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Cardiology > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

What are the two types of myocytes?

A

Conduction/ contraction

Myocytes can perform both functions but tend to favour one/ other

Most myocytes are contractile

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2
Q

Where does the SAN lie?

A

Between superior vena cava and right atrium

Spontaneously depolarises at a quicker rate than other cardiac cells and acts as the pacemaker of the heart

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3
Q

At what level does the inferior vena cava pass through the diaphragm?

A

T8

Via the vena caval foramen

The phrenic nerve can also be found running through this foramen

*Image shows inferior vena cava entering right atrium

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4
Q

What is shown in the image?

A

Right atrial appendage

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5
Q

What is the Vaughan Williams classification?

A

Classification of anti-arrhythmic drugs

Based on the effect the drugs have on the action potential of the cardiac cells

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6
Q

Phases of the action potentials of pacemaker cells

A

Phase 4: first upward slope due to opening of Na+ channels

Phase 0: Rapid up-slope due to opening of Ca2+ channels once there is enough Na+ inside cell and membrane is at -40mV

Phase 3: Once membrane potential reaches +10mV K+ channels open and K+ rushes out of cell, bringing it back down to starting point of -60mV

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7
Q

Phases of the cardiac myocyte action potential

A

Phase 4: resting potential of -90mV

Phase 0: neighbouring cell triggers opening of Na+ channels and there is a rapid upstroke to +40mV, Slow-type Ca2+ channels also open

At the top of phase 0 Na+ channels close

Phase 1: K+ channels open and allow a small amount of K+ out - bringing membrane potential down

Phase 2: 2 channels (K+ and Ca2+) working in equilibrium in opposite directions hence the plateau

Phase 3: Calcium channels close and K+ continues to exit cell - accounting for repolarisation

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8
Q

What is arrhythmia?

A

Deviation from a normal rhythm

Normal being regular and 60-100bpm

With each beat generated from SA node

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9
Q

How are arrhythmias broadly classified?

A

Bradyarrhythmia (<60bpm)

Tachyarrhythmia (>100bpm)

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10
Q

What are the main mechanisms responsible for tachyarrhythmias?

A

1. Abnormal automaticity: the pacemaker cells become abnormally permeable to Na+ during phase 4 resulting in an increase in the first upslope leading to disorganised firing of the cells

2. Triggered activity: abnormal leakage of + ions into the myocytes leading to a second bump on the myocyte action potential after depolarisation has occurred (= after depolarisations) This can trigger premature action potentials

3. Re-entry: an accessory pathway exists between the upper and lower chambers of the heart which allows the action potential to travel from the ventricles back to the stria causing them to contract before the SA node has fired (AVRT) - think Elliott think simple think one less letter

AVNRT: fast and slow pathways throguh the AV node - the signal from the SA node splits and half goes down the slow pathway, half goes down the fast pathway. The fast pathway signal reaches sooner than the slow pathway signal. The fast signal travels through the ventricles as well as up the slow pathway where it cancels the slow signal. Problems with the slow and fast pathway synchronisation leads to abberant conduction and repetetive firing of the AV node - leading to AV nodal re-entrant tachycardia

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11
Q

AVRT vs AVNRT

A

Both cause fast, irregular heart rates (tachyarrhythmias)

AVRT - think Elliott, think simple, think one less letter

AVRT: accessory pathway allows signal from ventricles to travel back to the atria and cause them to contract without firing of the SA node

AVNRT: involves de-synchronisation between fast and slow pathways of AV node - signals loops round AV node and causes ventricles to contract without SA node firing/ atrial contraction - there will not be a P wave before the QRS

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12
Q

Class 1 anti-arrhythmic drugs

A

Na+ channel blockers

Prolong phase 0 of AP, reducing the rate of depolarisation on non-nondal myocytes therefore reducing heart rate

Divided into 1A, 1B and 1C

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13
Q

Discuss class 1A antiarrhythmics

A

1 Na+, oK+ hun

Block Na+ & K+ channels

1A: block fast Na+ channels responsible for phase 0 of the cardiac myocyte action potential and block some K+ responsible for repolarisation

  • Class 1A agents cause a less-steep upstroke + a slower depolarisation (due to blockage of Na+ channels) and a longer effective refractory period (due to blockage of K+ channels, it takes more time before another AP can begin) PROCAINAMIDE, DISOPYRAMIDE
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14
Q

Discuss class 1B antiarrhythmic drugs

A

Minimal blockage of fast Na+ channels

Shorterns action potential and shortner effective refractory period

LIDOCAINE

Mainly used for ventricular arrhythmias

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15
Q

Discuss class 1C antiarrhythmic drugs

A

1C = powerful - think C think Charlotte think lots of salt blocked

They strongly block Na+ channels and therefore lead to a shallow upslope

Limited effect on the effective refractory period

FLECAINIDE

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16
Q

Problem with class 1 anti-arrhythmic drugs?

