Cardiac Arrhythmias Flashcards by Aliya Hussain

How are arrhythmias named?

Generally named for anatomical site or chamber of origin

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Types of arrhythmias?

Supraventricular - origin is above the ventricle, i.e: from the SA node, atrial muscle, AV node or of HIS origin. This is a non-specific-term and specifics are required

Ventricular - origin in the ventricle

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Electrical separation and connections between chambers?

Fibrous ring is electrically inert and electrically separates the chambers

AV node is the only physiological electrical connection between atria and ventricles

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What are ectopic beats/rhythms?

Beats/rhythms that originate in places other than the SA node

Ectopic focus may cause single beats or take over and pace the heart, dictating its entire rhythm - ectopic rhythms compete with normal sinus rhythm

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When are ectopic beats/rhythms dangerous?

May or may not be dangerous depending on how they affect the CO

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Types of supraventricular arrhythmias?

Supraventricular tachycardia:
Atrial Fibrillation
Atrial Flutter
Ectopic atrial tachycardia (area in atria fires indiscriminately)

Supraventricular bradycardia:
Sinus bradycardia (there can be issues with rhythm initiation and also block can occur somewhere)
Sinus pauses

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Pathological reasons for AV node arrhythmias?

AV node re-entry

Accessory pathway, e.g: Wolff Parkinson White syndrome (WPW) is due to Bundle of Kent

AV block:
1st degree
2nd degree
3rd degree

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Types of ventricular arrhythmias?

Premature Ventricular Complex (PVC) - initiated by purkinje fibres; ventricles contract first and before the atria have optimally filled the ventricles with blood (causes a transient decrease in BP)

Ventricular Tachcardia

Ventricular fibrillation

Asystole

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Number of fascicles in the bundle of His?

3 fascicles:
Left bundle has 2 - anterior and posterior fascicles
Right bundle has 1

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Clinical causes of arrhythmias?

Abnormal anatomy:
Left ventricular hypertrophy
Accessory pathways
Congenital heart disease

Autonomic:
Sympathetic stimulation - nervousness, exercise, CHF, hyperthyroidism
Increased vagal tone, causing bradycardia and potentially heart block

Metabolic:
Hypoxic myocardium, e.g: in COPD, PE (reduce threshold for arrhythmias)
Ischaemic myocardium, e.g: in acute MI and angina
Electrolyte imbalances, e.g: of K+, Ca2+ and Mg2+

Inflammation - viral myocarditis

Drugs, part. those that prolong the QT interval

Genetic - mutations of cardiac ion channels, e.g: the congenital long QT syndrome

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Physiological mechanisms by which tachycardias result?

Altered automaticity, e.g: due to ischaemia and catecholamines

Triggered activity, e.g: digoxin use

Re-entry, e.g: accessory pathway tachycardia (WPW syndrome), previous MI

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Symptoms of arrhythmias?

Palpitations
SoB
Dizziness
Syncope
Sudden cardiac death
Worsen a pre-existing condition, e.g: angina and CHF; angina can worsen if HR increases and increases cardiac work

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Investigations used in arrhythmia diagnosis?

12-lead ECG
CXR
Echocardiogram

Stress ECG to search for myocardial ischaemia and exercise-related arrhythmias

24 hour ECG holter monitoring
Event recorder
Electrophysiological study - induce arrhythmia to study it and map the pathway

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Why is ECG used in arrhythmia investigation?

To assess rhythm

Signs of previous MI, e.g: pathological Q waves, pre-excitation (via accessory pathway in WPW)

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Why is a 24 hour holter ECG used in arrhythmia investigation?

To assess for PAROXYSMAL arrhythmia; also, patient can press a button when they feel symptoms and these can then be linked to the underlying heart rhythm

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Why is an echo used in arrhythmia investigation?

Assess for structural heart disease, e.g:
Enlarged atria in AF
Left ventricle dilatation
Previous MI scar, aneurysm- disposes to arrhythmias

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What is the treatment and advice for ATRIAL ECTOPIC BEATS?

Can be asymptomatic or cause palpitations; generally, if asymptomatic, no treatment is given

β-blockers may help, by slowing down HR (target HR in for somebody on this drug is

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What is sinus bradycardia?

HR of

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Non-physiological causes of sinus bradycardia?

Drugs like β-blockers

Ischaemia - common in inferior STEMIs

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Treatment for sinus bradycardia?

If acute, atropine, e.g: in an aMI

Pacing can be used if there is haemodynamic compromise, e.g: in hypotension, CHF, angina, collapse

What is sinus tachycardia?

HR of >100 bpm and this can be physiological in anxiety, fever, hypotension, anaemia, hypoxia

When is sinus tachycardia inappropriate?

Drugs and stimulants

Syndrome Inappropriate Tachycardia - most common in young females; heart rate is reset

Acute management of supra-ventricular tachycardia?

