Impulses originate in the SA node regularly at a rate 60-100 per minute in adults and at faster rates in older children (90-110), small children (100-120) and infants (120-160). P waves upright in L2 and negative in AVR and of uniform size and contour from beat to beat. PR interval 0.12-0.20 sec and constant when A-V conduction normal; PR prolonged and/or variable when A-V block present. Each P followed by QRS with resulting P:QRS ratio 1:1 QRS ratio 1:1. QRS less than 0.11 sec or QRS wide and bizarre when bundle branch block present. RR intervals may be slightly irregular especially in the young and elderly.
Similar to normal sinus rhythm except that PP and RR intervals are irregular because the SA node discharges at a variable frequency. In children and young adults the irregularity is cyclic or related to respiration with the rate increasing during inspiration and decreasing during expiration. A cyclic sinus arrhythmia disappears upon exercise or breath holding and is accentuated by deep breathing. In elderly subjects the irregularity is frequently due to organic heart disease.
Similar to normal sinus rhythm except that the rate is less than 60/min in adults and older children or less than 80 in younger children. The PR interval may be slightly prolonged and/or P wave abnormally wide. Physiological bradycardia occurs in healthy individuals (usually athletes) with increased vagal tone. Exercise or atropine always increase the rate to normal. Pathological bradycardia occurs in subjects with acute myocardial infarction (especially inferior) or other heart disease involving the SA node, in subjects taking drugs such as digitalis or beta blockers and in elderly subjects. Exercise or atropine often fail to increase the rate to normal.
Impulses originate in the SA node at a rate 100-160/min in adults (and up to 200 or more in children). P upright in L2 and negative in AVR with identical or slightly different size and contour from beat to beat. At very rapid rates P superimposed on preceding T. When P recognizable, P:QRS ratio 1:1. Tachycardia usually appears and subsides gradually. Vagal stimulation produces gradual slowing which reverses when pressure is released. Exercise further increases the rate.
The impulse is discharged prematurely by some irritable focus in the atria giving rise to a distorted P wave (wide, narrow, notched, inverted or superimposed on the preceding T wave). The further from the SA node the ectopic focus is, the more abnormal will be P' configuration. PR interval normal or slightly prolonged. Premature P followed by QRS less than 0.11 sec except when very premature P is not conducted; occasionally QRS may be wide with RBBB configuration due to aberrancy. The pause between APB and the next sinus beat is usually noncompensatory, i.e., the RR interval between two QRS enclosing APB is less than twice the normal RR interval.
Impulses originate in an atrial pacemaker at a rate 140-250/min. Atrial activity may be represented by upright P in L2 or by P superimposed on T or ST segment of the preceding beat. At very rapid rates only every second P may be followed by QRS (2:1 AV block) with the resulting ventricular rate half the atrial. QRS usually less than 0.11 sec; wide and bizarre QRS mat be due to preexisting BBB or WPWS or due to aberrancy common at rapid rates. Onset and termination of AT is often abrupt. Vagal stimulation frequently terminates AT.
Impulses originate in an atrial pacemaker at a rate 240-340/min but some of them are blocked regularly at the AV junction. Atrial activity is represented by sawtooth-like deflections (F waves) not separated by an isoelectric segment and best seen in L2, L3 and AVF. Usually only every second F is conducted to the ventricles (2:1 AV block) with the resulting ventricular rate half the atrial rate; rarely the AV conduction is 3:1, 4:1, 1:1 or variable. Vagal stimulation may have no effect or slow ventricular rate by increasing AV block or terminate flutter. Exercise increases HR by decreasing the block.
Impulses originate in multifocal atrial pacemaker at a rate 300-600/min but only some of them are conducted to the ventricles. The atrial activity is represented by numerous, irregularly spaced small deflections of varying configuration (f waves) best seen in L2, L3 AVF and V1. Occasionally, f waves may be prominent ("coarse" fibrillation) resembling atrial flutter or no atrial activity is discernible ("fine" fibrillation). Only some f waves pass through the AV junction and activate ventricles in a completely irregular fashion. Vagal stimulation may have no effect or may slow the ventricular rate by increasing the AV block.
