causes of Arrhythmia
Name the 2 most common causes of Arrhythmia?
Abnormal Automaticity and abnormal impulse conduction
Name this class and how what are the sub classes
what is Sodium channel blockers and 1a, 1b, 1c
What are examples of B1 selective beta blockers
Atenolol, esmolol, Metoprolol
MOA of Potassium Channel Blocker
Prolongs refractory period by blocking K+ needed to repolarization.
What are Class IV and what are they used for
Calcium channel blockers, Reentry SVT, reduction of ventricular rate in A-fib and A- flutter
What sites of the heart are in control with Arrhythmias?
Sites other then the SA node may generate impulses
MOA of class 1a with example of the class, indications, when to avoid, and adverse effects
MOA is to decrease Na+ influx during depo that prolongs repo and slows conduction. Ex: Quinidine, procainamide, Dispyramide. Indications: A-fib, SVT, PAC's/ PVC's. Quinidine you want to avoid use in systolic HF or atherosclerotic HD. AE=lots of things and has many drug interactions
What are Non B1 selectives
Propranolol
What do all Class IIIs have the potential to do?
trigger arrhythmia as well as treat them
What are the non- dihydropyridines and which are the dihydropyridines
Verapamil and diltiazem are non and amlodipine, nifedipine, felodipine are dihydros
In what way do most AA drugs works
Block Na+, or Ca++, or K+ Channels and this prevents re-entry by slowing conduction or increasing refractory period
MOA of class 1b with example of the class, indications, when to avoid, and adverse effects
MOA is alter of signal conduction by blocking fast voltage-gated Na+ channels responsible for signal, with blockage it will fail to transmit. Ex=lidocaine, Has no inotropic effect, Indications=V-tach and V-fib AE=dizziness, sedation, slurred speech, blurred vision, n/v, seizures, psychosis, sinus arrest
What is the most common BB used
Metoprolol
Examples of Class III and what is the MOA
Amiodarone and Sotalol and IBUTILIDE--MOA is has some class I, II,III, IV and a-blocking activity with prolongation of action potential
adverse effects of CCB non- dihydropyridines
Bradycardia, Hypotension, peripheral edema, adjust dose in hepatic dysfunction
Describe Re Entry
this occurs if unidirectional block and an abnormal conduction pathway occurs
MOA of class 1c with example of the class, indications, when to avoid, and adverse effects
MOA suppresses purkinjie and myocardial fibers slowing the cardiac tissue- thus having no effect on action potential. Ex=flecainide . Indications=a-fib, a-flutter, SVT, and refractory ventricular arrhythmia. AE=Generally well tolerated, blurred vision, dizzy N/V
IV Tx during surgery or other emergent
Esmolol
Black box warning for Amiodarone
Proarrhythmic effect, Pulmonary toxicity, Hepatic toxicity
What is the drug of choice for Acute SVT
Adenosine
What is the main cause of Arrythmyias
what is Re- entry pathways of conduction
What is the Black box warning of Flecainamide
Excessive mortality or non-fatal arrest rates when used in pts with hx of MI
Indications For BB
A-fib, SVT, A-flutter, Tachycardias
Half life of Amiodarone
Several weeks but is really 40 days
Half life of Adenosine
15 seconds, very fast