Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pharmacology > Drugs for Cardiac Dysrhythmia > Flashcards

Drugs for Cardiac Dysrhythmia Flashcards

1
Q

Sodium channel blockers - MoA

A

Slow phase 0 depolarization and cardiac conduction –> increases QRS duration.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Class I sodium channel blockers - MoA and subdivision

A

Bind to sodium channels when the channels are in the open and inactivated states, and dissociate from the channels during the resting state.

Subdivided into 3 gr based on whether they have greater affinity for the open state or the inactivated state and based on their rate of dissociation from sodium channels (rate of recovery).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Class IA drugs - MoA

A

Greater affinity for the open state and have slow recovery.

Block the fast sodium channel and delayed potassium channels –> they slow phase 0 depolarization and phase 3 repolarization in ventricular tissue. These actions decrease ventricular conduction velocity and prolong the ventricular action potential duration and refractory period –> increases QRS duration and prolong QT interval.
They suppress abnormal automaticity, but they usually do not affect SA node automaticity and HR.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Class IA drugs - Special consideration + Interactions

A

All of class IA drugs have some degree of antimuscarinic (atropine-like) activity and reduce vagal inh of SA depolarization and AV node. Conduction –> increased HR.

Alcohol
Serum level increased by: Carbonic anhydrase inhibitors, Erithromycin, Antacids, Cimetidine
Serum level decreases by Rifampin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Class IA drugs - Adverse effects

A

Prodysrhythmic effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Class IA drugs + greatest to least antimuscarinic effect

A

Quinidine**
Procainamide*
Disopyramide***

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Quinidine - Indication

A

Suppress supraventricular and ventricular arrhythmias

Combination with dextromethorphan for treatment of emotional lability (pseudobulbar affect) in patients with neurodegenerative disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Quinidine - Adverse effects

A

Diarrhea
Excessive QT prolongation (torsade de pointes) –> syncope and decreased CO
Thrombocytopenia
Neurologic symptoms due to overdose- cinchonism; tinnitus, dizziness and blurred vision.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Procainamide - MoA

A

Converted to active metabolite N-acetylprocainamide –> Class III antidysrhythmic properties.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Procainamide - Indication

A

Terminate wide QRS complex form of acute ventricular tachycardia and convert atrial fibrillation to sinus rhythm.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Procainamide - Adverse effects + Special consideration

A

Reversible lupus erythematous like syndrome, with arthralgia and butterfly rash

Pt with slow-acetylator phenotype develop lupus-like syndrome more often and earlier during treatment than do rapid acetylators.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Disopyramide - Indication

A

Prevent life threatening ventricular dysrhythmias; sustained VT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Disopyramide - Contraindication/Caution

A

It should not be used to treat asymptomatic ventricular dysrhythmias because of its protentional prodysrhythmic effect. It has negative inotropic and antimuscarinic effects and should be used with caution in pat with HF and elderly persons.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Class IB drugs - MoA

A

Greater affinity for inactivated sodium channels and have rapid recovery.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Class IB drugs

A

Lidocaine

Mexiletine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Lidocaine - MoA

A

Local anesthetic. More pronounced effect on ischemic tissue then normal tissue. In ischemic tissue; cells are partly depolarized because they lack sufficient adenosine triphosphate to operate the sodium pump –> sodium channels in ischemic tissue spend more time in the inactivated state.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Lidocaine - Indication

A

Refractory ventricular tachycardia.

Ventricular arrhythmias during/after cardiac surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Lidocaine - Adverse effects and Interactions

A

CNS; nervousness, tremor, paresthesia.
Cardiac arrest

Toxic dose: slow cardiac conduction velocity –> cardiac arrest

Drugs that inhibit cyt P450; cimetidine, can increase levels and cause toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Mexiletine - MoA

A

Greater effect on normal cardiac tissue. Slows conduction in the heart and makes it less sensitive.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Mexiletine - Indication

A

Suppression of symptomatic ventricular tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Class IC drugs - MoA

