Pathophysiology of arrythmias Flashcards
How are disturbances in cardiac rhythm diagnosed?
ECG
either bradycardia or tachycardias
Discuss the conducting tissue of the heart
Obv all cardiac cells form a functional syncytium via desmosomes, but beyond that points of note are:
The SA node (pacemaker)
AV ring (insulating material)
AV node (decremental - the more frequently the node is stimulated the slower it conducts)
His Purkinge tissues (fast conduction)
Have a look at electrolyte changes over an ECG, its kinda cool
Nerd
Discuss Bradycardias
• Sinus Bradycardia – Drugs -• Beta Blockers, Diltazem – Vagal activity – Hypothyroidism – Sinus Node disease – Electrolyte abnormalities
• AV Block
– Vagal activity
– Myocardial infarction
– Electrolyte abnormalities
Discuss AV Block
• 1st Degree
– Lengthening of the PR interval
• 2nd Degree
– Mobitz Type 1 (Wenckebach block).
• Progressive lengthening of PR interval until P wave blocked and then PR short again
– Mobitz Type 2
• Block after 2 or 3 conducted beats in regular pattern
• 3rd Degree AV block
– Complete AV dissociation
What are the treatments for bradycardia
• Pacemakers
– Temporary
– Permanent
• Only if needed
– Symptoms of syncope dizziness
– Prophylactic at time of operations
– Post AMI
What are the types of tachycardias
- Narrow Complex / Supraventricular Tachycardias
* Broad Complex Tachycardias
Discuss Narrow complex/supraventricular tachycardias
– Atrial Tachycardias – Junctional Tachycardias – AVNRT + AVRT – Atrial Flutter – Atrial Fibrillation
Discuss broad complex tachycardia
– Ventricular Tachycardia
• Monomorphic and polymorphic VT
• Fascicular (RBBB and LAD and not very wide)
• RVOT (LBBB and RAD)
– SVT with aberration (= acquired, rate- dependent bundle branch block)
– SVT with a pre-existing BBB morphology on
ECG
– SVT of antedromic tachycardia in WPW
What are the basic mechanisms of tachycardias
- Ectopic Focus – i.e. tissue with rapid pacemaker function
- Re-entry / circus movement
- Fibrillation – independent wavelets of activity
Discuss tachycardias involving the AV node
• Narrow complex, usually no P waves, usually very fast, and no history of cardiac disease
• AVNRT = AV nodal re-entrant tachycardia
– Tachycardia where re-entry circuit is through juxtanodal material
• AVRT = AV re-entrant tachycardia
– Tachycardia where re-entry is through an accessory pathway
• Revealed accessory pathway means WPW 12 lead ECG
• Concealed accessory pathway means normal non- tachycardia 12 lead ECG (i.e. the accessory pathway only conducts in a retrograde manner)
• All are terminated by i.v. adenosine
Discuss Wolff-Parkinson-White syndrome
First of all, what a cool name, it is:
- Pre-excitation (of the ventricles)
- Anatomical atrio-ventricular bypass tract with non-decremental conducting properties
• Results in
– Shortened PR interval <0.12sec
– Slurred upstroke of QRS and widened QRS complex >0.12sec
What is the adenosine test in narrow complex / supraventricular tachycardias
Remember adenosine woman? Pretty sure this is that
- i.v. bolus of adenosine (3mg, then 6 mg then 12mg)
- Half life 4.5 secs
- Causes transient and complete AV block
Adenosine will stop any tachycardia with re- entry over the AV node i.e. AVNRT and AVRT
• Responses:
– No effect. = Wrong diagnosis. Sinus Tachy in case of narrow complex or VT in case of broad complex
– Transient slowing with (=atrial flutter or atrial tachycardia) or without revealed P waves (= AF)
– Restoration of sinus rhythm AVNRT or AVRT
Discuss atrial fibrillation
- Very common
- Irregular narrow complex tachycardia with no P waves
• Symptoms
– Fast ventricular response rate – SOB, hypotension – Slow conduction – dizziness and syncope
– Embolism of left atrial thrombus (CVA)
What causes atrial fibrillation
– Ischaemic Heart Disease – Hypertensive heart disease – Mitral Valve disease – Thyrotoxicosis – Cardiomyopathy – Alcohol – Post bypass – Myocarditis – Accessory pathways – Lone (no cause)
What are the mechanisms of atrial fibrillation
– Size of Left Atrium
- Uncommon in children, much more common in large mammals
- > 5 independent wavelets of activity
- Foci of wavelet generation around the insertion of the pulmonary veins
Discuss management of atrial fibrillation
- Rate control or rhythm control ?
- Prevention of thrombo-embolism (esp. CVA)
• Who gets which?
