Arrhythmias Flashcards
Define arrhythmia
- aka dysrhythmia
- A disturbance of the normal rhythmic beating of the heart-usually due to an ectopic pacemaker
What are the symptoms of arrhythmia?
- Palpitations
- breathlessness
- dizziness, faintness,syncope
Where is the pacemaker of the heart?
- SAN
- The entire conduction system is a latent pacemaker i.e in uncertain conditions it can take over from the SAN
What is the funny current
I(f)
- pacemaker current
- Most heavily expressed in the SAN
How can we classify arrhythmias?
- ) By rate:
- Inappropriate bradyarrhythmia (<60bpm)
- Inappropriate tachyarrhythmia (>100bpm) - ) By location:
- supraventricular (atrial or AV nodal origin)
- Ventricular( ventricular origin)-more severe - ) By cause:
- disorders of impulse generation
- disorders of impulse conduction
What are the causes of arrhthmias?
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
What is complete(3rd degree) heart block?
- 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
What are the symptoms of complete heart block?
-Temporary syncope as heart stops, followed by recovery , with breathlessness, fatigue & chest pain especially with effort
What is the treatment for complete heart block?
- 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
Outline the role of latent pacemakers in conduction
- 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
What happens to the ECG in 3rd degree heart block
- 3rd degree heart block= complete heart block
- The QRS complex becomes dissociated from the P wave as the atria & ventricles beat independently= atrioventricular dissociation
What are tachyarrhythmias?
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
How can we stop re-entry to prevent arrhytmia?
- ) Convert unidirectional block to bidirectional block by suppressing conduction
- ) Prolong the refractory period so the retrograde impulse cannot re-enter conducting myocardium
What is functional re-entry?
- 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
What complication can triggered automacity bring?
-Can initiate re-entry
What causes delayed after depolarisations( DADs)?
-excessive increases in calcium ion concentration due to e.g catecholamines, digoxin
What causes early after depolarisations (EADs)?
-Stimuli that increase the calcium ion current or AP duration e.g hypoxia, catecholamines, sotalol( an anti-arrhythmic)
Define atrial fibrillation
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
What causes atrial fibrillation
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
What is the effect of AF on the cardiac rhythm ?
- No organised atrial beating due to chaotic electrical activity
- ventricular excitation occurs when atrial depolarisations are sufficient to be conducted through the AVN
What are the symptoms of AF?
- palpitations
- breathlessness
- dizziness
- syncope
Describe the prognosis of AF
- 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
How can AF be treated?
- Class 1-4 anti-arrhytmic
- Radiocatheter ablation
- maze procedure
- Anti-coagulants or LA appendage closure
What happens to the ECG in AF?
- 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)
What does the term ‘irregularly irregular’ mean in terms of rhythm
-No clear pattern can be seen
Describe the Vaughan Williams& Singh anti-arrhytmic drug classification system
- 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
What pharmacological anti-arrhytmic strategies can be used for AF and other supraventricular tachycardias?
- ) 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 - ) 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
what is radiofrequency catheter ablation?
- 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
What is ventricular tachycardia?
A run of rapid (typically 120-200bpm) successive ventricular beats caused by an ectopic site in one of the ventricles
What is the cause of VT?
- 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
What is the effect of VT on cardiac rhythm?
- Tachycardia
- Rhythm may be regular( monomorphic VT) or irregular ( polymorphic VT)
What are the symptoms of VT?
- Chest pain
- SOB
- Syncope
What is the prognosis of VT
- Varied, depends on cause
- If persistent, may compromise cardiac pumping, leading to heart failure & death
- Can deteriorate into VF leading to sudden death
How can we treat VT?
- Implanted cardioverter defibrillator
- class 1,2 & 3 anti-arrhytmic drugs, radiocatheter ablation
What happens to the ECG in VT?
-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
What is ventricular fibrillation?
chaotic & disorganised electrical activity of the heart
What causes VF?
-Usually MI, ischaemic heart disease,cardiomyopathy, but can be idiopathic
What is the effect of VF on the cardiac rhythm?
-No organised ventricular beat so no CO
What are the symptoms and prognosis of VF
-Unconsciousness within seconds, death occurs rapidly
describe the ECG hallmark of VF
-Disorganised electrical activity which fades as the heart dies
What is defibillation used for?
- 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
What are implantable defibrillators?
- 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
