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Medicine 1 - Clinical > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

What are arrhythmias?

A

Abnormal heart rhythm due to an interruption to the normal electrical signals that coordinate the contraction of the heart muscle

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2
Q

What are the four cardiac arrest rhythms?

A

These are the four possible rhythms that you will see in a pulseless unresponsive patient.

They can be shockable or non-shockable (tells us if defibrillation will be effective or not)

Shockable rhythms:

Ventricular tachycardia
Ventricular fibrillation

Non-shockable rhythms:

Pulseless electrical activity (all electrical activity except VF/VT, including sinus rhythm without a pulse)
Asystole (no significant electrical activity)

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3
Q

Tachycardia treatment in an unstable patient

A

Consider up to 3 synchronised shocks
Consider an amiodarone infusion

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4
Q

Tachycardia treatment in a stable patient with a narrow complex (QRS < 0.125)

A

Atrial fibrillation – rate control with a beta blocker or diltiazem (calcium channel blocker)
Atrial flutter – control rate with a beta blocker
Supraventricular tachycardias – treat with vagal manoeuvres and adenosine

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5
Q

Tachycardia treatment in a stable patient with a broad complex (QRS > 0.125)

A

Ventricular tachycardia or unclear – amiodarone infusion
If known SVT with bundle branch block treat as normal SVT
If irregular may be AF variation – seek expert help

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6
Q

What causes atrial flutter?

A

Anaberrant macro-circuit within the right atrium which cycles at 300bpm.

This circuit activates the AV node but because this node has a relatively long refractory period it is not able to conduct impulses down the His-Purkinje system at such a fast rate.

Instead the there is a degree of block meaning that only 2:1, 3:1, 4:1 or rarely 5:1 atrial impulses is conducted to the ventricle.

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7
Q

What is atrial flutter?

A

Atrial flutter is a type of heart rhythm disorder in which the heart’s upper chambers (atria) beat too quickly

The atria beat regularly, but faster than usual and more often than the ventricles

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8
Q

How does atrial flutter look on an ECG?

A

Regular rhythm

Saw-tooth baseline with repetition at 300bpm (these are atrial flutter waves)

Narrow QRS complexes

Ventricular rate which depends on the level of AV block:
150bpm if 2:1
100bpm if 3:1
75bpm if 4:1
60bpm if 5:1

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9
Q

What can cause atrial flutter?

A

Causes are similar to atrial fibrillation (AF) but are more likely to occur with pulmonary disease such as:

COPD
Obstructive sleep apnoea
Pulmonary emboli
Pulmonary hypertension

Other causes include:

Ischaemic heart disease
Sepsis
Alcohol
Cardiomyopathy
Thyrotoxicosis

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10
Q

Symptoms of atrial flutter

A

Asymptomatic
Palpitations
Dizziness
Chest pain

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11
Q

Management of atrial flutter

A

Same as atrial fib.

Rate/rhythm control with beta blockers or cardioversion
Treat the reversible underlying condition (e.g. hypertension or thyrotoxicosis)
Radiofrequency ablation of the re-entrant rhythm
Anticoagulation based on CHA2DS2VASc score

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12
Q

What treatment is given to patients with atrial flutter who are haemodynamically unstable?

A

Emergency direct current synchronised cardioversion should be administered.

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13
Q

What are signs of haemodynamic instability in patients with atrial flutter?

A

Shock (suggests end organ hypoperfusion)
Syncope (evidence of brain hypoperfusion)
Chest pain (evidence of myocardial ischaemia)
Pulmonary oedema (evidence of heart failure)

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14
Q

Is electrical or pharmacological cardioversion more effective in atrial flutter?

A

Electrical cardioversion is more effective than pharmacological cardioversion (success rate of 95% v 40-70%)

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15
Q

What is atrial fibrillation?

A

Uncoordinated atrial contraction, typically at approximately 300-600 beats per minute.

