I. Field of the Invention
This invention relates generally to a device for stimulating cardiac tissue, and more particularly relates to an implantable cardiac rhythm management device capable of automatically detecting intrinsic and evoked response of a patient""s heart. The device of the present invention may operate in an automatic capture verification mode, wherein an electrocardiogram signal of a patient""s heart is received and used by the device to determine whether a stimulation pulse evokes a response by the patient""s heart. The rhythm management device may automatically adjust the detection threshold during a normal mode or an automatic capture verification mode. Also, the device may suspend the automatic capture verification mode and/or adjust the detection threshold dependent upon detected and/or measured noise, a determined amplitude of evoked response, a determined modulation in the evoked response, or detected and/or measured artifact. Further, the sensing circuit of the rhythm management device of the present invention reduces afterpotentials that result due to delivery of the stimulation pulses.
II. Discussion of the Prior Art
Cardiac rhythm management devices have enjoyed widespread use and popularity over the years as a means for supplanting some or all of an abnormal heart""s natural pacing functions. The various heart abnormalities remedied by these stimulation devices include total or partial heart block, arrhythmias, myocardial infarctions, congestive heart failure, congenital heart disorders, and various other rhythm disturbances within the heart. The cardiac rhythm management devices generally include a pulse generator for generating stimulation pulses to the heart electrically coupled to an electrode lead arrangement (unipolar or bipolar) positioned adjacent or within a pre-selected heart chamber for delivering pacing stimulation pulses.
Regardless of the type of cardiac rhythm management device that is employed to restore the heart""s natural rhythm, all operate to stimulate excitable heart tissue cells adjacent to the electrode of the lead. Myocardial response to stimulation or xe2x80x9ccapturexe2x80x9d is a function of the positive and negative charges found in each myocardial cell within the heart. More specifically, the selective permeability of each myocardial cell works to retain potassium and exclude sodium such that, when the cell is at rest, the concentration of sodium ions outside of the cell membrane is significantly greater than the concentration of sodium ions inside the cell membrane, while the concentration of potassium ions outside the cell membrane is significantly less than the concentration of potassium ions inside the cell membrane.
The selective permeability of each myocardial cell also retains other negative particles within the cell membrane such that the inside of the cell membrane is negatively charged with respect to the outside when the cell is at rest. When a stimulus is applied to the cell membrane, the selective permeability of the cell membrane is disturbed and it can no longer block the inflow of sodium ions from outside the cell membrane. The inflow of sodium ions at the stimulation site causes the adjacent portions of the cell membrane to lose its selective permeability, thereby causing a chain reaction across the cell membrane until the cell interior is flooded with sodium ions. This process, referred to as depolarization, causes the myocardial cell to have a net positive charge due to the inflow of sodium ions. The electrical depolarization of the cell interior causes a mechanical contraction or shortening of the myofibril of the cell. The syncytial structure of the myocardium will cause the depolarization originating in any one cell to radiate through the entire mass of the heart muscle so that all cells are stimulated for effective pumping. Following heart contraction or systole, the selective permeability of the cell membrane returns and sodium is pumped out until the cell is re-polarized with a negative charge within the cell membrane. This causes the cell membrane to relax and return to the fully extended state, referred to as diastole.
In a normal heart, the sino-atrial (SA) node initiates the myocardial stimulation of the atrium. The SA node comprises a bundle of unique cells disposed within the roof of the right atrium. Each cell membrane of the SA node has a characteristic tendency to leak ions gradually over time such that the cell membrane periodically breaks down and allows an inflow of sodium ions, thereby causing the SA node cells to depolarize. The SA node cells are in communication with the surrounding atrial muscle cells such that the depolarization of the SA node cells causes the adjacent atrial muscle cells to depolarize. This results in atrial systole wherein the atria contract to empty blood into the ventricles.
The atrial depolarization from the SA node is detected by the atrioventricular (AV) node which, in turn, communicates the depolarization impulse into the ventricles via the Bundle of His and Purkinje fibers following a brief conduction delay. In this fashion, ventricular systole lags behind atrial systole such that the blood from the ventricles pumps through the body and lungs after being filled by the atria. Atrial and ventricular diastole follow wherein the myocardium is re-polarized and the heart muscle relaxed in preparation for the next cardiac cycle. It is when this system fails or functions abnormally that a cardiac rhythm management device may be needed to deliver an electronic stimulation pulse for selectively depolarizing the myocardium of the heart so as to maintain proper heart rate and synchronization of the filling and contraction of the atrial and ventricular chambers of the heart.
