Electrical cardiac output forcer

Abstract

An electrical method and apparatus for stimulating cardiac cells causing contraction to force hemodynamic output during fibrillation, hemodynamically compromising tachycardia, or asystole. Forcing fields are applied to the heart to give cardiac output on an emergency basis until the arrhythmia ceases or other intervention takes place. The device is used as a stand alone external or internal device, or as a backup to an ICD, atrial defibrillator, or an anti-tachycardia pacemaker. The method and apparatus maintain some cardiac output and not necessarily defibrillation.

Description

RELATED APPLICATIONS

This is a continuation application of U.S. patent application Ser. No. 09/693,551, filed Oct. 20, 2000, entitled, “ELECTRICAL CARDIAC OUTPUT FORCER;” which is a continuation of U.S. patent application Ser. No. 09/139,822, filed Aug. 25, 1998, entitled, “METHOD AND APPARATUS FOR ELECTRICALLY FORCING CARDIAC OUTPUT IN AN ARRHYTHMIA PATIENT,” now U.S. Pat. No. 6,167,306, issued Dec. 26, 2000; which is a continuation of U.S. patent application Ser. No. 08/754,712, filed Dec. 6, 1996, entitled, “METHOD AND APPARATUS FOR TEMPORARILY ELECTRICALLY FORCING CARDIAC OUTPUT IN A TACHYARRHYTHMIA PATIENT,” now U.S. Pat. No. 5,978,703, issued Nov. 2, 1999; which is a continuation of U.S. patent application Ser. No. 08/543,001, filed Oct. 13, 1995, entitled, “METHOD AND APPARATUS FOR TEMPORARILY ELECTRICALLY FORCING CARDIAC OUTPUTIN A TACHYARRHYTHMIA PATIENT,” now abandoned; which is a continuation of U.S. patent application Ser. No. 08/251,349, filed May 31, 1994, entitled, “METHOD AND APPARATUS FOR TEMPORARILY ELECTRICALLY FORCING CARDIAC OUTPUTING A TACHYARRHYTHMIA PATIENT,” now abandoned; the entire disclosures of each of the above-referenced applications which are incorporated herein by reference.

FIELD OF THE INVENTION

The invention relates to the field of therapies for cardiac arrhythmias, and more particularly, to a method and an apparatus for forcing cardiac output by delivering a pulsatile electrical field to the heart during fibrillation of a hemodynamically compromising tachycardia.

BACKGROUND OF THE INVENTION

Approximately 400,000 Americans succumb to ventricular fibrillation each year. It is known that ventricular fibrillation, a usually fatal heart arrhythmia, can only be terminated by the application of an electrical shock delivered to the heart. This is through electrodes applied to the chest connected to an external defibrillator or electrodes implanted within the body connected to an implantable cardioverter defibrillator (ICD). Paramedics cannot usually respond rapidly enough with their external defibrillators to restore life. New methods of dealing with this problem include less expensive external defibrillators (and thus more readily available) and smaller implantable defibrillators. Since the first use on humans of a completely implantable cardiac defibrillator in 1980, research has focused on making them continually smaller and more efficient by reducing the defibrillation threshold energy level. The goal has been to reduce the size of the implantable device so that it could be implanted prophylactically, i.e., in high risk patients before an episode of ventricular fibrillation.

An ICD includes an electrical pulse generator and an arrhythmia detection circuit coupled to the heart by a series of two or more electrodes implanted in the body. A battery power supply, and one or more charge storage capacitors are used for delivering defibrillation shocks in the form of electrical current pulses to the heart. These devices try to restore normal rhythm from the fibrillation. While it works well at restoring normal function, the ICD is large in size and not practical for a truly prophylactic device. A small device capable of maintaining minimal cardiac output, in high risk patients, prior to admission into an emergency room is needed.

In addition, external defibrillators are limited in their performance. The typical paramedic defibrillation may be delayed by 10 minutes. At this time defibrillation may be irrelevant since the rhythm is often advanced to asystole. In asystole, there is little or no electrical activity and certainly no cardiac pumping.

There is a need for a new method and apparatus for dealing with ventricular fibrillation. The defibrillation approach does not work satisfactorily. External devices are too slow in arrival and implantable defibrillators are excessively large (and expensive) for prophylactic use.

