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Cardiovascular Medicine > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

Supraventricular tachycardia - refers to what?

A

A fast heart rate that’s caused by abnormal electrical signals above the ventricles (atria)

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2
Q

Pathophysiology of normal electrical activity of the heart

A 
Normal electrical activity in Sinoatrial node (SVC and RA)
Travel through RA and LA
Atrial contraction
Through atrioventricular node
To the ventricles
Ventricular contraction
One direction
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3
Q

Supraventricular tachycardia - what happens?

A

Refers to electrical signal re-entering the atria from the ventricles
Self-perpetuating electrical loop - fast narrow complex tachycardia

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4
Q

Paroxysmal supraventricular tachycardia

A

SVT remits over time in same patient

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5
Q

Narrow complex tachycardia - what does this mean?

A

Duration of QRS is less than 0.12s
Eg SVT
(3 small squares!!!)

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6
Q

Narrow complex tachycardia - 4 differentials

A
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7
Q

Sinus tachycardia - what is it?

A

Not an arrhythmia
Narrow complex tachycardia
Response to underlying cause e.g. sepsis/pain
Treat underlying cause

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8
Q

Supraventricular tachycardia vs Atrial fibrillation - QRS complex differences

A

QRS complexes are regular in SVT
QRS complex’s are irregularly irregular in AF
BOTH are narrow complex tachycardia

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9
Q

Atrial flutter - what is this?

A

Atrial rate 300bpm
Sawtooth pattern
QRS regular
Usually 2 atrial contractions: 1 ventricular contraction

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10
Q

SVT can cause a broad complex tachycardia in what circumstance?

A

If someone has a bundle branch block

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11
Q

Types of SVT (3)

A

Atrioventricular nodal re-entrant tachycardia - atria, AV node, ventricles, back through node into atria

Atrioventricular re-entrant tachycardia - accessory pathway, electricity back through - more common - Wolff Parkinson white = having an accessory pathway

Atrial tachycardia - abnormally generated activity in the atria, not sinoatrial node (atrial rate >100bpm)

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12
Q

Acute management of SVT in stable patients - stepwise approach to treat

A

Continuous ECG monitoring

1) Valsalva manoeuvre - blow hard against resistance
2) Carotid sinus massage - 2 fingers one side
3) Adenosine or verapamil in those contraindicated
4) (RARE) Electrical cardioversion

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13
Q

Adenosine - how does it work?

A

Slows cardiac conduction
Interrupts AV node or accessory pathway in SVT and resets into sinus rhythm
Half life <10secs - quickly metabolised
Given as a rapid bonus to reach heart quickly
Brief asystole

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14
Q

Contraindications to adenosine (5)

A 
Asthma
COPD
Heart failure
Heart block
Severe hypotension
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15
Q

With adenosine, warn the patient of…

A

Feeling of dying/doom during injection
Fast IV bonus into a large proximal cannula (grey in anti-cubical fossa)
Flushed fast to push it to heart
Doses - 6mg then 12mg then 12mg if no improvement between doses

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16
Q

Adenosine dosing

A

Doses - 6mg then 12mg then 12mg if no improvement between doses

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17
Q

Management of SVT in unstable patients (compromised by SVT) - what scenarios are considered ‘unstable’? (5)

A 
High RR
Chest pain
Hypotension
Heart failure
Poor perfusion
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18
Q

Management of SVT in unstable patients (compromised by SVT) - what do we do?

A

Synchronised cardioversion - defibrillator under sedation/general anaesthetic
Defibrillation monitors R waves, synchronised with ventricular contraction
If successful, sinus rhythms

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19
Q

Why is synchronised cardioversion used in SVT patients?

A

Avoid shocking during T-wave - send into VFib and cardiac arrest

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20
Q

What may be needed in addition to synchronised cardioversion to restore normal electrical activity in SVT? (Unstable patient)

A

Amiodarone

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21
Q

Long term management for SVT

A

Medication such as beta-blockers, calcium-channel blockers, amiodarone
Radio frequency ablation

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22
Q

What is radio frequency ablation?

