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.