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cardio boards > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

What phase of action potential is depolarization and what current affects this phase?

A

Phase Zero

Influx of Na current

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2
Q

What current makes up phase one of action potential?

A

Outward potassium via Ito current

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3
Q

What current(s) contribute to phase 2 of action potential?

A

Competition between inward calcium and outward potassium

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4
Q

What makes up phase three of action potential?

A

Efflux of K via IKr and IKs

-help get membrane back towards resting

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5
Q

What makes pacemaker cells different?

A

Automaticity via If (funny current)

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6
Q

Explain “reverse use dependence” in reference to IKr channels and how it differs from IKs.

A

By blocking either of these -> prolong phase 3 -> prolong QT, but when bradycardia repolarization mostly via IKr therefore if block IKr and are Brady -> very vulnerable for TdP

IKs contributes to repolarization as Hr increases

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7
Q

What occurs with 5CN5A up regulation vs blocking?

A

Up regulating -> long QT3 with increasing INa current

Blocking -> Brugada

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8
Q

What genes are affected, how are the genes affected and what currents are effected in:
Long QT type 1 - 3

A

Long QT1 = block KCNQ1 = IKs

Long QT2 = block KCNH2= heRG = IKr

Long QT3 = up regulates 5CN5A = INa

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9
Q

What is “early after depolarization”?

A

When action potential is prolonged so L-type Ca channels reopen during QT -> re-depolarization -> TdP
-dealing with IKr sonusually when Brady

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10
Q

What happens to the action potential/currents in Brugada?

A
  1. Impaired Na current -> decrease phase zero
  2. ItO is enhanced
  3. Mismatch voltage phase 1/early phase 2 -> coved ST
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11
Q

What medication can be used to treat Brugada and why?

A

Quinidine because it blocks ItO

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12
Q

These are Class 1 A antiarrhythmics:

How do they work and what can they cause?

A

Quinidine, procainamide, disopyramide

  • Na blockers
  • prolongs QT
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13
Q

These are Class 1B antiarrhythmics:

A

Lidocaine, mexiletine

  • Na blockers
  • no affect on atrial tissue
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14
Q

These are Class 1 C antiarrhythmics

  1. What do they do?
  2. How do they affect the QRS
  3. His are they affected by HR?
A

Flecainide, Propafenone

  • Na blockers
  • QRS prolonged -> AV block, cause AFib -> 1:1 Slow Aflutter (looks like VT)
  • use dependent = increase drug affect at higher HRs therefore must give with B.B. or CCB (only really with Flecainide because propafanone has some intrinsic BB)
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15
Q

Class 3 antiarrhythmics, what do they block?

-how are they affected by HR?

A

Sotalol, dofetilide, ibutilide

  • K channel blockers (IKr/IKs)
  • Reverse use dependence = increased drug affect at lower HRs -> TdP
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16
Q

Tx AFib with antiarrythmkics

  1. If no structural heart disease
  2. If LVH (>1.5cm)
  3. If CAD
  4. If CHF
A
  1. Dofetilide, dronedarone, flecainide, propafanone, Sotalol
    - if don’t work them Amio/ablation
  2. Dronedarone
    - if don’t work then Amio/abl
  3. Dofetilide, dronedarone, Sotalol
    - no type 1C
    - if don’t work then Amio/abl
  4. Amio, dofetilide
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17
Q

Dronedarone:

