29-09-22 – Pathophysiology of Arrhythmias Flashcards
Learning outcomes
- know why dysrhythmias may arise and how they are classified
- know how heart block arises and its classification
- know how circus re-entry may arise
- know the differences in the electrical activity of the different parts of the heart and between normal and abnormal pacemaker cells which allow antidysrhythmic drug treatment
- understand the importance of correct identification of location and nature of the dysrhythmia for proper choice of antidysrhythmic drug
- Understand genetic basis of VT and ionchannelopathies
- Understand the management of atrial fibrillation
What are the 2 main types of arrhythmias?
What is decremental conduction? What does this prevent?
- The 2 main types of arrhythmias are tachycardias and bradycardias
- Decremental conduction references the fact that the more frequently the AV node is stimulated, the slower it will conduct
- This prevents rapid conduction to the ventricle in cases of rapid atrial rhythms, such as atrial fibrillation or atrial flutter.
Where is fast conduction found in the heart?
What is fast conduction?
- Fast conduction is found in the His Purkinje system
- Fast conduction is where the His Purkinje System will conduct faster and faster until it stops conducting and enters its absolute refractory period where no more action potentials can be generated
What are the 5 phases of cardiomyocyte action potential?
How does pacemaker cell action potential compare with this?
What is pacemaker potential?
- 5 phases of cardiomyocyte action potential:
1) Phase 0 = rapid depolarisation
2) Phase 1 = partial repolarisation
3) Phase 2 = plateau
4) Phase 3 = repolarisation
5) Phase 4 = resting potential - Pacemaker cells do not have phases 1 or 2, but have an additional phase (phase 4 on the diagram) known as the pacemaker potential
- The pacemaker potential is the slow, positive increase in voltage across the cell’s membrane that occurs between the end of one action potential and the beginning of the next action potential
What are the 2 main type of bradycardia?
How do they each occur?
- 2 main types of bradycardia:
1) Sinus bradycardias
* Happens when your SA node generates a heartbeat less than 60 times a minute (60bpm)
2) AV blocks
* An AV heart block happens when the electrical impulses are delayed or blocked as they travel between your atria (the top chambers of your heart) and your ventricles (the bottom chambers of your heart)
* Occurs below the SA Node
What are the 5 causes of Sinus Bradycardia?
What are the 4 causes of AV heart block?
- 5 Causes of sinus bradycardia:
- Sinus Bradycardia is always a secondary event to:
1) Drugs (e.g. Beta Blockers, Diltazem(CCB))
2) Vagal activity
3) Hypothyroidism
4) Sinus Node disease
5) Electrolyte abnormalities - 4 Causes of AV heart block:
1) Vagal activity
2) Myocardial infarction
3) Electrolyte abnormalities
4) Degenerative diseases
What are the 3 types of AV block based on ECG abnormality?
How do they appear on an ECG?
- 3 types of AV block based on ECG abnormality:
1) 1st degree
* Lengthening of the PR interval
2) 2nd degree
* Has 2 types:
* Mobitz Type 1 (Wenckebach block) - Progressive lengthening of PR interval until P wave is blocked and then PR is short again
* Mobitz Type 2 - Block after 2 or 3 conducted beats in regular pattern
3) 3rd degree
* Complete AV dissociation
* Atrial activation (usually from the sinus node) is independent from ventricular activation (originating from the AV junction, His-Purkinje system, or ventricles)
What is the main type of treatment for bradycardia?
What 3 other treatments might be offered if needed?
- The main treatment for bradycardia is pacemaker (temporary or permanent)
- Only if needed, treatment for:
1) Symptoms of syncope dizziness
2) Prophylactic at time of operations
3) Post AMI (acute MI)
Based on ECG, what are the 2 main types of tachycardia?
How do they appear on an ECG?
Where do they each originate?
- 2 main types of tachcyardia based on ECG:
1) Narrow Complex / Supraventricular Tachycardias
* Whatever is causing it originates above AV node and sending it below AV node
* Occurs when the QRS complex is less than 0.12ms
* If its narrow, it must be conducted over the His/Purkinje tissue so must be an SVT
1) Broad Complex Tachycardias
* Origin is below AV node and therefore arising from ventricle)
* QRS complex is longer than 0.12ms
What are the 5 main types of narrow complex / supraventricular tachycardias?
