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CVPR Unit 1 > Clinical Treatment of Heart Failure > Flashcards

Clinical Treatment of Heart Failure Flashcards

1
Q

What are the major goals of therapy?

A

↑ quantity of life (improve survival)
↑ quality of life (reduce symptoms)
Decrease societal / financial burden of disease

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2
Q

How to therapeutically approach HF?

A

-Correction of the underlying cause of HF
-Elimination of precipitating factors (infection, anemia, etc)
-Reduction of congestion
-Improve blood flow:
Modulate neurohormal activation
Devices / transplantation

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3
Q

What lab studies could rule out reversible causes of HF?

A
  • Vitals BP / HR (hypertension)
  • EKG (tachyarrhythmia, AFib, PVCs)
  • CMP, CBC (renal failure, liver dysfunction, anemia, infxn)
  • CXR (coexistant lung disease, for future comparison)
  • BNP / NT-proBNP, troponin (prognosis)
  • Echo (dilation, LV function, wall motion, PHTN, prognosis)
  • Coronary angiogram v. CTA, stress testing, MRI (ischemia, scar)
  • Thyroid function tests
  • Iron studies (hemochromatosis, iron deficiency)
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4
Q

How do you reduce congestion?

A

Diuretics, Reverses fluid retention (Na loss)

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5
Q

The most common HF therapy

A

Diuretics

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6
Q

Pharmacokinetics of diuretics

A

Can be used chronically and acutely
Typically PO dose at baseline
Often use IV in the hospital (PO not absorbed, worsening renal function, also need higher dose)
Side effects: dehydration, hypokalemia, sulfa, tinnitis

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7
Q

Diuretics method of action

A

increase Salt (+Water) Excretion->decrease Intravasc Fluid Vol->decrease Venous Congestion->decrease dyspnea/edema

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8
Q

What are ACE inhibitors?

A
  • …prils (lisinopril, enalapril, benazepril)

- Block conversion of ATI to ATII

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9
Q

Effects of ACEIs

A

Direct vasodilation

Decreased aldosterone activation

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10
Q

Side effects of ACEIs

A

Hypotension
Worsening renal function (afferent vasocontraction)
Hyperkalemia
Cough (kinin potentiation): ~20%
Angioedema: <1%, can occur after months of use

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11
Q

What are ARBs?

A
  • …sartans (e.g. valsartan, candesartan, losartan)

- Effect: Block the receptor of angiotensin II

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12
Q

Clinical use of ARBs

A
  • In studies have been equivalent to ACEI
  • Controversial whether use in combination (ARB + ACEI) provides added benefit
  • Generally used when patients develop cough to ACEI
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13
Q

Side effects of ARBs

A

ARBs do not produce kinin potentiation (no cough)

Otherwise side effects are similar to ACEI

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14
Q

What are Mineralocorticoid Receptor Antagonists (MRA)?

A

-Spironolactone and eplerenone
-Effect: Block mineralocorticoid receptor
Kidney: ACEI/ARB aldosterone block is incomplete
Produces additional sodium loss (diuretic), Antifibrotic

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15
Q

Side effects of MRAs

A

Hyperkalemia (requires close monitoring)

Gynecomastia (spiro only)

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16
Q

What are beta-blockers?

A
  • olols (metoprolol, carvedilol, bisoprolol)
  • Effect: Antagonize effect of sypathetic system (epinephrine/norepinephrine)
  • β1 blockade:
  • Negative chronotrope (slow heart rate, less arrhythmia)
  • Negative inotrope (decreased metabolic demand)
  • [α1 blockade: vasodilation]
17
Q

Side effects of beta-blockers

A

Negative inotrope: short-term loss for long-term gain
Fluid retention
Hypotension
Decreased cardiac output, even cardiogenic shock
Bronchoconstriction

18
Q

End result of Adrenergic and RAAS blockers?

A 
-Anti-Remodeling Decreased:
Hypertrophy
Fibrosis
Apoptosis
-All 3 REDUCE MORBIDITYAND IMPROVE SURVIVAL
19
Q

What are the different Vasodilators for HF?