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16
Q

What is the difference between atrial flutter and atrial fibrillation?

A

In atrial fibrillation, the atria beat irregularly.

In atrial flutter, the atria beat regularly, but faster than usual and more often than the ventricles, so you may have four atrial beats to every one ventricular beat

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17
Q

What are cardiac causes of atrial fibrillation?

A

Ischaemic heart disease (most common cause in UK)

Hypertension

Rheumatic heart disease (typically affecting the mitral valve) (most common cause in less developed countries)

Peri-/myocarditis

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18
Q

What are non-cardiac causes of atrial fibrillation?

A

Dehydration

Endocrine causes (such as hyperthyroidism)

Infective causes (such as sepsis)

Pulmonary causes (such as pneumonia or pulmonary embolism)

Environmental toxins (such as alcohol abuse)

Electrolyte disturbances (such as hypokalaemia, hypomagnesaemia)

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19
Q

What are the four ways atrial fibrillation can be classified?

A

Acute (lasts <48 hours)
Paroxysmal (lasts <7 days and is intermittent)
Persistent (lasts >7 days but is amenable to cardioversion)
Permanent (lasts >7 days and is not amenable to cardioversion)

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20
Q

What are the symptoms of atrial fibrillation?

A

Palpitations
Chest pain
Shortness of breath
Dizziness

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21
Q

What are signs of atrial fibrillation?

A

An irregularly irregular pulse rate with a variable volume pulse.

A single waveform on the jugular venous pressure (due to loss of the a wave - this normally represents atrial contraction).

An apical to radial pulse deficit (as not all atrial impulses are mechanically conducted to the ventricles).

On auscultation there may be a variable intensity first heart sound.

Features suggestive of the underlying cause (e.g. hyperthyroidism, alcohol excess,sepsis)

Features suggestive of complications resulting from the AF (e.g. heart failure).

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22
Q

What is considered fast atrial fibrillation?

A

When ventricular rate is >100bpm it is considered to be fast AF which normally warrants some level of immediate treatment.

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23
Q

Management in fast atrial fibrillation

A

Always start by assessing the patient using an ABCDE approach

Assess for haemodynamic stability
Shock (suggests end organ hypoperfusion)
Syncope (evidence of brain hypoperfusion)
Chest pain (evidence of myocardial ischaemia)
Pulmonary oedema (evidence of heart failure)
If the patient is unstable then they should have immediate DC cardioversion

Consider reversible causes
Infection: Give antibiotics and fluids
Dehydration: Give fluids
Replace abnormal electrolytes

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24
Q

What is the first line treatment in those who have atrial fibrillation?

A

Offer rate control as the first-line strategy to people with AF, except in people:

Whose AF has a reversible cause.
Who have heart failure thought to be primarily caused by AF.
With new-onset AF.
For whom a rhythm control strategy would be more suitable based on clinical judgement.

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25
Q

What should be given for rate control in atrial fibrillation?

A

A beta-blocker such as bisoprolol or a rate limiting calcium-channel blocker (e.g. Dilitiazem) should be the initial monotherapy

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26
Q

What is the most commonly used beta blocker in atrial fibrillation?

A

Bisoprolol

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27
Q

Why can beta blockers not be used for atrial fibrillation treatment in those who have hypotension?

A

Drop blood pressure

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28
Q

What calcium channel blockers can be given for atrial fibrillation and why can they not be used frequently?

A

Diltiazem or verapamil

They are negatively ionotropic therefore it is contraindicated in heart failure

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29
Q

What medicine is used for atrial fibrillation treatment in patients who are hypotensive or have co-existent heart failure?

A

Digoxin

Should be avoided in younger patients because it increases cardiac mortality.

Often used second-line in conjunction with beta-blockers if fast AF remains refractory.

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30
Q

How can rhythm in atrial fibrillation be controlled?

A

Rhythm control can be achieved via two methods:

Electrical cardioversion
Pharmacological cardioversion

Note that patients in chronic AF or those who have failed cardioversion before are unlikely to be successfully cardioverted so this would not be considered in most of these cases.

