Arrythmias Flashcards

1
Q

What is the definiton of an arrythmia?

A

(AKA, dysrhythmia) is a disturbance of the normal rhythmic beating of the heart;

  • Usually due to an ectopic pacemaker.
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2
Q

Symptoms depend on the nature of an arrythmia, but what are the common symptoms?

A
  • palpitations;
    • (conscious sensation of pounding heart),
  • breathlessness,
  • dizziness, faintness,
  • syncope;
    • (unconsciousness).
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3
Q

What are the four main types of arrythmias?

(there are more)

A
  • Complete heart block,
  • Atrial fibrillation,
  • Ventricular fibrillation,
  • Ventricular tachycardia.
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4
Q

What are the components of the heart’s conducting system?

A
  • SA node initiates the impulse to the…
  • AV node
  • Then through the bundle branches to the…
  • Ventricles
  • Then Purkinje fibres to the…
  • Myocardium.
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5
Q

What current is the Phase 4 depolarisation casued by?

A

The funny current (If)

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6
Q

Where are If channels found in the heart?

What does this allow the area to do?

A

Found everywhere in the conduction system but are found at a higher concentration in the SA node.

This allows the whole of the conducting system to potentially be a pacemaker.

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7
Q

What are the three ways to classify an arrythmia?

(and sub classifiactions below them?)

A

By rate:

  • Inappropriate bradyarrhythmia (<60 bpm),
  • Inappropriate tachyarrhythmia (>100 bpm).

By location:

  • Supraventricular (atrial or AV nodal origin),
  • Ventricular (ventricular origin).

By cause:

  • Disorders of impulse generation,
  • Disorders of impulse conduction.
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8
Q

What causes brady/tachycardias?

A

Bradycardias (<60);

  • SA node (SAN) slows down,

or

  • Impulse from SA node is blocked, slower distal pacemaker takes over.

Tachycardias (>100);

  • Disorders of impulse generation,
  • Disorders of impulse conduction;
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9
Q

What is Complete (3rd degree) Heart Block?

And how can it be caused?

A

The blocked electrical connection between atria and ventricles.

Causes:

  • Idiopathic bundle branch fibrosis,
    • BBs become fibroses and cannot conduct.
  • Atherosclerotic coronary heart disease,
    • Causes ischemia to the conduction system.
  • Dilated cardiomyopathy.
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10
Q

How does complete heart block affect HR?

A

Heartbeat slows, degree of slowing depends on location of block.

  • Further along the conduction system, slower the beat.

Heart rhythm driven by ‘escape beats’ originating from distal pacemaker just below the block.

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11
Q

What are symptoms of a complete heart block?

A

Temporary syncope (stop), followed by recovery.

Breathlessness, fatigue and possible chest pain (especially with effort).

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12
Q

When is a complete heart block more likely to result in death?

A

Risk depends on the location of block;

More distal block → slower rhythm → greater risk of asystole (heart stopping).

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13
Q

Complete heart block treatment?

A

Pacemaker.

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14
Q

What does a complete heart block ECG look like?

A

QRS complex becomes dissociated from the P wave as the atria and ventricles beat independently.

Called atrioventricular dissociation.

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15
Q

What is tachyarrythmia majorly casued by?

A

Re-entry.

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16
Q

What is Re-entry?

(how can it present?)

A
  • When the impulse is delayed or ‘trapped’ in one region of the heart.
  • Meanwhile, the adjacent tissue finishes depolarising and is no longer refractory.

The delayed impulse then re-enters the adjacent tissue and then spreads throughout the heart.

  • So, two beats for every beat.

Presents:

  • once, creating a premature beat,
  • indefinitely, generating a sustained tachycardia.
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17
Q

How can you stop re-entry?

A
  1. Convert unidirectoinal block to bidirectional block by supressing conduction.
  2. Prolong the refractory period so the retrograde impulse cannot re-enter the conducting myocardium.
18
Q

Whats the difference between anatomical and functional re-entry?

A

Anatomical re-entry:

  • When the process of re-entry occurs along a conducting pathway with a non-excitable core.
    • Around which the impulse can cycle.
  • Has zones of differential conductivity.

Functional re-entry:

  • No defined anatomical pathway.
  • Typically occurs during or after an MI,
    • When cardiac conduction is slowed in some regions of the heart and therefore becomes spatially heterogeneous.
19
Q

What is atrial fibrillation?

A

Chaotic atrial rhythm with rapid and ‘irregularly irregular’ ventricular rhythm.

20
Q

What causes atrial fibrillation?

(and some associated risk factors)

A

Cause:

  • Most often an ectopic focus (pacemaker) located in the cardiac muscle layer.

Risk Factors:

  • Atrial dilatation during heart failure, hypertension, excessive alcohol intake, old age.
21
Q

Typical progression of Afib?

A

Paroxysmal (occasional) → persistentpermanent.

