Drugs for heart failure. Flashcards
DRUGS FOR HEART FAILURE
- Diuretics
- R A AS inhibitors
- Angiotensin-converting enzyme inhibitors
- Angiotensin II receptor blockers
- Aldosterone antagonists
- Direct renin inhibitors
- Beta blockers
- Digoxin
- Dopamine
- Hydralazine
DIURE TICS
Thiazide diuretics
• High-ceiling(loop)diuretics • Potassium-sparingdiuretics
DRUGS THAT INHIBIT THE RAAS
- Angiotensin-converting enzyme (ACE) inhibitors
- Hemodynamic benefits
- Arteriolar dilation
- Venous dilation
- Suppression of aldosterone release
- Impact on cardiac remodeling
- ACE inhibitors have a favorable impact
- ACE inhibitors
- Adverse effects
- Hypotension
- Hyperkalemia
- Intractable cough
- Angioedema
- Renal failure if patient has bilateral renal artery stenosis
- Can cause fetal injury
ANGIOTENSIN RECEPTOR NEPRILYSIN INHIBITOR: ENTRESTO
- Increasesnatriureticpeptideandsuppressnegativeeffects of RAAS.
- Betterendpoints:admissions,mortality
- ContainsanARBsoSEsimilar\
- Cannotusewithpreganancy
- Dose:24mg/26mgpoBID
- Start 36 hr ACE/ ARB stopped
Spironolactone [Aldactone] and eplerenone [Inspra]
Aldosterone antagonists
• Current studies recommend adding an aldosterone antagonist to standard HF therapy in patients with moderately severe or severe symptoms
BE TA BLOCKERS
- Action
- With careful control of dosage, can improve patient’s status
- Protect from excessive sympathetic stimulation
- Protect against dysrhythmias
- Adverse effects
- Fluid retention or worsening of HF
- Fatigue
- Hypotension
- Bradycardia or heart block
CORLANOR
- Stable,symptomaticHFwithEF<35inNSR • HR>70bpm
- 2.5–7.5mgBID
- SE:visualdisturbance
• Dopamine [Intropin]
• Sympathomimetics
• Catecholamine • Activates beta1-adrenergic receptors in the heart, kidney, and blood vessels • Increases heart rate • Dilates renal blood vessels • Activates alpha1 receptors
Dobutamine
Sympathomimetics
- Synthetic catecholamine
- Selective activation of beta1-adrenergic receptors
• Milrinone [Primacor]
• Phosphodiesteraseinhibitors
- Inodilator: Increases myocardial contractility and promotes vasodilation
- Reserved for patients with severe reduction in cardiac output resulting in decreased organ perfusion
- Arrhythmias, myocardial ischemia
VASODILATORS
Isosorbide dinitrate plus hydralazine
• Intravenous vasodilators for acute care
• Nitroglycerin
• Principal adverse effects
• Hypotension
• Resultantreflextachycardia
• Sodium nitroprusside [Nitropress]
• Principal adverse effect • Profoundhypotension
• Nesiritide [Natrecor] • Principal adverse effect
• Symptomatichypotension
Digoxin[Lanoxin,Lanoxicaps,Digitek]
CARDIAC (DIGITALIS) GLYCOSIDES
- Naturally occurring compound
- Profound effects on mechanical and electrical properties of the heart
- Increases myocardial contractility
- Increased cardiac output
- Adverse effect
- Can cause severe dysrhythmias
- Effects
- Positive inotropic action on the heart
- Increases force of ventricular contraction
- Increases myocardial contractility
- Relationship of potassium to inotropic action
- Potassium levels must be kept in normal physiologic range
- Hemodynamic benefits • Increased cardiac output
- Decreased sympathetic tone
- Increased urine production
- Decreased renin release
- Neurohormonal benefits
- Modulates the activity of the neurohormonal system
- Suppresses renin release in the kidney
- Decreases sympathetic outflow from the CNS
- Increases sensitivity of cardiac baroreceptors
- Electrical effects
- Alters electrical properties of the heart
- Increases firing rate of vagal fibers
- Increases responsiveness of sinoatrial (SA) node to acetylcholine
- Adverse effects
- Cardiac dysrhythmias
- Predisposing factors
- Hypokalemia
- Elevated digoxin level
- Narrow therapeutic range • Heart disease
- Diagnosing digoxin-induced dysrhythmias
- Managing digoxin-induced dysrhythmias
- Noncardiac adverse effects
- Anorexia, nausea, vomiting, fatigue • Measures to reduce adverse effects
- Education
- Drug interactions
- Diuretics
- ACE inhibitors and ARBs
- Sympathomimetics
- Quinidine
- Verapamil
- Pharmacokinetics
- Absorption
- Distributed widely and crosses placenta
- Eliminated primarily by renal excretion
- Half-life about 1.5 days