ECG tutorial Pacemakers


Atrial and ventricular pacing can be seen on the electrocardiogram (ECG) as a pacing stimulus (spike) followed by a P wave or QRS complex, respectively. The ECG has the ability to show normal and abnormal pacemaker function.


Atrial pacing appears on the electrocardiogram (ECG) as a single pacemaker stimulus followed by a P wave .

The morphology of the P wave depends upon the location of the atrial lead; it may be normal, diminutive, biphasic, or negative. The PR interval and configuration of the QRS complex are similar to those seen in sinus rhythm. They are independent of the atrial pacemaker; thus, the duration and configuration are determined by the intrinsic characteristics of the patient's conduction system.

There is 100 percent capture if the rhythm is entirely paced. However, there may be intermittent capture when the atrial pacemaker is in a demand mode and is activated only when the intrinsic atrial rate falls below a preset level. In these cases, a paced beat will be seen after a pause that is equal to this lower predetermined heart rate. For example, if the pacemaker is set at 60 beats/min, the pacemaker will only pace if the rate falls below 60 beats/min or there is a pause of one second (60 beats/min ÷ 60 sec/min).


Ventricular demand pacing appears on the electrocardiogram (ECG) as a single pacemaker spike followed by a QRS complex that is wide, bizarre, and resembles a ventricular beat.

The pacemaker lead is usually in the right ventricular apex; thus, the paced QRS complex has a left bundle branch block (LBBB) configuration since right ventricular activation occurs before activation of the left ventricle, and is negative in the inferior leads. Sometimes, the lead may be placed higher up in the right ventricular septum or outflow tract, and while there is still an LBBB pattern, the inferior leads may have variable axis. There may or may not be atrial activity noted, depending upon the nature of the patient's underlying rhythm, the atrial rate, and the occurrence of ventriculoatrial conduction via the atrioventricular (AV) node. If intrinsic or native atrial activity is present with a single chamber ventricular-only pacemaker, it occurs at a rate that differs from the ventricular rate since it is dissociated from the QRS complex. Frequently, ventricular demand pacing is used in association with atrial fibrillation.

There may be episodic pacing in patients who have a ventricular demand pacemaker. The pacemaker is activated and delivers a stimulus only when the intrinsic ventricular rate falls below a predetermined lower limit; pacemaker activity is suppressed when the intrinsic heart rate is faster (ventricular inhibited). The escape interval (the time between the last intrinsic beat and the paced beat) is equivalent to the rate at which the pacemaker is set to activate. Similar to atrial pacing, if the pacemaker is set at 60 beats/min, the pacemaker will only pace the ventricle if the rate falls below 60 beats/min or there is a pause of one second (60beats/min ÷ 60 sec/min). If the native rate is slow, there will be 100 percent ventricular pacing (figure 1). The ECG may have evidence of fusion or pseudofusion beats if the pacemaker rate and intrinsic heart rate are nearly identical, and the native and paced QRS complex occur simultaneously.

Fusion beats show a QRS morphology that is a mixture of the native and paced QRS complex. Pseudofusion beats show a native QRS with a pacing spike just after the beginning of the QRS complex, giving the appearance of pacing, but since the pacing spike is after the ventricle has started to depolarize, the pacing stimulus is delivered during the refractory period and does not capture the heart.


Atrioventricular (AV) sequential pacing appears on the electrocardiogram as pacemaker spikes before the P wave and QRS complex.

If the native atrial rate is faster than the programmed lower rate of the pacemaker, there will be no pacing spike prior to the P wave, since the P wave originates from the sinus node (or another atrial location). Depending on device programming and AV conduction, there is either a paced or a native QRS. The paced QRS has a bizarre morphology resembling a left bundle branch block (LBBB) or a ventricular complex

Every QRS complex is preceded by a pacemaker stimulus (marked by red lines). The QRS complex is abnormal, wide, and bizarre, resembling a ventricular beat. The QRS complexes usually have a left bundle branch block configuration since the ventricular lead is most commonly located in the right ventricle.

If there is a native QRS, the morphology is normal and narrow, but may be wide if there is an underlying bundle branch block.

The morphology of the P wave depends upon the location of the lead within the right atrium; it may be upright, biphasic, or negative and the amplitude may be normal, increased, or diminutive. The PR interval is determined by the pacemaker and represents the delay between the atrial and ventricular stimuli; the pacemaker is essentially functioning as the AV node. The second or ventricular spike is followed by a QRS complex that is bizarre and usually has an LBBB morphology since the ventricular lead is typically in the right ventricle.


Standard ventricular pacing is from the right ventricle. Hence, the QRS complex has a left bundle branch block (LBBB) morphology as the impulse originates from the right ventricle and is conducted to the left ventricle (a right to left direction). This produces a tall and broad R wave in leads I, V5, and V6, and a deep QS complex in lead V1.

With biventricular pacing, also known as cardiac resynchronization therapy, there are pacing leads in the right atrium, right ventricle, and the coronary sinus, which results in stimulation of the left ventricle.


Two pacemaker spikes are seen within each complex; there is an atrial spike (marked by red lines) and an associated P wave, followed by a ventricular spike (marked by green lines) and an associated paced QRS complex. The P wave morphology is variable, depending upon the location of the wire within the right atrium.

