Arrhythmias- Heart Block Flashcards

1
Q

Bradycardia (HR <60bpm) can be classified into absolute bradycardia and relative bradycardia; explain the difference

A
  • Absolute; HR <60bpm *CHECK WB SAYS 40bpm
  • Relative: HR is inappropriately slow for the haemodynamic state of the pt e.g. HR of 64 in a pt with septic shock
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2
Q

Alongside classifying bradycardias as absolute or relative, we can also classify them according to the pacemaker at fault. Which two pacemakers of heart could be at fault?

A

SA node or AV node

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3
Q

What is an arrhythmia?

A

Abnormal heart rhythm

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4
Q

Causes of sick sinus syndrome can be either extrinsic or intrinsic to the heart; state some extrinsic causes of sinus bradycardia

A
  • Drugs e.g. beta blockers
  • Hypothyroidism
  • Hypothermia
  • Cholestatic jaundice
  • Raised ICP

*Treat by treating underlying cause

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5
Q

Describe how we can classify tachy arrhythmias

A

Bradyarrhythmias

  • Sinus arrhythmia
  • Sinus bradycardia
  • Heart block

Tachyarrhythmias

  • SVTs
    • Sinus tachycardia
    • Atrioventricular junction tachycardias (AVNRT, AVRT)
    • Atrial tachycardias (AF, atrial flutter, atrial ectopics)
  • VTs
    • Ventricular tachycardia
    • Ventricular fibrillation
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6
Q

What is sinus arrhythmia?

Who is it common in?

A

Heart rate increases on inspiration (as on inspiration parasympathetic tone decreases) and heart rate decreases on expiration (as on expiration parasympathetic tone increases).

Normal particularly in children and young adults.

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7
Q

Sinus bradycardia can be either extrinsic or intrinsic to the heart; state some intrinsic causes of sinus bradycardia

A
  • Ischaemia & infarction of SA node as complication of MI
  • Chronic degenerative changes e.g fibrosis of atrium and SA node in the elderly

Both of the above can lead to sick sinus syndrome: intermittent failure of SA node depolarisation (sinus arrest) or failure of impule to propagate through perinodal tissue to atria (SA block)

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8
Q

What is sick sinus syndrome?

A
  • Usually caused by sinus node fibrosis
  • Sinus node becomes dysfunctional; in some cases it causes bradycardia and in others it can generate tachyarrhythmias e.g. AF, atrial tachycardia
  • Treat the manifestation e.g. bradycardia, AF etc..
  • Some pts develop tachy-bradysyndrome suffering from alternating tachycardic & bradcardic rhythms. Difficult to treat. May give pacing for bradycardic episodes combined with rate slowing meds for tachycardic episodes when pt is symptomatic
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9
Q

Bradycardias can be classified according to…?

A

Pacemaker which is at fault:

  • SA node (e.g. in sick sinus syndrome)
  • AV node (e.g heart block)
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10
Q

We have already said that bradycardias can be classified based on the pacemaker at fault (SA or AV node). If the problem is with conduction at the AV node we refer to this as heart block

Define heart block and state the 4 types of heart block

A
  • First degree AV block
  • Second degree AV block
    • Mobitz type I (Wenckebach)
    • Mobitz type II
  • Third degree heart block

*Remember heart block is delay, or failure, of conduction of impulses

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11
Q

State some risk factors/causes for developing heart block

A
  • Age
  • Chronic heart failure (CHF)
  • ACS (e.g. following inferior STEMI. If it is following an anterior MI- infranodal- it is more worrying)
  • Hypertension
  • Recent cardiac surgery
  • Cardiomyopathy
  • Medications e.g. beta blocker
  • Electrolyte imbalances
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12
Q

State some potential causes of heart block

A
  • Calcification & fibrosis of conducting system
  • AV nodal blocking medications e.g. beta blockers, CCBs
  • Some antiarrhythmics e.g. class I anti-arrhythmics
  • Blunt cardiac injury
  • Post catheter ablation for arrhythmias
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13
Q

If heart block is caused by an MI, will it resolve?

A

Yes, heart block following ACS event can resolve in hours to days

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14
Q

If heart block is caused by hyperkalaemia, how do we treat it?

A

IV calcium chloride (10ml of 10% solution over 3-5 mins)

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15
Q

State some medications which increase risk of heart block

A
  • Beta blockers
  • CCBs
  • Adenosine
  • Digoxin toxicity *COMMON
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16
Q

For first degree heart block, state:

  • What the problem is
  • ECG changes
  • Management
A
  • Slowing of conduction at AV node
  • Prolonged PR interval >0.2secs/5 small squares
  • No specific management but:
    • If pt on digoxin, check for toxicity
    • If there are symptoms of dizziness or syncope cardiac monitoring shoudl be considered to identify highter degrees of heart block
17
Q

For second degree heart block, Mobitz type I/Wenckebach type state:

  • What the problem is
  • ECG changes
  • Managment
A
  • Some of atrial depolarisations fail to pass through AV node to ventricles
  • Progressive lengthening of PR interval until a QRS is dropped
  • No specific management but:
    • If pt presents with syncope or dizziness then should investigate for higher degrees of heart block

