Chap 24 Heart Failure Drugs Flashcards
Heart Failure
Not a specific disease
Complex clinical syndrome resulting from any functional or structural impairment to the heart, specifically ejection of blood or ventricular filling
The heart is unable to pump blood in sufficient amounts from the ventricles to meet the body’s metabolic needs.
American College of Cardiology stages of heart failure
Foundation/American Heart Association (ACCF/AHA) Stages of Heart Failure
Stage A: At high risk for heart failure but no symptoms or structural heart disease
Stage B: Structural heart disease but no symptoms
Stage C: Structural heart disease with symptoms
Stage D: Refractory HF requiring interventions
Drug Therapy for Heart Failure
Positive* inotropic drugs: increase the force of myocardial contraction
Positive* chronotropic drugs: increase heart rate
Positive* dromotropic drugs: accelerate cardiac conduction
Phosphodiesterase inhibitors
Cardiac glycosides
Sinoatrial modulators
Angiotensin receptor-neprilysin inhibitors
Angiotensin-converting enzyme (ACE)* inhibitors*
Angiotensin receptor blockers (ARBs)*
Beta blockers*
Diuretics*
Positive Inotropic Meds
what do they do
strength heart muscle contraction
increase stroke volume
increase cardiac output
Cardiac Glycosides(digoxin)
Beta Agnoists(Dobutamine)
Phosphodiesterase Inhibitors(Milrinone) - heart cant pump enough blood to body’s tissue
Drugs of Choice for Early Treatment of Heart Failure
Dobutamine: positive inotropic drug
Hydralazine and isosorbide dinitrate combination, became the first drug approved for a specific ethnic group. Hydralazine/isosorbide dinitrate (BiDil) was approved specifically for use in the African- American population.
ACE Inhibitors
Inhibit angiotensin-converting enzyme.
Responsible for converting angiotensin I to angiotensin II
Prevent sodium and water resorption by inhibiting aldosterone secretion.
Diuresis results, which decreases preload, or the left ventricular end-volume, and the work of the heart.
Examples: lisinopril*, enalapril, fosinopril, quinapril, captopril, ramipril, trandolapril, and perindopril
Lisinopril (Prinivil, Zestril) Uses& Adverse Effects
Uses: hypertension, HF, and acute MI
Hyperkalemia
Common adverse effect: dry cough, hyperkalemia, decreased renal function
Angiotensin II Receptor Blockers (ARBs)
Potent vasodilators;* decrease* systemic vascular* resistance* (afterload)
Used alone or in combination with other drugs such as diuretics in the treatment of hypertension* or HF
Examples: valsartan (Diovan), candesartan (Atacand), eprosartan (Teveten), irbesartan (Avapro), telmisartan (Micardis), olmesartan (Benicar), and losartan (Cozaar)
Valsartan (Diovan)
Valsartan shares many of the same adverse effects as lisinopril.
ARBs* are not* as likely to cause* the cough* associated* with the ACE inhibitors.
ARBs are not as likely to cause hyperkalemia.
Beta Blockers
Cardioprotective quality of beta blockers: prevent catecholamine-mediated actions on the heart by reducing or blocking sympathetic nervous system stimulation to the heart and the heart’s conduction system
Intended effects: reduced heart rate, delayed AV node conduction, reduced myocardial contractility, decreased myocardial automaticity
Metoprolol*
Carvedilol (Coreg)
Aldosterone Antagonists
Spironolactone* (Aldactone): potassium- sparing diuretic and aldosterone antagonist shown to reduce the symptoms of HF
Eplerenone (Inspra): selective aldosterone blocker, blocking aldosterone at its receptors in the kidney, heart, blood vessels, and brain
B-Type Natriuretic Peptides
Nesiritide (Natrecor)**
Synthetic version of human B-type natriuretic peptide
Vasodilating effects on both arteries and veins
Effects of nesiritide
Diuresis (urinary fluid loss)
Natriuresis (urinary sodium loss)
Vasodilation
Indirect increase in cardiac output and suppression of neurohormonal systems such as the renin-angiotensin system
Nesiritide is used in the intensive care setting(ICU) as a final effort to treat severe, life-threatening HF, often in combination with several other cardiostimulatory medications.
Adverse Effects:
Hypotension
Dysrhythmia
Headache
Abdominal pain
Insomnia
Digoxin*
Derived from foxgloves
Used to treat:
A-Fib/Flutter
CHF
Mechanism of action:
Inhibits Na+K+ ATPase Enzyme
increases the force of heart’s contractions
Side Effects:*
Unusual tiredness and fatigue*
anxiety*
hallucinations*
Poisoning and Toxicity:*
visual disturbances*
nausea or vomiting*
arrhythmias*
electrolyte imbalances*
can be worsened by other meds
Preferred first-line txt:
ACE inhibitors
Beta Blockers
Contraindication:
V-Fib
Very narrow therapeutic window
Drug levels must be monitored.
0.5 to 2 ng/mL
Low potassium levels increase its toxicity.
Electrolyte levels must be monitored.
Adverse Effects
Cardiovascular: dysrhythmias, including bradycardia or tachycardia
Central nervous system: headaches, fatigue, malaise, confusion, convulsions
Eyes: colored vision (seeing green, yellow, purple), halo vision, flickering lights*
Gastrointestinal: anorexia, nausea, vomiting, diarrhea
Antiodote
Digoxin immune Fab (Digibind) therapy – Antidote for digoxin toxicity
Hyperkalemia (serum potassium greater than 5 mEq/L) in a digitalis-toxic patient
Life-threatening cardiac dysrhythmias
Life-threatening digoxin overdose
One vial of Digibind binds 0.5 mg of digoxin
Cardiac Glycosides: Mechanism of Action
Increase myocardial contractility
Change electrical conduction properties of the heart
Decrease rate of electrical conduction
Prolong the refractory period
Area between sinoatrial (SA) node and atrioventricular (AV) node
Cardiac Glycosides: Drug Effects
Positive inotropic effect
Increased* force and velocity* of myocardial contraction* (without an increase in oxygen consumption)
Negative chronotropic effect
Reduced* heart rate
Negative dromotropic effect
Decreased automaticity at SA node, decreased AV nodal conduction, and other effects
