JP2007503257A - Method and apparatus for cardiac resuscitation - Google Patents

Abstract

An apparatus for resuscitating the heart during a persistent episode of ventricular fibrillation, fine ventricular fibrillation, or asystole is provided.
An apparatus for resuscitating the heart during ventricular fibrillation, fine ventricular fibrillation, or persistent failure contraction delivers circulatory assistance during a time interval suitable to relieve cardiac myocardial hypoxia. And means for delivering a series of therapeutic electrical pulses capable of depolarizing at least a portion of the heart myocardium. Circulatory assistance may be delivered manually, for example, in the form of cardiopulmonary resuscitation (CPR), or in the form of, for example, a membrane oxygenator, the operation of an implantable ventricular assist device, or an automated CPR device May be mechanized. The apparatus can be implemented with an external or implantable cardiac electrical stimulation device and associated electrodes capable of delivering a series of pacing class pulses or defibrillation class pulses.
[Selection] Figure 1

Description

  The present invention relates generally to the field of cardiac resuscitation, and in particular, by delivering a combination of circulatory assistance or support and a series of cardiac stimulation pulses for depolarization, Alternatively, it relates to a method and apparatus for restoring cardiac activity after something close to asystole has occurred.

  Sudden cardiac death (SCD) kills an estimated 400,000 to 450,000 lives each year in the United States, and the incidence of SCD among young adults is increasing. SCD is usually caused by arrhythmia or coronary artery disease. Due to the unexpected nature of SCD, it is difficult to prevent SCD, and SCD continues to be a possible cause for the majority of heart-related deaths.

  Ventricular tachycardia (VT) or ventricular fibrillation (VF) often occurs before SCD. A defibrillation shock delivered within one minute of the beginning of fibrillation can be very effective in preventing death and restoring normal heart rhythm. Patients diagnosed as having a tendency to arrhythmia can benefit from an implantable cardioverter-defibrillator that quickly delivers life-saving electrical stimulation therapy after the onset of arrhythmia.

  However, patient risk for SCD is often unknown prior to the first arrhythmia episode and is often fatal if not treated quickly. The likelihood of successfully resuscitating from cardiac arrest using only cardiopulmonary resuscitation (CPR) is very low. Only 1-2% of patients treated with CPR in the hospital are discharged. CPR alone generally does not convert VF to sinus rhythm, but even if an external defibrillation shock is delivered to terminate VF, the result is asystole or pulselessness, also called electromechanical dissociation (EMD) Often becomes electrical activity (PEA). The success rate of defibrillation shock delivery is dramatically reduced over the first few minutes following the onset of VF. See August 2003 Annals of Emergency Medicine Volume 42, p242-250, entitled “Optimal Defibrillation Response Intervals for Maximum Out-of-hospital Cardiac Arrest Survival Rates” by V. DeMaio et al. The probability of a successful resuscitation using existing techniques is low, as there is little chance of emergency response personnel arriving within 4 minutes. The probability of emergency response personnel arriving within 15 minutes is good. Therefore, there is a need for new cardiac resuscitation techniques that allow a successful conversion to sinus rhythm after prolonged VF, fine VF, or asystole.

  The result of VF that limits the rate of successful resuscitation using current methods is hypoxia caused by perfusion damage during VF. During normal heart function, myocardial fiber contraction occurs when calcium enters cells through calcium channels (L-type channels). Calcium enters the cell when it is depolarized by the action potential across the cell membrane and increases its permeability to calcium via L-type channels. As calcium enters the cell, more calcium is released from the sarcoplasmic reticulum (SR) through the ryanodine channel into the muscle trait. This “calcium-induced calcium release” increases myoplasmic calcium concentration, whereby calcium interacts with myofilaments resulting in mechanical cycling of myofilaments and sarcomere shortening.

  Calcium requires the cellular fuel adenosine triphosphate (ATP) to operate and via an intracellular calcium pump known as “muscle endoplasmic reticulum or endoplasmic reticulum calcium ATPases” (or “SERCA”). It is stored again in the SR. Muscle filament cycling, especially during relaxation, also requires ATP. Both of these operations are affected by low oxygen as a result, as oxygen is required for ATP generation. During fibrillation, hypoperfusion of the heart results in a lack of available ATP for hypoxia and cellular function. If VF, asystole, or an episode close to asystole persists for several minutes, hypoxia becomes serious and becomes a limiting factor that prevents successful external defibrillation attempts.

  However, other mechanisms may play an important role. Ryanodine calcium channels that normally release calcium from SR during calcium-induced calcium release are “leaky”, that is, some calcium is released from the SR without a calcium-induced calcium release mechanism. Normally, SR calcium stores are replenished during each cardiac cycle by calcium re-uptake from the muscle trait via calcium entering the cells through L-type channels and via SERCA. In the absence of a constant sequence of action potentials, SR calcium storage can decrease as calcium leaks from the SR and is removed from the cell by sodium-calcium ion channels that maintain the cell's normal low electrostatic potential. As a result, this “leaked” calcium becomes unavailable to contribute to sarcomere shortening for the next action potential.

  In the past, this SR calcium leak was considered insignificant. However, recent studies suggest that this calcium leakage can be quite large. It can be theorized that, in large quantities, cardiac function gradually decreases by at least two mechanisms during fibrillation. First, hypoxia due to inadequate myocardial perfusion resulting from effective loss of circulation reduces the ATP available for SR calcium intake through myofilament cycling and SERCA. Second, SR calcium depletion due to calcium leakage is exacerbated by lack of sufficient cell depolarization and SERCA activity to supplement SR calcium storage, thereby reducing the available calcium for myofilament cycling. Therefore, both cumulative ATP loss and SR calcium depletion may contribute to exacerbating loss of function during the first 3-5 minutes following cardiac arrest, and successful resuscitation using known techniques It will be a hindrance.

