart failure

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19
Q

valsartan/sacubitril: Pharmacokinetics

none emphasized

A
  • twice daily
    dosing
  • LBQ657 has t1/2
    of ~ 11 hrs
  • valsartan has t1/2
    of ~9 hrs
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20
Q

Valsartan/Sacubitril: Toxicities

A 
Common 
- hypotension 
- hyperkalemia 
- increased serum
creatinine
also
- orthostatic
hypotension 
- dizziness, falling 
- decreased Hct, Hgb 
- angioedema (~ 2% of
black patients, <1% of
others) 
- renal failure 
-cough
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21
Q

Carvedilol: MOA

none emphasized

A 
a racemic
mixture, is a nonselective
beta- and
alpha-
adrenergic
blocker
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22
Q

Carvedilol: Effects

not in table

A

• Used to prevent down-regulation of the β
in the heart as a result of excessive sympathetic stimulation during heart failure

  • keeps heart responsive to sympathetic drive
  • protects against dysrhythmias
  • reduces renin secretion
  • reduces myocardial oxygen consumption
  • limits heart muscle remodeling and reduces necrosis and apoptosis of myocardial cells

• LOW DOSES are used at least initially, with caution in patient that
is stable

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23
Q

Carvedilol: Clinical Applications

A

• If clinically stable, it is recommended for:

  • recent or remote history of MI or ACS and reduced ejection fraction (rEF; <40%)
  • rEF to prevent symptomatic HF
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24
Q

Carvedilol: Clinical Applications (not in table)

A

•should be administered only to clinically stable patients
- patients with diastolic heart failure will benefit from a lower heart rate

  • β-blockers should be given to all patients with
    symptomatic CHF and LVEF < 40% unless contraindications…
    • bronchospastic disease
    • symptomatic bradycardia or heart block
  • unless contraindications, carvedilol should also be
    given along with ACE inhibitors to all patients with left ventricular systolic dysfunction caused by
    myocardial infarction to reduce mortality
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25
Q

Carvedilol: Common Adverse Effects

A

– allergy
– chest pain, discomfort, tightness, or heaviness
– dizziness, lightheadedness, or fainting
– generalized swelling or swelling of the feet, ankles, or lower legs
– pain
– shortness of breath
– bradycardia
– weight gain
– angina/heart attack if abruptly discontinued

26
Q

Ivabradine: MOA

none emphasized

A 
selective and
specific inhibition
of the hyperpolarization
-activated cyclic
nucleotide-gated
(HCN) channels
(f-channels) within the
sinoatrial (SA)
node of cardiac
tissue
27
Q

Ivabradine: Effects

none emphasized

A 
disrupts I(f)
(“funny” current) to prolong diastole and slow HR
28
Q

Ivabradine: Clinical Applications ***

A 
• treatment of resting HR
≥70 bpm in patients with
stable, symptomatic
chronic heart failure with
left ventricular ejection
fraction ≤35%, who are in sinus rhythm with:
  • maximally tolerated
    doses of beta blockers
    (or)
  • contraindication to
    beta-blocker use
29
Q

Ivabradine: Pharmacokinetics

none emphasized

A

Given PO

30
Q

Ivabradine: Toxicities

none emphasized

A 
• bradycardia 
• hypertension 
• increases risk of
atrial fibrillation 
• heart block 
• sinoatrial arrest
31
Q

Spironolactone: MOA

A
  • competitive
    antagonist of
    aldosterone
    receptors,
32
Q

Spironolactone: Effects

A

K+-sparing
diuretic

– decreases myocardial fibrosis
– reduces early morning rise in heart rate
– reduces mortality and morbidity in patients with severe
heart failure

33
Q

Spironolactone: Clinical Use

A

• cardioprotective, antifibrotic, and antiarrhythmic effects
have been proven in animal experiments

• effects on morbidity and mortality have been
demonstrated in randomized clinical trials

• APPROVED FOR TREATMENT OF SYMPTOMATIC HEART FAILURE WITH REDUCED SYSTOLIC FUNCTION but…

  • most underutilized of all classes of medications for
    heart failure, primarily because of fear of hyperkalemia
34
Q

Furosemide: MOA

A 
directly Inhibits
reabsorption of sodium
and chloride in the
thick ascending limb of
the loop of Henle (TAL)
by BLOCKING THE Na+-K+-2Cl- cotransporter
35
Q

Furosemide: Effects

none emphasized

A 
causes increased
excretion of
water, sodium, potassium,
chloride,
magnesium,
and calciu
36
Q

Furosemide: Clinical Applications

A 
• management of edema
associated with
- heart failure 
- hepatic disease 
- renal disease

• acute pulmonary edema by decreasing preload
- decreases EC vol
- rapid dyspnea relief due in part to PG-mediated venodilation (faster than
fluid excretion)

• treatment of
HYPERTENSION (alone or
combined with other
antihypertensives)
- unlike thiazides, also
works in patients with
low GFR
37
Q

Furosemide: Toxicities

A 
• hypokalemia
• hyponatremia
• hypocalcemia
• hypomagnesemia 
• hypochloremic
metabolic alkalosis 
• hyperglycemia 
• hyperuricemia 
• increased cholesterol
and triglycerides 
• ototoxicity: vertigo,
hearing impairment,
tinnitus
• ± reversible 
• SULFONAMIDE, so risk
of  hypersensitivity
38
Q

sulfonamide similar to furosemide with longer t1/2, better oral absorption and some evidence that it WORKS BETTER IN HEART FAILURE

