Impedance-gradient electrode reduces skin irritation induced by transthoracic defibrillation.

A new type of disposable external defibrillation electrode has been developed to reduce the skin irritation commonly associated with defibrillation and synchronised cardioversion. This design employs an impedance gradient to reduce the proportion of current delivered to the electrode periphery. The temperature distribution under the new electrode was compared with that of four other types of commercially available electrodes after repeated high-energy biphasic defibrillation discharges to domestic swine. Skin temperature distributions were acquired using non-invasive thermography. Measurements of the maximum temperature rise at each electrode site, taken 3.6s after the fifth defibrillation discharge, demonstrated that the new impedance-gradient electrode produced 50-60% less skin heating than two of the three uniform-impedance electrode designs. Histological examination of erythematous sites excised 24 h after defibrillation quantified the associated skin damage using a scoring protocol developed for this study. In contrast to previous studies, histological examinations demonstrated second-degree skin burns following defibrillation. The new electrode design, however, induced 44-46% less skin damage than two of the traditional uniform-impedance electrodes.

Electrophysiological control of ventricular rate during atrial fibrillation.

Thirteen anesthetized canine subjects (17-29 kg) were used to demonstrate that mild cervical left vagal stimulation could control ventricular rate effectively during atrial fibrillation (AF). Two studies are presented. The first study used six subjects to demonstrate the inverse relationship between (manually applied) left vagal stimulation and ventricular excitation (R wave) rate during AF. As left vagal stimulation frequency was increased, ventricular excitation rate decreased. In these studies, a left vagal stimulus frequency of 0-10 per second reduced the ventricular excitation rate from > 200/min to < 50/min. The decreasing ventricular excitation rate with increasing left vagal stimulation frequency was universal, occurring in all 26 trials with the six subjects. This fundamental principle was used to construct an automatic controller for use in the second study, in which seven subjects were used to demonstrate that ventricular rate can be brought to and maintained within a targeted range with the use of an automatic (closed-loop) controller. A 45-minute record of automatic ventricular rate control is presented. Similar records were obtained in all seven subjects.

Characterization of atrioventricular nodal response to electrical left vagal stimulation.

The dynamic effect of left vagal stimulation on atrioventricular conduction was studied in six isofluorane-anesthetized dogs ranging in weight from 22 to 29 kg. The cervical vagus nerve trunks were left intact and no beta-adrenergic blockade was produced so that any influences of the sympathetic nervous system and autonomic reflex activity could be observed. Atrial pacing was used to control the heart rate while single, short trains of left vagal stimulation were delivered and timed to occur at different instances during the cardiac cycle. The magnitude of the A-V delay depended on the instant of delivery of the train of vagal stimuli during the cardiac cycle. Vagal effect curves were constructed and fit to a mathematical equation which describes the pharmacokinetic behavior of a bolus injection of a drug whose onset time is of the same order as its half-life. The three parameters of this equation have physiologic significance and are related to nerve propagation time and synaptic delay, acetylcholine concentration rise, and the acetylcholineesterase mechanism. The maximum A-V delay occurred when the short train of left vagal stimuli was applied 200-300 ms after the atrial pacing stimulus and the total effect was virtually over by 800-1,000 ms.

Skin-temperature distribution under a new type of defibrillating electrode.

The temperature rises under a new type of x-ray-transparent, improved current-density-distribution defibrillation electrode applied to pig skin were measured at four sites with fiberoptic thermal probes. Three anesthetized pigs, ranging in weight from 79 to 92 lb, were used. Temperature-time curves were obtained and the maximum temperature was identified. For 17 measurements at each site, the maximum temperature rise for a 360-joule shock was 317.3 +/- 53.0 millidegrees Celsius.

Post-mortem changes after lead extraction from the ovine coronary sinus and great cardiac vein.

We investigated in sheep, non-thoracotomy extraction of leads which had been chronically implanted in the right atrium (RA), coronary sinus/great cardiac vein (CS/GCV) and right ventricle (RV) for atrial implantable defibrillation. Clinical success of extraction as well as gross and histologic findings in the heart are reported. Six of nine sheep had successful extractions. The major complication was laceration of the wall of the great coronary vein with hemorrhage into the pericardial space and cardiac tamponade. Tissue damage included several reversible changes: intra-tissue hemorrhage, thrombosis in the veins, and some necrosis of fat, vascular wall and myocardium. Myocyte necrosis was estimated as 0.03 to 0.3 grams of tissue. Osseous and cartilaginous metaplasia was more common around the RA lead than the CS/GCV lead. In cases where the lead must be removed, removal from the venous insertion site using lead extraction equipment should only be attempted with surgical back-up for emergency thoracotomy to control hemorrhage in the event of vessel laceration. Safer explantation of these leads from the vein entry site will require the development of new extraction procedures.

