Cardiac Arrhythmias Flashcards
What is a cardiac arrhythmia?
abnormality of the cardiac rhythm
*Clinical presentation of cardiac arrhythmias
- Sudden death
- Syncope
- Heart failure
- Chest pain
- Dizziness
- Palpitations
- No symptoms at all
2 main types of arrhythmia
Bradycardia
Tachycardia
Features of Bradycardia arrhythmia
Heart rate is slow (<60bpm during day and <50bpm at night)
Usually asymptomatic unless the rate is very slow
Normal in athletes owing to increased vagal tone and thus parasympathetic activity
Features of tachycardia arrhythmias
HR is fast (>100bpm)
More symptomatic if arrhythmia is fast and sustained
What are 2 types of tachycardia arrhythmias
Supraventricular tachycardias - arise from the atrium or the AV junction
Ventricular tachycardias - arise from the ventricles
What is the normal conduction pathway in the heart?
SAN → Action potential → Muscle cells of atria → Depolarisation of the AVN → Slow → Interventricular septum → Bundle of His → Right and left bundle branches → Free walls of both ventricles → Purkinje cells → Ventricular myocardial cells
Where is Sinoatrial node
Junction between the superior vena cava (SVC) and right atrium
What cell junctions are found between cardiac cells
Gap junctions
Where is Atrioventricular node?
Lower interatrial septum
Why is there slow spread of action potential between the AVN and ventricles?
Allow for complete contraction of atria before ventricles are excited and contract
SAN discharge rate is modulated by autonomic nervous system - is sinus rate faster in men or women
Women
What characterised normal sinus rhythm on an ECG?
Normal sinus rhythm is characterised by P waves that are upright in leads I & II of the ECG, but inverted in the cavity leads aVR & V1
How does HR change during inspiration
Parasympathetic tone falls and the heart rate quickens
How does HR change during expiration
Parasympathetic tone increases and so heart rate falls
Define atrial fibrillation
A chaotic irregular atrial rhythm at 300-600bpm; the AV node responds intermittently, hence an irregular ventricular rate
Epidemiology of Atrial fibrillation
Most common sustained cardiac arrhythmia
Males more than females
Around 5-15% of patients over age of 75
Clinical classifications of atrial fibrillation
Acute Paroxysmal Recurrent Persistent Permenant
Clinical classifications of atrial fibrillation: Acute
onset within the previous 48 hours
Clinical classifications of atrial fibrillation: Paroxysmal
stops spontaneously within 7 days
Clinical classifications of atrial fibrillation: Recurrent
2 or more episodes of AF
Clinical classifications of atrial fibrillation: Persistent
continuous for more than 7 days and not self-terminating
Causes of atrial fibrillation
- Idiopathic (5-10%)
- Any condition that results in raised atrial pressure, increased atrial muscle mass, atrial fibrosis, or inflammation and infiltration of the atrium may cause atrial fibrillation
- 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
Risk factors of atrial fibrillation
- Older than 60
- Diabetes
- High blood pressure
- Coronary artery disease
- Prior MI
- Structural heart disease (valve problems or congenital defects)
Pathophsyiology of atrial fibrillation
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.
What does ventricular response depend on?
Rate and regularity of atrial activity (particularly at entry to the AV node)
Balance between sympathetic and parasympathetic tone
How much can cardiac output drop if the ventricles are not primed reliably by the atria?
10-20%
Why are people with AF at higher risk of thromboembolic events e.g. stroke?
When the atria are spasming and some parts are not contracting, it causes blood to POOL in these parts and thus remain still. Here the blood doesn’t move and thus CLOT (or thrombus) begins to form. This could easily result in an EMBOLI and thus a stroke.
As people with AF are at higher risk of thromboembolic events, what can be given to help prevent these TE events?
Blood thinner e.g. Warfarin
*Clinical presentation of AF
- Symptoms are highly variable
- May be asymptomatic
- Palpitations
- Dyspnoea and or chest pains following the onset of atrial fibrillation
- Fatigue
- Apical pulse rate is greater than the radial rate
- 1st heart sound is of variable intensity
*Describe ECG of AF (diagnosis of AF)
No P Waves
Rapid and irregular QRS complex
*Differential diagnosis of AF
Atrial flutter
Supraventricular tachyarrhythmias
Acute management of AF
If AF due to acute precipitating event (e.g. alcohol toxicity, chest infection, hyperthyroidism), the provoking cause should be treated.
