- …sartans (e.g. valsartan, candesartan, losartan) - Effect: Block the receptor of angiotensin II

- 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

Clinical Treatment of Heart Failure Flashcards by Soliman Oushy

What are the major goals of therapy?

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

How well did you know this?

Not at all

Perfectly

How to therapeutically approach HF?

-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

How well did you know this?

Not at all

Perfectly

What lab studies could rule out reversible causes of HF?

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)

How well did you know this?

Not at all

Perfectly

How do you reduce congestion?

Diuretics, Reverses fluid retention (Na loss)

How well did you know this?

Not at all

Perfectly

The most common HF therapy

Diuretics

How well did you know this?

Not at all

Perfectly

Pharmacokinetics of diuretics

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

How well did you know this?

Not at all

Perfectly

Diuretics method of action

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

How well did you know this?

Not at all

Perfectly

What are ACE inhibitors?

…prils (lisinopril, enalapril, benazepril)

- Block conversion of ATI to ATII

How well did you know this?

Not at all

Perfectly

Effects of ACEIs

Direct vasodilation

Decreased aldosterone activation

How well did you know this?

Not at all

Perfectly

Side effects of ACEIs

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

How well did you know this?

Not at all

Perfectly

What are ARBs?

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

- Effect: Block the receptor of angiotensin II

How well did you know this?

Not at all

Perfectly

Clinical use of ARBs

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

How well did you know this?

Not at all

Perfectly

Side effects of ARBs

ARBs do not produce kinin potentiation (no cough)

Otherwise side effects are similar to ACEI

How well did you know this?

Not at all

Perfectly

What are Mineralocorticoid Receptor Antagonists (MRA)?

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

How well did you know this?

Not at all

Perfectly

Side effects of MRAs

Hyperkalemia (requires close monitoring)

Gynecomastia (spiro only)

How well did you know this?

Not at all

Perfectly

What are beta-blockers?

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]

Side effects of beta-blockers

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

End result of Adrenergic and RAAS blockers?

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

What are the different Vasodilators for HF?

Arterial vasodilation (antihypertensives)
Venous vasodilation (venodilators)
Pulmonary arterial vasodilation

Effect of pulmonary arterial vasodilation

Decrease in RV afterload

Effect of Venous vasodilation (venodilators)

Decrease in preload

Benefits of arterial vasodilatation

Decrease in LV afterload
Reduced cardiac work
Less mitral regurgitation

Use of Hydralazine / isosorbide dinitrate in HFREF

Hyd/ISDN < ACEI (V-HeFT II)

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

What is an ICD?

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

What is CRT therapy?

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

Indication for CRT use

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

CRT mechanism of action

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

Rx options for chronic (stable) HFrEF

``` BB ACEI/ARB Aldosterone antagonist Hydralazine / ISDN +/-Digoxin ICD/CRT ```

Rx options for Acute decompensated HF

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)

Types of Positive Inotropic Agents

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

Clinical use of positive inotropic agents

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)

T or F: inotropic agents Improve symptoms short-term | Long-term HF is worsened

True

Beta-Agonism v. Antagonism:

ACUTE v. CHRONIC, respectively

Stages of HF

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

What is LVAD?

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

Options for end-stage HFrEF

Transplant LVAD Inotrope infusion Hospice

What can you do to improve Sx in HFrEF?

``` Diuretics (furosemide) Digitalis PO (HFrEF with shock - dobutamine, milronone) ```

What can you do to prolong survival in HFrEF?

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

Therapy for HFpEF

- 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