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General med - Cardiovascular > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

Shockable rhythms

A

Ventricular tachycardia

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2
Q

Non-shockable rhythms

A

Pulseless electrical activity

Asystole(no significant electrical activity)

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3
Q

Treatment of tachycardia in an unstable patient

A

Consider up to 3 synchronised shocks

Consider amiodarone infusion

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4
Q

Definition of narrow complex

A

QRS < 0.12 secs

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5
Q

Definition of broad complex

A

QRS > 0.12s

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6
Q

What causes atrial flutter

A

Caused by a ‘re-entrant rhythm’ in either atrium

This is where electrical signals re-circulates in a self-perpetuating loop due to an extra electrical pathway(signal goes round and round the atrium without interruption stimulating atrial contraction at 300 rpm)

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7
Q

How does atrial flutter appear on an ecg

A

Sawtooth appearance on ECG with P wave after P wave

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8
Q

Conditions associated with atrial flutter

A

Hypertension
Ischaemic heart disease
Cardiomyopathy
Thyrotoxicosis

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9
Q

Treatment for atrial flutter

A

Rate/rhythm control with beta blockers or cardioversion

Treat reversible cause(HTN, thyrotoxicosis)

Radiofrequency ablation of the re-entrant rhythm

Anticoagulation based on CHA2DS2VASc score

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10
Q

What is an SVT

A

Caused by electrical signal re-entering atria from the ventricles

Signal then travels back through AV node and causes another ventricular contraction causing a self-perpetuating electrical loop resulting in a fast narrow complex tachycardia

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11
Q

What does paroxysmal SVT refer to

A

Describes a situation where SVT reoccurs and remits in the same patient over time

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12
Q

What are the three main types of SVT

A

Atrioventricular nodal re-entrant tachycardia(AVNRT)

Atrioventricular re-entrant tachycardia(WPW)

Atrial tachycardia

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13
Q

What is AVNRT

A

When the re-entry point is back through AV node

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14
Q

What is atrioventricular re-entrant tachycardia

A

When the re-entry point is an accessory pathway(WPW)

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15
Q

What is atrial tachycardia

A

Where the electrical signal originates in the atria somewhere other than SAN

Not caused by a signal re-entering from the ventricles but instead from abnormally generated electrical activity in the atria

The ectopic electrical activity causes an atrial rate of >100bpm

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16
Q

Acute management of stable patients with SVT

A

Continuous ECG monitoring
Valsalva manoeuvre
Carotid sinus massage
Adenosine
Verapamil as an alternative to adenosine
Direct current cardioversion if above fails

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17
Q

What is a valsalva manoeuvre

A

Ask patient to blow hard against resistance, for example into a plastic syringe

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18
Q

How does adenosine work in SVTs

A

Works by slowing cardiac conduction primarily through the AV node interrupting it and resetting it back to sinus rhythm

Will often cause a brief period of systole or bradycardia

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19
Q

How should adenosine be administered

A

Rapid bolus to ensure it reaches the heart with enough impact to interrupt the pathway

IV bolus into a large proximal cannula(grey annular in the antecubital fossa)

Initially 6mg, then 12 mg and then further 12 mg if no improvement

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20
Q

Who should adenosine be avoided in

A 
Asthma 
COPD 
Heart failure 
Heart block 
Severe hypotension
21
Q

Long term management of patients with paroxysmal SVT

A

Medication (beta blockers, calcium channel blockers or amiodarone)
Radiofrequency ablation

22
Q

What is the extra pathway present in WPW often called

A

Bundle of Kent

23
Q

Definitive treatment for WPW

A

Radiofrequency ablation of accessory pathway

24
Q

ECG changes in WPW

A

Short PR interval(<0.12 secs)
Wide QRS complex(>0.12 secs)
Delta wave which is a slurred upstroke on the QRS complex

25
Q

Why should anti arrhythmic meds be avoided in WPW with AF/atrial flutter

A

The meds promote conduction through accessory pathway by reducing conduction through AV node so they are contraindicated in patients with WPW that develop AF/flutter

26
Q

What is radio frequency ablation

A

Involves insertion of a catheter in to the femoral vein and feeding a wire through venous system under X-ray guidance to heart

Once identified, radio frequency ablation(heat) is applied to burn the abnormal area of electrical activity which leaves scar tissue that does not conduct electrical activity

27
Q

What is torsades de pointes

A

Type of polymorphic(multiple shape) ventricular tachycardia

Height of the QRS complexes progressively get smaller, then larger then smaller and so on

Occurs in patients with a prolonged QT interval

28
Q

Definition of prolonged QT interval

A

Anything greater than or equal to 0.5 seconds

29
Q

Pathophys behind prolonged QT interval

A

Prolonged repolarisation of the muscle cells in the heart after contraction

Longer repolarisation time can result in spontaneous depolarisation in some myocytes

