Arrythmias Flashcards
What is the main pacemaker in the heart?
The sinus node.
What controls the sinus node discharge rate?
The autonomic nervous system.
Define sinus rhythm.
Sinus rhythm - a P wave precedes each QRS complex.
Normal sinus rhythm: characteristics on ECG leads.
- P waves that are upright in leads I & II of the ECG
- Inverted P waves in the cavity leads, AVR & V1
What is sinus arrhythmia? Describe it during inspiration + expiration.
- Fluctuations of autonomic tone result in changes of the sinus discharge rate.
- During inspiration:
- Parasympathetic tone falls and the heart rate quickens.
During expiration:
* Parasympathetic tone increases and so heart rate falls.
- This variation is normal especially in children and young adults.
Name 4 causes of sinus tachycardia.
- Physiological response to exercise.
- Fever / sepsis
- Anxiety
- Anaemia.
- Dehydration.
- Pneumonia.
- Heart failure.
- Hypovolemia.
Give 4 causes of sinus bradycardia.
- Ischaemia.
- Fibrosis of the atrium.
- Inflammation.
- Drugs.
What lead(s) would you look in to assess sinus bradycardia/tachycardia?
Any - rhythm strip is best.
What is a cardiac arrhythmia?
An abnormality of the cardiac rhythm.
What is the most common cardiac arrhythmia?
Atrial fibrillation
What are the 2 main types of arrthymias?
- Bradycardia (slow HR)
- Tachycardia (fast HR)
What is classed as bradycardia?
Less than 60 bpm during the day and less than 50 bpm
at night
What happens in the autonomic nervous system to cause bradycardia?
Increased PARASYMPATHETIC TONE or decreased
SYMPATHETIC STIMULATION produces BRADYCARDIA
What is classed as tachycardia?
More than 100 bpm
What happens in the autonomic nervous system to cause tachycardia?
A reduction of PARASYMPATHETIC TONE or an increase in SYMPATHETIC STIMULATION leads to TACHYCARDIA
Give 3 potential consequences of arrhythmia.
- Sudden death.
- Syncope.
- Dizziness.
- Palpitations.
- Can also be asymptomatic.
Give the 2 broad categories of tachycardia.
- Supra-ventricular tachycardias
- Ventricular tachycardias.
Where do supra-ventricular tachycardia’s arise from?
They arise from the atria or atrio-ventricular junction.
Where do ventricular tachycardia’s arise from?
The ventricles.
Give the 5 types of supraventricular tachycardias.
Supraventricular tachycardias:
1. Atrial fibrillation.
2. Atrial flutter.
3. AV node re-entry tachycardia (AVNRT).
4. Accessory pathway / AVRT (WPW Syndrome).
5. Focal atrial tachycardia.
Give the 3 types of ventricular tachycardias.
Ventricular tachycardias:
1. Ventricular ectopic
2. Prolonged QT syndrome
3. Torsades de Pointes
Do supra-ventricular tachycardia’s have narrow or broad QRS complexes?
Supraventricular tachycardias are often associated with narrow complexes.
Do ventricular tachycardia’s have narrow or broad QRS complexes?
Ventricular tachycardias are often associated with broad complexes.
Name 2 things that may aggravate a supraventricular tachycardia.
Exertion, coffee, tea, alcohol
What is atrial fibrillation?
A chaotic irregularly irregular atrial rhythm at 300-600 bpm.
- The AV node responds intermittently, hence an irregular ventricular rate.
Give the 5 clinical classifications of AF.
- Acute: onset within the previous 48 hours
- Paroxysmal: stops spontaneously within 7 days
- Recurrent: two or more episodes
- Persistent: continuous for more than 7 days and not self terminating
- Permanent
Give 5 causes of AF.
- Idiopathic
- Hypertension (most common in developed world)
- Heart failure (most common in developed world)
- Coronary artery disease
- Valvular heart disease; especially mitral stenosis
- Cardiac surgery (1/3rd of patients after surgery)
- Cardiomyopathy (rare cause)
- Rheumatic heart disease
- Acute excess alcohol intoxication
Give 3 risk factors of AF.