Maintenance of atrial fibrillation in anesthetized and unanesthetized sheep using cholinergic drive.

Atrial fibrillation (AF) was induced electrically and the duration of AF was measured in six isoflurane-anesthetized sheep (weight range 54.5-72.7 kg), and in five unanesthetized sheep (weight range 60-75 kg). In the anesthetized sheep, AF was induced by direct electrical stimulation of the right atrium with a catheter electrode and the duration of AF was determined. Intravenous neostigmine (10 micrograms/kg IV) was administered and the duration of AF was again measured. Then cholinergic drive was increased by bilateral electrical vagal stimulation; AF was induced and the duration of AF was measured. In the anesthetized animals with no neostigmine or vagal stimulation, 34% of the episodes of AF lasted 10 seconds, 11% lasted 20 seconds, and only 1% lasted 200 seconds. However, in one anesthetized animal AF was sustained for 4,800 seconds with no drug or vagal support. The administration of neostigmine alone in 3 anesthetized animals more than doubled the average duration of AF. In the animals with vagal stimulation (after neostigmine), AF persisted throughout stimulation, but ceased shortly after vagal stimulation was terminated at 2,220, 4,500, and 3,840 seconds. The AF frequency ranged from 325-750/min. The unanesthetized sheep were lightly sedated with a small dose (200 micrograms/kg IM) of xylazine to make them less sensitive to environmental noise; then AF was induced and its duration was timed. After these measurements, neostigmine was administered (30 micrograms/kg IM) and cholinergic drive was produced reflexly by intravenous injection of 60-2,000 micrograms of phenylephrine. AF was electrically induced at the time of maximum reflex slowing in heart rate. For the control (no drug) studies, 64% of the AF episodes lasted 10 seconds, 20% lasted 20 seconds, and only 2% of the episodes lasted as long as 140 seconds. When phenylephrine was injected after neostigmine to provide increased cholinergic drive, the duration of fibrillation depended on the dose of phenylephrine. In a 60-kg sheep, the duration of AF increased from 1 second with an intravenous dose of 60 micrograms to 700 seconds with an intravenous dose of 2,000 micrograms. However, there was a considerable range in responsiveness to the reflex cholinergic drive provided by the intravenous phenylephrine; for example a single intravenous 500-micrograms dose produced AF ranging from 190-540 seconds among the sheep. The duration of AF was most controllable in the anesthetized sheep, following neostigmine administration and with bilateral vagal stimulation. In the unanesthetized sheep, AF could generally be sustained for more than the duration of the half-life (about 4 minutes) of phenylephrine following neostigmine. However, there was a large variation in the duration of AF among the animals for the same dose of phenylephrine. This study identifies two methods (direct vagal stimulation and reflex vagal stimulation) for providing the cholinergic drive needed to sustain AF in the adult sheep. The duration of AF is sufficiently long to enable the measurement of electrical atrial defibrillation threshold.

End-tidal CO2, CO2 production, and O2 consumption as early indicators of approaching hyperthermia.

To illustrate the abilities of several physiologic events to indicate a change in metabolic status, dinitrophenol was used to induce hyperthermia. Ten dogs were divided into two groups, one being mechanically ventilated and the other allowed to breathe spontaneously. End-tidal CO2 (ETCO2) and CO2 production, O2 consumption, mean blood pressure, and rectal temperature were monitored continuously in both groups. Respired volume was measured with a pneumotachograph. An infrared-absorption CO2 analyzer measured inspired and expired CO2 concentrations. An ultraviolet-absorption analyzer measured inspired and expired O2 concentrations. Of the physiologic events measured, CO2 production and O2 consumption were the earliest and most reliable indicators of increased metabolism and consequent approaching hyperthermia in the spontaneously breathing and mechanically ventilated animals. In the spontaneously breathing animals ETCO2 transiently decreased due to transient tachypnea. In the mechanically ventilated animals ETCO2 increased steadily. Mean blood pressure increased more in the mechanically ventilated animals than in the spontaneously breathing animals. The increase in rectal temperature required 6 minutes or more to occur, whereas the increases in CO2 production and O2 consumption appeared in only about 2 minutes. It is concluded that ETCO2 is a reliable indicator of increased metabolism in mechanically ventilated subjects only, but CO2 production and O2 consumption are excellent indicators of increasing metabolism in spontaneously breathing and mechanically ventilated subjects.

