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Yr 4 - ACC > Cardiology: SVT > Flashcards

Cardiology: SVT Flashcards

1
Q

What is a supraventricular tachycardia (SVT)?

A

A rapid heart rate that originates from above or within the atrioventricular (AV) node.

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2
Q

In general, SVT is caused by one of what three mechanisms?

A

1) Re-entry of signals

2) Increased automaticity

3) Triggered activity

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3
Q

What is a focal tachycardia?

A

The tachycardia originates from a single point (or points) in the atrium or AV node.

  • The sinus node is meant to be the most autonomic part of the heart and as such takes charge.
  • If another part of the heart becomes MORE autonomic (or the sinus node becomes LESS autonomic), it takes over and a focal tachycardia results.
  • There will be organised atrial contraction and a wave similar to a P wave will appear before the QRS complex.
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4
Q

What are some subtypes of focal tachycardias?

A

1) Sinus tachycardia

2) Atrial tachycardia

3) Multifocal atrial tachycardia

4) Junctional rhythms

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5
Q

What is sinus tachycardia?

A

The ‘focus’ is the sinoatrial node!

Usually regular.

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6
Q

What happens in atrial tachycardia?

A

A different focus in the atrium takes over from the sinoatrial node resulting in ABNORMAL P waves preceding QRS complexes.

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7
Q

Who is atrial tachycardia often seen in?

A

Patients with chronic lung disease e.g. COPD

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8
Q

Typical heart rate in atrial tachycardia?

A

Normally > 100 bpm and regular

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9
Q

What happens in multifocal atrial tachycardia?

A

The P waves will have different morphologies as the atrial focus changes from beat to beat.

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10
Q

What is the next most autonomic piece of tissue in the heart after the sino-atrial node?

A

AV node

I.e. If the sinoatrial node is not functioning (e.g. high vagal tone, sick sinus syndrome), the AV node takes over.

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11
Q

Where does the impulse originate from in junctional rhythms?

A

The impulse originates from the AV node and propagates to the atrium and the ventricles simultaneously.

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12
Q

Management of INAPPROPRIATE sinus tachycardia?

A

Can be slowed using:

1) beta blockers
2) ivabradine (selective sinus node blocker)

However it is usually best left alone.

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13
Q

Management of APPROPRIATE sinus tachycardia (e.g. due to concurrent sepsis/anaemia/thyrotoxicosis/pain)?

A

should be left alone and the underlying trigger treated.

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14
Q

What can atrial tachycardias usually be rate controlled with?

A

beta-blockers or calcium channel blockers

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15
Q

What is the most common type of SVT?

A

Re-entry tachycardias.

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16
Q

What happens in re-entry SVT?

A

1) There is normal electrical conduction from the atria to the ventricles in the normal pathway.

2) However, after this, retrograde conduction occurs via an accessory pathyway from the ventricles back up to the atria.

3) This leads to repetitive impulse propagation and subsequent tachycardia.

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17
Q

Which conditions is re-entry SVT seen in?

A

1) Atrial flutter

2) Atrial fibrillation

3) AVNRT (atrio-ventricular node re-entrant tachycardia)

4) AVRT (atrio-ventricular re-entrant tachycardia)

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18
Q

What is a macro-entrant tachycardia?

A

This means there is a single large re-entry circuit around the atrium which stimulates the AV node every time it passes.

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19
Q

What is a MICRO-RE-ENTRANT tachycardia?

A

There are lots of tiny circuits contributing to the chaotic and random fibrillation of the atrium.

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20
Q

Is atrial flutter a micro or macro-rentrant tachycardia?

A

Macro

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21
Q

What is the distinctive ECG pattern in atrial flutter?

A

sawtooth baseline

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22
Q

What are the risk factors for atrial flutter?

A

1) advanced age

2) structural heart disease

3) hypertension

4) diabetes

5) history of atrial fibrillation

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23
Q

Clinical features of atrial flutter?

A

1) Haemodynamic instablity: dyspnea, fatigue, lightheadedness, presyncope or syncope.

2) Palpitations

3) Chest Pain

4) Heart Failure Symptoms: orthopnea, PND, and peripheral oedema

5) Thromboembolic Complications: TIAs, strokes

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24
Q

What causes haemodynamic instability in atrial flutter?

A

The loss of coordinated atrial contraction results in reduced ventricular filling and subsequently diminished cardiac output.

