JPH0414005B2 - - Google Patents
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- Publication number
- JPH0414005B2 JPH0414005B2 JP58143601A JP14360183A JPH0414005B2 JP H0414005 B2 JPH0414005 B2 JP H0414005B2 JP 58143601 A JP58143601 A JP 58143601A JP 14360183 A JP14360183 A JP 14360183A JP H0414005 B2 JPH0414005 B2 JP H0414005B2
- Authority
- JP
- Japan
- Prior art keywords
- probe
- cardiac
- signal
- local
- circuit
- Prior art date
- Legal status (The legal status is an assumption and is not a legal conclusion. Google has not performed a legal analysis and makes no representation as to the accuracy of the status listed.)
- Expired - Lifetime
Links
- 230000000747 cardiac effect Effects 0.000 claims description 108
- 239000000523 sample Substances 0.000 claims description 92
- 210000002216 heart Anatomy 0.000 claims description 73
- 230000000694 effects Effects 0.000 claims description 70
- 230000000638 stimulation Effects 0.000 claims description 63
- 230000002861 ventricular Effects 0.000 claims description 59
- 230000001746 atrial effect Effects 0.000 claims description 58
- 230000004044 response Effects 0.000 claims description 48
- 230000028161 membrane depolarization Effects 0.000 claims description 40
- 230000002107 myocardial effect Effects 0.000 claims description 40
- 210000001519 tissue Anatomy 0.000 claims description 33
- 210000002837 heart atrium Anatomy 0.000 claims description 29
- 238000000034 method Methods 0.000 claims description 27
- 238000012545 processing Methods 0.000 claims description 16
- 210000005003 heart tissue Anatomy 0.000 claims description 10
- 230000001105 regulatory effect Effects 0.000 claims description 8
- 210000001008 atrial appendage Anatomy 0.000 claims description 6
- 230000001965 increasing effect Effects 0.000 claims description 6
- 230000008602 contraction Effects 0.000 claims description 5
- 210000003748 coronary sinus Anatomy 0.000 claims description 5
- 230000007423 decrease Effects 0.000 claims description 3
- 230000002123 temporal effect Effects 0.000 claims description 3
- 230000002169 extracardiac Effects 0.000 claims description 2
- 230000001939 inductive effect Effects 0.000 claims 2
- 230000033228 biological regulation Effects 0.000 claims 1
- 238000012790 confirmation Methods 0.000 claims 1
- 230000008878 coupling Effects 0.000 claims 1
- 238000010168 coupling process Methods 0.000 claims 1
- 238000005859 coupling reaction Methods 0.000 claims 1
- 238000005259 measurement Methods 0.000 claims 1
- 210000004165 myocardium Anatomy 0.000 description 20
- 230000004913 activation Effects 0.000 description 16
- 210000005245 right atrium Anatomy 0.000 description 16
- 230000005540 biological transmission Effects 0.000 description 14
- 239000012530 fluid Substances 0.000 description 14
- 238000010586 diagram Methods 0.000 description 11
- 210000005247 right atrial appendage Anatomy 0.000 description 11
- 238000002565 electrocardiography Methods 0.000 description 9
- 230000002159 abnormal effect Effects 0.000 description 8
- 210000001992 atrioventricular node Anatomy 0.000 description 8
- 210000001013 sinoatrial node Anatomy 0.000 description 8
- 238000011161 development Methods 0.000 description 7
- 210000005242 cardiac chamber Anatomy 0.000 description 6
- 230000005284 excitation Effects 0.000 description 6
- 238000000718 qrs complex Methods 0.000 description 6
- 230000033764 rhythmic process Effects 0.000 description 5
- 230000005856 abnormality Effects 0.000 description 4
- 210000005241 right ventricle Anatomy 0.000 description 4
- 230000004936 stimulating effect Effects 0.000 description 4
- 206010047302 ventricular tachycardia Diseases 0.000 description 4
- 208000001871 Tachycardia Diseases 0.000 description 3
- 239000008280 blood Substances 0.000 description 3
- 210000004369 blood Anatomy 0.000 description 3
- 238000006243 chemical reaction Methods 0.000 description 3
- 238000013461 design Methods 0.000 description 3
- 230000009177 electrical depolarization Effects 0.000 description 3
- 238000005516 engineering process Methods 0.000 description 3
- 238000007667 floating Methods 0.000 description 3
- 230000006794 tachycardia Effects 0.000 description 3
- 206010016654 Fibrosis Diseases 0.000 description 2
- 102100026827 Protein associated with UVRAG as autophagy enhancer Human genes 0.000 description 2
- 101710102978 Protein associated with UVRAG as autophagy enhancer Proteins 0.000 description 2
- 230000009471 action Effects 0.000 description 2
- 206010003119 arrhythmia Diseases 0.000 description 2
- 206010003668 atrial tachycardia Diseases 0.000 description 2
- 201000010099 disease Diseases 0.000 description 2
- 208000037265 diseases, disorders, signs and symptoms Diseases 0.000 description 2
- 230000009977 dual effect Effects 0.000 description 2
- 230000005672 electromagnetic field Effects 0.000 description 2
- 230000000763 evoking effect Effects 0.000 description 2
- 230000004761 fibrosis Effects 0.000 description 2
- 239000012634 fragment Substances 0.000 description 2
- 230000010247 heart contraction Effects 0.000 description 2
- 238000002513 implantation Methods 0.000 description 2
- 238000007914 intraventricular administration Methods 0.000 description 2
- 230000002028 premature Effects 0.000 description 2
- 230000004213 regulation of atrial cardiomyocyte membrane depolarization Effects 0.000 description 2
- 230000034225 regulation of ventricular cardiomyocyte membrane depolarization Effects 0.000 description 2
- 238000007920 subcutaneous administration Methods 0.000 description 2
- 208000003663 ventricular fibrillation Diseases 0.000 description 2
- 206010003130 Arrhythmia supraventricular Diseases 0.000 description 1
- 206010003662 Atrial flutter Diseases 0.000 description 1
- 206010033557 Palpitations Diseases 0.000 description 1
- 208000004301 Sinus Arrhythmia Diseases 0.000 description 1
- 206010040738 Sinus arrest Diseases 0.000 description 1
- 210000003484 anatomy Anatomy 0.000 description 1
- 238000004873 anchoring Methods 0.000 description 1
- 230000003288 anthiarrhythmic effect Effects 0.000 description 1
- 230000006793 arrhythmia Effects 0.000 description 1
- 230000009910 autonomic response Effects 0.000 description 1
- 210000004375 bundle of his Anatomy 0.000 description 1
- 206010061592 cardiac fibrillation Diseases 0.000 description 1
- 239000002327 cardiovascular agent Substances 0.000 description 1
- 229940125692 cardiovascular agent Drugs 0.000 description 1
- 230000008859 change Effects 0.000 description 1
- 230000001143 conditioned effect Effects 0.000 description 1
- 230000002950 deficient Effects 0.000 description 1
- 230000003111 delayed effect Effects 0.000 description 1
- 230000003205 diastolic effect Effects 0.000 description 1
- 239000003814 drug Substances 0.000 description 1
- 229940079593 drug Drugs 0.000 description 1
- 230000005684 electric field Effects 0.000 description 1
- 210000002615 epidermis Anatomy 0.000 description 1
- 239000000835 fiber Substances 0.000 description 1
- 230000002600 fibrillogenic effect Effects 0.000 description 1
- 208000019622 heart disease Diseases 0.000 description 1
- 230000005764 inhibitory process Effects 0.000 description 1
- 238000003780 insertion Methods 0.000 description 1
- 230000037431 insertion Effects 0.000 description 1
- 208000028867 ischemia Diseases 0.000 description 1
- 230000003902 lesion Effects 0.000 description 1
- 210000005244 lower chamber Anatomy 0.000 description 1
- 230000007246 mechanism Effects 0.000 description 1
- 238000012986 modification Methods 0.000 description 1
- 230000004048 modification Effects 0.000 description 1
- 210000003205 muscle Anatomy 0.000 description 1
- 210000000653 nervous system Anatomy 0.000 description 1
- 239000012811 non-conductive material Substances 0.000 description 1
- 210000000056 organ Anatomy 0.000 description 1
- 230000037361 pathway Effects 0.000 description 1
- 230000010287 polarization Effects 0.000 description 1
- 230000000750 progressive effect Effects 0.000 description 1
- 230000002035 prolonged effect Effects 0.000 description 1