SUMMARY OF THE INVENTION

The invention provides an electrical method of stimulating cardiac cells causing contraction to force hemodynamic output during fibrillation, hemodynamically compromising tachycardia, or asystole. Forcing fields are applied to the heart to give cardiac output on an emergency basis until the arrhythmia ceases or other intervention takes place. The device is usable as a stand-alone external or internal device or as a backup to an ICD, atrial defibrillator, or an anti-tachycardia pacemaker.

The goal of the invention is maintaining some cardiac output and not necessarily defibrillation. The method is referred to as Electrical Cardiac Output Forcing and the apparatus is the Electrical Cardiac Output Forcer (ECOF).

In the implantable embodiment, a forcing field is generated by applying approximately 50 volts to the heart at a rate of approximately 100-180 beats per minute. These fields are applied after detection of an arrhythmia and maintained for up to several hours. This will generate a cardiac output which is a fraction of the normal maximum capacity. The heart has a 4 or 5 times reserve capacity so a fraction of normal pumping activity will maintain life and consciousness.

The implantable embodiment is implanted in high risk patients who have never had fibrillation. If they do fibrillate, the ECOF device forces a cardiac output for a period of up to several hours, thus giving the patient enough time to get to a hospital. That patient would then be a candidate for an implantable cardioverter defibrillator (ICD). The ECOF differs from the ICD in that it is primarily intended for a single usage in forcing cardiac output over a period of hours, while the ICD is designed to furnish hundreds of defibrillation shocks over a period of years.

Insofar as is known, no prior attempts have been made at forcing pulses during any type of fibrillation. Some workers in the field have experimented for research purposes with local pacing during fibrillation. For example, Kirchhof did local pacing during atrial fibrillation in dog hearts (Circulation 1993; 88: 736-749). He used 0.5 mm diameter electrodes and pacing stimuli. As expected, small areas around the heart were captured but no pumping action was expected or detected. Similar results have been obtained in the ventricle by KenKnight (Journal of the American College of Cardiology 1994; 283A).

Various researchers have tried multiple pulse defibrillation without success in reducing the energy thresholds, for example, Schuder (Cardiovascular Research; 1970, 4, 497-501), Kugelberg (Medical & Biological Engineering; 1968, 6, 167-169 and Acta Chirurgica Scandinavia; 1967, 372), Resnekov (Cardiovascular Research; 1968, 2, 261-264), and Geddes (Journal of Applied Physiology; 1973, 34, 8-11).

More recently, Sweeney (U.S. Pat. No. 4,996,984) has experimented with multiple (primarily dual) shocks of timing calculated from the fibrillation rate. None of these approaches has been able to significantly reduce voltages from conventional defibrillation shocks. Importantly, none of these approaches anticipated the idea that the individual pulses might force cardiac output or could sustain life indefinitely. Some have considered the use of smaller pulses, before the shock, to reduce the energy required for a defibrillation shock (Kroll, European Application No. 540266), but never anticipated eliminating the defibrillation shock itself or anticipated that the pulses themselves could maintain cardiac output. Some have suggested using higher voltage pulses to terminate ventricular tachycardia, but no suggestion was made of an application with fibrillation or of obtaining cardiac output (Kroll WO 93/19809) and Duffin (WO 93/06886).

The benefits of this invention will become clear from the following description by reference to the drawings.

BRIEF DESCRIPTION OF THE DRAWINGS

FIG. 1 is a block diagram illustrating a system constructed in accordance with the principles of the present invention.

FIG. 2a shows the connection of an implantable embodiment of the device to the heart in an epicardial patch configuration.

FIG. 2b shows the connection of an implantable embodiment of the device to the heart using an endocardial lead system and the device housing as an electrode.

FIG. 3 shows the connection of an external embodiment of the invention.

FIG. 4 is a diagram showing a representative pulsatile electrical signal.

FIG. 5 is a flowchart illustrating one embodiment of the method of the invention.

FIG. 6 is a diagram showing the expected effect of a 50 V pulse on the heart during diastole.

FIG. 7 is a diagram showing the expected effect of a 50 V pulse on the heart during systole.

FIG. 8 is a diagram showing the expected effect of a 50 V pulse on the heart during fibrillation.

