ATRIAL TACHYARRHYTHMIAS

Def: A cardiac arrhythmia is a disturbance on the electrical rhythm or activity of the heart.
If there is an arrhythmia, then most often there is a structural cardiac disease, occasionally functional.

Mechanism
1. Increased automaticity
- SAN fibres are the fastest followed by atrial and ventricular fibres.
- SAN sets the pace for the cardiac activity and increased pace→ tachycardia. This may be due to an ectopic
focus.
2. Re- entry - Two alternative pathways with different conduction properties. This can occur in IHD →further
stimulation and tachycardia.
3. Triggered activity - Incompletely repolarized cell membrane →triggered activity and tachycardia.
Note:
Sinus arrhythmia- Parasympathetic activity is ↓in inspiration. Sinus arrhythmias are more predominant in
children.
Sinus bradycardia – HR <60/min
May be physiological as in – athletes or pathological as in
- Myocardial infarction
- Sic sinus syndrome/ sinus node dysfxn
- Hypothermia
- Hypothyroidism
- ↑ICP
- Cholestatic jaundice
- Drugs – digoxin, Beta Blockers, verapamil
Sinus tachycardia
i) Physiological
- Pregnancy
- Exercise increased sympathetic activity
- Emotion
ii) Pathological causes
- Anxiety disorders
- Fever
- Anaemia
- Heart failure
- Hyperthyroidism
- Phaeochromocytoma –paroxysmal tachycardia
- Drugs – beta adrenergic agonists e.g. salbutamol

Atrial Ectopic beats (Premature beats)

- Asymptomatic. There may be missed or extra strong heart beat.
- ECG – p-wave, one p-wave may be abnormal in one or some of the rhythms.
- Rx –rarely necessary

Atrial tachycardia
May be as a result of
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 - Increased atrial automaticity or
- SAN disease OR
- Digoxin toxicity
ECG – Abnormal p-wave which might not be accompanied by QRS complex
Rx – Beta blockers (To reduce automaticity)
- Class I (Disopyramide, flecainide, propafenone) and class III anti arrhythmias.
- Catheter ablation for recurrent or drug resistant AT.

Atrial flutter
- Is a re-entry circuit in the Rt atrium usually around the tricuspid annulus.
- Atrial rate may be up to 300/min and the ratio between atrial: ventricle rate may be 1:1, 2:1, 3:1 or 4:1.
- ECG findings – Saw toothed flutter p-wave.
NB: Any narrow QRS complex >150 is a suspect for a flutter even in the absence of saw toothed p-wave.
- To confirm the flutter -Massage carotid sinus OR Give IV adenosine to temporarily increase the degree of
AV block.

Treatment:
Aims
i) To achieve sinus rhythm
ii) To control ventricular rate so that they relax and fill
iii) To disrupt the circuit through cardioversion.

1. To achieve sinus rhythm

Cardioversion: A mechanical synchronized cardioverter. It’s a form of electrical shock but at a lower voltage.
Cardioversion is not the first choice of therapy. It is used if patient has HF or haemodynamic instability.

2. Rate control
- This is the main mode of therapy. It is the preferred mode of therapy.
i) Pharmacological; Amiodarone, propafenone, procainanide, flecainide are effective and should be
used to prevent recurrent episodes of atrial flutter.
- Flecainide should always be prescribed with AV node blocking drug (B- blocker).
ii) Catheter ablation – Gives a 90% cure rate.

ATRIAL FIBRILLATION
Def: Multiple interacting re-entry circuits in the atria leading to rapid uncoordinated, ineffective atrial contractions.
There is irregular atrial rhythm at between 300-600 and irregular ventricular rate.
The main risk is embolic stroke.

Epidemiology
This is the most common sustained cardiac arrhythmia.

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In the UK 0.5% of the adults suffer from this problem and the prevalence rises with age reaching 10% by the age of
80yrs.