  1. How is metabolized
  2. What happens to pt’s labs and what do you do about it?
  3. Which patients do you avoid giving to?
  4. What important substrate does it inhibit?
  5. What can it Tx and cannot Tx.
A
  1. Metabolized through the liver
  2. Will increase Cr but artifactually so don’t do anything about it
  3. Don’t use in CHF patients or patients with permanent AFib
  4. Blocks p-glycoprotein
  5. Only affective for Tx AF/Afl, not affective on VT/VF
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18
Q
  1. Which medications are metabolized via CYP3A4?
  2. Which inhibit it?
  3. Which induce it?
A
  1. Amio, dronedarone, quinidine, dofetilide, lido/mex, Xarelto/eliquis, simva/Atorva/lovastatins
  2. Verapamil, HIV PI, erythromycin, -azoles
  3. Rifampin, antieplieptics
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19
Q
  1. What medications are metabolized via CYP2D6?
  2. Which inhibit it?
  3. Which induce it?
A
  1. Propafanone, flecainide, mexiletine, metop/Tim/propranolol, codeine
  2. Quinidine, propafanone, dronedarone
  3. Rifampin
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20
Q
  1. Which medications are metabolized via p-glycoprotein?
  2. Which inhibit it?
  3. Which induce it?
A
  1. Digoxin, dabigatran (pradaxa)
  2. Amio, dronedarone, quinidine, erythromycin
  3. Rifampin, HIV PI
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21
Q

Treatment for bidirectional VT 2/2 Digoxin toxicity and why?

A

Lidocaine NOT Amio because Amio blocks pglycopro which will therefore increase dig levels

22
Q

Quinidine side effects:

A

Diarrhea, thrombocytopenia, cinchonism (tinnitus)

23
Q

Antiarrhythmics Treatment for AFib with WPW?

-what are some side effects of this drug?

A

Procainamide

-> lupus like reaction, TdP/LQT, induce Brugada

24
Q

Disopyramide:

  1. What class medication?
  2. What can it be used to treat?
  3. What are it’s side effects
  4. What type of patients should you avoid giving this medication to?
A
  1. Class 1A (Na blockers)
  2. Tx vagally mediated AFib, HOCM (b/c strong negative ionotrope)
  3. Anticholinergic therefore -> dry mouth, urinary retention ect.
  4. Avoid in pt with glaucoma, BPH and CHF
25
Q

What antiarrhythmics can be used to treat congenital LQT3?

A

Mexiletine (Na blocker)

B.B. are controversial

26
Q

Flecainide:

  1. Which patients can use this medication in?
  2. Which patients to avoid giving this medication to?
  3. Side effect of med?
A
  1. SVT, WPW, AFib, pregers
  2. Cannot use in pt with MIs or significant CAD (may need to do stress test before starting)
  3. Paresthesia, diplopia, CP
27
Q

Dofetilide:

  1. What class is it?
  2. Who can use this medication in
  3. How is it excreated
  4. Which medications are contraindicated with it?
A
  • Class III, pure IKr blocker
  • Tx persistent AF, can use in CHF and CAD patients, just not LVH
  • renally excreted (cant give if CrCl <20)
  • verapamil and thiazides (cautious with dig and metformin)
28
Q

What is biggest concern with AVNRT ablation?

A

Causing AV block requiring a PPM

-occurs <1%

29
Q

Wpw

  1. How do you know where pathway is coming from?
  2. What to do if Asymptomatic?
A
  1. If V1 looks RBBB then pathway on left. If II, III, aVF neg then it is coming from inferior/posterior vs superior/anterior
  2. If Asymptomatic put on treadmill and if delta disappears then it’s a weak pathway so just observe. Consider EP study and if leads to worrisome AFib then ablate.
30
Q

Pre-excited Afib:

  1. When do you worry?
  2. How to treat?
  3. Which medications to avoid and why?
A
  1. R-R <250msec = increase risk for VF
  2. If stable Tx Ibutilide or procainamide
    If plan to abl, abl accessory pathway not pulm veins
  3. Do not use Amio/B.B./CCB because impacts AV node and would then increase condition in accessory pathway -> VF or if drops BP -> increase catecholamines -> increase HR -> increase conduction down accessory pathway.
    Do not use digoxin because shortens refractory period in accessory pathways so increase conduction down it.
31
Q

SVT treatment in pregers:

A

Of unstable always cardiovert.
If stable/chronic Tx use dig, metop, propranolol, Sotalol, verapamil
-if no structural heart dz can use flecainide or propafenone.

