Arrythmia Flashcards
In AFib where is the signal originating
anywhere in the atria, not SAN and conducted through AVN but irregularly
What is AFib
Multiple atrial impulses and contractions transmitted randomly to the AVN but causing a normal ventricular contraction
What do you see on ECG in A.fib
No P waves, irregular rhythm, narrow complex
What is atrial flutter
Signal arises within atrial muscle as opposed to SAN at a set rate of 300bpm and either all pass through to cause a contraction or often one in 2 passed through (rate 150bpm)
What do you see on ECG with Atrial flutter
‘saw teeth’, usually regular rhythm, narrow complex, rate is most commonly 150 or 300bpm
What is the most common type of SVT
AV nodal re-entry tachycardia
How does AV nodal re-entry tacycardia (SVT) happen
Within the AVN there is another pathway which causes extra impulses to be transmitted through to the ventricles causing more ventricular contractions
What is AV re-entry tachycardia (SVT)
An extra pathway between the atria and ventricles by which extra signals are being transmitted along with the normal ones through the AVN resulting in more ventricular contractions e.g Wolff-Parkinson white
What does SVT look like on an ECG
Regular
Narrow complex tachycardia
Looks like ST depression but it’s an inverted P wave in a T wave
P waves are buried in T waves
what is ventricular tachycardia
Contractions are occurring within the ventricular tissue
What do you see on ECG in ventricular tachy
regular
broad complex - slow inefficient contraction
QRS is regular in height and width
No P or T waves
What is ventricular fibrillation
Arising within ventricular tissue but in a random pattern
What does V fib look like on ECG
Irregular
broad base
no P/T waves
Examples of narrow complex tacycardia
A fib
A flutter
SVT
Examples of broad complex tachycardia
V fib
V tachy
Regular, narrow complex tachycardia
a flutter
SVT
Irregular narrow complex tachycardia
A fib
Irregular broad base tachycardia
V fib
Regular broad complex tacycardia
Ventricular tachy
SVT with abberancy - SVT with a BBB
Management of stable Atrial fib and A flutter
- beta blocker to slow HR
- CHADVASC for anti-coagulation
( anti-arrhythmic in young with no co-morbidities e.g. digoxin)
What makes a patient in a tachy-arrhythmia unstable
Chest pain
Heart failure
hypotensive
reduction in consciousness
Management of an unstable tachy-arrhythmia
- cardioversion - DC shock
Management of stable SVT
- Vagal manoeuvres e.g. blowing on a syringe, carotid massage
- Adenosine - blocks of AVN temporarily
- DC shock
Do you need to anti-coagulate someone in SVT
no
What is the approach to diagnosing a tachycardia?
- Is it broad or narrow complex
2. Is it regular or irregular
Management of ventricular tachycardia with a pulse
- Amiodarone 300mg
- Amiodarone infusion 24h
- Cardiology involvement
Management of cardiac arrest with a shockable rhythm
- Compressions 30/2
- Shock
- Reassess rhythm every 2 mins + shock
- Adrenaline after third shock (1:1000) then every other shock
- Amiodarone after 3rd and 5th shock
Which are shockable rhythms
VF
VT (pulseless)
Non shockable rhythms
PEA
Asystole
Causes of cardiac arrest 4 T
- thrombosis
- tension pneumothorax
- tamponade
- toxins
Causes of cardiac arrest 4 H
- Hypoxia
- Hypovolaemia
- Hyperkalaemia (electrolyte disturbances)
- Hypothermia
Management of Non-shockable cardiac arres
- BLS
- Confirm un-shockable rhythm
- Adrenaline (1:1000)
- Reassess rhythm every 2 mins
- Adrenaline every alternate check
What conditions are associated with atrial flutter
Hypertension
Ischaemic heart disease
Cardiomyopathy
Thyrotoxicosis
How does adenosine work
Slows cardiac conduction primarily though the AV node. It interrupts the AV node / accessory pathway during SVT and “resets” it back to sinus rhythm. It needs to be given as a rapid bolus to ensure it reaches the heart with enough impact to interrupt the pathway. It will often cause a brief period of asystole or bradycardia.
