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Medicine - Year 2 > The cardiovascular system - Arrhythmias, syncope and arrest > Flashcards

The cardiovascular system - Arrhythmias, syncope and arrest Flashcards

1
Q

What is atrial fibrillation?

A

Uncoordinated atrial contraction. It is irregular and frequently fast ventricular rate

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2
Q

Describe the epidemiology of AF

A
  • Commonest cardiac arrhythmia
  • Prevalence increases with age
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3
Q

Aetiology of AF

a) Cardiac causes

b) Non-cardiac causes

A

a)
- Hypertension
- Ischaemic heart disease
- Valvular disease
- Myocardial infarction

b)
- Respiratory: COPD, pneumonia, PE
- Endocrine: hyperthyroidism (trigger), DM
- Acute infection: hypokalaemia, hypomagnesaemia, hyponatraemia
- Drugs: bronchodilators, thyroxine
- Lifestyle factors: alcohol, excessive caffeine, obesity, sleep apnoea
- Aging (structural remodelling)

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4
Q

ATRIALE PhIB is a pneumonic for the aetiology of AF. What does it stand for - Alcohol and caffeine
- Thyrotoxicosis
- Rheumatic fever and mitral valve pathology
- Ischaemic heart disease
- Atrial myxoma
- Lungs (pulmonary hypertension, pneumonia)
- Electrolyte disturbances

A

A - alcohol and caffeine
T - thyrotoxicosis
R- rheumatic fever and M - mitral valve pathology
I - ischaemic heart disease
A - atrial myxoma
L - lungs (pulmonary hypertension, pneumonia)
E - electrolyte disturbances

Ph- pharmacological
I- iatrogenic (drugs, surgery)
B - blood pressure (HTN)

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5
Q

What are two important concepts in the development of AF

A
  1. Trigger
  2. Maintenance
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6
Q

‘Trigger’ is an important concept in the development of AF. Describe this concept

A

Thought to be an initial focus of rapid atrial firing, usually around pulmonary veins, that ‘tigger’s the onset of AF. Other triggers include premature atrial complexes and other arrhythmias

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7
Q

‘Maintenance’ is an important concept in the development of AF. Describe this concept

A

In patients with persistent AF, once it has been ‘triggered’, alteration in the atrial myocardium enables maintenance of the abnormal arrhythmia.

Multiple factors contribute to the maintenance of AF including atrial structural remodelling (e.g., fibrosis, dilation, hypertrophy) and atrial electrical remodelling (e.g., alteration to atrial ‘refractoriness’) and contractile remodelling

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8
Q

Describe the relationship between AF and stroke

A
  1. Blood pools in the atria
  2. Blood clot forms
  3. Whole or part of the blood clot breaks off
  4. Blood clot travels to the brain and blocks a cerebral artery causing a stroke
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9
Q

Give the 5 different classifications of AF pattern

A
  1. First diagnosed AF
  2. Paroxysmal AF
  3. Persistent AF
  4. Long-standing AF
  5. Permanent AF
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10
Q

What is first diagnose AF?

A

AF that has not been diagnosed before, irrespective of the duration of the arrhythmia or the presence and severity of AF-related symptoms

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11
Q

What is paroxysmal AF?

A

Self-terminating, in most cases within 48 hours. Some AF paroxysms may continue for up to 7 days. AF episodes the are cardioverted within 7 days should be considered paroxysmal.

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12
Q

What is persistent AF?

A

AF that lasts longer than 7 days, including episodes that are terminated by cardio version, either with drugs or by direct current cardio version, after 7 days or more

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13
Q

What is long-standing AF?

A

Continuous AF lasting for a year or more when it is decided to adopt a rhythm control strategy

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14
Q

What is permanent AF?

A

AF that is accepted by the patient (and physician). Hence, rhythm control intervention are, by definition, not pursued in patients with permanent AF. Should a rhythm control strategy be adopted, the arrhythmia should be re-classified as ‘long standing persistent AF’

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15
Q

Atrial fibrillation

a) Symptoms

b) Signs

A

a)
- Asymptomatic
- Palpitations
- Dyspnoea
- Chest tightness
- Fatigue/lethargy
- Sleep disturbance
- Psychological effects

b)
- Irregular irregular pulse
- Absent ‘a’ wave on JVP
- Tachycardia
- Hypotension
- Features of heart failure: bibasal cracked, raised JVP, peripheral oedema
- Apical to radial pulse deficit -> occurs as not all atrial impulses (palpable at the apex) are mechanically conducted to the ventricles (palpable as a peripheral pulse)

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16
Q

Describe the level of symptoms and description of the following scores in modified European heart rate associate (EHRA) symptom scale of AF

a) I

b) 2a

c) 2b

d) 3

e) 4

A

a)
Symptom - none

Description - AF does not cause any symptoms

b)
Symptoms - mild

Description - normal daily activity not affect by symptoms related to AF

c)
Symptoms - moderate

Description - normal daily activity not affected by symptoms related to AF, but patient troubled by symptoms

d)
Symptoms - Severe

Description - Normal daily activity affected by symptoms related to AF

e)
Symptoms - disabling

Description - normal daily activity discontinued

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17
Q

When is a diagnosis of AF suspected clinically?

A

By can irregular pulse and confirmed on as 12-lead ECG

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18
Q

What are the 3 hallmark ECG features of AF

A
  • Irregularly irregular rhythm
  • Absence of P waves
  • Irregular, fibrillating baseline
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19
Q

Once AF is confirmed, investigations are completed to determine the underlying cause, guide management, and assess for complications.

What further investigations would you do?

