Pacemaker basics

Editor's Notes

• #3: A basic pacing system is made up of: Implantable pulse generator that contains: A power source—the battery within the pulse generator that generates the impulse Circuitry—controls pacemaker operations Leads—Insulated wires that deliver electrical impulses from the pulse generator to the heart. Leads also transmit electrical signals from the heart to the pulse generator. Electrode—a conductor located at the end of the lead; delivers the impulse to the heart.
• #5: Lithium-iodine is the most commonly used power source for today’s pacemakers. Microprocessors (both ROM and RAM) control sensing, output, telemetry, and diagnostic circuits.
• #14: Other sensors that measure QT interval, central venous temperature, stroke volume, etc., are largely investigational devices or have gained limited acceptance.
• #17: Pacing in the VVI/R mode and loss of AV synchrony can lead to pacemaker syndrome. Pacemaker syndrome can be defined as “an assortment of symptoms related to the adverse hemodynamic impact from the loss of AV synchrony.” Atrial pacemakers should only be used with patients who have proven AV conduction and regular follow-up testing available.
• #19: Studies have been done that demonstrate the differences in outcome, hemodynamic improvement, and quality of life assessment by using AV synchronous, or "atrial-based," pacing modes instead of VVI/R. Some of the benefits of using an atrial-based pacing mode include: AV synchrony–Clinical benefits such as increased cardiac output, augmentation of ventricular filling (especially important for the majority of the pacing population with LVD and reduced compliance from effects of aging). Providing AV synchrony minimizes valvular regurgitation, and preserves atrial electrical stability. In the Framingham Study, the development of chronic AF was associated with a doubling of overall mortality and of mortality from cardiovascular disease (Kannel, 1982) The following emphasize the importance of preventing atrial fibrillation: Patients with AF unrelated to rheumatic or prosthetic valvular disease have a risk of ischemic stroke about five times higher than those with normal sinus rhythm. AF is associated with over 75,000 cases of stroke per year. See bibliography for listing of studies cited.
• #20: Included is a summary of some studies depicting long-term results of AV synchronous (atrial based) and non-synchronous (VVI/R) pacing. Higano, et al. Hemodynamic importance of atrioventricular synchrony during low levels of exercise. PACE, 1990; 13:509 Abstract. Gallik DM, et al. Comparison of ventricular function in atrial rate adaptive versus dual chamber rate adaptive pacing during exercise. PACE, 1994; 17(2):179-185 Santini, et al. New Perspectives in Cardiac Pacing. Mount Kisco, NY: Futura Publishing, 1991. Rosenquist M, et al. Relative importance of activation sequence compared to atrioventricular synchrony during low levels of exercise. AM J Cardiology, 1991;67:148-156. Sulke N, et al. “Subclinical pacemaker syndrome: A randomized study of symptom free patients with ventricular demand (VVI) pacemakers upgraded to dual chamber devices. Brit Heart J, 1992; 67(1):57-64.
• #25: The stimulation process can be described in “phases:” The output voltage produces an electrical field at the electrode-tissue interface. The electrical field permeates cardiac cells via ionic movement and changes voltage on the cell membrane, which brings the cell membrane “above threshold” and alters its permeability. Phase 0 is the result of this part of the process. During Phase 0, sodium rushes in, which results in depolarization followed by cellular repolarization via sodium/potassium infusion. NOTE: The electrical field generated by the stimulation pulse must last long enough to excite the tissue. To effectively raise the membrane potential, the intensity of the stimulation must be balanced with the length of time it is applied.
• #27: Remind audience that amplitude had been discussed when voltage was described.
• #29: The greater the pulse width, the shorter the battery longevity. An increase in pulse width leads to an increase in total energy delivered. The longer the duration of the stimulus, the lower the amplitude required to capture the heart
• #30: The strength-duration curve illustrates the tradeoff of amplitude (intensity of stimulation, measured in volts) and duration (the length of time the stimulation is applied, measured in milliseconds). Capture occurs when the stimulus causes the tissue to react. On the graph, capture occurs on or above the curve. Anything below the curve will not capture. The lowest voltage on a stimulation curve which still results in capture at an infinitely long pulse duration is called rheobase. A voltage programmed below is inefficient and will lead to non-capture. The pulse duration at twice the rheobase value is defined as the chronaxie. Chronaxie time is typically considered most efficient in terms of battery consumption.