  Defibrillation alone may restore heartbeat when SR calcium storage is not depleted, which theoretically corresponds to a time course of up to 3-5 minutes where defibrillation can be effective. A single high voltage defibrillation shock depolarizes a large myocardial volume and allows it to enter into calcium, followed by a normal cardiac cycle if the ATP reserve is not yet exhausted A calcium treatment cycle is generated that can regenerate the process. However, when SR calcium storage is rather depleted, it is difficult to recover SR calcium loss without the contribution of extracellular calcium influx through L-type channels, which occurs only by repeated cell depolarization. Brelation alone may not be enough. When hypoxia begins, ATP becomes unavailable to myofilaments and SERCA. Many modern publications have emphasized the importance of CPR being enforced prior to shock delivery. It has been reported that when fibrillation has been present for longer than 4 minutes, 1 minute CPR delivered prior to delivery of the shock has resulted in better survival than immediate defibrillation.

  However, even when CPR is performed, individual defibrillation shocks usually do not restore sinus rhythm after prolonged fibrillation or asystole episodes. A single depolarization shock is not appropriate to restore cellular calcium treatment cycling because the calcium influx that occurs during a single depolarization may be insufficient to restore normal SR calcium concentration There is. Early studies in the development of percutaneous defibrillation therapy reported that a series of shocks was more effective than a single high energy shock. In one study, if the first shock failed to fully defibrillate, a series of shocks were uniformly successful. A series of depolarizations may be necessary to restore normal SR calcium concentration by the additive effect of a depolarization sequence that makes intracellular calcium available for SR retention.

  Despite early observations in the defibrillation study, subsequent studies focused primarily on single shock defibrillation currently being performed on implantable defibrillation devices. Single shock defibrillation requires less energy than a series of shocks and is therefore better suited to be implemented with implantable devices. Eventually, single shock defibrillation was found to be effective in scenarios of fibrillation detection within a few seconds of onset, with arrhythmia detection algorithms available on implantable devices.

  The use of multiple pulses during the treatment of cardiac arrhythmias has been proposed in some patients. Pulseless after performing defibrillation in a subject suffering from a fibrillating heart, including a first treatment waveform that is insufficient to defibrillate the heart and a second treatment waveform that defibrillates the heart A method for reducing the likelihood of initiating sexual electrical activity (PEA) is disclosed in its entirety in US Patent Application Publication No. 2002/0161407 to Walcott et al. A system and method for delivering a plurality of closely spaced defibrillation pulses to the heart is generally disclosed in US Pat. No. 5,620,464 issued to Kroll et al. Reduce overall size. Organize the activity of randomly contracting cardiomyocytes so that the defibrillation waveform applied after pretreatment can accomplish its task with less energy than would otherwise be required A process for applying electrical pretreatment to a fibrillating heart is disclosed in U.S. Pat. No. 5,314,448 issued to Kroll et al. In US Pat. No. 6,314,319 issued to Kroll et al., Cardiac cells are stimulated to force the contraction to produce hemodynamic output during fibrillation, and tachycardia or deflated contractions to hemodynamics. The electrical method of reducing the electrical power is disclosed in its entirety in the method referred to as “Electrical Cardiac output Forcing”.

  A method of treating the heart to restore blood flow, wherein electromechanical dissociation occurs after completion of ventricular tachyarrhythmia or ventricular fibrillation, the method comprising electromechanical after completion of ventricular tachyarrhythmia or fibrillation Identifying dissociation and providing electrical therapy, where the therapy includes a series of packets of electrical pulses, the method is disclosed in its entirety in WO 00/66222 issued to Rosborough and Deno . A series of pulse packets is delivered after ventricular tachyarrhythmia or fibrillation is terminated and an electromechanical dissociation is detected.

  However, there remains a need to address the problem of cardiac resuscitation after long-term episodes of ventricular fibrillation or asystole, and after long-term episodes, the severity of hypoxia is an electrical stimulus based on the method of defibrillating the heart. Plays an important role in limiting the success of In long-term, eg, fibrillation or asystole scenarios that exceed 1-2 minutes, the inventors of the present invention have found that both hypoxia and gradual SR calcium loss are the success rate of single shock defibrillation. Advocates that it is a cause of low. Therefore, in order to improve the success of cardiac resuscitation, the resuscitation method must deal with hypoxia and intracellular calcium loss. Therefore, it is thought that more calcium is made available to the pump by repeatedly sending electrical stimulation, so ATP can be made available to calcium pumps that depend on ATP, and SR calcium storage can be standardized. To achieve this, resuscitation methods that include a mechanism to mitigate hypoxia are needed.

  The present invention is particularly directed to providing systems and methods for performing cardiac resuscitation after long-term episodes of VF, fine VF, or asystole. The present invention provides circulatory assistance, which can be in the form of CPR or other perfusion or hemodynamic assistance delivered manually or automatically, and induces a series of cardiac depolarizations after a predetermined period of circulatory assistance In a system and method that includes: In one embodiment, a series of cardiac depolarizations are triggered by electrical stimulation pulses delivered with pulsed energy that depolarizes a mass of cardiomyocytes. Thus, a pulse train is referred to herein as a relatively low energy pulse, such as the energy normally associated with a cardiac pacing pulse, referred to herein as a “pacing class pulse”, and / or a “defibrillation class pulse” herein. It may include relatively high energy pulses normally associated with a called defibrillation shock. A series of cardiac stimulation pulses may be delivered at a constant or variable rate and constant or variable amplitude over a predetermined time interval or multiple pulses. In one embodiment, the series of stimulation pulses ends with a specified interval of high voltage defibrillation shock following the last stimulation pulse in the column.

  The apparatus for delivering the electrical stimulation portion of the resuscitation treatment may be embodied as a set of external stimulation devices and associated electrodes that deliver cardiac stimulation pulses percutaneously or esophagus. Alternatively, the device for delivering cardiac stimulation pulses may be an implantable heart capable of delivering cardiac stimulation pulses via intracardiac electrodes, epicardial electrodes, or electrodes placed subcutaneously or submuscularly. It may be embodied as a stimulation device and an electrode system. For programmable implantable devices, the resuscitation method provided by the present invention may be included in a menu of selectable arrhythmia treatments.

