Supraventricular Tachyarrhythmias
Tachyarrhythmias (tachycardias) and bradyarrhythmias (bradycardias)
are abnormalities in the origin, timing or sequence of cardiac depolarization
that result in a heart rate of >100 and <60 beats/ min, respectively. The
former are much more common and may be supraventricular, in which case
they arise in either the atria or the atrioventricular node (AVN), or are ventricular
in origin (see Chapter 50). Important bradyarrhythmias are described in
Chapter 12. Where appropriate, ECG leads that best illustrate the abnormalities
associated with each arrhythmia are shown here and in Chapter 50.
Most supraventricular tachycardias
(SVTs) are troublesome rather than life-threatening, although rarely sudden
death can occur. Common symptoms include lightheadedness, palpitations and
shortness of breath.
Supraventricular premature beats (Figure 49a) are caused by ectopic (i.e.
originating from a site other than the SAN) impulses arising in the atria or
AVN earlier in the cardiac cycle than would be expected from the normal heart
rate. They are typically conducted to the ventricles to cause a premature beat,
which is generally followed by a pause as the normal rhythm is reasserted. With
an atrial ectopic site the P wave is abnormally shaped because it is not
generated in the SAN, and it may be inverted or missing entirely if the ectopic
site is in or near the AVN.
Atrial tachycardia heart rate (120–240 beats/min) is frequently
caused by an ectopic pacemaker, and can arise in either atrium (e.g. often
close to the pulmonary veins in the left atrium). Other atrial tachycardias are
re-entrant in nature, frequently following surgery that involves incision into
the atrium. The tachycardia may start and stop suddenly or gradually. As with
atrial ectopics, the P wave is abnormally shaped (Figure 49b).
Atrial flutter results from re-entry in an atrium (usually the
right), often with an area of slowed conduction near the orifice of the
inferior vena cava and a circuit involving the whole atrium. The atrial rate is
typically ∼300 beats/min. As shown in Figure 49c, the AVN is often able to conduct
only every other atrial impulse (2:1 AV block) to the ventricles because it is
still refractory from the previous impulse, so that the ventricular rate is
typically ∼150 beats/min. Less commonly, 3:1 or 4:1 block can occur, leading to correspondingly
slower rates of ventricular contraction. The ECG has a ‘sawtooth’ appearance
due to the presence of rapid regular F waves representing atrial
depolarization; these become more obvious if AVN conduction and the QRS complex
are suppressed, for example, by adenosine (Figure 49c, right). Atrial flutter
is typically seen in patients with underlying cardiac disease, often associated
with atrial dilatation. It is particularly common in older hypertensive
patients, and may also be caused by acute pulmonary thromboembolism or
thyrotoxicosis, but can also develop paroxysmally in patients without
underlying heart disease (e.g. secondary to infection or alcohol excess).
Attempts to cardiovert (restore normal sinus rhythm) atrial flutter with
class IA drugs (see Chapter 51) may cause severe ventricular tachycardia and
sudden death by establishing 1:1 AVN conduction. This occurs because these
drugs suppress vagal firing, thereby increasing AVN conduction. This hazard is
avoided by pre-administering a drug that suppresses AVN conduction (e.g. a
β-blocker).
Atrial fibrillation (AF) is a chaotic atrial rhythm resulting in an atrial
rate of 350–600 beats/min and a lack of effective atrial con- traction. The
ventricular rate is described as ‘irregularly irregular’ and is fast but
typically less than 200 beats/min because the AVN is unable to conduct most of
the atrial impulses impinging upon it (Figure 49d). AF is the most common
arrhythmia, occurring in ∼10% of people over the age of 75, and has many
causes including but not limited to cardiac disease. Initially, AF is often
paroxysmal (episodic), but then becomes more persistent, and finally permanent.
