Abstract:
A method of treating hemodynamic disfunction by simultaneously pacing both ventricles of a heart. At least one ECG amplifier is arranged to separately detect contraction of each ventricle and a stimulator is then activated for issuing stimulating pulses to both ventricles in a manner to assure simultaneous contraction of both ventricles, thereby to assure hemodynamic efficiency. A first ventricle is stimulated simultaneously with contraction of a second ventricle when the first fails to properly contract. Further, both ventricles are stimulated after lapse of a predetermined A-V escape interval. One of a pair of electrodes, connected in series, in placed through the superior vena cava into the right ventricle and a second is placed in the coronary sinus about the left ventricle. Each electrode performs both pacing and sensing functions. The pacer is particularly suitable for treating bundle branch blocks or slow conduction in a portion of the ventricles.

Description:
CROSS REFERENCE TO RELATED APPLICATIONS 
     This is a continuation of Reissue application No.  08 / 547 , 691 , filed Oct.  19 ,  1995  now U.S. Pat. No. RE  38 , 119  E, which is a continuation of Reissue application No.  07 / 890 , 280 , filed May  29 ,  1992  now abandoned, which is a reissue of U.S. Pat. No.  4 , 928 , 688 , all of which are incorporated herein by reference. 
    
    
     BACKGROUND OF THE INVENTION 
     I. Field of the Invention 
     This invention pertains to medical devices, but more specifically, to a method for increasing the cardiac output of a patient suffering from congestive heart failure by stimulating the heart of the patient at multiple sites simultaneously. 
     II. Discussion of the Prior Art 
     Normally, impulses from the SA node affect contraction of the atria and then propagate to the AV node. The AV node, in turn, emits a second nerve impulse which affects contraction of the ventricles. These nerve impulses affect contraction, i.e., depolarization of the tissue of the heart, in a coordinated manner to circulate blood through the body. Cardiac pacers of the type herein described generally are useful for maintaining proper functional operation of a sick heart. Of many cardiac deficiencies which have in the past been diagnosed and treated, conduction difficulties have presented significant problems for which a pacer has been used for treatment. A particular conduction deficiency, known as AV branch block, inhibits the transfer of nerve impulses from the sinoatrial (SA) node to atrial-ventricular (AV) node. When a bundle block occurs, these nerve impulses are not properly transmitted from the SA node to the AV node and ventricles. 
     When this condition occurs, normal treatment is to employ a pacer which locks onto the rhythmic cycle of a atrial beating signal and supplies to the ventricles a stimulating impulse at a certain time thereafter to effect contraction of the ventricles. The time period between the occurrence of the atrial beat and the normal contraction of the ventricles is known as the A-V delay period. Generally, hemodynamic efficiency is somewhat dependent to the A-V delay period, thus the pacer must emit a stimulating pulse at a time to preserve an optimum A-V delay period. 
     Other forms of conduction deficiency, such as myocardial scarring and bundle branch block, cause slow conduction of nerve impulses, in which case, nerve impulses are indeed passed from the SA to the AV node, but in a time period which is slower than normal. The Q-R-S complex in this case would manifest itself in being very wide and hemodynamic efficiency also becomes lower than normal. 
     In each of the above-mentioned cardiac deficiencies, the heart does not contract in coordinated fashion. This uncoordinated movement increases depolarization time and results in more inefficient pumping rather than a more coordinated and simultaneous ventricular depolarization. In essence, such conduction deficiencies result in asynchrony between the left and right ventricle. 
