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 junctional rhythms present on EKG

A
  • retrograde P waves before, after or within the QRS.
  • gradual/abrupt onset and termination
  • HR 70-120
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3
Q

How do you treat junctional arrhythmias?

A

Treat underlying cause.

No need for PPM or A/C

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4
Q

What characterizes an accelerated idioventricular rhythm?

A

Regular, wide complex with rate of 60-120.

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5
Q

What ar ethe two possible mechanisms for an accelerated idioventricualr rhythm?

A
  1. Escape rhythm due to suppression of the higher pacemakers/depressed SA node function.
  2. Slow ventricular tachycardia due to increased automaticity
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6
Q

What are the two causes of accelerated idioventricular rhythms?

A
  • Acute MI/reperfusion injury post angioplasty
  • Digoxin toxicity
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7
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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8
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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9
Q

What is the usual rate of VTach?

A

160-240 BPM

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10
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

Long QT and brugada are not testable material.

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11
Q

What characterizes Long QT Syndrome?

A
  • Recurrent syncope
  • Long QT (0.5-0.7s)
  • Ventricular arrhythmias/TdP
  • Sudden death
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12
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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13
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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14
Q

When do most lethal cases of LQTS3 occur?

A

During sleep ):
or during high emotional stress

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15
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
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16
Q

How do we manage LQTS/Brugada?

A
  • Long-term BB sometimtes helps
  • ICD Implantation is first-line and only proven preventative measure
  • Avoiding QT prolongation meds
17
Q

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

A
  • Hemodynamically unstable
  • Immediate synchronized DC cardioversion and ACLS
18
Q

What is the first-line IV drug for acute, sustained, hemodynamically stable VT?

A
  1. IV amiodarone to convert to NSR
  2. IV lido if refractory
  3. IV Mg replacement
19
Q

How do you treat long-term VT?

A
  • ICD
  • 1st line: BBs
  • 2nd line: Amiodarone or sotalol
  • Catheter ablation
20
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.
21
Q

What is the leading cause of sudden death?

A

VF

Most people also have severe CAD.

22
Q

How do you treat VF?

A

Immediate defibrillation

23
Q

What is the primary artery related to LBBB?

24
Q

When is LBBB considered emergent to treat?

A

Occurring in the presence of ACS symptoms

Assume it is an MI until proven otherwise.

25
What are the etiologies of LBBB development?
* Structural HD/ischemia * Function (rate-related)
26
How do you treat symptomatic LBBB?
If low EF is also present, CRT may provide some benefit. ## Footnote Cardiac resynchronization therapy
27
What supplies most of the blood to a RBBB?
Septal branches of the LAD
28
What kind of processes lead to RBBB?
RV pressure increasing processes, like COPD.
29
What is the treatment for RBBB?
If isolated, usually asymptomatic and no tx needed.
30
How do most people with bifascicular blocks present?
Asymptomatic, no further diagnostics needed.
31
What concurrent condition would cause us to treat bifascular block?
Presyncope or syncope
32
How do we manage bifascicular block with syncope?
* Continuous EKG monitoring for 24-48 hrs * Echo * If CHB is identified, PPM is needed * If no symptoms or underlying ischemia, no tx needed :) ## Footnote CHB = complete heart block