• #35: Impedance is the sum of all resistance to the flow of current. The resistive factors to a pacing system include: Lead conductor resistance The resistance to current flow from the electrode to the myocardium Polarization impedance, which is the accumulation of charges of opposite polarity in the myocardium at the electrode-tissue interface. Resistance is a term used to refer to simple electric circuits without capacitors and with constant voltage and current. Impedance is a term used to describe more complex circuits with capacitors and with varying voltage and current. Therefore, the use of the term impedance is more appropriate than resistance when discussing pacing circuits.
• #37: Impedance in pacing is defined as everything that opposes the flow of current through a circuit. Although in strict engineering terminology, resistance and impedance are different things, in pacing the terms are used interchangeably. It is important to know a pacing lead’s impedance because it can be an early indicator of possible lead problems. Lead impedance is a measured value; you cannot adjust it. Lead manufacturers state acceptable impedance values in broad ranges rather than as specific values because many things can impact lead impedance.
• #38: Can be expressed in three ways: V = I x R R = V ÷ I I = V÷ R If any two values are known, the third may be calculated (cover the value you are seeking and the others appear in the appropriate format to calculate the unknown value).
• #41: Using the garden hose as an analogy, the higher the voltage, the greater the push, or “flow” of electrons (and the greater the current drain).
• #42: Resistance affects current flow. Leads with an insulation breach, such as the garden hose pictured in the middle, will measure a low resistance reading with a resultant high current flow, and possible premature battery depletion. Conversely, if there is a high resistance, such as a lead conductor break, the current flow will be low or non-existent.
• #44: There are three phases that make up the lead maturation process: The acute phase, where thresholds immediately following implant are low The peaking phase, where thresholds rise and reach their highest point, usually around one week post-implant; followed by a decline in the threshold over the next 6 to 8 weeks1 as the tissue reaction subsides. The chronic phase, where thresholds assume a stable reading to a level somewhat higher than that at implantation but less than the peak threshold.1 The lead maturation process occurs due to the trauma to cells surrounding the electrode, which causes edema and subsequent development of a fibrotic capsule. The inexcitable capsule reduces the current at the electrode interface, requiring more energy to capture the heart. 1Hayes DH et al. Cardiac Pacing and Defibrillation: A Clinical Approach. Armonk, NY: Futura Publishing Company; 2000. Page 7.
• #45: There are three phases that make up the lead maturation process: The acute phase, where thresholds immediately following implant are low The peaking phase, where thresholds rise and reach their highest point, usually around one week post-implant; followed by a decline in the threshold over the next 6 to 8 weeks1 as the tissue reaction subsides. The chronic phase, where thresholds assume a stable reading to a level somewhat higher than that at implantation but less than the peak threshold.1 The lead maturation process occurs due to the trauma to cells surrounding the electrode, which causes edema and subsequent development of a fibrotic capsule. The inexcitable capsule reduces the current at the electrode interface, requiring more energy to capture the heart. 1Hayes DH et al. Cardiac Pacing and Defibrillation: A Clinical Approach. Armonk, NY: Futura Publishing Company; 2000. Page 7.
• #46: Steroid eluting leads reduce inflammation by employing a capsule of dexamethasone sodium phosphate, which gradually emits steroid over time, nearly eliminating the peaking phenomenon of the lead maturation process.
• #47: This graph compares the stimulation thresholds of contemporary pacing leads. Older electrodes exhibited higher threshold peaking than that of steroid leads shown on the slide. The different types of electrodes exhibit a wide range of threshold peaking. Steroid-eluting electrodes continue to show lower chronic stimulation thresholds and no significant peaking. Threshold changes are shown here over a 12-week period post-implant, where a comparison is made between: • smooth metal electrode • textured metal electrode • steroid-eluting electrode Traditionally, implant stimulation thresholds are relatively low. Non-steroid-eluting electrodes exhibit a peaking phase from week 1 to approximately week 6, due to the maturation process at the electrode-tissue interface. Steroid-eluting electrodes exhibit virtually no peaking. The chronic phase of stimulation threshold occurs 8-12 weeks post-implant which is characterized by a plateau. This plateau is higher than the acute phase, due to fibrotic encapsulation of the electrode. Steroid-eluting lead chronic thresholds remain close to implant values.
