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Supporting life block > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

Define arrhythmia

A
  • aka dysrhythmia

- A disturbance of the normal rhythmic beating of the heart-usually due to an ectopic pacemaker

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2
Q

What are the symptoms of arrhythmia?

A
  • Palpitations
  • breathlessness
  • dizziness, faintness,syncope
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3
Q

Where is the pacemaker of the heart?

A
  • SAN

- The entire conduction system is a latent pacemaker i.e in uncertain conditions it can take over from the SAN

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4
Q

What is the funny current

A

I(f)

  • pacemaker current
  • Most heavily expressed in the SAN
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5
Q

How can we classify arrhythmias?

A
  1. ) By rate:
    - Inappropriate bradyarrhythmia (<60bpm)
    - Inappropriate tachyarrhythmia (>100bpm)
  2. ) By location:
    - supraventricular (atrial or AV nodal origin)
    - Ventricular( ventricular origin)-more severe
  3. ) By cause:
    - disorders of impulse generation
    - disorders of impulse conduction
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6
Q

What are the causes of arrhthmias?

A

Bradycardias:
-SAN slows down
-impulse from SAN is blocked, slower distal pacemaker takes over
Tachycardias:
-Disorders of impulse generation
-Disorders of impulse conduction-re-entry

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7
Q

What is complete(3rd degree) heart block?

A
  • Definition: blocked electrical connection between atria& ventricles
  • Causes: various e.g idiopathic bundle branch fibrosis, atherosclerotic coronary heart disease, dilated cardiomyopathy
  • Effect on cardiac rhythm: Heart beat is slow, degree of slowing depends on location of block. Heart rhythm driven by ‘escape beats’ originating from distal pacemaker just below the block
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8
Q

What are the symptoms of complete heart block?

A

-Temporary syncope as heart stops, followed by recovery , with breathlessness, fatigue & chest pain especially with effort

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9
Q

What is the treatment for complete heart block?

A
  • Implantation of a permanent pacemaker to generate the cardiac rhythm unless risk is low of block is likely to be temporary.
  • If risk of asytole is high, may need immediate temporary pacemaker
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10
Q

Outline the role of latent pacemakers in conduction

A
  • All parts of the conduction system are potential or latent pacemakers because they have the ion channels required for phase 4 depolarisation
  • This intrinsic automaticity normally remains latent because of overdrive suppression by the SAN ( the fastest pacemaker dominates)
  • If the conduction system is blocked between the atria& ventricles the heart will generally continue to beat, but more slowly. The region of the pacemaker just distal to the block will take over from the SAN
  • It paces the heart more slowly since its rate of intrinsic depolarisation is slower than that of the SAN
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11
Q

What happens to the ECG in 3rd degree heart block

A
  • 3rd degree heart block= complete heart block
  • The QRS complex becomes dissociated from the P wave as the atria & ventricles beat independently= atrioventricular dissociation
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12
Q

What are tachyarrhythmias?

A

Rapid heart rate generally caused by re-entry
-This is 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. This can occur once, creating a premature beat, or indefinitely, generating a sustained tachycardia
-Can occur wherever adjacent areas of the myocardium have different conduction rates& refractoriness ( can be caused by ischaemia, myocardial scarring, certain congenital conditions). Often triggered by premature impulses arising from triggered automaticity
Basic requirements for re-entry
1.) A conducting pathway with a non-excitable core around which the impulse can cycle
2.) Zones of differential conductivity or refractoriness within the path

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13
Q

How can we stop re-entry to prevent arrhytmia?

A
  1. ) Convert unidirectional block to bidirectional block by suppressing conduction
  2. ) Prolong the refractory period so the retrograde impulse cannot re-enter conducting myocardium
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14
Q

What is functional re-entry?

A
  • Re-entry can also occur without a defined anatomical pathway
  • This typically occurs during/after an MI, when cardiac conduction is slowed in some regions of the heart and therefore becomes spatially heterogenous
  • Interaction of waves of depolarisation with obstacles or zones of impaired conduction is thought to lead to breaking up the waves and formation of spiral waves of excitation: rotors
  • These may give rise to a chaotic electrical activity of the myocardium leading to fibrillation
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15
Q

What complication can triggered automacity bring?

A

-Can initiate re-entry

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16
Q

What causes delayed after depolarisations( DADs)?

A

-excessive increases in calcium ion concentration due to e.g catecholamines, digoxin

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17
Q

What causes early after depolarisations (EADs)?

A

-Stimuli that increase the calcium ion current or AP duration e.g hypoxia, catecholamines, sotalol( an anti-arrhythmic)

18
Q

Define atrial fibrillation

A

chaotic atrial rhythm with rapid and ‘irregularly irregular’ ventricular rhythm
-It is a major risk factor for stroke because a lack of atrial beat causes stasis of blood, and thrombi can form esp in LA appendage& then embolise to the cerebral circulation

19
Q

What causes atrial fibrillation

A

Most often an ectopic focus located in the cardiac muscle layer surrounding a pulmonary vein
-Risk factors: atrial dilatation, old age, heart failure, hypertension, excessive alcohol intake

20
Q

What is the effect of AF on the cardiac rhythm ?

A
  • No organised atrial beating due to chaotic electrical activity
  • ventricular excitation occurs when atrial depolarisations are sufficient to be conducted through the AVN
21
Q

What are the symptoms of AF?