Acute management:
Vagal manoeuvres and carotid massage (never do this in elderly people with cerebro-vascular disease) increase vagal tone

IV adenosine (drug of choice - slows AV node conduction)

IV verapamil (rate-limiting CCB - slows down AV node conduction)

Chronic management of supra-ventricular tachycardia?

Avoid stimulants

Radiofrequency ablation is preffered

Anti-arrhythmic drugs (class II or IV)

What is ablation?

Selective CAUTERY (burning) of cardiac tissue to prevent tachycardia, targeting either an automatic focus or part of a re-entry circuit

Radiofrequency ablation procedure?

Catheters placed in heart via femoral veins; catheter is placed over focus/pathway and the tip is heated An intracardiac ECG is recorded during sinus rhythm, tachycardia and during pacing manoeuvres

Causes of AV node conduction disease?

``` Ageing process Acute MI Myocarditis Infiltrative disease, e.g: amyloid Drugs, e.g: β-blockers, CCB ``` Calcific aortic valve disease - close to AV node and so it can be involved Post-aortic valve surgery Genetic: Lenegre's disease, myotonic dystrophy

What is 1st degree AV block?

Not really a block; PR INTERVAL IS PROLONGED (> 2 secs)

Treatment for 1st degree AV block?

Treatment: none Long-term follow up recommended, as more advanced block may develop over time

What is 2nd degree AV block?

Intermittent block at the AV node, so sometimes there are dropped beats

Types of 2nd degree AV block?

Mobitz type I - progressive lengthening of PR interval that eventually results in a dropped beat; usually vagal in origin Mobitz type II - pathological and can progress to complete heart block

Naming of Mobitz type II heart block?

Usually 2:1 or 3:1 but can be variable, e.g: if 3 APs are produced but only one gets through (3:1)

Treatment of Mobitz type II heart block?

Permanent pacemaker is indicated

What is 3rd degree AV block?

Complete heart block - no APs from the SA node/atria get through the AV node Requires ventricular pacing

Types of pacemakers and when they are used?

Single chamber (paces right atrium OR right ventricle only): Atrial pacemakers - used in isolated SA node disease when the AV node is normal Ventricular pacemakers - used in AF with a slow ventricular rate ``` Dual chamber (paces the right atrium AND right ventricle): Maintains AV synchrony to preserve atrial kick Used for AV node disease ```

Brief rule about pacemaker entry into heart?

Go into RIGHT SIDE of heart, not the left side (arterial risk of bleeding and thrombosis)

How do pacemakers affect the CO?

Cause contraction from bottom to top of heart (normally, contraction goes from top to bottom); this can decrease CO

What is and caution with broad complex tachycardia?

Wide QRS complex and patient is tachycardic Assume that all broad complex tachycardia are VENTRICULAR, UNTIL PROVEN OTHERWISE - in VT, there is a large, sustained reduction in arterial pressure

Outcome of Ventricular Tachycardia?

Life-threatening but may be haemodynamically stable

Causes of VT?

Most patients have significant heart disease: CAD Previous MI Rarer causes: Cardiomyopathy Inherited/familial arrhythmia syndrome, e.g: Long QT

Differentiating stable and unstable VT?

No chest pain, hypotension, CHF, altered conscious level

ECG characteristics of VT?

QRS complexes are rapid, wide and distorted T waves are large with deflections opposite the QRS complexes Ventricular rhythm is usually regular P waves are not usually visible PR interval is not measurable AV dissociation may be present VA conduction may or may not be present

Types of VT?

Monomorphic VT - same pattern and QRS distance; look for ischaemia/scarring Polymorphic VT - different QRS complexes, e.g: Torsades de pointe causes of which include hypokalaemia, hypomagnesaemia

Treatment of acute VT?

If unstable - DC cardioversion (converts to normal rhythm) If stable - consider pharmacologic cardioversion with anti-arrhythmic drugs If unsure if this is VT or something else, use adenosine to differentiate Correct triggers

What is ventricular fibrillation?

Chaotic, ventricular electrical activity causing the heart to lose ability to function as a pump - LIFE THREATENING

Treatment of ventricular fibrillation?

Defibrillation (only "treatment") | CPR

Management of VT?

Look for causes, e.g: electrolytes, ischaemia, hypoxia, medications (prolong QT interval, e.g: sotalol, arythromycin, quinidine) If it does not respond to Mg, it is not torsades Implantable Cardiovertor Defibrillators (ICD) if life-threatening - pacemaker + defibrillator Optimise CHF therapies

Functions of ICDs in atrium and ventricle?

``` Ventricle: VT prevention Anti-tachycardia pacing Cardioversion Defibrillation ``` Atrium and ventricle: Bradycardia sensing Bradycardia pacing