How do they each appear on ECGs?
- 5 main types of narrow complex / supraventricular tachycardias:
1) Atrial Tachycardias
* Focus in the atria
* There is a narrow complex tachycardia at 95 bpm.
* Each QRS complex is preceded by an abnormal P wave
* P wave morphology is consistent throughout.
2) Junctional Tachycardias
* Junctional mean associated with the AV node
* Arise at junction of the heart
* Retrograde P waves — inverted in II, III and aVF; upright in V1 and aVR.
3) AVNRT + AVRT
* Atrioventricular nodal re-entry tachycardia (AVNRT)
* AV re-entrant (or reciprocating) tachycardia (AVRT)
* Involves the AV node intrinsically or AV node and accessory pathway
* IN AVNRT, Regular, narrow complex tachycardia without P waves activity (p waves merge into QRS complex), or P-wave occurs after QRS complex in retrograde with a short RP interval (70ms)
* IN AVRT P-wave is visible in most cases.
* It is retrograde (inverted) in leads II, III and aVF and it occurs after the QRS complex (somewhere on the ST segment or early on the T-wave)
* Typically longer RP interval in AVRT (>70ms)
4) Atrial Flutter
* Narrow and regular
* Flutter waves are present, best seen in leads II, III, and aVF (*)
* The atrium can beat 300 times, making 3 p waves per QRS complex, which creates a saw tooth pattern
5) Atrial Fibrillation
* Narrow but irregularly irregular.
* Could still be AF is broad and irregular
What are the 3 main types of broad complex tachycardia?
How do they appear on an ECG?
How does bundle branch block appear on an ECG?
What is aberration?
- 3 main types of broad complex tachycardia:
1) Ventricular Tachycardia
* Can be monomorphic (every complex is the same) and polymorphic (complexes are different) VT
2) SVT (supraventricular tachycardia) with aberration
* Aberration is acquired, rate- dependent bundle branch block
* Rate-dependent left bundle branch block refers to a transient left bundle branch block (BBB) associated with an increase in heart rate
* If the QRS complex is widened and downwardly deflected in lead V1, a left bundle branch block is present.
3) SVT with a pre-existing BBB morphology on ECG
* e.g. SVT of antidromic tachycardia in WPW
What are the 3 basic mechanisms of tachycardias?
- 3 basic mechanisms of tachycardias:
1) Ectopic Focus (aka ectopic pacemaker)
* An excitable group of cells that causes a premature heart beat outside the normally functioning SA node of the heart
2) Re-entry / circus movement
3) Fibrillation – independent wavelets of activity
Explain the 12 steps in development of re-entry/circus movement.
Why is this important?
What occurs during ventricular tachycardia?
What 2 drugs could we used to correct this pathway?
What procedure could we used?
- Steps in development of re-entry/circus movement:
1) In connective tissue of the heart, there are two adjacent pathways with different electrophysiological properties, which are connected proximally and distally.
* One pathway has fast conduction and long refractory period
* The other pathways has slow conduction and short refractory period
* Absolute refractory period is a period when action potentials can not be generated, and cells can not be excited
2) Impulses (action potentials) split and go down the fast and slow pathway
3) Impulse conducted by the fast pathway reach the distal connection faster, and split, with one end going down the distal pathway, and the other going down the distal part of the slow conduction pathway
4) When these impulses meet here, the tissue on either side are in the refractory period, so the impulse cant be conducted on either side
5) If a premature beat occurs, the impulse conducted down the fast pathway doesn’t have any effect, as this pathway is in the refractory period
6) By the time the impulse travelling down the slow pathway reaches the point at which it would normally meet the Impulse down the fast conduction pathway, the refractory period of the fast conduction pathway has ended
7) This results in the action potential going onto the fast conduction pathway and going back around to the proximal connection
8) Once it reaches the proximal road, the action potential splits again, sending an action potential down the proximal route, and one down the slow conduction pathway
9) Once the action potential reaches the point at which it which it would meet the fast conduction action potential, the refractory period of the fast conduction pathway has ended, allowing it to continue
10) This cycle continues, resulting in a re-entry/circus movement, where action potentials are being send down the proximal and distal roads
11) When a normal AP is sent by the SA node, it is likely not going to be able to move down the pathway due to refractory periods set off by the AP circling round the pathway, which results in unidirectional blockade
12) These re-entry circuits will lead to ventricular tachycardias and arrhythmias
- This is important, as prolonged periods of ventricular tachycardia can lead to ventricular fibrillation, which can lead to death
- During ventricular fibrillation, disorganized heart signals cause the lower heart chambers (ventricles) to twitch (quiver) uselessly.