Aetiology
1. Coronary artery disease (CAD) especially AMI.
2. Valvular heart dz especially RHD (mitral valve).
3. Hypertensive heart disease.
4. Hyperthyroidism
5. Heavy alcohol consumption
6. Cardiomyopathy
7. Chest infxns e.g. pneumonia
8. Pulmonary embolism
9. Any patient with congestive heart disease.
10. Heart surgery –cardiac transplant, CABG
11. Electrolyte imbalance, K+, mg2+
12. Others
- Sino-atrial node dz – sic sinus syndrome
- Congenital heart disease
- Pericardial dz
- Idiopathic (zone atrial fibrillation) 20% of the cases.
- COPD
- Obstructive sleep apnoea
- Non cardiac surgery – intra-thoracic surgery
- Metabolic syndrome
- Obesity
- Autonomic neuropathy
- Diet especially caffeine
- Endocarditis
- Atrial myoxoma
- Haemochromatosis
- May be genetic
- Drugs – thiophilline, adenosine
- Digitalis
- Lung cancer
- Sarcoidosis

Pathophysiology
Ectopic beats originating from conducting tissues around pulmonary veins or from diseased atrial tissue in the
context of dilated atria or slow conducting area. This leads to a rapid, irregular, uncoordinated ineffective
contraction of the atrial tissue which will cause irregular ventricular activation. All this will give an irregularly
irregular pulse with an irregular QRS which is otherwise normal and also absent P waves.

Classification of atrial fibrillation

1. Paroxysmal atrial fibrillation; Intermittent and self-terminating.
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2. Persistent atrial fibrillation; Prolonged but can be terminated by cardioversion.
3. Permanent atrial fibrillation

Clinical features
A. fib may be asymptomatic
Symptoms include – palpitations, light headedness due to fall in Bp.
- Fatigue, breathlessness, chest pain
- Others – symptoms of the underlying disease, or cmxs e.g. HF or systemic embolism.
Signs – irregularly irregular pulse
Apical pulse > rapid pulse

Management
Aims
1. Restore sinus rhythm
2. Prevent recurrence
3. Optimize the HR during episodes
4. Reduce risk of thromboembolism
5. Treat the underlying disease

General measures
1. Full evaluation
- History
- Physical examination
- General
- Systemic
2. 12 lead ECG – Absent p waves, irregular QRS complex
3. Echo
4. Blood tests, Thyroid fxn tests, U/E, cardiac markers
5. Tests for aetiological pathology

Paroxysmal A. fib
i) Pharmacological therapy
- Rate control
- Beta blockers especially in IHD, hypertensive heart disease, heart failure and exercise related fibrillation.
- Rhythm control
- Propafenone and flecainide except in coronary heart disease and LV dysfxn
- Amiodarone is useful for prophylaxis

NB: Digoxin and verapamil –last option especially digoxin. These drugs do not prevent another episode. They
are purely for rate control. They are not effective for preventing paroxysmal A. fib.
Treat associated illness.
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 ii) Non-pharmacological therapy
- Radio frequency ablation
- Pacing
- Over drive pacing
- Cardioversion

Persistent and permanent A. fib

Rhythm control
- Infusion of flecainide 2mg/kg over 30min then amiodarone or BB to prevent relapse.
- Electrical cardioversion
Rate control
- Combination therapy; Two of the following
i) Digoxin
ii) Beta blocker
iii) Verapamil
If combination therapy fails, then put a pacemaker and permanently block the AV node.
Prevention of thrombo-embolism
i) Mod – High and very high risk patients.
1. Age > 75yrs with ↑Bp
2. Previous ischaemic stroke
3. Previous TIA or emboli
4. Co-morbidities; Mitral valve disease, HTN, HF (LV fxn / CCF), DM, Coronary or peripheral arterial
disease
Use Warfarin for prevention of thrombo-embolism in all the above cases.
ii) Low risk patients – use aspirin if warfarin is CI or <65yrs + no risk.

