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CARDIOLOGY > ARRYHTHMIAS > Flashcards

ARRYHTHMIAS Flashcards

1
Q

What are the four possible rhythms that you will see in a pulseless unresponsive patient?

A

Ventricular tachycardia
Ventricular fibrillation
Pulseless electrical activity
Asystole

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2
Q

What are the 2 shockable rhythms?

A

Ventricular tachycardia
Ventricular fibrillation

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3
Q

What are the 2 non-shockable rhythms?

A

Pulseless electrical activity
Asystole

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4
Q

What is pulseless electrical activity?

A

Cardiac arrest where the ECG shows a heart rhythm that should produce a pulse but it does not

All electrical activity except VF/VT, including sinus rhythm without a pulse

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5
Q

What is asystole?

A

no significant electrical activity

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6
Q

What are the symptoms of arrhythmias?

A

Asymptomatic
palpitations
Syncope
Decompensated cardiac disease
SOB
Chest pain - more common in tachyarrhythmias
Sudden death

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7
Q

What are the 2 types of Bradyarrhythmias?

A

sinus node dysfunction and atrioventricular (AV) blocks

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8
Q

What are the 2 types of tachyarrhythmias?

A

Broad complex >120ms
Narrow complex <120ms

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9
Q

What are the narrow complex tachyarrhythmias? Why do they cause narrow complex?

A

Supraventricular tachyarrhythmias

(A narrow QRS complex reflects rapid activation of the ventricles via the normal His-Purkinje system, which in turn suggests that the arrhythmia originates above or within the His bundle)

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10
Q

What are the broad complex tachyarrhythmias?

A

Ventricualr tachyarrhythmias
Can be Supraventricular if BBB

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11
Q

What is an arrhythmia?

A

Abnormality with rate, rhythm, sequence of conduction or origin of conduction
Or abnormality electrical activity within the hart

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12
Q

What are examples of supraventricular tachyarrhythmias?

A

Sinus tachycardia
AF
atrial flutter
Atrioventricular nodal re-entrant tachycardia
Atrioventricular re-entrant/reciprocating tachycardia
Supraventricular tachycardia or unknown origin
Focal atrial tachycardia
Multi focal atrial tachycardia
Sinus nodal re-entrant tachycardia
Junctional tachycardia

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13
Q

What are focal tachycardias?

A

The tachycardia originates from a single point (or points) in the atrium or AV node. Also known as ‘enhanced automaticity’. If another part of the heart becomes MORE autonomic than the SAN (or the sinus node becomes LESS autonomic), it takes over and a focal tachycardia results. This means there will be an organised atrial contraction and a wave similar to a P wave will appear before the QRS complex.
E.g. sinus tachycardia, atrial tachycardia, multifocal atrial tachycardia, junctional rhythm

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14
Q

What is PSVT?

A

paroxysmal supraventricular tachycardia
It’s a narrow complex tachycardia which involves episodic supraventricular tachycardia which typically ranges from 140-250bpm. Most common in young adults. Can be triggered by stress, anxiety, caffeine, nicotine, alcohol or exercise
There are many different types - AV nodal reentrant tachycardia, atrial tachycardia, atrioventricular reentrant tachycardia, junctional tachycardia,

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15
Q

What is atrial tachycardia and what are its ECG features?

A

A different focus in the atrium takes over from the sinoatrial node resulting in ABNORMAL P waves preceding QRS complexes
>100bpm and regular

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16
Q

Who is atrial tachycardia most common in?

A

Patients with concomitant lung disease e.g. COPD

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17
Q

What is multifocal atrial tachycardia and what are its ECG features?

A

Atrial impulses arise from multiple ectopic foci in the atria, resulting in an irregular ventricular response. It’s a type of SVT characterised by an irregular rhythm with 3 or more different P-wave morphologies on ECG.
Most common seen in pt with COPD or other lung disease, but can occur with heart disease or electrolyte imbalances

ECG findings:
Rapid, irregular HR >100bpm
Polymorphic P waves - at least 3 different P wave forms
P waves typically negative in V1 and have varying PR intervals
Irregular ventricular rhythm which is typically faster than atrial rate
Absence of a regular pattern of QRS complexes
Possible evidence of underlying lung disease/electrolyte imbalances

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18
Q

What are junctional tachycardias and what are its ECG features?

A

A type of SVT arising from the atrioventricular junction (AVN, bundle of His, and the bundle branches)

> 100bpm
Regular rhythm
P wave is typically inverted or absent and QRS is narrow

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19
Q

What are the types of re-entry tachycardia?

A

Atrial flutter
AF
AV node re-entrant tachycardia
AV re-entrant tachycardia
Reentrant Ventricualr tachycardias

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20
Q

What is a macro re-entrant tachycardia?

A

When there is a single large re-entry circuit around the atrium which stimulates the AV node every time it passes.
E.g. atrial flutter and AVRT

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21
Q

What is a micro re-entrant tachycardia?

A

Lots of small circuits within a small localised area of cardiac tissue that contribute to stimulating the AV node e.g. atrial fibrillation

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22
Q

What is a typical atrial flutter?

A

A single large re-entry circuit runs-around the right atrium and across the IVC and cavotricuspid valve isthmus
90% of cases this is anticlockwise. This produced inverted flutter waves in inferior leads

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23
Q

What is a atypical atrial flutter?

A

a single large re-entry circuit runs clockwise in the right atrium, left atrium or around sites of previous surgery
Lack the typical sawtooth appearance on ECG so suspect it for any regular tachycardia at or around 150bpm

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24
Q

Which leads is the sawtooth appearance for atrial flutter best seen? What causes this?

A

inferior leads
It is caused by the circuit alternately heading towards the inferior leads and away as it speeds around the atrium.

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25
Q

Outline the typical rate of atrial conduction in atrial flutter?

A

As the circuit is fixed, the rate of atrial contraction is constant (depending on the size of the atria – in a normal-sized chamber, flutter waves are around 300bpm but patients with dilated atria can have much slower circuits).

