Arrhythmias Flashcards

1
Q

What are the cardiac causes of arrhythmia?

A
MI
Coronary artery disease
LV aneurysm
Mitral valve disease
Cardiomyopathy
Pericarditis
Myocarditis
Abberant conduction pathwayds
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2
Q

What are non-cardiac causes of arrhythmia?

A

Caffeine
Smoking
Alcohol
Pneumonia
Drugs- Beta2-antagonists, digoxin, L-dopa, tricyclics)
Metabolic imbalance (potassium, calcium, magnesium, hypoxia, hypercapania, metabolic acidosis, thyroid disease)
Phaeochromocytoma

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3
Q

How is bradycardia treated?

A

If asymptomatic and rate is >40bpm, no treatment is required
Stop any drugs that may be contributing
If rate is <40bpm or patient is symptomatic, give atropine
If no response insert a temporary pacing wire
If necessary, start an isoprenaline infusion or use external cardiac pacing

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4
Q

What drugs may cause bradycardia?

A

Beta-blockers

Digoxin

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5
Q

What may cause bradycardia?

A

Drugs
Sick sinus syndrome
Hypothyroidism

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6
Q

What is sick sinus syndrome? How does it present? How is it treated?

A
  1. Arrythmia caused by caused by a malfunction of the sinus node
  2. Bradycardia +/- arrest, sinoatrial block or SVT alternating with bradycardia (tachy-brady syndrome)
  3. Pacing if symptomatic
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7
Q

Describe the acute management of SVT

A
  1. Vagal manoeuvres: e.g. valsalva manoeuvre, immersion of face in cold water or carotid sinus massage (all designed to stimulate the vagus nerve)
  2. IV adenosine (Verapamil if adenosine is contraindicated UNLESS patient is on beta-blocker)
  3. If vagal manoeuvres and medication fail to slow heart rate, and adverse signs are present, defibrilator conversion (DC) shock is done
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8
Q

What drugs are taken for long term management of SVT?

A

Beta blockers; verapamil

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9
Q

What treatment is recommended for recurrent SVT?

A

Catheter ablation

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10
Q

What are the DD’s for a narrow complex tachycardia?

A
  1. Sinus tachycardiac
  2. Supraventricular tachycardia
  3. Atrial fibrillation/flutter
  4. Atrial tachycardia
  5. Junctional tachycardia
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11
Q

What adverse signs seen in a SVT might indicate need for DC?

A
  1. Hypotension BP 200bpm
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12
Q

If adverse signs are not present and DC is deemed unnecessary, how is SVT treated following vagal manoeuvres and adenosine administration?

A
  1. Beta blockers
  2. Digoxin
  3. Amioderone
  4. Pacing (not AF)
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13
Q

If an SVT has an irregular rhythm, what is the likely diagnosis? How should this be treated?

A

AF. Control rate with either beta-blocker or digoxin. If onset <48h consider cardioversion with either amiodarone IVI or DC shock. Consider anticoagulation with heparin and/or warfarin to reduce risk of stroke

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14
Q

What are the relative contraindications of adenosine?

A

Asthma
2nd/3rd degree AV block
Sinoatrial disease

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15
Q

What are the interactions of adenosine?

A

Potentiated by dipyridamole

Antagonized by theophylline

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16
Q

In what condition is multi-focal atrial tachycardia most likely to occur? How should it be treated?

A
  1. COPD

2. Correct hypoxia and hypercapnia. Consider verapamil if rate remains >110bpm

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17
Q

What drugs are used in treatment of WPW?

A
  1. Fecainide
  2. Propafenone
  3. Sotalol
  4. Amiodarone
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18
Q

What is flecaininde?

A

A class 1C anti-dysrrhythmic

Works as a sodium channel blocker, slowing the upstroke of the cardiac action potential.[8] This thereby slows conduction of the electrical impulse within the heart, i.e. it “reduces excitability”.

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19
Q

What is amiodarone?

A

A class III antiarrhythmic agent, which prolongs phase 3 of the cardiac action potential, the repolarization phase where there is normally decreased calcium permeability and increased potassium permeability

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20
Q

What is sotalol?