A

They all have the potential to cause arrhythmia

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17
Q

Discuss class 2 anti-arrhythmics

A

Class 2 = beta blockers

Block the effects of adrenaline on the heart - they depress the automaticity of the SA node and slow conduction through the AV node

Decrease HR and decreased contractility

PROPRANOLOL, ATENOLOL

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18
Q

Class 3 antiarrhythmic drugs

A

K+ channel blockers

Slower efflux of K+ leaving cell means the absolute refractory period is prolonged and more time is needed before another action potential can occur

AMIODARONE, SOTALOL (which also works as a b-blocker 🙄🤨)

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19
Q

Which anti-arrhythmic is given for VT/ VF cardiac arrest in A&E?

A

Amiodarone

Class III agent - given after adrenaline to treat life-threatening arrhythmia

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20
Q

Side effects of amiodarone

A

Pulmonary fibrosis

Blue/ grey skin

Liver toxicity

Hyperthyroidism/ hypothyroidism (conatins iodine and is toxic to thyroid gland)

Long half life and lingers for months

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21
Q

Which anti-arrhytmics cause prolonged QT syndrome?

A

Class 1A and class 3

They prolong time for repolarisation and therefore prolong time between the depolarisation and repolarisation of the ventricular cells

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22
Q

Class 4 antiarrhythmic drugs

A

Block Ca channels particularly in the SA and AV nodes

Decrease sinus rate and reduce conduction through AV node

Reduce contractility of the heart

Decrease atrial rate

VERAPAMIL, DILTIAZEM

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23
Q

What is the difference between non-dihydropyridines and hydropyridines?

A

Non-dihydropyridines: work in the heart and cause a negative ionotropic effect

e.g. diltiazem, verapamil

Dihydropyridines: work on the periphery and cause vasodilation

e.g. nifedipine, amlodipine

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24
Q

Which drugs are used to treat AF?

A

Beta blockers e.g. propranolol or non-dihydropyridine Ca2+ blockers e.g. verapamil/ diltiazem

NICE doesn’t reccomend one over the other

They cana be used at the same time if monotherapy is ineffective

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25
Q

Class 5 antiarrhytmics

A

Drugs that don’t really fit elsewhere are grouped into class 5

DMSAD - doesn’t matter, sad because they don’t fit

Digoxin, Magnesium Sulphate, Adenosine

Digoxin: Na/K ATPase inhibitor: enhances contractility and stimulates vagus node - which slows the heart rate)

Magnesium sulfate: mechanism unclear but when given IV is very good for treateing torsades de pointes and digoxin-induxed arrhythmia

Adenosine: works by stimulating adenosine receptors on the SA and AV nodes - slowing conduction time through the AV node. It can also interrupt re-entry pathways through the AV node

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26
Q

What is digoxin especially good for?

A

Patients with heart failure and AF

Blocks NA/K ATPase, causes more calcium to enter cell and therefore increases strength of contraction (inotropic)

Digoxin also stimulates the vagus nerve which causes a slower rate of firing of the SA node thus slowing the HR in AF

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27
Q

What is adenosine mainly used for?

A

Supraventricular tachycardia

It is 1st line drug for AVNRT and AVRT

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28
Q

Define arrhythmias

A

Disturbance of electrical activity in the heart

Can be asymptomatic/ symptomatic/ deadly

Often paroxysmal (sudden/ unpredictable) meaning diagnosis can be difficult

Primary causes: the heart itself

Secondary causes: non-cardiac cause

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29
Q

Description of arrhythmias after feeling pulse

A

Regularly irregular: not a steady pattern but a predictable one

Irregularly irregular: no pattern

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30
Q

What is bradyarrhythmia?

A

An inappropriately low HR <60bpm

Sinus bradycardia is an appropriately low rhythm seen in athletes/ during sleep

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31
Q

What are the classic symptoms of bradyarrhythmias?