- Older than 60
- Diabetes
- High blood pressure
- Coronary artery disease
- Prior MI
- Structural heart disease (valve problems or congenital defects)
Explain the pathophysiology of AF.
- Atrial fibrillation (AF) is maintained by continuous, rapid (300 600/min) activation of the atria by multiple meandering re-entry wavelets.
- These are often driven by rapidly depolarising automatic foci, located predominantly within the pulmonary veins.
- The atria respond electrically at this rate, but there is NO COORDINATED MECHANICAL ACTION and only a proportion of the impulses are conducted to the ventricles
I.E. there is no unified atrial contraction instead there is atrial spasm. - The ventricular response depends on the rate and regularity of atrial activity, particularly at the entry to the AV node, and the balance between sympathetic and parasympathetic tone.
- Cardiac output DROPS by 10-20% as the ventricles are not primed reliably by the atria.
Describe the symptoms of AF.
Symptoms are highly variable.
- May be asymptomatic
- Palpitations.
- Dyspnoea and or chest pains following the onset of AF.
- Fatigue.
Diagnosis of AF.
ECG:
1. No P waves
2. Rapid & irregular QRS rhythm
3. Fine oscillation of the baseline.
The ECG taken from someone with atrial fibrillation shows a fine oscillation of the baseline and absent P waves.
Why?
The atria fire a lot, it is chaotic.
The AV node and ventricles can’t keep up -> irregularly irregular pulse.
What ECG features would you see in atrial fibrillation?
Absent P waves.
Irregular QRS complexes.
QRS less than 120 ms.
Atrial rate 300 bpm.
Acute management of AF.
- When AF is due to an acute precipitating events e.g. alcohol toxicity, chest infection or hyperthyroidism - the provoking cause should be treated.
- Cardioversion:
- Conversion to sinus rhythm achieved electrically by DC shock e.g. defibrillator
- NOTE: give low molecular weight heparin e.g. Enoxaparin or Dalteparin to minimise the risk of thromboembolism associated with cardioversion.
- If this fails, then achieved medically by IV infusion or anti-arrhythmic drugs e.g. flecainide or amiodarone - Ventricular rate control:
- Achieved by drugs that block AV node:
* Calcium channel blocker e.g. Verapamil
* Beta-blocker e.g. Bisoprolol
* Digoxin
* Anti-arrhythmic e.g. Amiodarone
Atrial fibrillation treatment: what might you give someone to help with rate control?
Beta blockers, CCB and digoxin.
Atrial fibrillation treatment: what might you give someone to help restore sinus rhythm (rhythm control)?
Electrical cardioversion or pharmacological cardioversion using flecainide.
Long term & stable patient management of AF.
2 strategies; which to choose should be decided based on individual patient needs.
- Rate control:
= AV nodal slowing agents + oral anti-coagulation
- Beta-blocker e.g. Bisoprolol
- Calcium channel blocker e.g. Verapamil or Diltiazem
- If above fails, then try Digoxin and then, consider Amiodarone - Rhythm control:
= Advocated for younger, symptomatic and physically active patients
- Cardioversion to sinus rhythm and use Beta-blockers e.g.
Bisoprolol to suppress arrhythmia
- Can use pharmacological cardioversion e.g. Flecainide if no
structural heart defect or use IV Amiodarone instead if there is
structural heart disease
- Appropriate anti-coagulation e.g. Warfarin due to
thromboembolism risk with cardioversion
What is the long term treatment of atrial fibrillation?
Catheter ablation - it targets the triggers of AF.
What score can be used to calculate the risk of stroke in someone with atrial fibrillation?
CHADS2 VASc.
What factors does the CHA2DS2-VASc score consider?
