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Cardiology > Lecture 11-12: Tachyarrhythmia, Atrial Fibrillation > Flashcards

Lecture 11-12: Tachyarrhythmia, Atrial Fibrillation Flashcards

1
Q

If you have an unstable tachycardia, the treatment is…Why does this work?

A

Electrical shock; depolarizes all cells together to 1. Interrupt reentry loops or 2. Restart sinus node of heart

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2
Q

Ventricular tachyarrythmias

A

Any rhythm originating in ventricles with rate >100 BPM

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3
Q

Three ventricular tachyarrythmias

A
  1. Monomorphic; 2. Polymorphic; 3. Ventricular fibrillating (no organized activity)
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4
Q

Which two ventricular tachyarrythmias do you almost always shock?

A

Polymorphic and ventricular fibrillation

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5
Q

Ventricular fibrillation

A

Disorganized electrical activity –> cardiac standstill

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6
Q

What is a trigger and what is a substrate for VF?

A

Acute cardiac injury (MI); structural abnormalities (myopathy)

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7
Q

If VF occurs after shock, what is treatment?

A

Difibrillator

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8
Q

Sudden cardiac death is caused by? % of total deaths

A

VF; 15%

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9
Q

Athletes > 35 die suddenly, it’s likely…

A

CAD

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10
Q

Athletes

A

Structural cause

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11
Q

What is congenital LQTS?

A

Inherited ion channelopathy that leads to a long QT interval

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12
Q

Romano Ward syndrome is

A

Autosomal dominant, no deafness

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13
Q

Jervell and Lange-Nielsen syndrome is

A

Autosomal recessive, sensorineural deafness

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14
Q

Brugada syndrome is…(4 points); what exacerbates it? EKG looks like…

A

Sodium channelopathy, variable penetrance, common in Asian males, SCD during SLEEP; alcohol and cocaine use; V1, 2, 3 –> ski slope late part of QRS

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15
Q

Torsade de points is a type of? Describe it in two ways

A

Polymoprhic VT: reentry arrhythmia with circuit continuously moving around the ventricles; when a PVC happens right on QT interval

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16
Q

Risk factors for Torsades (4)

A

QT prolonging medications (Class IA and III antiarrhythmics, antibiotics, antipsychotics), electrolyte abnormalities (hypocalcemia, magesemia, kalemia), genetic mutations of Na+ or K+ channels, bradycardia

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17
Q

What usualy happens in Torsades?

A

Generally gets better, if it doesn’t –> vfib

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18
Q

Torsades treatment (4)

A
  1. Magnesium; 2. Remove offending QT prolonging agent; 3. Cardiac pacing; 4. If unable to correct underlying cause, defibrillator implant
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19
Q

Most common form of monomorphic VT. This often? So you would…Classic example of a…

A

Scar-related; hemodynamically unstable; shock it! Reentry arrhythmia based on tissue that conducts slowly due to scarring

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20
Q

Treatment of scar-related VT? (4)

A

Shock, ablation of scar substrate, anti-arrhythmic medications, defibrillators

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21
Q

What is amiodarone used for and basic mechanism

A

Most common medication for VT that works by blocking all the channels

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22
Q

Does amiodarone cause Torsades?

A

Not generally due to its blocking of all the channels (though it does prolong QT)

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23
Q

Two things we should know about amiodarone

A
  1. 60 day half life; 2. Toxicities are significant (50% will have to come off) include pulm, liver thyroid (pneumonic is LFTs, TFTs, PFTs)
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24
Q

What is lidocaine used for and basic mechanism

A

Antiarrhythmic for VTs that works by blocking Na+ channels

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25
Q

Two cool things about lidocaine and one thing we need to know

A

Does not cause Torsades and works better in ischemic tissue; hepatically metabolized and can have toxicity if patient has low CO (poorly perfused liver)

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26
Q

What is procainamide used for and basic mechanism

A

Antiarrhythmic for VTs that works by blocking Na+

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27
Q

Can procainamide cause Torsade? Why?

A

Yes; metabolite (NAPA) is a K+ channel blocker

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28
Q

How do cardioverter-defibrillator works?

A

Also function as pacemakers, but can deliver a shock if it senses a fast HR

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29
Q

Because supraventricular arrhythmias use AV node/His system the QRS complex is __________ unless (2)

A

Narrow; aberrancy or pre-excitation

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30
Q

Regular supraventricular tachycardia is also called

A

Paroxysmal SVT

31
Q

The most common regular supraventricular tachycardia is… mechanism? Identify substrate/trigger

A

AVNRT (AV nodal reentrant tachycardia); both the fast pathway (quickly conducting w/ slow recovery) and slow pathway (slowly conducting w/ fast recovery) are engaged due to an early beat; substrate = dual pathways; trigger = PAC (premature atrial contraction)

32
Q

About what % of people have these two pathways?

A

70%

33
Q

Treatment for AVNRT (3)

A

Beta-blockers or Ca2+ channel blockers, ablation of slow pathways is very effective and safe (first-line)

34
Q

What is AVRT?

A

Reentry arrythmia due to abnormal congenital connection b/t atrium and ventricle outside AV node

35
Q

EKG in AVRT? Other name?