A

Symptoms often not present until HR <45bpm

  • Palpitations
  • Light-headedness
  • Dizziness
  • Fatigue
  • SOB
  • Chest pain
  • Syncope (Stokes-Adams attacks)
  • Cardiogenic shock and hypotension: late stage + life threatening
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32
Q

Outline some non-cardiac causes of bradycardia and bradyarrhythmias

A
  • Sleep and athletic training
  • Drugs: beta blockers, calcium blockers, amiodarone
  • Metabolic: hypothyroidism, hypothermia
  • Electrolyte disturbance: hyperkalaemia, hyponatremia, hypercalcaemia, hypomangesaemia

Others: raised ICP, obstructive sleep apnoea

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33
Q

What is sick-sinus syndrome?

A

Sinus node fails to pace the heart appropriately

Leads to:

Sinus pauses: cessation in electrical activity

Sinus tachycardia

Sinus bradycardia

Atrial tachycardia

Chronitropic incompetence: heart does increase rate in respond to exercise

Atrial fibrillation

Brady-tachy syndrome (

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34
Q

Brady-tachy syndrome suggests what specific disease?

A

Sick sinus syndrome

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35
Q

What causes sick sinus syndrome?

A

Mainly due to idiopathic fibrosis of the sinus node

MI, cardiomyopathy, myocarditis

Sarcoidosis, amyloidosis, haemachromatosis

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36
Q

How is brady-tachy syndrome managed?

A

Pacing for bradyarrhythmia, drugs for tachyarrhythmia

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37
Q

Types of bradyarrhythmia

A

Sick sinus syndrome

Heart block:

  • 1st degree
  • 2nd degree : Mobitz 1&2
  • 3rd degree
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38
Q

Normal ECG intervals

A
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39
Q

What is heart block?

A

Impaired conduction between the atria and ventricles

Caracterised into 1st, 2nd and 3rd degree

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40
Q

Where does geart block occur?

A

Can occur anywhere in the conduction system

AV node/ bundle of His = AV block

Block lower down = bundle branch block

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41
Q

Discuss 1st degree heart block

A

Prolongation of the PR interval >0.2seconds

0.2seconds = 1 large box

Considered more of a delay rather than a block because every atrial impulse eventually reaches the ventricles

ECG change: prolonged PR interval >0.2seconds

Husband comes home late every day ⌚️

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42
Q

Discuss 2nd degree heart block

A

Mobitz type 1

Longer and longer PR prolongation until a P wave fails to conduct - leading to a P wave that is not followed by a QRS

Only requires treatment if it is symptomatic, few cases progress to complete block

Husband comes home later and later until one night he doesn’t come home 🤨 🐍

Mobitz type 2

Regularly >1 P wave before every QRS e.g. 2:1 or 3:1

More likely to progress to complete heart block and is therefore often treated

Often symptomatic

Husband is home every now and again 😡

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43
Q

How is Mobitz type 2 managed?

A

Pacemaker

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44
Q

Discuss 3rd degree heart block

A

There is no association between atrial and ventricular actiivty

P waves = regular

QRS complexes = regular

But they are not associated at all

QRS rate is driven by spontaneous escape rhythm

Occasionally the atria and ventricles contract at the same time: atria contract but tricuspid vavle is closed - blood shoots back up jugular vein and causes canon waves

Serious and requires pacemaker

Husband and wife live separate lives 🧔🏻 ❌ 👩🏻‍🦱

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45
Q

Investigations for heart block

A

Bedside: 12-lead ECG

Bloods:

Troponin if thinking MI

U&E: derrangement can cause heart block

Calcium: derrangement can cause heart block

Thyroid function tests: hypothyroidism can cause heart block

If patient on digoxin, can check serum levels as this can cause heart block

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46
Q

How does digoxin cause heart block?

A

Digoxin enhances Vagus nerve activity, which slows conduction over the AV node.

Digoxin also has a direct effect on AV conduction, by slowing it.

This causes prolongation of the PR interval, which is considered a normal finding, unless severely prolonged.

Second- and third-degree AV block is evidence of intoxication

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47
Q

What causes a curved ST segment depression?

A

Digoxin toxicity

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48
Q

Management of bradyarrhythmia

A

Asymptomatic: often treated conservatively unless type 3

Symptomatic: pacemaker

Emergency treatment: transcutaneous pacing or IV atropine

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49
Q

Which drug is said to cause a feeling of impending doom?