• #48: When the heart functions normally, there is no need for the pacemaker to deliver artificial pacing impulses. A pacemaker must be able to sense and respond to normal and abnormal cardiac rhythms.
• #50: Pacemakers have programmable sensitivity settings that can be thought of like a fence: with a lower fence more of the signal is seen; with a higher fence less of the signal is seen.
• #56: Single chamber timing has three components: Lower rate interval Refractory period Blanking period Single chamber devices that are programmed to a rate responsive mode add a fourth component, the upper rate interval.
• #57: The lower rate defines the lowest rate that the pacemaker will pace. For example, if the lower rate is programmed to 60 ppm in the VVI mode, the pacemaker is required to pace at a rate of 60 ppm if the patient's intrinsic ventricular rate is less than 60 bpm. A paced or non-refractory sensed event restarts the rate timer at the programmed rate.
• #58: During refractory periods, the pacemaker “sees” but is unresponsive to any signals. This is designed to avoid restarting the lower rate interval in the event of oversensing. T-wave oversensing in VVI and AAI modes will occur if refractory periods are too short. In the AAI mode, the pacemaker may even sense the QRS complex (“far-field R wave”) if the refractory period is not long enough. Events that fall into the refractory period are sensed by the pacemaker (the marker channel will display a “SR” denoting ventricular refractory or atrial refractory in single chamber systems) but the timing interval will remain unaffected by the sensed event. A refractory period is started by a paced, non-refractory, or refractory sensed event.
• #59: A paced or sensed event will initiate a blanking period. Blanking is a method to prevent multiple detection of a single paced or sensed event by the sense amplifier (e.g., the pacemaker detecting its own pacing stimuli or depolarization, either intrinsic or as a result of capture). During this period, the pacemaker is "blind" to any electrical activity. A typical blanking period duration in a single-chamber mode is 100 msec*. Note: In Thera and Kappa devices, nonprogrammable blanking parameters are dynamic (ranging from 50-100 ms) depending on the strength/duration of the paced or sensed signal.
• #60: The upper sensor rate interval in single chamber pacing is available only in rate-responsive modes. The upper rate defines the limit at which sensor-driven pacing can occur.
• #62: VOO mode paces in the ventricle but will not sense and, therefore, has no response to cardiac events. Pacemakers programmed to the VVI, VVIR, and VDD modes will revert to VOO mode upon magnet application. In this example, an intrinsic beat occurs, but it has no effect on the timing interval and another ventricular pace is delivered at the programmed rate. No sensing occurs, thus, the entire lower rate interval is unresponsive to intrinsic activity.
• #63: In inhibited modes (VVI/AAI), intrinsic events that occur before the lower rate interval expires will reset the lower rate interval, as shown in the example above. As with paced events, sensed events will also initiate blanking and refractory periods.
• #64: Single chamber rate-responsive pacing is identical to non-rate responsive pacing operation, with the exception that the pacing rate is driven by a sensor. The sensor determines whether or not a rate increase is indicated, and adjusts the rate accordingly. The highest rate that the pacemaker is allowed to pace is the upper rate limit or interval. In this example, the pacemaker is pacing at the maximum sensor indicated rate of 120 ppm.
• #66: Knowing the basic A-V and V-A intervals will help in understanding the four modes or “faces” of dual chamber pacing. In the first example, the pacemaker is pacing in both the atrium and the ventricle–most likely a patient with sinus node dysfunction and AV block.
• #67: In this example, the atrium is being paced, but AV conduction is intact, so the ventricular output is inhibited by a sensed ventricular event.
• #68: In this example, the atrial rate is driving the ventricular rate–also called atrial tracking. This patient has adequate sinus node function with AV block.
• #69: In this example, the patient has adequate sinus node function and intact AV conduction, but may experience little to no increase in sinus rate with activity and/or AV block that occurs at increased rates. At appropriate rates, it is best to try and utilize the patient’s intrinsic rhythm when possible.
