Arrythmia Flashcards

1
Q

What is the most common sustained cardiac arrhythmia?

A

Atrial fibrillation (AF)

> 70-75 years (5%)

> 80-85 years (10%)

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2
Q

What is the most important important aspect of managing patients with Atrial Fibrillation?

A

reducing the increased risk of stroke

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3
Q

What can uncontrolled atrial fibrillation can result in?

A

symptomatic palpitations

inefficient cardiac function

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4
Q

What are the types of atrial fibrillation?

A

first detected episode

recurrent: 2 or more episodes of AF

permanent: continuous AF which cannot be cardioverted

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5
Q

two types of recurrent atrial fibrillation

A

paroxysmal: terminates spontaneously; episodes last less than 7 days (< 24 hours)

persistent: not self-terminating; episodes last greater than 7 days

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6
Q

treatment goals of permanent AF

A

rate control

anticoagulation if appropriate

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7
Q

AF signs and symptoms

A

symptoms: palpitations, dyspnoea, chest pain

signs: irregularly irregular pulse

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8
Q

conditions (other than AF) that can give an irregular pulse

A

ventricular ectopics or sinus arrhythmia.

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9
Q

What investigation is essential for diagnosis of AF?

A

ECG

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10
Q

key parts of managing patients with AF

A
  1. rate/rhythm control
  • rate control: accept pulse will be irregular but slow rate down to avoid negative effects on cardiac function
  • rhythm control: cardioversion (to maintain normal sinus rhythm) using drugs (pharmacological) or synchronised DC electrical shocks (electrical)
  1. reducing stroke risk
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11
Q

delete

A

delete

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12
Q

contraindications for rate control

A

coexistent heart failure

first onset AF

obvious reversible cause

(note: patients may have had a rate control strategy initially but switch to rhythm control if symptoms/heart rate fails to settle)

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13
Q

medications used for rate control in AF

A

beta-blocker or a rate-limiting calcium channel blocker (diltiazem)

combination therapy with any 2 of the following:
(if one drug does not control the rate adequately)
- a betablocker
- diltiazem
- digoxin

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14
Q

when is the highest risk for embolism leading to stroke in cardioversion ?

A

the moment a patient switches from AF to sinus rhythm

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15
Q

prior to attempting cardioversion, why must patients either have had a:

  • short duration of symptoms (less than 48 hours)
  • anticoagulated for a period of time
A

in cardioversion, the moment a patient switches from AF to sinus rhythm presents the highest risk for embolism leading to stroke.

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16
Q

how to identify most appropriate anticoagulation for reducing stroke risk in AF?

A

CHA2DS2-VASc

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17
Q

what does CHA2DS2VASc consist of

A

C ongestive ♡ failure (1)

H ypertension (or treated hypertension) (1)

A ge >= 75 years (2)

D iabetes (1)

S troke or TIA (2)

V ascular disease (1)

A ge 65-74 years (1)

S ex - female (1)

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18
Q

suggested anticoagulation strategy based on the CHA2DS2-VASc score

A

0: no treatment

1: males: consider anticoagulation
females: no treatment (as score only reached due to gender)

2 or more: anticoagulation

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19
Q

What is a common contraindication for beta-blockers

A

asthma

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20
Q

preferred rate control medication if there is coexistent heart failure

A

Digoxin

not considered first-line anymore as they are less effective at controlling the heart rate during exercise

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21
Q

rhythm control agents in patients with a history of atrial fibrillation

A

sotalol
amiodarone
flecainide

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22
Q

factors favouring rate control in AF

A

> 65 years

history of ischaemic heart disease

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23
Q

factors favouring rhythm control in AF

A

< 65 years

symptomatic

first presentation

lone AF or secondary to a corrected precipitant (e.g. Alcohol)

congestive heart failure

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24
Q

indications for catheter ablation

A

not responded or wish to avoid antiarrhythmic medication.

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25
Q

technical aspects of catheter ablation

A

aim is to ablate faulty electrical pathways- due to aberrant electrical activity between pulmonary veins and left atrium - that result in AF

procedure is performed percutaneously, typically via the groin

can use:
- radiofrequency (uses heat generated from medium frequency alternating current)
- cryotherapy

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26
Q

when should anticoagulation be started for patients undergoing catheter ablation

A

4 weeks before and during the procedure

therefore, patients still require anticoagulation afterwards as per theire CHA2DS2-VASc score

if score = 0: 2 months anticoagulation recommended
if score > 1: longterm anticoagulation recommended

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27
Q

complications of catheter ablation?

