Supraventricular trachycardias (SVT) - arise from atrium or AV junction
Ventricular tachycardias - arise from ventricles
When myocardial function is poor, arrhythmias are more symptomatic & are potentially life-threatening
P wave = sinus
A) SAN
B) AVN
Sinus arrhythmia is usually predictable - due to irregularities of pulse.
What is sinus bradycardia?
Sinus rate of less than 60 bpm
Usually asymptomatic unless rate is very slow
Sinus brachycardia is normal in athletes -> due to increased vagal tone
What are the 2 main types of arrhythmia production?
Distrubances in impulse generation
Distrubance in impulse propagation
Can cause bradycardia or tachycardia
What are the causes of EADs?
Slow HR
Prolonged APs
Ceratin antiarrhythmic drugs (e.g. quinidine) - prolongs AP
What causes DADS?
Increased serum Ca+2
Increasedadrenaline
Drug toxicity (e.g. digoxin)
MI
What could you see in pts with EADs?
Nothing
Prolonged QT
Sustained arrhythmia (Torsade's de pointes)
What could you see in pts with DADs?
Nothing
Ectopic beat
Sustained arrhythmia (ventricular tachycardia)
What is heart block?
Block in either the AVN or bundle of His -> AV block
Block lower in the conduction system -> Bundle branch block
What are the 3 forms of heart block?
1st degree
2nd degree
3rd degree
What is 1st degree AV block?
PR interval is uniformly prolonged (more than 0.2 s)
Every atrial depolarisation is followed by conduction to the ventricles, but with delay
What is are the 2 types of 2nd degree AV block?
Mobitz I
Mobitz II
What is Morbitz I AV block?
Sinus rhythm
PR interval lengthens progressively with successive beats, until 1 P wave is not conducted at all
PR interval before blocked P wave is much longer than the PR interval after blocked P wave
What is Morbitz II AV block?
Sinus rhythm present
PR interval is consistent
1 P wave is not conducted at all
Dropped QRS complex is not preceded by progressive PR interval prolongation ('no warning')
Usually, wide QRS complex (> 0.12 sec)
What is 3rd degree (complete) AV block?
Atrial rate is faster than ventricular rate
PR intervals are completely variable
Complete loss of signalling between atria & ventricles (each are contracting, but not in sync)
P waves fall on T waves or can be 'lost' in QRS complexes
Normal width QRS complexes
How can MI cause an AV block?
Right coronary artery (RCA) supplies SAN & AVN
So, blockage of RCA -> SAN & AVN ischaemia -> AV block
Bundle of His 'takes over' -> narrow QRS complex, rate 50-60 bpm
If Bundle of His is damaged, Purkinje fibres 'take over' -> broad QRS complex, rate < 40 bpm
What does Right Bundle Branch Block (RBBB) show on ECG?
Secondary R wave in V1
Slurred S wave in V5 & V6
Due to right bundle will be delayed -> left ventricle will depolarise first
When does RBBB occur?
Normal healthy individuals
PE
Right ventricular hypertrophy
Ischaemic Heart Disease
ASD (WHAT?)
VSD (WHAT?)
Tetrology of Fallot
What is WPW Syndome?
Wolff-Parkinson-White syndrome
Define flutter.
Regular, rapid atrial contractions
250 - 305 bpm
Define fibrillation.
Sawtooth (F waves)
Typically 2:1, 3:1 or 4:1 conduction ration
More than 300 bpm
What are the different mechanisms for producing disturbances in impulse generation?
Disorder in automaticity
Trigerred activity (EADs or DADs)
What are the different mechanisms for producing disturbances in impulse propagation?
Re-entry
Conduction block
Both (atrial flutter)
How does accelerated automaticity lead to arrhythmia?
Mechanism of slow depolarisation to reach threshold potential is altered (threshold increased/decreased)
Reduced threshold -> increased rapid AP firing
Increased threshold -> decreased AP firing
Can lead to sinus tachycardia, escape rhythms & accelerated AV nodal rhythms
How does triggered activity lead to arrhythmia?
Myocardial damage -> oscillations ('after-depolarisations') of transmembrane potential at end of AP -> may reach threshold potential & produce arrhythmia
If occurs before the transmembrane potential reaches its threshold -> early after-threshold AP (EADs)
If occurs after transmembrane potential is completed -> delayed after-threshold AP (DADs)
What can abnormal oscillations be exaggerated by?
Pacing
Catecholamines
Electrolyte disturbances
Hypoxia
Acidosis
Some medications
Describe re-entry.
Fibrous tissue/scar does not conduct electricity (electricity has to go around it)
Problem - one of the routes is slower than normal (image - alpha is fast & beta is slow)
Alpha pathway has a longer refractory period than beta
When AP travels along both pathways, by the time the b pathway has sent its activity around the fibrous tissue, the a pathway has recovered and the b pathway ends up activating the a pathway (and going back up)
When AP has reached the top (C), the b pathway will have recovered, AP goes back round -> ends up producing a run of tachycardia
What is sinus bradycardia due to?
Either extrinsic factors that influence a relatively normal sinus node, or to intrinsic sinus node disease
Can be acute & reversible OR chronic & degenerative
What are the common extrinsic causes of sinus bradycardia?