Patent Publication Number: US-8121680-B2

Title: Subcutaneous cardiac stimulation device providing anti-tachycardia pacing therapy and method

Description:
CROSS-REFERENCE TO RELATED APPLICATIONS 
     This application is a continuation of U.S. patent application Ser. No. 10/937,756, titled “Subcutaneous Cardiac Stimulation Device Providing Anti-Tachycardia Pacing Therapy and Method,” filed Sep. 8, 2004 and now U.S. Pat. No. 7,386,342, which is related to U.S. patent application Ser. No. 10/937,623, titled “Subcutaneous Cardiac Stimulation Device Providing Anti-Tachycardia Pacing Therapy and Method,” filed Sep. 8, 2004 and now U.S. Pat. No. 7,277,755; and U.S. patent application Ser. No. 10/937,656, also titled “Subcutaneous Cardiac Stimulation Device Providing Anti-Tachycardia Pacing Therapy and Method,” filed Sep. 8, 2004 and now U.S. Pat. No. 7,260,433. 
    
    
     FIELD OF THE INVENTION 
     The present invention generally relates to a cardiac stimulation device that provides electrical therapy to a patient&#39;s heart. The present invention more particularly relates to a subcutaneous device that provides anti-tachycardia pacing therapy while minimizing the perception of pain. 
     BACKGROUND OF THE INVENTION 
     Implantable cardiac devices are well known in the art. They may take the form of implantable defibrillators or cardioverters which treat accelerated rhythms of the heart such as fibrillation or implantable pacemakers which maintain the heart rate above a prescribed limit, such as, for example, to treat a bradycardia. Implantable cardiac devices are also known which incorporate both a pacemaker and a defibrillator. 
     A pacemaker may be considered as a pacing system. The pacing system is comprised of two major components. One component is a pulse generator which generates the pacing stimulation pulses and includes the electronic circuitry and the power cell or battery. The other component is the lead, or leads, having electrodes which electrically couple the pacemaker to the heart. A lead may provide both unipolar and bipolar pacing and/or sensing electrode configurations. In the unipolar configuration, the pacing stimulation pulses are applied or evoked responses are sensed between a single electrode carried by the lead, in electrical contact with the desired heart chamber, and the pulse generator case. The electrode serves as the cathode (negative pole) and the case serves as the anode (positive pole). In the bipolar configuration, the pacing stimulation pulses are applied or evoked responses are sensed between a pair of closely spaced electrodes carried by the lead, in electrical contact with the desired heart chamber, one electrode serving as the anode and the other electrode serving as the cathode. 
     Pacemakers deliver pacing pulses to the heart to cause the stimulated heart chamber to contract when the patient&#39;s own intrinsic rhythm fails. To this end, pacemakers include sensing circuits that sense cardiac activity for the detection of intrinsic cardiac events such as intrinsic atrial events (P waves) and intrinsic ventricular events (R waves). By monitoring such P waves and/or R waves, the pacemaker circuits are able to determine the intrinsic rhythm of the heart and provide stimulation pacing pulses that force atrial and/or ventricular depolarizations at appropriate times in the cardiac cycle when required to help stabilize the electrical rhythm of the heart. 
     Pacemakers are described as single-chamber or dual-chamber systems. A single-chamber system stimulates and senses in one chamber of the heart (atrium or ventricle). A dual-chamber system stimulates and/or senses in both chambers of the heart (atrium and ventricle). Dual-chamber systems may typically be programmed to operate in either a dual-chamber mode or a single-chamber mode. 
     Subcutaneous cardiac stimulation devices are also known in the art. In these devices, the device enclosure may also be implanted beneath the skin of a patient. However, in these systems, the electrodes are not implanted within the heart. Rather, the electrodes may still be placed beneath the skin of the patient but external to the heart. 
     Subcutaneous cardiac devices are generally easier to implant. They are not generally relied on for providing long term pacing because the pacing efficiency of subcutaneous electrodes is low. In order to reliably pace, for example, stimulation pulse energies may be required which would rapidly deplete the battery of the device. Also of significance is the potential pain that may be caused by the required stimulation energies and electrode placement. However, subcutaneous cardiac stimulation devices may be advantageous for use in patients who do not require long term pacing, but who may have the potential to require sporadic cardiac stimulation therapy, such as for the abnormally high heart rate of an occasional tachyarrhythmia. Such conditions may be treated with anti-tachycardia pacing (ATP) to return the heart rate to a normal rate. Without such ATP, the heart rate may continue to accelerate into a more life threatening arrhythmia, such as ventricular fibrillation. 
     ATP is well known in the art. In such therapy, the heart is paced at a rate faster than the intrinsic rate. The heart beat is captured by the ATP and the pacing rate is gradually decreased to return the heart to a normal rate. 
     Even though subcutaneous cardiac stimulation devices are well suited for delivering ATP to a heart, the pain that such therapy may cause remains an issue. It is to this issue and the improved delivery of ATP with a subcutaneous cardiac stimulation device that the present invention more generally relates. 
     SUMMARY OF THE INVENTION 
     The invention provides an implantable subcutaneous cardiac device. The device comprises at least two subcutaneous electrodes adapted for placement external to a heart, and a pulse generator that delivers pacing pulses to the subcutaneous electrodes. The pacing pulses have a waveform devoid of any exponential voltage decay. 