     Additionally, arrhythmias of the heart produce uncoordinated ventricular contraction that affects the hemodynamic efficiency of the heart. Specifically, the recent paper “Incomplete Filling and Incoordinate Contraction as Mechanisms of Hypotension During Ventricular Tachycardia in Man”, published in Circulation, Vol. 68, No. 5, in 1983, describes that left ventricular function is severely disturbed by the disorganization of wall motion in hearts undergoing ventricular tachycardias. Moreover, it was found that hearts with impaired functions show profound reductions in pumping ability due to incoordinate contraction of the ventricles. It appears reasonable to believe, therefore, that any abnormal functioning heart that requires pacemaking or which has QRS widening will have a better hemodynamic efficiency if both ventricles are paced to contract in coordination with each other. There have been systems developed in the past employing a plurality of electrodes attached to the heart for effecting stimulation of a plurality of regions of the heart. For example, the Funke U.S. Pat. No. 3,937,226 discloses a cardiac electrical stimulation defibrillation system including a plurality of electrode terminals connected in a spaced relation on the heart. The electrodes, which provide stimulating and sensing, are each connected to amplifiers. The amplifiers are connected to electronic control circuit means configured to cause stimulation of all of the electrode terminals simultaneously in response to a sensed depolrization signal on the heart by at least one electrode terminal. In addition, the electronic control circuit is provided with a multivibrator means to synchronize the stimulation signal with the Q-R-S complex. Although Funke does teach the concept of simultaneous stimulation of a plurality of spaced electrodes, he does not disclose its specific use as a method of improving the cardiac output of patients suffering from congestive heart failure, nor does he discuss the specfic placement of the electrodes about the heart. 
     The Rockland et al U.S. Pat. No. 4,088,140 discloses a similar system to Funke&#39;s although a specific use as a pacemaker is stated in the patent. Rockland, et al discloses a demand anti-arrythmia pacemaker including a plurality of sensing electrodes connected to the heart to sense ventricular depolarizations. Electronic circuitry is provided having two paths of operation. A first path provides stimulation to one area of the heart if depolarization of a naturally occurring heart beat fails to occur within a first predetermined time period. In this first path, it is stated that the circuitry acts as a pacemaker in the event of skipped natural heartbeats. A second path provides stimulation to a plurality of locations on the heart if a depolarization signal is sensed on the heart within a second predetermined time period. In this second path, it is stated that the circuitry acts as a synchronous multiple electrode pacemaker or a synchronous multiple electrode defibrillator. Although, one example of an electrode placed in the intraventricular section and others in a spaced relation on the heart ventricles is given, there are no teachings of the specific placement of the electrodes on the heart nor the improvement of cardiac output from a sick heart. In addition, the electrodes perform either stimulating or sensing, not both, therefore a large number of electrodes is required in this system. 
     The Tacker, Jr. et al and McCorkle U.S. Pat. Nos. 4,548,203, 4,458,677 and 4,332,259, respectively, disclose the specific placement of an electrode in or around both left and right ventricles of the heart. The Tacker, Jr. et al patent discloses the placement of a catheter having one electrode in the right ventricle and another outside the heart and a third electrode placed on the left ventricle. The catheter electrodes, each being paired with the left ventricular electrode, are pulsed in sequence with a predetermined time separation resulting in uniform current density delivered to the heart. However, this pulsing scheme and configuration is disclosed for use in a ventricular defibrillation device and not for cardiac pacing to improve cardiac output wherein a more precise synchronization of stimulation signals with the Q-R-S complex is required. 
     The McCorkle, Jr. patents disclose the specific placement of an electrode in the right ventricle and another electrode in the coronary sinus surrounding the left ventricle for connection to a pacemaker. However, there is no specific technique disclose of providing stimulating signals to the electrodes to perform a pacemaking function. 
     In light of the above difficulties and shortcomings of the prior art, an objective of the present invention is to provide a cardiac pacer for increasing hemodynamic efficiency of a heart experiencing a conduction deficiency. 
     Another objective of the invention is to ensure a more coordinated and simultaneous ventricular depolarization of both left and right ventricles of the heart. 
     A yet further objective of this invention is to provide a cardiac pacer suitable for being implanted in a manner so as to impose a minimal surgical risk during implantation thereof. 
     A further objective of this invention is to provide a method and apparatus of separately sensing and stimulating each ventricle of the heart in order for effecting simultaneous contraction automatically of both ventricles of the heart to narrow the QRS complex of a failing heart and thereby cause an increase in blood pressure and cardiac output. 
     SUMMARY OF THE INVENTION 
     The method of the present invention involves a procedure for pacing of the heart in a particular way so as to improve its contraction pattern, and thereby augment the movement of blood through the heart. Patients suffering from severe congestive heart failure, which is found not to respond well to conventional drug therapy and to have a conduction defect in the ventricle resulting in a widen Q-R-S complex have been aided by a pacing regimen in which stimulating pulses are simultaneously applied to both ventricles by way of a demand pacemaker or asynchronous pacemaker. 