FIGS. 9a and 9b show various waveforms useful for the electrical cardiac output forcing method and apparatus.

FIG. 10 shows the device used as a backup to an atrial defibrillator.

DETAILED DESCRIPTION OF THE PREFERRED EMBODIMENTS

The present invention will now be described more fully hereinafter with reference to the accompanying drawings, in which preferred embodiments of the invention are shown. This invention may, however, be embodied in many different forms and should not be construed as limited to the embodiments set forth herein. Rather, Applicants provide these embodiments so that this disclosure will be thorough and complete, and will convey the scope of the invention to those skilled in the art.

FIG. 1 is a block diagram illustrating a system 10 constructed in accordance with the principles of the present invention. The device circuitry is connected to the heart 40 via a series of leads; output lead 32, pressure sense lead 34, and ECG sense lead 36. The electronic circuit includes a conventional ECG amplifier 30 for amplifying cardiac signals. The amplified cardiac signals are analyzed by a conventional arrhythmia detector 20 which determines if an arrhythmia is present. The arrhythmia detector 20 may be one of several types well known to those skilled in the art and is preferably able to distinguish between different types of arrhythmias. For example; fibrillation, tachycardia or asystole. The circuit also contains an optional pressure sensing section 28 which amplifies and conditions a signal from an optional pressure sensor from within the heart or artery. The output of the pressure sense circuit 28 is fed to a cardiac output detection circuit 18 which analyzes the data and determines an estimate of the cardiac output. Data from the arrhythmia detector circuit 20 and the cardiac output detection circuit 18 is fed to the microprocessor 16. The microprocessor 16 determines if Electrical Cardiac Output Forcing (ECOF) is appropriate. If forcing is indicated, the microprocessor 16 prompts the output control 22 to charge a capacitor within the output circuit 26 via the capacitor charger 24. The output control 22 directs the output circuitry 26 to deliver the pulses to the heart 40 via the output leads 32. The microprocessor 16 may communicate with external sources via a telemetry circuit 14 within the device 10. The power for the device 10 is supplied by an internal battery 12.

FIG. 2a is a diagram showing the connection of an implantable embodiment of the device 130 to the heart 40 in an epicardial patch configuration. In this thoracotomy configuration, current passes through an output lead pair 32 to electrode patches 42 which direct the current through the heart 40. There is an optional pressure sense lead 34 which passes the signal from an optional pressure transducer 46 which lies in the heart 40. The ECG is monitored by sense electrodes 44 and passed to the device 130 by a lead 36. The area of the electrodes 42 is at least 0.5 cm². The size of the electrode is greater than that of a pacing lead and no more than that of a defibrillation electrode or between approximately 0.5 cm² and 20 cm² each.

FIG. 2b shows a non-thoracotomy system embodiment of the invention. In this system, the current passes from a coil electrode 52 in the heart 40 to the housing of the device 140. An endocardial lead 50 combines the ECG sensing lead and the pulse output lead. The ECG is monitored by sense electrodes 44 in the heart 40 and passes through the endocardial lead 50. There is an optional pressure transducer 46 in the heart 40 which passes a signal to the device 140 via optional lead 34.

FIG. 3 shows an external embodiment of the invention. External patch electrodes 54 are placed on the chest to deliver current to the heart 40 through output lead 32. The ECG is monitored by surface electrodes 56 and passed to the device 150 by a lead 36. Alternately, the ECG could be monitored by the external patch electrodes 54. An optional pressure sensor 46 passes a pressure signal via an optional pressure sense lead 34. This embodiment could be used as a substitute (due to its small size) for an external defibrillator and keep a patient alive until arrival at a hospital. Also, the system could precede the external defibrillator by generating output in patients in asystole until blood flow and rhythm are restored.

A series of forcing pulses 60 are shown in FIG. 4. The pulses are approximately 50 V in amplitude with a spacing of approximately 500 ms. The 50 V and the 500 ms pulse spacing are chosen as illustrative for an implantable embodiment. The forcing pulse interval is chosen to maximize cardiac output within the limits of device circuitry and the response of the heart muscle. An interval of 500 ms corresponds to a heart rate of 120 beats per minute. This will produce a greater output than a typical resting rate of 60 beats per minute. However, a rate of 240 beats per minute would produce a lower output due to mechanical limitations of the heart. Thus, a practical range of 60 to 200 beats per minute is appropriate. The pulses could also be timed to coincide with the natural pumping of the atria, thus improving overall cardiac output.