A

Catheter ablation in a catheter lab
Local or general anaesthetic
Femoral vein - wire under x-ray guidance
Wire in heart, placed to test signals in areas of the heart
Find abnormal pathways, try and induce arrhythmia to make it easier to find
Radio frequency ablation applied to burn the abnormal area
Scar tissue - wont conduct electrical activity

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23
Q

Radio frequency ablation can cure certain arrhythmias (4)

A

Supraventricular tachycardia
Wolff-Parkinson-white syndrome
Atrial flutter
Atrial fibrillation

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24
Q

An irregular broad complex tachycardia on the electrocardiogram is assumed to be ventricular fibrillation. This is always a … rhythm.

A

An irregular broad complex tachycardia on the electrocardiogram is assumed to be ventricular fibrillation. This is always a pulseless rhythm.

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25
Q

ECG features of VF

The QRS complexes are … and …

A

ECG features of VF

The QRS complexes are polymorphic and irregular

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26
Q

Management of VF

A

Management is according to the Advanced Life Support guidelines:

The initial priorities will be as for the Basic Life Support: ensure the airway is patent, check for signs of life (pulse and breathing), and commence CPR.

Ventricular fibrillation is a shockable rhythm: the next step is to administer defibrillation (unsynchronised cardioversion using a 200 J biphasic shock).
Chest compressions should then be resumed.
1 mg adrenaline (10 ml 1:10 000) plus 300 mg amiodarone should be administered after the 3rd shock. Adrenaline should subsequently be administered every 3-5 mins (after every alternate shock).

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27
Q

Is VF shockable?

A

Ventricular fibrillation is a shockable rhythm: the next step is to administer defibrillation (unsynchronised cardioversion using a 200 J biphasic shock).

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28
Q

ECG features of Ventricular tachycardia (VT)

A

Tachycardia (>100 beats per minute), plus
Absent P waves, plus
Monomorphic regular broad QRS complexes (>120 ms).

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29
Q

Management of pulseless Ventricular tachycardia (VT)

If there is no pulse the patient should be managed according to the Advanced Life Support algorithm:

A

VT is a shockable rhythm so a 200 J bi-phasic (unsynchronised) shock should be administered.
CPR should be resumed for 2 minutes before re-checking the rhythm.
Intravenous adrenaline (1 mg of 10 ml 1:10 000 solution) and amiodarone (300 mg) should be administered after delivery of the 3rd shock.
Adrenaline should be administered every 3-5 minutes thereafter (after every alternate shock).

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30
Q

Management of Ventricular tachycardia with a pulse with adverse features

If there is a pulse but the patient shows adverse features (shock, syncope, myocardial ischaemia, or heart failure) the patient should be managed according to the Resuscitation Council tachyarrhythmia algorithm:

A

Administer a synchronised DC shock (up to 3 attempts).
After seeking expert help amiodarone (300 mg intravenously over 10-20 minutes followed by 900 mg over 24 hours) should be administered.

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31
Q

Management of Ventricular tachycardia with a pulse with no adverse features

A

Management is with amiodarone (300 mg intravenously over 20-60 minutes followed by 900 mg over 24 hours).

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32
Q

Torsades de pointes (TdP) is a form of polymorphic ventricular tachycardia caused by QT …

A

Torsades de pointes (TdP) is a form of polymorphic ventricular tachycardia caused by QT prolongation.

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33
Q

Definition of Torsades de pointes

A

Torsades de pointes (TdP) is a form of polymorphic ventricular tachycardia caused by QT prolongation.

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34
Q

ECG features of Torsades de pointes?

A

The electrocardiogram characteristically shows QRS complexes ‘twisting’ around the isoelectric line.

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35
Q

Polymorphic ventricular tachycardia (PVT) is a form of ventricular tachycardia in which there are multiple ventricular foci with the resultant QRS complex varying in amplitude, axis, and duration. The most common cause of PVT is …

A

Polymorphic ventricular tachycardia (PVT) is a form of ventricular tachycardia in which there are multiple ventricular foci with the resultant QRS complex varying in amplitude, axis, and duration. The most common cause of PVT is myocardial ischaemia/infarction.

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36
Q

… is a specific form of PVT occurring in the context of QT prolongation — it has a characteristic morphology in which the QRS complexes “twist” around the isoelectric line.

