Arrhythmias Flashcards

1
Q

Is it common to see P waves in VT?

A

VT is characterised by mechanical and electrical dissociation, so P waves can sometimes be observed that are independent of the QRS complex (i.e. with no relationship between the two).

This happens because in VT, a scar site (usually from a previous MI) acts as an independent pacemaker independent of the SAN.

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2
Q

How can a VT be distinguished from an SVT with aberrant conduction?

A

Capture beats
Fusion beats
No response to carotid sinus massage or adenosine
Previous history of ischaemic heart disease
Extreme axis deviation
AV dissociation
Positive or negative concordance throughout precordial leads
Brugada sign

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3
Q

What are the features of VT on an ECG?

A

VT usually occurs in patients with CAD or cardiomyopathy and may cause haemodynamic compromise or degenerate into VF.

VT is characterised by a broad complex tachycardia with abnormal appearing QRS complexes with a rate >120/min

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4
Q

How is VT managed?

A

Emergency DC cardioversion is needed if SBP <90mmHg or any adverse features (e.g. myocardial ischaemia, syncope, signs of heart failure).
If VT is well tolerated then IV amiodarone can be tolerated - 300mg bolus followed by 900mg/24h
Hypokalaemia, hypomagnesaemia, acidosis and hypoxaemia should be corrected.
Beta blockers or amiodarone can be used for subsequent prophylaxis.

VT can occasionally occur in patients with normal hearts, in which case prognosis is good with catheter ablation.

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5
Q

What are the indications for ICD insertion in VT?

A

Usually indicated in refractory VT or those at high risk of sudden cardiac death (e.g. poor LV function, associated haemodynamic compromise.

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6
Q

What are capture beats?

A

This occurs when the ventricle is in a state of repolarisation and is activated by the normal firing of the SAN.

When this happens, QRS complexes look more normal.

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7
Q

What are fusion beats?

A

This is a complex formed from both activation of the ventricle from the scar site with simultaneous firing of the SAN.

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8
Q

How are the heart sounds and the JVP affected by VT?

A

Due to mechanical and electrical dissociation, there is often a variable intensity of the first heart sound.

Fusion beats cause a cannon A wave in the JVP.

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9
Q

What is torsades des pointes?

A

This is a polymorphic form of VT that occurs due to prolonged ventricular repolarisation.

The ECG shows rapid irregular complexes that oscillate from an upright to an inverted position, seeming to twist around the baseline. The ECG in sinus rhythm shows a prolonged QTc.

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10
Q

What can precipitate torsades?

A

Congenital
- Lange-Nielson (autosomal recessive associated with sensorineural hearing loss)
- Romano-Ward (autosomal dominant, no deafness)
Acquired/ secondary:
- Drugs (class Ia, Ic and III antiarrhythmics, macrolide antibiotics, opiates, TCAs and phenothiazines)
- Electrolyte disturbances (everything is low - Mg, Ca, K)
- MI/ IHD
- Hypothermia

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11
Q

How is torsades des pointes treated?

A

IV magnesium sulphate should be given in all cases.
Atrial pacing or isoprenaline shorten the QT interval by increasing the heart rate.
Otherwise, treatment is directed at the underlying cause.
Congenital long QT syndrome often needs ICD insertion.

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12
Q

What are the normal corrected QT intervals for a man and a woman?

A
Man = <440msec
Woman = <460msec
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13
Q

What are ventricular extrasystoles?

A

Ventricular ectopic beats produce a low stroke volume and premature, bizarre abnormal QRS complexes on the ECG.

Patients are usually asymptomatic but sometimes complain of irregular heart beats, missed beats or abnormally strong beats.

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14
Q

How are ventricular ectopics treated?

A

If the patient is symptomatic, then beta blockade can be useful.
Frequent VEBs in patients with heart failure or those who have survived the acute phase of an MI are associated with an adverse prognosis. Treatment should be directed at the underlying cause.

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15
Q

What is AVNRT?

A

This is a form of SVT.
AVNRT is due to re-entry in the right atrium and AVN and tends to occur in hearts that are otherwise normal (this is a functional, rathe than structure accessory pathway, cf. WPW). It produces episodes of regular tachycardia with a rate of 140-220/min that last from a few seconds to several hours.

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16
Q

What are the clinical features of AVNRT?

A

Patient is usually aware of a fast, regular heart beat and may feel faint or breathless. Polyuria may occur (due to release of ANP).

ECG shows narrow complex, regular tachycardia often with no visible P waves. Occasionally there can be rate dependent AV block.

Cannon A waves are sometimes visible as the atria are contracting against a closed tricuspid valve (these can also occur in other junctional rhythms).

17
Q

How are AVNRTs treated?

A

Attacks can be stopped by Vagal manouvres such as carotid sinus massage.
If this fails then IV adenosine is given (6-12-12) or verapamil if adenosine is contraindicated.
If there is severe haemodynamic compromise, then AVNRT should be treated with DC cardioversion.

If attacks are frequent or disabling, then catheter ablation is the best long term option rather than medication such as beta blockers.