The higher the voltage, the higher the forcing fields, and therefore a greater number of heart cells contracting producing greater cardiac output. However, the higher voltage produces greater patient discomfort and extraneous muscle twitching.

Implantable batteries are also limited to a certain power output and energy storage. If an output pulse is 50V and the electrode impedance is 50Ω, the power during the pulse is P=V²/R=50V*50V/50Ω=50 W. If the pulse has a duration of 2 ms then the energy perpulse is 0.1 J. If two pulses are delivered every second, the charger must be capable of delivering 0.2 J per second which is 200 mW. This is well within the limits of an implantable battery. An implantable battery can typically deliver 5 W of power. However, 200 V pulses at 3 per second would require 4.8 W which is near the limit of the battery and charging circuitry. A typical implantable battery energy capacity is 10,000 J. Delivering forcing pulses at a rate of 4.8 W would deplete the battery in only 35 minutes (10,000 J/4.8 W=2083 seconds). Thirty-five minutes may not be enough time to transport the patient to a hospital. Therefore 200 V represents the highest practical voltage for continuous operation in an implantable embodiment, although voltages of up to 350 V could be used for short periods and adjusted down when hemodynamic output is verified. A practical lower limit is about 10 V. During normal sinus rhythm, 10 V delivered through the patches would pace. However, during fibrillation the 10 V could not pace and only cells very near the electrodes would be captured. This would be insufficient for forcing cardiac output.

These calculations also suggest other differences between an implantable ECOF and an ICD. With a battery storing 10,000 J and an ECOF pulse having 0.1 J, this ECOF would be capable of delivering 100,000 pulses. An ICD can only deliver 200-400 shocks of about 30 J. The ECOF is also very different from an implantable pacemaker which typically delivers 150,000,000 pacing pulses (5 years at 60 BPM) each of about 0.00005 J.

For an external ECOF the calculations are similar, but scaled up. The typical ECOF pulse would have a voltage of 100 V with a range of 25-500 V. With electrode impedances of 50Ω the power during the pulse is P=V²/R=100V*100V/50Ω=200 W with a range of 12.5-5,000 W. If the pulse has a duration of 2-5 ms, then the energy per pulse is 0.02-25 J. This is much less than the American Heart Association recommended output of 360 J for an external defibrillator.

This is also different from an external transthoracic pacemaker. These devices are rated by current and typically have an output range of 30-140 mA. Most patients are paced by pulses of 40-70 mA of current. An example of a modem external thoracic pacemaker is given by Freeman in PCT Application No. WO 93/01861. Assuming an electrical impedance of 50Ω and the ECOF voltage range of 25-500 V, then the ECOF current range would be 500 mA 59 10 A. Since electrode impedance increases with lower voltage, the 25 V ECOF pulse would probably see an impedance of 100Ω thereby giving a lower current of 250 mA.

FIG. 5 is a flowchart illustrating the method of the invention, which is provided for purposes of illustration only. One skilled in the art will recognize from the discussion that alternative embodiments may be employed without departing from the principles of the invention. The flow diagram shown in FIG. 5 represents a method of automatically treating a heart which is in fibrillation, tachycardia, or asystole and thereby pumping inefficiently or not at all. Electrodes are attached 69 and diagnoses the presence of an arrhythmia 70. A series of cardiac output forcing electric pulses 72 is automatically delivered. It should be understood that the therapy 72 may be delivered for any output compromising cardiac arrhythmia. After delivery of 10 forcing pulses (at a rate of 60-200 BPM) in the first block 72, the status of the heart is determined 74. If an arrhythmia is still present and there exists low pressure within the heart, more forcing pulses are delivered 78. If the heart is pumping at a safe level, the therapy ceases and exits 76. Note that this means that the ECOF successfully defibrillated the patient's heart even though this is not a primary goal of the system. This could be tested in patients who were scheduled to receive an ICD, in a hospital setting. Those patients who are defibrillated by ECOF pulse therapy could then receive the ECOF instead of the larger ICD. After the therapy 78 has been delivered, the pressure and ECG is again monitored 74. If the therapy 78 is successful, it ceases and exits 76. If the therapy 78 is unsuccessful in producing a safe level of pumping efficiency, the method proceeds to a continuous cardiac assist mode 80. The therapy may only be stopped by an external command, for example, a telemetry signal or a magnet which is applied to the chest activating a magnetic reed switch 82 which terminates the therapy and exits 76. To minimize patient discomfort and maximize battery life, the forcing voltage could be adjusted down when sufficient pressure signals or adequate flow measured by other means were detected, for example, the pressure sense transducer could be replaced by an oxygen detector or a doppler flow measuring device. The pulse rate could also be adjusted to maximize output.

