United States Patent 3698398

An externally activated implantable rate-scanning heart pacer. Apparatus is disclosed for supplying to the heart of a patient a burst of stimulating pulses in which each successive interval between pulses of the burst is different in duration from the next previous interval. All of these intervals can correspond to repetition rates that lie within the physiological heartbeat range of the patient. The pacer comprises terminals for connection to the heart, a controllable electrical stimuli generator controlled internally by a discharging capacitor and controlled externally by a magnet. The pacer is particularly applicable to the treatment of paroxysmal supra-ventricular tachycardias, a rapid heartbeat condition originating in the atrium. The pacer can be temporarily activated by the patient.

Application Number:
Publication Date:
Filing Date:
Primary Class:
International Classes:
A61N1/362; (IPC1-7): A61N1/36
Field of Search:
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US Patent References:
3391697Runaway inhibited pacemaker1968-07-09Greatbatch
3253596Cardiac pacer1966-05-31Keller, Jr.
3209081Subcutaneously implanted electronic device1965-09-28Ducete
3195540Power supply for body implanted instruments1965-07-20Waller

Foreign References:
Other References:

Bilgutay et al., "Journal of Thoracic & Cardiovascular Surgery," Vol. 56, No. 1, July 1968, pp 71-82 .
Davies "British Institute of Radio Engineers-Journal" Vol. 24, No. 6, December 1962, pp. 453-456.
Primary Examiner:
Kamm, William E.
What is claimed is

1. A heart pacer for stimulating the heart of a patient, said pacer comprising terminal means for connection to the heart of said patient, pulse generator means for generating electrical stimuli on said terminal means at a varying repetition rate within the normal physiological heartbeat rate-range of said patient, said pulse generator means including means for automatically maintaining each interval between stimuli different in duration from the next most previous interval and from the next successive interval.

2. A heart pacer as recited in claim 1 and wherein said pulse generator means includes rate increasing means for causing said rate to continuously increase.

3. A heart pacer as recited in claim 1 and wherein said pulse generator means includes rate decreasing means for causing said rate to continuously decrease.

4. A heart pacer as recited in claim 1 further comprising control means for controlling duration of operation of said pulse generator means.

5. A heart pacer as recited in claim 4 and wherein said control means comprises a reed switch and a magnet, the field of said magnet arranged to operate said switch.

6. A heart pacer as recited in claim 5 and wherein said pacer, except for said magnet, is implantable within said patient and said magnet is adapted to be positioned externally adjacent said patient.

7. A heart pacer as recited in claim 1 further including a self varying source of voltage and said pulse generator being energized by said self-varying source of voltage.

8. A heart pacer as recited in claim 4 and wherein said control means includes automatic means for automatically terminating the generation of said stimuli after a predetermined time.


The subject matter of the present invention is related to the following three copending applications: Ser. No. 810,519, filed Mar. 26, 1969 which has matured into U.S. Pat. No. 3,595,242, entitled "Atrial and Ventricular Demand Pacemaker;" Ser. No. 884,825, filed Dec. 15, 1969, entitled "Atrio-Ventricular Pacer with Atrial Stimuli Discrimination," and Ser. No. 71,799 filed Sept. 14, 1970 entitled "Stimulator for Treatment of Tachycardia." Information disclosed in these three patent applications is incorporated herein by reference.

These applications were filed by the applicant of the present invention. All of these applications, including the present application, are assigned to the same assignee. Benefits of 35 USC 120 are claimed for the present invention with respect to the earlier applications.


1. Field of the Invention

The present invention relates in general to electrical pacing of a heart. More particularly, the present invention relates to electrical stimulation of the atria or ventricles of the heart for treating paroxysmal supra-ventricular tachycardia.

2. Description of Prior Art

The PQRST wave form complex depicted by electro-cardiograms is well known in the electro-medical art. The QRS portion of the wave form complex is associated with the ventricular action of the heart. The P-wave is associated with the atrial action of the heart. Toward the end of each heartbeat, the ventricular muscles repolarize, and this portion of the electrical activity of the heart corresponds to the T-wave in the electro-cardiogram.

