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Cardiovascular Medicine > Cardiac Arrythmias > Flashcards

Cardiac Arrythmias Flashcards

1
Q

From where do supraventricular tachycardias arise?

A

From the the atria or from the atrioventricular junction

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2
Q

What is the rate of sinus node discharge modulated by?

A

The autonomic nervous system

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3
Q

What does the parasympathetic system do to heart rate?

A

It decreases.

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4
Q

What part (or parts) of the nervous system lead to tachycardia?

A

Reduction of the parasympathetic system or increase in the sympathetic nervous system.

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5
Q

What are the components of the ‘Electrical System’ of the heart?

A

SA node, AV node, Bachmann’s Bundle, Bundle of His, L + R Bundles, Left posterior fascicle, Left Anterior Fascicle and Purkinje Fibres

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6
Q

What are the mechanisms of arrhythmogenesis?

A

1 - The Phase 4 slope is steeper or the threshold is reduced
2 - There can be another depolarisation after the initial one. this can be early (during phase 3) or delayed (after phase 3 is below the threshold)
3 - Scar tissue can cause depolarisation to move in rings causing re-entry or circus movements.

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7
Q

Bradycardia causes can be split into two categories, what are they?

A

Extrinsic and Intrinsic

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8
Q

What are the causes of extrinsic Bradycardias?

A

Hypothermia, hypothyroid, beta-blockers and Neurally Mediated Syndromes

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9
Q

What are the causes of intrinsic Bradycardias?

A

Acute Ischaemia of the SA node (from MI), Chronic degenerative fibrosis of the atrium (sick sinus syndrome)

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10
Q

Neurally mediated syndromes are due to a reflex called what?

A

Bezold-Jarisch

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11
Q

How to patients with with neurally mediated syndromes present?

A

Syncope and pre-syncope

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12
Q

What are the three neurally mediated syndromes? (Think about what happens)

A

Carotid Sinus Syndrome
Vasovagal Syncope
Postural orthostatic tachycardia syndrome (POTS)

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13
Q

How do we treat patients with bradycardia? (5)

A

If there an extrinsic cause this should be removed

Temporary pacemakers can be useful for reversible causes

If there is chronic SA nod disease a permanent pacemaker should be inserted

In patients with Brady-Tachy syndrome anti-coagulants should be used

Patients with vasovagal causes should avoid the stimulants or do a valsalva manoeuvre, beta-blockers can be considered

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14
Q

Where are heart blocks found and what are they called?

A

AV Node - AV Block
His Bundle - AV Block
Lower Bundles - Bundle branch block

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15
Q

What are the three forms of AV block?

A

1st degree, 2nd degree and 3rd degree (complete) AV block

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16
Q

What does 1st degree heart block mean?

A

That there is a delay of more than 0.22s in the PR interval

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17
Q

What are forms of 2nd degree heart block? (3)

A

Mobitz type I (wenckebach Phenomenon)
Mobitz type II
2:1 or 3:1 block

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18
Q

What Does Mobitz type I involve?

A

A progressively long PR interval followed by a dropped QRS complex

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19
Q

What does Mobitz type II involve?

A

A QRS complex is dropped with out a progressively prolonged PR interval

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20
Q

A Mobitz type I implies that the block is where?

A

The AV node

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21
Q

A Mobitz type II implies that the block is where?

A

The bundle of His

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22
Q

Which type of 2nd degree heart block is more likely to progress to complete heart block?

A

Mobitz type II

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23
Q

What is the leading cause of Mobitz type II?

A

Myocardial Infarction

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24
Q

How do the treatment strategies compare between Mobitz I + II

A

Mobitz I should be monitored and Mobitz II will require a pacemaker

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25
Q

How is life maintained during complete heart block?

A

With escape beats arising from the ventricles

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26
Q

In Complete heart block, what are the rhythms found in Narrow complex escape rhythm and broad complex escape rhythm?

A

Narrow complex - 50-60 bpm

Broad Complex - 15-40 bpm

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27
Q

How is Narrow complex complete heart block treated?

A

if it is acute then the underlying cause should be treated, temporary pacing or IV atropine can be useful
If it is chronic then permanent pacing should be used

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28
Q

What is atropine, how does it work and when is it used?

A

It is a competitive antagonist to acetyl choline. It therefor counters parasympathetic nervous stimulus. It is used to acutely raise heart rate

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29
Q

What are the causes of Complete Heart Block (6)

A

Congenital - Structural heart disease
Idiopathic Fibrosis - Lev’s Disease
Ischaemic Heart Disease
Non-ischaemic heart disease - calcific aortic stenosis, infiltrations (amyloidosis, sarcoidosis, neoplasia)
Cardiac Surgery - following valve replacement
Iatrogenic - Following ablation or pacemaker
Drug Induced - digoxin, beta blockers
Infections - endocarditis, Rheumatic heart disease,

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30
Q

In cardiology what is Lev’s Disease?

A

progressive fibrosis of the His-Purkije system in elderly patients

31
Q

How does Digoxin work and when is it used?

A

it is a cardiac glycoside which inhibits the the sodium potassium pump, this stops sodium calcium exchange and increases contractility. It is used in AF when no other medications are effective

32
Q

What is Bundle Branch Block?

A

A condition which stops the conduction below the level of His bundle inc left and right bundle and the anterior and posterior fascicles of the left bundle.

33
Q

What are the different variations of bundle branch Block? (4)

A

Bundle Branch conduction delay, complete bundle branch block, hemiblock and bifascicular block.

34
Q

What does bundle branch conduction delay show on an ECG?

A

Widening of the QRS complex up to 0.11s

35
Q

What width would the QRS complex but in complete bundle branch block?

A

> 0.12s

36
Q

What ECG pattern would a right bundle branch block show?

