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Cardiovacular > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

What are the two most common causes of AF?

A

Hypertension
Heart failure

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2
Q

How is the rhythm in AF described?

A

Irregularly irregular

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3
Q

Why is stroke risk increased in AF?

A

Irregular rhythm decreases filling time, thus cardiac output is decreased. This leads to stasis of blood - which is a risk of clotting (Virchow’s triad).

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4
Q

How long does parxoysmal AF last?

A

Less than 48 hours.

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5
Q

How long does persistent AF last?

A

Greater than 48 hours.

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6
Q

When is AF classed as permanent?

A

When cardioversion to normal sinus rhythm is not possible.

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7
Q

How does AF present on an ECG?

A

Atrial rate of 300bpm
Irregularly irregular rhythm
Absent P waves
Narrow (normal QRS)

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8
Q

What scoring system is used to determine stroke risk in AF?

A

CHA2DS2-VASc

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9
Q

What are options for rate control in AF?

A

Beta-blockers (atenolol is first line)
CCB
Digoxin (only given in sedentary patients)

An alternative is AV node ablation.

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10
Q

In which individuals should rate control not be offered for AF?

A

Underlying cause is reversible
The AF is of new onset
The AF is causing heart failure
Symptoms continue despite good rate control already

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11
Q

In which individuals should rhythm control be offered?

A

The AF has a reversible cause
The AF is of new-onset
The AF is causing heart failure
Symptoms persist despite good rate control

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12
Q

When is immediate cardioversion indicated in AF?

A

If AF is present for less than 48 hours, or the patient is severely haemodynamically unstable.

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13
Q

When is delayed cardioversion indicated in AF?

A

If AFD is present for more than 48 hours and the patient is haemodynamically stable.

Patient should be anticoagulated for atleast 3 weeks whilst waiting for cardioversion, as this will decrease clotting risk. Additionally, patient should have rate control during wait period.

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14
Q

What are pharmacological options for cardioversion?

A

Flecainide
Amiodarone (best in structural disease)

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15
Q

What condition is the ‘pill-in-the-pocket’ method applied in?

A

Paroxysmal AF

The pill used is normally flecainide - taken when symptoms start. If the CHA2DS2VASc score indicates so, take anticoagulants.

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16
Q

In AF, when is anticoagulation indicated?

A

In those with underlying valvular disease
When CHA2DS2VASc score is >2

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17
Q

What are risk factors for the development of atrial flutter?

A

Hypertension
IHD
Cardiomyopathy
Thyrotoxicosis

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18
Q

How does atrial flutter present?

A

Usually asymptomatic, although may have palpitations.

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19
Q

How does atrial flutter present on an ECG?

A

Sawtooth P waves (sometimes called F waves)
QRS is normal
Regular rhythm
Atrial rate 2:1 Ventricular rate

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20
Q

How is atrial flutter managed?

A

If acute presentation is symptomatic, cardiovert (either drug or electric).

If non-acute case, patient required 3 weeks of anticoagulation prior to cardioversion.

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21
Q

How is recurrent atrial flutter treated?

A

Catheter ablation
AV nodal blocking (e.g. beta blockers and amiodarone).

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22
Q

Does chronic atrial flutter progress?

A

Yes - progresses to AF.

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23
Q

What are precipitating factors in VT?

A

IHD
Previous MI
Cardiomyopathy
Iatrogenic

Can also be idiopathic.

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24
Q

What are the two forms of VT?

A

Polymorphic
Monomorphic

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25
Q

What causes monomorphic VT?

A

Increased automaticity (=spontaneous generation of APs).

Often due to scarring of the heart muscle from some mechanism.

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26
Q

What causes polymorphic VT?

A

Abnormal ventricular repolarisation.

Causes include long QT syndrome, drug toxicity, or electrolyte imbalances.

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27
Q

How does VT present?

A

Patient will have pre-syncope (dizziness), syncope, hypotension - will result in cardiac arrest.

Some may tolerate better than expected.

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28
Q

How does monomorphic VT present?

A

Will have constant QRS shape - wide complexes.

Rate is rapid.

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29
Q

How does polymorphic VT present?

A

QRS will be observed to be broad, with varying amplitudes.

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30
Q

What is Torsade de Pointes?

A

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

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31
Q

How is a patient with VT, whom is unstable but has a pulse, treated?

A

Cardioversion

32
Q

How is pulseless VT treated?

A

Defibrillation - this is cardiac arrest.

33
Q

How is a stable patient with VT treated?

A

Amiodarone/Lignocaine used first-line (medical therapy).

If not successful, then DCCV should be applied.

34
Q

What is VF?

A

Very rapid and irregular ventricular activation with no mechanical effect.

35
Q

What is primarily the underlying cause of VF?

A

IHD

May also be the result of:
Cardiomyopathy
Electrolyte imbalance
Overdose on cardiotoxic drugs

36
Q

What brings on VF?

A

Usually a ventricular ectopic.

37
Q

How does VF present?

A

Patient will have no pulse - they will become unconscious rapidly. Respiration will cessate.

Patient is in cardiac arrest.

38
Q

How does VF present on an ECG?

A

Will have bizarre irregular waveforms
There will be no regular QRS complexes
Waves present will be of random frequency and amplitude - uncoordinated activity.

39
Q

What is long-term management for VF?

A

ICD

40
Q

What is Brugada syndrome?

A

An inheritable condition causing idiopathic VF - there will be no evidence of a responsible structural abnormality/disease.

41
Q

What mode of inheritance is seen in Brugada syndrome?

A

Autosomal dominant

This makes it 8x more likely in men.

42
Q

What can trigger VF in Brugada syndrome?

