Normal rhythm, called sinus rhythm, is paced from the sinoatrial (SA) node. The heart rate for normal sinus rhythm is from 60 to 100 beats per minute. Sinus rhythm faster than 100 beats per minute is called sinus tachycardia; slower than 60 is called sinus bradycardia. Sinus rhythms show a normally oriented P wave before each QRS complex.
Ectopic atrial pacemaker:
The normal P wave should be upright in all leads except R. If the QRS is preceded by an abnormally-oriented P wave (often with a shortened PR interval) this indicates an ectopic atrial pacemaker. The heart is being paced by atrial tissue somewhere outside the sinus node. The ectopic P wave may have an odd shape.
Multifocal atrial rhythm:
If three or more different P wave shapes are seen, multifocal atrial pacing is diagnosed. This condition is often seen in chronic lung disease with right atrial enlargement. Several atrial locations are competing for control of the rhythm, resulting in P waves of differing shape and/or PR interval. Because the P waves occur at differing times, the rhythm tends to be irregular. If the rate is over 100, its called multifocal atrial tachycardia.
In this condition, clock-regular tachycardia occurs due to a circular motion of electricity within the atrioventricular (AV) node. QRS complexes are usually narrow, but if conduction blockage is present downstream from the AV node, the QRS may be wide, causing confusion with ventricular tachycardia. If electricity exits the node into the atrium after ventricular contraction, retrograde inverted P waves may be seen after the QRS complexes, but this is uncommon.
Atrial flutter is a fairly organized back-and-forth motion of electricity within the atria. The rate of atrial depolarization is typically 300 beats per minute. Usually every other atrial beat is blocked in the AV node, resulting in a typical ventricular rate of 150. With increasing AV block, the rate may slow to 50, 75, or 100 (if the rate is regular, it will be some fraction of 300). Occasionally, such as in WPW syndrome, atrial beats will be conducted 1:1, resulting in a ventricular rate of 300. When the ventricular rate is slowed enough to see the atrial activity, a typical sawtooth baseline is seen, with the peaks appearing 5 mm apart.
Atrial fibrillation is random electrical activity in the atrium, with ventricular beats occurring irregularly. Ventricular depolarization occurs whenever an electrical impulse arrives at the AV node when its ready to conduct. QRS complexes may be wide when conduction block is present. The rate in atrial fibrillation may be very rapid, or slow, depending on the conductivity of the AV node.
Wolff-Parkinson-White (WPW) syndome occurs when a band of conducting tissue bypasses the normal AV node path. This results in early activation of a portion of the ventricle. The PR interval will be abnormally shortened, with an abnormally-shaped wide QRS following. The QRS usually has a typical delta wave (an early slow upstroke of the R wave prior to a fairly normal-looking QRS).
WPW syndrome often results in paroxysmal supraventricular tachycardia. Other atrial arrhythmias may cause a severe tachycardia, as the extra conducting pathway delivers every atrial depolarization to the ventricle. For example, atrial flutter may result in a ventricular rate of 300 due to 1:1 conduction. Atrial fibrillation results in a chaotic tachycardia.
This rhythm originates in the AV conducting system. A regular, narrow QRS complex is seen, often at a rate of around 75, without normal P waves preceding it. Often an inverted P wave can be seen just after the QRS complex. Occasionally, the inverted P wave is seen at the beginning of the QRS complex, coupled too closely to be an ectopic atrial pacemaker. Junctional rhythm with atrial fibrillation and complete heart block usually indicates digoxin toxicity. [Chapter Menu]
This is an atrial-paced rhythm with a prolonged PR interval, but with conduction of every atrial beat to the ventricle. The PR interval exceeds 0.2 seconds.
Second degree AV block:
Second degree atrioventricular block is an atrial-paced rhythm where some, but not all, of the atrial beats are blocked from the ventricle. This type of block is further divided into Type I and Type II.
Type I second-degree AV block is often called Wenckebach block. This block occurs high in the AV node, and is usually caused by acute, reversible conditions. It is usually treatable and rarely goes on to complete heart block. In Wenckebach block, the AV node fatigues with each beat, causing a lengthening PR interval. Finally, a beat is blocked. Then the process begins again.
In Wenckebach block, the interval between QRS complexes actually shortens slightly until the dropped beat. This is because, while the AV delay becomes greater with each beat, the INCREASE in the AV delay is greatest with the first beat. The amount of extra delay added to the PR with each beat decreases after the first beat. This makes the R-R interval shorten until a beat is blocked.
Type II second-degree AV block is a blockage below the AV node. Often only one fascicle is conducting that is, the conducted beats may show LBBB or RBBB with hemiblock but is conducting only intermittently. If the block is above the junction between the left and right bundles, the QRS may appear normal, but this is rare. This type of AV block often progresses to complete (third degree) heart block.
Type II block can be diagnosed if two consecutive conducted beats have the same PR interval.
If the rhythm is 2:1 (i.e., every other P wave is blocked) it may be difficult to diagnose type I versus type II. The benign type I is more common. If the PR interval is prolonged and no bundle branch block is present, assume type I. If the PR interval is normal and there is a bundle block, assume type II. If the ECG shows both long PR and bundle block, the mechanism of second-degree AV block cant be diagnosed.