FIG. 6 is a diagram showing the effect of a 50 V forcing pulse on the heart 40 during electrical diastole (cells at rest). The current is passed through the heart 40 by the electrodes 42. Approximately 60% of cardiac cells 90 would be captured by a 50 V pulse if the cells were in diastole. The captured cells 90 mostly lie in the direct path between the electrodes 42 and near the electrodes 42 where the field strengths are highest. Of course over a time period of about 100 ms these directly captured cells then propagate an activation wavefront to stimulate the rest of the heart. This so called far-field pacing is irrelevant here as the hearts, of interest, are in fibrillation and not in diastole.

FIG. 7 is a diagram showing the effect of a 50 V forcing pulse on the heart during electrical systole (cells already stimulated). The current is passed through the heart 40 by the electrodes 42. Approximately 20% of cardiac cells 100 would be captured by a 50 V pulse if the cells were in systole. The captured cells 100 are nearest each electrode 42 where the field strengths are highest. Capture in systolic cells means that their activation potential is extended. This capture requires significantly higher fields (10V/cm) than those required for diastolic cell capture (1 V/cm).

FIG. 8 is a diagram showing the effect of a 50 V forcing pulse on the heart during fibrillation. During fibrillation there are always cells in systole and diastole simultaneously. But, the vast majority are in systole. This diagram assumes 50% of the cells are in diastole which applies only after several capturing pulses. The current is passed through the heart 40 by the electrodes 42. One hundred percent (100%) of the cells 110 nearest the electrodes 42 would be captured due to the high field strength. As shown in FIG. 7, even systolic cells are captured by high field strengths. Fifty percent (50%) of the cells 112 in the direct path between the electrodes 42 would be captured if it is assumed that 50% of all cells are in diastole. If roughly 60% of cardiac cells are captured by a 50 V pulse when the cells are in diastole, and 20% are captured when in systole, and if 50% are in systole and 50% in diastole, 40% would be captured during fibrillation. This calculation is shown in the following table. The last two columns give the mechanical action resulting and the contribution to forcing a cardiac output.

Considering the cardiac cells that are originally in diastole, (rows A & B) in the table below, the A row represents the diastolic cells that are not captured by the forcing pulse. If 50% of the heart's cells are in diastole and 40% of those are not captured that is 20% of the total cells. These cells will, however, shortly contract on their own (from previous wavefronts or new ones) providing a positive gain in mechanical action and therefore cardiac output. The B row corresponds to the diastolic cells that are captured. If 60% of the diastolic cells (50% of total) contract due to the forcing field this is 30% of the total heart cells. These cells provide the biggest gain in mechanical action and cardiac output. Next considering the activity of the systolic cells (rows C & D), if 50% of the heart's cells are in systole and 80% of those are not captured (row C), that is 40% of the heart's cells. These cells soon relax and negate a portion of the cardiac output. The systolic cells that are captured (row D) are 10% of the heart's cells (20% of 50%). These cells will hold their contraction and be neutral to cardiac output. The net result is a gain in contraction which forces cardiac output.

	Percentage	Status of	Percentage			Forcing
Original	of the	the	of the	Percentage		Cardiac
status of	cardiac	cardiac	original	of the total	Mechanical	Output
the cells	cells	cells	status	cells	Action	Effect
(A)	50%	Diastolic	40%	20%	Will start to	Positive (+)
Diastolic		non-captured	to 50%		contract on
(B)		Diastolic	60%	30%	own	positive
Diastolic		captured	of 50%		contract	(++)
(C)	50%	Systolic	80%	40%	Will start to	Negative
Systolic		non-captured	of 50%		relax on own	(−)
(D)		Systolic	20% of 50%	30%	hold	neutral
Systolic		captured				(0)
Total	100%		100%	100%	More	Positive
					contraction	(++)

The net result over a 200 ms mechanical response is given in the next table. The major contribution is in row (B) from the captured diastolic cells contracting.