A

A non-selective competitive β-adrenergic receptor blocker that also exhibits Class III antiarrhythmic properties by its inhibition of potassium channels

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21
Q

What are major side effects of amioderone?

A
  1. Interstitial lung disease
  2. Hypothyroidism
  3. Minor visual impairment
  4. Abnormal liver enzyme levels (hepatitis and jaundice occur rarely)
  5. Blue-grey tinge to the skin
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22
Q

What are the three types of junctional tachycardia?

A
  1. AV nodal re-entry tachycardia (AVNRT)
  2. AV re-entry tachycardia (AVRT)
  3. HIS bundle tachycardia
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23
Q

What is holiday heart syndrome?

A

Acute cardiac rhythm or conduction disturbances caused by binge drinking. Most commonly causes SVT, esp. AF. Diagnosis should be considered in patients with new onset AF without structural heart disease

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24
Q

What is the commonest cause of broad complex tachycardia?

A

Ventricular tachycardia

25
Q

What is a fusion beat in VT?

A

A normal beat which fuses with a VT complex to create an unusual complex?

26
Q

What is a capture beat in VT?

A

A normal QRS between abnormal beats

27
Q

Management of broad complex tachycardia

A
  1. Is there a pulse: No- use arrest protocol. Yes…
  2. …Give oxygen if sats sedate; DC shock; amioderone IVI
    No–> Correct electrolyte problems (esp. low K+). Assess rhythm- if regular assume VT and give amioderone IVI; if irregular diagnosis is probably AF with BBB- (treat for AF)
    If no response- DC
28
Q

What other drugs might be considered in refractory cases of VT? (i.e. other than amiodarone)

A
  1. Flecainide
  2. Lidocaine
  3. Procainamide
  4. Pacing
29
Q

What is lidocaine?

A
A class 1b anti-dissrhythmic
Works by blocking sodium channels to prolong upstroke of the action potention
30
Q

What are the important electrolyte abnormalities to check and correct in VT?

A

Low potassium and low magnesium

31
Q

What is procainamide?

A
A class 1a anti-disrhythmic
Works by blocking sodium channels to prolong upstroke of the action potention
32
Q

If VT occurs after MI, how should it be treated?

A

Amioderone IVI +/- oral anti-arrhythmic sotalol (if good AV function); amiodarone (if poor AV function)

33
Q

What is Torsade de pointes?

A

A form of VT with a constantly varying axis, often in the setting of long QT syndromes

34
Q

What causes Torsade de pointes?

A

Congenital

Drugs: some anti-arrhythmics, tricyclics, anti-malarials, antipsychotics

35
Q

How is Torsade de pointes treated?

A

Stop all contributing drugs

Give magnesium sulphate

36
Q

What is the main risk for atrial fibrillation?

A

Embolic stroke

37
Q

How is risk of atrial fibrillation reduced in patients who have had an embolic stroke?

A

warfarin

38
Q

Describe the ventricular rhythm in patients with atrial fibrillation

A

Irregular as AV conducts depolarization intermittently

39
Q

What causes atrial fibrillation?

A
Heart failure
MI
Hypertension
PE
Mitral valve disease
Pneumonia
Hyperthyroidism
Caffeine
Alcohol
Post-op
Low potassium
Low magnesium
40
Q

How does the pulse feel in a patient with atrial fibrillation?

A

Irregularly irregular.

41
Q

What are the two major signs of atrial fibrillation seen on the ECG?

A
  1. Absent P waves

2. Irregular QRS complexes

42
Q

Describe the management of acute AF

A
  1. Oxygen
  2. Check U&E
  3. Emergency cardioversion- DC or IVI amiodarone
  4. Treat associated illness e.g. MI, pneumonia
  5. Control ventricular rate:
    • first line verapamil or bisoprolol
      -second line- digoxin or amiodarone
  6. Start anticoagulation with LMWH
    N.B. if the 48 hour window has elapsed, cardioversion is OK it a trans-oesophageal echo is thrombus free
43
Q

When is atrial fibrillation described as “acute”? Why is this important?

A

Onset less than 48 hours previously. This is important as this is the window for cardioversion

44
Q

Which arrhythmias respond to defibrillation/cardioversion?

