Arrhythmias 1 + 2 Flashcards
What is an arrhythmia? What are arrhythmias names according to? (2) Examples? (2)
- Arrhythmia - no rhythm
- Anatomical site, mechanism
- Supraventricular (SVT), Ventricular
What is a supraventricular arrhythmia? Ventricular?
- Origin is above the ventricle e.g. SAN, atrial muscle, AV node or HIS
- Ventricular muscle or fascicles of the conducting system
Types of supraventricular arrhythmias? (2) Examples?
- Supraventicular tachycardia e.g. AF, atrial flutter, ectopic atrial tachycardia
- Bradycardia e.g. sinus bradycardia, sinus pauses
Types of ventricular arrhythmias? (4)
- Ventricular ectopics or Premature Ventricular Complexes (PVC)
- Ventricular Tachycardia
- Ventricular Fibrillation
- Asystole
Types of AV node arrhythmia? (3)
- AVN re-entry tachycardia
- AV reciprocating or AV Reentrant tachycardia
- AV block : 1st degree, 2nd degree, 3rd degree
Clinical causes of arrhythmias? (6)
- Abnormal anatomy (LVH, accessory pathways, congenial HD)
- Autonomic NS (sympathetic stimulation, increased vagal tone)
- Metabolic (hypoxia, ischaemia, electrolyte imbalances)
- Inflammation (viral myocarditis)
- Drugs (electrophysiologic effects, ANS)
- Genetic (congenital long QT syndrome)
Electrophysiological mechanisms of arrhythmia? (2)
- Ectopic beats
* Re-entry
What are ectopic beats? Examples? (2)
Beats or rhythms that originate in places other than the SA node
- Altered automaticity e.g. ischaemia, catecholamines
- Triggered activity, e.g. digoxin, long QT syndrome
What is re-entry? Example?
Requires more than one conduction pathway, with different speed of conduction (depolarization) and recovery of excitability (refractoriness)
* accessory pathway tachycardia (Wolf Parkinson White syndrome), previous myocardial infarction, congenital heart disease
Mechanisms of tachycardia? (2) Is tachycardia dangerous?
- Ectopic focus may cause single beats or sustained run of beats, that if faster than sinus rhythm, take over the intrinsic rhythm
- Re-entry: triggered by an ectopic beat, resulting in a self perpetuating circuit
May or may not be dangerous depending on how CO is affected
What is altered automaticity? How does altered automaticity change heart rate? (3)
Cells outside of SA node exhibit spontaneous electrical activity
- Change threshold
- Change resting membrane potential
- Changing phase 4 (pacemaker potential) slope
How does abnormal physiology and pathology cause arrhythmia? (2) Causes of this? (5 + 2)
Increases phase 4 slope causing increase in heart rate
- Hyperthermia
- Hypoxia
- Hypercapnia
- Cardiac dilation
- Hypokalaemia
Decreases phase 4 slope causing slowed conduction (bradycardia, heart block)
- Hypothermia
- Hyperkalaemia
What is triggered acivity?
In phase 3 (repolarisation), a small depolarisation called an AFTERDEPOLARISATION may occur, may reach depolarisation threshold and lead to sustained train of depolarisations called TRIGGERED ACTIVITY
Examples of causes of triggered activity? (3)
- Digoxin toxicity,
- Torsades de Pointes in long QT syndrome
- hypokalaemia
Do afterdepolarisations always lead to sustained train of depolarisations?
No, normally don’t come to anything
What can lead to re-entry? (2) examples?
- Structural abnormalities e.g. accessory pathways, scar from MI, congenital HD
- Functional abnormalities e.g. ischaemia, drugs
Does scar itself conduct electricity in re-entry circuits?