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26
Q

What does the ventricular rate in atrial flutter and fibrillation depend on?

A

The degree of AV block (ratio 2:1 means for every 2 beats in the atria, the ventricles beat once)
2:1 = 150bpm
3:1 = 100 bpm
Variable - can produce an irregularly irregular rhythm

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27
Q

What can be seen on ECG in AF?

A

Rapid fibrillation waves on the baseline
Absence of P waves
Irregularly irregular

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28
Q

What is atrio-ventricular nodal re-entrant tachycardia?

A

The most common regular SVT
It’s a paroxysmal supraventricular tachycardia that results due to the presence of a re-entry circuit within the AVN, or anatomically adjacent to - usually fibrosis or scarring in AVN. This repeating loop re-excites itself and passes on a rapid rate to the ventricles = no P waves as sinus node isn’t activating
More common in women 3:1
Precipitated by caffeine, alcohol, exercise, drugs, beta agonists, Sympathomimetics, hyperthyroidism
Sudden onset, sensation of regular palpitations, anxiety and SOB
Slow-fast pathway (alpha-beta) is most common

Because it is technically WITHIN the node, the resulting circuit activates both the ventricles and atria almost simultaneously. Two anatomical pathways next to the AV node (the slow and fast pathways) form a circuit with very rapid conduction that produces a rapid regular tachycardia.

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29
Q

What are the ECG findings for atrio-ventricular node re-entrant tachycardia?

A

pseudo R wave - this is actually the retrograde P wave superimposed on the QRS complex (may not see them as they may be buried in QRS)

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30
Q

What is atrio-ventricular re-entrant tachycardia?

A

A type of supraventricualr tachycardia
Most commonly associated with being the most common cause of tachycardia in Wolff-Parkinson-white syndrome, but also seen in permenant junctional reentrant tachycardia

A re-entrant circuit - Underlying accessory pathway between atria and ventricles (most commonly between left atrium and left ventricles - the bundle of Kent)

This requires two pathways – the normal AV conduction system and an accessory pathway (AP).
Accessory pathways can conduct ANTEGRADE (atria to ventricles) and RETROGRADE

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31
Q

What are ECG findings for AVRT?

A

Delta wave - pre-excitation on resting ECG due to antegrade accessory pathway

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32
Q

What are the types of AVRTs?

A

Orthodromic
Antidromic

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33
Q

What is the difference between orthodromic and antidromic AVRT?

A

ORTHODROMIC - antegrade conduction down the AV node and retrograde conduction up the accessory pathway. More common. Narrow QRS because ventricles depolarise at the same time
ANTIDROMIC – antegrade conduction down the accessory pathway and retrograde conduction up the normal AV conduction. Broad QRS

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34
Q

What are the ECG findings for Orthodromic AVRT?

A

Narrow QRS
Long PR interval - due to slow propagation across ventricular myocardium before reaching the accessory pathway and heading back to atrium = delay in atrial activation

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35
Q

What are the types of ventricular tachyarrhythmias?

A

Ventricular tachycardia
Ventricular fibrillation
Premature ventricular contractions

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36
Q

What are the 2 types of ventricular tachycardias?

A

monomorphic VT (1 firing area creating the abnormal Tachyarrhythmia) - most commonly caused by MI
polymorphic VT (multiple areas firing)

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37
Q

What are the 2 types of polymorphic ventricular tachycardia?

A

polymorphic VT with a normal QT interval
polymorphic VT with a prolonged QT interval (torsades de pointes)

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38
Q

What is ventricular tachycardia?

A

occurs due to rapid, recurrent ventricular depolarisation from a focus within the ventricles. This is commonly due to scarring of the ventricles following myocardial infarction.
. It has the potential to precipitate ventricular fibrillation and hence requires urgent treatment.

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39
Q

What are the ECG findings in ventricular tachycardia?

A

Regular, broad complex tachycardia
Uniform QRS complexes

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40
Q

What are ECG findings in ventricular fibrillation?

A

irregular unformed QRS complexes without any clear P waves

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41
Q

What are premature ventricular contractions?

A

Ventricular ectopic beats - an electrical stimulus of the ventricles which occurs within the ventricles themselves caused by a group of pacemaker cells operating independantly of normal stimulation
Common and usually benign
Can be unifocal or multifocal

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42
Q

What are some causes of premature ventricualr contractions?

A

Increased adrenaline due to exercise or anxiety
Alcohol or drug misuse
Electrolyte abnormalities - hypokalaemia, hypomagnesaemia, hypercalcaemia
Digoxin toxicity
Stimulants - Excessive caffeine intake or tobacco or illicit drugs
Sleep deprivation
Cardiac pathological causes - cardiomyopathy, MI, mitral valve prolapse
Non-cardiac pathological causes - hyperthyroidism, anaemia, hypertension

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43
Q

What are thr ECG changes in premature ventricular complexes?

A

Absence of P waves
Broad, premature QRS
Discordant large T wave

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44
Q

What are the types of Bradyarrhythmias?

A

Sinus bradycardia
Heart block 1st degree, 2nd degree type 1 and 2, 3rd degree

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45
Q

What is sick sinus syndrome?

A

Aka sinus node dysfunction
Condition where SAN doesnt function properly and causes Bradyarrhythmias or tachyarrhythmias
Predominantly affects older adults although can occur at any age
Can be caused by various factors including age-related degeneration of the SAN, medication side effects or underlying heart disease
Can cause tachy-Brady syndrome (- affects 50% of pt), Sinus bradycardia and sinus arrest, sinoatrial exit block, atrial fibrillation with a slow ventricular response

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46
Q

What can cause sick sinus syndrome?

A

Intrinsic factors - fibrosis or ischaemia
Extrinsic factors - anti-arrhythmic agents

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47
Q

Why does sick sinus syndrome comprise of both bradycardia and tachycardia?

A

As a result of dysfunction of the SAN leading to slower firing, associated supraventricular tachycardia can develop - compensatory mechanism

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48
Q

What is an escape rhythm?