  In other embodiments, the cardiac stimulation device further includes a cardiac stimulation therapy provided to improve cardiac output following cardiac resuscitation. In one embodiment, the cardiac stimulation device includes providing an extra-systolic stimulation pulse that is delivered to achieve the mechanical benefit of extra-systolic potentiation.

  In yet another embodiment, the system includes a physiological sensor that can generate a signal associated with the delivery of circulatory assistance. Sensors are provided as surrogate sensors, such as blood oxygen saturation (SaO2), or other metabolic parameters that directly or indirectly indicate lactate or hydrogen peroxide, pH or the extent of hypoxia. May be. In alternative embodiments, the sensor is provided as a mechanical sensor that generates a signal related to the presence of circulatory assistance, such as a blood pressure sensor, accelerometer, or mechanical sensor sensitive to chest compressions delivered during CPR. May be. The sensor signal may be used by an implantable stimulation device that automatically detects the presence and duration of circulatory assistance for use in determining an appropriate time to trigger the electrical stimulation portion of the resuscitation treatment. .

  FIG. 1 is a schematic diagram of a method for delivering cardiac resuscitation therapy after long-term episodes of VF, fine VF, or asystole. As used herein, VF refers to a coarse VF that appears on the ECG as a relatively high amplitude fibrillation wave that is usually readily observable on ECG monitoring equipment. “Fine VF” refers to the presence of relatively low amplitude fibrillation waves that may not be observable on some ECG monitoring equipment. As used herein, the term “asystole” refers to “bradycardia”, where there is no electrical activity and a very low rate of electrical activity present but less than about 10 depolarizations per minute. Refers to an activity that is sometimes referred to as "asystole".

  The method includes delivering a circulatory assist 52 that may be in the form of external chest compression used in CPR. Patient 50 is preferably provided with circulatory assistance 52 to prevent or alleviate hypoxia during long-term episodes of VF, fine VF, or asystole. By preventing or mitigating hypoxia, ATP is believed to be available for SERCA and other cellular functions. Moreover, maintaining cerebral perfusion is particularly important during long-term VF, fine VF, or asystole to avoid irreversible cerebral damage in the successful resuscitation of the heart.

  Chest compressions may be delivered manually by emergency responders or automatically using automated resuscitation equipment. If patient 50 is not spontaneously breathing, ventilatory assistance may also be required. Ventilation 54 may be delivered manually or using a ventilator according to known CPR techniques. Depending on the location of the patient, the equipment available in the field, and the skills of emergency responders, the type of ventilator 54 and the applied circulatory assistance 52 may vary. For example, in a hospital or emergency room environment, a patient can be placed on top of a ventilator and subjected to manual or automatic chest compressions. In a surgical environment, a direct cardiac massage may be provided for circulatory assistance, or another type of circulatory assistance mechanism, such as an intra-aortic balloon pump or membrane oxygenator (ECMO), is put in place. May be. In an out-of-hospital environment, manual CPR may be the only circulatory aid available.

  The resuscitation method further includes delivering cardiac stimulation pulses using 56, an external electrical stimulation device, in the embodiment shown in FIG. Stimulator 56 delivers cardiac electrical stimulation pulses via associated sets of leads 58 and electrodes 60. The electrode 60 can be provided as a skin electrode normally placed on the torso, generally in the thorax area, for performing percutaneous cardiac stimulation. The position of the electrode 60 shown is exemplary only, and alternative positions of the electrode 60 may be used to deliver cardiac stimulation pulses. The electrode 60 may alternatively be placed percutaneously or in the esophagus to stimulate the heart. For intraoperative cardiac resuscitation applications, the electrode 60 may take the form of an epicardial electrode that can be placed directly on the surface of the heart. Other known types of electrodes for applying cardiac electrical stimulation invasively or non-invasively may be utilized to deliver cardiac stimulation pulses when practicing the present invention.

  The stimulator 56 includes an interface 64 that couples the lead 58 to the pulse generation output circuit 62. The output circuit 62 may include a high voltage output circuit section that transmits a high voltage defibrillation class shock pulse and / or a low voltage output circuit that transmits a low voltage pacing class pulse. A high energy output circuit for use with an external defibrillator is described in its entirety in US Pat. No. 5,824,017 issued to Sullivan et al., Which is hereby incorporated by reference in its entirety. ing. The stimulator 56 may be a battery-powered device and may alternatively or additionally include a DC input with appropriate electrical shielding that allows connection to a wall socket.

  In the basic embodiment, the rate, pulse energy, pulse shape, and other characteristics of the electrical stimulation pulses delivered by the stimulator 56 are constant and enable or enable the stimulator 56 via the user interface 66. To be sent out by the output circuit 62. In an alternative embodiment, parameters that control the delivery of cardiac electrical stimulation pulse trains may be set by emergency responders via a user interface 66 coupled to output circuit 62. Various output parameters, including but not limited to pulse train pulse energy, pulse amplitude, pulse width, pulse rate, and / or duration, may be set by the emergency response personnel using the user interface 66.

  FIG. 2 is a functional block diagram of one embodiment of the cardiac stimulation device of FIG. In this embodiment, the stimulator 56 is an external stimulation device that includes a sensing circuit 70 that monitors the patient's ECG. Sensing circuit 70 is coupled to a lead interface 64 that receives the ECG signal from electrode 60. The ECG signal may be visually displayed on display 68 for viewing by emergency responders and / or used by external stimulator 56 to detect the presence of cardiac activity and classify heart rhythm. May be. Such information may be used by the stimulator 56 to select stimulation pulse parameters and control the time at which the depolarization stimulation pulse train is triggered. The stimulator 56 may also have the asystole detection capability disclosed in its entirety in US Pat. No. 6,304,773 issued to Taylor et al., Which is hereby incorporated by reference in its entirety. Good. Other rhythm detection and classification algorithms known for use in cardiac stimulation or monitoring devices are also used to detect and classify cardiac activity and to detect long-term VF, fine VF, or asystole. It may be performed when recommending resuscitation treatment based on and / or automatically selecting.

