Arrhythmias Flashcards
What are the two most common causes of AF?
Hypertension
Heart failure
How is the rhythm in AF described?
Irregularly irregular
Why is stroke risk increased in AF?
Irregular rhythm decreases filling time, thus cardiac output is decreased. This leads to stasis of blood - which is a risk of clotting (Virchow’s triad).
How long does parxoysmal AF last?
Less than 48 hours.
How long does persistent AF last?
Greater than 48 hours.
When is AF classed as permanent?
When cardioversion to normal sinus rhythm is not possible.
How does AF present on an ECG?
Atrial rate of 300bpm
Irregularly irregular rhythm
Absent P waves
Narrow (normal QRS)
What scoring system is used to determine stroke risk in AF?
CHA2DS2-VASc
What are options for rate control in AF?
Beta-blockers (atenolol is first line)
CCB
Digoxin (only given in sedentary patients)
An alternative is AV node ablation.
In which individuals should rate control not be offered for AF?
Underlying cause is reversible
The AF is of new onset
The AF is causing heart failure
Symptoms continue despite good rate control already
In which individuals should rhythm control be offered?
The AF has a reversible cause
The AF is of new-onset
The AF is causing heart failure
Symptoms persist despite good rate control
When is immediate cardioversion indicated in AF?
If AF is present for less than 48 hours, or the patient is severely haemodynamically unstable.
When is delayed cardioversion indicated in AF?
If AFD is present for more than 48 hours and the patient is haemodynamically stable.
Patient should be anticoagulated for atleast 3 weeks whilst waiting for cardioversion, as this will decrease clotting risk. Additionally, patient should have rate control during wait period.
What are pharmacological options for cardioversion?
Flecainide
Amiodarone (best in structural disease)
What condition is the ‘pill-in-the-pocket’ method applied in?
Paroxysmal AF
The pill used is normally flecainide - taken when symptoms start. If the CHA2DS2VASc score indicates so, take anticoagulants.
In AF, when is anticoagulation indicated?
In those with underlying valvular disease
When CHA2DS2VASc score is >2
What are risk factors for the development of atrial flutter?
Hypertension
IHD
Cardiomyopathy
Thyrotoxicosis
How does atrial flutter present?
Usually asymptomatic, although may have palpitations.
How does atrial flutter present on an ECG?
Sawtooth P waves (sometimes called F waves)
QRS is normal
Regular rhythm
Atrial rate 2:1 Ventricular rate
How is atrial flutter managed?
If acute presentation is symptomatic, cardiovert (either drug or electric).
If non-acute case, patient required 3 weeks of anticoagulation prior to cardioversion.
How is recurrent atrial flutter treated?
Catheter ablation
AV nodal blocking (e.g. beta blockers and amiodarone).
Does chronic atrial flutter progress?
Yes - progresses to AF.
What are precipitating factors in VT?
IHD
Previous MI
Cardiomyopathy
Iatrogenic
Can also be idiopathic.
What are the two forms of VT?
Polymorphic
Monomorphic
What causes monomorphic VT?
Increased automaticity (=spontaneous generation of APs).
Often due to scarring of the heart muscle from some mechanism.
What causes polymorphic VT?
Abnormal ventricular repolarisation.
Causes include long QT syndrome, drug toxicity, or electrolyte imbalances.
How does VT present?
Patient will have pre-syncope (dizziness), syncope, hypotension - will result in cardiac arrest.
Some may tolerate better than expected.
How does monomorphic VT present?
Will have constant QRS shape - wide complexes.
Rate is rapid.
How does polymorphic VT present?
QRS will be observed to be broad, with varying amplitudes.
What is Torsade de Pointes?
A specific form of VT associated with a long QT interval.
How is a patient with VT, whom is unstable but has a pulse, treated?
Cardioversion
How is pulseless VT treated?
Defibrillation - this is cardiac arrest.
How is a stable patient with VT treated?
Amiodarone/Lignocaine used first-line (medical therapy).
If not successful, then DCCV should be applied.
What is VF?
Very rapid and irregular ventricular activation with no mechanical effect.
What is primarily the underlying cause of VF?
IHD
May also be the result of:
Cardiomyopathy
Electrolyte imbalance
Overdose on cardiotoxic drugs
What brings on VF?
Usually a ventricular ectopic.
How does VF present?
Patient will have no pulse - they will become unconscious rapidly. Respiration will cessate.
Patient is in cardiac arrest.
How does VF present on an ECG?
Will have bizarre irregular waveforms
There will be no regular QRS complexes
Waves present will be of random frequency and amplitude - uncoordinated activity.
What is long-term management for VF?
ICD
What is Brugada syndrome?
An inheritable condition causing idiopathic VF - there will be no evidence of a responsible structural abnormality/disease.
What mode of inheritance is seen in Brugada syndrome?
Autosomal dominant
This makes it 8x more likely in men.
What can trigger VF in Brugada syndrome?