Key points to think about when administering adenosine
- Avoid if patient has asthma / COPD / heart failure / heart block / severe hypotension
- Warn patient about the scary feeling of dying / impending doom when injected
- Give as a fast IV bolus into a large proximal cannula
- Initially 6mg, then 12mg and further 12mg if no improvement between doses
What is the Long Term Management of patients with paroxysmal SVT
Medication (beta blockers, calcium channel blockers or amiodarone)
Radiofrequency ablation
What is Wolff Parkinson White
An extra electrical pathway connecting the atria and ventricles. Normally there is only one pathway connecting the atria and ventricles called the atrio-ventricular node. The extra pathway that is present in Wolff-Parkinson White Syndrome is often called the Bundle of Kent.
WHat are the ECG changes seen in Wolff Parkinson White
- Short PR interval (< 0.12 seconds)
- Wide QRS complex (> 0.12 seconds)
- “Delta wave” which is a slurred upstroke on the QRS complex
Which medications are contraindicated in patients with Wolff Parkinson White
- antiarrhythmic medications (beta blockers, calcium channel blockers, adenosine
Why are anti-arrhythmics contraindicated in patients with Wolff parkinson White
there is a risk that the chaotic atrial electrical activity can pass through the accessory pathway into the ventricles causing a polymorphic wide complex tachycardia
What is the definitive management of Wolff Parkinson White SYndrome
Radiofrequency ablation of the accessory pathyway
Which conditions can radiofrequency ablation be used to treat
- Atrial Fibrillation
- Atrial Flutter
- Supraventricular Tachycardias
- Wolff-Parkinson-White Syndrome
What is radiofreqeuncy ablation
- Heat is applied to burn the abnormal area of electrical activity. This leaves scar tissue that does not conduct the electrical activity. The aim is to remove the source of the arrhythmia.
- Done in the cath lab under local or GA
- May try and induce the arrhythmia to ensure the correct area is burned
What is Torsades de points
Polymorphic ventricular tachycardia
What causes Torsades de pointes
prolonged QT interval
What causes a prolonged QT
Long QT Syndrome (inherited)
Medications
Electrolyte Disturbance (hypokalaemia, hypomagnesaemia, hypocalcaemia)
What medications can cause a prolonged QT
Anti-psychotics ctialopram flecainide sotalol amiodarone marcolides
What electrolyte disturbances can cause a prolonged QT
Hypokalaemia
Hypomagnesaemia
Hypocalcaemia
What does torsades de pointes lead to
Often self terminating but can lead to ventricular tachycardia
What is the acute treatment of torsades de pointes
Correct the cause (electrolyte disturbances or medications)
Magnesium infusion (even if they have a normal serum magnesium)
Defibrillation if VT occurs
What is the long term treatment of torsades de pointes
Avoid medications that prolong the QT interval Correct electrolyte disturbances Beta blockers (not sotalol) Pacemaker or implantable defibrillator
What are ventricular ectopic beats
premature, weak ventricular contractions caused by random electrical charges outside the atria
How can you diagnose ventricular ectopic beats on an ECG
random, abnormal broad QRS complex on an otherwise normal ECG
What is bigeminy
- Ventricular ectopics happen after every sinus beat
- ECG: normal sinus beat followed immediately by an ectopic, then a normal beat, then ectopic
What is the management of ventricular ectopics
- check for anaemia, electrolyte imbalances and TFTs
- Reassurance
- Seek advice if underlying heart condition or concerning features e.g. syncope or chest pain
What is first degree heart block
- delayed atrioventricular conduction through the AV node
- Every P wave have a QRS
- PR interval >0.2 seconds: 5 small squares
What is second degree heart block
- some of the atrial impulses do not make it through the AV node to the ventricles.
