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ED Fellowship ECG/ABG/IX > Paeds Syncope > Flashcards

Paeds Syncope Flashcards

1
Q

Describe Brugada syndrome

A

Congenital condition due to NA channelopathy. Brugada symptoms can be transient or unsmasked by a host of things including

  • Fever
  • Ischaemia
  • Drugs
  • –Na channel blockers
  • –A agonists
  • –B blocker
  • –CA blocker
  • –Nitrates
  • –Cholinergic stimulation
  • – COcaine
  • –ALcohol
  • Hypokalaemia
  • Hypothermia
  • Post DC cardioversion
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2
Q

Describe Brugada type 1

A

Coved ST segment elevation of at greater than 2 mm in more than 1 of V1-3
Followed by -ve T-wave
Only sign that is potentially diagnositic - known as brugada sign

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3
Q

Describe Brugada pattern type 2

A

Type 2 has incomplete RBBB with greater than 2mm of st eleaveion
saddle

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4
Q

Describe Brugada patternt type 3

A

Can be either type 1 or 2 but with <2mm of elevation

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5
Q

Describe Brugada Syndrome

A

Brugada syndrome is Brugada pattern ECG with any of the following

  • Documented ventricular fibrillation (VF) or polymorphic ventricular tachycardia (VT).
  • Family history of sudden cardiac death at <45 years old .
  • Coved-type ECGs in family members.
  • Inducibility of VT with programmed electrical stimulation .
  • Syncope.
  • Nocturnal agonal respiration.
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6
Q

Discuss Management of Brugada Syndrome

A

The only proven therapy is an implantable cardioverter – defibrillator (ICD).
-Quinidine has been proposed as an alternative in settings where ICD’s are unavailable or where they would be inappropriate (eg: neonates).

Type 1 brugada can likley be discharged with EPS follow-up
Type 2-3 also

A japanese study of 98 people with Brugada sign were followed with 14000 others nil change in mortality seen

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7
Q

Discuss catecholaminerigic polymorhpic VT

A

Polymorphic VT is defined as a ventricular rhythm above 100 BPM with a continuously varying QRS morphology
Most are above 200 BPM, can cause HD instability, can deteriate into VF

History of Sudden cardiac death in the family
Typically begins in childhood to adolescence
Patients typically present after a physical or emotional stress with
-sudden cardiac death
- Syncope
-Seizure like activity
-Palpitations

Avoid stress
IACD
Propanalol

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8
Q

Describe the ECG of CPVT

A

Two types of polymorphic VT have been described in this condition

1) typical with continuing varying QRS morphology
2) Bidirectional VT

Bidirectional VT is generally pathognomic for digitalis intoxication but can also occur in CPVT both are thought ot be due to Ca overload leading to DADs

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9
Q

Discuss pre-excitation

A

Pre-excitation refer to early ventricular activation due to pathways that bypass the AV node
Can conduct antegrade towards the ventricle or retrograde towards the atria

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10
Q

Discuss ECG finding of WPW

A

Short PR <120
Delta wave
Wide QRS complex >110
ST segment and t-wave segment discordance
pseudo infarct pattern in up to 70% of cases

Type A: positive delta wave in all precordial leads with R/S > 1 in V1
Type B: negative delta wave in leads V1 and V2

IN retrograde only conduction nil ECG features will be seen as all APs are conducted throught the AV node – termed a concealed pathway

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11
Q

Discuss AVRT with orthodromic conduction

A

IN orthodromic ACRT conduction occurs throught the AV node

Narrow complex at a rate of 200-300 BPM
Can have QRS alternans
T-wave inversion common
St segment depression

Treatment depends on HD – if unstable shock the shit out of them
If stable as per SVT vagal maneuvers adenosine

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12
Q

Discuss AVRT with antedromic conduction

A

Antedromic AVRT conduction occurs through accessory pathway
Wide complex tachycard – 200-300 can be difficult to distinguish between this an VT
If seen in a child almost always re-entry with abherrency

Do not use AV nodal blockers as can detiorate into to VT/VF

Use flecanide or electicity

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13
Q

Discuss AF, aflut in WPW

A

Common occurs in 20% of patient with WPW for AF and 7% for A-flutter

Rate >200
Irregular if AF
Can have widecomplex if antedromic
QRS complex change in shape but does not alter axis as polymporphic VT would

Dont use AV nodal blockers as above
Flecanide or procainamide or shock

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14
Q

Discuss Mahaim type pre-excitation

A

Right sided accessory pathways connecting either AV node to ventricles, fascicles to ventricles, or atria to fascicles