No, scar is electrically inert but splits heart into different electrical pathways
Explain the normal action potential conduction down purkinje fibre to ventricular muscle (4)
- Conduction travels down purkinje fibres into (for simplicity) 2 pathways
- Conduction speed is the same down both pathways
- Conduction then meets in the middle and ventricular muscle contracts
Explain how ischaemia causes re-entry arrhythmia (6)
- Ischaemia slows down conduction in one of the pathways
- Currents will not meet in the middle to cause a single contraction
- Faster current will cause muscle to contract
- Slower current will cause an extra beat
- Current can then travel backwards and re-enter pathway causing re-entrant current and TACHYCARDIA
Symptoms of arrhythmias? (7)
- Palpitations, ”pounding heart”
- Shortness of breath
- Dizziness
- Loss of consciousness; ”Syncope”
- Faintness: “presyncope”
- Sudden cardiac death
- Angina, heart failure
Investigations for arrhythmias? (7)
- 12 lead ECG
- CXR
- Echocardiogram
- Stress ECG
- 24 hour ECG Holter monitoring
- Event recorder: (capture the arrhythmia)
- Electrophysiological (EP) study
What is ECG used for in arrhythmia?
- To assess rhythm
- Look for signs of revious MI (Q waves)
- Pre-excitation due to accessory pathway (Wolf Parkinson White syndrome)
What is an accessory pathway? What would indicate pre-excitation on ECG? What can it lead to? Why?
- Extra pathway that crosses atria to ventricle outside of fibrous ring
- Delta wave (reflects ventricle being depolarised early)
- Tachycardia
- Accessory pathway does not pass through AV node so current not slowed down
Purpose of exercise ECG? (2)
- To assess for ischaemia
* Exercise induced arrhythmia
Purpose of 24hr Holter ECG? (2)
- To assess for paroxysmal arrhythmia
* To link symptoms to underlying heart rhythm
Purpose of echocardiography? Examples? (3)
To assess for structural heart disease
e. g.
* enlarged atria in AF
* LV dilatation
* Previous MI scar, aneurysm
Purpose of electrophysiological study? (2)
- Trigger the clinical arrhythmia and study its mechanism/pathways
- Opportunity to treat the arrhythmia by delivering radiofrequency ablation to extra pathway
What is normal sinus arrhythmia? Is it something to be worried about?
- Variation in HR due to reflex change sin vagal tone during respiration i.e. inspiration reduces vagal tone and increases heart rate
- No, property seen in healthy people
What is sinus bradycardia? Causes? (3) Treatment? (2)
- <60 bpm
Causes
- Physiological e.g. athlete
- Drugs (b-bocker)
- Ischaemia - common in inferior STEMIs
Treatment
- Atropine if acute e.g. acute MI
- Pacemaker if haemodynamic compromise e.g. hypotension, CHF, angina, collapse
What is atropine?
Anti-vagal which will speed up HR
What is sinus tachycardia? Causes? (2) Treatment? (2)
- > 100 bpm
Causes
- Physiological e.g. anxiety, fever, hypotension, anaemia
- Inappropriate e.g. drugs, caffeine
Treatment
- Treat underlying cause
- B-blcokers
Symptoms of atrial ectopic beats? (2) Treatment? (2)
- Asymptomatic or palpitations
- Generally no treatment but b-blockers may help if symptomatic
- Avoid stimulants e.g. caffeine, cigarettes
Most common cardiovascular rhythm disturbance in paediatrics? Signs on ECG? (3)
- SVT
ECG
- Tachycardia - almost 300 bpm
- Non-sinus tachycardia because no P waves present
- Narrow QRS complex
Causes of regular supraventricular tachycardia? (3)
- AV nodal re-entrant tachycardia (AVNRT)
- AV reciprocating tachycardia/AV reentrant tachycardia (via an accessory pathway) (AVRT)
- Ectopic atrial tachycardia (EAT)
What does AVNRT and AVRT use? What is AVRNT? AVRT?
AV node
- AVRNT - circuit within AVN (micro-reentry)
- AVRT - circuit using AV node and accessory pathway (macro-reentry)
What are types of accessory pathway tachycardia? (3) Features on ECG?
- Pre-excitation - short PR interval
- Orthodromic AVRT (antegrade conduction through AV node) - normal QRS duration, no delta wave, retrograde P wave AFTER QRS
- Antidromic AVRT (retrograde conduction through AV node) - wide QRS, delta wave, no P waves (if P wave visible, it is retrograde and occurs just before QRS)
What does a wider QRS indicate?
Ventricular conduction slower
What is ectopic atrial tachycardia?