A

Torsades de pointes (TdP) is a specific form of PVT occurring in the context of QT prolongation — it has a characteristic morphology in which the QRS complexes “twist” around the isoelectric line.

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37
Q

Causes of Torsades de pointes?

A

Congenital Long QT syndromes such as Romano Ward syndrome and Jervell and Lange-Nielsen syndrome
Medication (antiarrhythmics, antibiotics such as erythromycin, tricyclics, antipsychotics, ketoconazole )
Myocardial infarction
Renal/liver failure
Hypothyroidism
AV block
Toxins

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38
Q

Management of TdP in haemodynamically unstable patients

A

If the patient displays adverse features (shock, syncope, myocardial ischaemia, or heart failure) emergency synchronised direct current shock should be administered, followed by intravenous amiodarone.

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39
Q

Management of TdP in haemodynamically stable patients

A

In haemodynamically stable patients, initial management is with intravenous magnesium sulphate (2 g over 10 minutes).

Offending drugs such as drugs that prolong the QT interval should be stopped and electrolyte abnormalities (particularly hypokalaemia and hypomagnesaemia) should be corrected.

Isoprenaline infusion and temporary or permanent pacing may be considered. These may be used in patients with recurrent TdP despite initial therapy with magnesium sulphate.

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40
Q

In irregular narrow complex tachycardias the most likely diagnosis is…

A

atrial fibrillation

Atrial fibrillation with onset <48 hours is typically managed with rhythm control (LMWH followed by flecainide if there is no structural heart disease, or amiodarone if there is structural heart disease).
Atrial fibrillation with onset >48 hours is typically managed with rate control (i.e. metoprolol or bisoprolol or verapamil, or digoxin if there are signs of heart failure) and anticoagulation.

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41
Q

In regular narrow complex tachycardias (SVTs) the first step is to trial vagal manoeuvres - such as?

A

Carotid sinus massage or Valsalva manoeuvre

If vagal manoeuvres fail, adenosine should be administered (initially as a 6 mg intravenous bolus, and if this fails 12 mg followed by a further 18 mg is trialled).

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42
Q

Management of tachycardia according to the Resuscitation Council adult tachycardia algorithm.

A

Patients should be assessed using the ABCDE approach.

If the patient shows adverse features (shock, syncope, heart failure, or myocardial ischaemia), emergency synchronised direct current (DC) cardioversion is indicated.

In haemodynamically stable patients management differs according to whether there is a broad (QRS duration >120 ms) or narrow (QRS duration <120 ms) QRS complex.

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43
Q

A tachycardia is defined as a heart rate greater than 100 beats per minute (bpm). In narrow complex tachycardias the QRS complex is shorter than …

A

A tachycardia is defined as a heart rate greater than 100 beats per minute (bpm). In narrow complex tachycardias the QRS complex is shorter than 120 ms (three small squares on the ECG). Narrow complex tachycardia is common.

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44
Q

Bradycardia is defined as a heart rate of

A

Bradycardia is defined as a heart rate of <60 beats per minute

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45
Q

Causes of acute bradycardia (4)

A

Sinus/AV nodal disease
Drug induced such as beta blockers, calcium channel blockers
Electrolyte abnormalities
Hypothyroidism

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46
Q

Clinical features of acute bradycardia (3)

A

Dizziness
Syncope
Tiredness

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47
Q

Initial management of acute bradycardia

A

According to the ALS adult bradycardia algorithm patients should first be assessed using DR ABCDE, ECG monitoring and any reversible causes should be identified and treated.
If there are any adverse features (shock, syncope, myocardial ischaemia or heart failure) then atropine 500 mcg IV is given.
Atropine blocks the vagus nerve activity on the heart, which increases the firing rate of the SA node.
Repeat boluses can be given up to 3mg

48
Q

Factors increasing the risk of asystole in bradycardia (4)

A

Mobitz type II block
Complete heart block + broad QRS
Recent asystole
Ventricular pause >3 seconds

49
Q

Atrial flutter is caused by an aberrant macro-circuit within the … atrium which cycles at 300bpm.

A

Atrial flutter is caused by an aberrant macro-circuit within the right atrium which cycles at 300bpm.

