Atrial Arrythmias Flashcards
What controls the rate of the SA node?
Parasympathetic: ‘puts the brakes on’.
Sympathetic: Increases HR.
Dominant extrinsic influence on heart is inhibition.
Sino-atrial block/pause
Blocks occur as a multiple of the p-p interval.
Measure out.
Non-conducted beat from normal pacemaker.
Rhythm before and after normal.
Sinus arrest
Time period without sinus node activation.
Clear pause in normal rhythm.
Often terminated by escape beat.
Rhythm before and after usually normal
Common causes / treatment of sino-atrial block
Most commonly acquired.
Ischaemia.
Fibrotic.
Inflammation.
Infiltrative.
Medication (B-blockers).
Genetic/congenital.
Treat underlying cause.
Symptoms / period of arrest determine intervention.
P wave
Should be rounded in shape (right atrium is activated before left atrium, so first part of p wave is RA, second part is LA)
Duration
< 0.12 s (<120ms or 3 small squares)
Amplitude
< 2.5 mm (0.25mV) in the limb leads
< 1.5 mm (0.15mV) in the precordial lead
Atrial abnormalities are most easily seen in the inferior leads and lead V1.
Premature Atrial Ectopic Beat
ECG criteria:
Premature firing of atrial cell (faster than SA node).
Premature, bizarre shaped P wave.
Normal, narrow QRS complex.
Compensatory pause.
The presence of an irritable focus in the atrial myocardium initiates the depolarisation of the atria before the next expected sinus discharge.
When your heart experiences an early beat, a brief pause often follows.
You generally become aware of it on the next beat – which feels much stronger.
Atrial Bigeminy
Every other beat.
Atrial trigeminy.
Can occur in short runs
Symptoms, Causes & Treatment
Symptoms:
Often asymptomatic.
Palpitations: skipped beats, fluttering, pounding.
Causes: Idiopathic
Lung Disease
Stimulants, alcohol, caffeine, smoking
Exercise
Stress – high adrenaline levels.
Treatment: Anti-arrhythmics (beta-blocker).
What causes long term atrial ectopics
More likely that there’s an underlying condition such as:
Heart disease
Chemical imbalances
Injury to the myocardium due to infection/ hypertension.
Wandering Atrial Pacemaker
Irregularly irregular rhythm.
Multiple atrial pacemakers firing at own rate.
Different p wave morphologies.
Different p wave distance from QRS.
Different QRS rate.
Multiple excitable areas.
Position determines P morphology and PR interval.
Often in very young, very old, athletes.
Cause: Unclear. ? varying vagal tone, digoxin toxicity, age.
Rarely symptomatic.
Atrial tachycardia
Atrial tachycardia is a supraventricular tachycardia (SVT).
Does not require the AV node, accessory pathways or ventricular tissue for its initiation and maintenance.
Can be unifocal or multifocal.
Usual atrial rate 160-250bpm.
Varying levels of conduction (1:1, 2:1, 3:1 etc).
or not easily seen.
Sudden onset and offset.
How does atrial tachycardia manifest?
Usually episodic or paroxysmal.
Sudden onset of palpitations.
Often due to enhanced automaticity.
May be non-sustained but repetitive.
Can be sustained/continuous (re-entrant forms).
Most common site of origin for AT: crista terminalis (smooth myocardium in RA).
Atrial tachycardia symptoms
Palpitations, which can be skipping, fluttering or pounding in the chest.
Chest pressure or pain.
Shortness of breath (dyspnoea) & fatigue
Syncope / near-syncope when V-rate is very fast.
Light-headedness or dizziness due to hypotension.
Frequent or incessant tachycardias can lead to reduced exercise tolerance and symptoms of heart failure due to tachycardia-induced cardiomyopathy.
Atrial tachycardia causes
Cardiomyopathy.
Chronic obstructive pulmonary disease.
Ischaemic and rheumatic heart disease.
Sick sinus syndrome.
Digoxin toxicity, cocaine, alcohol, caffeine, antihistamines, antidepressants, appetite suppressants.
Scar tissue which gives rise to the formation of a circuit.
ASD surgical repair.
Atrial tachycardia treatment
Depends on the type and severity.
Treat the cause! Assess medical history and meds.