Automaticity - tissues other than SA node exhibit spontaneous electrical activity
Acute management of supraventricular tachycardia? (2)
Chronic management? (4)
Acute
- Increase vagal tone e.g. valsalva, carotid massage
- Slow conduction in AVN e.g. IV adenosine, verapamil
Chronic
- Avoid stimulants
- Electrophysiologic study and radiofrequency ablation (first line in young, symptomatic patients) – surgery not given in elderly patients so drugs used instead
- Beta blockers
- Antiarrhythmic drugs
What is Radiofrequency Catheter Ablation ?
RFCA) Targets? (2
Selective cautery of cardiac tissue to prevent tachycardia
Targets include:
* automatic focus
* part of a re-entry circuit
Explain the procedure of electrophysiologic study and RFCA? (3)
- ECG catheters placed in heart via femoral veins
- Intracardiac ECG recorded during sinus rhythm, tachycardia and pacing manoevers to find location + mechanism of tachycardia
- Catheter placed over focus/pathway and tip heated to 55-65*C
Causes of AVN conduction disease (Heart Block)? (8)
- Ageing process
- Acute myocardial infarction
- Myocarditis
- Infiltrative disease e.g. amyloid
- Drugs e.g. B-blockers, calcium channel blockers, Digoxin
- Calcific aortic valve disease
- Post-aortic valve surgery
- Genetic : Lenegre’s disease, myotonic dystrophy
What is 1st degree A-V (heart) block? ECG sign? Treatment? (3)
- Not really a block - conduction following each P wave takes longer
- PR interval longer than normal (>0.2 sec i.e. big square)
Treatment
- No treatment
- Rule out other pathology
- Arrange follow-up as more advanced block may develop over time
What is 2nd degree A-V block? Types? (2)
Intermittent block at the AVN (dropped beats)
- Mobitz I
- Mobitz II
What is Mobitz I? (2)
- Progressive lengthening in PR interval eventually resulting in dropped beat
- Usually vagal in origin
What is Mobitz II? (2)
Treatment?
- Pathological - may progress to complete heart block (3rd degree)
- Usually 2:1 or 3:1 (2 P waves for every QRS)
- Treatment - permanent pacemaker
Difference between 3rd degree (complete heart block) and 2nd degree A-V block?
- In 2nd degree, only some APs fail to get through AV node - in 3rd degree, NO APs from atria get through AV node
What are the effects of 3rd degree A-V block? (2)
ECG sign?
Treatment?
- Heart either stops (asystole) or enters “escape rhythm” that allows CO and maintains survival
- Broad QRS - as conduction takes time spreading from gap junction to gap junction
- Ventricular pacemaker!!
What are pacemakers? Where are they positioned?
- Detects abnormal rhythm and delivers shock to return to sinus rhythm
- RA and RV
Types of pacemakers? (2)
Single chamber
* paces RA or RV only
Dual chamber
- Maintains A-V synchrony
- Used for AVN disease
Examples of ventricular arrhythmias? (4)
- Ventricular ectopic or Premature Ventricular Complex (PVC)
- Ventricular Tachycardia
- Ventricular Fibrillation
- Asystole
Causes of ventricular ectopics? (3)
- Structural causes: LVH, heart failure, myocarditis
- Metabolic: Ischaemic heart disease, electrolytes
- Inherited cardiac conditions
When do ventricular ectopics need to be investigated further? What is treatment for ventricular ectopics? (2)
- If worse on exercise need to investigate
Treatment
- B-blockers
- Ablation of focus
What does it mean if QRS complex is broad? QRS complex narrow?
- Problem in ventricles
* Problem with SA node
What is broad complex tachycardia likely to be?
Ventricular tachycardia
What is VT? Causes? (4)
Life threatening but may be haemodynamically stable
Causes
- Coronary artery disease
- Previous MI
- Cardiomyopathy
- Inherited/familial arrhythmia syndromes e.g. long QT
What are most causes of sudden death attributable to?
VT and VF
What is seen with ventricular tachycardia with haemodynamic compromise?
Large, sustained reduction of arterial pressure
What is monomorphic VT? Polymorphic VT?