The success of a stimulation pulse in depolarizing or xe2x80x9ccapturingxe2x80x9d the selected chamber of the heart hinges on whether the output of the stimulation pulse as delivered to the myocardium exceeds a threshold value. This threshold value, referred to as the capture threshold, is related to the electrical field intensity required to alter the permeability of the myocardial cells to thereby initiate cell depolarization. If the local electrical field associated with the stimulation pulse does not exceed the capture threshold, then the permeability of the myocardial cells will not be altered enough and thus no depolarization will result. If, on the other hand, the local electrical field associated with the stimulation pulse exceeds the capture threshold, then the permeability of the myocardial cells will be altered sufficiently such that depolarization will result.
Changes in the capture threshold may be detected by monitoring the efficacy of stimulating pulses at a given energy level. If capture does not occur at a particular stimulation energy level which previously was adequate to effect capture, then it can be surmised that the capture threshold has increased and that the stimulation energy should be increased. On the other hand, if capture occurs consistently at a particular stimulation energy level over a relatively large number of successive stimulation cycles, then it is possible that the capture threshold has decreased such that the stimulation energy is being delivered at level higher than necessary to effect capture. Alternatively, the electrocardiogram signal may be utilized to surmise whether a change in amplitude in the electrocardiogram signal at a particular time is the result of an intrinsic event or evoked response.
The ability of a rhythm management device to detect capture is desirable in that delivering stimulation pulses having energy far in excess of the patient""s capture threshold is wasteful of the rhythm management device""s limited power supply. In order to minimize current drain on the power supply, it is desirable to automatically adjust the device such that the amount of stimulation energy delivered to the myocardium is maintained at the lowest level that will reliably capture the heart. To accomplish this, a process known as capture verification must be performed wherein the rhythm management device monitors to determine whether an evoked depolarization occurs in the pre-selected heart chamber following the delivery of each pacing stimulus pulse to the pre-selected chamber of the heart.
At times, a stimulation pulse may be delivered coincidental to a depolarization by an intrinsic beat (hereinafter referred to as xe2x80x9cfusionxe2x80x9d or xe2x80x9ca fusion beatxe2x80x9d). From a surface ECG, the fusion beats manifest themselves by a pacing spike followed by an intrinsic QRS complex. Further, due to intrinsic detection latency, a stimulation pulse may be delivered after intrinsic activation has already begun (hereinafter referred to as pseudo-fusion). From a surface ECG, it is seen that the stimulation pulse falls inside the intrinsic QRS complex. The stimulation pulses may or may not capture the myocardium. During normal delivery of a stimulation pulse, fusion and/or pseudo-fusion beats may be of little consequence except some energy loss due to unnecessary pacing output. However, during autocapture or autothresholding, the impact of fusion or pseudo-fusion can be rather different.
During autocapture or autothreshold, fusion beats or noise may be detected as capture for amplitude-based detection methods. Thus, even though the stimulation pulse may be below threshold, the evoked response detection remains positive. As a result, the threshold may be identified at a lower amount than the actual threshold. Pseudo-fusion may be detected either as capture or non-capture depending upon timing of the occurrence of pseudo-fusion. If a stimulation pulse is delivered at an earlier portion of the QRS complex, then the stimulation pulse is more likely to be detected as capture and the consequence is the same as a fusion beat. If pseudo-fusion is detected as non-capture, a backup pulse may be issued between the QRS complex and a T wave which is undesirable.
During automatic threshold determination, pseudo-fusion beats may cause false detection of either capture or non-capture. When pseudo-fusion is detected as capture, an error in threshold measurement may arise. In many instances, occurrence of pseudo-fusion is caused by the inherent latency of sensing an intrinsic event. This latency often results from a sensing threshold level that is normally higher than front portions of the QRS complex of the endocardial signals, which prevents a detection by the rhythm management device of the front portions of the QRS complex. Other factors that may contribute to latency in intrinsic detection include sensing channel phase delay. Thus, there is a need for a method that reduces unnecessary autothresholding, error in threshold measurement, and other undesirable affects of fusion and pseudo-fusion during capture verification and autothreshold determination. There is a further need for a rhythm management device that manages the timing of delivery of backup stimulation that avoids stimulating during undesirable portions of a timing cycle.
Other factors, including afterpotential, affect the ability of a device to automatically set an accurate detection or sensing threshold. For example, the conventional pacemaker typically includes a pacing output circuit designed to selectively generate and deliver stimulus pulses through a lead to one or more electrodes positioned in the heart of a patient. The pacing output circuit includes a power supply, switches, a pacing charge storage capacitor, and a coupling capacitor, all of which cooperatively operate under the direction of a controller to perform a charging cycle, a pacing cycle, and a recharging cycle. The capacitance of the pacing charge storage capacitor typically ranges between 10-30 microfarads so as to develop a sufficient pacing charge for stimulating the heart. The capacitance of the coupling capacitor typically ranges between 15 to 40 microfarads with 33 microfarads being typical. A capacitor having a capacitance in this range was believed necessary to deliver sufficient energy to the heart.