A

Adenosine: causes complete AV block to terminate supraventricular tachycardias (AVRT, AVNRT

Idea is that it stops 2 hearts: that of the patient and that of the doctor…

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50
Q

How is bradyarrhythmia managed?

A

If symptomatic or type 3/ complete heart block: pacemaker

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51
Q

What is bundle branch block?

A

A block in conduction in the right/ left bundle branches

This causes a wide, biphasic QRS >0.12seconds (120ms or 3 small boxes)

The shape of the QRS depicts where the block is

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52
Q

Right bundle branch block

A

Produces a late activation of the right ventricle because the right ventricle is activated by secondary conduction vs the left ventricle

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53
Q

ECG change in RBBB

A

QRS is broad

Deep S wave in lead I and V6

Tall, late R wave in V1

VI change is said to look like an M (Rabbit ears in Right chest lead V1)

V6 change is said to look like a W

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54
Q

Causes of RBBB

A

Often benign and can be found in normal hearts

Important to look for a cause: anything that causes strain on right side of heart

  • PE
  • Pulmonary HTN
  • RV hypertrophy
  • Cor pulmonale
  • Inferior MI
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55
Q

Heart sound in RBBB?

A

S2 is split

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56
Q

Discuss LBBB

A

Delay in contraction of left ventricle due to conduction failure in left bundle branch

ECG: Deep S wave in V1 - ‘W’

Tall, late R wave in lead I, aVL, V5 and V6 - ‘M’

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57
Q

Can LBBB be normal?

A

NOOOOO - never occurs in normal hearts

It is a poor prognostic sign and needs investigating

New LBBB in a patient with chest pain - think MI

58
Q

Causes of LBBB

A
  • HTN
  • Aortic stensosis: causes LV hypertrophy and damage to left bundle branches
  • Coronary artery disease
59
Q

What are tachyarrhythmias?

A

Abnormal heart rhythms >100bpm

60
Q

How are tachyarrhythmias categorised?

A

Narrow complex: QRS <120ms/ 3 small squares

  • AKA supraventricular tachycardias, they reflect organised & efficient electrical activity originating above the AV node

Broad complex: QRS >120ms/ 3 small squares

  • Reflect disorganised and delayed electrical activity usually originating in the ventricles - more unstable than narrow complex tachycardias
61
Q

What is a supraventricular tachycardia?

A

Fast heart rates that arise from the atria or AV node

Can occur in healthy or diseased hearts

62
Q

Discuss sinus tachycardia

A

Persistent increase in HR unrelated to level of physical/ emotional distress

Acute causes: exercise, emotion, pain, fever, infection, acute HF, acute PE, hypovolaemia, drugs

Chronic causes: pregnancy, anaemia, hyperthyroidism, atrial tachycardia associated with COPD

Management: treat the cause, beta blockers, ivabradine

63
Q

Causes of narrow complex tachycardia?

A

Supra-ventricular tachycardia

  • Sinus tachycardia
  • Atrial flutter
  • Atrial fibrillation
  • AVRT
  • AVNRT
64
Q

What % of the population have a supraventricular tachycardia?

A

0.2%

65
Q

What is atrial tachycardia?

A

A rapid, regular rhythm arising from a discrete area in the atria

AKA focal atrial tachycardia

Due to a hyper-excitable focus in the atria that fires at a faster rate than the SA node meaning it takens control from the SA node

ECG: regular SVT (narrow complex tachycardia) with abnormal P wave morphology e.g. very upright or inverted P waves

*Can be difficult to diagnose by ECG alone

66
Q

What is multi-focal atrial tachycardia?

A

Same mechanism as atrial tachycardia but many foci for abnormal activity

ECG: an SVT with 3 different-looking P waves

Typically seen in COPD where the right side of the heart is dilated

67
Q

Which SVT is classically associated with COPD?

A

Multi-focal atrial tachycardia (MAT)

68
Q

Classification of atrial tachycardias

A
  1. Sinus tachy: regular tachycardia with regular and uniform P waves before every QRS
  2. Focal atrial tachycardia: recurrent, regular tachy, HR 100-250bpm. P waves are visible before every QRS but they are abnormal
  3. AVNRT: P waves may be visible but usually follow the QRS
  4. AVRT
  5. Multi-focal atrial tachycardia: irregular tachycardia, P waves before every QRS and at least 3 different P wave morphologies when looking at a single lead
  6. Atrial flutter: atrial activity is regular and ~300bpm, rate is usually ~150 bpm because every 2nd contraction propogates to ventricles
  7. Atrial fibrillation: irregular tachycardia with a beat-beat variation in heart rate
69
Q

How is atrial flutter sawtooth appearance sometimes more easily seen?