A

Failure to initiate electrical activity can cause another part of the heart to take over as the primary pacemaker. These are typically <60bpm
E.g. SAN fails to undergo spontaneous depolarisation then the AVN may initiate electrical activity

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49
Q

What are some intrinsic causes of bradycardia?

A

Failure to initiate or transmit electrical activity
Escape rhythms
Heart blocks
(Commonly due to degenerative fibrosis, ischaemia, hypertensive heart disease or infiltration e.g. amyloid)

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50
Q

What are some extrinsic causes of bradycardia?

A

Most commonly its an increase in parasympathetic activity which leads to a reduction in HR e.g. seen in athletes
Hypothermia
Increased intracerebral pressure
Autonomic dysfunction
Metabolic disturbances - hypocalcaemia, hyperkalaemia
Carotid sinus stimulation
Iatrogenic - rate-controlling meds

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51
Q

What is the vagal tone?

A

An index of how well the vagus nerve is functioning

When the vagal tone to the pacemaker is high, the vagus acts as a brake on the rate at which the heart is beating i.e. athletes have a high vagal tone

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52
Q

Outline the intrinsic rates of autorhythmicity within the SAN, AVN and ventricles?

A

SAN: 60-100 bpm
AVN: 40-60 bpm
Ventricles: 20-40 bpm

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53
Q

What can cause sinus bradycardia?

A

Normal in young, fit, healthy individuals
May be suggestive of an underlying SAN disease

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54
Q

How does sinus pause demonstrate itself on an ECG?

A

Absent P waves

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55
Q

What is sinus pause?

A

Failed initiation of conduction due to dysfunction of SAN (different to sinoatrial exit block which is failed transmission of electrical activity)

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56
Q

What is a sinus pause?

A

Transient absence of P waves that lasts from 2 seconds to several minutes. It is due to failure of the SAN to initiate electrical activity. It may be followed by resumption of normal electrical activity from the SAN or appearance of an escape rhythm (e.g. atrial or junctional escape).

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57
Q

What is first degree heart block?

A

Common and benign
Delayed conduction so there’s a consistent prolongation of PR interval >200ms
Abnormally slow conduction through the AV node

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58
Q

What is second degree heart block type 1?

A

Progressive prolongation of PR interval until a dropped beat occurs

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59
Q

What is second degree heart block type 2?

A

PR interval is constant but the P wave is often not followed by a QRS complex
Almost always progresses to third degree heart block so typically requires a pacemaker
Usually due to structural AV node disease

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60
Q

What is third degree heart block?

A

Aka complete heart block
Complete failure in conduction with AV dissociation. Ventricles start to pace themselves
No association between p waves and QRS complexes
Always due to structure disease of AV node
If untreated it will result in death within 6 weeks
P waves will occur at regular intervals. QRS will also occur at regular intervals but at a slower rate

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61
Q

What are clinical features associated with Bradyarrhythmias?

A

Asymptomatic
Fatigue, lethargy
Dizziness, pre-syncope
Syncope: transient loss of consciousness
Dyspnoea: may suggest pulmonary oedema
Chest pain: may suggest myocardial ischaemia
Shock: low BP (< 90 mmHg), pallor, sweating, cold
Impaired consciousness

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62
Q

What are the 4 cardinal features that suggest an unstable arrhythmia?

A

Syncope
MI
Heart failure
Shock

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63
Q

What is a reentrant circuit?

A

A continuous wave of depolarisation in a circular path. As the depolarising wave returns its site of origin, it reactivates that site leading to a continuous cycle.

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64
Q

What are the 3 types of arrhythmias that reentrant circuits can cause?

A

Ectopic beat
Paroxysmal tachyarrhythmias
Sustained tachyarrhythmias

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65
Q

How can you determine the origin of tachyarrhythmias based off ECG?

A

Supraventricular - narrow QRS
Ventricular - Broad QRS

(Exception to this is if there is an accessory pathway then a supraventricular tachycardia may have a broad QRS)

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66
Q

What can cause sinus tachycardia?

A

Normal physiological response to stress - exercise, inter current illness, underlyign pathology

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67
Q

what are ECG findings for AF?

A

Irregularly irregular rhythm
Absence of P waves (no coordinated atrial activity)
Irregular, fibrillating baseline

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68
Q

Whats the most common supraventricular tachycardia?

A

AVNRT - 50-60% of cases

(AVRT is second with 30% of cases)

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69
Q

What is Wolff Parkinson white syndrome? Whats the ECG pattern?

A

a preexcitation syndrome that is characterised by a congenital accessory pathway and episodic tachyarrhythmias

ECG - short PR (as no AV conduction delaye), delta wave, normal QRS after that as usually conduction ‘catches up’ with pre-excitated impulse

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70
Q

Whats the accessory o pathway in Wolff Parkinson white syndrome?

A

Usually referred to as the Bundle of Kent - it can allow conduction antegrade or retrograde. If there is antegrade conduction during normal electrical activity it can be seen on the resting ECG. Retrograde only conduction ‘conceals’ the accessory pathway.

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71
Q

Whats the main concern with WPW syndrome?

A

Development of AF due to rapid ventricular response

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72
Q

What is Supraventricular tachycardia with aberrant?

A

supraventricular rhythms with abnormal conduction and so presents with a broad QRS complex
Can be tricky to distinguish SVT with aberrant from a VT

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73
Q

What is Torsades de pointes?

A

a subtype of polymorphic VT that is characterised by ventricular tachycardia that ‘twists’ around the isoelectric line. This subtype occurs secondary to a prolonged QT interval.

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74
Q

How shold you manage torsades de pointes?

A

management is aimed at shortening the QT interval with intravenous magnesium sulphate.
If a patient is unstable with Torsades de pointes, they should undergo immediate DC cardioversion as with any unstable tachyarrhythmia.

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75
Q

What is ventricular fibrillation?