A

torsemide

39
Q

sulfonamide similar to furosemide, but MORE PREDICTABLE ORAL ABSORPTION

A

bumetanide

40
Q

NON-SULFONAMIDE LOOP DIURETIC reserved for those with sulfa allergy

A

ethacrynic acid

41
Q

hydrochlorothiazide (HCTZ): MOA

A

blockade of
Na+-Cl-
cotransporter

42
Q

hydrochlorothiazide (HCTZ): Effects

A

• also increases
urinary
excretion of K+,
and Mg2+

• i.e., K+ - losing

43
Q

hydrochlorothiazide (HCTZ): Clinical Applications

A 
• management of mild-
to-moderate
HYPERTENSION, ALONE OR IN COMBINATION
with other
antihypertensive
agents
-  NOT EFFECTIVE IN
PATIENTS WITH LOW
GFR

• treatment of edema
(adjunct role)

• off-label: CALCIUM
NEPHROLITHIASIS;
nephrogenic diabetes
insipidus

44
Q

hydrochlorothiazide (HCTZ): Pharmacokinetics

none emphasized

A

well absorbed

via oral administration

45
Q

hydrochlorothiazide (HCTZ): Toxicities

A 
• hypokalemia
• hypomagnesemia 
• hyponatremia 
• hypochloremic
metabolic alkalosis
• SULFONAMIDE drug, so hypersensitivity
reactions possible
46
Q

similar to HCTZ, but poor oral absorption

A

chlorothiazide

47
Q

similar to HCTZ, but half-life of 40-60 hrs… prolonged/stable response with
proven benefits is reason it is preferred by some hypertension specialists

A

chlorthalidone

48
Q

another long-acting thiazide diuretic, this is a favorite of cardiologists for use as an adjunct diuretic in the treatment of congestive heart failure

A

metolazone

49
Q

nitroglycerin: Effects

A 
produces a
vasodilator effect
on the peripheral
veins and arteries
with MORE
PROMINENT EFFECTS
ON THE VEINS
50
Q

nitroglycerin: Clinical Applications

none emphasized

A

• treatment or prevention of angina pectoris

• acute decompensated
heart failure (especially
when associated with
acute myocardial
infarction)

• perioperative hypertension
(especially during
cardiovascular surgery)

• induction of intraoperative
hypotension

• Intra-anal administration
(Rectiv ointment):
treatment of moderate-to-
severe pain associated
with chronic anal fissure

• off-label uses for short-
term for GI and pulmonary
arterterial smooth muscle
relaxation

51
Q

similar drug with slower onset of action, administered orally for prevention of angina and for heart failure with reduced ejection fraction.

A

isosorbide dinitrate

52
Q

hydralazine: MOA

A 
• old drug but
mechanism of
action remains
incompletely
understood… 
• recent study of
isolated
mesenteric
resistance arteries
from pregnant rats indicated:
- endothelium
dependent
- hyperpolarizes 
- requires
activation of
COX
- mediated by prostacyclin
(PGI2) receptor
53
Q

Hydralazine: Effects

A

DIRECT VASODILATION OF ARTERIOLES (with
little effect on veins) –> decreased
systemic
resistance

54
Q

Hydralazine: Clinical Applications

A 
• Management of
moderate to severe
hypertension
- NOT recommended
for the initial treatment of hypertension by JNC8

• off-label:
- heart failure with
reduced ejection fraction if intolerance to ACEI or ARB

  • HEART FAILURE with
    reduced ejection fraction NYHA Class III-IV (self-identified African-American)
  • HYPERTENSIVE
    EMERGENCY IN PREGNANCY
  • postoperative
    hypertension
55
Q

Hydralazine: Toxicities

A 
• ANGINA PECTORIS, FLUSHING,
orthostatic hypotension,
palpitations, PERIPHERAL
EDEMA, TACHYCARDIA, vascular collapse; increases intracranial
pressure

• pruritus

•drug-induced lupus-like
syndrome

56
Q

Digoxin: MOA

A

inhibition of the
Na+ - K+ ATPase
pump in myocardial
cells

57
Q

Digoxin: Effects

A
  • Increased
    contractility
  • direct suppression
    of AV node
    conduction
- positive inotropic
effect, enhanced
vagal tone, and
decreased
ventricular rate to
fast atrial
arrhythmias
58
Q

Digoxin: Clinical Applications

A
  • control of ventricular
    response rate in adults
    with chronic atrial
    fibrillation
- treatment of mild-to-
moderate (or stage C
as recommended by
the ACCF/AHA) HEART
FAILURE in adults and
pediatric PATIENTS TO
INCREASE MYOCARDIAL
CONTRACTILITY
59
Q

Digoxin: Pharmacokinetics

A

• administered orally

• t1/2: 36-48 hrs,
increased as cardiac
output and renal
function decrease…
so NEEDS A LOADING
DOSE
• widely distributed,
CROSSES THE
PLACENTA, but long
history of “safe”
use in pregnant
women with
supraventricular
tachycardia
60
Q

Digoxin: Noncardiac Adverse Effects

A

– anorexia, nausea, vomiting, salivation
– excessive urination
– fatigue, visual disturbances (blurred vision, HALOS, YELLOWISH OR GREENISH TINGE TO OBJECTS)

61
Q

Digoxin: Drug Interactions

A

– diuretics… the “biggie”; diuretics cause HYPOKALEMIA, WHICH LEADS TO INCREASED DIGOXIN BINDING, WHICH LEADS TO INCREASED DIGOXIN TOXICITY

– ACE inhibitors and ARBs - can increase plasma K+ levels, decreasing
digoxin effects

– sympathomimetics - beneficial interaction on contractility, detrimental
effects on arrhythmias

– quinidine, spironolactone, verapamil, propafenone and alprazolam are
among a range of drugs that interfere with clearance of digoxin

– cholesterol-binding resins block digoxin absorption from GI tract

Cardiopulm Exam 1 (13 decks)

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