	Status of the Cardiac	Change in	Description of
Row	Cells	Output	Activity
A	Diastolic	+5%	Positive. Some cells
	non-captured		will begin to contract
			on their own.
B	Diastolic captured	+30%	Positive. Cells
			contract due to
			forcing field.
C	Systolic	−5%	Negative. Some
	non-captured		cells will begin to
			relax on their own.
D	Systolic captured	0%	Neutral. Cells hold
			contraction due to
			forcing field.
Net Gain		+30%	A net gain in cardiac
			output due to forcing
			fields.

The 30% net pumping action should be sufficient to maintain survival and consciousness, because the heart has a 4-5 times reserve capacity.

FIG. 9 depicts examples of waveforms designed to minimize the twitching of the chest muscles which can be very uncomfortable to the patient. In FIG. 9a is seen a low harmonic pulse waveform 120 which has a very gradual “foot” 122 and a gradual peak 124. Such a pulse has less high frequency energy components and thus is less likely to stimulate the skeletal muscle.

FIG. 9b shows a technique of going to the opposite extreme. Here, each compound forcing pulse 126 is actually composed of 50 very short spikes 128 each of which is 20 μs in width with a 20 μs spacing. The heart will tend to average out these thin pulses and “see” a 2 ms wide forcing pulse. The skeletal muscle, however, is not efficiently stimulated by these extremely narrow pulses. The skeletal muscle will not average out this signal either. This approach could help minimize skeletal muscle twitching and discomfort.

An alternative system would be to charge the capacitor to 300 V for the first pulse to capture many cells therefore putting those cells into diastole after a delay of 100-200 ms. At this point the voltage could be lowered to 100 V and delivered every 100 ms. A 3 watt DC-DC converter with a 67% efficiency could provide 100 ms interval forcing pulses assuming a 50Ω resistance and 1 ms pulse (0.2 J). This rate is too fast for forcing cardiac output due to mechanical limitations, but is very effective for electrical capture. After sufficient capture, the rate of forcing pulses could be slowed down to 100-170 beats per minute for optimum cardiac output.

The Electrical Cardiac Output Forcing device (ECOF) could also be used to help patients with atrial fibrillation. As an alternative embodiment to the ventricular placement of FIG. 2b, the electrode coil 52 and sensing electrodes 44 could be placed in the atrium. The device could then function to force atrial output. Even though atrial fibrillation is not instantly fatal like ventricular fibrillation is, clots can build up in the atria which can eventually lead to strokes. Cardiac output forcing of the atria on a daily basis may limit this problem. It is also possible that after a number of forcing pulses the atria would return to a normal rhythm. There is however, no urgency as is the case with ventricular fibrillation.

A second use of this invention for atrial defibrillation is shown in FIG. 10. As before in FIG. 2b, the ECOF 160 is shown connected to the heart 40 via endocardial lead 50. Again, forcing coil electrode 52 and sensing electrodes 44 are in the right ventricle. In addition, a large atrial coil electrode 130 and atrial sensing electrodes 132 are in the right atrium. These would be used for conventional atrial defibrillation. One of the big concerns with atrial defibrillation is that in a few cases, an atrial defibrillation shock causes ventricular fibrillation. If this happens, the patient dies within minutes. With the ECOF approach, for the left ventricle, one could maintain output in the patient for several hours and thus have enough time for transport to a hospital or external defibrillation. Thus, the ECOF approach in the ventricle could provide a safety backup to atrial defibrillation.

Many cardiac patients have no known risk of ventricular fibrillation, but suffer regularly from ventricular tachycardia. Accordingly, these people can be treated with anti-tachycardia pacing (ATP). Unfortunately, occasionally ATP will cause a ventricular fibrillation. Then a large defibrillation shock must be applied. Thus, it is not considered safe to implant a pure ATP device and these patients instead receive a full size ICD. The ECOF approach also serves as a safety backup and thus allow the implantation of true ATP devices. The system is depicted in FIG. 2b, although the pressure sensor 46 would typically not be needed.

