METHOD AND APPARATUS FOR REDUCTION OF PAIN FROM ELECTRIC STIMULATION THERAPIES

Abstract: A method and apparatus that pretreat a patient prior to each therapeutic painful stimulus in a series of therapeutic painful stimuli, comprising the application of pain inhibiting stimuli to the patient prior to the application of each therapeutic painful stimulus in the series. Applying pain inhibiting stimuli comprises the steps of sensing a need for a next therapeutic painful stimulus in a series, preparing to deliver the pain inhibiting stimuli to the patient prior to applying the next therapeutic painful stimulus, and delivering the pain inhibiting stimuli to the patient prior to applying the next therapeutic painful stimulus. The method and apparatus are embodied in modern, noninvasive, transcutaneous or transesophageal pacing devices, either as stand-alone cardiac pacemakers, combination pacemaker-ECG monitors, or combination pacemaker-monitor-defibrillators. The pain inhibiting prepulse method is intended primarily for use in conscious patients but may also be used in sleeping patients.

Description: METHOD AND APPARATUS FOR REDUCTION OF PAIN FROM ELECTRIC STIMULATION THERAPIES BACKGROUND OF THE INVENTION 1. Field of the Invention. This invention relates generally to therapeutic painful stimuli such as electric pacing and subthreshold pulses, and more particularly to the process of reducing the pain associated with these therapeutic painful stimuli by modifying a patient's pain perception and response using prepulse inhibition (PPI). Specifically, the present in¬ vention relates to reducing the pain and discomfort associated with painful transcuta- neous and transesophageal cardiac pacing and subthreshold transcutaneous stimuli as provided using modern, noninvasive, transcutaneous or transesophageal pacing de- vices, either as stand — alone cardiac pacemakers, combination pacemaker — ECG monitors, or combination pacemaker — monitor — defibrillators. 2. Background Information. Implantable cardioverter-defibrillators (ICDs) deliver high-voltage electrical pulses (shocks) to terminate cardiac arrhythmias. This treatment is highly successful, but it is severely painful and may even stun a patient temporarily. Initially, painful and startling therapeutic shocks were considered acceptable only as a treatment of last resort. Because of this, ICD therapy was restricted to ventricular arrhythmias which were both life-threatening and refractory to all other therapies. Subsequently, how- ever, ICDs have become first-line therapy for patients with a history of life- threatening ventricular arrhythmias and patients at risk for life-threatening ventricular arrhythmias. Controlled studies have shown that ICDs are superior to alternative therapy for specific groups of these patients. These studies are the Multicenter Auto- matic Defibrillator Implantation Trial (Moss et al, N Engl J Med 1996; 335: 1933- 1940) and the Antiarrythmics Versus Implantable Defibrillators Trial (Zipes et al, N Engl J Med 1997; 337: 1576-1583). As ICD therapy has been applied to larger numbers of patients with ventricular arrhythmias, more attention has been paid to the painful and startling nature ofthe therapeutic shocks and the psychological complications of this therapy. These factors limit patient acceptance of ICD treatment of arrhythmias in conscious patients. A sig¬ nificant fraction of patients report anxiety and fear of painful ICD shocks ((1) Dough¬ erty, Psychological reactions and family adjustment in shock versus no shock groups after implantation of internal cardioverter defibrillator, Heart Lung 1995; 24: 281-291 — (2) Dunbar et al, Cognitive therapy for ventricular dysrhythmia patients, J Cardio- vasc Nursing 1997; 12: 33-44 — (3) Luderitz et al, Patient acceptance of ICD devices: Changing attitudes, Am Heart J 1994; 127: 1179-1184 — (4) Morris et al, Psychiatric morbidity following implantation ofthe automatic ICD, Psychosomatics 1991; 32: 58-64). Shocks correlate with anxiety, psychiatric morbidity and psychological dis- tress in ICD recipients. In one study 87.5% of patients experienced "nervousness" after a shock and 12.5% experienced "terror" or "fear." Patients who have experi¬ enced large numbers of repetitive shocks frequently suffer from a form of post- traumatic stress disorder. Recently, ICD therapy has been applied to treatment of atrial arrhythmias, particularly atrial fibrillation ((1) Lau et al, Initial clinical experience with an im- plantable human atrial defibrillator, PACE 1997; 20: 220-225 — (2) Timmersman et al, Early clinical experience with the Metrix automatic implantable atrial defibrillator, European Heart J 1997; 134). Although atrial fibrillation usually is not life- threatening, it is the most common arrhythmia requiring hospitalization in the United States. It causes potentially disabling symptoms of palpitations, shortness of breath, or chest pain and is an important cause of stroke. The painful and startling nature of ICD shocks are considered a particular limitation for patient acceptance of ICD treatment of atrial fibrillation. It has been stated in recent published literature (Cooper et al, Internal atrial defibrillation in hu¬ mans: Improved efficacy of biphasic waveforms and the importance of phase dura¬ tion, Circulation 1997; 96: 2693-2700) that the ultimate acceptance of a fully auto¬ matic atrial defibrillator will depend on the reduction of pain to acceptable levels. To this end, present state-of-the-art holds that a primary method of reducing the pain associated with these shocks is to reduce the strength ofthe shock pulse as measured by energy or voltage. This method requires a significant decrease in the shock strength required to defibriUate with a success rate of 50%. This shock strength is known as the defibrillation threshold. Recent studies have focused on reducing the atrial defibrillation threshold by altering the shape (waveform) ofthe delivered shock pulse or the locations ofthe electrodes (electrode configuration) through which these shocks are applied. The fundamental hypothesis is that lowering ofthe defibrillation threshold will permit atrial defibrillation with weaker shocks and thereby decrease the pain associated with these shocks in patients. The shock strength judged tolerable for defibrillation in conscious patients has differed in previous studies, but is generally in the range of 0.1 - 0.5 joules (J). Zipes (Zipes et al, Clinical transvenous cardioversion of recurrent life-threatening ventricu¬ lar tachyarrhythmias: Low energy synchronized cardioversion of ventricular tachycar- dia and termination of ventricular fibrillation in patients using a catheter electrode, Am Heart J 1982; 103: 789-794) reported that shocks of 0.5 J or less delivered be¬ tween electrodes in the superior vena cava and right ventricle were tolerable for treat¬ ment of ventricular tachycardia. However, using the same electrode system, Perelman ( Perelman et al, Assessment of prototype implantable cardioverter for ventricular tachycardia, Br Heart J 1984; 52: 385-391) found that 3 of 9 patients reported severe discomfort at a shock strength of 0.1 J. Nathan ( Nathan et al, Internal transvenous low energy cardioversion for the treatment of cardiac arrhythmias, Br Heart J 1984; 52: 377) delivered transvenous shocks to 19 conscious patients for various atrial and ventricular arrhythmias. Fourteen of 19 patients described severe discomfort with shock strengths 0.5 J. Murgatroyd (Murgatroyd et al, Efficacy and tolerability of transvenous low energy cardioversion of paroxysmal atrial fibrillation in humans, J Am Coll Cardiol 1995; 25: 1347-1353) determined the range of tolerable shock strengths for the most favorable electrode configuration for atrial defibrillation (right atrium to distal coronary sinus). Although the range of shock strengths tolerated without severe discomfort was 0.1 to 1.2 J, seven of 19 patients found even 0.1 J shocks intolerable. Using a different electrode system, Steinhaus (Steinhaus et al, Atrial defibrillation: are low energy shocks acceptable to patients? PACE 1996; 19: 625) delivered shocks of 0.4 J and 2.0 J shocks in randomized order. Patients reported no difference in perceived pain between the two shock strengths. Both shock strengths were given discomfort scores of approximately 7 on a scale of 0 - 10. However, Steinhaus found that the second shock was judged significantly more painful than the first shock, independent of shock strength. This observation is important because a strategy for reducing pain in defibrillation of arrhythmias which are not life-threatening (such as atrial fibrillation) contemplates clinical use of defi¬ brillation shocks with strength near the defibrillation threshold. The hypothesis is that, even if multiple shocks are required to terminate the arrhythmia, multiple weaker shocks will be better tolerated than one strong shock. Steinhaus' data suggest that any clinical benefit in pain reduction achieved by delivering clinical defibrillation shocks with strength near the defibrillation threshold is likely to be offset by the increased discomfort associated with subsequent shocks as weak as 0.4 J. Data reported for atrial defibrillation thresholds must be considered in the per¬ spective of these reported values for tolerable shock strengths. Cooper (Cooper et al, Internal cardioversion of atrial fibrillation in sheep, Circulation 1993; 87: 1673-1686) measured the atrial defibrillation threshold for multiple waveforms and electrode con¬ figurations in sheep. They showed that a specific biphasic waveform (3 ms phase 1 and 3 ms phase 2) and a specific electrode configuration (right atrial appendage to distal coronary sinus) resulted in the lowest atrial defibrillation threshold for the com- binations of electrode configurations and waveforms tested (1.3 ± 0.4 J). However, use of this waveform and electrode configuration in humans with paroxysmal (inter¬ mittent) atrial fibrillation, the principal treatment population for atrial ICDs, resulted in atrial defibrillation thresholds approximately twice as high as in sheep. Johnson (Johnson et al, Circulation 1993; I 592) reported a value of 2.5 ± 1.4 J and Murga- troyd (Murgatroyd et al, J Am Coll Cardiol 1995; 25: 1347-1353) reported a value of 2.2 ± 1.0 J. Therefore, the prior art does not teach a method sufficient for the reduc¬ tion of a patient's perceived pain during atrial defibrillation shocks. More recently, Cooper (Cooper et al, Internal cardioversion of atrial fibrilla- tion: Marked reduction in defibrillation threshold with dual current pathways, Circu¬ lation 1997; 96: 2693-2700) showed that sequential shocks delivered through two different sets of electrodes significantly decreased atrial defibrillation thresholds in sheep. The defibrillation threshold for this complex method (0.36 ± 0.13 J) was sig¬ nificantly lower than that ofthe best single-pathway method (1.3 ± 0.3 J). Since the average atrial defibrillation thresholds in sheep are approximately half that ofthe av¬ erage atrial defibrillation thresholds for patients with paroxysmal atrial fibrillation, it was estimated that this newly determined method would provide average atrial defi¬ brillation thresholds of slightly less than 1 J in patients. Thus, despite the additional complexity ofthe implant procedure and possible additional short and long-term mor- bidity associated with this new method, it is not likely to permit atrial defibrillation shocks without severe discomfort in the majority of patients. Therefore, this prior art does not teach a method sufficient for the significant reduction of a patient's perceived pain during atrial defibrillation. This prior art moreover requires the increased cost, surgical complexity, and risk associated with two additional electrodes. The method and apparatus of US Patent Number 5,332,400 issued to Alferness discloses an implantable atrial defibrillator that provides a warning to a patient prior to delivery of an atrial shock pulse to cardiovert or defibriUate the patient's atrial ar¬ rhythmia. The atrial defibrillator applies a warning electrical shock to the patient's atria when the apparatus determines that the atria require cardioversion or defibrilla- tion. The warning shock has an energy level lower than that required to treat the ar¬ rhythmia but high enough to be discerned by the patient without pain or other discom¬ fort. The purpose of this warning is to provide sufficient time in advance ofthe thera¬ peutic shock (in the range of 1 to 20 minutes) to afford a patient the opportunity to prepare for this painful and startling therapy. The Alferness method and apparatus demonstrate the limitation ofthe prior art to significantly reduce the extreme pain per¬ ceived by a patient when the defibrillation therapy is applied. The method and apparatus of US Patent Number 5,439,481 issued to Adams discloses an implantable atrial and ventricular defibrillator that diagnoses atrial and ventricular arrhythmias, automatically treats the ventricular arrhythmias, but allows discretionary treatment ofthe atrial arrhythmias. Such discretionary control permits the patient to forego painful atrial defibrillation shocks based on a medical assessment that the atrial arrhythmia is not significantly dysfunctional and is amenable to less immediate and less urgent medical treatment. The Adams method and apparatus fur- ther demonstrate the limitation ofthe prior art to alleviate the extreme pain perceived by a patient when atrial defibrillation therapy is applied. The method and apparatus of US Patent Number 5,630,834 issued to Bardy discloses an implantable atrial defibrillator that determines whether a patient is asleep prior to delivery of an atrial shock pulse. Defibrillation shocks that would be ex- tremely painful to a conscious patient are delivered only when a patient is asleep. Bardy states that although numerous patents and applications attempt to optimize shock waveforms and electrode systems to reduce defibrillation thresholds (and there¬ fore pain), the reliable accomplishment of low thresholds for all patients will remain a difficult and perhaps infeasible objective. This method may require a patient to re- main in atrial fibrillation for many hours until the patient falls asleep. Thus it is not practical for some patients who become symptomatic shortly after the onset of atrial fibrillation or for patients with ventricular arrhythmias who typically require treatment as soon as possible after the onset ofthe arrhythmia. Further, some patients have re- ported being awakened from sleep by painful and startling ICD shocks. Thus, ad¬ ministration of shocks during sleep is painful in some patients. In addition, a patient's knowledge that he/she may be shocked while asleep may result in anticipatory anxiety that interferes with sleep. The Bardy method and apparatus further demonstrate the limitation ofthe prior art to significantly reduce the extreme pain perceived by a con- scious patient when defibrillation therapy is applied. We therefore describe a method and apparatus to significantly diminish or eliminate the perceived pain by reducing the perceived intensity of defibrillation shocks and by inhibiting the startle response associated with these shocks. The clini¬ cal basis for the invention is the fundamental physiologic principal of PPL As will be appreciated from a review ofthe background discussion and the detailed description ofthe preferred embodiments, the invention overcomes the limitations and shortcom¬ ings ofthe prior art. In the field of neurophysiologic and neuropsychiatric research, it has been long appreciated that the experienced intensity of a strong, abrupt stimulus, and the behav- ioral (startle) response to this stimulus can be diminished by delivering a