Dysrhythmias part 3 Flashcards

(41 cards)

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

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?

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
long term therapy for v tach
ICD Beta blockers Amiodarone, Sotalol (Class III AAD) Catheter ablation
26
management for nonsustained VT
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
Over 75% of VFib victims of sudden cardiac death have what underlying condition
severe CAD
28
# ``` Other conditions besides Vfib that predispose to sudden death include:
* 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
management for Vfib
* **IMMEDIATE unsynchronized defibrillation** * Follow ACLS protocol, CPR, etc. * Treat underlying condition * Consider ICD if indicated
29
Intraventricular conduction defects are common in ?
individuals with otherwise normal hearts
30
Intraventricular Conduction Delays can also occur in many disease processes, including:
* ischemic heart disease * inflammatory disease * infiltrative disease * cardiomyopathy * postcardiotomy
31
LBBB most often occurs in patients with ?
* 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
which artery provides the primary blood supply for the LBB
left anterior descending artery
33
causes of LBBB
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
Evaluation of a patient with LBBB:
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
management for LBBB
* _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
The RBB receives most of its blood supply from ?
septal branches of L anterior descending coronary artery
37
RBBB conduction can be compromised by?
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
T/F: Patients with isolated chronic RBBB are generally asymptomatic and do not require further diagnostic evaluation or tx
T
39
presentation of bifascicular block
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
management for symptomatic bifascicular blocks
*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_