Rest/Sleep
Fever
Excessive alcohol
Large meals
Drugs
What drugs can trigger Brugada syndrome?
Beta blockers
Psychotropics
Analgesics
Anasthetics
How does Brugada syndrome present on an ECG?
ST elevation and RBBB in V1-V3 (may only appear on provocation testing).
May have AF - there is risk of progression to polymorphic VT or VF.
How is Brugada syndrome managed?
Avoid trigger
Fit an ICD
Test genetics of family for further cases
What are 2 examples of congenital causes of long QT syndrome?
Jervell-Lange-Nielsen syndrome (autosomal recessive)
Romano-Ward syndrome (autosomal dominant)
What may trigger QT prolongation/Torsades des Pointes?
Potassium-rich foods
Diarrhoea
Vomiting
Underwater breath-holding
Exercise
Sudden auditory stimuli
Sleep
Drugs
Diabetes
Acute MI
How does long QT syndrome present?
Will have syncope and palpitations (due to polymorphic VT).
Should spontaneously terminate, if not will progress to VF (with sudden death the result).
How is Long QT syndrome managed in the long-term?
Beta-blockers
Avoid drugs which may prolong drugs
Pacemaker therapy
What is responsible for AVNRT?
A re-entry circuit within the AV node.
What is the most common cause of SVT in a structurally normal heart?
AV nodal re-entrant tachycardia (AVNRT).
This is more common in women.
What is responsible for AVRT?
An accessory pathway, usually located in the valvular rings. It is most commonly caused by Wolff-Parkinson-White syndrome.
What is responsible for EAT?
When electrical signals originate outwith the SA node - but still within the atria.
What are the three main types of SVT?
AV nodal re-entrant tachycardia (AVNRT)
AV re-entrant tachycardia (AVRT)
Ectopic Atrial Tachycardia (EAT)
How does an SVT present clinically?
Palpitations
Dyspnoea
Wil have fast rate and narrow QRS on an ECG.
How is an EAT patient treated?
Usually, no treatment if no underlying issue - if it is troublesome, a beta blocker may help.
Should avoid stimulants (e.g. caffeine).
How is SVT managed in an acute setting - patient is stable?
First-step is valsalva manoeuvre, then carotid sinus massage. If still unsuccessful, try IV adenosine (or verapamil).
Last-line is DCCV - only used if above fails.
How does adenosine work?
Slows cardiac conduction through the AV node. It interrupts the AV node (and accessory pathway), resetting back to sinus rhythm.
How is a paroxysmal SVT treated in the long-term?
Can give beta blockers, CCBs or amiodarone.
In younger patients, radiofrequency ablation is preferred.
In which condition is a Bundle of Kent found?
Wolff-Parkinson-White Syndrome
Causes a re-entrant loop, predisposing to tachyarrhythmias.
How does WPW syndrome present on an ECG?
Will have slurred up-stroke of the QRS complex (called a delta wave). Accompanying this will be a short PR interval and wide QRS complex.
What is the definitive treatment for any disorder resulting from an accessory pathway?
Radiofrequency ablation
How does first degree heart block present?
Will have prolonged PR interval, but no change to rhythm AND no missing beats.
Usually asymptomatic, although the patient should be followed up for any progression to a more serious form.
In what conditions can first degree heart block present?
IHD
Digoxin toxicity
Electrolyte disturbance
What is second degree heart block?
An intermittent absence of QRS complexes - indicated a blockage between AV node and ventricles.
Two forms; Mobitz type 1 and Mobitz type 2.
Which form of Mobitz is referred to as Wenckebach?
Mobitz type 1
What occurs in Mobitz type 1?
Progressive prolongation of the PR interval, until a QRS is eventually dropped. Pattern will then reset after this.
Often due to high vagal tone - not a result of structural disease.
What occurs in Mobitz type 2?
When a QRS complex is regularly missed due to preceding P waves not being conducted properly. Often represented in a 2:1, or 3:1 ratio.
Likely to progress to third-degree heart block.
What is third-degree heart block?
Complete atrial block - atria contracts fine, but no beats conduct to the ventricles.
P waves and QRS complexes are completely unrelated in this - no pattern. Always indicates an underlying disease.
What rate is classed as sinus bradycardia?
Less than 60bpm.
Is sinus bradycardia always due to pathology?
No - can present normally in athletes.
What conditions may cause sinus bradycardia?
Acute/Previous MI
Sick sinus syndrome
Pericarditis
Hypothyroidism
Sleep apnoea
Medications (e.g. verapamil)
How is symptomatic sinus bradycardia treated?
Atropine, or if acute onset, identify and treat the underlying cause.
What is asystole?
The complete halt of electrical activity within the heart - thus blood is not being pumped around the body. It is usually irreversible.
What are premature ventricular contractions (PVCs)?
When abnormal heartbeats that originate from within the ventricles. Patient will have a flutter/missed beat feeling.
How is PVC treated?
Usually not needed - treat cause if identifiable.
How is PVC treated?
Usually not needed - treat cause if identifiable.