  Display 68 may include visual or audio signals related to cardiac electrical activity. During or after delivery of a series of depolarization stimuli, depolarization is initially expected to be accompanied by mechanically weak contractions, whether intrinsic or induced. A weak contraction will increase in strength with subsequent depolarization. Synchronizing chest or heart compression with weak heartbeats may provide hemodynamic benefits. Thus, the depolarization detected by the detection circuit 70 allows the display 68 to generate a signal that can be perceived by emergency response personnel under the control of the microprocessor 72. This signal may be an acoustic signal, a tactile signal, and / or a visual signal that indicates the occurrence of cardiac depolarization or other triggering events for the delivery of manual CPR. The emergency response personnel may then deliver chest or heart compressions, or another form of circulatory assistance that is generally pulsatile, synchronized with depolarization, to increase cardiac output of weak mechanical contractions. Good.

  External stimulator 56 is shown in FIG. 2 as a microprocessor controlled device that can control cardiac stimulation functions by microprocessor 72. However, it will be appreciated that the stimulator 56 may be provided as other types of pulse generating devices that are not microprocessor based, such as devices that utilize a dedicated digital or analog circuitry platform. The user interface 66 may allow entry of patient related data such as the start time of a VF / asystole episode and / or the duration of CPR or other circulatory assistance. Such data may be used by the stimulator 56 in conjunction with the cardiac activity detected at that time when automatically selecting or recommending when and what type of sequence of electrical pulses should be delivered.

  In an alternative embodiment, the cardiac stimulation device used when delivering the electrical stimulation portion of cardiac resuscitation according to the present invention may be provided as an implantable electrical stimulation device. FIG. 3 is an illustration of an implantable cardiac stimulation device 210 and associated cardiac leads 216 disposed within a patient's heart 208. Stimulation device 210 includes a connector block 212 that receives the proximal end of one or more cardiac leads operably disposed relative to a patient's heart 208. In FIG. 3, the right ventricular lead 216 senses cardiac activity and delivers a cardiac stimulation pulse that can include a relatively low energy pacing class pulse and / or a high energy cardioversion / defibrillation class shock pulse. Used to position the electrode for For these purposes, the right ventricular (RV) lead 216 includes a ring electrode 224, optionally a tip electrode 226 that is telescopically mounted within the electrode head 228, an RV coil electrode 220, and a superior vena cava (SVC). ) Comprising coil electrodes 230, each electrode being coupled to an insulated conductor housed within the body of the lead 216. The proximal end of the insulated conductor is coupled to a corresponding connector terminal held by lead connector 217 at the proximal end of lead 216 to provide an electrical connection to stimulation device 210.

  Electrodes 224 and 226 are commonly referred to as “tip-ring” configurations, as bipolar pairs for sensing cardiac activity or delivering low energy stimulation pulses, or generally “can” May be used individually in a monopolar configuration with a device housing 211 functioning as an indifferent electrode, referred to as a “case” electrode. Device housing 211 may also function as a subcutaneous electrode in combination with one or both of coil electrodes 220 or 230 to deliver high energy stimulation pulses to the atrium or ventricle.

  The locations shown by the RV lead 216 and electrodes 224, 226, 220, and 228 shown in FIG. 3 within or around the right heart chamber are approximate and are exemplary only. In addition, an alternative lead having a tip, ring, canister base, and / or other combination of coil electrodes provided for stimulation or sensing at a particular site within one or more heart chambers may be provided. It will be appreciated that it may be used with the invention. Although a specific implantable cardiac stimulation device and lead system is shown in FIG. 3, the methodology included in the present invention is positioned in the endocardium, epicardium, or coronary sinus. It may be applied in single-chamber, dual-chamber, or multi-lumen systems that include monopolar, bipolar, or multipolar leads. The present invention may alternatively be implemented in systems that do not employ leads that place electrodes in or on the heart. For example, a subcutaneously or submuscularly implanted device that is in an operable position relative to the heart, such as in the left or right pectoral muscle region, senses electrically and detects electrical stimulation to detect cardiac activity. A non-cardiac lead based method could be used. Such a system may employ subcutaneous or submuscular electrodes incorporated in or on the device housing.

  FIG. 4 is a functional block diagram of the implantable cardiac stimulation device of FIG. Device 210 includes a microprocessor 250, pacing output circuit 252, cardioversion / defibrillation output circuit 254, and stimulus timing and control circuit 256, which are linked by a control / data bus 258. In accordance with the present invention, device 210 delivers the depolarization stimulating portion of cardiac resuscitation therapy. A series of depolarized electrical stimulation pulses may be delivered by pacing output circuit 252 and / or cardioversion / defibrillation output circuit 254 under the control of stimulation timing and control circuit 256. Device 210 includes terminals 260, 262, 264, and 266 for electrical connection to electrodes operably placed relative to the heart. Terminals 260 and 262 may be coupled to a low voltage pacing / sensing electrode that delivers a relatively low voltage pacing class pulse within the pulse train. Terminals 264 and 266 can be coupled to high voltage electrodes that deliver relatively high voltage defibrillation class pulses within the pulse train. Parameters that control the delivery of the pulse train are programmed or stored in memory associated with the microprocessor 250 and communicated to the stimulus timing and control circuit 256 via the data bus 258.

  Device 210 may further be capable of sensing cardiac activity and delivering pacing, cardioversion, defibrillation, and / or other cardiac stimulation therapy according to methods known in the art. General sensing, pacing, and defibrillation functions are implemented according to the description provided in US Pat. No. 5,117,824 issued to Keimel, which is incorporated herein by reference in its entirety. May be.