A pressure-sensitive mat for measuring contact pressure distributions of patients lying on hospital beds.

The authors describe a novel system for sensing and displaying the distribution of contact pressure caused by a patient's lying on a hospital bed. The system includes a flexible, pressure-sensitive mat, electronics to activate the mat, a small computer to process data, and a color video display. The present prototypes can sense pressure at 1,536 discrete locations in a rectangular grid of 24 x 64 nodes, each node representing an area of 4 cm2. The computer receives data from each node and displays the results as a false-color map, refreshable every 5 seconds. The pressure-sensitive mat itself includes two orthogonal arrays of ribbon-like conductors, composed of silver-coated nylon fabric, which are separated by insulating open-cell foam rubber. The system monitors the electrical capacitance between selected pairs of horizontal and vertical conductors on opposite sides of the foam. The crossing points form pressure-sensitive nodes. Increased contact pressure compresses the foam, thereby decreasing the distance between the conductors and increasing the capacitance. Node capacitance is determined by measuring the current through it from a voltage source. The outputs of the various nodes are scanned, normalized, and converted to pressures using the known compressive stress-strain relationship for the foam, and the data are then displayed as a false-color image of the pressure distribution.

Oxygen uptake and mean blood pressure as indicators of induced hyperthermia.

This dog study was designed to identify which of two measurements (oxygen consumption, mean blood pressure) tracked the onset of hyperthermia as reflected by rectal temperature. The animals were anesthetized, paralyzed, and mechanically ventilated. Hyperthermia was induced with 2,4-dinitrophenol (5 mg/kg) injected intravenously in 5 dogs. It was found that the best and earliest predictor of approaching hyperthermia was the increase in oxygen consumption, which increased 10% in 1.72 min. Mean blood pressure was an insensitive indicator of approaching hyperthermia. Rectal temperature, not surprisingly, was found to be a late and undependable early indicator of developing hyperthermia, requiring about 15 minutes to exhibit a definite increase. It is concluded that among these indicators, monitoring oxygen consumption (ml/min) is the most reliable way to identify a metabolic change such as incipient hyperthermia.

End-tidal carbon dioxide concentration, carbon dioxide production, heart rate, and blood pressure as indicators of induced hyperthermia.

In 4 spontaneously breathing, barbiturate-anesthetized dogs, hyperthermia was induced with 2,4-dinitrophenol while rectal temperature, heart rate, mean blood pressure, end-tidal carbon dioxide, and carbon dioxide production (milliliters per minute) were measured continuously. The latter was determined with a pneumotachygraph (to obtain respired volume) and an infrared carbon dioxide analyzer that measured inspired and expired carbon dioxide concentration. Of the five physiologic measurements, the increase in carbon dioxide production preceded the increase in rectal temperature by more than 120 seconds. End-tidal carbon dioxide was an unreliable indicator in the spontaneously breathing animal of approaching hyperthermia during spontaneous breathing due to a transient tachypnea, which decreased end-tidal carbon dioxide. The carbon dioxide production (milliliters per minute) increased immediately and reached three to five times the control value. Blood pressure and heart rate were insensitive indicators of approaching hyperthermia.

Gastric insufflation during IAC-CPR and standard CPR in a canine model.

This study was undertaken to determine the effect of interposed abdominal compressions (IAC) during cardiopulmonary resuscitation (CPR) on gastric insufflation when the airway is not secured with an endotracheal tube. A canine model was used in which a common ventilation pressure was applied to separate cuffed esophageal and tracheal tubes. Gas entering the stomach was collected by a pre-placed gastrostomy tube leading to a bell spirometer. Gas entering the lungs was measured with a Wright Respirometer in series with the endotracheal tube. During standard CPR, measurable gastric gas volume was collected in 28 of 30 trials (mean 215 +/- 93 ml/ventilation). During IAC-CPR, in which abdominal pressure was maintained during ventilation after every 5th chest compression, measurable gastric gas was collected in 15 of 30 trials (mean 40 +/- 11 ml/ventilation). Interposed abdominal compressions as an adjunct to standard CPR may not only be of hemodynamic benefit, but may also reduce the incidence of gastric insufflation and attendant complications.