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Cardiac > Arrythmia > Flashcards

Arrythmia Flashcards

1
Q

In AFib where is the signal originating

A

anywhere in the atria, not SAN and conducted through AVN but irregularly

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2
Q

What is AFib

A

Multiple atrial impulses and contractions transmitted randomly to the AVN but causing a normal ventricular contraction

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3
Q

What do you see on ECG in A.fib

A

No P waves, irregular rhythm, narrow complex

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4
Q

What is atrial flutter

A

Signal arises within atrial muscle as opposed to SAN at a set rate of 300bpm and either all pass through to cause a contraction or often one in 2 passed through (rate 150bpm)

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5
Q

What do you see on ECG with Atrial flutter

A

‘saw teeth’, usually regular rhythm, narrow complex, rate is most commonly 150 or 300bpm

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6
Q

What is the most common type of SVT

A

AV nodal re-entry tachycardia

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7
Q

How does AV nodal re-entry tacycardia (SVT) happen

A

Within the AVN there is another pathway which causes extra impulses to be transmitted through to the ventricles causing more ventricular contractions

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8
Q

What is AV re-entry tachycardia (SVT)

A

An extra pathway between the atria and ventricles by which extra signals are being transmitted along with the normal ones through the AVN resulting in more ventricular contractions e.g Wolff-Parkinson white

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9
Q

What does SVT look like on an ECG

A

Regular
Narrow complex tachycardia
Looks like ST depression but it’s an inverted P wave in a T wave
P waves are buried in T waves

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10
Q

what is ventricular tachycardia

A

Contractions are occurring within the ventricular tissue

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11
Q

What do you see on ECG in ventricular tachy

A

regular
broad complex - slow inefficient contraction
QRS is regular in height and width
No P or T waves

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12
Q

What is ventricular fibrillation

A

Arising within ventricular tissue but in a random pattern

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13
Q

What does V fib look like on ECG

A

Irregular
broad base
no P/T waves

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14
Q

Examples of narrow complex tacycardia

A

A fib
A flutter
SVT

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15
Q

Examples of broad complex tachycardia

A

V fib

V tachy

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16
Q

Regular, narrow complex tachycardia

A

a flutter

SVT

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17
Q

Irregular narrow complex tachycardia

A

A fib

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18
Q

Irregular broad base tachycardia

A

V fib

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19
Q

Regular broad complex tacycardia

A

Ventricular tachy

SVT with abberancy - SVT with a BBB

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20
Q

Management of stable Atrial fib and A flutter

A
  • beta blocker to slow HR
  • CHADVASC for anti-coagulation
    ( anti-arrhythmic in young with no co-morbidities e.g. digoxin)
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21
Q

What makes a patient in a tachy-arrhythmia unstable

A

Chest pain
Heart failure
hypotensive
reduction in consciousness

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22
Q

Management of an unstable tachy-arrhythmia

A
  • cardioversion - DC shock
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23
Q

Management of stable SVT

A
  1. Vagal manoeuvres e.g. blowing on a syringe, carotid massage
  2. Adenosine - blocks of AVN temporarily
  3. DC shock
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24
Q

Do you need to anti-coagulate someone in SVT

A

no

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25
Q

What is the approach to diagnosing a tachycardia?

A
  1. Is it broad or narrow complex

2. Is it regular or irregular

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26
Q

Management of ventricular tachycardia with a pulse

A
  1. Amiodarone 300mg
  2. Amiodarone infusion 24h
  3. Cardiology involvement
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27
Q

Management of cardiac arrest with a shockable rhythm

A
  • Compressions 30/2
  • Shock
  • Reassess rhythm every 2 mins + shock
  • Adrenaline after third shock (1:1000) then every other shock
  • Amiodarone after 3rd and 5th shock
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28
Q

Which are shockable rhythms

A

VF

VT (pulseless)

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29
Q

Non shockable rhythms

A

PEA

Asystole

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30
Q

Causes of cardiac arrest 4 T

A
  1. thrombosis
  2. tension pneumothorax
  3. tamponade
  4. toxins
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31
Q

Causes of cardiac arrest 4 H

A
  1. Hypoxia
  2. Hypovolaemia
  3. Hyperkalaemia (electrolyte disturbances)
  4. Hypothermia
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32
Q

Management of Non-shockable cardiac arres

A
  • BLS
  • Confirm un-shockable rhythm
  • Adrenaline (1:1000)
  • Reassess rhythm every 2 mins
  • Adrenaline every alternate check
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33
Q

What conditions are associated with atrial flutter

A

Hypertension
Ischaemic heart disease
Cardiomyopathy
Thyrotoxicosis

34
Q

How does adenosine work

A

Slows cardiac conduction primarily though the AV node. It interrupts the AV node / accessory pathway during SVT and “resets” it back to sinus rhythm. It needs to be given as a rapid bolus to ensure it reaches the heart with enough impact to interrupt the pathway. It will often cause a brief period of asystole or bradycardia.