• #70: Dual-chamber pacing requires attention to these parameters: Lower rate AV and V-A intervals Upper rates Refractory periods Blanking periods
• #71: In order to provide optimal hemodynamic benefit to the patient, dual-chamber pacemakers strive to mimic the normal heart rhythm. In dual-chamber pacemakers, the lower rate is the rate at which the pacemaker will pace the atrium in the absence of intrinsic atrial activity. Similar to single-chamber timing, the lower rate can be converted to a lower rate interval (A-A interval), or the longest period of time allowed between atrial events.
• #72: The SAV is usually programmed to a shorter duration than the PAV to allow for the difference in interatrial conduction time between intrinsic and paced atrial events. Think of the difference in the activation sequence between a cycle initiated with an intrinsic atrial event versus a paced atrial event. The cycle starting with the intrinsic atrial event will use the normal conduction pathways between the right atrium and the left atrium. The cycle starting with the paced atrial beat will not use the normal interatrial conduction pathways but will instead use muscle tissue, which takes a little longer to reach the left atrium and causing it to contract. If the AV interval is timed to allow the appropriate amount of time for left ventricular filling when the cycle is initiated with a sensed atrial event, the same duration for the PAV may not be the appropriate amount of time to allow for left ventricular filling when the cycle is initiated by a paced atrial event. Proper LA-LV timing promotes left ventricular filling ("atrial kick") and prevents regurgitant flow through an open mitral valve. Therefore, it is beneficial to have separately programmable PAV and SAV intervals. In this example, the lower rate interval is terminated by a sensed atrial event, which initiates a SAV interval (and restarts the the lower rate interval).
• #73: Knowing the lower rate interval and the PAV interval (A-V interval after a paced atrial event), the V-A interval can be found: V-A interval = lower rate interval minus the AV interval. The V-A interval is the longest period that may elapse after a ventricular event before the atrium must be paced in the absence of atrial activity. The V-A interval is also commonly referred to as the atrial escape interval.
• #74: The A-V interval is employed to allow the appropriate amount of time to optimize ventricular filling and mimic the activation sequence of the normal heart. Knowing the lower rate interval and the PAV interval (A-V interval after a paced atrial event), the V-A interval can be found: V-A interval = lower rate interval minus PAV interval. The V-A interval is the longest period that may elapse after a ventricular event before the atrium must be paced in the absence of atrial activity. The V-A interval is also commonly referred to as the atrial escape interval.
• #75: This upper rate is defined as the upper activity rate, also known as the upper sensor rate or maximum sensor rate. Before mode switching was available, pacemakers utilized a separate activity/sensor rate and upper tracking rate to limit the rate to which the patient could track (e.g., in the presence of SVTs), but allow the patient to pace to higher rates if they were exercising.
• #76: The sequence of an atrial intrinsic event being sensed, starting an SAV interval, timing out the SAV interval, and pacing in the ventricle can be referred to as "tracking." If the atrial rate begins to increase and continues to increase, is it desirable to let the ventricle "track" to extremely high rates? No. It is desirable to limit the rate at which the ventricle can pace in the presence of high atrial rates. This limit is called the upper tracking rate.
• #77: The Post-Ventricular Atrial Refractory Period (PVARP) is the period of time after a ventricular pace or sense when the atrial channel is in refractory. In other words, atrial senses outside of blanking that occur during this period are "seen" (and marked “AR) on the marker channel), but do not initiate an AV interval. The purpose of PVARP is to avoid allowing retrograde P waves, far-field R waves, or premature atrial contractions to start an AV interval which would cause the pacemaker to pace in the ventricle at a high rate. The refractory period after a ventricular event (paced or sensed) is designed to avoid restarting of the V-A interval due to a T wave. Ventricular sensed events occurring in the noise sampling portion of the ventricular refractory period are "seen" (and marked “VR” on the marker channel) but will not restart the V-A interval. The atrial channel is refractory following a paced or sensed event during the AV interval. This allows atrial senses occurring in the AV interval to be "seen" but not restart another AV interval .