A

Ventricular fibrillation (VF) occurs when the ventricular muscle fibres contract independently due to multiple reentrance circuits. On the ECG, this is seen as no coordinated electrical activity with a chaotic, fibrillating baseline.
It’s incomparable with life and patients who develop this rhythm will go into cardiac arrest

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76
Q

What are the 3 most common causes of tachyarrhythmias?

A

Increased automaticity - increased sympathetic tone (hypovolaemic, hypoxia, sympathomimetic, pain, anxiety, fever, hyperthyroidism)

Triggered activity - EAD and DAD

Reentrance circuits

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77
Q

What are the 3 most common causes of bradyarrythmias?

A

Decreased automaticity - increased vagal tone, slow AV conduction (beta blockers, CCB, digoxin), slow down metabolic activity (hypothermia, hypothyroid), hyperkalaemia (alters resting membrane potential), high intracranial pressure (brain herniation can cause Cushing triad which causes bradycardia)

Conduction block - MI, fibrosis of AVN, hyperkalaemia, BB/CCB/digoxin, infiltration e.g. amyloidosis, sarcoidosis, lymes disease, cardiomyopathy etc

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78
Q

Outline the regulation of autorhythmicity?

A

Parasympathetic - Vagus nerve releases ACh which decreases conduction of SAN = decreases HR
Sympathetic - T1-T5 innervates SAN and contractile myocardial cells -> releases NA and Adrenaline -> increase sconduction of SAN -> increased HR -> increase automaticity

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79
Q

What is an EAD?

A

Early after depolarisation
occur with abnormal depolarization during phase 2 or phase 3, and can lead to a salvo of several rapid action potentials or a prolonged series of action potentials. and can lead to a salvo of several rapid action potentials or a prolonged series of action potentials. This form of triggered activity is more likely to occur when the action potential duration is increased
Simple - Early depolarisation that comes just after previous depolarisation
Commonly associated with torsades de pointes

80
Q

What causes EADs?

A

Electrolyte disturbances (hypokalaemia, hypomagnesaemia, hypocalcaemia)
anti-arrhythmics 1a/1c/3
antibiotics
antipsychotics
antidepressants (particularly TCA)
antiemetics

81
Q

What is delayed afterdepolarisation?

A

DAD
These begin during phase 4, after repolarization is completed but before another action potential would normally occur via the normal conduction systems of the heart. The triggered impulse can lead to a tachyarrhythmias. Associated with high intracellular calcium concentrations
Commonly associated with multifocal atrial tachycardia, focal atrial tachycardia and ventricular tachycardia with normal QT intervals i.e. not torsades de pointes

82
Q

What causes delayed after depolarisation?

A

Ischaemia - CAD or active MI
Hypoxia e.g. due to lung disease
Myocarditis
Stretch - Dilated cardiomyopathy and mitral regurgitation
Increased sympathetic tone
Digoxin toxicity

83
Q

What is the mechanism behind atrial fibrillation?

A

Multiple irritable areas in ventricles which create their own reentrance circuits

84
Q

What are the different types of paroxysmal supraventricular tachycardias?

A

AV nodal reentrant tachycardia - most common 60% of cases
Atrial tachycardia
Atrioventricular reentrant tachycardia
Junctional tachycardia

85
Q

What are the irregular supraventricular tachycardias?

A

Atrial fibrillation
Atrial flutter (variable block)
Multifocal atrial tachycardia

86
Q

Whats the most common cause of regular supraventricular tachycardia in patients with a structurally normal heart?

A

AV nodal re-entry tachycardia

87
Q

what is sinus arrest?

A

A pause of three seconds or more without any atrial activity (p waves)

88
Q

What are the differentials for narrow QRS with regular rhythm?

A

Atrial tach
Focal atrial tachycardia
Paroxysmal supraventricular tachycardias (AVRT and AVNRT)
Atrial flutter

89
Q

What are the differentials for narrow QRS with irregular rhythm?

A

Atrial fibrillation
Atrial flutter with a variable block
Multifocal atrial tachycarda

90
Q

What are the differentials for wide QRS with regular rhythm?

A

V.tachycardia (monomorphic)
SVT with abberancy (i.e. BBB)
Antidromic AVRT

91
Q

What are the differentials for wide QRS with irregular rhythm?

A

Polymorphic v.tach
A fib with wolf Parkinson white syndrome
A fib with abberancy (i.e. with a BBB)
Ventricular fibrillation

92
Q

How do you determine from an ECG that its sinus tachycardia?

A

Rate - >100
Rhythm - regular
P waves - upright in leads 1,2,aVL. Negative in aVR
Sinus - each P wave is followed by QRS which is followed by T waves
QRS - narrow

93
Q

How do you determine if an ECG is sinus rhythm?

A

P waves are upright in lead 2 and inverted in aVR.
After every P wave is a QRS complex and after every QRS wave is a T wave

94
Q

What does focal atrial tachycardia look like on ECG?

A

Rate - >100
Rhythm - regular
P waves - inverted in lead 2, 3 and aVF and upright in aVR
Sinus rhythm
QRS - narrow

95
Q

What does atrial flutter look like on ECG?

A

Rate - about 300bpm (ventricular rate depends on AV conduction ratio but whatever this is it will be constant!)
Rhythm - regular (can be irregular if with variable block)
P waves - saw-tooth waves (look in 2,3, aVF. May be upright flutter waves in V1)
QRS - narrow

96
Q

What does AVRT and AVNRT look like on ECG?

A

Rate - 140-280
Rhythm - regular
P waves - may be hidden in QRS or may be retrograde in inferior leads (in AVRT retrograde P waves occur later with a long RP interval so easier to see)
QRS - narrow

97
Q

How do you manage sinus tachycardia?

A

Treat underlying cause

98
Q

How do you treat ectopic beats ?

A

If ectopic beats are spontaneous and the patient has a normal heart, treatment is rarely required and reassurance to the patient will often suffice.
Beta blockers may be required

99
Q

How do you treat atrial flutter?