Cardioversion (conversion to sinus rhythm)
Ventricular rate control (by drugs that block AV node)
What is cardioversion?
Treatment of acute AF:
Conversion to sinus rhythm achieved by DC shock e.g. defrillator
What drugs should be given when having cardioversion and why?
LMW Heparin
e.g. Enoxaparin or Dalteparin to minimise risk of thromboembolism associated with cardioversion
If cardioversion fails, what can you do instead of cardioversion
Medical routes - IV infusion or anti-arrhythmic drug e.g. flecainide or amiodarone
What drugs can be given in acute management of AF to control ventricular rate?
Calcium Channel Blocker
Beta-blocker
Digoxin
Anti-arrhythmic
Example of calcium channel blocker
Verapamil
Example of Beta-blocker
Bisoprolol
Example of Anti-arrhythmic
Amiodarone
2 parts of long term and stable patient AF management
Rate control
Rhythm control
Long term and stable patient management AF: Rhythm control
- Cardioversion to sinus rhythm and use Beta-blockers e.g. Bisoprolol to suppress arrhythmia.
- Appropriate anti-coagulation e.g. Warfarin due to thrombo-embolism risk with cardioversion
- Can use pharmacological cardioversion e.g. Flecainide if no structural heart defect or use IV Amiodarone instead if there is structural heart disease
Long term and stable patient management AF: Rate control
AV nodal slowing agents plus oral anticoagulation
Beta-blocker e.g. Bisoprolol
Calcium channel blocker e.g. Verapamil or Diltiazem
If they fail try Digoxin and then consider Amiodarone
Long term and stable patient management AF - who would rhythm control be advocated for?
Younger, symptomatic and physically active patients
*What could you use to calculate stroke risk in AF patients (and thus need for anticoagulation)?
CHA2DS2-VASc score
*What is each part of the CHA2DS2-VASc score and how many points are needed for treatment
- Congestive heart failure (1 point)
- Hypertension (1 point)
- A2ge greater or equal to 75 (2 points)
- Diabetes mellitus (1 point)
- S2troke/TIA/thromboembolism (2 points)
- Vascular disease (aorta, coronary or peripheral arteries) (1 point)
- Age 65-74 (1 point)
- Scex Category: female (1 point)
- If score is 1 then it merits consideration of anticoagulation and or aspirin
- If score is 2 and above then oral anticoagulation is required
Define Atrial flutter
Usually an ORGANISED atrial rhythm with an atrial rate typically between 250-350bpm
Epidemiology of Atrial flutter
- Often associated with atrial fibrillation and frequently require a similar initial therapeutic approach
- Either paroxysmal or persistent
- Much less common than atrial flutter
- More common in men
- Prevalence increases with age
Aetiology of Atrial flutter
- Idiopathic (30%) (means unknown cause)
- Coronary heart disease
- Obesity
- Hypertension
- Heart failure
- COPD
- Pericarditis
- Acute excess alcohol intoxication
Risk factor for atrial flutter
Atrial fibrilation
Clinical presentation of atrial flutter
Palpitations Breathlessness Chest pain Dizziness Syncope Fatigue
Differential diagnosis of atrial flutter
Atrial fibrillation
Supraventricular tachyarrhythmias
*Diagnosis of atrial flutter
ECG
-Regular sawtooth-like atrial flutterwaves (F waves) between QRS complexes due to continuous atrial depolarisation
What can be done to diagnose atrial flutter if think patient has it but F waves are not showing on ECG
F waves may be able to be unmasked by by slowing atrioventricular conduction by carotid sinus massage or IV adenosine (AV nodal blocker)
Treatment of A Flutter
- Electrical cardioversion but anticoagulate (low molecular weight heparin e.g. Enoxaparin or Dalteparin) before if acute i.e. atrial flutter started <48 hours ago
- Catheter ablation - creating a conduction block to try an restore rhythm and block offending re-entrant wave
- IV Amiodarone to restore sinus rhythm and use a beta-blocker e.g. Bisoprolol to suppress further arrhythmias
