Describe the Vaughan Williams classification system for antidysrhythmic drugs.
Class I: Sodium Channel Blockers Class 2: Beta Blockers Class 3: Potassium Channel Blockers Class 4: Calcium Channel Blockers Other antidysrhythmic drugs: amiodarone and digoxin
Why is the use of antidysrhythmic drugs declining?
Benefits are limited to symptomatic relief; the risk of toxicity is substantial
What is the most common sustained dysrhythmia?
What is a-fib caused by?
Multiple atrial foci firing randomly, each contracting their local area of the atrium–results in a chaotic and irregular rhythm atrial rhythm
A-fib may cause an increased risk for ____ due to potential for _____ developing in the heart from this rhythm.
Stroke, blood clots
What fibrillation is a life threatening emergency that requires immediate treatment?
How does ventricular fibrillation occur?
Many different foci firing sporadically, each contracting their local areas of the ventricle–results in localized twitching taking place all over the ventricles, making coordinated ventricular contraction impossible!
What does PVC stand for?
Premature ventricular complexes
What are PVCs?
Beats that occur before they should in the cardiac cycle
How are PVCs causes?
Ectopic ventricular foci–perhaps one or several foci
Are PVCs a cause for concern?
No, UNLESS they are accompanied with additional signs of heart disease
What is atypical, rapid, undulating ventricular tachydsrhythmia that can evolve into potentially fatal ventricular fibrillation?
Torsades de pointes
What is the main factor associated with development of torsades?
Prolongation of the QT interval
What are some drugs that prolong the QT interval?
Class IA and class III antidysrhythmic agents
How do you acutely manage torsades de points?
IV magnesium plus cardioversion for sustained ventricular tachycardia
What class of anti-dysrhythmias are amiodarones?
Primarily Class III (K+ channel blockers)..but it works on all of the classes
Is amiodarone lipid soluble or polar?
HIGHLY lipid soluble
Does amiodarone have a short or long half life?
LONG–like 25-110 days long
T/F: Amiodarone has severe adverse effects.
What are the 6 adverse effects that may happen when taking amiodarone?
- Pulmonary fibrosis
- Optic neuropathy
Amiodarone: Adverse effect pulmonary fibrosis…What baseline data do we need to get to be able to monitor this effect?
Baseline chest x-ray and pulmonary function test; monitor throughout treatment
Amiodarone: Adverse effect dysrhythmias..What should be checked often and why?
Have blood levels checked often because of the risk of dysrhythemias with low or high levels; do not use if pre-existing HF
Amiodarone: Adverse effect hypo/hyperthyroidism.. What should be checked before giving this drug?
Baseline thyroid function test before and monitor thyroid levels closely
Amiodarone: Adverse effect hepatoxicity..What should be checked before giving this drug?
Check baseline liver function test before and monitor liver function levels closely
Amiodarone: Adverse effect optic neuropathy…what can this lead to? What needs to be checked prior to giving the drug?
Can lead to blindness; obtain ophthalmic tests at baseline and periodically thereafter
Amiodarone: Adverse effect photosensitivity..What do we need to teach the client?
Wear sunscreen or protective clothing, can make skin turn bluish grey
*if patients skin turns bluish grey, after stopping the drug it can take months before the discoloration goes away
Amiodarone is __% iodide.
Discuss the latest research regarding incidence of amiodarone hypersensitivity in patients with previous allergy to iodine.
Iodine is an atom which means its too small to be allergic too. People who claim to be allergic to iodine may not actually be allergic to it, but sensitive to something that the iodine is apart of.
What are the two major indications for digoxin therapy?
HF (blocks the Na-K-ATPase pump so it causes increased contractility)
Dysrhythmias (stimulates the vagus nerve, which releases an increased amount of Ach [parasympathetic], so it slows down the HR)
Does digoxin have a wide or narrow therapeutic range?
What is the therapeutic range for digoxin?
What if the digoxin levels are below 0.5 ng/mL?
The underlying dysrhythmia will continue
What if the digoxin levels are above 0.8 ng/mL?
Toxicity will result
What are the EARLY sings of digoxin toxicity?
What are the LATE sings of digoxin toxicity?
Dysrhythmias Visual changes (yellowing and "halos") Mental status changes (can progress to coma)
Both K and digoxin compete for the same sites of action. A normal K level is 3.5-5.0. What happens if someone who is taking digoxin has a K level is above 5?
What happens if someone who is taking digoxin has a K level below 3.5?
Above 5: Less digoxin binds to the Na-K-ATPase pump–>reduced therapeutic responses
Less than 3.5: More digoxin binds to the Na-K-ATPase bump–>toxicity
If your patient is to take digoxin, what needs to be done FIRST? Then what else will need to be done?
FIRST: Check the apical pulse (hold if HR below 60)
- Watch for early signs of toxicity (Anorexia,N/V)
- Monitor digoxin and K levels
If a patient is on digoxin, what can we teach them so they would know their K levels are too low?
They may experience muscle cramps and/or heart alterations
Digoxin is effective in treating the symptoms of HF, but does not prolong a client’s life. Why?
It helps to reverse the issues of HF, but doesn’t change the underlying cause of HR and may actually shorten the life of women!
Why do people who take digoxin also take an ACE?
ACE inhibitors are cardioprotective!