Antiarrhythmics

Question 1

what is cardiac arrhythmia

Answer 1

loss of cardiac rhythm

Question 2

what are the two types of cardiac action potentials

Answer 2

• those characteristic of atrial and ventricular muscle such as purkinje fibers are called fast response action potentials
• those observed in the sinoatrial (SA) node and atrioventricular (AV) node are called slow response action potentials

Question 3

resting potential in most myocardial cells

Answer 3

80 - 95 mV

Question 4

how are arrhythmias classified

Answer 4

supraventricular (atrial or AV junctional)

ventricular

Question 5

what are all arrhythmias a result of

Answer 5

• disturbances in impulse formation
• disturbances in impulse conduction
• or both

Question 6

what are the different types of arrhythmias

Answer 6

• premature atrial contractions
• premature ventricular contractions (PVCs)
• atrial fibrillation
• atrial flutter
• paroxysmal supraventricular tachycardia (PSVTs)
• ventricular tachycardia (V-Tach)
• ventricular fibrillation (V-fib)
• sinus node dysfunction

Question 7

describe premature atrial contraction, premature ventricular contractions, and atrial fibrillation

Answer 7

• premature atrial contraction is an early extra beat that originates in the atria and is harmless
• premature ventricular contraction is most common arrhythmias. it is a skipped beat caused by stress, exercise, nicotine, heart disease and etc and does not require treatment
• atrial fibrillation is irregular heart rhythm causing the atria to contract abnormally

Question 8

describe atrial flutter, paroxysmal supraventricular tachycardia, ventricular tachycardia

Answer 8

• atrial flutter is caused by one or more rapid circuits in the atrium. it is more regular than a-fib
• paroxysmal supraventricular tachycardia is a rapid heart rate with regular rhythm originating from above the ventricles
• v-tach is a rapid heart rhythm originating in ventricles and requires treatment immediately

Question 9

describe v-fib and sinus node dysfunction

Answer 9

• v fib is erratic disorganized firing of impulses from ventricle that prevents it from contracting and pumping out blood to the body and requires immediate response
• sinus node dysfunction is a slow heart rhythm due to abnormal SA node and requires treatment with a pace maker

Question 10

what is an electrical cardioversion

Answer 10

if drugs not controlling irregular heart rhythm, this is used to deliver electrical shock that synchronizes the heart and allows normal rhythms to restart

Question 11

why are the class I drugs classified into different subgroup and how does each subgroup differ?

Answer 11

classified based on their rate of drug binding and dissociation from the channel receptor

• class IA: intermediate in speed of binding and dissociation from receptor
• class IB: most rapid for both
• class IC: slowest for both

Question 12

mechanism of class I drugs

Answer 12

• blocks Na channels –> automaticity (ability to generate action potential) is decreased by shifting threshold to more positive potentials and decreasing slope of phase 4 depolarization
• basically it raises the threshold for action potential and slows the rate of depolarization

Question 13

what types of cells are not affects by class I drugs

Answer 13

nodal tissues because they do not rely on Na channels for depolarization

Question 14

what is the class IA drug and what do they do

Answer 14

QUinidine, PROCainamide, DISOPYRAMIDe

the QUeen PROClaims DISO’s PYRAMID

• they are sodium channel blockers thereby inhibiting phase 0 depolarization hence increased action potential duration
• they also block K channels in phase 3 (rectifying K channels) resulting in prolongation of the refractory period (unable to initiate another action potential) in atria and ventricles —-> increased QT interval
• antimuscarinic properties

Question 15

what is a big difference between the class IA drugs

Answer 15

quinidine and procainamide decrease vascular resistance while disopyramide increases vascular resistance

Question 16

what is the effect of a metabolite of procainamide called NAPA (n-acetyl procainamide)

Answer 16

it has little effect on sodium channels but still blocks the K channels so acts more like a class III drug

Question 17

clinical uses of class IA drugs

Answer 17

atrial fibrillation, supraventricular and ventricular arrhythmias

Question 18

adverse effects of quinidine

Answer 18

• precipitate arrhythmias
• increases toxicity of digoxin by decreasing its renal clearance
• Cinchonism (blurred vision, tinnitus, headache, tinnitus)
• thrombocytopenia purpura
• hemolytic anemia

Question 19

adverse effects of procainamide

Answer 19

• reversible lupus like syndrome
• aggravation of underlying HF
• induction of ventricular arrhythmias

Question 20

adverse effects of disopyramide

Answer 20

• heart failure
• hypotension
• severe antimuscarinic effects

Question 21

contraindications for quinidine

Answer 21

• complete heart block
• watch those with increased QT interval, history of torsades de pointes, incomplete heart block, uncompensated heart failure, myocarditis, severe myocardial damage

Question 22

contraindication for procainamide

Answer 22

• hypersensitivity
• complete heart block
• 2nd degree block
• SLE
• torsades de pointes
• heart failure and hypertension

Question 23

contraindication for disopyramide

Answer 23

-uncompensated heart failure

Question 24

what are the class IB drugs

Answer 24

Lidocaine
Mexiletine

I’d Buy LIDdy’s MEXican Tacos

Question 25

mechanism of class IB drugs

Answer 25

- slows phase 0 - shortens phase 3 repolarization - decrease slope of phase 4

Question 26

clinical applications of class IB drugs

Answer 26

ventricular tachyarrhythmias | mexiletine used with v-tachy and lidocaine in digitalis induced arrhythmias

Question 27

adverse effects of class IB drugs

Answer 27

lidocaine - convulsions/seizures and coma if in toxic range mexiletine - CNS and GI effects

Question 28

what are the class IC drugs

Answer 28

Flecainide Propafenone Can i have Fries Please

Question 29

mechanism of class IC drugs

Answer 29

-blocks sodium channels and due to its slow kinetics has a much higher increase in QRS propafenone also has beta blocking activity

Question 30

clinical applications of class IC drugs

Answer 30

- life threatening supraventricular tachyarrhythmias - ventricular tachyarrhythmias - prevention of paraoxysmal a-fib - maintenance of normal sinus rhythm - used exclusively for atrial arrhythmias

Question 31

adverse effects of flecainide and propafenone

Answer 31

- negative inotropic effects - CNS effects (headaches etc) - life threatening arrhythmias and ventricular tachycardia propafenone also has beta blocking activity so bronchospasm and aggravation of underlying heart failure

Question 32

what are class II drugs and name them

Answer 32

they are beta blockers | metoprolol, propanolol, and esmolol

Question 33

mechanism of class II drugs

Answer 33

- inhibit sympathetic tone which affects slow response tissues - slows conduction of impulses - reduce rate of spontaneous depolarization in cells with pacemaker activity

Question 34

clinical uses of class II drugs

Answer 34

- supraventricular arrhythmias (a-fib, a-flutter, AV nodal re-entrant tachycardia) - ventricular tachyarrhythmias - reduce incidence of sudden arrhythmic death after MI

Question 35

useful in tx of acute arrhythmias occuring during surgery or in emergency situations

Answer 35

esmolol

Question 36

adverse effects of beta blockers

Answer 36

sleep disturbances GI upset bradycardia hypotension

Question 37

contraindications of beta blockers

Answer 37

acute CHF severe bradycardia heart block severe hyperactive airway disease