- 230000001681 protective effect Effects 0.000 description 1
- 230000004043 responsiveness Effects 0.000 description 1
- 210000002027 skeletal muscle Anatomy 0.000 description 1
- 210000003491 skin Anatomy 0.000 description 1
- 238000010183 spectrum analysis Methods 0.000 description 1
- 230000009163 spontaneous depolarization Effects 0.000 description 1
- 230000002269 spontaneous effect Effects 0.000 description 1
- 201000002931 third-degree atrioventricular block Diseases 0.000 description 1
- 210000000591 tricuspid valve Anatomy 0.000 description 1
- 210000005243 upper chamber Anatomy 0.000 description 1
- 210000003462 vein Anatomy 0.000 description 1
- 230000002747 voluntary effect Effects 0.000 description 1
Classifications
-
- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61N—ELECTROTHERAPY; MAGNETOTHERAPY; RADIATION THERAPY; ULTRASOUND THERAPY
- A61N1/00—Electrotherapy; Circuits therefor
- A61N1/02—Details
- A61N1/04—Electrodes
- A61N1/05—Electrodes for implantation or insertion into the body, e.g. heart electrode
- A61N1/056—Transvascular endocardial electrode systems
-
- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61B—DIAGNOSIS; SURGERY; IDENTIFICATION
- A61B5/00—Measuring for diagnostic purposes; Identification of persons
- A61B5/24—Detecting, measuring or recording bioelectric or biomagnetic signals of the body or parts thereof
- A61B5/25—Bioelectric electrodes therefor
- A61B5/279—Bioelectric electrodes therefor specially adapted for particular uses
- A61B5/28—Bioelectric electrodes therefor specially adapted for particular uses for electrocardiography [ECG]
- A61B5/283—Invasive
- A61B5/287—Holders for multiple electrodes, e.g. electrode catheters for electrophysiological study [EPS]
-
- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61N—ELECTROTHERAPY; MAGNETOTHERAPY; RADIATION THERAPY; ULTRASOUND THERAPY
- A61N1/00—Electrotherapy; Circuits therefor
- A61N1/18—Applying electric currents by contact electrodes
- A61N1/32—Applying electric currents by contact electrodes alternating or intermittent currents
- A61N1/36—Applying electric currents by contact electrodes alternating or intermittent currents for stimulation
- A61N1/362—Heart stimulators
- A61N1/365—Heart stimulators controlled by a physiological parameter, e.g. heart potential
Landscapes
- Health & Medical Sciences (AREA)
- Life Sciences & Earth Sciences (AREA)
- Heart & Thoracic Surgery (AREA)
- Cardiology (AREA)
- Animal Behavior & Ethology (AREA)
- Veterinary Medicine (AREA)
- Public Health (AREA)
- General Health & Medical Sciences (AREA)
- Engineering & Computer Science (AREA)
- Biomedical Technology (AREA)
- Biophysics (AREA)
- Physiology (AREA)
- Nuclear Medicine, Radiotherapy & Molecular Imaging (AREA)
- Radiology & Medical Imaging (AREA)
- Molecular Biology (AREA)
- Surgery (AREA)
- Medical Informatics (AREA)
- Pathology (AREA)
- Physics & Mathematics (AREA)
- Vascular Medicine (AREA)
- Measurement And Recording Of Electrical Phenomena And Electrical Characteristics Of The Living Body (AREA)
- Electrotherapy Devices (AREA)
Description
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眮ã«é¢ãããDETAILED DESCRIPTION OF THE INVENTION BACKGROUND OF THE INVENTION The present invention relates to techniques and devices for sensing intracardiac electrical signals, and in particular to differentially sensing local intracardial electrical patterns under a sensing device;
It relates to techniques and devices for distinguishing it from all unwanted out-of-field electrical events.
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æ§ã§ããã The human heart is basically a pump, and the blood
Through this pump it is drawn into the atrium or upper chamber, which then fills the ventricle or lower chamber via a connecting valve. Blood is then pumped from the ventricle to the body's organs. Each cycle of this pump begins with a series of events occurring in a specific order. It is, in part, the order and relationship of these electrical events that determines the heart's particular efficiency as a pump.
The electrical cycle begins with spontaneous depolarization of cells in the sinoatrial node. The sinoatrial node refers to a small area of specific tissue adjacent to the superior vena cava-right atrium border. The depolarization front spreads slowly within the sinoatrial node and then through the perinodal tissue to activate the atrial myocardium. When the atrial myocardial tissue mass is activated, an electrical event occurs. this is,
When detected on the surface of the body, it is called P fluid. When detected from within the heart chamber, this same event is referred to as an "atrial electrogram." The properties of the atrial electrogram and surface recording P fluid are a function of the activated atrial myocardial mass and the specific activation mode that occurs within the human heart. It is this electrical activation mode that results in contraction of the atrial myocardium and at least partial filling of the ventricle.
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ã§ããã However, the atrial electrical excitation wave may terminate at the filamentous boundary if a specific multicomponent atrioventricular (AV) transmission system does not undertake the transmission of electrical information across the fibrillar boundary between the atria and ventricles. Probably. The AV node is a small 1- to 2-hole AV node located on the floor of the atrium midway between the entrance of the coronary sinus and the central fibrous body of the heart.
It is a cm structure. This structure, consisting of three distinct cell types, acts as an electrical filter and provides sufficient deceleration transmission area between the atrium and ventricle to allow adequate atrial filling. Electrical input to the AV node occurs partly through the normal atrial myocardium and partly through the transmission of electrical information between regions adjacent to the sinoatrial node and the upper, middle, and lower regions of the atrial-myocardial node. This occurs through three specific intraatrial pathways. Transmission within the AV node is highly sensitive to autonomic responses, cardiovascular drug processing, and the effects of heart disease.
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æã¯å³å¿å®€ã®è³ŠæŽ»ãåžãã As the front surface of the electrical depolarization advances through the AV node, it enters the AV or His bundle. this is,
Responsible for the transmission of electrical impulses between the anatomical atria and ventricles. This structure actually traverses the fibrous skeleton of the heart and advances several centimeters within the membranous intraventricular septum.
At the apex of the intraventricular septum, the special AV transmission system is divided into two main branches: the right bundle and the left bundle. The left bundle is divided into ventricular septal activation, specific fibers responsible for activation of the upper lateral ventricular myocardium, and a posterior portion responsible for activation of the septal mass and left ventricular myocardium. The right bundle controls activation of the right ventricle.
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ãã Electrical activity is detected from specific regions of the heart's conduction system by using special techniques, whereas surface electrocardiography techniques detect discrete electrical activity occurring in either the AV node, AV bundle, or bundle branch. It is not possible to indicate a specific event. The electrical activity continues until the ventricular myocardial mass begins to be activated and the QRS complex is formed.
Not observed on the surface electrogram following the P wave. This group of pulses, when recorded at the body surface, is generally P
It has a larger amplitude than the wave. This is because a fairly large ventricular myocardial mass causes this. When recorded from inside the pericardial chamber, this event is referred to as a "ventricular electrogram." Atrial myocardial lipolarization events, whether detected from the cardiac surface or from within the ventricles, are referred to as T waves.
