Tachycardia, generally defined as a heart rate ≥100 bpm, can be a normal physiological response to a systemic process or a manifestation of underlying pathology. The normal heart rate varies with age. The normal sinus rate in infants is 110 to 150 bpm, which gradually slows with age.
Classification of tachyarrhythmia
Several methods of classification of tachyarrhythmia are helpful in organising and assessing tachycardias. These include: sinus versus non-sinus causes; atrial versus ventricular arrhythmias; narrow- versus wide-complex tachycardias; regular versus irregular arrhythmias; and classification based on the site of origin of the arrhythmia.
Sinus versus non-sinus causes:
Sinus tachycardia is a common cause of tachycardia that can often be mistaken for an arrhythmia. Diagnosis depends on the P-wave morphology and the setting in which it occurs. Because each impulse originates in the sinoatrial node, the ECG shows a P wave preceding each QRS interval with a normal P-wave axis. In most cases, a secondary cause of sinus tachycardia can be identified. A careful assessment is important, to evaluate whether the sinus rate is appropriate for the clinical situation. Sinus tachycardia can be mistaken for other supraventricular arrhythmias, including atrial flutter, particularly with rapid tachyarrhythmias (when P waves are difficult to distinguish or when ectopic atrial foci originate near the sino-atrial node, such as near the superior vena cava or upper crista terminalis).
Atrial versus ventricular arrhythmia:
Whether the arrhythmia originates from the atrium or the ventricle is usually dependent on whether the QRS complex is wide or narrow, and on the atrial:ventricular relationship. Atrial arrhythmias usually conduct to the ventricle through the His-Purkinje system and result in a narrow QRS complex. Some overlap may occur when conduction occurs with aberrancy (left or right bundle branch block) and in the presence of anti-arrhythmic agents that may slow conduction (sodium channel blockers). If P waves are discernible, an atrial:ventricular relationship of <1 is highly suggestive of a ventricular arrhythmia, whereas a relationship >1 is highly suggestive of an atrial arrhythmia. A 1:1 atrial:ventricular relationship can occur with both atrial and ventricular arrhythmias.
Narrow versus wide QRS complex:
Classification can also be based on whether there is a narrow- (QRS interval <120 ms) or wide- (QRS interval >120 ms) complex tachycardia. Narrow-QRS-complex tachycardia suggests that anterograde conduction and thus depolarisation of the ventricle occurs through the atrioventricular (AV) node and His-Purkinje system. A wide-complex tachycardia suggests that conduction through the ventricle occurs through the slower myocyte-to-myocyte connections (because of either AV conduction via an accessory pathway or a ventricular origin) and can be seen even with sinus rhythm. However, atrial tachyarrhythmias that conduct aberrantly may present as a wide-complex tachycardia.
Regular versus irregular rhythm:
Whether a rhythm is regular or irregular is easy to determine clinically and can help guide diagnosis of the tachyarrhythmia. An irregular rhythm is defined as a beat-to-beat R-R variability of more than 30 ms. In general, irregular narrow-complex arrhythmias include: atrial fibrillation, atrial flutter with variable conduction, and multifocal atrial tachycardia. An irregular wide-complex tachycardia may be due to pre-excited atrial fibrillation (due to a rapidly anterograde-conducting bypass tract), polymorphic ventricular tachycardia and atrial fibrillation, or multifocal atrial tachycardia conducting with aberrancy.
Site of origin:
Tachyarrhythmias can be classified according to the site of origin: atrial, junctional, or ventricular.
Atrial impulses are characterised by initial depolarisation of the atrium, from a single focus, such as sinus tachycardia or atrial tachycardia; macro re-entry around an anatomical obstacle, such as in typical atrial flutter; or from multiple wavelets of re-entry, such as atrial fibrillation.
Arrhythmias that originate at the level of the junction of the atrium and ventricle (AV node and/or proximal His bundle), such as AV nodal re-entrant tachycardia or junctional ectopic tachycardia, are characterised by depolarisation of the ventricle and retrograde atrial activation (if present), manifested by a retrograde P wave.
