Cardiac Glycosides and Heart Failure Flashcards
What are the normal compensatory mechanisms the body has for someone in heart failure?
RAA system - increase in volume and vasoconstriction helps perfusion
Sympathetic stimulation - increases contractility and HR
What is the bad thing about the compensatory mechanisms our body has for heart failure?
In the long run our body wont be able to keep up these mechanisms and they will just end up making the heart failure worse.
What are some drug classifications that we use to treat heart failure? And if these fail to treat the heart failure what do we turn to? Why?
ACE inhibitors
ARBS
Diuretics
Beta-Blockers
If these dont work then we turn to cardiac glycosides, they are a last resort because of the risk for adverse effects
Where is digoxin originally derived from?
the foxglove/digitalis plant
What is the therapeutic action of cardiac glycosides?
increases the force of contraction, decreases the rate and conduction of the SA node
Decrase HR = Increased filling time = increased pre-load = increased contractility
How can digoxin be administered?
PO or IV
If digoxin is given IV, how long should it be pushed?
Infuse over 5 minutes
Other than treatment of heart failure, what other thing do cardiac glycosides have a therapeutic outcome for?
Atrial dysrhythmias
Does digoxin have a high risk for toxicity?
YES YES YES
What are some adverse effects of cardiac glycosides?
Dysrhythmias
Bradycardia (can be a sign of toxicity)
What are some things that cause the dysrhythmias in people taking cardiac glycosides?
hypokalemia (this medication doesnt cause it)
High serum drug levels (major decrease in HR = other pacemakers kick in)
Heart disease (damaged tissue = dysrhythmias)
MONITOR HEART RATE!!!!!!
Patients with this specific disorder are contraindicated for the use of cardiac glycosides.
ventricular dysrhythmias
What can bradycardia associated with taking cardiac glycosides be a sign of?
toxicity
Because of the risk for bradycardia what should the nurse do before administering a cardiac glycoside?
assess the apical HR of the patient before administration and if it is less that 60 HOLD the medication and call the physician
RATE AND RHYTHM
How would you describe the therapeutic range for cardiac glycosides? Give a range in numbers as well.
Very narrow (0.5-2.0)
Toxicity has occurred from 1.5-1.7
What does hypokalemia have to do with cardiac glycosides?
If the patient is hypokalemic the risk for toxicity increases, so it is crucial to monitor the patients potassium especially if taking a medication that lowers potassium
What are some general signs of toxicity from cardiac glycosides?
fatigue
weakness
vision changes (yellow/green/white halos around lights
What are some things that the patient might exhibit in early toxicity with cardiac glycosides?
Really tired, weak, no appetite
What are some GI effects that might occur with cardiac glycoside toxicity?
anorexia
nausea
vomiting
abdominal pain
What are some CNS effects that might occur from cardiac glycoside toxicity?
fatigue
weakness
visual changes (diplopia, blurred vision, yellow/green/white halos around lights)
what are some drug-drug interactions that cardiac glycosides have?
Thiazide and loop diuretics (cause hypokalemia)
ACE inhibitors and ARBS can cause hyperkalemia which decreases therapeutic effects
Quinidine and verapimil increase risk for toxicity
What are some main patient teaching points for cardiac glycosides?
eat high potassium foods (spinach, green leafy veggies, potatoes)
Check HR before administering (hold if below 60)
signs of hypokalemia (nausea, vomiting, weakness) and signs of toxicity
dont stop suddenly
dont double dose if a dose is missed (take it as soon as remembered then take scheduled dose
Keep lab appointments
Antidote - digibind
What is the mechanism of action for epinephrine?
Alpha 1, Beta 1 & 2 stimulation increase HR, contractility, vasoconstrict, and bronchdilate
alpha 1 - vasoconstrict
Beta 1 - Increase HR and contractility
Beta 2 - bronchodilate
When is epinephrine commonly used?
Shock
Asthma
Cardiac arrest
Anaphylaxis
USED IN ACUTE SITUATIONS
What are some nursing considerations for epinephrine?
continuous cardiac monitoring
monitor for dysrhythmias, angina, hypertension
watch out for extravasation - tissue necrosis around the site of administration
What is the mechanism of action for dobutamine?
beta 1 stimulation increases HR and contractility, also has a bit of vasodilation effect so the BP effects are less profound
when is dobutamine used?
Heart failure (for more chronic issues)
What is a primary nursing consideration for dobutamine?
continuous cardiac monitoring
What is the effect of low dose dopamine?
dilates renal arteries 1-3mcg/kg/minute
What is the effect of a moderate dose of dopamine?
(beta 1) - dilates renal arteries, increases HR, increases contractility, increases rate of conduction 3-10mcg/kg/minute
What is the effect of high dose dopamine?
Beta 1 and alpha 1 - vasoconstriction and renal artery constriction, increase in HR and contractility
USUALLY USED FOR CARDIOGENIC SHOCK
What are some nursing considerations for dopamine?
Closely monitor IV site for extravasation tissue necrosis
Many drug-drug interactions
Usually for emergent situations
Administer using IV pump and increase/decrease dose slowly (every 5 minutes) based on BP
