Exam 3 - Chronic HF Flashcards

1
Q

Define Heart Failure. What is #1 cause?

A

1 cause=CAD

Inability to provide enough oxygenated blood to body.

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2
Q

What is the most common form of HF and its result?

A

Systolic HF. LV can’t get blood to body due to dialation and hypertrophy.

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5
Q

Define Cardiac Index. Normal range? What is the CI in HF patients?

A

Measure of pumping ability from left ventricle to deliver O2. In HF patients their Cardiac Index is low.

Normal range: 2.5-4

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6
Q

What is Ejection Fraction? What percent is normal? Systolic and Diastolic HF values?

A

Amount of blood pumped/end diastolic volume. Below 40% is bad.
Normal=70%
Systolic HF is 3/10 and 30%
Diastolic HF is problem of filling, pumping 3 but can only hold 5, 3/5 for 60%. Looks normal but isn’t.

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7
Q

What is mortality of rate in 5 years of heart failure if nothing done? What if everything is done?

A

Nothing done=50% after 5 years

Everything done=35% after 5 years

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8
Q

What are the 4 compensatory mechanisms of HF?

A
  1. RAAS
  2. SNS
  3. Ventricular Hypertrophy
  4. Frank-Starling Law (increase end diastolic pressure)
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9
Q

Which four drugs reduce HF mortality?

A
  1. ACEI/ARBs
  2. BBs
  3. Aldosterone blocking agents
  4. Vasodilators (in AAs)
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10
Q

Two drugs which reduce HF morbidity?

A
  1. Digoxin

2. Diuretics

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11
Q

Treatments for Stages A and B of HF?

A

A=Treat risk factors. ACEI/ARBs

B=ACEI/ARBs or BBs

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12
Q

Routine treatment for Stage C HF? Selected PTs?

Treatment for Stage D HF?

A

Routine C: ACE/ARBs, BB, diuretics.
Selected C PT: Aldosterone antagonist, digitalis, hydralazine/nitrates

Stage D: End-of-life care. Hospice, transplant, IV Dobutamine

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13
Q

ACEI/ARB MOA? Effects on kidneys, H2O/Na, BP, Afterload? Place in therapy?

A

Interference with RAAS ending by disrupting Angiotensin II.

Decrease BP, decrease Na/H2O retention, decrease Afterload.

Highly excreted with kidneys. Only modify dose if K+ bad.
Used in all stages of HF.

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14
Q

ACEI/ARB absolute contraindications?

A

Preggers, K+ above 5, bilateral renal artery stenosis, angioedema

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15
Q

Sacubitril/valsartan (Ernesto) MOA and place in therapy? Time to convert from ACE to Ernesto?

A

Valsartarn=ARB
Sacubitril=Blocks neprilysin causing vasodilation
Together they add more vasodilation than ARB or ACEi alone.

Used in newly diagnoses with EF less than 40%. Wait 36 hours.

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16
Q

Beta-Blocker MOA? Effect on coronary areries? Which three can be used?

A

Block beta receptors decreasing HR and BP. Increased coronary artery blood flow.

  1. Metoprolol Succinate
  2. Bisoprolol
  3. Carvedilol
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17
Q

What stages are Beta Blockers used in? ADR? Why not Metoprolol Tartrate?

A

A, B, C.

ADRs=Bradycardia, worse HF is BB dose started too high, respiratory issues

Metoprolol Succinate has better outcomes.

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18
Q

MOA and place of Ivabradine?

A

MOA: selectively inhibits “funny channel” in SA and AV nodes and reduces HR

Place: All other meds maxed out and EJ less than 35%. Further enhances Beta-Blockers.

19
Q

Aldosterone MOA and place in which stages? Preload? CI?

A

MOA: Competes with Aldosterone for intracellular mineralcorticoid receptors. Decrease Na/H2O, increase K. Decreases Preload.

Place: In Stages C and D if on max ACEi/BB and still symptomatic.

CI: Hyperkalemia

20
Q

Hydrazaline and Isosorbide are what class of drugs? Where does each work? Who used in?

A

Vasodilators.
Hydrazaline=coronary, cerebral, renal arteries
Isosorbide=vasodilation via NO

Used in African Americans.

21
Q

Which diuretics best in HF? Does it improve morbidity or mortality?

A

Loop Diuretics best. Morbidity.

22
Q

Loop Diuretic MOA? Preload and edema effect? Kidneys?

A

Increase Na/H2O excretion in Loop of Henle. Reduce preload and edema. Can be used with bad kidneys!

23
Q

What stages get Loop Diuretics? What might you have to do with dose for diuretics and renal failure?

A

Stages C or D, only if symptomatic.

Increase dose with renal failure.

24
Q

Four most common Loop Diuretics electrolyte abnormalities?

A

Hyperglycemia, Hyperuricemia

Hypokalemia, Hypomagnesemia

25
Q

Digoxin MOA? Which VD and who gets toxic? How excreted?

A

MOA: Positive inotropic (+CO), negative chronotropic. Increased Intracellular Na and Ca causes inotrope.

Elderly become toxic due to small VD.
Renally excreted.

26
Q

Signs of Digoxin toxicity? Hyper/hypokalemia and Digoxin?

A

Bradycardia, heart failure, and hypokalemic.

Hyperkalemia=decrease effects of digoxin
Hypokalemia=increase effects of digoxin

27
Q

How to treat Diastolic HF?

A

No gold standard. Goal to treat underlying condition.

28
Q

What are 4 the ACC/AHA stages of HF? Which most commonly seen in hospital or clinic?

A

Class A=at risk, no structural changes
Class B=ventricular hypertrophy and found incidentally
Class C=the typical PT seen in clinicals
Class D=end-of-life

29
Q

Define Preload and Afterload. What happens to LV from afterload?

A

Preload=amount of blood at end of diastole (end diastolic volume)
Afterload=amount of pressure heart pumps against for systole (measurement of systemic resistance). LV hypertrophy.

30
Q

Define Pulmonary Capillary Wedge Pressure. What will it be in HF patients? Normal range?

A

Measurement of what’s happening in the capillaries as volume status in the lungs. In acute decom HF PCWP will be high!

Normal range: 8-12

31
Q

Which 4 meds renally excreted

A
  1. ACEi
  2. ARB
  3. Aldosterone blocker
  4. Digoxin
32
Q

When to reduce or d/c loop diuretics?

A

When excess fluid gone

33
Q

ACEi/ARB decrease which load?

Aldosterone-blocker deceases which load?

A

ACEi/ARB=Afterload

Aldosterone=Preload

34
Q

Most common ADE of Digoxin?

A

Stomach funk