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31
Q

Management of new Atrial fibrillation with onset less than 48 hours

A

DC cardioverted with sedation

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32
Q

Management of Atrial fibrillation with onset >48 hours with DC cardioversion

A

If the AF is >48 hours (or onset is uncertain) then the patient must be anticoagulated for at least 3 weeks before DC cardioversion can be done.

Alternatively the patient can have a transoesophageal ECHO to rule out a thrombus in the left atrial appendage before cardioversion.

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33
Q

Discuss the use of Flecainide in the treatment of atrial fibrillation

A

Can be either given regularly or as a “pill in the pocket” when symptoms come on.

Is preferred in young patients who have structurally normal hearts because it can induce fatal arrhythmias in structurally abnormal hearts.

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34
Q

Discuss the use of Amiodarone in the treatment of atrial fibrillation

A

Extremely effective drug in controlling both rate and rhythm.

However it comes with a massive list of significant side-effects so should normally only be given to older, sedentary patients.

35
Q

Discuss the use of Sotalol in the treatment of atrial fibrillation

A

This is a beta blocker with additional K channel blocker action

Used for those that don’t meet the demographics for either flecainide or amiodarone.

36
Q

Why should the need for long term anticoagulation be considered in atrial fibrillation?

A

The need for long term anticoagulation should also be considered as the main complication of AF is embolic stroke.

37
Q

What is used to estimate the risk of stroke in patients with atrial flutter?

A

CHADS2VASc

38
Q

How is the CHADS2VASc score used?

A

C: 1 point for congestive cardiac failure.
H: 1 point for hypertension.
A2: 2 points if the patient is aged 75 or over.
D: 1 point if the patient has diabetes mellitus.
S2: 2 points if the patient has previously had a stroke or transient ischaemic attack (TIA).
V: 1 point if the patient has known vascular disease.
A: 1 point if the patient is aged 65-74.
Sc: 1 point if the patient is female.

39
Q

How is the CHADS2VASc score interpreted?

A

The minimum score is 0 (associated with 0% annual stroke risk) and maximum score is 9 (15 annual risk)

Males who score 1 or more or females who score 2 or more should be anticoagulated.

0: no anticoagulation
1: consider anticoagulation
>1: offer anticoagulation

40
Q

What are HASBLED and ORBIT used for?

A

Stratifies bleeding risk of anticoagulation

41
Q

How is the HASBLED score used?

A

H: Hypertension 1 point
A: Abnormal renal or liver function 2 points if both are present
S: Stroke (previous) 1 point
B: Major bleed (previous) 1 point
L: Labile INR 1 point
E: Elderly (>65) 1 point
D: Drugs/alcohol 1 point for drug or alcohol use (2 points if both are present)

42
Q

What does the ORBIT tool screen?

A

Low haemoglobin or haematocrit
Age (75 or above)
Previous bleeding (gastrointestinal or intracranial)
Renal function (GFR less than 60)
Antiplatelet medications

43
Q

What are the two different diagno

A

Atrial fibrillation
Ventricular ectopics

Can be differentiated with an ECG

44
Q

MRS SMITH causes for atrial fibrillation?

A

Sepsis
Mitral Valve Pathology (stenosis or regurgitation)
Ischemic Heart Disease
Thyrotoxicosis
Hypertension

45
Q

What is valvular and non-valvular AF?

A

Valvular AF is defined as patients with AF who also have moderate or severe mitral stenosis or a mechanical heart valve.

AF without valve pathology or with other valve pathology such as mitral regurgitation or aortic stenosis is classed as non-valvular AF.

46
Q

Summarise option for rate control in atrial fibrillation

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)

47
Q

Who is rhythm control offered to? AF

A

There is a reversible cause for their AF
Their AF is of new onset (<48 hours)
Their AF is causing heart failure
They remain symptomatic despite being effectively rate controlled

48
Q

What is the aim of rhythm control and how can it be achieved?