Where can heart block occur in the conducting system
AV block:
AV node
His bundle
Block lower in conduction system produces a Bundle Branch Block
3 forms of AV block
First degree
Second degree
Third degree
Describe features of 1st degree AV block
Simple prolongation of the PR interval to greater than 0.22 seconds
Every atrial depolarisation is followed by conduction to the ventricles but without delay
Causes of 1st degree AV block
Hypokalemia
Myocarditis
Inferior MI
AV node blocking drugs e.g. Beta-blockers (Bisoprolol), Calcium channel blockers (Verapamil) and Digoxin
Treatment of 1st degree AV block
Asymptomatic so no treatment
2 types of 2nd degree AV block
Mobitz I block
Mobitz II block
2nd degree AV blocks generally occur when some P waves conduct and others do not
Describe featuers of Mobitz I block (2nd degree AV block)
A progressive PR interval prolongation until beat is ‘dropped’ and P wave fails to conduct i.e. excitation completely fails to pass through the AVN/bundle of His
The PR interval before the blocked P wave is much longer than the PR interval after the blocked P wave
Causes of Mobitz I block (2nd degree AV block)
- Atrioventricular node (AVN) blocking drugs e.g. beta blockers (Bisoprolol), calcium channel blockers (Verapamil) and Digoxin
- Inferior MI
Symptoms that result from Mobitz I block
Light headiness
Dizziness
Syncope
Describe features of Mobitz II block (2nd degree AV block)
- PR interval is constant and QRS interval is dropped
- Failure of conduction through the His-Purkinje system
Is a pacemaker required for Mobitz I or II block (2nd degree AV block)
Mobitz II block
as high risk of developing sudden complete AV block.
Mobitz I block only requires a pacemaker if poorly tolerated
Causes of Mobitz II block (2nd degree AV block)
- Anterior MI
- Mitral valve surgery
- SLE and Lyme disease
- Rheumatic fever
Symptoms that result from Mobitz II block
Shortness of breath
Mitral valve surgery
SLE and Lyme disease
Rheumatic fever
Describe 3rd degree AV block
Complete AV block
- When all atrial activity fails to conduct to the ventricles
- Ventricular contractions are sustained by spontaneous escape rhythm which originates below the block
- P waves are COMPLETELY INDEPENDENT of QRS complex
Causes of 3rd degree AV block
- Structural heart disease e.g. transposition of great vessels
- Ischaemic heart disease e.g. acute MI
- Hypertension
- Endocarditis or Lyme disease
What are 2 types of escape rhythm that can occur from 3rd degree AV block
Narrow-complex escape rhythm (QRS complex <0.12 seconds)
Broad-complex escape rhythm (QRS complex >0.12 seconds)
If a narrow-complex escape rhythm is shown for 3rd degree AV block, what can be be deduced about the location of the block
Implies block originates in the His bundle and thus the region of block lies more proximally in the AV node
Treatment of Narrow-complex escape rhythm (3rd degree AV block)
Recent onset (that has transient causes) - IV atropine Chronic narrow-complex escape rhythm - Permanent pacemaker (if symptomatic)
If a broad-complex escape rhythm is shown for 3rd degree AV block, what can be be deduced about the location of the block
Implies block originates BELOW the bundle of His and thus the region of
block lies more distally in the His-Purkinje system.
Treatment of Broad-complex escape rhythm (3rd degree AV block)
Permanent pacemaker implantation is recommended
In which type of escape rhythm do you get dizziness and blackouts
Broad-complex escape rhythm
*Which of these of false:
Bundle Branch blocks are usually asymptomatic
His bundle gives rise to right and left branches
Left branch subdivides into the anterior and inferior divisions of left bundle
Left branch subdivides into the anterior and POSTERIOR divisions of left bundle
What would be seen on an ECG to suggest incomplete bundle branch block
Incomplete block would cause bundle branch conduction delay.