A
  • palpitations
  • breathlessness
  • dizziness
  • syncope
22
Q

Describe the prognosis of AF

A
  • Typically progression is PAROXYSMAL—> PERSISTENT—->PERMANENT
  • This is associated with progressive electrical & structural remodelling of the atria which promotes more complex & refractory forms of re-entry
23
Q

How can AF be treated?

A
  • Class 1-4 anti-arrhytmic
  • Radiocatheter ablation
  • maze procedure
  • Anti-coagulants or LA appendage closure
24
Q

What happens to the ECG in AF?

A
  • Lack of p waves due to chaotic atrial electrical activity
  • Baseline shows small fibrillatory(‘f’) waves of varying amplitude
  • ‘Irregularly irregular’ high frequency QRS complexes cause fast irregular tachycardia (>150bpm)
25
Q

What does the term ‘irregularly irregular’ mean in terms of rhythm

A

-No clear pattern can be seen

26
Q

Describe the Vaughan Williams& Singh anti-arrhytmic drug classification system

A
  • Class 1: Na+ channel blockers- suppress conduction e.g flecainide
  • Class 2:Beta receptor blockers-reduce excitability, inhibit AVN conduction e.g bisoprolol
  • Class 3: drugs which prolong the AP and refractory period e.g amiodarone
  • Class 4: Ca2+ channel blockers- inhibit AVN conduction e.g verapamil

Adenosine: slows AV nodal conduction
Digoxin: stimulates vagus, slows AV nodal conduction
All inhibit conduction or reduce excitability in some way

27
Q

What pharmacological anti-arrhytmic strategies can be used for AF and other supraventricular tachycardias?

A
  1. ) RATE CONTROL: reduce proportion of impulses conducted through the AV node
    - atrial tachycardia continues, but the ventricles slow down, improving CO
    - Class 2, class 4,adenosine, digoxin - all of these drugs reduce the ability of the AVN to conduct impulse from atria to ventricles
  2. ) RHYTHM CONTROL: target the source of the arrhythmia or the conduction of the impulse away from the source by blocking the re-entrant pathway
    - class 3 or 1
    - anti-coagulant therapy to prevent stroke is required for AF
28
Q

what is radiofrequency catheter ablation?

A
  • Ectopic pacemaker or site along a re-entrant pathway is destroyed
  • Transvenois catheter is threaded into the heart, placed against the endocardium, and radio-frequency energy is delivered to the tip. This heats the tip causing a lesion~1cm wide
  • Cyroablation= a newer alternative used if the site to be ablated is very close to the AV node or conduction system
29
Q

What is ventricular tachycardia?

A

A run of rapid (typically 120-200bpm) successive ventricular beats caused by an ectopic site in one of the ventricles

30
Q

What is the cause of VT?

A
  • Varied
  • Almost always due to re-entry
  • Most often due to cardiac scarring after MI or dilated cardiomyopathy
  • Can be congenital e.g Brugada syndrome, LQT syndrome
  • May be caused by inappropriate use of anti-arrhythmic drugs
31
Q

What is the effect of VT on cardiac rhythm?

A
  • Tachycardia

- Rhythm may be regular( monomorphic VT) or irregular ( polymorphic VT)

32
Q

What are the symptoms of VT?

A
  • Chest pain
  • SOB
  • Syncope
33
Q

What is the prognosis of VT

A
  • Varied, depends on cause
  • If persistent, may compromise cardiac pumping, leading to heart failure & death
  • Can deteriorate into VF leading to sudden death
34
Q

How can we treat VT?

A
  • Implanted cardioverter defibrillator

- class 1,2 & 3 anti-arrhytmic drugs, radiocatheter ablation

35
Q

What happens to the ECG in VT?

A

-Broad complex rapid rhythm
-Complexes can be of regular(monomorphic) or varied shape( polymorphic/Torsades de pointes)
Atria usually beat more slowly and independently of the ventricles( AV dissociation)
-The p waves dont ‘capture’ the ventricles because when they get through the AV node the conduction system is usually refractory,since its been depolarised so frequently by the ventricular ectopic pacemaker

36
Q

What is ventricular fibrillation?

A

chaotic & disorganised electrical activity of the heart

37
Q

What causes VF?

A

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

38
Q

What is the effect of VF on the cardiac rhythm?

A

-No organised ventricular beat so no CO

39
Q

What are the symptoms and prognosis of VF

A

-Unconsciousness within seconds, death occurs rapidly

40
Q

describe the ECG hallmark of VF

A

-Disorganised electrical activity which fades as the heart dies

41
Q

What is defibillation used for?

A
  • To terminate VF or ‘pulseless’ VT
  • DC cardioversion: momentary discharge of large current across the chest via paddles placed at the sternum& RV apex
  • applied at onset of QRS complex(if present)
  • Stops the heart, allows the SAN to reassert itself
  • Combined with cardiopulmonary resuscitation,adrenaline can also be used
  • In the absence of equipment, a thump to the chest can occasionally terminate VF
42
Q

What are implantable defibrillators?

A
  • An implanted generator is connected to electrodes in the RV & SVC
  • The generator can sense and differentiate arrhythmias by rate and location, and delivers an appropriate shock or shock sequence, causing cardioversion( i.e. a return to sinus rhythm)
  • More successful than drug therapy in patients with serious ventricular arrhythmias
  • sometimes combined with drugs (e.g amiodarone) to reduce frequency of fibrillation episodes

Supporting life block (28 decks)

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