A

cardiac tamponade
stroke
pulmonary valve stenosis

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28
Q

success rate of catheter ablation

A

50%: early recurrence (3 months); often resolves spontaneously

55%: long term (3 years) sinus rhythm with one procedure

80%: long term (3 years) sinus rhythm with multiple procedures

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29
Q

When would cardioversion be used in atrial fibrillation?

A
  • emergency if patient is haemodynamically unstable (electrical cardioversion)
  • elective procedure where rhythm control strategy is preferred (electrical or pharmacological cardioversion)
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30
Q

why is electrical cardioversion is synchronised to the R wave

A

to prevent delivery of a shock during the vulnerable period of cardiac repolarisation when ventricular fibrillation can be induced.

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31
Q

AF onset <48 hours

indications prior to cardioversion

A

begin heparin

if risk factors for ischaemic stroke: lifelong oral anticoagulation.

may be cardioverted electrically or pharmalogically.

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32
Q

Following electrical cardioversion if AF is confirmed as being less than 48 hours duration then further anticoagulation is?

A

unnecessary

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33
Q

AF onset >48 hours

when should anticoagulation be given

A

at least 3 weeks prior to cardioversion

an alternative strategy:
- transoesophageal echo (TOE) to exclude a left atrial appendage (LAA) thrombus
- if excluded: patients may be heparinised and cardioverted immediately

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34
Q

AF onset >48 hours

which cardioversion?

A

electrical

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35
Q

What suggests a high risk of cardioversion failure?

A

Previous failure or AF recurrence

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36
Q

AF onset >48 hours & high risk of cardioversion failure

what should you do

A

4 weeks amiodarone or sotalol prior to electrical cardioversion

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37
Q

AF onset >48 hours

anticoagulation after electrical cardioversion ?

A

anticoagulation for at least 4 weeks.

after this time decisions about anticoagulation should be taken on an individual basis depending on the risk of recurrence

38
Q

pharmacological cardioversion agents (effective ones)

A

amiodarone

flecainide (if no structural heart disease)

39
Q

pharmacological cardioversion agents (less effective)

A

beta-blockers (including sotalol)

calcium channel blockers

digoxin

disopyramide

procainamide

40
Q

If CHA2DS2-VASc score suggests no need for anticoagulation it is important to ensure what?

A

transthoracic echocardiogram

to exclude valvular heart disease, which in combination with AF is an absolute indication for anticoagulation.

41
Q

NICE recommend that we offer patients a choice of anticoagulation

A

true

warfarin and the novel oral anticoagulants (NOACs)

42
Q

Aspirin is no longer recommended for reducing stroke risk in patients with AF

A

true

43
Q

A history of what make us consider whether warfarinisation is in the best interests of the patient?

A

falls, old age, alcohol excess and a history of previous bleeding

44
Q

NICE now recommend we formalise risk assessment for wararin prescription using what system?

A

HASBLED

45
Q

There are no formal rules on how we act on the HAS-BLED score

A

true

46
Q

A HASBLED score of what indicates ‘high risk’ of bleeding?

A

> = 3

defined as intracranial haemorrhage, hospitalisation, haemoglobin decrease >2 g/L, and/or transfusion.

47
Q

Outline HASBLED score

A

H Hypertension, uncontrolled, systolic BP > 160 mmHg 1
A Abnormal renal function (dialysis or creatinine > 200)
Or
Abnormal liver function (cirrhosis, bilirubin > 2 times normal, ALT/AST/ALP > 3 times normal 1 for any renal abnormalities

1 for any liver abnormalities
S Stroke, history of 1
B Bleeding, history of bleeding or tendency to bleed 1
L Labile INRs (unstable/high INRs, time in therapeutic range < 60%) 1
E Elderly (> 65 years) 1
D Drugs Predisposing to Bleeding (Antiplatelet agents, NSAIDs)
Or
Alcohol Use (>8 drinks/week) 1 for drugs

1 for alcohol

48
Q

following a stroke or TIA, what should be given as the anticoagulant of choice?

A

warfarin or a direct thrombin or factor Xa inhibitor (Rivaroxaban, Apixaban)
Antiplatelets should only be given if needed for the treatment of other comorbidities

49
Q

In acute stroke patients, in the absence of haemorrhage, anticoagulation therapy should be commenced after?

A

2 weeks. If imaging shows a very large cerebral infarction then the initiation of anticoagulation should be delayed

50
Q

Atrial flutter is a form of supraventricular tachycardia characterised by?

A

succession of rapid atrial depolarisation waves.