CHA2DS2-VASc score to calculate stroke risk and thus need for
anticoagulation:
- Congestive heart failure (1 point)
- Hypertension (1 point)
- Age greater or equal to 75 (2 points)
- Diabetes mellitus (1 point)
- Stroke/TIA/thromboembolism (2 points)
- Vascular disease (aorta, coronary or peripheral arteries) (1 point)
- Age 65-74 (1 point)
- Sex Category: female (1 point)
Results:
* If score is 1 then it merits consideration of anticoagulation and or aspirin
* If score is 2 and above then oral anticoagulation is required
What is atrial flutter?
Usually an ORGANISED atrial rhythm with an atrial rate
typically between 250-350 bpm.
What pathophysiological mechanism can cause atrial flutter?
The re-entry mechanism - there is blockage of the normal circuit.
Another pathway forms, takes a different course and re-enters the circuit within the right atrium -> tachycardia.
What are the 3 clinical classifications of atrial flutter?
- Paroxysmal
- Persistent
Give 4 causes of atrial flutter.
- Idiopathic (30%)
- Coronary heart disease
- Obesity
- Hypertension
- Heart failure
- COPD
- Pericarditis
- Acute excess alcohol intoxication
Describe the clinical presentation of atrial flutter.
- Palpitations
- Breathlessness
- Chest pain
- Dizziness
- Syncope
- Fatigue
Diagnosis of atrial flutter.
ECG:
* Regular sawtooth-like atrial flutter waves (F waves) between QRS complexes due to continuous atrial depolarisation
Describe what you would see on an ECG trace in atrial flutter.
‘Sawtooth’ flutter waves between QRS complexes.
300 bpm
Negative flutter waves in II, III and aVF (inferior)
Positive flutter wave in V1 (septal)
Narrow QRS
Treatment of atrial flutter.
- Electrical cardioversion but anticoagulate before
e.g low molecular weight heparin
e.g. Enoxaparin or Dalteparin if acute
I.E. atrial flutter started less than 48 hours ago - Catheter ablation
- creating a conduction block to try an restore rhythm and block offending re-entrant wave - IV Amiodarone + Beta-blocker (bisoprolol)
- To restore sinus rhythm and to suppress further arrhythmias
Amiodarone is used for pharmacological cardioversion, but it also chemically resembles a hormone made naturally by the body - what is this and what can this cause?
Thyroxine - can cause hyperthyroidism
What is the difference between atrial fibrillation and atrial flutter?
Atrial fibrillation = irregular ventricular conduction of atrial beats.
Atrial flutter = atrial rate of 300 bpm (same as AF), but ventricles conduct every other atrial beat - 150 bpm.
How does digoxin work in AF/atrial flutter?
Reduces heart rate and increases force of contraction (-vely chronotropic, +vely inotropic).
Works via indirect pathway - increased vagal tone, reduced contraction at AVN and preventing dome impulses travelling to the ventricles.
What are the 2 types of paroxysmal supraventricular tachycardia?
- AVRNT
- AVRT (accesory pathway)
What is AVRNT?
Atrioventricular Nodal Re-entrant Tacycardia
The most common type of supraventricular tachycardia. People with AVNRT have episodes of an irregularly fast heartbeat (more than 100 beats per minute) that often start and end suddenly.
Explain the pathophysiology of AVRNT.
2 pathways in the AVN in AVRNT:
1) Slow pathway:
- A short effective refractory period and SLOW conduction
2) Fast pathway:
- A longer effective refractory period (RFP) and FAST conduction
- Normal sinus rhythm: electrical impulse from atrium conducts through the fats pathway to the ventricles
- Early atrial impulse
- Happens when the fast pathway is still finishing the long RFP - Slow pathway takes over in electrical impulse propagation
- By the time the slow pathway has sent the impulse to the ventricles, the fast pathway has finished its long RFP.
- So, the fast pathway then sends the same impulse down to the ventricles + back up.
- At the same time, the slow pathway would have recovered from its slow RFP, and so the signal goes down the slow pathway as well.