CHADS score for risk assessment

C – Congestive heart failure – score 1
H – hypertension – score 1
A – Age >75 – score 1
D – Diabetes mellitus – score 1
S -Secondary prophylaxis for prior stroke or CVA – score 2
High risk 5-7 CHADS score – give warfarin unless CI
- Moderate risk 2-4 – warfarin unless CI
- Low risk 1-2 – junior ASA (Ascard)

Supraventricular tachycardia
Originates from atria and end up in the ventricles
May be
1. AVN re-entry tachycardia ( AVNRT), Rate 140 -220 regular
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 Management – Rx is not always necessary
- Terminate attack by use of carotid sinus pressure or vagal tone (valsalva manouvre)
- IV adenosine OR Verapamil OR
- B – blockers, flecainide and digoxin
- Emergency cases – cardioversion
- Catheter ablation
2. AVRT – Wolf Parkison White syndrome if symptomatic.
- Digoxin & verapamil – Not useful cos they shorten the refractory period of the accessory pathway.
- Patients for cardioversion must have been on warfarin and sustained INR of between 2-3
- Slowing the rate through vagal manourvers
i) Carotid massage
ii) Pressure over eye ball.
iii) Valsava maneuvers- Ask patient to bear down as if to pass stool or to blow out against a tube.
NB: Rate control is the most important thing in management.

VENTRICULAR TACHYARRHYTHMIAS
This is characterized by a long QRS complex & includes;
1. Ventricular ectopic beats (extra –systoles, premature beats).
2. Ventricular tachycardia (VT)
3. Ventricular fibrillation
4. Torsades de pointes

Ventricular ectopic beats

- These are premature broad –bizarre QRS complexes which may be unifocal (beats arising from a single
ectopic focus) or multifocal (varying morphology with multiple foci).
- Are the commonest post MI arrhythmias but they are also seen in healthy people.
Pathophysiology – ectopic trigger is located in the ventricles leading to a broad QRS complex that is ill
synchronized because the excitation has been distributed through H-Purkinje system.
Types of ventricular ectopic beats
1. Ventricular ectopic beats in normal people
Are due to Anxiety, Stress, Alcohol, Tea or caffeine ingestion
- Is prominent at rest and disappears with exercise.
- No treatment is required
- May require low dose BB in anxiety and palpitations.
- If it occurs in sub-clinical heart dz especially CAD then BBs are helpful.
2. Ventricular ectopic beats (VEBs) associated with heart conditions e.g MI (persistent type), Heart failure,
Digoxin toxicity
- Clinical features – mostly asymptomatic. Symptoms include- irregular heart beat, missed beats, irregular
beats, heavy beats.
- Investigations – ECG –fusion beats – two (2) irregular complexes then a normal complex
- Broad and bizarre QRS complex

Management – symptomatic
- Reassurance
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 - Beta blockers
- Angioplasty or CABG
Prognosis – good if no associated heart dz. Sudden death occurs in the presence of organic heart dz– HF, MI,
AS. The prognosis is worsened by class I anti – arrhythmic drugs. The prognosis depends on the frequency of
VEBs (> 10 beats/hr or >10 beats /min.

Ventricular tachycardia (VT)

Three or more consecutive ventricular pre-mature beats with an abnormal rate of 160- 240/min It is always
associated serious heart disease and may degenerate into ventricular fibrillation.
Pathology – re-entry
- Abnormal triggered rhythm as in AMI, Myocarditis, Cardiomyopathy, Chronic IHD
Types
1. Non Sustained – A VT that is equal or more than 5 consecutive beats but lasts <30sec. Is found in 6% of
normal individuals but in 60-80% in people with heart disease. Its associated with poor prognosis.
2. Sustained type - is symptomatic or sustained VT in the absence of reversible precipitating cause.

Clinical features - Palpitations, dizziness, dyspnoea, syncope

Investigations - ECG – Broad QRS complex tachycardia

Management –Immediate management is to restore sinus rhythm by;

i) Direct current cardioversion – Rx of choice or where not available then IV bolus of lidocaine.
Alternatively mexiletine, flecainide or disopyramide.
ii) Correct K+, PO4, acidosis, Mg2+ cos they may aggrevate the situation.
iii) Prophylaxis – BB
iv) If the above measures fail –than consider ICD