A typical frequency of occurrence of the wave form complex, or heartbeat rate, when the patient is at rest, is in the neighborhood of 70 times per minute. However, the frequency of occurrence of the wave form complex, due to improper heart functioning can exceed 160 occurrences per minute. This excessive rapidity of the heart's action is known as "Tachycardia." However, it should be understood that the physiological range with regard to normal heartbeat rate can vary considerably between individuals. For example, a child can have a normal physiological range comprised of heartbeat rates considerably higher than those of an adult.

"Atrial tachycardia" is the medical term assigned to the condition in which rapid and regular succession of P-waves of the wave form complex occur. The rate of occurrence is in excess of the physiological range of the particular patient.

"Paroxysmal supra-ventricular tachycardia" is the medical term assigned to the condition in which there is a sudden attack of rapid heart action in the atria or in the atrial-ventricular node. The main characteristics are the same as those in atrial tachycardia.

In normal heart operation the electrical activity begins with a nerve impulse generated by a bundle of fibers located in the sino-atrial node. The impulse spreads across the two atria while they contract and speed the flow of blood into the ventricle underneath them. The electrical impulse continues to spread across the atrial-ventricular node, which in turn stimulates the left and right ventricle.

During normal heart operation, tachycardia can arise when peculiar, unique conditions occur unpredictably. These conditions are associated with geometry of the atria, location of the nerve impulse, timing of the beat and impulse conduction velocity within the cardiac tissue. These conditions can set up a re-entry mechanism in the atria, for example, whereby the impulse continues to self-perpetuate. The self-perpetuation occurs at a rate above the physiological rate and is self-sustaining even after the "unique condition," (which permitted it to start), no longer exists. The self-perpetuation must then be interrupted by outside intervention interfering with the re-entry mechanism, thus permitting the heart to resume normal sequence.

Presently, treatments of the conditions of tachycardia include the mechanical message of the carotid sinus. This is an accepted therapy. however it has several drawbacks. For example, it requires a trained physician, who may not be readily available, to administer the massage.

Another treatment for tachycardia employs the use of drugs. However, this therapy has toxic effects on the body.

The self-perpetuation can be interrupted by electrical stimulation occurring at a critical time interval that is dependent on the patient's physiological condition at that time. The critical interval required is not predictable. Thus, one can apply a burst of stimuli, as was previously disclosed in my copending application Ser. No. 71,799, to the heart and for example to the right atrium to interrupt the self-perpetuating mechanism by interacting with the abnormal spread of an electrical impulse generated in the right atrium. Similarly, the stimuli could be applied to a ventricle. The stimuli were generated at a rate above the normal physiological heartbeat rate range. In particular embodiment, the stimuli were generated at a rate in the neighborhood of 1,000 per minute for a period of approximately 5 seconds duration. This amounts to individual bursts of approximately 83 pulses. Thus, some of the stimuli in the burst are properly spaced from each other to satisfy the critical interval.

However, the high repetition rate burst cannot be applied to all patients. In some patients with abnormal passways (such as a Kent bundle) the ventricle could respond to many of the fast stimuli, and produce a fast ventricular rate. In these patients, a high repetition rate burst of stimuli is dangerous and could result in fibrillation. Fibrillation can be fatal. The present invention is a therapeutic solution for these patients.

The present invention relates to a repetition rate scanning pacer that could be within the normal physiological rate range. the scanning pacer changes the interval between successive stimuli in a progressive manner. One of the increasing (or decreasing) intervals in the succession of intervals is expected to be the critical interval that will allow interruption of the paroxysmal tachycardia mechanism. Because the repetition-rate range can lie within the normal physiological rate range (i.e., 50 to 150 stimuli per minute) there is no danger to patients with abnormal passways. The pacer has no distinct rate.


The present invention relates to an externally activated implantable heart pacer for providing a series of stimulating pulses to the heart of a patient to treat a condition of tachycardia. The present invention incorporates an electrical stimuli generator and a control for controlling the generator. The stimuli are conducted to the heart via implantable terminals or electrodes. The control incorporates an external magnet and an implanted magnetic reed switch.