  Typically, electrical signals from terminals 260 and 262 are supplied to sensing circuit 280 on input lines 270 and 272. Terminals 260 and 262 provide an electrical connection to a sensing electrode pair, eg, a dipole tip-ring pair, which can be the same electrode pair used to deliver pacing class stimulation pulses, and thus terminals 260 and 262 may further be coupled to a pacing output circuit 252 as shown in FIG. In response to detecting a cardiac signal, such as a P-wave or R-wave, sensing circuit 280 provides a logic signal to stimulation timing and control circuit 256 on output line 274. The logic signal serves to reset the refill interval used to control the timing of the stimulation pulse delivery. The interval between sensing events may be used to detect and classify heart rhythms.

  According to a typical pacing operation, the stimulation timing and control circuit 256 receives a signal on the output line 274 for a predetermined time interval corresponding to the refill interval set to control the timing of the cardiac stimulation pulses. If not, the timing and control circuitry 256 will trigger the generation of pacing pulses by the pacing output circuit 252. The disable signal on line 276 prevents pacing pulses from being detected by default sensing circuit 280. The gain of the sensing circuit portion 280 is also controlled by the stimulus timing and control circuit 256 on the signal line 278.

  Terminals 264 and 266 provide an electrical connection to a high energy stimulation electrode configuration that will typically include another coil electrode and / or at least one coil electrode paired with the device housing. Terminals 264 and 266 are coupled to the cardioversion / defibrillation output circuit 254 and are used to deliver high energy cardioversion / defibrillation class pulses.

  In response to tachycardia detection, anti-tachycardia pacing therapy is delivered, if desired, by loading the therapy within the stimulation timing and control circuit 256 from the microprocessor 250 according to the type of tachycardia detected. May be. When a high voltage cardioversion or defibrillation shock pulse is needed, the microprocessor 250 activates the cardioversion and defibrillation output circuit 254. The timing of delivery of the defibrillation or cardioversion pulse is controlled by the stimulus timing and control circuit 256.

  Any known ventricular cardioversion or defibrillation pulse control circuit for use with an implantable cardioverter / defibrillator may be used with the present invention. In the illustrated device, the delivery of cardioversion or defibrillation pulses is accomplished by the cardioversion / defibrillation output circuit 254 via the control bus 258 under the control of the stimulus timing and control circuit 256. The cardioversion / defibrillation output circuit 254 determines whether a shock pulse waveform, eg, single phase, biphasic or multiphase pulse is delivered, which electrode is involved in delivering the pulse, the pulse shape and Determine slope, pulse energy, etc.

  In modern implantable cardioverter-defibrillators (ICDs), specific treatments are programmed into the device in advance by a physician and a treatment menu is usually provided. For example, if tachycardia is first detected, an anti-tachycardia pacing therapy can be selected. If tachycardia is detected again, a more aggressive anti-tachycardia pacing therapy may be scheduled. If repeated attempts at anti-tachycardia pacing therapy fail, then a high level cardioversion pulse therapy may be selected. As with currently available ICDs, in response to failure of the initial shock (s) to end fibrillation, the amplitude of the defibrillation shock may be incremented.

  If defibrillation shock therapy fails to convert VF to sinus rhythm using a single shock defibrillation technique within the first 1-2 minutes after VF detection, persistent VF, fine VF Or asystole may persist or occur. Cardiac resuscitation therapy according to the present invention is programmed to be triggered either after an interval of unsuccessful treatment of VF or by detection of fine VF or asystole following defibrillation therapy attempt. May be. Thus, the cardiac resuscitation therapy provided by the present invention may be included in a programmable menu of arrhythmia therapy.

  Resuscitation includes delivery of a series of stimulation pulses that are delivered either before hypoxia becomes serious or after circulatory assistance is provided to convert the hypoxia. The stimulation pulse train, which may include relatively low energy pacing class pulses and / or high energy defibrillation class pulses, is under the control of stimulation timing and control circuit 256 and / or pacing output circuit 252 and / or cardioversion / defibril. Output by the output circuit 254. The parameters that control the pulse train may be programmable and include, but are not limited to, the type of pulses (pacing class or defibrillation class) included in the train, pulse amplitude, pulse width, pulse shape, pulse rate, and pulse train. Or the total number of pulses. These parameters are applied by the stimulus timing and control circuit 256 according to the data received from the microprocessor 250 on the data bus 258.

  The device 210 further includes a cardiac event indicator 284 that includes circuitry that generates signals such as visual signals, tactile signals, and / or audible signals (such as beeps or tones) to direct emergency response personnel to develop a heartbeat. May be included. As mentioned earlier, during or after the delivery of a series of depolarizing stimuli, endogenous or induced depolarization is initially expected to be accompanied by a mechanically weak contraction, which is followed by a subsequent depolarization. The strength increases with polarization. Synchronizing chest or heart compression with weak heartbeats may provide hemodynamic benefits. Thus, under the control of the microprocessor 250, the event indicator 284 may be controlled by a depolarization detected by the detection circuit 280 or a depolarization pulse delivered by the pacing output circuit 252 or the cardioversion / defibrillation output circuit 254. A signal perceptible by emergency response personnel can be generated that indicates the occurrence of a cardiac event.

  The generation of such signals may be automatic or manually enabled after the stimulation pulse train is triggered, so that emergency response personnel can weak machine during and / or after a series of pulses. Chest or heart compression, or another form of pulsatile circulatory assist, can be delivered in synchrony with a cardiac event to increase the cardiac output produced by mechanical contraction. Generation of the cardiac event indicator signal may be automatically disabled after a predetermined time interval during which normal cardiac function is expected to recover and / or emergency response personnel using an external programming device May be manually disabled at any time.

  Relieving hypoxia with circulatory assistance before delivering a series of depolarizing stimuli is important in preparing muscle cells to benefit from the stimulating part of resuscitation therapy. Thus, it is possible to generate a signal indicating the delivery of circulatory assistance, or a sensor for detecting blood oxygen concentration is included in the implantable device provided to practice the present invention. May be. By detecting the delivery and duration of circulatory assistance and / or the concentration or change in arterial oxygen saturation, the implantable device can determine when it is appropriate to start the stimulating portion of the resuscitation therapy.