51
Q

What are the ECG findings in atrial flutter?

A

‘sawtooth’ appearance
as the underlying atrial rate is often around 300/min the ventricular or heart rate is dependent on the degree of AV block. For example if there is 2:1 block the ventricular rate will be 150/min
flutter waves may be visible following carotid sinus massage or adenosine

52
Q

How do you manage atrial flutter?

A

is similar to that of atrial fibrillation although medication may be less effective

atrial flutter is more sensitive to cardioversion however so lower energy levels may be used

radiofrequency ablation of the tricuspid valve isthmus is curative for most patients

53
Q

What is Ventricular tachycardia?

A

broad-complex tachycardia originating from a ventricular ectopic focus. It has the potential to precipitate ventricular fibrillation and hence requires urgent treatment.

54
Q

What are the two main types of VT?

A

monomorphic VT: most commonly caused by myocardial infarction

polymorphic VT: A subtype of polymorphic VT is torsades de pointes which is precipitated by prolongation of the QT interval.

55
Q

What are the congenital causes of prolonged QT interval?

A

Jervell-Lange-Nielsen syndrome (includes deafness and is due to an abnormal potassium channel)
Romano-Ward syndrome (no deafness)

56
Q

What are the drug causes of prolonged QT interval?

A
amiodarone, sotalol, class 1a antiarrhythmic drugs
tricyclic antidepressants, fluoxetine
chloroquine
terfenadine
erythromycin
57
Q

What are the other causes of prolonged QT interval?

A
electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia
acute myocardial infarction
myocarditis
hypothermia
subarachnoid haemorrhage
58
Q

What are the indications for cardioversion in VT?

A

If the patient has adverse signs (systolic BP < 90 mmHg, chest pain, heart failure) then immediate cardioversion is indicated.

In the absence of such signs antiarrhythmics may be used.

If these fail, then electrical cardioversion may be needed with synchronised DC shocks

59
Q

What drug therapy is used in VT?

A

amiodarone: ideally administered through a central line
lidocaine: use with caution in severe left ventricular impairment
procainamide

60
Q

Which drug should NOT be used in VT?

A

Verapamil
This is because Verapamil also blocks the calcium current responsible for sinus and AV nodal depolarization and can precipitate haemodynamic detoriaration, VF & cardiac arrest

61
Q

What to do if drug therapy fails in VT?

A
electrophysiological study (EPS)
implant able cardioverter-defibrillator (ICD) - this is particularly indicated in patients with significantly impaired LV function
62
Q

What is the key step in management of peri-arrest tachycardias?

A

Following basic ABC assessment, patients are classified as being stable or unstable according to the presence of any adverse signs:
shock: hypotension (systolic blood pressure < 90 mmHg), pallor, sweating, cold, clammy extremities, confusion or impaired consciousness
syncope
myocardial ischaemia
heart failure

63
Q

If there are adverse signs present in peri-arrest tachycardias what should be done?

A

synchronised DC shocks should be given
Treatment following this is given according to whether the QRS complex is narrow or broad and whether the rhythm is regular or irregular.

64
Q

How do you treat regular broad-complex tachycardias in the context of peri-arrest?

A

stable/unstable -> shock?
assume ventricular tachycardia (unless previously confirmed SVT with bundle branch block)
loading dose of amiodarone followed by 24 hour infusion

65
Q

How do you treat irregular broad-complex tachycardias in the context of peri-arrest?

A

stable/unstable -> shock?

  1. AF with bundle branch block - treat as for narrow complex tachycardia
  2. Polymorphic VT (e.g. Torsade de pointes) - IV magnesium
66
Q

How do you treat regular narrow-complex tachycardias in the context of peri-arrest?

A

stable/unstable -> shock?
vagal manoeuvres followed by IV adenosine
if above unsuccessful consider diagnosis of atrial flutter and control rate (e.g. Beta-blockers)

67
Q

How do you treat irregular narrow-complex tachycardias in the context of peri-arrest?

A

stable/unstable -> shock?
probable atrial fibrillation
if onset < 48 hr consider electrical or chemical cardioversion
rate control (e.g. Beta-blocker or digoxin) and anticoagulation

68
Q

What are possible causes of palpitations?

A

arrhythmias
stress
increased awareness of normal heart beat / extrasystoles

69
Q

What are first line investigations of palpitations?