Paroxysmal AF is usually driven by an ectopic focus or re-entrant pathway in
the cardiac muscle layer surrounding pulmonary veins where they enter the left
atrium. As AF progresses, it causes changes in the electrical and structural
properties of the atrial myocardium, promoting further and more complex forms
of re-entry, this rendering the arrhythmia more persistent and refractory to
treatment. Palpitations, dyspnoea, dizziness, chest pain or syncope (sudden
fainting) may occur as a result of the increased ventricular rate or the
absence of atrial systolic filling, which reduces ventricular stroke volume by ∼20%. Thrombi
may form in the left atrial cavity or appendage because the lack of coordinated
atrial contraction leads to stasis of blood. These can then embolize to the
systemic circulation, particularly the brain and limbs. For this reason, AF is
the most important cause of stroke in the elderly. Pharmacological treatment
aims to restore normal sinus rhythm (‘rhythm control’); amiodarone is often
used for this purpose. A class IV or other agent can also be used to suppress
AV conduction, thereby reducing the frequency of impulses that reach and excite
the ventricles (‘rate control’) even if the atria continue to fibrillate.
Atrioventricular nodal re-entrant
tachycardia (AVNRT) and atrioventricular
re-entrant tachycardia (AVRT) result in periodic episodes during which the
heart rate abruptly increases to 150–250 beats/min, and they are therefore
referred to as paroxysmal supraventricular tachycardias. Individuals
with AVNRT have an additional or accessory conduction pathway between the
atrium and the AVN. In most cases, the normal AV pathway (termed α) conducts
rapidly and has a long refractory period, while the accessory (β) pathway
conducts slowly and has a short refractory period. In these individuals, AVNRT
can be initiated by a premature impulse arising in an atrium. This impulse will
not be conducted by the α pathway if it is still refractory from the preceding
impulse. However, the impulse may travel slowly down the β pathway (which has
recovered from the preceding impulse), and then encounter the distal end of the
α pathway. Sufficient time has now elapsed for this pathway to be no longer
refractory, and the impulse is able to ascend the α pathway in a retrograde (back-
wards) direction, allowing it to return to the atrium. From here it can
continue to cycle through the α and β pathways, exciting the ventricles to
cause a heart beat with each circuit. An abnormal P wave is also generated each
time the impulse cycles through the atrium. This immediately follows the QRS
complex because the re-entrant circuit, and thus the cycle time, is very short
(Figure 49e).
An accessory pathway allowing impulse
conduction between an atrium and ventricle also exists in AVRT, but in this
case it is not located within the AVN. Those in whom this pathway can conduct
impulses in both directions may develop Wolff–Parkinson–White (WPW) or pre-excitation
syndrome, the mechanism of which is described in Chapter 48. When the
individual is in normal sinus rhythm, the atrial impulse is conducted in an anterograde
(forward) direction through both the accessory pathway and the AVN. Because
it is conducted more quickly through the accessory pathway, excitation of part
of one ventricle occurs more quickly than normal (i.e. pre-excitation occurs),
resulting in a shortened PR interval and an initial widening of the QRS complex
referred to as a delta wave (Figure 49f, left). During the tachycardia,
however, the accessory pathway conducts in the retrograde direction (see
Chapter 48) and so pre-excitation does not occur. Instead, premature P waves
(often superimposed on the T wave) caused by rapid excitation of the atria by
the retrograde impulse are observed. This type of accessory pathway is
particularly dangerous in people with atrial fibrillation, because it is often
better at conducting rapid impulses than the AVN bevause of its shorter
refractory period. Thus, the AVN ‘filter’ which protects the ventricles from
high- frequency atrial activity is bypassed, and the ventricular rate becomes
very fast. In this case, the ECG shows rapid and irregular QRS complexes, the
majority of which are widened by pre-excitation (Figure 49f, right).
Less common forms of AVRT also exist.
In antidromic AVRT, the accessory pathway conducts in an anterograde
direction during the tachycardia (Figure 49g). In other cases, the accessory
pathway is capable of conducting only in the retrograde direction. Thus,
pre-excitation does not occur, and the bypass pathway is said to be concealed.