Complete AV block:
Complete AV block is also called third-degree heart block. No atrial impulses reach the ventricles. The atrial P waves bear no relation to whats happening in the ventricles. The ventricles will usually develop an escape rhythm. If the lower AV node assumes the role of pacemaker, narrow regular QRS complexes may be seen. This is often called a nodal escape rhythm. If the ventricular muscle becomes the pacer, a wide-QRS ventricular escape rhythm will develop, at a rate of around 30.
Non-conducted extra beats originating the AV node may make the node refractory to the next electrical wave, causing a single-beat AV block. This may be an isolated prolonged PR interval, or a dropped beat. If these occult PVCs occur regularly, they can be differentiated from Type I second-degree block by the absence of lengthening PR prior to the dropped beat. [Chapter Menu]
Ventricular tachycardia is a regular, wide-complex tachycardia originating within the ventricles. It may be caused by an irritable area in the ventricle acting as a rapid pacemaker, or may originate via a circular motion of electricity in an area of damaged myocardium.
If atrial activity continues during the episode of V-tach, P waves may be seen deforming the ventricular complexes. Occasionally, an atrial depolarization may be conducted, resulting in a narrower QRS complex. This narrow QRS may resemble the patients standard QRS complex, or may be a hybrid between the V-tach QRS and the normal QRS, called a fusion beat. Either of these findings confirms that the tachycardia is V-tach rather than an aberrantly conducted supraventricular tachycardia.
V-tach that changes orientation (changes QRS axis) regularly over a period of many beats is called Torsades de pointes. This type of tachycardia may be caused by hypomagnesemia (among other etiologies), and is important to recognize because its treatment may differ from standard ventricular tachycardia.
Ventricular fibrillation is chaotic irregular electrical activity within the ventricles. No QRS complexes are seen. V-fib is referred to as course fibrillation if the waves of electricity cause large deviations of the ECG baseline, and as fine fibrillation if the electrical waves are of low amplitude. [Chapter Menu]
Premature beats (PVCs, extrasystoles) may be atrial, nodal, or ventricular in origin. The cause of premature beats can often be surmised from careful attention to preceding atrial activity, length of preceding R-R interval, length of the following R-R interval, and the QRS shape.
Premature beats preceded by a P wave (with a reasonable PR interval) are atrial premature beats. The P wave often has a different shape or size compared to the patients normal Ps. The pause after the QRS before the next beat is about the same as for the normal sinus R-R interval because the ectopic P wave will reset the sinus node.
AV node premature beats:
Premature beats that cause an inverted P wave to appear during the ST or T wave are originating in the AV node. The QRS is usually narrow. When the QRS is wide, the extra beat may be either an aberrantly-conducted nodal beat, or a ventricular extrasystole with retrograde conduction through the AV node. AV node premature beats may also be seen with an inverted P wave immediately in front of the QRS with an impossibly-short PR interval.
Ventricular premature beats:
Ventricular premature beats rarely disturb the underlying sinus rhythm. There will usually be a full compensatory pause after the extra beat: the distance from the previous normal beat to the normal beat following the PVC is the same as two normal R-R intervals. After the PVC, the sinus beat is blocked, and the pause occurs as the ventricle waits for the next sinus beat. With slower heart rates, a very early PVC may appear inserted between two normal sinus beats with normal R-R interval. PVCs usually have a wide QRS, often oriented all in one direction (monophasic). A PVC may have a normal-width QRS complex if it originates in the conducting system.
PVCs that occur at a regular interval, completely independent of conducted complexes, are called parasystole.
PVCs versus aberrant conduction:
Beats originating in the atrium may have a wide QRS complex due to abnormal (aberrant) conduction. Wide-QRS ectopic beats can be attributed to atrial extrasystoles if 1) an ectropic P wave is identified, 2) the beat occurs immediately following two normal beats separated by a longer R-R interval and has a bundle-branch block type QRS form.
In lead V1, most PVCs will tend to have a big-R, smaller R form. PVCs tend to be monophasic: the QRS complex is oriented all in one direction.
A small-R, bigger-R QRS form, or an rSR-prime, is usually aberrant conduction of a supraventricular beat. The initial portion of the QRS is usually identical to the normally-conducted beats.
An irregular-spaced, wide-complex tachycardia is almost always supraventricular in origin. Also, a run of wide-complex tachycardia is presumed to be atrial in origin if its immediately preceded by an ectopic P wave. [Chapter Menu]
Pacemaker spikes may be seen on the ECG. If possible, determine: Does the pacemaker SENSE? Does the pacemaker CAPTURE?
We will consider the standard VVI pacemaker: it paces the ventricle (V), senses spontaneous depolarization of the ventricle (second V), and is inhibited (I) from firing when it detects firing of the ventricle faster than a pre-set threshhold.
To determine sensing, find an area on the tracing where the heart rate is higher than the threshhold. See if the pacemaker turns off. Pacer spikes should disappear.
Find an area where the rate drops to the threshhold. To determine capture, see if each pacer spike is followed by a ventricular contraction. This linkage of spike to QRS is called capture.
If the patients own heart rate remains above the threshhold for pacing, you must induce the pacemaker to determine whether the pacer is functioning. A magnet (made specifically for this purpose) placed over the pacemaker turns sensing off. The pacemaker will fire as though the patients rhythm is too slow. When a spike occurs after the refractory period it should capture the ventricle.
The magnet rate will often be different from the pacing rate. A slowing magnet rate may indicate the need for pacemaker battery replacement. [Chapter Menu]
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