A

Controlling ventricular rate - beta-blocker, diltiazem hydrochloride, verapamil (digoxin can be added if inadequate)
Conversion to sinus rhythm - electrical cardioversion, pharmacological cardioversion or catheter ablation
Treat underlying condition
Radiofrequency ablation of re-entrant rhythm
Anticoagulation

100
Q

When should you not do cardioversion for converting atrial flutter to sinus rhythm? What should you do in this situation?

A

If duration of atrial flutter is unknown or had lasted >48 hours
Dont attempt until the pt had been fully anticoagulated for >3 weeks. If not possible then give parenteral anticoagulation and rule out a left atrial thrombus immediately before cardioversion
Oral anticoagulation should be given for at least 4 weeks after also

101
Q

Whats the treatment of choice for atrial flutter where rapid conversion to sinus rhythm is necessary?

A

Direct current cardioversion

102
Q

Whats the treatment of choice for recurrent atrial flutter?

A

Radiofrequency ablation of the tricuspid valve isthmus

103
Q

What anti-arrhythmic drugs can be used to convert atrial flutter to sinus rhythm? What should they be prescribed alongside and why?

A

Flecainide acetate or propafenone hydrochloride
They can slow atrial flutter, resulting in 1:1 conduction to the ventricles, and should therefore be prescribed in conjunction with a ventricular rate controlling drug

104
Q

How should you manage PSVT (AVRT and AVNRT)?

A
  1. vagal manoeuvres: Valsalva manoeuvre or carotid sinus massage
  2. IV adenosine
    rapid IV bolus of 6mg → if unsuccessful give 12 mg → if unsuccessful give further 18 mg
  3. electrical cardioversion

Prevention of episodes
beta-blockers
radio-frequency ablation

105
Q

What are ECG changes for atrial fibrillation?

A

Rate - >100
Rhythm - irregularly irregular
P wave - absent but fibrillation waves before QRS (most visible V1)
QRS - narrow

106
Q

What is atrial flutter with variable block?

A

Conduction ratio is variable which causes an inconsistent number of flutter waves between QRS complexes

107
Q

What are ECG changes in multifocal atrial tachycardia?

A

Rate - >100
Rhythm - irregularly irregular
P waves - 3 or more morphologially different P waves with isoelectric baseline
QRS - narrow

108
Q

How do we manage atrial fibrillation?

A

If haemodynamically unstable - electrical cardioversion

Haemodynamically stable but acutely unwell - rate or rhythm control if onset is <48 hours (if >48 hours/uncertain use rate control)

If haemodynamically stable but well -
Rate control first line
Rhythm control first line only in a certain subgroup of pt

CHADSVASC score and anticoagulation

Left atrial ablation if drug treatment failed or unsuitable - particularly in pulmonary veins

Surgery e.g. left atrial appendage occlusion

109
Q

Which groups of of should have their atrial fibrillation managed with rhythm control first?

A

If AF has a reversible cause
Who have HF thought to be primarily caused by AF
new‑onset atrial fibrillation
with atrial flutter whose condition is considered suitable for an ablation strategy to restore sinus rhythm
for whom a rhythm‑control strategy would be more suitable based on clinical judgement

110
Q

What rate control therapy is offered for AF?

A

Beta blocker (other than Sotalol) or a rate limiting CCB as mono therapy
Consider digoxin mono therapy if above is ruled out due to comorbidities

If monotherapy does not control the person’s symptoms, and if continuing symptoms are thought to be caused by poor ventricular rate control, consider combination therapy with any 2 of the following:
a beta‑blocker
diltiazem
digoxin

111
Q

What rhythm control is done for AF?

A

Antiarrhythmic drug therapy - beta blocker first line for long term (amiodarone if left ventricular impairment of HF)
If AF persisted >48 hours offer electrical cardioversion instead (consider starting amiodarone therapy 4 weeks before and continue 12 months after)
Consider left atrial ablation

112
Q

Why is it important that patients either have had a short duration of symptoms (<48 hours) or be anticoagulated for a period of time prior to attempting cardioversion>

A

the moment a patient switches from AF to sinus rhythm presents the highest risk for embolism leading to stroke

113
Q

Outline the CHA2DS2-VASc score?

A

Congestive HF - 1
Hypertension - 1
Age >= 75 - 2
Age 65-74 - 1
Diabetes - 1
Prior stroke, TIA or thromboembolism - 2
Vascular disease - 1
Sex female - 1

Score:
0 - no treatment
1 - consider anticoagulation in males but not females as this score of 1 is only reached by their gender
2 or more - anticoagulation

114
Q

How do you treat multifocal atrial tachycardia?

A

If ectopic beats are spontaneous and the patient has a normal heart, treatment is rarely required and reassurance to the patient will often suffice. If they are particularly troublesome, beta-blockers are sometimes effective and may be safer than other suppressant drugs.

115
Q

How can you distinguish between ventricular tachycardia and SVT with abberancy?

A

In V.tach QRS are >0.14 seconds and in SVT with abberancy its usually not as big
In V.tach you may see AV dissociation but this is not seen in SVT with abberancy
V.tach usually has extreme right axis deviation which SVT with abberancy does not
V.tach usually has a history of CVD whereas SVT with abberancy this is less likely and may be younger

116
Q

What are the ECG changes for ventricular tachycardia?

A

Rate - >100
Rhythm - regular
P waves - not visible
QRS - broad complex. Uniform
May have extreme right axis deviation
T waves - not visible

117
Q

How do you manage ventricular tachycardia?

A

If haemodynamically unstable - electrical cardioversion. If this fails give IV amiodarone and repeat cardioversion

If haemodynamically stable -
IV amiodarone first line.
If sinus rhythm not restored DC cardioversion or pacing should be considered.
If cessation is not urgent, catheter ablation can be used
Non-sustained v.tach can be treated with a beta blocker

Refer all pt to a specialist.
Most pt will require maintenance therapy with implantable cardioverter defibrillator

(Note this is a nasty arrhythmia that’s very unstable so put pads on pt as giving amiodarone in case they suddenly become haemodynamically unstable)

118
Q

What are ECG changes for polymorphic ventricular tachycardia?