- As a result, the heart doesn’t pump blood to the rest of the body.
- To correct this pathway, we could use:
1) Na+ channel blocker – slows conduction speed
2) K+ channel blocker – extends the refractory period - We could also use electrical cardioversion to shock the heart in order to return to Sinuous rhythm
What are AVNRT and AVRT?
What is the patient history associated with those diagnosed with AVNRT or AVRT?
How do AVNRT and AVRT re-entry circuits differ?
What is an accessory pathway?
What 2 ways can the accessory pathway of AVRT be?
How does this effect ECG findings?
How are AVRT and AVNRT terminated?
- Both AVNRT and AVRT are narrow complex / supraventricular tachycardias
- Those diagnosed with AVNRT or AVRT tend to have no history of cardiac diease
- AVNRT = AV nodal re-entrant tachycardia
- Tachycardia where re-entry circuit is through juxtanodal (nodal) material
- AVRT = AV re-entrant tachycardia where re-entry is through an accessory pathway
- An accessory pathway is His Purkinje material that has breached the AV ring somewhere other than the AV node
- The accessory pathway through which re-entry occurs in AVRT may either be
1) Revealed
* Means WPW (Wolff-Parkinson-White syndrome) on a 12-lead ECG
2) Concealed
* Means normal non-tachycardia on 12 lead ECG (i.e. the accessory pathway only conducts in a normal retrograde (backward moving) manner)
- AVRT and AVNRT are terminated through IV adenosine
What are the 3 different forms of AVRT?
Which one is associated with Wolff-Parkinson-White syndrome (WPW)
- Different forms of AVRT:
1) Orthodromic (most common)
* Anterograde (forward moving) conduction occurs via the AV node with retrograde conduction occurring via the accessory pathway
2) Antidromic
* Much less common AVRT in which the circuit is reversed
* Anterograde (forward moving) conduction occurs exclusively via the accessory connection and results in a “maximally pre-excited” QRS complex on an ECG
* This type is associated with Wolff-Parkinson-White syndrome (WPW)
3) Duodromic
What is Wolff-Parkinson-White syndrome (WPW)?
What is this due to?
What is the most common cause of WPW tachycardias?
What 3 ways characteristics does WPW have on an ECG?
- Wolff-Parkinson-White syndrome (WPW) is pre-excitation of the ventricles
- This is due to anatomical atrio-ventricular bypass tract with non-decremental conducting (conduction maintained) properties
- The most common cause of WPW tachycardias is antidromic revealed accessory pathway AVRT (narrow complex tachycardia)
- WPW appearance on an ECG:
1) Shortened PR interval <0.12sec
2) Slurred upstroke of QRS and
3) Widened QRS complex >0.12sec
How common if atrial fibrillation (AF)?
Describe the 3 features of AF appearance on an ECG? What are 3 signs of AF?
What are the associated symptoms?
What are 10 causes of AF?
What are 3 mechanisms that can contribute to AF?
- Atrial fibrillation (AF) is very common
- Appearance of AF on an ECG:
1) Usually a narrow QRS complex
2) Tachycardia
3) No P waves - 3 Signs of AF:
1) Fast ventricular response rate (causes SOB, hypotension)
2) Slow conduction (causes dizziness and syncope)
3) Embolism of left atrial thrombus (can cause CVA (stroke)) - 10 Causes of AF:
1) Ischaemic Heart Disease
2) Hypertensive heart disease
3) Mitral Valve disease
4) Thyrotoxicosis
5) Cardiomyopathy
6) Alcohol
7) Post bypass
8) Myocarditis
9) Accessory pathways
10) Lone (no cause) - 3 Mechanisms that can contribute AF:
1) Size of left atrium (common in large mammals, atria too small in children so doesn’t occur)
2) >5 wavelets of activity on an ECG
3) Focus of wavelet generation around the insertion of the pulmonary veins
What are the 3 main types of broad complex tachycardia?
