US-12616839-B2 - System and method to modulate phrenic nerve to prevent sleep apnea

Abstract

An implantable medical device for treating breathing disorders such as central sleep apnea wherein stimulation is provided to the phrenic nerve through a transvenous lead system with the stimulation beginning after inspiration to extend the duration of a breath and to hold the diaphragm in a contracted condition.

Inventors

• Mark Gelfand
• Howard R. Levin
• Andrew Halpert

Assignees

• ZOLL RESPICARDIA, INC.

Dates

Publication Date

20260505

Application Date

20220301

Claims (19)

1. 1 . A medical device for use in a patient comprising: a single transvenous stimulation lead comprising at least one stimulation electrode and configured to be placed in a vein adjacent to a phrenic nerve of the patient; an implanted medical device (IMD) configured to be implanted in a body of the patient, to be electrically connected to the single transvenous stimulation lead and to the at least one stimulation electrode via the single transvenous stimulation lead, and to receive a respiration signal via the single transvenous stimulation lead; and control logic incorporated within the IMD, the control logic configured to analyze the respiration signal and deliver stimulation pulses to maintain activation of at least a portion of a diaphragm of the patient, wherein the control logic is configured to be able to deliver consistent amplitude stimulation pulses, progressively increasing amplitude stimulation pulses, progressively decreasing amplitude stimulation pulses, and pulses in which an amplitude of the stimulation pulses increases and then decreases, and to be able to select for delivery one of the consistent amplitude stimulation pulses, the progressively increasing amplitude stimulation pulses, the progressively decreasing amplitude stimulation pulses, or the pulses in which the amplitude of the stimulation pulses increases and then decreases.
2. 2 . The medical device of claim 1 wherein the control logic is further configured to deliver the stimulation pulses at a time proximate a transition from an inhalation phase of respiration to an exhalation phase of respiration.
3. 3 . The medical device of claim 2 wherein the control logic is further configured to analyze the respiration signal and deliver the stimulation pulses at an end of naturally initiated inspiration.
4. 4 . The medical device of claim 2 wherein the control logic is further configured to analyze the respiration signal and deliver the stimulation pulses for a duration that exceeds naturally initiated exhalation.
5. 5 . The medical device of claim 2 wherein the control logic is further configured to analyze the respiration signal and deliver the stimulation pulses at an end of naturally initiated inspiration and for a duration that exceeds naturally initiated exhalation.
6. 6 . The medical device of claim 1 further comprising an implantable motion sensor capable of sensing motion of the patient, wherein the control logic is capable of sensing and analyzing motion signals.
7. 7 . The medical device of claim 6 wherein the control logic is further configured to deliver phrenic nerve stimulation based on the respiration signal and to disable the phrenic nerve stimulation based on the motion signals.
8. 8 . The medical device of claim 6 wherein the implantable motion sensor is an accelerometer.
9. 9 . The medical device of claim 1 wherein the control logic is configured to reject respiration signals indicative of cough, arousal, or movement.
10. 10 . The medical device of claim 1 wherein the control logic is configured to reject respiration signals that appear during a refractory period that follows a stimulation pulse.
11. 11 . The medical device of claim 1 wherein the single transvenous stimulation lead includes a plurality of stimulation electrodes, the plurality of stimulation electrodes including the at least one stimulation electrode.
12. 12 . The medical device of claim 11 wherein stimulation provided by the plurality of stimulation electrodes is bipolar.
13. 13 . The medical device of claim 1 wherein stimulation provided by the at least one stimulation electrode is monopolar.
14. 14 . The medical device of claim 1 wherein the single transvenous stimulation lead has at least one anchoring mechanism.
15. 15 . The medical device of claim 1 where the at least one stimulation electrode is coated with medication.
16. 16 . The medical device of claim 1 wherein the control logic is configured to calculate an observed breathing rate based on the respiration signal and to deliver the stimulation pulses at a fixed stimulation rate that is less than the observed breathing rate.
17. 17 . The medical device of claim 1 wherein the at least one stimulation electrode is configured to be retained in a pericardiophrenic vein.
18. 18 . The medical device of claim 1 , wherein the at least one stimulation electrode and a can of the IMD form a transthoracic impedance sensor to provide the respiration signal.
19. 19 . The medical device of claim 1 , wherein the phrenic nerve is a right phrenic nerve or a left phrenic nerve.

