Arrythmias Flashcards
What is the cardiac conduction pathway?
1) The electrical impulse begins in the SA node.
2) The impulse travels to the right and left atria, causing the atria contract.
3) The impulse continues through the Bundle of His and into the ventricles.
5) The signal continues to spread through the ventricles via the Purkinje fibers, which causes the ventricles to contract.
What causes the ventricles to contract?
Ventricular depolarization occurs when there’s an influx of Na.
QRS
What happens after the influx of sodium?
Polarization occurs from the closure of the sodium channels. A plateau is then formed due to the influx of calcium and an influx of potassium. This influx of potassium is what causes the repolarization of the ventricles (relaxation).
What are the atrial arrhythmias?
1) Atrial fibrillation
2) Atrial Flutter
3) Sinus tachycardia
What are the ventricular arrhythmias?
1) premature ventricular contractions (PVC)
2) Ventricular tachycardia
3) Ventricular fibrillation
What causes Torsade de Pointes?
QT prolongation is a risk factor
What drugs can cause QT prolongation?
1) higher doses
2) reduced drug clearance
3) additive effect of QT prolonging drugs
4) drug interactions that decrease clearance
5) hypokalemia
6) hypomagnesemia
What are the key drugs that can cause arrhythmias?
1) Antiarrhythmics (Class la and Class 3)
2) Antibiotics (quinolones and macrolides)
3) Azole antifungals
4) Antidepressants (tricyclics, citalopram, escitalopram etc)
5) Anti-emetic agents (5-HT3 receptor antagonists, droperidol)
6) Antipsychotics (especially haloperidol and ziprasidone)
What are the anti-arrhythmic medications?
Class 1: Sodium channel blockers
1a: disopyramide, quinidine, procainamide
1b: lidocaine, mexiletine
1c: flecainide, propafenone
Class 2: Beta blockers (indirectly block, calcium channels)
Class 3: Potassium channel blockers (Dronedarone, dofetilide, sotalol, ibutilide, amiodarone)
Class 4: Calcium blockers (verapamil, diltiazem)
Double Quarter Pounder, Lettuce, Mayo, Fries Please!
Because Dieting During Stress Is Always Very Difficult
What medications control Rate?
1) Beta blockers
2) non-DHP CCB
3) [sometimes] Digoxin
The patient stays in a fib with Rate Control. Guidelines suggest we try to control rate before rhythm.
Goal: 80 BPM (In patients with symptomatic AF)
HFrEF patients should not receive non-DHP CCB.
Digoxin may be added-on for refractory symptoms.
What medications control Rhythm?
Class 1a, 1c or Class 3 Antiarrythmics
Goal: Convert and Maintain NSR
Cardioversion meds: Amiodarone, Dofetilide, Flecainide, Ibutilide, Propafenone.
Maintenance meds: Dofetilide, Dronedarone, Flecainide, Propafenone, Sotalol
What is the mechanism of action of sodium channel blockers?
DISOPYRAMIDE, QUINIDINE, PROCAINAMIDE, LIDOCAINE, MEXILETINE, FLECAINIDE, PROPAFENONE
Reduces the speed of ion conduction through sodium channels
What is the mechanism of action of beta blockers?
Block the sympathetic activity that can trigger an arrhythmia; indirectly blocks calcium channels, which decreases ion conduction speed. Used primarily to slow ventricular rate in atrial fibrillation.
What is the mechanism of action of potassium channel blockers?
DRONEDARONE, DOFETILIDE, SOTALOL, IBUTILIDE, AMIODARONE
Amiodarone and Dronedarone block potassium channels, calcium channels, sodium channels, and alpha and beta receptors.
Amiodarone and dofetilide our preferentially used for a fib in patients with heart failure.
Sotalol potassium channels and is a beta blocker.
What is the mechanism of action of Ca-channel blockers (non-dhp)?
VERAPAMIL, DILITAZEM
These are used primarily to slow ventricular rate in atrial fibrillation.
Do not use verapamil or diltiazem in patients with heart failure rEF.
What is the mechanism of action of the digoxin?
Na-K-ATPase blocker
Suppresses AV node conduction (decreases heart rate) by enhancing vagal tone and increases force of contraction.
What is a mechanism of action of Adenosine?
Activates identity and receptors to decrease AV node conduction.
Used for superventricular re-entrant tachycardias
When should an anticoagulant use in a fib?
It should be started at least THREE WEEKS BEFORE cardioversion, and continued for at least FOUR WEEKS AFTER successful cardioversion to NSR.
Amiodarone half-life
T1/2: 40-60 days
What are the box warning for amiodarone?
1) Pulmonary toxicity
2) Hepatotoxicity
3) For life-threatening Arrhythmias only
What are the contraindications of Amiodarone?
1) Iodine hypersensitivity (amIODarone)
2) Bradycardia
3) Heart block (2/3)
What are the Warnings of amiodarone?
1) hyper and hypothyroidism
2) Optic neuropathy
3) photosensitivity (slate-blue skin discoloration)
4) severe skin reactions (SJS)
*Amiodarone is the drug of choice in patients with Heart Failure (rEF)
Drug interactions of Amiodarone
1) Digoxin, Warfarin, Statins
*When starting amiodarone, decrease digoxin by 50% and decrease warfarin by 30 to 50%.
*Amiodarone has an additive effect with other drugs that decrease heart rate rate, including digoxin, beta blockers
Diltiazem and Verapamil MOA
These block calcium channels, and is used to slow ventricular heart rate.
What are the contraindications of diltiazem and verapamil?
1) severe hypertension
2) 2nd/3rd degree hard block
3) cardiogenic shock
4) heart failure
What is the mechanism of action of digoxin?
Digoxin blocks Na-K-ATPase pump, increases contraction force (positive inotrope), and decreases heart rate (negative chronotrope).
Therapeutic range: 0.8 - 2 ng/mL
What are the symptoms of digoxin toxicity?
Nausea vomiting, loss of appetite, bradycardia, blurred/double vision, greenish-yellow halos around the lights or objects, neurological symptoms.
Hypokalemia, hypomagnesemia and hypercalcemia: Increases digoxin toxicity