A

Return the patient to normal sinus rhythm.

This can be achieved through a single “cardioversion” event that puts the patient back in to sinus rhythm or long term medical rhythm control that sustains a normal rhythm.

49
Q

When would you use immediate cardioversion vsdelayed cardioversion?

A

Immediate cardioversion if the AF has been present for less than 48 hours or they are severely haemodynamically unstable.

Delayed cardioversion if the AF has been present for more than 48 hours and they are stable.

50
Q

What are the options for pharmacological cardioversion in AF?

A

NICE guidelines (2014) say for pharmacological cardioversion first line is:

Flecanide
Amiodarone (the drug of choice in patients with structural heart disease)

51
Q

What is Paroxysmal Atrial Fibrillation?

A

Comes and goes in episodes, usually not lasting more than 48 hours.

Flecanide is the usual treatment for a “pill in the pocket” approach.

52
Q

What is Wolff-Parkinson White Syndrome?

A

Extra electrical pathway connecting the atria and ventricles

53
Q

What happens in WPWS?

A

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.

54
Q

What is the definitive treatment for Wolff-Parkinson White syndrome?

A

Radiofrequency ablation of the accessory pathway.

55
Q

ECG changes in WPWS?

A

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

56
Q

What can happen if someone presents with a combination of AF and WPW?

A

Risk that the chaotic atrial electrical activity can pass through the accessory pathway into the ventricles causing a polymorphic wide complex tachycardia.

Most antiarrhythmic medications (beta blockers, calcium channel blockers, adenosine etc) increase the risk by reducing conduction through the AV node and promoting conduction through the accessory pathway – therefore they are contraindicated in patients with WPW that develop atrial fibrillation or flutter.

57
Q

How is RFA carried out for WPW?

A

Insert a tube (catheter) into a vein through a small cut near the groin up to the heart area.

When the tip reaches the heart, the small area that is causing the fast heart rate is destroyed using a special type of energy called radiofrequency or by freezing it (cryoablation).

58
Q

What are clinical signs of WPW?

A

No symptoms - WPW is often asymptomatic
Palpitations
Dizziness
Syncope

59
Q

Management of WPW in unstable patients

A

Unstable patients (blood pressure <90/60mmHg or with signs of systemic hypoperfusion or fast atrial fibrillation) require urgent direct current (DC) cardioversion.

60
Q

What causes Supraventricular tachycardia (SVT)?

A

Electrical signal re-entering the atria from the ventricles.

61
Q

What exactly happens with electrical signals in SVT?

A

Normally the electrical signal in the heart can only go from the atria to the ventricles. In SVT the electrical signal finds a way from the ventricles back into the atria. Once the signal is back in the atria it travels back through the AV node and causes another ventricular contraction

62
Q

What does SVT look like on an ECG?

A

There is fast narrow complex tachycardia (QRS < 0.12).

It looks like a QRS complex followed immediately by a T wave, QRS complex, T wave and so on.

63
Q

What is Paroxysmal SVT?

A

SVT reoccurs and remits in the same patient over time

64
Q

What are the three main types of SVT - based on the source of electrical signal?

A

“Atrioventricular nodal re-entrant tachycardia” is when the re-entry point is back through the AV node.

“Atrioventricular re-entrant tachycardia” is when the re-entry point is an accessory pathway (Wolff-Parkinson-White syndrome).

“Atrial tachycardia” is where the electrical signal originates in the atria somewhere other than the sinoatrial node. This is not caused by a signal re-entering from the ventricles but instead from abnormally generated electrical activity in the atria. This ectopic electrical activity causes an atrial rate of >100bpm.

65
Q

What approach should you take when managing stable patients with SVT?

A

Stepwise approach trying each step to see whether it works before moving on.

Make sure they are on continuous ECG monitoring.