- Some instances where P waves don’t lead to QRS
- Can be split into TI or TII
What is Mobitz type I heart bock - Wenchebache
- Atrial contraction becomes progressively weaker until it does not transmit through to the ventricles
- Increasing PR interval until the P wave no longer conducts leading to absent QRS, then PR returns to normal
What is Mobitz TII heart block
- Intermitted failure or interruption of AV conduction
- missing QRS complex on ECG
- Can lead to asystole
- Usually in 3-1 block ( 3 p waves to each QRS)
What is 2:1 block
- 2 P waves for each QRS complex
- Caused by Mobitz Type 1 or Mobitz Type 2
What is third degree heart block
- AKA complete heart block
- no relationship between P waves and QRS complex
- significant risk of systole
What is the treatment of a stable person with bradycardia/AV node block
Observe
What is the treatment of an unstable person with bradycardia/AV node block
- Atropine 500 micrograms IV (can repeat up to 6 doses)
- Other inotropes e.g. noradrenalin
- Transcutaneous pacing - defib
What is Atropine
- Antimuscarinic
- Inhibits the PNS
- Side effects: pupil dilatation, urinary retention, dry eyes and constipation.
What is atrial fibrillation
Normal the sinoatrial node produces organised electrical activity that coordinates the contraction of the atria of the heart. Atrial fibrillation is where the contraction of the atria is uncoordinated, rapid and irregularly. This due to disorganised electrical activity that overrides the normal, organised activity from the sinoatrial node.
What are the features of AF
- Irregularly irregular ventricular contractions
- Tachycardia
- Heart failure: poor filling of the ventricles during diastole
- Risk of stroke
What are the presenting symptoms of AF
- Palpitations
- Shortness of breath
- Syncope (dizziness or fainting)
- Symptoms of associated conditions (e.g. stroke, sepsis or thyrotoxicosis)
What are the two differentials for an irregularly irregular pulse
- AF
- Ventricular ectopics
What does an ECG of a patient in AF show
Absent P waves
Narrow QRS Complex Tachycardia
Irregularly irregular ventricular rhythm
What are the most common causes of AF
S: sepsis M: mitral Valve Pathology (stenosis or regurgitation) I: Ischemic Heart Disease T: thyrotoxicosis H: hypertension
Which patients with AF should have rhythm control as first line
- Reversible cause
- New onset (within the last 48 hours)
- AF is causing heart failure
- Symptomatic despite being effectively rate controlled
What options are available for rate control of Fast AF
Beta blocker is first line (e.g. atenolol 50-100mg once daily)
Calcium-channel blocker (e.g. diltiazem) (not preferable in heart failure)
Digoxin (only in sedentary people, needs monitoring and risk of toxicity)
When do you do immediate cardioversion
- Onset <48 hours
- haemodynamically unstable
What happens in delayed cardioversion
- Patient anti-coagulated >3w
- rate control until anti-coagulated
- pharmacological/electrical cardioversion
Why must you anti-coagulate someone who has been in AF >48 hours
may have developed a blood clot in the atria and reverting them back to sinus rhythm carries a high risk of mobilising that clot and causing a stroke
What are the first line pharmacological cardioversion medications
- flecainide
- amiodarone - if structural heart disease
What does electrical cardioversion involve
- sedation/GA
- defibrillator
How do you manage long term medical rhythm control
- Beta blockers are first line for rhythm control
- Dronedarone is second line for maintaining normal rhythm where patients have had successful cardioversion
- Amiodarone is useful in patients with heart failure or left ventricular dysfunction
How do you manage paroxsymal AF
- Anti-coagulated based on Chad-Vasc
- Flecainide ‘pill in the pocket’ approach
Who can use the ‘pill in the pocket’ approach for paroxysmal AF
- Infrequent episodes
- No structural heart disease
- Able to identify when they are in AF
