Tachyarrhythmia

SINUS ARRHYTHMIA

Phasic alteration of the heart rate during respiration (the sinus rate increases during inspiration and slows during expiration) is a consequence of normal parasympathetic nervous system activity and can be pronounced in children. Absence of this normal variation in heart rate with breathing or with changes in posture may be a feature of autonomic neuropathy.

TACHYARRHYTHMIA

There are three main mechanisms of tachycardia:
Increased automaticity.
Re-entry. Most tachyarrhythmias are due to re-entry.
Triggered activity.

SINUS TACHYCARDIA

This is defined as a sinus rate of more than 100/min, and is usually due to an increase in sympathetic activity associated with exercise, emotion, pregnancy or pathology .





Sinus tachycardia

Anxiety

Fever
Anaemia
Heart failure
Thyrotoxicosis
Phaeochromocytoma
Drugs, e.g. β-adrenoceptor agonists

ATRIAL TACHYARRHYTHMIAS

ATRIAL ECTOPIC BEATS (EXTRASYSTOLES, PREMATURE BEATS)

These usually cause no symptoms but can give the sensation of a missed beat or an abnormally strong beat. The ECG shows a premature but otherwise normal QRS complex; if visible, the preceding P wave has a different morphology because the atria activate from an abnormal site. In most cases these are of no consequence, although very frequent atrial ectopic beats may herald the onset of atrial fibrillation. Treatment is rarely necessary.

ATRIAL TACHYCARDIA

Atrial tachycardia may be a manifestation of increased atrial automaticity, sinoatrial disease or digoxin toxicity. It produces a narrow complex tachycardia with abnormal P-wave morphology, sometimes associated with atrioventricular block if the atrial rate is rapid. It may respond to β-blockers, which reduce automaticity, or class I or III antiarrhythmic drugs




Multifocal atrial tachycardia : usually is associated with hypoxia as in COPD or may be due to electrolytes disturbance especially hypokalemia . The rate must be more than 100 b/min with at least three different morphologies of P wave . Treatment of the cause is needed .

Junctional ectopic :

Atrial flutter

Atrial flutter is characterised by a large (macro) re-entry circuit, usually within the RA encircling the tricuspid annulus. The atrial rate is approximately 300/min, and is usually associated with 2:1, 3:1 or 4:1 AV block (with corresponding heart rates of 150, 100 or 75/min). The ECG shows saw-toothed flutter waves . Carotid sinus pressure or intravenous adenosine may help to establish the diagnosis by temporarily increasing the degree of AV block and revealing the flutter waves
Management


Digoxin, β-blockers or verapamil can be used to control the ventricular rate . However, in many cases it may be preferable to try to restore sinus rhythm by direct current (DC) cardioversion or by using intravenous amiodarone. Beta-blockers or amiodarone can also be used to prevent recurrent episodes of atrial flutter. Catheter ablation offers a 90% chance of complete cure and is the treatment of choice for patients with persistent, troublesome symptoms.

Atrial fibrillation

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia. The prevalence rises with age, affecting 2-5% and 8% of those aged over 70 and 80 years respectively. Atrial fibrillation is a complex arrhythmia characterised by both abnormal automatic firing and the presence of multiple interacting re-entry circuits looping around the atria. Episodes of atrial fibrillation are usually initiated by rapid bursts of ectopic beats arising from conducting tissue in the pulmonary veins or from diseased atrial tissue. During episodes of AF, the atria beat rapidly but in an uncoordinated and ineffective manner. The ventricles are activated irregularly at a rate determined by conduction through the AV node. This produces the characteristic 'irregularly irregular' pulse.
AF can be classified as paroxysmal (intermittent, self-terminating episodes), persistent (prolonged episodes that can be terminated by electrical or chemical cardioversion) or permanent. When AF persists for a period of months, structural remodelling occurs with atrial fibrosis and dilatation that further predispose to AF. Thus early treatment of AF will prevent this and reinitiation of the arrhythmia.
Common causes of atrial fibrillation

Coronary artery disease (including acute MI)

Valvular heart disease, especially rheumatic mitral valve disease
Hypertension
Sinoatrial disease
Hyperthyroidism
Alcohol
Cardiomyopathy
Congenital heart disease
Chest infection
Pulmonary embolism
Pericardial disease
Idiopathic (lone AF)


About 50% of all patients with paroxysmal AF and 20% of patients with persistent or permanent AF have structurally normal hearts; this is known as 'lone atrial fibrillation'.