     The invention further provides an implantable subcutaneous cardiac device comprising at least two subcutaneous electrodes adapted for placement external to a heart, and an arrhythmia detector that detects a sustained tachyarrhythmia of the heart. The device further comprises a pulse generator that delivers anti-tachycardia pacing pulses to the subcutaneous electrodes in response to detection of a sustained tachyarrhythmia. 
     The invention still further provides an implantable subcutaneous cardiac device comprising at least two subcutaneous electrodes adapted for placement external to a heart, a cardiac output monitor that monitors cardiac output, and an arrhythmia detector that detects a tachyarrhythmia of the heart. The device further comprises a pulse generator that delivers anti-tachycardia pacing pulses to the subcutaneous electrodes in response to detection of a tachyarrhythmia and a decrease in cardiac output. 
     The invention further provides a method comprising detecting a tachyarrhythmia of a heart with at least two subcutaneous electrodes external to the heart, and delivering anti-tachycardia pacing pulses to the subcutaneous electrodes. The pacing pulses having a waveform devoid of any exponential voltage decay. 
     The invention still further provides a method comprising detecting a sustained tachyarrhythmia of a heart with at least two subcutaneous electrodes external to the heart, and delivering anti-tachycardia pacing pulses to the subcutaneous electrodes responsive to detecting a sustained tachyarrhythmia. A sustained tachyarrhythmia may be a tachyarrhythmia accompanied by a decrease in cardiac output 
    
    
     
       BRIEF DESCRIPTION OF THE DRAWINGS 
       Further features and advantages of the present invention may be more readily understood by reference to the following description taken in conjunction with the accompanying drawings, in which: 
         FIG. 1  is a simplified diagram illustrating a fully implantable stimulation device and a subcutaneous device in association with a patient&#39;s heart to be treated in accordance with the present invention; 
         FIG. 2  is a functional block diagram of the fully implantable device taking the form of a multi-chamber implantable stimulation device capable of providing cardioversion, defibrillation and pacing stimulation in four chambers of the heart according to one embodiment of the invention; 
         FIG. 3  is a functional block diagram of the subcutaneous device according to one embodiment of the present invention; 
         FIG. 4  is a simplified schematic diagram of a pulse generator circuit according to an embodiment of the present invention; 
         FIG. 5  shows a waveform of a pacing pulse which may be provided by the circuit of  FIG. 4 ; 
         FIG. 6  is a simplified schematic diagram of another pulse generator circuit according to another embodiment of the present invention; 
         FIG. 7  is another waveform of a pacing pulse according to an embodiment of the invention; and 
         FIG. 8  is a flow chart describing an overview of the operation of one embodiment of the present invention. 
     
    
    
     DETAILED DESCRIPTION 
     The following description is of the best mode presently contemplated for practicing the invention. This description is not to be taken in a limiting sense but is made merely for the purpose of describing the general principles of the invention. The scope of the invention should be ascertained with reference to the issued claims. In the description of the invention that follows, like numerals or reference designators will be used to refer to like parts or elements throughout. 
     As shown in  FIG. 1 , there is a fully implantable stimulation device  10  in electrical communication with a patient&#39;s heart  12  by way of three leads,  20 ,  24  and  30 , suitable for delivering multi-chamber stimulation and shock therapy. To sense atrial cardiac signals and to provide right atrial chamber stimulation therapy, the stimulation device  10  is coupled to an implantable right atrial lead  20  having at least an atrial tip electrode  22 , which typically is implanted in the patient&#39;s right atrial appendage. 
     To sense left atrial and ventricular cardiac signals and to provide left chamber pacing therapy, the stimulation device  10  is coupled to a “coronary sinus” lead  24  designed for placement in the “coronary sinus region” via the coronary sinus ostium for positioning a distal electrode adjacent to the left ventricle and/or additional electrode(s) adjacent to the left atrium. As used herein, the phrase “coronary sinus region” refers to the vasculature of the left ventricle, including any portion of the coronary sinus, great cardiac vein, left marginal vein, left posterior ventricular vein, middle cardiac vein, and/or small cardiac vein or any other cardiac vein accessible by the coronary sinus. 
     Accordingly, an exemplary coronary sinus lead  24  is designed to receive atrial and ventricular cardiac signals and to deliver left ventricular pacing therapy using at least a left ventricular tip electrode  26 , left atrial pacing therapy using at least a left atrial ring electrode  27 , and shocking therapy using at least a left atrial coil electrode  28 . 
     The stimulation device  10  is also shown in electrical communication with the patient&#39;s heart  12  by way of an implantable right ventricular lead  30  having, in this embodiment, a right ventricular tip electrode  32 , a right ventricular ring electrode  34 , a right ventricular (RV) coil electrode  36 , and an SVC coil electrode  38 . Typically, the right ventricular lead  30  is transvenously inserted into the heart  12  so as to place the right ventricular tip electrode  32  in the right ventricular apex so that the RV coil electrode will be positioned in the right ventricle and the SVC coil electrode  38  will be positioned in the superior vena cava. Accordingly, the right ventricular lead  30  is capable of receiving cardiac signals, and delivering stimulation in the form of pacing and shock therapy to the right ventricle. 
     Also shown in  FIG. 1  is a subcutaneous cardiac stimulation device  120 . The device  120  includes an enclosure  122  which encloses the electronic circuitry of the device which will be described subsequently with reference to  FIG. 3 . The device  120  further includes electrodes  124  and  126 . The electrodes  124  and  126  and the enclosure  122  are carried on a common substrate  128 . The device  120  is a subcutaneous device because the electrodes  124  and  128  are placed beneath the skin of the patient but are external to the heart. The device  10 , on the other hand, is fully implantable because its electrodes are not only beneath the skin of the patient, but are also implanted within the heart. The device  10  itself may be placed subcutaneously or submuscular. 