weak stimulus 30 - 500 ms prior to the strong stimulus ((1) Cohen et al, Sensory magnitude estimation in the context of reflex modification, J Exper Psychology 1981 ; 7: 1363- 1370 — (2) Swerdlow et al, "Neurophysiology and neuropharmacology of short lead interval startle modification," Chapter 6 of Startle Modification: Implications for Neu- roscience. Cognitive Science, and Clinical Science, Dawson et al, Cambridge Univ Press, 1997). This physiologic suppression ofthe startle reflex is referred to as pre- pulse inhibition (PPI). PPI decreases both the motor (startle) response and the sub¬ ject's perception ofthe intensity ofthe startling stimulus (pain). Normal human sub- jects consistently rate startling stimuli as significantly less intense if these stimuli are preceded by an appropriate weak prestimulus than if they were presented alone. The neural circuitry responsible for the sensorimotor modulation of PPI has been studied extensively. These studies indicate that PPI reflects the activation of ubiquitous, "hard-wired," behavioral gating processes that are regulated by forebrain neural circuitry. PPI occurs in virtually all mammals, and can be elicited in humans and humans and experimental animals using near-identical stimuli to produce strik¬ ingly similar response patterns (Swerdlow et al, Assessing the validity of an animal model of deficient sensorimotor gating in schizophrenic patients, Arch Gen Psychiatry 1994; 51 : 139-154). The importance of these findings is that optimal stimulus pa- rameters for PPI, and the neural substrates that regulate PPI, can be studied easily in animal models. This capability facilitates the application of PPI principles as dis¬ closed in the preferred embodiments ofthe invention. In one preferred embodiment ofthe invention, a single, low- voltage, short- duration pulse (the prepulse) precedes a high-voltage shock pulse. The time interval between the prepulse and the shock pulse is set between 30 to 500 ms. The specific time interval is determined by a testing method which identifies the optimal interval for PPI. The prepulse and therapeutic shocks may have arbitrary waveforms which are not necessarily identical. For example, these may include monophasic or biphasic capacitive-discharge pulses ofthe type presently used in ICDs, or a pulse waveform constructed specifically to reduce pain, such as a rounded, slow-rise time, or ascend¬ ing ramp waveform (Mouchawar et al, Sural nerve sensory thresholds of defibrillation waveforms, J Amer Coll Card 1998; 31(Suppl A): 373). At the time of implant of an atrial, ventricular, or dual-chamber ICD with the invention incorporated therein, a physician first determines an appropriate electrode system for a given patient and the appropriate cardioversion or defibrillation energy setting for that patient and electrode system. The physician then adjusts the amplitude ofthe prepulse and intervening time interval between the prepulse and the therapeutic shock pulse so as to significantly reduce or eliminate the patient's perceived pain and startle response caused by the shock pulse. Typically, the shock strength required for cardioversion or defibrillation is determined while the patient is under the influence of a short-acting anesthetic. The prepulse amplitude and time interval are adjusted in the conscious patient after the effects of any short-acting anesthetic has dissipated. Alternatively, the prepulse am¬ plitude and time interval are adjusted at a postoperative programming study. It is important to note that defibrillation shocks are associated with a promi¬ nent startle responses in many patients. Studies of other types of startle responses demonstrate that startle responses are actually increased when warning stimuli pre¬ ceded the startling stimuli at intervals (> 1 sec) that are adequate to evoke conscious anticipation ofthe startling stimulus (prepulse facilitation). Thus a "warning" pres- timulus which is sufficiently early to evoke a conscious response prior to an ICD shock is likely to increase the shock-induced startle effect. ICD recipients report se¬ vere discomfort related specifically to the startling effects of defibrillating shocks. A long-delay "warning" prestimulus is a programmable option in some ICDs. This fea¬ ture is rarely activated because patients experience anxiety during the anticipatory in- terval following the "warning" prestimulus. The invention overcomes these problems by suppressing the painful "jolt" associated with the defibrillation-induced startle re¬ flex, using automatic, preconscious mechanisms evoked during a time interval (30 - 500 ms) which is too short to stimulate anticipatory anxiety. The methods and devices ofthe prior art that most nearly approach the novel features ofthe invention, which uses PPI to reduce the perceived pain of therapeutic electrical stimuli delivered to a conscious patient, are, in fact, quite remote from it. Their marginal relevance can best be appreciated by a short, comparative description. The method and apparatus of US Patents Numbers 5,314,448 and 5,366,485 issued to Kroll and Adams disclose electrical pretreatment to a ventricular fibrillating heart to permit the applied shock pulse to defibriUate the ventricles with less energy than may otherwise be required. Pretreatment pulses and the treatment shock are de¬ livered through the same electrodes. The underlying hypothesis asserts that electrical pretreatment of a fibrillating heart is expected to achieve temporal organization ofthe ventricular cardiac cells, thereby diminishing the demands imposed on the defibrilla¬ tion threshold for the defibrillating shock pulse. As will become apparent in the de¬ scription ofthe preferred embodiments, the invention differs significantly from this prior art. The concept of electrical pretreatment of a fibrillating heart to assist the de¬ fibrillating shock pulse by reducing its level of required energy through temporal car- diac organization is completely absent from the invention. The method and apparatus of US Patent Number 5,425,749 issued to Adams discloses the delivery of an electrical preemptive cardioversion shock to a patient de¬ termined to have a life-threatening arrhythmia such as ventricular fibrillation. The underlying hypothesis asserts that the shock strength required for defibrillation is di- rectly related to the duration of fibrillation and that an electrical preemptive shock de¬ livered as soon as possible following the onset of an arrhythmia will reduce the total energy requirements for cardioversion or defibrillation. The preemptive shock is thus delivered several seconds before the main cardioverting or defibrillating pulse. As will become apparent in the description ofthe preferred embodiments, the invention differs significantly from this prior art. The concept of electrical preemptive cardio¬ version or defibrillation to quickly treat a patient and thereby to significantly reduce the size and energy requirements of a defibrillator is completely absent from the in¬ vention. Despite the need in the art for an ICD apparatus or methods which overcome the shortcomings and limitations ofthe prior art, none insofar as is known has been developed or proposed. Accordingly, it is an object ofthe invention to provide an im¬ plantable atrial, ventricular, or dual-chamber ICD method and apparatus that applies the clinical science related to sensorimotor gating to reduce or eliminate the perceived intensity of, and startle response to, the ICD's shock pulse. The invention reduces or eliminates the pain by delivering a timed prepulse that reduces the perceived intensity ofthe shock pulse, and inhibits the startle response to the shock pulse. There are no such teachings in the prior art. Patients often require emergency cardiac pacing in the form of temporary transcutaneous or transesophageal electrical pulses. Transcutaneous cardiac pacing (TCP) is commonly used in emergency medicine for immediate treatment of unstable bradycardia until a transvenous pacemaker can be established under more controlled circumstances. Transcutaneous or transesophageal cardiac pacing (TEP) may also be used to provide cardiac electrical activation during asystolic cardiac arrest as an ad- junct to cardiopulmonary resuscitation in either in-hospital or out-of-hospital settings. These techniques may also be used to terminate ventricular or supraventricular ar¬ rhythmias through overdrive pacing or other antitachycardia pacing methods. Rapid TEP atrial pacing is used with increasing frequency in conscious pa- tients to perform cardiac stress tests using echocardiographic or scintigraphic imaging ((1) Iliceto S et al, Prediction of cardiac events after uncomplicated myocardial in¬ farction by cross-sectional echocardiography during transesophageal atrial pacing, Int J Cardiol 1990; 28: 95 — 103, (2) Anselmi M et al, Usefulness of transesophageal atrial pacing combined with two — dimensional echocardiography (echo-pacing) in predicting the presence and site of residual jeopardized myocardium after uncompli¬ cated acute myocardial infarction, Am J Cardiol 1994; 73: 534 — 538, (3) Anselmi M et al, Comparison of left ventricular function and volumes during transesophageal atrial pacing combined with two-dimensional echocardiography in patients with syn¬ drome X, atherosclerotic coronary artery disease, and normal subjects, Am J Cardiol 1997; 80: 1261 — 1265, (4) Marangelli V et al, Detection of coronary artery disease by digital stress echocardiography: comparison of exercise, transesophageal atrial pacing and dipyridamole echocardiography, J Am Coll Cardiol 1994; 24: 117 — 124, (5) Marinsky G et al, Diagnostic value of synchronized transesophageal atrial pacing, PACE 1991 ; 14: 1228—1232, (6) Matiushin GV et al, [Combined use of left atrial transesophageal pacing and cordarone in atrial flutter], Ter Arkh 1998; 70: 71 — 73, (7) Santomauro M et al, Diagnosis of coronary artery disease with Tc 99m-methoxy isobutyl isonitrile and transesophageal pacing, Angiology 1992; 43: 818 — 825). However, the pain associated with this method has proved an important issue. TEP may also be used in conjunction with recording ofthe esophageal ECG as a simple and noninvasive means of diagnosing the mechanisms of cardiac rhythm disturbances (Deal BJ, Chapter 35, Esophageal pacing, in: Ellenbogen KA et al, Clini¬ cal Cardiac Pacing. Philadelphia, PA, W B Saunders Company, 1995, 701—705). TEP has also been used as a method of temporary pacing in patients who have re¬ quired removal of infected transvenous pacemaker electrodes or those undergoing magnetic resonance imaging (Hofman MB et al, Transesophageal cardiac pacing dur¬ ing magnetic resonance imaging: feasibility and safety considerations, Magn Reson Med 1996; 35: 413^22). It is well known in the art that the first method for external temporary cardiac pacing was introduced in 1952 by Zoll (Zoll PM, Resuscitation ofthe heart in ven¬ tricular standstill by external electrical stimulation, N Engl J Med 1952; 247: 768 — 771). Zoll developed the first reported transcutaneous cardiac pacemaker comprising an external DC pulse generator, a 2 ms pulse duration, and 3 cm diameter metal paddles. Zoll applied the device to patients suffering from asystole due to bradycardia. Discomfort and pain, however, from cutaneous nerve stimulation, pectoralis muscle contraction, and local soft tissue damage proved intolerable to many conscious patients. Despite its demonstrated efficacy, the procedure was abandoned because of these side effects in favor of newly developed transvenous pacing. Except for patients undergoing cardiac surgery, transvenous pacing is usually accomplished by placement of transvenous pacemaker leads through the internal jugular, subclavian, femoral, or antecubital veins. Significant complications can arise from these procedures, particularly in hemodynamically unstable patients. Techno¬ logical advances in the methods of TCP demonstrated that it was safe, effective, easy to use, reduced the pain and discomfort in some patients, and produced hemodynamic responses similar to those produced by right ventricular endocardial pacing (Zoll PM et al, External noninvasive temporary cardiac pacing: clinical trials, Circulation 1985; 71 : 937 — 944). These improvements lead to a resurgence of TCP use due to inade- quacies of transvenous pacing in the setting of cardiac arrest, asystole, and cardiopul- monary resuscitation. TCP improvements include (1) large surface area electrodes and (2) longer duration, lower intensity, constant — current pacing pulses. Despite these improvements in the art of TCP, there were no significant re¬ ductions in the associated pain and discomfort. A trial using a TCP device focused on patients with third — degree atrio ventricular block or asystole due to acute myocardial infarction requiring acute need for pacing or patients with third — degree atrioven- tricular block requiring a permanent implanted pacemakers either immediately or within 1 — 3 days (Madsen JK et al, Transcutaneous pacing: experience with the Zoll noninvasive temporary pacemaker, Am J Heart 1988; 116: 7 — 10). The researchers used a Zoll TCP device, which functioned as VVI demand pacemaker with separate pacing and sensing electrodes. The apparatus contained a pacing unit, an ECG moni¬ tor, screen, and paper recorder. The pacing pulse was a rectilinear constant current pulse of 40 ms duration and the amplitude varied from 0 to 140 mA. Pacing was achieved by two electrodes, one placed mid — chest (anterior apex) and one placed on mid — back (posterior). The front electrode was 75 cm 2 and the back electrode was 140 cm 2 in area. The Zoll TCP device contained all the presently known improvements. Regardless, pain and discomfort were felt by most patients to varying degrees. Some patients felt unacceptable pain at 40 mA and other patients felt slight irritation at pac¬ ing pulse of 80 mA. It was determined that 20 mA caused a prickly sensation ofthe skin, 40 mA was felt as a definite thump, 60 mA was slightly painful, and 80 mA was definitely painful. The median threshold for pacing determined for the patients in the trial was 55 mA, ranging from 30 to 110 mA. Sixteen of 29 conscious patients (55%) felt chest pain with threshold pacing. Sedation or analgesics were necessary for these patients, and it was the impression ofthe research physicians that sedation is required for any TEP output above 50 mA. Thus, to achieve a reliable safety margin, usually considered to be 1.5 — 2 X the pacing threshold, the vast majority of patients require sedation. Patient tolerance was measured in a second study using the Zoll TCP device (Klein LS et al, Transcutaneous pacing: patient tolerance, strength interval relations and feasibility for programmed electrical stimulation, Amer J Cardiol 1988; 62: 1126 — 1129). Ventricular pacing thresholds using TCP were determined in 11 of 16 patients. Thresholds could not be determined in 5 patients due to intolerable chest discomfort. In addition, 3 ofthe 11 patients in whom threshold was obtained could not tolerate the pacing for the duration required to complete the study. Therefore, only 8 ofthe 16 patients tolerated TCP in this study, and only one of these 8 patients tolerated pacing at more than 20 mA above threshold. The mean threshold was 61 mA (ranging from 45 mA to 80 mA) for these 8 patients. The three patients in whom threshold was obtained but were unable to tolerate the TCP had a mean threshold of 88 mA. The conclusions drawn were that TCP was not well tolerated, 15 of the 16 patients received conscious sedation, and therefore TCP appeared to be limited to a subset of patients with LOW TCP thresholds. Subjective discomfort levels were measured in a third study using a Marquette combination defibrillator — monitor — pacing device (Chapman PD et al, Efficacy and safety of transcutaneous low — impedance cardiac pacing in human volunteers using conventional polymeric defibrillation pads, Ann Emerg Med 1992; 21 : 1451 — 1453). Thirty healthy unmedicated adult volunteers were paced transcutaneously to the threshold of capture and beyond by an intensity factor of 125%. Pacing was contin- ued at the 125% level for two minutes, during which subjective discomfort levels were recorded on a 1 (minimal) to 5 (severe) pain scale. The pain assessment aver¬ aged 3.2, placing the mean discomfort level between moderate discomfort and moder¬ ately severe discomfort. The fact that pain is a limiting factor in TCP has been verified in multiple other studies. In a typical study by Altamura (Altamura G et al, Treatment of ven¬ tricular and supraventricular tachyarrhythmias by transcutaneous cardiac pacing, PACE 1989; 12: 331—338), the efficacy of TCP in the treatment of tachyarrhythmic events was evaluated. The experiment results showed that TCP was easily usable and immediately successful in the majority of atrio ventricular reentrant tachycardias and a relevant percentage of ventricular tachycardias. However, even though Altamura re¬ ported no clinically significant untoward effects, the clinical protocol was purpose¬ fully designed to minimize the painful discomfort ofthe overdrive pacing and the re¬ sults showed that the pacing was modestly tolerable if used for only a few seconds. Therefore, these devices demonstrate the limitation ofthe prior art to significantly re- duce the extreme pain perceived by a conscious patient when transcutaneous or trans¬ esophageal therapy is applied. Hence, the pain and discomfort of TCP is well recognized in the medical community. Despite this matter, TCP has been demonstrated to be safe and effica¬ cious across a wide range of important clinical circumstances and pacing modalities. The pacing parameters have not changed significantly since an improved version was clinically evaluated as reported by Zoll in 1985. TCP is routinely combined with a defibrillator to provide a complete cardiac arrest intervention system, offering anti- bradycardia and antitachycardia pacing combined with an external defibrillation capa- bility. This configuration results in a complete system connected with a single set of multifunction electrodes performing detection, pacing, and defibrillation. The pacing programmability range of available devices are pulse durations from 5 ms to 55 ms, current amplitude from 0 mA to 210 mA, and pacing rates from 30 to 180 ppm. The energy programmability is used to set the energy level at slightly above the pacing threshold to minimize discomfort to conscious patients. Therefore, pacing program¬ mability has broadened the applications of TCP in conscious patients, in spite ofthe patient's possibly severe pain and discomfort (Trigano JA et al, Noninvasive transcu¬ taneous cardiac pacing: modern instrumentation and new perspectives, PACE 1992; 15: 1937 — 1943). Most importantly, the clinical application of this kind of system is now incorporated into the standard cardiac life support guidelines (Standards and guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiac care (ECC), Am Med Assoc 1986; 255: 2905—2898). Specifically, the use of TCP for emergency cardiac pacing is described in Chapter 5 ofthe 1997 Textbook of Ad¬ vanced Cardiac Life Support, and this chapter is hereby incorporated by reference in its entirety. The methods and devices ofthe prior art that most nearly approach the novel features ofthe present invention, which uses PPI to reduce the perceived pain of therapeutic electrical stimuli delivered to a conscious patient, are, in fact, quite remote from it. Their marginal relevance can best be appreciated by a short, comparative de¬ scription. The method and apparatus of US Patent Number 4,349,030 issued to Belgard discloses a pulse generator that provides external noninvasive cardiac stimulation through design improvements comprising constant-current, spikeless electrical pulses with durations greater than 5 ms and large-surface, non-metallic, skin-contacting electrodes. With these design improvements focused on delivering a low current den¬ sity, it was proposed that the pulse generator and its preferred embodiments would overcome the limitations ofthe prior art by eliminating local sensory nerve stimula- tion and strong skeletal muscle contraction. The purpose of eliminating these effects as to reduce the extreme pain perceived by a patient when TCP is applied. How¬ ever, this method and apparatus are the Zoll TCP device evaluated in the clinical re¬ ports discussed above ((1) Madsen JK, Am J Heart 1988; 116: 7—10, (2) Klein LS, Amer J Cardiol 1988; 62: 1126 — 1129). The clinical reports clearly demonstrated the limitation of this prior art to significantly reduce the pain and discomfort perceived by a patient. In a series of US Patents numbered 5,193,537, 5,205,284, 5,282,843, and 5,431,688 each issued to Freeman, a general method and apparatus is disclosed re¬ garding transcutaneously pacing the heart with background stimuli occurring in the intervals between pacing stimuli to reduce patient discomfort during pacing. The pat¬ ents disclose a method and apparatus that feature a pacing pulse comprising of a series of pulses in which each pulse has a duration and amplitude that does not permit it to stimulate either skeletal or cardiac muscle. It is proposed that when these pulses are placed close enough together during output to form the equivalent of a single pacing pulse the series of pulses will capture the heart while reducing skeletal muscle stimu¬ lation. However, it is well known that the reduction ofthe skeletal muscle stimulation is highly variable and is extremely sensitive to electrode placement on a patient, par¬ ticularly athletes and patients with medium to highly defined muscular structure. The overall reduction of skeletal muscle stimulation is no more than 5% — 10% and has a nonlinear relationship to a patient's perceived pain. The patents further disclose a method and apparatus that feature background stimuli in the intervals between pacing stimuli. These background pulse trains are proposed to enhance accommodation of skeletal muscle and cutaneous nerves and discourage accommodation of cardiac mus- cle, thereby decreasing skeletal muscle and cutaneous nerve stimulation while simul¬ taneously achieving effective stimulation ofthe heart. However, as discussed in the background and clinical sections ofthe present invention, the combination of pacing and background pulse trains delivered by Freeman's apparatus in its preferred em¬ bodiments will in fact intensify the patient's perception of pain, particularly for two or more pacing pulses and for time periods greater than 1 second. Thus, the Freeman method and apparatus further demonstrate the limitation of prior art to significantly reduce the pain and discomfort perceived by a patient during transcutaneous or trans¬ esophageal cardiac stimulation. More recently, the method and apparatus of US Patent Number 5,782,882 is- sued to Lerman discloses a TCP system that includes a transcutaneous electrical nerve stimulation system (TENS) coupled to the TCP system to concurrently apply nerve stimulation pulses to the patient. The nerve stimulation pulses are proposed to miti¬ gate any discomfort that a patient may experience from the TCP. Again, as discussed in the background and clinical sections ofthe present invention, the combination of pacing pulses with TENS as delivered by Lerman' s apparatus in its preferred em¬ bodiments will in fact intensify the patient's perception of pain, particularly for two or more pacing pulses and for time periods greater than 1 second. Thus, the Lerman method and apparatus further demonstrate the limitation of prior art to significantly reduce the pain and discomfort perceived by a patient during transcutaneous or trans¬ esophageal cardiac stimulation. We therefore describe a method and apparatus to significantly diminish or eliminate the perceived pain by reducing the perceived intensity of transcutaneous or transesophageal cardiac pacing and by inhibiting the startle response associated with these pulses. The clinical basis for the present invention is the fundamental physiol¬ ogic principal of PPI as described in the background section above and the clinical section ofthe preferred embodiment below. As will be appreciated from a review of the background discussion and the detailed description ofthe preferred embodiments, the present invention overcomes the limitations and shortcomings ofthe prior art. BRIEF SUMMARY OF THE INVENTION The present invention provides a method and apparatus to pretreat a patient prior to a therapeutic painful stimulus, comprising the step of applying at least one pain inhibiting stimulus to a first part of a patient's body prior to an application ofthe therapeutic painful stimulus to the same part or a second part of a patient's body. This method is intended primarily for use in conscious patients, but it may also be used in sleeping patients. The benefits of this invention will become clear and will be best appreciated with reference to the detailed description ofthe preferred embodiments. Other ob¬ jects, advantages and novel features will be apparent from the description when read in conjunction with the appended claims and attached drawings. BRIEF DESCRIPTION OF THE SEVERAL VIEWS OF THE DRAWING FIGURE 1 illustrates a single, startling pulse, an associated measurement of perceived pain and startle reflex magnitude, a prepulse preceding the single, startling pulse by a 30-500 ms interval, and an associated, significant reduction ofthe per¬ ceived pain and startle response exhibited by a patient. FIGURE 2 illustrates a single, startling pulse, an associated measurement of perceived pain and startle reflex magnitude, a prepulse preceding the single, startling pulse by a 0.1-20 ms interval, and an associated, significant accentuation ofthe per- ceived pain and startle response exhibited by a patient. FIGURE 3 illustrates an empirically determined relationship of prepulse in¬ tensity to the percentage of PPI. FIGURE 4A illustrates an active housing ventricular ICD implanted pecto- rally and attached to transvenous electrodes placed into the superior vena cava, coro- nary sinus, and right ventricle of a patient's heart, and further attached to tip to ring pacing and sensing electrodes placed into the right ventricle of a patient's heart. FIGURE 4B illustrates an active housing atrial or dual chamber implanted pectorally and attached to transvenous electrodes placed into the superior vena cava, right ventricle and coronary sinus of a patient's heart, and further attached to bipolar pacing and sensing electrodes placed into the right atrium and right ventricle of a pa¬ tient's heart. FIGURE 5 illustrates the invention's primary defibrillation system compo¬ nents (analyzer — programmer, telemetry head, implantable cardioverter — defibrilla- tor, and electrode system) and their interconnection for operation to implant and monitor an atrial or ventricular ICD. FIGURE 6 illustrates the invention's primary ICD hardware and software elements and their interconnection for operation to diagnose atrial or ventricular fib¬ rillation and to deliver reduced-pain defibrillation therapy using the principle of PPI. FIGURE 7 illustrates first a monophasic atrial or ventricular defibrillation pulse, second a high amplitude, pain inhibiting, monophasic prepulse preceding the monophasic atrial or ventricular defibrillation pulse, and third a high amplitude, pain inhibiting, biphasic prepulse preceding the monophasic atrial or ventricular defibrilla¬ tion pulse. FIGURE 8 illustrates first a biphasic atrial or ventricular defibrillation pulse, second a high amplitude, pain inhibiting, monophasic prepulse preceding the biphasic atrial or ventricular defibrillation pulse, and third a high amplitude, pain inhibiting, biphasic prepulse preceding the biphasic atrial or ventricular defibrillation pulse. FIGURE 9 illustrates first a monophasic atrial or ventricular defibrillation pulse, second a low amplitude, pain inhibiting, monophasic prepulse preceding the monophasic atrial or ventricular defibrillation pulse, and third a low amplitude, pain inhibiting, biphasic prepulse preceding the monophasic atrial or ventricular defibrillation pulse. FIGURE 10 illustrates first a biphasic atrial or ventricular defibrillation pulse, second a low amplitude, pain inhibiting, monophasic prepulse preceding the biphasic atrial or ventricular defibrillation pulse, and third a low amplitude, pain inhibiting, biphasic prepulse preceding the biphasic atrial or ventricular defibrillation pulse. FIGURE 11 A illustrates control, charge, and discharge circuitry for charging and delivering a monophasic atrial or ventricular defibrillation pulse or a high ampli¬ tude, inhibiting prepulse. The circuitry illustrates charging and discharging each pulse from the same circuitry. FIGURE 11B illustrates control, charge, and discharge circuitry for charging and delivering a monophasic or biphasic atrial or ventricular defibrillation pulse or a high amplitude, inhibiting, monophasic or biphasic prepulse. The circuitry illustrates charging and discharging each pulse from the same circuitry. FIGURE 12 illustrates control, charge, and discharge circuitry for charging and delivering a monophasic or biphasic atrial or ventricular defibrillation pulse or a low amplitude, inhibiting, monophasic or biphasic prepulse. The circuitry illustrates charging and discharging each pulse from separate circuitry. FIGURE 13 A illustrates the effectiveness of prepulse inhibition in reducing the startling experience of electric stimulation. FIGURE 13B illustrates the effectiveness of prepulse inhibition in reducing the painful experience of electric stimulation. FIGURE 14A illustrates anterior to posterior transcutaneous pacing or sub- threshold stimulation as applied by a transcutaneous pacing or subthreshold stimula¬ tion apparatus and its electrode interconnection with a patient. FIGURE 14B illustrates atrial pacing or subthreshold stimulation as applied by a transesophageal pacing or subthreshold stimulation apparatus and its electrode interconnection with a patient. FIGURE 15 illustrates a block diagram ofthe invention's transcutaneous car- diac pacing system elements and their interconnection for operation to deliver re¬ duced — pain pacing therapy using the principles of PPI. FIGURE 16 illustrates a flow diagram of steps executed by the invention's transcutaneous cardiac pacing system elements to deliver alternating prepulses and pacing pulses according to the principles of PPI. DETAILED DESCRIPTION 1. Clinical Background and Theory of Operation Startle response is a well-understood simple behavior that has been studied systematically in the field of neurobiology. The systematic study has drawn on the characteristics of startle as a quantifiable, parametrically sensitive behavior of animals and humans. The startle response is regulated by forebrain circuitry and appears to exhibit striking similarities across species. The startle response demonstrates impor- tant forms of plasticity, including habituation and fear-potentiation. One form of startle plasticity relates to its amplitude modulation when the startle reflex is preceded by a prestimulus, or prepulse. The amplitude modulation is called PPI, which is the normal suppression ofthe startle reflex when the intense startling stimulus is preceded 30 to 500 ms by a relatively weak prestimulus. In PPI, a weak prestimulus inhibits a reflex response to a powerful sensory stimulus. Virtually all mammals and primates exhibit PPI. PPI reflects the activation