Ventricular Fibrillation
- A terminal rhythm of a dying heart.
- It is a very rapid and irregular ventricular activity with no mechanical effect.
- Patient is usually pulseless, becomes rapidly unconscious and respiration ceases.
- It is usually associated with VT
Categories
1. Primary V. fib – complicates AMI in the absence of shock or cardiac failure. The success rate of ICD is 95%.
– Short and long term prognosis is excellent
Lidocaine offers no benefit.
2. Secondary V. fib- occurs with AMI with shock with or without HF. It is associated with severe underlying
ventricular damage.
Treatment – As for cardiac arrest

Torsades de pointes (Twisting points)

A VT characterized by changing QRS vectors.
The arrhythmia is usually non- sustained and repetitive leading to long QT interval.
Causes
1. Electrolyte imbalance – K+, Mg2+, Ca+
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 2. Rare congenital syndromes e.g.
i) Jervell – Lange – Nielson syndrome – an autosomal recessive dz
ii) Romano – Ward syndrome- autosomal dorminant.
3. Drugs –Those that give prolonged QRS complex
- Class Ia anti-arrhythmias – Disopyramide
- Class III anti-arrhythmias – Sotalol, amiodarone
- TCA e.g. amitriptylline
- Phenothiazines – CPZ
- Macrolides – Erythromycin etc.
4. Bradycardia

Treatment
i) Treat underlying cause
ii) IV Mg2+ 8mmol over 15min, then 75mmol/24hrs in all cases.
iii) BB especially in congenital long QT syndromes
iv) ICD

HEART BLOCK
May be;
1. AV junction block
2. Accelerated conduction block
3. Bundle branch block

1. AV junction
The AV jnx is the only pathway for conduction of the heart. It consists of
i) AV node
ii) Bundle of His
From ECG, heart block is diagnosed on the degree of severity.
i) 1st degree heart block; Every p-wave is conducted through the AV jnx with a delay of >0.2 secs. The p-
wave is >5mm. every p-wave has a QRS following but the PR interval is prolonged.
ii) 2nd degree heart block; Some of the atrial currents are conducted through AV jnx to the ventricles
while some are not. Thus, some p-waves will have QRS complex following them and others will not.
a) Mobitz I- Progressive lengthening of successive PR interval culminating in a dropped beat (Wenkenbach
phenomenon) due to impaired conduction of AV node. It may be physiological at rest or during sleep in
athletes or young adults with high vagal tone.
b) Mobitz II – No progressive increase in PR interval but some p-waves have QRS complexes following them
while others don’t. It is a more serious variety of the 2 nd degree heart block that can lead to higher degree
of heart block or serious complications.
NB: Depending on ratio of p-waves to the number of QRS following them 2 0 heart block is described as 2:1, 3:1,
4:1.
iii) Third degree (complete) heart block; A more severe form of heart block.
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 There is no relationship between p-waves and QRS complex. No p-wave is conducted & there is no fixed PR
intervals as the P and QRS waves are entirely independent of each other.
In this condition, the QRS complexes are produced by the ventricles themselves but at a slow rate with a long
R-R interval (The ventricles have their own independent rhythmicity at a slow rate of 30-40/min. The atria,
being controlled by the SAN has higher rates of 60-100/min. 3 0 heart block requires careful observation and
treatment.
It requires insertion of permanent artificial pacemaker. The cause of delay of conduction in
AV jnx could be degeneration, fibrosis, destruction, inflammation

Aetiology of complete heart block

1. Congenital
2. Acquired
- Idiopathic fibrosis
- Myocardial infarction / ischaemia
- Inflammation
- Acute e.g. aortic root abscess, infective endorcarditis.
- Chronic –Sarcoidosis, Chaga’s dz
- Trauma especially cardiac surgery
- Drugs, BB, CIB and digoxin

2. Accelerated conduction
- Normally due to by-pass
- Diagnosis – shot PR interval <0.125 or <3mm
- Abnormal notes on the QRS complexes called delta waves.
- Accelerated conduction block occurs in
i) Wolf – Parkinson White syndrome (WPW)
ii) Lowen– Ganong – Levin syndrome
These conditions are associated with clinical & electrocardiographic features.
WPW Syndrome – The impulse is conducted through an accessory path called bundle of Kent.
Lowen – Ganong –Levin Syndrome – unlike in WPW there is no delta waves and QRS duration is normal.

