Failure to pace

The pacemaker fires but fails to pace the myocardium. This can again be dangerous for the patient as they can be subject to the condition the pacemaker was inserted to treat if the pacemaker fails to work correctly. This is seen on the ECG by the presence of pacing spikes without a subsequently paced QRS complex or P wave (Fig. 8.7). 

This is the complete absence of pacing spikes and paced complexes where expected. The ECG often shows a gap in between complexes. This can be problematic for patients as it can decrease cardiac ontpnt (Fig. 8.8). 

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Fig. 18.6 Posteroanterior radiograph (A) and close-up view (B) from a patient with intermittent failure to pace. Comparison of the upper and lower pins reveals that the lower of the two unipolar leads is not completely advanced. This difference is more evident on the close-up view. By convention, the lower of the two leads in the connector block is the ventricular lead, so that this patient must have had intermittent or permanent ventricular failure to output. An unrelated ohservation (arrowhead on 6 A) is the shallow positioning of the atrial lead, i.e., the J is much wider than 90°. (From Hayes DL. Pacemaker radiography. In Furman S, Hayes DL, Holmes DR Jr, editors. A practice of cardiac pacing, third edition. Mount Kisco [NY] Futura Publishing, 1993 361 100. Used with permission of Mayo Foundation for Medical Education and Research.)...

As with all manmade devices there is the possibility that the device can be faulty, either due to a fault in the manufacturing process or in the programming of the device. Pacemaker malfunctions can often be seen on the 12-lead ECG. The most commonly encountered problems associated with pacemaker systems include failure to sense, failure to capture, failure to pace and over sensing. 

Fig. 8.8 Failure to Pace. Arrows show the presence of a gap in between compiexes...

Interference with ventricular pacing occurred in a patient with a pacemaker who developed severe procainamide toxicity with a serum concentration of 36 ptglml the QRS widened from 0.20 to 0.26 sec and a delay of 0.18 sec appeared between the pacing stimulus and the QRS. Subsequently, periodic variation of the Wenkenbach type developed in the stimulus-QRS interval with intermittent failure to pace. Failure of pacemaker inhibition also occurred. Administration of 160 mM sodium bicarbonate intravenously led to immediate improvement in the abnormalities (37 ). 

Failure to pace can lead to asystole or a severe decrease in cardiac output in pacemaker-dependent patients. 

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Ideally, if symptomatic sinus node dysfunction occurs in the presence of drugs known to impair sinus node function, the first treatment is to discontinue the offending drug [29]. However, this is typically not feasible in patients with heart failure who are dependent on several medications to improve long-term outcomes, or may need antiarrhythmic drug therapy for symptomatic arrhythmias. Accordingly, the treatment usually becomes a question of whether to apply pacing to increase heart rate. This is further complicated by the appropriate pacemaker prescription once the decision to pace has been made. 

A series of pilot studies began with multisite pacing for patients with heart failure and dilated cardiomyopathy in the early 1990s [52, 105-111]. An improvement in LV function and symptoms of heart failure were demonstrated. This provided the interest in biventricular pacing for heart failure. The term cardiac resynchronization therapy was coined to refer to pacing therapies that attempt to enhance cardiac performance by using pacing to correct electrical conduction abnormalities in the heart. The most common form of this therapy is atrial-synchronous... 

Antidysrhythmic drugs increase the pacing threshold, but failure to capture is a rare consequence. It has, however, been reported twice with flecainide (28,29). 

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Loss of ventricular pacing occurs at or above the upper rate limit in patients with intact AV conduction and in sinus rhythm. In patients with intact AV conduction, this phenomenon has not been recognized in conventional pacing since it was of no hemodynamic consequence. In cardiac resynchronization therapy, it results in a failure to deliver pacing. In fact... 

Failure to Capture. The absence of myocardial depolarization despite appropriate stimulus delivery from the pulse generator defines failure to capture. Failure to capture is usually diagnosed fiom the ECG by the occurrence of visible pacing artifact without resultant paced P-waves or QRS complexes (Fig. 16.2). Failure to capture can, however, result in no visible stimulus artifact despite stimulus output from the generator when there is complete lead fracture (see above). Failure to capture results from lead failure, lead-tissue interface problems, and increases in myocardial stimulation threshold (Fig. 16.3). 

Fig. 16.2 Failure to capture due to insufficient current delivery in a patient with a pulse generator at end of life. The first and third QRS complexes are paced the second complex represents true fusion (the QRS complex resulting from both the pacing stimulus and spontaneous depolarization) the fourth complex represents pseudofusion (the QRS complex resulting from spontaneous depolarization despite pacing stimulus output) the remaining complexes are spontaneous.

If no abnormality is appreciated radiographically but there is a clinical abnormality, reassess the chest radiograph in a problem-oriented fashion. For example, if the patient has intermittent failure to output, the differential diagnosis includes a problem with the connector pin, such as a loose set screw or fracture of the conductor coil. Go back once again and inspect these elements of the pacing system. 

The purpose of inspecting the connector block is to determine that the connector and pin are firmly in contact. If the pin of the pacing lead is not firmly in the connector block, intermittent or permanent disruption of the circuit occurs. In Figure 18.6, the chest radiograph demonstrates a dual-chamber pacemaker with a lower pin that is only partially advanced. At presentation, the patient had intermittent failure to capture the ventricle and intermittent failure to deliver a ventricular pacing output. 

As early as the late 1700s, Physicians speculated that electrical current could be used to stimulate the heart. In 1882, von Ziemssen used electrical current to directly stimulate the heart of a woman whose anterior chest wall had been removed after resection of a chest tumor. In 1952, ZoU used transthoracic current to pace the heart, and in 1958 the first implantable pacanaker was placed by Ake Senning and Rune Elmquist. At the same time, Furman and Robinson demonstrated the feasibility of transvenous cardiac pacing. In the late 1960s, Mirowski and colleagues pioneered the concept of an implantable device that could be used to defibrillate the heart. Over the last 50 years, implantable cardiac devices have become the primary treatment for bradyarrhythmias and ventricular tachyarrhythmias and have emerged as an important adjunctive therapy for patients with heart failure. It is currently estimated that almost 400,000 pacemakers and defibrillators are implanted annually in the United States. 

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