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25
Q

How can atrial flutter induce HF symptoms?

A

Patients with pre-existing systolic or diastolic dysfunction may experience worsening heart failure symptoms due to the loss of atrial kick and tachycardia-induced cardiomyopathy.

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26
Q

How can atrial flutter predispose to thromboembolic complications?

A

Atrial flutter predisposes patients to thrombus formation within the left atrium and its appendage due to stasis from uncoordinated atrial contractions.

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27
Q

What is the atrial rate in atrial flutter?

A

250-350 beats per minute.

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28
Q

What does the ventricular rate depend on in atrial flutter?

A

The ventricular rate depends on the degree of atrioventricular node conduction.

  • 2:1 = 150bpm
  • 3:1 = 100bpm
  • Variable – can produce an irregularly irregular rhythm
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29
Q

What leads is the sawtooth appearance in atrial flutter best seen in?

A

Inferior leads (II, III, aVF)

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30
Q

Is atrial fibrillation a micro or macro-re-ntrant tachycardia?

A

Micro

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31
Q

What is the most common form of paroxysmal SVT?

A

Atrio-ventricular nodal re-entrant tachycardia (AVNRT)

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32
Q

What is paroxysmal SVT?

A

describes a situation where SVT reoccurs and remits in the same patient over time.

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33
Q

What is a narrow complex tachycardia?

A

a fast heart rate with a QRS complex duration of less than 0.12 seconds.

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34
Q

On a standard 25 mm/sec ECG, what does 3 small squares equal?

A

0.12 seconds

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35
Q

What are the 4 main differentials for a narrow complex tachycardia?

A

1) sinus tachycardia

2) SVT

3) atrial fibrillation

4) atrial flutter

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36
Q

What is sinus tachycardia usually a response to?

A

An underlying cause, such as sepsis or pain.

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37
Q

What does a SVT look like on an ECG?

A

1) QRS complex followed immediately by a T wave, then a QRS complex, then a T wave, and so on.

2) There are P waves, but they are often buried in the T waves, so you cannot see them.

3) Regular rhythm

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38
Q

When can SVT cause a broad complex tachycardia?

A

If the patient also has a bundle branch block –> consider this differential in patients with tachycardia and wide QRS complexes.

39
Q

What happens in atrioventricular nodal re-entrant tachycardia (AVNRT)?

A

where the re-entry point is back through the AV node.

40
Q

What is atrioventricular re-entrant tachycardia (AVRT)?

A

Where the re-entry point is an accessory pathway.

An additional electrical pathway, somewhere between the atria and the ventricles, lets electricity back through from the ventricles to the atria.

41
Q

What is having an extra electrical pathway connecting the atria and ventricles called?

A

Wolff-Parkinson-White syndrome.

42
Q

What happens in atrial tachycardia?

A

Atrial tachycardia is where the electrical signal originates in the atria somewhere other than the sinoatrial node.

This is not caused by a signal re-entering from the ventricles but from abnormally generated electrical activity in the atria.

43
Q

What is Wolff-Parkinson-White syndrome (WPW)?

A

This is caused by an extra electrical pathway connecting the atria and ventricles.

It is also called pre-excitation syndrome.

The additional pathway allows electrical activity to pass between the atria and ventricles, bypassing the atrioventricular node.

44
Q

What may the extra pathway in Wolff-Parkinson-White syndrome be called?

A

The Bundle of Kent

45
Q

What ECG changes are seen in WPW syndrome?

A

1) Short PR interval, less than 0.12 seconds

2) Wide QRS complex, greater than 0.12 seconds

3) Delta wave

46
Q

How does the delta wave appear in WPW syndrome?

A

As a slurred upstroke in the QRS complex.

47
Q

What is the delta wave caused by in WPW syndrome?

A

It is caused by the electricity prematurely entering the ventricles through the accessory pathway.

48
Q

What is the definitive treatment for WPW syndrome?

A

Radiofrequency ablation of the accessory pathway.

49
Q

What is the risk when a patient has a combination of atrial fibrillation or atrial flutter and WPW?

A

There is a risk that the chaotic atrial electrical activity can pass through the accessory pathway into the ventricles, causing a polymorphic wide complex tachycardia –> life-threatening medical emergency.

50
Q

What happens in polymorphic wide complex tachycardia?

A

The heart rate can get above 200, or even 300, beats per minute, and ventricular fibrillation and cardiac arrest can follow.