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ãã埮åçã«åŠçœ®ããåŸããšãããŸã§é²ãã ã Normal diastolic depolarization of the sinoatrial node followed by normal propagation of electrical excitation through the atria and ventricles, the frequency in response to the actions of the nervous system that change the discharge rate of the sinoatrial node and the rate of atrial and cardiac excitation. produces a normal heart rhythm with However, various disease states can affect the dominant natural cardiac pacemaker rhythm as well as the electrical excitation pattern. Abnormal rhythms occur in the following cases: That is, if sinoatrial node impulses are not derived intermittently from the sinoatrial node. In the case of atrial myocardial abnormalities, this results in rapid atrial arrhythmias such as palpitations and fibrillation. In the case of an abnormality or presence of AV nodal transmission, this causes an insufficiently slow intrinsic pacemaker to emerge from the lower part of the ventricle, resulting in an abnormally slow heart rhythm. In the case of disease of one or all of the bundle branches, this results in partial or complete AV block, which also results in a slow and inadequate heart rate. In the case of ventricular myocardial abnormalities, this results in rapid tachycardia, ventricular fibrillation and death. Modern medical technology has shown that this defective electrical depolarization mode of operation is more subtle than electronic stimulation of the heart using an external or implanted electronic device, commonly thought of as a pacemaker. It has progressed to the point where it can be treated.
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絊ããããã«äœ¿çšãããã The simplest and most frequently employed electronic device is the standard VVI pacemaker.
The device senses the ventricular electrogram and when the depolarization rate falls below a predetermined level, a stimulus is delivered to the ventricular myocardium, creating an electrical depolarization wave, followed by a cause contractions. Such electrical escape or assist devices can be used in ventricular (VVI) or atrium (AAI)
implanted at the level to correct abnormalities in AV transmission or sinus return node function. Newer pacemaker devices employ electrodes at the atrial and ventricular levels to sense and regulate at either or both locations in order to restore normal operating patterns of atrial and ventricular electrical excitation. Other implantable electrical devices may be used to convert atrial and/or ventricular tachycardia and provide a portion of the input to an implantable electrical device designed to terminate ventricular fibrillation. Ta.
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ã«ååèšèŒãããŠããã However, the ability of any of these devices to function properly is in no way determined by the adequacy of the electrical signals sensed from within the atria or ventricles. However, the appropriate pacemaker output is determined only by the appropriate signal or sensing input. Generally, most conventional devices utilize the same electrodes used for myocardial stimulation to sense myocardial depolarization in the absence of stimulation. Generally, most devices are implanted into the atrial or ventricular myocardium.
a second electrode in the form of a ring (bipolar sensing) or the pacemaker itself (unipolar sensing) placed in close proximity to the stimulation electrode along the same catheter body. The mean signal amplitudes of P and QRS complexes detected using unipolar or bipolar sensing have been well described in the cardiac literature for more than a decade.
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ã¯å€§ãªãèšåºç䟡å€ããããã The need to provide signals derived only from the myocardium in contact with which implanted electrodes are placed has been identified. The problem of electromechanical interference external to the patient, such as external magnetic and electric fields and the electromagnetic fields generated by electric shavers and microwave ovens, is also now well recognized by the general public. However, over the past decade there has been increasing recognition that it is easy to mismeasure cardiac electrical events due to other electrical events occurring within the body. See, for example, Electromagnetic Interference Symposium, PACE, Vol. 5, January-February 1982. Particularly in unipolar electrode devices, the sensing of electrical signals from the skeletal myocardium adjacent to the pacemaker anode itself (myopotential sensing) has been recognized as a frequent cause of false inhibition of these pacemakers. Although standard bipolar ring electrodes help reduce the rate at which myopotential and EMI sensing occurs, these devices are too insensitive to the outside world and to electrical phenomena generated in the patient and surroundings. A device that is insensitive to EMI would be of great clinical value.
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ãã Placing either a monopolar or bipolar contact electrode device within the ventricle to sense activation of the ventricular myocardium (ventricular electrogram) generally yields a sufficient ventricular electrogram signal of 10-12 mv, and the atrial myocardium Due to the large mass of the ventricular myocardium compared to the ventricular myocardium, electrical activity reflecting atrial depolarization is hardly detected by this catheter. However, this is not the case and electrograms are derived from various locations within the atrium. Contacting electrical sensing devices, whether unipolar or bipolar, all suffer from the same drawbacks: their location within the right atrial appendage, their location within the right atrium lateral wall or the proximal-distal coronary sinus is largely independent. . The problem appears to be unique to cardiac anatomy. That is, the mass of the atrium is small, and as a result, P fluid, even sensed from within the atrium, is generally quite small, 1-2 mv. Since the mass of ventricular myocardium exceeds the mass of atrial myocardium to some extent, ventricular depolarization can be captured as a separate electrical event even from within the atrium. This electrical event is thus distinguishable from the atrial electrical event in signal magnitude and form.
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ããèããé»å®³ãããã The development and development of atrial arrest (AAI) and P fluid gated (VAT or VDD) type systems has been very slow due to most of the drawbacks. This is important in the development of dual chamber demand pacemakers (DDD systems), which are designed to sense at both the atrial and ventricular levels.
It has become an almost insurmountable problem. The development of suitable rapid rate conversion pacemakers at the ventricular and atrial levels has also been severely hampered by the lack of signal discrimination between atrial and ventricular events sensed by standard pacemaker systems.
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æ¿ãé©åœãªé床ã§å¿å®€ã«äŸçµŠã§ããã These pacemaker technologies attempt to generate reliable trigger signals for stimulation pulses by sensing electrograms through catheters inserted into the heart via veins. Generally, a signal sensed in one heart chamber, or its absence, provided the information needed to govern that same heart chamber. It has long been the goal of cardiologists to create pacemaker systems that sense electrical activity in the upper part of the heart, the atria, and regulate the ventricles at a rate appropriate to the rate sensed in the atria. Most conventional systems employ two catheters, one placed in contact with the right atrial appendage and the other placed in contact with the right ventricular apex. In this way, the signal sensed in the atrium can be extracted by a pulse generator and stimulation can be delivered to the ventricle at the appropriate rate.
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ãããšèããããããã§ããã There are also several prior art descriptions of single catheters that can be used to sense atrial activity and regulate at the ventricular level. Generally, in each case the sensing element was an electrode similar to the stimulation electrode, but placed anywhere along the axis of the catheter. For example, placing one or two ring electrodes at the atrial level to sense the atrial electrogram is shown in Thaler, U.S. Pat. There is. Other similar designs include U.S. Pat.
U.S. Pat. No. 3,825,015 entitled "Single Catheter for Atrial and Ventricular Stimulation" to BerKovits;
Bures, US Pat. No. 3,865,118 entitled "Transvenous Axial Catheter." In most cases, it has hitherto been considered necessary to physically contact the electrode with the inner surface of the atrium. because,
Heart waves are generated within myocardial tissue, and O'Neill and
This is because contact was considered essential as shown in the Bures patent.
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A pacemaker is shown sensing P fluid and generating ventricular stimulation from two circumferential ring electrodes E1 and E2. The Thaler patent is illustrative of the complex circuits that the prior art attempted to devise to distinguish P fluid from the wave elements of ventricular depolarization and subsequent cardiac wave complexes. This is an important issue. This is because the P wave sensed from the non-contact ring electrode is substantially identical to the subsequent QRS complex. At the same time, there is no reliable way to distinguish P waves from their associated QRST wave trains by automated means, by spectral analysis or otherwise. Another complex circuit used in conjunction with cardiac pacers is U.S. Pat. No. 4,060,090 to Berkovits, Lin et al.
No. 3,937,226 to Funke, entitled "Anti-Arrhythmia Device."
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ãããããã The problem of signal discrimination at both the atrial and ventricular levels is further complicated when considering the effects of electrical stimulation by the pacemaker itself at the atrial or ventricular level. When attempting to sense myocardial depolarization induced by unipolar or bipolar 5 volt artificial electrical stimulation with the same electrode used for the stimulation, an electrical phenomenon (later (used as electric potential) is generated. This is a potential with an amplitude of a few volts and a duration of 200-500 msec. This will overwhelm the evoked adjacent myocardial response and, absent extremely complex circuitry, the stimulated myocardial event will not be sensed by the pacemaker itself. As a result,
In conventional technology, every stimulus or induced depolarization is followed by a "difficult period".