A

An rsR’ pattern in leads V1 and V2. The R’ wave is wide and late, this shows that the activation of the right ventricle is delayed.

37
Q

What ECG pattern would a left bundle branch block show?

A

In leads V1-V3 there will be a deep broad s wave, showing that there is early activation of the left ventricle (it is moving away from the right sided chest leads.

38
Q

What is Hemiblock?

A

A blockage of one of the branches of the left bundle branch (left anterior fascicle or the left posterior fascicle)

39
Q

What is the difference on ECG between left anterior and posterior division hemiblock?

A

Anterior will swing the axis to the left, posterior will swing it to the right. (QRS complexes are bigger on either the left or the right)

40
Q

What is Bifascicular block?

A

More than one bundle branch block

41
Q

Clinically, what would you find in a patient with bundle branch block? (signs and symptoms)

A

splitting of the second heart sound and syncope if there is intermittent complete block.

42
Q

What are the causes of right bundle branch block? (6)

A

Congenital, Cor pulmonale, PE, MI, conduction system fibrosis

43
Q

What are the causes of left bundle branch block? (3)

A

Aortic stenosis, Hypertension, MI

44
Q

What determines a sinus tachycardia on an ECG?

A

the presence of P waves

45
Q

What are the most common causes of inappropriate sinus tachycardia?

A

exercise, stress, pain, emotion, fever, hypovolaemia, hyperthyroid, catecholamine excess, anaemia

46
Q

what is the pathophysiology involved in Atrioventricular reciprocating tachycardia?

A

There is an abnormal communication between the atria and ventricles which occurs in utero, the atria contract before and after the ventricles have contracted

47
Q

What would be seen on an ECG in Atrioventricular reciprocating tachycardia?

A

Another P wave would be seen between the QRS and the T wave

48
Q

What are the most common accessory pathways in atrioventricular reciprocating tachycardia?

A

Kent Bundles

49
Q

If the p wave runs into the QRS complex and there is a history of palpitation what are these waves called and what is the name of the syndrome?

A

δ waves and it is called wolff-parkinson-white syndrome

50
Q

What is the main symptom in SVTs?

A

palpitations with sudden onset and termination, sometimes with caffeine or other stimulus

51
Q

Why might patients get polyuria with SVT?

A

Because of the release of atrial natriuretic peptide

52
Q

Might might patients get pulsating jugulars with SVT?

A

Because the atria are pumping against closed tricuspid and mitral valves.

53
Q

What is the difference between Atrioventricular Nodal Re-entry Tachycardia and Atrioventricular Reciprocating Tachycardia on an ECG?

A

In AVNRT there are no p waves

In AVRT the p waves can be part of the QRS (δ waves) or be after the QRS

54
Q

What is the immediate treatment of a patient with an SVT who is haemodynamically unstable?

A

DC cardioversion

55
Q

What is the immediate treatment of a patient with an SVT who is haemodynamically stable?

A

Emersion of face in cold water, Valsalva manoeuvre, carotid massage, if these do not work then 6mg of adenosine may be used

56
Q

What are the side effects of adenosine?

A 
Bronchospasm
Flushing
chest pain 
heaviness of the limbs
sense of impending doom
57
Q

What are the options for long term management of SVT?

A

Ablation, verapamil, Beta-blockers.

Amiodarone may also be used

58
Q

What underlying pathologies of the atria lead to atrial fibrillation?

A

raised atrial pressure, increased atrial muscle mass, fibrosis and inflammation

59
Q

What are the ‘classic’ causes of AF? (3)

A

Thyrotoxicosis, Rheumatic heart disease and Alcohol intoxication

60
Q

What are the most common causes of AF?

A

Congestive Heart failure and Hypertension

61
Q

What will an AF ECG show?

A

apparently random QRS complexes, f waves, no correlation between p waves and QRS complexes, sinus rhythm of 300-600 bpm

62
Q

What are the options for immediate treatment of AF?

A

treat the underlying cause (Throid, Chest infection, Alcohol), Cardioversion, IV infusion of anti-arrhythimic drug

63
Q

What should be considered before choosing treatment in AF? (3)

A

How well is AF tolerated?
Is anticoagulation required before cardioversion?
Will this patient resolve on their own? (has it happened before, is it a reversible cause?)

64
Q

How are patients anti-coagulated for DC cardioversion?

A

with warfarin before and after treatment. Transoesophageal echo maybe be used to check for clots, if there are none then no warfarin needed

65
Q

What are the two strategies for long term management of AF?

A 
rate control
rhythm control (both with warfarin)
66
Q

What drugs are used in rate control?

A

Digoxin, Calcium-channel blockers and beta-blockers

67
Q

What Calcium channel blocker may be used as an alternative to verapamil?

A

diltiazem

68
Q

What is the target INR for patients with AF?

A

between 2.0 and 3.0

69
Q

What drugs are used to anti-coagulate patients?

A

warfarin and rivaroxaban

70
Q

What is the CHA2DS2-VASc score?

A

Congestive heart failure, Hypertension, Age (65-74), Diabetes Mellitus, Stroke, Vascular disease, Age (again), Sex.

Anticoagulation is recommended in patients with a score of ≥2

71
Q

How should patients be treated who have sustained VT and haemodynamic comprimise?

A

DC cardioversion

72
Q

How should patients be treated who have sustained VT and no haemodynamic comprimise?

A

IV Lidocaine is first line (100mg over 5 minutes)
followed by lidocaine infusion of 4mg/min
Amiodarone 5mg/kg should be given for an hour. Cardioversion if this fails

73
Q

What is Brugada Syndrome?

A

Inherited idiopathic VF

74
Q

How does Brugada look on ECG?

A

ST segment elevation with apparent right bundle branch block

Cardiovascular Medicine (9 decks)

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