A

Rate - >100
Rhythm - irregular
P wave -
QRS - wide. different morphologies (all different heights etc)
QT - determine if its normal or prolonged before they entered this rhythm
Beat-to-beat acid deviation of QRS complexes around the baseline - ‘twisting of the points’

119
Q

Whats the most common wide QRS irregular rhythm?

A

Atrial fibrillation with a bundle branch block

120
Q

Why are wide QRS irregular rhythms so dangerous?

A

They can very quickly change into ventricular fibrillation

121
Q

How should you manage Torsade de pointes?

A

Episodes are usually self-limiting but are frequently recurrent
If not controlled, it can progress to V fib

IV infusion of magnesium sulphate
Beta blocker or atrial pacing can be considered
DONT GIVE ANTI-ARRHYTHMICS AS THESE CAN FURTHER PROLONG QT INTERVAL

122
Q

What are the ECG changes for sinus bradycardia?

A

Rate - <60
Rhythm - regular
P waves - sinus rhythm
PR interval - normal
QRS - regular

123
Q

What are the ECG changes for first degree heart block?

A

Rate - <60
Rhythm - regular
PR interval - prolonged >200ms

124
Q

What are the ECG changes for second degree heart block mobitz 1?

A

Rate - <60
Rhythm - irregular
PR - gets progressively longer until QRS complex is dropped

125
Q

What are the ECG changes for second degree heart block mobitz 2?

A

Rate - <60
Rhythm -
PR interval - normal
QRS - occasionally missing

126
Q

What are the ECG changes for third degree heart block?

A

rate - <60
Rhythm -
PR interval - normal
QRS - dropping and complexes are wide
I..e complex dissociation between atria and ventricles so atria and ventricles are beating at their own intrinsic rates

127
Q

How should you manage sinus bradycardia?

A

If haemodynamically unstable give IV atropine and seek expert help

If haemodynamically stable but risk of asystole then give IV atropine
If haemodynamically stable but no risk of asystole then observe

128
Q

What are risk factors for asystole?

A

complete heart block with broad complex QRS
recent asystole
Mobitz type II AV block
ventricular pause > 3 seconds

129
Q

How should you manage heart block?

A

Type 1 and 2.1 stop any AV blocking drugs
Type 2 mobitz 2 - cardiac monitoring but if haemodynamically stable dont treat
Type 3 - cardiac monitoring, transcutaneous pacing or isoprenaline infusion may be required. A permenant pacemaker is usually required

130
Q

What is Radiofrequency ablation?

A

It involves local/general anaesthetic, inserting a catheter in to the femoral veins and feeding a wire through the venous system under xray guidance to the heart. Once in the heart it is placed against different areas to test the electrical signals at that point. This way the operator can hopefully find the location of any abnormal electrical pathways. The operator may try to induce the arrhythmia to make the abnormal pathways easier to find. Once identified, radiofrequency ablation (heat) is applied to burn the abnormal area of electrical activity. This leaves scar tissue that does not conduct the electrical activity. The aim is to remove the source of the arrhythmia.

131
Q

What is bigeminy?

A

where the ventricular ectopics are occurring so frequently that they happen after every sinus beat. The ECG looks like a normal sinus beat followed immediately by an ectopic, then a normal beat, then ectopic and so on.

132
Q

What is a 2:1 heart block?

A

This is where there are 2 P waves for each QRS complex. Every second p wave is not a strong enough atrial impulse to stimulate a QRS complex. It can be caused by Mobitz Type 1 or Mobitz Type 2 and it is difficult to tell which.

133
Q

Whats the moa of atropine?

A

Inhibits muscarinic ACh receptors which inhibits vagal activity, alleviating parasympathetic depression of SAN activity - increases heart rate

134
Q

What are the 4 classes of antiarrhythmic agents?

A

1 - sodium channel blockers
2 - beta receptor blockers
3 - K+ channel blockers
4 - calcium channel blockers

135
Q

Whats the classification for antiarrhythmics?

A

Vaughan-William’s classification

136
Q

What are the 3 broad categories for why arrhythmias arise?

A

Increased automaticity
Re-entry circuits
Triggered activity - early or delayed afterdepolarisarions

137
Q

What are the proarrhythmic effects of class 1A antiarrhythmics and Sotalol?

A

They can’t cause prolonged QT and so increase the risk of polymorphic ventricular tachycardia (torsades des pointes)

138
Q

What are the pro-arrhythmic effects of class 1 C antiarrhythmics?

A

Not to be used in pt with coronary artery disease as have increase proarrhythmic effects

139
Q

Whats the moa of class 1 anti-arrhythmics?

A

They slow depolarisation and conduction byinhibition of fast sodium channels in cardiac myocytes

140
Q

What are the 3 different types of class 1 anti-arrhythmics?

A

Class 1 a- inhibit the Na+ channels and the K+ channels on atrial and ventricular myocytes and cells of the purkinje fibers. Because K+ channels are blocked there’s slower rates of repolairsation so a longer QRS and QT segment. Rarely used in UK due to adverse effects

Class 1B - inhibit the Na+ channels in purkinje fiber cells, ventricular myocytes, but not the atrial ones. decreases the duration of the action potential

Class 1c - inhibit the Na+ channels in atrial and ventricular myocytes and purkinje fiber cells. no effect on action potential. Most likely to cause arrhythmias

141
Q

What are examples of class 1a anti-arrhythmic agents?

A

Quinidine, Procainamide, Disopyramide.

142
Q

What are examples of class 1B anti-arrhythmic agents?

A

Lidocaine, Phenytoin.

143
Q

What are examples of class 1 c antiarrhythmics?

A

Flecainide

144
Q

What are the adverse effects of class 1 anti-arrhythmics?

A

Nausea & vomiting
Negative inotropic effect
Proarrhythmic effects
CNS toxicity (Class IB and IC in particular)
SLE-like syndrome (Procainamide)
Cinchonism (condition caused by Quinidine overdose)

145
Q

Whats the moa of class 2 anti-arrhythmics?