35
Q

Key points to think about when administering adenosine

A
  • Avoid if patient has asthma / COPD / heart failure / heart block / severe hypotension
  • Warn patient about the scary feeling of dying / impending doom when injected
  • Give as a fast IV bolus into a large proximal cannula
  • Initially 6mg, then 12mg and further 12mg if no improvement between doses
36
Q

What is the Long Term Management of patients with paroxysmal SVT

A

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

37
Q

What is Wolff Parkinson White

A

An extra electrical pathway connecting the atria and ventricles. Normally there is only one pathway connecting the atria and ventricles called the atrio-ventricular node. The extra pathway that is present in Wolff-Parkinson White Syndrome is often called the Bundle of Kent.

38
Q

WHat are the ECG changes seen in Wolff Parkinson White

A
  • Short PR interval (< 0.12 seconds)
  • Wide QRS complex (> 0.12 seconds)
  • “Delta wave” which is a slurred upstroke on the QRS complex
39
Q

Which medications are contraindicated in patients with Wolff Parkinson White

A
  • antiarrhythmic medications (beta blockers, calcium channel blockers, adenosine
40
Q

Why are anti-arrhythmics contraindicated in patients with Wolff parkinson White

A

there is a risk that the chaotic atrial electrical activity can pass through the accessory pathway into the ventricles causing a polymorphic wide complex tachycardia

41
Q

What is the definitive management of Wolff Parkinson White SYndrome

A

Radiofrequency ablation of the accessory pathyway

42
Q

Which conditions can radiofrequency ablation be used to treat

A
  • Atrial Fibrillation
  • Atrial Flutter
  • Supraventricular Tachycardias
  • Wolff-Parkinson-White Syndrome
43
Q

What is radiofreqeuncy ablation

A
  • Heat is applied to burn the abnormal area of electrical activity. This leaves scar tissue that does not conduct the electrical activity. The aim is to remove the source of the arrhythmia.
  • Done in the cath lab under local or GA
  • May try and induce the arrhythmia to ensure the correct area is burned
44
Q

What is Torsades de points

A

Polymorphic ventricular tachycardia

45
Q

What causes Torsades de pointes

A

prolonged QT interval

46
Q

What causes a prolonged QT

A

Long QT Syndrome (inherited)
Medications
Electrolyte Disturbance (hypokalaemia, hypomagnesaemia, hypocalcaemia)

47
Q

What medications can cause a prolonged QT

A 
Anti-psychotics
ctialopram
flecainide
sotalol
amiodarone
marcolides
48
Q

What electrolyte disturbances can cause a prolonged QT

A

Hypokalaemia
Hypomagnesaemia
Hypocalcaemia

49
Q

What does torsades de pointes lead to

A

Often self terminating but can lead to ventricular tachycardia

50
Q

What is the acute treatment of torsades de pointes

A

Correct the cause (electrolyte disturbances or medications)
Magnesium infusion (even if they have a normal serum magnesium)
Defibrillation if VT occurs

51
Q

What is the long term treatment of torsades de pointes

A 
Avoid medications that prolong the QT interval
Correct electrolyte disturbances
Beta blockers (not sotalol)
Pacemaker or implantable defibrillator
52
Q

What are ventricular ectopic beats

A

premature, weak ventricular contractions caused by random electrical charges outside the atria

53
Q

How can you diagnose ventricular ectopic beats on an ECG

A

random, abnormal broad QRS complex on an otherwise normal ECG

54
Q

What is bigeminy

A
  • Ventricular ectopics happen after every sinus beat

- ECG: normal sinus beat followed immediately by an ectopic, then a normal beat, then ectopic

55
Q

What is the management of ventricular ectopics

A
  • check for anaemia, electrolyte imbalances and TFTs
  • Reassurance
  • Seek advice if underlying heart condition or concerning features e.g. syncope or chest pain
56
Q

What is first degree heart block

A
  • delayed atrioventricular conduction through the AV node
  • Every P wave have a QRS
  • PR interval >0.2 seconds: 5 small squares
57
Q