ECG features:

Sinus rhythm ECG may be normal
May result in variation in ventricular morphology
Reentry tachycardia typically has LBBB morphology

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15
Q

Discuss ARVD

A

Second most common form of sudden cardiac death in young people after HOCM

Symptoms are caused by ventricular ectopic beats or sustained VT
Presenting complaint may be sudden cardiac death
if people survive often develop right sided heart failure

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16
Q

Discuss ECG finding of ARVD

A

ARVD is associated with characteristic ECG abnormalities:

  • Epsilon wave (most specific finding, seen in 30% of patients)
  • T wave inversion in V1-3 (85% of patients)
  • Prolonged S-wave upstroke of 55ms in V1-3 (95% of patients)
  • Localised QRS widening of 110ms in V1-3
  • Paroxysmal episodes of ventricular tachycardia with LBBB morphology (e.g. right ventricular VT).
17
Q

Described the epislon wave

A

Small positive deflection buried at the end of the QRS. Best seen in the precordial leads

Can use fontaine lead placement to exagerate epislon wave if present

18
Q

Discuss imaging modalities of ARVD

A

ECHO can show dilated, hypokinetic right ventricle with prominent apical trabeculae and dilatation of the RV outflow tract

Cardiac MRI can be diagnostic of the condition showing fibrofatty infiltrate

19
Q

Discuss risk assessment and management of ARVD

A

High risk groups

  • family history of sudden death - 1st degree relative
  • Recurrent arrythmias not suppressed by anti-arrythmics
  • History of syncope due to cardiac arrest

Patient at high risk should all have IACD
THose without high risk features can trial antiarryhthmics such as b blockers or amioderone to suppress cathecholamine triggered VT

20
Q

What is a long QT

A

QTc is prolonged if > 440ms in men or > 460ms in women
QTc > 500 is associated with increased risk of torsades de pointes
QTc is abnormally short if < 350ms

21
Q

List causes of a long QT

A

1) Drugs -Amioderone -antipsychotics (haloperidol, droperidol, TCAs,) -Many antibiotics (erythromycin, fluconazole) -antiemetics (metoclopramide, ondansetron) -antidepressants ( SSRI)
2) genetic -cardiac ion channel mutation -long qt syndrome
3) Myocardial disease -MI -RF -cardiomyopathy
4) electorlyte abnormalities -low, ca, mg, k

Raised ICP

22
Q

How do you caluculate a QTC

A

Bazett formula: QTC = QT / √ RR in seconds
Fridericia formula: QTC = QT / RR 1/3
Framingham formula: QTC = QT + 0.154 (1 – RR)
Hodges formula: QTC = QT + 1.75 (heart rate – 60)

23
Q

Discuss management of long qt

A 
beta-blockade
avoidance of increased sympathetic tone
cardiac pacing
treat cause and avoid agents that will prolong the QT 
ICD
24
Q

Discuss Short QTC

A

Patients are typically young and healthy, with no structural heart abnormalities; age at first presentation ranges from a few months to the sixth decade of life (median age = 30 years).
The most common initial presenting symptom is cardiac arrest (in one-third of cases); other patients may present with palpitations or syncope due to rapid atrial fibrillation or self-terminating ventricular arrhythmias.
Witnessed cardiac arrest within the first year of life and unexplained infant deaths have been observed in patients and families with SQTS, making it a possible cause of sudden infant death syndrome (SIDS).

25
Q

Describe ECG of short QTC

A

Short QT interval
Lack of the normal changes in QT interval with heart rate
Peaked T waves, particularly in the precordial leads
Short or absent ST segments
Episodes of atrial or ventricular fibrillation

26
Q

Management of short QTC

A

IACD however due to tall t -wave can given inappropriate shocks

Quinidine is medication of choice
Sotalol no good

27
Q

Discuss RVOT

A

Monomorphic VTY originating from the outflow tract of the RV or occasionally the tricuspid annulus

ECG:

  • LBBB morph
  • inferior acis
  • rs complex in V1 and R complex in V6
  • precordial transition usually > v3 with the exception of spetal origin
  • other general features of VT may also be present

RVOT Tachyacrdia is the most common form of idiopathic VT - whereby no strucutral heart disease, metabolic or electrolyte abnormalities or long QT can be found

The two most common froms are

1) repetitive unsustained monomorphic VT 60-90%
2) exercise induced sustained VT

Treatment

  • Vagal manoeuvres or adenosine
  • IV verapamil or beta blockers

ED Fellowship ECG/ABG/IX (8 decks)

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