Results in slight-widening of QRS complex (up to 0.11 seconds)
How could you tell a complete bundle branch block on an ECG
Wide QRS complex (larger than 0.12 seconds)
Shape of QRS depends on whether the right or left bundle is blocked
Causes of RBBB
Pulmonary embolism
Ischaemic heart disease
Atrial/Ventricular septal defect
*Describe physiological features of RBBB
Right bundle no longer conducts
Therefore 2 ventricles do not get impulses at the same time and instead spread from left to right
Produces late activation of the right ventricle
Also causes wide physiological splitting of the second heart sound
*ECG of RBBB
Deep S wave in leads I and V6 Tall late R wave in lead V1 MaRRoW (R for RightBBB): -M = QRS looks like an M in lead v1 -W = QRS looks like a w in V5 and V6
*Cause of LBBB
Ischaemic Heart Disease
Aortic valve disease
Describe physiological features of LBBB
Late activation of left ventricle
Causes reverse splitting of 2nd heart sound
Left bundle branch conduction is usually responsible for Initial ventricular activation so LBBB may also produce abnormal Q waves
*ECG of LBBB
Deep S wave in V1 Tall late R wave in I and V6 WiLLiaM (L for LBBB) W = QRS looks like a W in leads V1 and V2 M = QRS looks like an M in leads V4-V6
Define sinus tachycardia
HR >100bpm
Causes of sinus tachycardia
Anaemia Anxiety Exercise Pain HF Pulmonary embolism
Treatment of sinus tachycardia
Treat causes
If necessary, then can use Beta Blockers e.g. Bisoprolol
In what patients would you see Atrioventricular Junctional Tachycardias
Often seen in young patients with little or no structural heart disease.
First presentation is commonly between ages 12-30
AV node essential component to these tachycardias
What does AVNRT stand for
Atrioventricular nodal re-entrant tachycardia
Type of
Are AVNRTachycardias more common in men or women
Women
Risk factors of AVNRTs
Exertion Emotional stress Coffee Tea Alcohol
*Examples of paroxysmal Supraventricular tachycardias
AVNRT - Atrioventricular Nodal Re-entrant Tachycardia
AVRT - Atrioventricular Re-entrant Tachycardia
AVNRT - 2 pathways within the AV node
Short effective refractory period and SLOW conduction
Longer effective refractory period and FAST conduction
What is refractory period
window of time where
cells cannot be excited again after they have already been excited
*AVNRT - in sinus rhythm, which pathway does atrial impulse that depolarises the ventricles usually conduct through?
Fast pathway with longer effective refractory period.
By the time the impulse has been propagated to the ventricles, the FAST pathway has finished its refractory period and once again is able to transmit impulses
What happens in AV node if atrial impulse happens early e.g. atrial premature beat, while fast pathway is still in refractory period
Slow pathway takes over in propagating impulses of atria to the ventricles.
BUT
by the time the slow impulse has been propagated to the ventricles, the fast pathway would’ve finished its refractory period and is once again able to transmit pulses.
*Describe the Re-entrant loop at the AV node in AVNRT
2 pathways: Slow conduction but short refractory time
Fast conduction but long refractory time
Sinus rhythm - atria impulse that causes contraction of ventricles usually conducts through fast pathway.
If atrial impulse happens early, while fast pathway is still in refractory period, slow pathway takes over in propagating atrial impulses to the ventricles.
By the time the slow pathway has been propagated to the ventricles, the FAST pathway would’ve finished its refractory period and is once again able to transmit impulses.
This starts a cycle of fast and slow pathways sending signals through AV node and causing contractions at a much faster rate than a normal pacemaker would so you see Tachyarrhythmia
In AVNRT, what is expected heart rate due to re-entrant loop
100-250bpm
*AVNRT - clinical presentation
- Rapid regular palpitations (abrupt onset and sudden termination)
- Chest pain and breathlessness
- Neck pulsations (prominent jugular venous pulsations due to atrial contractions against closed AV valves)
- Polyuria (due to the realise of atrial natriuretic peptide in response to increased atrial pressures during the tachycardia)
*AVNRT - diagnosis
ECG
- QRS complexes can show typical BBB
- P waves are either not visible or are seen immediately before (normal) or after the QRS complex, due to simultaneous atrial and ventricular activation
What is AVRT
Atrioventricuar Re-entrant Tachycardia
Abnormal connection of myocardial fibres from posterior ventricle to atrium called accessory pathway or Bypass Tract.