of ubiquitous, "hard- wired," sensorimotor gating processes that are regulated by forebrain neural circuitry. Sensorimotor (startle response) modulation can also result in the potentiation ofthe startle reflex. Startle magnitude is increased when the startling stimulus is pre¬ ceded at very short (< 20 ms) or long intervals (> 1000 ms) by prestimuli. This modulation is called prepulse facilitation, and is most evident with weak prestimuli. Prestimulus modulation changes from facilitation to inhibition with increasing pre¬ pulse interval and intensity. Prepulse facilitation reappears as the time intervals be- come extended. It is not known whether PPI and prepulse facilitation are opposing forms of sensorimotor modulation that result from activity within either a single brain system or two separable substrates. The brain circuitry that mediates the inhibitory effect ofthe prestimulus does not deviate from the primary startle circuit by more than 1 to 2 neurons, with an ap- proximate 7.5 ms conduction time "out" from and 7.5 ms conduction time "back" to the primary startle circuit. The circuitry that mediates PPI is simple and is integrally related to the primary startle circuit. The forebrain circuitry "sets the gain" for PPI, involving several different neurotransmitter systems that regulate the amount of sen¬ sorimotor inhibition. Therefore, the regulation of startle facilitation is maximal with weak prestimuli at very short time intervals and startle inhibition is maximal with more intense prestimuli at relatively "longer" short time intervals. In addition to suppressing the motor component ofthe startle reflex response to intense, abrupt stimuli, prestimuli modify the perceived intensity of these stimuli. Subjects rate the intensity of loud noise bursts as being lower when those bursts are preceded by prepulses, compared to noise bursts without prepulses (Perlstein et al, Lead stimulation effects on reflex blink, exogenous brain potentials, and loudness judgments, Psychophysiology 1993; 30: 347-358). Thus, prepulses inhibit both the perceived intensity of, and the motoric response to, startling stimuli. Most important to the invention, the cardioversion or defibrillation pulse de¬ livered by an ICD result in subjective pain and discomfort perceived by a patient as well as an objective, physiologic, motoric, startle response by the patient. FIGURE 1 and FIGURE 2 illustrate the underlying neurobiologic principles in the attenuation or accentuation of pain through startle response modulation using an electrical prepulse. FIGURE 1 demonstrates the amplitude modulation of a patient's perception of or response to a painful stimulus due to PPI. The top time-versus-voltage graph in FIGURE 1 represents an intense, painful stimulus 10 to a patient, such as a defibril¬ lation shock pulse, and the patient's perception of or response to that stimulus illus¬ trated in the bar graph 12. Note that in FIGURE 1 and subsequent FIGURE 2 , bar graph 12 may represent a measure either of a patient's subjective perception ofthe painful stimulus lOor physiologic response to the painful stimulus 10, such as startle. The measured value ofthe patient's perception of or response to painful stimulus 10 is illustrated in the bar graph 12 as a "5" on a scale from 0 to 10, with 10 representing a measurement of greatest intensity. The bottom time-versus-voltage graph in FIGURE 1 represents an intense, painful stimulus 18 to a patient, such as a defibril¬ lation shock pulse. Painful stimulus 18 is preceded by a weaker prepulse 14 and sepa¬ rated by a predetermined time interval 16. The patient's associated perception of or response to the combined effects of painful stimulus 18 and prepulse 14 are illustrated in the bar graph 20, which corresponds to the bar graph 12 in the top panel. The measured value is illustrated in the bar graph 20 as a "1" on a scale from 0 to 10. FIGURE 1 thereby illustrates that the amplitude, duration, and preceding time inter¬ val for the prepulse were predetermined to modulate the patient's response in the form of PPI, thereby reducing a patient's pain, discomfort, or startle. Similarly, FIGURE 2 demonstrates the amplitude modulation of a patient's perception of or response to a painful stimulus due to prepulse facilitation. The top time-versus-voltage graph in FIGURE 2 again represents an intense stimulus 10 to a patient, such as a defibrillation shock pulse, and the patient's subjective perception of or physiologic response to the painful stimulus 10, such as startle. The measured value ofthe patient's perception of or response to painful stimulus 10 is illustrated in the bar graph 12 as a "5" on a scale from 0 to 10, with 10 representing a measurement of greatest pain. The top graph in FIGURE 2 is identical in all respects to the top graph in FIGURE 1. The bottom time-versus-voltage graph in FIGURE 2 represents an intense, painful stimulus 26 to a patient, such as a defibrillation shock pulse, which is preceded by a weaker prepulse 22. Prepulse 22 precedes intense stimulus 26 by predetermined time interval 24. Note that predetermined time interval 24 is much shorter than predetermined time interval 16 of FIGURE 1. The patient's associated perception of or response to the combined effects of painful stimulus 26 and prepulse 22 are illustrated in the bar graph 28, which corresponds to the bar graph 12 in the top panel and bar graph 20 in the bottom panel of FIGURE 1. This measured value is il¬ lustrated in the bar graph 28 as a "9" on a scale from 0 to 10. FIGURE 2 thereby il¬ lustrates that the amplitude, duration, and preceding time interval for the prepulse were predetermined to modulate the patient's response in the form of prepulse facili¬ tation, thereby accentuating a patient's pain, discomfort, or startle. Although both the prepulse and startling pulse are shown in FIGURES 1 and 2 as square waves for illustrative purposes, the pulses may have arbitrary waveform shape and varying amplitude and duration. Many studies have been conducted to characterize PPI in humans. In a typical method for demonstrating the increase in PPI with increased prepulse intensity (Swerdlow et al, Assessing the validity of an animal model of deficient sensorimotor gating in schizophrenic patients, Arch Gen Psychiatry 1994; 51 : 139-154), acoustic stimuli are delivered through headphones with a continuous 70-dB(A) background white noise. Startle pulses (40 ms-duration bursts of 118-dB(A) white noise) is pre- sented alone or 100 ms following a 20 ms-duration prepulse burst of white noise at 2, 4, 8, or 16 dB(A) above the background noise. Each startle pulse and prepulse com¬ bination is administered multiple times, in random order. PPI is defined as the per¬ centage of reduction in startle amplitude in the presence ofthe prepulse compared with the amplitude in the absence ofthe prepulse. Thus, a high percentage score indi- cates a high degree of PPI. Analysis of variance (ANOVA) with repeated measures on trial type can be used to reveal a significant effect of prepulse intensity on PPI Addi¬ tionally, a threshold sensitivity for the reduction of startle amplitude can be identified. Using the stimulus parameters described above, this typically occurs with prepulse intensities approximately 4 dB above the background noise. FIGURE 3 clearly illustrates the important relationship 48 between prepulse intensity and the percentage of PPI for a constant prepulse interval (time between pre¬ pulse and pulse). The reduction of startle amplitude increases with increasing pre¬ pulse intensity when prepulse interval is held constant. The results from the illustra¬ tive, acoustic trial have been repeated for other intense stimuli (e.g. air puff, shock and light flash) and their associated perceived pain or physiologic response. The results are consistent with the illustrated relationship and demonstrate a universal relationship of PPI to startle response across stimulus modalities. As importantly, it has been shown that PPI occurs when the prestimulus and the startling stimulus are in the same or different sensory modalities. One example would be an acoustically derived pres¬ timulus coupled with a startling stimulus that is electrically derived. Another example would be a tactile derived prestimulus coupled with a startling stimulus that is opti¬ cally derived. Preclinical studies suggest that certain medications can increase the amount of prepulse inhibition. For example, in some conditions, prepulse inhibition was en¬ hanced by the atypical antipsychotic clozapine. Because increased PPI may be asso¬ ciated with a reduction in the experience of, and response to a startling stimulus, it may be desirable, under certain circumstances, to utilize specific medications to en¬ hance the effectiveness of PPI in reducing the perception of, and/or response to a defi- brillation shock. Medication may be administered on an as-needed basis to patients in advance of a period of planned defibrillation, or on an ongoing basis to patients who require intermittent defibrillation. 2. Description ofthe Principle Physical Elements FIGURES 4A, 4B, 5 and 6 illustrate the principle physical elements ofthe invention. The figures illustrate a fully implantable atrial or ventricular cardioverter— defibrillator pulse generator (ICD) 30 that embodies the invention and shown in asso¬ ciation with a schematically illustrated human heart 34 and 38. The portions ofthe heart illustrated in FIGURES 4A and 4B are the right atrium 34 (RA), the left atrium (LA), the right ventricle 38 (RV), and the left ventricle (LV). ICD pulse generator 30 generally includes a housing 46 for hermetically seal¬ ing the internal circuits and programming 150 of ICD 30 to be described hereinafter, a right atrial/superior vena cava endocardial high-voltage lead 40, a coronary sinus/great cardiac vein, endocardial high-voltage lead 42, a right ventricle endocardial high- voltage lead 44, a right atrium pace/sense lead 50, and a right ventricle pace/sense lead 52. Each ofthe leads comprise an insulative lead body. The housing 46 of ICD 30 may be provided with some or all portions without plastic insulation (for example parylene or silicone rubber). The uninsulated portions ofthe housing 46 optionally serve as a prepulse or defibrillation electrode, used to deliver a prepulse or a high- voltage defibrillation shock pulse to the atria, ventricles or both atria and ventricles. High- voltage leads 40, 42, and 44 further comprise electrodes capable of conducting high voltage currents and defibrillation coil electrodes. They may be fabricated from platinum, platinum alloy, or other materials known to be usable in ICD electrodes. Leads 40, 42, and 44 are used to deliver a prepulse or a high- voltage defibrillation shock pulse to either the atria or ventricles. Lead 50 further comprise a tip electrode and a ring electrode, and is constructed to enable bipolar sensing of electrical activa¬ tions ofthe right atrium 34. Lead 52 further comprise a tip electrode and a ring elec- trode, and is constructed to enable bipolar sensing of electrical activations ofthe right ventricle 38. Although they are shown separately in FIGURE 4 for clarity, one or more ofthe high-voltage leads 40, 42, and 44 and one or more ofthe pace-sense leads 50 and 52 may be combined into a single multiconductor lead. The enclosure 46 and the endocardial leads 40, 42, 44, 50 and 52 are arranged for establishing electrical contact with the heart and to be implanted beneath the skin of a patient and so as to render ICD 30 fully implantable. Within the enclosure 46, ICD 30 includes electrode switching circuitry 188. Leads 40, 42, 44, 50 and 52 are coupled to the electrode switching circuitry via con- nector block 48. Leads 50 and 52 are further coupled communicatively to pacer tim¬ ing/control circuitry 174 and to electrogram sensing and conditioning circuitry 154. Lead 50 therefore forms a complete pace/sensing lead system for pacing and sensing electrical activations ofthe right atrium. Lead 52 therefore forms a complete pace/sensing lead system for pacing and sensing electrical activations ofthe right ventricle. The primary external components of ICD 30 are illustrated in FIGURE 5. These are contrasted with the implantable elements (ICD pulse generator 30 and en¬ docardial leads illustrated by right ventricle lead 44) which are shown within the hu¬ man thorax 47 in this Figure. An analyzer-programmer system 130 is comparatively remote from the patient. Analyzer-programmer system 130 is coupled to a telemetry relay 134 via communication means 132, thereby able to compute and transmit pro¬ gramming instructions and programmable parameters via telemetry relay 134 to ICD 30, and able to receive programmed parameters, patient-sensed parameters, and re¬ corded electrical activations in the form of atrial or ventricular electrograms via te- lemetry relay 134 from ICD 30. Telemetry relay 134 is employed near or on the pa¬ tient's body to communicatively couple analyzer-programmer system 130 with ICD 30 via telemetry signals 136. The instructions and parameters are transmitted to ICD 30 and received from ICD 30 using telemetry signals 136 comprising infrared, visible, radio-frequency electromagnetic, or ultrasound radiation. Analyzer-programmer sys- tern 130 and telemetry relay 134 are well appreciated by those skilled in the art. For purposes ofthe invention, these invention provisions and their general operation may correspond to inventions known in the prior art as disclosed in US Patent Number 4,809,697 issued to Causey and US Patent Number 4,958,632 issued to Duggan, both incorporated herein by reference in their entireties. The internal circuits and programming 150 of ICD 30 are illustrated in FIGURE 6, and generally include electrode switching circuitry 188, electrogram sensing and conditioning circuitry 154, pacer timing/control circuitry 174, sense am¬ plification and digitizing circuitry 156, microprocessor 152, random access memory 176, tachyarrhythmia and fibrillation detection software 158, address/data bus 178, address/data bus 184, pacing, cardioversion and defibrillation charging and delivery control software 160, charging and delivery control circuitry 180, charging circuitry 164, capacitor systems 162, discharge circuitry 168. A battery 166 is electrically and communicatively coupled to the internal circuits and programming 150 and provides a sufficient source of energy to meet all energy requirements for long-term operation of ICD 30. FIGURE 7 illustrates a monophasic atrial or ventricular defibrillation pulse 70, a high amplitude, pain inhibiting, short duration, monophasic prepulse 72 preced¬ ing the monophasic atrial or ventricular defibrillation pulse, and a high amplitude, short duration, pain inhibiting, biphasic prepulse 76 preceding the monophasic atrial or ventricular defibrillation pulse. The monophasic atrial or ventricular defibrillation pulse 70 serves as the intense, painful stimulus 18 of FIGURE 1. The high ampli¬ tude, short duration, pain inhibiting, monophasic prepulse 72 or the high amplitude, short duration pain inhibiting, biphasic prepulse 76 serves as the weaker prepulse 14 of FIGURE 1 and is separated by a predetermined time interval 74. FIGURE 8 il¬ lustrates a biphasic atrial or ventricular defibrillation pulse 78, a high amplitude, pain inhibiting, monophasic prepulse 72 preceding the biphasic atrial or ventricular defi¬ brillation pulse, and a high amplitude, pain inhibiting, biphasic prepulse 76 preceding the biphasic atrial or ventricular defibrillation pulse. In this illustration, the biphasic atrial or ventricular defibrillation pulse 78 serves as the intense, painful stimulus 18 of FIGURE 1. Note that in FIGURES 7 and 8 the weaker strength ofthe prepulses relative to the intense