The basis for water quality is decades out of date, given our current understanding of environmental data and availability of recently developed statistical models. The use of a single maximum concentration limit (MCL) for individual chemical elements does not reflect natural ecosystem function nor provide accurate indications of whether regulated industrial activities adversely impact the specific designated beneficial uses of surface or ground waters at specific locations. Water is a complex mixture of compounds, not individual ions, and concentrations vary with temperature, pH, binding and release with inorganic and organic substrata, and other factors. A sample of water represents a snapshot at a specific time and place. This is why aquatic ecologists have established data collection standards to minimize variability when measuring physical and chemical parameters of flowing and standing waters. Aquatic biota are much more reliable indicators of ambient water quality than are concentrations of chemical elements. The EPA considers aquatic life to be the highest and best use of water (that is, the use most sensitive to anthropogenic disturbance). Aquatic biota exist with the abiotic physical and chemical environments to form natural ecosystems. Natural ecosystems are highly complex; we cannot have complete knowledge of their variability and interactions among all components. About 50 years ago, when environmental laws began to be created, ecologists were moving from qualitative descriptions of ecosystems, communities, and populations to quantative measures of their dynamics. Also, appropriate statistical models did not exist, and computers were not as widely (or easily) used as they are today. To implement these statutes regulators had to assess and compare natural ecosystems in attempts to determine anthropogenic effects. The approach used then was to create methods producing a single numerical value assumed to summarize ecosystem quality and separate “good” from “bad” conditions. These species diversity and biotic integrity indices still are used today. And they still fail to describe ecosystem complexity, t quantify inherent natural variability, and to separate natural and anthropogenic changes to these systems. These faillings are overcome by applying appropriate, modern statistical models to biotic data. An important benefit of robust statistical analyses of ecosystems is that they integrate components of each drainage basin and its stream network. This integration provides insights that regulators and other stakeholders can use to make informed decisions. These statistical analyses do not produce a dichotomous decision point (less than this number is good, greater than this number is bad), but allow the use of Best Professional Judgment and adjusted as more data and knowledge become available. This monograph describes application of these ideas and protocols to several stream systems that drain the operational areas of the Jerritt Canyon Mine in the southern Independence Mountains, Elko County, Nevada. Each basin is described and characterized individually because they all differ. Inter-basin analyses could be accomplished with more data and the results would explain why the basins differ. The data available for each stream range from 4 to 8 years. Some statistical models could not be used because too few data were available. This conservative behavior discourages decision-making on weak or insufficient data. Over all the stream networks there was moderate to high variability in functional feeding group component ratios and explanatory variables. Any anthropogenic influences were within the variability range and did not modify biotic compositions in any distinctive way. The ideas, models, and analyses described in this document can be usefully applied in any drainage with suitable data; their power for regulators and the regulated public justifies the efforts and costs for obtaining such data for baseline and permit compliance monitoring.

Wetlands are difficult to understand by non-specialists, and by many specialists, too. There are differences among the general public perception of what is a wetland, the definitions used by wetland scientists, and the definitions used by regulators on jurisdictional wetlands. This primer is designed to provide an introduction to wetland defintions, how an area is determined to be wetland or upland, how the boundaries are determined, and wetland management considerations. Wetland management involves determining the functions and values of a wetland, criteria for enhancement, and design criteria for wetland creation.

Human exposure to external 50/60-Hz electric and magnetic fields induces electric fields within the body. These induced fields can cause interference with implanted pacemakers. In the case of exposure to magnetic fields, the pacemaker leads are subject to induced electromotive forces, with current return paths being provided by the conducting body tissues. Modern computing resources used in conjunction with millimeter-scale human body conductivity models make numerical modeling a viable technique for examining any such interference. In this paper, an existing well-verified scalar-potential finite-difference frequency-domain code is modified to handle thin conducting wires embedded in the body. The effects of each wire can be included numerically by a simple modification to the existing code. Results are computed for two pacemaker lead insertion paths, terminating at either atrial or ventricular electrodes in the heart. Computations are performed for three orthogonal 60-Hz magnetic field orientations. Comparison with simplified estimates from Faraday's law applied directly to extracorporeal loops representing unipolar leads underscores problems associated with this simplified approach. Numerically estimated electromagnetic interference (EMI) levels under the worst case scenarios are about 40 /spl mu/T for atrial electrodes, and 140 /spl mu/T for ventricular electrodes. These methods could also be applied to studying EMI with other implanted devices such as cardiac defibrillators.

