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CV <3 > Lecture 23: Dysrhythmias Part 3 > Flashcards

Lecture 23: Dysrhythmias Part 3 Flashcards

1
Q

What are the typical causes of junctional arrhythmias?

A
  • Digoxin toxicity
  • Lyte abnormalities
  • AAD toxicities
  • Ischemia
  • Myocarditis
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2
Q

How do you treat junctional arrhythmias?

A

Treat underlying cause.

No need for PPM or A/C

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3
Q

What characterizes an accelerated idioventricular rhythm?

A

Regular, wide complex with rate of 60-120.

Faster= VT, slower = V escape rhythm

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4
Q

What are the two possible mechanisms for an accelerated idioventricular rhythm?

A
  1. Escape rhythm due to suppression of the higher pacemakers/depressed SA node function.
  2. Slow ventricular tachycardia due to increased automaticity

VT would prob be > 120 BPM

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5
Q

What are the two causes of accelerated idioventricular rhythms?

A
  • Acute MI/reperfusion injury post angioplasty
  • Digoxin toxicity
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6
Q

How do you treat an accelerated idioventricular rhythm?

A

Do not treat unless hemodynamically unstable or more serious arrhythmia present.

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7
Q

What defines sustained vs nonsustained VTach?

A
  • Sustained = Lasts longer than 30s
  • Nonsustained = shorter than 30s

VTach = 3+ PVCs consecutively

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8
Q

What is the usual rate of VTach?

A

160-240 BPM

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9
Q

What are the causes of VTach?

A
  • Acute MI or CAD
  • Cardiomyopathy, valvular disease, myocarditis
  • Catecholaminergic polymorphic VT (No structural abnormalities)
  • Long QT syndrome, brugada (No structural abnormalities)
  • TdP due to severe hypokalemia or hypomagnesemia or QT prolongation drugs
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10
Q

What characterizes Long QT Syndrome?

A
  • Recurrent syncope
  • Long QT (0.5-0.7s)
  • Ventricular arrhythmias/TdP
  • Sudden death

Normal QT is 0.35s-0.45s

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11
Q

What congenital abnormality may occur alongside long QT?

A

Congenital deafness (Jervell-Lange-Nielsen syndrome) or absence thereof (Romano-Ward syndrome)

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12
Q

What kind of defect typically causes LQTS?

A
  1. Type 1 and 2 are due to K+ channel defects
  2. Type 3 is due to Na+ channel mutations

1 & 2 are the MC

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13
Q

When do most lethal cases of LQTS3 occur?

A

During sleep ):

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14
Q

What characterizes Brugada syndrome?

A
  • Sudden death
  • Incomplete RBBB + STE in anterior precordials
  • Young, male, asian
  • SCN5A gene mutation is often associated with brugada

Phillipines, Japan, Thailand

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15
Q

How do we manage LQTS/Brugada?

A
  • Long-term BB sometimes helps
  • ICD Implantation is first-line and only proven preventative measure
  • Avoiding QT prolongation meds
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16
Q

What is considered Unstable, acute, sustained VT and the treatment?

A
  • Hemodynamically unstable
  • Immediate DC cardioversion and ACLS

Unstable = hypotension, angina, AMS, or cardiac failure

Emailed her about the synchronized, and rice says synchronized is for monomorphic VT in which you can see a clear QRS and T wave. It is lower energy and is used to avoid shocking on the T wave, which could induce VF instead.

17
Q

What are the first-line IV drugs for acute, sustained, hemodynamically stable VT?

A
  1. IV amiodarone to convert to NSR
  2. IV lido if refractory
  3. IV Mg replacement
18
Q

How do you treat long-term VT?

A
  • ICD
  • BBs
  • Class 3: Amiodarone or sotalol
  • Catheter ablation

Prevents recurrence!

19
Q

If a patient has nonsustained VT with no HD, what is the tx? With HD?

A
  • Without HD, only treat with BBs if symptomatic.
  • With HD, treat with BBs no matter what.
20
Q

What is the leading cause of sudden death?

A

VF

Most people also have severe CAD.

21
Q

How do you treat VF?

A

Immediate defibrillation

22
Q

What is the primary artery related to LBBB?

23
Q

When is LBBB considered emergent to treat?

A

Occurring in the presence of ACS symptoms

Assume it is an MI until proven otherwise.

or with reduced EF

24
Q

What are the etiologies of LBBB development?

A
  • Structural HD/ischemia
  • Function (rate-related)
25
Q

How do you treat symptomatic LBBB?

A

If low EF is also present, CRT may provide some benefit.

Cardiac resynchronization therapy

26
Q

What supplies most of the blood to a RBBB?

A

Septal branches of the LAD

27
Q

What kind of processes lead to RBBB?

A

RV pressure increasing processes, like COPD.

28
Q

What is the treatment for RBBB?

A

If isolated, usually asymptomatic and no tx needed.

29
Q

How do most people with bifascicular blocks present?

A

Asymptomatic, no further diagnostics needed.

30
Q

What concurrent condition would cause us to treat bifascular block?

A

Presyncope or syncope

31
Q

How do we manage bifascicular block with syncope?

A
  • Continuous EKG monitoring for 24-48 hrs
  • Echo
  • If CHB is identified, PPM is needed
  • If no symptoms or underlying ischemia, no tx needed :)

CHB = complete heart block

CV <3 (25 decks)

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