What is called is recognized. "After potential" is
It acts at the ventricular level as a result of ventricular stimulation only, but at the atrial level, stimulation of either the atria or the ventricles results in obscuring the atrial electrogram for a significant period of time.
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ãç²ç®ãšãªã€ããšããäºå®ã«ããæªåãããã In any case, the prior art has had little success in devising acceptable P-synchronized, VDD, and DDD demand pacemakers because P fluid cannot be extracted well from the subsequent heart wave complex; Folded. This collapse was exacerbated by the fact that the sensing electrodes and associated circuitry were overwhelmed by the strong stimulation pulses generated by the pacemaker itself, thus blinding the pacemaker to whether or not depolarization had been successfully stimulated. It was done.
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ã«è€éãªåè·¯ã®äœ¿çšã«äŸåããã A problem encountered with increasing frequency in complex dual chamber pacer systems is that of abnormal retrograde activation of the atria. This results from spontaneous premature depolarization of the ventricles or slowing of retrograde or retrograde conduction across the ventricles and the AV node. Retrograde transmission is a normal ability of the AV node;
Occurs in 90% of patients with sinoatrial node dysfunction.
Therefore, this problem is of critical importance for DDD pacer systems. Attempts to determine whether retrograde transmission is responsible for a given P fluid require extremely complex circuits, essentially lacking common electrical sensors to accurately analyze the direction in which myocardial activation is occurring. Depends on usage.
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ãšãçžåœã®èšºæãšã©ãŒãçããããšã«ãªããã This same difficulty is compounded when attempting to utilize standard ventricular sensing systems to distinguish between normally conducted impulses and those generated by abnormal lesions within the ventricle, i.e., between normal forward conduction and premature depolarization of the ventricle. When trying to distinguish it from Shion,
It is also encountered in such systems. This latter capability becomes extremely important when considering the problems of tachycardia conversion pacemakers. Currently, lacking a suitable sensor, only the rate at which ventricular events occur can be used to distinguish desired from unwanted tachycardia.
Normal sinoatrial rhythm, atrial tachycardia with 1:1 transmission, atrial flutter with variable transmission, as well as ventricular tachycardia, will all occur at a rate that exceeds the preselected ratio to ventricular tachycardia conversion. Thus, using percentages alone to determine the presence of ventricular tachycardia would result in substantial diagnostic error.
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ãåŒå¥çã«æç¥ããåŸãããšã1 The local electrogram obtained from the tissue adjacent to the regulating catheter is differentiated from all external electrical events generated by other regions of the same chamber, the applied electrical stimulation or depolarization of the opposite chamber. something that can be sensed.
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圱é¿ã«äžæç¥ã«ãããããšã2. The local electrogram is rendered insensitive to the effects of EMI and myopotential sensing.
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ããæçã«åŒå¥ã§ããããšã4. Electrograms derived from the atrial myocardium can be recorded at fairly high amplitudes and can be clearly distinguished from atrial electrical events even though the magnitude of the electrical force causing the atrial events is essentially large.
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When applied to the problems encountered in handling electrical disturbances of the heart, it will lead to the development of accurate and reliable electrical devices for the treatment of cardiac arrhythmias.
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ãããæããä¿¡å·ãçºçããŠãå¯èœã§ãããSUMMARY OF THE INVENTION The present invention provides the ability to generate a desired electrical current through one or more points in a plane substantially perpendicular to a depolarization vector in cardiac tissue proximate to a pair of points at which localized excitation waves are sensed. Improving methods for sensing cardiac electrical activity, including discriminating desired local cardiac electrical events from complex series of waves, pacemaker stimulation, and/or extracardiac electrical events by sensing diagrams. It depends. The signals sensed at this pair or pairs of points are electrically compared to induce a difference signal that is specific to the desired local electrogram, but these signals are not unique to complex cardiac waves. Virtually independent of all elements or external electrical events. It depends on the fact that the latter is an "out-of-field" electrical event. According to this method, any cardiac electrical event is reliably and unambiguously sensed and selected from any complex cardiac wave or non-local electrical event. And this is possible even though these non-local events generate signals with fairly large magnitudes.
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ãå¯èœã«ããããšã«ããç¹åŸŽã¥ããããã The desired local electrogram discrimination is characterized in particular by not having a pair of sensing electrodes necessarily in contact with the myocardium (heart tissue). In other words, the sensing electrode is free floating within the cardiac cavity.
In particular, it is equipped with an electrode dedicated to electrogram sensing that is not used for myocardial stimulation, making it possible to sense electrical events evoked (stimulated) in a manner that is not hidden by the polarization effect (afterpotential sensing) at the electrode-myocardial interface. It is characterized by
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ã«èªç±ã«æµ®åããŠããã To explain in more detail, the intraatrial electrogram (P fluid) is
The stage that distinguishes it from all other depolarizations, such as depolarization that occurs at the ventricular level, is characterized by the absence of sensing electrodes in contact with cardiac tissue. Whether located in the right atrium or the right atrial appendage, the sensing electrode is free floating within the heart cavity.
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å·ãèªå°ãããã In a second embodiment of the invention, the step of discriminating P fluid also includes sensing P waves at two or more points in a plane perpendicular to the depolarization vector in adjacent cardiac tissue. In one embodiment, cardiac signals are sensed at three or four equally spaced points around a circle in this plane, and two or more signals are derived from this sensing.
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ããã«è«çãé©çšããããã®ãšããã In addition, normal atrial or ventricular activation behavior, that is, activation behavior that results from the normal spread of electrical activity within the heart, can be improved by utilizing two or more sensors in different parts of the atrium or ventricle. Rapid arrhythmias can be distinguished from abnormal activation modes such as single early depolarization and retrograde transmission. The characteristics of the sensor in each area are
This is the same as described above. However, the sensing signal that directs the activation mode of each induced electrogram is
Logic shall be applied to ensure that normal or abnormal activation patterns can be distinguished.
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ã®èª¬æããæãããšãªããã These and other objects of the invention will become apparent from the following description of preferred embodiments, taken in conjunction with the drawings.
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§ããŠè©³çްã«èª¬æããã Hereinafter, preferred embodiments of the present invention will be described in detail with reference to the accompanying drawings.
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æ¹æ³ãå«ãã The present invention distinguishes local cardiac signals from all other undesired electrical signals, whether these electrical signals are generated in other regions of the same heart chamber, in other heart chambers, or in skeletal muscle or external The method includes a method in which focal cardiac electrical activity is sensed in a manner that is identifiably sensed, regardless of whether it occurs as an electrical event external to the heart, such as generated by an electrical murmur.
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ãšãåã€ãã The electromagnetic field mechanism on which the methodology of the present invention is based is not well understood. However, sensing the heart waves at two or more points that lie substantially in a plane perpendicular to the direction of the local depolarization vector in the nearest or adjacent myocardial tissue, and It has been found that by differentially amplifying the signals, high-amplitude local electrograms can be generated with very high signal-to-noise ratios. For example, very high amplitude QRS complexes, accompanying T waves, or large stimulation pulses generated by an associated pacemaker reliably sense the very small P fluid in the heart;
It has been found that this does not in any way affect the efficacy of the methodology to reliably distinguish this P fluid from all other natural or artificially introduced electrical activity.
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This electrocardiogram shows a P wave 12 which is a surface representation of depolarization of the atrial myocardium, a QRS complex 14 following the P wave 12 which also reflects depolarization of the ventricular myocardium, and a ventricular lipolarization. , showing the T-wave 16 that follows. Line 18 is a normal atrium as measured typically by a prior art ring electrode probe floating within the atrium or in contact with the right atrial appendage.
