Venous pooling detection and therapy device

Details Venous pooling detection and therapy device Venous pooling detection and therapy device

1997-11-06

1999-06-22

Kamm, William E.

Surgery: light, thermal, and electrical application

Light, thermal, and electrical application

Electrical therapeutic systems

A61N 1368, A61N 136

Patent

active

059138793

DESCRIPTION:

BRIEF SUMMARY
BACKGROUND OF THE INVENTION

1. Field of the Invention
This invention relates to a detection device for detecting venous pooling in a human body and to the use of this detection device in a therapy device for preventing vasovagal syncope, particularly to the prediction of neurally mediated bradycardia and hypotension.
2. Description of the Prior Art
The exact etiology of vasovagal syncope remains unknown, but parasympathetic and sympathetic activity have been found to participate in the pathogenesis of vasovagal syndrome. Particularly, vasodepressor reaction is caused by the Bezold-Jarisch reflex. There are three modes of vasovagal responses: cardioinhibitory, vasodepressor and mixed response. Accordingly, patients may have profound bradycardia and a major component of vasodilation as well. It has been postulated that vigorous contraction of relatively empty ventricle activates myocardial sensory receptors, which, in susceptible persons, initiates an inhibitory reflex that results in hypotension, bradycardia or both. Vasodepressor reactions are believed to be caused by activation of unmyelinated left ventricular vagal nerve endings known as C-fibers normally being excited by catecholamines, sympathetic nerve stimulation and left ventricular pressure. The most important physiologic finding is that spontaneous vasodepressor reactions often occur in the context of a sympathetic stimulation as a response to the venous pooling. Accordingly, every vasovagal syncope is preceded by the venous pooling, the sudden heart rate increase, and by the vigorous ventricular contractions.
Bradyarrhythmias associated with vasovagal syncope must be treated by permanent pacing. Vasovagal syncope occurs usually in the erect body position with gravitational stress on venous return. The first pacing mode of choice was VVI pacing with hysteresis. U.S. Pat. No. 4,856,523, describes the inclusion of the hysteresis feature in a rate-responsive pacemaker, in an attempt to prevent competition between the pacemaker and the heart's SA node, when the anterograde conduction path is restored. This patent proposes to vary the hysteresis rate as a function of the pacemaker sensor rate, to a predetermined level upon sensing of the natural heart contraction during the escape interval. U.S. Pat. No. 4,363,325 discloses a multiple-mode pacer which automatically switches from an atrial synchronous mode to a ventricular inhibited mode when the intrinsic atrial rate drops below a preset hysteresis rate. Nevertheless, dual chamber pacing assures maximal contribution of atrial contraction to the ventricular filling, maintaining the natural sequence of cardiac activation. The majority of patients suffering from malignant vasovagal syndrome have intact retrograde atrioventricular conduction, which may cause the pacemaker mediated tachycardia. DVI mode of pacing may provoke atrial arrhythmias due to the fact that the atrial pacing pulse occurs irrespective of the atrial spontaneous activity. The best mode of pacing, preventing these problems in pacing therapy, is DDI mode, especially in patients having intact retrograde conduction. That is the mode when a pacemaker acts like the two independent pacemakers inhibited by spontaneous activity (DDI=AAI+VVI). When there is no vasovagal attack, there is no need for cardiac pacing. It is known in the art that the patient's baseline resting rate can fall as low as 50 beats per minute, especially during the sleep. Moreover, DDI pacing rate being 20 beats per minute higher than resting heart rate may provide significant hemodynamic improvement and maintain consciousness during a vasovagal attack. Accordingly, DDI pacing with hysteresis is the most appropriate pacing mode. However, allowing the patient to have a normal low sinus rate during the night and at rest, as well as starting to pace with 20 beats per minute higher frequency than basic rate (for instance during the day) would require special function of a pacemaker.
Such a pacemaker is disclosed in the U.S. Pat. No. 5,284,491. It has a programmable lower rate

REFERENCES:
"Characterization of Subcutaneous Microvascular Blood Flow During Tilt Table-Induced neurally Mediated Syncope," Benditt et al., JACC, vol. 25, No. 1, Jan. 1995, pp. 70-75.

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