Low energy cardioverters can also be used to treat ventricular tachycardias. These devices are also not considered safe as stand-alone devices due to the fact that they may not terminate the rhythm or that they may cause fibrillation. The ECOF method also could be used as a safety backup thus allowing the implantation of cardioverters without defibrillation capabilities. Such a system is shown in FIG. 2b.

It should be understood that various alternatives to the embodiments of the invention described herein may be employed in practicing the invention. For example, while most of the discussion is in the context of an implantable device, the concepts of the invention are also applicable to external delivery systems. It is intended that the following claims define the scope of the invention and that structures and methods within the scope of these claims and their equivalents be covered thereby.

Claims

1. A method for forcing cardiac output during hemodynamically compromising malfunction in a patient, comprising:

(a) detecting the presence of a hemodynamically compromising malfunction in the patient;

(b) delivering a first electrical signal through at least a portion of the patient's body, the first electrical signal including at least one pulse having sufficiently high energy for achieving a defibrillating effect in the patient; and

(c) delivering a second electrical signal through at least a portion of the patient's body, the second electrical signal having energy insufficient to achieve a defibrillating effect in the patient but sufficient to achieve a hemodynamic effect in the patient.

2. The method of claim 1, wherein delivering the second electrical signal includes causing cardiac output in the patient by forcing contraction in at least some of the patient's muscles.

3. The method of claim 1, wherein delivering the second electrical signal includes controlling the second electrical signal to have a periodicity that corresponds to a desired heartbeat rhythm in the patient.

4. The method of claim 1, and further comprising:

controlling the second electrical signal to correspond in time with pumping of the patient's atria.

5. The method of claim 1, further comprising the steps of reassessing the presence of a hemodynamically compromising malfunction and, if a hemodynamically compromising malfunction is detected, delivering a third electrical signal through at least a portion of the patient's body, the third electrical signal including at least one pulse having energy sufficient to achieve a defibrillating effect in the patient.

6. The method of claim 1, further comprising the steps of reassessing the presence of a hemodynamically compromising malfunction and, if a hemodynamically compromising malfunction is detected, continuing delivery the second electrical signal.

7. The method of claim 1, wherein delivering the first electrical signal is performed before delivering the second electrical signal.

8. The method of claim 1, wherein delivering the second electrical signal is performed before delivering the first electrical signal.

9. The method of claim 1, and further comprising:

positioning, in the patient's heart region, a plurality of electrodes through which the first electrical signal and the second electrical signal are conducted.

10. The method of claim 1, and further comprising:

providing at least one sensor adapted to detect a presence of a hemodynamically compromising malfunction in the patient.

11. The method of claim 1, and further comprising:

monitoring the patient's cardiac output; and

controlling the second electrical signal to maintain a desired level of cardiac output.

12. The method of claim 11, wherein the controlling includes adjustment of at least one parameter selected from the list consisting of:

signal amplitude pulse duration; and

pulse rate.

13. The method of claim 1, and further comprising:

shaping a waveform of the second electrical signal to reduce its effect on one of non-cardiac muscles, skeletal muscles, and cardiac muscles and skeletal muscles.

14. The method of claim 1, wherein the second electrical signal is delivered during at least a majority of a 30-minute period.

15. The method of claim 1, wherein the second electrical signal includes a plurality of pulses delivered at a rate of between about 60 and 200 pulses per minute.

16. The method of claim 1, wherein the second electrical signal includes pulses that are each between 2 and 100 ms in width.

17. The method of claim 1, wherein the second electrical signal includes electrical current pulses having a peak amplitude greater than 140 mA.

18. The method of claim 1, wherein the second electrical signal includes a train of at least 10 pulses.

19. The method of claim 1, wherein the second electrical signal includes a plurality of electrical bursts, wherein each burst includes a plurality of shorter pulses.

