Cardiac Pacing



Cardiac Pacing


Tyler L. Taigen



I. INTRODUCTION.

The indications and technology of cardiac pacing continue to evolve, leading to a rapid increase in the number of pacemakers implanted. Pacemaker implantation rates increased from 329 implants per million population in 1990 to 612 per million population in 2002. In 2011, 400,000 cardiac devices were implanted and over 3 million people in the United States had implantable cardiac rhythm management devices. It is imperative that the physician caring for the pacemaker patient understand the basic physiology and technology of cardiac pacing and be able to apply these principles to effectively manage the unique problems with which these patients may present.


II. BASIC COMPONENTS OF CARDIAC PACEMAKERS


A. Pulse generator


1. Power source (battery).

Lithium iodide is the most common chemical compound used. Lithium batteries deplete over a more predictable time course than other types of compounds, such as zinc mercuric oxide, that were used in prior generations of devices.


2. Circuitry


a. Output circuits.

These circuits control programmable features of the output pulse, including amplitude and pulse width.


b. Sensing circuits.

These circuits process the intracardiac electrogram, including amplification and filtering of the signal, and also provide other functions such as management of external electromagnetic interference (EMI). A bandpass filter allows signals of a certain frequency range to be passed while signals of other frequency ranges are blocked or attenuated. Pacemakers use a bandpass filter to distinguish between cardiac depolarization and repolarization signals from extracardiac signals, such as myopotentials from the chest wall musculature. Some appropriate signals that pass through the filter are small in amplitude, and a sense amplifier increases the appropriate signal for the device to process.


c. Timing circuits.

These circuits control the pacing intervals and sensing/refractory periods. They may be altered by input from the sensing circuits.


d. Telemetry circuit.

These circuits allow communication between an external programmer and the pulse generator for pacemaker programming or retrieval of information.


e. Microprocessor.

Most modern pacemakers have computer chips with memory (read only memory [ROM] and random access memory [RAM]) and therefore have enhanced capabilities, such as downloading of new features via telemetry and increased storage of diagnostic data.


f. Sensor circuit for rate-adaptive pacing.

See below.


B. Lead system


1. Terminal pin.

The male portion of the proximal lead that connects to the pulse generator.



2. Lead body.

Consists of conductor(s) and insulation. The conducting wire connects the stimulating and sensing electrodes to the terminal pin. The lead insulation is most commonly silicone rubber or a polyurethane material.


3. Stimulating/sensing electrode(s).

The distal end of the lead that connects via a fixation mechanism to atrial or ventricular myocardium.


4. Fixation device.

Passive fixation represents an attachment mechanism (e.g., “fins” or “tines”) that anchors electrodes to the endocardial trabeculae. Active fixation leads are secured to the endocardium using a “screw-in” mechanism. Over the past decade, active fixation leads have been implanted much more commonly. These types of leads have a lower rate of early dislodgement and yet higher chronic capture thresholds than passive fixation leads.


C. Polarity.

This refers to the electrode configuration of the pacing lead or the configuration of the pulse generator. Polarity may be unipolar or bipolar; however, some pacemakers can be programmed to pace in one polarity and sense in another (only if a bipolar lead is present).


1. Unipolar.

Configuration in which the cathode (negative) is on the lead, usually the lead tip, and the anode (positive) is the pacemaker can. This results in a large sensing “antenna” and produces large pacemaker artifact (spikes) on the electrocardiogram (ECG) due to proximity of the circuit to ECG electrodes.


a. Advantages.

Better sensing of premature ventricular contractions (PVCs), low-amplitude signals, and shifted axis.


b. Disadvantages.

Oversensing of extraneous signals, especially pectoralis muscle activity (myopotentials), and inadvertent skeletal muscle stimulation may occur. Moreover, large pacemaker artifacts on the ECG may obscure native electrical activity.


2. Bipolar.

Both electrodes are at the end of the lead—the cathode (negative) at the distal tip and the anode (positive) at the proximal ring. This results in a smaller sensing “antenna” with smaller pacemaker artifact (spikes) on the ECG. Myocardial stimulation occurs as electrons from the cathode travel through the myocardium and back to the anode.


a. Advantages.

Less myopotential oversensing and skeletal muscle stimulation, and the smaller pacemaker artifact on the ECG, do not obscure native wave morphology.


b. Disadvantages.

More complex lead design is more susceptible to malfunction/failure. Small pacemaker artifact on the ECG may be difficult to see.


D. Lead—heart interface.

This is equivalent to the site of energy transfer (pacing) and sensing functions.