- Morphology of each QRS is the same - fixed circuit
* Morphology constantly changing - multiple circuits, not re-entry (triggered activity or automaticity)
What are ECG characteristics of VT? (7)
- QRS complexes are rapid, wide and distorted
- T waves are large
- Ventricular rhythm usually regular
- P waves are usually not visible
- PR interval is not measurable
- A-V dissociation may be present
- V-A conduction may or may not be present
What is ventricular fibrillation? Treatment? (2)
- Chaotic ventricular electrical activity which causes the heart to lose the ability to function as a pump
- Defibrillation, Cardiopulmonary resuscitation
Acute treatment for VT? (4)
- Direct current cardioversion (DCCV) if unstable
- If stable: consider pharmacologic cardioversion with AAD
- If unsure if VT or something else, consider adenosine to make diagnosis
- Correct triggers/causes (electrolytes, ischaemia, hypoxia, pro-arrhythmic medications)
What are pro-arrhythmic medications? Example?
- Drugs that prolong the QT interval
* e.g. Sotalol
Long term treatment for VT? (5)
- Correct ischemia if possible (revascularisation)
- CHF therapies
- Anti-arrhythmic drugs to date have been shown to be INEFFECTIVE and are associated with worse outcomes!!!!!
- Implantable cardiovertor defbrillators (ICD) if life threatening
- VT catheter ablation
How is ICD inserted? Dual or single chamber device?
- Through SVC
* Dual chamber
What are therapies provided by ICDs? (4)
- Antitachycardia pacing
- Cardioversion
- Defibrillation
- Pacing for bradycardia
What is a wide QRS tachycardia with history of CAD/HF? What do most ventricular arrhythmias occur due to? What is the effectiveness of anti-arrhythmic drugs? What is an important part of treatment for VT/VF?
- VT until proven otherwise
- Structural heart disease (CHF, CAD)
- ineffective on survival, but are often used together with ICDs to reduce symptoms
- Optimal management of the underlying condition e.g. CHF, CAD
Prevalence and incidence of AF?
Increases with age
Appearance of AF on ECG? LVH?
AF
- Absence of P waves
- Irregularly irregular
LVH
- Very tall R waves
- ST depression
What is atrial fibrillation? Types? (3)
Why is it significant? Presentations?
- Chaotic and disorganized atrial activity causing irregular heart beat
- Paroxysmal, persistent or permanent
- Most common sustained arrhythmia
- Can be symptomatic or asymptomatic
Mechanism of AF?
Ectopic foci in muscle sleeves in the ostia of the pulmonary veins
Termination of AF? (3)
- Pharmacologic cardioversion with anti-arrhythmic drugs (30% effective) e.g. flecainide, sotalol and amiodarone
- Electrical Cardioversion (90% effective)
- Spontaneous reversion to sinus rhythm
3 types of AF? (3)
Paroxysmal
- Paroxysmal and lasting less than 48 hours
- Often recurrent
Persistent
- Lasting greater than 48 hours, can be cardioverted to NSR
- Unlikely to spontaneously revert to NSR
Permanent
* Inability of pharmacologic or non-pharmacologic methods to restore NSR
Associated diseases with AF? (13)
- Hypertension
- Congestive heart failure
- Sick sinus syndrome
- Coronary heart disease
- Thyroid disease
- Cardiac Valve disease
- Congenital heart disease
- COPD
- Pneumonia
- Septicaemia
- Pericarditis
- Tumors
- Vagal cause – high endurance athletes
Lifestyle/patient factors associated with AF?
- Obesity
- Inherited
- Alcohol abuse
- Cardiac surgery
What is lone (idiopathic) AF? How is it diagnosed? Cause? Why is this dangerous?
- Absence of any heart disease and no evidence of ventricular dysfunction
- Exclusion
- Genetic
- Significant stroke rate if >75 y/o
Symptoms of AF? (7) When are they worse?
Symptoms
- Palpitations
- Pre-syncope (dizziness)
- Syncope
- Chest pain
- Dyspnea
- Sweatiness
- Fatigue
Symptoms often worse at onset of AF
Appearance of AF on ECG? (5)
- Atrial rate >300 bpm
- Rhythm - irregularly irregular
- Ventricular rate - variable
- Absence of P waves
- Presence of f waves
What does ventricular rate in AF depend on? (3)
- AV node conduction properties
- Sympathetic and parasympathetic tone
- Presence of drugs with act on the AV node
Is AF a sinus arrhythmia?
No, as no underlying sinus beat
What is complicated about AF with slow ventricular rate? Treatment?