A

12-lead ECG: this will only capture the heart rhythm for a few seconds and hence is likely to miss episodic arrhythmias. However, other abnormalities linked to the underlying arrhythmia (for example a prolonged QT interval or PR interval, or changes suggesting recent myocardial ischaemia) may be seen.
thyroid function tests: thyrotoxicosis may precipitate atrial fibrillation and other arrhythmias
urea and electrolytes: looking for disturbances such as a low potassium
full blood count

70
Q

Palpitations presentation: What is the next step after first line investigations?

A
exclude an episode arrhythmia.
Holter monitoring
If no abnormality is found on the Holter monitor, and symptoms continue, other options include:
external loop recorder
implantable loop recorder
71
Q

In atrioventricular (AV) block, or heart block, there is impaired electrical conduction between the atria and ventricles.

A

true

3 types

72
Q

First-degree heart block?

A

PR interval > 0.2 seconds

asymptomatic first-degree heart block is relatively common and does not need treatment

73
Q

What is Mobitz I/ Wenckebach

A

type 1 Second-degree heart block

progressive prolongation of the PR interval until a dropped beat occurs

74
Q

What is mobitz II?

A

type 2 Second-degree heart block

PR interval is constant but the P wave is often not followed by a QRS complex

75
Q

Third-degree (complete) heart block?

A

there is no association between the P waves and QRS complexes

76
Q

What is Torsades De Pointes?

A

form of polymorphic ventricular tachycardia associated with a long QT interval. It may deteriorate into ventricular fibrillation and hence lead to sudden death.

77
Q

How do you manage Torsades De Pointes?

A

IV magnesium sulphate

78
Q

What is Wolff-Parkinson White?

A

syndrome is caused by a congenital accessory conducting pathway between the atria and ventricles leading to a atrioventricular re-entry tachycardia (AVRT). As the accessory pathway does not slow conduction AF can degenerate rapidly to VF

79
Q

What are the ECG features of Wolff-Parkinson White?

A

short PR interval
wide QRS complexes with a slurred upstroke - ‘delta wave’
left axis deviation if right-sided accessory pathway*
right axis deviation if left-sided accessory pathway*

80
Q

What are the two of Wolff-Parkinson White types

A
type A (left-sided pathway): dominant R wave in V1
type B (right-sided pathway): no dominant R wave in V1
81
Q

What are the associations of WPW?

A
HOCM
mitral valve prolapse
Ebstein's anomaly
thyrotoxicosis
secundum ASD
82
Q

What is the management of WPW?

A

definitive treatment: radiofrequency ablation of the accessory pathway
medical therapy: sotalol***, amiodarone, flecainide

sotalol should be avoided if there is coexistent atrial fibrillation as prolonging the refractory period at the AV node may increase the rate of transmission through the accessory pathway, increasing the ventricular rate and potentially deteriorating into ventricular fibrillation

83
Q

in the majority of cases, or in a question without qualification, Wolff-Parkinson-White syndrome is associated with left axis deviation

A

true

84
Q

The 2015 Resuscitation Council (UK) guidelines emphasise that the management of bradycardia depends on?

A
  1. identifying the presence of signs indicating haemodynamic compromise - ‘adverse signs’
  2. identifying the potential risk of asystole
85
Q

In Peri-arrest rhythms: bradycardia

The following factors indicate haemodynamic compromise and hence the need for treatment?

A

shock: hypotension (systolic blood pressure < 90 mmHg), pallor, sweating, cold, clammy extremities, confusion or impaired consciousness
syncope
myocardial ischaemia
heart failure

86
Q

What is the first line treatment of peri=arrest bradycardia with haemodynamic compromise?

A

Atropine (500mcg IV) is the first line treatment in this situation.

If there is an unsatisfactory response the following interventions may be used:
atropine, up to maximum of 3mg
transcutaneous pacing
isoprenaline/adrenaline infusion titrated to response

Specialist help should be sought for consideration of transvenous pacing if there is no response to the above measures.

87
Q

What are the risk factors for asystole?

A

complete heart block with broad complex QRS
recent asystole
Mobitz type II AV block
ventricular pause > 3 seconds

(in peri-arrest bradycardia) if there is a satisfactory response to atropine specialist help is indicated to consider the need for transvenous pacing:

88
Q

What are J waves and what are they associated with?

A

small bumps at the end of the QRS complex.

hypothermia

89
Q

What are features of hypothermia?

A
bradycardia
'J' wave - small hump at the end of the QRS complex
first degree heart block
long QT interval
atrial and ventricular arrhythmias
90
Q

Delta waves are associated with ?

A

Wolff-Parkinson-White Syndrome

91
Q

Saddle ST elevation is associated with?

A

pericarditis