The theoretical concepts of species diversity, biodiversity and their relatives were invented in an attempt to capture the complexity of natural ecosystems in a single number. This value represents the number of species present, the number of individuals in each species or similar numbers. Alternate approaches to the single-value index include statistical models of species abundances. With diversity indices calculated with equations taken from informa- tion theory, cryptoanalysis and thermodynamics, it is not surprising that these concepts cannot be validly applied to the real world. However, modern computer hardware and software allow for multiple, spatial variables to be examined simultaneously using map algebra for spatial analyses using a GIS (geographic information system). Mathematically rigorous analyses using spatial statistics and fuzzy logic permit us to objectively answer the questions that the diversity concepts tried to answer: why do we find the plants and animals where we do, and why do we observe the variations in distribution patterns?

The possibility of interference by low-frequency external electric fields with cardiac pacemakers is a matter of practical concern. For pragmatic reasons, experimental investigations into such interference have used contact electrode current sources. However, the applicability to the external electric field problem remains unclear. The recent development of anatomically based electromagnetic models of the human body, together with progress in computational electromagnetics, enable the use of numerical modeling to quantify the relationship between external field and contact electrode excitation. This paper presents a comparison between the computed fields induced in a 3.6-mm-resolution conductivity model of the human body by an external electric field and by several electrode source configurations involving the feet and either the head or shoulders. The application to cardiac pacemaker interference is also indicated.

THE OBJECT of this paper is to describe, quantitatively, differences in steady and pulsatile blood flow in terms of anenergy equivalent pressure, which is obtained by calculation from phasic flow and pressure measurements. Any project to develop an artificial heart or to aid the failing heart by surgical methods involves consideration of the nature of blood flow in the arterial system. The pulsatile properties of arterial flow and pressure have been thought by some investigators to be important and by others unimportant. It has been suggested that these properties influence the exchange rate between interstitial fluid and lymph, help maintain normal capillary flow and normal kidney function, and have an effect on cellular metabolism by aiding in the propulsion of lymph and in the exchange of cerebrospinal fluid.1The arterial pressure pulse has been found by numerous investigators to undergo characteristic changes in vascular disease. Its quantitative measurement,

A left ventricular assist device was placed as a bridge to cardiac transplantation in a 51-year-old man with cardiogenic shock. Placement of the left ventricular assist device occurred 5 years after implantation of an implantable cardioverter/defibrillator. The implantable cardioverter/defibrillator discharged appropriately during ventricular assist device support to terminate episodes of sustained ventricular tachycardia without causing malfunction of the ventricular assist device.

Background - Although the effects of epicardial implantable cardioverter-defibrillator (ICD) leads on underlying cardiac tissue have been reported, the gross and microscopic changes associated with endocardial ICD leads are less well described. This study describes the gross and microscopic changes associated with endocardial ICD leads in humans.Methods and Results - The hearts from 8 patients were examined. At the time of TCD implantation, the patients' mean age was 47 +/- 11 years, and the left ventricular ejection fraction was 0.24 +/- 0.10. Four patients had ischemic heart disease, and 4 had dilated cardiomyopathy, Five hearts were examined after transplantation; 3, after death. The electrode-myocardial interfaces were characterized by intense endocardial fibrosis and were remarkably consistent. Each lead was encased by a ring of fibroelastic tissue, and there was fibrosis of the right ventricular myocardium adjacent to the leads. Fibrosis involved the tricuspid valve in 5 patients, and 1 had perforation of the valve by the lead. Microscopically, interstitial fibrosis was adjacent to each lead in the current path of ICD shocks. Acute cell injury was present only in the hearts that had received recent shocks.Conclusions - The ICD electrode-myocardial interface is characterized by intense fibrosis. The fibrosis associated with endocardial ICD leads and the cumulative acute damage produced by defibrillation discharges may explain changes in the defibrillation and pacing thresholds and the difficulty of lead extraction that can be encountered with transvenous ICD systems.