     The subcutaneous electrodes  124  and  126  may take the form of small patch electrodes. They may be employed for sensing electrical activity of the heart, delivering pacing pulses to the heart, and, if need be, providing cardioverting or defibrillating shocks to the heart. 
       FIG. 1  illustrates that both the fully implantable device  10  and the subcutaneous device  120  may both be implanted within a patient. The device  10  may be implanted in the left chest as is common in the art and the device  120  may be implanted so as to be over the bottom ribs of the patient. As will be seen hereinafter, the devices  10  and  120  may coordinate their operating in providing therapy, such as ATP to the heart. However, as will also be seen, the device  120  alone may be provided with sufficient functionality to enable it to provide ATP solely on its own. 
     As illustrated in  FIG. 2 , a simplified block diagram is shown of the multi-chamber implantable stimulation device  10 , which is capable of treating both fast and slow arrhythmias with stimulation therapy, including cardioversion, defibrillation, and pacing stimulation. While a particular multi-chamber device is shown, this is for illustration purposes only, and one of skill in the art could readily duplicate, eliminate or disable the appropriate circuitry in any desired combination to provide a device capable of treating the appropriate chamber(s) with cardioversion, defibrillation and pacing stimulation. 
     The housing  40  for the stimulation device  10 , shown schematically in  FIG. 2 , is often referred to as the “can”, “case” or “case electrode” and may be programmably selected to act as the return electrode for all “unipolar” modes. The housing  40  may further be used as a return electrode alone or in combination with one or more of the coil electrodes,  28 ,  36  and  38 , for shocking purposes. The housing  40  further includes a connector (not shown) having a plurality of terminals,  42 ,  44 ,  46 ,  48 ,  52 ,  54 ,  56 , and  58  (shown schematically and, for convenience, the names of the electrodes to which they are connected are shown next to the terminals). As such, to achieve right atrial sensing and pacing, the connector includes at least a right atrial tip terminal (A R  TIP)  42  adapted for connection to the atrial tip electrode  22 . 
     To achieve left chamber sensing, pacing and shocking, the connector includes at least a left ventricular tip terminal (V L  TIP)  44 , a left atrial ring terminal (A L  RING)  46 , and a left atrial shocking terminal (A L  COIL)  48 , which are adapted for connection to the left ventricular ring electrode  26 , the left atrial tip electrode  27 , and the left atrial coil electrode  28 , respectively. 
     To support right chamber sensing, pacing and shocking, the connector further includes a right ventricular tip terminal (V R  TIP)  52 , a right ventricular ring terminal (V R  RING)  54 , a right ventricular shocking terminal (R V  COIL)  56 , and an SVC shocking terminal (SVC COIL)  58 , which are adapted for connection to the right ventricular tip electrode  32 , right ventricular ring electrode  34 , the RV coil electrode  36 , and the SVC coil electrode  38 , respectively. 
     At the core of the stimulation device  10  is a programmable microcontroller  60  which controls the various modes of stimulation therapy. As is well known in the art, the microcontroller  60  typically includes a microprocessor, or equivalent control circuitry, designed specifically for controlling the delivery of stimulation therapy and may further include RAM or ROM memory, logic and timing circuitry, state machine circuitry, and I/O circuitry. Typically, the microcontroller  60  includes the ability to process or monitor input signals (data) as controlled by a program code stored in a designated block of memory. The details of the design and operation of the microcontroller  60  are not critical to the present invention. Rather, any suitable microcontroller  60  may be used that carries out the functions described herein. The use of microprocessor-based control circuits for performing timing and data analysis functions are well known in the art. 
     As shown in  FIG. 2 , an atrial pulse generator  70  and a ventricular pulse generator  72  generate pacing stimulation pulses for delivery by the right atrial lead  20 , the right ventricular lead  30 , and/or the coronary sinus lead  24  via an electrode configuration switch  74 . It is understood that in order to provide stimulation therapy in each of the four chambers of the heart, the atrial and ventricular pulse generators,  70  and  72 , may include dedicated, independent pulse generators, multiplexed pulse generators, or shared pulse generators. The pulse generators,  70  and  72 , are controlled by the microcontroller  60  via appropriate control signals,  76  and  78 , respectively, to trigger or inhibit the stimulation pulses. 
     The microcontroller  60  further includes timing control circuitry  79  which is used to control the timing of such stimulation pulses (e.g., pacing rate, atrio-ventricular (AV) delay, atrial interconduction (A-A) delay, or ventricular interconduction (V-V) delay, etc.) as well as to keep track of the timing of refractory periods, blanking intervals, noise detection windows, evoked response windows, alert intervals, marker channel timing, etc., which is well known in the art. 
     The switch  74  includes a plurality of switches for connecting the desired electrodes to the appropriate I/O circuits, thereby providing complete electrode programmability. Accordingly, the switch  74 , in response to a control signal  80  from the microcontroller  60 , determines the polarity of the stimulation pulses (e.g., unipolar, bipolar, combipolar, etc.) by selectively closing the appropriate combination of switches (not shown) as is known in the art. 