A 
Have greater affinity for the open state and a very slow recovery.
Block both fast sodium channels and the rate of rise of the action potential during phase 0 to a greater extent than other class I drugs --> slow conduction throughout the heart and especially in the His-Purkinje system.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Class IC drugs

A

Flecainide

Propafenone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Flecainide

Propafenone - MoA

A

Also inhibit the potassium rectifier current (IKr) in ventricular tissue –> increases QT interval, but rarely cause torsades de pointes.
Prolongation of PR interval and QRS duration.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Flecainide - Indication

A

Supraventricular dysrhythmias

Documented life threatening ventricular dysrhythmias.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Flecainide - Adverse effects
VT | Brochospasm, leukopenia, thrombocytopenia, seizure
26
Flecainide - Special consideration
Increases mortality in pt who had experienced a MI
27
Propafenone - Indication
Long term; suppress supraventricular tachycardia and atrial fibrillation. Life threatening forms of ventricular dysrhythmias such as sustained ventricular tachycardia.
28
Propafenone - Adverse effects
Ventricular dysrhythmias, hematological abnormalities: agranulocytosis, anemia and thrombocytopenia.
29
Class II drugs - MoA
beta-adrenoceptor antagonists. Antiarrhythmic effect because of their ability to inhibit sympathetic activation of cardiac automaticity and conduction. They slow the HR, decrease AV node conduction velocity and increase AV node refractory period.
30
Class II drugs - Indication
Prevent and treat supraventricular dysrhythmias and to reduce ventricular ectopic depolarizations and sudden death in patients with MI
31
Class II drugs
Esmolol Metoprolol Propranolol
32
Esmolol - Indication
Acute supraventricular tachycardia & Ventricular arrhythmia Hypertension during or after surgery
33
Metoprolol and Propranolol - Indication
Suppress supraventricular and ventricular dysrhythmias | + In pat with MI; metoprolol is given IV during early phase of treatment
34
Class III drugs - MoA
They cause prolongation of the ventricular action potential duration and refractory period. Act by blocking potassium rectifier currents that repolarize the heart during phase 3 of the action potential (except Amiodarone)
35
Class III drugs
``` Amiodarone Dronedarone Dofetilide Ibutilide Sotalol ```
36
Amiodarone - MoA
Blocks potassium, sodium and calcium channels + beta-adrenoceptors. Decreases SA node automaticity, decreases AV node conduction velocity and prolongs AV node and ventricular refractory periods. Increases PR interval and QT interval and causes a slight prolongation of the QRS duration. Powerful inhibitor of ectopic pacemaker automaticity, and prolongs repolarization and refractory periods throughout the heart.
37
Amiodarone - Indication
Suppress supraventricular and ventricular dysrhythmias, incl atrial fibrillation, atrial flutter, supraventricular tachycardia and VT Effective adjunct to implantable cardioverter-defibrillators to reduce nr of shocks required to maintain sinus rhythm.
38
Amiodarone - Adverse effects
Bradycardia Impaired AV conduction QT interval prolongation --> torsades de pointes Corneal microdeposits Photosensitivity to UV light Blue-gray skin discoloration Hypothyroidism (managed w levothyroxine replacement therapy) Hyperthyroidsm Tremor, ataxia and optic or peripheral neuropathy Pulmonary fibrosis --> may be fatal.
39
Amiodarone - Interactions
Elevate plasma levels of: digoxin, Flecainide, phenytoin, procainamide, warfarin --> by inh P-glycoprotein mediated drug transport. Interacts w inhalation anesthetics and CNS depressants --> increases incidence of adverse cardiovascular effects like bradycardia contra: pregnancy
40
Dronedarone - Indications
Prevention of dysrhythmia in persons w paroxysmal atrial fibrillation or flutter
41
Dronedarone - Adverse effects and Contraindications
Liver injury Increase mortality pt w HF Contraindications: permanent atrial fibrillation, pt w HF must be monitored every 6 months. Pregnancy
42
Dofetilide - MoA