A

Rest/Sleep
Fever
Excessive alcohol
Large meals
Drugs

43
Q

What drugs can trigger Brugada syndrome?

A

Beta blockers
Psychotropics
Analgesics
Anasthetics

44
Q

How does Brugada syndrome present on an ECG?

A

ST elevation and RBBB in V1-V3 (may only appear on provocation testing).

May have AF - there is risk of progression to polymorphic VT or VF.

45
Q

How is Brugada syndrome managed?

A

Avoid trigger
Fit an ICD
Test genetics of family for further cases

46
Q

What are 2 examples of congenital causes of long QT syndrome?

A

Jervell-Lange-Nielsen syndrome (autosomal recessive)
Romano-Ward syndrome (autosomal dominant)

47
Q

What may trigger QT prolongation/Torsades des Pointes?

A

Potassium-rich foods
Diarrhoea
Vomiting
Underwater breath-holding
Exercise
Sudden auditory stimuli
Sleep
Drugs
Diabetes
Acute MI

48
Q

How does long QT syndrome present?

A

Will have syncope and palpitations (due to polymorphic VT).

Should spontaneously terminate, if not will progress to VF (with sudden death the result).

49
Q

How is Long QT syndrome managed in the long-term?

A

Beta-blockers
Avoid drugs which may prolong drugs
Pacemaker therapy

50
Q

What is responsible for AVNRT?

A

A re-entry circuit within the AV node.

51
Q

What is the most common cause of SVT in a structurally normal heart?

A

AV nodal re-entrant tachycardia (AVNRT).

This is more common in women.

52
Q

What is responsible for AVRT?

A

An accessory pathway, usually located in the valvular rings. It is most commonly caused by Wolff-Parkinson-White syndrome.

53
Q

What is responsible for EAT?

A

When electrical signals originate outwith the SA node - but still within the atria.

54
Q

What are the three main types of SVT?

A

AV nodal re-entrant tachycardia (AVNRT)
AV re-entrant tachycardia (AVRT)
Ectopic Atrial Tachycardia (EAT)

55
Q

How does an SVT present clinically?

A

Palpitations
Dyspnoea

Wil have fast rate and narrow QRS on an ECG.

56
Q

How is an EAT patient treated?

A

Usually, no treatment if no underlying issue - if it is troublesome, a beta blocker may help.

Should avoid stimulants (e.g. caffeine).

57
Q

How is SVT managed in an acute setting - patient is stable?

A

First-step is valsalva manoeuvre, then carotid sinus massage. If still unsuccessful, try IV adenosine (or verapamil).

Last-line is DCCV - only used if above fails.

58
Q

How does adenosine work?

A

Slows cardiac conduction through the AV node. It interrupts the AV node (and accessory pathway), resetting back to sinus rhythm.

59
Q

How is a paroxysmal SVT treated in the long-term?

A

Can give beta blockers, CCBs or amiodarone.

In younger patients, radiofrequency ablation is preferred.

60
Q

In which condition is a Bundle of Kent found?

A

Wolff-Parkinson-White Syndrome

Causes a re-entrant loop, predisposing to tachyarrhythmias.

61
Q

How does WPW syndrome present on an ECG?

A

Will have slurred up-stroke of the QRS complex (called a delta wave). Accompanying this will be a short PR interval and wide QRS complex.

62
Q

What is the definitive treatment for any disorder resulting from an accessory pathway?

A

Radiofrequency ablation

63
Q

How does first degree heart block present?

A

Will have prolonged PR interval, but no change to rhythm AND no missing beats.

Usually asymptomatic, although the patient should be followed up for any progression to a more serious form.

64
Q

In what conditions can first degree heart block present?

A

IHD
Digoxin toxicity
Electrolyte disturbance

65
Q

What is second degree heart block?

A

An intermittent absence of QRS complexes - indicated a blockage between AV node and ventricles.

Two forms; Mobitz type 1 and Mobitz type 2.

66
Q

Which form of Mobitz is referred to as Wenckebach?

A

Mobitz type 1

67
Q

What occurs in Mobitz type 1?

A

Progressive prolongation of the PR interval, until a QRS is eventually dropped. Pattern will then reset after this.

Often due to high vagal tone - not a result of structural disease.

68
Q

What occurs in Mobitz type 2?

A

When a QRS complex is regularly missed due to preceding P waves not being conducted properly. Often represented in a 2:1, or 3:1 ratio.

Likely to progress to third-degree heart block.

69
Q

What is third-degree heart block?

A

Complete atrial block - atria contracts fine, but no beats conduct to the ventricles.
P waves and QRS complexes are completely unrelated in this - no pattern. Always indicates an underlying disease.

70
Q

What rate is classed as sinus bradycardia?

A

Less than 60bpm.

71
Q

Is sinus bradycardia always due to pathology?

A

No - can present normally in athletes.

72
Q

What conditions may cause sinus bradycardia?

A

Acute/Previous MI
Sick sinus syndrome
Pericarditis
Hypothyroidism
Sleep apnoea
Medications (e.g. verapamil)

73
Q

How is symptomatic sinus bradycardia treated?

A

Atropine, or if acute onset, identify and treat the underlying cause.

74
Q

What is asystole?

A

The complete halt of electrical activity within the heart - thus blood is not being pumped around the body. It is usually irreversible.

75
Q

What are premature ventricular contractions (PVCs)?

A

When abnormal heartbeats that originate from within the ventricles. Patient will have a flutter/missed beat feeling.

76
Q

How is PVC treated?

A

Usually not needed - treat cause if identifiable.

77
Q

How is PVC treated?

A

Usually not needed - treat cause if identifiable.

Cardiovacular (13 decks)

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