  FIG. 5 is a functional block diagram of an implantable cardiac electrical stimulation device that includes a sensor used to determine when the stimulation portion of the resuscitation treatment is to be triggered. Sensor 290 may be included within and / or on the housing of implantable device 210 or may be implanted within the patient's body but external to device 210. Sensor 290 is connected to a sensor processing circuit 292 that receives and processes signals generated by sensor 290.

  Sensor 290 may be embodied as an oxygen sensor used to detect blood oxygen saturation levels to indicate a relative level of hypoxia. In this embodiment, the sensor 290 may be positioned on the lead and placed at a location within the heart or artery. Such leads may further include cardiac stimulation or sensing electrodes and may be coupled to device 210 via a connector block.

  A signal related to blood oxygen saturation may be adjusted and processed by sensor processing circuit 292. Hypoxic conversion during long term episodes of VF, fine VF, or systole, as expected after CPR or other circulatory assistance is delivered for a period of time, eg, about 1 minute or longer, The resulting oxygen saturation data is provided to the microprocessor 250 for use in determining whether the measured oxygen saturation level indicates. Upon detecting an oxygen saturation level increased by a specified amount beyond the previous hypoxic oxygen saturation level, or detecting an oxygen saturation level greater than a specified minimum level, the stimulating portion of the resuscitation treatment is 210 can be started.

  In an alternative embodiment, sensor 290 may be provided as a mechanical sensor capable of generating a signal indicating the presence of circulatory assistance. In one embodiment, sensor 290 may be embodied as a pressure sensor that can detect an increase in blood pressure that occurs during CPR or other circulatory assisted delivery. In another embodiment, the sensor 290 may be embodied as an accelerometer or piezoelectric sensor capable of generating a signal corresponding to the application of chest compression delivered during manual or automated CPR. Good. The output of the mechanical sensor is provided to a sensor processing circuitry 292 for adjusting and processing the signal so that data relating to the mechanical action of the circulatory assist can be provided to the microprocessor 250. Microprocessor 250 can trigger the stimulation portion of the resuscitation treatment after detecting circulatory assistance for some sustained time interval, for example, approximately 1 minute later.

  FIG. 6 is a timing diagram of one method for delivering cardiac resuscitation according to the method of the present invention. The ECG signal initially exhibits virtually no cardiac activity during the long-term asystole episode 100. The resuscitation method can be performed following long-term episodes of VF, fine VF, or asystole. Emergency responders begin delivering CPR or another form of circulatory assistance at 102 to mitigate hypoxia. If medical grade oxygen is available, ventilation of medical grade oxygen will convert hypoxia more quickly. CPR or other circulatory assistance is delivered for a period 104 before starting the stimulation portion of the resuscitation therapy. Current cardiac resuscitation techniques generally emphasize the delivery of defibrillation shock as quickly as possible following cardiac arrest. However, it is expected that ATP must be available to drive calcium processing functions such as SERCA in order to achieve a successful response to the stimulating portion of the resuscitation method. Thus, CPR or another form of circulatory assistance is provided for certain time intervals to relieve myocyte hypoxia and make ATP available to myocytes for calcium processing function. A suitable time interval for delivering circulatory assistance may be about 1 minute, but it may be longer or shorter depending on the severity of hypoxia and the duration of VF, fine VF, or asystole episode Good. The duration of circulatory assistance may be a reference time interval, such as 1 minute, or may be based on sensing another physiological indicator of hypoxia, such as blood oxygen concentration or pH.

  After the circulatory assist interval 104, the stimulation portion of the resuscitation treatment is performed by delivering a series of stimulation pulses 106. The stimulation pulse may be delivered by an external device or an implantable device, such as the devices described in connection with FIGS. The stimulation pulse may be a relatively low voltage electrical pacing class pulse that is high enough energy to depolarize a mass of cardiomyocytes. The pulse may alternatively be a high energy electrical shock pulse. The pulses are delivered at a predetermined pulse rate, for example, a rate of about 1 Hz. The pulses are delivered for some time interval 108, eg, about 1 minute or more. Without intending to limit the present invention to any particular theory, in order to restore normal SR calcium concentration by calcium influx during successive cell depolarization and its retention by the aerobic function of the calcium pump, It is currently believed that a series of depolarizing pulses is required.

  After pulse train 106 is delivered, cardiac activity is monitored to verify successful recovery of normal sinus rhythm 112. In some cases, an asystole or long-term state of fine VF may be converted to VF rather than sinus rhythm. FIG. 7 is a timing diagram illustrating events that occur during an alternative method of delivering cardiac resuscitation according to the present invention. In this example, the series of low voltage pulses 106 delivered after a period of circulation assist 102 is terminated by a defibrillation pulse 120 that may occur after a predetermined time interval 118 following the last pulse of pulse 106. When long-term, asystole or fine VF 100 is converted to VF 116 by pulse train 106, defibrillation pulse 120 is provided to convert VF 116 to sinus rhythm 122.

  After successful resuscitation treatment, when normal electro-mechanical association is restored but the intrinsic rate remains bradycardic, the implantable or external stimulation device It is further recognized that bradycardia pacing can be delivered to maintain the number.

  The interval of circulatory assistance 102 is shown to end before the start of pulse train 106 in FIGS. 6 and 7, but circulatory assistance does not interfere with stimulus delivery, and the pulse train does not provide CPR or other circulatory assistance. It is conceivable that circulatory assistance may be delivered continuously during depolarization stimulus delivery if not configured with high voltage electrical stimulation pulses that would pose a risk to the emergency response personnel to be delivered. It is further contemplated that the circulatory assistance intervals may be interspersed with the stimulation pulse intervals.