A

Antagonists of catecholamines at beta-adrenoceptors, possessing both negative inotropic and negative chronotropic effects; that is they reduce heart rate and the strength of contractions.

They act on the SA node to reduce the rate of spontaneous depolarisation (and so reducing the heart rate) by decreasing the slope of phase 4. In essence, slowing the spontaneous depolarisation of the pacemaker potential. They also act on the AV node to reduce conduction.

146
Q

What are the adverse effects of beta blockers?

A

Postural hypotension
Bradycardia
AV nodal block (heart block)
Bronchoconstriction (a particular consideration in severe asthma and COPD)
Hypoglycaemia
Erectile dysfunction
Insomnia, sleep disturbance

147
Q

Whats the moa of class 3 anti-arrhythmics?

A

Block potassium channels, which are responsible for the completion of repolarisation (phase 3) in contractile cells. Blockade leads to an extension of the refractory period, through the prolongation of phase 2.

148
Q

What are adverse effects of amiodarone?

A

Nausea
Constipation
Thyroid dysfunction (see our Hyperthyroidism and Hypothyroidism notes)
Peripheral neuropathy
Photosensitivity
Lung fibrosis
Proarrhythmic effects
Hepatitis / cirrhosis
Potentiates the effects of both digoxin and warfarin.

149
Q

Which type of CCB are more cardioselective and can exhibit anti-arrhythmic effects?

A

Non-dihydropyridines

150
Q

Whats the moa of non-dihydropyridines?

A

Block L-type calcium channels
Negative inotropes and negative chronotropes

151
Q

What are the adverse effects of CCBs?

A

Bradycardia
AV nodal block (heart block)
Negative inotropic effect
Constipation
Gum hyperplasia
Headaches, flushing, peripheral oedema - features associated with dihydropyridines (less common with non-dihydropyridines).

152
Q

Whats the moa of digoxin?

A

Cardiac glycoside derived from the foxglove plant

It inhibits a Na+/ K+ -ATPase pump on cardiomyocytes. This pump acts to take sodium out of the cell and pump potassium back in a ratio of 3:2. This helps drive calcium out of the cell via an exchanger This reduction in extracellular calcium results in an increase in intracellular calcium levels. As such, the contraction is more forceful (digoxin is a positive inotrope)

153
Q

What are the problems with digoxin?

A

Primarily excreted by the kidneys so care is needed in pt with renal impairment
Can cause ECG changes - ST depression and T wave changes
Toxicity can cause PR prolongation and arrhythmias
Narrow therapeutic window

154
Q

What are the adverse efefcts of digoxin?

A

Nausea and vomiting
Visual disturbances (yellow halos, changes to colour perception)
Insomnia and sleep disturbance
Proarrhythmic effects
Gynaecomastia

155
Q

What are the adverse effects of adenosine?

A

Sense of impending doom
Bradycardia, AV block
Flushing
Headache
Bronchospasm

156
Q

Whats the moa of adenosine?

A

its a purine nucleoside
Acts on SAN to reduce HR and on the AVN to slow conduction
Rapidly metabolised with a half life of <10 seconds

157
Q

What are adverse effects of atropine?

A

Nausea
Blurred vision
Dilated pupils, photophobia
Dry mouth

158
Q

When is magnesium Sulfate contraindicated?

A

AV block or bradycardia

159
Q

What causes right axis deviation?

A

Normal in children or thin/tall adults with a horizontally positioned heart
Right ventricular hypertrophy
Lateral MI
Acute lung disease e.g. PE
Chronic lung disease
WPW syndrome
Left posterior fascicular block

160
Q

What causes left axis deviation?

A

Left anterior fascicular block
Left BBB
Left ventricular hypertrophy
Inferior MI

161
Q

What does an inverted P wave on ECG typically mean?

A

Ectopic atrial rhythm

162
Q

What is a left bundle branch block?

A

The electrical activity occurs normally but is blocked at the left bundle branch.the septum becomes depolarised from right to left in order to depolarise the left bundle branch
Causes broach QRS as depolarisation takes longer

163
Q

What are the features of a left bundle branch block?

A

Broad QRS
V1 - deep S wave
Lateral leads V5, V6, I and aVL - broad dominant R wave

WiLLiaM
(W pattern in V1 and M pattern in V6)

164
Q

What is right bundle branch block?

A

No conduction occurs down right bundle branch but the septum is depolarised from the left side as usual. Excitation spreads from left ventricle.

165
Q

What are the features of a right bundle branch block?

A

Broad QRS
RSR pattern in V1, V2, V3 (M shape)
Wide slurred S wave in lateral leads

MaRRoW

166
Q

What is atrioventricular reentrant tachycardia?

A

Additional conductive pathway occurs somewhere between atria and ventricles (not AVN). Electrical signals pass down additional pathway and cause a recurring regular loop between that pathway and normal conducting pathway = ventricles at fast rate and no P waves

Classical example - wolf Parkinson white syndrome

167
Q

What are the 3 types of AF?

A

Paroxysmal AF - intermittent episodes that terminate spontaneously
persistent AF - can be terminated but requires medical intervention
Permenant AF - medical intervention does not re-establish sinus rhythm

168
Q

What is recurrent AF?

A

When a pt has 2 or more episodes of AF

169
Q

What is paroxysmal AF?

A

When episodes of AF terminate spontaneously
Each episode lasts less than 7 days, but typically <24 hours

170
Q

What is persistent AF?

A

Recurrent episodes that are not self-terminating i.e. lasts >7 days

171
Q

What is permenant AF?

A

Continuous AF which cannot be cardioverted or if attempts to do so are deemed inappropriate

172
Q

What is a pacemaker?

A

A box implanted under the skin with wires implanted into chambers of the heart
They deliver controlled electrical impulses to specific areas of the heart to restore the normal electrical activity and improve the heart function. They consist of a pulse generator (the little pacemaker box) and pacing leads that carry electrical impulses to the relevant part of the heart

173
Q

How long do pacemaker batteries last?