It's an EKG. A normal atrial EKG typically consists of a bipolar P-wave response, indicated generally by reference numeral 20, followed by a slightly smaller amplitude bipolar QRS response, indicated generally by reference numeral 22. have The waveform of QRS response 22 is P
It is roughly the same as wave response 20, but tends to be smoother and of lower amplitude. However, even among normal individuals, one person's heart waves may differ significantly from the measured heart waves of another individual, or from the same individual's heart waves measured at different times. There is. Slight variations in the intervals between the various component responses from the component responses shown by line 18 in the atrial EKG, including variations in the relative amplitudes of each component response, are to be expected in an abnormal heart. The waveform and amplitude fluctuations of the P-wave response 20 and the QRS response 22 make it extremely difficult for even a human observer to completely distinguish between the two in any environment. Therefore, the electronic circuits and logic are P wave response 20 and QRS response 2.
It is even more difficult to reliably distinguish between 2 and 2 than for a human observer, and this shortcoming has generally limited the development of current cardiac pacemakers.
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ã¯ååšããªãã Line 28 is an electrical diagram taken from the right atrial appendage by using the orthogonal probe devised by the present invention. The sensed signal is a response collectively indicated by the reference numeral 30, indicating a P wave, having the shape of a sharp recognizable spike of 2-10 mV, duration of 15-40 milliseconds, and similar to that of other cardiac There are virtually no other responses to electrical events. Line 32 is a ventricular electrogram sensed in accordance with the present invention, with a large recognizable QRS response, indicated generally by reference numeral 34, and a very small T, indicated generally by reference numeral 36.
There are no other discernible responses, including atrial P waves, to other cardiac events.
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and 32, the focal individual responses obtained in intracardiac electrograms retrieved in accordance with the present invention are significant when compared to those detectable by prior art devices and methods. For example: The electrical diagram shown by lines 28 and 32 of the present invention not only has a considerably better signal-to-noise ratio;
The duration of the response indicates only localized fields or nearby cardiac events. For example, a probe placed in the right atrial appendage would generate the response illustrated in line 28, in marked contrast to the normal atrial electrogram illustrated in line 18, and would respond to any cardiac activity in the ventricles. It is completely unaffected by twisting.
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å¿å®€ä¿¡å·ã«äºå®äžå¿çããªãã FIG. 2 further illustrates that the present invention senses only events near the field of the heart and provides sharp depolarization spikes in response with a very high signal-to-noise ratio. The surface EKG is reproduced as line 16 in FIG. 2, and the normal atrial electrogram is reproduced as line 18 in FIG. This is an electrogram sensed with a catheter having multiple orthogonal sensing electrodes, namely the electrogram exemplified by line 38 from the sensing electrode placed in the upper right atrium and the sensing electrode placed in the lower right atrium. A comparison is made with the electrical diagram illustrated by line 40. During normal progressive conduction, the P fluid response 42 sensed in the upper right atrium is clearly indicated by line 38, starting at some time during the early phase of the P wave. However, P of line 40 sensed by the electrode in the lower right atrium
The wave shows a P-wave response 44 that appears at a delayed time compared to response 42. This interval represents the normal propagation delay within the heart from the top to the bottom of the atrium. In each case, electrograms taken in the upper or lower regions of the right atrium are virtually unresponsive to large ventricular signals generated near the ventricles.
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ãã«ãªã€ãã®ã§ããã Continuing to refer to FIG. 2, the normal surface electrogram of a counter-propagating heart wave is illustrated by line 46, with the P-wave response 12' inverted and
The QRS complex continues. The same sensing electrodes used in FIG. 1, whose outputs are depicted at lines 38 and 40, produce electrograms as shown at line 48 from the upper right atrium and line 50 from the lower right atrium.
Generates an electrical diagram as shown. As mentioned above, the upper right atrium response is a sharp P wave response 52, and the lower right atrium response is a sharp P wave response.
This is a wave response 54. These EKG 48 and 50 waveforms are similar to EKG 38 and 4 except that their time sequences are opposite to each other.
It is essentially the same as the waveform of 0. The right atrial upper P-wave response 52 clearly lags in time than the right atrial lower response 54 (this retrograde atrial depolarization results in an inversion of the P-wave 12'). However, as shown by line 53,
A normal atrial electrogram corresponding to a retrograde heart wave is virtually indistinguishable from a normal atrial electrogram corresponding to a normal heart wave such as line 18. Thus, by using multiple sensing regions according to the present invention, for the first time, the propagation sequence of events within a particular cardiac chamber can be accurately detected and used to distinguish normal heart beats from abnormal heart beats. It became.
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It has been determined by the present invention that, regardless of the angular orientation of the electrodes 60 in the plane illustrated in FIG. 4, the electrodes 60 only sense electrical activity in their immediate vicinity. . Electrode 60 produces no response to cardiac activity occurring in other chambers of the heart, external to the heart, but occurring in adjacent muscle tissue, or to external electromagnetic interference. Although catheter 58 and electrode 60 are not in contact with the inner wall of heart 56 in FIG. 4, as was incorrectly believed in the prior art,
It should be noted that catheter 58 and electrode 60 do not need to contact the inner wall of heart 56 to generate a useful signal.
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Catheter 58 extends through atrium 70 and down through the tricuspid valve to apex 76 of heart 56 .
A stimulating tip 78 is provided at the end of the catheter 58 for implantation within the apex 76 of the ventricle, as shown enlarged in FIG. 6B illustrating the region of the heart 56 designated 6B in FIG. It is being A stimulating tip 78 is provided at the end of the catheter 58 for direct contact with the myocardial tissue at the apex 76 of the ventricle. High voltage stimulation pulses are applied to chip 78 by a conventional pacemaker to initiate the necessary ventricular contractions according to established medical principles. Stimulating tip 78 may be any conventional tip, including any fixation device (not shown) that facilitates implantation and anchoring of tip 8 within the myocardial tissue adjacent to ventricular apex 76.
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ãŒããä»ããŠçµåãããŠããã FIG. 7 schematically and fragmentarily illustrates an enlarged view of ventricle 72 in accordance with another embodiment of the present invention in which catheter 58 is shown as including a sensing electrode 80 contained within ventricle 72. exemplify. Electrode 8
0 is located in the ventricular wall of the heart 56 near ventricular myocardial tissue 82 . As mentioned above, the electrode 8
The signal sensed by 0 is coupled via conventional flexible leads to a conventional pacemaker circuit for subsequent processing and generation of stimulation pulses delivered to chip 78.
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The large stimulation pulses delivered to chip 78 will completely overwhelm the sensing circuitry associated with the stimulation means placed within the ventricle. Therefore, cardiac activity that may be initiated by the stimulation pulses applied to chip 78 cannot be reliably sensed by any method known in the art. however,
The electrical activity of the heart is sensed at a location of electrode 80 positioned in a plane approximately perpendicular to the nearest depolarization vector of adjacent myocardial tissue 82, and the sensed signal is differenced in a differential amplifier. 1, a discrete, localized electrogram response 34, as shown by line 32 in FIG.
Even in the application shown in FIG. 7, where 0 is within the 1-3 cm delivery range of the stimulation pulse, it is unaffected by the stimulation pulse delivered to the tip 78.
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åŒãèµ·ãããåŠãã«å¿çããŠã ãçºçã§ããã The method of the invention therefore results in the first true demand pacemaker. In other words, a stimulation pulse can only be generated in response to whether a previous ventricular stimulation pulse caused a contraction of the heart.
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ãã FIG. 8 shows a third embodiment of the invention in which stimulation of the heart is applied to the right atrial appendage, designated by the reference numeral 86, illustrated schematically and in fragments on an enlarged scale. Catheter 88 is J-shaped to allow atrial sensing by electrode 90 at the upper lateral atrial wall, ie at right atrial appendage 86 . Again, electrode 90 lies generally in a plane that is approximately perpendicular to the nearest depolarization vector of adjacent myocardial tissue (not shown). The end of the catheter 88 is shown in FIG. 7 and is provided with a stimulation tip 92 similar to the conventional stimulation tip 8 described in connection with FIG. The atrial appendage 86 illustrated in FIG. 8 is in close proximity to the right ventricular outflow tract designated by reference numeral 94. Despite electrical activity that may be associated with the ventricle or outflow tract 94, the atrial appendage 86
Electrodes 90 within the field sense only the nearest cardiac activity in the vicinity of the field and produce a large signal-to-noise output signal, as illustrated by line 28 in FIG.