The impulse prematurely discharged from an irritable focus in or near the AV junction spreads backward (retrograde) to the atria and forward (antegrade) to the ventricles. An inverted P wave may precede QRS by less than 0.12 sec ("upper" junctional beat ) or inverted P wave may follow QRS ("lower" junctional beat) or P wave may be buried in QRS ("middle" junctional beat). Premature QRS is less than 0.22 sec but often slightly distorted; occasionally QRS is wide and has RBBB configuration due to aberrancy. The pause following JPB is noncompensatory as explained for APB.
The SA pacemaker is suppressed or its impulses are blocked and the heart is controlled by impulses originating at the AV junction. Such impulses spread to the ventricles and also to the atria (in retrograde fashion). P waves are negative L2 and positive AVR and occur regularly at a rate 40-60. Depending upon whether retrograde conduction to the atria is faster, slower or similar to antegrade conduction to the ventricles, P waves either precede QRS complexes, the PR interval is less than 0.12 sec or follow QRS complexes by no more than 0.20 sec or are buried in the QRS complexes. Occasionally there is a block above the junctional focus so that the atria are under the control of sinus or atrial impulses (AV dissociation).
Impulses originate in the AV junctional pacemaker at a rate 140-220/min and are conducted retrograde to the atria and antegrade to the ventricles. P waves are negative in L2 and positive in AVR and may closely precede, follow or coincide with normal QRS complexes. When P waves precede QRS complexes, the PR interval is less than 0.12 sec; when P waves follow QRS complexes, they appear as splinters deforming the ST segment; when P waves coincide with QRS complexes, they are not discernible. The paroxysmal form of tachycardia is characterized by a ventricular rate 140-220, sudden onset and offset and sudden termination or no change upon vagal stimulation; the nonparoxysmal form is characterized by a ventricular rate 100-140, gradual onset and gradual slowing or no change upon vagal stimulation.
Impulses originate in a supraventricular pacemaker (above the bifurcation of the the common bundle) at a rate 150-250. P waves cannot be positively identified either because they merge with preceding T waves or because they are buried in QRS complexes so the the differentiation between atrial and junctional tachycardia is impossible. QRS complexes are less than 0.11 sec; occasionally QRS are wide and have RBBB configuration due to aberrancy. Vagal stimulation may have no effect or may terminate tachycardia abruptly.
An irritable focus in the left or right ventricle fires prematurely and the impulse spreads to the opposite ventricle with delay producing a bizarre QRS complex, wider than 0.11 sec and of bundle branch block configuration. The VPB originating in the LV usually produces the pattern of RBBB while that originating in the RV produces the pattern of LBBB. The P wave is usually buried in the VPB but occasionally it may be seen as a notch or splinter deforming some part of the QRS-T complex. The pause after the VPB is usually compensatory, i.e., the RR interval between the QRS complexes surrounding the VPB is twice the normal RR interval. VPB's are often the forerunners of ventricular tachycardia when they are frequent (more than 5/min), occur in groups of two or three, are multifocal or have a very short coupling (i.e. the VPB falls on a T wave). When every other beat is a VPB, the rhythm is called bigeminy. When every third beat is a VPB or when each normal beat is followed by two VPB's, the rhythm is called trigeminy.
Impulses originating in the SA node control the atria but fail to reach the ventricles; the latter are activated by their own pacemaker firing 100-250/min; rarely ventricle-borne impulses are also conducted to the atria. P waves are frequently indiscernible or may appear as notches at various points on the QRS-T complexes; if P waves are recognizable, they are usually of normal configuration, occur regularly at a rate 60-100 and bear no fixed relation to the QRS complexes (AV dissociation). Rarely, when the atria are controlled by the ventricular pacemaker, the P waves are inverted and follow QRS complexes at a constant RP interval. When the rate is less than 150, the SA-borne impulse may be occasionally conducted through the AV junction and it can activate the ventricles thus producing a QRS complex whose configuration and width are intermediate between the normal and abnormal complexes (fusion beat or partial capture). QRS complexes are usually wider than 0.12 sec and bizarre. RR intervals are usually regular but may vary up to 0.03 sec. Vagal stimulation has no effect on the rate. An ECG prior to tachycardia showing premature beats of identical configuration favors ventricular origin of the tachycardia.
Rhythmic impulses originating in the SA node are conducted abnormally slow through the AV junction to the ventricles. The rhythm pattern is similar to normal sinus rhythm except that the PR interval is prolonged beyond 0.20 sec in adults and 0.18 sec in children. With a severe (i.e. greater than 0.5 sec) lengthening of the PR interval or with a rapid rate, the P wave may be superimposed on the preceding T wave. Occasionally the rate may be slower than 60/minute. Frequently associated with vagotonia (in which case it disappears after exercise or atropine).
