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Cardio II Exam 3 > Drugs Used in Heart Failure > Flashcards

Drugs Used in Heart Failure Flashcards

1
Q

hx: 58 y/o man increasing SOB, sudden weight gain, dyspnea on exertion, ankle edema, PND, sleeps in sitting position, productive cough, edema, long hx of heart burn, depression, HTN, family hx of DM, cyanosis, pulse and BP are elevated

current meds: hydrochlorothiazide, ibuprofen, rantidine, citalopram

A
  • this is a classic cause of CHF
  • Ibuprofen is concerning: has 10 yr hx of osteoarthritis and takes a lot, but for this pt. it blocks prostaglandin synth, reduces vasodilation of arteries –> causing body to compensate by retaining sodium and water–> this is problematic for his CHF
  • HCTZ: diuretic that doesn’t appear to be working, need something else for BP
  • Rantidine: H2 histamine blocker for Heart burn
  • Citalopram is for depression
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2
Q

heart failure

A
  • it is a syndrome, not a disease
  • occurs when CO is inadequate to provide the O2 needed by the body
  • we are mostly talking about low output CHF, caused by stystolic failure –> this can be tx by pharmacotherapy

systolic failure:

  • reduced CO and contractility
  • reduced EF <45%
  • acute failure usually due to MI
  • responds to positive ionotropic agents

diastolic failure:

  • occurs as a result of hypertrophy and stiffening of myocardium, CO is reduced, EF may be normal
  • does not typically respond to positive ionotropic agents

signs of HF? tachycardia, decreased exercise tolerance, SOB, peripheral and pulmonary edema, cardiomegaly

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3
Q

historic focus on end-point components of CHF?

A
  • use diuretics with pt. who has congestion and volume overload
  • use positive inotropes, to tx myocardial dysfunction and heart failure
  • stabilize hemodynamic decompensation and reduce sx
  • ** THESE do NOT improve survival however***

Current therapies target organs other than heart: ACEI’s, ARBS, Aldo antagonists, Beta-blockers - have all been shown to reduce mortality

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4
Q

which class of diuretics are most effacacious in reducing volume overload and are an appropriate choice for pt. with CHF that has already been in HCTZ?

A

Loop diuretic- furosemide, bumetanide, torsemide, ethicrynic acid

inhibit the NKCC2 transporter in Loop of Henle –> results in increased sodium secretion, ion transport halts in TAL and LOTS of diuresis

  • with respect to HF they are excellent for reducing congestion which can be useful in chronic and acute, but they don’t reduce mortality. they are merely for stabilization!
  • they are indicated in edema, HF, HTN, acute renal failure, hypercalcemic states
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5
Q

prototypes of loop diuretics?

A

furosemide and ethacrynic acid** (only non sulfa loop diuretic)

AE’s: hypokalemia, alkalosis, hypocalcemia, hypomagnesemia, hyperuricemia

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6
Q

what results in nagging cough and swollen tongue and swollen face (angioedema)? it is used to control high BP and edema….

A

ACEI’s: enalapril (-prils)

Why nagging cough? b/c it inhibits ACE, which is also responsible for conversion of bradykinin to inactive peptides - thus it results in lots of active bradykinin (vasodilator)

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7
Q

which is appropriate replacement therapy if not using ACEI in combo with furosemide?

A

ARB’s: - sartan

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8
Q

what blocks bradykinin?

A

ACEI’s block bradykinin –> thus causing cough and angioedema

ARB’s work downstream of bradykinin, thus don’t cause cough

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9
Q

how can ACEI’s and ARBS help mortality?

A

reduce/prevent detrimental cardiac remodeling triggered by ANGII

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10
Q

third drug added to furosemide and losartan that reduces sx and improves survival in pt with CHF, may temporarily have worsened sx, but dramatic improvement should be seen in 3 most.

A

low doses of Beta blocker - metoprolol - Beta blockers improve contractile fn and have favorable effects on remodeling - also reduces myocardial O2 need - heart starts to produce more beta receptors and becomes MORE responsive

  • his sx may get temporarily worse due to the blockers taking a long time to see therapeutic effects of drugs

digoxin is not correct answer b/c it doesn’t reduce mortality, only reduces sx - there is actually a slight increase in SCD with its use

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11
Q

who don’t you ever give beta blockers to?

A

pt in acute heart failure - initially needs sympathetic activation, but chronically the symp activation is detrimental

  • but can be given to STABLE patients with CHF
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12
Q

what can you use in addition to beta blocker, ARB and loop?

A 
aldosterone antagonist (spironolactone, eplerenone)
- reduces mortality and hospitalizations

Hydralazinge + oral nitrate: reduced mortality in AA populations

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13
Q

pt develops palpitations and has third heart sound. is given a drug that may cause Parox. atrial tachy with block at toxic concentrations. which agent was given?

A

Digoxin - often used if diuretics and ACEIs fail to control sx (has positive inotropic effect on heart –> atrial tachycardia)

“digoxin” = “digitalis”

  • improves sx and reduces hospitalizations - but NO effect on mortality
  • VERY narrow therapeutic index

inhibits sodium potassium ATPase!