     It is theorized that a considerable part of the hemodynamic impairment in refractory congestive heart failure with conduction defects is due to an incoordinate contraction of the heart, so that a part of the heart muscle contracts and balloons out the part that is not contracting. When the latter area of the heart muscle does finally contract, the former has relaxed, so that a large part of the blood volume is merely shunted back and forth within the heart rather than being ejected as would happen with a more coordinate contraction pattern. 
     To attain the foregoing and other objectives, the present invention comprises, a bi-ventricular cardiac pacer having detecting and stimulating circuits for effecting substatially simultaneous contraction of both left and right ventricles of the heart. In the preferred embodiment, the bi-ventricular pacer comprises ECG amplifier means for separately processing sensed cardiac signals from each of the right and left ventricles. The amplified sensed signals are used to determined where possible abnormal conduction delays exist on the heart and to activate an electrical stimulator for stimulating the appropriate abnormally functioning part of the heart. More specifically, the stimulator responds to the control circuit to issue stimulating pulses simultaneously to either the left or right ventricle, as appropriate. The stimulator may be of the demand type wherein pacing pulses are only issued in the absence of a normal Q-R-S complex for one or the other of the two ventricles (e.g., occasional bundle branch block or slow conduction), or the nondemand type wherein pacing pulses are always issued (e.g., permanent bundle branch block or slow conduction). 
     To convey and sense signals to and from the heart, the present invention includes a pacing lead assembly comprising first and second separate electrodes. The first electrode is preferably introduced through the superior vena cava into the right ventricle and the second electrode is introduced through the coronary sinus to the left ventricle. Both lead segments include a sensing and pacing tip electrode which serves to both sense a cardiac depolarization signal or to apply a stimulating pulse from an implanted pulse generator to the ventricle. 
     Additionally, to preserve a predetermined A-V delay period, additional atrial sensing electrodes may be placed on or around the atrial chambers of the heart and connected to the control circuit. The control circuit responds to the sensed atrial and ventricular depolarization signals to provide simultaneous ventricular contraction signals applied to the left and right ventricles following a preset A-V delay period. 
     The advantages of the present invention include a more precise and coordinated simultaneous ventricular depolarization of both the right and left ventricular to thereby increase hemodynamic efficiency of a patient experiencing congestive heart failure or weak contractions. 
     These together with other objects and advantages which will become subsequently apparent reside in the details of construction and operation as more fully hereinafter described and claimed, reference being had to the accompanying drawings forming a part hereof, wherein like numerals refer to like parts throughout. 
    
    
     
       BRIEF DESCRIPTION OF THE DRAWING FIGURES 
         FIG. 1  depicts a functional block diagram of an apparatus for carrying out the teachings of this invention; and 
         FIG. 2  is a logic diagram of the “CONTROL” shown in FIG.  1 . 
     
    
    
     DETAILED DESCRIPTION OF THE PREFERRED EMBODIMENT 
       FIG. 1  illustrates the overall pacing system which may be employed for carrying out the teachings of the invention. A pair of leads  12  and  14  with corresponding sensing/stimulating tip electrodes  13  and  15  are electrically connected, via conductors  18  and  21 , to separate ECG sense amplifiers  16  and  17  (or to a single multiplexed amplifier). The amplifiers  16  and  17  are both connected to a control circuit unit  20 . A stimulator circuit  22  is connected to the control unit  20  and has two output conductor lines  24  and  26  which are electrically connected to the conductors  18  and  21 , respectively. From this structure, signals may be separately sensed by the electrodes  13  and  15  and stimulating pacing signals may be separately delivered to the electrodes  13  and  15 , via lead branches  12  and  14 . 
     In operation, the electrodes  13  and  15  are disposed in or about the right and left ventricles, respectively. A preferred surgical procedure for-implanting the lead  12  is to extend it through the superior vena cava  28  so that the sensing stimulating tip  13  thereof lodges in the internal chamber of the right ventricle of the heart  10 . A preferred surgical-procedure for implanting lead branch  14  is to extend it through the coronary sinus (not shown) of the heart  10  so that the sensing/stimulating tip  15  thereof lodges directly in or about the coronary sinus and left ventricle. Although it is described that electrodes  13  and  15  perform both sensing and pacing, it is possible for testing and examination, that separate unipolar or bipolar sensing and stimulating electrodes may be used. 
