Tachycardia

This is defined as a heart rate of > 100 bpm. Whilst it can be normal physiological response to increased demand (e.g., exercise), there are many arrythmias which also give rise to tachycardias.

Atrial fibrillation

This is a chaotic irregular atrial rhythm with an atrial rate which can exceed 400 bpm.

Small sections of atria are activated individually, resulting in the atrial muscle quivering instead of contracting in a synchronised manner.

The AV node allows intermittent impulses, which leads to an irregular ventricular contraction rate.

It is usually asymptomatic as the cardiac output only drops by about 10%, but it can lead to palpitations and haemodynamic compromise if severe.

Types

Atrial fibrillation can be classified into sub-categories:

First detected episode – this is the first time the patient experiences this arrythmia

Recurrent – this is when patient has multiple episodes of AF (in 2 subtypes):

Paroxysmal AF – when episodes of AF terminate spontaneously, usually < 7 days

Persistent AF – when episodes are not self-terminating and usually last > 7 days

Permanent AF – where the AF is unresponsive to cardioversion or other treatment

Causes

Many cases due to atrial hypertrophy/dilatation

Risk factors include hypertension, age, obesity, heart failure or mitral valve disease

Ischaemic heart disease, idiopathic and infection

Decreased K+, decreased Mg2+, caffeine, hyperthyroidism and regular alcohol use

Symptoms

Can be asymptomatic

Chest pain, palpitations, hypotension

Irregularly irregular pulse – this is caused by the fact that the AV node only allows intermittent pulses

ECG Features

P waves absent – replaced by f waves.

Rhythm is irregularly irregular

Patient usually tachycardic

Normal narrow QRS complexes 

Management

If hemodynamically unstable, electrical DC cardioversion with optional amiodarone

If hemodynamically stable, management consists of a rate or rhythm control strategy depending on the patient

Rate control

Here, it is accepted that the pulse will be irregular, but we give medications in order to slow the heart rate down.

1st choice is a beta-blocker (e.g., atenolol) or a rate-limiting Ca2+ blocker (diltiazem)

If not effective, dual therapy with drugs or addition of digoxin

Rhythm control

This attempts to get the patient back into normal sinus rhythm

Can use electrical cardioversion or drugs (Amiodarone or flecainide)

If onset is > 48 hours, it is advised to give anticoagulation for at least 3 weeks before performing cardioversion, unless the patient is haemodynamically unstable.

In addition, the main risk of AF is embolic stroke.

The CHA2DS2-VASc score is used to assess embolic stroke risk. Warfarin/NOACs is given to patients with a score of 2 or more (+ some men with score of 1):

Atrial flutter

This is a supraventricular tachycardia characterized by a fast atrial rate of around 200-400bpm.

The AV node again behaves intermittently, usually impeding many impulses

Crucially however, this delays impulses consistently and so the ventricular rate will probably be regular

Causes

Found in conditions that enlarge atrial tissue e.g., mitral disease, acute MI

Symptoms

Can be asymptomatic or cause chest pain, palpitations, hypotension

Clinical significance is determined by conduction ratio – number of impulses through node.

If it drops too low, cardiac output will be compromised –> can cause syncope, angina etc.

ECG Features

P waves lose distinction due to rapid rate and blend together

They give a “saw-toothed” appearance and are called flutter (F) waves.

Normal QRS waves

Management

Same management as atrial fibrillation. It is generally more difficult to rate-control than AF and therefore cardioversion is used more frequently.

If recurrent, radiofrequency ablation of the abnormal re-entrant circuit via ablating the cavo-tricuspid isthmus (CTI) is > 90% successful. 

Supraventricular Tachycardia (SVT)

An episodic tachyarrhythmia which has an unpredictable onset and termination.

It is typically an atrioventricular nodal re-entry tachycardia (AVNRT).

It leads to acute attacks of palpitations with symptoms which may then spontaneously resolve.

Symptoms

Episodes start and end suddenly but can be asymptomatic

Palpitations with chest pain

Sudden onset dyspnoea and feeling faint

Management

1st line is vagal maneuverers to increase parasympathetic tone slowing the heart rate, e.g., Valsalva manoeuvre, carotid sinus massage

If unresolving, IV adenosine 6 mg. If still unsuccessful, this can be repeated at a dose of 12 mg and third dose of 18 mg

If persistent, electrical cardioversion can be used

In the long term, these patients will likely need radio-frequency ablation to ablate the abnormal electrical circuit

Wolff-Parkinson White (WPW) syndrome

This is a condition in which there is an abnormal accessory conduction pathway between the atria and ventricles.

This means that the electrical impulse can bypass the delay at the AV node causing a fast heart rate.

As the accessory pathway does not slow conduction, it means atrial fibrillation can rapidly lead to ventricular fibrillation causing sudden death.

Any medication that blocks the AV node can potentiate the arrhythmia by promoting antegrade conduction down the accessory pathway.

Associations

HOCM

Mitral valve prolapse

Ebstein’s anomaly

ECG Features

Short PR interval

Wide QRS complex with a slurred upstroke = “delta wave”

Type A (left-sided pathway) gives right-axis deviation

Type B (right sided pathway) gives left- axis deviation

Management

If hemodynamically unstable, electrical cardioversion

Medical management involves medications like amiodarone and procainamide

Definitive management is radiofrequency ablation of the accessory pathway

Ventricular Tachycardia (VT)

This is a condition which occurs when the ventricular rate exceeds 100 bpm.

It is an unstable rhythm and can quickly progress to ventricular fibrillation.

As the rate originates in the ventricles, it causes broadening of the QRS complex.

On ECG, P waves are not seen as the ventricles overshadow the atrial impulse. 

Monomorphic VT

This is a broad complex tachycardia with a ventricular rate > 100 bpm.

It is most commonly due to ischaemia of the heart (e.g., MI) or a scar from previous ischaemic events providing a substrate for the VT.

Causes

Most commonly due to ischaemic to the heart (e.g. MI)

ECG features

Atrial rhythm/rate can’t be determined.

Rhythm regular and rapid >100bpm.

QRS is wide(>0.12s) and increased amplitude

Management

If patient is pulseless, treat as cardiac arrest

If hemodynamically unstable (BP < 90 mmHg, chest pain), electrical cardioversion

If hemodynamically stable, 1st line is IV amiodarone, 2nd line is lidocaine

If not due to an acute MI, the patient will likely need an implantable cardioverter-defibrillator (ICD)

Polymorphic VT (Torsades de pointes)

This is a type of VT which is associated with having a long QT interval.

The rate is again generated by the ventricles, but it does not give a consistent welldefined broad complex tachycardia like monomorphic VT.

Causes

Due to factors which increase the QT interval

Drugs (amiodarone, TCAs, erythromycin)

Hypothermia

Hypokalemia/Hypocalcaemia

ECG features

Hallmark is QRS complexes that rotate about the baseline, deflecting down and up for several beats.

Tachycardia (rate >100bpm)

Management

Intravenous infusion of magnesium sulfate is usually effective. Patients may require cardioversion or pacing.

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