32
Q

What is the reversal agent for dabigatran?

A

Idarucizumab

33
Q

What is the reversal for Xa blockers?

A

Andexanet

34
Q

Healthy patient with afib s/p DCCV was doing well for a few weeks but now developed SOB found to have rate controlled AFib. What should be the next step in treatment?

A

Start Flecainide and repeat DCCV!

- starting antiarrhythmics is Is recommendation while ablation is IIb, so first try meds!

35
Q

Patient had an ablation a few months ago and now presents with cough and hemoptysis?

  1. What are you concerned about?
  2. What imaging do you order?
A
  1. Worries about pulm vein stenosis post AFib abl. Occurrs 1% time
  2. Order CTA IMRA
36
Q

Complications of AFib ablation:

A
  1. 1% pulm vein stenosis -> cough/hemoptysis 1-6 mo post abl
    - check CTA IMRA
  2. 1% tamponade
  3. 0.5-1% stroke
  4. 1/500 right phrenic nerve injury-> dysphasia
    - check CXR, see elevated diaphragm
  5. 1/1000 LA-Esoph fistula -> symptoms 1mo post abl
  6. If clot forms at pulm vein -> pulm infarct
37
Q

How do Amio and digoxin interact?

A

Amio blocks Pglycopro so it will block dig excretion and increase dig levels

38
Q

What is sinus pause vs sinoexit block?

A

Sino-exit block = multiple of R-R while sinus pause is not

- p waves are not present in either

39
Q

If do carotid massage and AV block improves is this a good or bad sign and why?
-what acts in the opposite way than carotid massage?

A

Bad sign because carotid massage makes the his-perkinjie block better vs making the higher up AV block worse
-note:exercise and atropine do the opposite (make AV block better and His-perk block worse, therefore if exercise induced high degree block = his-perk and will likely need ppm)

40
Q

If Asymptomatic but high grade AV block, when do you still put in ppm?

A
  1. Asystole >3 sec
  2. Escape rate <40 bpm
  3. CHB with rate >40bpm but LV dysfunction
  4. Escape rhythm below AV node
41
Q

If don’t see pacing with it with ppm but then paces when magnet was placed, what is the problem?

A

Over sensing

42
Q

What are causes of bidirectional VT?

A

Dig tox, CPVT (catecholenenergic polymorphic vt) or Andersen-Tawil (LQT variant)

43
Q

What is the one type of wife complex tachycardia that it’s ok to use verapamil?

A

Left VT = RBBB with LAD and QRS is on narrower side. This is coming from Left fascicle

  • no ICD in these or because low risk for SCD
  • only time to use verapamil on wide complex tach, otherwise it’s a class III HARM
44
Q

Signs that rhythm are VT on EKG

A

Extreme RAD, atypical BBB such as RBBB like but R> or = r’, lbbb like but Q in V6, S> R in v6, very wide bundles, RS >100ms, notch in S wave

45
Q

What are the normal intracranial intervals:

  1. AH interval
  2. HV interval
A
  1. 50-140msec

2. 35-55msec

46
Q

Pt with RBBB, exercise induced VT, RV enlargement.

  1. What is dx?
  2. What to check to help with dx?
  3. What to check once dx is made?
A
  1. ARVC
  2. Check cMR
  3. Check genetics
47
Q

Patient has PPM now with SVT started on antiarrhythmic and now has loss of capture

  1. What antiarrhythmic was started?
  2. Why loss of capture?
A
  1. Flecainide

2. Flecainide increases ppm pacing thresholds. Will need to increase lead output to ensure myocardial capture

48
Q

How can you tell the difference between RVOT and LVOT PVCs/VT?

A

Both will have LBBB pattern with inferior axis but LVOT is posterior to RVOT so will have early transition of precordials

49
Q

ARVC EKG

A

RBBB with TWI V1-V4

50
Q

How to treat ARVC?

A

Avoid endurance training
B.B. is controversial
Ablation decreases arrhythmia but does not improve prognosis

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