Sometimes the coronary sinus lead is replaced by an epicardial or endocardial left ventricular lead. Ventricular pacing occurs from both the right ventricular and coronary sinus/left ventricular leads. The timing between the leads can be changed so that one lead is paced prior to the other or they can be paced simultaneously. Depending on the timing of pacing between the two leads, the QRS axis and morphology may change significantly.

Assuming left ventricular pacing occurs simultaneously or prior to right ventricular pacing, activation of the left ventricle precedes right ventricular activation. Therefore, the initial impulse direction is left to right. The most important electrocardiographic lead that demonstrates this impulse direction is lead I, which is a bipolar lead that looks at the impulse as it travels from the right to left. Initial activation of the left ventricle generates an impulse that is directed from left to right, producing a negative waveform (Q wave) in lead I. Therefore, with biventricular pacing lead, lead I will have an initial Q wave or a QS complex. In addition, leads V5-V6 also frequently demonstrate a QS complex. However, this is not definitive for biventricular pacing, as an LBBB may be associated with a QS complex in these leads. Biventricular pacing will also produce a tall R wave in lead V1, as the impulses are directed toward this lead. However, this QRS complex morphology may be seen with a right ventricular pacing electrode located at the interventricular septum. Therefore, while a QS complex in leads V5-V6 and a tall R wave in lead V1 are strongly suggestive of a biventricular pacemaker, an initial Q wave or a QS complex in lead I is definitive for left or biventricular pacing. In addition, if there is a significant difference between right and left ventricular pacing stimuli, two ventricular pacing spikes may be seen, with the second one occurring after the start of the QRS. This may be confused with pacemaker malfunction.


Pacemakers may malfunction either by failure of capture or sensing.

Loss of capture — Pacemaker malfunction with inconsistent capturing (atrium or ventricle) can be diagnosed from the electrocardiogram (ECG) when there are pacemaker spikes that are not followed immediately by either a P wave or QRS complex .

Non-capture may be intermittent, so that only occasional non-captured pacemaker stimuli are seen, or persistent, where no native complexes follow pacing spikes. In the latter cases, if intrinsic cardiac activity is present, the pacemaker stimuli are dissociated from the native P waves or QRS complexes. There may be no underlying cardiac activity in severe cases of loss of capture and asystole is seen. Loss of capture may be due to lead dislodgement or malposition, inflammation or fibrosis at the lead/tissue interface, low pacemaker output, lead failure, or battery depletion.

Failure of sensing — Pacemakers may have undersensing of native cardiac activity or oversensing of non-physiologic signal.


The second and fourth paced QRS complexes occur earlier than expected based upon the lower rate limit of the pacemaker. The pacemaker has failed to sense the preceding native complexes, and is therefore not inhibited by them. Thus, the pacemaker will fire and stimulate the atria or ventricles at its own predetermined rate, independently of the intrinsic rhythm. The interval between the native and paced complexes is variable while the intervals of the pacing spikes is constant.

In undersensing, the pacemaker does not see the native electrical signal in the chamber of interest, and will deliver a pacing stimulus at the lower rate for the atrium or after the programmed atrioventricular delay in the ventricle. Therefore, there will be a pacing spike in the middle of or after the beginning of the native P wave or QRS, or have no relation to the underlying cardiac activity. Depending on the refractoriness of the tissue, this pacing spike may or may not capture. The interval between the native and paced complexes is variable. Note that when pacemakers are turned to asynchronous modes (eg, AOO, VOO, DOO), they are programmed not to sense intrinsic cardiac signal and will have the appearance of undersensing.

It may seem that there is failure to sense a premature atrial or ventricular premature beat in some cases that are not actually representative of pacemaker malfunction. It may be dependent instead upon the timing of the premature beat, which may not be sensed by the pacemaker if the signal falls within a refractory period.

Oversensing may occur when the device sees a signal that does not originate from within the chamber of interest. This may be from electromagnetic interference, such as from electrocautery or other electrical interference, diaphragmatic myopotentials, pectoral muscle myopotentials if in a unipolar mode, lead fracture, or far field signals from another cardiac chamber. In oversensing, the device inhibits pacing. Therefore, no pacing spikes are seen at the expected time on the ECG, and unless there is intrinsic cardiac activity, there will be asystole.


Pacemaker leads may be placed in the right atrium, right ventricle, and coronary sinus/left ventricle.

If there is native cardiac activity faster than the programmed intervals, the P wave and QRS complex will resemble normal patterns. If there is slow cardiac activity, the electrocardiogram shows a pacing spike followed by a P wave or QRS complex. The morphology of a paced P wave may resemble or look different than the native P wave. The morphology of a paced QRS has a left bundle branch block configuration and is usually negative in the inferior leads.

The QRS complex with biventricular pacing will vary depending on right and left ventricular timing, but often has a tall R wave in V1 and an initial Q wave or QS complex in lead I.

Loss of pacemaker capture is defined by a pacing spike with no P wave or QRS complex, when the myocardium is physiologically capable of being depolarized.

Undersensing occurs when the pacemaker does not see native cardiac activity and paces inappropriately in the middle of or after a P wave or QRS complex, or has no relationship to the native cardiac signal.

Oversensing occurs when the pacemaker sees non-physiology activity and inhibits pacing. No pacing spikes are seen at the expected times.



Jordan M Prutkin, MD, MHS, FHRS