Medications: anti-arrhythmic drugs (sotalol, flecainide and amiodarone) .
Radio-frequency catheter ablation (RFA).
Cryo-ablation.
Atrial Flutter
Very rapid atrial impulses from atrial ectopic focus
Caused by Re-entrant circuit in the right atrium
The atria usually discharge at a regular rate of around 300bpm (~200-400bpm). Saw-tooth flutter waves.
The ventricular response is determined by the conducting ability of the AV node. Therefore regular or variable ventricular rate (quoted as a ratio -flutter waves: QRS, e.g. 2:1, 3:1 etc)
Features of AFl
Narrow complex tachycardia
Regular atrial activity at ~300 bpm
Flutter waves (“saw-tooth” pattern) best seen in leads II, III, aVF — may be more easily spotted by turning the ECG upside down!
- Flutter waves in V1 may resemble P waves
- Loss of theisoelectric baseline
- Fixed AV blocks
Ventricular rate is a fraction of the atrial rate, e.g.
2:1 block = 150 bpm
3:1 block = 100 bpm
4:1 block = 75 bpm
- Variable AV block
The ventricular response is irregular and may mimic AF
On closer inspection, there may be a pattern of alternating 2:1, 3:1 and 4:1 conduction ratios
Atrial flutter with a 3:1 block
Handy Tips For Spotting Flutter
- Rapid Recognition
Narrow complex tachycardia at 150 bpm (range 130-170)? Yes -> Suspect flutter!
Turn the ECG upside down and scrutinise the inferior leads (II, III + aVF) for flutter waves.
- VagalManoeuvres +/- Adenosine
Atrial flutter will not usually cardiovert with these techniques (unlike AVNRT), although typically there will be a transient period of increased AV block during which flutter waves may be unmasked.
- RR intervals
In atrial flutter with variable block the R-R intervalswill be multiples of the P-P interval — e.g. assuming an atrial rate of 300bpm (P-P interval of 200 ms), the R-R intervalwould be 400 ms with 2:1 block, 600 ms with 3:1 block, and 800 ms with 4:1 block.
Look for identical R-R intervals occurring sporadically along the rhythm strip; then look to see whether there is a mathematical relationship between the various R-R intervals on the ECG.
In contrast, atrial fibrillation will be completely irregular, with no patterns to be discerned within the R-R intervals.
How to differentiate between rhythms?
try some vagal manoeuvres or give a test dose of adenosine — AVNRT/AVRT will often revert to sinus rhythm, whereas slowing of the ventricular rate will unmask the underlying atrial rhythmin sinus tachycardia or atrial flutter.
Atrial Fibrillation
Common sustained arrhythmia (prevalence 2.5% in UK; 9% in over 65s).
Rapid firing foci – atria discharge at a rate between 350 and 600bpm – small irregular fibrillation waves.
Multiple re-entrant circuits or “wavelets” of electrical activity sweeping around the atrial myocardium.
Results in loss of effective atrial contraction
ECG – No P wave
Fibrillation waves
Irregular ventricular rate
Absence of an isoelectric baseline.
Irregularly irregular rhythm
Slow vs fast AF
Commonly AF is associated with a ventricular rate ~ 110 – 160.
AF is often described as having ‘rapid ventricular response’ once the ventricular rate is > 100 bpm.
‘Slow’ AF is a term often used to describe AF with a ventricular rate < 60 bpm.
Causes of ‘slow’ AF includehypothermia,digoxin toxicity, medications, andsinus node dysfunction.
AF/ Afl Symptoms
Breathlessness
Light-headedness & dizziness
Palpitations
Chest pain
(Stroke)
Reduced ability to exercise.
Fatigue.
Lightheadedness.
Dizziness.
Confusion.
Shortness of breath.
AF/ Afl Treatment
Rate (digoxin, beta blocker, CCB) and rhythm control (flecainide, beta blocker).
Cardioversion.
Ablation – PVI or Pace and ablate strategy (AVN ablation).
Anticoagulation.
CLASSIFICATION of AF
AF can be classified in terms of its duration:
Paroxysmal – terminates spontaneously in less than 7 days
Persistent – AF would continue but normal rhythm can be restored
Permanent – restoration of normal rhythm is likely impossible. Decision not to attempt to restore rhythm