     Atrial sensing circuits  82  and ventricular sensing circuits  84  may also be selectively coupled to the right atrial lead  20 , coronary sinus lead  24 , and the right ventricular lead  30 , through the switch  74  for detecting the presence of cardiac activity in each of the four chambers of the heart. Accordingly, the atrial (ATR. SENSE) and ventricular (VTR. SENSE) sensing circuits,  82  and  84 , may include dedicated sense amplifiers, multiplexed amplifiers, or shared amplifiers. The switch  74  determines the “sensing polarity” of the cardiac signal by selectively closing the appropriate switches, as is also known in the art. In this way, the clinician may program the sensing polarity independent of the stimulation polarity. 
     Each sensing circuit,  82  and  84 , preferably employs one or more low power, precision amplifiers with programmable gain and/or automatic gain control, bandpass filtering, and a threshold detection circuit, as known in the art, to selectively sense the cardiac signal of interest. The automatic gain control enables the device  10  to deal effectively with the difficult problem of sensing the low amplitude signal characteristics of atrial or ventricular fibrillation. The outputs of the atrial and ventricular sensing circuits,  82  and  84 , are connected to the microcontroller  60  which, in turn, are able to trigger or inhibit the atrial and ventricular pulse generators,  70  and  72 , respectively, in a demand fashion in response to the absence or presence of cardiac activity in the appropriate chambers of the heart. 
     For arrhythmia detection, the device  10  utilizes the atrial and ventricular sensing circuits,  82  and  84 , to sense cardiac signals to determine whether a rhythm is physiologic or pathologic. As used herein “sensing” is reserved for the noting of an electrical signal, and “detection” is the processing of these sensed signals and noting the presence of an arrhythmia. The timing intervals between sensed events (e.g., P-waves, R-waves, and depolarization signals associated with fibrillation which are sometimes referred to as “F-waves” or “Fib-waves”) are then classified by the microcontroller  60  by comparing them to a predefined rate zone limit (i.e., bradycardia, normal, low rate VT, high rate VT, and fibrillation rate zones) and various other characteristics (e.g., sudden onset, stability, physiologic sensors, and morphology, etc.) in order to determine the type of remedial therapy that is needed (e.g., bradycardia pacing, anti-tachycardia pacing, cardioversion shocks or defibrillation shocks, collectively referred to as “tiered therapy”). 
     Cardiac signals are also applied to the inputs of an analog-to-digital (A/D) data acquisition system  90 . The data acquisition system  90  is configured to acquire intracardiac electrogram signals, convert the raw analog data into a digital signal, and store the digital signals for later processing and/or telemetric transmission to an external device  102 . The data acquisition system  90  is coupled to the right atrial lead  20 , the coronary sinus lead  24 , and the right ventricular lead  30  through the switch  74  to sample cardiac signals across any pair of desired electrodes. 
     Advantageously, the data acquisition system  90  may be coupled to the microcontroller, or other detection circuitry, for detecting an evoked response from the heart  12  in response to an applied stimulus, thereby aiding in the detection of “capture.” Capture occurs when an electrical stimulus applied to the heart is of sufficient energy to depolarize the cardiac tissue, thereby causing the heart muscle to contract. The microcontroller  60  detects a depolarization signal during a window following a stimulation pulse, the presence of which indicates that capture has occurred. The microcontroller  60  enables capture detection by triggering the ventricular pulse generator  72  to generate a stimulation pulse, starting a capture detection window using the timing control circuitry  79  within the microcontroller  60 , and enabling the data acquisition system  90  via control signal  92  to sample the cardiac signal that falls in the capture detection window and, based on the amplitude, determines if capture has occurred. 
     Capture detection may occur on a beat-by-beat basis or on a sampled basis. Preferably, a capture threshold search is performed once a day during at least the acute phase (e.g., the first 30 days) and less frequently thereafter. A capture threshold search would begin at a desired starting point (either a high energy level or the level at which capture is currently occurring) and decrease the energy level until capture is lost. The value at which capture is lost is known as the capture threshold. Thereafter, a safety margin is added to the capture threshold. 
     The microcontroller  60  is further coupled to a memory  94  by a suitable data/address bus  96 , wherein the programmable operating parameters used by the microcontroller  60  are stored and modified, as required, in order to customize the operation of the stimulation device  10  to suit the needs of a particular patient. Such operating parameters define, for example, pacing pulse amplitude, pulse duration, electrode polarity, rate, sensitivity, automatic features, arrhythmia detection criteria, and the amplitude, waveshape and vector of each shocking pulse to be delivered to the patient&#39;s heart  12  within each respective tier of therapy. 
     Advantageously, the operating parameters of the implantable device  10  may be non-invasively programmed into the memory  94  through a telemetry circuit  100  in telemetric communication with the external device  102 , such as a programmer, transtelephonic transceiver, or a diagnostic system analyzer. The telemetry circuit  100  is activated by the microcontroller by a control signal  106 . The telemetry circuit  100  advantageously allows intracardiac electrograms and status information relating to the operation of the device  10  (as contained in the microcontroller  60  or memory  94 ) to be sent to the external device  102  through an established communication link  104 . The telemetry circuit  100  may also be employed to support communication with the subcutaneous device  120 . Through such communication, coordination between the devices in providing desired therapy may be maintained. Such coordination will be described subsequently. 
     In the preferred embodiment, the stimulation device  10  further includes a physiologic sensor  108 , commonly referred to as a “rate-responsive” sensor because it is typically used to adjust pacing stimulation rate according to the exercise state of the patient. However, the physiological sensor  108  may further be used to detect changes in cardiac output, changes in the physiological condition of the heart, or diurnal changes in activity (e.g., detecting sleep and wake states). Accordingly, the microcontroller  60  responds by adjusting the various pacing parameters (such as rate, AV Delay, V-V Delay, etc.) at which the atrial and ventricular pulse generators,  70  and  72 , generate stimulation pulses. 
