Surgery: light – thermal – and electrical application – Light – thermal – and electrical application – Electrical therapeutic systems
Reexamination Certificate
2001-05-03
2003-11-11
Sykes, Angela D. (Department: 3762)
Surgery: light, thermal, and electrical application
Light, thermal, and electrical application
Electrical therapeutic systems
C607S017000
Reexamination Certificate
active
06647295
ABSTRACT:
FIELD OF THE INVENTION
The invention generally relates to cardiac pacing techniques and in particular to techniques for preventing vasovagal syncope using cardiac pacing.
BACKGROUND OF THE INVENTION
Syncope is a sudden loss of strength or consciousness caused by reduced cerebral circulation, itself typically the result of vasodilation. Vasovagal syncope is a type of syncope referred to as a neurocardiogenic syncope wherein the syncope is triggered by an interaction between the heart and nerve tissue connected to the heart. Neurocardiogenic syncope may also be referred to as neuromediated syncope, neurally mediated syncope, cardioinhibitory syncope, cardioneurogenic syncope, vasodepressor syncope, malignant vasovagal syndrome, neurally mediated hypotension/bradycardia and cardiovascular neurogenic syncope. For vasovagal syncope, the interaction occurs between the heart and the vagus nerve.
Evidence suggests that vasovagal syncope is initially triggered by a sudden reduction in peripheral vascular resistance, perhaps resulting from stress, pooling of blood in the extremities, or other factors. As a result of the reduction in peripheral vascular resistance, the pressure of blood entering the heart drops and the amount of blood filling the ventricles prior to ventricular contractions therefore also drops. With less blood in the ventricles, the ventricles thereby contract much more quickly and vigorously than would otherwise occur in an effort to maintain a constant stroke volume. The more vigorous ventricular contractions have the effect of stimulating ventricular mechanoreceptors, also known as C fibers, that normally only respond to ventricular expansion or stretching, rather than contraction. The activation of the ventricular mechanoreceptors results in a surge in neural traffic to the brainstem, particularly to the nucleus tractus solitaries, via the vasovagal nerve.
For most people, the neurological system properly interprets the increase of activity of the mechanoreceptors as being in response to a drop in peripheral vascular resistance and compensates by increasing the heart rate and constricting the blood vessels. However, in certain patients, as a result of a neurological condition within the vagus nerve or for some other reason, the surge in neural traffic is falsely perceived by the neurological system as being representative of hypertension. In response thereto, the brainstem triggers an increase in peripheral vasodilation and a reduction in heart rate. The vasodilation and the drop in heart rate, in turn, cause a still further reduction in blood pressure, i.e. hypotension. In other words, the actions taken by the brainstem exacerbate the problem. If the degree of hypotension is sufficiently severe, cerebral hypoperfusion occurs wherein brain cells do not receive enough oxygen and, consequently, the victim loses consciousness. Accordingly, within these patients, any sudden drop in peripheral vascular resistance can trigger vasovagal syncope and the patients suffer from recurrent vasovagal syncope. Further information regarding vasovagal syncope may be found in S. Serge Barold and Jacques Mugica,
Recent Advances in Cardiac Pacing
, Futura Publishing Company, 92-95, 1997.
As can be appreciated, loss of consciousness can be particularly dangerous for the patient if occurring while the patient is driving a motor vehicle, climbing a flight of stairs or engaged in any other activity wherein the loss of consciousness could result in injury or death. Accordingly, it is highly desirable to provide techniques for preventing vasovagal syncope or other forms of neurocardiological syncope. One possible technique for preventing vasovagal syncope is to employ a pacemaker, or other implantable cardiac stimulation device, to pace the heart to prevent the reduction in blood pressure associated with vasovagal syncope from occurring. Indeed, the American College of Cardiology-American Heart Association suggested in 1991 that vasovagal syncope in patients should be used as a Class 2 indication for pacing therapy. However, conventional cardiac pacemakers have had only limited success in preventing recurrent vasovagal syncope. (See David G. Benditt et al.,
Cardiac Pacing for Prevention of Recurrent Vasovagal Syncope
, Ann Intern Med. 1995; 122; 204-209.)
With many conventional techniques for preventing vasovagal syncope, the cardiac pacemaker analyzes a sequence of intrinsic heart beats (i.e. natural or non-stimulated heart beats) to determine whether the sequence of heart beats indicates an episode of vasovagal syncope and, if so, the pacemaker paces the heart. In one example, if the intrinsic heart rate falls below a lower threshold, the pacemaker then analyzes the immediately preceding heart beats to determine whether a sharp drop in heart rate has occurred. If so, the pacemaker then continues to monitor intrinsic heart beats to determine whether the heart rate remains at a stable rate below the threshold rate. If the rate remains stable for a predetermined number of heart beats, the pacemaker then concludes that an episode of vasovagal syncope may be occurring and begins pacing at an elevated heart rate. Unfortunately, by the time the pacemaker has had the opportunity to analyze a sufficient number of heart beats to determine whether an episode of vasovagal syncope is occurring, the blood pressure of the patient has likely dropped to the point where an elevated heart rate will not remedy the vasovagal syncope and the patient will become unconscious. In this regard, the drop in blood pressure results in significantly less blood filling the ventricles, such that there is simply not enough incoming blood to pump. Hence, overall blood pressure is not significantly increased merely by pumping the heart faster, and the aforementioned cerebral hypoperfusion still occurs resulting in unconsciousness. Indeed, depending upon the programming of the pacemaker, it may take five to eight seconds or more before the pacemaker begins increasing the heart rate.
Moreover, vasovagal syncope detection techniques, which require analysis of numerous heart beats, can be fairly elaborate thereby requiring considerable computing resources, particularly memory space. Within many pacemaker or implantable cardioverter defibrillator (ICD) designs, all or most of the available processing resources are devoted to pre-existing software programs. Examples include programs for: detecting ventricular and atrial arrhythmias and administering responsive therapy; performing automatic mode switch operations between an atrial tracking mode and a non-atrial tracking mode; monitoring the battery or other power supply; and storing diagnostic information such as a list of pacing events along with the internal electrocardiogram (IEGM). Another example is a rate hysteresis program that temporarily paces the heart at a Base Rate whenever the intrinsic heart rate falls below a Hysteresis Escape Rate so as to permit the heart to typically beat with an intrinsic heart rhythm as opposed to a paced rhythm. In addition to these examples, many, many other programs are usually provided in state of the art stimulation devices, typically consuming most or all available computing resources. Hence, to add a complex vasovagal syncope detection algorithm, the stimulation device may need to be re-designed to provide additional computing resources, such as a more powerful processor, larger memory system or faster bus system. Moreover, even if the hardware of the stimulation device need not be modified, additional costs will arise in the design, development and de-bugging of the complex vasovagal syncope detection software.
Accordingly, it would be highly desirable to provide an improved cardiac stimulation device capable of promptly pacing the heart at an elevated rate upon detection of possible vasovagal syncope, so as to prevent a significant drop in blood pressure to thereby more effectively prevent loss of consciousness. It would also be highly desirable to provide an improved cardiac stimulation device capable of detecting and responding to a
Bornzin Gene A.
Florio Joseph J.
Hauck Gregory
Droesch Kristen
PaceSetter, Inc.
Sykes Angela D.
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