Advantages of the present invention include immediate and self-initiated treatment. The patient can sense when tachycarida occurs by his dizziness, perspiration and weakness. The patient can recognize these symptoms readily. Instead of going to a hospital for treatment, as is usually necessary at present, the patient can apply stimulation himself via an externally controlled implanted stimulator.

It is thus an object of the present invention to provide a new treatment for the physiological condition known as tachycardia, and more particularly for the physiological condition known as paroxysmal supra-ventricular tachycardia.

It is another object of the present invention to provide a new and improved heart pacer.

It is a further object of the present invention to provide a pacer for providing a burst of stimuli to the heart of a patient, where the repetition rate is self-controlled and can lie within the patient's physiological rate range.

Other objects and advantages of the present invention will become apparent to one having reasonable skill in the art after referring to the detailed description of the appended drawings herein:


FIG. 1 is a block diagram of an illustrative embodiment of the present invention indicating the implantable stimulator and external magnet; and

FIG. 2 is a schematic diagram of the circuit of an illustrative embodiment of the present invention.


In FIG. 1, a functional block diagram of an illustrative embodiment of the present invention is depicted. Oscillator control 11 controls oscillator 12 as shown. Oscillator 12 triggers stimuli pulse generator 13 once with each oscillation. Stimuli pulse generator 13 provides an electrical stimulus to heart 14 with each oscillation. Heart 14 is stimulated in response thereto. Control 11, oscillator 12, generator 13, and heart 14 are depicted as enclosed by phantom line 10. Phantom line 10 is intended to represent the surface of a patient in whom the stimulator is implanted. Magnet 15 is depicted as external to the patient. It is positioned in close proximity to the oscillator control 11, and dashed line 16 is intended to indicate the dependence of oscillator control 11 on magnet 15.

FIG. 2 is a circuit diagram of an illustrative embodiment of the present invention. Batteries 3 through 7 are connected in series aiding. (The dashed line between batteries 3 and 7 indicate that the exact number of batteries used may vary.) The positive terminal of battery 7 is connected to the junction of one end of resistor 23 and one end of resistor 24. The negative terminal of battery 3 is connected to a junction comprised of one side of capacitor 28, the emitter of transistor T9, electrode E2, one end of resistor 25, and one end of resistor 63. The other end of resistor 23 is connected to terminal 30 of reed switch 32. Reed element 31 makes contact with terminal 30 in the normally closed position, and connects terminal 30 with the other side of capacitor 28.

Terminal 29 is the normally open contact of reed switch 32, and is connected to the junction consisting of one end of resistor 35 and the anode of diode 27. The cathode of diode 27 is connected to the anode of diode 26 whose cathode is connected to a junction comprised of resistor 25, the base of transistor T7, and the collector of transistor T8. The other end of resistor 35 is connected to the emitter of transistor T7 and to one end of resistor 37. The collector of transistor T7 is directly connected to the base of transistor T8.

The other end of resistor 37 is connected to one side of capacitor 57 the other side being connected to a junction consisting of the emitter of transistor T8 and one end of resistor 61. The other end of resistor 61 is connected to a junction comprised of the other end of resistor 63 and the base of transistor T9. The collector of transistor T9 is connected to a junction comprised of the other end of resistor 24, and one side of capacitor 65. The other side of capacitor 65 is connected to electrode E1. Electrodes E1 and E2 are both connected to heart 14.

In operation, consider reed switch 32 to initially be in its normally closed position as depicted. In this position, capacitor 28 charges to a value of voltage equal to the sum of potentials of the batteries or to full battery voltage. The charging circuit includes resistor 23, the contact made between terminal 30 and reed element 31, and capacitor 28.

When reed element 31 is in the position depicted, there is no energization provided to the circuitry to the left of capacitor 28. Thus, transistor T9 is non-conducting because of zero base current and T9 behaves like an open switch. The open switch maintains capacitor 65 charged to full battery voltage. Resistor 24, capacitor 65, electrode E1, heart 14, electrode E2 and the conductive path returning to the negative terminal of battery 3 comprise a charge path for capacitor 65. Capacitor 65 charges through the heart. The relatively slow charging of capacitor 65, (due to resistor 24,) through the heart does not cause any stimulation to the heart. (It is the rapid discharge of capacitor 65, to be described later, which provides stimulation to the heart.)