     The stimulation device additionally includes a battery  110  which provides operating power to all of the circuits shown in  FIG. 2 . For the stimulation device  10 , which employs shocking therapy, the battery  110  must be capable of operating at low current drains for long periods of time, and then be capable of providing high-current pulses (for capacitor charging) when the patient requires a shock pulse. The battery  110  must also have a predictable discharge characteristic so that elective replacement time can be detected. Accordingly, the device  10  may employ lithium/silver vanadium oxide batteries. 
     As further shown in  FIG. 2 , the device  10  is shown as having an impedance measuring circuit  112  which is enabled by the microcontroller  60  via a control signal  114 . The impedance measuring circuit  112  is not critical to the present invention and is shown for only completeness. 
     As will be seen hereinafter, the subcutaneous device  120  is fully capable of providing cardioverting/defibrillating therapy to the heart on its own. Hence, it is not necessary for the fully implantable device  10  to also provide such therapy. However, in the case where the stimulation device  10  is also intended to operate as an implantable cardioverter/defibrillator (ICD) device, it is preferable that it be able to detect the occurrence of an arrhythmia, and automatically apply an appropriate electrical shock therapy to the heart aimed at terminating the detected arrhythmia. To this end, the microcontroller  60  may further control a shocking circuit  116  by way of a control signal  118 . The shocking circuit  116  generates shocking pulses of low (up to 0.5 joules), moderate (0.5-10 joules), or high energy (11 to 40 joules), as controlled by the microcontroller  60 . Such shocking pulses are applied to the patient&#39;s heart  12  through at least two shocking electrodes, and as shown in this embodiment, selected from the left atrial coil electrode  28 , the RV coil electrode  36 , and/or the SVC coil electrode  38 . As noted above, the housing  40  may act as an active electrode in combination with the RV electrode  36 , or as part of a split electrical vector using the SVC coil electrode  38  or the left atrial coil electrode  28  (i.e., using the RV electrode as a common electrode). 
     Cardioversion shocks are generally considered to be of low to moderate energy level (so as to minimize pain felt by the patient), and/or synchronized with an R-wave and/or pertaining to the treatment of tachycardia. Defibrillation shocks are generally of moderate to high energy level (i.e., corresponding to thresholds in the range of 5-40 joules), delivered asynchronously (since R-waves may be too disorganized), and pertaining exclusively to the treatment of fibrillation. Accordingly, the microcontroller  60  is capable of controlling the synchronous or asynchronous delivery of the shocking pulses. 
     Referring now to  FIG. 3 , it is a simplified block diagram of the circuitry of the subcutaneous device  120 , which may be enclosed within the enclosure  122 . 
     The enclosure or case  122  for the stimulation device circuitry is shown schematically in  FIG. 3  and may be conductive and programmably selected to act as the return electrode for “unipolar” pacing modes when desired. The enclosure  122  may further be used as a return electrode alone or in combination with one or more of the electrodes  124  and  128  for cardioversion or defibrillation purposes. The enclosure further includes a connector (not shown) having terminals  144  and  146  for connection to electrodes  124  and  126  respectively. 
     Also at the core of the subcutaneous stimulation device  120  is a programmable microcontroller  160  which controls the stimulation therapy. The microcontroller  160  typically includes a microprocessor, or equivalent control circuitry, designed specifically for controlling the delivery of stimulation therapy and may further include RAM or ROM memory, logic and timing circuitry, state machine circuitry, and I/O circuitry. Typically, the microcontroller  160  includes the ability to process or monitor input signals (data) as controlled by a program code stored in a designated block of memory. The details of the design and operation of the microcontroller  160  are not critical to the present invention. Rather, any suitable microcontroller  160  may be used that carries out the functions described herein. The use of microprocessor-based control circuits for performing timing and data analysis functions are well known in the art. 
     As further shown in  FIG. 3 , a pulse generator  170  generates anti-tachycardia pacing stimulation pulses for delivery by one or more of electrodes  122 ,  124 , and  126  via an electrode configuration switch  174 . The microcontroller  60  further includes timing control circuitry  179  which is used to control the timing of such stimulation pulses. 
     The switch  174  includes a plurality of switches for connecting the desired electrodes to the appropriate I/O circuits. The switch  174  operates in response to a control signal  180  from the microcontroller  160  for making the desired electrode connections. 
     A sensing circuit  182  may also be selectively coupled to desired ones of the electrodes through the switch  174  for detecting the presence of cardiac activity. It may include dedicated sense amplifiers, multiplexed amplifiers, or shared amplifiers. 
     The sensing circuit  182  preferably employs one or more low power, precision amplifiers with programmable gain and/or automatic gain control, bandpass filtering, and a threshold detection circuit, as known in the art, to selectively sense the cardiac signal of interest. The automatic gain control thus enables the device  120  to reliably sense the ventricular cardiac activity to support detection of tachycardia and fibrillation. The output of the sensing circuit  182  is connected to the microcontroller  160 . 
