Chronic Heart Failure Flashcards

(47 cards)

1
Q

What is Heart failure?

A

– Inability to provide enough oxygenated blood to the rest of the body

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2
Q

What is Preload?

A

– Amount of blood at end of diastole (end diastolic volume)

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3
Q

What is Afterload?

A

– Amount of pressure the heart has to pump up against for systole

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4
Q

What is Ejection fraction (%)?

A

– Amount of blood pumped / end diastolic volume

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5
Q

What are two ways to lower mortality rate due to Chronic Heart Failure?

A
  • Pharmacological

* Non-Pharmacological

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6
Q

What are some of Pharmacological ways to tx HF?

A
  • ACE I/ARBs
  • BB
  • Aldosterone Blockers
  • Vasodilators
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7
Q

Incidence of HF is Increasing at a dramatically fast rate, Why?

A
  • Baby Boomers
  • We do great job at tx’ing CAD
  • Better screening, catching it earlier
  • Untreated HTN
  • Older life expectancy, more opportunity to develop HF
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8
Q

What are ACC/AHA Stages of HF?

A

A. At high risk for HF but w/o structural heart disease or symptoms of HF (CAD, HTN, DM, Obese, Metabolic Syndrome OR Using Cadriotoxins, FHx)

Therapy: ACE I or ARBs for Vascular dz of DM

B. Structural heart disease but w/o s&s of HF (Previous MI LVH w/o symptoms)

Therapy: ACE I or ARBs + BB (to delay progression)

C. Structural heart disease but with prior or current symptoms of HF (Known Structural H. dz w/ symptoms ie: SOB, Fatigue, DOE)

Therapy: Diuretics (loop), ACE I or BB (Select pt’s Aldosterone, ARB’s digitalis, hydralazine/nitrates)

D. Refractory HF requiring specializing interventions (N-Stage HF – Marked Symptoms at rest despite maximum medical therapies)

Therapy: Hospice Care, Heart Transplant, IV Inotropes, Mechanical Support, Experimental Surgery or drugs

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9
Q

What are NYHA functional classification?

A

Class I – Ordinary activity does not cause symptoms

Class II - Ordinary activity does not cause symptoms

Class III – Less than ordinary activity causes symptoms

Class IV – Symptoms are present at rest

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10
Q

Types of HF?

A

– Systolic

– Diastolic

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11
Q

About Systolic HF?

A
  • EF < 40% → poor EF & CO
  • Most common
  • Problem with ejection of blood to the lungs or systemic circulation
  • Result of hypertrophy and dilation of ventricle
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12
Q

About Diastolic HF?

A
  • EF >55% → normal EF w/ poor CO
  • Inability of the heart to fill appropriately
  • Usually results from stiffness of myocardium
  • More difficult to treat
  • Treatment not well defined
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13
Q

What are the 4 compensatory mechanisms of HF?

A
  • RASS
  • SNS
  • V. Hypertrophy
  • Frank-Starling Law (increase End diastolic Vol.)
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14
Q

How do Compensatory mechanisms affect Heart?

A

They delay symptoms as result of HF…….

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15
Q

How doe Frank-Starling Law effect Heart?

A

For a very short time Heart will stretch longer (increase Radius of Ventricle/Increase End diastolic Vol.) to compensate for reduced CO.

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16
Q

What’s the major contradiction of CCB’s in a pt w/ Systolic HF?

A

CCB’s can cause death if used in a pt w/ Systolic HF

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17
Q

ACEi/ARBs MOA?

A

– Interference with RAAS ending with disrupting angiotensin II

– Produces decreases BP, Na/H2O retention

– Afterload reducer

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18
Q

ACEi/ARBs Key PK notes?

A

– Highly excreated via kidneys; dose reductions often necessary as long as K is within normal limits

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19
Q

ACEi/ARBs Dosing?

A

–Used in all stages of HF:

  * All ACEi/ARBs have been used in HF
  * Goal doses are essential in maximizing mortality/morbidity benefit

  * Lisinopril: start at 5 mg daily, goal dose of 20-40 mg daily
          * Start at 5mg, double to 10mg, than double to 20mg……
          * Wait at least 2 weeks before you add BB (takes about 6 mo to reach goal)
          * Every two weeks, you should either do something w/ ACE I or BB. 
          * Never start ACE I & BB together at the same time unless you’re in hospital setting
20
Q

ACEi/ARBs ADRs?

