Antiarrhythmics

Question 1

Name the 4 Classes of Antiarrhythmic drugs.

Answer 1

Sodium Channel Blockers, BBs, Potassium Channel Blockers, CCBs (Specifically Verapamil and Diltiazem).

Question 2

Key to understanding Antiarrhythmic agents is what?

Answer 2

Depolarization and Repolarization of the myocyte.

Question 3

Class I Antiarrhythmics are which drugs and block which channels?

Answer 3

Voltage gated fast sodium channels responsible for upstroke in Phase 0. This decreases the slope and velocity of Phase 0. You cannot forget that they also block Potassium channels that mediate Repolarization at phase 3.

Question 4

Sodium channels fluctuate between which 3 states? Class IA bind the channel during which state?

Answer 4

Resting, Open, then Closed. Quinidine, Procainamide, and Disopyramide bind channels in the Open state.

Question 5

Class IB Antiarrhythics bind sodium channels during which states?

Answer 5

Both Open and Closed states.

Question 6

Class IC Antiarrhythmics are potent blockers of which state?

Answer 6

Open state, and take the longest to dissociate.

Question 7

Class IA Sodium channel blockers are especially helpful for which cardiac condition?

Answer 7

SVT or Vtach

Question 8

ADRs of Class IA Antiarrhythmics are very High Yield. What are Tinnitus, HA, and visual problems, possible hearing loss part of?

Answer 8

Cinchonism.

Question 9

Describe Cinchonism and DIL. Which drugs in Class IA can have these adverse effects on the pt?

Answer 9

Cinchonism is HA, tinnitus, hearing, loss, visual changes. DIL has fever, arthralgias, myalgias, rash.

Question 10

What can Disopyramide cause as an adverse effect? And what can all 3 of Class IA cause?

Answer 10

Disopyramide can result in Heart Failure. All three can cause the fatal Torsades de Pointes due to the QT prolongation that occurs by blocking the repolarization of the Potassium channels at Phase 3.

All 3 can also cause Thrombocytopenia, tho mechanism is not well understood.

Question 11

Which drugs fall under Class IB Sodium Channel Blockers and what is their mechanism?

Answer 11

Lidocaine and Mexiletine. (Technically also Phenytoin but it is more of an antiseizure drug). These drugs shorten the action potential.

Question 12

When do we clinically prefer to use Class IB antiarrhythmics?

Answer 12

Especially post-MI and Digitoxin induced arrhythmias. Also used in Acute Vtach.

Question 13

1B is Best Post-MI is to remind you of what?

Answer 13

That Lidocaine and Mexilitine are the DOC for post-MI or ischemic pts.

Question 14

What is a serious potential adverse effect of Class IB drugs?

Answer 14

Anytime there is too much sodium, there is a risk of Cardiovascular depression. Both are also very lipophilic and can stimulate or depress the CNS as well.

Question 15

Which of the Class IB Antiarrhythmics is classically known for triggering seizures?

Answer 15

Lidocaine think Seizures.

Question 16

Flecainide and Propefenone are rarely used clinically due to dangerous side effects. Which class of drugs is this?

Answer 16

Class IC. NEVER GIVE POST-MI. Can cause serious arrhythmias.

Question 17

Post MI you want to decrease the ARP by using what class of drugs?

Answer 17

A class IA drug will prolong the ARP because it increases the action potential (AP) duration. A class IB drug will decrease the AP and therefore decrease the ARP. A class IC drug will not change the ARP. Regardless of ARP action, all class I drugs decrease the slope of phase 0.

Question 18

Describe the G protein pathway of Beta blocking in the heart.

Answer 18

β-Receptor antagonists work by inhibiting β-receptors, hindering the G-protein/cAMP mechanism. By reducing the amount of cAMP and protein kinase A (PKA) produced, β-receptor antagonists decrease the Ca2+ currents within the AV node. (Decreased production of cAMP and PKA reduces the Na+ current via phosphorylation-mediated downregulation of expression and other mechanisms)

Question 19

In which phase do BBs decrease the slope? How do BBs affect the HR?

Answer 19

β-receptor antagonists decrease the slope of phase 4 and phase 0. β-Receptor antagonists are known to slow the heart rate (negative chronotropic effect).

Question 20

Describe the phases of the AV node cardiac potential.

Answer 20

Phase 0: L-type calcium channels open, causing depolarization.
Phases 1 and 2 are absent.
Phase 3: Potassium channels open, causing repolarization. These channels can be affected by a number of pharmacologic mechanisms.
Phase 4: Funny channels with a slow leak of potassium out of the cell cause a transient depolarization toward threshold.

Question 21

How do Beta blockers affect cAMP and Protein Kinase A?

Answer 21

β-Receptor antagonists cause a decrease in cAMP.

β-Receptor antagonists cause a decrease in PKA.

Question 22

What does Torsades de Pointes look like on ECG?

Answer 22

Google images.

Question 23

ADRs of Adenosine?

Answer 23

Adenosine is not known to cause TdP. Causes flushing, dyspnea, and chest pain, as well as high-grade atrioventricular (AV) block.