pulses is determined by pulse duration. FIGURE 9 illustrates a monophasic atrial or ventricular defibrillation pulse 70, a low amplitude, pain inhibiting, monophasic prepulse 98 preceding the monopha¬ sic atrial or ventricular defibrillation pulse, and a low amplitude, pain inhibiting, bi¬ phasic prepulse 100 preceding the monophasic atrial or ventricular defibrillation pulse. The monophasic atrial or ventricular defibrillation pulse 70 serves as the in¬ tense, painful stimulus 18 of FIGURE 1, the low amplitude, pain inhibiting, mono- phasic prepulse 98 or the low amplitude, pain inhibiting, biphasic prepulse 100 serves as the relatively weaker prepulse 14 of FIGURE 1 and is separated by a predeter¬ mined time interval 74. FIGURE 10 illustrates a biphasic atrial or ventricular defi¬ brillation pulse 78, a low amplitude, pain inhibiting, monophasic prepulse 98 preced¬ ing the biphasic atrial or ventricular defibrillation pulse, and a low amplitude, pain inhibiting, biphasic prepulse 100 preceding the biphasic atrial or ventricular defibril¬ lation pulse. In this illustration, the biphasic atrial or ventricular defibrillation pulse 78 serves as the intense, painful stimulus 18 of FIGURE 1. Note that in FIGURES 9 and 10 the weaker strength ofthe prepulses relative to the intense pulses is determined by pulse amplitude. This contrasts with FIGURES 7 and 8 in which the weaker strength ofthe prepulses relative to the intense pulses is determined by pulse duration. FIGURE 11A illustrates hardware and software elements that implement the delivery of a monophasic atrial or ventricular prepulse from high- voltage defibrilla- tion circuitry primarily designed for monophasic atrial or ventricular defibrillation waveforms. FIGURE 11 A illustrates charge circuitry 82, capacitor system 84, dis¬ charge control circuitry 80, monophasic discharge control lines 86, and monophasic discharge switching circuitry 88 for solid-state switching control of charging and de¬ livering a monophasic atrial or ventricular defibrillation pulse or a high amplitude, inhibiting prepulse. Charging and delivery controller 160 of ICD 30 is coupled com¬ municatively to the circuitry via address/data bus 184 (which may be separate from address/data bus 178). The charging portion of controller 160 operates charging cir¬ cuitry 82 via control lines 182. Charge circuitry 82 charges capacitor system 84 to predetermined energy and voltage levels prior to discharge. The delivery portion of controller 160 first utilizes discharge control circuitry 80 and operates switching cir¬ cuitry 88 via control lines 86 to output a monophasic, truncated exponential prepulse 72, second operates an internal timer for a predetermined amount of time to imple¬ ment predetermined time interval 74, and third operates switching circuitry 88 to out¬ put a monophasic, truncated exponential cardioversion or defibrillation shock pulse 70. The circuitry illustrates charging and discharging a prepulse and a cardioversion or defibrillation pulse from the same circuitry. Prepulse 72 and 76 have leading-edge voltages equivalent to leading-edge voltages for cardioversion or defibrillation shock pulse 70. Discharge control circuitry 80 modulates the prepulse waveform duration and modulates the predetermined time interval 74. FIGURE 11B illustrates hardware and software elements that implement the delivery of a monophasic or biphasic atrial or ventricular prepulse from high- voltage defibrillation circuitry primarily designed for biphasic atrial or ventricular defibrilla¬ tion waveforms. FIGURE 11B illustrates charge circuitry 82, capacitor system 84, discharge control circuitry 80, monophasic or biphasic discharge control lines 90 and 92, and monophasic or biphasic discharge switching circuitry 94 and 96 for solid-state switching control of charging and delivering a monophasic or biphasic atrial or ven¬ tricular defibrillation pulse or a high amplitude, inhibiting, monophasic or biphasic prepulse. Charging and delivery controller 160 of ICD 30 is coupled communica- tively to the circuitry via address/data bus 184 (which may be separate from ad¬ dress/data bus 178). The charging portion of controller 160 operates charging cir¬ cuitry 82 via control lines 182. The charge circuitry 82 charges capacitor system 84 to predetermined energy and voltage levels prior to discharge. The delivery portion of controller 160 first utilizes discharge control circuitry 80 and operates switching cir- cuitry 94 and 96 via control lines 90 and 92 to output a monophasic 72 or biphasic 76 truncated exponential prepulse, second operates an internal timer for a predetermined amount of time to implement predetermined time interval 74, and third operates switching circuitry 94 and 96 to output a monophasic 70 or biphasic 78 truncated ex¬ ponential cardioversion or defibrillation shock pulse. FIGURE 11B illustrates charging and discharging circuitry that implements biphasic waveforms using an H- bridge design. FIGURE 11B further illustrates charging and discharging circuitry that output a prepulse and a cardioversion or defibrillation pulse from the same deliv¬ ery circuits. Prepulse 72 and 76 have leading-edge voltages equivalent to leading- edge voltages for cardioversion or defibrillation shock pulse 70 and 78. Discharge control circuitry 80 modulates the prepulse waveform duration and modulates the pre¬ determined time interval 74. Capacitor system 84 illustrated in FIGURES 9A and 9B represents a conven¬ tional capacitor system for ICD 30. Capacitor system 84 is implemented with one or more electrically coupled capacitors of up to 1000 microfarads (μF) each. The elec¬ trical coupling circuitry implements effective capacitance values for ICD 30 in the range of 10 to 250 microfarads (μF), preferably in the range 60 to 120 μF. Capacitor system 84 stores 0 to 40 joules (J) of energy, preferably 2 to 20 J for ventricular defi¬ brillation and 0.05 to 15 J for atrial defibrillation, and may be charged to 1000 V for the leading-edge voltage of prepulses 72, 76 and defibrillation shock pulses 70, 78. FIGURE 12 illustrates hardware and software elements that implement the delivery of a monophasic or biphasic prepulse from low-voltage, low-energy circuitry substantially different from high-voltage defibrillation circuitry that implement the delivery of high- voltage, high-energy monophasic or biphasic defibrillation wave- forms. FIGURE 12 illustrates charge and capacitor circuitry 104, discharge control circuitry 102, discharge control lines 108 and 110, and discharge switching circuitry 116 and 118 for a low amplitude, low-energy, monophasic or biphasic atrial or ven¬ tricular prepulse. FIGURE 12 further illustrates charge and capacitor circuitry 106, discharge control circuitry 102, discharge control lines 112 and 114, and discharge switching circuitry 120 and 122 for a monophasic or biphasic atrial or ventricular de¬ fibrillation pulse. Charging and delivery controller 160 of ICD 30 is coupled commu¬ nicatively to the circuitry via address/data bus 184 (which may be separate from ad¬ dress/data bus 178). The charging portion of controller 160 operates charging cir¬ cuitry 104 and 106 via control lines 182. The charge circuitry 104 charges its capaci- tor system to a predetermined energy and voltage level for a low- voltage, low-energy prepulse. The charge circuitry 106 charges its capacitor system to a predetermined energy and voltage level for a high- voltage, high-energy cardioversion or defibrilla¬ tion shock pulse. The delivery portion of controller 160 first utilizes discharge control circuitry 102 and operates switching circuitry 116 and 118 via control lines 108 and 110 to output a monophasic 98 or biphasic 100 truncated exponential prepulse, second operates an internal timer for a predetermined amount of time to implement predeter¬ mined time interval 74, and third utilizes discharge control circuitry 102 and operates switching circuitry 120 and 122 via control lines 112 and 114 to output a monophasic 70 or biphasic 78 truncated exponential cardioversion or defibrillation shock pulse. The circuitry illustrates charging and discharging each pulse from separate circuitry. Prepulse 98 and 100 are programmable to permit the ability to have stored energies, delivered energies, leading-edge voltages, and prepulse waveform shapes substantially different from the stored energies, delivered energies, and leading-edge voltages for cardioversion or defibrillation shock pulse 70 and 78. Discharge control circuitry 102 modulates the prepulse waveform phase durations and amplitudes, and modulates the predetermined time interval 74. Capacitor systems 104 and 106 illustrated in FIGURE 12 represent conven¬ tional capacitor systems for ICD 30. Capacitor systems 104 and 106 may each be im- plemented with one or more electrically coupled capacitors of up to 1000 microfarads (μF) each. Electrical coupling circuitry for each capacitor system implements effec¬ tive capacitance values for ICD 30 in the range of 10 to 250 microfarads (μF), pref¬ erably in the range 60 to 120 μF. Capacitor systems 104 and 106 each store 0 to 40 joules (J) of energy, preferably 2 to 20 J for ventricular defibrillation and 0.05 to 15 J for atrial defibrillation, and each system may be charged to 1000 V for the leading- edge voltage of prepulses 98, 100 and defibrillation shock pulses 70, 78. Independent capacitor systems 104 and 106 provide for prepulse waveform design substantially similar or substantially different from cardioversion and defibrillation waveform de- signs, as illustrated in FIGURES 7, 8, 10 and 11. In a preferred embodiment, ca¬ pacitor system 104 is designed with different capacitive values and energy capabilities from the capacitance and energy capabilities of capacitor system 106. Capacitor sys¬ tem 104 implements the prepulse therapy with different capacitor values, stored and delivered energies, leading-edge voltages, and waveform shapes. Alternatively, ca- pacitor system 104 implements a square waveform and rounded waveform as a pre¬ pulse. Capacitor systems 104 may be implemented as a pacing circuit and provide pacing pulses for prepulses 98 and 100. The remainder ofthe invention is dedicated to the provision of cardiac pacing, cardioversion, defibrillation therapies, and apparatus programming techniques. For purposes ofthe invention, these invention provisions may correspond to inventions known in the prior art. An exemplary apparatus is disclosed of accomplishing pacing, cardioversion, defibrillation, and programming functions. The general operation of the apparatus may correspond to that apparatus disclosed in US Patent Number 5,549,642 issued to Min, incorporated herein by reference in its entirety. As cited earlier, the exemplary apparatus is illustrated by FIGURES 4A through 12. As illustrated in FIGURE 4A, sensing electrodes 52 are located on or in the right ventricle 38 and are coupled to the R — wave detection section ofthe electrogram sensing and conditioning circuitry 154, which preferably takes the form of an auto¬ matic threshold controlled sensing circuit providing an adjustable sensing threshold as a function ofthe measured electrogram amplitude. As illustrated in FIGURE 4B, sensing electrodes 50 are located on or in the right atrium 34 and are coupled to the P — wave detection section ofthe electrogram sensing and conditioning circuitry 154, which preferably takes the form of an automatic threshold controlled sensing circuit providing an adjustable sensing threshold as a function ofthe measured electrogram amplitude. The general operation ofthe P — wave and R — wave sensing and condi¬ tioning circuitry 154 may correspond to circuitry disclosed in US Patent Number 5,117,824 issued to Keimel and US Patent Number 5,282,837 issued to Adams, incor¬ porated herein by reference in their entireties. Electrode switching circuitry 188 is used to select which ofthe available electrodes are coupled to the electrogram sensing and conditioning circuitry 154 for use in digital signal analysis. Selection of elec¬ trodes is controlled by microprocessor 152 using the data and address bus 178, which selections may be varied as desired. Signals from the selected electrodes are provided to the wide band (0.02 — 200 Hz) amplifier, multiplexer, and analog to digital con- verter circuitry 156 for conversion to multi-bit digital signals and to the random ac¬ cess memory 176 under the control ofthe microprocessor 152 for storage. Micro¬ processor 152 may employ digital signal processing techniques to characterize the digitized signals stored in memory 176 to recognize and classify the patient's heart rhythm. Microprocessor 152 may employ any ofthe numerous signal processing methods known to the art. The pacer timing/control circuitry 174 includes programmable digital counters which control the basic time intervals associated with DDD, VVI, DVI, VDD. AAI, DDI, and other modes of single and dual chamber pacing well known to the art. Cir¬ cuitry also controls escape intervals associated with anti-tachyarrhythmia pacing in both the atrium and the ventricle, employing any anti-tachyarrhythmia pacing thera¬ pies known to the art. Intervals defined by pacing circuitry 174 include atrial and ventricular pacing escape intervals, the refractory periods during which sensed P — waves and R — waves are ineffective to restart timing ofthe escape intervals and the pulse widths ofthe pacing pulses. The durations of these intervals are determined by microprocessor 152, in response to stored data in memory 176 and are communicated to the pacing cir¬ cuitry 174 via address/data bus 178. Pacer circuitry 174 also determines the ampli¬ tude ofthe cardiac pacing pulses under the control ofthe microprocessor 152. During pacing, the escape interval counters within pacer timing/control cir¬ cuitry 174 are reset upon sensing of R- waves and P-waves as indicated by signals on address/data bus 178, in accordance with the selected mode of pacing on time-out trigger generation of pacing pulses by pacer output circuitry, which are coupled to electrodes 50 and 52. The escape interval counters are also reset on generation of pacing pulses, and thereby control the basic timing of cardiac pacing functions, in¬ cluding tachyarrhythmia pacing. The durations ofthe intervals defined by the escape interval timers are determined by microprocessor 152, via address/data bus 178. The value ofthe count present in the escape interval counters when reset by sensed R — waves and P — waves may be used to measure the durations of R — R intervals, P — P in- tervals, P — R intervals, and R — P intervals, which measurements are stored in mem¬ ory 176 and used to detect the presence of tachy arrhythmias. Microprocessor 152 operates as an interrupt driven device, and is responsive to interrupts from pacer timing / control circuitry 174 corresponding to the occurrence sensed P-waves and R- waves and corresponding to the generation of cardiac pacing pulses. These interrupts are provided via address/data bus 178. Any necessary mathematical calculations to be performed by microprocessor 152 and any updating ofthe values or intervals controlled by pacer timing / control circuitry 174 take place following such interrupts. For example, in response to a sensed or paced ventricular depolarization or R — wave, the intervals separating that R — wave from the immediately preceding R — wave, paced or sensed (R — R interval) and the interval separating the paced or sensed R — wave from the preceding atrial depolarization, paced or sensed (P — R interval) may be stored. Similarly, in response to the occurrence of a sensed or paced atrial de- polarization (P — wave), the intervals separating the sensed P — wave from the imme¬ diately preceding paced of sensed atrial contraction (P — P interval) and the interval separating the sensed P — wave from the immediately preceding sensed or paced ven¬ tricular depolarization (R — P interval) may be stored. Preferably, a portion ofthe memory 176 is configured as a plurality of recirculating buffers, capable of holding a preceding series of measured intervals, which may be analyzed in response to the oc¬ currence of a pace or sense interrupt to determine whether the patient's heart is pres¬ ently exhibiting atrial or ventricular tachyarrhythmia. The tachyarrhythmia and fibrillation detector 158 operates the algorithms that process the arrhythmia signal data stored in memory 176. Detection of atrial or ven- tricular tachyarrhythmias, as employed in the invention, may correspond to tachyar¬ rhythmia detection algorithms known to the art. There are many algorithms known in the art for processing arrhythmia data to determine if an atrial or ventricular tachyar¬ rhythmia is present. For example, presence of atrial or ventricular tachyarrhythmia may be confirmed by means of detection of a sustained series of short R — R or P — P intervals. The average cycle length, median cycle length, or cycle length of a certain percentage of intervals (e.g. 75% or 100%) is less than the corresponding, pro¬ grammed tachyarrhythmia detection interval and thus indicative of a tachyarrhythmia. The suddenness of onset ofthe detected high rates in each chamber, the interval sta- bility ofthe high rate P — P and R — R intervals the presence or absence of P — R asso¬ ciation, information related to the morphology ofthe electrograms corresponding to P and R waves in each chamber, or a number of other factors known to the art may also be measured at this time. Appropriate ventricular tachyarrhythmia detection method¬ ologies measuring such factors are described in US Patent Number 4,726,380 issued to Vollmann, US Patent Number 4,830,006 issued to Haluska, US Patent Number 4,880,005 issued to Pless, US Patent Number 5,251,626 issued to Nickolls, and US Patent Number 5,545,186 issued to Olson, all incorporated herein by reference in their entireties. An additional set of tachycardia recognition methodologies is disclosed by Olson (Onset and stability for ventricular tachyarrhythmia detection in an implantable pacer-cardioverter-defibrillator, Computers in Cardiology, October 7-10, 1986, IEEE Computer Society Press, pages 167-170) also incorporated herein in its entirety. However, the advantages ofthe invention is clearly practicable in conjunction with most prior art tachycardia detection algorithms. Atrial fibrillation detection method¬ ologies in particular are disclosed in US Patent Number 5,205,283 issued to Olson and US Patent Number 5,282,837 issued to Adams, in the publication by Arzbaecher (Arzbaecher et al, Automatic tachycardia recognition, PACE 1984; 541-547), and in the publication by Thakor (Thakor et al, Ventricular tachycardia and fibrillation de¬ tection by a sequential hypothesis testing algorithm, IEEE Trans Biomedical Engi¬ neering 1990; 37: 837-843), all of which are incorporated herein by reference in their entireties. Implementing such atrial and ventricular arrhythmia detection algorithms by a microprocessor is well within the preview of one skilled in the art. In the event that an atrial or ventricular tachyarrhythmia is detected, and an anti-tachyarrhythmia pacing regimen is desired, appropriate timing intervals for con- trolling generation of anti-tachyarrhythmia pacing therapies are loaded from micro¬ processor 152 into the pacing timing and control circuitry 174 to control the operation ofthe escape interval counters therein and to define refractory periods during which detection of P — waves and R — waves is ineffective to restart the escape intervals. Alternatively, circuitry for controlling the timing and generation of anti- tachycardia pacing pulses as described in US Patent Number 4,577,633 issued to Berkovits, US Patent Number 4,587,970 issued to Holley, US Patent Number 4,726,380 issued to Vollman, and US Patent Number 4,880,005 issued to Pless, all of which are incorporated herein by reference in their entireties, may also be used. In the event that generation of a cardioversion or defibrillation pulse is re- quired, microprocessor 152 employs an escape interval counter to control timing of such cardioversion and defibrillation pulses, as well as associated refractory periods. In response to the detection of atrial or ventricular fibrillation or tachyarrhythmia re¬ quiring a cardioversion pulse, microprocessor 152 activates the therapy charging and delivery controller 160 and the therapy charging and delivery control circuitry 180, which initiates charging ofthe high voltage capacitor systems 162 via the charging circuit 164 powered by the battery 166 and under the control of high voltage charging control lines 182. The voltage on the high voltage capacitors is monitored, and in re¬ sponse to reaching a predetermined value set by microprocessor 152, results in gen¬ eration of a logic signal that terminates the charging ofthe capacitor systems 162. Thereafter, timing ofthe delivery ofthe defibrillation or cardioversion pulse is con¬ trolled by the therapy charging and delivery controller 160 and the therapy charging and delivery control circuitry 180. Following delivery ofthe fibrillation or tachycar¬ dia therapy the microprocessor 152 then returns the device to cardiac pacing and awaits the next successive interrupt due to pacing or the occurrence of a sensed atrial or ventricular depolarization. As described in preceding paragraphs, the control, charging, and delivery circuitry and logic for the pain-suppressing prepulse therapies ofthe invention are embodied within the structural framework ofthe modern im¬ plantable cardioverter — defibrillator as described herein. One embodiment of an appropriate system for delivery and synchronization of ventricular cardioversion and defibrillation pulses and for controlling the timing func¬ tions related to them is disclosed in more detail in US Patent Number 5,188,105 is¬ sued to Keimel, incorporated herein by reference in its entirety. Embodiments of ap¬ propriate systems for delivery and synchronization of atrial cardioversion and defi- brillation pulses and for controlling the timing functions related to them are disclosed in more detail in US Patent Number 4,316,472 issued to Mirowski and in US Patent Number 5,269,298 issued to Adams, both incorporated herein by reference in their entireties. However, any known cardioversion or defibrillation pulse control circuitry is believed usable in conjunction with the invention. For example, circuitry control- ling the timing and generation of cardioversion and defibrillation pulses as disclosed in US Patent Number 4,375,817 issued to Engle, in US Patent Number 4,384,585 is¬ sued to Zipes, and in US Patent Number 4,949,719 issued to Pless, all incorporated herein by reference in their entireties, may also be employed. In the illustrated apparatus, delivery ofthe cardioversion or defibrillation pulses is accomplished by the therapy discharge circuitry 168, under control of cir¬ cuitry 180 via control bus 186. Therapy control circuitry 180 determines whether a monophasic or biphasic pulse is delivered, the polarity ofthe electrodes, and which electrodes are involved in delivery ofthe pulse. Therapy discharge circuitry 168 in¬ cludes high voltage switches which control which electrodes 40, 42, 44, and 46 are coupled together during delivery ofthe pulse. Alternatively, electrodes intended to be coupled together during the pulse may simply be permanently coupled to one another, either exterior to or interior ofthe device housing, and polarity may similarly be pre- set, as in current implantable defibrillators. An example of output circuitry for deliv¬ ery of biphasic pulse regimens to multiple electrode systems may be found in US Pat¬ ent Number 4,727,877 issued to Kallok and in US Patent Number 4,953,551 issued to Mehra, both incorporated herein by reference in their entireties. An example of cir¬ cuitry which may be used to control delivery of monophasic pulses is set forth in US Patent Number 5,163,427 issued to Keimel, incorporated herein by reference in its entirety. However, output control circuitry as disclosed in the previously cited US Patent Number 4,953,551 issued to Mehra, or US Patent Number 4,800,883 issued to Winstrom, incorporated herein by reference in its entirety, may also be used in con¬ junction with a apparatus embodying the invention for delivery of biphasic pulses. In the event that both atrial and ventricular defibrillation are available, ven¬ tricular defibrillation may be accomplished using higher pulse energy levels than re¬ quired for atrial defibrillation and may employ the same or a different electrode set as those electrodes used for atrial defibrillation. For example, electrodes 40 (right atrial/superior vena cava) and 42 (coronary sinus/great vein) may be employed for atrial defibrillation. Electrodes 40 and 44 (right ventricle) might be employed for ventricular defibrillation, with electrode 40 coupled to electrode 46 (device housing). One particularly desirable embodiment ofthe invention employs only the right atrial/superior vena cava electrode 40, the coronary sinus/great cardiac vein electrode 42 and the right ventricular electrode 44. During atrial defibrillation, electrodes 40 and 46 are coupled in common to one another, and the atrial defibrillation pulse is de¬ livered between these electrodes and electrodes 42. During ventricular defibrillation, electrodes 40 and 46 are coupled in common with one another, and the ventricular de¬ fibrillation pulse is delivered between these electrodes and electrode 44. This par- ticular set of electrodes thus provides optimized defibrillation pulse regimens for both atrial and ventricular defibrillation, by simply switching the software or hardware controlled connections ofthe coronary sinus/great vein electrode 42 and the right ventricle electrode 44. In another particularly desirable embodiment ofthe invention the same lead configuration is used for both atrial and ventricular defibrillation. Electrodes 40 and 46 are coupled in common with one another, and the atrial or ven¬ tricular defibrillation pulse is delivered between these electrodes and electrode 44. This particular set of electrodes avoids the need for a coronary sinus/great vein elec¬ trode 42 and facilitates delivery of an atrial defibrillation shock with a strength that exceeds the ventricular upper limit of vulnerability. Functional switching circuitry well known in the art may be employed in high voltage output circuit 168, such that the circuitry includes high voltage switches indi¬ vidually controlled by signals on control bus 186. These switches allow connection of any ofthe described electrodes to either the positive or the negative terminals ofthe capacitor systems 162. As illustrated, any combination of electrodes may be selected, any polarities desired may be provided, and monophasic or biphasic pulses may be delivered, depending upon control signals on control bus 184. In the event that a re¬ duced set of available electrode configurations is desired, the switching circuitry may be simplified. An example of switching circuitry may be found in the cited patent is- sued to Min (US Patent Number 5,549,642). In modern ICDs, the particular therapies are programmed into the device at the time of implant or later by the physician, and a menu of therapies is typically provided for such programming by the analyzer-programmer system 130. For example, on ini¬ tial detection of an atrial or ventricular tachycardia, an anti-tachycardia pacing therapy may be selected and delivered to the chamber in which the tachycardia is diagnosed or to both chambers. On redetection of tachycardia, a more aggressive anti-tachycardia pacing therapy may be delivered. If repeated attempts at anti-tachycardia pacing therapies fail, a higher voltage cardioversion pulse may be selected thereafter. Thera¬ pies for tachycardia termination may also vary with the rate ofthe detected tachy car- dia, with the therapies increasing in aggressiveness as the rate ofthe detected tachy¬ cardia increases. For example, fewer attempts at anti-tachycardia pacing may be un¬ dertaken prior to delivery of cardioversion pulses if the rate ofthe detected tachycar¬ dia is above a preset threshold. The cited references in conjunction with descriptions of prior art tachycardia detection and treatment therapies are applicable here as well. As described in preceding paragraphs, the programming logic and algorithms for the pain-suppressing prepulse therapies ofthe invention are embodied within the struc¬ tural framework for programming modern ICDs as described herein. In the event that atrial or ventricular fibrillation is identified, the typical ther¬ apy will be delivery of a high amplitude defibrillation pulse, typically 10 joules or more in the case of ventricular fibrillation and 10 joules or less in the case of atrial defibrillation. Lower energy levels will be employed for cardioversion. As in the case of currently available implantable pacemakers and ICDs, and as discussed in the cited references, it is envisioned that the amplitude ofthe defibrillation pulse may be incremented in response to failure of an initial pulse to terminate fibrillation. Prior art patents illustrating such pre-set therapy menus of anti-tachycardia therapies include the previously cited US Patent Number 4,587,970 issued to Holley, US Patent Num¬ ber 4,727,380 issued to Vollmann, and US Patent Number 4,830,006 issued to Ha- luska. While the invention that is disclosed is embodied in a dual chamber pacemaker and ICD, the invention may also be usefully practiced in substantially simpler de¬ vices. For example, the illustrated defibrillation electrodes may simply be coupled to an implantable atrial cardioverter as disclosed in US Patent Number 3,738,370 issued to Charms and US Patent Number 5,282,837 issued to Adams, incorporated herein by reference in their entireties. Similarly, while the electrodes employed for atria sensing and pacing are disclosed as mounted to the atrial lead, these electrodes might alterna¬ tively take the form of ring electrodes mounted to either the ventricular lead or the coronary sinus/great vein lead or on a separate electrode. From the foregoing preferred embodiments, it can be seen that the invention provides a new and improved fully implantable atrial defibrillator and a new and im¬ proved fully implantable cardioverter — defibrillator, each of which is fully automatic and which is safe in use. 3. Description ofthe Principle Methods ICD pulse generator 30 is implanted in a pectoral or abdominal pocket. When an arrhythmia occurs, ICD 30 detects it and charges the output capacitors. ICD 30 also activates the circuits required to deliver the prepulse. After the output capacitors for the therapeutic pulse are charged, ICD 30 may optionally confirm that the ar¬ rhythmia persists. In atrial fibrillation, ICD 30 may also wait until the interval be¬ tween sensed QRS complexes exceeds a predetermined, programmable value to minimize the risk of inducing ventricular fibrillation by a shock in the ventricle's vul¬ nerable period. A typical minimum interval is 500 ms. The prepulse is delivered synchronously with the sensed QRS complex. The prepulse is synchronized to the local bipolar electrogram recorded from the right- ventricular sensing electrodes 52 or to a far-field electrogram which uses the active housing 46 or right-ventricular defibrillating electrode 44. ICD 30 may transmit a te¬ lemetry pulse at the time of prepulse delivery. This telemetry pulse can be detected by analyzer-programmer system 130 and telemetry relay 134 for ICD 30. The thera¬ peutic shock is delivered 20 - 200 ms later. The preferred interval between the pre¬ pulse and therapeutic pulse is the shortest interval which optimizes PPI. Optimal PPI occurs at time intervals of approximately 100 ms, well within the ventricle's absolute refractory period. A shortest, optimal prepulse interval eliminates the risk of inducing ventricular fibrillation by a therapeutic shock delivered during atrial fibrillation or ventricular tachycardia. The strength of therapeutic shocks can be less than a ventri¬ cle's upper limit of vulnerability, and therefore the therapeutic shock is delivered with a sufficiently short interval after the sensed QRS complex to precede the inner limit of vulnerability at the therapeutic shock strength. Therefore, the prepulse is synchro- nized at QRS complex onset (Hou et al, Determination of ventricular vulnerable pe¬ riod and ventricular fibrillation threshold by use of T- wave shocks in patients under¬ going implantation of cardioverter — defibrillators, Circulation 1995; 92: 2558-2564). In patients with right- ventricular conduction delays, synchronization to a far-field electrogram may be required because the bipolar right- ventricular electrogram occurs late in the QRS complex. The prepulse may be an electrical, auditory, or vibro-tactile stimulus. ICD 30 may deliver the prepulse over the same electrode system used to deliver the therapeu¬ tic shock or over a different pathway. Prepulses may include the following: (1) elec- trical pulses delivered between two cardiac (endocardial, epicardial, or extrapericar- dial) electrodes or between one intracardiac electrode and an extracardiac electrode, for example right atrial/superior vena cava electrode 40, housing electrode 46, or a subcutaneous electrode (not illustrated); (2) electrical pulses delivered between two extracardiac electrodes including any combination ofthe housing 46, small electrodes suspended from and electrically coupled to ICD 30, an additional electrode in the ICD pocket or an adjacent pocket, or an electrode implanted at a distance from the pocket; (3) acoustic pulses delivered from a speaker in ICD 30; or (4) vibro-tactile stimuli de¬ livered to muscle, bone, or nerve via ICD 30 or from a remote stimulator controlled by the pulse generator. In the last case, communication between the pulse generator and ICD 30 may be described by standard wire or wireless methods in a same manner as telemetry communications. If an electrical prepulse is used, the range of prepulse stimulus strengths vary from 5 V to 1000 V and the duration of prepulse stimuli from 0.1 ms to 25 ms. The preferred strengths are in the range of 10 V to 100 V with preferred durations from 1 ms to 10 ms. Auditory stimuli vary in intensity from 0.1 dB(A) to 100 dB(A) above ambient noise and from 0.1 ms to 100 ms in duration. The preferred strengths range from 5 dB(A) to 15 dB(A) above ambient noise with durations from 15 ms to 25 ms. Optimal prepulse characteristics are determined on a patient-specific basis or are preset with default parameters. The method for programming a patient-specific prepulse intensity and interval is as follows: The initial prepulse interval is set near the median optimal interval for the population (about 100 ms), and the initial intensity is set slightly below the median sensory threshold. The prepulse is then delivered synchronously with a QRS complex. If it is below the patient's sensory threshold, the stimulus strength is incremented, and the process is iterated until the patient identifies the prepulse reliably. The prepulse intensity is further increased in small increments until the patient judges the prepulse to be slightly uncomfortable. It is then pro¬ grammed to a level slightly below this discomfort level. 4. Further Clinical Background Normal human subjects consistently rate startling stimuli as significantly less intense if these stimuli are preceded by an appropriate weak prestimulus than if they were presented alone ((1) Peak H, Time order error in successive judgements and in reflexes. I. Inhibition of the judgement and the reflex, J Experimental Psychology 1939; 25(6): 535 — 565, (2) Swerdlow NR et al, Effects of discrete acoustic prestimuli on perceived intensity and behavioral responses to startling acoustic and tactile stim¬ uli, Psychobiology 1999 (in press)). We therefore sought to assess the effectiveness of prepulses in reducing the startling and painful experiences of electric stimulation such as transcutaneous or transesophageal cardiac pacing or subthreshold stimulation. Electromyographic re¬ sponses of orbicularis oculi (eyeblink) and pain ratings were measured in response to transcutaneous 5 V and 15 V electric shocks (1 ms duration) applied to the left supra- orbital area in seven healthy adult male volunteers. These electric shock levels were selected based on their ability to consistently produce both a robust startle reflex and a sensation rated as "moderate pain". Prior to testing, electric stimuli were applied in 0.1 V increments, starting from 0.1 V, to determine a perceptual threshold (PT). Electromyographs were recorded from left orbicularis oculi for 200 ms after electric shock delivery, during which time mean and peak output were assessed. Immediately after each electric shock, the subjects recorded their perceived pain by making a mark on a 250 mm visual analog scale. Subjects experienced 36 trials, with a variable inter- trial interval (averaging 20 s), that consisted of 5 V or 15 V electric shocks presented alone, or preceded 60 ms by prepulses that were either 0.7 PT or 1.0 PT in intensity. These six trial types were presented in six consecutive blocks, with trial order ran¬ domized in each block. Startle magnitude was analyzed by repeated measure analysis of variance (ANOVA) with trial type and block as within-subject measures. Pain scores using the visual analog scale were analyzed similarly, and were also normal- ized for each subject by dividing each score by the score range (maximum minus minimum) for each test subject. Results were considered significant if p < 0.05. As illustrated in FIGURES 13A and 13B, both startle magnitude and pain (visual analog scale scores) were significantly reduced by 1.0 PT prepulses. For star¬ tle magnitude, ANOVA revealed a significant effect of prepulse intensity (F=7.56, df 2,12, p<0.008), a significant effect of trial block (F=3.36, df 5,30, p<0.02), and no significant intensity x block interaction (F<1). The significant effect of block reflected the process of reflex habituation, the response reduction across repeated stimulus presentations. Post — hoc comparison revealed significantly reduced startle magnitude after 1.0 PT prepulses, compared to trials without prepulses (p<0.04). For visual analog scale scores, ANOVA revealed a significant effect of prepulse intensity (F=19.04, df 2,12, p<0.0005), a significant effect of trial block (F=5.82, df 5,30, p<0.001), and no significant intensity x block interaction (F<1). The significant effect of block reflected increased pain ratings across the course ofthe test session with re- peated shocks (sensitization). Post — hoc comparisons revealed significantly reduced visual analog scale scores after 1.0 PT prepulses, compared to trials without prepulses (p<0.005). Electric shocks resulted in pain responses that were at least of "moderate" intensity, and this particular type of prepulse (1.0 PT, 0.1 ms, 60 ms prepulse interval) results in a reduction in overall visual analog scale scores by approximately 27%. The prepulse effects were evident across the entire session, including the initial block, and were also evident for every subject (7 out of 7), and for each electric shock strength (both 5 V and 15 V). Therefore, in the 14 different conditions (7 subjects x 2 electric shock levels), 1.0 PT prepulses effectively reduced perceived pain. 5. Further Detailed Description. FIGURE 14A illustrates a pulse generator 210 serving as a transcutaneous cardiac pacing (TCP) system for delivering electrical pulses to a patient's heart 200. The TCP system 210 includes a set of two cutaneous electrodes 212 attached to the skin at anatomically selected locations. The electrodes are connected to the TCP sys¬ tem via standard ECG electrical connections 214. To administer TCP, the electrodes are typically placed at the anterior chest wall and back ofthe patient, or at the pa¬ tient's sternum and apex ofthe heart. The pulse generator 210 serving as a TCP sys- tern can deliver electrical pulses at a subthreshold level for pacing, depending on the amplitude settings for the device at the time of use. Similarly, FIGURE 14B illustrates a pulse generator 220 serving as a trans¬ esophageal cardiac pacing (TEP) system for delivering electrical pulses to a patient's heart 200. The TEP system 220 includes an esophageal electrode system 222 located in the patient's esophagus and within pacing range ofthe patient's heart 200. The electrode system is connected to the TEP system via standard ECG electrical connec¬ tions 222. The TCP system 210 generates pacing pulses effective to stimulate cardiac activity in a patient. The pulse generator provides ventricular sensing and extensive programmability. The pacing mode is most commonly programmed to the VVI pac¬ ing mode. A square wave, trapezoidal, or exponential pulse is used for either a pre¬ pulse or a pacing pulse and is programmable. A prepulse can have a different shape than a pacing pulse if the TCP system 210 is programmed accordingly. The prepulse and pulse durations are programmable from 1 to 500 ms. The prepulse and pulse cur- rent amplitudes are programmable from 1 to 250 mA. The prepulse and pulse pacing rates are programmable from 1 to 250 ppm. High pacing rates permit overdrive pac¬ ing for tachycardia termination. The programmable pacing parameters are adjustable continuously or step by step. Each pulse type (prepulse or pulse) has separate pro¬ grammable parameters, permitting the TCP system 210 operator to program duration and current amplitude value for the prepulse that are different from those parameter values for the pacing pulse. Ventricular sensing is performed when desired to prevent competition and ventricular arrhythmias after spontaneous rhythm restoration. Asyn¬ chronous pacing is applied by programming or by removing the sensing electrodes if the sensing electrodes are separate from the pacing electrodes. FIGURE 15 illustrates a block diagram ofthe present invention as a typical pulse generator 230. The internal circuits and programming ofthe pulse generator 230 generally include pacer timing/control circuitry 232, pacer oscillator 234, pacer pulse — shaping circuitry 236, pacer isolation circuitry 238, and pacing electrode sys- tern 240, 242, and 242. The pulse generator 230 as described serves to deliver transcutaneous or trans¬ esophageal cardiac pacing pulses. An example of a pulse generator 230 designed to delivery transcutaneous or transesophageal pulses is set forth in US Patent Number 4,349,030 issued to Belgard, incorporated herein by reference in its entirety. Refer- ring to FIGURE 15, the electrodes 240 are attached to a patient's chest and electrically connected 242 and 244 to the pulse generator 230. The input for the pulse generator 230 is a trigger signal provided by the timing circuitry 232. In a synchronous mode QRS signals from a standard cardiac monitor controls the trigger signal. In an asyn¬ chronous mode the trigger signals are provided at an adjustable uniform rate. A switch (not shown) also permits the operator to trigger signals manually. Means for generating single or multiple signals in any complex timing pattern desired is pro¬ vided. An adjustable rate limit control in the synchronous mode prevents rapid stimulation of frequency synchronizing signals, and it is also allows the production of stimuli only after alternate or after three or more QRS synchronizing signals. The pulse generator 230 as a TCP system generally comprises a trigger amplifier, pulse width monostable multivibrator, oscillator, amplifier, isolation transformer, and out¬ put circuitry, comprising a rectifier, attenuator, and filter, as primary components to the pacer timing and control circuitry 232, pacer oscillator and drive circuitry 234, and the pacer pulse — shaping circuitry 236. FIGURE 1 illustrates the combination of a prepulse 14 and a pacing pulse 18 as a pretreating pacing unit. The pulse generator 230 as a TCP system outputs a pre- treating pacing unit at a rate of 1 to 250 ppm, creating a continuous series of pretreat¬ ing pacing units that are used to stimulate the patient until such time that the TCP system 230 operator stops pacing or stimulation output. FIGURE 16 further illus¬ trates this method of operation for the present invention. At each starting time for a next pretreating pacing unit, the pulse generator 230 outputs a prepulse 250. The pulse generator 230 then delays output for a first predetermined period of time 252, ranging from 20 ms to 500 ms in length. The pulse generator 230 then outputs a pac- ing pulse or subthreshold stimulation pulse 254. The pulse generator 230 then delays output for a second predetermined period of time 256. In this way, the pulse genera¬ tor 230 creates a continuous stream or sequence of prepulse — pulse pacing units com¬ prising a pretreating prepulse 14 prior to a painful therapeutic pulse 18 in accordance with PPI. The pulse generator 230 incorporates a blanking circuit that filters out the sig¬ nal — distorting prepulse and pacing stimuli to allow ECG monitoring. A monitor or a strip — chart recorder can be integrated with the pulse generator 230. An external de¬ fibrillator can also be integrated with the pulse generator 230 to provide a complete cardiac arrest intervention system, offering antibradycardia and antitachycardia pacing combined with a defibrillation capability. The combined pacemaker — defibrillator can be connected to a patient with a single set of multifunction electrodes used to per¬ form arrhythmia detection, pacing, and defibrillation. Other modules can be inte¬ grated with the pulse generator 230 as well, including such devices as a blood pres- sure monitor, an oximeter, and temperature and respiratory monitors. In one preferred embodiment, the same set of electrodes are used to administer both the prepulses and the pacing pulses. An example of such a multiple purpose electrode may be found in US Patent Number 5,205,297 issued to Montecalvo , incor¬ porated herein by reference in its entireties. In another preferred embodiment, a first set of electrodes are used to administer the pacing pulses and a second set of elec¬ trodes are used to administer the prepulses. Those skilled in the art will recognize that the preferred embodiment or em¬ bodiments thereof disclosed herein are exemplary in nature and that various changes can be made therein without departing from the scope and the spirit of this invention. In that regard, as many changes as are possible to the embodiments of this invention utilizing the teachings thereof, the descriptions above, and the descriptions above and the accompanying drawings should be interpreted in the illustrative and not the lim¬ ited sense. In particular, it should be understood that there may be other embodiments which fall within the scope ofthe present invention as defined by the following claims. Where a claim, if any, is expressed as a means or step for performing a speci¬ fied function it is intended that such claim be construed to cover the corresponding structure, material, or acts described in the specification and equivalents thereof, in¬ cluding both structural equivalents and equivalent structures, material-based equiva¬ lents and equivalent materials, and act-based equivalents and equivalent acts.