A

Turn the ECG upside down…

70
Q

ECG showing a regular SVT with P waves that have an unusual axis e.g. inverted?

A

Think focal atrial tachycardia

71
Q

ECG showing regular SVT with P waves before every QRS but the P waves all appear different?

A

Multifocal atrial tachycardia

72
Q

What are re-entrant tachycardias?

A

Occur when electrical activity conducts through abnormal circuits which loop back on themselves to form a re-entry loop which is self stimulating

Often occurs around a circuit of scar tissue

Key features: seen in youn patients, tend to be short-lasting, rarely life-threatening but are often symptomatic

73
Q

Types of re-entrant tachycardias

A

Atrioventricular nodal re-entry tachycardia (AVNRT)

Atrioventricular re-entry tachycardia

74
Q

Discuss AVNRT

A

Most common SVT - 80%

  • AV node has 2 tracks;
    • Fast conducting track=long refractory period; P wave normally conducted through this pathway.
    • Slow conducting track=short refractory period.
  • If have an ectopic immediately after a normal P wave it will conduct through slow tract (as fast is still refractory).
  • By time has reached bottom of slow-track, fast will have recovered so it travels back up the fast track, which then re-stimulates the slow-track
75
Q

ECG in AVNRT

A

Typical appearance = absent P waves and tachycardia

Normal QRS with rhythm of 140-240bpm

Atria and ventricles depolarise almost simultaneously so P waves are hidden in the QRS or seen immediately before/ after QRS

*P waves can sometimes be seen within the QRS as a pseudo R wave

76
Q

Difference between atrial tachycardia and other SVT?

A

Atrial tachycardia is defined as a supraventricular tachycardia (SVT) that does not require the atrioventricular (AV) junction, accessory pathways, or ventricular tissue for its initiation and maintenance

77
Q

What is the classic presenting rhythm in patients with digoxin toxicity?

A

Focal AT

78
Q

Which type of patient is AVNRT classically seen in?

A

75% of cases are in women

Can occur in young patients as well as those who are older with heart disease

79
Q

Investigations for AVNRT

A

Patient often presents with palpitations

ECG: tachycardia with normal and regular QRS complex + either

a) no P wave
b) P wave immediately before QRS
c) P wave immediately after QRS

Bloods: U&E to look for electrolyte causes

Echo: look for any structural damage

80
Q

Typical clinical presentation of AVNRT in A&E

A

Middle aged or older female

Pounding sensation in neck, palpitations, lightheadedness, syncope, SOB

Canon A waves - referred to as ‘frog sign’ because the JVP with buldge like a frog’s neck 🐸

81
Q

How are AVNRT and AVRT managed?

A

Medical: if patient haemodynamically stable

Valsalva manoeuvre: ask patient to push down/ bear down as if having a poo while glottis is closed

Dive reflex: ice-cold cloth to face

Carotid sinus massage: 5-10 seconds

Pharmacological:

  • Adenosine: rapid bolus, works in 80-95%

If patient is haemodynamically unstable emergency cardioversion is needed

Long term management

Beta blockers, verapamil, diltiazem, ablation therapy (1st line in WPW)

82
Q

Why does polyuria occur in patients with AVNRT and AVRT

A

Increased levels of atrial-natriuretic peptide - typically occurs once the episode is over

83
Q

Appearance of ECG in AVRT

A

P waves clearly seen between QRS and T wave - Impulse travels back up and causes atrial contraction after ventricular contraction

84
Q

On which side of the heart are accessory pathways found?

A

Left

Called the bundle of Kent in WPW

85
Q

Which SVT is esecially common in women?

A

AVNRT

86
Q

Good way to try and manage AVNRT/ AVRT in children?

A

Get them to blow into a syringe

87
Q

What would cause a new normall-narrow complex tachycardia to be broad?

A

Pre-existing BBB

88
Q

What is Wolf-Parkinson White?