51
Q

Why are most anti-arrhythmic medications (e.g., beta blockers, calcium channel blockers, digoxin and adenosine) contraindicated in patients with WPW that develop atrial fibrillation or flutter?

A

As these drugs increase the risk of polymorphic wide complex tachycardia by reducing conduction through the AV node and promoting conduction through the accessory pathway.

52
Q

Management of SVT in patients WITHOUT life-threatening features?

A

Stepwise approach:

1) Vagal manoeuvres

2) Adenosine

3) Verapamil or a beta blocker

4) Synchronised DC cardioversion

53
Q

Management of SVT in patients WITH life-threatening features (e.g. syncope, muscle heart ischaemia, severe HF)?

A

Synchronised DC cardioversion under sedation or general anaesthesia.

54
Q

If initial shocks with synchronised DC cardioversion are unsuccessful in life-threatening SVT, what can be added?

A

IV amiodarone.

55
Q

What drugs should patients with WPW syndrome with possible atrial arrhythmias (e.g., atrial fibrillation or atrial flutter) NOT have?

A
  • adenosine
  • verapamil
  • beta blocker

As these block the AV node, promoting conduction of the atrial rhythm through the accessory pathway into the ventricles, causing potentially life-threatening ventricular rhythms.

56
Q

What is indicated instead of adenosine, verapamil or a beta blocker in patients with WPW with possible atrial arrhythmias?

A

1) procainamide (does not block the AV node)

2) electrical cardioversion (if unstable)

57
Q

What are vagal manoeuvres?

A

These stimulate the vagus nerve, increasing the activity in the parasympathetic nervous system.

This can slow the conduction of electrical activity in the heart, terminating an episode of SVT.

58
Q

What are the 3 vagal manoeuvres used in SVT?

A

1) carotid sinus massage (CSM)

2) Valsalva maneuver (VM)

3) diving reflex

59
Q

What do Valsalva manoeuvres involve?

A

These involve increasing the intrathoracic pressure.

This can be achieved by having the patient blow hard against resistance, for example, blowing into a 10ml syringe for 10-15 seconds.

60
Q

What does a carotid sinus massage involve?

A

This timulating the baroreceptors in the carotid sinus by massaging that area on one side of the neck (not both sides at the same time).

61
Q

Who is carotid sinus massage avoided in?

A

Patients with carotid artery stenosis (e.g. with a carotid bruit or previous TIA).

62
Q

What does the diving reflex involve?

A

The diving reflex involves briefly submerging that patient’s face in cold water.

63
Q

Mechanism of adenosine?

A

1) Causes transient heart block in the AV node

2) It is an agonist of the A1 receptor in the AV node, which inhibits adenylyl cyclase and reduces AMP, causing hyperpolarisation by increasing outward potassium flux

64
Q

How does adenosine treat SVT?

A

Adenosine works by slowing cardiac conduction, primarily through the AV node.

It interrupts the AV node or accessory pathway during SVT and “resets” it to sinus rhythm.

65
Q

What is adenosine’s half life?

A

<10 secnds: needs to be given as a rapid bolus

66
Q

Who is adenosine avoided in?

A

1) asthma
2) COPD
3) HF
4) heart block
5) severe hypotension
6) potential atrial arrhythmia with underlying pre-excitation (WPW)

67
Q

How must adenosine be given?

A

Adenosine must be given as a rapid IV bolus into a large proximal cannula (e.g., grey cannula in the antecubital fossa).

68
Q

How many doses of adenosine are attempted until sinus rhythm returns?

A

Three:

1) Initially 6mg
2) Then 12mg
3) Then 18mg

69
Q

Adverse effects of adenosine?

A

1) chest pain

2) bronchospasm

3) transient flushing

4) can enhance conduction down accessory pathways, resulting in increased ventricular rate (e.g. WPW syndrome)

5) can cause a brief period of asystole or bradycardia (scary for patient and doctor)

70
Q

Why is adenosine contraindicated in asthma/COPD?

A

Can cause bronchospasm

71
Q

What does synchronised DC (direct current) cardioversion involve?

A

An electric shock applied to the heart to restore normal sinus rhythm.

1) A defibrillator machine monitors the electrical signal, particularly identifying the R waves.

2) An electric shock is synchronised with a ventricular contraction, at the R wave on the ECG. If successful, the shock will be followed by sinus rhythm.