These depolarisations spread throughout the ventricle leading to ventricular contraction prior to proper repolarisation

30
Q

End result of torsades de pointes

A

Will either terminate spontaneously and never back to sinus rhythm or progress in to ventricular tachycardia

Usually, they are self limiting but if they progress to VT, it can lead to cardiac arrest

31
Q

Causes of prolonged QT

A

Long QT syndrome(inherited)
Meds
Electrolyte disturbances

32
Q

Which medications can cause prolonged QT

A 
Antipsychotics 
Citalopram 
Flecainide 
Sotalol 
Amiodarone 
Macrolides
33
Q

Electrolyte disturbances which can cause prolonged QT

A

Hypokalaemia
Hypomagnesaemia
Hypocalcaemia

34
Q

Acute management of torsades de pointes

A 
Correct cause(electrolyte disturbances or meds) 
Magnesium infusion(even if normal serum magnesium) 
Defib if VT occurs
35
Q

Long term management of prolonged QT syndrome

A 
Avoid meds that prolong QT interval 
Correct electrolyte disturbances 
Beta blockers(not sotalol) 
Pacemaker or implantable defibrillator
36
Q

What are ventricular ectopics

A

Are premature ventricular beats caused by random electrical discharges from outside atria

Appear as individual random, abnormal, broad QRS complexes on a background of a normal ECG

37
Q

What is bigeminy

A

This is where ventricular ectopics are occurring so frequently that happen after every sinus beat

ECG looks like a normal sinus beat allowed immediately by an ectopic, then a normal beat, then ectopic and so on

38
Q

Management of ventricular ectopics

A

Check bloods for anaemia, electrolyte disturbance and thyroid abnormalities
Reassurance and no treatment in otherwise healthy people
Seek expert advice in patients with background heart conditions or other concerning features or findings (e.g. chest pain, syncope, murmur, family history of sudden death)

39
Q

What is first degree heart block

A

Occurs where there is delayed AV cofunction through AV node

Every p waves results in a QRS complex. On an ECG this presents as a PR interval greater than 0.20 seconds (5 small or 1 big square).

40
Q

What is second degree heart block

A

Second-degree heart block is where some of the atrial impulses do not make it through the AV node to the ventricles. This means that there are instances where p waves do not lead to QRS complexes.

Divided into mobitz type 1 and 2

41
Q

What is mobitz type 1/wenckebach’s

A

On an ECG this will show up as an increasing PR interval until the P wave no longer conducts to ventricles. This culminates in absent QRS complex after a P wave. The PR interval then returns to normal but progressively becomes longer again until another QRS complex is missed. This cycle repeats itself.

42
Q

What is mobitz type 2

A

intermitted failure or interruption of AV conduction. This results in missing QRS complexes. There is usually a set ratio of P waves to QRS complexes, for example 3 P waves to each QRS complex would be referred to as a 3:1 block. The PR interval remains normal. There is a risk of asystole with Mobitz Type 2.

43
Q

What is third degree heart block

A

This is referred to as complete heart block. This is no observable relationship between P waves and QRS complexes. There is a significant risk of asystole with third-degree heart block.

44
Q

Treatment for bradycardias/AV node blocks

A

Stable - observe

Unstable or risk of asystole - 1st line - Atropine 500mcg IV

No improvement:

Atropine 500mcg IV repeated, other inotropes(noradrenaline), transcutaneous cardiac pacing(using a defibrillator)

45
Q

Management of patients with a high risk of systole due to heart block

A

Temporary transvenous cardiac pacing

Permanent implantable pacemaker when available

46
Q

How does atropine work

A

is an antimuscarinic medication that works by inhibiting parasympathetic nervous system

Leads to side effects of pupil dilatation, urinary retention, dry eyes and constipation

47
Q

What is brugada syndrome

A

ECG abnormality with a high incidence of sudden death in patients with structurally normal hearts.

It is caused by a mutation in the cardiac Na+ channel gene, known as a sodium channelopathy

48
Q

Diagnosis of brugada syndrome

A

Diagnosis can only be made with the characteristic Brugada ECG patterns (Coved ST-segment elevation >2mm in >1 of V1-V3 followed by a negative T wave) and one of the clinical criteria

49
Q

Clinical criteria for diagnosis of brugada syndrome

A

Documented ventricular fibrillation (VF)
Polymorphic ventricular tachycardia (VT)
A family history of sudden cardiac death at <45 years old
Coved-type ECGs in family members, Inducibility of VT with programmed electrical stimulation
Syncope
Nocturnal agonal respiration

General med - Cardiovascular (13 decks)

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