Arrhythmias Flashcards
Shockable rhythms
Ventricular tachycardia
Non-shockable rhythms
Pulseless electrical activity
Asystole(no significant electrical activity)
Treatment of tachycardia in an unstable patient
Consider up to 3 synchronised shocks
Consider amiodarone infusion
Definition of narrow complex
QRS < 0.12 secs
Definition of broad complex
QRS > 0.12s
What causes atrial flutter
Caused by a ‘re-entrant rhythm’ in either atrium
This is where electrical signals re-circulates in a self-perpetuating loop due to an extra electrical pathway(signal goes round and round the atrium without interruption stimulating atrial contraction at 300 rpm)
How does atrial flutter appear on an ecg
Sawtooth appearance on ECG with P wave after P wave
Conditions associated with atrial flutter
Hypertension
Ischaemic heart disease
Cardiomyopathy
Thyrotoxicosis
Treatment for atrial flutter
Rate/rhythm control with beta blockers or cardioversion
Treat reversible cause(HTN, thyrotoxicosis)
Radiofrequency ablation of the re-entrant rhythm
Anticoagulation based on CHA2DS2VASc score
What is an SVT
Caused by electrical signal re-entering atria from the ventricles
Signal then travels back through AV node and causes another ventricular contraction causing a self-perpetuating electrical loop resulting in a fast narrow complex tachycardia
What does paroxysmal SVT refer to
Describes a situation where SVT reoccurs and remits in the same patient over time
What are the three main types of SVT
Atrioventricular nodal re-entrant tachycardia(AVNRT)
Atrioventricular re-entrant tachycardia(WPW)
Atrial tachycardia
What is AVNRT
When the re-entry point is back through AV node
What is atrioventricular re-entrant tachycardia
When the re-entry point is an accessory pathway(WPW)
What is atrial tachycardia
Where the electrical signal originates in the atria somewhere other than SAN
Not caused by a signal re-entering from the ventricles but instead from abnormally generated electrical activity in the atria
The ectopic electrical activity causes an atrial rate of >100bpm
Acute management of stable patients with SVT
Continuous ECG monitoring
Valsalva manoeuvre
Carotid sinus massage
Adenosine
Verapamil as an alternative to adenosine
Direct current cardioversion if above fails
What is a valsalva manoeuvre
Ask patient to blow hard against resistance, for example into a plastic syringe
How does adenosine work in SVTs
Works by slowing cardiac conduction primarily through the AV node interrupting it and resetting it back to sinus rhythm
Will often cause a brief period of systole or bradycardia
How should adenosine be administered
Rapid bolus to ensure it reaches the heart with enough impact to interrupt the pathway
IV bolus into a large proximal cannula(grey annular in the antecubital fossa)
Initially 6mg, then 12 mg and then further 12 mg if no improvement
Who should adenosine be avoided in
Asthma COPD Heart failure Heart block Severe hypotension
Long term management of patients with paroxysmal SVT
Medication (beta blockers, calcium channel blockers or amiodarone)
Radiofrequency ablation
What is the extra pathway present in WPW often called
Bundle of Kent
Definitive treatment for WPW
Radiofrequency ablation of accessory pathway
ECG changes in WPW
Short PR interval(<0.12 secs)
Wide QRS complex(>0.12 secs)
Delta wave which is a slurred upstroke on the QRS complex
Why should anti arrhythmic meds be avoided in WPW with AF/atrial flutter
The meds promote conduction through accessory pathway by reducing conduction through AV node so they are contraindicated in patients with WPW that develop AF/flutter
What is radio frequency ablation
Involves insertion of a catheter in to the femoral vein and feeding a wire through venous system under X-ray guidance to heart
Once identified, radio frequency ablation(heat) is applied to burn the abnormal area of electrical activity which leaves scar tissue that does not conduct electrical activity
What is torsades de pointes
Type of polymorphic(multiple shape) ventricular tachycardia
Height of the QRS complexes progressively get smaller, then larger then smaller and so on
Occurs in patients with a prolonged QT interval
Definition of prolonged QT interval
Anything greater than or equal to 0.5 seconds
Pathophys behind prolonged QT interval
Prolonged repolarisation of the muscle cells in the heart after contraction
Longer repolarisation time can result in spontaneous depolarisation in some myocytes