     When attached to the heart, the electrodes  13  and  15  sense cardiac signals in the form of well-known Q-R-S complex at separate sites within the left and right ventricles. The ECG amplifiers  16  and  17  feed the amplified versions of these signals to the control circuit  20 . 
     The control circuit  20  analyzes the cardiac signals to determine whether an abnormal conduction exists. Specifically, if a cardiac signal is received from the left ventricle but not from the right ventricle, the control circuit  20  provides a control signal to the stimulator  22  to issue a stimulating pacing pulse over conductors  24  and  18  and lead branch  12  to the right ventricle, via the sensing/stimulating tip electrodes  13 . Similarly, the control circuit  20  provides a control signal to the stimulator  22  to issue a stimulating pacing pulse over lead branch  14  to the left ventricle, via sensing/stimulating tip electrode  15 , if a cardiac depolarization signal is received from the right ventricle, but not from the left ventricle. It is also possible to sense a depolarization signal from only one ventricular chamber and then unconditionally stimulate both ventricular chambers. This is wasteful of power which is a concern only if the stimulator is totally implanted and must rely on an implanted battery power source. 
     The timing of the stimulating pacing pulse from the stimulator  22  is such that both ventricles will contract substantially simultaneously. Where both ventricles are unconditionally stimulated upon the occurrence of a QRS complex on only one side, the fact that ventricular site which had produced a Q-R-S complex is immediately stimulated along with the other ventricle does not cause a problem since the site producing that complex is still refractory at the time it is stimulated. 
     It is also possible that no cardiac signals are sensed from either ventricle, possibly resulting from complete conduction failure between the sinoatrial node and the atrialventricular node. In this case, the control circuit  20  will again activate the stimulator  22  to provide stimulating signals to both ventricles simultaneously. 
     In an alternative embodiment of the invention, the issuance of pacing pulses to the ventricles is time-coupled to the rhythmic cycle of the atrial beat of the heart to preserve a preset atrial-ventricular delay period of about 120 to 200 milliseconds. Additional atrial sensing is accomplished, via lead  23  and a sense electrode  25  similar to the ventricular leads  12  and  14 , but disposed in or about the right atrial chamber and connected to the control circuit  20 , via atrial sense amplifier  27 . The control circuit  20  may be configured to respond to the sensed atrial and ventricular signals to activate the stimulator for providing appropriate simultaneous stimulating signals to the ventricles as described above in accordance with the predetermined A-V delay period. 
     In the case where the conduction of the natural stimulating signal originating at the sinoatrial node of the heart  10  is only partially blocked or slowed, the ventricles may partially or incompletely contract, in which case hemodynamic efficiency is reduced. Under these circumstances, provision is made in the control circuit  20  for determining whether a Q-R-S cardiac signal, although present, is weak or slow, and if so, to activate the stimulator  22  to stimulate the ventricles of the heart by passing pacing pulses simultaneously thereto. 
       FIG. 2  shows one embodiment of the control circuitry  20  of  FIG. 1  required to perform bi-ventricular pacing. Also shown in the circuit of  FIG. 2  are means for interconnecting the bi-ventricular control circuitry with conventional demand pacing circuitry to implement various additional pacing modes. It is understood that in the preferred embodiment, the circuitry shown in  FIG. 1  would be preferably incorporated directly into the design of a pacer rather than its adjunctive form shown here for purposes of illustration. 
     To accomplish bi-ventricular pacing, activity is sensed in both the left and the right ventricle. When a ventricular contraction is sensed in either ventricle, a timer is initiated. If within a time window established by said timer, the contraction is sensed in the other ventricle, all pacing is inhibited because the natural contractions are deemed to be simultaneous. On the other hand, if ventricular contractions are not sensed in both ventricles within a period of coincidence defined by the time delay, at the end of this delay, the pacing pulse will be emitted, but only to the ventricle for which a QRS complex has not been sensed. Generally, ventricular contractions which occur within 5-10 milliseconds of each other result in sufficient hemodynamic efficiency so as to not require treatment. Hence, the delay window may be of this order of magnitude. As used herein, the term “substantially simultaneous contraction” includes the occurrence of natural contractions of both ventricles within the window period or an evoked contraction of one or both ventricles immediately following the expiration of the window period. 