Thus, two charge paths exist, and capacitors 28 and 65 are each charged to and for this condition remain at the total battery potential. But, when reed element 31 is caused to make contact with terminal 39, a different situation exists.

Consider magnet 15 to be brought in close proximity to magnet reed switch 32. This causes element 31 to move and to make contact with fixed terminal 29. Circuit operation may best be understood by assuming that magnet 15 is held in close proximity to switch 32 so that element 31 is in contact with terminal 29 for a sufficient period of time for capacitor 28 to substantially discharge to a predetermined voltage.

Upon contact between element 31 and terminal 29 charged capacitor 28 becomes the effective D.C. power supply for the circuitry to its lefthand side in the diagram. However, the charged capacitor is an unusual D.C. power supply in the sense that its "output" voltage is a decreasing function of time rather than a fixed function of time. Thus, at some predetermined time during discharge of capacitor 28 through the circuitry to its left, the capacitor voltage will fall below some predetermined voltage that is required to maintain operation of the circuitry to its left.

Considering circuitry to the left of capacitor 28, the series circuit of diode 27, 26 and resistor 25 establish a biasing network for transistor T7 and T8. Current flow from capacitor 28 through both diodes and resistor 25 establish a potential at the cathode of diode 26 that is approximately 1 volt less than voltage at the anode of diode 27. This voltage difference is due to the forward voltage drop of diodes 26 and 27 being approximately 0.5 volts each and being approximately constant for different forward current values. There is nothing unique about 1.0 volts. An approximately constant 1.2 volts would work equally well. The actual value of voltage drop is a function of the diodes employed, (As voltage on capacitor 28 decreases, current through resistor 25 decreases but the 1-volt drop across the diodes remains approximately constant.) This voltage at the cathode of diode 26 is a threshold voltage which must be exceeded by voltage at the emitter of transistor T7 by approximately 0.5 volts (since the base-emitter junction of transistor T7 requires a forward bias voltage similar to the 0.5 volt drop of the diodes) before transistor T7 and T8 conduct.

Capacitor 57 charges through resistors 35 and 37 until the voltage across it causes transistors T7 and T8 to conduct. Transistors T7 and T8, connected as shown, operate in a similar fashion to that of a silicon controlled rectifier. Both are normally non-conducting. When the emitter electrode of transistor T7 goes sufficiently positive to exceed threshold voltage at the base of transistor T7 by approximately 0.5 volts, the transistors conduct and current flows through the emitter circuit of transistor T8. Current coming from both capacitors 28 and 57 continues to flow through the emitter of transistor T8 until the potential difference between the emitter and base of transistor T7 drops below approximately 0.5 volts due to sufficient discharge of capacitor 57. Note that the current drain from capacitor 28 during this operation contributes to its discharge.

When transistors T7 and T8 stop conducting, capacitor 57 is made to charge from the value of voltage across it at the time of turn off of these transistors toward a "new" (and lower) value of voltage on capacitor 28. When the voltage across capacitor 57 is sufficiently positive, transistors T7 and T8 conduct once again and the cycle is repeated. This circuitry comprises an oscillator and can be thought of as a type of relaxation oscillator.

The frequency of this particular oscillator increases with each cycle of oscillation (or the time interval between each stimuli pulse decreases with each cycle). The oscillator has no distinct rate. The reason for this decrease of interval with each cycle is due to unequal rates of voltage decrease at the base and at the emitter of transistor T7. The voltage drop across diodes 27 and 26 are approximately constant and the voltage at the cathode of diode 26 (the base of T7) decreases at the same rate as the voltage decrease on capacitor 28. But, the voltage at the emitter of transistor T7 decreases at a slower rate due to voltage divider action of resistors 35 and 37. Although the base and emitter voltages of transistor T7 both decease as capacitor 28 discharges, the base voltage decreases faster. Thus, transistor T7 returns to a conducting state sooner due to earlier forward biasing of its base-emitter junction with each cycle.