What is second degree heart block

A
  • some of the atrial impulses do not make it through the AV node to the ventricles.
  • Some instances where P waves don’t lead to QRS
  • Can be split into TI or TII
58
Q

What is Mobitz type I heart bock - Wenchebache

A
  • Atrial contraction becomes progressively weaker until it does not transmit through to the ventricles
  • Increasing PR interval until the P wave no longer conducts leading to absent QRS, then PR returns to normal
59
Q

What is Mobitz TII heart block

A
  • Intermitted failure or interruption of AV conduction
  • missing QRS complex on ECG
  • Can lead to asystole
  • Usually in 3-1 block ( 3 p waves to each QRS)
60
Q

What is 2:1 block

A
  • 2 P waves for each QRS complex

- Caused by Mobitz Type 1 or Mobitz Type 2

61
Q

What is third degree heart block

A
  • AKA complete heart block
  • no relationship between P waves and QRS complex
  • significant risk of systole
62
Q

What is the treatment of a stable person with bradycardia/AV node block

A

Observe

63
Q

What is the treatment of an unstable person with bradycardia/AV node block

A
  • Atropine 500 micrograms IV (can repeat up to 6 doses)
  • Other inotropes e.g. noradrenalin
  • Transcutaneous pacing - defib
64
Q

What is Atropine

A
  • Antimuscarinic
  • Inhibits the PNS
  • Side effects: pupil dilatation, urinary retention, dry eyes and constipation.
65
Q

What is atrial fibrillation

A

Normal the sinoatrial node produces organised electrical activity that coordinates the contraction of the atria of the heart. Atrial fibrillation is where the contraction of the atria is uncoordinated, rapid and irregularly. This due to disorganised electrical activity that overrides the normal, organised activity from the sinoatrial node.

66
Q

What are the features of AF

A
  • Irregularly irregular ventricular contractions
  • Tachycardia
  • Heart failure: poor filling of the ventricles during diastole
  • Risk of stroke
67
Q

What are the presenting symptoms of AF

A
  • Palpitations
  • Shortness of breath
  • Syncope (dizziness or fainting)
  • Symptoms of associated conditions (e.g. stroke, sepsis or thyrotoxicosis)
68
Q

What are the two differentials for an irregularly irregular pulse

A
  • AF

- Ventricular ectopics

69
Q

What does an ECG of a patient in AF show

A

Absent P waves
Narrow QRS Complex Tachycardia
Irregularly irregular ventricular rhythm

70
Q

What are the most common causes of AF

A 
S: sepsis
M: mitral Valve Pathology (stenosis or regurgitation)
I: Ischemic Heart Disease
T: thyrotoxicosis
H: hypertension
71
Q

Which patients with AF should have rhythm control as first line

A
  • Reversible cause
  • New onset (within the last 48 hours)
  • AF is causing heart failure
  • Symptomatic despite being effectively rate controlled
72
Q

What options are available for rate control of Fast AF

A

Beta blocker is first line (e.g. atenolol 50-100mg once daily)
Calcium-channel blocker (e.g. diltiazem) (not preferable in heart failure)
Digoxin (only in sedentary people, needs monitoring and risk of toxicity)

73
Q

When do you do immediate cardioversion

A
  • Onset <48 hours

- haemodynamically unstable

74
Q

What happens in delayed cardioversion

A
  • Patient anti-coagulated >3w
  • rate control until anti-coagulated
  • pharmacological/electrical cardioversion
75
Q

Why must you anti-coagulate someone who has been in AF >48 hours

A

may have developed a blood clot in the atria and reverting them back to sinus rhythm carries a high risk of mobilising that clot and causing a stroke

76
Q

What are the first line pharmacological cardioversion medications

A
  • flecainide

- amiodarone - if structural heart disease

77
Q

What does electrical cardioversion involve

A
  • sedation/GA

- defibrillator

78
Q

How do you manage long term medical rhythm control

A
  • Beta blockers are first line for rhythm control
  • Dronedarone is second line for maintaining normal rhythm where patients have had successful cardioversion
  • Amiodarone is useful in patients with heart failure or left ventricular dysfunction
79
Q

How do you manage paroxsymal AF

A
  • Anti-coagulated based on Chad-Vasc

- Flecainide ‘pill in the pocket’ approach

80
Q

Who can use the ‘pill in the pocket’ approach for paroxysmal AF

A
  • Infrequent episodes
  • No structural heart disease
  • Able to identify when they are in AF

Cardiac (7 decks)

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