Deja Review Pharmacology by Jessica Gleason
Author:Jessica Gleason
Language: eng
Format: epub
Publisher: McGraw-Hill Education
Published: 2010-09-14T16:00:00+00:00
CONGESTIVE HEART FAILURE AGENTS
What is the cardiac output equation?
Cardiac output (CO) = heart rate (HR) × stroke volume (SV)
What is normal CO?
5 L/min
What is the most common cause of right-sided heart failure?
Left-sided heart failure
Name three compensatory physiologic responses seen in congestive heart failure (CHF):
1. Fluid retention
2. Increased sympathetic drive
3. Hypertrophy of cardiac muscle
Define preload:
The pressure stretching the ventricular walls at the onset of ventricular contraction; related to left ventricular end-diastolic volume/pressure
Define afterload:
The load or force developed by the ventricle during systole
What drugs are used to decrease preload?
Diuretics; vasodilators; angiotensin-converting enzyme inhibitors (ACEIs); angiotensin II receptor blockers (ARBs); nitrates
What drugs are used to decrease afterload?
Vasodilators; ACEIs; ARBs; hydralazine
What drugs are used to increase contractility?
Digoxin; phosphodiesterase inhibitors (amrinone and milrinone); β-adrenoceptor agonists
What is the mechanism of action of digoxin?
Inhibition of the Na+/K+-ATPase pump which leads to positive inotropic action (via increased intracellular sodium ions that exchanges with extracellular calcium ions; resulting increase in intracellular calcium ions leads to increased force of contraction)
What are the two digitalis glycosides?
1. Digoxin
2. Digitoxin
What are the adverse effects of digoxin?
Arrhythmias; nausea; vomiting; anorexia; headache; confusion; blurred vision; visual disturbances, such as yellow halos around light sources
What electrolyte disturbances predispose to digoxin toxicity?
Hypokalemia; hypomagnesemia; hypercalcemia
Digoxin can cause what types of arrhythmias?
Supraventricular tachycardias; AV nodal tachycardias; AV block; ventricular tachycardias; ventricular fibrillation; complete heart block
Can digoxin be used in WPW syndrome?
No. Since digoxin slows conduction through the AV node, the accessory pathway present in WPW is left unopposed, leading to supraventricular tachycardias and atrial arrhythmias.
How is digoxin toxicity treated?
Correction of electrolyte disturbances; antiarrhythmics; anti-digoxin Fab antibody (Digibind)
What drugs can increase digoxin concentrations?
Quinidine; amiodarone; erythromycin; verapamil
What drugs can decrease digoxin concentrations?
Loop diuretics; thiazide diuretics; corticosteroids
Does digoxin therapy in CHF lead to prolonged survival?
No. It is of symptomatic benefit only, improving quality, but not necessarily duration of life.
What classes of medications have been shown to increase survival in CHF patients?
ACEs/ARBs; β-blockers
How does dobutamine work in CHF?
β-Adrenergic agonist (sympathomimetic that binds to (β1-adrenoceptors) that increases force of contraction and vasodilation via increased cAMP
How do amrinone and milrinone work in CHF?
Inhibits phosphodiesterase (PDE) thereby increasing cAMP levels; increased cAMP leads to increased intracellular calcium; increased intracellular calcium leads to increased force of contraction; increased cAMP also leads to increased vasodilation
What are the side effects of the PDEIs?
Milrinone may actually decrease survival in CHF; amrinone may cause thrombocytopenia.
How do diuretics work in CHF?
Decrease in intravascular volume thereby decrease in preload; reduce pulmonary and peripheral edema often seen in CHF patients
How can increased sympathetic activity in CHF be counteracted?
β-Blockers
What two β-blockers have specific indications for the treatment of CHF?
1. Metoprolol
2. Carvedilol (mixed α-/β-blocker)
What is the mechanism of action of nesiritide?
Recombinant B-type natriuretic peptide that binds to guanylate cyclase receptors on vascular smooth muscle and endothelial cells, thereby increasing cyclic guanosine monophosphate (cGMP) levels; increased cGMP leads to increased relaxation of vascular smooth muscle
How do ACEIs work in CHF?
Inhibition of angiotensin-II (AT-II) production thereby decreasing total peripheral resistance (TPR) and thus afterload; prevents left ventricular remodeling
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