Mechanisms of Arrhythmias Flashcards
Bradycardia= Tachycardia= 3 types of tachycardia 1) 4 within 2) eg... 3) other types such as...
4 reasons/ causes for arrhythmia which lead to TWO KEY DISTURBANCES
Bradycardia < 60bpm
Tachycardia > 100bpm
types:
1) Narrow complex tachycardia:
- atrial fibrillation
- atrial flutter
- atrial tachycardia
- sinus tachycardia
2) broad complex tachycardia eg. ventricular tachycardia
3) ventricular fibrillation tasardes
Causes of arrthymias:
- structural abnormalities
- cell damage
- electrolyte damage
- ion channel modification/ change
leads to…
disturbance in IMPULSE GENERATION
disturbance in IMPULSE PROPAGATION (or both
Who’s at risk:
Cell structure changes (3/5 eg’s)
Ion channel alterations (2)
Also environmental such as (2/4)
cell structure changes:
MI, Fibrosis, Toxins, Chemo, Myocarditis
ion channel alterations:
drugs, Long QT syndrome
Environmental:
Temp, hypoxia, academia, metabolic abnormalities such as low or high K+, Ca2+, Mg2+
Disturbance in impulse generation:
What is automaticity?
eg’s such as ectopic atrial tachycardia=
or junction tachycardia=
DAD- What does is stand for?
what's happening? 1) when does it happen? 2) 3) what does it cause? (3)
automaticity- the property of a fibre to initiate an impulse without prior stimulation
ectopic atrial tachycardia= P waves inverted, tissue firing in atria when shouldn’t be
junction tachycardia= AV firing when it shouldn’t be
DAD- Delayed After-Depolarisation
1) Action potential generated at the end of Phase 4 BEFORE the voltage-gated Ca2+ have recovered (should be resting)
2) therefore next circuit will have a shorter long-shoulder and a high of intra-cellular Ca2+ levels
3) activation of Na+/ Ca2+ exchanger could trigger an AP too early
causes:
- ventricular tachycardia
- arrhythmia
- ectopic beat
Disturbance in impulse generation:
EAD- What does is stand for?
what’s happening?
1) when is it occurring?
2) inc. in
3) inc. in
4) therefore
5) ALSO…. ->
what does it cause? (3 some mentioned)
EAD- Early After-Depolarisation
1) occurs in phase 2/3 of the circuit
2) inc. in Ca2+ opening -> therefore longer long-shoulder
3) Na+ do not close (H gates) more Na+ influx
4) leads to Elongated QT complex meaning a slower re-polarisation rate.
5) ALSO another heart beat can potentially be triggered TOO EARLY -> lead to Tarsades de pointes
causes:
- prolonged QT
- arrhythmia
- tarsades de pointes
Disturbances in Conduction Propagation:
Re-Entry Tachycardias:
requirements for re-entry (2)
why would one pathway be slower than another? ;) (2)
requirements:
1) 2 possible routes for AP to flow down- slow + fast route
2) impulse flows down one route, up another and gets caught in a loop
why?
1) central area block -> eg. scar tissue, refractory cells
2) variable blocking -> dead myocytes or myocytes with differing refractory periods/times
Disturbances in Conduction Propagation:
Supra-ventricular tachycardia:
characteristics (3)
mechanism
1) what is present and why?
2)
3)
4) wave front meet to form ->
5)
two types and they differ because
- regular tachycardia (130-250 bpm)
- one P wave for each QRS (might not see it though)
- QRS narrow in duration
mechanism
1) Accessory route present due to anatomical anomoly
2) Atrial systoe and AVN holds impulse (normal)
3) But AP travels down accessory route elsewhere and is not held, reaching ventricles early, normal AP then follows
4) wave fronts meet to form -> Delta wave
5) AP travels back up accessory route and forms a loop circuit
two types:
AVNRT- accessory pathway near AVN (circuit around AVN)
AVRT- accessory pathway not near AVN
Disturbance in impulse generation:
Atrial Fibrillation
what is it and how does it usually occur?
seen on ECG by: (2)
type of rhythm= …. because
Atrial Flutter
what is it and what is it caused by?
whats seen on ECG? (1)
ratios represent?
Atrial Fibrillation
mini-circuits in atria caused by scarring in atria
seen as:
No clear P waves
wobbly line
-irregularly irregular QRS complexes as impulses are hitting the AV node at random times
Atrial Flutter
Macro-circuit around right atrium caused by extra conduction tissue near AV valve
on ECG seen as Saw Tooth Motion
3:1 block -> every third AP from atria reaches ventricles
2:1 block
Disturbances in Conduction Propagation:
Conduction Block
The Heart Block Story
Normal conduction: (2)
First Degree
what’s happening? (4)
Second Degree Type 1 aka Wanke bach
what’s happening? (4)
Second Degree Type 2
what’s happening? (4)
Third Degree (3)
Normal Conduction:
QRS always after P wave
0.2s between P wave and QRS or less
First Degree: P wave present QRS always present but late same every beat >0.2s (5 small squares
Second Degree Type 1 aka Wanke bach:
- P wave present
- QRS becomes later and later until doesn’t show
- PR interval increases each time until QRS dropped
- two P waves consecutively
Second Degree Type 2
- P wave present
- sometimes QRS present sometimes not- unpredictable
- seen by random P waves without QRS
- need pacemaker
Third Degree
- Regular P waves at one rate
- QRS regular at another rate, both on completely separate schedule
- usually their escape rhythms so QRS slower
Disturbance in impulse generation:
Broad complex tachycardia
what is it?
why? (2)
whats seen on ECG? (2)
what is it?
ventricles have mini-circuit and dictate HR
why? (2)
- scar tissue (from MI) some cardiomyocytes are dead and others partially dead -> one pathway quicker
- causes a re-entry circuit around scar
whats seen on ECG?
big broad QRS complex
v high HR (150 bpm)
Ischaemic heart disease causes AV block: mechanism (v brief) 1) what artery supplies AVN? 2) then... 3)
consequences of arrhythmia 1) due to 2 reasons can lead to 2) KEY WORD therefore (3/4 egs)
Right coronary artery supplies AVN
blocked via atheroslerosis -> inferior MI
AVN ischaemia -> damage
consequences: 1) dec. CO because low HR or low SV from a decrease in diastolic filling can lead to... heamodynamic compromise and therefore -HF - Cardiac ischaemia - hypo tension - dec. renal/liver/ perfusion so failure of these organs
