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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
Two cool things about lidocaine and one thing we need to know
Does not cause Torsades and works better in ischemic tissue; hepatically metabolized and can have toxicity if patient has low CO (poorly perfused liver)
26
What is procainamide used for and basic mechanism
Antiarrhythmic for VTs that works by blocking Na+
27
Can procainamide cause Torsade? Why?
Yes; metabolite (NAPA) is a K+ channel blocker
28
How do cardioverter-defibrillator works?
Also function as pacemakers, but can deliver a shock if it senses a fast HR
29
Because supraventricular arrhythmias use AV node/His system the QRS complex is __________ unless (2)
Narrow; aberrancy or pre-excitation
30
Regular supraventricular tachycardia is also called
Paroxysmal SVT
31
The most common regular supraventricular tachycardia is... mechanism? Identify substrate/trigger
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
About what % of people have these two pathways?
70%
33
Treatment for AVNRT (3)
Beta-blockers or Ca2+ channel blockers, ablation of slow pathways is very effective and safe (first-line)
34
What is AVRT?
Reentry arrythmia due to abnormal congenital connection b/t atrium and ventricle outside AV node
35
EKG in AVRT? Other name?
EKG = very short PR interval w/ slurred upstroke of QRS (delta wave); pre-exciation
36
How do you establish reentry in AVRT? (2, also give QRS results and alternative names for both)
Either by blocking AVN (--> wide complex/antidromic) or accessory pathway (--> narrow complex/orthodromic)
37
Special name for AVRT EKG pattern
Wolf-Parkinson-White (WPW) pattern: short PR interval + delta wave
38
Describe WPW syndrome and treatment
WPW pattern + palpitations that has slight increase of SCD, but generally benign condition; ablation
39
Describe Focal Atrial Tachycardia and treatment
Abnormal focus anywhere in atrium that's firing; treat with beta blockers or calcium channel blockers; cure w/ ablation
40
How to determine regular supraventricular tachycardia diagnoses (3)
Induce AV block w/ valsalva, carotid sinus massage, or give adenosine
41
If AV block terminates arrhythmia?
Likely AVRT or AVNRT because reentry circuit is dependent on AVN
42
If AV block reveals atrial activity? What does "reveal atrial activity" mean?
Focal atrial tachycardia/sinus tachycardia --> AV block revealed p wave of the outta whack focus
43
Don't give adenosine to...
An asthmatic (causes bronchoconstriction)
44
Multifocal atrial tachycardia is...EKG definition...treatment?
Always the consequence of something else going on (pulmonary disease/ischemia); at least three different p wave morphologies; treat underlying cause!
45
How is typical atrial flutter initiated?
Unidirectional block across the cavo-tricuspid isthmus --> reentry loop in right atrium
46
How is the AV node protective against atrial flutter?
Decremental --> the atrial rate is 300BPM, but only a proportion of the impulses get transmitted
47
Atrial flutter EKG
"Saw tooth" pattern in inferior leads
48
Atrial flutter can be either...
Regular or irregular depending on conduction through AV node
49
Is ablation used in atrial flutter treatment?
Yes, and it's very effective
50
T/F: Atrial flutter can occur in structurally normal hearts
True
51
Describe atrial fibrillation; rate; QRS?
Irregular, chaotic, continuous atrial depolarization; irregularly irregular tachycardia; narrow QRS
52
What is the most common arrhythmia? Most important risk factor? Risk factors? Pathophysiology?
A fib; age; another structural heart abnormality; micro-fibrosis of atrium
53
Symptoms of A fib
Broad: asymptomatic --> acute heart failure; normally present w/ fatigue, chest pain, dyspnea
54
Four classes of A fib by duration
Paroxysmal; Persistent (> week); Long-standing persistent (> year); Permanent
55
What is difficult about management for A fib or A flutter?
Stasis of blood in left atrial appendage --> thrombus risk
56
% of strokes caused by A fib
20%
57
Treatment for A fib
Decision: blood thinners or not
58
What is the CHADS-VASC scoring system
Assigns points based on risk factors: CHF, HT, diabetes, stroke, vascular disease, age, female; 2+ points, anticoagulation is recommended
59
Rate control strategy. What bpm? Justificiations (2)?
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
Rhythm control strategy
To accomplish a normal sinus rhythm; require anti-arrhythmic medications, electrical conversion, ablation
61
Why would you use a rhythm control strategy?
Symptoms persist after rate is controlled
62
Class 1C agents (2) and their mechanism
Propafenone and flecainide; bind to open/inactive Na+ channel states and prolong QRS complex
63
Class 3 agents (2)
Dofetilide and sotalol
64
Other drug used for rhythm control in A fib
Amiodarone
65
What does use dependence mean?
Na+ channel blockers favor depolarized cells (aka faster rates or injured cells, which are "leaky")
66
Flecainide does what to phase 0? SEs?
Decreases CV by decreasing slope of phase 0; dizziness (30%) and can slow HR
67
Propafenone also has this effect; Weird SE?
Beta-blocker effect; dysgeusia (bad taste in mouth)
68
What can happen with exercise and Na+ channel blockers? What is the solution for this!
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
Class IC agents are contraindicated in the setting...
Of any structural heart abnormality including CAD
70
Sotalol is an...How is it cleared and why is this important?
IKr channel blocker + beta blocking abilities; renally cleared and contraindicated in pts with renal disease
71
Major SE of sotalol
Torsades (prolongs QT interval + beta blocking acton)
72
Dofetilide is just a...How is it cleared and why is this important? SE of doeftilide is just like...
IKr blocker; renally cleared and contraindicated in pts with renal disease; sotalol (torsades)
73
Class III agents have what kind of use dependence? Why is this bad?
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
Is ablation useful for a fib?
Yes: it works for some patients whose paroxysmal arrhythmias are triggered by pulmonary veins tachycardias

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