• #79: DDD/R modes have four types of blanking periods: A non-programmable atrial blanking period (varies from 50-100 msec) is initiated each time the atrium paces or senses. This is to avoid the atrial lead sensing its own pacing pulse or P wave (intrinsic or captured). In Thera and Kappa devices, this blanking period is dynamic, depending on the strength of the paced/sensed signal. The PVAB-(Post-Ventricular Atrial Blanking Period) is initiated by a ventricular pace or sensed event (nominally set at 220 msec) to avoid the atrial lead sensing the far-field ventricular output pulse or R wave. In dual-chamber timing, a non-programmable ventricular blanking period occurs after a ventricular paced or sensed event to avoid sensing the ventricular pacing pulse or the R wave (intrinsic or captured). This period is 50-100 msec in duration and is dynamic, based on signal strength. There also is a ventricular blanking period after an atrial pacing pulse in order to avoid sensing the far-field atrial stimulus (crosstalk). This period is programmable (nominally set at 28 msec). This blanking period is relatively short because it is important not to miss ventricular events (e.g., PVCs) that occur early in the AV interval. Ventricular blanking does not occur coincident with an atrial sensed event. This is because the intrinsic P wave is relatively small and will not be far-field sensed by the ventricular lead. The issue of ventricular safety pacing and cross-talk will be addressed later on in the presentation. A note of caution in programming long ventricular blanking periods after an atrial pace should be mentioned. If the ventricular blanking period after an atrial pace is excessively long, conducted ventricular events may go unsensed and cause the pacemaker to pace in the ventricle after the AV interval expires. This pace could occur before the ventricle has recovered from depolarization and may induce a ventricular arrhythmia (R on T phenomena).
• #81: This ECG depicts Wenckebach operation.
• #82: Pacemaker Wenckebach has the characteristic Wenckebach pattern of the PR (AV) interval gradually extending beat-to-beat until an atrial event falls into the PVARP and cannot restart an AV interval. In effect, a ventricular beat is “dropped”. In this graphic, starting from the left side of the ECG, the pacemaker senses an atrial beat and starts an SAV. Because no ventricular event occurs by the end of the SAV, a ventricular pace is delivered. Now the pacemaker is looking for a sensed atrial beat. An atrial beat is sensed outside of the PVARP and starts an SAV. This time, when the SAV times out, the upper rate interval has not yet expired. Since the pacemaker can never violate the upper tracking rate, the ventricular pace has to be delayed until the end of the upper rate interval, at which time a ventricular pace is delivered. This pattern of sensing a P wave, starting an SAV, waiting for the upper rate interval to time out, and pacing in the ventricle repeats until a P wave falls into the PVARP and does not start an SAV. The amount of delay created by the time from the sensed P wave until the upper rate interval expires is a little longer each time, producing the gradually lengthening of the P wave to ventricular pace intervals. Once a P wave falls into the PVARP and does not initiate an SAV, the pacemaker looks for the next sensed P wave and the pattern starts all over again. This is how the classic Wenckebach pattern develops. The rate at which the pacemaker will exhibit Wenckebach behavior is at the upper tracking rate (or upper rate if the pacemaker does not have a separate upper tracking rate and upper activity rate).
• #85: Pacemaker 2:1 block is characterized by two sensed P waves per paced QRS complex. This pattern develops because every other P wave falls into PVARP. Starting on the left side of this ECG, the sequence begins with a sensed P wave. This P wave initiates a SAV, followed by a paced ventricular event. The next P wave falls into the PVARP, started by the ventricular pace, so no SAV is initiated. The following P wave is sensed outside of the PVARP, so a SAV is started. Again, no ventricular event occurs during the SAV, so the pacemaker paces in the ventricle. In this manner, a 2:1 block pattern is created. The rate at which the pacemaker will exhibit a 2:1 block pattern is determined by the SAV and the PVARP (or the TARP). Atrial rates with a P-P coupling interval shorter than the TARP will result in 2:1 block. To determine at what rate the pacemaker will go into 2:1 block, the TARP is simply converted from an interval to a rate. Therefore, the rate the pacemaker will go into 2:1 block is: 60,000/TARP.
• #86: The total time that the atrial chamber of the pacemaker is in refractory is during the AV interval and during the PVARP. The Total Atrial Refractory Period (TARP) is equal to the SAV interval plus the PVARP. The TARP is important to understand as it defines the highest rate that the pacemaker will track atrial events before 2:1 block occurs.