50
Q

Causes for atrial flutter

Causes are similar to atrial fibrillation (AF) but are more likely to occur with pulmonary disease such as: (4)

A

COPD
Obstructive sleep apnoea
Pulmonary emboli
Pulmonary hypertension

51
Q

Other less likely causes of atrial flutter include:

A 
Ischaemic heart disease
Sepsis
Alcohol
Cardiomyopathy
Thyrotoxicosis
52
Q

Symptoms of atrial flutter (4)

A

Asymptomatic
Palpitations
Dizziness
Chest pain

53
Q

ECG features of atrial flutter

A

Regular rhythm
Saw-tooth baseline with repetition at 300bpm (these are atrial flutter waves)
Narrow QRS complexes
Ventricular rate which depends on the level of AV block:
150bpm if 2:1
100bpm if 3:1
75bpm if 4:1
60bpm if 5:1
Note that sometimes patients might have variable block which makes the rhythm appear irregular and can be hard to distinguish from AF.

54
Q 
Atrial flutter - 
Ventricular rate which depends on the level of AV block:
…bpm if 2:1
…bpm if 3:1
…bpm if 4:1
….bpm if 5:1
A 
Ventricular rate which depends on the level of AV block:
150bpm if 2:1
100bpm if 3:1
75bpm if 4:1
60bpm if 5:1
55
Q

Management of atrial flutter?

A

Initial management is similar to that AF and therefore the exact distinction between AF and flutter is academic in the acute setting (i.e. it doesn’t matter if you are not sure which one it is!)

56
Q

Signs of haemodynamic instability in atrial flutter (4)

A

Shock (suggests end organ hypoperfusion)
Syncope (evidence of brain hypoperfusion)
Chest pain (evidence of myocardial ischaemia)
Pulmonary oedema (evidence of heart failure)

57
Q

Management in haemodynamically unstable patients (atrial flutter)

A

If the patient is haemodynamically unstable emergency direct current synchronised cardioversion should be administered.

58
Q

Management in haemodynamically stable patients - atrial flutter

A

If the patient is haemodynamically stable then reversible causes can be treated. Often fluid resuscitation in septic or dehydrated patients can reverse atrial flutter into sinus rhythm.
Rate control with an AV node blocking agent (a beta blocker or calcium channel blocker) should be attempted first line.
If the atrial flutter fails to respond to rate control therapy and correction of the underlying cause, cardioversion is attempted.

59
Q

Cardioversion for atrial flutter

A

Electrical cardioversion is more effective than pharmacological cardioversion (success rate of 95% v 40-70%).

Pharmacological cardioversion is therefore indicated if the patient is unsuitable for electrical cardioversion or if electrical cardioversion is not available.

Pharmacological cardioversion can be performed using a number of different drugs including amiodarone, sotalol, verapamil, digoxin and a few others.

60
Q

Further management of atrial flutter

A

Recurrent or refractory atrial flutter is managed with catheter ablation of the cavotricuspid isthmus.
Suitable patients include those who are symptomatic despite rate control and those in which at least 1 drug has failed.
The success rate of catheter ablation is high (approximately 90%).

61
Q

Anticoagulation in atrial flutter?

A

Anticoagulation in atrial flutter

The guidelines for anticoagulation are as for atrial fibrillation (i.e. in accordance with the CHA2DS2 VASc score).

62
Q

Atrial fibrillation - what is this?

A

Atrial fibrillation (AF) occurs when there is uncoordinated atrial contraction, typically at approximately 300-600 beats per minute.

Delay at the atrio-ventricular node means that only some of the atrial impulses are conducted to the ventricles, resulting in an irregular ventricular response.

63
Q

Epidemiology of AF

A

Epidemiology

AF is the commonest sustained cardiac arrhythmia.

The prevalence of AF roughly doubles with each advancing decade of age, from 0.5% at age 50–59 years to almost 9% at age 80–89 year

64
Q

Pathophysiology of AF

A

The exact pathophysiology of AF is unclear, but factors that cause dilation of the atria through inflammation and fibrosis result in discrepancies in the refractory periods within the atrial tissue. This causes electrical re-entrant pathways within the atria, and recurrent uncoordinated atrial contraction.

The atrioventricular node (AVN) only conducts some of these atrial impulses, resulting in an irregular ventricular response (hence the irregularly irregular pulse).