A

– Cough (ACEi)
– Hyperkalemia
– Hypotension

21
Q

ACEi/ARBs Absolute contraindications?

A

– Pregnancy
– Hyperkalemia (K>5.0 meq/L)
– Bilateral renal artery stenosis
– Angioedema

22
Q

Which drug class is prefered in HF, ACEi or ARBS?

A

• ACE I are recommended no efficacy diff but a cost diff

23
Q

Which BB can be used for HF?

A
  • Metoprolol succinate
  • Bisoprolol
  • Carvedilol 2/day
24
Q

What can BB cause?

A

HF is started in high dosage

25
BB MOA?
– Blockage of beta receptors leading to decreased heart rate, BP, increase coronary artery blood flow
26
BB Dosing?
* Metoprolol succinate: 6.25-12.5 mg/day; goal 200 mg/day * Bisoprolol: 1.25 mg/day; goal 10 mg/day * Carvedilol: 3.125 mg twice daily; goal 25 mg twice daily
27
Aldosterone Blockers Drugs?
– Spironolactone | – Eplirinone
28
Aldosterone Blockers MOA?
* Competes with aldosterone for intracellular mineralcorticoid receptors → Na and H2O excreation (this also increases K in the blood) * Decreases preload
29
Aldosterone Blockers Key PK notes?
– Highly protein bound – Primarily renally excreated – Aldosterone Blockers
30
Aldosterone Blockers ADRs?
– Hyperkalemia | – Gynecomestia
31
Aldosterone Blockers Absolute contraindication?
– Hyperkalemia
32
Vasodilators Drugs?
– Hydralazine: direct arterial vasodilator | – Isosorbide dinitrate: direct vasodilator
33
Vasodilators MOA?
* Predominately vasodilates in coronary, cerebral, and renal arteries * Converts into nitric oxide which produces vasodilation
34
Vasodilators Key PK notes?
–Used in place of ACEi contraindications; not renal excreted • Evidence shows this drug combination is useful in African American patients with HF (along with other traditional meds-ACE, BB, etc).
35
Vasodilators ADRs?
– Tolerance to nitrates | – hypotension
36
When do you use Vasodilators?
When you can't use ACE I or ARDs
37
Why would Vasodilators benefit being seen only in African Americans but not in Caucasians?
Because you're more likely to use ACE I or ARBs for Caucasian
38
Which drug class is most effective in HF?
Loop Diuretics
39
Loop Diuretics MOA?
– Exerts their action at the loop of Henle. Increase Na and H2O excreation. Since all diuretics reduce pre-load and edema why are loop diuretics prefered over other agents (such as thiazide diuretics)
40
Loop Diuretics Key PK notes?
– May require higher than usual doses to induce diuresis in patients with renal failure
41
Loop Diuretics Goal?
– After initial diuresis and reduction of fluid, try to get to the lowest dose possible or even consider discontinuing
42
Loop Diuretics ADRs?
``` –Electrolyte imbalances (most common) • Hyperglycemia • Hyperuricemia • Hypokalemia • Hypomagnesemia ```
43
Digoxin MOA?
–Positive inotropic activity and negative chronotropic activity • Increase in intracellular Na and Ca→ increase in force of contraction
44
What is the driving force behind Digoxin producing negative chronotropic activity?
• Reduced intracellular K & Increases intracellular Ca+
45
Which is more likely to have unintended toxicity using Digoxin?
• Elderly – Smaller VD leads to increased concentration in the blood
46
Digoxin ADRs?
``` – High potential for digoxin toxicity – Electrolyte disturbances • Hypomagnesemia • Hypokalemia – Bradycardia – GI disturbances (most common side effect) ```
47
Digoxin Additional comments?
– Hypokalemia increases the effects of digoxin – Hyperkalemia decreases the effects of digoxin – How can digoxin interfere with maximizing mortality reducing medications?