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Heart Failure Drugs Flashcards

1
Q

Forward failure?

A
  • systolic dysfunction
  • contractility is reduced
  • reduced CO, EF
  • decreased BP
  • fatigue
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2
Q

Backward failure?

A
  • diastolic dysfunction
  • stiffening, hypertrophy causing inadequate relaxation and filling
  • cardiac/pulmonary congestion (dyspnea) and fluid accumulation (edema)
  • CO reduces, EF normal
  • do not use positive inotropic drugs, don’t want to increase contractility
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3
Q

What is heart failure?

A
  • pump failure with decreases CO
  • usually involves both systolic and diastolic failure plus remodeling which includes loss of myocytes, hypertrophy, fibrosis
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4
Q

How does stroke volume relate to preload and afterload?

A
  • positively related to contractility and preload

- negatively related to after load

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5
Q

How does preload relate to heart failure?

A
  • preload increases due to increased blood volume and venous tone
  • this reduces stroke volume and worsens congestion and edema in a depressed heart, heart is already tired so don’t want to increase preload
  • use venodilators (nitrates), diuretics (thiazides), and salt restriction to treat heart failure
  • also can use positive inotropic drugs
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6
Q

How does after load relate to heart failure?

A
  • increased after load, decreases CO and SV
  • depends on arterial stiffness, BP
  • for someone with heart failure, want to decrease after load and BP with arterial vasodilators (calcium channel blocker)
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7
Q

Compensatory actions of heart failure? (when CO decreases)

A
  1. CO decreases which decreases BP
  2. RAAS and SNS is activated which results in increased force, HR, preload
  3. circulating catecholamines and Angiotensin II increases after load and remodeling
  4. cardiac performance decreases over time
    - the point is that with heart failure patients, you want to decrease sympathetic nervous system by using a beta blocker
    - can also use ACE inhibitor
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8
Q

Stage A, pre failure?

A
  • no symptoms but risk factors present

- treat obesity, hypertension, diabetes, hyperlipidemia

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9
Q

Stage B, I?

A
  • symptoms with severe exercise

- treat with ACE inhibitor, beta blocker, diuretic

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10
Q

Stage C, II, III?

A
  • symptoms with high exercise (II)
  • symptoms with mild exercise (III)
  • treat with aldosterone antagonist, digoxin, CRT, hydralazine, nitrates
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11
Q

Stage D, IV?

A
  • severe symptoms at rest

- treat with transplant, LVAD

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12
Q

Therapies for chronic systolic heart failure?

A
  1. beta blocker *
    - slows progression of heart failure, reduce SNS
  2. diuretics
  3. aldosterone receptor antagonist
  4. ACE inhibitor
  5. cardiac glycosides
  6. vasodilators
  7. resynchronization
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13
Q

Therapies for acute heart failure?

A
  1. beta agonist*
    - increase contractility and CO, stimulate heart function
  2. diuretics
  3. vasodilators
  4. bipyridines
  5. cardiac glycosides
  6. natriuretic peptide
  7. LVAD
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14
Q

Types of drugs used for heart failure?

A

combination of diuretics, ionotropics, vasodilators

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15
Q

Digoxin?

A

Effects:

  • positive inotropic effect, increased contractility
  • negative chronotropic effect, stimulates Vagus nerve to slow HR at SA node and AV node
  • PR interval increases

Mechanism:

  1. inhibits Na/K ATPase pump which increases intracellular NA
  2. this alters the gradient for the Na/Ca exchanger
  3. less calcium is removed so increased calcium in cell
  4. increase in myocardial contraction

ADR:
-high doses could cause bradycardia and heart block

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16
Q

ECG effects of Digoxin?

A
  • action potential duration is shortened, refractory period reduced
  • shortened QT interval
  • ST segment depression
  • phase 4 automaticity is increased, coupled with increased calcium promotes development of after potentials that can lead to ectopic beats and arrhythmogenic effects, extra contractions (Oubain study)
17
Q

Pacemaker and Nodal ECG related effects of Digoxin?

A
  1. Conducting cells
    - increased PR interval (slow HR)
    - Digoxin stimulates Vagus nerve which effects SA and AV nodes decreasing HR and AV conduction
  2. Cardiac muscle
    - shortened refractory period
    - increased automaticity
    - activates latent ventricular pacemaker activity resulting in ectopic beats
18
Q

Pharmacokinetics of Digoxin?

A
  1. narrow therapeutic window
    - therapeutic and toxic doses are very close
  2. long half life (40 hours)
    - give loading dose followed by maintenance does PO or parenteral
  3. factors that effect toxicity
    - large amount excreted via kidneys unchanged
    - kidney damage or drugs that reduce renal function increases toxicity
    - 40% CL for liver metabolism
    - reduce drugs that compete with Digoxin
19
Q

Clinical uses of Digoxin?

A
  1. Acute heart failure
    - inotropic for systolic dysfunction
  2. chronic heart failure
    - alleviates symptoms
    - monitor carefully for toxicity
  3. Atrial fibrillation/Paroxysmal supra ventricular tachycardia (PVST)
    - slows AV conduction, increases PR interval to slow ventricular rate and increase filling
20
Q

ADR of toxicity of Digoxin?

A
  1. GI irritation
  2. Visual effects
    - blurring, halo effect
  3. CNS effect
    - confusion, hallucinations, psychosis
    - lipid soluble so crosses BBB
  4. Cardiac arrhythmias
    - heart block from vagal stimulation
    - may induce any type
  5. Electrolyte drug interactions
    - hyperkalemia
    - hypokalemia
    - hypercalcemia
    - quinidine
21
Q

What electrolyte interactions decrease Digoxin effects?

A
  1. Hyperkalemia
    - increased K+ in blood competes with Digoxin for ATPase binding
    - caused by ACE inhibitors, K sparring diuretics
  2. Hypermagnesemia
22
Q

What electrolyte interactions increase Digoxin effects?

A
  1. Hypokalemia
    - less K+ in blood to compete for ATPase binding caused by K+ losing diuretics
  2. Hypercalcemia
    - increased Ca in blood and inside cells
    - more Ca to stimulate contraction
  3. Quinidine
    - competes with Digoxin for renal CL, decreases CL of Digoxin
23
Q

How to treat Digoxin toxicity?

A
  1. K+ salts when low in K+
  2. Antiarrhythmics if arrhythmia is induced
  3. Digoxin immune, antibodies that bind Digoxin inactivating them
24
Q

Mechanism of action of beta agonist and phosphodiesterase inhibitor?

A
  1. beta 1 agonist binds G coupled receptor
  2. increased cAMP and PKA
  3. calcium channel phosphorylated
  4. increased in calcium and contraction
25
Q

Dobutamine?

A
  • beta 1 agonist
  • parenteral administration

Mechanism:

  • increases cAMP and PKA
  • causes phosphorylation and calcium influx
  • force of contraction and HR increase

Clinical use:
-acute heart failure

ADR:
-tolerance develops with long term usage

26
Q

Milrinone and Inamrinone?

A
  • phosphodiesterase inhibitors (PDE)
  • Bipyridines
  • IV administration

Mechanism:

  • inhibits PDE III in cardiac muscle and smooth muscle
  • causes increase in cAMP and intracellular calcium

Clinical use:

  • acute heart failure
  • potent vasodilator, decreases preload and after load, increases CO

ADR:

  • GI, nausea and vomiting
  • arrhythmias, Ca increased in cell
  • liver damage, enzymes changed
  • thrombocytopenia

Pharmacology (9 decks)

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