Clinical Treatment of Heart Failure Flashcards

1
Q

Goals of patients in stage A & B is all about prevention. What about patients in stage C?

A

Control symptoms, prevent hospitalization/ mortality!

HFpEF: identify comorbitities, diuresis, quality of life
HFrEF: patient education, diuretics, beta blockers, etc

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2
Q

What are the specific HF goals of Rx?

A
  • Correction of underlying cause (if possible)
  • Elimination of precipitating factors
  • Reduction of congestion (ie. diuretics)
  • Improve blood flow
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3
Q

Again (from last lecture) what tests/ procedures are done?

A
  • Vitals
  • ECG
  • CBC
  • Chest X ray (CXR)
  • BNP
  • Echo
  • Coronary angiogram
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4
Q

What is the most common therapy for all HF patients?

A

Diuretics: reverses fluid retention

  • Loop diuretics preferred because more potent
  • Can be used chronically (oral) and acutely (IV in hospital)
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5
Q

Okay so diuretics decrease venous congestion, but describe with a SV (y axis) end-diastolic pressure (x axis) the FUNDAMENTAL treatment of heart failure…

A

The graph is logarithmic (increases fast then slows down)
-So large increases in diastolic pressure don’t increase SV very much and screw over your heart. But this is how your body compensates to increase SV (Na retention)

-Decreasing end-diastolic pressure to a degree saves the heart with only minimal decrease in stroke volume

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6
Q

Diuretics half short half lives and are pretty cheap, but what’s the big difference between furosemide vs bumetanide or torsemide

A

Furosemide doesn’t absorb as well in intestines

-bumetanide/ torsemide have better oral bioavailability

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7
Q

Grandpa eats at the brazilian steakhouse again and can’t breath (HFrEF) and vomits all night because of food poisoning. What do you give him?

A

Don’t use diuretics because he’s dehydrated

- Use IV Fluids (has lower stroke volume because low fluid)

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8
Q

Review: How does your body respond to low CO?

A

RAAS activation = vasoconstriction + Na retention > increased fluid volume/ pressure

Adrenergic = vasoconstriction + increase HR

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9
Q

What medications block the RAAS pathway? How?

A

ACE inhibitors (“-pril”)

  • Blocks conversion of ATI => ATII (Angiotensin Converting Enzyme)
  • Effects: direct vasodilation, decreased aldosterone release
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10
Q

What are the side effects of ACE inhibitors?

A
Hypotension
Worse renal function
Hyperkalemia
COUGH
Angioedema
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11
Q

What other medications block the RAAS pathway by blocking the receptor of angiotensin II?

A

ARBS (“-sartan”)

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12
Q

ARBS are essentially equivalent to ACE inhibitors. When would you decide to use these instead?

A

To avoid cough (not a side effect)

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13
Q

He talked a lot about LCZ696 as a new hot medicine. What is it?

A

ARB + sacubutril (neprolysin inhibitor)

Supposedly had better effects in ACEI

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14
Q

Mineralocorticoid Receptor Antagonists (MRA) are also pretty dope diuretics. What do they do?

A

The name just told you…

  • block mineralocorticoids in kidney
  • Also have some antifibrotic effects

=spironolactone and eplerene

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15
Q

What medications do you use to block the adrenergic pathway? How do they work?

A

Beta blockers (“-olols”)
-antagonize sympathetic system
Beta 1 block:
-negative chronotrope (slow HR)
-negative inotrope (decrease metabolic demand)
[sometimes block alpha 1, beta 2]

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16
Q

T/F: You should put someone on all three drugs (ACE/ARB, Beta blockers, aldosterone inhibitors) to reduce morbidity and death?

A

True

  • Together they decrease remodeling best
    - hypertrophy
    - fibrosis
    - apoptosis
17
Q

If you have an african american patient that is using all three of these drugs and still has hypertension, what could you give him?

A

Hydralazine/ isosorbide dinitrate (arterial vasodilator)

There are other venous dilators and pulmonary arterial vasodilators too

18
Q

Again, what are the 2010 guidelines for treating someone with stage 3 (NYHA Class I-IV) HfrEF?

A

Loop diuretics +
ACEI or ARB or ARB-neprolysin inhibitor +
aldosterone antagonist +
hydral-nitrates (African Americans)

19
Q

Who should get an Implanted Cardioverter Defribillator (ICD)?

A

Patients with LVEF (left ventr. ejection fraction)

20
Q

What other electrical therapy can you use to restore ventricular synchrony? Who should get it?

A

Cardiac Resynchronization Therapy (CRT) aka Bi-ventricular pacemaker (BiV)
-Shocks ventrical/ septal wall to contract together

> Patients with left bundle branch block, QRS > 120 msec

21
Q

For an acute patient that comes in and is warm and wet (congested), you give IV diuretics. What about an acute patient that is cold and wet (ie. in shock)?

A

You need to give them a positive inotrope!

-also, address their precipitants to bring up their CO before using diuretics

22
Q

Alright ER doc, summarize your plan of action for an acute hospitalized HF patient?

A

1) IV diuretics
2) IV vasodilators (if BP allows)
3) Ventilation (for hypoxia)
4) cut back beta blockers (severe cases)
5) IV inotropes (shock only)

23
Q

So what’s the big difference between chronic vs. acute treatment

A

Chronic: trying to slow heart down (ie. beta blocker)
Acute: trying to stabilize (opposite effect of beta blocker)
-increase inotropy to bring SV back up

24
Q

What are some good positive inotropes to use in an acute setting?

A
Epinephrine
Norepinephrine
Dopamine
Dubutamine
Digoxin
(milrinone)
25
Q

What happens if the patient moves into stage D?

A
Transplantation
mechanical support (LVAD)
Supportive care (shorter life - better quality)
Inotrope infusion (shorter life - better quality)
26
Q

That was all HFrEF. But with HFpEF the problem is lusitropy. What do you do to treat them?

A

-ACEI and ARBs don’t work!
=volume control (diuretic/ vasodilators) and treat underlying disease (hypertension, diabetes, kidney dysfxn)

**Not much you can do with HFpEF