     Operation of the circuit of  FIG. 2  will now be described. Electrical activity originating in the left ventricle is sensed by electrode  15  on lead  14  coupled to amplifier  16 . It is assumed that amplifier  16  contains all of the thresholding and inhibiting provisions commonly utilized in existing pacing systems to inhibit all electrical activity, save valid ventricular contractions. Similarly, electrical activity in the right ventricle is sensed by electrode  13  on lead  12  and processed by ECG amplifier  17 . 
     Let if first be assumed that a left ventricle contraction procedes that of the right. In this case, an R-wave signal propagates through amplifier  16  to set the Set-Reset type flip-flop  30 . a logical “1” signal passes through OR gate  32  to clock D-type of flop  34  to the “set” state which, in turn, initiates the aforementioned delay timing. Window register  36  is loaded with a digital count value which is representative of the desired delay window, e.g., 5-10 ms. This may be either a fixed, hard-wired register or, alternatively, a programmable register which may be set by telemetry means in a known manner. When the preset enable input (PE) in high, counter  38  is held at a digital count corresponding to the value held in window register  36 . When flip-flop  34  is set, the PE on counter  38  is removed, allowing the counter to be decremented with each clock pulse provided on clock line  40 . At the end of the preprogrammed window delay interval, counter  38  is decremented to zero, causing the zero detect (ZD) line  42  to go high. The leading edge of the zero detect pulse is used to trigger a ventricle pacing pulse from pulse generator  44 , via gates  54  and  56 , as required. The pulse generator circuitry  44  converts this leading edge trigger to a pulse of the proper amplitube and duration for effective stimulation of the right ventricle. Note that, since under the assumed conditions flip-flop  30  has been set, AND gate  48  is disabled and, therefore, pulse generator  50  is inhibited from generating a left ventricle pacing pulse. 
     Next to be considered is the case where a right ventricle contraction has not been sensed within the prescribed window interval. In this case, flip-flop  52  remains reset and AND gate  54  is enabled which allows the zero detect pulse ZD to propagate through OR gate  56  to trigger pulse generator  44 , thus stimulating the right ventricle. If, however, a right ventricle contraction has been detected, flip-flop  52  would have been set prior to the generation of the ZD pulse and, in this case, both AND gates  48  and  54  are disabled and no pacing pulse in either ventricle is generated. 
     It can be seen from the symmetry of the circuit that the operation is identical if the right ventricle contraction precedes the left ventricle contraction by more than the preprogrammed delay interval. In either case, the setting of either flip-flop  30  or  52  causes  52  causes the initiation of the timing window delay interval. When one of these flip-flop sets, the other must set within the window period, otherwise a pacing pulse will be generated in the unsensed ventricle. 
     The bi-ventriclar pacing control circuitry may be combined with other well-known pacer control circuitry such that the bi-ventriclar mode can be realized in combination with any other pacing mode, such as VVI, DDD, VOO. Line  58  is the logical OR of either of left ventricle event or a right ventricle event. It may be connected to other pacing control circuitry  62  in place of the signal which is normally responsive to only activity in the left ventricle. A sensed ventricle event thus inhibits the generation of a pacing trigger from another pacing circuitry and leaves the control of pacing in the alternate ventricle, as required, to the circuitry of FIG.  1 . If line  58  is not activated within the escape interval of the other pacing control circuitry, a paced ventricle trigger signal on line  60  is produced which propagates through both OR gate  62  and OR gate  56  to trigger pacing pulses in both ventricles. 
     It is also contemplated that when a ventricular depolarization signal is sensed in one or the other of the ventricles, that a stimulating pulse may also be immediately delivered, on an unconditional basis, to both ventricles, via the implanted leads  13  and  15 , thus resulting in a coordinated contraction of both ventricles. 
     The foregoing illustrate preferred arrangements for carrying out the objectives of this invention. Modifications and variations can obviously be made by those skilled in the art without departing from the true spirit and scope of the invention. For instance, the circuit may be employed to simultaneously pace the auricles, instead of ventricles, if such is required to improve pumping efficiency. The arrangement may also be employed as an improvement of conventional pacers thereby to improve their performance. As stated herein, the inventive arrangement can be used in an implanted device or in an external treating, diagnostic or testing device. Accordingly, the invention is limited only by the scope of the appended claims rather than by what is shown and described. Therefore, it is the intent to cover all such modifications and alternate embodiments as may come within the true scope of this invention.