  To assist hemodynamic recovery after resuscitation, some form of circulatory assistance may be continued or restarted after the series of stimulation pulses has ended. In some embodiments, a cardiac stimulation therapy directed to improving cardiac hemodynamic performance may be delivered by a stimulation device after a pulse train to increase cardiac output. Such stimulation therapies include, but are not limited to, cardiac resynchronization therapy and / or extrasystolic stimulation. FIG. 8 illustrates a method for performing cardiac resuscitation according to the present invention, comprising delivering an extra systolic stimulus to improve hemodynamic function after successful resuscitation of the heart. FIG.

  Long-term, VF or asystole episodes 100 are initially treated with CPR 102 or other circulatory assistance to relieve hypoxia. Circulation assistance is followed by a series of depolarization stimulation pulses 106 currently believed to mitigate SR calcium loss. After the series of pulses 106 is completed and the sinus rhythm 112 is restored or the electromechanical coupling is restored and it is verified that the heart rate is maintained by bradycardia pacing, post-extra systolic enhancement An extra systolic stimulus 140 is delivered to enhance the heart pumping function by accomplishing the action. Aspects and benefits of extrasystolic stimulation to achieve the mechanical benefits of post-extrasystolic enhancement are described in PCT patent application publication WO 03/020364 to Deno et al., Which is incorporated herein by reference in its entirety. The

  The extra systolic stimulation 140 may be applied by delivering an extra systolic stimulation pulse 136 following a ventricular event (VE) 134, which may be a sensed R wave or a ventricular pacing pulse. The extra systolic stimulation pulse 140 may be delivered every paced or intrinsic cardiac cycle, or less frequently, eg, at a constant rate of the intrinsic heart rate or paced heart rate. . In the example of FIG. 8, extra systolic (ES) stimulation pulses 136 are delivered after every other R wave 130 detected as a ventricular event (VE) 134 to induce extra systolic depolarization 132. The Further details regarding the control of extra systolic stimulation pulse delivery are provided by US patent application by Burnes et al.

  The pulse train 106 shown in FIGS. 6, 7 and 8 is shown to consist of pulses of constant pulse amplitude delivered at a constant rate. It will be appreciated that the pulse train may consist of pulses of different or varying pulse energy or amplitude, and may be delivered at a different or varying rate within the pulse train. A series of pulses delivered with the intention of restoring normal SR calcium levels and myocyte calcium processing may be adjusted to provide the most effective recovery of normal heart activity, The activity may depend in part on the initial cardiac activity that exists when the resuscitation method begins and / or the cardiac activity that exists during or after the interval between circulatory assistance and the initial pulse train.

  In one embodiment, the cardiac stimulation device monitors for a return of VF during the resuscitation procedure and changes the stimulation portion of the resuscitation treatment if VF is detected. FIG. 9 is a timing diagram illustrating a method of delivering cardiac resuscitation including delivering both pacing class pulses and defibrillation class pulses. After the pulse train 106 is triggered, the systolic episode 100 is converted to VF at 142. When VF is detected, a high energy shock pulse is delivered instead of a low energy pulse in the pulse train. To convert and prevent VF, many high energy shock pulses 146 may be replaced by low energy pulses in the pulse train, or all remaining pulses in the pulse train are delivered as high energy shock pulses. May be. Alternatively or additionally, the pulse train may include a sequence of pulses 148 that vary in rate. During or after the pulse train, trying to convert the VF or prevent the VF from restarting, the sequence of pulse 148 with varying rate is sent at a higher rate that gradually drops to a slower rate. Also good.

  In the example of FIG. 9, circulatory assistance 102 is provided during a certain time interval 104 prior to the start of the stimulation pulse train 106 until a high voltage defibrillation class pulse 146 is delivered in response to detection of VF 142. Continue during the pulse train. When the VF ends, a low energy pulse 148 is delivered and circulation assistance resumes at 103.

  FIG. 10 is a timing diagram illustrating an alternative method of performing cardiac resuscitation according to the present invention. Persistent, VF or fine VF episode fibrillation waves are not mechanically effective, but still require energy and may contribute to depletion of intracellular calcium. The result of a defibrillation shock delivered long after the start of VF or fine VF may result in asystole. However, this conversion to asystole may be advantageous in reducing ATP loss due to the generation of fibrillation waves. Thus, in FIG. 10, a long-term VF episode 152, which may be a coarse VF or a fine VF, may first be treated with a defibrillation shock 154 to convert VF to asystole 156. When an asystole 156 is triggered, an interval of circulatory assistance 102 is delivered, followed by a series of depolarization pulses 106, as described above in connection with FIG.

  FIG. 11 is a graph of the experimental results obtained from the separated muscle cell specimen. Continuously perfused, isolated guinea pig myocytes were stimulated using a 1 Hz supra-threshold pulse until a steady state mechanical response was reached. Stimulation was stopped for 1, 2.5, 5, 10, 15, and 20 minute intervals, after which 1 Hz stimulation was resumed. The results of the 20 minute rest period experiment are shown in the graph of FIG. The sarcomere length is plotted over a predetermined period. Baseline steady state shortening 10 was established during 1 Hz stimulation, followed by a 20 minute rest period at 12. At 14, when 1 Hz stimulation was resumed, sarcomere shortening was initially impaired, but recovered to 16 baseline steady-state responses in the course of approximately 1 minute of sustained 1 Hz stimulation. Thus, in the presence of appropriate oxygenation, normal muscle cell shortening recovery can be obtained even after 20 minutes of inactivity.

  It is important that there is considerable mechanical damage after 20 minutes of depolarization with proper oxygenation. As such, hypoxia may not be the only cause of electromechanical dissociation (EMD) that occurs after persistent fibrillation or asystole. The result for a shorter rest period of 5 minutes or more shows that myocyte shortening is reduced to about 10% of baseline shortening after the rest period, and full recovery of baseline shortening is after about 1 minute of sustained 1 Hz stimulation. The results achieved were similar to the results shown in FIG. The mechanical damage was smaller and recovery towards baseline shortening occurred more rapidly following a downtime of less than 5 minutes. These results support the theory that SR calcium loss increases with increasing periods of inactivity due to calcium leakage and a sustained series of depolarizations is required to replenish calcium stores. These results further support the need for resuscitation methods that switch both hypoxia and SR calcium loss.