We describe how a single defect in a new model transvenous lead for an implantable curdiuverter defibrillator can result in malfunction of the sensing and defibrillation circuits. The patient had received shocks during atrial fibrillation without premonitory symptoms. At least one shock was delivered and not fell by the patient. In addition, late in the course, a shock was delivered during atrial fibrillation documented to be with a slow ventricular response. In the transvenous lead, a distal spring functions as the anode for rate sensing and the cathode for defibrillation. The wire from this spring bifurcates near the proximal end of the catheter. One wire from the bifurcation leads to the positive (anode) rate‐sensing socket of the pulse generator, and the other wire leads to the negative (cathode) high voltage output socket of the defibrillator for defibrillation and cardioversion. After the inappropriate and unperceived shocks were documented, intraoperative and postoperative electrical testing indicated that intermittent discontinuity of the distal spring system within the proximal yoke of the catheter caused faulty sensing and potentially unreliable defibrillation. This dual malfunction was possible because the distal spring of the lead functions in the high‐voitage output and the rate‐sensing iow‐vollage input circuits of the implantable defibrillator.

During implantable defibrillator (ICD) operations, we measured acute and chronic transpericardial bipolar pacing thresholds through standard myocardial surface electrodes sewn on the pericardium for chronic ICD QRS rate‐sensing use. We compared observations in 24 patients on day 0 with chronic measurements in seven patients at 27,4 ± 12.1 (median 31.7) months. The leads were used only for QRS rate‐sensing, not for pacing, during the time between acute and chronic measurements. Acute transpericardial pacing threshold at 0.5‐msec stimulus duration on day 0 was 4.5 ± 2.19 V (standard deviation), median 3.5 V, and at median time 964 days postimplantation was 3.8 ± 2.07 V, median 3.5 V. Mean acute pacing current threshold was 3.7 ± 1.90 mA, n = 23, and chronic was 2.7 ± 1.73 mA, n = 6. Acute bipolar impedance was 1,209 ± 383 ohms, median 1,138 ohms, and chronic was 1,550 ± 358 ohms, median 1,410 ohms, n = 7. Acute bipolar QRS amplitude was 12.3 ± 5.93 mV, median 12.1 mV, n = 24, and chronic was 13.5 ± 8.5 mV, median 17.2 mV, n = 7. None of the changes between the acute and chronic states was statistically significant, with the exception of bipolar impedance (P = 0.054). We concluded that: (1) transpericardial pacing threshold did not increase with time; (2) initial and chronic pacing impedances were high and current low; (3) QRS amplitudes were highly satisfactory for defibrillator rate‐sensing; and (4) this approach to ICD implantation left the surgically virgin heart unscarred to make future transplantation easier, and enhanced safety when previous cardiac operations had been done.

The pathology associated with an investigational transvenous defibrillating and sensing lead is described. The lead system had delivered a total of 865 J from the time of implantation to the time of patient death from a noncardiac cause 7 months after implantation and 1 month after his last defibrillator shock. There was mild, superficial fibrous thickening on the endothelial surface of the superior vena cava adjacent to the proximal spring electrode, which did not extend into the vessel wall. The distal portion of endocardial lead was embedded in the interventricular septum near the apex of the right ventricle, surrounded by fibrous thickening, and partially covered by endocardial tissue. Microscopically, there was a thick bed of fibrous connective tissue surrounding the lead with extensive interstitial fibrous connective tissue radiating into the adjacent myocardium. Since this pattern is different from the more generalized fibrotic scarring produced by myocardial infarction, we speculate that the mechanism for the observed interstitial fibrosis is replacement fibrosis following acute myocyte injury that resulted from prior defibrillator shocks and possibly from the trauma produced by the lead compressing adjacent myocardium during systole. Potential effects on device efficacy of these fibrotic changes at the bioelectric interface include their representing a new arrhythmia substrate, the possibility that fibrosis could increase both defibrillation and pacing thresholds, and that the inflammatory reaction may cause deterioration of intracardiac electrograms and interfere with sensing and tachycardia recognition.

Surgical approaches for implantation of the automatic cardioverter defibrillator are sternotomy, left thoracotomy, subxiphoid, and subcostal. Although any one of these may be combined with insertion of one or more of the electrodes transvenously, surgical entry into the chest is required for every noninvestigational defibrillator implantation operation. The approaches differ in exposure provided for selecting electrode sites and for handling untoward events, in amount and location of tissue that must be divided or dissected, and in average time required. The operation is an electrical one. Its purpose is to obtain reliable rhythm sensing so that defibrillation or cardioversion shocks will occur only when necessary, and to obtain low enough defibrillation thresholds for shocks of 30 joules or less to have a 10-joule defibrillation safety margin. Many of the patients have had previous cardiac operations. They usually have low or very low ejection fractions. Intraoperative electrophysiological testing with often multiple defibrillation episodes is required. The choice of approach varies with the state of the patient, the institutional experience, and the surgeon. This article describes technique, and the advantages and disadvantages of the four approaches as used by four surgeons in four different institutions.