66
Q

Acute management of stable patients with SVT - step wise

A

Valsalva manoeuvre. Ask the patient to blow hard against resistance, for example into a plastic syringe.

Carotid sinus massage. Massage the carotid on one side gently with two fingers.

Adenosine

An alternative to adenosine is verapamil (calcium channel blocker)

Direct current cardioversion may be required if the above treatment fails

67
Q

How does adenosine work?

A

By slowing cardiac conduction primarily though the AV node. It interrupts the AV node / accessory pathway during SVT and “resets” it back to sinus rhythm

68
Q

Key points about 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 (e.g. grey cannula in the antecubital fossa)

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

69
Q

What is the long term management of paroxysmal SVT?

A

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

70
Q

What is first degree heart block?

A

Occurs where there is delayed atrioventricular conduction through the AV node.

Despite this, every atrial impulse leads to a ventricular contraction, meaning 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).

71
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.

72
Q

What are the types of second degree heart block?

A

Wenckebach’s phenomenon (Mobitz Type 1)
Mobitz Type 2
2:1 Block
Third Degree Heart Block

73
Q

What causes first degree heartblock?

A

High vagal tone (e.g. athletes)
Acute inferior MI
Electrolyte abnormalities (e.g. hyperkalaemia)
Drugs: NHP-CCBs, beta-blockers, digoxin, cholinesterase inhibitors

74
Q

What is the management of first degree heart block?

A

First degree heart block itself is benign and does not need treating. However, any pathological underlying cause should be reversed.

75
Q

Causes of Mobitz Type I

A

MI (mainly inferior)
Drugs such as beta/calcium channel blockers, digoxin
Professional athletes due to high vagal tone
Myocarditis
Cardiac surgery

76
Q

Causes of Mobitz Type II

A

Infarction: particularly anterior MI which damages the bundle branches

Surgery: mitral valve repair or septal ablation

Inflammatory/autoimmune: rheumatic heart disease, SLE, systemic sclerosis, myocarditis

Fibrosis: Lenegre’s disease

Infiltration: sarcoidosis, haemochromatosis, amyloidosis

Medication: beta-blockers, calcium channel blockers, Digoxin, amiodarone

77
Q

Mobitz Type I treatment

A

It is generally asymptomatic and does not require any specific management as the risk of high AV block/ complete heart block is low.

If symptoms do arise, ECG monitoring may be required, exclude precipitating drugs and if bradycardic may require atropine.

78
Q

What is Mobitz Type I?

A

Wenckebach phenomenon or Mobitz type I is a type of second degree heart block that is usually due to reversible conduction block at the AV node.

It is characterised by progressive lengthening of the PR interval which results in a P wave that fails to conduct a QRS.

79
Q

What is Mobitz Type II?

A

Mobitz type II block is a type of second degree AV block where there are intermittent non-conducted P waves.

The PR interval is constant and there may no pattern or fixed ratios such as 2:1 or 3:1 block.

In most cases there is a broad QRS indicating a distal block in the His-Purkinje system and many patients have pre-existing left bundle branch block/ bifascicular block.

80
Q

What causes Mobitz Type II?

A

Conduction system failure, especially at the His-Purkinje system

81
Q

How is Mobitz Type II managed?

A

Permanent pacemaker as these patients are at risk of risk of complete heart block and becoming haemodynamically unstable

82
Q

What is complete (third) heart block?

A

Atrial impulses fail to be conducted to the ventricles.

Sufficient cardiac output may be secondary to a ventricular or junctional escape rhythm.

83
Q

What are clinical features of third degree heart block?

A

Patients may present with syncope or cardiac arrest.

ECG shows severe bradycardia and dissociation between the P waves and the QRS complexes.

84
Q

What can cause third degree heart block?

A

Myocardial infarction (especially inferior)
Drugs acting at the AV node (beta blockers, calcium channel blockers)
Idiopathic fibrosis.

Medicine 1 - Clinical (41 decks)

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