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Alaska Nurse Practitioner Annual Conference 2009
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LAURIE RACENET, RN, MSN, ANP,
CEPS, CCDS
Alaska Heart Institute
Member: Boston Scientific Allied Professional Advisory
Board
Participant in Industry Sponsored Research: Boston
Scientific, Medtronic and St. Jude Medical
Speaker for Boston Scientific Corporation and
Medtronic, Inc
No pharmaceutical relationships to disclose
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Action Potential
Movement of Potassium, Sodium and Calcaim ions across the cell membranes of the myocardium
Anti-arrhythmic medications work on these ion channels
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Automaticity
Re-entry
Triggered Activity
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Caused by an abnormal acceleration of phase 4
These arrhythmias often warm up and slow down gradually
Often, an underlying metabolic cause can be determined
Think of this as an “itch”, that anti-arrhythmic drugs can sometimes help sooth
Examples Multifocal atrial tachycardia
VT in the acute MI (ischemia)
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Common metabolic causes of automatic arrhytmias Cardiac ischemia
Hypoxemia
Hypokalemia
Hypomagnesemia
Acid-base disturbance
High sympathetic tone
Use of sympathomimetic agents
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Most clinically significant arrhythmias are re-entry arrhythmias
3 things that must be present for re-entry to occur 2 parallel pathways that are connected proximately and distally 1 pathway must have a longer refractory period than the other The pathway with the shorter refractory period must conduct
electrical impulses more slowly than the other
If all these are present, a properly timed premature impulse can set off the arrhythmia circuit
Examples of re-entry arrhythmias WPW AVNRT VT in patients with scar from previous MI
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Resembles automaticity in that new action potentials are created by a “leakage” of positive ions into the cell
Similar to re-entry in that it is not always spontaneous and can be triggered by properly timed premature beats
Cannot be overdrive paced
Examples: Dig toxic arrhythmias
Torsades de Pointes (think patients with Long QT)
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Classes are based on their effect on the action potential
Classed as I –IV
Easiest to remember and study by class than individually
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Class I (A, B and C)- sodium channel blockers
Class II – beta blockers
Class III – potassium channel blockers
Class IV – calcium channel blockers
Miscellaneous – digoxin, adenosine, magnesium
Dronedarone (Multaq) just released Aug 2009
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Quinidine
Procainamide
Disopyramide (Norpace)
Prolong the QRS (Phase 0, slows the influx of sodium ions into the cell) and the QT intervals
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Action Potential of
Class 1A drugs
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Dosages for Class IA Drugs
Quinidine Sulfate
300 – 600mg every 6 hours
Quinidine Gluconate
324 – 972mg every 6 – 8 hours
Procainamide
500 – 1250mg every 6 hours
Disopyramide
100 – 200mg every 6 hours
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Nausea and diarrhea
Constipation
Heart block
Decreased appetite
Widened QRS
Prolonged QT interval
Ventricular arrhythmias
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Complete AV block
Congential Long QT Syndrome
Dig toxicity
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Lidocaine
Mexiletine
Phenytoin
Does not change the QRS, but shortens the QT interval
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Action Potential of
Class 1B drugs
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Dosages for Class IB Drugs
Lidocaine
per ACLS Protocol
Mexiletine
150 – 200mg every 8 hours
Phenytoin
300 – 500mg per day in divided doses
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Tingling sensations
Visual changes
Slurred speech
Headache
Decreased appetite, GI upset
Confusion and mental changes
Ventricular arrhythmias
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2nd of 3rd degree block
Use caution in patients with epilepsy or heart failure
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Flecainide
Propafenone
Prolongs the QRS, but not the QT interval
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Action Potential of
Class 1C drugs
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Dosages for Class IC Drugs
Flecainide
100 – 200mg every 12 hours
Propafenone
150 – 300mg every 8 hours
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Tingling sensations
Slurred speech
Blurred vision
Decreased appetite, GI upsets
Headache
Bradycardia
Widened QRS
Ventricular arrhythmias
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Known coronary artery disease
2nd or 3rd degree heart block
Bifasicular block
Profanenone has some beta blocker activity
These drugs can organize atrial fib into atrial flutter. May want to add a small dose of beta blocker just in case.
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Little effect on the Action Potential – effect is primarily on sinus node and secondarily on the AV node
Use bisoprolol (Zebeta), acebutelol (Sectral), pindolol for younger patients (less sleepiness, fatigue associated with these drugs)
If using for rate/arrhythmia control, it is OK to use generic and cheap.
