Cardiology (Arrhythmia con.) Flashcards

1
Q

Wolff-Parkinson-White (WPW) syndrome is

A

a congenital disorder characterised by an accessory pathway that allows the conduction of electrical impulses from the atria to the ventricles directly, bypassing the atrioventricular (AV) node.

This leads to AV re-entry tachycardia (AVRT) and can cause paroxysmal supraventricular tachycardia.

This can also trigger ventricular fibrillation and cause sudden cardiac death.

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2
Q

WPW syndrome is associated with:

A
  • Ebstein’s anomaly
  • Hypertrophic obstructive cardiomyopathy
  • Hyperthyroidism
  • PRAKAG2 – this is a gene associated with a familial form of WPW syndrome
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3
Q

WFW ECG findings

A
  • PR interval is short
  • QRS complexes are wide with a slurred upstroke known as a delta wave
  • Associated left axis deviation or right axis deviation
  • Non-specific ST changes
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4
Q

management of WPW

A

The definitive management step involves radiofrequency ablation of the accessory pathway.

Initial management steps of an acute episode are similar to supraventricular tachycardia such as vagal manoeuvres except adenosine is not used if co-existing atrial fibrillation is suspected:

This is because adenosine blocks the AV node which can increase the ventricular rate potentially leading to ventricular fibrillation.

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5
Q

Ventricular tachycardia (VT)

A

is a broad complex tachycardia that originates from a ventricular ectopic focus. It is defined as 3 or more consecutive beats at a rate of >100 bpm. It requires urgent treatment as it can lead to ventricular fibrillation and cardiac arrest.

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6
Q

types of VT

A

Monomorphic VT:
* Stable SQRS morphology with no variation between beats
* Most commonly caused by myocardial infarction

Polymorphic VT:
* QRS morphology changes with each beat
* A subtype of polymorphic VT is torsades de pointes.

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7
Q

Presentation of VT

A
  • Palpitations
  • Breathlessness
  • Chest pain or tightness
  • Anxiety
  • Dizziness
  • Syncope
  • Fatigue
  • Haemodynamic instability
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8
Q

ECG findings VT

A
  • Rate >100 bpm
  • Wide QRS complexes (>120 ms)
  • Atrioventricular dissociation
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9
Q

management of VT

A

Haemodynamically unstable

  • Manage as per the Resuscitation Council UK Tachycardia guidelines. These are discussed in Adult Tachycardia.

Haemodynamically stable

  • IV amiodarone through a central line
  • Other options include lidocaine and implantable cardioverter-defibrillators
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10
Q

Torsades de Pointes

A

translates to “twisting of the points”. It is a polymorphic ventricular tachycardia. It is polymorphic because the QRS amplitude varies and the QRS complexes look like they are twisting around the baseline.

Torsades de pointes is associated with a prolonged QT interval and may degenerate into sustained ventricular tachycardia or ventricular fibrillation. Torsades de pointes is a life-threatening arrhythmia that may present as cardiac arrest in people with structurally intact hearts.

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11
Q

risk factors for torsades de pointes

A

1) Congenital QT syndromes (described in Long QT Syndrome)

2) Acquired QT syndromes (described in Long QT Syndrome):

  • Myocardial infarction
  • Drugs e.g. erythomycin
  • Electrolyte imbalances
  • CNS lesions e.g. subarachnoid haemorrhages
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12
Q

presentation of Torsades de pointes

A

Patients may be asymptomatic or have recurrent episodes of symptoms which are usually triggered by stress, fear, or physical exertion. Some recurring features may be:

1) Palpitations
2) Dizziness
3) Syncope:
* Preceded by: palpitations, shortness of breath, and dyspnoea
* During: pallor and cyanosis
* After: recovery period brief and there is flushing

4) Sudden cardiac death
5) Features of a congenital disorder e.g. sensorineural hearing loss in Jervell and Lange-Nielsen syndrome

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13
Q

ECG for Torsades de pointes

A
  • Shows polymorphic ventricular tachycardia consistent with Torsades de pointes
  • May show QT prolongation
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14
Q

management of Torsades de Pointes

A
  • 1st line: IV magnesium sulfate
  • Also withdraw offending drugs and correct electrolyte abnormalities
  • Management of long QT syndrome
  • In recurrent torsades de pointes, temporary or permanent pacing may be indicated
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15
Q

management of bradycardia if evidence of life-threatening signs e.g. shock, syncope, MI, HF

A

Give IV atropine 500 micrograms

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16
Q

management of adult tachycardia with life threatening features e.g. shock, syncome, MI, HF

A
  • Give up to 3 synchronised DC shocks
    Give sedation or anaesthesia if conscious

If unsuccessful:
* Amiodarone 300mg IV over 10-20 minutes
* Repeat synchronised DC shock

17
Q

shockable rhythms

A

VF and VT

18
Q

non-shockable rhythms

A
  • pulseless electrical activity
  • asystole
19
Q

initial management of all patients who are unrepsonsive and not breathing properly

A
  • Call the resuscitation team/ambulance
  • Commence CPR at a ratio of 30 compressions:2 breaths (30:2)
  • Attach the defibrillator/monitor and assess rhythm
  • Obtain IV access
  • If this isn’t possible, deliver drugs through the intraosseous (IO) route
20
Q

4 Hs

A
  • Hypoxia
  • Hypovolaemia
  • Hypokalaemia, hyperkalaemia, hypoglycaemia, hypocalcaemia and other metabolic disorders
  • Hypothermia
21
Q

4 Ts

A
  • Thrombosis – coronary or pulmonary
  • Tension pneumothorax
  • Tamponade (cardiac)
  • Toxins
22
Q

management of shockable rhythm

A

If “witnessed” cardiac arrest i.e. in a coronary care unit: 3 stacked shocks then 2 minutes CPR then check rhythm then give single shocks instead and repeat

If not witnessed: 1 single shock then 2 minutes CPR then check rhythm then repeat

After third shock:
* adrenaline 1mg and amiodarone 300mg
* Repeat adrenaline 1mg every 3-5 minutes i.e. during alternate cycles of CPR

After fifth shock: further 150mg dose of amiodarone

Use lidocaine if amiodarone is not available

23
Q

If non-shockable (asystole/PEA)

A

Adrenaline 1mg as soon as possible followed by CPR then check rhythm
Repeat adrenaline 1mg every 3-5 minutes i.e. during alternate cycles of CPRIf non-shockable (asystole/PEA)

24
Q
A