Content – Supraventricular Tachycardias

Sinus tachycardia is a physiologic response, with increased sympathetic tone, following a variety of conditions.

There are many causes of sinus tachycardia:

ECG findings include:

• a heart rate above 100 in adults, or above the normal range for children
• normal P waves and QRS complexes
• the P wave may be hidden in the T wave from the previous beat

AV Nodal Reentrant Tachycardia (AVNRT) is a common cause of paroxysmal tachycardia. In contrast to AVRT (below), reentry is through the AV node.

AVNRT is normally paroxysmal – occurring in healthy hearts without known cause. It is more common in women.

It may be precipitated by:

• exercise
• caffeine
• alcohol
• salbutamol
• amphetamines

Heart rate is normally between 140-280, and is regular.

The QRS is normally narrow, < 120 ms. It may be wide if a bundle branch block is present, if there           is aberrant conduction, or if there is an accessory pathway.

If the P wave is visible, it is normally inverted, due to retrograde conduction through the atria. However, the P wave may be buried within, after, or before the QRS complex.

The ST segment may be depressed if there is sufficient cardiac demand to cause ischemia.

It may terminate on its own, or may persist without intervention.

In AVNRT, there is a reentry loop involving the AV node. Two pathways exist. A slow pathway is slowly conducting, but with a short effective refractory period (ERP). A fast pathway is rapidly conducting, but with a long refractory period.

Reentry circuit, slow-fast AVNRT, courtesy of Life in the Fast Lane

Slow-fast AVNRT (80-90% of cases): anterograde conduction occurs down the slow AV pathway, and retrograde conduction occurs up the fast pathway.

With depolarization through the atria, signals are sent down both slow and fast pathways. Normally, during sinus rhythm, the fast impulse begins to travel up the slow pathway in a retrograde manner. The impulses, when they meet each other, cancel each other out.

If a second signal from the atria (a premature contraction, for example) occurs immediately after the first, the fast pathway will still be refractory. As a result, it will only travel down the slow pathway. This impulse will travel in a retrograde fashion up the fast pathway, establishing a rapid cycle within the AV node. With each cycle, impulses will pass into the ventricles and back to the atria, causing a rapid heart rate.

Fast-slow AVNRT (10% of cases): anterograde conduction occurs down the fast pathway, while retrograde conduction occurs up the slow pathway. Inverted P waves commonly occur after the QRS, given the slow rate of retrograde conduction.

Slow-slow AVNRT (1-5% of cases), anterograde conduction occurs down the slow pathway, while retrograde conduction occurs up the atria.

Atrioventricular reentrant tachycardias describe tachycardias that result from reentry into the atria through accessory pathways. One of the most important of the AVRTs is termed Wolff-Parkinson-White (WPW) syndrome, in which an accessory pathway results in pre-excitation of the ventricles from the atria.

Pre-excitation may be present during a normal heart rate; however, with tachycardia, the accessory pathway may act as a reentry circuit.

Orthodromic conduction occurs down the AV node, and in a retrograde fashion through the accessory pathway.

Antidromic conduction occurs through the accessory pathway, and in a retrograde fashion through the AV node.

Pre-excitation may be increased with:

• increased vagal tone (eg Valsalva maneuvers)
• AV blockade

The heart rate may be as high as 200-300 during periods of AVRT.

P waves may be buried in the QRS complex, or may be retrograde.

The QRS complex is normally <120ms, unless there is:

• antidromic conduction
• bundle branch block
• aberrant conduction

Delta wave in WPW, courtesy of James Heilman

In WPW, the PR interval is <120 ms.

The QRS is prolonged and a Delta wave is evident, resulting from a slurring of the initial portion of the QRS due to re-excitation.

ST segment and T waves are discordant.

WPW syndrome, classified as a form of AVRT, is caused by an accessory electrical conduction pathway between the atria and the ventricles. That accessory pathway is typically known as the “bundle of Kent.”  Essentially, that accessory pathway has the capability to conduct action potentials which directly bypass the AV node and allow ventricular pre-excitation, or earlier activation.  This leads to the shortened PR interval and classic delta-wave, suggesting a slightly longer transition of conduction through the accessory pathway, rather than the quicker AV node.

Accessory Pathway in WPW; used with permission

Atrial tachycardia is normally due to a single ectopic area within the atria, in which the case will be regular. More rarely, the beats may originate from a number of areas, causing multifocal atrial tachycardia.

Atrial tachycardia may be idiopathic, though may also be caused by:

• atrial scarring
• coronary artery disease
• valvular heart disease
• cardiomyopathies
• cor pulmonale
• COPD (especially multifocal atrial tachycardia)
• congenital abnormalities
• increased sympathetic tone
• digoxin toxicity
• hypokalemia and hypomagnesemia

ECG normally shows:

• rate >100 bpm; normally > 120 bpm
• abnormal P wave morphology
• identical P waves in atrial tachycardia; varying P wave morphology in multifocal atrial tachycardia
• narrow QRS, unless BBB, accessory pathway, or aberrant conduction
• isoelectric baseline

Atrial tachycardia can occur through increased automaticity, reentry, or triggered activity.

Multiple atrial tachycardia normally is seen in quite ill patients, and may lead to atrial fibrillation or flutter. The right atrial stretch (Cor pulmonale), along with hypoxia, sympathetic tone and medications, and electrolyte abnormalities, lead to an irritable atria.

Atrial fibrillation, or AF, is a supraventricular arrhythmia caused by uncoordinated atrial activity and resulting in an irregular ventricular response. The rate is frequently rapid.

Atrial flutter is similar to AF but the atria remain coordinated while contracting at a very high rate – often 240-340 bpm.

AF can have significant short and long term effects. One immediate concern is sufficient cardiac output, which can be affected by reduced atrial activity, ventricular irregularity, and excessive ventricular rate.

AF also predisposes to thrombus formation in the heart, potentially leading to dangerous thromboemboli (eg stroke).

Atrial fibrillation and flutter have a number of potential causes, including:

• stress states, both physiologic or drug-induced
• hypertension
• heart disease: coronary heart disease, valvular disease, heart failure, cardiomyopathy
• electrolyte abnormality, especially hypokalemia, hypomagnesemia
• thyroid disease
• lung disease: acute or chronic
• alcohol overuse
• trauma (cardiac contusion)
• cardiac surgery

Atrial fibrillation classically causes an irregularly irregular heart rate, resulting from small, irregular waves in the place of coordinated P waves. The QRS is typically narrow, but will be irregular and often is rapid. The QRS may also be wide with a bundle branch block, with an accessory pathway, or if there is a rate-related conduction aberrancy. The ventricular rate is often 110-160, though may also be ‘slow’, at <60.

Atrial fibrillation, courtesy of Life in the Fast Lane

Atrial flutter normally causes saw – tooth flutter waves at a very high rate – normally 240 – 340 bpm. These flutter waves are normally inverted in leads II, III and aVF and upright in V1. If a 2:1 block is present, as is often the case, the ventricular rate is often 120 – 160 bpm.

Atrial flutter with 2:1 block, courtesy of Life in the Fast Lane

courtesy of Life in the Fast Lane

Mechanisms that cause AF and flutter include:

• focal activation due to increased automaticity or re-entry circuits
• multiple wavelets with wandering re-entry circuits; exacerbated by atrial dilatation

Atrial flutter is normally caused by a re-entry circuit within the right atrium.