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phamacology - cardiology > Therapy of Heart Failure > Flashcards

Therapy of Heart Failure Flashcards

1
Q

What symptoms, clinical presentation, and treatment are associated with NYHA class I?

A

Symptoms:
• None

Presentation:
• Low EF below 50%

Treatment:
• Ace I or ARB, ß-blocker

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2
Q

What symptoms, clinical presentation, and treatment are associated with NYHA class II?

A

Symptoms:
•on Moderate exertion

Clinical Presentation:
• Dyspnea on exertion, edema

Treatment:
• DIURETIC, Ace I or ARB, ß-blocker

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3
Q

What symptoms, clinical presentation, and treatment are associated with NYHA class III?

A

Symptoms:
• on Minimal Exertion

Clinical Presentation:
•Dyspnea, ORTHOPNEA, PND, edema

Treatment:
• DIGOXIN, diuretic, ACE I or ARB, ß-blocker, Spironolactone

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4
Q

What symptoms, clinical presentation, and treatment are associated with NYHA class IV?

A

Symptoms:
• At rest

Clinical Presentation:
• Refractory Edema

Treatment:
• Digoxin, diuretic, ACE I or ART, ß-blocker, Spironolacter + COMBINATION DIURETICS, IV VASODILATORS, TRASPLANTATION/ASSIST DEVICES

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5
Q

What preventative measures should be taken at all stages of heart failure?

A

prevent: HTN, Lipids, Smoking, Diabetes, EtOH

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6
Q

Which of the ACE inhibitors are NOT prodrugs?

A
  • Captopril

* Lisinopril

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7
Q

What drug directly inhibits the protease activity of renin?

A

• Aliskiren

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8
Q

What general effect do the ACE inhibitors, ARBs, and renin blockers have?

A

Decreased Aldosterone => Natriuresis = Loss of Na+ in Urine

**Reduction in Total Peripheral Resistance (vasodilation)

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9
Q

What substrate besides angiotensin in acted on by ACE?

• Potential Implications?

A

Bradykinin - normally broken down by ACE, but it builds up with ACE I’s

• Bradykinin increases Prostaglandin Production and may contribute to Vasorelaxation

This is a good effect unless it induces angioedema

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10
Q

African Americans are less likely to benefit from ACE therapy. What modifications can be made to make therapy with ACE I drugs effective?

A

• Administer them with an ACE-I with a THIAZIDE

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11
Q

What are some major advantages of ACE I therapy over other HF therapies?
• Contraindications?

A

Benefits:
• Little Effects on Lipids and Sexual Function

Disadvantage:
• FETOTOXICITY - don’t give to pregnant or breastfeeding women or those that are expecting to conceive

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12
Q

What are some of the MOST common adverse effects of ACE Inibitors?

A

MOST COMMMON:
• 1st Dose Hypotension
• Na+ depletion

NEXT MOST COMMON: 
• Dry Irritating Cough
• HyperKalemia 
• Angioedema 
• RENAL INSUFFICIENCY

others: proteinuria, rashes, fever, bone marrow depression, hepatotoxicity pancreatitis

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13
Q

If someone develops a Cough what drug could you give that acts on the same pathway to prevent this?

A

Angiotensin Receptor Antagonists because they don’t act on Bradykinin

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14
Q

What side effects are associated with ARBs?

A
  • 1st Dose Hypotension
  • Hyperkalemia
  • Hepatic Dysfunction
  • FETOTOXICITY

**Olmesartan - can cause spruelike enteropathy (chronic nausea and diarrhea)

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15
Q

What are the side effects of the Renin Inhibitors?

•Drug Interactions?

A
  • 1st dose Hypotension
  • Hyperkalemia
  • Angioedema
  • Fetotoxicity

Drug-Drug Interactions:
• p-glycoprotein inhibitor so don’t give with Erythromcin or Amiodarone (or other p-gp inhibitors)

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16
Q

What adverse effect is common to Renin inhibitors are ACE inhibitors, but not to ARBs?

A

ANGIOEDEMA: this is because both ultimately prevent ACE from breaking down bradykinin

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17
Q

What adverse effects are seen with ARBs, ACE I, and Renin Inhibitors?

A
  • 1st Dose Hypotension
  • Hyperkaleia
  • Fetotoxicity
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18
Q

What 3 things happen with Angiotensin II is allowed to bind its receptor?

A
  • Vasoconstriction => inc. BP
  • Aldosterone Production => Na+/H2O retention => inc. BP
  • Cell Growth => Left Ventricular Hypertrophy, Vascular Remodeling
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19
Q

T or F: Angiotensin II causes Cardiac and Vascular Fibrosis and Atheroslcerosis.

