Method of detecting and predicting neurocardiogenic syncope

Abstract

A method of detecting an early onset of neurocardiogenic syncope in a patient uses respiratory functions as a predictor of the syncope. According to the method, at least one sample of baseline minute ventilation, tidal volume and respiratory rate of the patient is obtained. The detection unit is set to detect an increase in tidal volume and in minute ventilation over a predetermined respiratory period. The detecting unit also detects any rate of change in respiratory rate and sends a signal to a microprocessor to determine whether the increase in minute ventilation is a sole function of increased tidal volume. The impending syncope is diagnosed if variance in respiratory rate is less than 25% in relation to the sampled baseline during the predetermined period of time.

Description

CROSS-REFERENCE TO RELATED APPLICATIONS[0001]This application is a continuation-in-part of my co-pending application Ser. No. 12 / 998,056 filed on Mar. 10, 2011 entitled “Pacemaker with Neurocardiogenic Syncope Detection and Therapy Utilizing Minute Ventilation Input,” which is based on my Provisional Application Ser. No. 61 / 096,494, filed on Sep. 12, 2008, the full disclosures of which are incorporated by reference herein and priority of which is hereby claimed.BACKGROUND OF THE INVENTION[0002]Neurocardiogenic syncope (vasovagal syncope, the common “fainting spell”) is a common but complex physiologic disorder. An estimated 6% of the population are recurrent fainters. The condition is marked by a sudden drop in heart rate and blood pressure, resulting in decreased cerebral perfusion and subsequent loss of consciousness and postural tone. This condition is unpleasant and limiting for the patient as well as potentially dangerous; unexpected episodes of syncope may result in injury fro...

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Problems solved by technology

The condition is marked by a sudden drop in heart rate and blood pressure, resulting in decreased cerebral perfusion and subsequent loss of consciousness and postural tone.

This condition is unpleasant and limiting for the patient as well as potentially dangerous; unexpected episodes of syncope may result in injury from falls.

In addition, when frequent, it can lead to disability due to prohibitions on driving as well as certain types of employment and activities.

Behavioral treatment for recurrent neurocardiogenic syncope has been limited to lifestyle limitation, avoidance behaviors and abortive maneuvers, and liberalization of fluid and sodium intake.

Medical therapy has been limited to selective serotonin reuptake inhibitors and the “off label” use of fludrocortisone, a mineralocorticoid that enhances sodium and water retention.

The latter therapy is often unacceptable in older patients with preexisting heart disease or hypertension.

However, as a whole, these therapies have yielded disappointing results.

Although monitoring of heart rate and rhythm is accomplished simply with a set of three leads applied to the chest (as is used on telemetry units and outpatient monitoring), there is as of yet no practical way of monitoring of intracranial blood flow, the final common pathway that is interrupted when syncope occurs.

Additionally, monitoring of systemic blood pressure on a continuous basis, a less than ideal surrogate for intracranial blood flow, is also impractical or difficult in ambulatory individuals.

Vasomotor instability preceding syncope has been previously discussed; however, early work did not show a convincing relationship between respiration and syncope in healthy volunteers.

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