A

EKG = very short PR interval w/ slurred upstroke of QRS (delta wave); pre-exciation

36
Q

How do you establish reentry in AVRT? (2, also give QRS results and alternative names for both)

A

Either by blocking AVN (–> wide complex/antidromic) or accessory pathway (–> narrow complex/orthodromic)

37
Q

Special name for AVRT EKG pattern

A

Wolf-Parkinson-White (WPW) pattern: short PR interval + delta wave

38
Q

Describe WPW syndrome and treatment

A

WPW pattern + palpitations that has slight increase of SCD, but generally benign condition; ablation

39
Q

Describe Focal Atrial Tachycardia and treatment

A

Abnormal focus anywhere in atrium that’s firing; treat with beta blockers or calcium channel blockers; cure w/ ablation

40
Q

How to determine regular supraventricular tachycardia diagnoses (3)

A

Induce AV block w/ valsalva, carotid sinus massage, or give adenosine

41
Q

If AV block terminates arrhythmia?

A

Likely AVRT or AVNRT because reentry circuit is dependent on AVN

42
Q

If AV block reveals atrial activity? What does “reveal atrial activity” mean?

A

Focal atrial tachycardia/sinus tachycardia –> AV block revealed p wave of the outta whack focus

43
Q

Don’t give adenosine to…

A

An asthmatic (causes bronchoconstriction)

44
Q

Multifocal atrial tachycardia is…EKG definition…treatment?

A

Always the consequence of something else going on (pulmonary disease/ischemia); at least three different p wave morphologies; treat underlying cause!

45
Q

How is typical atrial flutter initiated?

A

Unidirectional block across the cavo-tricuspid isthmus –> reentry loop in right atrium

46
Q

How is the AV node protective against atrial flutter?

A

Decremental –> the atrial rate is 300BPM, but only a proportion of the impulses get transmitted

47
Q

Atrial flutter EKG

A

“Saw tooth” pattern in inferior leads

48
Q

Atrial flutter can be either…

A

Regular or irregular depending on conduction through AV node

49
Q

Is ablation used in atrial flutter treatment?

A

Yes, and it’s very effective

50
Q

T/F: Atrial flutter can occur in structurally normal hearts

A

True

51
Q

Describe atrial fibrillation; rate; QRS?

A

Irregular, chaotic, continuous atrial depolarization; irregularly irregular tachycardia; narrow QRS

52
Q

What is the most common arrhythmia? Most important risk factor? Risk factors? Pathophysiology?

A

A fib; age; another structural heart abnormality; micro-fibrosis of atrium

53
Q

Symptoms of A fib

A

Broad: asymptomatic –> acute heart failure; normally present w/ fatigue, chest pain, dyspnea

54
Q

Four classes of A fib by duration

A

Paroxysmal; Persistent (> week); Long-standing persistent (> year); Permanent

55
Q

What is difficult about management for A fib or A flutter?

A

Stasis of blood in left atrial appendage –> thrombus risk

56
Q

% of strokes caused by A fib

A

20%

57
Q

Treatment for A fib

A

Decision: blood thinners or not

58
Q

What is the CHADS-VASC scoring system

A

Assigns points based on risk factors: CHF, HT, diabetes, stroke, vascular disease, age, female; 2+ points, anticoagulation is recommended

59
Q

Rate control strategy. What bpm? Justificiations (2)?

A

Patient remains in a fib but pulse rate is controlled using medications (beta blockers, Ca2+ blockers); below 80 bpm at rest; pts will often become asymptomatic; large studies show that this might be the best method

60
Q

Rhythm control strategy

A

To accomplish a normal sinus rhythm; require anti-arrhythmic medications, electrical conversion, ablation

61
Q

Why would you use a rhythm control strategy?

A

Symptoms persist after rate is controlled

62
Q

Class 1C agents (2) and their mechanism

A

Propafenone and flecainide; bind to open/inactive Na+ channel states and prolong QRS complex

63
Q

Class 3 agents (2)

A

Dofetilide and sotalol

64
Q

Other drug used for rhythm control in A fib

A

Amiodarone

65
Q

What does use dependence mean?

A

Na+ channel blockers favor depolarized cells (aka faster rates or injured cells, which are “leaky”)

66
Q

Flecainide does what to phase 0? SEs?

A

Decreases CV by decreasing slope of phase 0; dizziness (30%) and can slow HR

67
Q

Propafenone also has this effect; Weird SE?

A

Beta-blocker effect; dysgeusia (bad taste in mouth)

68
Q

What can happen with exercise and Na+ channel blockers? What is the solution for this!

A

Because of use dependence, if your HR increases you can fall into VF and need to be shocked; an AV nodal agent such as a Ca2+ channel or beta blocker needs to be administered with a 1 C agent

69
Q

Class IC agents are contraindicated in the setting…

A

Of any structural heart abnormality including CAD

70
Q

Sotalol is an…How is it cleared and why is this important?

A

IKr channel blocker + beta blocking abilities; renally cleared and contraindicated in pts with renal disease

71
Q

Major SE of sotalol

A

Torsades (prolongs QT interval + beta blocking acton)

72
Q

Dofetilide is just a…How is it cleared and why is this important? SE of doeftilide is just like…

A

IKr blocker; renally cleared and contraindicated in pts with renal disease; sotalol (torsades)

73
Q

Class III agents have what kind of use dependence? Why is this bad?

A

Reverse use dependence: work worst when heart is beating fast and best when heart is beating slowly; maximal chance of toxicity at bradycardia w/ minimal chance of fixing arrhythmia

74
Q

Is ablation useful for a fib?

A

Yes: it works for some patients whose paroxysmal arrhythmias are triggered by pulmonary veins tachycardias

Cardiology (22 decks)

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