72
Q

Why is it important that cardioversion is synchronised in SVT?

A

Synchronised cardioversion is used in patients with a pulse to avoid shocking the patient during a T wave. Delivering a shock during a T wave can result in ventricular fibrillation and, subsequently, cardiac arrest.

73
Q

Why is there no need for the shock to be synchronised in cardiac arrest?

A

During a cardiac arrest scenario with pulseless ventricular tachycardia or ventricular fibrillation, where the patient does not have organised electrical activity or a pulse, there is no need for the shock to be synchronised.

74
Q

Patients with recurrent episodes of SVT can be treated to prevent further episodes.

What are the 2 main options?

A

1) Long-term medication (e.g., beta blockers, calcium channel blockers or amiodarone)

2) Radiofrequency ablation

75
Q

What is radiofrequency ablation?

A

Catheter ablation is performed in a catheter laboratory, often called a “cath lab”.

It involves a general anaesthetic or sedation.

1) A catheter is inserted into a femoral vein and fed through the venous system under x-ray guidance to the heart.

2) The catheter tip is placed against different areas to test the electrical signals

3) The operator attempts to identify the location of any abnormal electrical pathways

4) Once identified, radiofrequency ablation (heat) is applied to burn the abnormal electrical pathway.

5) This leaves scar tissue that does not conduct electrical activity.

76
Q

Radiofrequency ablation can permanently resolve certain arrhythmias in what conditions?

A

1) atrial fibrillation

2) atrial flutter

3) SVTs

4) WPW syndrome

77
Q

What are the 4 main differentials of a narrow complex tachycardia?

A

1) Sinus tachycardia

2) SVT

3) Atrial fibrillation

4) Atrial flutter

78
Q

Pathophysiology of SVT?

A

In most cases, caused by electrical signal RE-ENTERING the atria from the ventricles.

The signal then travels back through the AV node to the ventricles again, causing another ventricular contraction.

This causes a self-perpetuating electrical loop (without an end point) –> fast narrow complex tachycardia.

79
Q

What is paroxysmal SVT?

A

SVT reoccurs and remits in patient over time.

Period of normal sinus rhythm in between.

80
Q

How can SVT be differentiated from AF on an ECG?

A

In SVT –> QRS complexes are regular

In AF –> QRS complexes are irregularly irregular

81
Q

What is atrial rate in atrial flutter?

A

around 300bm

82
Q

Ventricular rate in atrial flutter?

A

Depends on how often there is conduction from the atria to ventricles.

Normally 2 atrial contractions to 1 ventricular contraction (i.e. 2 p waves to 1 QRS complex)

83
Q

When can SVT cause a broad complex tachycardia?

A

If patient also has a bundle branch block.

84
Q

What are the 3 main types of SVT?

A

1) Atrioventricular nodal re-entrant tachycardia

2) Atrioventricular re-entrant tachycardia

3) Atrial tachycardia

85
Q

What happens in atrioventricular nodal re-entrant tachycardia?

A

When the re-entry point is back through the AV node into the atria again.

86
Q

What happens in atrioventricular re-entrant tachycardia?

A

When the re-entry point is an accessory pathway (somewhere between the atria and ventricles that lets electricity back through).

87
Q

What is the most common type of SVT?

A

Atrioventricular re-entrant tachycardia

88
Q

What is having an additional electrical conducting pathway in the heart called?

A

Wolff-Parkinson-White syndrome.

This might not cause any symptoms or may cause episodes of SVT.

89
Q

How may the accessory pathway be seen on an ECG?

A

1) Slurred upstroke in the QRS complex (delta wave)

2) Short PR interval

90
Q

What happens in atrial tachycardia?

A

Electrical signal originates in the atria somewhere other than the SA node.

This is NOT from the signal re-entrying the atria but from abnormally generated electrical activity in the atria (ectopic).

91
Q

How does adenosine work?

A

Slowing cardiac conduction primarily through the AV node.

Interrupts the AV node or accessory pathway during SVT and resets it back to sinus rhythm.

92
Q

During synchronised DC, what is the timing of the shock avoiding?

A

Avoids shocking the patient during a T wave (this can cause VF and cardiac arrest).

93
Q

What may unstable patients with SVT require alongside synchronised cardioversion?

A

Amiodarone

94
Q
A

Yr 4 - ACC (73 decks)

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