A

Bedside
- Observations
- Blood pressure
- ECG

Bloods
- FBC (anemia, infection)
- U&Es (electrolyte disturbances)
- TFTs (hyperthyroidism)
- Coagulation
- Cholesterol
- Bone profile
- Magnesium
- Troponin: if MI suspected
- CRP/ESR: if acute infection suspected

Imagine
- CXR: can assess for acute infection or cardiac failure
- CT/MRI: if embolic event suspected
- Echocardiography: needed in patients with high risk suspicion of underlying structural defect e.g., valvular heart disease

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20
Q

What are the 4 principles of AF management?

A
  1. Rate control
  2. Rhythm control
  3. Management of acute AF
  4. Prevention of thromboembolic events
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21
Q

Discuss the options for rate control for AF?

A

Beta-blockers (e.g., metoprolol, bisoprolol, carevdiolol) - contraindicated in acute HF, asthma, COPD and hypotension

Non-dihydropyridine/rate-limiting calcium channel blockers (e.g., verapamil, diltiazem) - contraindicated in HF

Digoxin - usually for patients who are hypotensive or have co-existant HF

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22
Q

Rate control should be offered as the first-line strategy to people with AF. However exceptions. What are these exceptions?

A

Except in people

  • Whose AF has a reversible cause
  • Who have heart failure though to be primarily caused by AF
  • With new-onset AF and haemodynamically unstable
  • For whom a rhythm control strategy would be more suitable based on clinical judgement
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23
Q

Discuss the options for rhythm control for AF

A
  1. Pharmacological
    - Amiodarone: has significant side-effects so normally only given to older, sedentary patients
    - Flecainide: can be give regular or as a “pill in the pocket” for paraxosymal AF
    - Sotalol: a beta blocker with additional K channel blocker action. For those who don’t meet requirements for amiodarone/flecainide
  2. Electrical - DC cardioversion
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24
Q

What type of patients may be suitable for rhythm control?

A
  • New onset AF
  • Identifiable reversible cause
  • Heart failure (exacerbated by AF)
  • Associated with atrial flutter and ablation strategy appropriate
  • Rhythm control felt more suitable (clinical judgement)
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25
Q

What is an alternative treatment to long-term anti-arrhythmic drugs to maintain sinus rhythm?

A

Catheter ablation

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26
Q

Describe the process of catheter ablation

A

It involves passing a small catheter via a transferral venous approach to eventually reach the left atrium

Several mechanisms (e.g., radio-frequency ablation or cyroablation) may then be used to damage left atrial tissue and prevent electrical transmission

This is predominately focused around area where AF is ‘triggered’ such as the pulmonary vein

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27
Q

Describe the management of acute AF

A
  1. Perform a clinical assessment (ABCDE) and determine haemodynamic stability
  • Haemodynamic stability: emergency DC cardioversion
  • Haemodynamic stability: rate or rhythm control strategies
  1. In patients who are stable, the key determinant to further management is precise time of onset. This is because cardioversion is associated with an increased risk of embolic events
  • Onset > 48 hours: increased risk of thromboembolism. Patients need adequate anticoagulation (minimum 3 weeks) to reduce thromboembolic risk prior to cardioversion
  • Onset < 48 hours: low risk of thromboembolism. Patients’ can be considered for immediate electrical or pharmacological cardioversion
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28
Q

Describe the algorithm for anticoagulation for cardioversion in AF

A

If unstable then immediate help emergency cardioversion

If stable check anticoagulation status. If therapeutic then immediate or delayed cardioversion

If no anticoagulation status then initiate anticoagulation. If onset <48 hours then do early cardioversion. If onset > 48 hours then do elective cardioversion (min. 3 weeks)

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29
Q

Why is the time of onset of acute AF in stable patients important?

A

This is because cardioversion is associated with an increased risk of embolic events. Therefore time of onset determines whether anticoagulation is required.

If onset <48 hours then low risk of thromboembolism so you can then do early cardioversion

If onset > 48 hours then high risk of thromboembolism so anticoagulation for a minimum of 3 weeks is required. Therefore you’ll do an elective cardioversion (min. 3 weeks)

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30
Q

What risk stratification tool is used to asses stroke in patients with AF?

A

CHA2DS2-VASc score

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31
Q

a) What are the components of the CHAD2DS2-VASc score? and how many points does each score?

b) Evaluate the scores

c) What anticoagulation is first line?

A

a)
C- Congestive heart failure +1
H - Hypertension +1
A - Age 75 years or older +2
D - Diabetes +2
S - Stroke, TIA or thromboembolism previously +1

b)
Va - vascular disease (previous MI, PAD, or aortic plaque)+1
A- Age 65-74 years +1
Sc - Sex category (female) +1

b) Anticoagulation should be considered in men with a score of 1 and greater

Anticoagulation should be considered in females with a score of 2 or greater

c) DOAD

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32
Q

If a DOAC is not suitable or tolerated (e.g., mechanical heart valve), in patients with AF what is the second line anticoagulant?

A

Vitamin k antagonist e.g., warfarin

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33
Q

Patients with AF should undergo a formal risk assessment for major bleeding with anticoagulation using what score?