The charging cycle involves manipulation of switches such that the pacing charge storage capacitor is charged up to a predetermined voltage level. The pacing cycle involves manipulating the switches such that the voltage within the pacing charge storage capacitor may be discharged through the coupling capacitor to the electrodes of the pacemaker. The recharging cycle involves further manipulation of the switches for a predetermined period of time following the pacing pulse to allow the coupling capacitor to be discharged.
While the conventional pacing circuit is generally effective in delivering stimulus pulses to a selected chamber of the heart, it has been found that the detection of evoked depolarization or capture verification is rendered very difficult due to polarization voltages or xe2x80x9cafterpotentialxe2x80x9d which develop at the heart tissue/electrode interface following the application of the stimulation pulses. The ability to verify capture is further affected by other variables including patient activity, body position, drugs being used, lead movement, noise etc.
In the past, the large capacitance of the coupling capacitor was believed necessary in order to sufficiently block any DC components from the heart and to minimize pace pulse voltage droop. However, the large capacitance of the coupling capacitor causes a charge dissipation or xe2x80x9cafterpotentialxe2x80x9d which is relatively large (100 mV or greater) and which decays exponentially over a relatively long period of time (100 milliseconds). This is particularly troublesome due to the fact that the evoked potential of the heart tissue is small in amplitude relative to the polarization voltage or xe2x80x9cafterpotentialxe2x80x9d (100 mV). The amplitude of the evoked potential corresponding to a P-wave typically ranges between 1-5 mV and the amplitude of the evoked potential corresponding to an R-wave typically ranges between 5-2 mV.
Further, the long decay period of the polarization voltage or xe2x80x9cafterpotentialxe2x80x9d effectively masks the evoked potential, which typically begins within approximately (10-40) milliseconds after the stimulation pulse to a selected chamber of the heart. It will be appreciated that this creates difficulty in detecting the evoked response of the heart following the delivery of stimulus pulses. In that evoked response is indicative of capture, the undesirable masking of the evoked response by xe2x80x9cafterpotentialxe2x80x9d thus hampers the ability of the pacemaker to conduct automatic capture verification. Hence, there is a need for a rhythm management device that decreases and/or shortens the pacing afterpotential with minimal increase of the leading edge voltage pacing threshold. It is also desirable to reduce the number or complexity of the implanted components and, thus, there is a need for a system having a stimulation/sensing circuit that minimizes the number of required electrodes positioned within the heart for sensing a response evoked by a stimulation pulse directed to a pre-selected chamber of the heart.
U.S. Pat. No. 4,686,988 to Sholder teaches the use of a separate sensing electrode connected to a detector for detecting P-waves in the presence of atrial stimulation pulses, wherein the P-wave detector has an input bandpass characteristic selected to pass frequencies that are associated with P-waves. U.S. Pat. No. 4,858,610 to Callaghan et al. teaches the use of charge dumping following delivery of the stimulation pulse to decrease lead polarization and also the use of separate pacing and sensing electrodes to eliminate the polarization problem on the sensing electrode. The techniques of the ""610 patent and ""988 patent, which involve using a separate electrode located at some distance from the stimulating electrode for the purpose of isolating the polarization voltages or xe2x80x9cafterpotentialxe2x80x9d are not completely desirable in that they require the additional cost and complexity of the additional sensing electrode.
U.S. Pat. No. 5,324,310 to Greeninger et al. teaches the use of the xe2x80x9cring-to-ringxe2x80x9d sensing with corresponding atrial and ventricular EGM amplifiers whose outputs are multiplied and compared to a predetermined threshold to determine capture. U.S. Pat. No. 5,486,201 to Canfield discloses an active discharge circuit having a switching device which sequentially and repeatedly couples a charge transfer capacitor to the coupling capacitor to transfer charge therebetween and thereby actively discharge the coupling capacitor. None of these devices reduce or shorten the pacing afterpotentials through the use of a simplified pacing output. The present invention addresses these and other needs that will become apparent to those skilled in the art.
Hence, there is a need for a cardiac rhythm management device that attenuates polarization voltages or xe2x80x9cafterpotentialsxe2x80x9d which develop at the heart tissue/electrode interface following the delivery of a stimulus to the heart tissue, and which minimizes the number of required components of the cardiac pacing system. There is a further need for a device that automatically adjust the detection threshold during a normal mode or an automatic capture verification mode. There is a still further need for a device capable of suspending the automatic capture verification mode and/or capable of adjusting the detection threshold dependent upon detected and/or measured noise, a determined amplitude of evoked response, a determined modulation in the evoked response, and detected and/or measured artifact.