Rhythmic impulses originating in the SA node are conducted through the AV junction at progressively slower (decremental) speed. P waves are positive in L2 and negative in AVR and occur regularly at a rate 60-100. A blocked P wave occurs after 2-5 conducted P waves and this so-called Wenckebach cycle or period is repeated. The P:QRS ratio of 3:2, 4:3, 5:4 may be constant in all cycles or may vary from cycle to cycle. The PR interval immediately following a dropped QRS complex is the shortest and may be normal or prolonged; with each successive beat the PR interval becomes progressively longer until a P wave is blocked. QRS complexes may be normal or wide and bizarre if BBB is present.
Rhythmic impulses originating in the SA node are intermittently blocked at the AV junction. P waves are positive in L2 and negative in AVR and occur regularly at a rate 60-100. Only every second (or rarely third, fourth, etc.) P wave is followed by a QRS complex resulting in the P:QRS ratio 2:1, 3:1, 4:1, etc. and the ventricular rate 20-60. Rarely the AV conduction and the P:QRS ratio may be 3:2, 4:3, 5:2 or other and may vary in the same tracing. The PR interval of the conducted beats is normal or prolonged and usually constant. QRS complexes are frequently wide and have RBBB configuration because the lesion extends below the AV junction.
Impulses originate in the SA node or in an atrial pacemaker but none of them is conducted through the AV junction to the ventricles. P waves are positive in L2 and negative in AVR and occur regularly at a rate 60-100; rarely atrial activity is represented by inverted (ectopic) P waves, F waves of f waves. Since all P waves are blocked, the ventricles are activated by impulses activated by impulses arising (through escape mechanism) in pacemaker cells below the bifurcation of the common bundle. The resulting QRS complexes are wide, slurred, frequently of RBBB configuration and occur regularly at a rate 20-40 (the so-called idioventricular rhythm). P waves occurring at a faster rate are completely unrelated to QRS complexes (AV dissociation).
There is no fixed temporal relationship between P waves and QRS complexes due to the existence of two independent pacemakers, one in the SA node (or in the atria) which controls the beating of atria and other in the AV junction (or in the ventricles) which controls the beating of ventricles. When the atria are beating faster than the ventricles, AV dissociation is due to complete AV block; when the ventricles are beating faster than the atria, AV dissociation is due to ectopic tachycardia (junctional or ventricular). In complete AV dissociation no atrial impulse is conducted to the ventricles; in incomplete AV dissociation some atrial impulses may be conducted to the ventricles resulting in ventricular captures.
Impulses originate in the SA node and spread normally through the atria and AV junction, however, the conduction through the right (R) or left (L) branches of the bundle of His is blocked. In RBBB the right ventricle is activated late through the septum this being reflected by M-shaped QRS complex or wide notched or slurred R in V1-V2 and wide slurred S in V5-V6. In LBBB the left ventricle is activated late through the septum this being relected by M-shaped QRS or wide notched or slurred R in V5-V6 and wide slurred S or QS in V1-V6. QRS duration 0.11 sec or more. ST segment depressed and T inverted in leads with M-shaped QRS.
Also called Wolff-Parkinson-White Syndrome (WPWS). Impulses originating in the SA node spread over the atria and then bypass the AV junction through an accessory bundle. Premature activation of a small portion of the ventricles produces stepwise notching or slurring of the initial part of the QRS complex (the delta wave). QRS complexes and delta waves upright in all precordial leads are associated with type A of WPWS; QRS complexes and delta waves negative in V1-V2 and positive in V5-V6 are associated with type B. The QRS duration 0.11 sec or more. The PR interval usually less than 0.12 sec due to early onset of QRS as a delta wave. ST segment depressed and T wave inverted in leads with tall R waves. Frequent attacks of supraventricular tachycardia.
July 11, 1997
|AUTHOR:||Joseph Wartak MD|
|SOURCE:||Tables of Cardia Arrhythmias, 3rd Revised Edition, 1983 (Courtesy of Squibb Canada Inc.)|
|HTML:||D. John Doyle MD PhD, Ciorsti MacIntyre|