A

True

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20
Q

In the treatment of heart failure are ARBs or ACE I’s better?

A
  • ACE I’s are considered better
  • possible because of Bradykinin buildup causing Vasodilation

Note: there is no added benefit of combining ACE I’s with ARBs

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21
Q

T or F: Beta blockers used to be contraindicated in CHF because we didn’t want to DECREASE inotropy of an already defective heart.

A

True

22
Q

Why are Beta Blockers now inidicated in CHF management?

A

Blocking NE and E from binding is advantageous b/c these cause:
•Arrhythmias
• Myocardial O2 consumption => ischemia
• Myocyte apoptosis => Fibrosis of heart

23
Q

Why is it so important that Beta blockers prevent arrhythmias?

A

• Arrhythmias are the leading cause of death in class II and III heart failure

24
Q

Differentiate the short term and long term effects of beta blockers in CHF patients?

A

Short Term:
• Lower CO and BP

Long Term:
• Increased CO and Decreased Left Ventricular End Diastolic Pressure

This means patients may experience worsening symptoms before things get better

25
Q

What 3 general effects do beta blockers have on the receptor pathways in myocytes?

A
  • Reversed Desensitization (caused by persistent NE/E signaling)
  • Increases Receptor Number
  • Restores Fast Signaling Modes (contractility) over slow signaling modes (gene expression)
26
Q

What contraindications are there for giving a beta blocker in heart failure?

A
  • Heart Block
  • Bradycardia
  • DECOMPENSATED CHF (i.e. if they need IV inotropes like dobutamine to stay alive)
  • Volume overload
27
Q

What Beta blockers are used in CHF?

A

• Metoprolol
• Carvedilol
• Bisoprolol
*Nebivolol - used in CHF in Europe

28
Q

*****What are the guidelines for CHF managment by stage in ACC/AHA? What NYHA classes do these fit into?

A

Stage A - At Risk (NO SYMPTOMS):
• Eat Better, Stop Smoking, Manage Diabetes/HTN
• ACE I, ARBs

Stage B - NYHA I (NO SYMPTOMS - Low E.F.):
• Stage A + Beta Blockers

Stage C - NYHA II/III (SYMPTOMS w/ EXERTION):
• Stage B + Diuretic/Digoxin/Spironolactone

Stage D - NYHA IV (SYMPTOMS at REST):
• IV Inotropes/Transplant

29
Q

T or F: Measuring serum levels of digoxin is useful for meeting a set dose for all CHF patients

A

False, there is no set dose - serum measurements are useful only for meeting the dose that has been adjust for a particular CHF patient

30
Q

What is the MOA of DIGOXIN?

A

DIGOXIN
• Blocks the Na+/K+ pump causing INCREASED INTRACELLULAR sodium. This triggers increased Ca2+ influx during the depolarized state and decreased Ca2+ efflux during the

31
Q

What is the effect of Digoxin on the pressure volume curve?

A

• Shifts the Curve up and to the left

32
Q

Digoxin
• administration
• % absorption (per method)
• Half-life

A

Administration/Absorption:
• Tablet (55-60% abs.) or Capsule (100% abs.)

Half-life = 36 hours

33
Q

T or F: Digoxin plasma concentrations correlate to therapeutic effect

A

Truish - might contribute to therapeutic effect in a particular patient but not across patients

34
Q

What Adverse effects are seen with Digoxin toxicity?

•why is it so hard to manage these effects?

A

DIGOXIN has a VERY narrow therapeutic window so seeing effects of drug toxicity probably aren’t uncommon.

  • Atrial and Ventricular Arrhythmias
  • BLURRING/YELLOW-GREEN HALO IN VISION
  • headach, fatigue, drowsiness, confusion, seizures
35
Q

In the case of SEVERE digoxin toxicity what drug can you use? MOA?

A

Digibind = antibody used to neutralize digoxin

***Really only used in life-threatening Situations

36
Q

Mutiple drug-drug interactions is a major drawback of digoxin. Name a few drugs that are likely to cause adverse effects?

A
  • NON-K+ sparing Diuretics - may increase potential for arrhythmias
  • Verapamil cause cause Slowing of HR and digoxin tox.
  • Amiodarone - inc. digoxin by decreasing elmination
  • Quinidine - Decreases Digoxin Elimination
37
Q

Who benefits the most from digoxin therapy?

A

Patients with:
• Ejection Fraction below 0.25
• Cardiac Enlargement
• NYHA class III, IV

38
Q

What effect do Diuretics have on the survival and prognosis of CHF patients?
• what are they given for?
• possible exceptions?

