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Breathing therapy device and method

Breathing therapy device and method description/claims

This application is a continuation-in-part of U.S. application Ser. No. 10/686,891 filed Oct. 15, 2003, fully incorporated herein by reference.

The invention relates to a device and method for detection, diagnosis and treatment of breathing disorders and to the management of pulmonary or cardiac rhythms, heart failure and other cardiac and/or respiratory related conditions.

Diaphragm stimulation has been used to provide breathing in patients unable to breath on their own. Diaphragm stimulation has also been proposed to treat sleep apnea. However, these uses of diaphragm stimulation have not provided optimal breathing responses or control of breathing.

Accordingly it would be desirable to provide improved diaphragm stimulation.

Breathing is typically intrinsically controlled by complex brain control and feedback sensing by the body. The body's involuntary control of respiration is mediated by the brain's respiratory center located in the brainstem, particularly in the medulla oblongata and pons. The respiratory center regulates the rhythmic alternating cycles of inspiration and expiration. The dorsal respiratory group within the medulla is responsible for the generation of respiratory rhythm through a reciprocal inhibition with other cell groups.

In addition, various central and peripheral receptors, e.g., chemoreceptors and mechanoreceptors play important roles in regulation of inspiration.

Central chemoreceptors of the central nervous system located on the ventrolateral medullary surface, are sensitive to pH of their environment. It is believed that these chemoreceptors act to detect a change in pH of the cerebral spinal fluid. An increase in carbon dioxide tension of the arteries will indirectly cause the blood to become more acidic; the cerebral spinal fluid pH is closely comparable to plasma pH, as carbon dioxide easily diffuses across the blood/brain barrier. The detection of variation in the arterial carbon dioxide tension acts as a quick response system, useful in short term regulation. This system utilizes a negative feedback system, therefore if the pH of the cerebral spinal fluid is too low, then the receptor is believed in effect send an error signal to the medulla and respiration is adjusted accordingly.

Peripheral chemoreceptors are believed most importantly to act to detect variation of the oxygen in the arterial blood, in addition to detecting arterial carbon dioxide and pH. These receptors are typically referred to as aortic or carotid bodies, and respectively are location on the arch of the aorta and on the arch of the common carotid artery. A continuous signal is sent, via cranial nerves from the peripheral chemoreceptors. With a decrease in arterial oxygen tension, the signal intensifies, calling for an increase in respiration. However, increase in respiration typically results in falling PCO2 and hydrogen ion concentration which creates strong respiratory inhibitory effects that oppose the excitatory effects of diminished oxygen.

Mechanoreceptors are located for example, in the airways and parenchyma, and are responsible for a variety of reflex responses.

Pulmonary Stretch Receptors are located in smooth muscles of the trachea down to the terminal bronchioles. They are innervated by large, myelinated fibers and they discharge in response to distension of the lung. Their vagally mediated inhibition of inspiration and promotion of expiration is believed to be sustained as long as the lung is distended. They contribute to what is known as the Hering-Breuer reflex which prevents over-inflation of the lungs, by providing feedback signals that cause termination of inspiration.

Other receptors, such as respiratory proprioreceptors located in muscle spindle endings and tendon organs of the respiratory muscles, are stimulated in response to rib movement or intercostals/diaphragmatic tendon force of contraction.

In addition to involuntary control of respiration by the respiratory center, respiration can be affected by conditions such as, e.g., emotional state via input from the limbic system, or temperature, via the hypothalamus. Voluntary control of the respiration is provided via the cerebral cortex, although chemoreceptor reflex is capable of overriding conscious control.

Known diaphragm stimulation techniques have not interacted with this complex respiratory control system to override, influence or work with the system.

Accordingly improved stimulation devices and methods would be desirable.

The invention provides a device and method for electrically stimulating the diaphragm to control breathing while inhibiting respiratory drive. According to the invention, a stimulation phase is identified. The stimulation phase is a period of time within the breathing cycle in which stimulation will inhibit respiratory drive and most likely will occur during a first fraction of the rest phase. Baseline breathing is sensed and stored. The length of the rest period in a breathing cycle is identified and a stimulation phase is determined.

The baseline is used to determine when to stimulate. EMG or other respiratory indicators may be sensed on a breath by breath basis or over time to determine when to stimulate within the respiratory phase. For a given tidal volume stimulation amplitude, duration and respiratory rate may be varied to inhibit respiratory drive when stimulating.

The respiratory drive inhibition may be used in a number of applications such as improving or remodeling the heart in heart failure patients, treating apnea, chronic obstructive pulmonary disorder (COPD), and hypertension.

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