STOKES –ADAM’S
Episodes of ventricular asystole may complicate complete heart block or Mobitz II.
It can also occur in patients with sino-atrial disease leading to recurrent syncope called ‘Stoke’ Adam’s attacks.
It is characterized by sudden loss of consciousness which occurs without warning and results in a fall.
Convulsions can occur if there is prolonged asystole. Pallor & death like appearance during the attack will
occur but when the heart starts beating again, there is a characteristic flush.
Carotid sinus syndrome and vaso-vagal syndrome may also have similar features.

3. Bundle branch block and hemiblock

There is interruption of the Rt or Lt branch bundle of His which delays activation of the appropriate ventricles,
broadens QRS complex > 0.1sec and produces characteristic alteration in QRS morphology.
RBBB (Rt bundle branch block) can be a common normal variant but Lt bundle branch block (LBBB) signifies an
important underlying dz.

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Both forms may be due to a conduction tissue disease or a feature of other heart diseases. The Lt branch of His is
divided into ant. and post. fascicles. Damage to conduction tissue at this point (Hemiblock) does not broaden QRS
complex and alters the mean direction of ventricular depolarization causing a left axis deviation in Lt anterior
hemiblock and a Rt axis deviation in left posterior hemiblock. The combination of the Rt and Lt block is known as
Bifascicular block.

Common causes of bundle branch block

a. RBBB
1. Normal variant
2. RVH or strain e.g. PE, embolism
3. CHD e.g. ASD
4. Coronary artery disease (CAD)

b. LBBB
1. CAD
2. HTN
3. Aortic valvular disease
4. Cardiomyopathy

Management of heart block (AV block)

1. AV block complicating AMI
Acute inferior MI – Usually has a reliable escape rhythm and if asymptomatic, no Rx is required.
Symptomatic 20 or complete heart block may respond to:-
i) Atropine 0.6mg IV; repeat PRN. If atropine fails, give temporary pacemaker. In most cases AV block
will resolve in 7-10days
2. Chronic AV block
- Symptomatic bradyarrhythmias associated with AV block →permanent pacemaker.
- Asymptomatic heart (10 or Mobitz I) requires no treatment. However:
i) Reverse the underlying cause
ii) Stop any medication slowing the HR
iii) Reverse any condition that increases vagal output.
- Permanent pacemaker is indicated in Mobitz II or complete heart block except in young asymptomatic
patients with long, complete heart block which mean daytime rate of >50/min. In Mobitz II- the defect is
always below the AV node & management is by giving permanent pacemaker.

Causes of heart block

1. Congenital causes
- Fibrosis and sclerosis of conduction e.g.
- Lev’s dz – sclerosis of Lt side of the cardiac skeleton
- Lenegre’s dz - progressive fibrotic sclerodegenerative changes of the conduction system.
2. Ischaemic heart disease – 40% of AV blocks may be acute or chronic
3. Drugs – mainly
Beta blockers, CCB mainly non-dihydropyridines, Digitalis, Amiodarone, adenosine, quinidine,
procainamide, disopyramide
4. Increased vagal tone due to Pain ,Carotid sinus manage, Hypersensitivity carotid sinus syndrome
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 5. Valvular heart disease; Aortic or mitral valve calcification
6. Congenital heart disease
7. Familial – Association with mutations in the Na+ and K+ channels
8. Cardiomyopathies
9. Myocarditis
10. Hyperkalaemia
11. Neuromuscular diseases
Dermatomyositis, Rheumatoid arthritis
12. Hypothyroidism
13. Cardiac tumours
14. Myocardial trauma

Clinical features
1. Syncope – due to bradyarrhythmias
2. Sudden fainting
3. Chest pain
4. Dizziness
5. Pre- syncope – sweating, restless before patient falls.

Management
- Asymptomatic cases – No treatment
- Atropine – usually the last option
- 20 heart block – Mobitz II or complete heart block – pacemaker
- Reverse the underlying cause.

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