Claims: CLAIMS The invention claimed is: 1. A therapeutic method, comprising the steps of: (a) applying a preceding stimulus to a patient's body; (b) waiting a first predetermined time period; (c) applying a painful stimulus to the patient's body, whereby the patient per¬ ceives pain associated with said painful stimulus as being reduced; and (d) continuing steps (a) through (c) for a second predetermined time period. 2. The method of claim 1 , wherein said preceding stimulus is selected from the group of preceding stimuli consisting of an electrical stimulus, an auditory stimulus, and a vibro — tactile stimulus. 3. The method of claim 1, wherein said painful stimulus is selected from the group of painful stimuli consisting of a transcutaneous pacing pulse, a transcuta¬ neous subthreshold pulse, a transesophageal pacing pulse, and a transesophageal sub- threshold pulse. 4. The method of claim 1 , wherein said first predetermined time period is between 20 and 500 milliseconds. 5. The method of claim 1 , wherein said first predetermined time period is between 50 and 250 milliseconds. 6. The method of claim 1 , wherein said second predetermined time period is selected from the group of time periods consisting of a second, a minute, an hour, a day, a week, and a month. 7. The method of claim 1 , wherein said step of applying said preceding stimulus comprises delivering said preceding stimulus for a duration from 0.1 milli- second to 50 milliseconds. 8. The method of claim 1 , wherein said step of applying said preceding stimulus comprises delivering said preceding stimulus for a duration from 1 millisec¬ ond to 10 milliseconds. 9. The method of claim 1 , wherein said step of applying said preceding stimulus comprises delivering an electrical preceding stimulus at an amplitude from 1 millivolt to 100 volts. 10. The method of claim 1 , wherein said step of applying said preceding stimulus comprises delivering an electrical preceding stimulus at an amplitude from 1 millivolt to 10 volts. 11. The method of claim 1 , wherein said step of applying said preceding stimulus comprises delivering an auditory preceding stimulus at an intensity from 0.1 dB(A) to 100 dB(A) above an existing ambient noise level. 12. The method of claim 1 , wherein said step of applying said preceding stimulus further comprises delivering an auditory preceding stimulus at an intensity from 5 dB(A) to 15 dB(A) above said existing ambient noise level. 13. The method of claim 1, wherein said preceding stimulus is applied to a first body part and wherein said painful stimulus is applied to a second body part. 14. The method of claim 13, wherein said first body part and said second body part are the same body part. 15. The method of claim 1 , wherein said steps of applying preceding stimulus and said painful stimulus have the same sensory modality. 16. The method of claim 1 , wherein said steps of applying said preceding stimulus and said painful stimulus have different sensory modalities. 17. The method of claim 1 , wherein said step of applying said preceding stimulus includes at least one first stimulus which has a sensory modality which is the same as that of said painful stimulus and at least one second stimulus that has a differ¬ ent sensory modality than that of said painful stimulus. 18. The method of claim 1 , used for pretreating a patient prior to a painful electrical stimulus for treatment of a cardiac arrhythmia of said patient, wherein said preceding stimulus is a relatively small electrical stimulus applied to the patient prior to applying a relatively large electrical stimulus as said painful electrical stimulus to treat said patient's arrhythmia. 19. The method of claim 1 , used for pretreating a patient prior to a painful electrical stimulus for treatment of a cardiac arrhythmia of said patient, wherein said preceding stimulus is an auditory prepulse adapted to be audible by said patient prior to said application of said painful electrical stimulus to treat said patient's arrhythmia. 20. The method of claim 1 , used for pretreating a patient prior to a painful electrical stimulus for treatment of a cardiac arrhythmia of said patient, wherein said preceding stimulus is a vibro-tactile prepulse adapted to be felt by said patient prior to said application of said painful electrical stimulus to treat said patient's arrhythmia. 21. The method of claim 18, further comprising the steps, conducted prior to applying said preceding stimulus and said painful stimulus, of: (a) preparing a first energy source and circuitry to deliver said painful electrical stimulus; and (b) preparing a second energy source and circuitry to deliver said preceding electrical stimulus. 22. The method of claim 21 , wherein said step of preparing said first en¬ ergy source and circuitry occurs simultaneously with said step of preparing said sec¬ ond energy source and circuitry. 23. The method of claim 21 , wherein said first energy source and circuitry and said second energy source and circuitry are unitary, whereby said electrical pre¬ ceding stimulus is delivered using the same energy source and circuitry as said elec¬ trical painful stimulus. 24. The method of claim 1 , further comprising the step of administering a predetermined medication which is pharmacologically effective at enhancing said re¬ duction in said patient's perceived pain associated with said painful transcutaneous stimulus due to said preceding stimuli, prior to said step of applying said preceding stimuli. 25. The method of claim 1 , further comprising the step of administering a predetermined medication which is pharmacologically effective at enhancing said re¬ duction in said patient's physiological response to said painful transcutaneous stimu¬ lus due to said preceding stimulus, prior to said step of applying said preceding stim- uli. 26. A method of pretreating a patient during a series of painful electrical stimuli delivered from a stimulation device, comprising the steps of: (a) detecting a need to provide painful electrical stimulation; (b) preparing an electrical prepulse to pretreat said patient; (c) preparing said painful electrical stimulus to treat said need; (d) delivering said electrical prepulse to pretreat said patient; (e) waiting a predetermined interval of time; (f) delivering said painful electrical stimulus to treat said need, whereby said patient physiologically and psychologically responds to said pain¬ ful electrical stimulus at a reduced level; and (g) continuing steps (b) through (f) until said painful electrical stimuli are no longer required to treat said need. 27. A method of pretreating a patient during a series of painful transcuta¬ neous pulses delivered from a transcutaneous pacemaker to treat an arrhythmia, com¬ prising the steps of: (a) detecting an occurrence of an arrhythmia; (b) preparing a prepulse to pretreat said patient; (c)preparing said painful transcutaneous pacing pulse to treat said arrhythmia; (d) delivering said prepulse to pretreat said patient; (e) waiting a predetermined interval of time; (f) delivering said painful transcutaneous pacing pulse to treat said arrhythmia, whereby said patient physiologically and psychologically responds to said painful transcutaneous pacing pulse at a reduced level; and (g) continuing steps (b) through (f) until said painful transcutaneous pacing pulses are no longer required to treat said arrhythmia. 28. A method of pretreating a patient during a series of painful transcuta¬ neous pulses delivered from a transcutaneous pacemaker to treat an arrhythmia, com¬ prising the steps of: (a) detecting an occurrence of an arrhythmia; (b) preparing a prepulse between 1 millivolt to 100 volts to pretreat said patient; (c) preparing said painful transcutaneous pacing pulse to treat said ar¬ rhythmia; (d) delivering said prepulse to pretreat said patient for between 0.1 and 50 milliseconds; (e) after step (d), waiting between 20 and 500 milliseconds; (f) delivering said painful transcutaneous pacing pulse to treat said ar¬ rhythmia, whereby said patient physiologically and psychologically re¬ sponds to said painful transcutaneous pacing pulse at a reduced level; and (g) continuing steps (b) through (f) until said painful transcutaneous pac¬ ing pulses are no longer required to treat said arrhythmia. 29. A method of pretreating a patient during a series of painful trans- esophageal pulses delivered from a transesophageal pacemaker to treat an arrhythmia, comprising the steps of: (a) detecting an occurrence of an arrhythmia; (b) preparing a prepulse to pretreat said patient; (c) preparing said painful transesophageal pacing pulse to treat said arrhythmia; (d) delivering said prepulse to pretreat said patient; (e) waiting a predetermined interval of time; (f) delivering said painful transesophageal pacing pulse to treat said arrhythmia, whereby said patient physiologically and psychologically responds to said painful transesophageal pacing pulse at a reduced level; and (g) continuing steps (b) through (f) until said painful transesophageal pacing pulses are no longer required to treat said arrhythmia. 30. A method of pretreating a patient during a series of painful trans- esophageal pulses delivered from a transesophageal pacemaker to treat an arrhythmia, comprising the steps of: (a) detecting an occurrence of an arrhythmia; (b) preparing a prepulse between 1 millivolt to 100 volts to pretreat said patient; (c) preparing said painful transesophageal pacing pulse to treat said ar¬ rhythmia; (d) delivering said prepulse to pretreat said patient for between 0.1 and 50 milliseconds; (e) after step (d), waiting between 20 and 500 milliseconds; (f) delivering said painful transesophageal pacing pulse to treat said ar¬ rhythmia, whereby said patient physiologically and psychologically re¬ sponds to said painful transesophageal pacing pulse at a reduced level; and (g) continuing steps (b) through (f) until said painful transesophageal pac¬ ing pulses are no longer required to treat said arrhythmia. 31. A medical therapeutic apparatus, comprising: (a) at least one transmission element adapted for connection to a patent's body; (b) a pulse generator coupled to said at least one transmission element; and (c) a controller coupled to said pulse generator and to said at least one transmission element for applying, via said at least one transmission element, an alternating series of (i) a preceding stimulus to the patient's body and for applying, via said at least one transmission element, (ii) a painful therapeutic stimulus to the patient's body a predetermined time period after application of said preceding stimulus, whereby the patient perceives pain associated with said series of painful therapeutic stimuli as being reduced. 32. The apparatus of claim 31 , wherein said preceding stimulus includes an electrical stimulus and said at least one transmission element includes an electrode. 33. The apparatus of claim 31 , wherein said preceding stimulus includes an auditory stimulus and said at least one transmission element includes a speaker de¬ vice. 34. The apparatus of claim 31 , wherein said preceding stimulus includes a vibro-tactile stimulus and said at least one transmission element includes a vibrator device. 35. The apparatus of claim 31 , wherein said predetermined time period is between 20 and 500 milliseconds. 36. The apparatus of claim 31 , wherein said predetermined time period is between 50 and 250 milliseconds. 37. The apparatus of claim 31 , wherein said preceding stimulus is applied to the patient's body for a duration from 0.1 millisecond to 50 milliseconds. 38. The apparatus of claim 31, wherein said preceding stimulus is applied to the patient's body for a duration from 1 millisecond to 10 milliseconds. 39. The apparatus of claim 32, wherein said electrical preceding stimulus is applied to the patient's body at an amplitude from 1 millivolt to 100 volts. 40. The apparatus of claim 32, wherein said electrical preceding stimulus is applied to the patient's body at an amplitude from 1 millivolt to 10 volts. 41. The apparatus of claim 33, wherein said auditory preceding stimulus is applied to the patient's body at an intensity from 0.1 dB(A) to 100 dB(A) above an existing ambient noise level. 42. The apparatus of claim 33, wherein said auditory preceding stimulus is applied to the patient's body at an intensity from 5 dB(A) to 15 dB(A) above said ex¬ isting ambient noise level. 43. The apparatus of claim 31 , wherein said preceding stimulus is applied to a first body part and wherein said painful therapeutic stimulus is applied to a sec¬ ond body part. 44. The apparatus of claim 31, wherein said preceding stimulus and said painful therapeutic stimulus are applied to the same body part. 45. The apparatus of claim 31 , wherein said painful therapeutic stimulus comprises a transcutaneous cardiac pacing pulse. 46. The apparatus of claim 31, wherein said painful therapeutic stimulus comprises a transesophageal cardiac pacing pulse. 47. The apparatus of claim 31 , wherein said preceding stimulus and said painful therapeutic stimulus have the same sensory modality. 48. The apparatus of claim 31, wherein said preceding stimulus and said painful therapeutic stimulus have different sensory modalities. 49. The apparatus of claim 31 , wherein said preceding stimulus includes a stimulus which has the same sensory modality as that of said painful therapeutic stimulus and a stimulus which has a different sensory modality than that of said pain¬ ful therapeutic stimulus. 50. The apparatus of claim 31 , wherein said pulse generator includes: (a) a first energy source for applying said painful therapeutic electrical stimulus; and (b) a second energy source for applying said preceding electrical stimulus. 51. The apparatus of claim 50, wherein said first energy source is activated simultaneously with activating said second energy source. 52. The apparatus of claim 50, wherein said first energy source and said second energy source are unitary, whereby said electrical preceding stimulus is deliv¬ ered using the same energy source and circuitry as said electrical painful therapeutic stimulus. 53. A medical therapeutic apparatus for pretreating a patient during a series of painful transcutaneous pulses, comprising: (a) at least one first electrode adapted for location selected from the group of locations consisting of said patient's lower left chest, left side, and apex ofthe heart; (b) a second electrode adapted for location selected from the group of lo- cations consisting of said patient's back, right side, and right upper chest; (c) a pulse generator coupled to said first and second electrodes; and (d) a controller coupled to said pulse generator and to said first and second electrodes for applying, via said first and second electrodes, an alter- nating series of (i) preceding electrical pulses and (ii) painful transcu¬ taneous pacing pulses to the patient's body a predetermined time pe¬ riod after application of said preceding electrical pulses, whereby the patient perceives pain associated with said painful transcutaneous pac¬ ing pulses as being reduced. 54. A medical therapeutic apparatus for pretreating a patient during a series of painful transcutaneous pulses, comprising: (a) at least one first electrode adapted for location selected from the group of locations consisting of said patient's lower left chest, left side, and apex ofthe heart; (b) a second electrode adapted for location selected from the group of lo¬ cations consisting of said patient's back, right side, and right upper chest; (c) a pulse generator coupled to said first and second electrodes; and (d) a controller coupled to said pulse generator and to said first and second electrodes for applying, via said first and second electrodes, an alter¬ nating series of (i) preceding electrical pulses with a duration from 0.1 millisecond to 50 milliseconds and with an amplitude from 1 millivolt to 10 volts and (ii) painful transcutaneous pacing pulses to the patient's body between 20 and 500 milliseconds after application of said pre¬ ceding electrical pulses, whereby the patient perceives pain associated with said painful transcutaneous pacing pulses as being reduced. 55. A medical therapeutic apparatus for pretreating a patient during a series ul transesophageal pulses, comprising: (a) at least one first electrode adapted for location inside said patient's esophagus; (b) a second electrode adapted for location inside said patient's esophagus; (c) a pulse generator coupled to said first and second electrodes; and (d) a controller coupled to said pulse generator and to said first and second electrodes for applying, via said first and second electrodes, an alter¬ nating series of (i) preceding electrical pulses with amplitudes from 1 millivolt to 10 volts and (ii) painful transesophageal pacing pulses to the patient's body a predetermined time period after application of said preceding electrical pulses, whereby the patient perceives pain associ¬ ated with said painful transesophageal pacing pulses as being reduced. 56. A medical therapeutic apparatus for pretreating a patient during a series of painful transesophageal pulses, comprising: (a) at least one first electrode adapted for location inside said patient's esophagus; (b) a second electrode adapted for location inside said patient's esophagus; (c) a pulse generator coupled to said first and second electrodes; and (d) a controller coupled to said pulse generator and to said first and second electrodes for applying, via said first and second electrodes, an alter¬ nating series of (i) preceding electrical pulses with a duration from 0.1 millisecond to 50 milliseconds and with an amplitude from 1 millivolt to 10 volts and (ii) painful transesophageal pacing pulses to the pa¬ tient's body between 20 and 500 milliseconds after application of said preceding electrical pulses, whereby the patient perceives pain associ¬ ated with said painful transesophageal pacing pulses as being reduced. 57. A therapeutic method, comprising the steps of applying a preceding stimulus to a patient's body, waiting a predetermined time period, and applying a painful therapeutic stimulus to the patient's body, whereby the patient perceives pain associated with said painful therapeutic stimulus as being reduced and/or the patient physiologically responds to said painful therapeutic stimulus at a reduced level. 58. A medical therapeutic apparatus, comprising: (a) at least one transmission element adapted for connection to a patent's body; (b) a pulse generator coupled to said at least one transmission element; and (c) a controller coupled to said pulse generator and to said at least one transmission element for applying, via said at least one transmission element, a pre¬ ceding stimulus to the patient's body and for applying, via said at least one transmis¬ sion element, a painful therapeutic stimulus to the patient's body a predetermined time period after application of said preceding stimulus, whereby the patient perceives pain associated with said painful therapeutic stimulus as being reduced and/or the patient physiologically responds to said painful therapeutic stimulus at a reduced level.

Applicants: IMPERCEPTION INC, IMPERCEPTION, INCORPORATED
Application year: 1999
Main classification: A61N
IPC codes: A61N1