20. The method of claim 1, wherein the second electrical signal is delivered at a voltage of between 10 and 350 volts.

21. An at least partially implantable device for maintaining some cardiac output of a patient's heart during hemodynamically compromising malfunction using electrical forcing fields, comprising:

a power supply circuit;

a hemodynamically compromising malfunction detector circuit (HCMD) operatively coupled with the power supply circuit;

electrotherapy circuitry operatively coupled with the HCMD and the power supply circuit, and adapted to deliver first type and second type electrotherapy signals to at least a portion of the patient's upper body region, wherein the first type electrotherapy signal includes at least one pulse having sufficiently high energy for achieving a defibrillating effect in the patient and the second type electrotherapy signal has energy insufficient to achieve a defibrillating effect in the patient but sufficient to achieve a hemodynamic effect in the patient; and

a controller circuit operatively coupled with the power supply circuit and interfaced with the HCMD and the electrotherapy circuitry, the controller circuit configured to: recognize a hemodynamically compromising malfunction in the patient based on an indication from the HCMD; and cause the electrotherapy circuitry to deliver at least one of the first type and second type electrotherapy signals.

22. The method of claim 21, wherein the second type electrotherapy signal is adapted to cause cardiac output in the patient by forcing contraction in at least some of the patient's muscles.

23. The device of claim 21, wherein the controller circuit is further configured to control the second type electrotherapy signal to have a periodicity that corresponds to a desired heartbeat rhythm in the patient.

24. The device of claim 21, wherein the controller circuit is further configured to control the second type electrotherapy signal to correspond in time with pumping of the patient's atria.

25. The device of claim 21, wherein the controller circuit is further configured to reassess the presence of a hemodynamically compromising malfunction based on an indication by the HCMD and, if a hemodynamically compromising malfunction is detected, to cause delivery of one of the first type electrotherapy signal, the second type of electrotherapy signal and the first type of electrotherapy signal before causing delivery of the second type electrotherapy signal to at least a portion of the patient's upper body region.

26. The device of claim 21, wherein the controller circuit is configured to cause delivery of the second type electrotherapy signal before causing delivery of the first type electrotherapy signal.

27. The device of claim 21, wherein the HCMD includes at least one circuit selected from the group consisting of the following sensor circuits:

an electrophysiological signal sensing circuit;

a pressure sensing circuit;

an oxygen sensing circuit; and

a flow measuring circuit.

28. The device of claim 21, wherein the HCMD is adapted to detect an arrhythmia.

29. The device of claim 21, further comprising a therapeutic effectiveness measuring circuit.

30. The device of claim 29, wherein the therapeutic effectiveness measuring circuit includes a blood pressure sensor adapted to monitor cardiac output.

31. The device of claim 29, wherein the controller circuit is configured to adjust at least one electrotherapy parameter to maintain a desired therapeutic effect on the patient.

32. The device of claim 31, wherein the at least one electrotherapy parameter is selected from the list consisting of:

signal amplitude

pulse duration; and

pulse rate.

33. The device of claim 21, wherein the controller circuit is configured to stop administration of electrotherapy signals in response to an indication by the HCMD indicating an absence of a hemodynamically compromising malfunction.

34. The device of claim 21, wherein the controller is configured to assess the hemodynamically compromising malfunction based on indication from the HCMD and, based on the assessment, to select from among the first type and the second type electrotherapy signals to administer.

35. The device of claim 21, wherein the power supply circuit and the electrotherapy circuitry are adapted such that electrotherapy signaling can be maintained for at least 30 minutes.

36. The device of claim 21, wherein the electrotherapy circuitry is adapted to deliver the second type electrotherapy signal at a periodicity of between about 60 and 200 pulses per minute.

37. The device of claim 21, wherein the electrotherapy circuitry is adapted to deliver second type electrotherapy signals that include pulses that are between 2 and 100 ms in width.

38. The device of claim 21, wherein the second type electrotherapy signal has a wave shape adapted to stimulate cardiac muscles to a greater degree than non-cardiac muscles.

39. The device of claim 21, wherein the second type electrotherapy signal has a wave shape that includes pulses, each pulse comprising a plurality of narrow pulses.

40. The device of claim 21, wherein the second type electrotherapy signal has a wave shape in which edges are rounded.

42. The device of claim 21, wherein the second type electrotherapy signal has a peak voltage between 10 and 100 volts.

43. The device of claim 21, wherein the electrotherapy circuit operates to produce a cardiac output of between about 10% and about 90% of the normal maximum cardiac output for the patient.