- Sets up a RE-ENTRANT LOOP at the AV NODE
- This loop sends signals through the AVN at a MUCH FASTER RATE than a normal pacemaker would
= TACHYARRHYTHMIA with a HR of 100-250 bpm
- Signal goes back via the fast pathway (recovers from its RFP)
- Initiates the slow-fast AVNRT:
= the atria contract SLOWLY in 1 cycle and then FAST in the next
Give 4 symptoms of AVNRT.
- Sudden onset/offset palpitations.
- Neck pulsation - prominent jugular venous pulsations due to atrial contractions against closed AV valves
- Chest pain.
- Shortness of breath.
- Polyuria - (due to the realise of atrial natriuretic peptide in response to increased atrial pressures during the tachycardia)
What is seen on the ECG for AVRNT?
No P wave.
Narrow QRS
Do you see P waves in AVNRT?
No - the P waves are within the QRS complex.
What is AVRT?
Atrioventricular Re-entrant Tachycardia
AKA Accessory pathway; Wolff-Parkinson-White sydrome
What happens in AVRT?
Atrial activation occurs after ventricular activation
Describe the pathophysiology of accessory pathway arrhythmias (AVRT).
Congenital muscle strands connect the atria and ventricles - accessory pathway.
This can result in pre-excitation of ventricles.
Describe 3 characteristics of an ECG taken from someone with accessory pathway arrhythmia (AVRT).
- Delta wave.
- Short PR interval.
- Slurred QRS complex.
What is an example of AVRT?
Wolff-Parkinson-White syndrome.
What is Wolff-Parkinson-White syndrome (WPW)?
Pre excitation accessory pathway - AVRT
What causes Wolff-Parkinson-White?
Congenital accessory conduction pathway between atria and ventricles.
What is the mechanism in Wolff-Parkinson-White?
Accessory pathway, usually from left atria, allows direct transmission of signal, bypassing AVN (hence short PR)
Give 4 symptoms of AVRT and WPW.
- Palpitations
- Severe dizziness
- Dysponea
- Syncope
Describe the features of a resting ECG in a patient with WPW.
- Short PR interval
- Wide QRS complex that begins as a slurred part known as a delta wave
(Best seen in V3 + V4)
Treatment of stable AVRT and AVRNT.
Vagal manoeuvres:
- Breath-holding
- Carotid massage
- Valsalva manoeuvre
- Abrupt voluntary increase in intra-abdominal and intrathoracic pressure by straining
- Several seconds after the release of the strain, the resulting intense vagal effect may terminate the AVNRT or AVRT
How to treat AVRT/AVRNT when vagal manoeuvres fail?
IV adenosine
- Causes complete heart block for a fraction of a second and is highly effective at terminating AVNRT and AVRT
What are the surgical options for AVRT + AVRNT?
Surgery:
* Catheter ablation of the accessory pathway in AVRT
* Modification of the slow pathway in AVNRT
How do you treat sudden episodes of supraventricular tachycardia?
Carotid sinus massage
IV adenosine
In supraventricular tachycardia, adenosine is administered IV to bring the heart back into normal rhythm.
How does it work on the heart?
What type of arrhythmias should it be used for?
It works via the A1 receptor, which reduces cAMP - so causes cell hyperpolarisation by pushing potassium out of the cell.
also relaxes the smooth muscle of the heart causing vasodilation.
Only used for ventricular tachycardias.
Why do you need to warn the patient that they may get a sense of ‘impending doom’ after you administer adenosine?
Because it induces transient heart block in the AV node so the heart stops for a beat or so.
What are ventricular ectopic premature beats?
A premature beat arising from an ectopic focus in the ventricles - this focus depolarises before the SAN, leading to a premature and inefficient beat.
Premature ventricular contraction.
What is a risk factor for ventricular ectopic beats?
MI
- These are the most common POST-MI arrhythmia
Explain the pathophysiology of ventricular ectopic beats.