– Rate control unless
• Symptomatic with high ventricular response rates refractory to treatment
• Acute presentation with clear precipitating cause
– Rate control
• Drugs to slow AV conduction
– Diltiazem, Verapamil, Beta blockers, (Digoxin)
• AV node ablation and permanent pacemaker
– Rhythm control
• Cardioversion
– Electrical DC cardioversion
– Chemical – Flecainide, Propafanone, Amiodarone
• Maintainance of Sinus Rhythm – Class 3 Sotalol, Amiodarone
– Class 1c Flecainide
– Radio frequency/cryo ablation
» Pulmonary Vein ablation with or without atrial lines
• Prevention of thrombo-embolism (esp. CVA)
– High incidence of CVA (embolic stoke) in AF
• First noticed in mitral stenosis
– Warfarin/NOACs therapy became standard
• Non-rheumatic AF
– Less than MS but still very significant
– Warfarin/NOACs causes a 66-70% reduction in stroke risk attributable to AF
– Aspirin (300mg a day) has a weak/no beneficial effect
– Who gets Warfarin/NOACs in non-rheumatic AF? Risk based
• Appreciable risk of stoke other than AF – Age (>65yr)
– Hypertension
– Previous stroke – CHA2DS2-VASc
• No contraindiactions to anticoagulation
– Peptic ulcer disease, Contact sports, alcoholism etc.
What atrial fibrillation pts should get anticoagulants
Those with a CHA2DS2-VASc score of 2 or more
Discuss ventricular tachycardia
• Serious
Ventricular Tachycardia
– Often fast
– Can degenerate into VF (and death)
• Inherently Unstable rhythm
• Often provokes ischaemia as associated with CAD
• Usually associated with previous LV damage
– MI, hypertensive heart disease, cardiomyopathy, previous heart surgery etc
How to tell if broad complex tachycardia is VT or SVT with aberration
- Is the distinction important? - If fast and the patient unwell the treatment is the same DC cardioversion
- Width of QRS – >140msec VT
- If RBBB: RSR’, R’>R favours SVT
• AV relationship
– Independent P waves, fusion or capture beats diagnose VT. Cannon waves in JVP
• NB these are not invariable as there is quite often 1:1 retrograde conduction
• Irregular
– Nearly always AF
• Is there a history of LV damage? – If so statistically a broad complex tachycardia will be VT whatever the ECG looks like
Discuss ventricular tachycardia mechanisms
• AcuteLVdamage
– Ischaemia, trauma
• Specific mechanisms that interfere with cell membrane electrophysiology
• Chronic LV damage
– (micro) Re-entry around fibrotic areas of non- conduction
• Abnormalities of the Na and K channels (Ion channelopathies) = Long QT interval syndrome
– Changes in intracellular K altering the cellular action potential
• Usually polymorphic
Discuss management of acute VT
• If haemodynamically compromised: – DC synchronised cardioversion
• Haemodynamics OK
– i.v.Amiodarone
– i.v. lignocaine (only to works in acute ischaemia)
– i.v.Class 1 agents (procainamide)
Discuss management of VT long term
• Management of the cause underlying it:
– Active ischaemia in IHD
– Pulmonary regurgitation post Fallot repair – Heart Failure
• Prevention of recurrence
– Implanted cardioverter defibrillator (ICD)
– Drugs Beta blockers, Class 1 agents (?prognosis),, Amiodarone
– Ablation
– Anti-tachycardia pacemaker (ATP)
Discuss ventricular fibrillation
- Invariably fatal
- ECG chaotic often fine movements
- No detectable cardiac output
- Often (but not always) preceded by VT
- Blow to the chest
- DC cardioversion
- IV adrenaline + DC cardioversion
- Treatment of any acute underlying cause
- ICD implanation
What is Torsade de Pointes - polymorphic ventricular tachycardia
- Tachycardia that can degenerate and cause death
* Cause of sudden death with normal heart at autopsy
What are the mechanisms of Torsade de Pointes
• Congenital
– Ion channelopathy, Brugarda, Catacholaminergic Polymorphic VT, ARVC
• Plus a provocation – adrenalin, facial immersion, exercise, hypokalaemia
• Acquired
– Drugs that inhibit inward rectifying K channel
• Erythromycin, antihistamines, antifungal (..conazoles), some anti-malarials and some anti-psychotics
– Drugs that lengthen QT inetrval
• Antiarrhythmics, Amiodarone, sotalol
– Slow AF with hypokalaemia and long-slow coupling interval
Discuss long QT syndrome diagnosis
- 1in5,000
- Family history of sudden death
- Death is associated with adrenergic setting
- <1 point low prob.
- 2-3 intermediate
- 4 or more high
What is brugada syndrome?
a genetic disorder in which the electrical activity within the heart is abnormal.[2] It increases the risk of abnormal heart rhythms and sudden cardiac death due to serious abnormal heart rhythms such as ventricular fibrillation or polymorphic ventricular tachycardia.
Discuss drug-induced Torsad
• Many drugs which may be linked by effects on inward rectifying Potassium channel
• Pause-dependent initiation
Its Torsade de Pointes
What are some risk factors for drug-induced LQTS
• Female gender 66% • Heart Failure 25% • LVH 14% • Hypokalaemia 18% • Hypomagnesaemia 9% • Digoxin 29% • Ca2+ Chan. Blockers 14% • Beta blockers 11% • Culprit drugs – Antiarrhythmics 77% – Quinidine 32% – Sotalol 17% – Non-antiarrhythmics 23%
LQT Syndrome Management
- Identify risk
- Avoid precipitating events
- Betablockers
- Pacemaker
- ICD
Conclusions
- The 12 lead ECG and Holter testing allow the precise diagnosis of disturbance of the cardiac rhythm
- Cardiac rhythm disturbances are potentially fatal and require specialist treatment
- Both drugs and device therapy are involved in the management of cardiac rhythm disturbance