- May co-exist with periods of fast VR
* Pacemaker req to allow for pharmacologic control of fast VR
What is AF with fast ventricular response known as?
Pseudo-regularisation
What does AF lead to? How? What condition can AF result in?
- Reduced CO
- Lost ‘atrial kick’ and decreased filling times (reduced diastole)
- Can result in CCF, esp with diastolic dysfunction
What can ventricular rates <60 bpm suggest in AF? Treatment? (2)
- AV conduction disease
- Caution with anti-arrhythmic and rate-controlling drugs
- May require permanent pacing
What can AF in patients with pre-excitation e.g. Wolf-parkinson-White syndrome result in?
- Ventricular fibrillation and sudden cardiac death
Management of AF? (3)
- Rhythm control (maintain sinus rhythm)
- Rate control (accept AF but control ventricular rate)
- Anti-coagulation for both approaches if high risk of thromboembolism
What treatments are used for rate control in AF? (3) What do they do? What if medications are unsuccessful? (2)
- Digoxin, b-blockers and verapamil/diltiazem
- Slow down AVN conduction
- More invasive efforts - electrophysiolgy and ablation
What are the 2 goals of rhythm control? What are treatments? (2 + 3)
Restoration of NSR and maintenance of NSR
Restoration of NSR
- Pharmacologic cardioversion (anti-arrhythmic drugs e.g. amiodarone)
- Direct Current Cardioversion (DCCV)
Maintenance of NSR
- Anti-arrhythmic drugs
- Catheter ablation of atrial focus/ pulmonary veins
- Surgery (Maze procedure)
What is electrical cardioversion? What does success depend on?
- Aims at immediate restoration of sinus rhythm
* the time the patient has been in atrial fibrillation
What are classes of anti-arrhythmic drugs? (4) Examples?
- Class 1 - reducing Na+ channel current e.g. lignocaine, quinidine, flecainide, propafenone
- Class II - B-Adrenergic antagonists e.g. propranalol
- Class III: action potential prolongation e.g. amiodarone, sotalol, DRONEDARONE
- Class IV - Ca channel antagonists e.g. Verapamil
What are AF patients at high risk of thromboembolism? (7)
What is the biggest risk of AF?
- Valvular heart disease
- Age >75 esp female
- Hypertension
- Heart failure
- Previous thromboembolism/ stroke
- Coronary artery disease/ diabetes and > 60 years old
- Thyrotoxicosis
Biggest risk = stroke
Indication for anti-coagulation in AF if valvular? Non-valvular? (6)
Valvular
* Mitral valve disease - MS and MR
Non-valvular
- Age >75
- Hypertension
- Heart failure
- Previous stroke/ thromboembolism
- CAD / DM
- Diabetes
Purpose of radiofrequency ablation in AF? (2)
- To maintain Sinus Rhythm by ablating AF focus (usually in the pulmonary veins)
- For rate control by ablation of the AVN to stop fast conduction to the ventricles
What is atrial flutter? How is atrial flutter sustained? How long to episodes last?
- Rapid and regular form of atrial tachycardia - usually paroxysmal
- Macro-reentrant circuit
- Episodes can last from seconds to years
What are complications of atrial flutter?
- Chronic atrial flutter usually progresses to atrial fibrillation
- May result in thrombo-emblism
Difference between hearts of patients with paroxysmal atrial flutter and chronic atrial flutter?
Patients presenting with paroxysms of atrial flutter often have normal hearts, whereas patients with chronic atrial flutter usually have underlying heart disease
Appearance of atrial flutter on ECG? (4)
- Saw-tooth pattern
- Atria beating fast ~300 bpm
- AV node cannot conduct that fast (heart block) so 2:1 physiologic pattern
- Ventricle possibly beating half as fast ~150 bpm
Atrial flutter mechanism? Treatment? (4)
Counter-clockwise macro-reentrant circuit
- RF ablation (80-90% long term success)
- Pharmacologic therapy (slow the ventricular rate, restore sinus rhythm, maintain sinus rhythm once converted)
- Cardioversion
- Warfarin for prevention of thromboembolism
Goals in AF management? (2)
- Symptom control
- Improve cardiovascular outcomes e.g. stroke prevention with anti-coagulatns, optimal treatment of underlying CVS disease, lifestyle risk reduction