- Patient complains of extra beats, missed beats or heavy beat
- Following a premature beat, there is usually a complete compensatory pause because the AV node or ventricle is refractory (i.e. cannot accept new impulses) to the next sinus impulse - resulting in missed beat.
- Can provoke VENTRICULAR FIBRILLATION - potentially fatal
Describe the clinical presentation of ventricular ectopic beats.
- May be uncomfortable especially when frequent
- Pulse is irregular owing to the premature beats
- Usually are asymptomatic
- Can feel faint or dizzy
What does a ventricular ectopic beat look like on ECG?
Broad or double waved QRS
- > 0.12 s
Why do ventricular ectopic beats have a broad QRS on an ECG?
Because they arise from an abnormal (ectopic) site in the
ventricular myocardium.
Describe the clinical and ECG features of a premature ventricular ectopic beat.
Broad, abnormal QRS complex before you would expect it.
Patient complains of extra/missed beats/heavy beats - palpitations
Treatment of ventricular ectopic beats.
- Reassure patient
- Give beta-blockers e.g. Bisoprolol if symptomatic
How would you treat a symptomatic ventricular ectopic beat?
What are patients with ventricular ectopic beats at a higher risk of?
Beta blockers.
Ventricular fibrillation.
Causes of ventricular tachycardia?
Ventricular fibrosis or dilatation
Describe the ECG changes that may be seen in a ventricular tachycardia.
Very broad, abnormal QRS (>160ms)
No P waves
T waves difficult to identify
Rate > 200bpm (rapid).
What is the treatment for ventricular tachycardia in an urgent situation?
DC cardioversion.
How do sodium channel blockers work in the treatment of ventricular tachycardia?
They block the inactivation gate of the sodium channel.
What is the long term treatment for ventricular tachycardia in high risk patients?
Implantable defibrillator.
What is ventricular fibrillation (VF)?
Involves very rapid and irregular ventricular activation with NO MECHANICAL EFFECT i.e NO CARDIAC OUTPUT
Causes of VF
Myocardial iscahemia/infarction
Electrolyte abnormalities
Cardiomyopathy (dilated, hypertrophic, restrictive)
Long QT
Brugada syndrome
Drugs
Environmental - electrical shock, drowing, hypothermia
PE
Cardiac tampnoade
Blunt trauma
Describe the ECG changes seen in ventricular fibrillation (VF).
Chaotic irregular deflections of varying amplitude
No identifiable P waves, QRS complexes or T waves
Rate 150-500bpm
What is torsaides des pointes?
Ventricular tachycardia with long QT
Normally caused by mutations in ion channels or drugs – ventricular depolarisation is longer
What is long QT syndrome?
Describes an ECG where the ventricular repolarisation - QT interval is greatly prolonged
Give 2 signs of long QT syndrome.
- Palpitations.
- Syncope.
Give 3 causes of long QT syndrome.
- Congenital
- Electrolyte disturbances
- Hypokalaemia
- Hypocalcaemia
- Hypomagnesaemia - A variety of drugs
- Tricyclics
- Macrolides
Name 2 drugs that can prolong the QT interval.
- Sotalol.
- Amiodarone.
Give 5 potential side effects of drugs that prolong the QT interval.
- Pro-arrythmic effects.
- Interstitial pneumonitis.
- Abnormal liver function.
- Hyper/hypothyroidism.
- Sun sensitivity.
- Grey skin discolouration.
- Corneal micro-deposits.
- Optic neuropathy.
Treatment of long QT syndrome.
- Treat underlying cause
- If acquired long QT: then give IV isoprenaline (contraindicated for congenital long QT)
Describe the pathophysiology of focal atrial tachycardia.
Another area of the atrium becomes more autonomic than the sinus node and so sinus node function is taken over -> focal atrial tachycardia.
What might you see on an ECG taken from someone with focal atrial tachycardia?
Abnormal P waves appear before a normal QRS.