Clinical features : AF can cause palpitation, anxiety , breathlessness and fatigue. In patients with poor ventricular function or valve disease it may precipitate or aggravate cardiac failure (tachycardia induced cardiomyopathy ) because of loss of atrial function and heart rate control. A fall in BP may cause lightheadedness and syncope . Chest pain may occur with underlying coronary disease. However, AF is often completely asymptomatic, in which case it is usually discovered as a result of a routine examination or ECG.

AF is associated with significant morbidity and a twofold increase in mortality that are largely attributable to the effects of the underlying heart disease and the risk of cerebral embolism. Careful assessment, risk stratification and therapy can improve the prognosis.
Management

Assessment of patients with newly diagnosed AF includes a full history, physical examination, 12-lead ECG, echocardiogram and thyroid function tests. Additional investigations such as exercise testing may be needed to determine the nature and extent of any underlying heart disease.

When AF complicates an acute illness (e.g. chest infection, pulmonary embolism), effective treatment of the primary disorder will often restore sinus rhythm. Otherwise, the main objectives are to restore sinus rhythm as soon as possible, prevent recurrent episodes of AF, optimise the heart rate during periods of AF, minimise the risk of thromboembolism and treat any underlying disease.

Paroxysmal atrial fibrillation

Occasional attacks that are well tolerated do not necessarily require treatment. Beta-blockers are normally used as first-line therapy if symptoms are troublesome . Class Ic drugs such as propafenone or flecainide, are also effective at preventing episodes but should not be given to patients with coronary disease or left ventricular dysfunction. Amiodarone is the most effective agent for preventing AF but its side-effects restrict its use to patients in whom other measures fail. Digoxin and verapamil are not effective drugs for preventing paroxysms of AF. In patients with AF in whom β-blockers or class Ic drugs are ineffective or cause side-effects, catheter ablation can be considered. Ablation prevents AF in approximately 70% of patients with prior drug-resistant episodes, although drugs may subsequently be needed to maintain sinus rhythm.

Persistent and permanent atrial fibrillation

There are two options for treating persistent AF:
rhythm control: attempting to restore and maintain sinus rhythm
rate control: accepting that AF will be permanent and using treatments to control the ventricular rate and to prevent embolic complications.
Rhythm control
An attempt to restore sinus rhythm is particularly appropriate if the arrhythmia has precipitated troublesome symptoms and there is a modifiable or treatable underlying cause.
Electrical cardioversion to restore and maintain sinus rhythm are most successful if AF has been present for < 3 months, the patient is young and there is no important structural heart disease.


Immediate DC cardioversion after the administration of intravenous heparin is appropriate if AF has been present for < 48 hours.
Chemical cardioversion : An attempt to restore sinus rhythm by infusing intravenous flecainide is a safe alternative to electrical cardioversion if there is no underlying structural heart disease. DC cardioversion should be deferred until the patient has been established on warfarin, with an international normalised ratio (INR) > 2.0 for a minimum of 4 weeks, and any underlying problems, such as hypertension or alcohol excess, have been eliminated. Anticoagulation should be maintained for at least 3 months following successful cardioversion; if relapse occurs, a second (or third) cardioversion may be appropriate. Concomitant therapy with amiodarone or β-blockers may reduce the risk of recurrence. Catheter ablation is sometimes used to help restore and maintain sinus rhythm in resistant cases, but it is a less effective treatment for persistent AF than for paroxysmal AF.

Rate control

If sinus rhythm cannot be restored, treatment should be directed at maintaining an appropriate heart rate. Digoxin, β-blockers or rate-limiting calcium antagonists such as verapamil or diltiazem

In exceptional cases, poorly controlled and symptomatic AF can be treated by deliberately inducing complete AV nodal block with catheter ablation; a permanent pacemaker must be implanted beforehand. This is known as the 'pace and ablate' strategy.

Prevention of thromboembolism

Loss of atrial contraction and left atrial dilatation cause stasis of blood in the LA and may lead to thrombus formation in the left atrial appendage. This predisposes patients to stroke and other forms of systemic embolism.

How to assess risk of thromboembolism in atrial fibrillation: the CHADS score

Congestive heart failure (1 point)
Hypertension (1 point)
Age > 75 (1 point)
Diabetes mellitus (1 point)
Stroke or transient ischaemic attack (2 points)


Score: 0 = aspirin therapy only, 1 = warfarin or aspirin, ≥ 2 = warfarin