Signal‐averaged electrocardiography has been used to identify patients at risk for arrhythmic death after myocardiaJ infarction. Since patients with implantable Cardioverter defibrillators (ICDs) are at high risk for arrhythmic events, they should also be expected to have a high incidence of abnormal signal‐averaged electrocardiograms (SAECGs). However, whether the SAECG can discriminate patients who will have arrhythmia recurrence and receive appropriate ICD shocks from those who will have no recurrence and no shocks is unknown. This study examines the usefulness of the SAECG to separate appropriate users from non‐users of the ICD. Fifty patients with ICDs participated in this study. Those who received a shock preceded by symptoms, a shock without preceding symptoms but with electrocardiographic documentation of ventricular fibrillation or ventricular tachycardia, or a shock while asleep were classified as ICD users. All other patients were classified as nonusers. The SAECG was classified as normal if the QRS duration on the standard electrocardiogram was ≤ 110 msec and if the total filtered QRS duration was < 120 msec, the root‐mean square voltage of the terminal 40 msec was > 25 μV, and the terminal low amplitude signal duration measured < 38 msec. The SAECG was classified as abnormal if the QRS duration on the standard electrocardiogram was ≤ 110 msec and any one of these three criteria were outside the “normal range.” The SAECG was classified as indeterminate if the QRS duration on the standard 12‐lead electrocardiogram was > 110 msec. For the entire group of 50 patients, 8 (16%), 12 (24%), and 30 (60%) had normal, abnormal, and indeterminate SAECGs, respectively. Of the 22 ICD users, 1 (5%), 5 (23%), and 16 (73%) patients had normal, abnormal, and indeterminate SAECGs, respectively. Of the 28 ICD nonusers, 7 (25%), 7 (25%), and 14 (50%) patients had normal, abnormal, and indeterminate SAECGs, respectively. ICD users had lower left ventricular ejection fractions (P = 0.0002J, a higher incidence of ventricular tachycardia (P = 0.04J, prior exposure to a greater number of antiarrhythmic drugs (P = 0.04), and a lower likelihood for survival (P = 0.02) compared to the ICD nonusers. There was no statistically significant difference between the ICD users and nonusers as stratified by SAECG classification regardless of whether or not the indeterminate studies were included or excluded from the analysis. When the analysis was restricted to the 35 patients with coronary artery disease and mono‐morphic ventricular tachycardia, again there was no statistically significant difference between the ICD users and nonusers as stratified by the SAECG classification. In a Cox analysis no SAECG parameter entered the model to predict ICD use. Thus, appropriate ICD discharges occurred regardless of the outcome of signal‐averaged electrocardiography. The data suggest that the SAECG should not be used in the decision analysis whether to implant or deny ICD implantation for patients who have demonstrated life‐threatening ventricular arrhythmias.

To determine patterns of variation in chronic pacing thresholds, we made 4,942 threshold measurements in 257 patients with 312 leads, at times from implant to 295 months (median 17 months) including 1,053 determinations in 46 children < 12 years old. Motivation was late sudden death in two single‐ventricle pacemaker‐dependent children with multiple possible death causes. At stimulus duration 0.5 ± 0.04 msec, mean of the thresholds, measured 1 month or more after implant, was 1.3 ± 0.66 volts (V) for endocardial electrodes and 2.8 ± 1.39 V for epicardially applied electrodes. Highest mean thresholds were in the 6 to 12‐year‐old age group. In 34 leads studied at implant, again within a month and for at least three years thereafter, time of maximum threshold occurred after one month in 59%, independent of lead type or patient age. Of 107 leads with five or more measurements after 3 months use, gradual increase in threshold continued after 3 months in 24%. An additional 21% had at least one threshold that exceeded the post‐three‐months individual patient lead mean by three standard deviations. Most striking was the occurrence of transient several‐volt increases and decreases in threshold as late as 8 years after lead implantation in at least three children. These temporary changes were detected initially transtelephonically by the vario method of threshold measurement. They occurred during minor illnesses such as summer colds, yet similar illnesses also occurred without threshold elevation. We suggest further study of pacing threshold variations in highly pacemaker‐dependent children whose cardiac anatomy makes use of epicardial electrodes necessary.