A

ORBIT score

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34
Q

a) What are the components of the ORBIT score and how many points does each score?

b) Evaluate the score

A

a)
O - older age > 74 +1
R - reduced haemoglobin +2
B - bleeding history (GI bleeding, intracranial bleeding, haemorrhagic stroke) +2
I - insufficient kidney function +1
T - treatment with antiplatelets +1

B) Score of 4-7 is considered high risk, 3 is medium risk and 0-2 is low risk

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35
Q

Describe the treatment of paroxysmal AF

A
  • Patients with infrequent paroxysmal may be treated with a ‘pill-in-pocket’ regimen
  • Patients can self-administrate of flecainide or sotalol at the onset of AF to induce pharmacological cardioversion
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36
Q

Complications of AF

a) Cardiac

b) Non-cardiac

A

a)
- Heart failure
- Tachycardia-induced myopathy
- Ischaemia
- Sudden cardiac arrest

b)
- Thromboembolic events: stroke, TIA, mesenteric ischemia, limb ischaemia
- Bleeding events

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37
Q

What are the risk factor contributors of AF?

A
  • Hypertension
  • Diabetes mellitus
  • Obesity
  • Obstructive sleep apnea (OSA)
  • Smoking
  • Alcohol
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38
Q

Describe the risk factor management of AF

A
  • Blood pressure control
  • Weight reduction
  • Lipid control
  • Blood sugar level control
  • treat/manage obstructive sleep apnea
  • Smoking cessation
  • Alcohol reduction
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39
Q

What is tachycardia defined by?

A

> 100 bpm

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40
Q

Differential diagnosis for narrow complex tachycardia?

A
  • Sinus tachycardia
  • AF
  • Atrial flutter
  • Focal atrial tachycardia
  • Atrioventricular re-entrant tachycardia (AVRT)
  • Atrioventricular nodal re-entrant tachycardia (AVNRT)
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41
Q

Differential diagnosis for broad complex tachycardia?

A
  • Ventricular tachycardia
  • Ventricular fibrillation
  • “SVT” with aberration
  • Pre-excited tachycardia
  • Pacemaker associated tachycardia
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42
Q

What a narrow complex tachycardia defined as?

A

QRS complex shorter than 120 ms (three small squares on the ECG)

43
Q

Describe the management of narrow complex tachycardias

A
  1. Patients should be assesses using the ABCDE approach
  2. If haemodynamically unstable (shock, syncope, acute pulmonary oedema or myocardial ischaemia) then emergency DC cardioversion required
  3. Haemodynamically stable and regular rhythm (SVT)
    - vagal manoeuvres (carotid sinus massage or valsalva manoeuvre)
    - If that fails then administer adenosine (initially 6mg iV bolus, if this fails 12mg followed by a further 18mg) - asthma, COPD and heart failure and some of the contraindications for using adenosine so verapamil 2.5-5mg instead
  4. Haemodynamically stable and irregular - most likely AF
    - onset <48 hrs usually managed with rhythm control
    - onset >48 hrs usually managed with rate control
44
Q

a) Give 3 contraindications of adenosine

b) What can you give to a patient who has irregular narrow come tachycardia and cannot take adenosine?

A

a) Asthma, COPD, decompensated heart failure

b) verapamil 2.5-5mg

45
Q

Sinus tachycardia

a) Definition

b) Epidemiology

c) Aetiology

d) Pathophysiology

e) Clinical features

f) ECG appearance

g) Management

A

a) An increase in the heart rate to more than 100 bpm in adults. Normal sinus rhythm is observed

b)
- Majority of patients (90%) are female
- Peak incidence of 38 years old

c)
Common causes:
- Physiological: exercise, pain, anxiety, pregnancy
- Drugs: adrenalines, salbutamol, antihistamines, tricyclic antidepressants
- Pulmonary embolism

Other causes
- Cardiac: heart failure, ischaemic heart disease, cardiomyopathies
- Metabolic - hyperthyroidism, anaemia
- Infection
- Substances - cocaine, amphetamines, cannabis, caffeine
- Psychological - anxiety

d) Increased automaticity because of sympathetic activation and/or parasympathetic inhibition

e) May present with palpitations, breathlessness, and light-headedness

f)
- Rate of more than 100 bpm
- Normal visible p waves often buried in preceding t waves (‘camel hump’ appearance)

g)
- Treat underlying cause for remove offending agent
- Pharmacological therapy: beta-blockers or ivabradine may be used in symptomatic patients with chronic sinus tachycardia
- Surgical: radiofrequency ablation of SA node is performed if patient is resistant to medical therapy. The treatment modality for sinus tachycardia are exceedingly rare

h)

46
Q

Sinus tachycardia

a) Definition

b) Epidemiology

c) Aetiology

d) Pathophysiology

e) Clinical features

f) ECG appearance

g) Management

A

a) An increase in the heart rate to more than 100 bpm in adults. Normal sinus rhythm is observed

b)
- Majority of patients (90%) are female
- Peak incidence of 38 years old

c)
Common causes:
- Physiological: exercise, pain, anxiety, pregnancy
- Drugs: adrenalines, salbutamol, antihistamines, tricyclic antidepressants
- Pulmonary embolism

Other causes
- Cardiac: heart failure, ischaemic heart disease, cardiomyopathies
- Metabolic - hyperthyroidism, anaemia
- Infection
- Substances - cocaine, amphetamines, cannabis, caffeine
- Psychological - anxiety

d) Increased automaticity because of sympathetic activation and/or parasympathetic inhibition

e) May present with palpitations, breathlessness, and light-headedness

f)
- Rate of more than 100 bpm
- Normal visible p waves often buried in preceding t waves (‘camel hump’ appearance)

g)
- Treat underlying cause for remove offending agent
- Pharmacological therapy: beta-blockers or ivabradine may be used in symptomatic patients with chronic sinus tachycardia
- Surgical: radiofrequency ablation of SA node is performed if patient is resistant to medical therapy. The treatment modality for sinus tachycardia are exceedingly rare

47
Q

Atrial flutter

a) Definition

b) Epidemiology

c) Aetiology

d) Pathophysiology

e) Clinical features

f) ECG appearance

A

a) Atrial tachyarrhythmia which is characterised by a regular, rapid atrial rate

b)
- Less common than AF
- More common in males
- Incidence increase with age

c)
Common causes
- Right atrial dilatation: pulmonary embolus, mitral and/or tricuspid pathologies, congestive heart failure
- Ischaemic heart disease
- Idiopathic
- Normal variant: tall males
- Patients with a history of endurance sports (causing atrial enlargement)

Other causes
- Drugs: flecainaide, propefoneone
- Metabolic disturbances: hyperthyroidism, alcohol
- Iatrogenic: previous catheter ablation, cardiac surgery

d) Macro re-entrant circuit within the right atrium, most commonly around the tricuspid annulus in an anti-clockwise fashion. This results in a rapid regular atrial activity at a rate of around 300 bpm

e)
- Breathlessness
- Palpitations
- Syncope
- Severe dysponea

f)
- Narrow complex tachycardia with a classic atrial rate of 300bpm
- Regular ‘sawtooth’ pattern of future waves
- Fixed conduction ratios (2:1, 3:1 etc)

g)
- Adenosine unmasks flutter waves
- Management is similar to AF so first-line is beta-blockers
- Radiofrequency ablation highly recommended in patients with chronic atrial flutter

48
Q

Atrioventricular nodal re-entrant tachycardia (AVNRT)

a) Definition

b) Epidemiology

c) Aetiology

d) Pathophysiology

e) Clinical features

f) ECG appearance

g) Management

A

a) A type of paroxysmal supraventricular tachycardia (SVT) caused by an aberrant circuit within the AV node

b)
- Most common cause of paroxysmal SVT
- Female predominance

c) Idiopathic

d)
- In AVRNT, a re-entrant circuit occurs within the AV node
- It most commonly involving dual pathways of different conduction velocities (i.e., a slow and fast pathway)
- Typically, a conduction via the slow pathway will be anterograde (forward direction) and retrograde (backward direction)
- In AVNRT every time it goes around the circuit an electrical signal is fired down into the ventricle (slow pathway), which depolarises normally, and backwards up into the atrium (fast pathway) which depolarise with an inverted p wave
- This leads to depolarisation of ventricle and atrium at the same time
- This is known as the slow-fast type and is the most common cause of AVRNT observed in clinical practice

e)
- Sudden onset of rapid palpitations
- Dizziness
- Breathlessness
- Syncope occasionally occurs

f)
- Regular narrow complex tachycardia
- P waves may not visible as they buried in QRS complexes

g)
- Some AVNRTs can be terminated by vagal manoeuvres
- IV adenosine or rate-limiting calcium channel blockers may be used if vagal manoeuvre fails
- In emergencies, when patients present with haemodynamic compromise, DC cardioversion is advised
- Catheter ablation - indicated in patients with recurrent episodes; associated with a less than 1% risk of heart block

49
Q

Atrioventricular re-entrant tachycardia (AVRT)

a) Definition

b) Epidemiology

c) Aetiology

d) Pathophysiology

e) Clinical features

f) ECG appearance

g) Management

A

a)
- A form of paroxysmal SVT caused by anatomically defined re-entrant circuit involving one or more accessory pathways

b)
- Wolff-Parkinson-White (WPW) syndrome often leads to AVRT
- 60-70% of patients with WPW have no evidence of heart disease

c)
- Congenital
- Associated with hypertrophic cardiomyopathy and Epstein’s anomaly

d)
- Accessory pathways (e.g., Bundle of Kent in WPW) are fibres of abnormal myocytes extending across the atrioventricular groove forming an aberrant connection between the atria and ventricles
- This results in an anatomical re-entrant circuit comprising the normal AV conduction system and the accessory pathway
- Therefore a beat arises in atrium and conducted into ventricles but then goes back up through accessory pathway into the atrium and depolarises it

e)
- Palpitations
- Chest pain
- Syncope

f)
- ‘Delta’ wave (slurring of the QRS uspstroke)
- Short PR interval (<0.2 s)

g)
- In the acute setting vagal manoeuvre, IV adenosine and procainamide or rarely DC cardioversion may be used to terminate the tachyarrythmia
- Flecainide and amiodarone may also be useful in the acute setting
- Catheter ablation of the accessory pathway is the definitive therapy

50
Q

Why is the PR interval short in atrioventricular re-entrant tachycardia

A
51
Q

Explain the different between the p waves in AVRT and AVRNT

A

In AVRT retrograde p wave is usually more distinct from the QRS complex than in AVRNT (this is because of sequential depolarisation of the atrium and ventricle)

52
Q

Why is there a short PR interval in AVRT?

A

Accessory pathways do not have that time delay property that AV nodes so there is rapid conduction of accessory pathways

53
Q

What is the definitive treatment of AVRT?

A

Catheter ablation of the accessory pathway

54
Q

Describe the two forms of AVRT and the affect of the QRS complex

A

Orthodromic
- most common type that involves anterograde conduction via the AV node (down AV node) and retrograde conduction via the accessory pathway (back up the accessory pathway) -> narrow QRS complex

Antidromic
- anterograde conduction occurs via the accessory pathway and retrograde conduction through the AV node -> broad QRS complex

55
Q

Ventricular tachycardia

a) Definition

b) Epidemiology

c) Aetiology

d) Pathophysiology - 3 mechanisms underlying VTs?

A

a) VT refers to tachyarrhthmias that originate from the ventricles producing three or more successive broad QRS complexes at a rate of more than 100 beats per minute

b) Peak incidence in middle-aged patients

c)
Common causes
- Ischaemic heart disease: scarring post MI
- Structural heart disease: cardiomyopathies, valvular heart disease
- Electrolyte disturbances: hyper-/hypokalaemia, hyper-hypomagneasaemia

Other causes
- Drugs and substances - digoxin toxicity, cocaine
- Channelopathies - long QY syndrome, Brugarda syndrome
- Idiopathic

d)
1. Re-entrant circuit (most common) - usually due to post-MI scarring
2. Trigger activity
3. Increase automaticity

56
Q

Ventricular tachycardia

a) Symptoms

b) Signs

A

a)
Haemodynamically stable patients
- Palpitations
- Dizziness/light-headedness
- Syncope

Haemodynamically unstable patients (severely hypotensive and tachycardia)
- Low cardiac output symptoms: severe dyspnoea, dizziness, syncope
- Eventually leading to cariogenic shock and cardiac arrest

b)
- JVP may be elevated,
- Intermittent cannon A waves may be seen

57
Q

Describe the ECG appearance in ventricular tachycardia

A
  • Broad QRS complexes (>0.12s)
  • Slurred initiation of QRS
  • Positive/negative concordance
  • Basically regular
  • Extreme axis
  • Not a typical bundle branch block
  • AV dissociation
  • Fusion beat (a P wave happens to get conducted through the AV node to start depolarisation of the ventricles via the conduction tissue at the same time as a beat of VT, giving a combination of the two, which is narrower than a normal VT complex)
  • Capture beat (a P wave is conducted through the AV node time exactly so that it depolarises the ventricle normally)
58
Q

a) Explain how the type of infarct affects the concordance on ECG of a VT

b) How relevant is the concordance?

A

a) A scar at back of the heart will cause all depolarisation to be towards the chest leads V1 to V6, which will be positive in polarity - hence “positive concordance”

A scar on the anterior surface will cause depolarisation away from all the chest leads - hence “negative concordance”

b) Not essential to diagnose VT - but if it is present, it make VT more likely

59
Q

Describe the management of a VT in:

a) Hameodynamically unstable patient

b) Haemodynamically stable patient

c) Ongoing recurrent VT

A

a)
1. Immediate resuscitation (100-230 chest compressions with 2 rescue breaths) - if no pulse
2. Emergency DC cardioversion - synchronised shock recommended if there is a pulse
3. After seeking expert help, amiodarone (300mg IV over 10-20 minutes, followed by 900mg over 24 hours) should be administrated
4. ICD implantation

b)
Management deepends on underlying cause:
1. IV amiodarone (non-idiopathic VT)  300 mg IV over 20-60 minutes followed by 900 mg over 24 hours
2. Elective synchronised DC cardioversion may be indicated if resistant to medical therapy

c)
Non-idiopathic VT - consider ICD or catheter ablation (patients with structural heart disease)

Idiopathic VT - pharmacological therapy (beta-blockers, rate-limiting calcium channel blockers) may be considered

60
Q

How long should patients not drive for after a VT/VF?

A

6 months

61
Q

Torsades de point

a) Definition

b) Epidemiology

c) Aetiology

d) Pathophysiology

e) Clinical features

f) ECG appearance

g) Management

A

a) A form of polymorphic VT associated with a prolonged QT interval. Torsos de pointes is French for “twisting of the point”

b) Female predominance (females have a longer baseline QT interval)

c)
- Congenital long QT syndrome
- Acquired QT syndrome e.g., electrolyte imbalance
- Drugs e.g., clarithomycin and fluoxetine

d) Derangeemnt of cardiac ions, particularly sodium, potassium and calcium increase the duration of action potential, resulting in early after-depolarisation

e)
- Usually asymptomatic
- Commonly presents with self-limiting episodes of palpitations, light-headedness or syncope

f)
- Broad QRS comps
- Peaks of the QRS twist around the isoelectric line (corkscrew appearance)
- Irregular intervals
- Tachycardia with ventricular rate of 160 to 250 bpm
- Prolonged QTc

g)
- Treat underlying cause
- IV magnesium sulphate (given as a slow infusion) - 2mg magnesium sulphate over 10 mins IV if no adverse effects
- If resistant to medical therapy, consider temporary pacing
- If patient is haemodynamically unstable, non-synchronised electrical cardioversion may be indicated

62
Q

Brugarda syndrome

a) Definition

b) Epidemiology

c) Clinical features

d) ECG appearence

f) Management

A

a)
- An autosomal sodium channelopathy associated with sudden cardiac deaths
- Defective sodium channels impair influx of sodium ions resulting in shorter action potentials

b)
- Most prevalent in Asia
- High male predominance (8:1)

c)
- Syncope and cardiac arrest in otherwise normal asymptomatic panic

d)
‘brugarda’ sign -> downscoping coved ST elevation followed by an inverted T wave - only presents in leads V1 and V2

d)
- ICD implantation is the only definite treatment

63
Q

Ventricular fibrillation

a) Definition

b) Epedmiology

c) Aetiology

d) Pathophysiology

e) ECG appearence

f) Management
i) immediate
ii) long-term

A

a) A rapid, uncoordinated and life-threatening arrhythmia resulting in more myocardial contraction, eventually leading to cardiac death

b) Has a bimodal distribution peaking at under 6 months and 45-75 years

c)
Common causes
- Ischaemic heart disease
- Electrolyte abnormalities (particularly hypokalaemia)
- Idiopathic

Other causes
- Long QT syndrome
- Structural heart disease
- Systemic - PE, sepsis

d)
- Multiple wavelets – continuous micro re-entrant circuits are formed within the ventricles
- Very rapid (up to 500 bpm) irregular electrical activity results in unsynchronised ventricular contractions
- Cardiac output will be significantly reduced and ultimately the patient will go into cardiogenic shock

e)
- Chaotic waveforms with varying amplitude
- Unidentifiable P waves, QRS complexes or T waves

f)
i) Immediate management
- adavancec cardiac life support - most important shockable rhythm
- IV amiodarone (1st line) or procainamide (2nd line) can be sued as a last resort if all measures have failed

ii) Long-term management
- ICD insertion
- Amiodarone may be used when ICDs are contraindicated

64
Q

Aside from the ‘saw tooth’ appearance, when should atrial flutter be suspected

A

Atrial flutter should always be suspected in tachycardias with a fixed atrioventricular conduction ratio (2:1).

Atrial flutter classically produces an atrial rate of approximately 300 bpm and a ventricular rate of 150 bpm

So if heart rate is exactly 150 bpm - think atrial flutter

65
Q

a) What does adenosine do?

b) Describe the affect of adenosine if the tachycardia originates from and provide examples

i) Above the AV node

ii) Within the AV node

iii) Below the AV node

A

a) Block the AV node

b)
i) Adenosine blocks the AV node, and you can see the the atrial activity underlying, but does not terminate the tachycardia e.g., AF, atrial flutter

ii) Adenosine terminates tachycardia e.g., AVNRT, AVRT

iii) Adenosine has no effect on tachycardia e.g., VT

66
Q

Describe the electrical supply of the heart

A

Only the SA and AV nodes are well supplied by parasympathetic nerves.

The rest of the cardiac conduction system (bundle of His, left and right bundle branch and purkinje fibres ) is supplied by sympathetic nerves

67
Q

Different areas of the heart have differing rates of automaticity. What is the hierarchy of the pacemakers?

A

Fastest: SA node

Second fastest: AV junction

Slowest: Purkinje network

68
Q

What is bradycardia defined as?

A

Heart rate < 60 bpm

69
Q

Describe the aetiology of bradycardia

A

Physiological
- Sleep
- High level athletic conditioning

Pathological
- Congenital
- Acquired e.g., degenerative, ischaemic heart disease, drugs, electrolyte/metabolic, infection, (e.g., endocarditis), iatrogenic (ablation, cardiac surgery), infiltrative diseases (e.g., sarcoid, amyloid), neuromuscular disease (e.g., myotonic dystrophy)

70
Q

Describe the symptoms of bradycardia

A
  • Fatigue
  • Difficult concentrating
  • Exercise intolerance
  • Falls
  • Syncope
  • Breathlessness
  • Dizziness
71
Q

Sick sinus syndrome/sinus node disease

a) Definition

b) Aetiology

c) Pathophysiology

d) Clinical features

e) Management

A

a) A group of arrhythmias due to a syndrome of SA node dysfunction that encompasses sinus bradycardia, sinus pause and sinoatrial block

b)
Common causes
- Idiopathic fibrosis of the SA node (because of ageing)
- Myocardial ischaemia

Other causes
- Infiltrative conditions: sarcoidosis, amyloidosis
- Drugs: beta-blockers, digoxin, calcium channel blockers, amiodarone
- Metabolic: hypothyroidism, hyperkalaemia

c) Degenerative and ischaemic changes in the SA node, nerve supply, and the surrounding atrial tissue can result in abnormalities of impulse formation, conduction or both

c)
- Chronic frequent episodes of intermittent bradycardia and tachycardia
- Fatigue
- Palpitations
- Dizziness
- Syncope

d)
- Treat underlying cause of present
- IV atropine may be useful in patients with severe symptoms
- Dual chamber pacemaker implantation recommended for patients with symptomatic chronic disease

72
Q

First degree heart block

a) Definition

b) Epidemiology

c) Pathophysiology

d) Clinical features

e) ECG appearance

f) Management

g) Prognosis

A

a) Delayed atrioventricular conduction resulting in a constant prolong PR interval (>0.2s) on ECG

b) Commonly affects patients over age of 65

c)
Common causes
- Idiopathic degeneration (fibrosis) of the conduction system
- Physiologcal: ncreased vagal tone (e..g, athletes, during sleep)
- Myocardial ischaemia (RCA supplies the AV node e.g., inferior MI)
- Drugs (beta-blockers, calcium channel blockers, digoxin)

d) Usually, asymptomatic

e)
- Prolonged PR interval
- Sinus rhythm

f) Benign condition, treatment is not usually required

g) Normal, although some patient will progress to higher degrees of AV block over time

73
Q

Second degree heart block: Mobitz type I (also known as the Wenckebach block)

a) Definition

b) Epidemiology

c) Aetiology

d) Pathophysiology

e) ECG appearance

f) Management

A

a) Atrioventricular conduction deficit resulting in progressive prolongation of the PR interval until one p wave is not followed by a QRS complex

b)
- Occurs in 45% of post-inferior MI
- More common than Mobitz type II

c)
Common causes
- Idiopathic fibrosis of conduction system
- Drugs (beta-blockers, calcium channel blockers, digoxin, procainamide)
- Increased vagal tone – athletics, children, during sleep

Other causes
- Iatrogenic – transcatheter aortic valve implantation (TAVI)
- Post-Inferior MI

d)
- Caused by progressive induction block, more commonly within the AV node itself (70%) and sometimes distally in the conduction system (30%)

e)
- Progressive prolongation of the PR interval until QRS is not followed
- Narrow QRS complex
- PR interval longest before the dropped beat (QRS and shortest after

f)
- Treatment not usually required unless symptomatic
- IV atropine ma be used in emergency situations of severe Brady cardia
- Permanent pacemaker implantation is indicated in patients with non-resolving symptomatic block

74
Q

Second degree heart block: Mobitz type II (also known as the non-Wenckebach block)

a) Definition

b) Aetiology

c) Pathophysiology

d) Clinical features

e) ECG appearance

f) Management
i) Haemodynamic compromise
ii) Definite treatment

g) Prognosis

A

a) An atrioventricular conduction deficit resulting in intermittent dropped beats without changes in the PR interval, until one p wave is not followed by a QRS

b)
Common causes
- Idiopathic fibrosis of the conduction system
- Anterior MI

Other causes
- Drugs (beta-blockers, calcium channel blockers, digoxin)
- Infiltrative disease (sarcoidosis, amyloidosis, hemachromatosis)

c) In contrast Mobitz type I, the conduction block in kibitz type II tends to occur infra-nodally, in the His bundles (20%) or Purkinje fibres (80%)

d)
- Dizziness
- Syncope
- May present with haemodynamic instability and sudden cardiac death in some cases

e)
- Constant PR interval and then a p wave is not followed by QRS
- QRS complex may be broad if the AV block occurs at the Purkinje fibres
- May be associated with a fixed ration 2:1, 3:1 etc

f)
i) Treat haemodynamic compromise with:
1. IV atropine
2. IV adrenaline
3. IV isoprenaline infusion
4. If all measures fail, and permanent pacing is not immediately consider temporary external pacing

ii) Permanent pacemaker implantation is indicated for all patients (even as asymptomatic patients)

g)
- Commonly progress to third degree heart block

75
Q

Third degree (complete) heart block

a) Definition

b) Aetiology

c) Pathophysiology

d) Clinical features

e) ECG appearance

f) Management
i) Haemodynamic compromise
ii) Definite treatment

A

a) Refers to complete failure of the AV conduction system resulting in a loss of communication between the atria and ventricles, causing them to beat independently of one another

b)
Common causes
- Idiopathic degeneration of the conduction system (ageing)
- Anterior and inferior MI - due to interruption of the blood supply to the AV node
- Drugs (beta-blockers, calcium channel blockers, digoxin, anticholinesterase inhibitors e.g., Donepezil)

Other causes
- Congenital: maternal SLE
- Iatrogenic: cardiac surgery, cardiac catheterisation

c)
- Complete failure of the AV conduction system results in complete AV block
- Latent pacemaker cells in the His-purkinje fibres system will resume the role of the AV node as a physiological compensatory mechanism to ensure ventricular contractions and maintain cardiac output.

d)
- Symptoms of low cardiac output: dizziness, breathlessness, fatigue
- Stokes-Adams attacks 9episode of syncope characterised by a sudden unexpected collapse, accompanied by a transient loss of consciousness
- Palpitations

e)
- Rate tends to be less than 50bpm
- Constant P-P and R-R intervals but apparent AV dissociation
- QRS complexes may be narrow (junctional escape rhythm) or wide (subjuntional escape rhythm)

f)
i)
1. Emergency iV atropine
2. IV isoprenaline infusion

ii)
- Correct reversible causses
- Permanent pacemaker implantation is indicated for all patients

76
Q

Outline the emergency treatment of bradycardia

A
  1. Assess with ABCDE approach
  2. Give oxygen if appropriate and obtain IV access
  3. Monitor ECG, BP, SpO2, record 12-lead ECG
  4. Identify and treat reversible causes e.g., electrolyte abnormalities
  5. If evidence of life threatening signs (shock, syncope, MI, HF) - atropine mcg IV and if no satisfactory response interim measures: atropine 500 mcg IV repeat to maximum 3 mg, isoprenaline 5 mcg min-1 IV, adrenaline 2-10 mcg min-1 IV, alternative drugs or transcutaneous pacing. If that fails the seek expert help and arrange transvenous pacing
  6. If no evidence of life threatening signs and risk of a aystole (recent asystole, mobitz II AV block, complete heart block with broad QRS, ventricular pass > 3 s) then carry out interim response. If no risk of asystole, then observe
  7. Alternatives include: Aminophyline, dopamine, glucagon (if beta-blockers or calcium channel blocker overdoes), glycopyrrolate can be used instead of atropine
77
Q

What are cardiac devices?

A

Devices that we implant for either diagnosis or treatment of cardiac arrhythmias and unexplained syncope

78
Q

Name cardiac devices for

a) Diagnosis

b) Treatment

A

a) Loop reorder

b)
- Permanent pacemaker
- Implantable cardioverter defibrillator (ICD)
- Cardiac resynchronisation therapy (CRT)

79
Q

Implantable cardioverter defibrillator (ICD)

a) Purpose

b) Indications

c) Variation

A

a) Delivers overdrive pacing and/or DC shocks to restore sinus rhythm

b) Used to treat ventricular tachyarrhythmias and primary and secondary prevention of sudden cardiac deaths

c) Single chamber (RV), dual chamber (RA and rv)

80
Q

Who needs an ICD?

A

Primary prevention of sudden cardiac death from ventricular arrhythmias
- Severe LV impairment
- Inherited cardiac conditions

Secondary prevention of sudden cardiac death from ventricular arrhythmias
- Survivor of VF/VT
- Cardiac arrest
- Sustained VT with haemodynamic compromise
- Sustained VT and severe LF impairments

81
Q

How does the ICD recognise ventricular arrhythmias?

A
  1. The first thing the ICD looks at is the heart
  2. If this is above a certain threshold (e.g., 200 bpm) then the ICD will deliver a shock
  3. If the heart rate is not quite as high but still fast (e.g., above 180bpm) the ICD will look at other parameters including:
    - how did the arrhythmia start? (was it gradual or sudden)
    - Is it regular or irregular?
    - is the QRS narrow or broad?
82
Q

What are the limitations of coventional ICDs? How are they overcome?

A

In conventional ICDs the leads can become damaged and may not be straightforward to removed

They are overcome by subcutaneous ICD - which are easier to remove

83
Q

How are ICDs deactivated

A

ICD deactivation involves turning off shock therapies. This is best done by pacing physiologists. But in an emergency a doughnut magnet can be strapped over the ICD

84
Q

What is a pacemaker?

A

An electronic device that regulates the heart rate.

It consists of a generator (battery and circuit) and pacing leads (insulated electrodes)

85
Q

What are the two roles of a pacemaker?

A
  1. To detect the patient’s own intrinsic impulses - “Sense”
  2. To depolarise the heart if there isn’t any impulses - “Capture”
86
Q

What are the two forms of pacing that is usually performed for the treatment of bradycardia?

A
  1. Temporary pacing
  2. Permanent pacemaker
87
Q

Name the two types of temporary pacing

A
  1. Transvenous
  2. Transcutaneous
88
Q

Permanent pacemaker (PPM)

a) Purpose

b) Indications

c) Variation

A

a) Prevent bradycardia

b) Sinus node disease and AV node disease (conduction block)

c)
- Single chamber (RA or RV)
- Dual chamber (RA and RV)

89
Q

Permanent pacemaker - single chamber

a) Chamber being paced?

b) Chamber being sensed?

c) Pacing response to a sensed beat

A

a) Ventricle (V)

b) Ventricle (V)

c) Inhibited (I)

= VVI pacemaker

90
Q

Permanent pacemaker - dual chamber

a) Chamber being paced?

b) Chamber being sensed?

c) Pacing response to a sensed beat

A

a) Atrium and ventricle (D)

b) Atrium and ventricle (D)

c) Inhibited or triggered (D)

= DDD pacemaker

91
Q

What are the limitations of traditional pacemakers and how are these overcome?

A

Traditional pacemakers can become infected and leads can fail overtime

This is overcome by headless pacemakers

92
Q

What are the 2 roles of a pacemaker?

A
  1. To detect the patient’s own intrinsic impulses “Sense”
  2. Tod polarise the heart if there isn’t any impulses “Capture”
93
Q

What does a pacemaker do?

A

The pacemaker senses the patient’s own natural heartbeat and withholds the heartbeat

  1. It then sets a timer and if that timer expires without it seeing any electrical activity in that chambers of the heart, then it will stimulate that chamber of the heart to depolarise (capture)
  2. There will be a pacing spike followed by a broad QRS
94
Q

Describe the ECG changes in a single atrial pacemaker

A

Pacing spikes preceding the p wave

95
Q

Describe the ECG changes in a single ventricular pacemaker

a) Right ventricle

b) Left ventricle

A

a)
- Pacing spikes preceding the QRS complexes.
- Broad QRS complexes with an rS’ in V1 and notched R wave in V6
(In right ventricular pacing the QRS morphology is similar to left bundle branch block ) (William marrow -W complex in V1 and M shaped complex in V6)

b)
- Pacing spikes preceding QRS complexes
- Broad QRS complexes with an rSr’ pattern in V1
(In left ventricular pacing the QRS morphology is similar to right bundle branch block ) (wiliam marrow -M complex in V1 and normal/slurred S in V6)

96
Q

Describe the ECG changes in a dual pacemaker

A

May be features of atrial pacing - pacing spikes preceding p wave

May be features of ventricular pacing - pacing spikes preceding QRS complex

May eb features of atrial and ventricular pacing

97
Q

Cardiac resynchronisation therapy (CRT)

a) Purpose

b) Indications

c) Variation

A

a) Co-ordinates and synchronise atrial RV and LV contractions

b) Heart failure

c)
- CRT pacemaker
- CRT ICDs for patients at high risk of ventricular arrhythmias

98
Q

What is cardiac arrest?

A

The abrupt cessation of activity of the heart, with subsequent loss of cardiac output and haemodynamic collapse

99
Q

What are the four main non-perfusing rhythm abnormalities

A

Shockable
- VF
- Pulseless VT

Non-shockable
- Pulseless electrical activity
- Systole

100
Q

What are the clinical features of a cardiac arrest?

A
  • Patients lose consciousness within 10-15 seconds secondary to cerebral hypoxia
  • Rarely symptoms prior to arrest
101
Q

Describe the management of a cardiac arrest

A
  • CPR
  • Early defibrillation (if shockable rhythm - VF/ pulseless VT)
  • Maintain oxygenation
102
Q

Describe the late management of cardiac arrest

A

Two questions: what is the cause? Is it reversible? - if yes treat reversible cause

History - of the event, PMH, Family

Tests - ECG, Echo, Monitoring, imaging (angio/CT/MRI)

103
Q

What are the reversible causes of cardiac arrest?

A

4 H’s

  • Hypoxia
  • Hypovolaemia
  • Hypothermia
  • Hyper/hypokalaemia & hypocalcaemia

4 T’s
- Tension pneumothorax
- Tamponade
- Toxins
- Thrombo-embouls

Medicine - Year 2 (27 decks)

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