*NOTE: may occur in young fit patients with high vagal tone or post inferior MI

18
Q

For second degree heart block, Mobitz type II state:

  • What the problem is
  • ECG changes
  • Management
A
  • Some of atrial depolarisations fail to pass through AV node to ventricles
  • Constant PR interval followed by sudden drop of a QRS. This may be in a fixed ratio e.g. 3:1 (every 3rd atrail depolarisation is conducted)

Management

  • Stop any drugs that may be causing heart block
  • In the absence of a recent acute coronary event, permanent pacing should be arranged as Mobitz type II, in comparison to Mobitz type I, indicates more serious involvement of conduction pathways and has a high risk of progression to third degree heart block
19
Q

Which coronary artery supplies the SA node?

Which coronary artery supplies the AV node?

A
  • SA node: sinoatrial nodal artery from RCA (60%) or from LCA (40%)
  • AV node: atrioventricular nodal branch of RCA (in over 80% of people)

*This is why heart block more common following inferior STEMI as RCA supplies inferior heart

20
Q

For third degree heart block, state:

  • What the problem is
  • ECG
  • Management
A
  • No conduction from atria to ventricles. Block can occur above the AV node at the His region or beneath the AV node. It can also be intermittent therefore you should look for ECGs with trifasicular and bifasicular block
  • No relationship between P waves and QRS complexes

Management of Stable Pt

  • Stop any medications which may be causing the heart block
  • Urgent pacemaker (should be considered within 24 hours) in all patients except those who have reasonable likelihood of recovery of conduction e.g. those who have heart block following MI

Management of Haemodynamically Unstable Pt

  • Try atropine (600mg up to max of 3mg)
  • Isoprenaline (at 5ug/min) can also be tried
  • Consider temporary transvenous or transcutaneous pacing
21
Q

Do people with first degree heart block often have symptoms?

A

No, pts with first degree heart block are generally asymptomatic and only find out they have heart block when they have e.g. ECG

22
Q

Do people with Mobitz type I/Wenkebach second degree heart block have any symptoms?

A

Most people don’t experience symptoms but some may experience:

  • Light headedness
  • Dizziness
  • Fainting
23
Q

Do people with Mobitz type II second degree heart block often experience symtoms?

A

Likely to experience symptoms of:

  • Light headedness
  • Dizziness
  • Fainting
  • Chest pain
  • SOB
  • Fatigue (particularly on exertion)
24
Q

Do people with third degree heart block experience symptoms? If so, state some.

A

Yes, will experience symptoms similar to second degree heart block:

  • Light headedness
  • Dizziness
  • Fainting
  • Chest pain
  • Fatigue (particulary during physical exertion/activity)
  • SOB
  • Palpitations
  • Nausea & vomitting
  • Slow HR
25
Q

Describe what you would find on examination of someone with heart block

A
  • Bradycardia
  • Hypertension (often) or hypotension (more acute/emergency)
  • Other signs of cardiac disease (as cardiac disease is a risk factor for heart block)
26
Q

If someone presents with suspected heart block, state:

  • Bedside tests
  • Bloods
  • Imaging

*For each one, explain why you would request it

A

Bedside tests

  • ECG

Bloods

  • FBC
  • U&Es (mainly to look at K+ and Ca2+)
  • Troponin (check no other cause for chest pain)
  • Serum digitalis levels (if pt taking digoxin as digoxin toxicity is a cause of AV block)
  • Serum pH (abnormal values can cause AV block)

Imaging

  • ECHO (check for structural heart disease. Transthoracic echo also required prior to pacemaekr insertion)
  • CXR (rule out any lung disease and check for signs of other cardiac pathology)
27
Q

State some potential complications of heart block

A

Prognosis if treated with pacemaker (if required) is generally good. Increased risk of AF with type 1 and Mobitz type 1. Risk of asystole if third degree untreated.

28
Q

Discuss the treatment for heart block, include treatment for:

  • Stable pts
  • Pts who are unstable or at risk of asytole (e.g. Mobitz type II, complete heart blok)
  • Pts with high risk of astyole (e.g. Mobitz type II, complete heart block or previous asystole)
A

Stable

  • Observe

Unstable or at risk of astyole

  • Atropine 500ug IV

Unstable or risk of asytole

  • Atropine 500ug IV repeated (can give up to 6 doses)
  • Other inotropes e.g. Noradrenalin
  • Transcutaenous cardiac pacing (use a defib)

High risk of astyole

  • Temporary transvenous cardiac pacing (use electrode on end of wire that is inserted into a vein and fed through venous system to right atrium or ventricle to simtulate directly)
  • Permanent implantable pacemaker
29
Q

Describe the mechanism of action of atropine

State some ADRs

A

Antimuscarinic which inhibits parasympathetic nervous system; it is a competitive antagonist of muscuranic receptors

ADRS

  • Pupil dilation
  • Urinary retention
  • Dry eyes
  • Constipation