Arrhythmia

Question 1

Aim of therapy

Answer 1

To reduce ectopic pacemaker activity

To modify conduction or refractoriness in reentrant circuits to disable the circular movement

Question 2

Antiarrhythmic agents generally alter:

Answer 2

Diastolic potential in pacemaker cells and/or resting membrane potential in ventricular cells (phase 4)
Phase 4 depolarization
Threshold potential
Action potential duration

Question 3

Effect on Automaticity:

Answer 3

• Can slow spontaneous discharge by:
  Depressing diastolic depolarization
  Otherwise known as phase 4
  Shifting threshold voltage to zero
  Hyperpolarizing resting membrane potential
• Affects ectopic sites more than sinus node

Question 4

Effect on Reentry:

Answer 4

• Improves or depresses conduction
  Eliminate unidirectional block
  Facilitate conduction so returning wavefront reenters when cells still refractory
  Depress conduction to transform unidirection to bidirectional block
• Prolong refractoriness relative to action potential duration

Question 5

Vaughan Williams Classification of Antiarrhythmic Drugs Class I

Answer 5

block sodium channels

 works mostly on Phase 0, but also works on the latter parts

Question 6

T/F: Vaughan Williams Classification of Antiarrhythmic Drugs Class Ia example: Lidocaine

Answer 6

F:
Ia (quinidine, procainamide, disopyramide)
Ib (lidocaine)
Ic (flecainide)

Question 7

Vaughan Williams Classification of Antiarrhythmic Drugs Class II

Answer 7

β-adrenoreceptor antagonists
works on Phase 4, keeps slope less steep (flattens the slope)
Atenolol, sotalol

Question 8

Vaughan Williams Classification of Antiarrhythmic Drugs Class III

Answer 8

prolong action potential and prolong refractory period
Works on Phase 0 to 3
Amiodarone, sotalol

Drugs which prolong ERP (effective refractory period) by prolonging action potentials

Question 9

Vaughan Williams Classification of Antiarrhythmic Drugs Class IV

Answer 9

Calcium channel antagonists
Works on Phase 2
verapamil

Question 10

T/F: Lidocaine Low toxicity high effectiveness in arrhythmias associated with MI

Answer 10

T

Question 11

Lidocaine toxicity

Answer 11

Toxicity: one of the least cardiotoxic drugs
May precipitate hypotension by depressing myocardial contractility in large doses in patients with heart failure
Neurologic: parethesias, convulsions, dizziness

Question 12

T/F Flecainide is a potent Na and K channel blocker

Answer 12

T

Question 13

Very effective in suppressing premature ventricular contractions and  premature atrial contractions

Answer 13

Class Ic: Flecainide

Question 14

T/F Class Ic May exacerbate arrhythmias in patients with ventricular arrhythmias + patients with previous MI and ventricular ectopy

Answer 14

T

Question 15

Flecainide route, half-life, metabolism

Answer 15

oral, 20 hours, hepatic and renal metabolism

Question 16

main use is for patients with paroxysmal AF and those without structural heart diease

Answer 16

Class Ic: Flecainide

Question 17

Prototype of Class II

Answer 17

propranolol, esmolol

Question 18

MOA of class II

Answer 18

indirectly reduce the phase 4 slope by blocking positive chronotropic action of norepinephrine

Question 19

therapeutic use of class II

Answer 19

suppression of ventricular ectopic depolarizations

Question 20

Amiodarone cardiac effect

Answer 20

Broad spectrum of cardiac actions, high efficacy
Markedly prolongs APD (QT interval)
Significantly blocks inactivated Na channels
Has weak β-adrenergic and calcium channel blocking actions

Question 21

Indications of amiodarone

Answer 21

Preventing recurrent VT
Adjuvant therapy in patients with ICD
Maintaining sinus rhythm in atrial fibrillation patients with structural heart disease

Question 22

Amiodarone cardiac toxicity

Answer 22

Symptomatic bradycardia and heart block in patients with preexisting sinus or AV node disease
Prolongs QT interval

Question 23

Amiodarone toxicity

Answer 23

Pulmonary fibrosis (dose-related)
Hypothyroidism or hyperthyroidism
Amiodarone has iodine in it, so you have to check the patient’s thyroid function every so often.
Abnormal liver function tests and hepatitis
Skin deposits, photodermatitis

Question 24

T/F: Sotalol is not cardioselective

Answer 24

T
 both class II and class III effects

Question 25

Sotalol route, half-life, excretion

Answer 25

oral, 12 hours, renal excretion

Question 26

Sotalol toxicity

Answer 26

further depression of LV function

Question 27

Sotalol use

Answer 27

life-threatening ventricular arrhythmias maintaining sinus rhythm in AF

Question 28

Class IV prototype

Answer 28

Verapamil

Question 29

Effects of verapamil

Answer 29

Block both activated and inactivated L-type Ca channels Prolongs AV nodal conduction time and ERP Slows the SA node Peripheral vasodilation

Question 30

Verapamil indication

Answer 30

Termination of SVT (if adenosine not available) | Control heart rate in AF

Question 31

Verapamil toxicity

Answer 31

Dangerous in patients with VT misdiagnosed as SVT, may cause hypotension and VF Negative inotropic effects Can induce AV block

Question 32

Adenosine half life

Answer 32

<10 seconds

Question 33

Adenosine cardiac effect

Answer 33

Marked hyperpolarization Suppression of Ca-dependent AP Directly inhibits AV nodal conduction

Question 34

DOC for prompt conversion of SVT to sinus

Answer 34

Adenosine

Question 35

Magnesium MOA

Answer 35

not well known

Question 36

use of magnesium

Answer 36

Digitalis-induced arrhythmias if low Mg | Torsade de pointes even if Mg normal (1g/IV)

Question 37

Main indication of digoxin

Answer 37

Slow the ventricular rate in chronic AF (not very effective in acute setting)

Question 38

MOA of digoxin

Answer 38

Slowing the sinus node discharge rate | Prolonging AV nodal refractoriness

Question 39

Toxicity of digoxin

Answer 39

Headache, nausea/vomiting, diarrheas and arrhythmias

Question 40

Pharmacologic Treatment of Arrhythmias

Answer 40

``` Eliminate the cause if possible Make a firm diagnosis Determine baseline condition Evaluate need for therapy Weigh benefits vs risks of therapy ```

Question 41

T/F Antiarrythmics can be proarrhythmics.

Answer 41

T