Selectively block the rapidly activating delayed rectifier channel (IKr) responsible for repolarizing (rectifying) myocardial tissue during phase 3 of the action potential. By inh this outward potassium current --> prolongation of ventricular repolarization and increases refractory periods and QT interval of the ECG.
43
Dofetilide - Indications
Convert atrial fibrillation, long term suppression of dysrhythmia
44
Dofetilide - Adverse effects
QT-prolongation | torsades de pointes
45
Ibutilide - MoA
Activates the slow (late), inward sodium current --> increases sodium influx and counteracts the outward potassium current so as to slow atrial and ventricular repolarization.
46
Ibutilide - Indication
Rapid conversion of atrial fibrillation or flutter to normal sinus rhythm. Before cardioversion in pt that do not respond to cardioversion alone
47
Ibutilide - Adverse effect + Contraindication
Can induce torsades de pointes Contra: in pat with prolonged QT interval (QTc>440 ms) and polymorphic VT.
48
Sotalol - MoA
Nonselective B-antagonist, that prolong the cardiac action potential duration and QT interval by blocking the delayed potassium rectifier current during Phase 3 of ventricular action potential. Decreases HR, slows AV node conduction velocity and increase AV node refractory period without affecting the ventricular conduction and QRS duration Modest (-) inotropic effect
49
Sotalol - Indication
Supraventricular dysrhythmias Rhythm control in persons w atrial fibrillation and flutter Adjunctive therapy in pt w implantable cardioverter-debrillator (facilitates defibrillation by lowering the defibrillation threshold and decreases nr of shock required. Ventricular dysrhythmia
50
Sotalol - Lower dose VS higher dose
Lower dose: acts through beta-receptor blockade | Higher dose: Class III action and prolongation of ventricular repolarization
51
Sotalol - Adverse effects
``` Bradycardia Bronchospasm Dyspnea Pulmonary edema and heart failure Dose dependent torsades de pointes ```
52
Class IV drugs
Diltiazem | Verapamil
53
Class IV drugs - MoA
Decrease AV node conduction velocity and increase AV node refractory period. Smaller effect on SA node and HR
54
Class IV drugs - Indication
Controlling/converting supraventricular dysrhythmias Control ventricular rate in pt w atrial fibrillation or flutter and a rapid ventricular response. Verapamil (IV): Terminate paroxysmal supraventricular tachycardia
55
Class IV drugs - Adverse effects
Exacerbate wide QRS complex VT- must be diagnosed before giving the drugs
56
Miscellaneous drugs
``` Adenosine Digoxin Magnesium sulfate Ivabradine Ranolazine ```
57
Adenosine - MoA
Derived from ATP and activates specific G protein-coupled adenosine receptors. Stimulation of these receptors leads to activation of acetylcholine sensitive potassium channels and blockade of calcium influx in the SA node, atrium and AV node. Causes cell hyperpolarization, slows AV node conduction velocity and increases AV node refractory period. Av node conduction can be completely blocked for few seconds --> brief period of asystole
58
Adenosine - Indication
Terminate supraventricular tachycardia by preventing retrograde conduction of reentrant impulses through AV node. Cardioversion Terminate acute PSVT including Wolff-Parkinson white syndrome
59
Adenosine - Adverse effects and Interactions
Bronchospasm Vasodilatory effects: facial flushing, rash, diaphoresis Metallic taste Dipyridamole inh cellular uptake and increases its cardiac effects.
60
Digoxin - Indication
Slow ventricular rate in atrial fibrillation
61
Magnesium sulfate - Indication and Adverse effect
Suppress drug induced torsades de pointes, treat digitalis induced ventricular dysrhythmias and supraventricular dysrhythmias associated with magnesium deficiency. Low BP Skin flushing Low blood calcium
62
Ivabradine - MoA
Blocks funny current in the SA node which is a mixed Na/K inward current that is activated by hyperpolarization, modulated by the autonomic nervous system and responsible for diastolic depolarization and cardiac impulse initiation.
63
Ranolazine - MoA
Blocks late sodium current in ventricular tissue
64
Ivabradine and Ranolazine - Indication
Angina pectoris Heart failure Inoperative sinus tachycardia
65
Ivabradine and Ranolazine - Adverse effects
Excessive bradycardia | Slow AV conduction in some patients.

Pharmacology (55 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions