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Yr 5 - CVS > Revision - Heart Block, SVT & Arrhythmias > Flashcards

Revision - Heart Block, SVT & Arrhythmias Flashcards

1
Q

Define a prolonged PR interval

A

> 0.2s

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2
Q

Define 1st degree heart block

A

Consistent prolongation of PR interval due to delayed conduction via AV node

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3
Q

What is the PR inverval on an ECG?

A

From the beginning of the P wave to the beginning of the QRS complex

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4
Q

What does the PR interval represent?

A

The time between atrial depolarisation and ventricular depolarisation

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5
Q

What drugs can cause 1st degree heart block? (4)

A

1) beta blockers

2) rate-limiting CCBs e.g. diltiazem

3) digoxin

4) magnesium

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6
Q

What occurs in Mobitz type I AV block?

A

There is progressive prolongation of the PR interval until eventually the atrial impulse is not conducted, and the QRS complex is dropped.

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7
Q

Why can an inferior MI cause AV block?

A

As the RCA supplies the AV node

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8
Q

Mx of Mobitz type I if patient is asymptomatic?

A

No mx required

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9
Q

Mx of Mobitz type I if patient is symptomatic?

A

Pacemaker may be considered

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10
Q

What happens in Mobitz type II?

A

There is consistent PR interval duration with intermittently dropped QRS complexes due to a failure of conduction.

The intermittent dropping of the QRS complexes typically follows a repeating cycle of every 3rd (3:1 block) or 4th (4:1 block) P wave.

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11
Q

Is Mobitz type II sometimes a normal variant?

A

No - always pathological

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12
Q

ECG findings in second-degree AV (type 2)?

A

1) Rhythm: irregular (may be regularly irregular in 3:1 or 4:1 block)

2) P wave: present but there are more P waves than QRS complexes

3) PR interval: consistent normal PR interval duration with intermittently dropped QRS complexes

4) QRS complex: normal (<0.12 seconds) or broad (>0.12 seconds)

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13
Q

When will the QRS complex be broad in second-degree AV block (type 2)?

A

The QRS complex will be broad if the conduction failure is located DISTAL to the bundle of His.

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14
Q

Symptoms & exam findings in second-degree AV block (type 2)?

A

Symptoms:
- palpitations
- pre-syncope
- syncope

Exam:
- ‘regularly irregular’ pulse

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15
Q

Management of second-degree AV block (type 2)?

A

1) Patients should be placed on a cardiac monitor as soon as possible (due to risk of progression to complete AV block).

2) Investigate underlying cause

3) Temporary pacing or isoprenaline may be required if the patient is haemodynamically compromised due to bradycardia.

4) A permanent pacemaker is usually inserted if there are no reversible causes identified.

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16
Q

What 2 types of escape rhythms can 3rd degree (complete) heart block consist of?

A

1) narrow complex escape rhythms

2) broad complex escape rhythms

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17
Q

Narrow complex escape rhythms in complete heart block:

a) QRS interval?
b) where do they originate?
c) typical HR?

A

a) <0.12s
b) above bifurcation of bundle of His
c) >40bpm

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18
Q

Narrow complex escape rhythms in complete heart block:

a) QRS interval?
b) where do they originate?
c) typical HR?

A

a) >0.12s
b) below bifurcation of bundle of His
c) <40bpm (more significant clinical features e.g. heart failure, syncope)

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19
Q

What 3 infections can cause complete heart block?

A

1) Lyme disease

2) Chagas disease

3) Infective endocarditis

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20
Q

ECG findings in 3rd degree heart block?

A

1) Rhythm: variable

2) P wave: present but not associated with QRS complexes

3) PR interval: absent (as there is atrioventricular dissociation)

4) QRS complex: narrow (<0.12 seconds) or broad (>0.12 seconds) depending on the site of the escape rhythm (see introduction)

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21
Q

Management of 3rd degree heart block?

A

1) Place on cardiac monitor

2) Transcutaneous pacing/temporary pacing wire or isoprenaline infusion may be required. Some rhythms (particularly narrow-complex escape rhythms) may respond to atropine.

3) A permanent pacemaker is usually required.

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22
Q

What is the main complication of 3rd degree heart block?

A

Sudden cardiac death due to ventricular arrhythmias

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23
Q

What do the following ECG components represent:

1) p wave
2) PR interval
3) QRS complex
4) T wave

A

1) Atrial depolarisation

2) Conduction through the AVN to the ventricles (i.e. time between atrial and ventricular depolarisation)

3) Ventricular depolarisation

4) Ventricular repolarisation

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24
Q

What is the main feature of bundle branch blocks?

A

Broad QRS complexes

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25
Q

What are the causes of damage to the right bundle branch?

(i.e. causing RBBB)

A

1) lung pathology:
- COPD
- pulmonary emboli
- cor pulmonale

2) Primary heart muscle disease (ARVC)

3) Congenital heart disease (e.g. ASD)

4) Ischaemic heart disease

5) Primary degeneration of the right bundle

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26
Q

What does the left bundle branch split into?

A

Anterior & posterior fascicles

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27
Q

Each branch of the left bundle branch may be damaged in isolation.

Is anterior or posterior fascicular block more common?

A

Anterior

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28
Q

In the mx of angina in patients already taking a beta blocker, but a CCB is contraindicated, what can be given next?

A

A long-acting nitrate, ivabradine, nicorandil or ranolazine

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29
Q

When is aortic valve replacement considered in aortic stenosis?

A

1) patient is symptomatic

2) if asymptomatic but valvular gradient >40 mmHg and with features such as LV systolic dysfunction

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30
Q

ECG features of WPW syndrome?

A

1) Short PR interval

2) Broad QRS

3) Delta wave

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31
Q

How does the delta wave appear in WPW syndrome?

A

Slurred upstroke of QRS

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32
Q

What is the delta wave caused by in WPW syndrome?

A

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

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33
Q

What is the definitive treatment for WPW syndrome?

A

Radiofrequency ablation of accessory pathway

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34
Q

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

A

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

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35
Q

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

A

1) adenosine
2) beta blockers
3) verapamil

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36
Q

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

A

1) procainamide

2) electrical cardioversion

37
Q

Mechanism of adenosine?

A

Causes transient heart block in the AV node.

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

38
Q

What is adenosine’s half life?

A

<10 seconds –> needs to be given as a rapid bolus

39
Q

Who is adenosine avoided in?

A

1) asthma
2) COPD
3) HF
4) heart block
5) severe hypotension
6) WPW syndrome

40
Q

How must adenosine be given?

A

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

41
Q

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

A

Three:

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

42
Q

Adverse effects of adenosine?

A

1) flushing

2) bronchospasm

3) feeling of impending doom

4) chest pain

43
Q

Why is it important that cardioversion is synchronised in SVT?

A

To avoid delivering a shock during a T wave –> can result in VF and cardiac arrest.

44
Q

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

A

In pulseless VT or VF, where the patient does not have organised electrical activity or a pulse, there is no need for the shock to be synchronised.

45
Q

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

What are the 2 main options?

A

1) Radiofrequency ablation

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

46
Q

VT can be divided in monomorphic VT and polymorphic VT.

What is the difference?

A

Monomorphic: characterised by a single, stable QRS morphology with no beat-to-beat variation.

Polymorphic: has beat-to-beat variation in QRS shape and multiple QRS morphologies.

47
Q

What is monomorphic VT most commonly caused by?

A

MI

48
Q

How is ventricular tachycardia of unclear cause treated?

A

IV amiodarone

49
Q

How is atrial fibrillation with bundle branch block treated?

A

Treat as AF

50
Q

How is supraventricular tachycardia with bundle branch block treated?

A

Treat as SVT

51
Q

How is polymorphic ventricular tachycardia, such as torsades de pointes treated?

A

IV magnesium

52
Q

What is the QT interval?

A

From beginning of QRS complex to end of T wave

53
Q

What is the corrected QT interval (QTc)?

A

This estimates the QT interval if the heart rate was 60bpm.

54
Q

What is a prolonged QTc?

A

Men: >440ms

Women: >460ms

55
Q

What does a prolonged QT interval represent?

A

Prolonged repolarisation after a contraaction.

56
Q

What is torsades de pointes?

A

A form of polymorphic VT associated with a long QT interval.

57
Q

Complications of torsades de pointes?

A

1) Will terminate spontaneously and revert to sinus rhythm

OR

2) Will progress to VT (can lead to cardiac arrest)

58
Q

What are some causes of a prolonged QT?

A

1) Drugs e.g. macrolides, citalopram, ondansetron, antipsychotics, amiodarone

2) Long QT syndrome (inherited)

3) SAH

4) Myocarditis

5) Hypothermia

6) Electrolytes e.g. hypokalaemia, hypocalcaemia, hypomagnesaemia

59
Q

Why are dilitazem and verapamil contraindicated in patients with ventricular tachycardia?

A

Can precipitate cardiac arrest

60
Q

What is sick sinus syndrome often caused by?

A

Idiopathic degenerative fibrosis of the SA node.

61
Q

There is a risk of asystole in which heart conditions?

A

1) Mobitz type II

2) Complete heart block

3) Previous asystole

4) Ventricular pauses longer than 3 seconds

62
Q

1st line mx of unstable patients with bradycardia?

A

IV atropine

63
Q

2nd line mx of unstable patients with bradycardia?

A

1) Inotropes (e.g. isoprenaline or adrenaline)

2) Temporary cardiac pacing

64
Q

What are 2 options for temporary cardiac pacing?

A

1) Transcutaneous pacing

2) Transvenous pacing

65
Q

Mechanism of atropine?

A

Antimuscarinic –> inhibits the PNS

66
Q

1st line medical management of asystole (or severe bradycardia)?

A

IV atropine

67
Q

What adverse signs indicate haemodynamic compromise and hence the need for treatment in extreme bradycardia?

A

HISS:

1) HF

2) Ischaemia

3) Syncope

4) Shock: hypotension (systolic blood pressure < 90 mmHg), pallor, sweating, cold, clammy extremities, confusion or impaired consciousness

68
Q

1st line management of extreme bradycardia with adverse signs?

A

IV atropine 500mcg (repeat up to 3mg)

69
Q

Stepwise management of severe bradycardia with adverse signs?

A

1) Atropine 500mcg

2) Repeat atropine 500mcg up to 3mg (i.e. up to 6x)

3) Transcutaneous pacing

4) Isoprenaline/adrenaline infusion titrated to response

5) Transvenous pacing (seek expert help)

70
Q

If there is a satisfactory response to IV atropine in severe bradycardia, what is the next step?

A

Figure out is there a risk of asystole?

If yes –> go back to other intermin measures:
- atropine 500mcg IV, repeat to maximum of 3mg
- transcutaneous pacing
- isoprenaline/adrenaline infusion titrated to response
- transvenous pacing (seek expert help)

If no –> observe

71
Q

What are some risk factors for asystole in patients with severe bradycardia?

A

1) mobitz type II

2) complete heart block

3) recent asystole

4) ventricular pause >3s

72
Q

What is the approach to adult tachycardia?

A

1) ABCDE approach

2) Identify is there are any life-threatening features (adverse signs)?

3) If yes –> Synchronised DC shock up to 3 attempts

4) If no –> is the QRS narrow or broad (< or >0.12s)

5) For both broad and narrow QRS, is it regular or irregular?

Manage accordingly.

73
Q

What adverse signs indicate the need for synchronised DC shock in adult tachycardia?

A

HISS

74
Q

How many synchronised DC shocks can be given in tachycardia with adverse signs?

A

Up to 3

75
Q

If tachycardia is broad complex with REGULAR rhythm, what should you assume it is?

A

Assume VT unless previously confirmed SVT with bundle branch block.

76
Q

Management of ventricular tachycardia?

A

Loading dose of amiodarone (300mg IV) followed by 24h infusion

77
Q

If tachycardia is broad complex with IRREGULAR rhythm, what are the possibilities of causes?

A

1) AF with BBB –> most common in stable patients

2) Torsades de pointes (polymorphic VT)

3) AF with ventricular pre-excitation

78
Q

If tachycardia is NARROW complex with REGULAR rhythm, what is the immediate management?

A

1st line –> vagal manoeuvres

2nd line (if ineffective) –> give adenosine:
- 6mg rapid IV volus
- if unsuccessful, give 12mg
- if unsuccessful, give 18mg

3rd line (if ineffective) –> give verapamil or beta blocker

4th line (if ineffective) –> synchronised DC shock up to 3 attempts (sedation or anaesthesia if conscious)

79
Q

What drug should be given as soon as possible for non-shockable rhythms?

A

Adrenaline 1mg

80
Q

How often should adrenaline be given in cardiac arrest?

A

Repeat adrenaline 1mg every 3-5 mins whilst ALS continues

81
Q

What are the reversible causes of cardiac arrest? (H’s & T’s)

A

1) Hypoxia
2) Hypovolaemia
3) Hypothermia
4) Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia and other metabolic disorders

5) Tension pneumothorax
6) Cardiac tamponade
7) Thrombosis
8) Toxins

82
Q

When is amiodarone given in cardiac arrest?

A

300mg given after the third shock to patients in VF/pulseless VT

83
Q

What can be used as an alternative if amiodarone is not available?

A

Lidocaine

84
Q

What is alternative to IV adenosine in asthmatics?

A

IV verapamil

85
Q

What can be added as 2nd line treatment for rate control in AF?

A

Digoxin (after a beta blocker)

86
Q

How does a tension pneumothorax cause a cardiac arrest?

A

1) Increased air in the pleural space

2) Impairment of venous return to the heart

3) Results in reduced cardiac output

4) Leads to PEA as the heart is no longer able to pump properly, but the conducting system of the heart is intact.

87
Q

What is the dose of adrenaline given in ALS?

A

1mg

88
Q

Mx of an irregular broad complex tachycardia?

A

Seek expert help

89
Q
A

Yr 5 - CVS (8 decks)

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