When using for heart failure metoprolol succinate (not tartarate) Carvedilol (for patients with financial concerns, use generic
carvedilol with BID dosing instead of once a day Coreg CR) bisoprolol
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Fatigue
Sleepiness
Bradycardia
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Underlying bradycardias or advanced heart block
Use caution with diabetes
Use caution in patients with reactive airway disease
In heart failure patients, it may be best to diurese them before starting beta blocker
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Tikosyn
Sotalol
Ibutalide
Bretyllium
Amiodarone
Prolongs the QT interval = risk for torsades
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Action Potential of
Class III drugs
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Dosages for Class III Drugs
Tikosyn
500mg every 12 hours
250mg every 12 hours for impaired renal function
Sotalol
80 – 160mg every 12 hours
Amiodarone
800 – 1600mg per day for 3 – 10 days, the 100 – 400mg per day
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CLASS III DRUG CALCULATOR
9/2/2009 Age Wt, Lbs Creatinine
Enter data in yellow boxes:
Estimated Creatinine Clearance:
Male: #DIV/0! ml/min
Female: #DIV/0! ml/min
If Creatinine Clearance is: Tikosyn dose: Sotalol dose:
>60 500 bid 80-160 Q12
40-60 250 bid switch to Q24
20-40 125 bid stop drug
<20 stop drug stop drug
Most recent QTc interval: msec
QT limits during maintenance: Tikosyn Sotalol
-narrow QRS 500 520
-wide QRS (>100ms) 550 JT interval 330
May refill prescription:
____________________________, MD Laurie Racenet ANP
9/2/2009
Do not refill:______________________________________, MD
9/2/2009
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Prolonged QT interval Ventricular arrhythmias, including torsades Amiodarone
Blue skin, pulmonary hypertension, liver dysfunction, hyper or hypothyroid, blindness
Also be aware of effect on heart rate. Will cause bradycardia
Be very cautious of interaction between amiodarone and Coumadin – cut Coumadin dose in half when starting amiodarone
Recently there has been evidence of an interaction between amiodarone and simvastatin at doses of 40mg and higher. Change to different cholesterol treatment when starting amiodarone
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Long QT Syndromes
Tikosyn should not be given if a QTc has ever been greater than 440ms
Severe renal impairment
Uncontrolled CHF (sotalol only)
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Cardiazem
Verapamil
Beware of calcuim channel blockers in systolic heart failure, but they may have some benefit in diastolic heart failure
Good rate controlling drugs
Very helpful in atrial fib
Use generic formulations
These are also anti-anginal drugs and may be a good choice if the patient has rapid heart rates and CAD with stable angina
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Fatigue
Ankle Swelling (cardiazem)
Constipation
Worsening heart failure
Daytime sleepiness
Bradycardias
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Severe LV dysfunction
2nd or 3rd degree heart block
Atrial fib with a known accessory pathway, such as WPW (verapamil)
Severe hypotension
Acute MI
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Unclassified Anti-Arrhythmic Agents
Digoxin
Adenosine
Magnesium
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Digoxin
Increases intracellular contraction
Increases parasympathetic tone
Use lower dose in elderly
Monitor for subtle signs of toxicity
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Adenosine
In high concentrations has a dramatic, but short depressive effect on the SA and AV nodes
Produces high grade AV block 10 – 30 seconds after IV administration
Can terminate re-entrant arrhythmias and is useful in diagnosing atrial flutter and fib
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Magnesium
Precise mechanism is not established
Most useful in treating TDP
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Dromadarone (Multaq)
“Cousin” to Amiodarone
Approved for atiral fib
Has properties belonging to all 4 Vaughan-Williams Classes
Just approved for use August 2009
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Dronedarone
Dosage: 400mg twice a day with the morning and evening meals
Most common side effects:
nausea, diarrhea, abdominal pain, vomiting and asthenia
Contraindications: Class IV heart failure or Class II – III heart failure with a recent decompensation requiring hospitalization or referral to a specialized heart failure clinic
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Other Precautions
•Pregnancy – woman of child bearing age should use effective contraception while on drug
•Stop if QTc greater or equal to 500ms
•Maintain normal serum levels of potassium and magnesium
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Drug Interactions
Simvastatin
Any drug that can prolong the QT interval is contraindicated
Calcium channel blockers
Beta blockers
Digoxin
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Atrial flutter Membrane Active AADs are not a 1st line choice – ablation
has fewer side effects and is considered curative if successful (95%)
May choose to use beta blockers, calcium channel blockers or dig to slow the heart rate
Supraventricular arrhythmias Membrane active AADs are usually not indicated Consider patient circumstances – may not be 1st line
treatment
Ventricular arrhythmias Be aware that membrane active AADs do not have a
mortality advantage If EF < 35%, patient should be considered for ICD
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Atrial fib
Rate control vs rhythm control
Heart failure
HRS and ACC recommend patient fail one membrane active AAD before being considered for curative ablation
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Get a base line QTc (if QTc has EVER been greater than 440ms do not use Tikosyn)
Consider whether another treatment might have a stronger indication
Be sure you have ruled out treatable causes of arrhythmias
Consider Co-morbidities: Do not use class IC drugs in patients with CAD Use caution with beta blockers in patients with
diabetes or asthma Do not use calcium channel blockers in patients with
heart failure (systolic dysfunction)
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Hospital admission for 3 days Serial EKGs and bloodwork QRS widening QTc prolongation BMP –watch creatinine clearance Flecainide levels Liver and thyroid function with amiodarone Baseline and yearly PFTs with amiodarone Baseline and yearly vision exam with amiodarone
EKG and blood work every 3 months Only give 3 months supply of the drug at a time Consent prior to giving drugs (?) If patients experience ventricular arrhythmias, consult EP –
the drug may need to be stopped
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Be aware of potential side effects Amiodarone is a wonderfully effective drug for both
ventricular and supra-ventricular arrhythmias, BUT, it has ugly and potentially permanent side effects. Consider stopping the drug for any of the following reasons:
Unexplained SOB Vision changes Change in liver function test Symptoms of thyroid disorder Breakthrough arrhythmia requiring cardioversion
Monitor arrhythmia burden: if there is a lot of break-through arrhythmia, may need to consider the drug a failure
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Bottom line:
Class I and Class III AADs are serious business. It is best to consult EP prior to initiating these meds 561-3211 – ask to speak to EP on call
Class II and Class IV drugs have a better safety profile and can be safely used to treat most arrhythmias. May want EP consult to determine if the patient is a candidate for curative ablation.
Safe monitoring of AADs can be done very effectively by NPs
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Questions?