Cardiology- torsades de pointes Flashcards

1
Q

What is torsades de pointes?

A

Torsades de Pointes is a type of polymorphic ventricular tachycardia characterized on electrocardiogram by oscillatory changes in amplitude of the QRS complexes around the isoelectric line. Torsades de Pointes is associated with QTc prolongation, which is the heart rate adjusted lengthening of the QT interval

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2
Q

Torsades De Pointes
Pathophysiology of drug induced prolonged QT interval?

A
  • Involves inhibition of the rapid component of the delayed rectifier potassium current (IKr-potassium current)
  • Blocking IFr leads to prolongation of the ventricular action potential duration (VAPD), leading to an excess sodium influx or decreased potassium efflux.
  • Excess of positively charged ions leads to an extended repolarization phase of VAPD, resulting in prolonged AT interval.
  • TdP trigger is seen as a premature ventricular complex (PVC) that is generated during the prolomnged repolarisation phase, also known as the R on T phenomenon.
  • in contrast to ventricular fib, tdP is a unique ventricular arrhythmia because it can spontaneously end. However, it is possible for TdP to degenerate to ventricular fibrillation and cause sudden death
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3
Q

What are the common drugs that can cause Torsades de Pointes?

A

Important ones to remember are the antiarrhythmics!

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4
Q

Is long QT prolongation accquired or congenital?

A

Both

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5
Q

What causes long QT syndrome?

A
  • heterogeneity of tranmural ventricular repolarization among different cell types of the heart
  • medication
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6
Q

What is the RF for TdP?

A
  • congestive heart failure wih a reduced ejection fraction
  • bradycardia
  • prior MI
  • female gender
  • Age older than 65 years
  • chronic renal insufficiency
  • hypokalemia
  • diuretic treatment
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7
Q

TdP prevention

A

Careful what drugs you give

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8
Q

What is a wide complex tachycardia?

A

QRS widens as the normal ventricular depolarisation through the His-Pirkinjw system is either impaired or bypassed, and the ventricles rely on myocyte to myocyte currens for depolarization, which is much slower

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9
Q

What are the common causes of WCT (wide complex tachycardia)?

A

Ventricular tachycardia (VT)

supraventricular tachycardia with aberrant conduction (SVT)

Pre-excitation tachycardia (especially WPW)

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10
Q

Causes of aberrant conduction?

A

Bundle branch blocks

hyperkalaemia

sodium channel blocking drugs

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11
Q

What are the features of an ECG that increases the likelihood of VT?

A

very broad complexes (>160ms)

Extreme axis deviation

AV dissociation (p and ARS complexes at different rates)

capture Beats

Fusion beats

Positive or negative concordance through the chest leads

Brugada Algorith,

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12
Q

WHat is a Postive Concrdance in VT

A

V1-6 showing entirely postive R waves

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13
Q

What si Negative Concordance in VT?

A

Entirely negative QS complexes with no RS complexes seen from V1-6

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14
Q

WHat is acute management for all wide complex tachycardia?

A

Depends on the hemodynamic stability of the patient. After recognising the rhythm on cardiac monitor or 12- lead ECG, immediately assess the patient fir signs of hypoperfusion and shock: hypotension, tachycardia, hypoxia, chest pain, SOB, railes, mottling, cold extemities, altered mental state etc

-Immediate electrical cardioversion is required to restore adequate cardiac output in such hemodynamically unstable patients regardless of the specific WCT.

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15
Q

What are the classification of antiarrhythmic drugs?

A
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16
Q

What is the mechanism of SVT

A
  • Re-entry- 2 pathways of differing electrophysiological properties (conduction velocity and refractory period)
  • Increased automaticity (from a group of cells with changes in resting membrane potential- SA node, AV node)
  • Triggered activity (extra- depolarisation ollwoing ellular repolarisation eg digoxin toxicity)
17
Q

What are the pneumonia patterns

A
18
Q

Which pneumonia pattern is most common?

A

Lobar pneumonia