Voltage at the junction of resistors 35 and 37 varies with voltage on capacitor 57. Capacitor 57 charge time is primarily determined by resistors 35 and 37; its discharge time is primarily determined by resistor 37. Resistors 35 and 37 are in the charge path of capacitor 57 but only resistor 37 is in the discharge path.

With each oscillation, the "power supply voltage" provided by capacitor 28 is decreased in value. Thus after a predetermined period of time, capacitor 28 will "run down" to a predetermined voltage and there will be insufficient energy stored in capacitor 28, in view of the biasing constraints imposed by its "load" circuitry, to provide another single oscillation. At this point, there will be no further energizations supplied to the heart unless capacitor 28 is recharged.

When the magnet is removed, by spring action or other means, element 31 moves back to its normally closed contact element 30. Thus, the position of magnet 15 controls the state of switch 32.

If magnet 15 were removed prior to capacitor 28 discharging to the predetermined voltage (where it no longer acted like a power supply), reed switch 31 would have been returned to its normally closed contact earlier in time. Thus, the number of stimulations supplied to the heart would have been reduced, and capacitor 28 would have been recharged.

Thus, there are two controls over the oscillator. First, if magnet 15 is held in position long enough, a finite number of oscillations are allowed beyond which no further oscillations are permitted unless the magnet is removed to allow capacitor 28 to recharge.

Second, the number of oscillations can be controlled or limited by removing the magnet prior to discharge of capacitor 28 to the predetermined voltage.

Transistor T9 is a simple current amplifier which is normally non-conducting. When transistor T8 conducts the emitter current flowing through resistors 61 and 63 causes the potential at the base of transistor 59 to increase.

At such a time, transistor T9 is biased to conduction and capacitor 65 can discharge through it through the heart. Capacitor 65 discharges more rapidly than it charges since resistor 24 is not involved in the discharge path. Capacitor 65 discharges through an essentially short circuited transistor switch. Transistor T9 operates in response to each oscillation. The combination of the oscillator, transistor T9, and capacitor 65 comprise a pulse generator.

The frequency (repetition-rate) range can be made as large as desired. It can be made to scan through a wide range from below the physiological rate range to above the physiological rate range. However, for a patient with abnormal passways, the range is limited to within the physiological rate range of that patient. A typical rate range would be 90 to 130 cycles per minute.

After magnet 15 is removed, reed switch 32 assumes the depicted state. Capacitor 28 is recharged and capacitor 65 is recharged as previously described. Only if the patient or another person places magnet 15 in proper position once again will there be another burst of stimuli to the heart. The patient can perform this operation himself in response to an uncomfortable feeling when he goes into tachycardia. (Paroxysmal supra-ventricular tachycardia is a disorder which is not lethal but which does cause temporary discomfort to the patient.) When the magnet is in position once again, capacitor 28 assumes its role as power supply and once again a burst of stimuli is applied to the heart.

If a second burst is needed, in the event that one burst did not interrupt the re-entry mechanism, the decreasing intervals in the second burst will not correspond exactly in duration to the decreasing intervals in the first burst. This difference (although slight) is attributed to variations in the semiconductors due to some self-heating, and to variations in the amounts residual voltage on the capacitors. This change in corresponding intervals between bursts is usually desirable as it can result in a greater liklihood of the critical interval occurring during the second burst. Also, the patient's critical interval requirements may vary between bursts, i.e., the critical interval required by the patient can vary from burst to burst which can further enhance the chance of the pulse generator's supplying pulses at the critical interval.

The invention may be embodied in other specific forms without departing from the spirit or essential characteristics thereof. For example, the oscillator need not be of the relaxation variety, the output could be transformer coupled, and other means for controlling turn on and turn off of the oscillator could be employed. It should be understood that other biasing arrangements could be used so that the frequency of oscillation could decrease instead of increase, and could even randomly increase or decrease. The essential requirement is to cause the critical interval to occur.

The present invention can, of course, be extra corporeal (external) having the terminals implanted or the entire mechanism, with the exception of the control, can be implanted.

The present embodiments are therefore to be considered in all respects as illustrative and not restrictive, the scope of the invention being indicated by the appended claims rather than by the foregoing description, and all changes which some within the meaning and range of equivalency of the claims are therefore intended to be embraced therein.