Antiarrhythmics pt 2

Question 1

what phase is being prolonged, what channels, and what class of drugs cauase this?

Answer 1

phase 0: fast action depoloarization in the myoctes

Na blocking drugs

class I (abc)+class III drugs

Question 2

Left to right

Answer 2

A. class 1a: QRS increased; QT increased ; AP increased; ERP increased

B. class 1b: QRS no change; QT decreases; ERP+AP both decrease

c. class 1c: QRS increases; QT no change; ERP+AP no change

red line = after drug administration

Question 3

which class 1 drug effects sodium channels largely during their depolarized state?

Answer 3

class 1b: bind above 0mv

RAPIDLY unbinds- unbound by the time the next impulse arrives; therefore works better in fast heart rates

Question 4

which drug can be used to treat re-entry and what is the MOA of this induced state?

Answer 4

Re-entry occurs when there is an accessory route refracting a depolarizing wave back to the atria: lidocaine inhibits this “two way” electrical route and permits only unidirectional electrical flow.

re-entry pathways look like this

unidirectional (normal)–> bidirectional (pathological)

Question 5

which class 1 causes CNS toxicity? what is its bother AE?

Answer 5

class1b: tremor and agitation

class 1b also causes heart block, bradycardia

Question 6

MI-associated arrhythmia and Ic drugs

Answer 6

CAST trial showed almost 4x mortality in patients using class 1c antiarrhythmics following MI: DONT USE THEM

therefore ONLY USE DRUG IN NORMAL HEARTS

Monitor patient so QRS does NOT PROLONG

Question 7

bradycardia vs tachycardia: which of these conditions will class 1 drugs be beneficial?

Answer 7

tachycardia for class 1 drugs: they all have USE-dependence but especially class 1c drugs, meaning they only act when the channels are open/activated

Question 8

which drug class causes these changes?

Answer 8

K+ (repolarization) channel blockers: class III: amidarone, sotalol, dofetilide, ibutilide

Question 10

torsade de pontes

Answer 10

may be induced by class III and Class 1a because these drugs prolong AP, therefore QT interval

Question 11

prolongs QRS, slows AV conduction, slows HR

Answer 11

Amiodarone: has class I (prolonged class I character), class II+IV (delays HR and AV conduction) characteristics.

Amiodarone is the class III drug with the lowest risk of TDP induction torsade.

Question 12

half life of amiodarone

Answer 12

58 days; lipid soluble, so accumulates in tissues

Question 13

Answer 13

amiodarone: photosensitivity to sun is the most common affect of amiodarone

Question 14

Answer 14

least common side effect of amidarone: blue man syndrome

Question 15

Answer 15

pulmonary fibrosis- SE of amiodarone, “honeycombing” cxr: foamy macrophages fllled with phospholipids

Question 16

tests needed for px on amiodarone

Answer 16

LVTs, TFTs, PFTs

Question 17

class III drugs for cardiomyopathy

Answer 17

sotalol, dofetilide: they have reverse use dependence; this permits them to bind during the potassium resting state, when they aren’t in use. They have the greatest effect in bradycardic patients

Question 18

Ibutilide

Answer 18

Class III drug, Intravenous (Ibut..), 2-4 hr half life, used predominantly for cardioversion

terminates arrhythmia but can induce torsades

Question 19

Answer 19

Class II drugs (beta blockers)

Question 20

Answer 20

class II drugs (BB): blue is before red is after

Question 21

AV block drugs

Answer 21

Class II BB and Class IV CCBs: decrease AV conduction –> type 1 AV block or type II (Mobitz 1; wenckebach)

used soley for anti-arrhythmic rates

Question 22

VTac/Vfib–>SCD. which drug would decrease rates of SCD among antiarrhythmics?

Answer 22

beta blockers: they not only slow AV conduction down but also work on ventricular myocytes as well, so they improve outcomes for patients.

Question 23

Answer 23

adenosine

Question 24

adenosine receptors, use, and mode of delivery, SE

Answer 24

located in the AV node and blood vessels

used for AVNRT (most common SVT)

used via IV

because of vascular receptors–> vasodilation, flushing

Question 25

Magnesium

Answer 25

only used in Trsades: blocks calcium influx during phase 2

Question 26

Answer 26

atropine: can be used as an anti-arrhythmic.

Hot as a hare: increased body temperature
Blind as a bat: mydriasis (dilated pupils)
Dry as a bone: dry mouth, dry eyes, decreased sweat
Red as a beet: flushed face
Mad as a hatter: delirium

Question 27

adenosine block

Answer 27

theophylline and caffeine

Question 28

patient has reduced EF: this drug is available. what is it?

Answer 28

digoxin

Question 29

what is the outcome and drug used in this scene?

Answer 29

digoxin; increases contractility by decreasing Ca2+ loss by inhibiting K/Na ATPase

in other words, more Calicum inside myocyte

Question 30

Answer 30

second MOA of Digoxin (not the same as the Na/K pump inhibitor

Question 31

hypokalemia and renal clearance

Answer 31

digoxin: patients will need K sparring diuretics

Question 32

GI: N/V

Neuro: confusion/delerious

Visual changes: scotomas, blindness

Answer 32

digoxin

Question 33

Answer 33

digoxin

Question 34

Answer 34

digoxin toxicity

Question 35

Fab binding, produced by sheep, bound to albumin as haptan –> leading to antibody against ____

Answer 35

Digibind: synthetic anitbody that binds digoxin and corrects HYPERkalemia.