Question 24

Esmolol is known for…

Answer 24

Esmolol is extremely short acting (15–20 minutes) BB, so it has few major adverse effects

Question 25

Lidocaine toxicity cardiac associations...(ignore the seizures for a second ;)

Answer 25

ADRs of lidocaine are third-degree AV heart block, altered AV node conduction, and depressed SA node automaticity.

Question 26

Propranolol can cause what on the heart...

Answer 26

Bradycardia and HoTN.

Question 27

Side effects of verapamil include...

Answer 27

Bradycardia, dizziness, and transient hypotension, if it is administered without calcium pretreatment.

Question 28

Name drugs most commonly associated with causing TdP's fatally rapid ventricular rhythm by elongating the QT interval (by blocking K+'s repolarization in Phase 3 of the slope)

Answer 28

Procainamide, Quinidine, fluoroquinolones, amiodarone, sotalol, tricyclic antidepressants, risperidone, SSRIs, methadone, ondansetron, and erythromycin.

Question 29

What is a typical rate for Torsades?

Answer 29

Fatally rapid ventricular rate is variable between 250 and 350 and is usually transient.

Question 30

Causes of TdP?

Answer 30

Low potassium level and potassium channel blockers such as Amiodarone or Sotalol. It can also occur as a result of congenital abnormalities, such as long QT syndrome. Administration of quinidine. Quinidine is a class Ia sodium channel blocker. It also has a concentration-based potential to block potassium channels, extending the QT interval and causing torsades. This can occur at even subtherapeutic levels.

Question 31

Amiodarone's MOA is prolonging phase 3 repolarization of potassium, but also affects other phases. Most high yield however are its toxicities...

Answer 31

Pulmonary fibrosis, hepatotoxicity, and hypothyroidism or hyperthyroidism. And Corneal deposits. Blue/gray skin deposits, photodermatitis. In pts taking Amiodarone, remember to check pulmonary function, liver function, and thyroid function tests.

Question 32

If defibrillation convert the Vtach to sinus rhythm...what do we give the pt according to ACLS?

Answer 32

Epinephrine followed by Amiodarone.

Question 33

What Sxs are suggestive of DIL? Which medications can induce it?

Answer 33

Pleuritic chest pain, a right pleural effusion, and positive antinuclear antibodies and antihistone antibodies (but not anti-double-stranded DNA [anti-dsDNA] antibodies). A collection of fluid around the lungs or heart. Other Sxs include fever, fatigue, myalgia, rash, arthralgia, and arthritis.

Question 34

SHIPPPEM mnemonic.

Answer 34

Sulfa drugs, Hydralazine, Isoniazid, Procainamide, Penacillamine, Phenytoin, Etanercept, Methyl-Dopa.

Question 35

Adenosine is a very short-acting drug useful in terminating certain forms of SVT by hyperpolarizing the cell and decreasing atrioventricular (AV) node conduction. Adverse Effects are...

Answer 35

Flushing, hypotension, chest pain, bronchospasm, and a sense of impending doom

Question 36

MOA of Ivabradine and what is its special clinical use?

Answer 36

is used to treat stable angina in patients who cannot take β-blockers. It works by inhibiting funny channels, thus prolonging phase IV of the cardiac action potential.

Question 37

DOC for Paroxysmal SVT? What are its ADRs?

Answer 37

Adenosine. Flushing, Chest pain, Bronchospasm, Impending doom, Coronary Steal Syndrome.

Question 38

What is Adenosine's structure and which 2 other chemicals have a similar structure and can inhibit its effects?

Answer 38

Purine structure. Caffeine and Theophylline (asthma drug) are also purines and can inhibit the Adenosine receptor.

Question 39

Ivabradine's MOA?

Answer 39

Inhibits funny Na+ channels in Phase 4, thereby slowing down SA nodal firing and depolarization.

Question 40

What are Ivabradine's clinical uses?

Answer 40

Treatment of angina in those who are not able to take beta blockers. May also be used in HF. But Ivabradine is not involved in contractility, just chronotropy.

Question 41

What are the ADRs of Ivabradine?

Answer 41

Visual light disturbances. And due to slowing of SA node, could cause possible bradycardia or reflex increase in BP.

Question 42

Mg++ is whose babysitter and how so?

Answer 42

Mg is K+'s babysitter in that whenever Potassium is abnormal, Mg is given to adjust the situation. Mg helps eliminate K+ in the urine and is a cofactor for the ubiquitous Na-K+ ATPase.

Question 43

What are two serious events in which Mg++ is given as an antiarrhythmic?

Answer 43

1. TdP! 2. Digoxin toxicity - to stimulate the action of Na-K ATPase being inhibited by digoxin.

Question 44

How does Adenosine cause bronchospasm?

Answer 44

Adenosine can cause mast cell degranulation in the lungs and thereby leading to the anaphylactic response.

Question 45

What is an ideal antiarrhythmic for Wolff-Parkinson-White?

Answer 45

Ibutilide or Sotalol but these are also infamous for causing TdP.