A
  1. Ventricular tachycardia
  2. Ventricular fibrillation
  3. Atrial fibrillation
45
Q

How is cardiversion/defibrillation carried out in atrial fibrillation?

A
  1. Give patient oxygen
  2. Unless critically unwell. patients require general anesthetic or monitored heavy sedation
  3. If elective cardioversion of AF, ensure adequate anticoagulation beforehand
  4. Using a biphasic defibrillator, discharge the machine to 120-200J. Three shocks are normal for AF
46
Q

How is drug cardioversion carried out?

A

Amiodarone IVI (5mg over 1 hour then 900mg over 24 hours) OR amiodarone PO (200mg/8hr for 1 week; 200mg/12 hours for 1 week; 100- 200mg/24 hours maintenance.

Alternatively, if patient is stable and has no known IHD or WPW, flecainide may be used.

47
Q

What are the main goals in managing chronic AF?

A
  1. Rate control

2. Anticoagulation

48
Q

What 2 drug classes are first line for rate control in AF? What additional treatments may be used?

A

Beta-blocker or rate limiting calcium channel blocker are first line

If this fails, add digoxin then consider amiodarone

49
Q

How is rhythm control carried out when treating AF?

A

If cardioversion is chosen, first do an echo, then pretreat with sotalol for >4 weeks. If there is increased risk of cardioversion failure (previous failure or recurrence), pre-treat with amiodarone for >4 weeks.

Flecainide is the first line treatment for pharmacological cardioversion if there is no structural heart disease. If there is structural heart disease, IV amiodarone is used

50
Q

How is anticoagulation carried out in acute AF?

A
  1. Use heparin until a full risk assessment for emboli is made
  2. Use warfarin if risk of emboli is high
  3. Use no anticoagulation if stable sinus rhythm is restored and no risk factors for emboli and AF recurrence unlikely
51
Q

How is risk of stroke calculated? Why is this useful?

A
Risk is calculated using the CHA2DS2VASc score.
C= Congestive heart failure= 1
H= Hypertension= 1
A= Age >75= 2
D= Diabetes= 1
S= Stroke/TIA= 2
V= Vascular disease= 1
Age= 64-75= 1
S= female= 1

A score of 1 or more (or 2 or more in older patients) indicates that oral anticoagulation should be considered

This is useful in deciding whether to use warfarin in AF patients who are also at risk of bleeding.

52
Q

Anticoagulation in chronic AF

A
  1. Use warfarin unless contraindicated

2. If warfarin is contraindicated can use aspirin although less effective.

53
Q

What contraindications are there for warfarin use in AF?

A
  1. Bleeding diathesis (bleeding tendency)
  2. Low platelet count
  3. High BP
  4. Compliance issues around dosing or INR monitoring
  5. Issues such as >75-80 years old, frequent falls, NSAID use, polypharmacy, low Hb and past intracranial bleeds may also be considered but have less evidence base
54
Q

What is dabigatran?

A

A thrombin inhibitor which does not need regular lab monitoring and dose adjustment. Expensive but may be used as an alternative to warfarin e.g. if warfarin is declined or has CI/SE

55
Q

How are atrial flutter waves ‘unmasked’?

A

Carotid sinus massage or IV adenosine as both transiently block the AV node

56
Q

What is the characteristic sign of atrial flutter on an ECG?

A

Sawtooth baseline

57
Q

How is atrial flutter treated?

A
  1. Cardioversion may be indicated (anticoagulate before)

2. Anti-AF drugs may not work but consider amiodarone to restore sinus rhythm and amiodarone or sotalol to maintain it

58
Q

When is temporary pacing required?

A
  1. Symptomatic bradycardia unresponsive to atropine
  2. After acute anterior MI, prophylactic pacing is required in complete AV block, Mobitz type I and II AV block and bi-/tri-fascicular block
  3. Supression of drug reisistant arrhythmias
  4. Special situations: during GA, during cardiac surgery, drug overdose (e.g. digoxin, verapamil, beta-blockers)
59
Q

When is permanent pacing required?

A
  1. Complete AV block
  2. Mobitz II AV block
  3. Persistent AV block after anterior MI
  4. Symptomatic bradycardia
  5. Heart failure
  6. Drug resistant tachyarrhythmias