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14
Q

Digoxin sodium potassium ATPase block?

A

sodium out, brings Ca2+ in - thus if ATPase is blocked, sodium builds up internally, sodium/calcium exchanger doesn’t get out, so must be pumped more into the SR (this a good thing for failing heart!) - thus is results in more calcium being pumped in and release up depolarization of membrane

but b/c these are located all over, there are many other adverse effects of blocking this pump

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15
Q

effects of digoxin: therapeutic levels

A
  • brief prolongation of AP, followed by AP shortening
  • increased intracellular Ca2+
  • increases cardiac contractility
  • increases PS tone and reduces symp tone
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16
Q

effects of digoxin on AV node?

A

slows things down in AV node by increasing refractory period

at toxic doses this refractory period is reduced and can cause nearly ANY arrhythmia

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17
Q

which of pt. current meds might be expected to potentiate the toxic effects of digoxin? Losartan, ibuprofen, furosemide, rantidine, citalopram

A

furosemide: hypokalemia potentiates the toxic effects of the drug - the less potassium you have around the more likely digoxin will bind

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18
Q

hyperkalemia and digoxin?

A

inhibits abnomal cardiac automaticity (ie hyperkalemia decreases pacemaker arrhthmogenesis)

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19
Q

bipyridines

A

inhibit PDE3 phosphodesterase which degrades cAMP
in heart: cAMP promotes relaxation and promotes calcium influx (thus can increase contractility and cause relaxation)

* used in acute decompensated heart failure*

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20
Q

digoxin

A

cardiac glycosides = inotropic agent

  • used to tx HF and Afib through
    1. improving contractility
    2. prolonging the refractory period of AV node

mechanism: causes inhibition of membrane-bound Na+/K+ ATPase, ultimately causing an increase in contraction due to increasing releasable Ca2+ from SR
- see brief prolongation of AP, followed by AP shortening
- increased CA2+ and increased contractiliy
- increased PS tone and reduced symp tone

Note: PS effects of digoxin predominate at therapeutic doses

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21
Q

inamrinone

A

bypiridine = IA

  • short term support of circulation in acute decompensated heart failure

MOA: selective inhibition of phosphodiesterase 3 (PDE3) which increases cAMP –> increases CA2+ concentrations –> increased force of contraction and accel. of myocardial relaxation

toxicity: nausea, vomiting, bone marrow toxicity and thrombocytopenia, liver enzyme changes

22
Q

Milrinone

A

bipyridine = IA

  • short term support of circulation in acute decompensated heart failure

MOA: selective inhibition of phosphodiesterase 3 (PDE3) which increases cAMP –> increases CA2+ concentrations –> increased force of contraction and accel. of myocardial relaxation

toxicity: nausea, vomiting, arrhythmias

23
Q

dobutamine

A

beta-adrenergic agonist = IA

MOA: stimulation of B1 receptors, resulting in increased SV and increased CO

SE’s: xs tachycardia, arrhythmias

24
Q

dopamine

A

dopaminergic agonist = IA

  • useful if need to raise BP *
  • low dose: cause vasodilation through D1
  • intermediate doses: stimulates B receptors
  • high dose: causes peripheral and venous contstriction via alpha receptors

SE: pronounced tachycardia
* short term therapy *

25
Q

Bumetanide

A

loop diuretic

26
Q

Furosemide

A

loop diuretic

27
Q

Torsemide

A

loop diuretic

28
Q

Hydrochlorothiazide

A

thiazide diuretic

*most freq. used in tx of systemic HTN

29
Q

Eplerenone

A

Aldo antagonist diuretic–>decreased water/Na+ reabsorption in DT/CD

  • has been shown to improve survival in pts with advanced CHF
  • reduces mortality, may be most useful after MI

toxicity: hyperkalemia and met acidosis

30
Q

spironolactone

A

Aldo antagonist diuretic –> decreased water/Na+ reabsorption in DT/CD

  • has been shown to improve survival in pts with advanced CHF
    toxicity: hyperkalemia and met acidosis
31
Q

conivaptan

A

vasopressin (ADH) antagonist of ADH receptors in cortical collecting tubule

  • use not universally recommended
    toxicity: hypernatremia, nephrogenic diabetes insipidus
32
Q

Tolvaptan

A

vasopressin (ADH) selective antagonist

  • use not universally recommended
    toxicity: hypernatremia, nephrogenic diabetes insipidus
33
Q

-pril

A

ACE inhibitors: captopril, enalapril, fosinopril, lisinopril, quiapril, ramipril

MOA: suppress ANGII production by inhibiting ACE and decrease ALDO production, reduce salt and water retention and reduce preload as well as afterload. Also decrease sympathetic NS activity.
** Reduce long term remodeling of heart and vessels (degredation of bradykinins which stimulate NO and growth factors)

SE: angioedema, cough, mild hyperkalemia

34
Q

isosorbide dinitrate

A

venodilator

MOA: NO released when drug is metabolized causing venodilation and reduced preload and ventricular stretch

  • used in acute AND chronic HF as well as angina and HTN emergencies
  • often given with Hydralazine and reduces mortality

AE’s: postural hypotension, tachycardia, h/a

35
Q

hydralazine

A

arteriolar dilator

MOA: stimulates NO release from endothelium and reduces BP and afterload, resulting in increased CO

** used in combination with nitrates to reduce mortality in patients with HF, due to reducing damaging remodeling

AEs: tachycardia, fluid retention, lupus-like synd.