A

Around 5 years

174
Q

What are pacemakers a contraindication for?

A

MRI scans (although many modern ones are MRI compatible)
Electrical interventions e.g. TENS machine and diathermy
Cremation

175
Q

What are the indications for a pacemaker?

A

Symptomatic bradycardias
Mobitz Type 2 AV block
Third degree heart block
Severe heart failure (biventricular pacemakers)
Hypertrophic obstructive cardiomyopathy (ICDs)

176
Q

What are the different types of pacemakers?

A

Single-chamber
Dual-chamber
Biventricular (triple-chamber)
Implantable cardioverter defibrillators

177
Q

What are single-chamber pacemakers and how do they work?

A

They have leads in a single chamber, either in the right atrium or the right ventricle.
They are placed in the right atrium if the AV conduction in the patient is normal and the issue is with the SA node. This way they stimulate depolarisation in the right atrium and this electrical activity then passes to the left atrium and through the AV node to the ventricles in the normal way.
They are placed in the right ventricle if the AV conduction in the patient is abnormal and they stimulate the ventricles directly.

178
Q

What are dual-chamber pacemakers and how do they work?

A

Dual-chamber pacemakers have leads in both the right atrium and right ventricle. This allows the pacemaker to synchronise the contractions of both atria and ventricles.

179
Q

What are biventricular pacemakers and how do they work?

A

They are also called cardiac resynchronisation therapy (CRT) pacemakers.

Biventricular pacemakers have leads in right atrium, right ventricle and left ventricle
These are usually in patients with heart failure. The objective is to synchronise the contractions in these chambers to try to optimise the heart function.

180
Q

What are implantable cardioverter defibrillators?

A

They continually monitor the heart and apply a defibrillator shock to cardiovert the patient back in to sinus rhythm if they identify a shockable arrhythmia.

181
Q

What ECG changes do you see with a pacemaker?

A

Sharp vertical line on all leads on the ECG trace
I.e. a line before each p-wave indicates a lead in the atria
A line before each QRS complex indicates a lead in the ventricles

182
Q

How can you tell what type of pacemaker a pt has from their ECG?

A

A line before either the P or QRS but not the other indicates a single-chamber pacemaker
A line before both the P and QRS indicates a dual-chamber pacemaker
Often no P waves
(Larger QRS can also be normal)

183
Q

How common is AF?

A

2.5% prevalence in England
12% of over 65s and 22% at age 80

184
Q

What are the complications of AF?

A

Ischaemia
Tachycardia-induced cardiomyopathy
Heart failure
Thromboembolic events - stroke
Mortality
Reduces quality of life due to reduced exercise tolerance and impaired cognitive function

185
Q

where do clots develop in atrial fibrillation?

A

Left atrial appendage

186
Q

What is pAF?

A

Paroxysmal AF

187
Q

What is the HAS-BLED score?

A

A scoring system that estimates the risk of major bleeding for patients on anticoagulation to assess risk-benefit in AF care

Hypertension?
Abnormal renal or liver function? Age?
Stroke Previously

Bleeding predisposition or major bleed in past
Labile INR
Ethanol use
Drugs that predispose to bleeding

0-1 points - anticoagulation should be considered as pt relatively low risk for major bleed
2 points - anticoagulation can be considered but pt moderate risk for major bleed
3 points or more - high risk for major bleed dont give anticoagulation

188
Q

What anticoagulation is given for AF?

A

If CHAD2VASC score of 1 consider and 2 or more give…

First line - DOAC
(Warfarin used to be first line so lots of pt on it, also used first line for metal heart valves)
LMWH may be used as a bridging therapy or used in pt with severe renal failure i.e. Cr <15 (who can’t take DOAC)

189
Q

What are the 4 main choices of DOAC for AF?

A

Edoxaban (OD dosing)
Apixaban (TD dosing)
Rivaroxiban (OD dosing and must be taken alongside food)
Dabigatran (TD dosing)

190
Q

Where is the foci in most AF?

A

Near pulmonary veins

191
Q

How do you calculate ventricular rate in atrial flutter?

A

Ventricular rate is a fraction of the atrial rate, for example:
2:1 block = 150 bpm
3:1 block = 100 bpm
4:1 block = 75 bpm

192
Q

What electrolyte disturbances can cause atrial fibrillation?

A

Hypomagnesaemia
Hypokalaemia

193
Q

What metabolic diseases can cause tachyarrythmias?

A

Hyperthyroidism
Phaeochromocytoma

194
Q

What are the 2 functions of pacemakers?

A

Sensing - can sensing intrinsic depolarisations which is used to inhibit or trigger pacing pulses so that pacing is appropriate
Pacing - depolarisation of atria or ventricles resulting from an impulse delivered from the generator down a lead to the heart

Different pacemakers can utilise this differently e.g. in AF you want to override the heart’s rhythm completely so you only need pacing and not sensing

195
Q

Where is the scar for an implantable Cardioverter defibrillator?

A

Usually infraclavicular on the left

196
Q

What are the indications for ICD?

A

VT or VF
Familial cardiac condition with a high risk of sudden death e,g. Long Qt syndrome, hypertrophic cardiomyopathy, brugada syndrome
Undergonme surgical repair of congenital heart disease
HF with EF<35% - to prevent sudden cardiac death

197
Q

What is ORBIT score?

A

Predicts the bleeding risk in pt on anticoagulation for atrial fibrillation (similar to HAS-BLED)

Age >74 (+1)
Hb <130 or Hct <40% (+2)
Bleeding history (+2)
GFR <60 (+1)
Treatment with antiplatelet agents (+1)

Score 0-2 low risk (2.4 bleeds per 100 patient-years)
Score 3 - medium (4.7 bleeds per 100 patient-years)
Score 4 or more (8.1 bleeds per 100 patient-years)

CARDIOLOGY (19 decks)

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