  Of course, the present invention is easily implemented as instructions stored on a computer-readable medium and can be executed under computer control in an implantable or external medical device. Computer readable media can be any form of storage media, such as random access version, read only version, serial access version, dynamic version, and erasable version (eg, RAM, ROM, SAM, DRAM, EPROM, EEPROM, etc.) These include magnetic storage media, optical storage media, and other storage media currently known or later developed.

  Thus, cardiac resuscitation methods have been described that address the need to resuscitate the heart after long-term episodes of VF, fine VF, or asystole. The methods and apparatus described herein for practicing the present invention have been described according to particular embodiments. These embodiments are intended to be illustrative and not limiting with respect to the appended claims.

FIG. 6 is a schematic diagram of a method for delivering cardiac resuscitation therapy after VF, near asystole, or a long-term episode of asystole. FIG. 6 is a functional block diagram of an embodiment of an external stimulation device that can be used when delivering cardiac resuscitation therapy. 1 is an illustration of an implantable cardiac stimulation device and associated cardiac leads placed within a patient's heart that can be used when delivering cardiac resuscitation therapy. FIG. FIG. 4 is a functional block diagram of the implantable cardiac stimulation device of FIG. 3. 1 is a functional block diagram of an implantable cardiac stimulation device that includes a sensor used to determine when the electrical stimulation portion of a resuscitation treatment should be triggered. FIG. FIG. 4 is a timing diagram of one method for delivering cardiac resuscitation according to the method of the present invention. FIG. 6 is a timing diagram illustrating events that occur during an alternative method of delivering cardiac resuscitation according to the present invention. FIG. 4 is a timing diagram of a method for performing cardiac resuscitation according to the present invention comprising delivering an extra systolic stimulus to improve hemodynamic function after a successful resuscitation of the heart. FIG. 5 is a timing diagram illustrating a method for delivering cardiac resuscitation including delivering both pacing class pulses and defibrillation class pulses. FIG. 6 is a timing diagram illustrating an alternative method of performing cardiac resuscitation according to the present invention. It is a graph of the experimental result obtained from the separated myocyte sample.

Claims (15)

A method of resuscitating the heart during a ventricular fibrillation, fine ventricular fibrillation, or persistent asystole episode,
Delivering circulatory assistance for a time interval suitable to relieve myocardial hypoxia in the heart; and
Delivering a series of therapeutic electrical pulses capable of depolarizing at least a portion of the myocardium of the heart;
To resuscitate the heart including. The sending step includes:
Manually delivering cardiopulmonary resuscitation, delivering extracorporeal oxygenation assistance via a device coupled to the patient; activating an implantable ventricular assist device fluidly coupled to a portion of the patient's vasculature; and The method of resuscitating a heart according to claim 1, comprising at least one of activating an automated cardiopulmonary resuscitation device coupled to a patient.   The method of resuscitating a heart according to claim 2, wherein the step of manually delivering the cardiopulmonary resuscitation further comprises initiating a chest compression with a signal.   The method of resuscitating a heart according to claim 3, wherein the signal includes at least one of an audible signal, a tactile signal, and a visual signal.   The periodic manual compression trigger signal is wirelessly provided from an implantable pulse generator to an external device, which transmits the signal to a person attempting to manually resuscitate a patient. To revive your heart.   The method of resuscitating a heart according to claim 1, wherein the series of therapeutic electrical pulses includes pacing class pulses.   The method of resuscitating a heart according to claim 6, wherein a portion of the pacing class pulse has at least one common characteristic, the common characteristic including a pulse width characteristic, a polarity characteristic, pulse energy, and pulse amplitude.   The method of resuscitating a heart according to claim 1, wherein the series of therapeutic electrical pulses are conducted through at least one of the following electrodes: intracardiac, epicardial, subcutaneous, and submuscular electrodes. .   Clinician operating telemetry programming device, detection of potentially lethal arrhythmia, mechanical sensor, detection of arrhythmia by external defibrillator, detection of unsuccessful previous defibrillation attempt, The method of resuscitating a heart according to claim 1, induced by at least one of a relatively low heart rate, a relatively low cardiac output state, and a relatively low saturated oxygen state.   The mechanical sensor is coupled to an accelerometer adapted to sense cardiac activity, a pressure sensor coupled to sense cardiac activity, and coupled to sense cardiac activity 10. The method of resuscitating a heart according to claim 9, comprising at least one of an impedance based sensor.   The method of resuscitating a heart according to claim 1, further comprising displaying one or more parameters associated with the delivery of the circulatory assist or associated with the delivery of the series of therapeutic electrical pulses. . A method for reviving the heart,
Providing the patient with cardiopulmonary resuscitation, and
A method for resuscitating a heart comprising applying a series of electrical pulses capable of depolarizing at least a portion of the patient's myocardium. A device that revives the heart during ventricular fibrillation, fine ventricular fibrillation, or persistent failure contraction,
Means for delivering circulatory assistance during a time interval suitable for relieving myocardial hypoxia in the heart;
Means for delivering a series of therapeutic electrical pulses capable of depolarizing at least a portion of the myocardium of the heart;
A device for resuscitating the heart. A device for resuscitating the heart following unsuccessful high-voltage defibrillation therapy delivered as a result of a ventricular fibrillation state, a fine ventricular fibrillation state, or a persistent asystole state,
Means for delivering circulatory assistance during a predetermined time interval to relieve myocardial hypoxia in at least a portion of the heart;
Means for delivering a series of therapeutic electrical pulses capable of depolarizing at least a portion of the myocardium of the heart;
A device for resuscitating the heart. A computer readable medium for performing a method of resuscitating a heart,
Instructions to deliver circulatory assistance during a time interval suitable to relieve myocardial hypoxia in the heart;
Instructions for delivering a series of therapeutic electrical pulses capable of depolarizing at least a portion of the myocardium of the heart;
A computer readable medium including:

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