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Cardiovascular > Dysrhythmias part 3 > Flashcards

Dysrhythmias part 3 Flashcards

1
Q

what are Junctional Arrhythmias

A
  • Rhythm originating from junction/AV node
  • gradual or abrupt onset, with change in rate, followed by abrupt termination
  • 70-120 bpm
  • Retrograde P waves either immediately preceding QRS, immediately following QRS, or buried in the QRS and not visible
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2
Q

causes of Junctional Arrhythmias

A
  • Digoxin toxicity
  • Electrolyte abnormalities
  • Other AAD toxicities
  • Ischemia, Myocarditis
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3
Q

presentation of junctional arrhythmias

A

May be asymptomatic
Palpitations, dizziness, near syncope

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4
Q

management for junctional arrhythmias

A

Treat underlying cause
Usually no need for pacemaker or other management

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5
Q

2 mechanisms of Accelerated Idioventricular Rhythm

A
  1. escape rhythm due to suppression of higher pacemakers resulting from sinoatrial and AV block or from depressed sinus node function
  2. slow ventricular tachycardia due to increased automaticity
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6
Q

causes of accelerated idioventricular rhythm

A
  • In acute MI and following reperfusion with angioplasty or thrombolytics
  • Also common with digoxin toxicity
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7
Q

tx for accelerated idioventricular rhythm is not indicated unless ?

A

there is hemodynamic compromise or more serious arrhythmias.

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8
Q

what is V tach?

A
  1. Defined as 3+ consecutive ventricular premature beats
    - Nonsustained – < 30 s, terminates spontaneously
    - Sustained – > 30 s
  2. 160–240 bpm
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9
Q

causes of V tach

A
  1. Acute MI, CAD
  2. Cardiomyopathy, valvular disease, myocarditis
  3. May occur in structurally normal hearts
    - Catecholaminergic Polymorphic VT
    - Long QT syndromes, Brugada
  4. Torsades de pointes - severe hypokalemia, hypomagnesemia, or after administration of a drug that prolongs the QT interval
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10
Q

what are Congenital Long QT Syndromes

A
  • Rare in US – may be autosomal recessive or dominant, depending on underlying genetic disturbance
  • Characterized by recurrent syncope, a long QT interval (0.5–0.7 s), documented ventricular arrhythmias, and sudden death.
  • Specific genetic mutations affecting membrane potassium and sodium channels have been identified
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11
Q

Congenital Long QT Syndromes may occur in the ____ or ___ of congenital deafness.
What are the official syndrome names?

A

presence (Jervell-Lange-Nielsen syndrome) or absence (Romano-Ward syndrome)

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12
Q

Congenital Long QT Syndrome is mainly characterized by ____ that are often triggered by adrenergic stimulation, which can be brought about by physical exertion or mental or emotional stress.

A

episodes of torsades de pointes

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13
Q

MC forms of congenital LQTS are caused by ?

A

ion channel defects

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14
Q

which LQT is a Na channel mutation?

A

LQT 3

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15
Q

which LQT are K+ channel abnormalities

A

LQT1 and LQT2

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16
Q

Proposed as one of the causes of sudden infant death syndrome

A

Congenital Long QT Syndromes

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17
Q

which type of congential LQT is MC

A

LQT1and LQT2account for 80% of the cases.
Exercise and sudden auditory stimuli are triggers

18
Q

which LQT is only seen in 10% of the cases, but it accounts for most of the lethal cases of LQTS.
Most of the events occur during sleep at slower heart rates

A

LQT 3

19
Q

Characterized by sudden death associated with one of several ECG patterns characterized by incomplete RBBB and ST-segment elevations in the anterior precordial leads

A

Brugada Syndrome

20
Q

Brugada Syndrome is MC in who?

A

The typical patient is young, male, and otherwise healthy, with normal general medical and CV PE.
Also more common in Asians (Philippines, Thailand, Japan)

21
Q

Brugada syndrome has been associated with alterations in what gene?