These depolarisations spread throughout the ventricle leading to ventricular contraction prior to proper repolarisation
End result of torsades de pointes
Will either terminate spontaneously and never back to sinus rhythm or progress in to ventricular tachycardia
Usually, they are self limiting but if they progress to VT, it can lead to cardiac arrest
Causes of prolonged QT
Long QT syndrome(inherited)
Meds
Electrolyte disturbances
Which medications can cause prolonged QT
Antipsychotics Citalopram Flecainide Sotalol Amiodarone Macrolides
Electrolyte disturbances which can cause prolonged QT
Hypokalaemia
Hypomagnesaemia
Hypocalcaemia
Acute management of torsades de pointes
Correct cause(electrolyte disturbances or meds) Magnesium infusion(even if normal serum magnesium) Defib if VT occurs
Long term management of prolonged QT syndrome
Avoid meds that prolong QT interval Correct electrolyte disturbances Beta blockers(not sotalol) Pacemaker or implantable defibrillator
What are ventricular ectopics
Are premature ventricular beats caused by random electrical discharges from outside atria
Appear as individual random, abnormal, broad QRS complexes on a background of a normal ECG
What is bigeminy
This is where ventricular ectopics are occurring so frequently that happen after every sinus beat
ECG looks like a normal sinus beat allowed immediately by an ectopic, then a normal beat, then ectopic and so on
Management of ventricular ectopics
Check bloods for anaemia, electrolyte disturbance and thyroid abnormalities
Reassurance and no treatment in otherwise healthy people
Seek expert advice in patients with background heart conditions or other concerning features or findings (e.g. chest pain, syncope, murmur, family history of sudden death)
What is first degree heart block
Occurs where there is delayed AV cofunction through AV node
Every p waves results in a QRS complex. On an ECG this presents as a PR interval greater than 0.20 seconds (5 small or 1 big square).
What is second degree heart block
Second-degree heart block is where some of the atrial impulses do not make it through the AV node to the ventricles. This means that there are instances where p waves do not lead to QRS complexes.
Divided into mobitz type 1 and 2
What is mobitz type 1/wenckebach’s
On an ECG this will show up as an increasing PR interval until the P wave no longer conducts to ventricles. This culminates in absent QRS complex after a P wave. The PR interval then returns to normal but progressively becomes longer again until another QRS complex is missed. This cycle repeats itself.
What is mobitz type 2
intermitted failure or interruption of AV conduction. This results in missing QRS complexes. There is usually a set ratio of P waves to QRS complexes, for example 3 P waves to each QRS complex would be referred to as a 3:1 block. The PR interval remains normal. There is a risk of asystole with Mobitz Type 2.
What is third degree heart block
This is referred to as complete heart block. This is no observable relationship between P waves and QRS complexes. There is a significant risk of asystole with third-degree heart block.
Treatment for bradycardias/AV node blocks
Stable - observe
Unstable or risk of asystole - 1st line - Atropine 500mcg IV
No improvement:
Atropine 500mcg IV repeated, other inotropes(noradrenaline), transcutaneous cardiac pacing(using a defibrillator)
Management of patients with a high risk of systole due to heart block
Temporary transvenous cardiac pacing
Permanent implantable pacemaker when available
How does atropine work
is an antimuscarinic medication that works by inhibiting parasympathetic nervous system
Leads to side effects of pupil dilatation, urinary retention, dry eyes and constipation
What is brugada syndrome
ECG abnormality with a high incidence of sudden death in patients with structurally normal hearts.
It is caused by a mutation in the cardiac Na+ channel gene, known as a sodium channelopathy
Diagnosis of brugada syndrome
Diagnosis can only be made with the characteristic Brugada ECG patterns (Coved ST-segment elevation >2mm in >1 of V1-V3 followed by a negative T wave) and one of the clinical criteria
Clinical criteria for diagnosis of brugada syndrome
Documented ventricular fibrillation (VF)
Polymorphic ventricular tachycardia (VT)
A family history of sudden cardiac death at <45 years old
Coved-type ECGs in family members, Inducibility of VT with programmed electrical stimulation
Syncope
Nocturnal agonal respiration