Description

CROSS-REFERENCE TO RELATED CASES This application is a continuation of U.S. patent application Ser. No. 14/715,128, filed May 18, 2015, and titled “System and Method to Modulate Phrenic Nerve to Prevent Sleep Apnea,” now U.S. Pat. No. 11,305,119, which is a continuation of U.S. patent application Ser. No. 13/538,713, filed Jun. 29, 2012, and titled “System and Method to Modulate Phrenic Nerve to Prevent Sleep Apnea,” now U.S. Pat. No. 10,518,090, which is a continuation of U.S. patent application Ser. No. 11/601,150, filed Nov. 17, 2006, and titled “System and Method to Modulate Phrenic Nerve to Prevent Sleep Apnea,” now U.S. Pat. No. 8,244,359, which claims priority from and the benefit thereof and incorporates entirely: U.S. Provisional Application 60/737,808, filed Nov. 18, 2005, and titled “System and Method to Modulate Phrenic Nerve to Prevent Sleep Apnea;” U.S. Provisional Application 60/743,062, filed Dec. 21, 2005, and titled “System and Method to Modulate Phrenic Nerve to Prevent Sleep Apnea;” and U.S. Provisional Application 60/743,326, filed Feb. 21, 2006, and titled “System and Method to Modulate Phrenic Nerve to Prevent Sleep Apnea.” FIELD OF THE INVENTION The present invention relates generally to implantable medical devices and more particularly to a device and method for controlling breathing and for treating Central Sleep Apnea. BACKGROUND OF THE INVENTION History Sleep Disordered Breathing (SDB) and particularly Central Sleep Apnea (CSA) is a breathing disorder closely associated with Congestive Heart Failure (CHF). The heart function of patients with heart failure may be treated with various drugs, or implanted cardiac pacemaker devices. The breathing function of patients with heart failure may be treated with Continuous Positive Air Pressure (CPAP) devices or Nocturnal Nasal Oxygen. These respiratory therapies are especially useful during periods of rest or sleep. Recently, implanted devices to directly address respiration disturbances have been proposed. Some proposed therapeutic devices combine cardiac pacing therapies with phrenic nerve stimulation to control breathing. Phrenic nerve pacing as a separate and stand alone therapy has been explored for paralyzed patients where it is an alternative to forced mechanical ventilation, and for patients with the most severe cases of central sleep apnea. For example, Ondine's Curse has been treated with phrenic nerve pacemakers since at least the 1970's. In either instance, typically, such phrenic nerve pacemakers place an electrode in contact with the phrenic nerve and they pace the patient's phrenic nerve at a constant rate. Such therapy does not permit natural breathing and it occurs without regard to neural respiratory drive. Motivation for Therapy SDB exists in two primary forms. The first is central sleep apnea (CSA) and the second is obstructive sleep apnea (OSA). In OSA the patient's neural breathing drive remains intact, but the pulmonary airways collapse during inspiration, which prevents air flow causing a form of apnea. Typically, such patients awake or are aroused as a result of the apnea event. The forced airflow of CPAP helps keep the airways open providing a useful therapy to the OSA patient. CSA patients also exhibit apnea but from a different cause. These CSA patients have episodes of reduced neural breathing drive for several seconds before breathing drive returns. The loss of respiratory drive and apnea is due to a dysfunction in the patient's central respiratory control located in the brain. This dysfunction causes the patient's breathing pattern to oscillate between too rapid breathing called hyperventilation and periods of apnea (not breathing). Repeated bouts of rapid breathing followed by apnea are seen clinically and this form of disordered breathing is called Cheyne-Stokes breathing or CSR. Other patterns have been seen clinically as well including bouts of hyperventilation followed by hypopneas only. In patients with CHF, prognosis is significantly worse when sleep apnea is present. A high apnea-hypopnea index (a measure of the number of breathing disturbances per hour) has been found to correlate to a poor prognosis for the patient. The swings between hyperventilation and apnea characterized by central sleep apnea have three main adverse consequences, namely: large swings in arterial blood gases (oxygen and carbon dioxide); arousals and shifts to light sleep; and large negative swings in intrathoracic pressure during hyperventilation. The large swings in blood gases lead to decreased oxygen flow to the heart, activation of the sympathetic nervous system, endothelial cell dysfunction, and pulmonary arteriolar vasoconstriction. Arousals contribute to increased sympathetic nervous activity, which has been shown to predict poor survival of patients with heart failure. Negative intrathoracic pressure, which occurs during the hyperventilation phase of central apnea, increases the after load and oxygen consumption of the l