A 
Arterial vasodilation (antihypertensives)
Venous vasodilation (venodilators)
Pulmonary arterial vasodilation
20
Q

Effect of pulmonary arterial vasodilation

A

Decrease in RV afterload

21
Q

Effect of Venous vasodilation (venodilators)

A

Decrease in preload

22
Q

Benefits of arterial vasodilatation

A

Decrease in LV afterload
Reduced cardiac work
Less mitral regurgitation

23
Q

Use of Hydralazine / isosorbide dinitrate in HFREF

A

Hyd/ISDN < ACEI (V-HeFT II)

Hyd/ISDN+ACEI/BB in blacks good (A-HeFT)

24
Q

What is an ICD?

A

Implanted Cardioverter Defibrillators
Patients with LVEF <=35% or prior dangerous heart rhythms
Abort sudden cardiac death from ventricular tachycardia / fibrillation

25
Q

What is CRT therapy?

A

Cardiac Resynchronization Therapy
Biventricular pacemakers (CRT or BiV)
LV lead placed through the coronary sinus

26
Q

Indication for CRT use

A

For patients with QRS duration > 120 msec (bundle brank block)

27
Q

CRT mechanism of action

A

Cause the LV lateral wall and septal wall to contract together, which produces a more efficient contraction / ↑ stroke volume
Usually placed with ICD

28
Q

Rx options for chronic (stable) HFrEF

A 
BB
ACEI/ARB
Aldosterone antagonist
Hydralazine / ISDN
\+/-Digoxin
ICD/CRT
29
Q

Rx options for Acute decompensated HF

A

IV diuretics
IV vasodilators (nitrates / nitroprusside, if BP allows)
Positive pressure ventilation (CPAP/BiPAP, intubation) for hypoxia
May also reduce preload
IV inotropes for shock only
May need to cut back on beta-blockers (only in severe cases)

30
Q

Types of Positive Inotropic Agents

A

Digoxin (PO) - K/Na exchange
Dobutamine (IV) – β agonist (opposite of BB)
Milrinone (IV) – phosphodiesterase inhibitor (effect is similar to dobutamine)

31
Q

Clinical use of positive inotropic agents

A

ACUTE: IV agents used short term to reverse shock
Long-term they worsen remodeling
CHRONIC: Digoxin has no effect on mortality but may reduce symptoms and hospitalization (also some decrease in heart rate in AFib)
In high doses causes dig toxicity (mostly arrhythmias)

32
Q

T or F: inotropic agents Improve symptoms short-term

Long-term HF is worsened

A

True

33
Q

Beta-Agonism v. Antagonism:

A

ACUTE v. CHRONIC, respectively

34
Q

Stages of HF

A

Asymptomatic HF (late “prevention”)
Chronic stable HF (ambulatory)
Acute decompensated HF (hospitalized)
End-stage heart failure (advanced)

35
Q

What is LVAD?

A

Left Ventricular Assistance Device mechanical circulatory device that is used to partially or completely replace the function of a failing heart, can be used in CHF

36
Q

Options for end-stage HFrEF

A

Transplant
LVAD
Inotrope infusion
Hospice

37
Q

What can you do to improve Sx in HFrEF?

A 
Diuretics (furosemide)
Digitalis PO (HFrEF with shock - dobutamine, milronone)
38
Q

What can you do to prolong survival in HFrEF?

A

ACE Inhibitors / Angiotensin Receptor Blockers
Beta Blockers
Aldosterone Receptor Antagonists
Other Vasodilators (hydralazine + nitrates)
Cardiac Resynchronization Therapy (biventricular pacing)
Implantable Cardioverter Defibrillator (ICD)

39
Q

Therapy for HFpEF

A
  • treating the underlying disorder (hypertension, diabetes, kidney dysfunction)
  • Diuretics are used to keep volume normal (sodium retention is common)
  • Vasodilators are used to maintain normal blood pressure
  • neurohormonal antagonists (e.g. ACEI, ARB) not successful

CVPR Unit 1 (27 decks)

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