Drugs Used in Heart Failure Flashcards by Tyler Soulek

Characteristics of HF

Progressive and often fatal
Left ventricular dysfunction, reduced CO, insufficient tissue perfusion, signs of fluid retetion
5 million americans
Heart is unable to pump sufficient blood to meet the metabolic need of tissues
- Volume overload
- Inadequate tissue perfusion

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The two forms of heart failure

Left ventricular systolic dysfunctions

Diastolic heart failure, also known as heart failure with preserved LV ejection fraction

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HF: Causes

Chronic hypertension
MI
CAD
dysarrhythmias
ageing of the myocardium

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HF: Physiologic adaptations

Reduced CO
Cardiac dilation
Increased sympathetic tone 
Water retention and increased blood volume
Natriuretic peptides

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HF: Signs and Symptoms

Decreased exercise tolerance
Fatigue
Shortness of breath
Tachycardia
Pulmonary and peripheral edema
Hepatomegaly
Distension of jugular veins
Progressive disorder

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HF: Pathogenesis

Decreased contractility
Increased cardiac workload
- Increases in HR, preload, afterload

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HF: Compensatory mechanisms

RAA stimulation
ADH release, ANF release
Sympathetic stimulation
Cardiac dilation and hypertrophy

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Remodeling

Changes in cardiomyocytes, extracellular matrix, changes in heart size, shape and function

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Drugs Used to Treat HF

Thiazide Diuretics
Loop (high-ceiling) diuretic
Potassium- sparing diuretic

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Drugs that inhibit RAAS

ACE inhibitors
Angiotensin II receptor blockers
Aldosterone antagonists
Direct renin inhibitors

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ACE inhibitors: Hemodynamic benefits

Arteriolar dilation
Venous adilation
Suppression of aldosterone release

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ACE Inhibitor: Impact on cardiac remodeling

Favorable impact

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ACE Inhibitors: Adverse effects

Hypotension
Hyperkalemia
Intractable cough
Angioedema
Renal failure if patient has bilateral renal artery stenosis
Can cause fetal injury

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Angiotensin II receptor blockers

ARBs improve LV ejection fraction, reduce HF symptoms
Increase exercise tolerance
Decrease hospitalization
Enhance quality of life
Reduce mortality

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Aldosterone antagonists: drugs

Spironolactone

Eplerenone

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Aldosterone antagonists: Recommendations

Adding an aldosterone antagonist to standard HF therapy in patients with moderately severe or severe symptoms

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Direct Renin Inhibitors

Benefits in HF about equal to ACE/ARBs

Aliskiren

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What is the most common cause of secondary hyperaldosteronism?

Congestive heart failure

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Beta-blockers: Action

With careful control of dosage, can improve patient status
Protect from excessive sympathetic stimulation
Protect against dysrhythmias

Beta-blockers: Adverse effects

Fluid retention or worsening of HF
Fatigue
Hypotension
Bradycardia or heart block

Digoxin (other cardiac glycosides): Actions

Positive inotropic
- Increase myocardial contractile force
- Alter electrical activity of the heart
- Favorably affect neurohormonal systems
Second-line agents

Inotropic agents [acute care]

Dopamine
Dobutamine
Phosphodiesterase inhibitors

Dopamine: Mechanism

Activates beta-adrenergic receptors in the heart, kidney ,and blood vessels
Increase HR
dilates renal blood vessels
Activates alpha1 receptors

Dobutamine

Synthetic catecholamine

Selective activation of beta1- adrenergic receptors

Phosphodiesterase inhibitors: Drugs

Inamrinone | Milrinone

Vasodilators

Isossorbide dinitrate plus hydralazine | Intravenous vasodilators

Intravenous vasodilators for acute care: Drugs

Nitroglycerin Sodium nitroprusside Nesiritide

Nitroglycerin: Adverse effects

Hypotension | Resultant reflex tachycardia

Sodium nitroprusside: Adverse effect

Profound hypotension

Nesiritide: Adverse effect

Symptomatic hypotension

Cardiac Glycosides: Drugs

Digoxin

Digoxin: Origination

Foxglove plant

Digoxin: Effects

``` Positive inotropic action on the heart Increases the force of ventricular contraction Increases myocardial contractility Inhibits sodium potassium ATPase promoting calcium accumulation in the myocytes Increases exercise tolerance Increased CO Increased contractility DOES NOT PROLONG LIFE ```

Digoxin: Adverse Effects

Can cause severe dysrhytmias Arrhythmia Increases automaticity

Digoxin: Status

alternative status

Digoxin: Ionic interactions

K ( competes with digoxin to bind to Na-K-ATPase) - Hyperkalemia reduces action of digoxin - Hypokalemia increases digoxins action Calcium - Facilitates toxic effects of digoxin - Hypercalcemia results in an increase risk of dig-induced arrhythmias Magnesium - Hypomagnesemia may cause arrhythmia

Digoxin: Positive Inotropic Effects

Increased force and efficiency of contractions - Increases CO - Decreases heart size, venous pressure and BV - Diuresis and relief from edema Vagal effect - Intensifies effect of vagus on the heart - Increases sensitivity of SA node to negative chronotropic effects of Ach - Reflex decrease in sympathetic tone - Slow AV conduction

Digoxin: Effects on ECG and contraction

Slowed AV and Bundle of HIS conduction (Prolongs PR interval) Prolonged refractory period of AV node Increased automaticity - Premature ventricular contractions

Digoxin: Effects on CHF

``` Increased CO - Decreased sympathetic tone - Increased urine production - Decreased renin release Bradycardia Decreases afterload and preload ```

Digoxin: Adverse Effects

Narrows margin of safety and therapeutic range | Cardiac dysrhythmias

Digoxin: Cardiac dysrhythmias

Arterioventricular block, ventricular flutter, ventricular fibrillations Predisposing factors - Hypokalemia - Elevated digoxin level

Digoxin: Noncardiac adverse effects

Anorexia, nausea, vomiting, fatigue, visual effects | Useful warning symptoms early in digoxin toxicity so baseline assessment

Digoxin: Measures to reduce adverse effects

Education

Digoxin: Drug interactions

Diuretics (hypokalemia) Beta blockers (decrease in contractility resulting in higher dose needed) ACEI and ARBs (hyperkalemia) Sympathomimetics (arrhythmia) Quinidine (anticholinergic effects, sometimes used to decrease the bradycardia of digoxin, can increase digoxin levels) Verapamil (can increase digoxin levels)

Digoxin: Managing adverse effects

Withdraw digoxin Monitor serum potassium or administer K Administer lidocaine or phenytoin for arrhythmias Cholestyramine, activated charcoal ( can bind digoxin in the gut where it wont be absorbed)

Digoxin: Management of patients with AV block or bradycardia

Atropine

Digoxin: Pharmacokinetics (absorption)

``` Tables variable Patients not switch brands Crosses the placenta Renal excretion Digitalization ```