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ã®åŠçãçããããã The present invention can implement a fourth embodiment shown in FIG. 9 in which sensing local myocardial depolarization from multiple regions can be achieved. Electrograms are recorded by electrode 100 from the lower right atrial region 98 and by electrode 104 from near the atrial bed 102. As mentioned above, the upper right atrial signal is sensed by electrode 60. electrodes 60, 100,
and 104 are approximately perpendicular to the nearest depolarization vector in the adjacent myocardial tissue. Electrodes 60, 100 and 104
each produces an individual spike-shaped response indicative of local cardiac activity, of the type shown in lines 38, 40, 48, and 50 of FIG. These electrodes 60, 100 and 10
Each of 4 is coupled to a pacemaker circuit (not shown) through a corresponding flexible lead within catheter 106 for subsequent processing and appropriate generation of stimulation pulses. The use of multiple sensing electrodes, as illustrated in FIG. 9, results in processing of the heart that is not based on the mere absence or presence of cardiac activity within the heart, but is based on the sequential progression of cardiac activity. .
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ãã®å¹²æžãªãã«ç¢ºå®ã«ç£èŠã§ããã Thus, it is clear that the methodologies and probes of the present invention can be used anywhere in or near cardiac structures and with a wide variety of probe shapes. For example, although shown sensing in the atrial appendage, various locations within the atrium, and in the ventricle, the probe can also be placed in the coronary sinus. Again, only events local or near the field of the coronary sinus are received by the probe, ensuring that these events can be monitored without interference from nearby large amplitude signal sources.
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8 and 110. Each electrode plate 1
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8 and 110 are on the surface of the virtual cylinder 118,
They are arranged circumferentially around catheter 116. The surface of cylinder 118 may actually be directly beneath the physical surface 120 of catheter 116. Catheter 116 with external protective and insulating sheathing
The epidermis of the electrode plate 108 and 110 is excised to expose the electrode plates 108 and 110, which are in direct contact with the surrounding blood.
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極ãããã«çµåãããã In this way, the electrode plates 108 and 110 are connected to the tenth electrode via the leads 112 and 114, respectively.
It is coupled to a differential amplifier 122, which is shown schematically in the figure. The output of this differential amplifier 122 is the trigger pulse shown and described in FIGS. 1 and 2.
Although leads 112 and 114 are shown schematically as straight lines, in reality these leads are multi-land, with very high fatigue tolerances developed to accommodate the expected curvature within the human heart. Consists of coil wire. In the case illustrated in FIG. 10 where only two points, electrode plates 108 and 110, are used to sense the nearest depolarization vector 150, the two signals are input to a conventional differential amplifier 122. used as. The output of the differential amplifier 122, ie, the spike-shaped response, is passed to a processing and pulse generation circuit 124, which may be of conventional design, contained within a subcutaneous pacemaker, generally indicated by the reference numeral 126. be combined. Processing and pulse generation (logic) circuitry 124 generates stimulation pulses in response to trigger pulses provided by differential amplifier 122 according to principles well known in the art. The stimulation pulses are coupled by a conventional flexible lead 128 through catheter 116 (not shown) to the stimulation electrode tip.
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ãšãã§ããããã³ïŒ¹ä¿¡å·ãæ§æããã FIG. 11 schematically illustrates a portion of catheter 130 with four sensing electrodes 132-138. Electrode plates 108 and 1 in FIG.
10, the electrodes 132-138 each have a virtual cylinder 1 defined within the catheter 130.
It is on the surface of 40. In reality, the cylindrical support surface, described herein as virtual cylinder 140, may be a sheathing on the underside of catheter 130 or a non-conductive material that acts as a mold for supporting electrodes 132-138. It may also be a cylindrical ring. If four electrodes are used as shown in FIG. 11, true orthogonal sensing signals can be extracted. For example, electrodes 132-138 are equally spaced around the circumference of catheter 130, and thus are 90 degrees apart from each other. Electrode 13
4 is paired with electrode 138, and electrode 136 is paired with electrode 132. Each pair is routed to an associated differential amplifier via their corresponding flexible leads. For example, electrodes 134 and 138
provides the input signal to differential amplifier 142, while electrodes 136 and 132 provide the input signal to differential amplifier 1.
44. Differential amplifiers 142 and 144
The output of is provided as an input signal to a processing and pulse generation circuit 146, similar to circuit 124, contained within subcutaneous pacemaker 148.
The outputs of the two differential amplifiers are shown in Figures 10 to 1.
2 can be subsequently processed to obtain a signal whose absolute magnitude is independent of the angular orientation of catheter 130 in a plane perpendicular to the local depolarization vector, illustrated symbolically as arrow 150 in FIG. Configure the X and Y signals.
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ãæ§æããã In the embodiment of FIG. 12, electrodes 152-156 are located within a virtual cylinder 158 defined within catheter 160.
are arranged at equal intervals on the surface. In this example where three electrodes are used, each electrode is 120° apart, but two of these electrodes, e.g.
It has been found that sensing is also possible when electrodes 152 and 156 are placed diametrically opposite each other, with electrode 154 spaced midway therebetween and spaced 90 degrees from each of electrodes 152 and 156. In either case, electrodes 152-156 may be associated in any logical manner to form electrode pairs for deriving quasi-orthogonal signals. For example, electrode 156 can optionally be selected as a common electrode, and a first signal is generated between electrodes 152 and 156 in differential amplifier 162. A second signal can similarly be generated between electrodes 156 and 154 and provided as an input to differential amplifier 164. The outputs of differential amplifiers 162 and 164 are thus routed to circuit 14 in the manner described in connection with FIG.
Construct pseudo X and Y signals that can be subsequently processed by 6.
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It has been experimentally determined that the optimal area for each electrode is approximately 1-4 mm2 . It has been found that the amplitude of the signal decreases as the area of each electrode is increased to, for example, 10 mm 2 .
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50 symbolically represents the direction of the depolarization vector in the adjacent myocardial tissue closest to the sensing electrode of each catheter. The angular orientation of the electrodes with respect to the depolarization vector is determined as long as these electrodes are close to each other, i.e.
It does not matter, as long as they are within cm and as long as the geometric center of each electrode lies generally in a plane substantially perpendicular to the depolarization vector 150. Maximum sensing appears to occur when the plane of each electrode's surface is approximately parallel to the imaginary plane in which the depolarization vector lies. Small variations from this ideal condition do not materially reduce the operational ability or effectiveness of the present invention.
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ããã Furthermore, in each of the embodiments described in connection with FIGS. 1-9, the sensing electrodes were placed within the heart so as not to contact adjacent myocardial tissue. This is contrary to the prior art belief that the electrode must be in contact with tissue to obtain a reliable and useful signal. This has been largely true when it comes to delivering stimulation pulses to the heart, but has been found to be false when it comes to sensing signals. Indeed, the effectiveness of sensing local electrical heart facts from the nearest myocardial tissue is increased in the absence of contact. Prolonged contact can lead to fibrosis, resulting in covering all or part of the contacting portion of the catheter with bodily tissue. It has been found that fibrosis generally attenuates the signal that can be sensed from such covered electrodes. Although it is only incompletely understood,
It appears that local electrical cardiac events can be sensed more effectively when the electrodes are not in direct physical contact with adjacent myocardial tissue. Thus, provision for contacting or securing the electrode to adjacent tissue is not included within the methodology of the present invention, contrary to the teachings of the prior art. In fact, the electrodes described in connection with each of the embodiments shown in FIGS. 10-12 are slightly recessed within their respective catheters, thus
Even if the catheter were to make physical contact with adjacent tissue, the electrodes themselves would not be in physical contact.