Arrhythmias that originate from the ventricle may originate from the distal His-Purkinje system or ventricular myocardium. The site of origin within the ventricle further defines some arrhythmias within the ventricle. Examples include right ventricular out-flow tract ventricular tachycardia and bundle branch re-entry ventricular tachycardia. Haemodynamic stability is not a helpful factor in differentiating atrial and ventricular arrhythmias. Some cases of ventricular tachycardia may be initially well tolerated haemodynamically. Misdiagnosis and inappropriate treatment (i.e., calcium channel blockers) may have catastrophic consequences.
When a patient with a wide-complex tachycardia is being evaluated and the diagnosis is not certain, the arrhythmia must be initially regarded as ventricular tachycardia until it is proven to be otherwise.
Sinus tachycardia is the most common cause of tachycardia, as it is usually a normal physiological response to emotional or physical stimulation.
Atrial fibrillation is the most common arrhythmia in clinical practice, with an estimated prevalence of 0.5% to 1% in the general population and increasing with age. Up to 9% of patients aged 80 years or older have atrial fibrillation. As the proportion of older people in the population increases, the number with atrial fibrillation is likely to increase significantly.
The incidence of atrial flutter has been reported as 88 cases per 100,000 person-years; it is more common in men, with increasing age, and in those with heart failure or chronic obstructive pulmonary disease (COPD). It has been estimated to be 2.5 times more common than paroxysmal supraventricular tachycardia (PSVT).
PSVT, defined as intermittent supraventricular tachycardia (AV node re-entry tachycardia, AV reciprocating tachycardia, or atrial tachycardia) has an incidence of 36 cases per 100,000 person-years and a prevalence of 2.29 cases per 1000 people. Females are twice as likely to develop PSVT, and the incidence is five times greater in people older than 65 years compared with younger people. Most cases of supraventricular tachycardia are due to AV nodal re-entrant tachycardia (60% of cases); the remainder are due to AV reciprocating tachycardia (30%) and atrial tachycardia (10%).
The prevalence of inappropriate sinus tachycardia is not well known and the underlying mechanisms are likely to be multifactorial, but patients are often young (age 15 to 50 years) and female.
The prevalence of ventricular tachyarrhythmia is highly dependent on its type and duration. In patients with a history of previous MI, the incidence of sustained monomorphic ventricular tachyarrhythmia depends on the size of the infarction and the overall left ventricular function.
- Sinus tachycardia
- Acute atrial fibrillation
- Chronic atrial fibrillation
- Atrial flutter
- Atrial tachycardia
- AV nodal re-entrant tachycardia
- AV re-entry tachycardia/Wolff-Parkinson-White syndrome
- Multifocal atrial tachycardia
- Junctional ectopic tachycardia
- Monomorphic ventricular tachycardia with prior myocardial infarction
- Monomorphic ventricular tachycardia with non-ischaemic cardiomyopathy
- Ventricular fibrillation
- Polymorphic ventricular tachycardia with normal QT interval
- Idiopathic ventricular tachycardia: structurally normal heart
- Sinus node re-entry tachycardia
- Inappropriate sinus tachycardia
- Permanent junctional reciprocating tachycardia
- Torsade de pointes
- Bidirectional ventricular tachycardia
- Accelerated idioventricular rhythm
Ramin Shadman, MD, FACC
Southern California Permanente Medical Group
Assistant Professor of Medicine
RS declares that he has no competing interests.
Robert W. Rho, MD, FACC
RWR is an author of a reference cited in this topic.
Mark M. Gallagher, BSc, MD
Consultant Cardiologist and Electro-physiologist
St George's Hospital
MMG declares that he has no competing interests.
Fred Kusumoto, MD
Associate Professor of Medicine
FK declares that he has no competing interests.
Zachary D. Goldberger, MD
University of Michigan Health System
ZDG declares that he has no competing interests.
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