Therefore there are 2 circuits: normal AV circuit and Accessory circuit (both transmitting impulses from atria to ventricles)
*What causes Accessory pathway in AVRT
Incomplete separation of the atria and the ventricles during fetal development.
True or False: The accessory circuit impulse in AVRT can travel from atria to venticle or ventricle to atria
True
Atria to ventricle is Anterograde
Ventricle to Atria is Retrograde
Atrial activation can occur after ventricular activation.
Patients more prone to AF or Ventricular Fibrillation
*Example of AVRT
Wolff-Parkinson-White (WPW) syndrome
Pathophysiology of Wolff-Parkinson-White (WPW) syndrome (AVRT) and formation of re-entry circuit
SAN depolarises
Impulse travels to AVN via atria or travels by accessory pathway.
Accessory pathway conducts from atrium to ventricle during sinus rhythm and the electrical impulse can conduct QUICKLY over this abnormal connection to depolarise part of the ventricles ABNORMALLY (PRE-EXCITATION).
Accessory pathway would be in refractory period (cant transmit to signal).
Normal impulse will travel down the AVN, down the Intra-ventricular septum via the Bundle of His and through the left and right bundle branches and into the free walls of the ventricles via the Purkinje cells until it meets the Accessory Pathway, the ventricles innervated by abnormal pathway have already contracted and cant again.
At the point the acessory pathway will be out of its refractory period and will thus be able to conduct the impulse BACK to atria.
Once back in the atria the impulse can then travel back to AVN, thereby setting up a re-entry circuit and the signal cycle will repeat resulting in tachyarrhythmia.
Describe Pre-Excitation in AVRT
Accessory pathway conducts impulse from atrium to ventricles during sinus rhythm.
Electrical impulse can conduct quickly over this abnormal connection to abnormally depolarise part of the ventricles (this is while normal atria is depolarising)
Describe what an ECG showing Pre-Excitation would look like
Short PR interval
Wide QRS complex (begins as a slurred part called a delta wave)
Clinical presentation of AVRT (WFW syndrome)
Palpitations
Severe dizziness
Dysponea
Syncope
*Diagnosis of AVRT or Wolff-Parkinson-White syndrome
ECG:
Short PR interval
Wide QRS complex that begins as a slurred part known as a DELTA wave
*Treatment of AVRT or WFW syndrome
- Patients presenting haemodynamic instability require emergency cardioversion
- If stable then vagal manoeuvres
- If vagal manoeuvres unsuccessful the IV ADENOSINE - causes complete heart block for a fraction of a second and is highly effective at terminating AVNRT and AVRT
- Surgery
What is meant by haemodynamic instability
Hypotension
Pulmonary oedema
Describe surgery in AVRT
Catheter ablation of accessory pathway
Describe surgery in AVNRT
Modification of the slow pathway
Give example of vagal manoeuvres
Breath-holding
Carotid massage
Valsalva manoeuvre - abrupt voluntary increase in intra-abdominal and intra-thoracic pressure by straining - several seconds after the release of the strain, the resulting intense vagal effect may terminate AVNRT or AVRT
Examples of ventricular tacharrhythmias
Ventricular ectopics Ventricular tachycardia Sustained ventricular tachycardia Ventricular fibrillation Some cardiac channelopathies e.g. Long QT syndrome
What are cardiac channelopathies
Congenital disorders that are caused by mutations of the function of cardiac ion channels and hence the electrical activity of the heart e.g. long QT syndrome
What are most common POST-MI arrhythmias
Ventricular ectopics
What are ventricular ectopics
premature ventricular contraction
Ventricular ectopic risk factors
MI
can occur in healthy patients
Pathophysiology of ventricular ectopic
(Extra beats, missed beats or heavy beats)
*These premature beats have a broad and bizarre QRS complex (>0.12 seconds) as they arise from an abnormal (ectopic) site in the ventricular myocardium.