A

Condition where an accessory pathway (bundle of Kent) results in ventricular pre-excitation

Signal from pathway and AVN combine to contract ventricles - on ECG pre-excitation is seen as a delat wave and a PR interval <120ms with a QRS >110ms

Usually benign but can lead to other arrhythmias and is often symptomatic so treated

89
Q

Clinical features of SVTs

A

Palpitations: flitter in chest, fast beat, start and stop suddenly, commonly terminated by Valsalva manoeuvre

*Many patients with palpitations are due to extrasystole (both atrial and ventricular extrasystoles are common)*

  • If palptations occur immediately after/ during exercise they need referring to cardio, also if the palpitations are associated with pain/ syncope
  • Dyspnoea, fatigue, polyuria due to increased ANP, raised JVP
90
Q

What are extrasystoles?

A

AKA ectopic beats, contractions that occur out fo the normal rhythm when there is electrical discharge from somewhere in the heart other than the SAN

Common

Atrial extrasystoles: seen in >60% adults

Ventricular extrasystoles: 40-75% adults, common in structural heart disease (nost common type of arrhythmia after MI

91
Q

Risk factors for extrasystoles

A

HTN

Heart disease

Electrolyte disturbance

Alcohol

Drugs

Stress

Infection

Hyperthyroidism

Caffeinr

92
Q

Presentation of patient with extrasystole

A

Palpitations = main symptom

  • Worse at rest, dissapear with exercise - if they get worse with exercise this is a worrying feature
  • Syncope, atypical chest pain, fatigue, chronic cough
93
Q

History taking for extrasystoles

A
  • Onset, duration, associated symptoms and recovery
  • Other cardiac symptoms: chest pain, breathlessness, syncope or pre-syncope
  • Exertional syncope = alarming
  • FHX: cardiac death/ disease
  • CHD risk factors
94
Q

Investigations for extrasystoles

A

12-lead ECG resting/ ambulatory/ holter (24hr ECG)

FBC, TFTs

U&Es

Echo

95
Q

ECG finding in atrial extrasystole

A

Premature P waves which look different to normal P wave

96
Q

Ventricular extrasystole ECG

A

Wide, abnormally shaped QRS complexes

If they occur at every 2nd or third beat they are called bigeminy/ reigeminy respectively

97
Q

In the context of extra systole, which patients need referring

A

Urgent symptoms: chest pain, SOB, LOC

Syncope/ pre-syncope

Significant ECG abnormality

Significant cardiac disease

FHx

Troublesome symptoms

98
Q

Managament of extrasystole

A

Low risk with no symptoms/ cardiac problems: reassure

Medication: beta blockers, catheter ablation of ectopic focus

Lifestyle: avoid caffeine

99
Q

What is atrial flutter?

A

A type of atrial tachycardia due to a macro re-entrant curcuit where the atria contract at a very high rate (typically ~300bpm)

Many patients with flutter have associated atrial fibrillation

Typical flutter: origin is in right atrium, classic saw-tooth pattern and rates of 240-350 bpm

Atypical flutter: origin is in right or left atrium, ECG is variable and rates may be faster than those seen in typical flutter

100
Q

Epidemiology of atrial flutter

A

2nd most common arrhythmia after AF

Commonly associated with AF

Increases with age

80% cases in men

Systemic thromboembolism less likely to occur in atrial flutter than AF

101
Q

Aetiology of atrial flutter

A

Age is most common risk factor

  • Structural anomalies: left-atrial dilatation = strongest predictor for developing flutter
  • CHD, atrial dilatation, cardiac surgery/ ablation, obesity, alcohol, COPD, cardiomyopathy, myxoma, pericarditis, sick sinus syndrome, obstructive sleep apnoea, very high-intensity sport
102
Q

Presentation of atrial flutter

A

Varies, can be an incidental ECG finding, can be found after patient has had a stroke

Palpitations, fatigue, dyspnoea, pre syncope

Syncope

TIA/ stroke

Pulse: can be regular/ irregular, AV conduction usually 2:1 so ventircular rate is 150bpm - if. AV conduction is 1:1 this can cause haemodynamic collapse

Associated with symptoms of underlying disease e.g. alcoholism, thyrotoxicosis

103
Q

Where is the saw-tooth pattern of atrial flutter best seen?