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瀺ãããã®ã§ããã FIG. 13 is a flowchart generally summarizing the implementation of the method described in connection with the embodiments described in FIGS. 2-9 with the probe illustrated in FIGS. 10-12. The flow diagram of FIG. 13 illustrates a single cardiac cycle.
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åšãã倿¥µæ§ä¿¡å·ãçºçãããã The heart wave is sensed at step 166 and a local electrogram obtained as described above. In the case of the catheter of FIG. 10, a single signal is generated as the output of differential amplifier 122, whereas in each of the embodiments of FIGS. 11 and 12, a multipolar signal is generated from a corresponding plurality of differential amplifiers. is generated.
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66 and the difference of each associated pair is taken at step 168 to generate one or more trigger or response pulses. In the illustrated embodiment, the difference taking is described as being performed by an analog differential amplifier. However, any equivalent means can be used, such as digitizing the sensed signals and taking an arithmetic average of them in step 166.
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ãããŠäºæã§ããããšã§ããã One way the signal can be processed in step 168 is to provide variable amplitude adjustment. The voltage of the series of stimulation pulses can be varied depending on the success of the immediately preceding pulse or the percent success of the previous series of pulses in stimulating responsive heart contractions. Thus, if the stimulation pulse is unable to depolarize the myocardium due to insufficient strength, this failure will be sensed and there will be no response or trigger pulse at the output of the differential amplifier coupled to the sensing electrode. This is detected by the processing circuitry in step 168. The next pulse can be generated with a predetermined increase in stimulation intensity. It can be repeated until a successful pulse output is obtained, at which point the regulated pulse output can be held stable until the cardiac condition changes again. This is to be expected, for example, in situations where the responsiveness of myocardial tissue is altered by drugs or ischemia.
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2 may include decision logic to reset the pacemaker to its initial state. On the contrary, a decision is made to generate or trigger a cardiac stimulus based on objective criteria, whereby an appropriate stimulus is generated and delivered step 17.
It may be set to 4. Thereafter, the pacemaker is reset to its default state at step 176.
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å®çŸã§ããã As a result of the processing at step 170, a decision is made in accordance with processing rules as to whether or not a stimulation pulse should be generated, and if so, what type of stimulation pulse. Not only can the timing and amplitude of the pulses be varied as described above, but the location of the pulses can also be selected. For example, two stimulation electrodes may be provided on the same or different catheters, allowing for selection of points at which stimulation is applied to adjacent heart tissue. Alternatively, a two- or multiple-tip catheter may provide suitable stimulation to any one of a plurality of cardiac locations, eg, one to the apex of the ventricle and one to the atrial appendage. Similarly, selective stimulation of the atria and ventricles can be easily achieved depending on the cardiac activity observed according to the invention at any point within the heart.
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FIG. 1 shows the temporal relationship between a conventional surface electrogram and atrial and ventricular electrograms obtained from the right atrial appendage and right ventricular apex for comparison with the electrogram recorded by the sensing probe of the present invention. graph,
FIG. 2 shows the temporal relationship between the normal surface electrogram of a normal heartbeat, the standard atrial appendage electrogram, and the upper and lower right atrium electrograms obtained with the sensing probe of the present invention. Graphs, FIG. 3 is a fragmentary schematic perspective view showing a catheter containing a sensor of the present invention adjacent to myocardial tissue, and FIG.
A cross-sectional view taken along line -4, Figure 5 is the same as Figure 3.
6 is a schematic diagram showing the right atrium and right ventricle of a human heart with the catheter of the present invention inserted, and FIG. 6A is an enlarged view of the circled area 6A in FIG. 6. Figure 6B is an enlarged view of the circled area 6B in Figure 6, Figure 7 is a fragmentary schematic of the ventricular sensing and stimulation probe at the apex of the ventricle, and Figure 8 is the right atrial appendage. FIG. 9 is a fragmentary schematic diagram of a J-shaped atrial sensing and stimulation probe positioned in the atrium; FIG. is a fragmentary schematic diagram showing an enlarged portion of a catheter in which two electrodes are provided for sensing;
FIG. 11 is an enlarged schematic diagram of a catheter showing an embodiment in which four electrodes are used; FIG. 12 is an enlarged schematic diagram of a portion of the catheter showing an embodiment in which three electrodes are used; FIG. The figure is a flowchart outlining the methodology of the present invention. 56... Heart, 58... Single filament catheter, 60... Electrode, 62... Depolarization vector, 64... Myocardial tissue, 70... Right atrium,
72...Right ventricle, 76...Apex of the heart, 78...
Stimulation tip, 80... Sensing electrode, 82... Myocardial tissue, 86... Right atrial appendage, 88... Catheter, 90... Electrode, 92... Stimulation tip, 94
...Right ventricular outflow tract, 98 ...Lower right atrial region, 1
00... Electrode, 102... Atrial floor, 104... Electrode, 108, 110... Electrode plate, 112, 114
... flexible wire lead, 116 ... catheter, 118 ... virtual cylinder, 120 ... physical surface of catheter 116, 122 ... differential amplifier, 1
24... Processing and pulse generation circuit, 126...
pacemaker, 130...catheter, 132
~138...Sensing electrode, 140...Virtual cylinder, 1
42,144...Differential amplifier, 146...Processing and pulse generation circuit, 148...Pacemaker, 152-156...Electrode, 158...Virtual cylinder, 160...Catheter, 162,164...
Differential amplifier, 165...pacemaker.
Claims (1)
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ïŒïŒé èšèŒã®ãããŒãããã³åè·¯çµåãè£ çœ®ã[Scope of Claims] 1. Local cardiac signals are transmitted to other cardiac tissues by sensing local cardiac waves at a pair of points in a plane substantially perpendicular to the depolarization vector in adjacent cardiac tissue. a probe that discriminates from intracardiac signals and signals sensed at the pair of points of the probe in the plane are compared to each other to determine the local cardiac signal and to differentiate it from the other intracardiac signals. and a circuit for inducing a differential signal that is unrelated to the other intracardiac signals to reliably and unambiguously sense and select the local heart wave signal from the other intracardiac signals,
A device for sensing heart activity. 2 the probe for discriminating the local cardiac signal,
2. The cardiac activity sensing of claim 1, wherein the cardiac activity is sensed at a location in the plane proximate to the cardiac tissue, and neither of the pair of points in the probe is in contact with the cardiac tissue. Device. 3. The cardiac activity sensing device according to claim 1 or 2, wherein the probe for discriminating local cardiac signals senses the cardiac activity at two or more points within the plane within the probe. 4. The cardiac activity sensing device according to claim 3, wherein the probe for discriminating local cardiac signals senses the cardiac activity at three points within the probe. 5. The cardiac activity sensing device according to claim 4, wherein the cardiac activity is sensed at three equally spaced points around a circle existing in the plane within the probe. 6. The cardiac activity sensing device of claim 1, wherein the probe for discriminating the local cardiac signal senses the cardiac activity in close proximity to ventricular tissue. 7. The cardiac activity sensing apparatus of claim 1, wherein said circuit processes said difference signal to generate a response to said differentially sensed local cardiac signals obtained from said probe. 8. The cardiac activity sensing device of claim 7, wherein said circuit generates a ventricular regulating signal as said response. 9. Generation of a ventricular regulating signal in said circuit is conditional on confirmation of the presence of said differentially sensed local cardiac signal at said probe, said circuit comprising:
9. The cardiac activity sensing device of claim 8, wherein said ventricular regulating signal is generated in the absence of said differentially sensed local cardiac signal obtained from said probe. 10 said circuit at a rate determined by calculated measurements of a plurality of previously differentially sensed local cardiac signals obtained from said probe;
Claim 9 for generating the ventricular rate regulating signal