65
Q

Causes of Atrial fibrillation (cardiac causes - 4)

A

Cardiac:

Ischaemic heart disease
Hypertension
Rheumatic heart disease (typically affecting the mitral valve) (most common cause in less developed countries)
Peri-/myocarditis

66
Q

List 6 non-cardiac causes of AF

A 
Dehydration
Endocrine causes (such as hyperthyroidism)
Infective causes (such as sepsis)
Pulmonary causes (such as pneumonia or pulmonary embolism)
Environmental toxins (such as alcohol abuse)
Electrolyte disturbances (such as hypokalaemia, hypomagnesaemia)
67
Q

Classifying AF - 4 types

A

Acute (lasts <48 hours)
Paroxysmal (lasts <7 days and is intermittent)
Persistent (lasts >7 days but is amenable to cardioversion)
Permanent (lasts >7 days and is not amenable to cardioversion)

68
Q

Symptoms of AF (4)

A

Symptoms

Palpitations
Chest pain
Shortness of breath
Dizziness

69
Q

Signs of AF

A

An irregularly irregular pulse rate with a variable volume pulse.
A single waveform on the jugular venous pressure (due to loss of the a wave - this normally represents atrial contraction).
An apical to radial pulse deficit (as not all atrial impulses are mechanically conducted to the ventricles).
On auscultation there may be a variable intensity first heart sound.
Features suggestive of the underlying cause (e.g. hyperthyroidism, alcohol excess,sepsis)
Features suggestive of complications resulting from the AF (e.g. heart failure).

70
Q

What is fast AF?

A

When ventricular rate is >100bpm it is considered to be fast AF which normally warrants some level of immediate treatment.

71
Q

Management of Fast Atrial Fibrillation

A

Always start by assessing the patient using an ABCDE approach

Assess for haemodynamic stability
Shock (suggests end organ hypoperfusion)
Syncope (evidence of brain hypoperfusion)
Chest pain (evidence of myocardial ischaemia)
Pulmonary oedema (evidence of heart failure)
If the patient is unstable then they should have immediate DC cardioversion

Consider reversible causes
Infection: Give antibiotics and fluids
Dehydration: Give fluids
Replace abnormal electrolytes
If AF persists or reversible causes are not present then decisions should be made about rate control, rhythm control or electrical cardioversion
72
Q

If the patient is unstable with AF then they should have immediate …

A

DC cardioversion

73
Q

Consider reversible causes of AF such as…

A

Consider reversible causes
Infection: Give antibiotics and fluids
Dehydration: Give fluids
Replace abnormal electrolytes

74
Q

When to offer rate control in AF

Offer rate control as the first-line strategy to people with AF, except in people:

A

Whose AF has a reversible cause.
Who have heart failure thought to be primarily caused by AF.
With new-onset AF.
For whom a rhythm control strategy would be more suitable based on clinical judgement.

75
Q

Rate control in AF - what is used?

A

A beta-blocker such as bisoprolol or a rate limiting calcium-channel blocker (e.g. Dilitiazem) should be the initial monotherapy
Consider digoxin monotherapy for people with non-paroxysmal AF only if they are sedentary (do no or very little physical exercise).

76
Q

Beta-blockers - what is most commonly used for AF?

A

The most commonly used beta-blocker in AF is bisoprolol
Commonly used medication for acute treatment and chronic management.
Technically contraindicated in COPD and asthma (in reality unless the conditions are considered brittle it is not a problem).
Cannot be used in hypotension because it will drop blood pressure.
Note that sotalol CANNOT be used as a rate control agent because of its rhythm control action.

77
Q

Non-dihydropyridine calcium channel blockers - Which ones are used in AF?

A

Calcium channel blockers used in AF are diltiazem or verapamil
They are not frequently used in hospital settings because it is negatively ionotropic therefore it is contraindicated in heart failure

78
Q

When is digoxin indicated in AF?

A

Usual for patients who are hypotensive or have co-existent heart failure
Should be avoided in younger patients because it increases cardiac mortality.
Often used second-line in conjunction with beta-blockers if fast AF remains refractory.