     The device  120  includes an arrhythmia detector  175  that utilizes the sensing circuit  182  to sense cardiac signals to determine whether a rhythm is physiologic or pathologic. Again, as used herein “sensing” is reserved for the noting of an electrical signal, and “detection” is the processing of these sensed signals and noting the presence of an arrhythmia. The timing intervals between sensed events are then classified by the microcontroller  160  by comparing them to predefined rate zone limits and various other characteristics including cardiac output in order to determine the presence of a sustained tachycardia, or fibrillation requiring anti-tachycardia pacing or cardioversion shocks or defibrillation shocks. 
     In accordance with this embodiment, the device  120  provides ATP therapy much later than a standard fully implantable device. For example, the device  120  may provide ATP therapy responsive to a sustained tachycardia characterized by tachycardia detection accompanied with a decrease in cardiac output instead of providing ATP upon the first detection of tachycardia. 
     Cardiac signals are also applied to the inputs of an analog-to-digital (A/D) data acquisition system  190 . The data acquisition system  190  is configured to acquire intracardiac electrogram signals, convert the raw analog data into a digital signal, and store the digital signals for later processing and/or telemetric transmission to an external device  202 . The data acquisition system  190  may be coupled through the switch  174  to sample cardiac signals across any pair of desired electrodes. 
     Advantageously, and in accordance with this embodiment, the data acquisition system  90  is coupled to the microcontroller for detecting an evoked response from the heart  12  in response to an applied ATP stimulus for detection of capture. The microcontroller  160  detects a depolarization signal during a window following an ATP stimulation pulse, the presence of which indicates that capture has occurred. The microcontroller  160  enables capture detection when the pulse generator  172  generates an ATP stimulation pulse. This starts a capture detection window using the timing control circuitry  79  within the microcontroller  60 , and enables the data acquisition system  190  to sample the cardiac signal that falls in the capture detection window and, based on the amplitude, determines if capture has occurred. Capture detection may occur on a beat-by-beat basis or on a sampled basis. If an evoked response is not detected, the pulse generator output is preferably increased. 
     The microcontroller  160  is further coupled to a memory  194  by a suitable data/address bus  196 , wherein the programmable operating parameters used by the microcontroller  60  are stored and modified, as required, in order to customize the operation of the subcutaneous stimulation device  120  to suit the needs of a particular patient. Such operating parameters define, for example, pacing pulse amplitude, pulse duration, electrode polarity, rate, sensitivity, automatic features, arrhythmia detection criteria, and the amplitude, waveshape and vector of each shocking pulse to be delivered to the patient&#39;s heart. 
     Advantageously, the operating parameters of the implantable device  10  may be non-invasively programmed into the memory  194  through a telemetry circuit  200  in telemetric communication with the external device  202 , such as a programmer, transtelephonic transceiver, or a diagnostic system analyzer. The telemetry circuit  200  is activated by the microcontroller by a control signal  206 . The telemetry circuit  200  advantageously allows intracardiac electrograms and status information relating to the operation of the device  120  (as contained in the microcontroller  60  or memory  94 ) to be sent to the external device  202  through an established communication link  204 . 
     In accordance with this embodiment, the telemetry circuit  200  may also be used for coordinating ATP therapy with a fully implanted device, such as device  10  of  FIG. 1 . In this regard, the telemetry circuit  200  may send a command to the fully implanted device to administer ATP therapy first before initiating therapy on its own. Hence, if the device  120  is informed by the fully implanted device  10  that it was unsuccessful at terminating the tachycardia, the subcutaneous device  120  may then take the therapy over and administer its ATP therapy. 
     Of course, the arrhythmia detector  175  of the subcutaneous device  120  could determine the success or failure of the implanted device  10  through its own arrhythmia detector  175 . 
     Before the device  120  delivers ATP therapy, in accordance with this embodiment, it may administer electrical nerve stimulation such as that used in transcutaneous electrical nerve stimulation (TENS) to first treat the patient for possible pain caused by the ATP therapy. The electrical nerve stimulation (ENS) may be delivered from the pulse generator  172  to the electrodes  124  and  126  in the form of, for example, 5 to 10 volt pulses at 100 Hz. TENS is well known in the art. 
     In the preferred embodiment, the subcutaneous device  120  further includes a physiologic sensor  208 , commonly referred to as a “rate-responsive” sensor. However, the physiological sensor  208  may be used to advantage in this embodiment to detect changes in cardiac output to support detection of a sustain tachycardia. 
     The subcutaneous device  120  additionally includes a battery  210  which provides operating power to all of the circuits shown in  FIG. 3 . The battery may again be lithium/silver vanadium oxide batteries. 
     Further in accordance with this embodiment, the device  120  is shown as having an impedance measuring circuit  212  which is enabled by the microcontroller  60  via a control signal  214 . The impedance measuring circuit  212  may be used to advantage as an alternative measure in monitoring cardiac output. The impedance measuring circuit  212  is coupled to the switch  174  for selective coupling to electrodes  122 ,  124 , and  126 . 
     When the subcutaneous device  120  is called upon to operate as an implantable cardioverter/defibrillator (ICD) device, it must detect the occurrence of an arrhythmia, and automatically apply an appropriate electrical shock therapy to the heart aimed at terminating the detected arrhythmia. To this end, the microcontroller  60  further controls a shocking circuit  216  by way of a control signal  218 . The shocking circuit  216  generates shocking pulses of between 200 and 2,000 volts and more preferably between 500 and 1,000 volts for cardioversion/defibrillation. As used herein cardioversion is meant to be generic for both cardioversion and fibrillation. The shocking pulses are applied to the patient&#39;s heart  12  through at least two of the electrodes  122 ,  124 , and  126 . 