Digoxin can cause both hyperkalemia and hypokalemia

Question 36

A rapid form of polymorphic VT associated with the evidence of prolonged
ventricular repolarization (long QT syndrome).

Answer 36

torsades de pontes: class 1a and class III drugs may induce, amiodarone has the lowest risk

Question 37

a triggered activity resulting from
early afterdepolarizations

Answer 37

torsades: a triggered activity resulting from early afterdepolarizations that prolongs the QT interval
1. Triggered activity: depolarizing oscillations in the membrane potential induced by the preceding action potentials
2. Early afterdepolarizations:

• Often associated with the impaired function of potassium channels leading to a prolonged period of repolarization
• Abnormal depolarizations occur during phase 2 or phase 3 of AP
  
  • due to the opening of Ca2+ (2) or Na+ (3) channels, respectively

Question 38

A type of a triggered activity resulting from delayed afterdepolarization

Answer 38

1. Digoxin:
   
   1. Occur during phase 4
      
      1. results from increased cytosolic Ca2+ due to Ca2+ overload
   2. Spontaneous Ca release from SR
      
      1. activates 3Na+/Ca2+ exchange leading to a net depolarizing current

Question 39

Atrial fibrillation RATE control: mnenomic

Answer 39

• Atrial fibrillation:
  
  • Ventricular rate control
    
    • Calcium channel blockers
    • Beta-blockers
    • Digoxin
    • Amiodarone
  • “D CABs are slower”

Question 40

Paroxysmal/Persistant AF: Step 1 –> two PWs + the “goal” of this tx

Answer 40

1. assess liver function —>
2. No HF and LVEF is = or > 40%
   
   1. –> CCB or BB
      
      1. Worked? No–> CCB AND Digoxin or BB and Digoxin
         
         1. Worked? No–> Amiodarone
3. HF + LVEF less than 40%
   
   1. bb
      
      1. worked? no–> bb + digoxin
         
         1. worked? no –> amiodarone
4. Goal less than 100 bpm or 20% reduction rate reduction with symptom relief.

HINT: Heartfailure + is treated the same way as heartfailure - but without the CCB. End of.

Question 41

Rhythm control (conversion to sinus rhythm)

Answer 41

1. Rhythm control (conversion to sinus rhythm)
   
   1. Cardioversion using direct current cardioversion
   2. Pharmacologic (chemical) cardioversion
      
      1. Amiodarone
      2. Flecainide
      3. Dofetilide
      4. Ibutilide
      5. Propafenone
   3. “I FAPD”

Question 42

Maintenance of sinus rhythm after the conversion to sinus rhythm

Answer 42

1. Maintenance of sinus rhythm after the conversion to sinus rhythm: FAPD + drone + soda + catheter ablation
   
   1. Dronedarone
   2. Flecainide
   3. Propafenone
   4. Sotalol
   5. Amiodarone
   6. Dofetilide
   7. Catheter ablation
2. All the drugs used for cardioversion EXCEPT ibutilide
3. New additions include dronedarone, sotalol, and catheter ablation

Question 43

Decision algorithm for conversion of hemodynamically stable AF to sinus rhythm

Answer 43

1. 2. 1. AF < or equal to 40 hrs
      2. direct current cardioversion
         
         1. feasible/desirable?
            
            1. no
               
               1. No HF and LVEF > or = 40%?
                  
                  1. yes
                     
                     1. IFAPD
                  2. No​​​​
                     
                     1. IDA

Question 44

AFIB: which two things do you need to control

Answer 44

Ventricular rate (D-CAB), SA rhythm (I FAPD)

Question 45

SVT

Answer 45

1. Paroxysmal supraventricular tachycardia
   
   1. termination
      
      1. – Adenosine
      2. – Verapamil or diltiazem
      3. – Beta-blockers
      4. – Digoxin
      5. – Amiodarone
   2. Prevention
      
      1. – Verapamil
      2. – Digoxin
      3. – Catheter ablation

Question 46

PSVT termination

Answer 46

1. PSVT
   
   1. Vagal maneuvers. Worked?
      
      1. No–> adenosine
         
         1. Worked? No–>
            
            1. No HF and LVEF above/equal to 40%?
               
               1. Yes–> Verapimil + Diltiziem
                  
                  1. worked? no–> BBlocker
                     
                     1. worked? no –> digoxin
               2. No–> Digoxin
                  
                  1. worked? no –> amiodarone
                     
                     1. worked? no–> diltiazam
                        2.

Question 47

Tx for AV block

Answer 47

1. mostly asymptomatic, just monitor
2. Acute high grade AV block that is symptomatic
3. atropine–> epinephrine if needed
4. Long-standing AV second or third degree block–> if patient is on drugs, discontinue them –> pacemaker if that doesnt work

Question 48

Polymorphic Ventricular Tachycardia

Answer 48

Torsades

1. if drug induced, discontinue
2. if hemodynamically unstable, DCC
3. if hemodynamically stable:
   a. correct electrolyte imbalance
   b. MgSulfate (regardless of Mg status)
   c. Transvenous temporary pacemaker for overdrive pacing or isoproterenol i.v.

Question 49

Polymorphic Ventricular Tachycardia: prevent

Answer 49

1. prevent QT prolongation
2. Do not give TdP-inducing drugs if QTc is >450 ms
3. If a completely reversible cause cannot be identified, consider
   implantation of ICD (implantable cardioverter defibrillator)

Question 50

1. Tx Digoxin overdose Digoxin-induced arrhythmias
   
   1.  Cancel digoxin
   2.  Anti-digoxin antibodies (Digibind, Digifab)
   3.  Potassium supplementation to upper normal levels