79
Q

Rhythm control

Rhythm control can be achieved via two methods in AF

A

Electrical cardioversion
Pharmacological cardioversion
Note that patients in chronic AF or those who have failed cardioversion before are unlikely to be successfully cardioverted so this would not be considered in most of these cases.

80
Q

Management of new Atrial fibrillation with onset less than 48 hours

A

If the AF is acute (<48 hours) then the patient can be DC cardioverted with sedation.

81
Q

Management of Atrial fibrillation with onset >48 hours with DC cardioversion

A

If the AF is >48 hours (or onset is uncertain) then the patient must be anticoagulated for at least 3 weeks before DC cardioversion can be done.

Alternatively the patient can have a transoesophageal ECHO to rule out a thrombus in the left atrial appendage before cardioversion.

82
Q

Specific drugs used in AF ?

A

Flecainide
Can be either given regularly or as a “pill in the pocket” when symptoms come on.
Is preferred in young patients who have structurally normal hearts because it can induce fatal arrhythmias in structurally abnormal hearts.
Amiodarone
Extremely effective drug in controlling both rate and rhythm.
However it comes with a massive list of significant side-effects so should normally only be given to older, sedentary patients.
Sotalol
This is a beta blocker with additional K channel blocker action
Used for those that don’t meet the demographics for either flecainide or amiodarone.

83
Q

Anticoagulation in AF? WHY?

A

The need for long term anticoagulation should also be considered as
the main complication of AF is embolic stroke. Anticoagulation reduces this risk.

84
Q

CHADS2VASc score components

Patients should be risk stratified using the CHADS2VASc score with AF

A

C: 1 point for congestive cardiac failure.
H: 1 point for hypertension.
A2: 2 points if the patient is aged 75 or over.
D: 1 point if the patient has diabetes mellitus.
S2: 2 points if the patient has previously had a stroke or transient ischaemic attack (TIA).
V: 1 point if the patient has known vascular disease.
A: 1 point if the patient is aged 65-74.
Sc: 1 point if the patient is female.

85
Q

Interpretation of the CHADS2VASc score?

A

The minimum score is 0 (associated with 0% annual stroke risk) and maximum score is 9 (15 annual risk)
Males who score 1 or more or females who score 2 or more should be anticoagulated.

86
Q

Assessing bleeding risk (AF + anticoagulation)

A

In their 2021 AF guidelines NICE suggested the use of the ORBIT score which takes into account:

Sex
Haemoglobin (<13mg/Dl in males, <12mg<dl>74) 1 point
Bleeding history 2 points
Renal function (eGFR <60) 1 point
Concomitant use of anti-platelets 1 point</dl>
87
Q

Anticoagulation options in AF

A

Direct oral anticoagulants (DOACs) for AF
Are currently generally considered to be the drugs of choice
Examples of DOACs are edoxaban, apixaban, rivaroxaban & dabigatran
Do not require monitoring
Generally associated with less bleeding risks than warfarin.
Most have approximately 12 hour half-lives therefore if patients miss doses they are not covered.
Warfarin
Requires cover with LMWH for 5 days when initiating treatment (because warfarin is initially prothrombotic).
Requires regular INR monitoring.
INR can be affected by a whole host of drugs and foods.
Has 40 hour half-life therefore anticoagulant effect lasts days.
Is the only oral anticoagulant licenced for valvular AF.
Low Molecular Weight Heparin (LMWH) for AF
An example of a LMWH is enoxaparin.
A rare option in patients who cannot tolerate oral treatment.
Involves a daily treatment dose injections.

88
Q

Direct oral anticoagulants (DOACs) for AF

A

Are currently generally considered to be the drugs of choice
Examples of DOACs are edoxaban, apixaban, rivaroxaban & dabigatran
Do not require monitoring
Generally associated with less bleeding risks than warfarin.
Most have approximately 12 hour half-lives therefore if patients miss doses they are not covered.

89
Q

What is the only oral anticoagulant licenced for valvular AF?

A

Warfarin
Requires cover with LMWH for 5 days when initiating treatment (because warfarin is initially prothrombotic).
Requires regular INR monitoring.
INR can be affected by a whole host of drugs and foods.
Has 40 hour half-life therefore anticoagulant effect lasts days.
Is the only oral anticoagulant licenced for valvular AF.