III. PACEMAKER CLASSIFICATION.

The North American Society of Pacing and Electrophysiology and the British Pacing and Electrophysiology Group initially published a “pacemaker code” in 1983. Guidelines were later revised in 2002 and the five-position code remains the accepted nomenclature for pacemaker therapy (see Table 54.1). The first two positions (chamber paced and chamber sensed) are straightforward. The third position, however, is often misunderstood. As outlined in Table 54.1, the third position reflects the device response to a sensed event (labeled “I,” “T,” or “D”). ‘I” (Inhibited)—the device will pulse the given chamber unless it senses an intrinsic event. Thus when programmed DDI, atrioventricular (AV) synchrony will only exist if the atrial chamber is paced. If the atrial activity is intrinsic and the ventricular response depends only on the sensed activity in that chamber, then AV synchrony will not be provided. “T” (Triggered)—this mode is used during device testing where a sensed event results in the device producing a pulse. “D” (Dual)—atrial and ventricular sensing and pacing with dual-chamber devices. When programmed DDD, a sensed atrial beat inhibits atrial pacing and, after a programmed time interval, triggers ventricular pacing. This mode enables tracking of intrinsic atrial activity and corresponding ventricular pacing to allow AV synchrony.









TABLE 54.1 Revised NASPE/BPEG Generic (NBG) Code for Antibradycardia, Adaptive Rate, and Multisite Pacing






















































Position


I


II


III


IV


V


Category


Chamber(s) paced


Chamber(s) sensed


Response to sensing


Programmability, rate modulation


Multisite pacing


Letters


0 = none


0 = none


0 = none


0 = none


0 = none



A = atrium


A = atrium


T = triggered


R = rate modulation


A= atrium



V = ventricle


V = ventricle


I = inhibited



V = ventricle



D = dual (A + V)


D = dual (A + V)


D = dual (T + I)



D = dual (A + V)


Manufacturers’ designation only


> S = single (A or V)


S = single (A or V)





BPEG, British Pacing and Electrophysiology Group; NASPE, North American Society of Pacing and Electrophysiology. Pacing Clin Electrophysiol. 2002;25:260-264.



IV. INDICATIONS FOR PACEMAKER IMPLANTATION.

The American College of Cardiology (ACC)/American Heart Association (AHA)/Heart Rhythm Society (HRS) published updated guidelines for indications for pacemaker implantation in device-based therapy of cardiac rhythm abnormalities in 2008 (see Table 54.2).


V. PHYSIOLOGY OF CARDIAC PACING


A. Pulse generator output.

This is determined by the output voltage and duration of the stimulating pulse (pulse width). Most implanted cardiac pacemakers use constant-voltage output (as opposed to most temporary cardiac pacemakers, which use constant-current output).


B. Strength—duration relation.

There is an exponential relationship between the stimulus amplitude for myocardial stimulation and the pulse width, such that there is a rapidly rising strength—duration curve at pulse widths < 0.25 millisecond and a flatter curve at pulse widths > 1.0 millisecond (see Fig. 54.1).


1. Rheobase.

The flattened portion of the strength—duration curve indicating the point at which increasing pulse width is no longer associated with a progressive decrease in stimulus amplitude (voltage) required for myocardial stimulation. In general, the rheobase voltage is determined by assessing the threshold stimulus voltage at a pulse width of 2.0 milliseconds.


2. Chronaxie.

This corresponds to the threshold pulse width at twice the rheobase voltage. The chronaxie pulse duration approximates the point of minimal threshold energy on the strength—duration curve.


C. Safety margins


1. Voltage.

The voltage output should be programmed to a level that is approximately twice the capture (stimulation) threshold for a 2:1 output safety margin.


2. Pulse width.

The pulse duration should be programmed to a level approximately three times the pulse width capture threshold for a 3:1 output safety margin. The typical range for pulse width is 0.2 to 1.0 millisecond.


D. Temporal changes in stimulation threshold.

Typically, the stimulation threshold rises within 24 hours following implantation of a permanent pacemaker lead. The




threshold peaks at 1 to 2 weeks, then gradually declines and plateaus at approximately 6 weeks at a level less than the acute peak, but greater than that measured at implantation. The absolute value of the temporal changes in stimulation thresholds varies between individuals and also between various types of electrodes.








TABLE 54.2 Indications for Cardiac Pacing
















































































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Jun 7, 2016 | Posted by in CARDIOLOGY | Comments Off on Cardiac Pacing

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Class I


Class II


Class III


SND


1. SND with documented symptomatic bradycardia,


IIa:


1. Permanent pacemaker



including frequent sinus pauses that produce


1. SND with heart rate < 40 bpm when a


implantation is not indicated for



symptoms.


clear association between significant


SND in asymptomatic patients.



2. Symptomatic chronotropic incompetence.


symptoms consistent with bradycardia


2. Permanent pacemaker implantation



3. Symptomatic sinus bradycardia that results from


and the actual presence of bradycardia


is not indicated for SND in



required drug therapy for medical conditions.


has not been documented.


patients for whom the symptoms




2. Syncope of unexplained origin when clinically


suggestive of bradycardia have




significant abnormalities of sinus


been clearly documented to occur




node function are discovered or provoked


in the absence of bradycardia.




in electrophysiological studies.


3. Permanent pacemaker implantation




IIb:


is not indicated for SND with symptomatic bradycardia due to




In minimally symptomatic patients with chronic heart rate < 40 bpm while awake.


nonessential drug therapy.


Acquired AV


1. Permanent pacemaker implantation is indicated for


IIa


1. First-degree AV block.


block


third-degree and advanced second-degree AV block


1. Permanent pacemaker implantation is


2. Asymptomatic type I seconddegree



at any anatomic level associated with the following