The present invention provides for a cardiac rhythm management device capable of automatically detecting intrinsic and evoked response of a patient""s heart during a normal mode or capture verification mode. The implantable cardiac rhythm management device of the present invention generally includes a pulse generator that generates stimulation pulses, a controller having a timing circuit, sensing circuit and stimulation circuit for controlling activation of the pulse generator and delivery of the stimulation pulses, and an electrode lead arrangement electrically coupled to the controller. The rhythm management device further includes an adjustable detection threshold operable in a normal or autocapture verification mode, that may be adjusted or suspended dependant upon one or more of the following: detected and/or measured noise, a determined amplitude of evoked response, a determined modulation in the evoked response, and detected and/or measured artifact. The electrode lead arrangement of known suitable construction is positioned within the patient""s heart and is electrically coupled to the controller, wherein electrocardiogram signals are electrically conducted to the controller from the electrodes. The electrocardiogram signal includes electrical impulses corresponding to a cardiac depolarization and noise.
In an embodiment of the present invention, the controller detects an evoked response of the patient""s heart from the electrocardiogram signal, determines an amplitude associated with the evoked response, and adjusts the detection threshold dependent upon the determined amplitude. Further, the controller may determine a value associated with modulation of the evoked response, wherein the value is determined from the amplitude of a detected evoked response. Once the value associated with modulation is determined, the controller may adjust the detection threshold dependant upon the value associated with modulation. The value associated with modulation may be determined from a respiration modulation index and evoked response filter index.
In another embodiment of the present invention, the controller may also include a means for determining an amount associated with an artifact baseline of the electrocardiogram signal. In this embodiment the detection threshold is set greater than the amount associated with the artifact baseline and less than a minimum of maximum amplitudes of the evoked response over a predetermined number of beats. The minimum of maximum amplitudes of the evoked response is determined from the electrocardiogram signal as described below in greater detail.
The sensing circuit includes a sense amplifier electrically connected to the electrodes and controller in a manner wherein a polarity of an amplitude of the electrocardiogram signal corresponding to an evoked response is opposite a polarity of an amplitude of the electrocardiogram signal corresponding to afterpotential. Also, a positive pole of the sense amplifier is coupled to an indifferent contact, and a negative pole of the sense amplifier is coupled to the electrodes. The peaks associated with evoked response are thus distinguished from peaks related to afterpotential, thereby eliminating the need for peak to peak detection. The stimulation circuit may also include a coupling capacitor arrangement that reduces afterpotentials, wherein the coupling capacitor arrangement includes a capacitor having a capacitance less than 5 microfarads.
In another embodiment of the present invention, the sensing circuit includes a pre-amplifier electrically coupled to the electrodes, a first high pass coupling capacitor electrically coupled between the electrodes and the pre-amplifier, a blanking switch electrically coupled between the high pass coupling capacitor and the pre-amplifier, and a dedicated evoked response amplifier. Alternatively, the sensing circuit may include a first coupling capacitor operatively coupled to a second coupling capacitor, and a switching means for selectively coupling the second coupling capacitor in series with the first coupling capacitor so as to reduce the effective capacitance of the first and second coupling capacitor and thereby attenuate afterpotentials.
In still another embodiment of the rhythm management device of the present invention, the controller detects the presence of noise in the electrocardiogram signal. Further, the controller may determine a value associated with an amplitude of the detected noise. Once the value associated with an amplitude of the detected noise is determined, the controller may adjust the detection threshold dependant upon the value associated with the amplitude of the detected noise. The controller may also include a memory means for storing the determined value associated with an amplitude of noise over a plurality of detected cardiac depolarization, wherein the controller adjusts the sensing threshold dependant upon the determined value associated with an amplitude of noise corresponding to prior detected cardiac depolarization.
It is accordingly a principal object of the present invention to provide a rhythm management device that may automatically adjust the detection threshold on a beat by beat basis.
Another object of the present invention is to provide a rhythm management device capable of automatically adjusting the detection threshold during an automatic capture verification sequence.
A further object of the present invention is to provide a rhythm management device capable of suspending an autocapture sequence dependent upon detected and/or measured noise, a determined amplitude of evoked response, a determined modulation in the evoked response, or detected and/or measured artifact.
Still another object of the present invention is to provide a rhythm management device that automatically adjusts the detection threshold without iterating the detection threshold level.
Yet another object of the present invention is to provide a rhythm management device that reduces potential error in autocapture and autothreshold determination.
A further object of the present invention is to provide a rhythm management device that reduces the effects of afterpotentials during autocapture verification.
These and other objects and advantages of the present invention will become readily apparent to those skilled in the art from a review of the following detailed description of the preferred embodiment especially when considered in conjunction with the claims and accompanying drawings in which like numerals in the several views refer to corresponding parts.
USPTO Backgrounds
USPTO Backgrounds