A

SCN5Agene

22
Q

management of congenital LQT/brugada

A
  1. Refer to Cardio or EP ASAP
  2. Long-term tx - BB - Propranolol & Nadolol preferred
  3. ICD implantation, esp Brugada
    - also recommended in recurrent syncope, sustained ventricular arrhythmias, or sudden cardiac death occurs despite medical therapy.
  4. Avoid prolonging QT meds
23
Q

s/s of v tach

A
  1. Patient may be asx, esp with nonsustained
  2. Majority with sustained VT have sx
    - Palpitations, heart racing
    - Near syncope, syncope
    - Confusion, fatigue
    - Chest pain, SOB

PE findings and diagnostic study results depend on the underlying cause

24
Q

management for Acute Sustained VT

A
  1. hemodynamically unstable - immediate synchronized direct current cardioversion
  2. stable – IV amiodarone
    - IV Lidocaine if refractory
    - IV magnesium replacement
  3. Manage any underlying causes
25
Q

long term therapy for v tach

A

ICD
Beta blockers
Amiodarone, Sotalol (Class III AAD)
Catheter ablation

26
Q

management for nonsustained VT

A

If no heart disease – BB if sx only
If due to structural HD (low EF) - BB, even if no sx, d/t increased risk of sustained VT and sudden death

27
Q

Over 75% of VFib victims of sudden cardiac death have what underlying condition

A

severe CAD

28
Q

```

Other conditions besides Vfib that predispose to sudden death include:

A
  • Severe LVH, hypertrophic cardiomyopathy, dilated cardiomyopathy
  • Severe AS
  • Primary pulmonary hypertension, cyanotic congenital heart disease
  • Hypoxia, electrolyte abnormalities
  • Long QT, Brugada syndrome, ARVD, catecholaminergic VT
28
Q

management for Vfib

A
  • IMMEDIATE unsynchronized defibrillation
  • Follow ACLS protocol, CPR, etc.
  • Treat underlying condition
  • Consider ICD if indicated
29
Q

Intraventricular conduction defects are common in ?

A

individuals with otherwise normal hearts

30
Q

Intraventricular Conduction Delays can also occur in many disease processes, including:

A
  • ischemic heart disease
  • inflammatory disease
  • infiltrative disease
  • cardiomyopathy
  • postcardiotomy
31
Q

LBBB most often occurs in patients with ?

A
  • underlying heart disease and may be associated with progressive conducting system disease.
  • However, LBBB can also be seen in asx pts with a structurally normal heart
32
Q

which artery provides the primary blood supply for the LBB

A

left anterior descending artery

33
Q

causes of LBBB

A
  1. Structural Heart Disease
    - not usually the result of a single clinical entity, except in acute MIs.
    - conditions that contribute to myocardial fibrosis (HTN, CAD, cardiomyopathies) can contribute to LBBB.
    - may result following acute myocardial insult = worse prognosis
  2. Functional LBBB
    - Rate-related aberrancy
34
Q

Evaluation of a patient with LBBB:

A
  1. In the setting of CP/ACS sx, MIs are difficult to determine with EKG alone
    - Assume MI until proven otherwise, unless old LBBB
  2. Thorough H&P to assess for causes: HTN, CAD, CM, Valve disease, Myocarditis
  3. Diagnostic testing should be based on H&P
    - Echo
    - Stress test or LHC
35
Q

management for LBBB

A
  • asx w/ isolated LBBB, no evidence of cardiac disease - no therapy required
  • Otherwise, treat any underlying cause
  • Sx pts w/ LBBB and low EF - CRT
36
Q

The RBB receives most of its blood supply from ?

A

septal branches of L anterior descending coronary artery

37
Q

RBBB conduction can be compromised by?

A

both structural and functional factors:

  1. Structural heart disease –
    - Processes that increase RV pressure, like COPD, PE, Pulm HTN
    - MI, HTN, CM, Myocarditis, Congenital heart defects
  2. Rate-related aberrancy is possible
38
Q

T/F: Patients with isolated chronic RBBB are generally asymptomatic and do not require further diagnostic evaluation or tx

A

T

39
Q

presentation of bifascicular block

A

asymptomatic and fairly benign

  • asx - no further diagnostic evaluation or therapy is required
  • Pts should be screened carefully for s/s suggesting occult cardiac disease
40
Q

management for symptomatic bifascicular blocks

A

present with presyncope or syncope and are noted to have bifascicular block on ECG

  1. additional monitoring and eval are required - intermittent complete heart block may result occur
    - Continuous ECG monitoring x 24-48 h - inpatient
    - Echo - assess for underlying structural heart disease
    - CHB is identified - PPM

Otherwise, if no sx and no underlying ischemia, then no tx is necessary

Cardiovascular (24 decks)

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