90
Q

An example of a LMWH is ….
A rare option in patients who cannot tolerate oral treatment.
Involves a daily treatment dose injections.

A

An example of a LMWH is enoxaparin.
A rare option in patients who cannot tolerate oral treatment.
Involves a daily treatment dose injections.

91
Q

Low Molecular Weight Heparin (LMWH) for AF
An example of a LMWH is enoxaparin.
A rare option in patients who cannot tolerate oral treatment.
Involves a … treatment dose injections.

A

Low Molecular Weight Heparin (LMWH) for AF
An example of a LMWH is enoxaparin.
A rare option in patients who cannot tolerate oral treatment.
Involves a daily treatment dose injections.

92
Q

Atrial ablation in AF

A

Atrial ablation

Atrial ablation is an option for some patients who do not have uncontrolled symptoms and have an identifiable locus in their left atrium.

93
Q

Complications of Atrial fibrillation

A

Most complications are either from uncontrolled heart rate, embolism or from anticoagulation. They include:

Heart failure
Systemic emboli:
Ischaemic Stroke
Mesenteric ischaemia
Acute limb ischaemia
Bleeding:
GI
Intracranial
94
Q

Cautions and contra-indications to the use of Adenosine?

A

IV Adenosine 3mg should not be administered to heart transplant patients, those who have central line access, or patients on medications that can potentiate the effects of Adenosine such as Dipyridamole or Carbamazepine.

Asthma is a contra-indication to the use of Adenosine so Verapamil should be used instead.

95
Q

Complcations of SVT can include:

A 
Syncope
Deep vein thrombosis
Embolism
Cardiac tamponade
Congestive cardiac failure
Myocardial infarction
Death
96
Q

Atrial Fibrillation (AF), AV Re-entry Tachycardia (AVRT) and AV Nodal Re-entry Tachycardia (AVNRT) are examples of ….

A

Atrial Fibrillation (AF), AV Re-entry Tachycardia (AVRT) and AV Nodal Re-entry Tachycardia (AVNRT) are examples of SVTs.

97
Q

Emergency Management of Torsades de pointes

A

In unstable patients with haemodynamic compromise, DC cardioversion can be done. In stable patients, the choice of treatment is IV Magnesium Sulphate 2g over 1 to 2 minutes.

98
Q

Wolff-Parkinson-White (WPW) is caused by a congenital accessory electrical pathway which connects the atria to the ventricles bypassing the AV node.

This accessory pathway leads to the potential for re-entrant circuits to form leading to…

A

Wolff-Parkinson-White (WPW) is caused by a congenital accessory electrical pathway which connects the atria to the ventricles bypassing the AV node.

This accessory pathway leads to the potential for re-entrant circuits to form leading to supraventricular tachycardias.

99
Q

The prevalence of WPW syndrome is approximately 100-300 per 100000 individuals worldwide. … are more commonly affected with WPW syndrome than …, with the ratio being approximately 2 to 1.

A

The prevalence of WPW syndrome is approximately 100-300 per 100000 individuals worldwide. Men are more commonly affected with WPW syndrome than women, with the ratio being approximately 2 to 1.

100
Q

Clinical features of WPW

A

Patients may present with:

No symptoms - WPW is often asymptomatic
Palpitations
Dizziness
Syncope

101
Q

Features on ECG in WPW?

A

Delta waves (slurred upstroke in the QRS)
Short PR interval (<120ms)
Broad QRS
If a re-entrant circuit has developed the ECG will show a narrow complex tachycardia

102
Q

Diagnosis of WPW?

A

Patients with suspected WPW may benefit from the following:

ECG
24 hour ECG monitoring if paroxysmal symptoms
Routine bloods including TFTs if non-cardiac causes of tachycardia are suspected
ECHO - to assess ventricular function
Intracardiac electrophysiological studies to map the location of the accessory pathway

103
Q

Management of WPW

A 
Radiofrequency ablation of the accessory pathway
Drug treatment (such as amiodarone or sotalol) to avoid further tachyarrhthmias. These are contraindicate din structural heart disease.
Surgical (open heart) ablation - rarely done and only used in complex cases
104
Q

Contraindications in WPW

A

Digoxin and NDP-CCBs (e.g. verapamil) are contraindicated for long term use because they may precipitate ventricular fibrillation.

