ECG Arrhythmias Flashcards
ECG provides info on
about rate, rhythm and the timing of events in the cardiac cycle
– arrhythmias, conduction blocks
heart muscle
what do increased voltage in ECG suggest
increased muscle mass - hypertrophy
what do wider waves suggest
slowed conduction
what does left axis deviation mean
left ventricle hypertrophy
more muscle mass pulls depolarisation to the left
deflections in lead I get bigger but aVF get smaller
what does right axis deviation mean
– right axis deviation
– right ventricle hypertrophy
– more muscle mass, pulls depolarisation to the right
– deflections in AvF get bigger, while lead I gets smaller
how is delayed conduction conveyed
elongated PR interval, QRS or QT
when is ST depression seen
– only seen in leads pointing towards damage ischaemia
when is ST elevation seen
(infarction)
– only seen in leads pointing towards damage
– acute infarction, full thickness of the myocardium
tachycardia
> 100 bpm
bradycardia
<60 bpm
name 2 types of irregular rhythms
regularly irregular - irregular pattern
irregularly irregular - does not repeat an irregular pattern
arrhythmia
It collectively describes a change in the normal sequence of electrical impulses
causes if arrhythmia
altered rate - too fast or too slow
irregular patterns
conduction problems
how does ischaemia affect the heart
disrupt individual membrane potential in individual myocytes
• Sinus tachycardia and cause
: increased rate but normal rhythm
– mainly sympathetic as in exercise or secondary to low blood pressure
– also increased high temperatures or cardiac toxicity
Sinus bradycardia
decreased rate but normal rhythm
– seen in athletes, low rate but larger stroke volume
– increased vagus (PNS) activity (e.g. carotid sinus syndrome)
Sinus arrhythmia:
a regularly irregular rhythm from the SA node
– Cross talk between cardiorespiratory signals
– heart rate increases on inspiration
Arrhythmias may arise due to a number of reasons
- Changes in automaticity
- Triggered activity (after depolarisation)
- Conduction delay and appearance of re-entry circuits
is the SA alone in its automaticity
The SA node is not alone in its automaticity
– but it is the fastest
SA node depolarisation rate what does the its rate depend on?
depolarisation rate 60-100/min
– depends on the autonomic nervous system
AV node depolarisation rate
depolarisation rate 40-50/min
Purkinje fibres depolarisation rate
depolarisation rate ~35/min
Afterdepolarisations
abnormal stimuli outwith the normal activity
types of afterdepolarisations
early (EAD) or delayed afterdepolarisations (DAD
when do EADs occur
EADs occur when stimulation occurs during the plateau (Phase 2) or repolarisation phase (Phase 3)
when do DADs occurs
DADs occur during Phase 4 (resting) and trigger depolarisation, but
before the time normally expected
– due to elevated Ca2+
levels
what parts of the heart DONT depolarise
blood vessels, damaged fibrotic tissue
what happens when depolarisation in regions of heart that dont typically depolarise
When depolarisation hits these areas it cannot go through, but must go around
can be a problem if there new route is longer than typical path of conduction
issues that can arise when typical path of conduction is deviated to longer path of conduction
– fibrous plaques or dilated heart increases path length
– ischaemia slows conduction, due to high K+ and depolarisation
– this goes back to the refractory period
paroxysmal tachycardia
• Bursts of tachycardia due to re-entry pathways
– classified by origin: either ventricular or supraventricular
types of paroxysmal tachycardia
ventricular and supraventricular
what can ventricular paroxysmal tachycardia lead to?
what is ventricular paroxysmal tachycardia?
what are its causes?
may lead to fibrillation and death
– fibrillation is the uncoordinated depolarisation
– usually due to ischaemic damage or some drugs
supraventricular paroxysmal tachycardia
it originates above the ventricles so is either atrial or AV node
– atrial (inverted P wave) or AV node (hidden P wave)
– more common in young, seldom has morbidity
fibrillation
• Rather than the coordinated spread of depolaristion through the
heart this is uncoordinated and sporadic
Atrial fibrillation
no coordinated depolarisation of the atria, so no P wave
– irregular transmission to ventricles, irregularly irregular tachycardia
Ventricular fibrillation
individual myocytes depolarising so no discernible waveform
– no coordinated contraction, no cardiac output
ectopic beats of the atria
These are premature contractions due to abnormal impluses from
ectopic (abnormal) foc
causes of ectopic beats of atria
– areas of ischaemia (altered membrane potential)
– excessive stretch of muscle fibres
– drug actions
what does ectopic beats of atria look like on ECG
– show up as extra P wave and weak pulse on the ectopic beat
Looks similar to premature AV node contraction
weak pulse no P wave
ectopic beats of ventricle
premature ventricular contractions (PVCs)
what does ectopic beats of ventricles look like on ECG
• Present as a widened and QRS and inverted T wave
– conduction through muscle is slower than conducting system
– the slow conduction means fibres that depolarised first also repolarise first
causes of Ectopic beats
Minor PVCs caused by drugs (nicotine/coffee) but others are major
and may lead to fibrillation
heart block
• Decreased or total block of AV conduction
– due to ischaemia/compression/inflammation of AV-node
how is 1st degree heart block characterised
the delay in conduction
– characterised by an increased PR interval (>0.2 sec or one large box)
how is 2nd degree heart block characterised
the increased delay
– so that now some QRS complexes are dropped (PQRS > P > PQRS > P…)
how is 3rd degree heart block characterised
3rd Degree is the complete block
– ventricles contract (automaticity /”ventricular escape”) but slower (~40 bpm)
– SA node still firing but no relationship between P and QRS