A

II, III and aVF - usually shows atrial rates of 240-340bpm

104
Q

Investigations for atrial flutter

A

ECG: no isoelectric baseline, saw tooth waves between the QRS complexes, variable AV conduction e.g. 2:1, 3:1 etc

Look for causes: CXR, TFTs, ESR, renal function and LFTs

Echo

105
Q

Management of atrial flutter

A

If haemodynamically unstable: direct current cardioversion (DCCV)

Acute, haemodynamically stable: B-blocker/ Ca2+ blocker - often not as effective as with other SVTs, anticoagulate with a NOAC, cardioversion is 2nd line - patient must have been anti-coagulated for at least 3 weeks

Recurrent flutter: catheter ablation

Ongoing: antithrombotics, same as AF

106
Q

What is atrial fibrillation?

A

Most common sustained arrhythmia characterised by irregularly irregular atrial pulse and loss of association between cardiac apex beat and radial pulse

Conducts rapidly to the ventricles resulting in an irregular ventricular rate

High risk of thromboembolic disease and stroke due to poor atrial contractions leading to blood stagnation

107
Q

Classification of atrial fibrillation

A
  • Paroxysmal: lasts <7 days
  • Persisten: lasts >7 days
  • Long-standing: lasts >1yr
  • Permanent: lasts >7 days and can’t be cardioverted
108
Q

Epidemiology of AF

A

Most common sustained cardiac arrhythmia with increasing prevalence

3% of adults aged 20+

10% those aged 80+

Greater prevalence in those who are older and have conditions such as HTN, HF, CAD, valvular heart disease, obesity, DM, CKD

More common in men

109
Q

Aetiology of AF

A

Triggering event: any condition resulting in raised atrial pressure, increased atrial mass, atrial fibrosis, infiltration or inflammation

HTN is most common cause

HF is 2nd most common cause

IHD, valvular disease, hypothyroidism, hyperthyroidism, alcohol, caffeinem pneumonia, PE

110
Q

Foci that cause AF are often located where?

A

Pulmonary veins - the myocardial tissue of the left atrial wall extends in to the pulmonary venous walls

111
Q

Presentation of patient with AF

A

30% cases AF is an incidental finding

Breathless

Palpitations

Dizziness

Chest discomfort

Stroke/ TIA

112
Q

Signs of AF

A

S1 is variable in intensity

Irregularly irregular pulse

ECG: no clear P waves, fine oscillations of the baseline, rapid and irregular QRS - described as a worn out saw

113
Q

Investigations for AF

A

ECG: in all who have an irregular pulse, where symptomatic or not

  • This can either be a 12 lead, ambulatory, holter or event recorder

- Bloods: TFTs, CXR, echo

- Coagulation screen if considering patient for anti-coagulants

Echo to exclude structural heart disease

114
Q

Management of atrial fibrillation

A

Haemodynamic instability: direct current cardioversion (DCCV)

Acute but haemodynamically stable:

Offer rate/ rhythm control if started <48hrs ago: DCCV or pharmacological cardioversion (with amiodarone/ felecainide or only amiodarone for those with structural heart disease)

Offer rate control (metoprolol, verapamil, diltiazem) if started >48hrs ago: if patients with an unknown duration of AF are considered for long-term rhythm control, do not do this until they have been on an anti-coagulant for 3 weeks minimum

Anti-coagulation if AF is new: offer heparin at initial presentation and continue until full assessment and anti-thrombotic therapy started

Anti-coagulation if AF diagnosis confirmed: offer oral anti-coagulant if there is high risk of AF recurrence or sinus rhythm isn’t restored within 48hrs of onset

115
Q

Which type of AF on ECG is particularly dangerous?

A

Pre-excited AF

Occurs when an accessory pathway conduction the atrial fibrillation to the ventricles - this can quickly degrade into ventricular fibrillation

*Important not to give patients with pre-excited AF drugs that block the AV node because this increases conduction through the accessory pathway*

116
Q

Difference between AF and other SVTs?

A

AF has an irregularly irregular rhythm

117
Q

What is a delta wave?

A

Slurring of the QRS upstroke - occurs because the action potential from the SAN is able to conduct very quickly to the ventricles via the accessory pathway (usually the AV node slows it down)

This results in a short PR interval

Seen in WPW

118
Q

When is WPW espeically life threatening?

A

When it occurs in addition with AF

If medication is sued that temporarily blocks the AV node - the ectopic foci continue firing but the fibrillation is sent down the accessory pathway leading to ventricular fibrillation

119
Q

What are the AV node-blocking agents?