     Cardioversion shocks are provided if an ATP therapy is found to be unsuccessful. Additional tachyarrhythmia criteria may be imposed before a cardioversion shock is delivered. 
     Referring now to  FIG. 4 , it illustrates a schematic circuit diagram of a pulse generator  220  which may be used in pulse generator  170  for providing the ATP according to this embodiment of the present invention. The pulse generator  220  includes a filter  222  including an inductor  224  and a capacitor  226 . The push-pull arrangement  232  of transistors  228  and  230  delivers a chopped full amplitude signal to the filter  222  formed by inductor  224  and capacitor  226 . Representative chopping frequencies may be, for example, in the range of 5 to 20 kHz, but frequencies in the range of 1 to 300 kHz may also be used as well. 
     The filter  222  is coupled to an output H-bridge circuit  234  which is formed by solid state switches  236 ,  238 ,  240 , and  242 . The common junction of switches  236  and  240  form a first output terminal  244  and the common junction of switches  238  and  242  forms another output terminal  246 . 
     The output H-bridge  234  will deliver a negative version of the signal coming out of filter  222  by turning on switches  238  and  240 . A positive version of the signal coming out of the filter  222  is provided with the turning on of switches  236  and  242 . The switches  236 ,  238 ,  240 , and  242  may, for example, be FET transistors, as are known in the art. 
     The pulse generator  220  may be utilized for delivering ATP pulses to the electrodes  124  and  126 , for example, for treating tachycardia with minimum pain. 
       FIG. 5  illustrates a pacing pulse  250  provided by the pulse generator  220  of  FIG. 4  according to this embodiment of the present invention. The pacing pulse  250  has a generally rounded waveform  252  which, by virtue of the H-bridge  234 , includes a first phase  254  and a second phase  256 . As will be noted in  FIG. 5 , the waveform  252  is rounded in both the first phase  254  and the second phase  256  by virtue of the filter  222  of the pulse generator  220  and hence, is devoid of any exponential voltage decay. The first or positive phase  254  is fairly wide having a width, of, for example, 3 milliseconds. The rounded and very wide waveform of the first phase  254  will reduce nerve stimulation as nerves have a higher frequency response than do cardiac cells. 
     The second or negative phase  256  of the waveform  252  has about half of the voltage of the first or positive phase  254 . The width of the second phase  256  is also about twice the width of the first phase  254 . 
       FIG. 6  is a simplified schematic diagram of another pulse generator  260  according to a further embodiment of the present invention. The pulse generator  260  includes a filter  262  including an inductor  264  and a capacitor  266 . The filter  262  is within an H-bridge  268  formed by solid state switches  270 ,  272 ,  274 , and  276 . Again, the solid state switches  270 ,  272 ,  274 , and  276  may be field effect transistors as known in the art. 
     The common junction of inductor  264  and capacitor  266  forms a first output terminal  278 . The common junction of switches  272  and  276  forms the other output terminal  280 . 
     Here, all of the waveform chopping is done within the bridge  268 . Rather than having separate transistors perform the chopping function, and then have the H-bridge provide polarity inversion, the pulse generator  260  of  FIG. 6  performs the waveform chopping by pulsing of the appropriate switches  270 ,  272 ,  274 , and  276 . This is then followed by the filtering effect of inductor  264  and capacitor  266  which are in parallel with the pacing electrodes. 
     Hence, the pulse generator  260  of  FIG. 6  is capable of providing an output pacing pulse having a rounded waveform similar to that shown in  FIG. 5 . With appropriate control of switches  270 ,  272 ,  274 , and  276 , an output waveform having a rounded positive first phase and a rounded negative second phase, such as that shown in  FIG. 5 , may be provided to prevent nerve stimulation and thus pain. 
       FIG. 7  shows another pacing waveform  290  which may be employed to advantage in accordance with another embodiment of the present invention. The waveform  290  has been referred to as a plateau waveform and is fully described in copending application Ser. No. 10/855,840, filed May 26, 2004, titled “System and Method for Reducing Pain Associated with Cardioversion Shocks Generated by Implantable Cardiac Stimulation Devices,” which is incorporated herein in its entirety by reference. The waveform  290  is biphasic and has a first phase  292  and a second phase  294 . The first phase  292  is longer in duration than the second phase  294 . The first phase  292  may have a duration of, for example, 10 milliseconds, as illustrated, but its duration may be in a range of, for example, 8 milliseconds to 12 milliseconds. The second phase  294  may have a duration of 5 milliseconds, as illustrated, but its duration may be in a range, for example, of 5 milliseconds to 8 milliseconds. The first phase  292  of the waveform  290  has a substantially constant or clamped positive amplitude  296  of, for example, 10 volts to 50 volts. The second phase  294  of the waveform  290  has a substantially constant or clamped negative amplitude  298  of, for example, 2 volts to 4 volts. It may be noticed in  FIG. 7  that that waveform  290  is devoid of any exponential voltage decay characteristic of standard capacitive discharge waveforms. The waveform  290  has been found to substantially reduce the perception of pain when used to stimulate the heart as compared to standard capacitive discharge waveforms. Alternatively, the negative portion  294  of waveform  290  may be deleted as some arrhythmias appear to be better treated by monophasic instead of biphasic shocks. 