The automatic implantable cardioverter-defibrillator (AICD) effectively prevents death due to ventricular tachycardia or ventricular fibrillation. Some patients who need an AICD also require cardiac pacing to treat symptomatic bradycardia, bradycardia after defibrillation, or to provide a rate floor to reduce the frequency of bradycardia-related ventricular arrhythmias. Some patients also can benefit from antitachycardia pacing. A mapping technique to implant a pacemaker and AICD sensing leads is presented. For patients with a pacemaker who later need an AICD, the left ventricle is mapped with use of the AICD rate-sensing electrodes to identify a site at which the minimal pacemaker stimulus and maximal ventricular electrogram amplitudes are recorded. An external cardioverter-defibrillator that has amplifiers similar to those in the AICD is used to monitor the rate-sensing electrogram. For patients with an implanted AICD, pacemaker implantation is undertaken by mapping the right ventricle with the pacemaker lead while the AICD is in standby mode; the AICD beep monitor is then used to determine a site where pacemaker stimulus detection by the AICD does not occur. Eight patients underwent implantation of a combined AICD-pacemaker system (four ventricular antitachycardia pacemakers, three ventricular demand pacemakers and one atrial demand pacemaker). Neither inhibition of AICD arrhythmia detection nor double counting occurred. Satisfactory AICD-pacemaker function was shown in all patients postoperatively, and no pacemaker malfunction was observed. Thus, with currently available technology, a combined AICD-pacemaker system can be implanted with satisfactory function of both devices and without adverse device-device interactions.

LR was a patient, followed over a 16‐year period, who presented with an atrial tachycardia which was initially intermittent, but became incessant. Neither the atrial tachycardia nor the associated rapid ventricular response rate could be treated successfully with available drug therapy, resulting in a dilated cardiomyopathy and New York Heart Association (NYHA) class III‐IV congestive heart failure. Acute induction of atrial fibrillation with rapid atrial pacing demonstrated that the associated ventricular rate could be satisfactorily slowed with digitalis therapy. Initially, short bursts from an implanted, radiofrequency controlled, patient activated pacemaker programmed to a rate of 600 bpm and connected to a permanent endocardial atrial J lead successfully interrupted the tachycardia and precipitated atrial fibrillation. Over a period of 3 months, this therapy changed the patient's heart failure to NYHA class II status. Subsequently, precipitation of atrial fibrillation with this technique failed, resulting in return to NYHA class III‐IV congestive heart failure. Therefore, a custom‐designed, high rate, rate‐programmabie pacemaker was implanted to pace the atria rapidly and continuously to maintain atrial fibrillation. A pacing rate of 375 bpm plus digoxin slowed the ventricular rate to 70–80 bpm, with stabilization of the congestive heart failure to NYHA class II. The pacemaker generator was replaced 6 months later, and after another 5 months, pacing was discontinued. The patient's subsequent rhythm remained stable atrial fibrillation with clinically successful control of both the ventricular rate and heart failure (NYHA class II) until the patient's death 72 months later. This unique case demonstrates another form of chronic therapy which, in selected cases, can be used for the long term control of rapid ventricular response rates to supraventricular arrhythmia.

A major limitation in the use of the automatic implantable cardioverter‐defibrillator (AICD) is limited battery longevity and the absence of an accurate and precise end‐of‐life indicator. An elective replacement indicator, or ERI, was proposed by the manufacturer of the AICD in 1985. This ERI was evaluated in nine patients with AICDs. The ERI was exceeded at a mean of 10.9 ± 3.0 months after implantation. Although 0.6 ± 0.4 months of battery life were predicted to remain before battery failure, the devices were followed for 6.0 ± 3.8 months (p = 0.002) during which time no device failed. Although 28.9 ± 21.9 seconds of charging time were predicted to remain, 103.5 ± 67.9 seconds were shown to be available by magnet charge time testing (p = 0.01). Thus, the EHI of the AICD, as originally proposed by its manufacturer, consistently underestimated both the predicted time to end‐of‐life as well as the cumulative charging time remaining before end‐of‐life for each AICD examined. We propose that this ERI not be used to predict end‐of‐life of the AICD. A “new” ERI has been recommended.

A calibration equation describing the relationship between electrical resistance and gravimetric soil moisture was generated for resistance-type soil-moisture-sensing units to be used in a high-clay-content soil. Soil moisture percentages measured gravimetrically and percentages predicted by entering resistance values from a validation set of moisture-sensing units into the equation did not differ. Subsequent analyses indicated that with a calibration set of five soil moisture units, a reliable equation could be generated with data from as few as three wetting-drying cycles in a high-clay-content soil.