A

Adenosine, Amiodarone

Beta-blockers

Calcium channel blockers

Digoxin

ABCD

120
Q

What is ventricular tachycardia?

A

Broad complex (>120ms or 3 small squares) tachycardia originating from a ventricular focus

Defined as >=3 successive ventricular beats occurring at >100bpm

Dangerous as can lead to VF, cardiac arrest and death 🫀

121
Q

What is Torsades de Pointe?

A

Polymorphic VT in which the QRS complexes appear to twist around an imaginary baseline

122
Q

Broad complex tachycardia with an irregularly irregular rhythm?

A

Think about AF with bundle branch block

**Ventricular tachycardia is regular

123
Q

Aetiology of VT

A

Monomorphic VT resulting from an abnormal re-entry circuit often caused by scarring e.g. due to sichaemic heart disease. cardiomyopathy, myocarditis, long QT syndrome

124
Q

What are the shockable rhythms?

A

Heart rhythms associated with cardiac arresr are divided into 2 groups

Shockable: VF, pulseless VT

Non shockable: asystole (flat line) and pulseless electrical activity (electrical activity of the heart is not accompanied by a palpable or effective pulse

125
Q

Classification of VT

A

Pulsed (palpable pulse) or pulseless

Non-sustained <30s or sustained >30s

Monomorphic: QRS always same

Polymorphic: QRS appearance frequently changes

126
Q

Key characteristics of sustained VT

A

>30 seconds

Often results in syncope, pre-syncope, hypotension, cardiogenic shoch and cardiac arrest

127
Q

Management of VT

A

Haemodynamically unstable

  • DCCV (3 attempts).
  • Amiodarone.

Haemodynamically stable

  • If cause identifiable
    • Lidocaine and procainamide are other options.
    • Amiodarone 1st line.
    • If medication fails then DCCV.
    • Can attempt radiofrequency catheter ablation to certain pt.
  • If pt. has high risk of recurrence then give implantable defibrillator.

All patients with Torsades de Pointes require urgent DCCV

128
Q

What % of broad complex tachycardias are caused by VT?

85%

The remainder are SVT with BBB

A
129
Q

Which features suggest VT rather than SVT with BBB?

A

Very broad QRS >160ms

Extreme axis -90 to -180 degrees

  • Capture beats: where a SAN beat captures the ventricles and produces a normal looking beat

Bizarre QRS morphology

AV dissociation

*Treat as VT until proven otherwise

130
Q

You see an ECG with broad complex tachycardia - what is it?

A

VT until proven otherwise

131
Q

What are ICDs?

A

Implantable cardioverter defibrillators

Used for secondary prevention in patients with VT/ VF causing syncope or cardiac arrest

Used for primary prevention in patients with high-risk conditions e.g. severe heart failure

  • They do not prevent VT but they restore sinus rhythm when it occurs
132
Q

What is VF?

A

Myocardium devoid of any coordinated electrical or mechanical activity and cardiac output ceases 🫀❌

133
Q

Management of VF

A

VF always results in cardiac arrest so alays requires DCCV to prevent asystole and death

Long term treatment = ICD

134
Q

What is Brugada syndrome?

A

Inherited AD channelopathy that occasionally presents with sudden cardiac death due to VT/ VF

More common in males in SE Asia

135
Q

How is Brugada syndrome diagnosed?

A

presence of:

  • VT/ VF
  • FHx of sudden cardiac death
  • Family members with Brugada syndrome
136
Q

ECG findings Brugada syndrome

A

ST elevation in V1-V3, without ischemia

137
Q

Management of Brugada syndrome

A

ICD

Avoid drugs that can cause the arrhythmia: anti-arrhythmics, psychotropics and anaesthetic agents

138
Q

What is the CHA2DS2-VASC score?

A

Annual stroke risk in patients with AF

139
Q

What is the HASBLED score?

A

Estimates the risk of bleeding in patients on warfarin

140
Q

Medication used for tate control in AF

A

Beta blockers

Calcium channel blockers

Digoxin (reserved for more sedentary patients because it doesn’t allow the heart rate to rise with exercise)

141
Q

What are the priorities when treating AF?

A

Reduce stroke risk

Control HR

Control symptoms

  • Restoring sinus rhythm has not been shown to improve prognosis
142
Q

Which arrhythmia is commonly seen in systemic illness and following surgery?

A

AF

Cardiology (8 decks)

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