If the patient is experiencing supraventricular tachycardia the management depends on whether the patient is stable or unstable, and if stable the type of arrhythmia:

105
Q

Management of WPW in unstable patients

Unstable patients (blood pressure <90/60mmHg or with signs of systemic hypoperfusion or fast atrial fibrillation) require …

A

Unstable patients (blood pressure <90/60mmHg or with signs of systemic hypoperfusion or fast atrial fibrillation) require urgent direct current (DC) cardioversion.

106
Q

Management of WPW in stable patients

If the patient is stable they are managed according to the rhythm:

A

In patients with an orthodromic AV reciprocating tachycardia (narrow QRS complex with short PR interval) management is with vagal manoeuvres (carotid sinus massage or Valsalva manoeuvre) in the first instance. If this fails IV adenosine should be administered.
Note that in orthodromic AV reciprocating tachycardias one limb of the aberrant circuit involves the AV node so slowing conduction through the AV node helps terminate the tachycardia.
In patients with antidromic AV reciprocating tachycardia (wide QRS complex), atrial fibrillation, or atrial flutter intravenous anti-arrhythmics (such as procainamide or flecainide) help prevent rapid conduction through the accessory pathway.
DC cardioversion may be used if symptoms persist.

107
Q

WPW ECG features

A

PR interval < 120ms
Delta wave: slurring slow rise of initial portion of the QRS
QRS prolongation > 110ms
Discordant ST-segment and T-wave changes (i.e. in the opposite direction to the major component of the QRS complex)
Pseudo-infarction pattern in up to 70% of patients — due to negatively deflected delta waves in inferior/anterior leads (“pseudo-Q waves”), or prominent R waves in V1-3 (mimicking posterior infarction)

108
Q

Wolff-Parkinson-White is associated with a small risk of what?

A

Associated with a small risk of sudden cardiac death

109
Q

There are only two main forms of tachyarrhythmias that occur in patients with WPW — these are discussed separately:

A

Atrial fibrillation or flutter. Due to direct conduction from atria to ventricles via an AP, bypassing the AV node
Atrioventricular re-entry tachycardia (AVRT). Due to formation of a re-entry circuit involving the AP

110
Q

Focal atrial tachycardia (FAT) is a form of supraventricular tachycardia (SVT) originating from a single ectopic focus within the atria but outside of the …

A

Focal atrial tachycardia (FAT) is a form of supraventricular tachycardia (SVT) originating from a single ectopic focus within the atria but outside of the sinus node

111
Q

… - Consistent, abnormal P wave morphology indicating an ectopic focus

A

Focal atrial tachycardia (FAT): Consistent, abnormal P wave morphology indicating an ectopic focus

112
Q

Pathophysiology of FAT (focal atrial tachycardia)

A 
Due to a single ectopic focus
The underlying mechanism can involve increased automaticity, triggered activity or reentry
May be paroxysmal or sustained
Multiple causes including:
Digoxin toxicity
Atrial scarring due to ischaemic heart disease
Catecholamine excess
Stimulants including cocaine, caffeine
Alcohol
Congenital abnormalities
Idiopathic
Sustained atrial tachycardia may rarely be seen and can progress to tachycardia-induced cardiomyopathy
113
Q

ECG Features of Atrial Tachycardia

A

Atrial rate > 100 bpm
Abnormal P wave morphology and axis (e.g. inverted in inferior leads) due to ectopic origin
Unifocal, identical P waves
Isoelectric baseline (unlike atrial flutter)
Normal QRS morphology (unless pre-existing bundle branch block, accessory pathway, or rate-related aberrant conduction)

114
Q

Tachyarrhythmias - ECG differences (QRS and rhythm)

A

Narrow QRS, regular rhythm
Narrow QRS, Irregular rhythm
Wide QRS, regular rhythm
Wide QRS, Irregular rhythm

115
Q

Narrow QRS, regular rhythm
Narrow QRS, Irregular rhythm
Wide QRS, regular rhythm
Wide QRS, Irregular rhythm

Examples of each?

A
116
Q

What does this show?

A

Atrial flutter

Cardiovascular Medicine (28 decks)

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