36
Q

nitroprusside

A

combined arteriolar venodilator
- MOA: converted to NO and causes profoudn reduction in BOTH preload and afterload

**used for ACUTE cardiac decompensation in HTN emergencies!!

37
Q

-olol

A 
beta-adrenergic receptor blocker: 
bisoprolol - B1 antagonist* off label
carvedilol - alpha and Beta antagonist
metoprolol- B1 antagonis
nebivolol - B1 antagonist*

-in HF see symp. hyperactivation which supports circulatory fn and increases HR

MOA: Beta blockers have been shown to:

  • improve contractile fn by upregulating beta receptors
  • favorable remodeling
  • reduced myocardial O2 demand
  • decreased freq. of tachyarrhythmias

Therapy is administered at low doses, and it may take several months for effects to be noted: will see slight rise in EF, slower HR, improved exercise tolerance and reduced sx

38
Q

nesiritide

A

natriuretic peptide that causes vascular smooth mm. cell relaxation

results in vasodilation, natriuresis and diuresis

AEs: xs hypotension, IV admin of nitroglycerin/nitroprusside usually preferred vasodilator

39
Q

what are most helpful in long-term tx of heart failure?

A

ACE inhibitors (-pril), ARBs (-sartan), Beta-blockers (-olol), Aldo receptor antagonists (-one)

40
Q

digoxin toxicity?

A

heart: changes in AV junctional rhythm, premature ventricular depolarization, bigeminal rhythm, second degree AV block: decreased rate of AV node, decreased refractory period and arrhythmias

GI: anorexia, nausea, vomiting, diarrhea

CNS: disorientation, hallucinations, visual changes

** give antidigoxin immunotherapy (antidigoxin fab Ab) in case of overdose

41
Q

how does digoxin interact with ions?

A

dig and K+ compete for binding sites on Na+/K+ ATPase

  • hyperkalemia can reduce effects of digoxin
  • hypokalemia can potentiate toxic effects
42
Q

what do diuretics do?

A

help with “congestive sx” - through reducing EC fluid volume –> decreased ventricular preload and reduction of edema

*** loop diuretics are most frequently used and most effecacious

HOWEVER. use of diuretics with exception of aldosterone antagonists does NOT reduce mortality in heart failure!

43
Q

which diuretic most freq. used in tx of systemic HTN?

A

thiazide diuretics - though have more reduced use in tx of HF

44
Q

what does ANGII do? What drugs prevent its actions?

A

ANGII is a arterial vasoconstrictor, increases retention of sodium and water and ALDO secretion, potentiates catecholamine release and promotes pathological myocardial hypertrophy and stimulates myocyte death.

** Antagonism of ANGII is a main form of HF tx

Inhibition of ANGII reduces both preload (intravascular volume is reduced by blocking its secretion) and afterload (via vasodilation)

45
Q

ACEI’s vs ARBs?

A

** these are first choice in patients with HF without associated edema**

ACEI’s + diuretics should be considered first-line tx in CHF!!!

ACEI’s (-pril): lower BP by decreasing peripheral vascular resistance, thus CO and heart rate aren’t changed (good for athletes) - SE of dry cough

ARB’s (-sartan): have no effect on bradykinin (no dry cough), and thus are more selective antagonists of ANGII- used to tx HTN

46
Q

-sartans

A

ex. candesartan and valsartan

ARBs: block ANGII and its deleterious effects on heart.

MOA: ARBs are selective at blocking AT1 receptors and thus do not alter bradykinin metabolism

** use in pt. that are intolerant to ACEI’s b/c don’t have cough or angioedema

47
Q

how are vasodilators helpful in tx of HF?

A
  • provide reduction in preload through venodilation
  • reduction in afterload through arteriolar dilation
  • relax smooth mm. by supplying NO
48
Q

what can be dangerous to use with loop diuretics/thiazides?

A

these diuretics cause sodium loss and secondary loss of K+ which can be hazardous if pt. is given digoxin! (hypokalemia can cause prolonged AP’s, increased HR and increased pacing)

49
Q

what might be good in AA’s?

A

use of hydralazine + isosorbide dinitrate

  • this combo should be used in patients with high filling pressures in whom the principal sx is dyspnea, venous dilators will be most helpful in reducing filling pressures and sx of pulmonary congestion
  • in patients with fatigue due to low left ventricular output, consider arteriolar dilators to increase CO
50
Q

First line tx in CHF?

A

ACEI’s + diuretics should be considered first-line tx in CHF!!! (digoxin given if these fail to control sx - it has no net effect on mortality but does reduce hospitalizations and deaths from progressive heart failure)

51
Q

which drugs shown to improve survival?

A 
ACE Inhibitors
ARBs
β-blockers
Aldosterone antagonists
Hydralazine + nitrate

Cardio II Exam 3 (15 decks)

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