     In  FIG. 8 , a flowchart  300  is shown describing an overview of the operation and novel features implemented in one embodiment of the subcutaneous device  120 . In this flowchart, the various algorithmic steps are summarized in individual “blocks.” Such blocks describe specific actions or decisions that must be made or carried out as the algorithm proceeds. Where a microcontroller (or equivalent) is employed, the flowchart presented herein provides the basis for a “control program” that may be used by such a microcontroller (or equivalent) to effectuate the desired control of the stimulation device. Those skilled in the art may readily write such a control program based on the flow chart and other descriptions presented herein. 
     The process of the flowchart  300  initiates with a decision block  302 . In decision block  302  it is decided if ATP therapy is required. To implement decision block  302 , the arrhythmia detector  175  of the device  120  may utilize the electrogram generated by the sensing circuit  182  to determine if a ventricular tachycardia is present. The arrhythmia detector  175  may determine that therapy is required upon the onset of a detected ventricular tachycardia. Alternatively, the arrhythmia detector  175  may also condition the requirement for therapy upon evidence of a sustained ventricular tachycardia. In accordance with this alternative, the arrhythmia detector  175  may call upon the impedance measuring circuit  212 , for example, to monitor for a decrease in cardiac output. Upon the detected ventricular tachycardia accompanied by a decrease in cardiac output, the arrhythmia detector  175  may declare a sustained ventricular tachycardia in need of therapy. 
     As an alternative to utilizing the impedance measuring circuit  212  for monitoring cardiac output, the arrhythmia detector  175  may call upon the physiologic sensor  208 . The use of physiologic sensors for determining changes in cardiac output is well known in the art. 
     If therapy is not required, the process returns as illustrated. However, if therapy is needed in accordance with decision block  302 , the process immediately advances to activity block  304  wherein the telemetry circuit  200  of the subcutaneous device  120  is utilized to communicate a command to the fully implanted device  10  to begin ATP therapy. The telemetry signal used may be a traditional radio frequency (RF) signal, an inductive signal, Galvanic signal or an acoustic signal. After the device  10  has delivered its ATP therapy, the process advances to decision block  306  to determine if the fully implanted device  10  was successful in terminating the ventricular tachycardia. If the device  10  was successful, the process returns. However, if the fully implanted device  10  was not successful in terminating the ventricular tachycardia, the process advances as described subsequently. 
     As an alternative to having the arrhythmia detector  175  determine if the fully implanted device  10  was successful in terminating the ventricular tachycardia, the fully implanted device  10  may make that determination on its own. Once the fully implanted device  10  has determined if it was successful, it would then communicate through its telemetry circuit  100  to the telemetry circuit  200  of the subcutaneous device  120  the status of the detected ventricular tachycardia. If the device  10  is successful in terminating the ventricular tachycardia, the message of success received by the telemetry circuit of the subcutaneous device  120  will cause the process of flowchart  300  to return. However, if the message from the implanted device  10  indicates that its efforts were unsuccessful, the subcutaneous device  120  will respond as indicated in flowchart  300  by advancing to activity block  308 . 
     In activity block  308 , the subcutaneous device  120  delivers electric nerve stimulation (ENS). In carrying out activity block  308 , the subcutaneous device  120  may utilize its pulse generator  170  to provide electrical pulses to subcutaneous electrodes  124  and  128  for delivering the electrical nerve stimulation therapy. As previously mentioned, the electrical nerve stimulation therapy may be used to block pain and may take the form of electrical pulses at a rate of 100 Hz with amplitudes of 5 volts to 10 volts. 
     After the subcutaneous device  120  has delivered the electrical nerve stimulation therapy, the process then advances to activity block  310  wherein the subcutaneous device  120  delivers its ATP therapy. During delivery of the ATP therapy, as illustrated by the decision block  312 , the subcutaneous device  120  continuously detects for evoked responses to the pacing pulses of the ATP therapy being delivered by the pulse generator  170  of the subcutaneous device  120 . If there is a failure to detect evoked responses, the process advances to activity block  314  wherein the output of the pacing pulses is increased. Hence, if there is a failure to capture the heart during the ATP therapy, the output of the pacing pulses is increased until the heart is captured. 
     When the ATP therapy is completed, the process then advances to decision block  316  where it is determined if the ATP therapy was successful. If the ATP therapy was successful, the process returns. If the ATP therapy delivered by the subcutaneous device  120  is not successful in not terminating the ventricular tachycardia, the process then advances to activity block  318  to apply a cardioverting or defibrillating shock to electrodes  124  and  128 . Once the cardioverting or defibrillating shock is applied to the heart, the process returns. 
     Instead of the subcutaneous device  120  delivering the cardioverting or defibrillating shock, it may alternatively communicate a command through its telemetry circuit  200  to the implanted device  10  to cause it to deliver the cardioverting or defibrillating shock using its implanted shock electrodes. The subcutaneous device  120  may either detect the delivery of the cardioverting or defibrillating shock by the fully implanted device  10  or wait until it receives a communication from the device  10  through its telemetry circuitry before causing the process of flowchart  300  to return. Of course, if the patient does not have a fully implanted device as, for example, device  10 , requiring the subcutaneous device  120  to operate on its own, it will of course perform the electrical nerves stimulation and ATP therapy immediately upon determining that therapy is needed and will also apply the cardioverting or defibrillating shock if its ATP therapy is unsuccessful in terminating the ventricular tachycardia. 
     While the invention has been described by means of specific embodiments and applications thereof, it is understood that numerous modifications and variations could be made thereto by those skilled in the art without departing from the spirit and scope of the invention. It is therefore to be understood that within the scope of the claims, the invention may be practiced otherwise than as specifically described herein.