Premature atrial complexes (PACs)
These may occur as single or repetitive events and may be unifocal or multifocal in origin. The premature P wave (P’ wave) differs in contour from the normal sinus wave, which is usually followed by a normal QRST sequence.
The P'R interval is normal or prolonged because the AV junction is often partially refractory when the premature impulse enters it.
PACs may have three different outcomes:
1) Normal conduction: similar to normal QRS complexes in the ECG.
2) Non-conducted: no QRS complex because the PAC meets the AV node when still refractory.
3) Conducted with aberration: the PAC makes it into the ventricles but finds one or more of the conducting fascicles or bundle branches refractory, hence the resulting QRS is usually wide.
The pause after a PAC is usually incomplete - i.e. the PAC usually enters the sinus node and resets its timing, causing the next sinus P to appear earlier than expected (premature ventricular complexes, by contrast, are usually followed by a complete pause because they do not usually disturb the sinus node).
Clinical significance: PACs are commonly seen during anaesthesia and during the postoperative period. Not uncommonly, they may be misdiagnosed as AV junctional premature beats, ventricular premature beats or sinus arrest.
Multi-focal atrial tachycardia (MAT)
This arrhythmia is characterised by the following features:
- Multiple and multifocal PACs at rates of 100-250/min with varying PR intervals.
- Ventricular response is irregularly irregular (rate of 100-200/min).
- MAT may be intermittent, alternating with periods of normal sinus rhythm
1) MAT indicates diffuse atrial disease, including atrial distension with/without sinus node degeneration.
2) Seen commonly in association with advanced chronic obstructive pulmonary disease.
3) MAT may cause significant haemodynamic compromise due to impaired atrial and ventricular filling.
4) The rhythm usually returns to normal once the underlying acute medical problem subsides.
The ECG features of atrial flutter are:
1) An atrial rate between 250-350 bpm
2) A saw-tooth appearance (F waves) is seen in leads II, III, aVF and V1. Variable degrees of AV block is seen (2:1 being more common).
1) Atrial flutter usually results from a re-entrant circuit located totally within the atrial wall.
2) It is generally associated with heart disease - e.g. rheumatic heart disease (with mitral stenosis).
3) 1:1 ventricular conduction may compromise cardiac output significantly.
4) Haemodynamic compromise may warrant electrical cardioversion.
5) Digitalis is very effective in slowing ventricular rate, while ß-blockers or verapamil slow the ventricular rate and sometimes revert it to sinus rhythm.
Atrial fibrillation (AF)
The ECG features of atrial fibrillation include:
- Rapid, irregular fibrillating atrial waves (f waves) at a rate of 300-600 bpm, best seen in leads II, III, aVF and V1. The fibrillation is probably caused by numerous microentry circuits within the atrial muscle.
- Ventricular rate is irregularly irregular, with a rate of 140-200 bpm due to a certain degree of AV block which is always present.
- The differential diagnosis includes atrial flutter with an irregular ventricular response and multi-focal atrial tachycardia, which is usually irregularly irregular.
- AF is usually associated with chronic heart disease (valvular, myocardial or pericardial).
- Also seen in hyperthyroidism, pulmonary embolism and chronic lung disease.
- Electrical cardioversion may be required in the acute setting with haemodynamic compromise.
Paroxysmal supraventricular tachycardia (PSVT)
These arrhythmias occur due to circus movements, thus utilising the mechanism of reentry. The onset and resolution are sudden and usually initiated by a premature beat, thus the term "paroxysmal". They are generally narrow-QRS tachycardias (unless there is pre-existing bundle branch block or aberrant ventricular conduction). There are several types of PSVT, depending on the location of the reentry circuit.
AV nodal reentrant tachycardia (AVNRT)
This is the most common form of PSVT accounting for approximately 50% of all symptomatic PSVTs. It is the most common cause of SVT in patients with structurally normal hearts.
It is accompanied by the following features:
1) ECG shows normal regular QRS complexes with a rate of 140-240 bpm.
2) QRS complexes may sometimes show typical bundle branch block/aberration.
3) P waves are either not visible or are seen immediately before or after the QRS complex.
4) An attack may be spontaneously triggered but exertion, tea, coffee or alcohol may trigger an AVNRT.
5) Vagal manoeuvres may terminate an acute attack.
6) Beta-blockers or calcium channel blockers may help to suppress recurrent attacks.
The diagram illustrates the probable mechanism involving dual AV nodal pathways, alpha and beta, with different electrical properties. In the diagram, alpha is a fast AV nodal pathway with a long refractory period (RP), and beta is the slow pathway with a short RP. During sinus rhythm, alpha is always used because it conducts faster. An early PAC, however, finds alpha still refractory and must use the slower beta pathway to reach the ventricles. By the time it traverses beta, however, alpha has recovered, allowing retrograde conduction back to the atria. The retrograde P wave (called an atrial echo, for obvious reasons) is often simultaneous with the QRS and, therefore, not seen on the ECG, but it can re-enter the AV junction because of beta's short RP.
AV reciprocating tachycardia (extranodal bypass pathway)
This is the second most common form of PSVT and is seen in patients with Wolff-Parkinson-White (WPW) syndrome. The WPW ECG, seen in the diagram, shows a short PR, delta wave and a somewhat widened QRS.