Following a premature beat, there is usually a complete compensatory pause because the AV node or ventricle is refractory so can’t accept next sinus impulse - resulting in missed beat.
(LV dysfunction can develop from frequent ectopics)
Clinical presentation of ventricular ectopic
May be uncomfortable (especially if frequent)
Irregular pulse owing to premature beats
Usually are asymptomatic
Can feel faint or dizzy
Diagnosis of ventricular ectopic
ECG
Widened QRS complex >0.12 seconds
Treatment of ventricular ectopic
Reassure patient
Give Beta-blockers e.g. Bisoprolol if symptomatic
Define (differential diagnosis of) ventricular tachycardia
Pulse >100bpm with at least 3 irregular heart beats in a row
What patients can have ventricular tachycardia
Patients with structurally normal hearts commonly have this (idiopathic ventricular tachycardia)
In these cases it’s usually a benign condition with an excellent long-term prognosis
What can result from untreated ventricular tachycardia
Cardiomyopathy
Ventricular tachycardia aka Gallavardin’s tachycardia
Pathophysiology of ventricular tachycardia
Rapid ventricular beating results in inadequate blood filling of ventricles since they are filled in between beats and if beating was
faster there would be less time to fill (thus less blood fills).
Results in decreased cardiac output and thus a decrease in the amount of
oxygenated blood that is circulated around the body
*Symptoms of ventricular tachycardia
- Breathlessness (lack of lung perfusion)
- Chest pain (lack of heart perfusion)
- Palpitations
- Light headed or dizzy (lack of brain perfusion)
*Treatment of ventricular tachycardias
Beta-blockers e.g. Bisoprolol
What is sustained ventricular tachycardia
Ventricular tachycardia for longer than 30 seconds
Symptoms of sustained ventricular tachycardia
- Dizziness (pre-syncope)
- Syncope
- Hypotension
- Cardiac arrest
What is syncope
Temporary loss of consciousness usually related to insufficient blood flow to the brain
Pulse rate of someone with sustained ventricular tachycardia
120-220bpm
Diagnosis or ECG of sustained ventricular tachycardia
ECG:
- Rapid ventricular rhythm
- Broad and abnormal QRS complex (>0.14 seconds)
Treatment of sustained ventricular tachycardia
Emergency electrical conversion if haemo-dynamically unstable (e.g. hypotensive or pulmonary oedema)
IV beta-blocker e.g. esmolol
IV Amiodarone
Prevented by the use of beta-blockers and implantable cardiac defibrillator
Example of an IV beta-blocker
Esmolol
What can cause ventricular fibrillation
a ventricular ectopic beat
Pathophysiology of ventricular fibrillation
Rapid and irregular ventricular activation with NO MECHANICAL
EFFECT i.e NO CARDIAC OUTPUT
Patient is pulseless and becomes unconscious and respiration ceases (CARDIAC ARREST)
ECG of patient with ventricular fibrillation
Shapeless
Rapid oscillations
No hint of organised complexes
Treatment of ventricular fibrillation
ELECTRICAL DEFIBRILLATION
(only effective treatment)
Management of survivors:
Give long-term, implantable cardioverter-defibrillators
Congenital causes of long QT syndrome
Jervell-Lange-Nielsen syndrome (autosomal recessive) - mutation in cardiac potassium and sodium-channel genes.
Romano-Ward syndrome (autosomal dominant)
*Acquired causes of long QT syndrome
Hypokalemia Hypocalcaemia Bradycardia Acute MI Diabetes Drugs
What drugs can give you a long QT interval
Amiodarone
Tricyclic anti-depressants e.g. Emitriptyline
*Clinical presentation of long QT syndrome
Syncope
Palpitations
Patient may have had Polymorphic ventricular tachycarida that has degenerated into ventricular fibrillation this (or terminates spontaneously)
Diagnosis of long QT
ECG
Treatment of long Qt syndrome
Treat underlying cause
If ACQUIRED long QT, then give IV Isoprenaline (contraindicated for congenital long QT)
