Implantable cardiac stimulator with safe noise mode

Details Implantable cardiac stimulator with safe noise mode Implantable cardiac stimulator with safe noise mode

1999-06-15

2001-03-06

Schaetzle, Kennedy (Department: 3762)

Surgery: light, thermal, and electrical application

Light, thermal, and electrical application

Electrical therapeutic systems

C128S901000, C607S017000

Reexamination Certificate

active

06198968

ABSTRACT:

BACKGROUND OF THE INVENTION
1. Field of the Invention
The present invention relates generally to cardiac stimulating devices. More particularly, the present invention relates to an implantable cardiac pacemaker or cardioverter/defibrillator with a safe mode of operation during the occurrence of externally generated noise or interference.
2. Description of the Related Art
In the normal human heart, illustrated in
FIG. 1
, the sinus (or sinoatrial (SA)) node generally located near the junction of the superior vena cava and the right atrium constitutes the primary natural pacemaker by which rhythmic electrical excitation is developed. The cardiac impulse arising from the sinus node is transmitted to the two atrial chambers (or atria) at the right and left sides of the heart. In response to excitation from the SA node, the atria contract, pumping blood from those chambers into the respective ventricular chambers (or ventricles). The impulse is transmitted to the ventricles through the atrioventricular (AV) node, and via a conduction system comprising the bundle of His, or common bundle, the right and left bundle branches, and the Purkinje fibers. The transmitted impulse causes the ventricles to contract, the right ventricle pumping unoxygenated blood through the pulmonary artery to the lungs, and the left ventricle pumping oxygenated (arterial) blood through the aorta and the lesser arteries to the body. The right atrium receives the unoxygenated (venous) blood. The blood oxygenated by the lungs is carried via the pulmonary veins to the left atrium.
This action is repeated in a rhythmic cardiac cycle in which the atrial and ventricular chambers alternately contract and pump, then relax and fill. Four one-way valves, between the atrial and ventricular chambers in the right and left sides of the heart (the tricuspid valve and the mitral valve, respectively), and at the exits of the right and left ventricles (the pulmonic and aortic valves, respectively, not shown) prevent backflow of the blood as it moves through the heart and the circulatory system.
The sinus node is spontaneously rhythmic, and the cardiac rhythm it generates is termed normal sinus rhythm (“NSR”) or simply sinus rhythm. This capacity to produce spontaneous cardiac impulses is called rhythmicity, or automaticity. Certain other cardiac tissues possess rhythmicity and hence constitute secondary natural pacemakers, but the sinus node is the primary natural pacemaker because it spontaneously generates electrical pulses at a faster rate. The secondary pacemakers tend to be inhibited by the more rapid rate at which impulses are generated by the sinus node.
If the body's natural pacemaker performs correctly, blood is oxygenated in the lungs and efficiently pumped by the heart to the body's oxygen-demanding tissues. However, when the body's natural pacemaker malfunctions, an implantable pacemaker often is required to properly stimulate the heart. Disruption of the natural pacemaking and propagation system as a result of aging or disease is commonly treated by artificial cardiac pacing, by which rhythmic electrical discharges are applied to the heart at a desired rate from an artificial pacemaker. An artificial pacemaker (or “pacer” as it is commonly described) is a medical device which includes an electronics assembly and one or more leads connecting the electronics assembly to the heart. Electrodes on the distal end of the leads include an exposed conducting surface adjacent to or in contact with the heart tissue. The pacemaker delivers electrical pulses via the electrodes to the patient's heart in order to stimulate the heart to contract and beat at a desired rate.
Pacemakers originally were designed to operate asynchronously. That meant the pacemaker emitted an electrical pulse that was delivered to the heart through the pacemaker's electrodes at a constant rate. Asynchronous pacemakers paced the heart at a constant, preselected rate generally thought to be sufficient for the particular patient (e.g., 70 pulses per minute). This type of pacing protocol, however, unnecessarily expended the energy of the pacemaker's battery (which has a limited life) because the hearts of many patients were capable of beating on their own, at least occasionally, without the need for an artificially generated pacemaker pacing pulse. Thus, an asynchronous pacemaker may expend energy pacing the heart at a time when the heart's natural pacemaker and conduction system are functioning properly and not in need of artificial stimuli.
Pacemakers today typically are provided with the capability to determine whether the heart is able to beat on its own, and if so, the pacemaker will not pace the heart. If, however, the heart cannot beat on its own, the modern pacemaker will pace the heart instead. This type of pacemaker is referred to as a “demand” pacemaker because pacing pulses are generated by the pacemaker only as needed by the heart (i.e., on “demand”).
Some patients have disease processes that may cause an “arrhythmia,” which is an abnormal cardiac rhythm. For some of these patients the arrythmias may be characterized by an excessively slow heart rate (termed “bradycardia”) or an excessively fast and irregular heart rate (termed “tachyarrhythmia”). Tachyarrhythmia may degenerate into fibrillation in which the affected cardiac chamber merely quivers and loses all of its blood pumping capability. If the fibrillation condition occurs in a ventricular chamber of the heart (a condition commonly called “ventricular fibrillation”)
1
the patient will normally die within minutes. In patients undergoing pacing therapy, a tachyarrhythmia hopefully can be terminated with an antitachyarrhythmia pacing protocol which generally includes a fast pacing rate to interfere with the focus of the arrhythmia. If antitachyarrhythmia pacing does not stop the arrhythmia, a defibrillation pulse is necessary to terminate the arrhythmia.
Patients that are susceptible to tachyarrhythmias are candidates for an implantable cardioverter/defibrillator (“ICD”) which is a device that senses the onset of tachyarrhythmias and generates antitachyarrhythmia pacing pulses and, if needed, a subsequent defibrillation pulse to terminate the arrhythmia. Patients that require an ICD also generally require pacing support such as that provided by pacemakers. Thus, in addition to a defibrillation capability, an ICD typically also includes a pacing capability to pace the heart on demand.
In some patients with pacemakers/ICD's observed that the pacemaker/ICD itself has demonstrated the propensity to induce a tachyarrhythmia which may degenerate into a fatal fibrillation. The reason for this phenomenon can be described with respect to
FIG. 2
in which a ventricular repolarization wave (during which the ventricle relaxes after contracting) is detected by the surface electrocardiogram (“ECG”) as the so-called “T-wave”. The T-wave occurs approximately 150-400 milliseconds after the occurrence of the ventricular depolarization wave shown on the surface ECG as the QRS complex. Around the time the T-wave is detected, various portions of the ventricles are undergoing repolarization, and as such are not sensitive to stimulation. This period of time in which cardiac tissue is not sensitive to electrical stimulation is called the refractory period.
If pacing occurs during the refractory period, a slowly propagating action potential initiated by tissue which is sensitive to stimulation may cause the stimulation of tissue which was not viable for stimulation at the time the original stimulus was generated. This propagating wave may later reach the tissue which was originally stimulated at a time when it has already repolarized, and thus cause its depolarization anew. If this sequence of events occurs, a reentrant loop is created which causes the ventricle to beat at a rate determined by the period of the reentrant loop. This sequence causes what is known as a “reentrant tachycardia,” and may degenerate into fibrillation. The period of time during which a pacing pu

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