  • This is associated with progressive electrical and structural remodelling of the atria.
  • Creates more rotors and fibrillation until eventually it becomes permanent.
22
Q

Afib is a major risk factor for another cardiovascular issue. What is it?

A

Stroke.

Increases chance of a stroke by x5!

  • Lack of atrial beat causes stasis of blood, and thrombi can form and then embolise to the cerebral circulation.
23
Q

What does the Afib ECG look like?

A

Lack of P waves due to chaotic atrial electrical activity.

  • The small bumps you see are actually t-waves.

Baseline shows small fibrillatory (‘f’) waves of varying amplitude.

  • These are not large enough to cause full depolarisation.
  • Occasionally, an f wave is large enough to trigger the QRS complex.

Eventually over time, ‘f’ waves become smaller and QRS complexes occur less frequently, so HR slows down.

24
Q

There are four classes of antiarrythmic drugs - Class 1-4.

What is Class 1?

A

Na+ channel blockers;

  • suppress conduction.
    e. g. Flecainide.
25
Q

There are four classes of antiarrythmic drugs - Class 1-4.

What is Class 2?

A

β receptor blockers;

  • Reduce excitability, inhibit AVN conduction.
    e. g. bisoprolol.
26
Q

There are four classes of antiarrythmic drugs - Class 1-4.

What is Class 3?

A

K+ channel blockers;

  • Drugs which prolong the AP and refractory period.
    e. g. amiodarone.
27
Q

There are four classes of antiarrythmic drugs - Class 1-4.

What is Class 4?

A

Ca2+ channel blockers;

  • Inhibit AVN conduction.
    e. g. verapamil.
28
Q

What are the two pharmalogical strategies for Afib?

A

Rate control and Rhythm control.

Rate control - Reduce proportion of impulses conducted thru the AV node.

  • Class 2 and class 4.

Rhythm control - Target the source of the arrhythmia by blocking the re-entrant pathway.

  • Class 1 and class 3.
29
Q

What type of drug must always be given in the treatment of Afib?

What does it prevent?

A

Anti-coagulant therapy.

To prevent stroke.

30
Q

What are a couple of non-parmacological ways to treat Afib?

A

Ablation and cryoablation.

Ablation -

  • Transvenous catheter is placed against the endocardium, and the tip is heated.
  • Causing a lesion ~1 cm wide.

Cryoblation -

  • Same thing as ablation but the tip is super-cooled.
  • Used if the site is very close to the AV node or conduction system (i.e. safer).
    *
31
Q

What is Ventricular Tachycardia?

A

A run of rapid (typically 120-200 bpm) successive ventricular beats.

Caused by an ectopic site in one of the ventricles.

32
Q

What causes the ectopic sites that result in Ventricular Tachycardia?

A

Varied, but most often due to cardiac scarring after MI or dilated cardiomyopathy.

Can be congenital (e.g. Brugada syndrome, LQT syndrome), or caused by some anti-arrhythmic drugs(!).

Almost always due to re-entry.

33
Q

Prognosis for Ventricular tachycardia?

A

Varied, depends on the cause.

If persistent, may compromise cardiac pumping, leading to heart failure and death.

Can deteriorate into ventricular fibrillation = sudden death.

34
Q

The ECG in ventricular tachycardia.

A

Broad complex rapid rhythm.

Complexes can be of regular (monomorphic) or varied shape (polymorphic).

35
Q

Why is the ECG broad in Ventricular Tachycardia?

A

The wave of conduction (from the ectopic site) is travelling through the cardiac muscle not the conducting system and so is a lot slower.

36
Q

Pharmacological anti-arrhythmic strategies for VT.

A

Inhibit conduction in the conduction system or cardiac muscle or increase the refractory period.

  • Class 1 or Class 3.

Reduce excitability.

  • Class 2.

These therapies are not particularly effective!!

37
Q

What is a non-parmacological way to treat Ventricular arrythmia?

A

Implantable defibrillators.

An implanted generator is connected to electrodes in the right ventricle and the superior vena cava.

The generator can sense and differentiate arrhythmias, and delivers an appropriate shock or shock sequence, causing cardioversion.

38
Q

What is Ventricular fibrillation?

A

Chaotic and disorganised electrical activity of the heart.

There is no organised ventricular beat so no cardiac output.

39
Q

What causes Vfib?

A

Usually MI, ischaemic heart disease, cardiomyopathy, but can be idiopathic.

40
Q

Ventricular fibrillation prognosis?

A

Unconsciousness within seconds, death occurs rapidly.

41
Q

What does the ECG of Ventricular fibrillation look like?

A

Disorganised electrical activity which fades as the heart dies.

42
Q

What is the treatment for Ventricular fibrillation?

How does it work?

What should it also be combined with?

A

Defibrillation.

  • Applied at onset of QRS complex (if present).
  • Stops the heart, allows the SAN to reassert itself.

Should be combined with cardiopulmonary resuscitation.