The cardiac activity sensing device described in Section 1. 11 the circuit variably varies the magnitude of the current in response to the presence or absence of a previously differentially sensed local cardiac signal obtained from the probe to generate the ventricular regulating signal; A cardiac activity sensing device according to claim 8. 12. The cardiac activity sensing device of claim 1, wherein the probe for discriminating local cardiac signals senses the cardiac activity in close proximity to atrial heart tissue. 13. The cardiac activity sensing device according to claim 12, wherein the local cardiac activity sensing probe senses the cardiac activity in close proximity to a posterior lateral region of the atrium. 14. The cardiac activity sensing device of claim 12, wherein the cardiac activity sensing probe senses the cardiac activity in close proximity to an atrial appendage. 15. The cardiac activity sensing device according to claim 12, wherein the probe for sensing cardiac activity senses the cardiac activity in close proximity to the coronary sinus. 16. The cardiac activity sensing device according to claim 12, wherein the probe for sensing cardiac activity senses the cardiac activity in close proximity to the atrial floor. 17. The cardiac activity sensing of claim 1, wherein said circuit processes said difference signal to selectively generate a response to said differentially sensed local cardiac signals obtained from said probe. Device. 18. The cardiac activity sensing device of claim 17, wherein said circuit generates a ventricular regulating signal as said response. 19. The cardiac activity sensing device of claim 17, wherein said circuit generates an atrial cadence signal as said response. 20 a probe that senses cardiac activity within the heart at at least two proximate locations in a plane, and a difference between signals sensed at at least two locations within the probe to determine the local cardiac signal; a circuit for inducing instructive trigger pulses to reliably and unambiguously sense and distinguish the local cardiac signal from the heart wave with a probe, regardless of the source of the local cardiac signal within the heart. A probe and circuit combination device for discriminating local cardiac signals from intracardiac signals within the heart, characterized in that: 21 The cardiac activity sensing probe senses the local cardiac signal at three locations within the probe in or near the plane, and the three locations within the probe are located within the probe. are related to include two pairs of positions,
21. The probe and circuit combination of claim 20, wherein one of said three locations within said probe serves as a common location within said probe for this association. 22. The probe and circuit combination of claim 21, wherein said cardiac activity sensing probe senses said localized cardiac signals at three equally spaced locations within said probe. 23. A probe that senses the local cardiac signal at the location on the probe is configured to detect the local cardiac signal in the probe by an electrode that lies generally in a plane generally parallel to the depolarization vector in myocardial tissue proximate the probe. 21. The probe and circuit combination of claim 20, wherein the probe and circuit combination senses the local cardiac signal at each location. 24. The probe according to claim 20 or 23, wherein the cardiac activity sensing probe senses the local cardiac signal at each position within the probe by an electrode within the probe having a rotating surface. Circuit combination device. 25. Sensing the local cardiac signals by the electrodes in the probe; wherein the probe senses the local cardiac signals by electrodes having a geometry defined by a flat geometric plane in the range of 1 to 4 mm2 ; 25. The probe and circuit combination device of claim 24, wherein each of said locations within said probe is separated from each of said locations within said probe by less than 10 mm. 26. A probe for sensing localized electrical activity at a plurality of closely spaced points in or near a plane perpendicular to a depolarization vector in adjacent myocardial tissue; taking a difference in the local electrical activity sensed at a plurality of points to obtain at least one trigger pulse indicative of a local cardiac signal; and processing the at least one trigger pulse signal to generate a stimulation pulse. a circuit for determining whether the true demand of the heart should be met, generating said stimulation pulses, and coupling said stimulation pulses to the heart via said probe to stimulate contractions of the heart; A probe and circuit combination device for differentially sensing local cardiac signals from cardiac wave complex signals and extracardiac electromagnetic noise, characterized by speed regulation. 27. The electrical activity sensing probe senses at the plurality of points within the probe with a plurality of corresponding electrodes positioned at the plurality of points within the probe; 27. The probe and circuit combination of claim 26, wherein said probe and said myocardial tissue adjacent to said probe are not contacted. 28. The probe and circuit combination of claim 26, wherein the signal processing portion of the circuit determines whether to generate a stimulation pulse depending on the presence or absence of a P-wave following a preceding stimulation pulse. Device. 29 The signal processing portion of the circuit determines whether a particular local cardiac signal from the probe was present at the cardiac wave complex at the location sensed by the probe at a time following the occurrence of the previous stimulation pulse. Thus, determining whether to increase or decrease the magnitude of the stimulation pulse, and when the probe and circuitry indicate the absence of the particular local cardiac signal from the probe, increase or decrease the magnitude of the stimulation pulse. when increasing and indicating the presence of the particular local cardiac signal from the probe;
29. A probe and circuit combination according to claim 26 or 28, wherein the magnitude of the stimulation pulse is reduced. 30. Claim 26, wherein said circuitry determines the temporal interval between successive stimulation pulses depending on whether the circuit indicates the presence or absence of a particular local cardiac signal from the probe. probe and circuit combination equipment. 31 The probe sensing said electrical activity is
sensing the electromagnetic activity at a plurality of locations in the probe, each location in the probe being on or near a plane generally perpendicular to a depolarization vector in myocardial tissue proximate to the probe; 27. The probe and circuit combination device of claim 26, which is arranged at a plurality of closely spaced points. 32. The circuit of claim 31, wherein the circuit takes the difference in electrical activity at each position of the probe at the plurality of corresponding points on the probe to generate a plurality of corresponding trigger signals. probe and circuit combination equipment. 33. Claim 31, wherein a signal processing portion of said circuit processes said plurality of trigger signals to detect differentially sensed local sequential patterns of cardiac activity obtained from said probe. or the probe and circuit combination device according to item 32.
Applications Claiming Priority (2)
| Application Number | Priority Date | Filing Date | Title |
|---|---|---|---|
| US40569582A | 1982-08-05 | 1982-08-05 | |
| US405695 | 1989-09-11 |
Publications (2)
| Publication Number | Publication Date |
|---|---|
| JPS5982831A JPS5982831A (en) | 1984-05-14 |
| JPH0414005B2 true JPH0414005B2 (en) | 1992-03-11 |
Family
ID=23604818
Family Applications (1)
| Application Number | Title | Priority Date | Filing Date |
|---|---|---|---|
| JP58143601A Granted JPS5982831A (en) | 1982-08-05 | 1983-08-05 | Apparatus for sensing signal in hart |
Country Status (5)
| Country | Link |
|---|---|
| JP (1) | JPS5982831A (en) |
| DE (1) | DE3322900A1 (en) |
| FR (1) | FR2533817B1 (en) |
| IT (1) | IT1161941B (en) |
| NL (1) | NL8302742A (en) |
Families Citing this family (3)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| DE4126363B4 (en) * | 1991-08-06 | 2004-11-04 | Biotronik Gmbh & Co. Kg | Cardiac pacemaker with means for effectiveness detection |
| US6240307B1 (en) * | 1993-09-23 | 2001-05-29 | Endocardial Solutions, Inc. | Endocardial mapping system |
| EP2401031B1 (en) * | 2009-02-06 | 2015-07-01 | Cardiac Pacemakers, Inc. | Cross-channel noise detector in implantable devices |
Family Cites Families (1)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| US4365639A (en) * | 1980-02-07 | 1982-12-28 | Applied Cardiac Electrophysiology | Catheter, cardiac pacemaker and method of pacing |
-
1983
- 1983-06-15 IT IT21642/83A patent/IT1161941B/en active
- 1983-06-25 DE DE19833322900 patent/DE3322900A1/en not_active Withdrawn
- 1983-08-03 NL NL8302742A patent/NL8302742A/en not_active Application Discontinuation
- 1983-08-04 FR FR8312910A patent/FR2533817B1/en not_active Expired
- 1983-08-05 JP JP58143601A patent/JPS5982831A/en active Granted
Also Published As
| Publication number | Publication date |
|---|---|
| JPS5982831A (en) | 1984-05-14 |
| DE3322900A1 (en) | 1984-04-26 |
| IT1161941B (en) | 1987-03-18 |
| IT8321642A0 (en) | 1983-06-15 |
| NL8302742A (en) | 1984-03-01 |
| FR2533817B1 (en) | 1988-11-25 |
| FR2533817A1 (en) | 1984-04-06 |
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