How do they appear on an ECG?
How does bundle branch block appear on an ECG?
What is aberration?
- 3 main types of broad complex tachycardia:
1) Ventricular Tachycardia
* Can be monomorphic (every complex is the same) and polymorphic (complexes are different) VT
2) SVT (supraventricular tachycardia) with aberration
* Aberration is acquired, rate- dependent bundle branch block
* Rate-dependent left bundle branch block refers to a transient left bundle branch block associated with an increase in heart rate
* If the QRS complex is widened and downwardly deflected in lead V1, a left bundle branch block is present.
3) SVT with a pre-existing BBB morphology on ECG
* e.g. SVT of antidromic tachycardia in WPW
How do we differentiate between VT and SVT with aberration?
How serious and fast is VT?
What can it degenerate into?
Why is this deadly?
What is VT usually associated with in patients?
What does VT normally appear on an ECG?
What is the difference between monomorphic and polymorphic VT on ECGs?
What is Torsades do Pointes?
How does it present on an ECG?
- We differentiate between VT and SVT with aberration using an adenosine test, with there being no response for VT
- VT is very serious and often fast
- VT can degenerate into VF, which is an inherently unstable rhythm that can promote death through ischaemia in CAD
- VT is Usually associated with previous LV damage e.g MI
- On an ECG, VT has a broad complex, with no P waves associated with the QRS complex
- Monomorphic VT usually looks regular on an ECG
- Polymorphic VT is usually very irregular on an ECG (known as Torsades de Pointes – many morphologies)
- Torsades de Pointes is a type of polymorphic ventricular tachycardia characterized on electrocardiogram by oscillatory changes in amplitude of the QRS complexes around the isoelectric line.
- Torsades de Pointes is associated with QTc prolongation, which is the heart rate adjusted lengthening of the QT interval.
How fatal is VF?
How does it affect Cardiac output?
What is it often preceded by?
How does VF appear on an ECG?
- VF is Invariably fatal
- There is no detectable cardiac output in VF
- VF is Often (but not always) preceded by VT
- VF appears on an ECG as chaotic irregular deflections of varying amplitude
What is the most likely cause of sudden death with normal heart at autopsy?
What is Torsades de Pointes?
How does it appear on an ECG?
- The most likely cause of sudden death with normal heart at autopsy is Polymorphic Ventricular Tachycardia
- Torsades de Pointes is a type of polymorphic ventricular tachycardia
- It is characterized on electrocardiogram by oscillatory changes in amplitude of the QRS complexes around the isoelectric line.
- Torsades de Pointes is associated with QTc prolongation, which is the heart rate adjusted lengthening of the QT interval.
What is another name for ion channelopathies?
What is the distinctive feature of ion channelopathies on an ECG?
Which phases of the AP change in a long QT interval syndrome?
- Another name for ion channelopathies is Long QT interval syndrome
- The distinctive feature of ion channelopathies on an ECG is a Long QT interval
- In long QT interval syndrome phases 2 and 3 are altered (determined by activity in sodium and potassium channels which is where mutations happen)
What is Brugada syndrome?
How is it characterised on an ECG?
How is it associated with Torsades de Pointes?
- Brugada syndrome is A type of channelopathy in which people with no known heart problems or defects suffer sudden cardiac death or aborted sudden cardiac death.
- Characterised by Right bundle branch block, with persistent ST-segment elevation.
- One of the congenital causes of Torsades de Pointes.
What is sudden cardiac death?
What are the 2 best tests to diagnose disturbance of the cardiac rhythm?
What is Holter monitoring?
- Sudden cardiac death is unexpected death due to heart problems, which occurs within one hour from the start of any cardiac-related symptoms
- 2 best tests to diagnose disturbance of the cardiac rhythm:
1) 12 lead ECG
2) Holter testing
* a technique for long-term, continuous usually ambulatory, recording of ECG signals on magnetic tape for scanning and selection of significant but fleeting changes that might otherwise escape notice.