A
  • NO effect on survival or prognosis in CHF patients on ACE I’s and Beta Blockers changes these factors
  • DIURETICS are ONLY given to manage the CONGESTIVE EFFECTS (like pulmonary congestion)

Exceptions would be Spironolactone/eplerenone because they have effects on Aldosterone too, but these effects are not linked to the diuretic actions of these drugs

39
Q

What are the effects of diuretics on preload and cardiac output?

A

• Diuretics - Decrease Preload (overall less fluid volume), but have NO effect on Afterload (this is because Afterload is affected by pressure in the arterial end which has more to do with vasodilation?)

40
Q

What are the 4 potassium sparing diuretics?
• which are used in CHF?
• What are some loop diuretics?

A

Used in CHF = the aldosterone antagonists:
•Spironolactone
• Eplerenone
since aldosterone is toxic to the heart this effect is important

Loop Diuretics:
• Furosemide
• Bumetanide

41
Q

T or F: combination of diuretics is not a good medical practice.

A

False, combination of diuretics is commonly used in treatment of CHF

42
Q

What combinations are typically used?

A
  • Loop Diuretic plus Meolozone (not K+ sparing) or

* Loop Diuretic plus Spironolactone

43
Q

What are some adverse effects and possible drug-drug interactions that may result from diuretics?

A
  • Problems associated with XS fluid and Electrolyte loss including hypotension
  • OTOTOXICITY - tinnitus, hearing loss (loop diuretics)
44
Q

What do ACE I’s, ARB’s and Spironolactone have in common?

• what does this mean about ACE I’s and ARB’s?

A
  • They inhibit the release of Aldosterone**
  • Aldosterone has a mitogenic and fibrinogenic effect on the heart*
  • aldosterone is important in both Na+ and H2O retention, this means ACE I’s have somewhat of a Diuretic Effect
45
Q

What is the benefit of vasodilation in CHF?
•Main Vasodilator used in CHF?
• Venous or Arterial action?

A

• Reduced AFTERLOAD => increased ventricular emptying

  • HYDRALAZINE - acts on arterial side of things
  • Nitrates - act both on veins and arteries but are usually given IV

To have effects on preload and afterload the vasodilator must dilate both veins and arteries

46
Q

T or F: decreasing preload is a good thing in CHF

A

True, we don’t want to the heart to work harder so decreasing preload will decrease frank starling mechanism so that heart won’t try to overwork

***Nitrates - main vasodilator useful in reducing preload

47
Q

Hyralazine:
• Adverse Effects
• Toxicity

A

Adverse Effects:
• Stimulate RAAS (so give with ACE I) - can stimulate peripheral edema, circulatory congestion

Toxicity:
• NAUSEA, ANOREXIA = frequent
• Drug-Induced Lupus
• Exacerabate Angina (by reflex tachycardia - so give witha Beta blocker)

48
Q

What nitrate is commonly given IV in CHF?

A

• Nitroprusside (reduces preload and afterload)

49
Q

What drugs are only given as short-term therapy in CHF? MOA?
• Administration?

A

Dobutamine, Milrinone, Nitrates, Nseritide

Nitrates - Veno/Arterio dilation

Dobutamine - acts to to agonize BETA-1 primarily and Alpha-1 (racemic angonist/antagonist) to VASODILATE and increase IONOTROPY

Milrinone - INHIBITS phosphodiesterase so that cAMP stays active and you get increased effects of Beta Stimulation

Nesiritide - B-type natriuretic peptide

BOTH drugs are given IV and are only given in an EMERGENCY situations

50
Q

What phosphodiesterase inhibitor would you give to someone with Stage IV CHF?

A

Milrinone

51
Q

What are the effects of giving the 4 end-stage drugs?

•specify by drug.

A

Nitrates - Decreased preload (red. venous pressure) Decrease Afterload (red. arteriole pressure)

Dobutamine - Stimuation of Inotropy, Chronotropy => increased CARDIAC OUTPUT (shorterm)

Milrinone - increased cAMP enhances Sympathetic stimulation (inc. CO)

Nesiritide - Reduced blood volume and vasodilation- Decreased PRELOAD and AFTERLOAD

52
Q

What are the general effects of (A and B) Natriuretic Peptides? MOA?
• when is Nesiritide used?

A

Induce Peeing out of Sodium (as the name implies)
• binds to BNP receptor in smooth muscle and causes vasodilation via cGMP

  • Increased GFR and reduced Na+ reabsorption
  • Suppressed RAAS

SAME EFFECTS AS NITROGLYCERINE BUT LONGER ACTINGONLY GIVE AFTER NITROGLYCERINE HAS FAILED***

phamacology - cardiology (11 decks)

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